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NOPAUSE:
Female Hormones in Context
By Raymond Peat, PhD

From PMS to Menopause: Female Hormones in Context
PART ONE: ESTROGEN IN CONTEXT

1. Estrogen: The Pill--Simply Dangerous .......... ........................ .. ............. ..... 3
2. Estrogen: The Hoax of "Replacement" .......... ..... ....... ...... ..... ................... 10
3. Agi ng ovaries: Not the eggs... ...... .. ... .. ....... .. ............... ............................ 27
4. Menopause and its Causes ... .......... .... ... ........ ..... .. .... ................................. 37
S. Not the "Female HomlOne" .. ... ...... ..... ........ .. ....... .................... ...... ...... .. ... 43
6. Just One Clots... ... .. .... ...... ...................... ....... ... .... ...................... 54
PART TWO; PROGESTERONE IN CONTEXT

7. Symptoms that Respond to Progesterone Therapy ............ ...... .. ................ 60
8. The Origins of Progesterone Therapy ........................... .... ..... ................ .... 63
9. Alltiaging Hormones: Steroids ill General.. ... ........ ..... ........ ... .................... 67
10. Youth-Associated Hormones ... ....... .... .. ...... .. ....... ............ .......... .. .. .... .. ..... 7 1
11. Thyroid ... ..... .......... ..................................................... .... ..... .................... 76
12. Progesterone's Bio logical Genera lity .. ....... .. .................... ...... ................... 79
13. Dosage ......................... .. .... .. ... .... ...... .. .. ...... ... .... ................................. .... 89
14. An Effi cient Oral Therapy................................................... .... .......... .. .. .. 92
15. Transdennal Therapy for PMS .................................... ....................... .. .. . 94
16. The Progesterone Deceptions ......... ....................... .............. ...... ... ... .. ... ... .97
PART THREE: "MYSTERIOUS" DISEASES IN CONTEXT

17. Preserving Tissues: Osteoporosis and the SkilL ... .......... ........ .... .... .... . 102
18. Natural Hormones and Arthritis .. .... ... .. ..... .. .... ... .................... ........... .... 11 0
19. The Cervical Cancer Scare and Other Approaches to C41ncer.. ... ...... ...... 115
20. Warburg's Cancer Theory and Thyroid ........................ .... .. ..... ........... .... 117
21. Migraine, Varicose Veins, & Epilepsy ............... .. ..... .... .... .................... 120
22. Nerves ........ .. ... ........................................................ ........ .. ................... 121
23. Alzheimer's Disease............................................................... ... ........... 122
24. Eclampsta in the real Organism ......... .... .... ........................................ .... 124
PART FOUR: SOME PRODUCTS IN CONTEXT

25 . Estriol & Phytoestrogens ............................ ... ........... ........ ..................... 134
26. Using Sunlight to Enhance Life .......... ....... ... ........................ ...... ..... ..... . 144
27. Unsaturated Oils: Toxic and Estrogenic .............. ... .. .. ........ ....... ....... 153
28. The Dangers of Iron: Exacerbated by Estrogen ..... .... .. ...................... 164
29. Coconut Oil.. ........................... .......... ............................................. ..... .. 175
Concl usion ........................... .. ..... ..... ........... .... ...... .... .......................... ...... . 190
Copyright 1997 Raymond Peat, PO Box 5764 Eugene, OR 97405

Introduction
Most of the ideas about health and hormones that are being
propagated are fraudu lent commercial invent ions. In this setting, it is
impossible to have any sense of security about the way you are living
unless you make the effort to critically examine the claims you hear
everywhere.
Occasionally, someOne complains that they "don't wanl to read a
lot of technical stuff." (These people prefer to do what "the authorities"
leI! them. Where would the authorities be without them? I wouldn't want
to interfere in their relationships with the aLlthorilies, except that the
system they sustain is tending to kill everyone.) I have defined some of
the technical words, so it shouldn't be necessary to use a dictionary too
frequently . Generally, physicians have found my writing more challenging
than the average woman does, because my purpose is at odds with the
medical culture, and women are realizing that much of the medical culture
is at odds with them.
The history of conventional medicine is mainly a history of
unscientific and dangerous practices. Medical alternatives were
introduced by conscientious workers to avoid the dangers of conventional
medicine. But alternative approaches to medicine, especially nutritional
therapies, have come to be influenced or even dominated by the same
giant industries that control conventional medicine.
Many of the "preventive medicine" and "alternative health" ideas
are dangerous-· "estrogen replacement therapy," low protein diets, fear of
milk, fear of salt, fear of shell-fish, fear of coconut oil, the avoidance of
all of the best foods, emphasis on legumes and "complex carbohydrates,"
supplementation with fish oils and polyunsaturated seed oils, with
"complete mineral supplements" (consisting of earth), with minerals
"chelated" with toxins such as orotate, glutamate, and aspartate, the use
of supplements containing dangerous amounts of iron and manganese,
etc.
By putt ing the idea of eating dirt ("mined in Utah") or pond scum
(various algaes) into a very limited context, the advertisers convince
people that their product meets a need. Bad ideas don't look so bad, if
you can write the presentation without mentioning certain drawbacks.
Good ideas are almost invariably twisted into profit-making
schemes. People have come up with the idea that progesterone can be
turned into a lucrative product, and--by attaching their products to the
deeply entrenched ideolob'Y of "hormone replacement
convince people that they should keep using progesterone indefinitely, "to
prevent osteoporosis." Many of these marketers advise their customers
to avoid milk, and to substitute "plant proteins." (Milk actually helps to
prevent and even to cure osteoporosis, becl',use of its optimal content of
calcium, protein, progesterone, thyroid, and vitamins.) Big drug
companies long ago saw that progesterone wasn't appropriate for their
involvement, since "a good drug is one you have to keep taking for the
rest of your life."
Progesterone can relieve disabilities with great speed and safety.
Since it is a protective substance that stabilizes structures and functions at
many levels, it can be useful in almost any situation. It even helps the
body regain its ability to produce more progesterone. But if there is a
progesterone deficiency, something has caused that deficiency, and it is
important to find out what the basic problem is. A diet that is deficient in
high quality protein, or that contains natural food toxicants, often is
responsible for a progesterone deficiency. If your diet is killing you,
supplementing progesterone is of limited value.
For example, a pregnant vegetarian who has produced a long
series of children with "attention deficit disorder" wants to use
progesterone preventively, without changing her diet; the progesterone
would undoubtedly improl'f:' the outcome of the pregnancy, but without
an adequate diet it is certain that the outcome will not be entirely good.
When such people use a "wild yam cream" during pregnancy, they are
likely to blame the baby's birth defects on "progesterone," when in fact
they were probably not absorbing a measurable amount of progesterone.
If progesterone is used as part of an appropriate physiological
program, it isn't necessary to keep using it Once it has helped to restore a
balanced hormone metabolism.
This book is intended to help you preserve and promote your
natural ability to produce an optimal hormonal balance. Since the
greatest threat for many people is coming from the medical and
nutritional industries, it is necessary to learn enough about the hormOnes
and their physiology to be able to critically reject the impostures that are
all around us. A scientific attitude is of great importance, but we must
recognize that science has absolutely nothing to do with the "consensus of
the authorities." You are less likely to do the wrong thing if you believe
that "the authorities are always wrong," because then you will begin to
question their assumptions, evaluate their evidence, and examine their
reasomng.
J
PART ONE: ES'IROGEN IN CONTfXT
I
ESTROGEN: SIMPLY DANGEROUS
The lJUCSlinns f('f Ihis chapler fru1\! a .1 d"y cnnfcrcn..:e in Los
An g..:lc$ in 1995.
GLOSSARY:
The pituitary gland sits at the base oflhe brain. where it
receives signals from the brain, and secretes hormones thai
regulate the production of various other hormones and
secretions.
Prolactin is a hormone secreted by the pituitary gland
during pregnancy, and during stress. It promotes milk
production, removes calcium from the bones, and inhibits
progesterone formation.
Progesterone is the main female hormone, and is a
protective hormone during pregnancy, but it is also
important in men since it is a general brain regulating and
protective hormone.
DnEA, known as the youth honnone, is very similar to
progesterone but is present in both men and women at
very high levels. It can be turned into either estrogen or
testosterone.
The thymus gland is the main regulator of the immune
system. Estrogen causes it to shrink , while progesterone
protects it.
Estrogen is a honnone that stimulates cell division
(mainly in the breast, uterus, and prostate gland, and in the
pituitary gland) and is normally produced in a monthly
surge at the time of ovulation and during pregnancy.
Women nonnally have higher levels in their blood than
men do.
Q: What are (he harmful effects of taking estrogen?
Just naming some of estrogen's effects on the body and mind that
have been described in scientific and medical publications will give you at
least an indication of the possibilities:
4
Breast cancer, uterine cancer, ovarian cancer, fibroid
tumors, pituitary tumors, lung cancer, liver cancer,
bowel cancer, kidney cancer, malignant melanoma,
meningioma and other brain cancers, cancers of other
organs, osteoarthritis, lupus, rheumatoid arthritis,
allergies, porphyria , optic neuritis, epilepsy, depression,
suicide, aCcidents, anxiety, agoraphobia, amnesia, nerve
cell damage, low blood pressure, fainting , shock,
migraine, varicose veins, irregular heart beat, blood
vessel spasms, intestinal spasms, inflammatory bowel
disease, gall stones, gall bladder spasms, blood sugar
disturbances, hypothyroidism, blood clots, strokes,
heart attacks, miscarriage, birth endometriosis,
excess hair and loss of hair, skin discoloration, thinning
of the skin, water retention and obesity.
About 50 years ago, Hans Selye (known for his discovery of the
stress syndrome) gave large doses of individual steroid hormones to rats
to study the range of their effects_ He had previously analyzed the
physiology of the stress reaction, and he observed that estrogen treatment
exactly duplicated the shock phase of the stress reaction. This interferes
with circulation and energy metabolism, and its physiological purpose is
to cause ti ssue to take up water which stimulates cell division, for
example in the uterus to prepare for pregnancy, and in the breasts to
prepare fo r lactation . But none of the physiological functions of estrogen
suggests that it could be beneficial in situations other than
reproduction·*and then only when its "shock" effect is tightly regulated by
a well balanced possibly in wound healing, where its abi lity
to stimulate cell division could be useful.
Q: YOIl mE-nlion that estrogE'n can causE' both {"XCE'SS hair and loss of
hair. What do you mE-an?
By suppressing the thyroid and st imulating the pituitary's secretion

of prolactin, estrogen can have a variety of complex effects on hair
growth ; usually, thinning of the hair on the head is a consequence of
hypothyroidism. In both men and women, loss of hair flom the scalp is
associated with low thyroid. but "male pattern baldness" has been held to
be produced by a male hormone; but even the male hormones can be
turned into estrogen by enzymes in the skin, and experiments show that it
5
is estrogen which causes the h,air follicle to become inactive, while an
can stimulate the renewal of hair. (R. C. Sman, III £II..
Pro,:. NCII/. Acad. o.fScif:m..:e:i, Oct. 29, 1996.)
By stimulating the adrenal glands. estrogen can increase the
production of the "male" hormones that are associated wi th whiskers and
chest hair. [E. C. Ditkoft: et aI. , "The impact of estrogen on adrenal
androgen sen sitivity and secretion in polycystic ovmy syndrome," J. Clin .
Endocrinol. Metab. 80(2), 603-607, 1995 .] This usually happens when a
progesterone deficiency is combined wit h an excess of estrogen, as in the
polycystic ovary syndrome and sometimes at menopause. In animals,
polycystic ovaries afC caused by a deticiency of the thyroid hormone, and
the same regulatory mechanisms seem to operate in women. The
polycystic ovary syndrome is the most common endocrine disorder in
women during the reproductive years, and may occur in 10% of them. [A.
Dunaif, et aI. , eds. The Polycystic Ovary Syndrome. Cambridge, MA :
Blackwell Scientific; 1992.]
Q: You mentioned thai estrogen causes pituitary tumors, If the

pituitary is the "master gland," isn't that very serious?
In the early 1970s. researchers at Johns Hopkins studied a group

of 300 young women living in their region who had pituitary tumors.
Previously, that kind of tumor was very rare, and the researchers
suggested that the estrogen in the oral contraceptive was causing this
epidemic. Estrogen's ability to produce this kind of tumor is now firmly
established. This type ofturnor secretes prolactin . Prolactin is a hormone
which is known to cause osteoporosis, and which also has a role in breast
abnormalities, including cancer. It can suppress the ovaries' ability to
make progesterone, and it affects sweat glands and hair follicles . If the
tumor is very large, its pressure on the optic nerve can cause visual
disturbances.
Normally, by the age of 50, most people have an enlargement of
the pituitary, and this is undoubtedly a factor in the menopause and other
conditions that occur in aging. A blood test for prolactin will usually
show whether a tumor is forming or not . A drug is available that will
shrink the tumor and nonnalize the gland's function.
Q: What are some of the emotional symptoms of excess estrogen?

6
Estrogen excess can cause suicidal depression, or milder forms of
depression and lethargy, as .well as irritability, aggressiveness, anxiety,
fear of public places, forgetfulness, a feeling of confusion, and a tendency
to cry easily_ Post ·partum depression (following childbirth) is associated
with high estrogen and low thyroid, and insomnia is common at that time,
and during menopause. Sometimes insomnia is associated with night-time
•
worrymg. .
Migraine headaches are strongly associated with high estrogen
and low thyroid. The traditional view that they are caused by emotions
probably came from the observation that migraines are frequently
associated with the monthly hormone cycle.
According 10 Germltn documents lim·e!l·tigated by Jean Jofen of
Baruch College, reportea at the Fifth World of Jewish
Stu die!)' in the Nazi... put in the food at
concentratitm camps, to make the prisoners he/pIes... and unable to
()rganize resistllnce. They certainly weren't doing it to slow the aging
process.
Q: What caused your interest in estrogen?
Between }950 and the early 1960s I knew three women who used
estrogen. One developed an extreme case of rheumatoid arthritis, which
got worse with each dose of estrogen, and disappeared when she stopped
using it. Another woman had a mental breakdown within an hour of her
estrogen injection, and was hospitalized for six months. Her daughter
began using the contraceptive pill, and died of a stroke at the age of 28 .
It was clear to me that estrogen had harmful effects, and that it was being
promoted without adequate warnings. Magazine articles described
massive testing programs in Puerto Rico and claimed that the women
were healthier after using the pills, but in reality the contraceptive Enovid
was approved on the basis of only 135 women who were studied for a
year or more; three young test subjects died. When I went to graduate
school in 1968, I began projects in brain physiology, aging, and cancer,
and in each of those areas I found that estrogen was an important factor.
Q: What should I do if I want to stop the pill?
In the case of birth control pills, you can simply stop taking them,
with few symptoms of withdrawal, but it is important to be alert to the
possibility that your own hormone balance might not spontaneously
7
return to ncnnal. Some women are unable to get pregnant after using the
pill. If your normal cycles don't resume within a few months, it would be
useful to have tests done for prolactin, progesterone, and thyroid, since
those hormones are modified by estrogen usc. And you should be aware
that estrogen lise increases the risk of birth defects. Since natural
progesterone has been found to reduce the incidence of birth defects, it
would seem reasonable to be sure that your own progesterone has
returned to normal before getting pregnant.
Q: How can I tell if my natural estrogen level is too high?
Only a blood test can tell for sure whether your estrogen is higher
than it should be, and it is necessal)' to measure your progesterone at the
same time, since it is best to have five or ten times as much progesterone
as estrogen. If your progesterone level is low, even an average estrogen
level can cause serious symptoms, because its effects are not balanced and
opposed by progesterone.
Generally, people whose temperature (measured by an oral
thermometer) is below normal or whose thyroid function is tow are likely
to have high estrogen and low progcstcronc. (Low temperature
stimulates the ovaries to produce excess estrogen, and retards the liver's
ability to excrete it.) A deficiency of protein and B vitamins can make it
impossible for your liver to excrete estrogen, leading to a chronically high
estrogen level. Excess fat tissue, especial1y after the age of 40 when
progesterone and thyroid may be low, is a major cause of chronically high
estrogen levels, and therefore is associated with an increased incidence of
breast and uterine cancer.
Estrogen usually causes fat to he deposited on the thighs and hips.
Q: How can I get my natural estrogen level to be lower?
Adequate protein and B vitamins are essential. Vitamin A

protects some tissues, such as the breasts, against estrogen's effects,
including cancer, and general1y offers protection against estrogen by
increasing progesterone. Several studies found that vitamin E protects
against estrogen's harmful effects. A thyroid supplement can reliably
lower estrogen, by increasing the liver's ability to excrete it. Unsaturated
oils have a strongly estrogen· promoting act ion, and should be avoided.
Raw carrots can help, by preventing the reabsorption of estrogen which
has been secreted into the intestine with the bile. Adequate sunlight helps
8
10 maintain a healthy balance of the hormones_ In certain circumstances,
natural progesterone can help to reestablish a balance ofhonnones
Q : Wililowt'rill g my estrogclI have a uy harmful eITects?

No Natural estrogen is closely associated with stress, and this
"anti*cstrogcn" program is essentially an antisl ress progmnl, which is
likely to improve many aspects of your health_
Q : What llr(" my options for birth cOlllml if I don 't take estrogen?
Human fCI1i1ity. Iih' that of birds, repliles, fish. and other animals.
has declined so steeply during the last 20 years, as a result of the
indust rial pollutants with harmful estrogen-l ike efTeets. that it is very
likely that every form of birth control has become more etl'ective than il
was found to be in the 1960s and 1970s. This means that even the
rhythm method, using temperature or mucous tests to determine the
fel1i le lime, should be more effective than it used to be. The barrier
methods--condoms, diaphragms, and cervical cars--will tend to be more
effective even without the toxic spermicida l drugs that are now normally
used with them.
The traditional cervical cap was illegal in the United Slates lor
Illany years. (In fac t, contraception was a crime not vcry long ago. And
when I lirs! considered including contraception in a coursc I taught I
learned that even teaching about it would have been illegal. It was
undoubtedly lobbying by the pharmaceut ical indu stry that contributed to
the changed legal situation .) When a so-called cervical cap was finall y
approved tor use in this count I)'. it was actually an unworkable.
ludicrously designed receptacle for a spermicidal dnlg, and not actually an
etlective barrier. The actual cervical cap, if it can be obtained "il legally,"
is a safe. easy, cornfonable and eflective means or contraception .
The IUD (intrauterine device) actually works by causing serious
hormonal disruptions, blocking the ability to produce progesterone.
Natural progesterone has been added to plastic IUDs, but this
doesn't correct the general hormone imbalance tllilt can be produced by
the presence of an object in the uterus.
Synthetic hormones which are implanted under the skin increase
the risk of cancer, and can calise disfiguring injury at the sit e of
implantation.
Natural progesterone placed in the vagina during intercourse has
been very effective in my st udies, but is not officially approved .
9
Progesterone's nannal effects include maintenance of pregnancy, and that
requires the prevention of additional pregnancies during the course of an
established onc. Its presence in the vagina during intercourse causes the
cells to react as if there were already an established pregnancy. There are
various reasons that this method of contraception hasn't been generally
accepted; for example. progesterone's very name suggests thai it
promotes pregnancy. and the bureaucratic mentality sees things in
simplistic ways
Incidentally, I think the evidence is absolutely clear that the
estrogen pills are not contraceptives. They don't prevent conception, they
prevent implantation of the embryo into the uterus. That is abortion, so
the industry had to make up a theory in which the pills could be marketed
as a contraceptive, to avoid the religious reaction to the abortion pill.
This theoretical gimmick took nearly twenty years to develop.
SUMMARY
There is no valid scientific evidence of its safety in any

amounts.
Estrogen's contraceptive action is just one aspect of its

general toxic effect.
Estrogen is dangerous, in any amounts, unless it is balanced

by an abundance of the natural forms of thyroid,
progesterone, and DHEA.
Estrogen is a cumulative toxin, because it causes changes in

every system of the body, even when present in normal
amounts. These cumulative changes appear to accelerate
aging in all tissues.
10
2
ESTROGEN: THE HOAX OF
"REPLACEMENT"
GLOSSARY:
Progesterone is the main female hormone, and is a
protective honnone during pregnancy, but it is also
important in men since it is a general brain-regulating and
protective hormone.
DH EA, known as the youlh hormone, is very similar to
progesterone but is present in both men and women at very
high levels. It can be turned into either estrogen or
testosterone.
The thymus gland is the main regulator of the immune
system,
Testosterone is the main male hormone, though it is
present in females too.
Free radicals are parts of molecules that can react
destructively with other molecu les to cause damage to
cells.
HDL and LDL are often called "good cholesterol" (High
Density Lipoproteins) and "bad cholesterol" (Low Density
Lipoprotei ns) because of a slight association between their
ratio and heart disease, but in fact the ratio that suggests
freedom from heart disease suggests susceptibility to
cancer. LDL ("bad") is extremely good because it is used
as the source for producing progesterone and DHEA.
Q: You point out the dangers or estrogen, but don', women need to
replace it at menopause?
"Replacement" is a trick word in this context. At a European

conference, a researcher asked "why do you Americans use the word
'replacement,' when you are administering doses that give them 15 times
more estrogen than normal young women have naturally?" Rather than
bringing the blood level of estrogen up to normal, most physicians ignore
the amount of estrogen already present in the blood, and give a dose of
II
estrogen suflicient to suppress the p1tUltary hormones, FSH and LH,
which are sometimes called "the menopause hormones."
But the menopausal excess of those pituitary hormones is caused
by estrogen's chronic damage to the nerve cells that regulate the pituitary,
which causes the nerves to become insensitive to normal stimulation by
estrogen.
Cholesterol is tllmed into honnanes such as progesterone in the
brain and the adrenal glands, as well as in the ovaries and testicles, hut
estrogen can be produced in practically every part of the body. For
example. 1;?1'I:n when Ihe omries (ll'e I'emol'l!d, hormones from the adrenal
glands can be turned into estrogen in fat cells. In general, the fatter a
person is, the higher their estrogen levels are. This is why the risk of
cancer increases in proportion to obesity.
The stimulating effect some women experience when they are
given large, unphysiological doses of estrogen seems to be produced
partly by an eflect of estrogen that resembles stimulation by cocaine. In a
variety of ways, estrogen is a powerful brain excitant: it can provoke
epileptic seizures. and it increases the effects of some of the excitatory
substances and processes that contribute to brain aging.
Q: How saf(> is it for a wOnlan to take estrogen?
It simply isn't safe to take estrogen. Safety implies that adequate

studies have been performed, and have found that the treatment has done
no harm . The first such large scale study to examine the general effects
of estrogen replacement is just beginning. Many studies which looked for
particular effects in humans have already found harm, and the huge
amount of research that has been done on animals strongly indicates that
the over-all effects of estrogen will be found to be harmful.
During the 20th century, animal studies have revealed almost an
infinite variety of harmful effects of estrogen. Cancer, blood clots,
miscarriage, shock-like effects, and accelerated aging are among its
longest-established toxic effects. Some publications have claimed
that estrogen-treated women live longer than untreated women, but as
Or. Elizabeth Barrett-Connor (UCSD) has obselVed, the women who
received estrogen were healthier before the study began than the women
who didn't receive estrogen, and in such a biased situation no meaningful
conclusion is possible, except that some women can survive treatment
with estrogen. There are many scientifically sound studies that show
estrogen treatment to be seriously harmful to women. Even some of
12
estrogen's less deadly effects, such as memory impairment and water
retention, should be taken more seriously_
Q: How saft' is estrogen in very low dost's?
[t's not safe even in low doses.

"Low estrogen" birth control pills contain about 30 micrograms of
estrogen, and since this amount prevents pregnancy, it is significantly
"large" in physiological tenns. It is low only by reference to earlier pills.
Even young women have had strokes caused by the estrogen in birth
control pills, and tumors of the pituitary and liver have been linked to use
of the pill, as have cancer, heart disease, inflammatory bowel disease,
suicides, and accidental death. Since many environmental pollutants
(DDT, phenolic compounds, smoke and dioxins, for example) act like
estrogen, it is increasingly difficult to distinguish the effects of medical
estrogens from the general effects of pollution, but the higher background
level of estrogenic stimulation suggests that more and more people will be
injured by the additional burden of "low dose" estrogen treatments. (Skin
patches for menopause treatment are intended to deliver 50 or 100
micrograms of the powerful natural estrogen, estradiol, per day, vaginal
creams deliver similar amounts (probably causing higher blood
concentrations at times, because of the greater permeability of vaginal
membranes), and the suggested oral dose of estradiol for menopause
symptoms is I or 2 mg., that is, 1000 or 2000 micrograms per day.
Tablets of conjugated estrogen for oral use range from 300 micrograms
to 2,500 micrograms. As a vaginal cream, the applied dosage suggested
is 1,250 or 2,500 micrograms per day for the conjugated estrogen,
somewhat lower than the suggested amount of estradiol cream .)
Q: Why would th e medical establishment prescribe estrogen if it's

not safe?
Hundreds of millions of dollars of annual profits from estrogen

products allow the drug companies to subsidize medical conferences,
medical research, medical journals, and medical schools. The information
physicians receive is heavily biased in favor of estrogen treatment by that
funding . Physicians are not regularly taught in medical schoo l or in
continuing education courses, that they should measure the amount of
estrogen in the blood before they prescribe a treatment to "replace" it ,
and the amount commonly prescribed has no meaningful relatio nship to
13
the amount which is normal in young women. Many women have told me
that their doctors have measured their estrogen level, but when they look
at their medical records they often find that only the pituitary hormones
or the vaginal cells have been examined.
Q: Doesn't taking estrogen prevent aging and increase energy?
Because of the claims that estrogen protects the skin against

aging, investigators have tested its effects when rubbed onto guinea pigs
(Pliske, \953), or injected into rats (Hooker and Pfeiffer, 1943). It
caused hair loss and thinning of skin in the rats, and in guinea pigs it
caused degeneration and vacuolization of connective tissue. Animal
experiments show clearly that estrogen accelerates the aging of
connective tissues, and it causes the accumulation of "age pigment."
When a rat is treated with estrogen, it is likely to run 30 miles a
day, because of the brain excitation it causes. Some women like this
sensation of "energy," but biochemlcally, the stimulation isn't unlike that
received from cocaine, and accordingly the estrogen-induced excitation
seems to be addictive. Cocaine doesn't have some of estrogen's side
effects. Estrogen tends to deprive all tissues of an adequate supply of
oxygen, sO the "energy" it provides isn't protective in the way that a good
reserve of biological energy is, and in fact it activates brain pathways that
involve potentially deadly over-excitation, which arc responsible for the
aging and death of brain cells.
Q: Why do so many women 1 know look and feel better when they
take estrogen?
Cows and other animals that have been given estrogen treatments
to make them put on extra weight, are fat and waterlogged, but none of
their functional systems are improved. When a woman's skin is aging and
slack, it becomes tighter and smoother if she gains weight, even if the
weight consists of fat and retained water. But the skin itself becomes
thinner, less elastic, and "older" in several structural and functional ways
when it is treated with estrogen.
Estrogen, as discussed above, can act as a stimulant, and give an
increased sense of energy. Estrogen can be metabolized into a form
which promotes the actions of the catecho/amine,\·, such as adrenalin. In
this form, estrogen produces toxic free radicals, which contribute to aging
and cancer.
14
In those senses--tightening the aging skin by causing water
retention and obesity, and acting as a stimulant--estrogen can make you
"look better" and "feel better." But personality studies show that women
who trust their physicians more than they trust themselves are the ones
who are likely to use estrogen. What they say they feel tends to be what
their physicians have told them they should feeL
Q: Doesn', estrogen prevent osteoporosis?
No . It is said that estrogen slows the rate of bone loss, while

progesterone, thyroid, and DHEA actually shift bone metabolism into the
growth phase. (Around the time of menopause, there is a steep decline in
the levels of these three protective hormones.) But there are serious
reasons for believing that estrogen is a factor in causing bone loss.
Young women have thinner bones than men of the same age, because
even at a young age estrogen is acting to inhibit bone growth. (Men's
bones are 50% bigger.) Prolactin, a pituitary honnone which is increased
by estrogen, has a powerful bone*weakening effect and it is often
produced in excess around menopause. Cortisone, another
bone-weakening hormone, also tends to be increased by estrogen. The
thyroid hormone, which fundamentally supports the bone-building
process, is inhibited by estrogen. And progesterone, which has a
bone-protecting and bone*building effect. is inhibited by these
estrogen-induced hormonal changes. When bone loss begins at the onset
of menopause, it is progesterone (which normally keeps estrogen in
balance) which has suddenly decreased. leaving estrogen undiminished
and unopposed, usually for years, during which the worst symptoms of
menopause occur.
In egg-laying chickens, estrogen promotes the storage of calcium,
largely in the soft interior of bones, but if combined with a high calcium
imake, extra estrogen can be toxic . To the extent that estrogen does
increase the mineral content of bone, it seems to be in the spongy
cancellous bone around the marrow, rather than in the strong cortical
bone. In the complexly organized hormonal environment of pregnancy,
estrogen's ability to st imulate the retention of iron and calcium fits into
the whole scheme, in which the growing baby is consuming those
substances. Poisoning by cyanide, or oxygen deprivation, can increase
the retention of calcium by tissue, and since an immediate effect of
estrogen is to decrease the oxygenation of tissue, I see estrogen's effect
on calcium metabolism as analogous to its effect on iron: In stress,
15
organisms absorb calcium and iron . In dying cells, both calcium and iron
tend to be deposited together. Estrogen has its place in normal growth
and development, but the people who advocate its use as a supplement
seem to have no respect for the complexity of its relation to the
developing organism.
In young animals, estrogen retards the growth of cartilage.
Physicians sometimes give estrogen to tall children, when their parents
want their growth to stop, because it does stop bone growth.
Estrogen is not an anabolic hormone, like testosterone, which
builds up bone and muscle. In fact, it strongly opposes the effects of
those hormones. In the polycystic ovary syndrome, an excess of estrogen
stimulates the adrenal glands to produce a large amount of the androgenic
steroids, probably to balance estrogen in the way progesterone does when
the ovaries are fimctioning properly. These anabolic/androgenic
hormones apparently have some of the good effects of progesterone, such
as reducing the incidence of cancer, but many women are disturbed by the
increased growth of body and facial hair; facial features also tend to be
masculinized. In France, progesterone lotions have been in use for
several years for reversing some of these effects of the adrenal hormones,
and for balancing estrogen .
Considering this sort of information, it is very unfortunate lor
women that the osteoporosis problem is so often seen simply as an
opportunity for prescribing estrogen. In some countries, old women don't
have a problem with osteoporosis. Shouldn't physicians pay ':I10re
attention to emulating the factors that prevent osteoporosis, instead of
thinking that it is a p'harmacological problem?
Studies of both animals and humans show that estrogen
contributes to a variety of inflammatory degenerative diseases, and one
condition known to be aggravated by estrogen is osteoarthritis.
Osteoarthritis is sometimes referred to as a matter of "wear" of the joints,
but estrogen's contribution seems to be that it structurally weakens the
joint tissues, after binding to estrogenwsensitive receptors. This research
should be kept in mind when listening to the claims about its "protecting
the bones. " Other studies have implicated estrogen in other types of
arthritis.
Q: What about laking estrogen to avoid Alzheimer's disease and

heart attacks?
16
Several years ago it was noticed that estrogen treatment caused
changes in the types and amounts of fat carried in the blood. Ordinarily,
unexpected changes caused by drugs are treated as abnormalities, and
bring the drug into question . But with estrogen, the situation is different:
Recently, a reviewer noted that estrogen alters the triglyceride (simple
fat) levels in the blood, but dismissed the change as "probably benign."
In the case of cholesterol, the abnormality was interpreted as a
virtue. Estrogen increased the ratio of HDL (high density
lipoprotein--"good" --cholesterol) to LDL (low density lipoprotein--
"bad"--cholesterol), In other situations. a high ratio ofHDL to LDL has
been found to be associated with a lower incidence of he an attacks (but a
higher incidence of cancer), and this single trait has been considered
alone, out of context, to allow many people to claim that estrogen
"protects against heart altacks," since it shifts that indicator in the
direction associated w it h fewer heart attacks. But estrogen also does
many things that are more directly associated with hean attacks: It
increases the tendency to form blood clots, and it increases the tendency
of blood vessels to go into spasm during st ress (synergizing with
adrenalin). When men were given estrogen following a heart attack , it
was found to increase--rather than decrease-·the lisk of another heart
attack.
In the famolls Framingham study, it was found that
post-menopausal estrogen use increased heart attacks by 50% and
increased strokes by 100'%. "Estrogen's heart protective effect" is a clear
example of tak ing one feature (the cancer-associated HDLlLDL ratio) oul
of context for the purposes of advertising a product. It is a good idea 10
read the literature that comes with estrogen prescription products,
because even though it is printed by the pharmaceutical company, the law
requires that some truthful warning information must be provided .
It is known that cancer (and other degenerative diseases) take a
long time to develop. often more than 20 years after the crucial damage
was done. Many studies have been able to lind that estrogen has no
harmful effect by stopping the study at an age at which no damage would
be expected to show.
In 1993 , a sludy in California found Ihal women who took
estrogen were less likely to develop Alzheimer's disease. The lirst study
was done in a little town where J had done some lectures and
consultations, and I was aware that a local doctor was giving his patients
natural progesterone whenever he prescribed estrogen, and thaI he usually
gave estrogen only when they specifically asked for it. J suspect t hat the
17
women who chose to use estrogen were (as in other studies) morc
amUCO! and healthier, and that many of them were at the same time taking
natural progesterone.
Another morc recent study showed that women who take
estrogen are not less likely to develop Alzheimer's disease, but were morc
highly educated than those who don't use estrogen. Several studies have
found that poorly educated people are much more likely 10 be diagnosed
with Alzheimer's disease, because of the way the mental tests are
designed and interpreted. These relationships show how it is possible to
get a mistaken impression oflhe effects of estrogen treatment.
Since it is harder to do an accurate study of humans than of
animals, we should examine the effects of estrogen on the brains of
animals much more carefully before making any more claims about its
"protective" effects. We should remember that it was claimed to prevent
miscarriages (it actually causes them), to prevent skin aging (it accelerates
it), to delay menopause (in animals, it accelerates the onset of sterility and
the loss of cyclic pituitary function), and to prevent heart attacks in men
(it caused them). As far as the brain is concerned, estrogen is known to
"erase" memories, to induce seizures, to cause the exhaustion or death of
particular types of nerve cell , and to be very toxic to the developing fetal
brain, retarding its growth. The derivative of estrogen
which is responsible for much of its action is known to
produce toxic free radicals. Free radicals are considered to play an
important role in the development of both Alzheimer's disease and heart
disease.
Q: Do you melln estrogen might accelcl'atc brain aging?
In animal studies, it accelerates changes in every organ

examined . In P. M. Wise's studies, it appeared to exhaust and kill specific
brain cells that are involved in fertility. Recent studies of brain physiology
show that estrogen and cortisol both promote the "excitotoxic" processes,
which are increasingly believed to be implicated in the processes of brain
aging and degeneration .
Since excess iron is now thought (as discussed in the chapter on
iron) to contribute to cancer and heart disease, and is a factor in brain
degeneration, and since iron assimilation is promoted by estrogen, I
would expect there to be an intensification of the toxic eiTects of dietary
iron supplementation by estrogen treatment. For example, both iron and
estrogen can destabilize liver protein synthesis, they are both involved in
18
the fannalian of "age pigment," they both seem to fac ili tate epileptic
seizures, and so on.
Menstnaation, I suspect, is protective (by causing some iron loss),
and estrogen (hy promoting iron retention), harmfiJ1.
The incidence of Azheimer's disease is higher in lVomen than in
mcn [A. F. Jorm, 1990; W . A. Rocca, et aI., 1991], osteoporosis is mainly
a disease of American and European women, and men have more hean
attacks when they are given estrogen. According to the Framingham
st udy, women who use estrogen have more heart attacks and strokes than
those who don't. Consideri ng those simple facts, one has to wonder how
the estrogen promoters came up with the theory that estrogen is
"protective" against heart di sease, Alzheimer's disease, and osteoporosis.
Q: My doctor said estrogen is safe if I take it with "progesterone"

or progestin or testosterone.
Physicians often confuse the synthetic progestins with natural

progesterone. The brand of medroxyprogesterone acetate called Provera
is often mistakenly ca lled progesterone. Each steroid hormone has a
range of biological effects, and generally the synthetic progestins contain
some very powerful estrogen-l ike or testosterone-like effects. Natural
progesterone's effects on the uterus can be achieved to some extent by
some of the synthetic hormones, but the natural substance also has a
powerful and pervasive balancing effect on 01her hormones, and serves as
the material out of which other natural hormones can be formed . The
synthetic progestins lack that balancing etTect, and can't bc transfonned
biologically into any of the other natural hormones.
The synthetic progestins can protect the utenls from the
carci nogenic effect of estrogen. Even testosterone's anti-estrogen action
seems to protect the uteru s and the breast from estrogen's effects. But
the famous studies on female beagles showed that a commonly used
synthetic progestin can cause breast cancer, and similar results have been
seen with other synthetics. One of progesterone's most important ell""ects
is its protection of the brain's structure and function ; the use of a synthetic
substitute for it often causes nervous and emotional symptoms, and I
think it is reasonable to be concerned that the synthetic may have harmful
10ng-ral1ge effects on the brain that haven't been discovered yet.
Adding testosterone to estrogen treatment reduces some of the
risks of estrogen treatment, and it definitely improves bone metabolism.
Testosterone is a powerful sexual stimulant, and this has probably
19
increased the popularity of the treatment , but many women dislike the
growth of whiskers that testosterone stimulates. [Estrogen itself can
sometimes stimulate the growth of whiskers, by over-stimulating the
adrenal glands_ E C. Dilkolf. el al.. "The impact of estrogen on adrenal
androgen sensitivity and secretion in polycystic ovary syndrome," J. elin.
Endocrino]. Metab . 80(2). 603-607, 1995.] Both testosterone and
estrogen cause the thymus gland to shrink, with serious consequences fo r
immunity, and they also seem to have some similar toxic effects on the
brain.
If estrogen is not balanced by hormones such as progesterone,
DHEA. pregnenolone. and testosterone, even a vcry small amount of the
substance has a very l:lrge efrect on the body. Even when the oVMies
h:lve been removed, the body's fM tissues can produce significant
quantities of estrogen. Various stresses and injuries can cause the body
to produce more estrogen. When large amounts of estrogen arc given,
the body is unable to produce enough of the other hormones to balance it,
and Ihese olher hormones fail at an earlier age than estrogen production
does. "Ovarian failure" always involves a progesterone deficiency, but it
doesn't necessarily mean that there is an estrogen deficiency .
N:ltural progesterone is a cheap material which is effective when
taken orally diHOh,t'd (not just packed) in oil, but many physicians are
confused about it, because the FDA lists only the injectable form (which
is in a toxic solvent) as the "approved" form . Natural progesterone, when
not in an injectable fOfm , doesn't /let'd the FDA's approval, because il is a
natural hormone which was in use before the FDA law was passed .
To be effective. it has to be fully dissolved and not visible as a
white powder. This is why some studies have claimed that it is not
effective. or is effective only when administered in very large doses.
.
Q : What about tstriol and ot her estrogt'lt choices, such as
ph)·toestrogens (estrogens d erived from pla nts such as soybeans)?
Estriol is a slightly weaker variant of the stronger natural

estradiol. It is more water soluble than estradiol, so it is slightly easier to
excrete in the urine. When it is used as a drug, the body can change it
into the more active estradiol.
The phytoestrogens, or plant·derived estrogens, have been
promoted recently as safer alternatives for therapeutic use. In the sense
that these weaker estrogens can modify the actions of st rong estrogens,
they mi!{hl be protective in ceria;" circumstances involving excess
20
estrogen, but this protection is more theoretical than practical, and the
harm they can do is real. Sheep farmers learned long ago that the
phytoestrogens in clover can cause miscarriages, animal studies show t hey
cause genital deformities, and recent tests are suggesting that they are,
like ot her estrogens. carcinogenic . This is similar to the situation with
Tamoxifen, which is an anti-estrogen used to treat breast cancer. It , in
itself. is carcinogenic . (See my discussion of est ri ol and other "weak"
estrogens in section 4 .)
Q: Doesn't everyone hllve the right to deride what is best for them?
What if they feel estmgen is working fOl' Ihem and t'liminatt'S
symptoms?
That is reasonable, if you have access to the best information on

the beneticial and harmful effects of the treatment. This book is to help
you to decide whether you have the information you need on questions of
this sort . Many people have felt that they understood a treatment, and
benefitted from it, bu t later learned that it had seriously harmed them .
For example, many people were given large doses of X-rays to treat their
acne or ringworm or sinus inflammation or "enlarged thymus gland," with
their physicians' assurance that it was the safe and effective and
un iversally accepted treatment, only to discover that the treatment caused
cancer or brain damage or deformity or loss of immunity_ Many people,
including physicians, do not realize that there is a very large and
persuasive scientific literalUre that indicates that estrogen is neither safe
nor effective for the ,various uses which are current ly advertised .
Q: Whal are the pros and cons of other treatment regimes if I go ofT
estrogen?
Many physicians prescribe c10nidine patches to prevent hot flashes

in women who don't want to use est rogen . Clonidine is a drug that
blocks adrenalin. Since hot flashes can be caused by excess cortisone,
and adrenalin triggers the release of cort isone, this procedure seems to
have a logical foundation. Cortisone excess causes osteoporosis, so
c!onidine could protect the bones while preventing hot nashes.
Natural progesterone strengthens the bones by blocking cort isone
and prolactin, it normalizes thyroid and energy metabolism and thereby
helps with insomnia, it prevents the growth of excess facial hair, steadies
the emotions, and sometimes even helps to control hot flashes.
21
Natural thyroid supplements can help to avoid weight gain.
depression, and hot flashes ; this will be discussed in the chapter on
thyroid. The claims that thyroid contributes to osteoporosis are not true,
according to the relevant human and animal studies (for example,
Franklyn. 1994), and that myth was based on a few unscientific reports.
There is a drug which is sometimes morc powerful than thyroid
and progesterone in correcting abnormal pituitary function , and this has
been used 10 relieve some of the symptoms of menopause, including
osteoporosis.
The diet should support optimal functioning of the thyroid and
other glands, as discussed in other chapters.
Q: How do I gel ofT eSl rogen?
Keeping estrogen's stimulating action in mind. women who want

to stop using estrogen prescribed "for menopam;e" usually find that they
can withdraw from it by decreasing the dose gradually over a period of
two or three months, while using some harmless stimulants such as tea or
coffee as needed to smooth the process of withdrawal.
SU M MA RY
Estrogen can cause breast cancer, heart disease, strokes,
accelerated aging, and many other serious problems .
There is no valid scientific evidence of its safety in any

amounts.
Estrogen is dangerous, in any amounts, unless it is balanced

by an abundance of the natural forms of thyroid,
progesterone, and DHEA.
Estrogen can be produced in practically every part of t he

body, especially in fat tissue.
Estrogen's only clearly established useful functions are to

prepare for reproduction by stimulating growth of the uterus,
the breasts, and the pituitary gland, and to influence behavior
during reproduction. Even in these specialized functions , it
22
•
has an absolute requirement for a complex and precise
balance of other hormones.
The body's normal defenses against estrogen fail with aging,

causing many symptoms associated with menopause.
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circulation than they had bd"or<: the menopause."
79. Prior, 1. C. Cl <II.. "l'rogcst...-ronc as f GnRh anlagonist on lymphoc yte in priuwry
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"slcopcnia, and Ihe adminislrali"n of o,;,;lr(lgens 10 poslmcnopalls:tI womcn leads lu
hyPerpro Illel i n.:m i a .....,
27
3
AGING OVARIES; NOT THE EGGS
A few months ago public television ran a long program on the
menopause, in which a rather glamorous woman physician said some
shockingly ignorant things about the ovaries and menopause. I went to
some book shops., to see what she might have been reading, or hearing in
conversal ions.
One writer thought it would be nice to change the name of the
menopause to "the pause," Another said it is too judgmental to say that
the ovaries "tail" at menopause, and that they are really just maturing.
Those concerns with Icnninological politeness remind me of Woody
Allen's remark about it is nature's way of telling us to slow
down ,
All of these current paperback books about menopause subscribe
to the same doctrine about reproductive aging. Uniformity of opinion
creates an environment in which publishers who want to sell a lot of
books feel that they have to publish things that don't disturb the reading
public. Books about menopause become books about an attitude toward
menopause.
Even people who like to say that the ovaries "don't fail" at
menopause describe a theory in which menopause and its consequences
are the result of the disappearance of eggs from the ovary. That theory is
so simple it can be described in three short sentences, none of which is
true: (I) the ovary runs out of eggs; (2) ovulation produces hormones,
so you can tcll when ovulation stops because the ovaries stop producing
hormones; (3) menstruation stops because ovulation has stopped. Those
principles are surrounded by various corollaries. "Estrogen is the female
hormone." "Estrogen deficiency acceleratcs aging." "Treatment with
estrogen makes you more feminine." "Progesterone deficiency is the
result of anovulatory cycles."
Many experimenters have demonstrated that old animals that have
become infertile keep producing eggs. Several experimenters (e.g., R. R.
Maurer and R. H. Foote,l 1971 , "Maternal ageing and embryonic
mortality in the rabbit," J. Reprod . Fert . 25, 329-341) have removed eggs
from the ovaries of old animals, and transplanted the fertilized eggs into
young animals, where the embryos were able to implant and develop
normally.
28
I found that old animals had too little oxygen in their uterus to
keep the embryo alive at the time it would normally be ready to implant
itself in the uterus. Giving estrogen to a young animal causes a similar
lack of oxygen in the uterus, and prevents implantation of the embryo.
AI the time old animals would normally have become infertile.
they remain fertile jf they are given a supplement of vitamin E and
progesterone. II is now established that aging animals, at the time they
become infertile, are deficient in progesterone, hut still produce estrogen .
Even in young individuals, when stress occurs around the time of
ovulation, interference with progesterone production will prevent
implantation. If progesterone becomes deficient after the embryo has
become implanted, miscarriage occurs.
Estrogen, acting alone or with insufficient progesterone, causes
spasms in the spiral arteries that provide oxygen and nUllients to the
endometlium. This seems to be the basis for menstruation, and is also
believed to be a factor in miscarriage.
About 30 years ago, researchers began to understand that
reproductive aging was not caused by the lack of eggs, and the aged
utems was able to support pregnancy ifit had the light hormonal support .
Interest turned tn the brain cells in the which regulate the
pituitary. G. H. Zeihnaker ("Effects of prolonged feeding of an ovulation
inhibitor (Lyndiol) on ageing of the hypothalamic-ovarian axis and
pituitary gland tumorigenesis in rats," J. Endocrin . 43 , xxi, 1969i was
one or the first to suggest that ovarian hormones caused the brain to age.
More recently, P.M. WiSCH has clearly demonstrated that estrogen
exhausts the cells which inhibit the pituitary gonadotropins, with the
result tl.lat even abnormally high levels of estrogen are unable to turn off
the pituitary secretion of the hormones that drive the ovary. Estrogen
itself can impair the ovary's ability to produce progesterone, but the
continuously high secretion of gonadotropins disturbs the ovary, the
adrenals, and (according to recent observations) even the uterus.
Stress, especially when augmented by estrogen, leads to injury,
exhaustion, and aging. The uterus and ovaries participate in the response
to stress, but (as Zeilmaker and Wise have shown) the brain proves to be
more directly involved in menopause than the ovaries or uterus.
Coordination turns out to be crucial ror complex processes such as
ovulation, fertilization , and implantation. The destruction of the nerve
cells that regulate the pituitary makes coordination impossible.
The issue of "running out of eggs" can be settled simply by
demonstrating the presence of viable eggs at the time reproductive ability
29
has ended. In the 19405, menopause was "explained" in terms of an
estrogen deficiency, without a basis in fact, and now an "egg deficiency"
is combined with the "estrogen deficiency," compounding the confusion .
Facts aren't everything in science;'" it is necessary to look at the context
from which these ideas develop.
Two of America's most productive researchers in reproductive
physiology, Edgar Allen and Herbert M. Evans, made observations that
they believed showed that the germinal epithel ium of the ovary goes
through a cycle of cell proliferation that produces a new generation of
oocytes during each menstrual cycle. It is recognized that new egg cells
appear in the ovaries of adult prosimian primates, and at puberty in cats
and pigs. Observations of newly developed egg cells have been reported
in some other species. But the dominant view prefers to see the number
of egg cells declining from birth, or earlier, with absolutely no new egg
cells being formed later.
During gestation and infancy, the gonadotropins are very high.
These hormones decline during childhood, during the time that the
number of egg cells is so visibly declining. The high level of the
gonadotropins during infancy hasn't been explained, but it is reasonable to
suppose that it has something to do with the development oflhe ovaries,
since a "developmental" function can be demonstrated for the
gonadotropins in the ovaries and testes of older animals.
The number of brain cells peaks a few months before birth, just as
the number of egg cells does. Many people have argued that this
somehow means that brain cells are incapable of dividing after infancy,
though there is no factual basis for making that argument, and in fact
adult brain cells are now known to be able to divide. (That is true of
heart cells, too.)
In a variety of tissues, it can be shown that the presence of mature
cells inhibits the division of other cells. If part of the liver is removed, the
remaining cells divide to replace the lost tissue. If the skin is cut, cells
divide to help fill in the defect. If there is an adequate number of egg
cells, this principle suggests that there is no need to produce more. There
is a treatment for polycystic ovaries called "wedge resection." This can
reduce the production of masculinizing hormones. By analogy with other
tissues, it seems likely that the removal of a mass of malfunctioning ti ssue
leads to the growth and development of new cells which function the way
a new ovary would. Regeneration seems to be a capacity of every tissue,
given the right environment. If the ovary were studied after such
treatment, I suspect that "new eggs" would be found . (But even in the
30
seemingly simple process of healing a wound in the skin. there is still
disagreement as to the relative contribution made by local cell division,
and the invasion of the region by structural cells from elsewhere in the
body. The appearance of a cell can be misleading•.histology is often a
matter of making educated guesses. For example, white blood cells can
look like epithelial cells.)
Although the question of whether all the woman's eggs are in
existence at or before birth doesn't logically have anything to do with the
other question, whether there are still eggs in the ovary at menopause,
there is a reason that people connect them. This has to do with the idea
of a "germ line" as distinct from the "somatic cells." The eggs are "from
the germ line," all the rest of the body (and much of the ovary) is a
different SOl1 of stuff The "germ line" has the spedaJ property of
immortality and it is "isolated" and independent. The body is susceptible
to being modified by the environment, and is mortal. These are the
traditional fonnulations of the idea, and the people who learn their
orientation from textbooks are not necessarily conscious of how the ideas
fit together. For biologists of my professors' generation, these ideas
seemed to be a sacred core of biology, but with their death, maybe
biology can he liberated
August Weismann, working at the end of the last century and the
beginning of the 20th century, created the basic ideology of genetics, to
combat the idea of the inheritance of acquired characteristics, which had
been supported by Darwin and others. He argued that the hereditary
substance, or geml plasm, was derived only from preexisting germ plasm,
and couldn't be formed anew, or modified by the environment. It created
every part of the perishable body, by a process in which traits were
segregated, so that the germ plasm contained the full complement of
hereditary material, and each part oflhe body contained only the limited
fraction needed for its characteristics. Thus, the body was inferior
created material , while the germ line was the immortal creative stuff'.
Since the body adapts in response to the environment , it had seemed that
these changes would be passed on to descendants, until Weismann's
argument showed that it was only the perishable, dead-end body tacking
the hereditary principle which was adapting. The germ line was somehow
isolated from the body and from the environment.
Weismann's theoretical germ line became identified with the
chromosomes and the genes. His theory was shown to be simply wrong,
in that each type of cell in the body contains a full complement of
chromosomes and genetic information. Although his facts were wrong,
31
his ideology became deeply embedded in the culture of genetics. To keep
the idea that the "germ line" is somehow something distinct from the body
required a special effort, once the chromosomes were seen to be identical
in every part of the body. Weisman's whole point in his "germ line" idea
was to show an absolute distinction between the body and the hereditary
substance. If his ideology that had been built to deny the inheritance of
acquired characteristics were to be saved, the isula/f!cJ germ line would
have to be found elsewhere than in the chromosomes.
The idea of "germ line (or Keimhal1l1) determinants" (lOW took
over, and was believed to be something in a certain spot in the egg. As
the egg divided, into cells that look very much like each other, the cells
which came from Ihal part of the egg represented the germ line. As the
embryo developed. the region that seemed to be traceable back to that
part of the egg, represented the germ line. As the gonad began to grow,
cells from the region representing the germ line were thought to tfavel
over and invade the gonad, where they multiplied into vast numbers, but
always remained the same isolated strain of germ cells with their
"separate" history that could be traced back to the determinants in the
special place in the egg. During the early days of embryonic
developmcm. these immigrant cells looked exactly like their neighbors
which were somatic cell sprouts from the cmbryonic kidney rcgion.
If it weren't for the ideology of absolute isolation oflhe hereditary
substance, an embryologist might have suggested that cells or material of
one part of the embryo illduced a specialized, differentiated state in some
cells that happened to be suitably located . If the cells derivcd Irom that
certain part of the egg didn't carry unique genetic material--and they
didn't--then what they carried with them was an incipient state of
differentiation. Why the big deal about that particular history of
differentiation? It was because the ideology that motivated Weismann
was still active, and its purpose was to argue that only the "gene" was the
creative productive source, and that the body--the "somat ic cells"··was
the passive product, whose adaptations meant nothing in the long run .
This has been called the "central dogma" of genetics, that infomlatian
flows only from the gene to the cell, and nat back from the cell to the
gene. That ideology forced geneticists to deny the existence of RNA
viruses (including retroviruses such as the HIV-"AIDS" virus). and is still
active in blocking research on the plion or scrapie virus, which is a
protein. To say it bluntly. many highly respected biologists acted stupidly
because they blindly believed in a false ideology.
32
Incidentally, this ideology was always impossible for
horticulturists to accept, since they were in the habit of grafting (cloning)
vegetative (somatic) parts of plants, which would then produce flowers
and fruits . For them, the "germ" was often a product of the "body."
Luther Burbank's work was consistently ridiculed by the academic
biologists, who believed his achievements were impossible, that is,
fraudulent. Many of Burbank's perceptions have been supported by
recent evidence, but they couldn't be accepted by people whose ideology
of the genn line/somatic distinction seemed to be contradicted by his
work.
Another problem with the doctrine of the germ line was revealed
when embryologists separated the embryo at a very early stage into two
groups of cells, and found that each was able to grow into a complete
animal. The idea of the germ line predicts ,that one member of the pair of
twins could get the ability to reproduce while the other would be sterile.
Some important ideas can survive their disproof.
It is exactly the · same academic ideology of the priority of the
germ line which blames the whole complex process of reproductive aging
on the mechanical process of an "ovary nmning out of eggs." The ovary
doesn't run out of eggs, and running o ut of eggs would have no great
consequences if it did happen, because the main events in ovulation are
produced by CP.l1s other than the eggs. But the ideology says that the
"germ line" controls everything, and the eggs are the germ line. In other
words, genes control the organism. and eggs control the woman.
After I had written the preceding paragraphs, Ian Wilmut's
success in cloning a sheep trom an adult's cell was announced. Those
who still argued for Weismann's genetic interpretation of the germ line
wiil probably stop talking about it, but generally, the "germ line"
advocates will keep their doctrine (as empty as it is) by acknowledging
the role of the cytoplasm in differentiation. The cytoplasm of the egg is
constructed with the assistance of the surrounding cells of the ovary, so
the important questions regarding the production of eggs will no longer
be quite so obstructed by the ideology of the "germ line."
Another idea about aging of the ovary was that "old eggs"
contained "old DNA," and so were defective. This was just a derivative
of the idea that aging was a genetic phenomenon, and it appears that
Wilmut's cloning experiment will make that argument extremely difficult
to sustain. According to two variants of this theory ("Hayflick's limit,"
and "telomere depletion"), the cells of an adult had exhausted their
"quota" of cell divisions, and so wouldn't be able to undergo enough
33
divisions to multiply into a new animal. The end of a dogma was mildly
recognized by Professor Franklin Stahl's comment, "One often had reason
to imagine that DNA suffered from irreversible changes during
development." One could have imagined many things, if dogmas such as
Weismann's hadn't obstructed biology for a century.
I think it will be instnlctive to consider the three steroid secreting

glands· -ovaries, testes, and adrenals--together, to see what they might
have in common. In the testis, it is generally believed that pituitary
gonadotropins regulate steroid synthesis and gametogenesis. In the
ovaries, the gonadotropins also regulate Ihe production of steroids,
and--to some extent--the production of eggs, if not the whole
gametogenic process. In the adrenal, ACTH govems the production of
conisol and sex steroids, and the transformation of the glomerulosa cell
type into the other types, which secrete those hormones.
The outer layer of cells in the adrenals can form the other two cell
types, and since stress-ACTH converts them to the other types, new ones
must be formed . If the inner layers are removed, the whole adrenal
cortex can regenerate from the outer layer. Obviously, jf stress causes
cells to multiply and differentiate, cells are disappearing from the inner
layers.
When I was in graduate school, immunologists were aware that
new cells were continually appearing in the thymus gland, but the gland
didn't get bigger, and there was no visible trace of dying cells. At that
time, it was considered a ma.ior puzzle, but gradually it came to be
understood that a special kind of cell dissolution (called apoptosis) was
occurring that accounted for the missing cells.
In the testes, apoptosis or cell-dissolution is always occurring,
even though sperm cells are being produced and leaving the organ .
In the ova!)', "waves" of egg cell degeneration are constantly
taking place in young women. Radioactive labelling that has been used to
argue that egg cells aren't being replaced seem to show that there is
continual cell division in all the other ovarian cells. Interestingly, those
researchers didn't seem to be interested in this apparent regeneration of
the other parts of the ovary.
Apoptosis always seems to be part of a shaping process of the
organ in which it occurs. Regeneration provides new cells, apoptosis
recycles the substance of certain fraction of the tissue's cells. We are
just starting to notice that various hormones inhibit or promote apoptosis,
and so participate in the of the organism. In many systems, it
34
seems that the need for a cell type or function cans it into existence, while
idleness makes a cell susceptible to dissolution_
I have been referring to the "pituitary gonadotropins," and
deliberately avoided referring to them as LH--Iuteinizing hormone--and
FSH--follic1e stimulating hormone--because their names reflect a theory
of what they do. In some textbook descriptions of testicular function, for
example, it has been said that LH produces testosterone, and that
negative feedback from testosterone suppresses LH, while FSH governs
the formation of sperms. That description is completely worthless, and
probably was largely built up by analogy with their supposedly neatly
divided functions in the ovary, reflected in their names. These
gonadotropins participate in the development, maintenance, and
functioning of the ovaries, and their effects depend on their timing, their
balance with each other and with the steroids produced by the ovaries in
response to their stimulation, and their actions are modified by many
other factors, ovarian, nervous, pituitary, uterine, and immunological.
During youth, the system functions in a coordinated way, with ovulation
as a consequence. During aging, the crucial changes appear to be a
decreased ability of the ovary and the brain to produce progesterone.
Thyroid hormone, cholesterol, vitamin A and efficient cellular respiration
are essential factors for synthesizing progesterone. Accumulated iron,
unopposed estrogen, and impaired use of cholesterol and oxygen are
factors known to contribute to the widespread and variable damage to the
system of coordination .
Two things can cause the pituitary to secrete excessive amounts
of the gonadotropins: A deficiency of the steroids, and damage to the
steroid-sensing nerves that regulate the pituitary. When an ovary is
moved (transplanted into the spleen) so that its honnones are destroyed
before getting to the brain, there is hypersecretion of gonadotropic
hormone/·6.7 and tumors develop in the ovary. The interpretation, that
hypersecretion causes the tumors, is supported by other observations,
e.g ., that removal of one ovary increases the chance of developing a
cancer in the other ovaryl and that prolonged use of estrogen (known to
create the conditions for later hypersecretion of gonadotropinH ) increases
the risk of ovarian cancer after menopause.9
Psychologists have noticed that naming an object according to a
certain function often limits the way people will be able to use it . This
happens in science. If we know one function of a substance, and name it
for that function, we will find it harder to think of its other possible roles.
Hans Selye argued that steroids, for example, should be named according
35
to their place of origin, rather than by a single aspect of their function . I
think this applies even to the phrases "male hormone" and "female
hormone": it's better to think of them in terms of their origin, and not to
count on them to promote femininity or masculinity .
A note about "the female hormone." In the absence of the

testicular or "male" hormones, animals differentiate as females. Recent
evidence indicates that the mechanism by which testosterone masculinizes
the brain requires that it be converted (in the brain) into estrogen . In this
crucial event, estrogen is functioning as "the male hormone." Over the
last 20 years, some types of experiment indicate that estrogen is necessary
for the aggression-promoting effect of testosterone.
Progesterone is an and blocks testosterone's
effects. When testosterone is given to newborn or very young rats, it sets
up a male pattern of hormone development, but if progesterone is given
at the same time, that doesn't happen. Progesterone prevents the
differentiation . away from the basic female path into the male
specialization. Later in life, a deficiency of progesterone in a woman can
again lead to masculinization of some features, such as musculature and
facial or body hair. When progestcronc is givcn to mcn in largc doses, it
blocks various typically male processes, such as growth of whiskers. In
the brain, it has a protective function in both sexes.
Estrogen promotes cell division, and is involved in essentially
every tissue, in both males and females. If it is to be called a ''female
hormone," maybe it also has to be called "a male hormone." It does have
to be present for breast development, though it is just one of many
factors. In this instance, it is contributing to feminization. In other
instances, it seems to contribute to virilization.
At menopause, estrogen excess can promote the production of
androgens, in the absence of progesterone, which tends to defeminize the
woman . This is often a result of stress, and sometimes is a consequence
of hypothyroidism. In situations of this sort, estrogen is seen not to be a
feminizing hormone; it is unable to neutralize the male hormones the body
produces in response to the estrogen excess.
NOTE AND REFERENCES:
... Since the 1930s. estrogen's toxic potential has become \'ery clear. Howc\"cr.
the cstrogen industry doesn't want people to understand that estrogen is a shock
hormone with pro-aging effects. Hist..1lninc mimics estrogen's effects on the uterus,
36
and antihistamines block estrogen's effects (Szego. 1%5, S7.ego and Davis. 1%7).
Estrogen mimics the shock reaction. Stress. c:-.:crcisc, and toxins cause a rapid
increasc in estrogen. Males oftcn have as much estrogen as females. especially when
they arc tired or sick. Estrogen increases the brain's to epileptic seizures.
and recent research shows thai it (a nd cortisol) promote the effects of the
which arc increasingly implicated in degenerative brain diseases.
Currently. estrogen marketing emphasizcs appe;!rancc and the danger of
osteoporosis. Evidence occasionally turns up implic.'lling estrogen in thinning of the
sk in and bones. '0
REFERENCES
I. R. R. Muurer and It H. Foole,' "M(I\cmal Ugc111g aud embryonic moT1ulity in the r"hbit ," J.
Rcprod. F\,'ft. 25, 329-341 . 1971.
2. G. H. l.cilmak.:r ("Effects of prolonged lcooing or an ovulation inhibitor (Lyndiol) on 3gcing
of thc axis and pitn ita'Y gland tnmorigen.::sis in rats," J. Endocrin." 3, xxi ,
196').
3. Wi>sc, P. M .. "In!lu.:ncc of Oil aging of the central nen'ous s,'stem: Its role in
dcdinillg lcmak rcprodw;tiw function: in MClIOJXIuSt!: Evaluation, Treatment. and llealth
Conccms, pages 5J-70, 19&9.
4. Wi ....:, P.M., c\ a!. , "N':UfOelldocrille illllucm;es on aging of the femalc reprOductive
Fronti<..'fS ill Neurocm\ocrinology 12, 323- 1991 .
5 M. H. Li nnd W. 11. Gardncr, "£xpo:.'Timental Studi.:;; on th.: and histogenesis of
ovarian tumors in mice: Cancer Research 7, 549-566, 1947.
6. W. 11. Gardm.'T, "Honnonul imbalance in tumorigenesis," CnnceT Research 8, 397-411, 1948.
7. M. I I. Li and W . U. Garwlcf, "Fwth<'r studj<,s on the l:>athog"ncsis of ovarian tumors in
mice," CUn«:r Rcsearch 9, SJ2-S36, 1'./49.
8. H. S. Kaplan, "Influcncc of ovarian fWICtiOn on incidencc of radiation-inducl..'d ovarial!
tumoninmice: J. NatI.Cam;crlnsl., 1\ , 125-132, 1950.
9. l..x, N. C., et aI. , therapy and the risk of breast, ovary and endometrial cancer," iu
IIging, Reproduction , and the Climactl..nc," L. Mas!wialUl;' Jr., and C. II. Paulsen, I..,(\i!ors,
Plenum. N.Y. & London , 191:\6. To tlle c.x!el11 that oral rontroct:ptivo:s suppress the pituitary
gonadotropic homIOllCl;, the ovary is protected from the stimulation th3t c..'1n produce cancer.
Ilowever, the estrogen used to treat menopause doubles the risk of ovarian cancer alter ten
Tfthe estrogen WdS used for more than 6 )"eunI, the risk tripkd .
10. BaUC!, D. c. , ct aI. , ' Skin thickness, estrogen lISC and bone mass in older women,"
Menopause 1(3), 13 1-136, 1991. found no evidence that cstrogen prc.'«!fVeS skin
thickness: iTKieo:d, estrogen usc is associatoo with thitu1<.'T skin.· "Our findings further support
an association between skin thickness and bone mMS." "Skin thickne.<;s and bone mass arc
reiak'd, but skin thicknl!Ss cannot be used to predict bone mass."
37
4
MENOPAUSE AND ITS CAUSES
When I was in graduate school at the University of Oregon,
everyone in our lab was working on the problem of reproductive aging.
Previously, people in the lab had established that the ovaries didn't "run
out of eggs." There was never really any basis for that ridiculous belief.
Many people just said it, the way they said "old eggs" (but never old
spenns) were responsible for birth defects, or that "estrogen is the female
honnone," a deficiency of which is the cause of menopausal infertility.
(Old sperms have been implicated in some birth defects. People who are
newly married, for example, were found to have children with fewer birth
defects than people of the same age who had been married a long time,
suggesting that more frequen t intercourse involves fresher sperms.)
When ovaries have been treated with to destroy their ability to
ovulate, they have been found to produce more estrogen than before.
Ovulation is one thing, and the production of hormones is another thing.
You can't determine whether ovulation has occurred by measuring the
hormones.
Knowing the large amount of work that has gone into our
understanding of the age·related decline in fertility, it is disturbing to see
people on television and in popular health books saying that menopause
occurs when the "ovaries run out of eggs."
Around 1970, many people were saying that aging was caused by
the loss of brain cells. There is a glinuner of truth in that silly idea, just as
there would be in saying that "aging is caused by the death of skin cells,"
making the skin thinner and drier and less elastic. Both the brain and the
skin are sources of steroid honnones, and it is possible that the death of
skin cells and neurons is one factor in the age·related decline in the "sex
steroids." An organism would be an easier thing to understand if cells
just did their job for a certain period of time, and then died . A man
named Hayflick has given people some publications to cite, when they
want to simplify things by saying that aging occurs when cells have used
up their quota of 50 divisions, but there are many more studies that
clearly show that Hayflick's limit is nothing but a product of the cells'
environment. The celt's environment, the signals and substances and
energy it receives, is complex, but real progress is being made in
understanding the things involved in the aging process. Luckily, the
38
infinite complexity of the environment is channeled into an understandable
array of processes by the cell's systematic ways of responding.
I knew, from talking with L. C. Strong,l that early reproductive
maturity was associated with early death; in his strains of cancer-prone
mice, he showed that high estrogen was the cause of early puberty, a high
cancer incidence, and a relatively short life. D. A Snowdon, et aI. ,
showed that the occurrence of menopause al an early age in women is
associated with a greater risk of death from all causes, including strokes
and coronary heart disease.2 (They saw ovarian aging as an indicator of
general aging.) P. W. F. Wilson, el al., reponed that postmenopausal
estrogen use was associated with an increased incidence of heart disease
and stroke.'! P . M. Wise showed that estrogen accelerates aging of the
central nervous system, destroying the nerves which regulate the pituitary
gonadotropins, and causing ovarian failure and infertility."' Many other
studies of particular tissues show that estrogen accelerates the rate o f
.
agmg.
In my work with hamsters, r found that the infertility that
developed at middle age was caused by a high rate of oxygen
consumption in the uterus, causing the oxygen needed by the developing
embryo to be consumed by uterine tissues, and causing suffocation of the
embryo . This is the central mechanism by which the estrogen·containing
contraceptives work: at any stage of pregnancy, a sufficient dose of
estrogen kills the embryo.
Polvani and Nencioni/ among others, found that in women, the
onset of menopause (the fir st missed period, sudden ly increased bone
loss, nervous symptoms such as depression, insomnia, and flushing)
corresponds 10 the failure to produce progesterone, while estrogen is
produced at normal levels. This results in a great functional excess of
estrogen, because it is no longer opposed by progesterone. Typically, it
takes about fOllr years for the monthly estrogen excess to disappear.
They suggested that the bone loss sets in immediately when progesterone
fails because cortisol then is able to dominate, causing bone catabolism;
progesterone normally protects against cortisol. Other researchers have
pointed out that estrogen dominance promotes mitosis of the
cells of the pituitary, and that prolactin causes
osteoporosis; by age 50, most people have some degree of tumefaction of
the prolactin·secreting part of the pituitary. But estrogen dominance (or
progesterone deficiency) also clearly obstructs thyroid secretion, and
thyroid governs the rate of bone metabolism and repair. Correcting the
39
thyroid and progesterone should take care of the cortisol/prolactin/osteo-
porosis problem .
P. M. has demonstrated that the "menopausal" pituitary
hormones, high levels of LH and FSH, are produced because the
regulatory nerves in the hypothalamus have lost their sensitivity to
estrogen, not because estrogen is deficient. In fact , he showed that the
nerves are desensitized precisely by their cumulative exposure to
estrogen . If an animal's ovaries are removed when it is the
regulatory nerves do not atrophy, and if ovaries are transplanted into
these animals at the normally infertile age, they arc fertile. But if animals
are given larger doses of estrogen during youth, those nerves atrophy
prematurely, and they become prematurely infertile.
The mechanism by which estrogen desensitizes and kills brain cells
is now recognized as the "excitotoxic" process, in w hich the excitatory
transmitter glutamic acid is allowed to exhaust the nerve cells. (This
explains the older observations that glutamic acid, or aspartic acid, or
aspartame, can cause brain damage and reproductive failure.) Cortisol
also activates the excitotoxic system, in other brain cells, causing
stress-induced atrophy of those cells.6 Progesterone and pregnenolone
are recognized as inhibitors of this excitotoxic process.
Besides estrogen's promotion of excitotoxic cell death, leading to
the failure of the gonadotropin regulatory system, estrogen's
stress-mimicking action probably tends to increase the secretion of LH, in
ways that can be corrected by supplementing progesterone and thyroid.
Since Selye's work, it has been known that estrogen creates the same
conditions as occur in the shock phase of the st ress reaction. (And shock,
in a potential vicious circle, can increase the level of estrogen. 7) It has
recently been demonstrated that est rogen stimulates the adrenal glands,
independently of the pituitary'S ACTH. This can increase the production
of ad renal androgens, leading to hirsutism, and other male traits, including
anabolic effects.'
It was establiShed in the 1950s that estrogen "erases" memories in
well trained animals. I suppose that acute effect is related to the chronic
toxicity that leads to cell death. (In the 1940s, DES was sold to prevent
miscarriages, though it was already known that it caused them; then there
was the argument that it slowed aging of the skin, despite the Revlon
studies at the University of Pennsylvania showing that it accelerates all
aspects of skin aging; lately there has been talk of promot ing estrogen to
improve memory.)
40
Estrogen's nerve-exCIting action is known to lower seizure
thresholds; premenstrual epilepsy is probably another acute sign of the
neurotoxicity of estrogen .
When fatigue and lethargy are associated with aging, the brain
stimulating action of estrogen can make a woman feel that she has more
energy. (Large doses given to rats will make them run compulsively;
running wheels with odometers have shown that they will run over 30
miles a day from the influence of estrogen.) Estrogen inhibits one of the
enzymic routes for inactivating brain amines, and so it has more general
effects on the brain than just the glutamate system. This generalized
effect on brain amines is more like the effects of cocaine or amphetamine.
If that is a woman's basis for wanting to use estrogen, a monoamine
oxidase inhibitor would be safer.
The reason for the menopausal progesterone deficiency is a
complex of stress-related causes. Free-radicals (for example, from iron in
the corpus luteum) interfere with progesterone synthesis, as do prolactin,
ACTH, estrogen, cortisol, carotene, and an imbalance of gonadotropins.
A deficiency of thyroid, vitamin A, and LDL-cholesterol can also prevent
the synthesis of progesterone. Several of the things which cause early
puberty and high estrogen, also tend to work against progesterone
synthesis. The effect of an intra-uterine irritant is to signal the ovary to
suppress progesterone production, to prevent pregnancy while there is a
problem in the uterus. The logic by which ACTH suppresses
progesterone synthesis is similar, to prevent pregnancy during stress.
Since progesterone and pregnenolone protect brain cells against the
excitotoxins, anything that chronically lowers the body's progesterone
level tends to accelerate the estrogen-induced excitotoxic death of brain
cells.
Since progesterone and pregnenolone protect brain cells against
the excitotoxins, anything that chronically lowers the body's progesterone
level tends to accelerate the estrogen-induced excitotoxic death of brain
cells.
Chronic constipation, and anxiety which decreases blood
circulation in the intestine, can increase the liver's exposure to endotoxin.
Endotoxin (like intense physical activity) causes the estrogen
concentration of the blood to rise. Diets that speed intestinal peristalsis
might be expected to postpone menopause. Penicillin treatment, probably
by lowering endotoxin production, is known to decrease estrogen and
cortisone, while increasing progesterone. The same effect can be
achieved by eating raw carrots (especially with coconut oil/olive oil
41
dressing) every day, to reduce the amount of bacterial toxins absorbed,
and to help in the excretion of estrogen. Finally, long hours of daylight
are known to increase progesterone production, and long hours of
darkness are stressful. Annually, our total hours of day and night are the
same regardless of latitude, but different ways of living, levels of artificial
illumination, etc., have a strong influence on our hormones. In some
animal experiments, prolonged exposure to light has delayed some
aspects of aging.
General aging contributes to the specific changes that lead to
menopause, but the animal experiments show that fertility can be
prolonged to a much greater age by preventing excitotoxic exhaustion of
the hypothalamic nerves. The question that still needs to be more clearly
answered is, to what extent can general aging be prevented or delayed by
protecting against the excitotoxins? Minimizing estrogen (and cortisone)
with optimal thyroid activity, and maximizing pregnenolone and
progesterone to prevent excitotoxic cell fatigue, can be done easily. A
diet low in iron and unsaturated fats protects the respiratory apparatus
from the damaging effects of excessive excitation, and--since
pregnenolone is formed in the mitochondrion--also helps to prevent the
loss of these hormones
REFERENCES
I. L. C. Strong, Biological ofC(luecr lind Aging. Pergamon Press. 1%8.

2 O. A Snowdon. cl al.. "[:; carly naIHral menopause (I biologic mmi;<.'T of he<llih nnd aging?
Am . J. Public Health 79. 709-714, 1089 .
.1. 1'. W. F. Wilson, t:I a!. rlllC framingham Study), N. E. J. M. 313(J7), 1038-11143, 1985
4. P. M. Wise. "Inlluell\:c of cStrogt:lI on aging of the c<.'1ltral nervous system: Its role in
,kc1ining female r<.'j)TOdudivt: funclion: in Menopause: Treatment, and Health
COllcems, p,a ges 19119.
5. Nencioui , T., l'. Poh'oni , Calcilonin, p. 297 -3U5, A. Peci le , editor. Elscvier, N. Y ., 1985.
6. T I. & Io\'a, 'St mcturnl damage to the mesenccphalic reticular lonl1(1tion induced hy
immobilization st russ: Bull. E:>:J>. BioI. & M<.'(\. lOS{ 7), 126030. 1989.
7. f, Fourricr. c t al. . "Scx steroid honnones in circul<lIO!)' shock, sepsis s}udrornc. and $Cptk
shock," ei rc. Shock 43(4 ), 171-178. 1994.
ll. E. C. \)il kot1', ct nt.. "'Illc imp<lel of eSlrogeu on adn:nnl androgen sCllsitivit y and secrction in
pol ycyslk ovary syndrome: J. C lill. Endocrillol. Mctab. 8tJ( 2), 603-607, 1995.
9. C. 8i!in, et a l.. "Use of !X"'tmel1opausaJ honnoncs and risk of myocardial infarction:
Circu lation 64. 42-46, 1981 .
10. T. L. [lush, <.'I a I. , "Estrogen and a!l-causc mortality: l'rcliminmy rcsnl!s from Ihe
Lipid Re'iCarch Clinics I'rolf<un foll ow_np study," JAMA 24 9, 903-906, 1983.
I I, C. Rodriguez, c1 aI. , "Estrogen rcploet.111cut therapy and falal ovarian cancer," Am. J.
Epidcmiol. 14\ (9). 828·835, 1995, Long-l<.'tlIl u<sc of estfOi!:en replact.1nC1!t tht.'Tllp)' is assoc iated
with incrca:;cd death from o\'arian cancer.
12. 1.<.'C, N. C , et aI. , "Estrogen therapy and Ihe risk of breast, QI'ar}, and endometrial in
Agiug, Reproductioll , and Ill<: Cli nl3ct<.'Tic ," L Mastro iatUli, Jr.. and C. A, Paulsen, cditON,
42
Plenulll, N.Y. &. London. 19&6. To the extent thaI owl contraccptives suppress the pituitary
gonadotropic honnoncs, the OVlIry is prol<!Cloo lfom Ihe stimulolion Ilml ron produ.x: cancer.
1I0we\"er, Ihe us.:d 10 trcal rncnopallS<: double;; Ihe risk of 0\'1Iri1l11 cancer an ..'f h.m
yean<. If the estrogen was IIscd for mOTe than 6 years. Ih.:: risk is tripled.
13. M. S Ihmk'f lind K. I. . M. LillO, "Intentions 10 WiC honnon.:: themp)' in 11
cotlilmmity sumple of 45-year-old women," Muturitas 20( 1). 13-23, 1'>94. (WOml.'11 who
cxpre;,sed un int..111ion 10 usc honnonc rcp1I1CL'lllcnllllt:rupy III mcnopmlse reponed
lower sclf-csICl."I11, more dcprcsS<..'<.I mood, allxi':l)" amI m:gllli\"\: attimdcs townrd m<!llopunsc_
The abo c"prl!sscd stronger bdid" in their doctors' ability-as oppos.:d 10 lll.::i r 0\\11-\0 control
tIlL>ir m,-'uopausc
14. L. o..:lul.:rslein, C! a!. , \\cll-h.:ing, mid-Ii Ie and 1hc mCllopause,"
MaturilaslO(l ). 1-11. 1994.
43
5
NOT THE "FEMALE HORMONE," BUT
THE SHOCK HORMONE
Estrogen, at least when it is not opposed by a very large
concentration of progesterone, creates all of the conditions known to be
involved in the aging process. These effects of estrogen include
interference with oxidative metabolism, fonnation of lipofuscin (the
age-pigment). retention of iron, production of free radicals and lipid
peroxides, promotion of excitotoxicity and death of nerve cells, impaired
leaming ability, increased tendency to form blood clots and to have
vascular spasms, increased autoimmunity and atrophy of the thymus,
elevated prolactin, atrophy of skin, increased susceptibility to a great
variety of cancers, lowered body temperature, lower serum albumin,
increased tendency toward edema, and many of the features of shock . In
recent years, it has been found to be responsible even for neonatal
masculinization and the masculinization of the polycystic ovary syndrome.
Although the phannaceutical industry has often referred to it as "the
female hormone." I don't know of any competent scientist who has ever
called if that.
Since the 1930s, estrogen's toxic potential has become very clear.
However. the estrogen industry doesn't want people to understand what
estrogen is, because it is the source of billions of dollars per year for
them. Estrogen is a shock hormone with pro-aging effects. In the 1930s
and 1940s Loeb. Lipschutz. the Shutes, Selyc, LC. Strong, and others
showed that it causes cancer, excessive clotting of the blood, shock,
miscarriage, and tissue degeneration. but at the same time, the shills of the
drug companies were promoting its use for preventing miscarriages and
even for pn:vl!lIlillK the complications of pregnancy and toxemia it was
•
known to C(/llse.
The diuretic induslTY complemented the estrogen industry in its
assault on pregnancy. creating a myth of pregnancy as a sodium-retention
syndrome. when in fact an increased intake of salt is highly protective
against the effects of excess estrogen and toxemia of pregnancy. (In
hypovolemic shock. even a hyperton ic salt solution is known to be
therapeutic, and hypovolemia with hypoalbuminemia was clearly
recognized as a feature of eclampsia). Thousands of well-meaning
teachers and physicians helped to spread and perpetuate the fraudu lent
44
ideas originating with the corrupt pharmaceutical industry. (The U.S.
Dept . of Justice and FBr found fraud in connection with research on
diuretics, but it didn't affect the FDA's approval.) After Tom Brewer's
work (which built on R. Ross' and M. B. Strauss's 1935 work, and many
other studies in the 19405 and 1950s), the FDA's continued approval of
those drugs could only be characterized as malfeasance. (In 1834, J.
Lever recognized that malnutrition and restricted salt intake could cause
eclampsia. "Cases ofpucrpera\ convulsions," Guy's Hospital Report s vol.
1, series 2, 495·517, 1843 .) By 1950, there was sufficient knowledge
available for controlling I his disease of estrogen·excess, hut the mere
concept of too much estrogen was anathema to the industry-agency
conspirators_ This is a disturbing issue. because even in 1996, prestigious
professors of medicine (NPR's "Science Friday") are pretending that
toxemia and eclampsia are mysterious.
Histamine mimics estrogen's effects on the uterus, and
antihistamines block estrogen's effects (Szego, 19.65, Szego and Davis,
1967). Estrogen mimics the shock reaction. Stress, exercise, and loxins
cause a rapid increase in estrogen. Males often have as much estrogen as
females, especially when they are tired or sick_ Estrogen increases the
brain's susceptibility to epileptic seizures, and recent rcscarch shows that
it (and cortisol) promote the effects of the "excitotoxins," which are
increasingly implicated in degenerative brain diseases.
Just after Szego's work was published, I suggested that
antihistamines might be used to resist some of estrogen's toxic effects,
including cancer. A few people tried the idea, with some benefit, but the
basic idea of a physiological counterforce is opposed by the ideology of
"specific chemotherapy," in cancer, epilepsy, arthritis, infertility,
osteoporosis, immunodeficiency, Alzheimer's disease, etc .
The pooling of blood in veins, a basic feature of shock, has
recently become another of estrogen's "protective" features for the
circulatory system--the reasoning seems to be that reduced circulation of
blood makes life easier for the circulatory system. The relevant contexts,
though, are the contribution this makes to the formation of blood clots,
and the quality of oxygenation of all tissues.
Besides causing stress, estrogen levels are increased by stress.
For example, a male runner's estrogen is often doubled after a race. Men
and women who are hospitalized for serious sickness typically have
greatly increased estrogen levels. Estrogen's role in terminal illness, a
vicious circle in which stress decreases the person's ability to tolerate
stress, is seldom appreciated. Circulatory collapse, multi-organ failure,
45
intravascular coagulation (and the consequent depletion of fibrinogen,
leading to internal bleeding) are so commonly seen in the people who die
in hospitals that it would seem scandalous to suspect that estrogen could
be a major contributing factor. The willingness to cover up estrogen's
involvement in strokes was evident in a recent newspaper report in which
a woman won a large financial settlement after her husband died from a
series of strokes, caused by a phannacy's mistakenly giving him "a female
sex hormone." The mass media seem to have a "speak no evil about
estrogen" policy.
Estrogen marketing involves manipulation of the mass media and
the medical media. Currently, there is emphasis on appearance, heart
disease, and the danger of osteoporosis. Undesirable evidence is simply
ignored . 1 have never met a physician who had considered that estrogen
might contribute to thinning of the skin and bones. Why are women's
skeletons lighter than men's? This issue is sometimes noted in a tangential
way (for example, see the discussions of osteoporosis and prolactin, and
of prolactin and estrogen, in the Yearbook of Endocrinology, in the
1980s), but the relevant information is ignored by the influential media.
Estrogen's effects have been known since the I 950s,
or earlier. Text-books in the 1960s discussed experiments in which either
estrogen or insulin stopped growth of the fetus's brain, and also in the
1960s experiments were showing that progesterone fosters brain growth
and intelligence. Zamenhoff's work showed that the prenatal abundance
of glucose is a central factor in brain growth. Since estrogen and insulin
lower blood sugar, and progesterone and thyroid sustain it, Zamenhoff's
work showed that the level of glucose was a common factor in many of
the previous experiments, though other factors, including blood volume
and body temperature, are also important . The epidemiological evidence
is clear that women with toxemia of pregnancy, which involves
inadequate delivery of glucose to the fetus, have babies with subnormal
intelligence. Among obstetricians, it used to be common knowledge
(before insulin treatment became common) that diabetic women were
likely to have intellectually precocious children. As the work of Shanklin,
Hodin, and the Brewers shows, there is a large group of Americans with
neurological damage resulting from their mothers' treatment during
pregnancy.
While I was studying the effects of light on health, many of the
women with the pre- or peri-menstrual syndrome told me thai they had
few symptoms during the summer months, so I began in the 1960s to
examine the role of progesterone in health, because its synthesis is
46
promoted by long days. I saw that many of the sicknesses that mainly
affect women had often been described as the consequence of an excess
of estrogen, When animal experiments ,support the clinical reports and
epidemiological evidence, as they do in the case of the "estrogen
sicknesses," the goal of research becomes understanding the mechanisms
involved, and discovering the safest way to avoid or 10 correct the
problem. Tn the period between 1940 and 1960, thyroid, progesterone,
and vitamins E and A had often been described as antiestrogenic
substances, and some of this information persists in classical textbooks, in
spite of the efforts of the drug industry to suppress the facts by giving
their financial support to journals and symposia which exclude research
which uses the concept of excess estrogen. For example, Goodman and
Gilman's text on pharmacology discusses the ability of estrogen to make
animals susceptible to seizures, and progesterone's opposing effect . One
might suppose that the fact that all oj Ihe "C!/ficial" approved dnw; for
Irealing epi/ep.\y are teratogens should have been mentioned at that
point, so that it would be brought to the attention of physicians that they
had the option of using natural hormones to prevent seizures during
pregancy, instead of making women choose between having a baby with
birth defects, or having sei:£ure.s durillg pregnallcy. But Lhat is not how
the subject of epilepsy is presented to medical students.
It turns out that the meaning of "excess estrogen" has to be
interpreted in relation to the balance of estrogen (and the multitude of
factors which mimic estrogen's effects) with all of the antiestrogen
factors. I have concentrated o n thyroid, progesterone, and red light as
the most important factors that protect against estrogen, and these all tum
out to be protective against stress, shock, ionizing radiation, free radicals,
lipid peroxidation, thymic atrophy, osteoporosis, arthritis, sclerodenna,
apoptotic cell death, and other problems that arc involved in tissue
degeneration or aging.
A Better Name is Needed
If animals grow up with female traits simply because testosterone

is lacking, what can a "female homlOne" be? If too much estrogen can
make women grow whiskers, what should estrogen be called?
If we named hormones according to their place of origin, as Selye
suggested, we could call estrogen folliculin (as Selye did, because it is
produced abundantly in the ovarian follicle) , or adipin, because it is
47
sometimes produced in fat cells. But it can be produced by many cells
when they are under stress, and it seems to be normal for some to be
produced in the testicle. (I have heard that stallions produce more
estrogen than mares, though I haven', read the studies.)
If estrogen is produced by so many different cell types, could it be
named according to its etfects? Sclye objected to that approach to
naming hormones, because every hormone has a variety of functions .
Nearly every type of tissue in the body contains the proteins thai are
called "estrogen receptors," though the receptors are not the only way
estrogen affects cells. For example, it reacts with some common enzymes
in cycles which produce free radicals .
I studied many different systems, tl)'ing to characterize estrogen's
functions in a general way. In every system that I examined, estrogen
seemed to "wasle oxygen," resulting in a tendency for the tissue to be
de-energized . Recent studies have used estrogen's ability to lower the
cell's "energy charge" to study its ability to promote tumor growth: It
lowers the energy charge in cells when it is stimulating their growth.
My results, in which estrogen interfered with respiration, made me
think of Warburg's description of cancer metabolism. He saw cancer's
"respiratory defect" as depriving it of the energy it needed to function as a
useful tissue_ leaving it only the primitive function of growth. I
considered many ways in which estrogen might be a cancer hormone,
including its promotion of the oxygen-wasting age pigment, and its
stimulation of porphyrin metabolism, since some researchers had seen an
association between cancer and porphyrins. At that time, it wasn't known
that the breakdown of the porphyrin, heme. produced carbon monoxide.
But beyond the possibility that estrogen was deeply involved in
the nature of cancer, I felt that its biological role had to do with its
interference with oxidative metabolism. Selye had characterized
estrogen's effect as "like the shock phase of the stress reaction ." Estrogen
does act in conjunction with histamine, and histamine alone tends to cause
circulatory collapse by allowing fluid to leak out of blood vessels. Lack
of oxygen probably relates more generally to the shock reaction than does
histamine.
The reduction of cellular energy is probably estrogen's central
action, and in Warburg's scheme, this would be the way to turn on cell
division and growth. In the absence of oxygen, cells take up water, and
when water-logged (even from being placed in a hypotonic fluid) , they
begin to divide.
48
Since some pituitary honnones (including prolactin, ACTH, and
the gonadotropins) cause cell division in their "target organs," I suspect
that they function much the way estrogen does, except that they have
different affinities and so act on different types of ceiL
The thyroid hormone is opposed to estrogen in many ways,
promoting the delivery of oxygen to tissues, reducing tissue edema, etc.
ft is also antagonistic to some of the pituitary hormones, especially
prolactin. In bones, prolactin causes osteoporosis, estrogen blocks bone
forming processes as well as bone destroying processes, while thyroid
increases bone turnover, activating both formation and removal. I'm not
sure how far this generalization can be applied, but it seems that some
hormones can be understood largely in terms of their pro-energy or
anti-energy functions. Estrogen turns on a primitive type of growth by
lowering cellular energy and function. Thyroid turns on cellular energy
and function, and controls the rate of c.ell growth .
Some mysteries, such as the high levels of gonadotropins during
infancy, might be explained by this principle: Their primary function is to
regulate energy and growth. After prolonged stress or in old age, their
hypersecretion would tend to cause tumors, or to de-energize cells
further, causing atrophy.
Note: Although the so-called regulatory agencies have served the giant
drug corporations well, by suppressing their competition and approving
the most profitable drugs, in exchange, for lucrative drug industry jobs
offered to the officials· who do their jobs satisfactorily. the current trend
in the US is to remove all constraints from the powerful corporations.
Vice President Quail, with major family interests in the drug business, was
put in charge of a commission to make it even easier for businesses to
avoid the regulations, and similar favors are being done for the timber
industry, the mass media, the banks, and the insurance industry.
New channels must be found to inform the public about the
threats to their health. Even the "health food" industry is dominated by
the giant corporations, so their publications don't present the alternative
that used to exist, thirty years ago, in a few magazines like Prevention .
>I<The revolving-door between the agency and the industry--the delayed

bribe--applies only for the well qualified officials. The basic function of
allowing industry to do what it waniS is also served by staffing the agency
at lower levels with ridiculously unqualified people. The technical
"training" given to people who lack any formal background in the field
49
apparently consists mainly of teaching them to scoff at evidence because
it was published in a British or French or German or Japanese or Russian
or Italian scientific journal, or because it hasn't been discussed recently in
an American journal. And at a!llevels, the institutional principle is that if
a drug doesn't cause cancer or Azheimer's disease within five years, then
it is proven to be safe. At the highest level, when the agency is presented
with clear evidence of fraud or malfeasance, the final response is that the
agcncy doesn't handle complaints by individuals I have been lorced to
believe that something more than incompetency is involved when officials
refuse to say in writing things they have lold me orally, and when they
make misstatements in writing. or make deletions from documents
provided under the Freedom of Information Act. And these are the guys
that "work for us,"
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50
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HonnOllal changes at menopause "may represent the swn of IWlctionai abermtions that were
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51
estradiol·induced formation of free radicals. ' ", ..this bcta-cndorphin ce1110ss is followed by
IirompelL'l3tory upregullition of mil opioid receptors in the vicinity of LHRH cell bodies.'
Resulting superserusitivity of the cells f<..'$u!ts 'in chronic opioid suppression of tho: pattern of
LHRH release, and subS<!(j\le]ltly Ihat of H I." Tbe neurotoJ:ic effects of estradiol CIIuse II
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·_ ..molecular o;>,:ygcn is consumed by a sequence of reactions initiated by the glutathione thiyl
radicaL ... the estradiol phenoxyl radical abstracts hydrog<."Il from ... NADH to generate the NAD
radicaL ' " ... the futile metabolism of micromolar quantities of estradiol catalyzes the
oIldation of much greater concentrations of biochemical reducing cofactorl, such as
glutathione and NADH, y,ith hydrogen peroxide produced as a conse<jUCllCC."
33. S. Santagllti, ct aI , 'Estrogen r<.'Ceplor is expfess...'<.1 in different types of glial cells in
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almost L-qual .. ."
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35. J. Owens and r . A. Schwartziaoin, 'Suppression of evoked IPSPs by arachidonic acid and
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36. E. A. Quail and G. C. T. Yeoh, "The effect of iron status 011 g1yc..'faldehyd<: 3-phoophate
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over.:x"Pression of GAPDH mRNA in iron deficiency is probahly due to increased mes..'Nl.ge
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USA 92(20), 9220-9224, 1995. • ... elicits biological activities distinct from estradiol, most
notably WI oxidant strell$ re$ponse induced by free radicals generated by metabolic redoI
cycling reactions."
38. 1. G. Lichr and D. Roy, "Free radical generation by redOl tyding of estrogeru," Free
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39. P. Aschheim, "Resultats foumis par la grelIe hcterochrone des ovaires dan I'etude de la
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1964/65. ·Our last experiment, grafting ovaries... into senile rats which had been castrated
(ovariectomized) when young, and its result, the appearance of estrous cycles, seems e:>;plicable
by this hypothesis. Everything happens as If the long absence of ovarian hormones ... had
kept the ce\l$ of the hypothalamus in tbe ,tate of youth. It's a$ If the messlIgu of the
circulating ,terolds fatigued the hypothlamic memory." "What are the factors thai cause
thi$ diminution of the hypothalamic SCllllitivity... ? Kennedy incriminates a decrease in the
cellular metabolism in generaL .. •
52
HI I' 1\,..:II..:un. "i\)!IIl)! 111 h)p"11",kIlIlK·hl'I"'physc,,I·(lnulan a\IS in Ih..: ral: I'p..'7(,-41)0;
III II, V b','rill mld.l /I. I . ..:,hl",-". I h pOI h"lmlllls. I'll IIi I'ln Hllli ('. C '1lI'Hila"
Spnuj.!l;dd. I 'nh
-II , <:. 1\ !-rn,; ,mJ J I) SllIr!!,s. "N.' uru\' c ruj,h ,,1'1.... (\ 'fl,lI ia l n orking, ant!
tllu::-t c rm ur fl' m"k n lt l," N"""nh,,,L I "afH. I). 1'195. !! <:111'11.:
rals llluV..:r hI ",'pm..: a SP'llli"II",l dunn)! bdl"I'I<>Ial (' /\ 1"11":. hUslon un;\",. d":]11
1",,1. h"II,I\'I<)I,,1 11":111..,,<1:1 !ah. hush '" 15 I • J-,slrlls''''SI"mlcd in a \\"Iel' m<l/e task
",..: Il1ll1kd tu acqUlslllUlL" I'I!IslOL Ikll<ll . 57( I L 5-1-1. 1')')5 .
.\2 II, I. S M "11.1 I) I(m. "SC I 11lld.::o, I lNfI dama)!..: and hpid r><.:r<l'IJnl iOIl
III dOl'sol<l1cI'<l1 or Nohk nih: CLII(..:r 1...:11 S.t(2). I 1')<)-1
·0. (" A f.;ns1cIIs<'·II, cl al _ ··l-:IlC...·1 or lIillllJra\\al 011 ellcrgl -ndl alld
"r del',:",kIK": 1I1""Ii<>r..:d HI 1'1\·u 1'-."1 lIIagnetic' r..:s"n:IIK": SPU'If(IS<.·OP)
"l" ('mr hlll1l"n hie:'" \ell"gl;llk " ( '"nc..:1' ({":>'<!Hr..:h 55( 1(,(>-1_1 (>l;') . I
·I·/. C. 1,_ I' i ndl . "Thc C",IUIIIl" or ,Wanall (1,>0;\ k' in,' "llh "1!-'lIg ;md p(l"sihk r..:l:il io"ships
In I >.m II ndrnillc :lIld AI/hclI"":,'s Ilisc",;c " le"I' (;":1'1>111 2'!(h 1. 1'. 2')'). 19\)·1.
II I I,hll . cl 111.. Twwcrsi"" orcslr,,"c 10 2- ;md h}' hamster hidtlcI ;lUd
11\":1' hnpl"'aliun Ii>! Iii..: 1I\,,<:hanism or eSlrngcn-indll\'cd ,'artill<lgcn":sls,-
1'.nd"'lIl1ul"j!.' 1-'5(51.1772-177'). 1')'1-1
·1(, I' A. Mall' _c! :II. . -'fh t: dkds ol-"T""I<>.:riplill": ,II"II'",I;'clin ill
Ih, 11"l'den<l1l gblld (If Ill<' male t.kS(>.:rk<!lI1S ann,llls: J_ "I' C01l1p.
11·- II1<>.:h,m ieal "",J EII,-imlllllc»lal I'h\ sl"h'l!.' )(,,1(71. 52-1-52')_ 11)1)5.
·17. C]{ Ilal'l,. CI ,II.. -Opioid lIl,I<l"I"I'<>1I (If !!"Hadulr<>l'in rd,,,sin!! 1l0l'lnun..: rckas..: fmm Ihe
hn">1 h,,!a1l11l' I'r..... 'pl;( !!r"::1 III Ih, Ill!!: ! )0I11C-,1 An illl , EU(I,>o;r;m)1 I 1(-1) . .<7;·.lS2. I <)9·1.
N Ni Isscm and I I. ("(nisku. "I mUII,'cs sHl'pr,SSlI'H oj' ""luml killcr ,dl ()
aud of 1'",: dUlIal )1 <xli ;I,'lil":l1 ion." Cd I hllUlllllol. 151\( 1). I J I_I.">. 19')-1 .
-1':1. X_ L Ilan ;lIld .1. ( i . "1;_1 h'dru\\l:iI ;ol1 "r ;n kidllc' mull,,'er DNA 01'
Ircat..'1.1 \\1111 cslrmh"L ]t"k of Ircc r(I,!i\'als in ..... l ":an;iIlOj!,ncsis:
('<Ull'er Res_ 5(21). 5515-5(7. I'N-I
50. 1\ T 1.1111 . .:I "I . -coll'crsion uf .:sln>l1' It> 2- and Iv, hmllstcr Iddu<!)- and
II\'cr mi'f'oslIu>e.<: hnl'!i":<llions j(>r Ilic 1I1,-'Ch'lIlism of esllOgcll-indut;C(1 l,'an:inog.!Ilcsis:
F.mlocril1ohl!1) !.lSl51. 1772-171'J. 11)')-1,
51 {, C. cl al. . l'>Lla-clld"'llhill n":IITOIl loss: A
IX)ssih!.: modd IIi" hypothalami;: "l!inl!." ,il ':"p ("ronlnl"g" -,O(,V-I I, 25.1_2(,7. 11)95.
52. w (, Rnsslllitililh. "( i()tladOI ropin S<....Tclioll dnring llping ill R"::l"ic\\ aT1kk - I::-;p_
(,,,!'\,nloh>IlY _lO( lI-I J.. 1. I ')'J5 ,
53, W IS<;, 1'. M . "A kml;(lIls in Ih, procslrolls pallcm of m,,,lian .:miIlCII(<.' U II{!I. seOUll, U I.
[·SII. cslraui,,1 mid ,'(lllwnlr:ltolls ill nliddlc-ag.:d n'ls ." Sd. .11, 165-1 n.
1'182
54. SlIn;ud. M .. ct al.. "An i11lr:lClahl" impaion..::nl in Ihc h)llOlhulamo-
pilnllary uf Ih" cSlmdio!·\'aleral..:: O\'<lrian condilion in Ihc Tnt" BioI.
Ikprod. )h, 122 'J-12 .n. 1
E. W Ilahn anu W 1·_ Wanl. --nIC incl,kn..:<! of ill x_imldia1L'I.I rats: J.
FCI1_ 20. I SI- I>I. 1%1. and Wuru mid 11<llm. ({mi. I{",,_33,57-1_ 1%7.
,)J1li-mdiatj<>n (11111111"'): Val":lIl and Hahn. ISIW 20( .• ). 25 'J-2h7, 1971. "lnl!eneml, irrndial ..-.'
kma!.:s <.'xpcricllcc a pc:riod of 10110\\ ..'1.1 Iw a n:dllction U'
ccssalioll of l'ydinp._ · "o.:Slrous (k1)rcss ion is dW!'<Id,ril.cd b\ prolollfU'lioll I!f vagina
wmi!k'llioH . 1clllling to OOIlSIH1ll and linall y pcmmncnl di-oc"tros .... • "Exposur·
of uuring I1IctOt.'Slms 10 SO 10 2()() R X·m)·s has Ix:cn found 10 I"pical signs"
p;;yclhk acti\"i1>"-loru()sis, ":;If 4')''10 or Ihe animals, ... •
5(,. R. nischoO: ci al . '111C illnll<.'1ICC of irradialion of Ih, ,"';!ri"s upon eslrus and neupl"s1i
,k"'do]lme1)t in Ihe Marsh-Bullalo l1li(,: -1.1 , 55. ]'}-I-I ..
57. S. I-I. Geist , al . "Vag;nal in irratli3k'd lIli,..:: Endll,rinolo!1' 2<). 59. I 'J.l1.
5)
58. W,G. Salle and J. T. [lradbuTY. "Ovarian histology alkr irradiation 01\
alhino Em.locrinolo!!y 10, I. 1962.
59. D. L Ingram awl A M. Mondl, ""nil! conlro! of x-ray Slcri!i7cu ovary'- J.
Endocrin. 17. 1-12, !<,is!;. "'1llis finding imlicalc, that in Ihe ao;;.mc.: of th.:: pimiuu.... Illc
x-irradiated QI"UT)' Cltll proolloc more O\!slrogcn Ih:m a o\"ary, or Ihat the
il produces is biologicaJ!v more active"
6/), Mandl ZUCko:nlUlll. 1956: "After the C'\POSUfC of their ovmlcs \0 sterili zing doses of
x-rays. adult rats CXporiC1KC 11 pllas.: of vaginal wmificalion which begins II ilhin 40 <11,,; and
lasts up \0 14 w<.'l::ks." ".. .in 1011111:<."11 of tile fiJlccn litter-pairs (on.: animal irradiated: one
oontrol ) kiHoo a\ intervals of 5.7() days the uterus in the
irmdiatt:J animal. ... " "(11 is of interest thai the one control :minJaI whose uterus wus the heavier
of liller-pair was later found to hU\'e a mild Jcgrc.: of glandular
61. C. A. Frye and J. I). Sturgis, "N.:urostcroids spatial rderenee. working, and
mi..'1nol)' of rats: NCHTohiol. L.:arn. Memory 64( 1), lD-96, I ')\15. I
take longer to aC<juir.: a spatial task during Ix:havioral estrus.] and (C. 11.. Frye, Boston Univ.
I),.:pt. BioI.. lkh3\"ioral Neurmci. Lab, Boston U2215) "Es\rUs-1l>neiated ,k.:rements in a ""liter
ma;>;e lask arc limit.:d 10 acquisiliO!I," PhY5iol . Bellav. 57( I), 5· 14, 1995 .
54
6
JUST ONE PROBLEM: CLOTS
A stage magician can produce surprising illusions by directing the
audience's attention to where something is nOI happening, or to a
distracting gesture. The billion-dollar estrogen industry has learned the
trick of directing the public's attention to where some plausible benefit
might be expected, and of politely ignoring the areas where death and
destruction are in fact being produced.
Interestingly, another billion-dollar industry--thc edible oil
industry--is using the same prestidigitation to profitably misinform the
public . Decades ago, unsaturated oils were found to lower cholesterol.
However, studies showed that adding the polyunsaturated oils to the diet
didn't prevent death from heart disease, but that it did increase cancer
deaths. There were also warnings that the oils could cause
problems with blood clotting. There was silence from the industry, the
government, and the medical profession in response 10 the bad news.
When evidence of an association between blood lipids and heart
disease was found. the blood tests. rather than actual health. became the
focus of publicity. A high ratio of HDL (High density lipoprotein) to LDL
(low density lipoprotein) came to be identified with "health," because of
its association with lower risk of heart disease. although it was also an
indicator of a risk of death from cancer. By ignoring evel)'thing but heart
disease, it could be argued that "If high HDL equals health , and estrogen
and PUF A (polyunsaturatcd finty acids) cause HDL to incrcase, then
these things promote health."
Concerning estrogen, similarly twisted reasoning led to its trial in
the 1960s to prevent heart atlacks in men, but the experiment was
stopped when the rate of he an attacks increased sharply.
Focus on the positive. Ignore the HDL-cancer association.
Ignore the association of estrogen with thrombosis. embolism, stroke.
edema, obesity. depression, myocardial infarction, eclampsia, epilepsy,
brain damage, and immunodeficiency. Ignore the implications of thyroid
suppressIOn.
In her comedy routine, Judy Tenuto describes a most implausible
situat ion, and then belligerently pleads: "It could happen; it could
happen ."
The ignorance or mendacity which allows experts to plead the
importance of one possible benefit, in the face of clear evidence of a
55
multitude of serious dangers, defies any sort of conventional scientific
response.
The recent corruption scandal involving the FDA's generic drug
division might come to mind when I suggest that Tenuta's satire
illuminates the attitude of the FDA (and the medical industry), but I
believe the indictments are pan of the prestidigitation .
Marvin Scife, who was head of the generic drug division, was
indicted for perjury. The indicated intent of Congress had been to support
generic dnlgs to break the monopoly of the biggest drug companies, but
for the last six years there has been an intense campaign by the
monopolies to keep generic drugs off the market, and Scife's indictment
must be evaluated in this context.
Earlier, an FDA official who was too friendly toward DMSO and
its developer, Dr. Jacob, was exposed for accepting a loan ITom the
doctor. While keeping new entrepreneurs from intruding into the
fabulously lucrative drug business, those little prosecutions allow the
public to believe thaI the government is policing itself (If your
corporation could expect an additional $4,000,000,000 in profits in the
next 10 years, but only if a few men would narrow the scope of their
judgment, how do you suppose you could encourage those few men to go
in the right direction?)
Fony five years ago the Shutes found that estrogen promotes the
clotting of blood . AI the same time, Knisely was studying the
phenomenon of blood sludging, which occurs under many types of stress,
At that time it was recognized that there is an equilibrium between clot
formation and clot removal (fibrinolysis). Vitamin E and magnesium and
some substances produced by the body shift the balance away fi'om clots.
Estrogen, calcium, altered water content and blood volume, and sluggish
!low of blood encourage the formation of clots. Some contemporary
anicles acknowledge that estrogen can calise thrombophlebitis or
thromboembolism and can exacerbate gallbladder and liver disease and
breast cancer, but these warnings are subordinated {O praising the benefits
of estrogen replacement therapy. (Valery Miller, Veronica Ravnikar. and
Chrystie Timmons, "ERT: Weighing the risks and benefits," Pafielll Carr: ,
June I S, ! 990.)
Some quotations from the ERT anic\e by Miller, e/ al.. illustrate
current medical attitudes:
56
"Allhaugh the reasons for its apparent protective effect on the
heart are not fully understood, oral estrogen does decrease low-density
lipoprotein cholesterol and increase high-density lipoprotein cholesterol."
"Although no prospective study has yel shown thai estrogen protects
against cardiovascular disease, other studies show that women who use
est rogen or who have ever used estrogen have a reduced risk of heart
disease_ The only study that has not confirmed thest' results is the
Framingham Heart Study, which contained smaller numbers of older
women and classified chest pain--a notoriously poor identifier of heart
disease in women--as a cardiovascular end point" (p. 47).
The prospective long-term Framingham study noted above used
to be highly praised as a source of reliable information on heart disease.
In contrast, some of the studies that are praised in prestigious journals are
wildly unscientific. For example, the heart disease in Marin County
women receivi ng estrogen has been compared with that of women in the
East Bay not getting estrogen. Marin County is a rich residential area,
which is swept by ocean breezes, while across the bay there are more
working class people (and work ing class men afe known to have nearly
50010 more heart disease than white collar workers), and the wind from
one direction blows smoke from a concentration of industries and
refineries, from another direction it carries the pollution from San
Francisco's traffic, and from another direction it brings the agricultural
poisons of the Salinas area.
If enough women die from strokes, pulmonary embolisms,
accidents, suicide, cancer, and loss of immunity caused by estrogen
excess, it is possible that some competent study will eventually show that
estrogen treatment reduces the mortality from heart attacks, but this is
not likely.
It is the estrogen in oral contraceptives which correlates with their
effects on the clotting system. In the last 20 years there has been general
agreement that increased risk of cardiovascular disease, rather than cancer
or immunodeficiency or depression, is the most important concern about
the effects of oral contraceptives. l . ll
There are many ways that estrogen can contribute to a
hypercoagulable state (leading to cardiovascular disease). Some of these
involve altered liver function, including disturbed production or
metabolism of 8 different coagulation controlli ng factors. I2.13 Since
estrogen can stimulate endothelial proliferation (often cited as crucial in
heart disease) and reduces the rate of venous it is necessary to
57
consider the whole complex circulatory system, and nol just the clotting
factors .
The thyroid and other hormones such as insulin and adrenalin are
influenced by estrogen, and must be taken into account. Although I'm not
sure what clinical perceptions led the Shutes to study estrogen's affect on
clotting, pregnancy and lactation are notoriously associated with
hypercoagulability (eclampSia and thromboembolism, for example)
produced by the body's high eSlrogen production at those limes. I.,..!.' The
very high doses of estrogen that were once used to suppress lactation
were found to produce cloning problems ..!-' Postmenopausal use of
estrogen causes changes in cOilgulability. I.',N;
In the mid-l <no's when I pointed out that menopause resembles
Cushing's syndrome,17 [ haon't invest igated that disease of
enough to know the full extent of the parallel: For example, hot !lushes.
night sweats. and insomnia. such comlllon menopausal symptoms. are
also COllllllon symptoms in Cushing's syndrome. Estrogen's tendency to
increase cortisol production should be considered in connection with the
brain-aging elfeets of both estrogen and eortisol l$.l<l
Both estrogen and cortisol weaken the stnJc{Ural components of
tissue. and the bruising which is so commonly associat.ed with the
premenstrual syndrome seems 10 involve the unopposed action of both of
these hormones. The women who otten have bnJised thighs in their
twenties are later susceptible to hemorrhages into the white part of thc
eye, and still later to bleeding into the brain. presumably because there is a
hierarchy of protection against the tissue-weakening clrects of thosc
hormones, with the brain being the last to lose its resistance.
For example, the brain content of progesterone. pregnenolone and
DHEA is normally 20 or 30 times higher than the serum concentration.
and these hormones arc protective against both estrogen and cortisone.
As far as I know, if is possible to have fragile blood vessels at the
same time as an excessive tendency 10 clot, though when the vessels
break the extent of the bleeding will be smaller in the hypercoaglllable
state. The observation that low cholesteral is associated \\·ith increased
risk of hemorrhagic slroke.lO suggests that the age-related decline in
progesterone. pregnenolone. and DHEA occurs earlier when there is a
low level of the precursor substance. cholesterol.
Clotting too easily is just one of the problems that can be caused
by an excess of estrogen. and I don't mean to give it too much emphasis.
since I consider its toxic effects on the brain. and its acceleration of brain
aging to be its worst effects--though its cancer inducing
58
effects on the uterus, the breast, the lung, the bowel and liver, and brain,
are certainly serious. BUI at present, estrogen's cardiovascular toxicity is
probably the aspect that people need to be reminded of.
The effects of estrogen on calcium metabolism--stimu lating cells
to take up an excess of ca!cium--have been known for a very long time,
but accumulating knowledge shows that this excess calcium is a very
important aspect of estrogen's contribution to blood clotting, heart
necrosis, and tissue aging, especially brain aging. Magnesium, which is
absorbed under the influence of thyroid hormone, is onc of our basic
defenses against the toxic effects of calcium.
REFERENCES
I, &ls, (leta, -The OIUj'lg" of AnlilhlOmbins," eRe Pr.:ss, Hoca Raton, 199(),
2 . IlIl11al1 , W. II. W._ <it (d., --rlU"ombo.::mbolic diwaS<! und the st.:roidal conkllt of ural
A r..:por! to the COllullillee un Salet)' of Dn'gs," Br..Ife"- .1. 1, 20\ 19711.
3 Shapiro, S._ "Oral -- a time to luke stock: .\:. EIli!/. J . ,I It'd. 3J5 , 450, 1986.
4 . Stadel, 13 V., "Oral (>lld C<lrdiOl"as<;a1ar disease: ,V. 1:lIgl..I. ,Ih'(l. .W.! , 6 12,
I ')1I I.
5 Meade , T.W., I?I al. , -lJacmoslalic lipid and blood press ure profiles of women on oral
conlmccpti\'es ng or.w IIg 1-tlllcl?t 2, 94l!, 1977.
(,. Sahra , It. lUld Bunnar, J. , "Hacmostntie system t>y 51) uf!. lInd 30 ug
estrOf!cn/ pTOJ!estagcn oral COlltroC<!pti .1. /leprod ,lh'(l. 2'( RS, I 9R3.
7 Ileller, I· ,K. and [ her! , C. "F.fl':cl S of ora! oolltwcepti vcs on hlood coogulatioll, A review,"
Obs/e/. G)1lfxol. Sun', -10,425 , 1985.
R. NOlelOl'i ls, M , "Oro I oontruc.;:ptioll and ( '/il/. Obste/. Gyllco/. 2x, 73, 19R5.
9 , BOlliger, L E, el al., "Orol contraceptives and IhrombocullXllic di sease: cl1'cct of lowering
oestrogen content," l.ancel I , 1097, 19R I .
10 Bonnar, 1. "CO(Igulution effects of 01<11 cOlllr&:eption: , 1//1,.1. O.llet. qWI£'Col. Jj7. 1042 ,
1'11\7.
II . ,'on Kalilla . I': . and ,'on Kaulla , K.N. '"Oral conlraccpt;"es and low 3ntithromhinlll
!-til/eel f, 36, In!).
12 . IJonnar. J eI al.. "Coagulatiml system in postmenopausal "omen rccci"ing
oestrogen preparallons," l'o,<Ir,rod. .l/ed. J. j2, 30, 197(,.
13. ,'()II Kaulla , I' , e/ al.. "Conjugated oestrogens and Alii. J.
Gymxol. J22, 6R'I:I, 1975.
14. Ire\' , N S I!t "'. "Va<;cular lesions in women lak ing oral Arch. l'mlwl. 89,
J, I'!71).
J 5. N S and Norri s, HJ , "[ntimal l"aw ulur aSi;ociutcd with l<:malc rcprudll(\ivc
steroids," Arc-I!. I>alilol. 96, 22 7,
I (). Ullery, J C , "l1iromhocmbolic diSC<lsc complio.:.11ing pregnancy and the pucrperium: , I", . .I.
Oh,I/I!/. ( iy"ecol. /Iii. 124 3, 1954.
17 S,l( et ai" "Antepartum pulmonarv cmlXllism," Am, .I. ( iwl£,("oI. ifill,
27f), 1'!7 1. . -
III Ilonnar, J , "Venous thromboemboli sm and pregnancy," in Rec. Adv. in Ob,<t. (/1/(/
( iyrh!coiri1{Y. J. Stallworth and G, BOUl11c, I :Us , Chun;hill !.i "ingstone, Edinburgh , 197<), 173.
1'I. j ldlgrcn , M, and Rlomback . M. "Studies on hlood and fihrinolysis in preWl"ncy
during del ivel)' and in the pucrp<:rium," (ly"ecol. Ohstet, ll1ve.l"l, 11, 141; 1<'R I.
59
20. !-Iall, J el al., "Maternal and fetal sequelae of anticoagulation during pregnancy," Am. J.
Med. (;8, 122. 1980.
21 . WCitll.T, C. P.• "Diagllosis and manag<.'1n ..'tl1 of thromboembolic disease during p"-'gIl3nC)''-
C/in, Ob.!ief. GYllecol. 28. 107, 1985.
22. Dc Sv.;ct. M " Illfomboc:mbolism,' in Aled. Di.fOroer$ in Obsletric Praclice, M . De Swiel,
Ed , Blackwell Scientific, Oxford, 1984, 95.
23. Hcllgreu, M.. , 11lYomixJemb{Jlism and pregllw/{:y, Thesis, Karolinsku Institute, Stockholm,
198 L
24. Kunie!, D.G. e/ ClI., "Pucrpernl and of lactation," Wllcel 2,
287, 1%7.
25. lkls\on Col1aoorntjvc Dnlg SUfvcilhmcc Program: SW"gically OOIlfinncd gallbladder dis.:asc,
veuous thromboembolism, and breast tumors in relation to menopausal oestrogen therapy, N.
ElIgl.J.M('(/.290,1 5, 1974.
26. Boruulr, J. el al .. ·Coagulation system chnng<!s in postinCllopausal women TeCeII'mg
preporatioIlS," P05fgmd ".fed. J. 51,30, 1976.
27. Peat, R. .NulriliOl'for Womm. 3rd edition 1980, Blake College, Eugene, Oregon.
28. Belol'a, T . I., "Struetuml damage to the meso.."1le'."phalic reticular formation induced by
inunubili:rlliion stress: Bull. Exp. BioI. olldMed. 108(7), 1989.
29. Wise, P. W., "ln11u("'1tcc of estrogen on aging of tile eentrul neTl'OU$ its role in
dI..'Clining fcmuk reproductive fWK:tion," in j\{euopal/se: E,·oiu(.Itioll, Tft'Ulmelll. and lIooltil
COlic-ems, pages 53-70, 1989.
30. Shinmmolo. T. , et al., CirculmiOlI. March. 1959.
60
PART TWO: PROGESTERONE TN CONTEXT
7
A LlST OF SIGNS AND SYMPTOMS
THAT RESPOND TO PROGESTERONE
THERAPY
Many people found the list of signs and symptoms in the first
edition of this book either useful or interesting; at least it is an emphatic
way of pointing out that progesterone has so many functions it can't be
considered to be just a "reproductive hormone," Since I now understand
better the biological meaning of these signs, I want to emphasize more
strongly the importance of normalizing nutrition, thyroid function, light
exposure, and bowel action in correcting the problems behind these signs
and symptoms. It is really a kind of index of physiological disorders, and
it happens that progesterone is a major tool for physiological adaptation.
Abdominal bloating Depression

Accident proneness Diabetic vascular problems
Acne (cyclic) Edema
Aggressiveness Endometriosis, cervical
Alcoholic or drug addiction dysplasia
Allergic rhinitis Epilepsy, venigo
Appetite disturbance Facial hair
Arthritis l Facial pallor, puffiness,
Asthma, especially in darkening under the eyes
adolescence & menopause Fainting
Bleeding gums Fatigue, lethargy
Breast symptoms2 Fibroids
Bruising spontaneously Fluctuations in weight
Capillary fragility Formication (crawling
Carpal tunnel syndrome sensation on the skin)
Cold hands & feet Gall bladder symptoms
Colitis, regional enteritis Glaucoma (high eye pressure)
Conjunctival or retinal Goiter
hemorrhage Headache, eye pain, flashes
Constipation, colicky pain of light, photophobia
61
Heart murmur Palpitations or paroxysmal

High blood pressure tachycardia
Hypoglycemia Paraesthesias
Hysteria (many emotional Pituitary abnormalities
symptoms) Porphyria
Infertility Sciatica
Inflammatory and "fibrous" Skin disorders: facial pigmen-
disease tation, erythema, urticaria
Inner ear dizziness Stroke symptoms
insomnia Sweat glands: fewer func-
Irritability tional
Low blood pressure Toxemia of pregnancy.
Lethargy and clumsiness Urinary frequency, etc.
Menopause Varicose veins, tired leg
Mittelschmerz.l Vascular abnormalities:
Migraine flushing, capillary fragility,
Nymphomania, loss of clotting, kidney undert'unc-
libido tion, varicosities.
Optic neuritis
Panic, weepiness, night-
worry
I. Antibodies to joint material are found after even a mechanical or

thermal injury to the joint; twisting cart ilage makes it antigenic;
autoimmune disease is probably nothing very special, and cSirogen is now
known to be responsible for many forms of it, including osteoarthritis.
"Rheumatism" is an early sign of stress damage to joints. See H. Selye's
publications on arthritis and scleroderma.
2. See A,male.\· d'Elldm:rillologie 37. p. 309; Cancer 33 , p. 1506; AliI/. N.
Y. Acad Sci .. 1977. Progesterone deficiency predisposes to cancer.
3. Cramping at ovulation, often mistaken for appendicitis: in a 1962
study, 62% of all appendices removed from girls ages 11-20 were normal.
REFERENCES
I, Kalharina l)allOn. Th" ilIlIl I'n>!,-cslcr"n" Therapy. Ye"r n""k

Mctlircall'uhfishcrs. Illc .. 1977.
2. Ashk)' M"nlagu, I!um;'n IIcrIXlily. New Amcri.:an J.,hra ry, New Y"rk. 1" 0.' .
62
J . It F. ]>"", A J.. S"dcl"I':all. Tstr"l-tcn Sll111Ubkd ra1hw"y changes:' I'hysio].'gieal
Chclll is!r), nlld 4{1 I. 1')72.
4 . R. f. I'cal, "A apr,.,,;!.:h h' ahcr.:.! J. ()f OnJwJl1"kcubr
1<)75.
5. S. R"S<l. ''!:Uvirutllllcnta] "ll hrain antllx:h;winr." .: haplcr in Ra.::e and Intelligcnce.
,,<li"'d hy Rlch;mj:;,)n :md Spears,l'cnguin 1I""b, lI:JlIinwrc. 1972.
(, _ A . E. "1"11<: (,r"wlh I'r,'<:6s in '\n;I11"I,;, Van N<>Slrantl.l'rim:<lloll. N . J. 1%4.
7. Max R"IS" J>sydu'cmlucrilwl"gy. {;run..: and Slrath'll. N.:w York. I 95X.
63
8
ORIGINS OF PROGESTERONE
THERAPY
By the beginning of the 20th century, the idea of extracting
regulatory substances from apimal tissues was coming into general
acceptance in Western medicine. J. A. Lebreton, in Paris, was one of the
first to argue for the therapeutic use of an extract of the corpus luteum.
Around 1904, C. F. Burnam, of Baltimore, began using corpus luteum of
the sow, administered orally, to treat the nervous symptoms associated
with menopause or with the menstrual cycle, and also to treat functional
amenorrhea, obesity, sterility, and habitual miscarriage. (1912 edition of
New and Nonofficial Remedies, and J.A.M .A. , Aug. 31 , 1919, !ix, p.
698.) By the 19205, tablets of desiccated corpus iuteum were generally
available, and the daily dosage recommended (representing 6 to 18 grams
of fresh tissue) contained a very substantial quantity ofprogesteronc.
The chemical structure of pure crystalline progesterone was
determined in 1934 (by Butenandt), and within 2 years many publications
were reporting the beneficial effects of injections of the purified material .
By 1935, animal research was confirming that the therapeutic work
previously done with the crude extract had been on the right track.
Although the early research showed that progesterone was very beneficial
in threatened miscarriage, arthritis, infertility, cancer and functional
diseases of the nervous system, interest in this generic,
material faded as the pharmaceutical industry found methods for
converting it into proprietary synthetic glucocorticoids, estrogens, and
progestins.
Animals are generally more sensitive to progesterone than humans
are, and in animals no toxic level has been found , except that in the
highest doses it is anesthetic. In humans, even this effect has never been
reported in the medical literature, and it is clearly anti-toxic in nature.
Besides preventing acute poisoning of many kinds, it also reduces the
incidence of birth defects and cancer.
Progesterone. the Protective Substance of Youth
In 1971 , I discovered that vitamin E and progesterone work

together to sustain efficient production and use of biological energy. (1)
64
In the mid· 19705, I found that progesterone is the most powerful
order-preserving substance (anti-chaotropic) on the cellular level, and that
this explains its range of protective actions, from anti-toxic to anti-stress.
(2,3)
Around 1980, I discovered that vitamin E, with its crucial effect
on the mitochondrial respiratory enzymes, is a uniquely powerful, stable,
and biologically compatible solvent for progesterone.(4) Their iniimate
association at certain cellular sites requires mutual solubility. This
property of mutual affinity extends to all biological areas, meaning that
the solution of progesterone in vitamin E can be administered with
exceptional efficiency by application to the skin or other membranes, or
by ingestion, where normal digestive processes convert it into
chylomicrons and distribute it to all tissues, allowing it to escape the
tendency of the liver to convert it rapidly to an excretory fonn, as occurs
when progesterone is administered in other forms .
Because of its profound biological compatibility, the
progesterone-vitamin E solution permits otherwise impossibly high doses
to be given, increasing by as much as 2,000% progesterone's already
dramatic effects in a wide range of major biological problems, including
epilepsy, habitual miscarriages, auto-immune diseases, and cancer of the
uterus, breast, and kidney.
Some Aspects of Basic Progesterone Research
By 1945, Hans Selye had demonstrated that progesterone in itself

has the full spectrum of regulatory and anti-stress functions of the adrel1al
steroids. A little later, Albert Szent-Gyorgyi showed that progesterone is
able to regulate the heart, in a manner similar to digitalis. In the 1970s, I
demonstrated that it acts similarly on vascular smooth muscle, regulating
its tone and preventing venous pooling of blood, and maintaining normal
filling of the heart, opposing shock. The immediate improvement in
circulation can have dramatic effects, which include restoration of kidney
function, elimination of fluid from the lungs, restoration of sensation in
the feet , and healing of gangrenous toes. It restores normal tone to other
smooth muscles, including the gall bladder, urinary bladder, intestine,
sphincters, and uterus.
Progesterone's ability to regulate thresholds of cellular excitation
operates in nerves, as well as in smooth and cardiac muscle. It sensitizes
6S
nerves that regulate respiration, and has been used to treat infant apnea,
sleep apnea in adults, and polycythemia vera in men.
In cases of specific progesterone deficiency in men, small doses
can cure impotence. It has been used effect ively to treat benign prostatic
enlargement .
It normalizes fluid pressure, as in bursitis and glaucoma treatment .
This effect on tissue fluid contcnt is probably involved in its ability to
improve oxygenation in emphysematous lungs, and to normalize swollen
cartilage.
It restores many of the functions of aged skin, and is the normal
defense against calcium loss from bones. It is one of the few essential
requirements, besides nutrients, for nerve (brain) cell growth and survival.
In young people of both sexes, the brain contains more progesterone than
other organs do.
lt is reasonable that progesterone, the dominant hormone in
pregnancy, should have a full range of protective functions to protect the
vulnerable organism during its intra-uterine life.
Praclical Issues
A typical dose of progesterone/vitamin E, 20mg.lday for 10
consecutive days, costs about $1 .00 per month, at the present retail price.
Pharmacists have the authority \0 compound drugs as they choose, just as
physicians can prescribe the formulation they prefer. (And beyond that
principle. is the fact natural hormones have never been legally even
prescription drugs. Even potentially deadly injectable insulin is available
everywhere without a prescription. The FDA acknowledged that they
had en·oneously been listing insulin as a prescription drug, when it wasn't .
Federal law prohibits labeling a non-prescript ion drug as a prescription
drug. When I asked for a copy of their policy discussions regarding
natural hormones, they claimed the records were "old," and unavailable,
then they said that those poticy discussions were done elsewhere, so they
couldn't get access to the record. It's a touchy subject; the Freedom of
Information office claimed they couldn'l find those old documents, and
some related things they sent me were incomplete, wi th no explanation
for the missing pages.)
Neither progesterone nor vitamin E has any toxicity when used
orally. Under federal law. a prescription is needed for a dosage form of a
drug that is potentially harmnJI. The very dangerous injectable insulin is
always sold without need for a prescription, because something overrides
the principle of danger. presumably that its use is conceived as akin to
66
nutritIOn, providing an essential natural substance to restore a natural
function of the body. By analogy with insulin, the infinitely less
dangerous progesterone should not require a prescription . The most
useful terms for regulatory obfuscation are "Approved New Drug," and
"not an approved drug." Most legal drugs under the 1938 FDA law have
not been under the special category of" Approved New Drugs," but thaI
is a subject the regulators just won't talk about. They talk about what
they control, and hope people will assume they control everything.
Economic Questions and Pharmaceutical Efficacy

Because of its absorption by a natural digestive route which
distributes it to all of the tissues, progesterone di ssolved in vitamin E is
almost 100% absorbed when taken orally. Less than 1% is absorbed from
some types of suppositories, and less than 5% absorption is typica1.
Taken orally as a micronized powder, 'pharmaceutical efficiency is only
slightly better.
Most of the valid human research before 1981 used intramuscular
injections of progesterone dissolved in vegetable oil and benzyl alcohol.
Benzyl alcohol has a high affinity for water, and in contact with the tissue
fluid , it leaves the mixture, causing progesterone crystals to fonn, since
vegetable oil is a poor solvent for progesterone. Therapeutic blood levels
of progesterone can be achieved by intramuscular injections, but at the
cost of leaving toxic debris at the site of injection . Benzyl alcohol is a
powerful neuro·toxin, but its harm is reduced by progesterone's anti·toxic
action . The cost of the injectable progesterone, and especially of the
injection itself, has been the main factor preventing wider acceptance of
this form of progesterone in the United States, since the solvent's toxicity
has never been discussed officially.
The chemistry for converting crude diosgenin into pregnenolone,
and for converting pregnenolone into progesterone, is simple enough that
it can be done with little capital, at the site of production of the raw
material.
REFERENCES
1. R. Peat, BiQlollY i)('p«rt!Ucnt, University "fOrcl!-"o, 1972.

2. R. Pcal and A. L Sodcrwall. Cohl·inactival.:d Enzymes. ("hcm. and I'hysks.
1971 and 1972.
3. R. Peal, A biQphysical approach to altcred coosciouSIIc!lS, Jour. of
Psychiatry, 1975.
4. R. Peal,u.s. f'UletJI No. 4.432.437. /984.
67
9
ANTI-AGING HORMONES: STEROIDS,
IN GENERAL
This type of molecule might be the most common carbon
compound in the universe. It is made by single celled organisms, by
plants, and by animals, and has many kinds of function . The steroid
hormones are involved in all aspects of animal physiology, and overlap
with control functions of the nervous system, peptide hormones,
metabolites, prostaglandins, cyclic nucleotidcs, etc. (I suspect that their
ubiquity reflects a special kind of physical influence on biological water,)
Sometimes people speak of "steroids" when they mean glucocorticoids
such as cortisol or a symhetic like dexamethasone, or, among athletes,
when they mean anabolic steroids or synthetic androgens; and so it is
common to associate "steroids" with harmful side effects. Oddly, many
people who are afraid of toxic steroids fail to realize that estrogen is a
steroid, and is the most toxic steroid normally found in animals. All foods
contain steroids and sterols (a major type, containing an alcohol group
and a side-chain) some of which are beneficial and some of which are
toxic or allergenic.
In animals, cholesterol is the basic sterol molecule, which is
massively converted into other substances, including the steroid
hormones. (In plants, cholesterol in very small amounts appears to serve
as a hormone.) Thyroid hormone and vitamin A are required for this
conversion. The first step occurs in the energy-producing mitochondrion,
where cholesterol loses its side-chain and is slightly oxidized, producing
pregnenolone. Being less fat soluble than cholesterol, pregnenolone
leaves the mitochondrion, so it tends not to inhibit its own synthesis.
Rather, it seems to stimulate its own synthesis, though this isn't as
clearly established as in the case of progesterone. Depending on the
tissue, pregnenolone will be converted by enzymes in the cytoplasm
into either progesterone or Dl·IEA (dehydroepiandrosterone). The fact
that progesterone (and probably pregnenolone) stimulates its own
synthesis means that taking it does not suppress the body's ability to
synthesize it, as happens with cortisoL Sometimes, one dose or a few
doses can restore the body's ability to produce enough of its own.
Progesterone also allows the thyroid gland to secrete its
hormones, especially when the thyroid function has been inhibited by
68
estrogen. Since thyroid hormone is needed to produce progesterone,
a supplement of either tcnds to normalize both thyroid and progesterone
production.
Progesterone and DHEA aTC the precursors for the other more
specialized steroid hormones, including cortisol , aldosterone
(sodium-retaining hormone), estrogen, and testosterone. The formation
of these other hormones is lightly regulated, so that taking the precursor
will correct a deficiency of a specialized hormone, but will not create an
excess. At least in tne case ofprogestcrone, an excess tends to balance or
neutralize an excess of the specialized hormone, so it has been described
as having anti-androgenic. anti-estrogen, anti-aldosterone, and
anti-cortisol functions .
Many steroids nave a protective {"cat atoxic"} action against a
wide varicty of poisons. Some of the quick effects (e.g., within 10
minutes) of progesterone and pregnenolone probably represent a
catatoxic action, as well as a neutralizing or balancing of excessive
estrogen or cortisol. Improved metabolic efficiency, sparing oxygen and
glucose, will have a quick effect in reducing edema .
During pregnancy, very large amounts of progesterone are made.
It protects and stabilizes practically all functions of both the mother and
the fetus. Progesterone, glucose and the thyroid hormones powerfully
influence the brain development and intelligence oftne baby, probably by
influencing both the number and the size of brain cells, and the quality of
their functioning.
Pan of progesterone's protective effect is a result of its quieting
effect on cells. For example, it tends to prevent seizure activity in brain
cells. During childbirth, its normal function is to act as an anesthetic_
When the level of estrogen is too high, progesterone can't achieve this
effect. In a non-pregnant person, it is important to determine the
minimum effective dose by taking only a few drops at a time, and
repeating this small dose about every 20 minutes until symptoms have
been controlled . Otherwise, serious "drunkenness" can be produced, with
loss of coordination, and even unconsciousness.
The only solvent for progesterone which isn't toxic and which will
dissolve an effective quantity, is vitamin E. In this form, it can be
absorbed through the skin or other membranes, or can be taken orally.
Taken orally, it is absorbed as chylomicrons, going into the general
circulation (as vitamin E does), instead of to the liver where it would be
prepared for excretion. In this form, therefore, it is fully and quickly
available to all tissues. It is approximately 20 times more powerful in its
69
action than olher preparations. so il is important to use it in physiological
quantities, rather than in the huge doses commonly given rectally or by
Injection. Tell or 20 mg. is often an effective dose, though people with
low thyroid or high estrogen sometimes lise 50 to 100 mg. per day_ In
the customary 10% solut ion, one drop contains about 3 mg.
progesterone. and J ml. (] /4 !Sp.) contains 100 mg. The first dose should
never be more than I 5 mg .
Pregnenolone, taken orally, does nothing noticeable to a healthy
animal or person. but if the stress-related hormones are elevated, they
return to normal when pregnenolone is taken . The brain contains much
Illore pregnenolone, DHEA, and progesterone than do other organs or
the blood, and these levels decrease progressively with age. Older people
are more likely to fcc! an elTect fi·om pregnenolone. than are young
people. A tenth of a gram is a reasonable first dose, though some people
seem to need as much as I gram per day, po!>sibly because of poor
ilbsorption. (The amount produced daily in a healthy young adult is
roughly 30 mg.)
Normalizing the stress hormones with pregnenolone often seems
to have the effect ofcolTecting the fum.;tion of the thyroid gland , probably
because it is suppressed by stress. Since pregnenolone is the precursor
for progesterone and DHEA (and all the other steroid hormones), it oftcn
has the same effects as progesterone or DHEA. and it has the advantage
that it allows the body to produce just an optimum amount of those
hormones. In very old people. or people with special enzyme
deficiencies. it might be neces!>ary to supplement all three to achieve their
normal physiological concentration in the tissues.
Pregnenolone and progesterone are known to protect nerves
against the damaging effects of the "excitotoxi ns," which activate nerve
cells to the point of cumulative injury during stress and fatigue. The need
for pregnenolone is probably what is described as "agitated depression,"
in which the person feels unable to cope with ordinary life, and when the
body is unable to produce enough pregnenolone, the
distress leads to increased production of cortisol.
The clinical depression, which so typically involves elevated conisol
production, is probably primarily a pregnenolone deficiency . The active
fraction of the thyroid hormone, triiodothyronine, or tiothyroninc (Tj ). is
essential for the conversion of cholesterol to pregnenolone, as is the
retinol form of vitamin A. Butyric acid is known to facilitate the entry of
T3 into the mitochondrion.
70
Since progesterone and pregnenolone protect against the
excilOtoxins which damage neurons, and estrogen and cortisol promote
excitotoxic damage, it seems reasonable to see this opposition as relating
to their known physiological actions. For example, estrogen damages
memory, and pregnenolone restores memory in old animals. Although
the exciloloxins might not be involved in other organs, I suspect that
something analogous (possibly the cyclic nucleotide ratio) is involved in
the opposite effects of these substances on. for example, the thymus,
vascu la r tone, and liver function .
71
10
YOUTH ASSOCIATED HORMONES
PROGESTERONE
Sixty years ago, progesterone was found to be the main hormone

produced by the ovaries. Since it was necessary for fertility and for
maintaining a healthy pregnancy, it was called the
hormone," and its name sometimes leads people to think that it isn't
needed when you don't want to get pregnant. In fact , it is the most
protective hormone the body produces, and the large amounts that are
produced during pregnancy result from the developing baby's need for
protection from the stressful environment. Normally, the brain contains a
very high concentration of progesterone, reflecting its protective function
for that most important organ. The thymus gland, the key organ of our
immune system, is also profoundly dependent on progesterone_
In experiments, progesterone was found to be the basic hormone
of adaptation and of resistance to stress. The adrenal glands use it to
produce their hormones, and when there is enough
progesterone, they don't have to produce the potentially harmful
cortisone. In a progesterone deficiency, we produce too much cortisone,
and excessive cortisone causes osteoporosis, aging of the skin, damage to
brain cells, and the accumulation of fat , especially on the back and
abdomen .
Experiments have shown that progesterone relicves anxiety,
improves memory, protects brain cells, and even prcvents epileptic
seizu res. It promotes respiration, and has been used to correct
emphysema. In the circulatory system, it prevents bulging veins by
increasing the tone of blood vessels, and improves the efficiency of the
heart. It reverses many of the signs of aging in the skin, and promotes
healthy bone growth It can relieve many types of arthritis, and helps a
variety of immunological problems.
If progesterone is taken dissolved in vitamin E, it is absorbed very
efficiently, and distributed quickly 10 all of the tissues. If a woman has
ovaries, progesterone helps them to produce both progesterone and
estrogen as nceded, and also helps to restore normal functioning of the
thyroid and other glands_ If her ovaries have been removed, progesterone
should be taken consistently to replace the lost supply. A progesterone
deficiency has often been associated with increased susceptibility to
cancer, and progesterone has been lIsed to treat some types of cancer.
72
It is important to emphasize that progesterone is noi just the
hormone of pregnancy . To use it only "to protect the uterus" would be
like telling a man he doesn't need testosterone if he doesn't plan to father
children, except that progesterone is of far greater and more basic
significance than testosterone. While men do naturally produce
progesterone, and can sometimes benefit from using it, it is not a male
hormone. Some people get that impression, because some physicians
recommend combining estrogen with either testosterone or progesterone.
to protect against some of estrogen's side effects, but progesterone is the
body's natural complemcni to estrogen . Used alone, progesterone often
makes it unnecessary to use estrogen for hot flashes or insomnia, or other
symptoms of menopause.
When dissolved in vitamin E, progesterone begins entering the
blood stream almost as soon as it contacts any membrane. such as the
lips, tongue, gums, or palate, but when it is swallowed . it continues to be
absorbed as part of the digestive process. When taken with food. its
absorption occurs at the same rate as the digestion and absorption of the
food .
PREGNENOLONE
Pregnenolone, which is the raw material for producing many of

the hormones of stress and adaptation, was known as early as [934. but
for several years it was considered to be an "inert" substance. A reason
for this belief is that it was first tested on healthy young animals. Since
these animals were already producing large amounts of pregnenolone (in
the brain. adrenal glands, and gonads), additional pregnenolone had no
effect.
In the 1940s, pregnenolone was tested in people who were sick or
under stress, and it was found to have a widE' range of beneficial actions,
but the drug industry never had much interest in it. Its very generality
made it seem unlike a drug, and its natural occurrence made it impossible
to patent. Thus, many synthetic variants, each with a more specialized
action and some serious side effects, eame to be patented and promoted
for use in treating specific conditions. The dnlg companies created an
atmosphere in which many people felt that each disease should have a
drug, and each drug. a disease_ The side effects of some of those
synthetic hormones were so awful that many people carne to fear them _
For example, synthetic varieties of "cortisone" can destroy immunity. and
73
can cause osteoporosis, diabetes, and rapid aging, with loss of pigment in
the skin and hair, and extreme thinning of the skin .
Natural pregnenolone is present in young people of both sexes at
a very high concentration, and one rcason for the large amount produced
in youth is that it is one of our basic defenses against the harmful side
effects that an imbalance of even our natural hormones can produce. [n
excess, natural cortisone or estrogen can be dangerous. but when there is
an abundance of pregnenolone, their side effect s are prevented or
minimized.
In a healthy young person or animal. taking even a large dose of
pregnenolone has no hormone·like or drug-like action at aiL It is unique
in this way. But if the animal or person is under stress, and producing
more conisone than usual , taking pregnenolone causes the cortisone to
come down to the normal level. After the age of or 45. it seemS that
everyone lives in a state of continuous "stress," just as a normal part of
aging_ This coincides with the body's decreased abilit y to produce an
abundance of pregnenolone.
When aging rats are given a supplement of pregnenolone. it
immediately improves their memory and general performance. Human
studies, as early as the 1940s, have also demonstrated improvc_d
performance of ordinary tasks. It is now known that pregnenolone is one
of the major hormones in the brain . II is produced by certain brain cells.
as well as being absorbed into the brain from the blood . It protects brain
cells from injury caused by fatigue, and an adequate amount has a calming
effect on the emotions, which is part oflhe reason that it protects liS from
the stress response that leads 10 an excessive production of cOl1isone_
People feel a mood of resilience and an ability to confront challenges.
Many people have noticed that pregnenolone has a "tace-lifting"
action . This effect seems 10 be produced by improved circulation to the
skin, and by an actual contraction of some muscle-like cells in the skin _ A
similar effect can improve joint mobility in anhritis, tissue elasticity in {he
lungs. and even eyesight . Many studies have shown it to be protective of
"fibrous tissues" in general, and in this connection it \'1' 115 pro\'cn to
prevent the tumors that can be caused by estrogen_
Pregnenolone is largely converted into two other
"youth-associated" protective hormones. progesterone and DHEA . AI
the age of 30, both men and women produce roughly 30 10 50 mg. of
pregnenolone daily, When taken orally. even in the po\\dered fonn. il is
absorbed fairly well . One dose of approximately 300 mg (the size of an
aspirin tablet) keeps acting for about a week. as absorption continues
74
along the intestine, and as it is "recycled" in the body. Part of this long
lasting effect is because it improves the body's ability to produce its own
pregnenolone. It tends to improve function of the thyroid and other
glands, and this "normalizing" effect on the other glands helps 10 account
for its wide range of beneficial effects.
DHEA: ANOTHER YOUTH-ASSOCIATED HORMONE
DHEA (dehydroepiandrosterone) has a technical-sounding name

because it has never been identified with a single dominant function, in
spite of its abundance in the body. Many researchers still think of it as a
substance produced by the adrenal glands, but experiments show that
animals without adrenals are able to produce it in normal amounts. Much
of it is formed in the brain (from pregnenolone), but it is probably
produced in other organs, including the skin. The brain contains a much
higher concentration of DHEA than the blood does.
In old age, we produce only about 5% as much as we do in youth .
This is about the same decrease that occurs with progesterone and
pregnenolone. The other hormones (for example, cortisone) do not
decrease so much; as a result, our balance shifts continually during aging
toward dominance by hormones such as con isone, which use up more
and more body substance, without rebuilding it . Protection against the
toxic actions of these specialized honnones is a major function of DHEA
and the other youth-associated hormones.
For example, starvation, aging, and stress cause the skin to
become thin and fragile. An excess of cortisone--whether it is from
medical treatment, or from stress, aging, or malnutrition--does the same
thing. Material from the skin is dissolved to provide nutrition for the
more essential organs. Other organs, such as the muscles and bones,
dissolve more slowly, but just as destructively, under the continued
influence of cortisone. DHEA blocks these destructive effects of
cortisone, and actively restores the normal growth and repair processes 10
those organs, strengthening the skin and bones and other organs.
Stimulation of bone-growth by DHEA has been demonstrated ill pi/to (in
laboratory tests). and it has been used to relieve many symptoms caused
by osteoporosis and arthritis, even when applied topically in an oily
solution.
Estrogen is known to produce a great variety of immunological
defects, and DHEA, apparently by its balancing and restorative actions, is
75
able to correct some of those immunological defects, including some
"autoimmune" diseases.
It is established that DHEA protects against cancer, but it isn't yet
understood how it does this. It appears to protect against the toxic
cancer-producing effects of excess estrogen, but its anti-cancer properties
probably involve many other functions.
Diabetes can be produced experimentally by certain poisons which
kill the insulin-producing cells in the pancreas. Rabbit s were
experimentally made diabetic, and when treated with DHEA their diabetes
was cured. It was found thaI the insulin-producing cells had regenerated .
Many people with diabetes have used brewer's yeast and DHEA to
improve their sugar metabolism. In diabetes, very little sugar enters the
cells, so fatigue is a problem. DHEA stimulates cells to absorb sugar and
to burn it, so it increases our general energy level and helps to prevent
obesity.
Young people produce about 12 to 15 milligrams ofDHEA per
day. and that amount decreases by about 2 mg. per day for every decade
after the age of30. This is one of the reasons that young people eat more
without getting fat , and tolerate cold weather better: DHEA, like the
thyroid honnone, increases our heat production and ability 10 bum
calories. At the age of 50, about 4 mg. of DHEA per day will usually
restore the level ofDHEA in the blood to a youthful level. It is important
to avoid taking more than needed, since some people (especially if they
are deficient in progesterone, pregnenolone, or thyroid) can turn the
excess into estrogen or testosterone, and large amounts of those sex
hormones can disturb the function of the thymus gland and the liver.
76
11
THYROID
Measuring the amount of thyroid in the blood isn't a good way to
evaluate adequacy of thyroid function, since the response of tissues to the
honnone can be suppressed (for example, by unsaturated fats) ,
In the 19305 accurate diagnosis was made by evaluating a variety
of indications, including basal oxygen consumption, serum cholesterol
level, pulse rate, temperature, carotenemia, bowel function, and quality of
hair and skin. A good estimate can be made using only the temperature
and pulse rate. (Pul se rate should be thought of as an indicator of the
rate of blood circulation, meaning that the strength of the pulse should
increase with the rate; a rapid but weak, shock*like pulse gives useful
information, but has a different meaning.)
Oral or armpit temperature, in the morning before getting out of
bed, should be around 98 degrees F. and it should rise to 98.6° by
mid-morning. This is not valid if you sleep under an electric blanket, or if
the weather is hot and humid. A person who is hypothyroid produces
heat at a low rate, but doesn't lose it at the normal rate, since there is less
sweating, and the skin is relatively cool. Many hypothyroid people
compensate with high adrenalin production (sometimes 40 times higher
than normal), and this tends to keep the skin cool, especially on the
hands, feet, and nose. The high adrenalin is the consequence of low
blood glucose, so a feeding of carbohydrate, such as a glass of orange
juice, will sometimes lower the pulse rate momentarily Since thyroid is
essential for producing progesterone, and progesterone is "thermogenic"
in the sense of setting the temperature control system higher, the body
sometimes maintains a subnormal temperature even in wann weather,
Healthy populations have an average resting pulse rate of about 85 per
minute. Especially in hot weather it is useful to consider both
temperature and pulse rate.
The Achilles tendon reflex is another quick way to estimate
thyroid function . This reflex is used because of the insignificant weight of
the toes in relation to contraction of the gastrocnemius muscle. The T
(repolarization) wave o n the electrocardiogram is a similar indicator of
the rate of energy production. Thumping the Achilles tendon causes the
muscle to contract (unless it is already in a semi·contracted state, which
isn't uncommon). The contraction consumes energy, and the muscle can't
relax until enough energy has been produced to restore the threshold and
77
the readiness for a new contraction , (Creatinine levels are a vague
indicator of the activity of this system, and are often a little low in
hypothyroidism.)
If energy production is efficient, relaxation is faster than the
passive return motion of the foot, so the foot swings freely back to its
original position, and over·shoots slightly, causing a slight swinging
action . In hypothyroidism, the foot returns as if controlled by a
pneumatic door-closer, and settles slowly and precisely into its relaxed
position, sometimes with a hesitating, intermittent motion . This slow
replenishment of energy, and slow relaxation, can cause muscles to cramp
easily. The aching leg muscles of children at the end of an active day are
often a sign of hypothyroidism, and sometimes the gastrocnemius muscle
become vel)' swollen and hypertrophied in hypothyroid children. The
same process, of slow energy regeneration, can cause rhythm disturbance
in the heart, and often causes insomnia and restless sleep .
The thyroid gland secretes about 3 parts of thyroxin to one part of
triiodothyronine, and this allows the liver to regulate thyroid function , by
converting more of the T4 to tile active T J when there is an abundance of
energy. Glucose is essential for the conversion, so during fasting there is
a sharp decrease ;n metabolic rate, and in experiments, 200 or 300
calories of carbohydrates can be added to the diet without causing fat
storage.
When the liver is the main cause of hypothyroidism, your
temperature (and especially the temperature of your nose, hands and feet)
will fall when you are hungry, and will rise when you eat carbohydrates.
If a hypothyroid person has a very slow pulse, and feels lethargic, it seems
that there is little adrenalin; in this case, a feeding of carbohydrate is likely
to increase both the pulse rate and the temperature, as the liver is
permitted to form the active T:; hormone.
Women often have above-average thyroxin, with symptoms of
hypothyroidism. This is apparently because it isn't being converted to the
active form (TJ Before using a Cytomel (T,) supplement, it might be
possible to solve the problem with diet alone. A piece of fmit or a glass
of juice or milk between meals, and adequate animal protein (or potato
protein) in the diet is sometimes enough to allow the liver to produce the
hormone . If Cytorne[ is used, it is efticient to approximate the
physiological rate of T , formation, by nibbling one ( J 0 or 15 meg.) tablet
during the day. When a large amount is taken at one time, the liver is
likely to convert much of it to the inactive reverse-T., form, in a norma!
defensive response.
78
Women normally have less active livers than men do. Estrogen
can have a directly toxic effect on the liver, but the normal reason for the
difference is probably that temperature and thyroid function strongly
influence the liver, and are generally lower in women than in men.
Estrogen inhibits the secretion of hormone by the thyroid gland itself,
probably by inhibiting the proteolytic enzyme which dissolves the colloid.
Progesterone has the opposite effect, promoting the release of the
hormones from the gland . AI puberty, in pregnancy, and at menopause,
the thyroid gland often enlarges, probably as a result of estrogen
dominance.
Thyroid function stimulates the liver to inactivate estrogen for
secretion, so estrogen dominance can create a vicious circle, in which
excess estrogen (or deficient progesterone) blocks thyroid secretion,
causing the liver to allow estrogen to accumulate to even higher levels.
Progesterone (even one dose, in some cases) can break the cycle.
However, if the gland is very big, the person can experience a few months
of hyperthyroidism, as the gland returns to normal. It is better to allow
the enlarged gland to shrink morc slowly by using a thyroid supplement.
If an enlarged gland does begin to secrete too much thyroid hormone, it
can be controlled with tablets of propylthiouracil, or even with raw
cabbage or cabbage juice, and cysteine-rich meats, including liver.
Besides fasting, or chronic protein deficiency, the common causes
of hypothyroidism are excessive stress or "aerobic" (i .e., anaerobic)
exercise, and diets containing beans, lentils, nuts. unsaturated fats
(including carotene), and undercooked broccoli, cauliflower, cabbage, or
mustard greens. Many health conscious people become hypothyroid with
a synergistic program of undercooked vegetables, legumes instead of
animal proteins, oils instead of butter, carotene instead of vitamin A, and
breathless exercise instead of a stimulating life.
A good diet, plus a supplement of either thyroid or progesterone,
can olien break the cycle of hormonal imbalance.
If a person has at least a normal level of cholesterol, it is very
likely that a progesterone deficiency can be corrected by normalizing thc
thyroid function, since thyroid, vitamin A, and cholesterol are the main
factors in the synthesis of progesterone. If the problem is that the ratio of
estrogen to progesterone is too high. though progestcrone might itself be
at a reasonable level, thyroid becomes crucial, 10 bring the estrogen level
down to normal. In hypothyroidism there is a tendency to develop cystic
ovaries, and low thyroid nmclion normally leads to estrogen dominance,
even if the ovaries seem normal.
79
12
PROGESTERONE'S BIOLOGICAL
GENERALITY
t. Intrinsic general properties.
All of the steroid functions, except those of estrogen and
testosterone, are included , though weakly, in the progesterone molecule
itself. These include lysosome stabilization, salt regulation, blood sugar
elevation, and anesthesia (or, in physiological amounts, modulation of
nerve functions). It is unusual among the steroids in promoting
enlargement, rather than atrophy, of the thymus gland . Progesterone, like
testosterone is anti·estrogenic.
A weak hormone activity in the absence of the stronger hormone
will act as a substitute, but in the presence of the stronger hom10ne will
weaken the strong hormone's effect by competition or "ditution" at the
point of action, and possibly by suppressi ng the trophic pitu it ary agent
which regulates synthesis. By thus opposing both deficiencies and
excesses, such a hormone wil! tend to protect against pathological
extremes. There is, for example, supposed to be competition bel\veen
progesterone and aldosterone for the "aldosterone receptors" which cause
water retention by the kidneys, so that in many situations, progesterone
will relieve edema; but when the adrena l cortex is removed or fails to
function (as in Addison's disease), progesterone will promote relatively
normal retention of sodium and water, keeping the individual alive as long
as large doses are given regularly.
Some hormones which are both progestins and anti-testosterones
seem to work both at the tissue "receptor" level, and at the pituitary level.
Though progesterone itself will suppress menopausal pituitary
gonadotrophins, and (my observations) reduces excessive facial hair, it
has nOI been found to have anti-testosterone effects in men when used in
low doses, and in appropriate doses it can improve sexual functions in
some impotent men who are deficient in progesterone. Pregnenolone
(produced from cholesterol in the mitochondria), which is the precursor
to progesterone and other steroids. has been used successfully to restore
fertility (sperm count and motility, and, according to the wives·-libido) in
men.
80
All of the natural steroids have functions that overlap to some
extent--e.g" testosterone has some progestational functio n--but
progesterone's generality is the most remarkable.
2. Steroid precursor fun ction.
The second aspect of progesterone's biological generality, besides

its intrinsic hormonal activity, is its role as precursor for all of the other
steroid hormones (see chart). When consumed in food (e.g., butter,
brains, milk, ovaries--some cultures cat pork ovaries, many cal sea-urchin
ovaries), it, like cholesterol, only morc efficiently, enters the cycle of
steroid synthesis ncar the beginning, so that it is a raw material, allowing
normal amounts of the other hormones to be produced . This aspect of
progesterone distinguishes it most strongly from the other progeslins
(e,g" medroxyprogesterone), which have had atoms introduced al
unusual positions to inhibit metabolism and prolong activity (as weI! as to
create a patentable and thus highly profitable substance). When we eat
protein, we support the production of all the peptide hormones; likewise,
natural progesterone (and pregnenolone, which is also found in brains,
endocrine glands, and probably skin) serves to allow the body to produce
an appropriate and balanced amount of all the other steroid hormones.
3. Anti-estrogen fun ctions.
A third aspect of progesterone's generality is a little less clear than

its intrinsic generality and its function as a general steroid precursor,
because this third form has to do with its overall antagonism to estrogen,
and gains significance only to the extent that we sec estrogen as havi ng a
very broad physiological role--for males as well as for females. 1 wil! just
mention some of the many effects of estrogen, and some reasons for its
ubiquity .
Estrogen causes water retention, even when dietary salt is restricted:

hyposmotic blood has been ubserved under estrogen influence.
Estrogen causes "erasure" of memory, as docs prolactin, which is formed
under the influence of estrogen_
Estrogell promotes the formation of prolactin, which normally increases
with aging and s!ress, and which is a known contributor to osteoporosis.
81
Estrogen causes hypoxia at many levels--pulmonary diffusion,
intracellular metabolism, and various points between .
Estrogen synergizes with insulin, lowering blood sugar, promoting fat
synthesis.
Estrogen opposes actions arthyroxin, elevates the bound proportion, and
blocks its secretion from the gland.
Estrogen causes reproductive aging, by exhausting neurons which
regulate the pituitary.
Estrogen contributes to the risk of miscarriage and infertility_
Estrogen retards prenatal brain growth.
Estrogen promotes histamine release.
Estrogen shifts the balance of prostaglandins and cyclic nucleotides,
impOitant cellular regulators.
Estrogen and its metabolites are carcinogenic, in every sense oflhe word.
Estrogen promotes development of fibroids and many other kinds of
tumor, including pituitary prolactin-secreting tumor.
Estrogen promotes blood clotting and increases embolism incidence.
Estrogen synergizes with adrenaline in causing vascular spasm.
Estrogen atters blood lipids and promotes galt bladder disease.
Estrogen accelerates the aging of cotlagen.
Estrogfn mimics the shock phase of the stress reaction.
Estrogen is produced by many tissues--possibly by every tissue under
certain circumstances. Stress hormones promote liver synthesis of
estrogen .
Estrogen lowers the seizure threshold of nerve cells, increasing
susceptibility to epileptic convulsions.
Estrogen shrinks the thymus, and contributes to many auto-immune
conditions and tissue alterations including osteoarthritis.
Men and women, especially as they age, are susceptible to liver damage
from toxins which can cause elevated estrogen levels by interfering with
metabolism and excretion.
Malnutrition can cause signs of high estrogen.
Various physical factors, including ionizing radiation, mimic estrogen
actions.
Many environmental pollutants--phenolic compounds, dioxins, PCBs,
polycyclic hydrocarbons, chlorinated hydrocarbons, DDT, etc.--are
estrogenic.
Estrogen promotes the n;.tention of iron, which accumulates with aging
and promotes the free-radical damage caused by stress.
82
In relating progesterone's effects to those of estrogen, we should

avoid being misled by the opinions expressed in many textbooks,
describing symptoms of the luteal phase of the menstrual cycle as
symptoms "caused by progesterone." For example. many medical books
promote the erroneous idea that progesterone causes edema, because
edema often occurs during the luteal phase of the cycle, which is too
often conceptualized as "the progesterone dominance phase," Actually.
is the time when the estrogen/progesterone ratio frequently reaches
its pathological height, for four common reasons:
1. failure to eliminate estrogen;

2. failure to produce enough progesterone;
3. overproduction of estrogen;
4. excessive metabolism of progesterone.
Failure of the liver to metabolize or detoxify estrogen is equivalent

to the older idea of an "elevated kidney threshold for estrogen," which
was proposed as the cause of the "pre-menstrual syndrome. "I Probably
the main for liver sluggishness (lI.pll.rt from the direct action of
estrogen itself, discussed in liver monographs, and often noticed in the
post-ovulatory increase of susceptibility to intoxication by alcohol or
other chemicals) is low thyroid, which itself is related to estrogen--about
five times more women have thyroid abnormalities than men. Protein
deficiency has been shown to cause the liver to fail to detoxify estrogen. 2
Thyroid therapy nonnally increases assimilation of nutrients and
stimulates synthesis of steroids though it lowers estrogen by promoting its
metabolism in the liver. However, it increases metabolic activity
systemically and can exacerbate a nutritional deficiency or a failure of
steroidogenic tissue, so thyroid therapy should always be accompanied by
nutritional optimization, and sometimes should be used with a steroid,
preferably progesterone, to promote adrenal and other glandular function .
Thyroid honnone is one of the essential factors for the conversion of
cholesterol to progesterone. Progesterone promotes its own synthesis,
and provides stability during adaptation.
Failure of the corpus luteum to produce adequate quantities of
progesterone has been observed under various circumstances. A lack of
vitamin and reduced circulation resulting from the prostaglandin F1
(resulting from estrogen action, or from uterine irritation) have been
proposed as causes of luteal failure. ) There is no doubt that vitamin A is
83
essential for the conversion of cholesterol to progesterone; its action can
be competitively blocked by an excess of carotene. Luteolysis has been
demonstrated to result from uterine irritation by a foreign object.4 A
uterine infection probably would have the same effect. (Penicillin has
been found to relieve PMS, but the mechanism by which it increases
progesterone and decreases estrogen and cortisone isn't clear, and
probably involves endotoxin and the liver.) The IUD often causes the
same kind of symptoms as the oral contraceptive pill··obesity, depression,
etc., and this seems to be the result of progesterone deficiency from
\uteolysis. An excess ofproiactin, which is now recognized as a sequel to
use of the estrogen contraceptive pill (estrogen induces mitoses in the
prolactin secreting pituitary cells) has been found to block progesterone
synthesis. (Incidentally, Korenchevsky demonstrated 50 years ago that
progesterone would cause regression of the estrogen-induced pituitary
tumor.) Logically, since it isn't desirable to get pregnant during stress,
the stress honnones ACTH and cortisone inhibit progesterone
production . Lack of sunlight , short photoperiod, or staying indoors can
probably contribute to a progesterone deficiency, since both progesterone
and testosterone synthesis (the latter in men) are increased in summer.
Excessive production of estrogen can result from a large mass of
adipose tissue, or from a sick liver.3 Olfactory stimuli seem to increase
estrogen production in female mice, sufficient to induce spontaneous
abortion; pheromonal activation of estrogen synthesis in humans might be
another possible cau'se of estrogen excess.'; Stress is probably a common
cause of elevated estrogen especially when it is prolonged enough to
cause significant protein loss. Stress also stimulates liver estrogen
synthesis_7
Excessive metabolism of progesterone, e.g., by its conversion to
cortisol and other anti-stress hormones, can probably explain the
increasingly common observations of "athlete's amenorrhea" and the
development of excess facial hair in some women working under pressure
(the alternate honnonal disturbance in stress appears to result in obesity) .'
Besides losing the effects of progesterone on the endometrium, pituitary
gonadotrophins would be increased, and would drive various synthetic
pathways at a higher rate, shifting the ratio of progesterone to other
hormones, but I do not think the ovaries have been studied very much
during ordinary stress. (In the stress of ionizing radiation, the ovaries
produce excessive estrogen; with the stress of high levels of
gonadotrophins, they tend to be cancerized.) While large doses of
progesterone have been shown to have anti-stress effects without hanning
84
the adrenals (and probably protecting them, by lowering the demand for
adrenal hormones), large doses of estrogen were found to destroy certain
areas of the adrenal cortex,? possibly in a reaction similar to luteolysis by
estrogen.
4. Effects on development.
The three aspects of progesterone's biological generality discussed

above disregard the time dimension, i.c., the effect of progesterone on the
developing organism, which is, according to popular belief (deriving
largely from its name), its only role. All of the points discussed above are
relevant to the developing organism . For example, the fetus is highly
dependent on glucose for growth--especially brain growth--and the
oxygen supply and maternal metabolism both affect Ihe glucose supply.
Animal studies have shown that an excess of estrogen, late in the
gestation period, like oxygen deprivation and insulin-induced
hypoglycemia, can cause brain damage, in the form of reduced cel!
number and brain weight. Stress during can produce
(apparently hormonal) defects in the offspring.!O L. C. Strong showed
transgenerational effects, apparently acting through hormone balance, in
his cancer-prone (high-estrogen) mice which were treated with a liver
extract (personal communication). Many older studies showed
transgenerationai effects which I believe can be traced to gestational
hormonal modification, affecting metabplism at a variety of levels,
including the liver. For example, feeding thymus to rats for several
generations caused each generation to be more precocious in
development . The known transgenerational influences of starvation
(Zamenhoff, et a\.,11 with rats, and more recently--1978--in human studies)
are similar to the first generation effects of estrogen or hypoglycemia. I
suspect that these effects are part of a general system of physiologically
adjusting the metabolism of offspring to the availability of nutrients.
One of the physiological effects of progesterone is its suppon of
the thymus (opposing the effects of glucocorticoids and sex steroids). In
animal experiments (dog and rat), results so far indicate that the same
types of precocity are induced by progesterone in these animals as were
reponed for thymus feeding .u Dalton's (and others') studies in humans
show the same generalized precocity, e..xcept that in humans the
intellectual precocity is the most noticeable. Rat studies show that
increased prenatal exposure to progesterone increases rats' learning ability
and the thickness of their cerebral cortex, bUI the scientific community's
85
lack of interest in these studies has been great The owner of an afghan
dog which gestated with extra progesterone commented that the dog had
learned to retrieve a stick by watching another dog, while "normal"
afghans dislike learning anything, especially retrieving (though they have a
remarkable geographic memory).
Since the brain is dependent on glucose for its growth, the ability
of progesterone to promote maternal fat metabolism and to spare glucose
(elevating blood glucose) for fetal use is a logical part of its role as a
gestational hormone. Other pregnancy hormones, including "placental
lactogen," also promote elevation of blood glucose.
I propose that there is a "developmental trajectory" (analogous to
a ballistic trajectory) which is set by the availability of biological energy
during gestation, and that we could. by measuring brain weight and the
ratio of brain weight to body weight during gestation, predi¥t (given
stable post·natal conditions for growth) such things as the ages at
puberty, full growth, and approximate lifespan . Good prenatal conditions
would increase the rate of development (IQ, etc.), but would delay
maturity, allowing achievement of a higher level of development by the
rapid and prolonged development of higher abilities. Bright people
develop faster Ihan dul! people, but bright monkeys, at first. develop even
faster (see chart). Our species characteristics would include setting the
angle of our developmental trajectory, but the availability of biological
energy during gestation determines the rate of ascent and the "altitude"
achieved, as the explosive charge determines velocity and altitude of a
ballistic trajectory. The effect of nutrition on brain size is known, as are
the relationships between relative brain weight and and
between rate of sexual development and life· span (Strong, and others), so
what I am suggesting is simply that the amount of energy early in life
might organize in an orderly way the liming of, and quality of,
development throughout the rest of one's life.
A "Medical News" item in a 1976 issue of the J.A.M.A.14 reports
a study showing that progesterone probably plays a critical role in
preventing rejection of the fetus by the mother. In reviewing the scientific
and medical literature, I have found no side effects attributed to natural
progesterone, except for sometimes altering the menstrual rhythm
temporarily. Its use before and during pregnancy is associated with a
reduced incidence of birth defects. (Since all of the drugs used to treat
epilepsy are known to cause birth defects, it would certainly seem
reasonable to take advantage of progesterone's anti·seizure effect,
especially during pregnancy. It wouldn't be hard to ascribe liability for
86
the prenatal injury of thousands ofpeopJe, to the pharmaceutical industry
and regulatory agencies, who seem to conspire to keep this information
away from the medical profession.) Some publications fail to distinguish
between natural progesterone and the frequently harmful synthetic
progestins.
Some recent animal studies are showing that prenatal
progesterone increased body size, but even more, it increased brain size,
for an improved brainlbody ratio. First, it was established that good
prenatal nutrition produced big, healthy babies with big heads, high
intelligence, and good disposition. Then, experiments with rats showed
that prenatal treatment with prolactin, which stimulates progesterone
synthesis in that species (but blocks it in humans) produced large brained,
intelligent animals (95th percentile for brain size and intelligence). It has
since been established that a large brain is associated with a long life span .
Prenatal stress produces many minor physical "stigmata," and
these have been shown to be associated with hyperactivity. Excess
estrogen (and other toxins, and associated deficiencies) reduces brain size
and damages behavior. (In animals, the effects of prenatal stress can be
passed on to the third generation.)
Progesterone opposes estrogen, and promotes. prenat(ll nutrition.
Dalton's studies of babies whose mothers received natural progesterone
showed greatly improved intelligence. U Another researcher, deliberately
attempting to improve intelligence (Dalton simply intended to treat PMS
and toxemia of pregnancy) claims "his" babies have a 200 IQ. Other
investigators find that progesterone babies have strong, serene,
independent characters.
There is increasing recognition that prenatal conditions, whether
good or bad, can be passed on to at least one subsequent generation. A
reduced ability to produce progesterone is probably often a consequence
of prenatal stress, which can lead to pregnancy difficulties, and another
stress-injured generation. I feel that progesterone can reverse the trend
toward more hyperactive and brain damaged children, and that it can
make a great contribution to the mental and physical health of future
generations.
5. Progesterone and magnesium .
In considering the general biological effects of progesterone, it is

interesting 10 compare some of its functions with those of the magnesium
ion, and to contrast them with the effects of calcium and estrogen.16
87
Uptake of magnesium is promoted by thyroid, and progesterone promotes
thyroid fhnction, while tending to block the stress-induced loss of
magnesium. Estrogen increases the uptake of calcium.
Blood clotting (especially excessive): promoted by estrogen and calcium,

restrained by magnesium and progesterone.
Blood sugar: depressed by estrogen and calcium, sustained by
progesterone and magnesium .
Kidn ey fun ction, diuresis: promoted by magnesium and progesterone,
decreased by estrogen; excess calcium appears to damage kidneys.
Hist amine release: decreased by progesterone and magnesium, increased
by estrogen, and calcium probably facilitates it.
Phagocytosis a nd other immune fun ctions: increased by magnesium
and progesterone, decreased by estrogen; calcium is involved in t riggering
thymocyte death.
G lucagon: magnesium promotes, calcium inhibits.
Insulin: magnesium and progesterone restrain its secretion, calcium and
estrogen promote it.
Vascular spasms: decreased by progesterone and magnesium, promoted
by estrogen and calcium.
Vascular ton e: stabilized by progesterone and magnesium, often
decreased by estrogen, possibly acting through histamine, leading to the
tendency of blood to pool in the legs. Estrogen is believed to contribute
to varicose veins.
Nerve stabilization or anesthesif! : magnesium and progesterone are
anesthetic in very large amounts and are protective inhibitors in
physiological amounts. Calcium ' pposes the anesthetic effect of
magnesium, and is always involved in toxic or excitotoxic cell death.
Estrogen even in physiological amounts is nerve-exciting, and eventually
contributes to the excitotoxic death of brain cells.
Hans Selye demonstrated that calcification of various tissues
(kidneys, blood vessels, and skin, for example) could be produced by
interactions of stress and hormones. Selye and his associates, and F. Z.
Meerson's group in Russia, have demonstrated numerous toxic
interactions of iron, calcium, and unsaturated fats. Magnesium, vitamin
E, thyroid, and progesterone tend to protect against those toxic effects.
88
REFERENCES
I. DaUon. The I'r<!IIIt'lIslnw{ Sy",fr",,,t' <IIuf PrGgeslerum- TIIC'm py. Year Buok
Medical Puhlishers.IIIC .. Chkasu, 1977.
2. Alc){:mdcr Lipsdmtt. SI<'roiJ I/urll/O""S alld "fill/lOr.<. ;'011 Wilkins Company.
llallimorc,
3. COJlstaO<.:c Marl in. 1".Ylf,uok 4 P"'/<Jt"rine Physiology. Oxfurd l)nivt-...sil y !'res.... 1976.
4. S. N. Chal1crjce. ;:1 al.. "En,:cl of intrauterine conlr:<ccl'live sUlure on corpora lutea of
(jui!)"" pigs," II/diull JOIm,," 'if Rxperi"Il'II(<<1 Bi"f,1gj' 9.- 105, 1971.
5. J. M. (in,din. e\ aL "Origin (If CStrug..11 in the J. <ifOillioll "",Joe rjllofoX)'
allel M<!I<I/mlistII .l6( 2): I '>73.
6. C . n. Turner 1Imi J; T . fbgnara. Gel/<-{II{ Elldocriuology. SHumlcn; Publishing \0 ., 1971 .
7. C. Martin. 01". cil. p'lfI,e Ss.
8. MOII,,:r Jones MaR".;"'" 1978.
9. D. 1. Kimddorfand A. I., So(lo:rwall. "Changes in the adrenal enr1ical ZOlles hy ovari,tIl
bonnones:' EII(t.)( ·I·;I1,n"XJ· 4/( I): 21 -26.
IO. L. R.. fkrrcnkohl. Psyehol"gy ])epartment. Temple 11niycrsity.
I L S. Zal1\enbolT. ct al.. "DNA (cdl numhcr) and protein in neonatal rat brain: ,1 lh:ration by
timing or maternal ,Iidary protein J . of Nutrit ion 10 I: 1265_1270. 197 1.
12. Ciha Foundation S}1np""illlll. The ThyllIllS. Ev,,'rim('nl,,1 lind Clinic"l Sflldil's. Mdhoumo:.
1975.
D. G. A. "Molc.:ular wrsus systelll ic theories on the go:ncsis "r aging," E-rperillll'lII,t/
Gemnlology .1: 2OS. 1968.
14, J. oJlhe Allier. M.:di,."l AssOt!. JJI\(R): 905. August 23, 1976.
15. K. Dallon. or. cit.. chapter XVI!.
16. Ilans $ely.." Hnt:yrIOfl.:di" "J ElldQ("riIlO/"g)' \·o/s. 1-4. Fran ks !>Ublishing Cu.. Montreal.
194 3.
17. R. P<:-at, NII/rili<m for W(llIIl'n . make ('<,Uege . EugcDI:. Oreg,'Il. 1978.
89
13
DOSAGE OF PROGESTERONE
Since progesterone has nonc of the harmflll side effects of other
hormones (except for alteration orthe menstrual cycle ifil is taken at the
wrong time of month), the basic procedure should be to usc it in sutlicient
quantity to make the symptoms disappear, and to time its use so that
menstrual cycles are not disrupted. This normally means using it only
bet ween ovulation and menstruation unless symptoms are suffi ciently
serious that a missed period is not imponanl. The basic idea of giving
enough to stop the symptoms can be refined by some information on a
few of the factors that condition the need for progesterone.
If a person has an enlarged thyroid gland, progesterone promotes
secretion and unloading of the stored "colloid," and can bring on a
temporary hyperthyroid state. This is a corrective process, and in itself
isn't harmfuL A thyroid supplement should be used to shrink the goiter
before progesterone is given . Normal amounts of progesterone facilitate
thyroid secretion, while a deficiency, with unopposed estrogen, causes the
thyroid to enlarge_ The production of euphoria has been mentioned as a
side effect, but I think euphoria is simply an indication of a good
physiological state. Very large doses that are given in vitamin E solution,
allowing complete absorption, can reach the level that is sometimes
achieved late in pregnancy, producing both euphoria and a degree of
anesthesia. To avoid unexpected anesthesia, the correct dose should be
determined by taking about 10 mg. at a time, allowing it to spread into
the membranes of the mouth, and repeating the dose after 10 minutes
until the symptoms are controlled_
An excessive estrogen/progesterone ratio is more generally
involved in producing or aggravating symptoms than either a simple
excess of estrogen or a deticiency of progesterone, but even this ratio is
conditioned by other factors, including age, diet, other steroids, thyroid,
and other hormones. The relative estrogen excess seems to act by
producing tissue hypoxia (as reported in my dissertation, University of
Oregon, 1972), and this is the result of changes induced by estrogen in
alveolar diffusion, peripheral vascular changes, and intracellular oxygen
wastage.
Hypoxia in turn produces edema (as can be observed in the cornea
when it is deprived of oxygen, as by a contact lens) and hypoglycemia
(e.g ., diminished ATP acts like insulin), because glycolysis must increase
90
greatly for even a small deficiency of oxygen. Elevated blood lactic acid
is one sign of tissue hypoxia. Edema, hypoglycemia, and lactic acidemia
can also be produced by other "respiratory" defects, including
hypothyroidism, in which the tissue does not use enough oxygen . In
hypoxia, the skin will be bluer (in thin places, such as around the eyes),
than when low oxygen consumption is the main problem . Low thyroid is
one cause of excess estrogen, and when high estrogen is combined with
low thyroid, the skin looks relatively bloodless.
Symptoms in cycling women are most common around ovulation
and in the premenstrual week, when the estrogen/progesterone ratio is
normally highest. At puberty, in the early twenties and in the late thirties
and menopause are the ages when the ratio is most often disturbed--and
these are also the ages when thyroid disorders are commonest in women.
The individual who suffers from one aspect of the progesterone
(andlor thyroid) deficiency will tend to develop other problems at
different times_ With cyclic depressions or migraine headaches at age 22,
there will possibly be breast disease later, and often there will be problems
with pregnancy. These people with a history of severe symptoms are the
ones most likely to have severe problems around menopause. Prenatal
exposure to poorly balanced homlones seems to predispose the child to
later hormone problems. .
Excess stress (which can block progesterone synthesis and elevate
estrogen) may bring on symptoms in someone who never had them.
Spending a summer in Alaska, with an unusually long day, may relieve the
symptoms of a chronic sufferer. Dark cloudy winters in England or the
Pacific Northwest are powerful stressors, and cause lower production of
progesterone in women, and testosterone in men. Toxins can produce
similar symptoms, as can nutritional deficiencies. A very common cause
of an estrogen excess is a dietary protein deficiency--the liver simply
cannot detoxify estrogen when it is under-nourished.
With a diet high in protein (e.g., 70- 100 grams per day, including
eggs) and vitamin A (not carotene), I have found that the dose of
progesterone can be reduced each month. Using thyroid will usually
reduce the amount of progesterone needed. Occasionally, a woman won't
feel any effect even from 100 mg. of progesterone; r think this indicates
that they need to use thyroid and diet, to normalize their estrogen,
prolactin, and cortisol.
Progesterone stimulates the ovaries and adrenals to produce
progesterone, and it also activates the thyroid, so one dose can sometimes
have prolonged effects. It shouldn't be necessary to keep using
91
progesterone indefinitely, unless the ovaries have been removed. In
slender post-menopausal women, 10 mg. per day is usually enough to
prevent progesterone deficiency symptoms.
In a 10% solution of progesterone in vitamin E, one drop contains
about three milligrams of progesterone. Normally, the body produces 10
to 20 milligrams per day. A dose of 3 or 4 drops usualJy brings the blood
levels up to the normal range, but this dose can be repeated several limes
during the day if it is needed to control symptoms.
For genera! purposes, it is most economical and effective to take
progesterone dissolved in vitamin E orally, for example taking a few
drops on the lips and tongue, or rubbing it into the gums. (It is good for
the general health of the gums.) These membranes are very thin, and the
progesterone quickly enters the blood. When it is swallowed, the vitamin
E allows it to be absorbt..'<i through the walls of the stomach and intestine,
and it can be assimilated along with food, in the chytomicrons, permitting
it to circulate in the blood to all of the organs before being processed by
the liver. These droplets are smaller than red blood cells, and some
physicians seem to forget that red blood cells pass freely through the
liver.
For the topical treatment of sun damaged skin, or acne, wrinkles,
etc. , the oil can be applied directly to the affected area.
For topical treatment of arthritis, osteoporosis, tendinitis, bursitis,
or varicose veins, to speed absorption it is best to apply a few drops of
olive oil to the area, and then to rub the progesterone-vitamin E solution
into and around the affected area. Some of the progesterone will be
absorbed systemically, but the highest concentration is sustained in the
local area, helping to correct the problem locally.
REFERENCES
I. Kalharillu Dullon, Pmllmsrnw/ .\)1Idrome 1111</ Progesreroll<' nreropy. Ycar !look Medical
Inc. , Chkngo, 1977.
2. Alexander Lipschutz, Steroid 1/017111:»1('.5 III/d r llmol"$. mId WiU;clls Compa ny,
Baltimore, 1950.
3. R. F. Peat, Nlltrition fi)I" H·omen, Illll.'I1IIllional College. 1992.
4. R. F. Peat, Age Udal ...1 Oxilimil'(1 C/ulIIges ill Ihe 1/('"1$/<'1" {hems. Univ<:rsilY of Oregon
Ihcsis, Eugt.'1lc, Orcgon, 1972.
92
14
AN EFFICIENT ORAL THERAPY
As early as 1912, Armour & Co. sold desiccated corpus luteum
for use in cases of ovarian failure, and said that it prevented "nervous
symptoms accompanying" menstrual abnonnalities. 1 It was also used to
treat obesity and other physical conditions sometimes associated with
"ovarian deficiency."
In early reports on the use of synthetic progestins, they were
praised as being active when taken orally, unlike natural progesterone,
which was said to be "destroyed in the stomach ." Although I have looked
carefully, I have never found the study which demonstrated that
progesterone was inactive when taken orally. No source was cited for the
claim. I am convinced that the idea was invented by the promoters of the
patented new compounds. The most "popular" (i.e. , profitable) of the
synthetic "progestins," medroxyprogesterone acetate, is not a
progestagen, causes cancer, impairs circulation to the heart, causes birth
defects, and suppresses the production of progesterone. I feel that the
involvement of the various government agencies in the promotion of this
poison, and the suppression of information about natural progesterone,
has been conspiratorial and deliberately criminal, and those involved
should be identified as criminals.
When fats are eaten, they are almost 100% absorbed by the small
intestine. They break up in the intestine into mkroscopic droplets, called
chylomicrons, and reach the general circulation in that fonn . If
progesterone is perfectly dissolved in oil, it is absorbed in that way, and is
not immediately exposed to enzymes in the wall of the intestine or in the
liver. People often speak of "avoiding the liver on the first pass," but in
fact chylomicrons pass through the liver many times before they are
destroyed; after an hour, at least 10% of the chylomicrons are still
circulating.
While dissolved progesterone circulates in the chylomicrons, it
will be distributed to the various tissues. Unlike other steroid hormones,
progesterone tends to become concentrated inside cells. Its concentration
in red blood cells is twice as high as its concentration in serum/ and the
brain contains a still higher concentration. These intracellular reservoirs
of progesterone prolong the elevated blood levels, so that the observed
hormone level after a single oral dose is much more stable than are the
triglyceride levels after a fatty meal . The perfect absorption, and the
93
prolonged action make the oil-dissolved Ofa! progesterone much more
etlicient and economical than injected or suppository forms.
Since progesterone tends to promote its own synthesis, it
shouldn't be necessary to keep using it, unless the ovaries have been
removed, or the thyroid or cholesterol level is very low, or aging has
damaged their ability to convert cholesterol to progesterone. While an
excess of carotene can inhibit progesterone synthesis, a carrot salad
(grated carrots, vinegar, coconut oil, and salt) can often help to normalize
progesterone, apparently by protecting against intestinal absorption of
bacterial endotoxin, and by helping to reduce the reabsorption of estrogen
which has been excreted in the bile,
The beneficial hormonal effects that have been seen during
antibiotic therapy (raising progesterone while lowering cortisol and
estrogen) can be achieved safely with the carrot salad in most cases,
without the possible toxic effects of the antibiotics.
REJ1ERENCES
1. New alld NOli-Official Remeriks, 1912, Supplement, 158 , 160.
2. E. M"Io.k;. , c. ,d., " Mcl<lbuliMU "I' Ii"" mloJ CQUjugalW by in''',,1 ""oJ hucmolyS1e<l
mamnl<llian CJ)1hrocytcs," mochem. Hiophy.f . .kla 16fJ: 290_297, 1972 .
94
15
TRANSDERMAL PROGESTERONE FOR
PREMENSTRUAL SYNDROME
For many years, Katharina Dalton studied the use of injected
progesterone as therapy for the premenstrual syndrome. A typical patient
required several progesterone injections per momh, more or less
pennanently. While this was feasible in her practice in London, it is not
comfortable or convenient, in some cases leads to serious reactions at the
injection sites, and in the United States would be too expensive for
general use. When the syndrome is disabling, even the burden of frequent
and expensive injections was usually seen as a welcome alternative.
However, a less expensive and more pleasant form of administration
could make the therapy available to millions of women who are now
disabled for one or more days each month. A satisfactory alternative to
injections for many women is to use a dissolved form of progesterone in a
vitamin E base for transdermal use. (This form is especially suitable for
treating localized problems, including arthritis, varicose veins, and facial
or body hair that has developed from excess androgens.)
After animal experiments revealed that progesterone in vegetable
oil was absorbed effectively through the skin, in 1977 I began
experiments with women who suffered with the premenstrual syndrome.
The first three were completely disabled by epilepsy, suicidal depression,
and optical neuritis, and they all had dramatic, immediate recoveries.
The effectiveness of the transdermal absorption route of
administration varies with the individual, but compares favorably with
injections in the amount assimilated. (Neither method is as economical as
oral use. ) Thickness of skin or degree of circulation in the skin (these can
be very abnormal in hypothyroidism, for example) and the amount of
adipose tissue apparently make some difference in the rate of absorption
and response. When a small daily dose (e.g. , 5 or 10 mg.) is sufficient,
this can be taken as about 1/8 teaspoonful of a 10 percent solution rubbed
into the skin, for example on the front of the neck, or the inside of the
anns, where the skin is thin, after having spread a few drops of olive oil
or coconut oil over the skin to make the viscous solution spread more
easily. For large doses, the appropriate amount can be applied to a larger
area of skin after a hot bath, once or twice a day if necessary.
9S
Although progesterone will dissolve in warm vegetable oil, when
the oil cools nearly all of the progesterone crystallizes out of solution.
This is why vitamin E is necessary as the solvent, for transdennal use as
well as oral use.
Over the years I have seen transdermal progesterone used in
hundreds of women suffering from the full range of perimenstrual
symptoms, including migraine, acne, depression, mastalgia, edema, and
lethargy. Nearly all the women, applying the lotion themselves, are able
to find the appropriate dosage for controlling their symptoms.
Often thyroid therapy or a change in diet or light-exposure or
amount of activity is necessary for complete relief from symptoms.
Progesterone therapy can offer quick relief to many people whose real
problem is diet·induced hypothyroidism, but it shouldn'! be considered as
a substitute for the correct diet, or for thyroid supplementation when that
is needed_
It is necessary to be clear in describing the amounts that can be
used, while leaving it up to the patient to find the dose which controls her
symptoms, because some women have an exaggerated idea of the power
of a "hormone." The behind-the·ear scopolamine patch has had its
influence on the idea of trans dermal therapy, and many women have tried
just touching the oil to their wri sts_
It is sometimes helpful for the physician to administcr one dose
(sometimes using a twenty percent solution) in the office, and to wait 30
or 40 minutes to make sure that it was large enough to take effect . Once
having felt sudden relieffrom the eOtTect dose, it is casier for the patient
to understand how it should be used . (This trial dose in the office is a
good idea when using oral doses, too, but for an additional reason,
namely, to watch for signs of an overdose. It is probably impossible to
overdose using the transdermal method .)
Many of the solvents which hold progesterone stably in a
concentrated solution are highly allergenic_ Injectable progesterone in oil
could be used transdermally except for this problem. If necessary,
micropulverized progesterone can be dissolved in warm olive oil for
patients who react to other materials, or who have a history of skin
allergies_ Progesterone usually corrects such allergies, but some women
have found that taking it orai1y in oil was preferable.
The French have two standard topical progesterone preparations
that have been used for many years for breast pain and facial hair.
Besides the slow and steady absorption permitted by the
transdermal method, and the fact that many women with PMS are
96
exaggeratedly sensitive to ingesting anything that tastes odd, there is a
special set of problems that make the topical use of progesterone very
valuable. As I mentioned above, the French advocate topical
progesterone for mastalgia, but I think thyroid supplementation is the
more general solution to that problem. But in the case of bursitis,
arthriti s, tendonitis, "fibrositis," and varicose veins, it is possible to
achieve a higher local concent ration with transdermal use, than can
conveniently be achieved by oral administration. (Though two can be
combined usefully.)
As with oral progesterone, it is important to correct a goiter
before using transdermal progesterone, because progesterone acfs directly
on the thyroid gland to facilite its secretion, and the sudden correction of
thyroid function can lead to a hyperthyroid state, as the goiter unloads the
stored hormone.
Progesterone is so insoluble in water that it can penetrate tissue to
a remarkable depth, before a significant amount of it is carried away in the
body fluids. Tissue proteins have a great affinity for oils. Failure to
consider these points has made many people doubt that topical treatment
could affect the underlying tissues.
97
16
THE PROGESTERONE DECEPTIONS
In the 19305, it was demonstrated that estrogen, even in small
doses, produced abortions, and that when it is given early enough, even a
very small dose will prevent implantation of the fertilized embryo.
Progesterone was known, by the early 19405, to protect against the many
toxic effects of estrogen, including abortion, but it was also known as
nature's contraceptive, since it prevents pregnancy without hannful
side-effects, by different mechanisms, including prevention of sperm entry
into the uterus. That is, progesterone prevents the miscarriages which
result from excess estrogen,(1 ,2) but if used before intercourse, it
prevents conception, and thus is a true contraceptive, while estrogen is an
abortifacient, not a contraceptive.
In the 1950s, there was a search for chemicals which would
prevent ovulation. According to Carl Djerassi,(3) drug companies were
extremely reluctant to risk a religious backlash against their other
products, and so hesitated to market contraceptives. Obviously, the
induction of monthly abortions would have been even harder to sell.
According to Djerassi,(3) "Until the middle 1940s it was assumed
that progesterone's biological activity was extremely specific and that
almost any alteration of the molecule would diminish or abolish its
activity." This would obviously discourage interest from the drug
companies, who could patent a substance which they had chemically
modified. but could not patent a simple natural substance. However,
many substances--even non-steroidal chemicals--tumed out to have
estrogenic action.(4)
By 1942, Hans Selye had demonstrated that natural steroids retain
their activity when administered orally. But every drug company with a
steroid patent had an obvious interest in having the public believe that
there is a reason that natural steroids cannot be conveniently used .
The doctrine that natural steroids are destroyed by stomach acid
appeared, was promoted, and was accepted. In the manufacture of
progesterone. the precursor steroid is boiled in hydrochloric acid to free it
from its glucose residue; no one seriously believed that stomach acid
hurts progesterone, except the public.
The real issue is solubility. Hydrocortisone is reasonably soluble in
water, but progesterone is extremely insoluble in water, and, though it is
98
vastly morc soluble in vegetable oil than in water, it does not stay in
solution at room temperature even at the low concentration of 1 part in
1000 parts ofvegelable oil .
When people speak of an allergy to progesterone (or even to
penicillin) they generally arc not aware of the presence of a very toxic
solvenl .(5) A few years ago. progesterone was often sold dissolved in
benzyl benzoate: the Physician's Desk Reference warned of possible
allergic reaction to progesterone. Now, it is supposedly sold dissolved in
vegetable oil, with about \0% benzyl alcohol as a bacteriostatic agent .
Bacteriostatic water contains 0.9% to 1.9% benzyl alcohol, and can
irreversibly harm nerves.( 6, 7) Awareness of benzyl alcohol's toxicity gocs
back to 1918 at least ; it was proposed as an effective insecticide, and was
found to be toxic to many animal systems. The safe systemic dose(7) is
excecded with an injection of I 50 mg. of progesterone, yet the local
concentration is far higher. It can cause a severe reaction even when used
at a lower concentration. in bacteriostatic water.(5)
Other alcohols, including ethanol , have been used as solvents, but
since thcy (ethanol even morc than benzyl alcohol) have an affinity for
water, the solution decomposes in contact with tissue water.
In spite of the toxicity of the vehicle, several beneficial effects can
be obtained with injected progesterone, in serious conditions such as
epilepsy or cancer of the breast or lItems. Many researchers have
commented on the very obvious difficulty of giving very large amounts of
progcsterone.(8} My comparisons of oral progesterone in tocopherol with
other form s and methods of administration show a roughly similar
efficiency for oral and injected progesterone, and about 1/20 the effect for
suppositories. Crystals of progesterone are visible in the suppositories I
have examined, and this material is obviously wasted .
An old theory of vitamin E's mechanism of action in improving
fertility was that it spares progesterone.(9) It is established that some of
the effects of vitamin E and progesterone are similar; for example, both
prevent oxygen waste and appear to improve mitochondrial coupling of
phosphorylation with respiration. I suspected that if they actually both
work at the same mitochondrial site, then they must have a high mutual
solubility. Knowing the long-standing problem of administering large
doses of progesterone without a toxic solvent , I applied for and was
granted a patent for the composition of progesterone in tocopherol. One
of my reasons for publishing in the form of patents is that I have had
many years of experience in having my discoveries taken up by others
without acknowledgment. My dissertation research, which established
99
that an estrogen excess kills the embryo by suffocation, and that
progesterone protects the embryo by promoting the delivery of both
oxygen and glucose, didn't strike a responsive chord in the journaJs which
are heavily influenced by funds from the drug industry.
According to a consultant for a major medical journal, the idea
" .. .of dissolving progesterone, a fat soluble steroid hormone, in vitamin E
which is then incorporated into chylomicrons absorbed via the lymphatics,
and thus avoids the liver on the so called first pass ... .. .is so simple it is
amazing that the pharmaceutical companies have not jumped on it."
In the powder Conn, direct and intimate contact with a mucous
membrane allows lipid phase to lipid phase transfer of progesterone
molecules. Instead of by-passing the liver, much of the progesterone is
picked up in the portal circulation, where a major part of it is
glucuronidated, and made water soluble for prompt excretion. Since this
glucuronide form cross-reacts to some extent with ordinary progesterone
in the assay process, and since 50% of the ordinary free progesterone is
carried inside the red blood cells,(IO, II) and 50% is associated with
proteins in the plasma, while the glucuronide hardly enters the red blood
cells at all, it is better to judge by c1inicaJ efficacy when comparing
different oral forms _ My comparisons show several times higher potency
in the tocopherol composition than in powder fonn .
Since progesterone's use as a drug antedates the 1938 law
requiring special federal approval, its legal status is similar to that of
thyroid honnone. Unfortunately, for both thyroid and progesterone, there
is a tendency to cut corners for the sake of a bigger profit margin.
For example, steroid acetates are generally a little cheaper than
the simple natural steroid . Some people assume that an acetate or
butyrate can be substituted for the steroid itself. This can cause dangerous
reactions.
Medroxyprogesterone acetate is considered a progestin (though it
is not . supportive of gestation), because it modifies the uterus in
approximately the way progesterone does, but it is luteolytic, and lowers
the ovaries' production of progesterone while progesterone itself has a
positive effect on the corpus luteum, stimulating progesterone synthesis.
Defining "progestin" in a narrow way aJlows many synthetics to be sold as
progestagens, though some of them are strongly estrogenic, allowing
them to function as contraceptives--it is odd that contraceptives and
agents which suppress progesterone synthesis should be officially called
Ksupporters of pregnancy." It is probably partly the acetate group in the
medroxyprogesterone acetate molecule which makes it bind finnly to
100
receptors, yet causes it to block the enzymes which would nonnally be
involved in progesterone metabolism. (I think testosterone, even, might
be a safer progestin than medroxyprogesterone acetate.) Pregnenolone
acetate similarly blocks the enzymes which nonnaJly metabolize
pregnenolone.(12) In aspirin, it has been found that it is the acetyl group
which (by a free radical action) blocks an enzyme involved in
prostaglandin synthesis.
If the category called "progestogens" or "progestins" is to be
defined on the basis of a single tissue reaction, then it is possible to
classity progesterone with the toxic synthetic substances, but then it
becomes highly deceptive to imply that progesterone is jllst a progestin,
or that it has any of the olher of the toxic synthetics, but Ihis
continues to be done. The warnings about "progestins causing birth
defects," for example, cause epileptic women to use conventional
ami-seizure drugs (all of which cause birth defects) during pregnancy, and
to avoid natural progesterone, which generally could control their
seizures. Thus, a false message attached to progesterone creates
precisely the hann it claims to want to prevent . In my communications
with the regulatory agencies, I have concluded that their attempts to
deceive arc too blatant to ascribe to incompetency. Whether it's the
Forest Service or the FDA, the principle is the same: the regulatory
agencies have been captured by the regulated industries.
Another place to cut costs is in the tocopherol. Tocopherol
acetate does have vitamin E activity, but since it is only about half as
efficiently absorbed as the simple tocopherol,(13) it is a mistake to save a
few dollars an ounce, at the expense of losing half of the therapeutic
effect . People who have compared natural progesterone in natural
tocopherols with other compositions have insisted that the other
compositions must not contain progesterone.
The taste of natural vitamin E is stronger than that of the synthetic
fonns, but since the mixture is absorbed by any tissue it contacts,
including various parts of the bowel, it can be taken in a capsule. If a
small amount of olive oil is used with it, absorption through the skin is
very rapid. Many women use it vaginally, spread onto a diaphragm, to
hold it in contact with the membranes. The efficiency of abso(ption by all
routes is so high that patients should be warned against its anesthetic
effect, until their dosage requirement is known approximately. Some
physicians prefer concentrations higher than 10%, but the risk of
accidental drunkenness or anesthesia is higher with the stronger solutions.
101
It is an indication of the tocopherol solution's high availability that
medical researchers such as Roy Hertz,(S) who thought they were
administering maximal doses by combining injections with suppositories.
never mentioned the problem of an anesthetic effect from an overdose.
Similarly, it is evidence of the extremely poor availability of the
micropulverized progesterone that the researchers have administered
hundreds of milligrams per day, without mentioning the symptoms of an
overdose. Because of the difficulties involved in scient ifically studying the
clinical eft'tx:tiveness of various formulations, I think the most practical
way of evaluating the effectiveness of diflerent progesterone formulat ions
is to measure the amount extractable from the red blood cells. a few
hours after the peak serum level has been reached. This will reasonably
reflect the amounts reaching brain cells, adrenal glands, and the various
other cells on which progesterone has its therapeutic action .
REFERESCES
1. A. A. Ui<llcy-lIairJ. el al.. Fai lure of implantativn in in vitro l"rt i!irat inn ,mJ em hry,'
thc "ll"c<::ts vi" alh:reJ prng<:stervneA:str"gcn in and mice.
Fertility Sterility 45( I): 69-74. 1<»)16.
2. J. I.. y,.>v;,·h. e\ 1.. serum pr"ge""",,,,n,, """""n!r:H i"ns ;Ire h'gh,.,. i" pre""":o,,,,>,
cycles, Fertility and SlerililY 44( I): 1K5-llI9. 19X5 .
C njerllssi. The mak ing or the pill. Science 84: 127-129. 1<lX4 .
4. R. Keil1. lA-OS (ilimdes Endrx:rines. l lniversitaires .Ie Fnlllw. ParIS. 1<;152 .
5.1. A. (irant. ct a1.. New England kumal of Medidne 30(.(2): lUX. 1<)Kl. lInsusp<.:.:ted t>clllyl
ilkoh ..l hypo.:rscnsitivily.
O. T. E. Fe:.shy. d a!.. Ncur.,lnxidty "r .... aler, New Fnghlnd J"urn,,j or i\.kdki ne
JOK(6): <')fi6-7, IORJ.
7. F. T. Kimura, ct a!.. Parenteral toxidty siudies wilh ocllI.}'1 aknlhIU"" .,k"I '\PI'I 1'lmrm,I\;,'1
18: 00-61:1.1 '171.
K. A. Whitc , e,ji!oT. Symposium ,m in Expcrimcll'" l :lnd ("Iin;";a! ['w.:t,.:e. Thc
Hlakiston Cu.• N. Y.. 1\151. p. 4tH.
\I. A. Fraschini. 11 MC\"tio lliolugieo <Ii Rinvigorimenhl. Ftlizinni r-.kdi.: .. , Mil an .
1954.
10. E. Mu!.ler, cl ill., d f Ire.; "lid .:onjllgatcd stcr,.ids hy intact <Iud
mamOialian crythu><:ytes. Hioo.:him. Hiophys. Ada 21'1 .' : 2'JO-2'n, 1')72.
I I. M. lIolzl>;'lI..,r. The associati(lJI (If with ill""d ceUs in yin'. J. <.f Stc",id
J: 579-502. 1972.
12. S. Liebcrm:m. et A heurist ic pwp"s<l1 I('r untlerst:tndin!! skwidog..,nic
F.ntl,....:rine R..,views 5( I): 121:1· 141:1. 19X4.
13 . L. J. Machlin 3ml E. Kin<..1ics or tisslle ;llph:I-1<....:"ph.:wl lIpl"kc :md Jepkti<'n.
foll(,willg adm inislr.!linn "rhigh )c"cls ,,!'vit:ullill E. p. 411 in Annals "fth.: N.Y. or
Sd.:n..,c 393. R. Lubin and L. J. /l.1:I.:hlin. New Yurk, I <) it2.
J02
PART THREE, "MYSTFJlJOUS" DISEASES IN CONTEXT
17
PRESERVING THE TISSUES: Osteoporosis
and the Skin
While I was working on my dissertation, around 1970, the
opposition between stress-injury and energetic resistance became
increasingly apparent to me. Estrogen (like X-irradiation, aging, or
trauma) called up the cortisone response, and other factors, especially
progesterone and thyroid, allowed the organism to restore itself in ways
that neutralized the cortisone response. Therefore, when I saw that the
estrogen-like processes became more and more dominant after
middle-age, it was natural to think of progesterone and thyroid as the
main factors that should be replaced. This is why in 1975 I described
menopause as resembling Cushing's syndrome, which is caused by a toxic
excess of cortisol. Osteoporosis, hot flashes, insomnia, and mood
disorders are caused by cortisol, and so I tried using progesterone and
thyroid--the anticortisol factors--for those conditions. The results were
so profound that I began to study the general implications for health, and
to try to understand the mechanisms so that prevention might replace
treatment.
Several people who had been abandoned as hopeless terminal
cases--with "epileptic brain damage," inflammatory degeneration of hip
and thigh bones, diabetic gangrene, senility--recovered their health within
a few days, and went on with their lives in productive and pleasant ways.
I knew that intense and frequent epileptic seizures cause the
exhaustion and death of brain cells. A 52 year old woman had been
having seizures for over 15 years. Her neurologist gave her a mental
exam every year, and considered her to be hopelessly demented . After
using progesterone for a few days, she functioned normally. After about
a year, she returned to graduate school at the University of Oregon, and
got a master's degree with straight As.
A 79 year old woman had had artificial hip joints implanted when
she was in her fifties, but her bones had weakened to the point that no
further surgical repair was possible. She settled her affairs, and didn't
expect to get out of bed again. After using progesterone topically and
orally, after two weeks she was able to get out of bed and return to her
103
normal activities. At the age of 85, she went camping on the beach in
Mexico, and travelled to Scotland.
An 82 year old man was agitated and confused, and was
apparently suffering from senile dementia. After being given
progesterone and pregnenolone for a few days, his mind became clear,
and he returned to work on scientific projects he had begun decades
earlier. A squamous cell cancer on his lip regressed, and never bothered
him again.
A 60 year old woman had "osteoporosis" (shrinking) of the jaw
bone that was causing her teeth to loosen. After applying progesterone
solution to her gums daily for a few months, her teeth became firm.
When bones had almost disappeared ITom X-rays, yet became firm
and functional within a few weeks, it was obvious that regeneration had
taken place. But when brains went in a very short time from imbecility or
idiocy to intellectual productivity, I could only guess what might be
happening to the cells. But I got a useful perspective on the mechanism
of progesterone's action by seeing some recoveries that were even faster
than those I have mentioned.
In animal experiments, I knew that estrogen causes cells to take
up water within a few minutes after it reaches the tissue, and that this is at
least partly the result of its interfering with the availability of oxygen.
Within 40 minutes of administering a large dose of estrogen, the lungs
become extremely inefficient at oxygenating the blood. This involves a
sudden thickening of the alveolar membranes and the walls of capillaries,
simply by taking up water. So, when I saw bulging veins disappear a few
minutes after women took progesterone. along with a sudden lifting of
extreme depression, I guessed that their circulation had become more
efficient, and that beller oxygenation had changed their mood.
Then, I repeatedly saw physical changes in other people that were
visible within an hour, and that involved a sudden movement of water out
of edematous tissues. In many people with damaged joint cartilage
(confirmed by various types of examination, including arthroscopy), the
joints became mobile in an hour, and by the next day, the defect no longer
existed. A man who was purple from emphysema changed color within a
few hours, and within a few days was going to work. The bulging eyes of
exophthalmic Graves' disease receded into their sockets noticeably within
an hour, and were normal the nexl day. Simply improving the circulation
couldn't have done those things. Opposing estrogen's edema· promoting
action was involved, but I couldn't imagine any mechanism that could
104
explain such rapid movement of water from the swollen tissue into the
blood stream.
One of estrogen's effects is to lower the amount of albumin in the
blood . Estrogen causes the liver to synthesize less albumin, panly by
causing the messenger RNA to be destabilized and degraded . ( Iron can
have some similar effects on liver RNA.) When there isn't enough
albumin in the blood, water moves from the blood into the tissues.
Albumin binds oily substances, and its conformation seems to be opened
when it binds them. Progesterone is known to adsorb strongly to
proteins--it has been called a "cardinal adsorbant ," meaning that it can
bind in ways that cause the protein's adsorptive capacity to change I
believe that progesterone and pregnenolone oppose estrogen in many
ways, but the amazing speed with which they can cause major structural
changes in the soft tissues convinces me that one of their first sites of
action is the albumin molecule, causing its conformation to open in such a
way that it is able to more strongly bind water molecules. This physical
change in albumin would change the blood's osmotic/oncotic pressure,
causing water to flow into capillaries. As the edema is reduced,
oxygenation is more efficient, because the pathway for oxygen diffusion
becomes shorter.
Albumin has been described as a first line of defense against
toxins, since it binds them until the liver is able to degrade them
chemically. Progesterone, pregnenolone, and cholesterol are known to
increase thc organism's resistance to a great variety of toxins. (Sclye
coined the name "catatoxic steroids" to describe steroids of this type.) If
these steroids bind to albumin in a way that opens the protein to increase
its binding capacity, that single process could explain the "catatoxic"
effect, as well as the anti-edema effect.
When the blood is unable to retain its normal amount of water
because of insufficient albumin/sodium, the blood volume is reduced as
the tissues become water-logged . This causes the hematocrit (the
proportion of cells in a volume of blood) to rise, and this increased
packing of red blood cells causes the blood to become more viscous.
(Knisely studied this phenomenon in a great variety of sickness.)
Increased viscosity and slower flow decreases the bloods ability to deliver
oxygen and nutrients to the tissues, including the blood vessel walls,
modifying their tone. Slower flow, even without any changes in the
fibrin-fiblinogen system itself, increases the formation of clots.
This description of progesterone's immediate action is intended to
take some of the mystery out of its dramatic effects, but it isn't intended
105
to argue against any of its actions within cells. It serves to give a general
picture of how progesterone can systematically reduce stress and its
harmful consequences, just by making blood circulation more efficient.
At first I most "often used progesterone dissolved in olive oil to
stop the stress-induced processes of deterioration, with a high protein diet
to support the processes of repair. Now, I have added a variety of other
techniques, including the use of progesterone in vitamin E.
There always seems to be a rough balance between tissue
regeneration and tissue degeneration, with growth and repair occurring
when the equilibrium shifts in one direction, and with atrophy or
degeneration occurring when the balance shifts in the other direction. If
we can understand the mechanisms of atrophy, and how to retard or to
block tissue destruction, then we can restore the balance to a degree
which might allow regeneration to occur, even if we don't clearly
understand the mechanisms of growth.
Skin and bones are such different types of tissue that it will be
useful to start with them, because if we can see similar processes of
degeneration or regeneration in them, then the chances are good that the
same processes will occur in other tissues too. Bone is a relatively stable
tissue, while skin is a tissue whose cells divide rapidly.
It is common medical knowledge that cortisone and related
glucocorticoid-type hormones cause skin to atrophy, becoming thinner.
Using topical applications of a synthetic derivative of cortisone, C. M.
Papa and A M. Kligman showed that the atrophy ext.ended to the pigment
cells, reducing their size and eliminating most of their dendritic branches.
They also found that estrogen suppressed sweating and hair growth. The
other steroids they tested, progesterone, testosterone, and pregnenolone,
acted in the opposite direction, making aged and atrophied skin thicker
and more regular. They also made the pigment cells larger, and increased
their branching. I
Since these hormones were already known to have protective
actions against cortisone and · estrogen, these results were not too
surprising, though they did directly contradict the claims of people who
made estrogen-containing cosmetics.
Since progesterone and pregnenolone do not cause healthy, young
skin to thicken, their effect in damaged skin is probably partly to replace
the deficiency of that type of steroid which occurs with aging, and to
offset the damaging effects of the catabolic hormones, whose influence
does not decrease with age. l
106
Many years ago it was tound that in old age a woman's estrogens
were increased relative to the steroids adrenal androgens. Later.
it was found that the conversion of androgen to estrogen increases with
age in both men and women, and that this occurs largely in fat cells.
Several years ago. P. K. Siiteri found that low thyroid modified the
enzymes of fat cells in a way that would tend to increase the conversion
of androgen to estrogen . More recently, it was found thai adding
progesterone to the enzymes had the opposite effect of aging and
hypothyroidism, prOiecting the androgen from conversion to estrogen.
These researchers (c. J. Newton and colleagues, of London) concluded
that the decreased output of progesterone after the menopause might
account for the increased production of estrogen .-' Since progesterone
declines in aging men, too, this could account for the same process in
men .!
Vitamin A's effect on the skin opposes that of estrogen .1 There
are several mechanisms that could account for this. Vitamin A is used in
the formation of steroids, and since the skin is a major site of steroid
metabolism, vitamin A might help to maintain the level of the
anti-catabolic steroids A deficiency of vi tamin A causes excessive
release of the lysosomal enzymes. acid hydrolases, reslilting in tissue
catabolism.·' Also, vitamin A is necessary for the proper differentiation of
cells in skin and other membranes. A deficiency tends to cause an
increased rate of cell division, with the production of abnormal cells, and
a substitution of keratinized cells for olher types. Estrogen also promotes
keratinization and speeds cell division. A deficiency of vitamin A can
cause leukoplakia in the mouth and on the cervix of the uterus; although
this is considered "pre-cancerous," I have found it 10 be very easily
reversible, as I have discussed elsewhere.6 I suspect that the intracellular
fiber, keratin, is produced when a cell can't afford to do anything more
complex . Adequate vitamin A speeds protein synt hesis/ and allows it to
be used more efficiently.
Prolactin (which is promoted by estrogen, and inhibited by
progesterone) increases with stress and with age. It probably affects
every tissue, but it seems to have its greatest efecls on the secretory
membranes. It is known 10 have strong effects on the kidney, gut and
skin (sweat and oil glands, hair follicles, and feathers inbirds), and on the
gills of fish. Its involvement with milk production suggests that it might
mobilize calcium ITom bones, and inf fact it does contribute to
osteoporosis. This was foreseen by G. Bourne, in his book on the
107
metabolism of hard tissues, when he suggested that estrogen, actmg
through the pituitary, might be expected to promote osteoporosis.
Since reading Bourne's book, I have doubted thai it was rational
to use estrogen to prevent osteoporosis, especially when it is known to be
carcinogenic and when the ratio of estrogen to and androgens and
progesterone increases after menopause. Now that severa l publications
have appeared clearly showing that estrogen increases prolactin. that
prolactin increases with aging, and that prolactin contributes to
osteoporosis, the postmenopausal use of estrogen is worse than dubious .
But this was exactly when the pharmaceutical companies needed help in
continuing to sell their profitable estrogens, and this was exactly the time
when the FDA came out with its olTtcial approval of estrogen for
preventing osteoporosis.'
Some doctors combine estrogen with testosterone, and this is
much safer and more likely to keep the bones healthy. But since
testosterone, like estrogen and cortisone, causes the thymus gland to
atrophy, it is not a very good idea fo r chronic use, even if it doesn't cause
masculinization . The other anti-estrogens, which are present al high
levels in young women, include progesterone and DH EA. I have seen
several publications which I think would justify the use of physiological
amounts of DHEA to prevent or to treat osteoporosis,9 and a few which
support the use of progesterone. 10 My own observations on their use in
osteoporosis have been presented many times al alternat ive medical
conferences since the 1970s, but the main-line medical journals and
conferences have declined to accept my reports, even when they advertise
that all papers submitted will be presented in some form; many physicians
believe that they are being presented with a fair sampling of the work
being done in endocrinology, when in tact t hey are being g iven intensive
advertising sessions.
Since it is known Ihal cortisol causes bone loss, and it is widely
accepted that progesterone has an "antiglucoc0l1icoid" action, it is
reasonable to think that progesterone should protect against bone loss,
and that it is a progesterone deficiency after menopause which is a major
factor in the ddevelopment of osteoporosis. In the first edition of
Nllirilioll/or Womell (1975) I pointed this out, in comparing menopause
to Cushing's disease. Nencioni and Po lvani have more recently made
observations wh ich support this mechanism, in which progesterone
"exerts a protective effect ," by blocking the corticosteroid rC{:eptors.
They observed "that the process of rapid bone resorption starts before the
108
onset of amenorrhea and the abrupt fall in the estrogen levels and
coincides wit h decline in progesterone secretion "
By improving circulation of the blood and oxygenation of the
tissues. progesterone and pregnenolone will decrease the need for the
body to produce conisol. Pregnenolone acts in the brain to lower the
basal secretion of ACTH . This protective effect is more basic than that
achieved by blocking the conisol receptors.
The early tests of the toxicity of vitamin A used cartilage in tissue
culture. The same enzymes which are released by a deficiency of vitamin
A are released by a large excess, causi ng dissolution of the cartilage.
Other studies showed that a vitamin A deificiency caused similar changes
in both bone and cartilage. Although much vitamin A is consumed in the
production of progesterone, these studies show a direct effect of the
vitamin on tissue stability. Although I believe that a vitamin A
supplement will oOer considerable protection against osteoporosis (and
also against aging of the skin). it is important to remember thai excessive
vitamin A inhibits the thyroid, and that there is less risk of toxicity when
vitamin E is supplemented too. I think many of the headaches currently
associated with vitamin A use are the result of a preservative in the
capsules (probably a sulfi le), since people who reast to the vitamin in
capsule form don't react when they use a specially ordered bulk form
prepared without preservatives,
Things whIch damage skin and bones also damage other tissues,
and things which protect them also protect other ti ssues. The protective
factors include hormones (thyroid, DHEA, progesterone, and
pregnenolone), vitamins A and E, and magnesium,
calcium, and sodium. Sodium spares magnesium, and helps to make
albumin function in regulating blood and tissue water content. Under
some conditions, sodium can act as an antioxidant . Since the unsaturated
oils (and their prostaglandin derivatives) decrease f-::spiration, cause stress
to be more harmful, and have some specific effects that promote aging of
skin, bones, and other tissues, the use of coconut oil is especially
important. I think its use is one of the factors that prevents osteoporosis
in tropical countries,
REFERENCES
I. C M. Papu and A. M, Kligman, d mptcr XI in Advances in the Biologl' orSkill. 1'01. VI,
Aging .....:1 by W. MOn!llgnll . Pergamon Press, N. Y.. 1% 5.
2. C. N, GhCl'QnUache, el a I. , "SI\!roid honnon..:s in aging men," chupler 5 in Endocrint.: s and
Aging . .::d. by Gilman. 1%5.
109
3. C. J. NC\\.'lon, et aI., 'Aromatase activity and coucentrlltiOIlS of cortisol, progcsteronO! and
testosterone in breast and abdominal adipose tissue," 1. Steroid Biochem. 24(5), 1033-\039,
\986.
4. W. 1. 80, :Relation of vitamin A deficiency and estrogen to induction of k.:ratinizing
metaplasia," Amer. J. Clin. Nutt. 516, p. 666, 1957. Also, Proc. Soc. Exp. BioI. Med. 76,1951.
5. O. A Roels, "Present knowledge of vitamin A," chapter XIll in Present Knowledge in
Nutrition (third edition), Nutrition Foundation, N.Y., 1967.
6. R. Peat, Nutrition for WOITh!II, 1981 .
7. S. B. Porter, ct ai., 'Vitamin A status affects chromatin structure," Intcmatl. J. ViI. and Nulr.
Res. 56, \1·20, 1986.
8. "Estrogens for osteoporosis,' FDA Drug Bulletin 16(1), pages 5-6, June 1986.
9. S. Arody, cl ai., Maturitas (NetllcrJands) 4(2), 113-122, 1982; M. Boross, el as., Aktuclle
Geronlo!ogie (Stuttgart) 13( 1). 15-18, 1983.
10. F. P. Mandel, et ai , J. Reprod. Moo. 27(8), 511-519, 1982; T Ncncioni and F. Polvani,
Calcitonin, p. 297-305, A Pecilc, editor, Elsevier, N. Y., 1985.
110
18
ARTHRITIS AND NATURAL HORMONES
A very healthy 71 year-old man was under his house repairing the
foundation, when a support slipped and let the house fall far enough to
break some facia l bones. During his recovery, he developed arthritis in his
hands. It is fairly common for arthritis to appear shortly after an accident ,
a shock, or surgery, and Han Selye's famous work with rats shows that
when stress exhausts the adrenal glands (so they are unable to produce
normal amounts of cortisone and related steroid hormones), arthritis and
other "degenerative" diseases are likely to develop.
But when this man went to his doctor 10 "get somet hing for his
arthritis," he was annoyed that the doctor insisted on giving him a
complete physical exam, and wouldn't give him a shot of cortisone. The
examination showed low thyroid function, and the doctor prescribed a
supplement of thyroid extract , explaining that arthritis is one of the many
symptoms of hypothyroidism. The patient agreed to take the thyroid, but
for several days he grumbled about the doctor 'fixing something that
wasn't wrong' with him, and ignoring his arthritis. But in less than two
weeks, the arthritis had entirely disappeared . He lived to be 89, wit hout a
recurrence of arthritis. (He died iatrogenically, while in good health.)
Selye's work with the diseases of stress, and the anti-stress
hormones of the adrenal cortex, helped many scientists to think marc
clearly about the interaction of the organism with its environment, but it
has led others to focus too narrowly on hormones of the adrenal C0I1ex
(such as cortisol and cortisone), and to forget the older knowledge about
natural resistance. There are probably only a few physicians now
practicing who would remember to check for hypothyroidism in an
arthritis patient, or in other stress-related conditions. Hypothyroidism is a
common cause ofadrenaJ insufficiency, but it also has some direct efl'ects
on joint tissues. In chronic hypothyroidism (myxedema and cretinism),
knees and elbows arc often bent abnormally.
By the 1930's, it was well established that the resistance of the
organism depended on the energy produced by respiration under the
influence of the thyroid gland, as well as on the adrenal hormones, and
that the hormones of pregnancy (especially progesterone) could substitute
for the adrenal hormones. In a sense, the thyroid honnone is the basic
anti-stress honnone, si nce it is required for the production of the adrenal
and pregnancy hormones.
III
A contemporary researcher. F. Z. Meerson, is putting together a
picture of the biological processes involved in adapting to stress.
including energy production, nutrition, hormones, and changes in cell
structure.
While one of Sclye's earliest observations related gastrointestinal
bleeding to stress, Meerson's work has revealed in a detailed way how the
usually beneficial hormone of adaptation, conisone, can cause so many
other harmful effects when ils action is too prolonged or too intense.
Some or the harmful effects of the cortisone class of drugs (other
than bleeding) are: Hypertension, osteoporosis, delayed
healing, atrophy of the skin, convulsions, cataracts, glaucoma, protruding
eyes, psychic derangements, menstrual irregularities, and loss of immunity
allowing infections (or cancer) to spread.
While normal thyroid function is required for the secretion of the
adrenal hormones, the basic signal which causes cortisone to be formed is
a drop in the blood glucose level. The increased energy requirement of
any stress tends to cause the blood sugar to fall slightly, but
hypothyroidism itself tends to depress blood sugar.
, The person with low thyroid function is more likely than a normal
person to relluire cortisone to cope with a certain amount of stress
However, if large amounts of cortisone are produced for a long time, the
toxic effects of the hormone begin to appear. According to Meerson.
heart attacks are provoked and aggravated by the cortisone produced
during stress. (Meerson and his colleagues have demonstratcd that the
progress of a heart attack can be halted by a treatment including natural
substances such as vitamin E and magnesium .)
While hypothyroidism makes the body requirc morc cortisone to
sustain blood sugar and encrgy production, it also limits the ability to
produce cortisone, so in some cases stress produces symptoms resulting
ITom a deficiency of cortisone. including various forms of arthritis and
more generalized types of chronic inflammation .
Often. a small physiological dose of natural hydrocortisone can
help the patient meet the stress, without causing harmful side-effects.
While treating the symptoms with cortisone for a short time. it is
important to try to learn the basic cause of the problem, by checking ror
hypothyroidism, vitamin A deficiency, protein deficiency, a lack of
sunlight, etc. (I suspect that light on the skin directly increases the skin's
production of steroids, without depending on other organs. Different
steroids probably involve different frequencies of light, but orange and
red light seem to be important frequencies .) Using conisone in this way,
I 12
physiologically rather than pharmacologically, it is not likely to cause the
serious problems mentioned above.
Stress-induced cortisone deficiency is thought to be a factor in a
great variety of unpleasant conditions, from allergies to ulcerative colitis,
and in many forms of arthritis. The stress which can cause a cortisone
deficiency is even more likely to disturb formation of progesterone and
thyroid hormone, so the fact that cortisone can relieve symptoms does not
mean that it has corrected the problem .
According !() the Physicians' Desk Referenc, hormones similar to
cortisone arc useful for treating rheumatoid arthritis. post-traumatic
osteoarthritis, synovitis of osteoarthritis, acute gouty arthritis. acute
nonspecific tenosynovitis, psoriatic arthritis, ankylosing spondylitis, acute
and subacute bursit is, and epicondylitis.
Although cortisone supplementation can help in a great variety of
stress-related diseases. no curewit1 take place unless the basic cause is
discovered. Besides the thyroid, the other class of adaptive hormones
which are often out of balance in the diseases of stress, is the group of
hormones produced mainly by the gonads: the "reproductive homlones."
During pregnancy these hormones scrve to protect the developing baby
from the stresses suffered by the mother. hUI the same hormones function
as part to the protective anti-stress system in the non-pregnant individual,
though at a lower level.
Some forms of arthritis are known to improve or even to
disappear during pregnancy. As mentioned above, the hormones of
pregnancy can make up for a lack of adrenal cortex hormones. During a
healthy pregnancy, many hormones are present in increased amounls,
including the thyroid hormones. Progesterone. which is the most
abundant hormone of pregnancy, has both anti-inflammatory and
anesthetic actions, which would be of obvious benetit in arthritis.
There arc other naturally anesthetic hormones which are increased
during pregnancy, including DHEA, which is being studied for its
anti-aging, al}ti-cancer, and anti-obesity effects. (One of the reasons that
is frequently given for the fact that this hormone hasn't been studied more
widely is that , as a natural suhstance, it has not been monopolized by a
drug patent . and so no drug company has been willing to invest money in
studying its medica! uses.) These hormones also have the ability to
control cell division, which would be important in forms of arthritis that
involve invasive tissue growth.
While these substances. so abundant in pregnancy, have the ability
to substitute for cortisone, they can also be used by the adrenal glands \0
113
produce cortisol and related hormones. But probably the most surprising
property of these natural steroids is that they protect against the toxic
side-effects of excessive adrenal hormones. And they seem to have no
side-effects of t heir after about fifty years of medical use, no toxic
side effects have been found for progesterone or pregnenolone.
Pregnenolone is the material the body uses to form either
progesterone or DHEA Others, including DHEA, haven't been studied
for so long. but the high levels which are normally present in healthy
people would suggest that replacement doses, to restore those normal
levels, \vould not be likely to produce toxic side effects. And, considering
the terrible side etTects of the drugs that are now widely used, these drugs
would be justifiable simply to prevent some
of the toxic effects of conventional treatment.
It takes a new way of thinking to understand that these protective
substances protect against an excess of the adrenal steroids, as well as
making up for a deficiency. Several of these natural hormones also have a
protective action against various poisons; Selye called this their
"calatoxic" effect .
Besides many people whose arthritis improved with only thyroid
supplementation , I have seen 30 people use one or more of these other
natural hormones for various types of arthritis, usually with a topical
application. Often the pain is relieved within a few minutes. I know of
several other people who used progesterone topically for inflamed
tendons, damaged cartilage, or other inflammations. Only one of these, a
woman with rheumatoid arthritis in many joints, had no significant
improvement. Though she used only a small amount, an hour after she
had applied it to her hands and feet , she enthusiastically reported that her
ankle had stopped hurting, but after this she said she had no noticeable
Improvement.
We often hear that "there is no cure for arthritis, because the
causes are not known." If the cause is an imbalance in the normal
hormones of adaptation and resistance, then eliminating the cause by
restoring balance will produce a true cure. But if it is more profitable to
sell powerful drugs than to sell the nutrients needed to form natural
hormones (or to supplement those natural hormones) we can't expect the
drug companies to spend any money investigating that sort of cure. And
at present the arthritis market amounts to billions of dollars in drug sales
each year.
Fasting has been found to relieve rheumatoid arthritis, and there is
good evidence that a variety of bowel bacteria are involved in arthritis
114
and other "autoimmune diseases." Bacterial toxins and antigens interact
with hormones and the immune systems, and intestinal health should be
considered as an integral part of hormone therapy. Raw carrots, by
stimulating the intestine, often help to lower estrogen and increase
progesterone. One of the thyroid hormone's important functions is to
improve digestion and bowel health.
Rheumatoid arthritis, osteoarthritis, lupus, sclerodenna, and a
variety of other "autoimmune" diseases and connective tissue diseases
respond well to these hormonal treatments.
REFERENCE S
1. T, D. Koepscll, <;!! aI., "Non-cOLlIra«:ptivc lionnOllCS aud L1IC risk of rheumatoid arthritis in
menopausal women ," [nl. 1. EpidcmioL 23(6),1 248-1255, 1994.
2. 1. D, Taurog, ct Ill., Cel!, No\'<:mbcr, 1990.
3. R. Dalt.:y and H. G. Miller, Progres.! ill CIi"ical Medici"". Sceond Edi tion. J. &. A. Churchill,
London , 1952.
4. T. lJshiyama, ct aI., "F.xprc.<;sion of estrogen !"e(:eptor rclat...-d protein (p29) lind estradiol
binding in human arthritic syno\"imn: 1. Rhcumatol. 22,421-426, 1995.
III
19
THE CERVICAL CANCER SCARE AND
OTHER APPROACHES TO CANCER
Many women with abnonnal Pap smears, even with a biopsy
showing the so·called "carcinoma in situ," have returned to nonnal in just
two months with a diet including the following: 90 grams of protein, 500
mg. of magnesium as chloride, 100,000 units of vitamin A, 400 units of
vitamin E. 5 mg. folic acid, 100 mg. pantothenic acid, 100 mg. of B6 and
niacinamide, and SOD mg. of vitamin C, with progesterone and thyroid as
needed. Liver should be eaten once a week, because of its high B-vitamin
content . Some of the women apply vitamin A (not carotene) directly to
the cervix.
Estrogen is known to cause uterine cancer, but the pervasive
marketing of estrogen led to solving that problem by the mass removal of
American uteruses. The evidence is clear, however, that many tissues
have estrogen receptors, and can be cancerized by exposure to estrogen.
Breast, lung, brain, and liver are coming to be widely recognized as sites
of estrogen-induced cancers in humans, 50 years after Lipschutz
demonstrated the extensive nature of estrogen carcinogenesis in animals.
The pancreas, which has estrogen receptors, is another organ that I
believe is significantly cancerized by estrogen.
Progesterone's anti-estrogen effect has been successfully used to
treat some uterine and breast cancers, but the doses were never high
enough to duplicate the levels that exist in late pregnancy . I believe it is
irrational to use less than the maximum physiological level, in attempting
to reverse a condition which resulted from years of severe deficiency .
When progesterone dissolved in benzyl alcohol with sesame oil is
injected, progesterone crystals are deposited, inertly, in the tissue. Even
this limited approach has produced some visible results.
I believe the fact that the cancer death rate keeps rising disproves
the claim that there has been progress in the cure of cancer. Everyone
over 50 contains some tissue that can be diagnosed as cancer. Though
not everyone dies from cancer, it could be diagnosed in everyone, if a
sufficient diagnostic effort were made. Then, 75% of "all cancers" could
be "cured," though just as many people would die from it . The cancer
situation is so thoroughly unscientific that I am not convinced that it is
worthwhile to make any effort to diagnose cancer. At a cancer
116
conference, a very high proportion of the male physicians, when asked
what they would do if they had prostate cancer, said they would do
nothing; that response seems to be justified by the evidence accumulated
for several decades, that treatment for prostate cancer hasn't clearly
prolonged life. More aggressive diagnosis will certainly improve the
"cure rate," but until the population's death rate from prostate cancer
decreases, it is hard to have confidence in therapies based on
fundamentally confused notions of the biology of cancer. If something
harms your vitality, and is just as toxic to your immune system, your liver,
and your brain, as it is to cancer cells, the medical situation seems
analogous to that of the anny that destroys a town to save it.
Benign breast disease, breast cancer and pre· cancerous conditions
have been found to be associated with a progesterone deficiency and
excess estrogen .{l) Some additional references are given in Nutritioll
for Womell. Since progesterone deficiency and excess estrogen can be
caused by either a thyroid deficiency or a protein deficiency, the most
important cause of the steroid imbalance, and of the hormone related
cancers, is hypothyroidism. Broda Barnes has discussed this issue in his
books. (Protein deficiency is one cause of hypothyroidism.) Vitamin A,
vitamin E, and thyroid have all been used effectively to relieve benign
breast disease. Caffeine actually has been repeatedly shown to protect
against cancer. Minton's so-called study which led to a generalized fear
of coffee as a cause of breast disease was based on confused reasoning. I
believe anti-inflammatory drugs such as aspirin or prostaglandin inhibitors
such as indomethacin have a rational place in cancer therapy, especially if
(like aspirin) they have some antihistamine activity. (The prostaglandins
have now been implicated in all of the major types of cancer.) Estrogen
tends to be deposited in inflamed tissues, and in that sense those drugs
might be considered as part of an anti-estrogenic program.
Simple derivatives of glucose, glucuronic acid and glucaric acid,
have been proposed as substances that might limit the deposition of
estrogen in inflamed tissues. Recent studies using glucarate and variou s
fomls of vitamin A have produced good effects in breast cancer.
REFERENCE
L Cowan, L. D.. cl al.. "Bre<lSI cancer ineii.lence in women with a history of pr,'ges!<.-"I'(ln<'
i.leficicncy," Am. 1- Epidt;mio logy 114.209-217_ 1981.
11 7
20
W ARB URG'S CANCER THEORY,
CACHEXIA
AND THYROID THERAPY
Guo Warburg l demonstrated that all cancers have defective
respiration, by which he meant that glucose is consumed too rapidly. even
when there is adequate oxygen. The excessive consumption of glucose in
the presence of oxygen is called aerobic glycolysis. and is typical of
canceL Oxygen may be consumed. but it does not result in . the
production ofsufficicnt AT P 10 inhibit glycolysis (by the Pasteur effect),
This generally means that excess lactate will be produced and will leave
the celL will be detected by other tissues, and will be processed by the
liver into glucose. Lactate is a sumcient stimulus to trigger the stress
reaction, and in many people causes an anxiety syndrome. Since
resynthesis of glucose from lactate by the liver requires much morc
energy than is derived from conversion of glucose to lactate. the tumor's
fonnation of lactate a large hurden 10 the organism. Totlll
energy consumption would increase, because of intense bu t inetlicient
metabolism in the tumor and in the liver, and also possibly because of
stress-induced brain excitation and the catabolism of muscle and other
tissue proteins. Cortisol elevates blood glucose and would inhibit the
thyroid. Since there is evidence of thyroid deficiency in various cancers.
and since thyroid supplementation reduces the incidence of spontaneous
or induced tumors in animal studies, thyroid therapy \vould be desirable in
cancer. especially if there is cachexia. Gerson. 1 Tallberg.-' and others have
reported good results from using thyroid as part of supponive therapy .
The stereotype of the hypothyroid person as over-weight will lead
the typical physician to believe that metabolic stimulation by thyroid
would be exactly the opposite of what the cachectic patient needs. The
relevant effects of thyroid (especially with progesterone, to promote
tissue response to thyroid, to block cortisol production. and \0 provide
general anti-stress physiological support) however. are stimulation of
protein synthesis and the prevention of lactate fortnation--or the
st imulation of its oxidation, either by the tumor itself or by other tissues,
to prevent its entry into the Cori cycle. for gluconeogenesis. Cachexia
strumipriva, the wasting disease that used to result following removal of
the thyroid gland when the thyroid hormone wasn't replaced. should be
118
kept in mind, since it is a situation in which thyroid cures cachexia,
stimulating anabolic processes.
There has been publicity in recent decades about various
substances produced by cancers that induce the growth of blood vessels,
providing the tumors with the circulation needed for growth , Since lactic
acid is an adequate stimulus for such growth, and is produced by tumors,
it is remarkable that it has been so consistently ignored as a reasonable
point of intervention for limiting tumor growth. Thyroid and magnesium
make respiration efficient, in the sense of producing ATP, which is
required for the Pasteur effect to turn off glycolysis. Lactic acid can't be
made (in humans) from fats or alcohol, a point which is often overlooked
by biochemists who work with bacteria. and so the use of acetic acid,
butyric acid, and other fatty acids (as in coconut oil, for example),
combined with adequate thyroid hormone and magnesium, should make a
significant contribution toward removing the lactate stimulus for
increased blood supply to the tumor. The carbon dioxide produced by
the action of thyroid is itself involved in the suppression of lactic acid
formation.
Progesterone and pregnenolone, by reducing the
cancer-induced excess of the glucocorticoid hormones, would also make
a contribution to decreasing the supply of glucose to the tumor.
Warburg believed that a riboflavin deficiency was an important
contributor to the development of defective respiration, but he also
pointed out that the simple lack of oxygen would promote the
development of cancer. I have emphasized the role of estrogen in
creating an oxygen deficiency. Since it inhibits the secretion of thyroxin
at the glandular level , and antagonizes thyroxin at the cellular level,
estrogen is a good candidate for the main cause of the respiratory defect.
It also antagonizes other respiratory factors , such as magnesium and
vitamin E, and excess estrogen actually impedes oxygenation of Ihe
blood . (Both low thyroid and high estrogen are known to cause an
emphysema-like interference with ditrusion of oxygen into the lung
capillaries.)
Radioactive estrogen has been shown to accumulate selectively in
(liver) cancer cells, which is remarkable since that behavior is so untypical
of liver cells. One of my first research projects had to do with the fact
that estrogen promotes the formation of beta-glucuronidase, an enzyme
which can reverse the reaction which normally occurs in the liver,
detoxifying estrogen by combining it with glucuronic acid . Irritated
tissues, and all cancers, contain beta-glucuronidase, with the capacity to
119
're-toxify" estrogen in the irritated or cancerous site, depositing it locally
and negating the liver's protective function . More recently, breast cancer
cells have been found to contain sulfatase enzymes, with the same kind of
function, since the liver's other main fOllte of estrogen detoxication is by
combining it with sulfate. A systematic anti -estrogen program (including
adequate protein to sustain liver funct ion) would help to minimize the
cancer-promoting action of this locally deposited estrogen. I think of the
appearance of these estrogen-releasing enzymes in irritated tissue as part
ofa system for promoting regeneration. In the uterus, estrogen promotes
simple growth, and progesterone promotes differentiation . I t hink
something analogous happens in other tissues, with a variety of
substances supporting differentiation.
Once we accept Warburg's thesis, that damaged respiration is the
prime cause of cancer, the therapeutic use of thyroid in cancer seems
obvious, Aging and estrogen-dominance are other states in which cell s
seem to bc relatively insensitive to thyroid honnones. (Unsaturated fats
are involved in resistance to thyroid, and promote the incidence of cancer
in a variety of ways, ) [fthe liver is a main site ofT4's conversion to T l ,
cancer patient s may require very large doses of thyroid hormone, or else
direct usc o f T .• (possibly in large doses), since the liver is so likely to be
inefficient. Incidentally, thyroid's abi lity to improve digestion and
peristal sis is important for liver function ; endotoxin absorbed from the
intestine can be a serious burden to the li ver, and it is known to cause a
large increase in the blood estrogen level.
REFERE." 'CES
I, (III" II. n,,· Md«""'"m "rr",,,on. R. R. Smolh, N,Y., 1'1,1.

2 Max (jer,,,n ..1 1 '''!('('r l'iI("nlPY. !lonk> , N.Y., 1'I5H. (i<:r.",,,n ,lk,l m "nd
"j"hls h" " k h;.v" a lkrctl Ins conclus io ns; I ",'ns;,ic, UII:1ll I" b..:
111",,, for{lcrics, Ii,r P' lJUi<Jliunal pu rpuscs.
1. I [ / 'r"'ld(" <"/Ilre /I"dy /.'iI",/\ I 'J7l! ,
4. K. ;.nd J\, S. J""b<)ll. "S"l1lc c" ncer and Ih yr"IJ (\clici c lH:Y:'
121') J, 11 74- \1 i (" 1'1(,4.
5 I.. A ( ;lIcrrcT" ,md f{ , ( 'am .. "" Ic, "f{ c)!1c;;sl"n "r pi IlI il"ry 111m", " Iler Ihyr,,,d
in primary hypnlh Y"Jldlsm :' S('UI hcm J. 71,14), 52')- 1, I, I'll! 1.
( , j Y !<e;:lOhh, S Rud \'cll , un oJ I'. M (ila/cr, 1·(ltl,·",.JlI/.I(-ardl. Dec. 15, 1')<)(" l il is s\ wly
lh;'l Ihe oxytlell-poor cll"ir<>llIncnl n' lumor' 1\ J. ( ;I"ce la , e/
a/. . h,,"e 11M hvp"x,;, i;" ',,rs Ihe growth or tUlllnf w!h. "f'hc<;o..: n;suU , ,"o"finn Ihc
'Hnk Wa rhllrg did sc"cral
120
21
MIGRAINE, VARICOSE VEINS, EPILEPSY
This group of problems relates to the behavior of the muscles in
the walls of blood vessels. Estrogen tends to decrease the muscle tone in
veins, while increasing it (especially if adrenalin is present) in arteries, and
progesterone increases the tone of veins. One aspect of estrogen's
production of increased problems with blood clots is that it slows
circulation, allowing clots to form in the slow moving blood of the large
veins. especially in the legs.
The times (premenstrually, in pregnancy, around menopause, in
hypothyroidism, for example) when estrogen is high and progesterone is
low, are the times of increased incidence of migraines, epileptic seizures,
and development of varicose veins.
There is increasing recognition that progesterone can cure
migraines and epilepsy, but there is a mechanistic dogma about varicose
veins. largely based on a strange idea that has been perpetuated by
medical schools that veins "don't have muscular walls." Believing that
veins don't have muscles, many physicians can't conceive of any way in
which an enlarged vein could correct itself: "The valves are defective."
But when they have enough progesterone in relation to estrogen, the
walls contract, narrowing the channel so the valves are able to function .
Visible veins around the ankles often disappear, even in older people,
when the hormone balance is improved.
Since migraine and epilepsy can be debilitating, I always urge
people to use progesterone to get rid of their symptoms, SO they can
focus on correcting the basic metabolic problems, which usually relate to
diet and thyroid function .
A quick demonstration of progesterone's effect on the veins can
be done by holding the hands at waist level. If the veins on the back of
the hand bulge visibly, an appropriate oral dose of progesterone wilt
regulate the tone of the smooth muscles in the veins, causing them to
contract and become relatively invisible within a few minutes. Once, I
watched a woman whose hands were disfigured by gnarled purple blood
vessels. who took about 30 mg. of progesterone every 10 minutes. After
the fifth dose, her hands suddenly (in a moment when we weren't
watChing them closely) were transformed into perfectly beautiful young
hands. Progesterone's effects can be similarly quick in migraine and
epilepsy.
121
22
NERVES
Almost everyone knows that estrogen causes water retention and
edema, but few people seem to be aware that the edema associated with
either high estrogen or low thyroid (which go together so closely)
involves the retention of water without a sufficient amount of sodium to
balance it--the edema is "hypotonic" This means that the water in the
blood in effect forces itself into cells and connective ti ssues, causing them
to swell . Some celts aren't damaged very much by a little swelling, but
when cells are enclosed by a rigid container of bone or connective tissue,
the pressure will tend to prevent the entry of blood, and will cause
structural changes, simply because the contents are too big for the
container.
The carpal tunnel syndrome involves the pinching of nerves by
ligaments in the wrist, damaging their function . The spinal cord and brain
are enclosed, and extreme swelling can cut off the blood supply, causing
death. Before that point is reached, swelling can cause a great variety of
nervous symptoms.
Swelling of the lower spinal cord can cause weakness or paralysis
of the legs, or various sensory or circulatory problems. Veterinarians
have recognized conditions in dogs and horses caused by spinal swelling
(and in dogs the problem was traced to hypothyroidism), but analogous
symptoms in people are often ascribed to the mysterious "multiple
sclerosis. "
Multiple sclerosis is strongly associated with hormone imbalances,
and disproportionately affects women in their reproductive years.
Progesterone and thyroid are crucial for maintaining and repairing the
myelin sheath that deteriorates in MS. Blood clots are known to be
associated with the "plaques" in the brain, and a low protein diet
predisposes to abnormal clotting, partly through its effect on the balance
of estrogen and the anti-estrogens. One of the first people I knew who
used progesterone was a woman who had cured her multiple
sclerosis/optic neuritis with progesterone. Often, thyroid
supplementation by itself eliminates the symptoms of MS.
Since the edema of estrogen excess and thyroid deficiency is
hypotonic, eating extra salt is appropriate, but the body can't retain the
salt unless the hormone balance is corrected.
122
23
ALZHEIMER'S DISEASE
The results seen in several Alzheimer's studies could have a
significance larger than what has been suggested by the investigators. A
diagnostic bias has been reported to result from the use of standardized
tests based on vocabulary, because education increases vocabulary, and
lends to cover up the loss of vocabulary that occurs in dementia. In the
Framingham study, it was concluded that there was a real association of
lower educational level with dementia, but the suggestion was made that
self-destructive practices such as smoking were more common among the
less educated.
The Seattle study of the patients in a health maintenance
organization showed a very distinct difference in educational level
between the demented and the both of whom had roughly
similar frequency of prescriptions for estrogen. The features that seemed
important to me, that weren't discussed by the authors, were that the
demented women had a much lower rate of progestogen use, and a much
higher incidence of hysterectomy, which interferes with natural
progesterone production.
Although Brenner, et aI., in the Seattle study concluded that "this
study provides no evidence that estrogen replacement therapy has an
effect on the risk of Alzheimer's disease in postmenopausal women," they
reported that "Current estrogen use of both the oral and the vaginal
routes had odds ratios below I, while former use of both types yielded
odds ratios above 1.... " (They seem to neglect the fact that
disease in old people has a long developmental history,
so it is precisely the "former" use that is relevent. 3 I% of the demented
women had formerly used estrogen, and only 20% of the control group.
Since estrogen is a brain excitant, present use creates exactly the same
sort of effect on verbal fluency and other signs of awareness of the
environment that a little cocaine does. Anyone who neglects this effect is
probably deliberately constructing a propaganda study.) This
observation, that the demented had 155% as much former estrogen use as
the normal group, as well as the difference in rates of progestogen use
(nonnal patients had 50% more progestogen use than demented) and
hysterectomy (demented had 44.1% vs. 17% in the nonnals, i.e., 259% as
many; the incidence of hysterectomies after the age of 55, which is a
strong indication of a natllral excess of estrogell, ill the demented was
123
.P-I% (?f Ihl.! ;/IC.:idcl}(:e ill Ihl.! l/oll-dclIIl!lIlcd) , should call for a larger
study to clarify these observatons, which tend to indicate that exposure to
estrogen in middle-age increases the risk of Alzheimer's disease in old
age, and that even medical progestogens offer some protection against it .
(Although this study might have been bigger and better, it is far
better than the junk-studies Ihat have been promoted by the
pharmaceutical publicity machine. I have seen or heard roughly 100
mentions of the pro-estrogen anti-scientific "studies," and none
mentioning this one.)
REFERENCES
I. n. E. Brclln..:r. cl 111. "l'oslm..:nolX!usal eSlrop,en rcplllC<.'1n....ui therap)' aud the risk of
Alzh..:imcrs discasc: A pOJlnlalion-hlIStX! casc-(;onlml study: Am. J. EpidcmioL 140, 262·267,
199.\ , "Wumen Il'nU 10 higher ag .... specific lnclllence rale'S of
do men."
2, IIF. Jonn , The l:pidemiologl' ,{Alzheimer's D;.'oo.,e (md Refufed Disorrlers. Charmm1 and
Ilal!. London. I99(). and W, A. cl "I., Ann, NCllrol. 30, 3S 1-190, 1991 .
.1. H. C. Lin, el al.. "1\;:rfonn1lllce on a dementia scf<.:ening tcsl in relalion 10 demographic
of 5297 cOllllllunit y residcnts in Taiwan: Arch. NcnToL 1(9), 910-915, 1994.
"Com1\lonly used tests may Ile Imf:1ir to poorly edncaled individuals,
eSl">I!dall y women and mm] n:sidcnts:
4. n. L. "rui]ur<; I)f nulmcfcnc "lid II) improvc m.::mOT)" in di:<Ctl:l<!.'
Am. J ofPs),chialry 144. 31\6·7. 1987.
124
24
ECLAMPSIA IN THE REAL ORGANISM:
A Paradigm of General Distress Applicable to
Infants, Adults, Etc.
To prevent the appropriation and abuse of our language by
academic and professional cliques, I like to recall my grandparents'
speech. When my grandmother spoke of eclampsia, the word was still
normal English, that reflected the Greek root meaning, "shining out,"
referring to the visual effects that are often prodromal to seizures. The
word was most often used in relation to pregnancy, but it could also be
applied to similar seizures in young children . The word is the sort that
might have been coined by a person who had experienced the condition,
but the experience of seeing hallucinatory lights is seldom mentioned in
the professional discussion of "eclampsia and preeclampsia ."
Metaphoric comparisons, models, or examples··js
our natural way of gaining new understanding. Ordinary language, and
culture, grow when insightful comparisons are generally adopted,
extending the meaning of old categories. Although the free growth of
insight and understanding might be the basic law of language and culture,
we have no institutions that are amenable to that principle of free
development of understanding. Institutions devoted to power and control
are naturally hostile to the free development of ideas.
Among physicians, toxemia (meaning poisons in the blood) has
been used synonymously with preeclampsia, to refer to the syndrome in
pregnant women of high blood pressure, albumin in the urine, and edema,
sometimes ending in convulsions. Eclampsia is reserved for the
convulsions themselves, and is restricted to the convulsions which follow
preeclampsia, when there is "no other reason" for the seizure such as
"epilepsy" or cerebral hemorrhage. Sometimes it is momentarily
convenient to use medical terms, but we should never forget the quantity
of outrageous ignorance that is attached to so many technical words when
they suggest the identity of unlike things, and when they partition and
isolate things which have meaning only as part of a process. Misleading
tenninology has certainly played an important role in retarding the
understanding of the problems of pregnancy.
In 1974, when I decided to write Nutrition for Women, I was
motivated by the awful treatment I saw women receiving, especially
125
during pregnancy, from physicians and dietitians. Despite the research of
people like the Shutes and the Biskinds, there were slil1 "educated" and
influential people who said that the mother's diet had no influence on the
baby. (That strange attitude affects many aspects of behavior and
opinion.)
How can people believe that the mother's diet has no effect on the
baby's health? Textbooks used to talk about the "insulated" fetus. which
would gel sufficient nutrients trom the mother's body even if she were
starving. To "prove" the doctrine, it was pointed out that the fetus gets
enough iron to make blood even when the mOl her is anemic. In the last
few years, the recognition that smOking, drinking, and using other drugs
can harm the baby has helped to break down the doctrine of "insulation,"
but there is still not a medical culture in which the effects of diet on the
physiology of pregnancy are appreciated. This is because of a mistaken
idea about the nature of the organism and its development. "Genes make
the organism," according to this doctrine, and jf there are congenital
defects in the baby, the genes are responsible. A simple son of causality
flows from the genes to the finished organism, according to that idea. It
was taught that if "the genes" are really bad, the defective baby can
make the mother sick, and she contributed to the baby's bad g("nes,
The idea isn't completely illogical, but it isn't based on reality, and it is
demonstrably false. (Race, age and parity have no effect on incidence of
cerebral palsy; low birth weight and complications of pregnancy are
associated with it : J. F. Eastman, "Obstetrical background of753 cases of
cerebral palsy," Obstet. Gynecol. Surv. 17,459-497, 1962.)
Although Sigmund Freud sensibly argued in 1897 thai it was more
reasonable to think that an infant's cerebral palsy was caused by the same
factors that caused the mother's sickness, than to think that the baby's
cerebral palsy caused maternal sickness and premature labor, more than
50 years later people were still taking seriously the idea that cerebral
palsy might cause maternal complications and prematurity. (AM .
Lil ienfield and E. Parkhurst, "A study of the association of factors of
pregnancy and parturition with the development of cerebral palsy," Am. J.
Hyg. 53, 262-282, 1951.)
Medical textbooks and articles still commonly list the conditions
that are associated with eclampsia: Very young and very old mothers, a
first pregnancy or a great number of previous pregnancies, diabetes,
twins, obesity, excessive weight gain, and kidney disease. Some authors,
observing the high incidence of eclampsia in the deep South, among
126
Blacks and on American Indian reservations, have suggested that it is a
genetic disease because it "runs in families." 'fpoverty and malnutrition
are also seen to "run in families," some of these authors have argued that
the bad genes which cause birth defects also cause eclampsia and poverty.
(L C. Chesley, et aI., "The familial factor in toxemia of pregnancy,"
Obstet. Gyoce. 32, 303-311, 1968, reported that women whose mothers
suffered eclampsia during their gestation were likely to have eclampsia
themselves. Some "researchers" have concluded that eclampsia is good"
because many of the babies die, eliminating the "genes" for eclampsia and
poverty.)'" Any sensible farmer knows that pregnant animals must have
good food if they are to successfully bear healthy young, but of course
those farmers don't have a sophisticated knowledge of genetics.
The inclusion· of obesity and "excessive weight gain" among the
cond]tions associated with eclampsia has distracted most physicians from
the fact that malnutrition is the basic cause of eclampsia. The pathologist
who, knowing nothing about a woman's diet, writes in hi s autopsy report
that the subject is "a well nourished" pregnant woman, reflects a medical
culture which chooses to reduce "nutritional adequacy " to a matter of
gross body weight. The attempt to restrict weight gain in pregnancy has
expanded the problem of eclampsia beyond with poverty,
into the more affluent classes.
Freud wasn't the first physician who grasped the idea that the
baby's health depends on the mother's, and that her health depends on
good nutrition . Between 1834 and 1843, John C. W. Lever, M.D. ,
discovered that 9 out of 10 eclamptic women had protein in their urine.
He described an eclamptic woman who bore a premature, low-weight
baby, as having "... been living in a state of most abject penury for two or
three months, subsisting for days on a single meal of bread and tea. Her
face and body were covered with cachectic sores." of puerperal
convulsions," Guy 's Hospital Repuns, Voillme I, series 1, 495-5 17,
1843.) S. S. Rosenstein observed that eclampsia was preceded by
changes in the serum (Tmite Pr((liqlle des Maladies des ReiIlS,
1874). L. A. A. Charpentier specifically documented low serum albumin
as a cause of eclampsia (A Practical Treatise 011 Obstetrics, Volume 2.
William Wood & Co. , 1887). Robert Ross, M.D., documented the role
of malnutrition as the cause of proteinuria and eclampsia (Sollthem
Medical Journal 28, 120, 1935).
In outline, we can visualize a chain of causality beginning with a

diet deficient in protein, impairing liver function, producing inability to
127
store glycogen, to inactivate estrogen and insulin, and to activate thyroid.
Low protein and high estrogen cause increased tendency of the blood to
clot. High estrogen destroys the liver's ability to produce albumin (G.
Belasco and G. Braverman, COIl/ro/ of Messenger RNA Stability,
Academic Press, 1994). Low thyroid causes sodium to be lost. The loss
of sodium albuminate causes tissue edema, while the blood volume is
decreased. Decreased blood volume and hemoconcentration (red cells
form a larger fraction of the blood) impair the circulation. Blood pressure
increases. Blood sugar becomes unstable, cortisol rises, increasing the
likelihood of premature labor. High estrogen, hypoglycemia, viscous
blood, increased tendency of the blood to clot cause seizures . Women
who die from eclampsia often have extensive intravascular clotting, and
sometimes the brain and liver show evidence of earlier damage, probably
from clots that have been cleared. (Sometimes prolonged clotting
consumes fibrinogen, causing inability to clot, and a tendency to
hemorrhage.) M. M. Singh, "Carbohydrate ml!labo/ism 11/
Br. J. Obslel. Gynaecol. 83, 1976. Sodillm
decrease, R. L. Seany, Diagnostic Biochemistry, 1969.
Vi.w.:osily, L. C. Chesley, 'Hypertensive Disorders ill Pregnancy,
Appleloll-Cenlury-Crojts. 1978. Claffing. r Cha flerjee. et al.. "Studies
on plasma fibrinogen lew/ ill preeclampsia and eclampsia. Expericlllia
3{ 562-3. 1978; D. M. Haynes, "Medical Complications D/lring
Pregnancy, M(:Craw-Hill Co. Blakisloll Dil'., 1969. Progesterolle
decrease. n. V S'milh, el al., "Estrogen alld progestill ill
pregnallf womell, with espec:ia/ reference to pre-eclamptic toxemia alld
'he effect (!f hormolle adminislratioll." Am. J. Ohstet. CYllecol. 39. 405.
1940: U. l.. Searcy. Diagnosfic fJiochemislry. McGraw-Hii/. 1969.
But the simple chain of causality has many lines of feedback ,
exacerbating the problem, and the nutritional problem is usually worse
than a simple protein deficiency. B vitamin deficiencies alone are enough
to cause the liver's underact ivity, and to cause estrogen dominance, and a
simple vitamin A deficiency causes an inability to use protein efficientlyor
to make progesterone, and in itself mimics some of the effects of
estrogen .
The clotting which sometimes kill s women, can, if it is not so
extensive, causc spotty brain damage, similar to that seen in "multiple
sclerosis," or it can occur in the liver, or other organ, or in the placenta,
or in the fetus, especially in its brain and liver. Some cases of supposed
"post-partum psychosis" have been the result of multiple strokes. When
large clots occur in the liver or placenta., the fibrinogen which has been
128
providing the fibrin for disseminated intravascular coagulation can appear
to be consumed faster than it is produced by the liver. I think its
disappearance may sometimes be the result of the liver's diminished blood
supply, rather than the "consumption" which is the way this situation is
usually explained. It is at this point that hemorrhages, rather than clots,
become the problem . The undernourished liver can produce seizures in a
variety of hemorrhages, hypoglycemia, and brain edema, for
example, so eclampsia needn't be so carefu lly discriminated from "the
other c:mses of seizures."
Because I had migraines as a child, I was interested in their cause.
Eating certain foods, or skipping meals, seemed to be involved, but I
noticed that women often had migraines premenstrually. Epilepsy too, I
learned, often occurred premenstrually.
In my experience of migraine, nausea and pain followed the visual
signs, which consisted of a variable progression of blind spots and lights.
When I eventually learned that I could stop the progression of symptoms
by quickly eating a quart of ice cream, I saw that my insight could be
applied to other situations in which similar visual events played a role,
especially "eclampsia" and "epilepsy." For example, a woman who was 6
months pregnant called me around 10 o'clock o ne morning, to say that
she had gone blind, and was alone in her country house. She said she had
just eaten breakfast around 9 AM, and wasn't hungry, but I knew that the
6 month fetus has a great need for glucose, so I urged her to eat some
fruit. She called me ! 5 minutes later to report that she had eaten a
banana, and her vision had returned .
Early in pregnancy, "morning sickness" is a common problem , and
it is seldom thought to have an)1hing to do with eclampsia, because of tile
traditional medical idea that the fetus "causes" eclampsia, and in the first
couple of months of pregnancy the conceptus is very small . But salty
carbohydrate (soda crackers, typica!\y) is the standard remedy for
morning sickness. Some women have "morning sickness" premenstrually,
and it (like the nausea of migraine) is eased by salt and carbohydrate.
studies have demonstrated that there are spasms of the small
intestine (near the bile duct) associated with nausea.
Hypoglycemia is just one of the problems that develops when the
liver malfimctions, but il is so impOllant that orange juice or ('oca Colu or
ice cream can provide tremendous relief from symptoms. S0dium
(orange juice and Pepsi provide some) helps to absorb the sugar,
essential for helping to restore the blood volume.
Pepsi has been recommened by the World Health Organization for the
129
rehydration of babies with diarrhea, in whom hypovolemia (thickening of
the blood from loss of water) is also a problem.
The problem of refeeding starving people has many features in
common with the problem of correcting the liver malfunction and
hormone imbalances which follow prolonged malnutrition of a milder
sort. The use of the highest quality protein (egg yolk or potato juice, or
at least milk or meat) is important, but the supplementation of thyroid
containing T, is often necessary. Intravenous albumin, hypertonic
solutions of glucose and sodium, and magnesium in an effective fonn
should be helpful (magnesium sulfate injected intramuscularly is the
traditional treatment for eclampsia, since it is quickly effective in stopping
convulsions). While the sodium helps to restore blood volume and to
regulate glucose, under some circumstances (high aldosterone) it helps to
retain magnesium; aldosterone is not necessarily high during eclampsia..
Triiodothyronine directly promotes cellular absorption of magnesium.
Hypertonic glucose with minerals is known to decrease the destruction of
protein during stress: M. Jeevanandam, et aI., Melabolism 40,
1199-1206,1991.
Katherina Dalton observed that her patients who suffered from
PMS (and were benefitted by treatment) were likely to
develop "toxemia" when they became pregnant, and to have problems at
the time of menopause. In these women, it is common for "menstruation"
to continue on the normal cycle during the first several months of
pregnancy. This cyclic bleeding seems to represent times of an increased
ratio of estrogen to progesterone, and during such periods of cyclic
bleeding the risk of miscarriage is high. Researchers found that a single
injection of progesterone could sometimes eliminate the signs of toxemia
for the remainder of the pregnancy. Katherina Dalton, who continued to
give her patients progesterone throughout pregnancy, later learned that
the babies treated in this way were remarkably healthy and bright, while
the average baby delivered after a "toxemic" pregnancy has an IQ of only
85 .
Marian Diamond's work with rats clearly showed that increased
exposure to estrogen during pregnancy reduced the size of the cerebral
cortex and the animals' ability to learn, while progesterone increased the
brain size and intelligence. Zamenhofs studies suggested that these
hormones probably have their effects largely through their actions on
glucose, though they also affect the availability of oxygen in the same
way, and have a variety of direct effects on brain cells that would operate
toward the same end .
130
If Katherina Dalton's patients' IQs averaged 130, instead of the
expected 85, the potential social effects of proper health care during
pregnancy are enormous.
But there is evidence that healthy gestation affects more than just
the IQ . Strength of character, ability to reason abstractly, and the
absence of physical defects, for example, are strongly associated with
weight at birth .
Govemmcnt studies and Social Security statistics suggest the size
of the problem. The National Institute of Neurological Diseases and
Stroke found that birth weight was directly related to 10 at age four, and
that up to half of all children who were undenveight at birth have an 10
under 70.(Chase.) According to standard definitions, about 8% ofbahies
in the U.S. have low birth weight.
Among people receiving Social Security income because of
disability that existed at the age of 18, 75% were disabled before birth . In
94% of these cases, the abnormally was neurological. (HEW .)
A study of8 to IO-year-old children found that abstract verbal reasoning
and perceptual/motor integration are more closely related to birth weight
than they are to IQ. (Wiener.)
National nutritional data that in Ihe U.S. the development
of at least a million babies a year is "substantially compromised" by
prenatal malnutrition. Miscarriages, which are also causally related to
poor nutrition, occur at a rate of a few hundred thousand per year.
(Williams.)
When a muscle is fatigued, it swells, taking up sodium and water,

and it is likely to become sore. Energy depletion causes any cell to take
up water and sodium, and to lose potassium. An abnonnal excess of
potassium in the blood, especially when sodium is low, affects nerve,
muscle, and secretory cells; a high level of potassium can stop the heart,
for example. Cellular energy can be depleted by a combination of work,
insufficient food or oxygen, or a deficiency of the honnones needed for
energy production. When the swelling happens suddenly, the movement
of water and sodium from the blood plasma into cells decreases the
volume ofbtood, )Nhite the quantity of red cells remains the same, making
the blood more viscous.
During the night, as adrenalin, cortisol, and other stress hormones
rise, our blood becomes more viscous and clots more In rats, it
has been found that the concentration of serum proteins increases
significantly during the night, presumably because water is moving out of
131
the circulatory system. Even moderate stress causes some loss of water
from the blood.
If a person is malnourished, a moderate stress can overcome the
body's regulatory capacity. If tissue damage is extreme, or blood loss is
great, even a healthy person experiences hypovolemia and shock.
C.A Crenshaw, who was a member of the trauma team at Parkland
Hospital in Dallas that worked on Kennedy and Oswald, had been
involved in research with G. T. Shires on traumatic shock. In his words,
"we made medical history by discovering that death from hemorrhagic
shock (blood loss) can be due primarily to the body's adjunctive depletion
of internal salt water into the cells." (Shires' work involved isotopes of
sodium to show that sodium seems to be taken up by cells during shock.)
According to Crenshaw, "Oswald did not die from damaged
internal organs. He died from the chemical imbalances of hemorrhagic
shock. From the time he was shot... until the moment fluids were
introduced into the body... " [19 minutes] "there was very little blood
circulating in Oswald's body. As a result , he was not getting oxygen, and
waste built up in his cells. Then, when the fluids were started, the
collection of waste from the cells was dumped into the bloodstream,
slIrldenly increasing the acid level, and delivering these impurities to his
heart . When the contaminated blood reached the heart, it went into
arrest .... " The "waste" he refers to includes potassium and lactic acid .
Crenshaw advocates the use of Ringer's lactate to replace some of the lost
fluid . Since the blood already contains a large amount of lactate because
the body is unable to consume it, this doesn't seem reasonable. I think a
hypertonic version of Locke's solution, containing glucose and sodium
bicarbonate as well as sodium chloride, would be better, though I think
the potassium should be omitted too, and extra magnesium would seem
desirable. Triiodothyronine, I suspect, would help tremendously to deal
with the problems of shock , causing potassium, magnesium, and
phosphate to move back into cells, and sodium to move out, helping to
restore blood volume and reduce the wasteful conversion of glucose to
lactic acid.
Albumin has been used therapeutically in preeclampsia (Kelman),
to restore blood volume. Synthetic polymers with similar osmotic
properties are sometimes used in shock, and might also be useful in
eclampsia, but simply eating extra protein quickly restores blood albumin.
For example, in a group of women who were in their seventh month of
pregnancy, the normal women's serum osmotic pressure was 247 mm. of
water, that of the women with nonconvulsive toxemia was 215 mm., and
132
in the women with eclampsia, the albumin and osmotic pressure were
lowest, with a pressure of 175 rum. In the eighth month, the toxemic
women who atc 260 grams of protein daily had a 7% increase in osmotic
pressure, and a g roup who ate 20 grams had a decline of5}O/o.(Strauss) In
a group of preeclamptics, plasma volume was 39% below that of normal
pregnant women .
Besides protein deficiency and other nutritional deficiencies,

excess estrogen and low thyroid can also limit the liver's ability to
produce albumin . Hypovolemia reduces liver function, and (like hepatic
infarcts) will reduce its ability to maintain albumin production ..
The studies which have found that hospitalized patients with the
lowest albumin are the least likely to survive suggest that the
hypovolemia resulting from hepatic inefficiency is a problem of general
imponance, and that it probably relates to the multiple organ fa!!ure
which is an extremely common form of death among hospitalized
patients. A diet low in sodium and protein probably kills many more
people than has been documented. Ir old age is commonly a hypovolemic
condition, then the common salt restriction for old age hypertension is4
just as irrational as is salt-restriction in pregnancy or in shock. Thyroid

(T.l)' glucose, sodium, magnesium and prolein should be considered in
any state in which weakened homeostatic control of the composition of
plasma is evident.
"'Note: Although Konrad Lorenz (who lalcr rccci\'cd the Nobel Prize) was Ihe
architect of the Naz i's policy of "racial hygiene" (cx1crmination of those wilh
unwanted physical. cultural. or politic.11 trailS which ""ere supposedly detcrmined by
"gencs") he took his ideas from the leading U.S. geneticists. whose works wcre
published in the main genctics journals. Following the Nazi's defeat, some of these
journals werc renamed. and the materials on eugenics werc often remo\"ed from
librarics. so Ihat a new historical resume could be prcsented by the proression.
AOOITIONAL REFERENCES
I. G. et al. . "Correlate:; of low birth w.::ight: Psychologic.. 1 at eigllt to tell

of age: Pcdiatr. Res. 2. 110-101. 1968.
2 , A Chas.::. "The great pellagra co\·...'r-up." Psychol. Today, pp. 83-86, Feb., 1975.
3. Pn:vention Handbook. Natl. Assoc, for Ci tizens. 1974.
4. US HEW, The WOlllcn and Their Pregnancies, W.u. Saundcr"l; Co .• 1972.
5. M. Winick aud 1'. Rosso, "The efti:cl of severe early malnutrition on cellular grov.th of
hmnan brain: p....diatr. R(.'S. 3. 181 · 184. 1969.
6. Roger Williams, Nutrition Disease, Pitman Publ. , 19 71 .
7. H.M. &luneck, Jr., "Brain hann in US laid to food lack," N. y , times, Nov. 2, 1975.
III
8. [(. Hurley, PQverty and Rdardation : A Causal Relationship , Random Ilouse , 197U,
9. n . Shuilkliu [Iud J. l1ooil\, Mutemal NUlrition ami Child Ikahh, C . C. lliomas,
11). 11.11. RccS<.', 1/. A. I'askind, and E. I.. 1936 Yi:.1r Book of NCUT010¥)'.
:md Endocriuoiogy. Year I300k Publishers, Chicago, 1937.
I I . M. lI. "OhS<!rvations on Ih.: of the IOM:mias of pregnancy: The relationship
of hypoproteinemia , and clcval,:d venous pn.:;;su]'c 10 rd<.'1llion in
pregnancy," Am J. M....J. S<;;j, 190.811-&24.19.,5.
11. "Albumin i:onCcnlnltion can t>.: USl.'d lor mild Ob,tct. Gyncool. News,
Oclol:J<:r l. 1974.
lJ. L. Kelman. d aL. "En"'C1S of dietaf}' pro!.::ill n:strictioll on albumin albumin
call,holism, and Ihe pl1ls!l111 aminogram ," Am. J. Clin. Nlltr. 25, I 174·1 1710:, 1972.
14. T. II. Rr.:wcr, "Rot..: of mulnmrition, dysfu!lction, and bactcria in Ihc
pathogenesis (If acule lox.::miu 01 Ant J. Obslct. Gyn.::col. 84, 12:>3-1256, 1962
15. "Plasll1u volume 'a clnt' 10 hypo::rtension ri s}';;: OOsle\. GI'Ilc\;ol. Ohs..:r\"er,
1975.
16. C A. C'r.::nslww, MD. J. I lanscn 1. G. ShUll". JFK: Conspiracy ojSUence. 1992.
17. 1'. Bilckstrum. "Epileptic seizures in women relaled to plasma cslrogl11 and progc;krone
during (he iIlcnslJ1.);l1 cycle." Acta N.... urol. SC<lnd, S4, 321-347, 1976.
C. Mullcr, el aI. , ·Rcl'ersib!.... bilul .... rul C<.."TChral clmng.... s on magnetic rCSOIUII1CC imaging
during cciampsiil," J,)culschc Wochell,;chrift 121 (39), I \84-1 188, ! 996. (Brain
edema was
134
PART FOUR: SOME IN CON'lEXT
25
ESTRIOL, DES, DDT, ETC.
As the result of industrial promotion, including product
advertising and granlS for research, "weak estrogens" and "antioxidants"
derived from soy are being discussed as means to prevent breast and
prostate cancer, heart disease, stress and aging.
Japanese women used to be very free of breast cancer, and when
their children grew up in the U.S., their incidence of the disease was like
that of Americans. How odd that the soybean should be singled out for
responsibility. Japanese breast cancer incidence has risen sharply in
recent years. Did they stop eating tofu? Did their traditional use of
seaweed as food have nothing to do with their health? Did the traditional
home-bound isolation of Japanese women, their avoidance of smoking
and drinking, have no effect on hormones and cancer? Their calorie
intake? Iodine and trace minerals? What types of protein and fat, in what
quantities, did they use?
Another so-called weak estrogen, estriol, is being promoted by
drug companies for the "alternative medical" market, with the circulation
of an editorial from lAMA, recommending it for preventing breast cancer.
A review of the use of estrogens reported in JAMA (only up to 1987)
found nearly 200 different "indications" for its use. (Palmlund, 1996.)
Using the conservative language of that journal, such use could be said to
constitute wildly irresponsible "empirical" medical practice. More
appropriate language could be used .
Pollution of the environment and food supply by est rogenic
chemicals is getting increased attention. Early in the study of estrogens, it
was noticed that soot, containing polycyclic aromatic hydrocarbons, was
both estrogenic and carcinogenic. Since then, it has been foun d that
phenolics and chlorinated hydrocarbons are significantly estrogenic, and
that many estrogenic herbicides, pesticides, and industrial by-products
persist in the environment, causing inferti lity, deformed reproductive
organs, tumors, and other biological defects, including immunodeficiency.
In the Columbia River, a recent study found that about 25% of the otters
and muskrats were anatomically deformed.
Estrogenic pollution kills birds, panthers, alligators, old men,
young women, fish, seals, babies, and ecosystems. Some of these
chemicals are sprayed on forests by the US Department of Agriculture,
135
where they enter lakes, underwater aquifers, rivers, and oceans. Private
businesses spray them on farms and orchards, or put them into the air as
smoke or vapors, or dump them directly into rivers. Homeowners put
them on their lawns and gardens.
Natural estrogens, from human urine, enter the rivers from
sewage. Many tons of synthetic and pharmaceutical estrogens,
administered to menopausal women in quantities much larger than their
bodies ever produced metabolically, are being added to the rivers.
In the same way that weak estrogens in the environment may
become hundreds of times more estrogenic by synergistic interactions 0.
A. McLachlan, ct aI. , Sdence, June 7, 1996), combinations of natural,
medical, dietary, and environmental estrogens are almost certain to have
unexpected results. The concept of a "protective estrogen" is very similar
to the idea of "protective mutagens" or "protective carcinogens," though
ill the case oj estrogens, their promoters don't even know what the
1I0rmal, natllral jUllctions oj estrogen are.
In November, 1995, an international conference was held to study
the problem of "Environmental endocrine-disrupting chemicals," and to
devise strategies for increasing public awareness of the seriousness of the
problem . Their "Statement from the work session" says "New evidence is
especially worrisome because it underscores the exquisite sensitivity of
the developing nervous system to chemical perturbations that result in
functional abnonnalities. " "This work session was convened because of
the growing concern that failure to confront the problem could have
major economic and societal implications." "We are certain of the
following: Endocrine-disrupting chemicals can undermine
neurological and behavioral development and subsequent potential
of individuals .... " "Because the endocrine system is sensitive to
penurbation, it is a likely target for disturbance." "Man-made
endocrine-disrupting chemicals range across all continents and oceans.
They are found in native populations from the Arctic to the tropics, and,
because of their persistence in the body, can be passed from generation to
generation." " ... many endocrine-disrupting contaminants. even if less
potent than the natural products. are present in living tissue at
concentrations millions of times higher than the natural hormones."
"The developing brain exhibits specific and often narrow windows during
which exposure to endocrine disruptors can produce permanent changes
in its stl1Jcture and function ."
In spite of this increased exposure to estrogens, there is a new
wave of advertising of estrogenic substances, based on the idea that weak
136
estrogens will provide protection against strong estrogens. The
environmental background of estrogenic pollution already provides a
continuous estrogenic exposure. In the 1940s, Alexander LipshulS
demonstrated that a continuous, weak estrogenic stimulus was immensely
eft'eclive in producing, first fibromas, then cancer, in one organ after
another, and the effect was not limited to the reproduct ive system. How
is it possible that the idea of "protection" from a weak estrogen seems
convincing to so many? Isn't this the same process that we sa.w when the
nuclear industry promoted Luckey's doctrine of "radiation hormesis,"
literally the claim that "a little radiation is positively good for us"?
DES (diethyl stilbestrol) is one of the most notorious estrogens,
because studies in humans revealed that its use dU1;ng pregnancy not only
caused cancer, miscarriages, blood clots., etc., in the women who used it,
but also caused cancer, infertility, and defonnities in their children, and
even in their grandchildren. (But those transgenerational effects are not
unique to it. )
Besides the absurd use of DES to prevent miscarriages, around
1950 it was also used to treat vulvovaginitis in little girls, for menstrual
irregularity at puberty, to treat sterility, dysfunctional bleeding,
endometriosis, amenorrhea, oligomenorrhea, dysmenorrhea, migraine
headaches, nausea and vomiting, and painful breast engorgement or
severe bleeding after childbirth.
DES is a "weak" estrogen, in the sense that it doesn't compete
with natural estrogens for the "estrogen receptors." (Estriol binds more
strongly to receptors than DES does: "Cytosolic and nuclear estrogen
receptors in the genital tract of the rhesus monkey," J. Steroid JJiach.
8(2), 151-155, 1977 .) Pills formerly contained from 5 to 250 mg. of DES.
The 1984 PDR lists doses for hypogonadism and ovarian failure as 0.2 to
0.5 mg. daily. In general, dosage of estrogens decreased by a factor of
100 after the 1960s.
An aggressively stupid editorial by Alvin H. Follingstad, from the
Jan. 2, 1978, issue of JAMA, pages 29-30, "Estriol, the forgotten
estrogen?" is being circulated to promote the use of estriol, or the
phytoestrogens. It argues that women who secrete larger amounts of
estriol are resistant to cancer.
By some tests, estriol is a "weak estrogen," by others it is a
powerful estrogen.
When estriol was placed in the uterus of a rabbit, only 1.25 meg.
was sufficient to prevent implantation and destroy the blastocyst.
(Dmowski , et aI. , 1977.) Since the effect was local, the body weight of
137
the animal doesn't make much difference, when thinking about the
probable effect of a similar local contentration of the hormone on human
tissues. The anti-progestational activity of estriol and estradiol are
approximately the same. (Tamotsu and Pincus, J 958 .)
When 5 mg. of estriol was given to women intravaginally, this
very large dose suppressed LH within 2 hours, and suppressed FSH in 5
hours. Given orally, 8 mg. had similar effects on LH and FSH after 30
days, and also had an estrogenic effect on the vaginal epithelium .. These
quick systemic effects of a "weak estrogen" are essentially those of a
strong estrogen, except for the size of the dose. (Schiff, et aI. , 1978)
When administered subcutaneously, estriol induced abortions and
stillbirths (Velardo, et al.)
Another indication of the strength of an estrogen is its ability to
cause the uterus to enlarge. Estriol is slightly weaker, in tems of
milligrams required to cause a certain rate of uterine enlargement, than
estradiol. (Clark, et aI. , 1979.) But isn't the important question whether
or not the weak estrogen imitates all of the effects of estradiol , including
carcinogenesis and blood clotting, in addition to any special hannful
effects it might have?
When added to long-term culture of human breast cancer cells,
estriol stimulated their growth, and overcame the antiestrogenic effects of
tamoxifen, even at concentrations hundreds of times lower Ihan that of
tamoxifen . "The data do not support an anliestrogenic role for estriol in
human breast cancer." (Lippman, et al. . 1977.)
Studies of the urinary output ofestriollestradiol in women with or
without breast cancer do not reliably show the claimed association
between low estriol/estradiol and cancer, and the stimulating effect of
estriol on the growth of cancer cells suggests that any alteration of the
estrogen ratio is likely to be a consequence of the disease, rather than a
cause. The conversion of estradiol to other estrogens occurs mainly in
the liver, in the non-pregnant woman, as does the further metabolism of
the estrogens into glucuronides and sulfates. The hormonal conditions
leading to and associated with breast cancer all affect the liver and its
metabolic systems. The hydroxylating enzymes are also affected by
toxins. Hypothyroidism (low T3), low progesterone, pregnenolone,
DHEA, etiocholanolone, and high prolactin, growth hormone, and
cortisol are associated with the chronic high estrogen and breast cancer
physiologies, and modifY the liver's regulatory ability.
The decreased output of hormones when the fetal-placental
system is dying is a natural consequence, since the placenta produces
138
hormones, and during pregnancy converts estradiol to estriol. Since
estradiol in excess kills the fetus, its conversion by the placenta to estriol
is in accord with the evidence showing that estriol is the more quickly
excreted form. (G. S. Rao, 1973.) The conversion of 16-hydroxy
androstenedione and 16-hydroxy-DHEA into estriol by the placenta
(Vega Ramos, 1973) would also cause fetal exhaustion or death t.o result
in lower estriol production. But a recent observation that a surge of
estriol production precedes the onset of labor, and that its premature
occurrence can identify women at risk of premature delivery (McGregor,
et ai. , 1995) suggests that the estriol surge might reflect the mother's
increased production of adrenal androgens during stress. (This would be
analogous to the situation in the polycystic ovary syndrome, in which
excessive estradiol drives the adrenals to produce androgens.)
Estetrol, which has one more hydroxyl group than estriol, is a
"more sensitive and reliable indicator of feta l morbidity than estriol during
toxemic pregnancies," because it starts to decrease earlier, or decreases
more, than estriol. (Kundu, et aI. , 1978.) This seems to make it even
clearer that the decline of estriol is a consequence, not a cause, of fetal
sickness or death .
A 1994 publication (8. Zumoff, "Hormonal profiles in women
with breast cancer," Obslet. GYllecol. Clill. Nor/h. Am. (U.S.) 2/(4),
751-772) reported that there are four honnonal features in women with
breast cancer: diminished androgen production, luteal inadequacy,
increased 16-hydroxylation of estradiol, and increased prolactin. The
16-hydroxylation converts estradiol into estriol.
A new technique for radiographically locating a
hormone-dependent breast CMcer is based on the fact that estriol-sulfate
is a major metabolite of estradiol. The technique showed the tumor to
have about a six times higher concentration of estriol-sulfate than liver or
muscle. (N. Shimura, et aI., "Specific imaging of honnone-dependent
mammary carcinoma in nude mice with ( 131 1]_anti_estriol 3-sulfate
antibOdy," Nue/. Med BioI. (Eng/and) 22(5),547-553,1995.)
Another association of elevated conversion of estradiol to estriol
with disease was found to occur in men who had a myocardial infarction,
compared to controls who hadn't. (W. S. Bauld, et aI., 1957.)
The estrogens in clover have been known for several decades to
have a contraceptive action in sheep, and other phytoestrogens are known
to cause deformities in the genitals, feminization of men, and anatomical
changes in the brain as well as functional masculinization of the female
brain. (Register, et aI. , 1995; Levy, et ai, 1995; Clarkson, et al., 1995;
139
Gavaler, et a!. , 1995.) The effects of the phytoestrogens arc very
complex, because they modify the sensitivity of cells to natural estrogens,
and also modify the metabolism of estrogens, with the result that the
effects on a given tissue can be either pro-estrogenic and anti-estrogenic.
For example, the flavono ids, naringenin, quercetin and kaempherol
(kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify
the metabolism of estradiol, causing increased bioavailability of both
estrone and estradiol. (w. Schuben, et al ., "Inhibition of
17-beta-estradiol metabolism by grapefruit juice in ovariectomized
women," Mafllrifm" (ire/aI/d) 30(2-3), 155-163, 1994.)
Since phenolic compounds often function as "antioxidant s," as
well as estrogens, we are seeing an epidemic of marketing claims for plant
substances that are "better than vitamin E" and "better than Premarin,"
but something that these super-antioxidants have in common with all
estrogens is that they are easily oxidized, fonning cycles of
oxidation-reduction that consume oxygen, waste energy, and produce
immense quantities of free radicals, causing genetic damage as well as
other changes. That the damage might lead to cancer or seizures is bad
enough, but the awful thing is that some of the changes are passed on in
heredity, as cancer, or anatomical or neurological abnormalities._ L.e .
Strong pioneered in the study of the hereditary toxicity of estrogen,
generations ago, and transgenerational effects have been seen with DES
and other estrogens.
Why do plants make phytoestrogens? There is some infonnation
indicating that these compounds evolved to regulate the plants'
interactions with other organisms--to attract bacteria, or to repel insects,
for example, rather than just as pigment-forming materials. (Baker,
1995.) The fact that some of them bind to our "estrogen receptors" is
probably misleading, because of their many other effects, including
inhibiting enzyme functions involved in the regulation of steroids and
prostaglandins. Their biochemistry in animals is much more complicated
than that of natura! estrogens, which is itself so complicated that we can
only guess what the consequences might be when we change the
concentration and the ratio of substances in that complex system. (See
quotation from Velardo, et ai. , page 6)
These "natural" effects in sheep were forerunners of the observed
estrogenic effects in wild animals, caused by pollutants_ Twenty-five
years ago I reviewed many of the issues of estrogen's toxicity, and the
ubiquity of estrogenic substances, and since then have regularly spoken
about it, but I haven't concentrated much attention on the phytoestrogens,
140
because we can usually just choose foods that are relatively free of them.
They are so often associated with other food toxins--antithyroid factors,
inhibitors of digestive enzymes, immunosuppressants, etc.--that the
avoidance of certain foods is desirable. Recently an advocate of soybeans
said "if they inhibit the thyroid, why isn't there an epidemic of
hypothyroidism in Asia?" I happened to hear this right after seeing
newspaper articles about China's problem with 100,000,000 cret ins; yes,
Asia has endemic hypothyroidism, and beans arc widely associated with
hypothyroidism.
When I first heard about clover-induced miscarriages in sheep, I
began reading about the subject, because it was relevant to the work I
was doing at that time on reproductive aging. Sheep which are adapted
to living at high altitude, where all animals have reduced fertility, have an
adaptive type of hemoglobin, with a greater affinity for O"1'gen. Fetal
hemoglobin, in animals at sea-level, has a great affinity for oxygen,
making it possible for the fetus to get enough oxygen, despite its
insulation from the mother's direct blood supply. The
high-altitude-tolerant sheep have hemoglobin which is able to deliver
sufficient oxygen to the uterus to meet the needs of the embryo/fetus,
even during relative oxygen-deprivfltion. These sheep fire ahle to sllstain
pregnancy while grazing on clover. It seemed evident that estrogen and
high altitude had something in common, namely, oxygen deprivation, and
it also seemed evident that these sheep provided the explanation for
estrogen's abortifacient effects.
Estrogen's effects, ranging from shock to cancer, all seem to relate
to an interference with the use of oxygen. Different estrogens have
different affinities for various tissues, and a given substance is likely to
have effects other than estrogenicity, and the presence of other substances
will modify the way a tissue responds, but the stressful shift away from
oxidative production of energy is the factor that all estrogens have in
common. Otherwise, how could suffocation and x-irradiation have
estrogenic effects?
Pharmaceutical misrepresentations regarding the estrogens rank,
in terms of human consequences, with the radiation damage from faJI·out
from bomb tests and reactor-leaks, with industrial pollution, with
degradation of the food supply--with genocide, in fact.
Advertising gets a bad name when it can't be distinguished from
mass murder. At a certain point, we can't afford to waste our time
making subtle distinctions between ignorance and malevolence. if we
begin pointing out the lethal consequences of "stupid" or quasi-stupid
141
commercial/governmental policies, the offenders will have the bw"den of
proving that their actions are the result of irresponsible ignorance, rather
than criminal duplicity. From the tobacco senators to the
chemical/pharmaccuticai/foodfcnergy industries and their agents in the
governmental agencies. those who do great harm mllst be held
responsible.
The idea of corporate welfare, in which public funds are given in
massive subsidies to rich corporations, is now generally recognized .
Next, we have to increase our consciousness of corporate responsibility,
and that ordinary criminal law, especially RICO, can be directly applied to
corporations. It remains to be seen whether a government can be made
to stop giving public funds to corporations, and instead, to begin
enforcing the law against them·-and against those in the agencies who
participated in their crimes.
[n the U.S., the death penalty is sometimes reserved for
"aggravated homicide." If those who kill hundreds of thousands for !he
sake of billions of dollars in profi!s are not committing aggravated
homicide, then it must be that no law wriuen in the English language can
be objectively interpreted, and the legal system is an Alice in Wonderland
convenience for t he corporate state.
REFERENCE S
I. Or. lkrnard wciss , Dep!. of Em'iromncnta l Unh·..:rsity or i{Ql.:hest..:r School of

Medicine, RQl.:hestcr, NY . amI 17 othcrs, work session on cl]\'ironmental
d\<;!micals, 5-10, 1995.
2. 1s,1ac Schill, et aI. , of estriol administration on the woman ," Fen il.
Ster;l. 30(3), 278-2!12, 1978.
3. N. P. 1. Knndn, e! ai. , · Scqnentiol determination of human placental lae((Jgcn , estriol,
und estctrnl for assessment of morbidity," Obste! G)llL·WI. 52(5), 5 D-S20, 1978 .
4 . M. E. Licbennan. ct aI. , ' Estrogen control of prolactin i<yIlthesis in vitro," PNA.s. (USA)
75(12),5946·5949,1978.
5 Murc Lippman. ct aI. , of estrone, and ,;:striol on I'';: human
c.. in long kml tisslle Cancer Res. 37(6). I '.10 1_! 907. 1977.
6. W. P. JAllowski, et :11., "En':.: t of intrauterine estriol on rejJrodnctil'c tlll)Clion in Ih,;: m!>bi!. ·
F<.'J1iL Stcril. 28(3), 262-8. 1977.
7 . W. S. Baliid. cl ai , "Abnol1nnlity mctnbolism in human sultiL'<:h witll mynCilrdlal
inC1rctiotl: Crm(ldi(1It JOI/I". lJiOc/II!III. (111(/ Physiol. ]5(/2). 12TI-1 288. 1957. (Th,;:
of estrmlio! to wus higher in men II ilh prcl'iolli; mYIX'"rdial inf;lrction than ill l"Ontrols.)
8. R A. Edglcn and D. W. Ca lhoun , '"lmcr;'ctioll of on Ihe I'agina l $m ...-nr or sp"ycd
rat"," ilm. J . Phys;ol. 189(2i. 355-337, 1957. "Employmg Ihe \"a<1iI1111 smear liS all index or
cn-"d , wmbmat ions or various substances" erc tested ((If iutct;iclion. Ilere
concentmtcu at the approximnte 50% response k,·ct." "'!llC;;C d!i1i1 arc iuterprc\cd:ls illdkltinJ,!
simple additivc rdutiOl1 Ship, !lllIOlIg, thc cf'm ponuds tcsted.' "Curiously theil, cstmgens that
showcd inhibitory when ..:d on ut.:rille gm"lh ImJ simple ad(!itil'<:
intera'·'.i OllS "hen !cst.:<.1 Of! the I'aginul " ..it secm, r..:asonabk 10 that :,
142
gh-<''11 honnon.:: combination may evoke dillCring levels of response in lilTgi:l ol1!ans,
and that increase of one COnl!X'llcnl mlly increase n::spous.: :11 nne sil': while
d.:.'Creasing it 111 Ollolilcr. Many stcroidg, ..arc present in the 11l!Hlml<llian circulation Juring
various pha.'><!s of the sex cycle lind arc knO\\11 10 modiry the of any gi\'cn -nlis
hon nona] muUiplicity appan::ntly consti tutes an CSlrogcn-buO<'-:ring system lind snpports the
hypothesis that 'lCxlIal responscs ' ... upon a rotllt::r prt..'Cise lionncn!!1 homeostasis.'"
9. R. C . Merrill, "Estriol: A fCvieW," Phvsiol. Rei'S. 38(3), 463-480, 1958. " ... c§triol itself i) 8
potent estrogen , to the (onco:ption of ih being just a metabolite o f the mort'"
potent estrone lind estradi ol. Allhongh ordinari ly less eflectil'e than estrone and estmdio[ in
promoting \"3{!.illal eomiJicution, eslIiol, Wlili.>r optimum conditions, upproa<.:hes thdr
ctlix:ti \'ClIO:SS for this purposc, Estnol is nlore potent than estrone Of estradiol in causing
establishment und op,.."llillj! of th.;: vag.inal ontke, in promoting imbibition of uterine Ilnid, in
incro.1sing lactic dchydrogcna"'c! activity in Ille lind ill stimulating mitotic acti vity in the
cpidcnn is ofthc mouse ,:ar. 111C octivity of cstriol is ofthc same of<kr of magnitude as that of
cstronc and ...'Stmdio l in olh...'!' cSlrogenic aclious, 10 promotc utenne gro\\1h at low
oouccmm tiO)lS (although less e!)",<:ti\'c (It high to inCTCIISC b.!ta-glucuronidase mid
rcducc::d diphosphop,1'idine nuc1CQtidt: activity in thc uterus, to reduce Ulotili1r of Ihc
uterus in vi\'o, and to stimulate ovarian gfO\.\1h , body wcight , phagoc)1osis of carbon by
rdiculocndolhci ial cells, cilia£)' 1l\O\'emcnts of thc bUl;copharyllgcal m\J{,'ose of the frog, and new
bone fonnalion. The fibromatog...llic aetivity or cslriO! in thc guine3 pig is llI\1l;h koss than that
of .:.'S tronc or Recent expcrimcllts suggest and JXlrtly \'eriry hypolhesis that estriol
stinllllat.:.'S the <.:eTvix, \'agina and \'u\I'<I ,Il\OfC ctl,,'Cth'ely thun cstrone or estradiol, wh ... Ihe
arc much more c!TCCti\'c on the corpus ut ...-ri."
10_ T. Miyake and G_ Pinctls, "Anti-progestaliolllll aClivily of estrogens in rabbit ClldotllelIilun,"
Proc. Soc. h'Xflll. mol. ami M".!. 99(1) 478 -482, 1958. "The nnli-progeslationa! activily of.:l
.. '-'strn<liol , ,",slriol, :md slilbeslro\_aomin;skrcd \.\;\h
progcstcrolle into rabbils has b..."Cu ..'(L · " Tht anti-progestational
aelh'il!es uf these are th(' ", .. estrogen may
real'ttvity of the endolllelrill11l to progesterone mther thun ncutmlize or inactivate prog.csk-rone
in the body."
II, J. T . Velardo, d aI. , 'EITL'<:t of I'mious steroids on g...'Slation and litter size ill mts," Fertili/y
tim/ Sterility 7(4), 30 1-311 , 1956, • ... I;ertain mctabolites of estrogCllic and prog.eslatil'C
substllllces that \\-L'Te prcviously considered 10 b.: \\'C/lJ.:' or in ert may well play (I rolc ill the
rcprodllail'c process." "W(' han' been impressfi'tl with the probability Ihat an)' ('ndocrille
receplor-organ Is n(lt ac complished by the indq}l'ntlt'nt !!ction of one hormone
alone, It Hpp ear,; more Iike1)' that s ue h is tlie physiologic!!1 express ion of the
tOlltl of tlil' biologic liormones and their metaho1itcs in coneen on the re«ptor organs,"
"The cll'cct of ...'>Itnol on Ihe birth nilc of IheS<! \1'(1, moTt! drnmatic ." " _.when L'Striol was
ll!iCd mating, it r<!duc ...'<i Ihc !ilk-r size 10 66 PCI' C"'''llt of thl; controls." "J-lowcv<!r, I\1lCli
th..: same \\us employed from thc day of mating and daily thereatk'r the tiille of
implantatioll. 6 days \alL-r. a reduction of Ii\'<! births 10 33 pcr celli of thc controls was
produc .......1. [Htllis eXIJ<.'1'imclli Ih" Oled;,'aliou \Il! ;; l\ithhcl<J \l util aftcr O\'ulatioa ha.1 preslUnnbly
occurr...'d. 'lllC prescnce or plac",'uta! so::afS and (Ill incrcaS<..'y th..: I;slrogen in the tubc,.'
".. .Ihe or plllcl;nlal scar>;, abortions, and ,Ii!lbirths lilrthcr bears witn..:ss to lhc
possibi lity tlU!t the st<!roids cmploycd intcrfercd wilh thc oplirmun dit)\.'Tcmiutiotl of
progestational endometrial chfll\gL'S, mth ..... than any suppression of ovuh1tory
mechanisms ."
12. D_ Rcgister, c\ ul., ' En<:ct of !lcona!.11 e .... flOSur..: to dicthylstilbclitrol, COll11lcstrol, and
!:>eta-sitostcrol ()f\ pituitary and sexually dimorphic Iluclcus \'olullle," /'.SH.B.,If.
208. 72,1995 .
143
13. J. It Levy, et a!. , "DYee! of prenatal exposure to the ph}1ocstrogcll genistein 011
dilli:I\.'IItialiOIl ill rats: I'.S.EB.AI. 208, 60 , 1995.
14. B.O. L}11-Cook, d aI. , "M.::thylatioll promc lind mlll,1;lication of pro\(}.{)lll.-'Q\!,cncs in r..t
pancreas induced with phytocstmg..:ns," J'SEJJ:l11Q8, 116,
IS. J. S. Ga,'akr, d al., "l'hytOC»trogCll of alcoholic CIII1\.'1\1 stalus,:
PSEBM lQ8, 9&, 1995.
16. A. I. NWanncnna, d aI. , "Cliuku! changes in OVl'Irit:'':lomized C\\,(."i> CXj)()SI.>U 10
ph)1U<.'Slrogcns and 17OCla-c::;tmJ iol implmlls: I'SEBM 208. 92 , 1995.
17. P. L. Whitten , .::1 al.. "lnflucuw of phytoc51rogcn dids Oil cslr<ldioJ <lclioll in Ille mt
Steroids 59, 443--449, 1994. did not anta gonize the utcrolrophic action of
estradiol when adminbtert"d either prior to, or joinlly with, E2 treatment, or when
admini5tered orally or parenterally," " These finuings eontraui(t the anumption that all
phylOCltrogenJ are necessarily anliprollferatiH agents .... "
18. M. E. Baker, "Endocnue activity of plant-deri\'ed compounds: An elull,ltiOllar;.'
perspe<.:th'C," J>SERH 208,13 1, 1995.
19. I. Palmluud, "To cell from elwiromnclll," Chapt",'\" 19 in Cell"I",' (md Molecular
,\·k 'dlal/isms ojHomrollal Carcjllog(''1lesiJ, published by Wiky-Liss.
20. J . H. Clark . et aI. , "Nuclear binding of the estfl)gen "-"'«-'Plor: I·!ct",-rogcn<.'ily of sitcs and
uterotropic responsc," Sleroid Hom wlle R,,'ceplOI" SY.TIL'IIIS. pngc 17, 1979.
21. P. Vega Ramos. ct at.. "Fonnation of o<:striol from (;19 , 16-oxygenah..-d steroids by
microsomal preparation;; of hwuan placenta," Re.I. (l/I SIi:rojds. vol. V, page 79, Pn)\;. of the
Fmh Mcctinl,l of U1I:: International Study Group lor SK'mid L-diled by M . l'inkelstcin,
dal..19H
22. G . S. Rae, "EI17.ymes in st<.."foid metabolism," Re.f. "11 Sleroids, wll. V, page 175, 1973.
23. !.. I I. Cuner and C. B. Hanington, Admilri.<lmlil'e l..aw mrd Politics HurpcrCollins, 1991 .
"Cllplur" "hen infonnally promote Ih" in"'..."sts they are ollie;:>!!y
rc"pollsible for f<!gulating." In 1925, Cooli<lge's appoililmeni of "anli-public" W. E J JUlllphrcy
10 Ih" FT(; kd some of ils fonner support",-n; 10 ca.l! for the abolition oftbc FT<':'
"If ncarly II century of regulllt(lr)" history telts us it that th e
agcndcli of lire almost jm'lI riably captured by the industrie)
which they established to control. " Rob<..'!1 Heilbroner, [n the Name of Profil, 1972 , p .
239. 'Federal economic regulation was g"''U<."nIlt)' dt!SigJlL'<.1 b)' the regulated to its
01\11 (.'lId, and not those of the pllhlic or Ihe commonweal." Gabriel Kolko, rho! Tl'iumph oj
Consen·atism: A Reill/o!rprelolicm ojAmeriC(/It Ws/ory, /'100-19/6, 1%3.
"It is a given in tlte modem doctrine of most ton laws the of potential
liability if anything encouragL'l! citizens to U:le gn:aler IhllllghtlilJr1l:SS lind care in their ilitily
actions. and no obvious I\!lIsons suggest the salllC dynamic should not al1':ct puhl;c nfficinls. "
Adm. Law. & Pob .. p. 404. "That Congress d<:cidcd. after the pilssage of the FIlUrtt!<.'11th
Amendment, to enact legislation s]ledfica!! y requiring state to respond in fcJt'Tal court
for their lailure:; 10 obs...,-ve tb.:: collslitutionallimi talions ou their hardly reason lllr
exc llsing their fe<kn! L"Olmtcrparts for the identical constitutional tmosgr;..'Ssions· "In
situations of abuse, an aCllon fQr damages against the res ponsible official can t.e an
important of "indicating constitutional .. ,." Ju stice White, Butt v.
Economou, p, Adm. Law & Pols.
144
26
SUNLIGHT: USING IT TO ENHANCE LIFE
GLOSSARY:
Mutations are changes in DNA molecules which can kill
cells, or accelerate their aging, or contribute to the
development of cancer.
Cellula.- respiration: the ability of cells to consume
oxygen and produce useful biological energy.
Free radicals are parts of molecules thai can be produced
by radiation (including sunlight), which contribute to cell s'
aging, cancer, and mutations.
The thymus gland is an essential part of our immune
system, and it shrinks when we don't get enough light .
Melatonin, or pineal hormone: the pineal gland in the brai n
responds to an absence of light (or to any stress which
increases the adrenalin systems) by secreting a hannone
call ed melatonin, which lightens the skin, makes the brain
sluggish, turns off thyroid and progesterone production, and
suppresses immunity and fertility.
Immunosuppression refers to any process that lowers the
efficiency of our immune system, such as stress, radiation, or
. .
pOisonmg.
Q: You mention sunlight as beneficial to your health. How?
For example, it can cure depression, improve immunity, stimulate

our metabolism while decreasing food craving, and increase our
intelligence.
Although exposure to sun does contribute to aging of the skin,
people who spend years working outdoors have a reduced incidence of
cancer of internal organs. For many years, it has been known thaI the
death rate increases during the winter months and also increases at night
(winter or summer). Most deaths occur just before dawn when the body
is in it s least efficient Sl<ll c. It is just in the last few decades that we have
been learning the reasons lor this beneticial ctfect of light. It turns out
that daylight stimulates our ability to use oxygen for energy product ion,
and protects our tissues from some of the free-radical toxins that are
produced by normal metabolism, by stress, or by radiation.
145
While ultraviolet light. and even blue light, tend to suppress our
cells' ability to produce energy, those types of light penetrate only a short
distance into living tissue, and so it is mainly the skin which is damaged
by too much sunlight. Since blood does circulate in the layers of skin
which receive ultraviolet rays, prolonged sun exposure can damage the
immune system by injuring white blood cells, but usually the stimulating
effect of the other types of light that penetrate more deeply offset this
effect on the immune system.
Many health food stores are now selling melatonin, to induce
sleep and "prevent cancer." They have taken some infonnation out of
context, and don't realize how dangerous melatonin is. It makes the brain
sluggish, causes the sex organs to shrink, and damages immunity by
shrinking the thymus gland. It suppresses thyroid and progesterone, and
increases estrogen . It is the hormone of darkness and winter, and is
produced in the pineal gland by any stress which increases adrenalin.
Adequate sunlight suppresses the formation of melatonin.
This means that the immune system is most responsive in the
summer, when days are long. Daylight stops the stress reaction, and
protects our immune system .
Long hours of daylight increase progesterone production , and Ihis
contributes to a sense of well-being, and to the protection of all our
tissues.
Q: Doesn't exposure to the sun age you?
This effect is variable, and depends on our honnones and diet.

The unsaturated oils have been identified as a major factor in skin
aging. For example, two groups of rabbits were fed diets containing
either corn oil or coconut oil, and their backs were shaved, so sunlight
could fall directly onto their skin. The animals that ate corn oil developed
prematurely wrinkled skin, while the animals that ate coconut oil didn't
show any harm from the sun exposure. In a study at the University of
California, photographs of two groups of people were selected, pairing
people of the same age, one who had eaten an unsaturated fat rich diet,
the other who had eaten a diet low in unsaturated fats. A panel of judges
was asked to sort them by their apparent ages, and the subjects who
consumed larger amounts of the unsaturated oils were consistently judged
to be older than those who ate less, showing the same age-accelerating
effects of the unsaturated oils that were demonstrated by the rabbit
experiments.
146
While it is important to avoid overexposure to ult raviolet light,
the skin damage that we identifY with aging is largely a product of our
diet.
Q: Don't you have 10 avoid sunlight because of skin cancer?
The type of skin cancer which is clearly caused by sunlight is a

relatively harmless type of cancer, which appears only in sun-damaged
skin. Melanoma, which is often called a skin cancer, because it
sometimes begins in moles, does not have such a simple relationship to
sunlight, and its incidence is significantly increased by the use of estrogen .
It is often said that the great increase in deaths from melanoma
during the last 60 years has been caused by an increased popularity of
sunbathing, but during the same time there has been a great increase in
the incidence of cancer of the prostate, which is in a location that gets
very little exposure to light. What these two cancers have in common is a
sensitivity to estrogen, and it is during this same period of time that we
have been exposed to increased amounts of estrogenMlike chemicals in the
environment as a result of industrial pollution: Dioxins, phenols,
chlorinated hydrocarbons, DDT, smoke, etc. It is likely that these
cancers (and others) are caused by the estrogenic pollutants.
The incidence of melanoma is consistently lower at greater
elevations, where ultraviolet light is more intense, than at lower
elevations. It is common for melanoma to develop on relatively shaded
areas, including the middle of the back and the inside of the thigh, unlike
the ordinary less malignant skin cancers, which develop most often on the
forehead , nose, ear, cheek, and lip, where sun exposure is greatest.
People who work outside have a low incidence of melanoma according to
some studies, and this is sometimes said to be because they don't get
sunburned, as pale people do when they spend time in the sun after being
indoors for long periods. Sunburn does cause freckling, which is a
clumping of pigment cells, but recent studies show that children who get
sunburned are not at increased risk for melanoma. Sunburn causes
complex Changes in the tissue, including weakened immunity.
To avoid the aging and immunosuppressive effects of sunlight, it
seems best for sunlight to come through a window glass which removes
most of the ultraviolet light, and some of the blue light. Plastic film is
available which contains copper that removes this hannful ,part of
sunlight, and can be applied to ordinary window glass. Sitting in sunlight
coming through a window of this sort, for short times during the day. is
147
very protective. Besides protecting against cancer, it helps to keep the
mood and energy level high, by keeping melatonin low and stimulating
metabolism.
Recently, the polyunsaturated oils have been identified as the main
thing in cells that radiation interacts with, to cause cellular damage.
Vitamin E, taken internally or even applied to the skin, has been found to
reduce the damage produced by exposure to ultraviolet radiation, which
is logical, since it interrupts the chain reactions of toxic free·radicals
produced when unsaturated oils are oxidized by radiation or other injury.
Aspirin has been found to have a similar effect in reducing the hannful
effects which develop in the skin after sunlight over-exposure. Coconut
oil has been used for generations in "suntan lotions," and whether it is
absorbed through the skin or eaten as a food , it clearly has a protective
antioxidant function . Carotene seems to work with vitamin E in the skin
to reduce injury by ultraviolet radiation. Caffeine also has shown a
protective action against radiation, but its mechanism of action isn't
clearly understood.
Q: Why not use so you can get light without getting

burned?
If a sunscreen lotion is based on the use of an opaque reflective

material, such as zinc oxide or titanium oxide, that substance remains
mostly on the surface of the skin. This should make it fairly hannless,
though it is possible that traces of titanium could be absorbed with oils
into the skin, where it could be made toxic by interaction with ultraviolet
rays.
However, other chemicals used in the sunscreen lotions, such as
PABA derivatives, also react dangerously with light, and are easily
absorbed in significant quantities into the deeper layers of the skin, where
they can cause mutations.
For example, several recent studies have found that the
which decrease the ordinary skin damage caused by
ultraviolet rays., actually increase the risk of developing melanoma, by
causing mutations when the cells' chromosomes interact with the
sunscreen and the light. (Something similar happens in the disease,
porphyria. A pigment that accumulates causes the skin to become very
sensitive to the sun. Estrogen is known to intensify the disease.)
148
Even natural colored compounds, which have sometimes been
used in suntan lotions, should be avoided, since they might be able to
transmit the energy of light to the chromosomes, causing mutations.
Radiation from the sun reacts with the unsaturated fats you have
eaten to cause oxidative damage to skin cells. Vitamin E, vitamin A and
carotene arc antioxidants that prevent skin cell damage, when they arc
taken internally or applied to the surface of the skin.. None of these
causes any harmful effects in the sun.
Aspirin reduces the iron content of the blood serum, and also
inhibits the formation of the sometimes-toxic prostaglandins from fatty
acids. Coconut oil is very resistant to radiation damage and, like vitamin
E, tends to stop the chain reactions that occur in unsaturated fats. The
old formula for suntan oil, cocount oil with iodine, might turn out to be a
safe sunscreen, since the brown iodine absorbs light, as other "U. V .
blockers" do, but iodine is also an effective chain breaker that inactivates
free radicals, and it can't be absorbed into cells in its brown form. It
doesn't have the potential for causing cancer that the popular sunscreens
do
Q: Is sunlight still beneficial if you use a safe sun blocker?
The popular chemical sun blockers are meant to stop the

ultraviolet rays. If they can do that, without increasing the risk of
melanoma, then they are very beneficial, because this will allow you to get
a long exposure to direct sunlight, which penetrates deeply and has an
antistress effect . But so far, there is no research that shows any of the
chemical ultraviolet blockers is safe.
Q: Why do people seem to get sicker in the wintertime. often right

after Christmas?
Nights are much longer in the winter, and even in the summer,
death rates are higher during the night than in daytime. December 21 is
the day with the fewest hours of sunlight, but the cumulative damage of
prolonged darkness reaches its peak about a month later. Cold
temperatures do have some harmful effects, but by keeping people
indoors, or bundled up in thick clothing, cold weather also causes us to
get very little expOSure to sunlight. Winter sickness is mainly the result of
a "light deficiency"
149
When young sailors spent 6 months in {he continuous polar night
of Antarctica, Ihey developed the same signs of nocturnal stress that are
common in old people during the night. Many old people habitually get
up before dawn, because they find it impossible 10 stay asleep. Even
healthy young people (and animals) experience some degree of nocturnal
stress as SOon as the light is turned off at night, and their body responds
with an increased production of adrenalin and cortisol.
The energy-producing pan of cells, the mitochondrion. shows
signs of being increasingly damaged as the night progresses. but they lire
gradually restored to their normal condition during the daytime light
hours. This means that our greatest ability to resist stress is in the late
afternoon, and we are most susceptible to injury at dawn. In the wiT)ter,
nights arc long and days are shon, so we experience a cumulative
increase in our susceptibility to stress-injUJ)' during the winter months.
The light which penetrates deeply into our ti ssues (mainly orange
and red light) is able to improve the efficiency of energy production, and
to suppress the toxic free-radicals that are always being fonned in cells.
Q: Can you get enough sunlight d u ring the summer to hold YOll
throug h the winte r ?
No, many of the beneficial effects of bright light disappear during

just a few hours of darkness. though the restoration of our tissues that
happens during the summer puts us into a better state for surviving the
wimer, for example by allowing massive regeneration of the thymus to
occur. (This occurs in adults, not just in children. The idea that the
thymus disappears after puberty is based on autopsies. If a person lives
for even 3 hours after an accident or the onset of sickness, the thymus has
had time to shrink.)
Frequent short exposures to bright light is almost as valuable as
continuous sunlight, and it is less likely to cause skin aging.
Q. How mllr h sunlight do we nE't>d a day for gtneml htalth ?

If artificial light is bright enough, it is as effective as sunlight at
stopping the stress reaction, but people seldom use light s that are bright
cnough . Generally, people and animals are healthier when days are longer
than 12 hours. that is, after March 21 and before September 20. When
days are shorter than 12 hours, al1ificial lights should be used from sunset
until bedtime, but the greatest brightness probably doesn't have to be
continuous. Studies on isolated organs and tissues suggest that a few
150
seconds of penetrating bright light are enough! to break the free radical
chain reactions, slowing the production of toxic substances, which tend to
increase in concentration during nocturnal stress. A few seconds'
exposure to the direct light of ten 1SO Watt incandescent bulbs, for just a
few minutes every two or three hours, might provide more effective
protection than continuous exposure to a single 100 Watt light.
SUMMARY
In fall and winter, use very bright incandescent lights daily

from sunset until bedtime.
Expose as much skin as possible to the bright light; even a

minute is better than nothing. Thin, light-colored clothing
transmits a considerable amount of light.
Infrared bulbs, with clear glass, are especially beneficial.

Special low temperature red lights are available.
It is better to get your sunlight through windows, because it

has less ultraviolet light than direct sunlight.
Don't use lotions, other than the simply

refl ective type (zinc oxide or titanium oxide).
Decrease the use of unsaturated oils in the diet, and use

coconut oil as food and also on the skin during exposure to
direct sunlight.
Vitamin E and aspirin reduce the harmful effects of

sunburn, even when used after exposure to the sun, they can
be applied topically to the burned skin. Vitamin E often
contains some soy oi l, so I recommend small doses o f about
100 mg. per day.
REFF.REN C ES
B. K. Annstrong. "!' rralospIH:ri<: oz"nc:md lnl. J. Epi,lcmiol. 23( 5). 117.'1-')95. 1')')4 .
I5 I
2 R. J. DCf..:cr and N. H. Phillips, "Constanl light suppresses stoep and cin::adian rhythms in
without consequent sh.."Cp rebound in darkness," Amer . 1. Physiol..ReguL ll1tcgr. C
36(4), R945 ·0/0952. 1994. "Sleep pallcms ... no evidence of prior deprivation
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1')<)5.
4 L IJolognani . .:1 aI., "Effocls of low-pow.:r 632 nm radilllion (HtNI': laser) on a human cell
line: Influence on adcnylnuclcotldcs and cytoskcielal S!!uclurcs," J. l'holo.:hcUl. l'hotobioJ.
B-Iliol. 26(3), 257-264. 1994.
5 N. V. Bulyakova and M. F. I'opova, "Stimulation of p"st-tr.mll1alic regeneration lIf
"fold rats x-ray irr.. diation," Bull. Exp. BioI. & Moo. \03(4),546-550,1987.
6 A. R. Soldani. C. Romagno lo, and S.S.c. Yen, "'Melatonin-induced o.Iecrea.w of
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26(3), 257-264. 1994.
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10 V. A. Frolov, "Scasonal stmctural functional changes in the rabbit heart ," Bulletin of
Expcrim(!nlal Oio logy and M(!dicinc, 420-423. 19!W.
II V. 1\. Frolov, V.I'. ?ukhlyanko, and T. A. Kanskaya, "Chang...-s in len ventricular
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12 R. 1'. ct aI., "'Sunlight exposuro.:, pigmcntalio.ln factors. amI risk of
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1995. r"'lbe of as:><.x:iati"n betwc<:n cUlllulative sun ,:x]"l<'sllte anll Bee contradicts
wisdom about the cause ohhis twnor .... "1
13 R. P. Gallagher. el aI. , "Sunlight exposure, pigmcntation fadors, risk of
nonmcianoo::ytic skin 2. Squamous cdl carcinoma," Arch. 131(2), 164- I 69,
[" ...No m;,<;{)(:iation W<tS !lCcn bo..1we<:n rigk t)f sec <aulllliativc lifetime sun
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14 S. L !larrison, <)1 "Sun exp<\Sllto,l an,j m(!lanocyt ie in young Australian children, ,.
Lan.::et 344 (89.36), 1529-1532, 1994. (Sunburn.)
15 M. lIascgawa. A. Adachi, T. Yoshimura, and S. "Retinally perceived light is not
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mkrllliialysis." J. Comp. I'bysiol. A 175(5),581-586,1994.
16 J. I. Kitay and M. D AII5(;l1ul<:. "{1w /';m",,! Glalld. Harvard Univ. Press. C1ll1hridge. 1954.
17 I.. II. Kligman. I'.S. Zheng, "The efrco.;t ofa bT<Xld-spt..-..:tnun against
chronic UVA radiation in hairless mi ce: A hi stologic and assessment." J. So..:.
(·osmd. Ch..."n. 45( 1), 21-n. 1994. IOXYBFNZONE more skin damage th.,n was .'S(..'Cn
in unpr"h_'Cted mice. J
18. Kunkel and Williams. Ch"mistry, 1951.
19. W. Malomi. et al.. "!loth INi\ an,] lNH iodu<;c slirface h!chhing
in cpid"mlo id cells."' J. I'holocheill. Photobiol. B-Oio l 26(3), 265-270. 1994.
20 A. J.. Maksimov and T. fl. ChenlOnk. "BiorhytlUllic aspt.'Cls of intercontinental Anlarctic
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21. F. Nac!llxsr and !I. C. Kortin1!. "The wk or vitamin E in Ju>rm,,( ;mll dmnagcd skin." J.
Molecular Mcd.-Juuu. 7.1(1), 7·11,1995.
22 It. l'aS<lu"li. ct al.. Ada EndIH.:rin (lioJl,ica 107.42-4)1, 19X4.(111yroiL[ S\:3sonal in
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23 n. M. V. A. l'..:1mgallo. and S. Passarella. "'uucase in II IIc{-) r!llio III
rnitoc]wudri;, irr3,liatcd with helium-neon Bi<)chcm. Mol. BioI. lnt. 34(4), 1994.
24 A. T. ['ikulcv. .;1 at, Ka<Jiubiology 24( I J, 29-34, 1984. Krd)S cyek enzymcs.
25 Yu. J. Prokopenko, uigiyena i Sanilariya 12, pp. 8-10, 1982 ... Adaplogcnic light."
2(> J. M. RivilS and S. E. U!!rkh. "The wI<:: of 11..-4. IL-lU. ;md TNF-alpha in the illullunc
surrrc>sioll induced by uilraviolcl J. Leuk<><.:ytc BioI. 56(,), 11/94.
27 E. S. R"hinwrl. d al.. " Malignant melanoma in ultraviolet ..:d 0POi<SlllllS:
Init iation in sud:linj! young. mdastasis in adults, and x..,nograft lNhaviM in nude mi.., ... ,"
C<lw.:er R..:s. 54(22), 598(,-5991,1994.
28 G. L. So.:hi..:ven and J. A. L..,dooHCf, "Activation of tyrosine kinase signal pathways hy
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2') H. J. V.... M. Hurks, "The dini.., .. l r .... or imnlunu5uppressi,\U oy IN
irradiation," 1. l'h"[ochem. Phntob iol. B-RioL 24(3),149-154.1994.
30 1-'. Watll>crg and E. Skug, "Incrcasinj! incid.mce of basal eell ean:inoma," IIr. 1. Ikmla\ol,
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153
27
UNSATURATED VEGETABLE OILS: TOXIC
GLOSSARY:
Immunodeficiency of the immune system ) can
take many fonns. AIDS. for example, refers to an
immunodefickncy which is "acq uired," rather than
"inborn." Radiation and vegetable oil s can cause "acqu ired
immunodeficiency." Unsaturated oils, especiall y
polyunsaturates, weaken the immune system's fu nction in
ways thai afC similar to the damage caused by radiation,
hormone imbalance, cancer, aging, or viral infections. The
media discuss sex ually transmitted and drug-induced
immunodeficiency, but it isn't yet considered polite to
discuss vegetable oi l-induced immunodeficiency .
Unsaturated oils: When an oi l is saturated, that means
that the molecule has all the hydrogen atoms it can hold.
Unsaturation means that SQme hydrogen atoms have been
removed , and Ihi s opens the structure of the molecule in a
way that makes it susceptible to attack by free radica ls.
Free radicals are reactive molecular fragments that occur
even in healthy cells, and can damage the cell. When
unsaturated oil s are exposed to free radicals they can create
chain reactions of free radicals that spread the damage in the
cell, and contribute to the cell's aging.
Rancidify of oi ls occurs when they arc exposed to
oxygen , in the body just as in the bottlc. Hannful free
radicals are formed, and oxygen is used up.
Essential fatty acids (EF A) are, according to the
textbooks, linoleic acid and lino lenic acid, and they are
supposed to have the status of "vitamins," which must be
taken in the diet to make life possible. However, we are
able to synthesize our own unsaturated fats when we don't
eat the "EFA," so they are not "essenti al. " The term thus
appears to be a misnomer. [M. E. Hanke, "Biochemi stry,"
Encycl. Brit. Book of the Year, 1948.]
Q: You say vegetable oils are hazardous to your health. What

vegetable oils are you talking about?
154
Mainly, I'm referring to soybean oil, corn oil. safflower oil, canola,
sesame oil, sunflower seed oil, palm oil, and any others that are labeled as
"unsaturated" or "polyunsaturated." Almond oil, which is used in many
cosmetics, is very unsaturated.
Chemically, the material that makes these oils very toxic is the
polyunsaturated fat itself These unsaturated oils are found in very high
concentrations in many seeds, and in the fats of animals that have eaten a
diet containing them. The fresh oils, whether cold pressed or consumed as
part of the living plant material, are intrinsically toxic, and it is not any
special industrial treatment that makes them toxic. Since these oils occur
in other parts of plants at lower concentration, and in the animals which
eat the plants, it is impossible to eat a diet which lacks them, unless
special foods are prepared in the laboratory.
These toxic oils are sometimes called the "essential fatty acids" or
"vitamin F," but this concept of the oils as essential nutrients was clearly
disproved over 50 years ago.
Linoleic and linolenic acids, the "essential fatty acids," and other
polyunsaturated fatty acids, which are now fed to pigs to fatten them, in
the form of com and soy beans. cause the animals' fat to be chemically
equivalent to vegetable oil . In the late 19405, chemical toxins were used
to suppress the thyroid function of pigs, to make them get fatter while
consuming less food. When that was found to be carcinogenic, it was
then found that corn and soy beans had the same antithyroid effect,
causing the animals to be fattened at low cost . The animals' fat becomes
chemically similar to the fats in their food , causing it to be equally toxic,
and equally fattening.
These oils are derived from seeds, but their abundance in some
meat has led to a lot of confusion about "animal fats." Many researchers
still refer to lard as a "saturated fat," hut this is simply incorrect when pigs
are fed soybeans and corn.
Q: How are these oils hazardous to your health?

Ultimately. all systems of the body are harmed by an excess of
these oils. There are two reasons for this. One is that the plants produce
the oils for protection, not only to store energy for the germination of the
seed . To defend the seeds from the animals that would eat them, the oils
block the digestive enzymes in the animals' stomachs. Digestion is one of
our most basic functions, and evolution has built many other systems by
155
using vanatlons of that system: as a result, aU of these systems are
damaged by the substances which damage the digestive system.
The other reason is that the seeds are designed to germinate in
early spring, so their energy stores must be accessible when the
temperatures are cool , and they normally don't have to remain viable
through the hot summer months. Unsaturated oils are liquid when they
are cold, and this is necessary for any organism that lives at low
temperatures. For example, {ish in cold water would be stiff if they
contained saturated fats, These oils easily get rancid (spontaneously
oxidizing) when they are wann and exposed to oxygen. Seeds contain a
small amount of vitamin E to delay rancidity. When the oils are stored in
our tissues, they are much warmer, and more directly exposed to oxygen,
than they would be in the seeds, and so their tendency to oxidize is very
great . These oxidative processes can damage enzymes and other parts of
cells, and especially their ability to produce energy.
The enzymes which break down proteins are inhibited by
unsaturated fats, and these enzymes are needed not only for digestion, but
also for production of thyroid hormones, clot removal, immunity, and the
general adaptability of cells. The risks of abnormal blood clotting,
inflammation, immune deficiency, shock, aging, obesity, and cancer are
increased . Thyroid and progesterone are decreased. Since the
unsaturated oils block protein digestion in the stomach, we can be
malnourished even while "eating well."
Plants produce many protective substances to repel or injure
insects and other animals that eat them. They produce their own
pesticides. The oils in seeds have this function . On top of this natural
toxicity, the plants are sprayed with industrial pesticides, which can
concentrate in the seed oils.
It isn't the quantity of these polyunsaturated oils which governs
the harm they do, but the relationship between them and the saturated
fats. Obesity, free radical production, the formation of age pigment,
blood clotting, inflammation, immunity, and energy production are all
responsive to the ratio of unsaturated fats to saturated fats, and the higher
this ratio is, the greater the probability of harm there is.
There are interesting interactions between these oils and estrogen.
For example, puberty occurs at an earlier age if estrogen is high, or if
these oils are more abundant in the diet. This is probably a factor in the
development of cancer.
156
All systems of the body are harmed by an excess of these oils.
There are three main kinds of damage: one, hormonal imbalances, two,
damage to the immune system, and three, oxidative damage.
Q: How do they cause hormonal imbalances?
There are many changes in honnones caused by unsaturated fats.

Their best understood effect is their interference with the function of the
thyroid gland. Unsaturated oils block thyroid hormone secretion, its
movement in the circulatory system, and the response of tissues to the
hormone. When the thyroid hormone is deficient. the body is generally
exposed to increased levels of estrogen . The thyroid hormone is essential
for making the "protective honnones" progesterone and pregnenolone, so
these hormones are lowered when anything interferes with the function of
the thyroid. The thyroid honnone is required for using and eliminating
cholesterol, so cholesterol is likely to be raised by anything which blocks
the thyroid function . [8 . Barnes and L Galton, Hypothyroidism, 1976,
and 1994 references.)
Q= How do 'hey damage the immune system?
Vegetable oil is recognized as a drug for knocking out the

immune system. Vegetable oil emulsions were used to nourish cancer
patients, but it was discovered that the unsaturated oils were suppressing
their immune systems. The same products, in which vegetable oil is
emulsified with water for intravenous injection, are now marketed
specifically for the purpose of suppressing immunity in patients who have
had organ transplants. Using the oils in foods has the same harmful effect
on the immune system. [E . A. Mascioli, et al .,Lipids 22(6) 421 , 1987.]
Unsaturated fats directly kill white blood cells. [c. 1. Meade and 1.
Martin, Adv. Lipid Res., 127, 1978.]
Q: How do they cause o:lidative damage?
Unsaturated oils get rancid when exposed to air; that is called

oxidation, and it is the same process that occurs when oil paint "dries."
Free radicals are produced in the process.
This process is accelerated at higher temperatures. The tree
radicals produced in thi s process react with parts of cells, such as
157
molecules of DNA and protein and may become attached to those
molecules, causing abnormal ities of structure and function.
Q: What if' eat only organically grown vegetable oils?
Even without the addition of agricultural chemicals, an excess of

unsaturated vegetable oils damages the human body. Cancer can't occur,
unless there are unsaturated oils in the diet. rc.II', ci al. . Cancer Res, 45 ,
1985.} Alcoholic cirrhosis of the liver cannot occur unless there arc
unsaturated oi ls in the diet. [Nanji and French, Life Sciences. 44, 1989.1
Heart disease can be produced by unsaturated oils, and prevented by
adding saturated oils to the die!. [1. K. O. Kramer, et aI. , Lipids 17,372,
1983.J
Q. What oils are safe?
Coconut and olive oil are the only vegetable oils that are really
safe, but butter and lamb fat , which arc highly sat urated, are generally
very safe (except when the animals have been poisoned). Coconut oil is
unique in its ability to prevent weight-gain or cure obesity, by stimulating
metabolism. It is quickly metabolized, and functions in some ways as an
antioxidan't. Olive oil, though it is somewhat fattening, is less fattening
than corn or soy oil, and contains an antioxidant whi ch makes it
protective against heart disease and cancer.
Israel had the world's highest incidence ofbreasl cancer when they
allowed the insecticide lindane to be used in dairies, and the cancer rate
decreased immediately after the government prohibited its use. The
United States has fairly good laws to control the use of cancer-causing
agents in the food supply, but they are not vigorously enforced. Certain
cancers are several times marc common among corn farmers than among
other farmers, presumably because corn "requires" the use of more
pesticides. This probably makes corn oil's toxicity greater than it would
be othel"Vlise, but even the pure, organically grown material is {oxic,
because of its intrinsic unsaturation .
In the United States, lard is toxic because the pigs are fed large
quantities of corn and soy beans. Besides the intrinsic toxicity of the seed
oils, they are contaminated with agricultural chemicals. Corn farme rs
have a very high incidence of cancer, presumably because of the
pesticides they use on their crop.
158
Although I don't recommend "palm oil" as a food , because I think
It ISless stable than coconut oil, some studies show that it contains
valuable nutrients. For example, it contains antioxidants similar to
vitamin E, which lower both LDL c ho lesterol and a platelet clotting
factor. (B . A. Bradlow, University of Illinois, Chicago; Science News
139, 268, 1991.] Coconut oil and other tropical oils also contai n some
hormones that are related to pregnenolone or progesterone.
Q: Isn'l coconut oil fattening?
Coconut oil is the least fattening of all the oils. Pig farmers tried
to use it to fatten their animals, but w hen it was added to the animal feed,
coconut oil made the pigs lean [See Encycl . Brit. Book of the Year,
1946J.
Q: What about olive oil? Isn't it more fallening than other vegetable
oils?
In this case, as with coconut oil, "fattening" has more to do with

your ability to bum calories than with the caloric value of the oil . Olive
oil has a few morc calories per quart t han corn or soy oil, but since it
doesn't damage our ability to burn calories as much as the unsaturated oils
do, it is less fattening . Extra virgin olive oil is the best grade, and
contains an antioxidant that protects against cancer and heart disease.
{1994, Curr. Conts.J
Q: Does that mean that using olive oil helps to prevent cancer?
Some studies in Europe suggest that, but studies in animals

show that when the total calorie intake is excessive, even a smail
amount of linoleic acid is enough to increase the incidence of cancer,
and olive oil contains some linoleic acid. The people who use more
olive oil might eat less bread and pasta, and as a result might be less
obese, and so less likely to get cancer. Eating any fat with a starch
makes the starch less hannful, and it's clearly better to use olive oi l
than the more highly polyunsaturated seed oils.
1S9
Q: Is "light" olive oil okay?
No. Now and then someone learns how to make a profit from
waste material. "Knotty pine n boards were changed ITom a discarded
material to a valued decorative material by a little marketing skill. Light
olive oil is a low grade material which sometimes has a rancid smell and
probably shouldn't be used as food.
Q: Is margarine okay?
There are several problems with margarine. The manufacturing

process introduces some toxins, including a unique type of fat which has
been associated with heart disease. [Sci . News, 1974; 1991.] There are
likely to be dyes and preservatives added to margarine. And newer
products contain new chemicals that haven't been in use long enough to
know whether they are safe.
However, the basic hardening process, hydrogenation of the oils,
has been found to make the oils less likely to cause cancer. If r had to
choose between eating ordinary corn oil or corn oil that was J 00%
saturated, to make a hard margarine, I wuuld l:hoose lhe hard margarine,
because il resists oxidation, isn'l suppressive to the thyroid gland, and
doesn't cause cancer.
Q: What about butter?
Butter contains natural vitamin A and 0 and some beneficial

natural hormones. It is less fattening than the unsaturated oils. There is
much less cholesterol in an ounce of butter than in a lean chicken breast
[about 1/ 5 as much cholesterol in fat as in lean meat on a calorie basis,
according to R. Rei ser o f Texas A & M Vniv., 1979].
Q: Are fish oils good for you?
Some of the unsaturated fats in fish are definitely less toxic than
those in corn oil or soy oil, but that doesn't mean they are safe. Fifty
years ago, it was found that a large amount of cod liver oil in dogs' diet
increased their death rate from cancer by 20 times, from the usual 5% to
100%. A diet rich in fish oil causes intense production of toxic lipid
peroxides, and has been observed to reduce a man's sperm count to zero.
[H. Sinclair, Prog. Lipid Res. 25, 667, 1989.}
160
Q: What about lard?
In this country. lard is toxic bcause the pigs are fed large
quantities of com and soy beans_ Besides the natural toxicity of the seed
oils, the oils are contaminated with agricultural chemicals. Corn farmers
have a very high incidence of cancer, presumably because corn "requires"
the use of more pesticides. This probably makes com oil's toxicity
greater than it would be otherwise. but even the pure, organically grown
material is loxic, because ofilS unsaturation .
Women with breast cancer have very high levels of agricultural
pesticides in their breasts [See Science News. 1992, 1994].
Israel had the world's highest incidence of breast cancer when they
allowed the insecticide lindane to be used in dai ries, and the cancer rate
decreased immediately after the government prohibited its use. The
United States has fa irly good laws to control the lise of
agents in the food supply, but they are not vigorously enforced . [World
Incid . of Cancer, 1992.J
Q: I havc no control over oils when eating out. What can I do to

offset the harmful effects of polyunsaturated oils?
A small amount of these oils won't kill you . rt is the proportion of

them in your diet that matters. A litt le extra vitamin E (such as 100 units
per day) will take care of an occasional American restaurant meal. Based
on ani mal studies, it would take a teaspoonful per day of com or soy oil
added to a diet to significantly increase our risk of cancer.
Unfortunately, it is impossible to devise a fat-free diet outside of a
laboratory. Vegetables, grains, nuts, fish and meats all naturally contain
large amounts of these oils, and the extra oil used in cooking becomes a
more serious problem.
Q Why are the unsaturated oils so popular if they are dangerous?
It's a whole system of promotion, advertising, and protitability.

50 years ago, paints and varnishes were made of soy oil, safflower
oil , and linseed (flax seed) oil. Then chemists learned how to make paint
from petroleum, which was much cheaper. As a result, the huge seed oil
industry found its crop increasingly hard to sell . Around the same lime,
farmers were experimenting with poisons to make their pigs get fatter
161
with less food , and they discovered that com and soy beans served the
purpose, in a legal way. The crops that had been grown for the paint
industry came to be used for animal food . Then these foods that made
animals get fat cheaply came to be promoted as foods for humans, but
they had to direct attention away from the fact that they are very
fattening. The "cholesterol" focus was just onc of the marketing tools
used by the oil industry. Unfortunately il is the one that has lasted the
longest, even after the unsaturated oils were proven to cause heart disease
as well as cancer. [Study at L.A. Veterans Hospital, 1971.]
I use some of these oils (walnut oil is very nice, but safflower oil
is cheaper) for oil painting, but I am careful to wash my hands thoroughly
after I touch them, because they can be absorbed through the skin.
SUMMARY
Unsaturated fats cause aging, clotting, inflammation,
cancer, and weight gain .
Avoid foods which contain the polyunsaturated oils, such

as com, soy, safflower, flax, cottonseed. canola, peanu!. and
sesame oil.
Mayonnaise, pastries, even candies may contain these oils:

check the labels for ingredients.
Pork is now fed corn and soy beans, so lard is usually as

toxic as those oils: use only lean pork.
Fish oils are usually highly unsaturated: "dry" types of fish,

and shel1t1 sh, used once or twice a week, are good. A void
cod liver oil.
Use vitamin E.
Use coconut oil, butter, ,md olive oil.
Unsaturatcd fats intcnsify estrogen's harmful effects.

162
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164
28
DANGERS OF IRON--EXACERBATED BY
ESTROGEN
'Ill\!: questions in this <;hapt"r lrom a Iw(' w y W III.:r<:n<.:c in ]nJian"JX,1 is. in I <N"' .
GLOSSARY:
Free radicals are fragments of molecules that are very
destructive to all cells and system of the body.
Respiration refers to the absorption of oxygen by cells,
which releases energy. The SlruClure in side the cel l in which
energy is produced by respiration is called the
mitochondrion.
Oxidation refers to the combination of a substance with
oxygen . This can be beneficial , as in nonnal respiration that
produces energy, or harmful, as in rancidity, irradiation, or
stress reactions.
Antioxidants: Vitamin E and vitamin C are known as
antioxidants, because they stop the harmful free· radical
chain reactions which o ften involve oxygen, but they do not
inhibit normal oxidation processes in cells. "Chain
breaker" would be a more suitabl e term. It is often the
deficiency of oxygen which unleashes the dangerous
free-radical processes. Many substances can function as
antioxidants/chain breakers: thyroxine, uric acid, biliverdin,
-selenium, iodine, vitamin A, sodium, magnesium, and
lithium, and a variety of enzymes. Saturated fats work with
antioxidanrs to block the spread of free-radical chain
reactions.
Age pigment is the brown material that forms spots on
aging skin, and that accumulates in the lens of the eye
forming cataracts, and in blood vessels causing hardeni ng of
the arteries, and in the heart and brain and other organs,
causing their functions to deteriorate with age. It is made up
of oxidized unsaturated oils with iron.
Anemic means lacking blood, in the sense of not having
enough red blood cell s or hemoglobin . It is possible to have
too much iron in the blood while being anemic. Anemia in
itself doesn't imply that there is a nutritional need for iron.
165
Q: You believe iron is a deadly substance. Why?
Iron is a potentially tox.ic heavy metaL In excess, it can cause

cancer, heart disease, and other illnesses.
Q: Could you tell us about some of these studies?
[n the 19605 the World Healt h Organization found that when iron
supplements were given to anemic people in Africa, there was a great
increase in the death rate from infectious diseases, especially malaria.
Around the same time, research began to show that the regulation afiron
is a central function of the immune system, and t hat this seems to have
evolved because iron is a basic requirement for the survival and growth of
cells of all types, including bacteria, parasites, and cancer. The pioneer
researcher in the role of iron in immunity believed that an excess of
dietary iron contributed to the development of leukemia and lymphatic
cancers.
For about 50 years, it has been known that blood transfusions
damage immunity, and excess iron has been suspected to be one of the
causes for this. People who regularly donate blood, on the other hand,
have often been found to be healthier than non-donors, and healthier than
they were before they began donating.
Just like lead, mercury, cadmium, nickel, manganese and other
heavy metals, stored iron produces destructive free radicals. The harmful
effects of iron-produced free radicals are practically indistinguishable
from those caused by exposure to X-rays and gamma rays; both
accelerate the accumulation of age-pigment and other signs of aging.
Excess iron is a crucial element in the transformation of stress into tissue
damage by free radicals.
In one of Hans Selye's pioneering studies, he found that he could
experimentally produce a form of scleroderma (hardening of the skin) in
animals by administering large doses of iron, fo llowed by a minor stress.
He could the development of the condition by giving the animals
large doses of vitamin E, suggesting that the condition was produced by
iron's oxidative actions.
Many recent studies show that iron is involved in degenerative
brain diseases, such as Parkinson's, ALS (Lou Gehrig's disease),
Huntington's chorea, and Alzheimer's disease. Iron is now believed to
166
have a role in skin aging, atherosclerosis, and cataracts of the lenses of
the eyes. largely through its formation of the "age pigment."
Q: flow does excess iron accelerate our aging process?
During aging, OUf tissues tend to store an excess of iron. There is

a remarkably close association between the amount of iron stored in our
tissues and the risk of death from cancer, heart disease, or from all
causes. This relationship between iron and death rate exists even during
childhood, but the curve is downward until the age of 12, and then il rises
steadily until death_ The shape of this curve, representing the iron
hurden, is amazingly similar to the cUlVes representing the rate of death in
general, and the rate of death from cancer. There is no other relationship
in biolot,'Y that I know ofrha! has this peculiar shape, with its minimum at
the age of 12, and its maximum in old age at the time of death .
One of the major lines of aging research, going back to the early
pan of this century, was based on the accumulation of a brown material in
the tissues known as "age-pigment." The technical name for this material,
"lipofuscin," means "fatty brown stuff." In the 1960s, the "free radical
theory" of aging was introduced by Denham Harman, and this theory has
converged with the age-pigment theory, since we now know that the
age-pigment is an oxidized mass of unsaturated fat and iron, formed by
uncontrolled free radicals. Until a few years ago, these ideas were
accepted by only a few researchers, but now practically eveT)' doctor in
the countly accepts that free radicals are important in the aging process.
A nutrition researcher in San Diego suspected that the
lite-extending effects of calorie restriction might be the result of a
decreased intake of toxins. He removed the toxic heavy metals from
foods. and found that the animals which ale a normal amount of
food lived as long as the semi-stan:ed animals. Recenlly. the iron
content of food has been identified as the major life-shortening
factor, rather than the calories. [ehoi and Yu, Age vol. 17, page 93 ,
1994J
Q: Exactly how much iron do we need to eat?
Children's nutritional requirements arc high, because they are

growing, but there are indications that in the U.S. even children eat too
much iron . Some researchers are concerned that the iron added to cereals
is contributing to the incidence of leukemia and cancers of the lymphatic
167
tissues in children. [Goodfield, 1984.] During the time of rapid growth,
children are less likely than adults to store too much iron. At birth, they
have a large amount of stored iron, and this decreases as they "grow into
it." It is after puberty, when growth slows and the sex hormones are
high, that the storage afiron increases. [Blood, Sept. , 1976.}
In a study of the "malnourished" children of migrant fruit pickers
in California, these children who were "seriously anemic" were actually
morc resistant to infectious diseases than were the "well nourished"
middle class children in the same region .
If the normal amount of dietary iron causes an increased
susceptibility to infections even in children, and if a subnormal amount of
iron slows the aging process, I think we are going to have to reconsider
our ideas of nutritional adequacy, to look at the long range effects ordiel,
as well as the immediate effects. My current studies have to do with
analyzing our ability to handle stress safely, in relation to our diet. r
believe our nutritional recommendations for iron have to be revised
sharply downward.
Q. Don'l women need extra iron?
That's a misunderstanding. Doctors generally don't realize that

only a few milligrams of iron are lost each day in menstruation. The real
issue is that you can hardly avoid getting iron, even when you try.
Women absorb iron much more efficiently than men do. From a
similar meal , women will normally absorb three times as much iron as
men do . When pregnant , their higher estrogen levels cause them to
absorb about nine times as much as men . Every time a woman
menstruates, she loses a little iron, so that by the age of 50 she is likely to
have less iron stored in her tissues than a man does at the same age, but
by the age of 65 women generally have as much excess iron in their
tissues as men do. (During those 15 years, women seem to store iron al a
faster rate than men do, probably because they have more estrogen.) At
this age their risk of dying from a hean attack is the same as that of men.
Some women who menstruate can donate blood regularly without
showing any tendency to become anemic .
Since the custom of giving large iron supplements to pregnant
women has been established, there has been an increase in jaundice of the
newborn. It has been observed that women who didn't take iron
supplements during pregnancy have healthy babies that don't develop
jaundice. I have suggested that this could be because they haven't been
168
poisoned by iron. Those supplements could also be a factor in the
increased incidence of childhood cancer.
Q: Don', you need iron supplements if you are anemic?
In general, no.
Many doctors think of anemia as necessarily indicating an iron
deticiency, but that isn't correct. 100 years ago, it was customary to
prescribe arsenic for anemia, and it worked to stimulate the formation of
morc red blood cells_ The fact that arsenic, or iron, or other toxic
material stimulates the formation of red blood cells doesn't indicate a
"deliciency" of the toxin. but simply indicates that the body responds to a
variety o f harmtul factors by speeding its production of blood cells. Even
radiation can have this kind of stimulating effect, because growth is a
natural reaction to injury. Between 1920 and 1950, it was common to
think of "nutritional growth factors" as being the same as vitamins, but
since then it has become com mon to use known toxins to stimulate the
growt h of farm animals, and as a result, it has been more difficult to
define the essential nutrients. The optimal nutritional intake is now more
often considered in terms of resistance to disease, longevity or rate of
aging, and even mental ability.
An excess of iron, by destroying vitamin E and oxidizing the
unsaturated fats in red blood cells, can contribute to hemolytic anemia, in
which red cells are so fragile that they break down too fast. In aging, red
cells break down faster, increasing the tendency to become anemic, but
additional iron tends to be more dangerous for older people.
Anemia in women is caused most often by a thyroid deficiency (as
discussed in the chapter on thyroid), or by various nutritional deficiencies.
Estrogen (even in animals that don't menstruate) causes dilution of the
blood, so that it is normal for females to have lower hemoglobin than
males.
Q. What should I do ir my doctor tells me I'm anrmie? Is therr any

situation in which a person needs to take iron supplements?
Iron deficiency anemia does exist, in laboratory situations and in

some cases of chronic bleeding, but I believe it should be the
last-suspected cause of anemia, instead of the first. It should be
considered as a possible cause of anemia only when very specific blood
tests show an abnormally low degree of iron saturation of certain
169
prot eins. Usually_ physicians consider the amount of hemoglobin or of
red cells in the blood as the primar), indicator of a need for iron. but thaI
jllsi isn't biologically reasonable ,
If a large flmOllnt of blood is lost in surgery. a temporary anemia
might be pr0duced. but even then it would be best to know whether the
iro n stores are really depicted before deciding whether an iron supplement
would be reasonable. Liver (or even a waler extract of wheat germ) can
supply as ll1uch iron as would be given as a pill , and is safer.
Q . \ Vhal foods contaill iron?
Flour, pasta. elc .. almost always contain iron which has been
artificially added as ferro us sulfate. because of a fede ral law. Meats,
grains, eggs, and vegetables naturally contain large amounts of iron , A
few years ago, someone demonstrated that they could pick up a certain
breakfast cereal with a magnet because of the added iron. Black olives
contain iron. which is used as a coloring material. You should look for
"ferrous" or "ferric" or "i ron" on the label. and avoid foods with any
added iron . Many labels list "reduced iron," meaning that iron is added in
the lerrous form. which very reactive ami ea<;ily ab<;orbed
Q. : Why does federal law require the addition of iron to Ihose

foods?
Industrially proccs<;cd grains have most of the nutrients, such as

vitamin E, the B vitamins. manganese, magnesium, etc., removed to
improve the products' shelf life and eHiciency of processing, and the
government required Ihal certain nutrients be added to them as a measure
to protect the public's health, but the supplementation did not reflect the
best science even when il was first made law, since food industry
lobbyists managed to impose compromises that led to the use of the
cheapest chemicals, rather than those that offered the greatest health
benefits. For example, studies of processed animal food had
demonstrated that the addi tion of iron (as the highly reactive form,
fer rOllS sulfate, which happens to be cheap and easy to handle) created
disease in animals, by destroying vitamins in the food. You should read
the label of ingredients and avoid products thaI contain added iron, when
possible,
Q: Can cooking in an iron fryin g pan pul iron inlo food?

170
Yes, especially if the food is acidic, as many sauces arc. The

added iron will destroy vitamins in the food, besides being potentially
toxic in it self.
Q: What about aluminum?
Aluminum and iron react similarly in cell s and are suspected

causes of Alzheimer's disease.
The aluminum industry started propagandizing more than 50 years
ago about the "safety" of aluminum utensils, claiming that practically none
of the toxic metal gets into the food . Recent research showed that coffee
percolated in an aluminum pot contained a large amount of dissolved
aluminum, because of coffee's acidity.
Q: What kinds of cooking pots or utensils are safe?
Glass utensils are safe, and certain kinds of stainless steel are safe,
because their iron is relatively insoluble. Teflon-coated pans are safe
unless they are chipped .
Q: How do I know which stainless steels are safe?
There are two main types of stainless steel, magnetic and

nonmagnetic. The nonmagnetic form has a very high nickel content , and
nickel is allergenic and carcinogenic . It is much more toxic than iron or
aluminum . You can use a little "refrigerator magnet" to test your pans.
The magnet will stick firmly to the safer type of pan.
Q: Why is there iron in most multi-vitamin and mineral products?
Although several researchers have demonstrated that iron destroys

vitamins, there is enough wishful thinking in industry, government, and
the consuming public, that such mistakes can go on for generations before
anyone can mobilize the resources to bring the truth to the public . Ten
years ago, I thought it was a hopeful sign of increased awareness of iron's
danger when the manufacturer of a new iron product mentioned in the
Physician's Desk Reference that it hadn't yet been reported to cause
cancer.
I 7I
•
Q. I can'l avoid all those foods, especially the bread and grams.
What can' do to keep tht> iron I ingest from harming me?
Iron destroys vitamin E, so vitamin E should be taken as a

supplement. It shouldn't be taken at the same time as the
iron-contaminated food , because iron reacts with il in the stomach ,
About 100 mg. per day is adequate. though our requirement increases
with age, as our tissue iron stores increase. Coffee, when taken with food ,
strongly inhibits the absorption of iron, so I always try to drink coffee
with meat. Decreasing your consumption of unsaturated fats makes Ihe
iron less harmful.
Vitamin C sti mulates the absorption of iron, so it might be a good
idea to avoid drinking orange juice at the same meal with iron-rich foods_
A deficiency of copper causes our tissues to relain an excess of iron, so
foods such as shrimp and oysters which contain abundant copper should
be used regularly.
Q: How does copper help us?
Copper is the crucial element for producing the color in hair and
skin, for maintaining the elasticity of skin and blood vessels, for
protecting against certain types of free radical, and especially for aHowing
us to use oxygen properly for the production of biological energy. It is
also necessary for the normal functioning of certain nerve cells (substantia
nigra) whose degeneration is involved in Parkinson's disease. The shape
and texture of hair, as well as its color, can change in a copper deficiency_
Too much iron can block our absorption of copper, and loa little
copper makes us store too much iron. With aging, our ti ssues lose
copper as they Slore excess iron. Because of those changes, we need
more vitamin E as we age.
SUMMARY,
[ron is a potentially toxic heavy metal; an excess can cause
cancer, heart disease, and other illnesses.
Other heavy metals, including lead and aluminum, are toxic;

pans and dishes shoul d be chosen carefully.
[ron causes cell aging.

172
Drinking coffee with iron rich foods can reduce iron's toxic
effects.
Use shrimp and oysters, etc., to prevent the copper

deficiency which leads to excess storage of iron.
Avoid food supplements which contain iron .
Take about 100 units of vitamin E daily; your vitamin E

requirement increases with your iron consumption .
REFERESCES
l. Allen, O. R., Cl aI., "Cateo.:ho] adrenergic agents enhance hydroxyl radical genllration in
xanthine oxidase systems containing ferritin: Implications fot ischemia n:po.:rfusi on," Arch.
Biochem. Biophys. 315(2), 235-243, 1994.
2. M. Bartal. el ai., "Lipid peroxidalion in iron deficiem.:y anemia··Reply," Acta Hacm31ol.
91(3),1 70, 1994.
1 R. 1. ct aI., of iron on in vivo proliferation and lethality of Ll210
cells," 1. Nutrition 115(3), 369·374. 1985.
4. P. Carthcw and A. G. Smith. "Pathological mechanisms of hepalic twuor formation in rats
exposed chronically to dietary he:o;achlorobenzene: J. Applied To:o;icolo8Y 14(6), 447·S2,
1994.
S. Chen, Y., et aI., "Weak antio:o;idant defenses make the heart a target for damage in
copper-deficient rat!," Free Radical BioI. Med. 17(6), 529-536, 1994.
6. J. J. C. Chiao, et ai., "Iron de1ocalization occurs during ischemia and persists on
reo:o;ygenation of skeletal musc le," J. Lab. Clin. Med. 124(3), 432-438, 1994.
7. Choi, J. H. and B. P. Yu, "Modulation o f age-rela ted alterations of iron, ferritin, and lipid
peroxidalion in rat $Cf\U\l," Age 17(3), 93-97, 1994.
8. P. C. Elwood. "Iron. magnesium. and ischemic heart disease: Proc. of Nutrition Society
53(3), 599-603, 1994.
9, J. Goodfield, An Imagined World, 1'enguin Books, N.Y.• 1984.
10. M. Galleano and S. Puntarulo, "Mi ld iron overload effect on rat liver nuclei," Toxicol.
93(2-3), 125-34,1994.
I I. E. C. Hirsch, "Biochemistry of Parkinson's disease with sptX:ial reference to the
dopaminergic systems." Mol. Neurohiol. 9(1-3), 135-1 42. 1994.
12. G. M. Kainova , et at, "Activation of endogenous lipid pew:o;idalion in thc bt-din durin&
o:o;idation stress induced by iron and preve ntion by vitamin E." Bull. Exp. BioI. & Moo.
109( 1).43-45, 1989.
13. S. Kiochl. et aI., "Body iron stores and presence of carotid athcrosclerosis--resuHs from the
Broneck study," Arterioscler. Thrornb. 14(10), 1625-1 630, 1994.
14. L. H. Kligman and P. S. Zheng, "The protective cITect of a broad-sptX:trum sunscreen
against chronic UV A radiation in hairlcss mice: A histologic and ultrastructural
J. Soc. Cosme!. Chern. 45(1 ), 21 -33, 1994. [ ..... mice protected ....' th the oxybcnzoue contain ing
sunscreen, sU!Jlrisingly, had damage that what was seen in unprotected mice."
IS. S. KaminlUra, ct aI., "Hepatic fibrosis in rats red a liquid did with ethanol and <.:arb<myl
iron," Inl.lk-patol. Commun. 3(2), 70-76, 1995.
\73
16. Y. Kondo, et aI., "Regional differences in late-onset iron ferritin, transferrin,
astrocyte proliferation, and microglial activation after transient forebrain ischemia in ral
brain," J. Cereb. Blood Flow Metab. 15(2), 216-226, \995.
\7. A. V. Kozlov. et aI., of endogenous [fCC iron in a<..1.ivlllion of lipid peroxidation
Bull. Exp. BioI. Med. 99(1), 1984.
18. D. J. Lamb and D. S. I.eake, "Iron released from transferrin al acidic pH can calalyse the
oxidation oflow density lipoprotein," FEBS Len 352(1). 15-18, 1994.
19. E. E. Letendre, "Importance of iron in tile pathogenesis of infection and m:oplasm," Trends
in Bi()l;beinicai S<.;i., April, 1985, \66-163.
20. V. M. Mann, et aI., "Complex I, iron and ferritin in Parkinson's diseas.: nigra,"
Ann. of Neurology 36(6), 876-81,1994.
21. Z. Maskos and W. H, Koppeno\, "Oxyradicals and multivitamin tablets," Free Radical
BioI. & Med. 11,669-670, 1991.
22. S. Ozsoylu, "Lipid po:roxidation in iron dclici&:llCY am.:mia;· Acta llaematol. 91(3), 170.
1994.
23. Pecci, 1.., et aI., H Aminoethylcystein ketimine decarboxylated dimer protects
submitochondrial particles from lipid peroxidation at a .;on.;entralion not inhibitory of eie<:tron
transpon," Biochem. Diophys. Res. CommlUl. 205(1 ), 264-268, 1994.
24. R. A. Sabroe, et aI., "Polymyositis and malignant melanoma," Br. 1. Dermatol. 132(2),
3 12-3\3,1995.
25. J. T. Saionen, et aI., "Lowering of body iron stores hy blood leIting and oxidation
resistance of serum lipoprotcimi: A randomized cross-over trial in male smokers:' J. Intern.
Med. 237(2), 16 1-168, 1995.
26. M. Savoiardo, ct aI., "Magnetic re$onan.;e imaging in supr.muclear palsy and
other parkin.. J. Neur.tl Trans. (suppl. 42), 93-110, 1994.
27.1. J. Strain, "Putative role of dietary trace elements in .;oronary heart disease and
Brit. J. Biomed. Sci. 51(3).24 1-251, 1994.
28. Vanrensburg, S. J., et aI., "Upid peroxidation and platelet membrane tluidlty- imp!l.;ations
for AlZheimer's disease?", Neuroreport S(17), 2221-2224, 1994.
29. G. F. Vile and R. M. Tyrrell, "UVA radiatioll-indu.;ed oxidative damage to lipids and
proteins in vitro and in human skin fibroblasts deendcnt on iron and singlet oXY8en," Free
Radical BioI. Moo. 18(4),7).1-730, 1995.
30. M. Vlad, et aI. , "Concentration of copper, zinc, chromium, iron Md nickel in the
abdominal aorta ofpatients deceased with coronary hean disease," 1. Troce Elcm. Electr. Hlth.
Dis. 8(2), 111-114, 1994.
31. 1. J. Wesselius, el aI., "Increased release of ferritin and iron by iron-loaded alveolar
macrophages in dgarette smokers:' Amer. J. Respir. ent. Care Moo. IS0(3), 690-69S, 1994.
Transfusions: Amer. J. of Surgery ISS, p. 43. 1988.

-A Finnish study, two years ago, indicated that high iron stores may increase bean
atta<:k risk: In People magazine, 1994: "Is iron a killer? " Dr. Jerome L. Sullivan, diredor of
dinical Jabs of Veterans Affairs Medical Center at Charleston, S.c.. in 1983 proposed that
excess iron contributes to heart attacks. University of Kuopio in Finland: l.arge-scale study
(nearly 2,000 men, for up 10 five years; next to smok.ing. ..'Xcess stored iron is the most
significant identifiable risk. factor for beart attacks. (t is a stronger risk factor for heart attack.
than high blood pressure and cholesterol.
-[)e,;: . 7, page 6E, Register Guard ( Eugene, OR): US studies showed a weak
connection between iron and heart discase, and a weak. connection with the iron in red meal.
Epidemiologists at the Pacific Nonhwest Laboratory in Washington have reponed that the
greater the concentration of iron in a person's blood, the greater his or her r isk. of cancer.
Richard Stevens and his co-workers found the connection from e:>(amining .;am:er rat.;s in more
174
than K,UOO (\<:"p!c who parlidpatc<J in the 1<)71 NatiOll.11 HClllih Hnd Nutrition Fllamimdion
surv"''Y. A St:(;ond Finnish study with similar findings accompanied Stevens's report in the
Journal orc.mccr, and rugsclS thallhcre may be cause for concern.
Register Guard (Eug...'1IC, OR), Jan . J 6, 95; P 11\: Numh<:r uf heart failures doubles.
AP: 1')K2-'J2, heM! <.iiscasc ,katb Me dropped 24.5 n;.; num her of cases of congcslivc heaTt
failur;: ,\ouhkd during roughly tbe sam.: pt,>fiod. H killed 39,000 Americans in 1991. cus1s
$<tO billion p.::r year. Cancer is the higgest kilkr or w,>llIen under 64, h.earT disease I!lT
sUTP<.gSCS c:tOcct in w"men o f 65-lt4.
175
29
COCONUT OIL
I have already disclissed the many toxic effects of the unsaturated
oils, and I have frequently mentioned that coconut oil doesn't have those
toxic effects, though it does contain a small amount of the unsaturated
oils_ Many people have asked me to write something on coconut oil. I
thought I might write a small book on it, but I realize that there are no
suitable channels for distributing such a book--if the seed-oil industry can
eliminate major corporate food products that have used coconut oil for a
hundred years, they certainly have the power to prevent dealers from
selling a book that would affect their market morc seriously. For the
present, I will just outline some of the virtues of coconut oil.
The unsaturated oils in some cooked foods become rancid in just
a few hours, even at refrigerator temperatures, and are responsible for the
stale taste of left-over foods . (Eating slightly stale food isn't particularly
harmful , since the same oils, even when eaten absolutely fresh , will
oxidize at a much higher rate once [hey are in the body, where they are
heated and thoroughly mixed with an abundance of oxygen .) Coconut oi l
that has been kept at room temperature for a year has been tested for
rancidity, and showed no evidence ofil. Since we would expect the small
percentage of unsaturated oils naturally contained in coconut oil to
become rancid, it seems t hat the other (saturated) oils have an
antioxidative effect: J suspect that the dilution keeps the unstable
unsaturated fat molecules spatially separated from each other, so they
can't interact in the destructive chain reactions that occur in other oils.
To interrupt chain-reactions of oxidation is one of the functions of
antioxidants, and it is possible that a sufficient quantity of coconut oil in
the body has this function . It is well established Ihat dietary coconut oil
reduces our need for vitamin E, but I think its antioxidant role is more
general than that, and that it has both direct and indirect antioxidant
activities.
Coconut oil is unusually rich in short and medium chain fatty
acids. Shorter chain length allows fatty acids to be metabolized without
use of the carnitine transport system. Mildronale, which I discussed in an
article on adaptogens, protects cells against stress partly by opposing the
action of carnitine, and comparative studies showed that added camitine
had the opposite effect, promoting the oxidation of unsaturated fats
during stress, and increasing oxidative damage 10 cells. I suspect that a
176
degree of saturation of the oxidative apparatus by short-chain fally acids
has a similar effect--that is. that these very soluble and mobile short-chain
saturated fats have priority for oxidation, because Ihey don't require
carnitine transport into the mitochondrion, and that this will lend to
inhibit oxidation orlhe unstable, peroxidizable unsaturated fatty acids.
When Albert Schweitzer operated his clinic in tropical Africa, he
said it was many years before he saw any cases of cancer, and he believed
that Ihe appearance of cancer was caused by the change to the European
type of diet. In the 1920s, German researchers showed that mice on a
fat-free diet were practically free of cancer. Since then. many studies
have demonstrated a very close association between consumption of
unsaturated oils and the incidence of cancer.
Heart damage is easi ly produced in animals by feeding them
linoleic acid : this "essential" fatly acid turned Ollt to be the heart toxin in
rape·seed oil. The addition of saturated fat to the experimental
heart·toxic oil·rich diet protects against the damage to heart cells.
Immunosuppression was observed in patients who were being
"nourished" by intravenous emulsions of "essential fatty acids," and as a
resu lt coconut oil is used as the basis for intravenous fat feeding, except
in organ·transplant patients. For those patients, emulsions of unsaturated
oils are used specifically for their immunosuppressive effects.
General aging, and especially aging of the brain, is increasingly
seen as being closely associated with lipid peroxidation .
Several years ago I met an old couple, who were only a few years
apart in age, but the wife looked Illany years younger than her doddering
old husband. She was fi'om the Philippines, and she remarked that she
always had to cook two meals at the same time, because her husband
couldn't adapt to her traditional food. Three times every day, she still
prepared her food in coconut oil. Her apparent youth increased my
interest in the effects of coconut oil.
In the 1960s, Hartroft and Porta gave an elegant argument for
decreasing the ratio of unsaturated oil to saturated oil in the diet (and t hus
in the tissues). They showed that the "age pigment" is produced in
proportion to the ratio of oxidants to antioxidants, multiplied by the ratio
of unsaturated oils to saturated oils. More recently, a variety of studies
have demonstrated that ultraviolet light induces peroxidation in
unsaturated fats, but not saturated fats, and that this occurs in the skin as
well as ill vitro. Rabbit experiments, and studies of humans, showed that
the amount of unsaturated oil in the diet strongly affects the rate at which
aged, wrinkled skin develops. The unsaturated fat in the skin is a major
177
target for the aging and carcinogenic effects of ultraviolet light, though
nol necessarily the only one.
In the 19405. farmers attempted to use cheap coconut oi1 for
fattening their animals, but they found that it made them lean, active and
hungry. For a few years, an antithyroid drug was found to make the
livestock get fat while eating less food . but then it was found to be a
strong carcinogen. and it also probably produced hypothyroidism in the
people who ale the meat. By the late 1940s, it was found that the same
antithyroid effect. causing animals to gel fat without eating much food ,
could be achieved by using soy beans and corn as feed .
Later, an animal experiment fed diets that were low or high in
lotal fat, and in dilTerent groups the fat was provided by pure coconut oil,
or a pure unsaturated oil , or by various mixtures of the two oils. At the
end of their lives, the animals' obesity increased directly in proportion to
the ratio of unsaturated oil to coconut oil in their diet, and was not related
to the total amount of fat they had consumed. That is, animals which ate
just a little pure unsaturated oil were fat, and animals which ate a lot of
coconut oil were lean.
In the 1930s, animals on a diet lacking the unsaturated fatty acids
were found to be "hypermetabolic." Eating a "normal" diet. these animals
were malnourished, and their skin condition was said to be caused by a
"deHciency of essential fatty acids." But other researchers who were
studying vitamin 8 6 recognized the condition as a deficiency of that
vitamin . They were able to cause the condition by feeding a fat-free diet.
and to cure the condition by feeding a single B vitamin . The
hypermetabolic animals simply needed a better diet than the "normal,"
fat-fed , cancer-prone animals did .
G . w. Crile and his wife found that the metabolic rate of people in
Yucatan. where coconut is a staple food , averaged 25% higher than that
of people in the United States. In a hot climate, the adaptive tendency is
to have a lower metabolic rate, so it is clear that some factor is more than
offsetting this expected efrect of high environmental temperatures.· The
people there are lean, and recently it has been observed that the women
there have none of the symptoms we commonly associate with the
menopause.
By ]950, then, it was established that unsaturated fats suppress the
metabolic rate, apparently creating hypothyroidism. Over the next few
decades, the exact mechanisms of that metabolic damage were studied.
Unsaturated fats damage the mitochondria, partly by suppressing the
repiratory enzyme, and partly by causing generalized oxidative damage.
178
The more unsaturated the oils arc. the morc specifically they suppress
tissue response to thyroid hormone, and tTanspon of the hormone on the
thyroid transport protein_
Plants evolved a variety of toxins designed to protect themselves
from "predators," such as grazing animals. Seeds contain a variety of
toxins. that seem to be specific for mammalian enzymes, and the seed oils
themselves function to block proteolytic digestive enzymes in the
stomach. The thyroid hormone is formed in the gland by the action of a
proteolytic enzyme, and the unsaturated oils also inhibit that enzyme.
Similar proteolytic enzymes involved in clot removal and phagocytosis
appear to be similarly inhibited by these oils.
Just as metabolism is "activated" by consumption of coconut oil,
which prevents the inhibiting effect of unsaturated oils, other inhibited
processes, such as clot removal and phagocytosis, will probably tend to
be restored by continuing use of coconut oiL
Brain tissue is vel)' rich in complex forms of fats. The experiment
(around 1978) in which pregnant mice were given diets containing either
coconut oil or unsaturated oil showed that brain development was
superior in the young mice whose mothers ate coconut oil. Because
coconut oil supports thyroid function, and thyroid governs brain
development , including myelination, the result might simply reflect the
difference between normal and hypothyroid individuals. However, in
1980, experimenters demonstrated that young rats fed milk containing
soy oil incorporated the oil directly into their brain cells, and had
structurally abnormal brain cells as a result . Lipid peroxidation occurs
during seizures, and antioxidants such as vitamin E have some
anti-seizure activity Currently, lipid peroxidation is being found to be
involved in the nerve cell degeneration of Alzheimer's disease.
Various fractions of coconut oil are coming into use as "drugs,"
meaning that they are advertised as treatments for diseases. Butyric acid
is used to treat cancer, lauric and myristic acids to treat virus infections,
and mixtures of medium-chain fats are sold for weight loss. Purification
undoubtedly increases certain effects, and results in profitable products,
but in the absence of more precise knowledge, I think the whole natural
product, used as a regular food , is the best way to protect health. The
shorter-chain fatly acids have strong, unpleasant odors; for a couple of
days after I ate a small amount of a medium-chain triglyceride mixture,
my skin oil emitted a rank, goaly smell. Some people don't seem to have
that reaction, and the benefits might outweigh the stink, but these things
just haven't been in use long enough to know whether they are safe. We
179
have to remember that the arguments made for aspartame, monosodium
glutamate, aspanic acid, and they are like the amino
acids that make up natural proteins·-are dangerously false. In the case of
amino acids. balance is everything. Aspartic and glutamic acids promote
seizures and cause brain damage, and are intimately involved in the
process of stress-induced brain aging, and tryptophan by itself is
. .
carclnogemc.
Treating any complex natural product as the drug industry does,
as a raw material to be fractionated in the search for "drug" products, is
risky, because the relevant knowledge isn't sought in the search for an
association between a single chemical and a single disease.
While the toxic unsaturated oils, especially safflower,
soy, com and linseed (flaxseed) oils, have been sold to the public
precisely for their drug effects, all of their claimed benefits were false ,
When people become interested in coconut oil as a "health food ," the
huge indu stry··operating through their shills··is likely to attack it
as an "unproved drug"
While components of coconut oil have been found to have
remarkable physiological effects (as antihistamines,
antiinfecrivesiantiseptics, promoters of immunity, glucocorticoid
antagonist, nontoxic anticancer agents, for example), I think it is
important to avoid making any such claims for the natural coconut o il,
because it very easily could be banned from the import market as a "new
drug" which isn't "approved by the FDA. " We have already seen how
money and propaganda from the soy oil industry eliminated
long·established products from the U.S. market. I saw people lose
weight stably when they had the habit of eating large amounts of tortilla
chips fried in coconut oil, but those chips disappeared when their
producers were pressured into switching to other oils, in spite of the short
shelf life that resulted in the need to add large amounts of preservatives.
Oreo cookies, Ritz crackers, potato chip producers, and movie theater
popcorn makers have experienced similar pressures.
The cholesterol-lowering fiasco for a long time centered on the
ability of unsaturated oils to slightly lower serum cholesterol. For years,
the mechanism of that action wasn't known, which should have suggested
caution. Now, it seems that the effect is just one more toxic action, in
which the liver defensively retains its cholesterol, rather than releasing it
into the blood. Large scale human studies have provided overwhelming
evidence that whenever drugs, including the unsaturated oils, were used
to lower serum cholesterol, mortality increased, from a variety of causes
180
including accident s, but mainly from cancer. Since the 1930s, it has been
clearly established that suppression of the thyroid raises serum cholesterol
(while increasing mortality from infections, cancer, and heart disease),
while restoring the thyroid hormone brings cholesterol down to nonnal.
In this situation, however, thyroid isn't suppressing the synthesis of
cholesterol, bUI rather is promoting its use to form hormones and bi le
salts. When the thyroid is functioning properly, the amount of cholesterol
in the blood entering the ovary governs Ihe amount of progesterone being
produced by the ovary, and the same situation exists in all steroid-forming
tissues. such as the adrenal glands and the brain . Progesterone and its
precursor, pregnenolone, have a generalized protective functio n:
antioxidant, anti-seizure, antitoxin, ami-spasm, anti-dOl , anti-cancer,
pro-memory, pro-myelination, pro-attention, etc. Any interference with
the lormation of cholesterol will interfere with all of these exceedingly
imponant protective functions.
As far as the evidence goes, it suggests that coconut oil, added
regularly to a balanced diet , lowers cholesterol to normal by promoting its
conversion into pregnenolone. (The coconut family contains steroids that
resemble pregnenolone, but these are probably mostly removed when the
fresh oil is washed with water to remove the enzymes which would digest
the oil.) Coconut-eating cultures in the tropics have consistently lower
cholesterol than people in the U.S. Everyone that I know who uses
coconut oil regularly happens to have cholesterol levels of about 160,
while eating mainly cholesterol rich foods (eggs, milk , cheese, meat,
shellfish). I encourage people to eat sweet fruits, rather than starches, if
they want to increase their production of cholesterol, since fructose has
that effect.
Many people see coconut oil in its hard, white state, and--as a
result of their training watching television or going to medical
school--associate it with the cholesterol-rich plaques in blood vessels.
Those lesions in blood vessels are caused mostly by lipid peroxidation of
unsaturated fats, and relate to stress, because adrenaline liberates fats
from storage, and the lining of blood vessels is ex.posed to high
concentrations of the blood-borne material . In the body, incidentally, the
oil can't exist as a solid, since it liquefies at 76 degrees. (Incidentally, the
viscosity of complex materials isn't a simple matter of averaging the
viscosity of its component materials; cholesterol and saturated fats
sometimes lower the viscosity of cell components.) Most of the images
and metaphors relating to coconut oil and cholesterol that circulate in our
culture are false and misleading. I offer a counter-image, which is
I8I
metaphorical, but it is tnlC in thai it relates to lipid peroxidalion. which is
profoundly important in our bodies. After a bottle of saOlower oil has
been opened a few limes, a few drops that gel smeared onto the out side
of the bottle begin to get very sticky, and hard 10 wash off This property
is why it is a valued base for paints and varnishes. but this varnish is
chemically closely related to the age pigment that form s "liver spots" on
the skin. and similar lesions in the brain, heart. blood vessels. lenses of the
eyes, etc . The image of "hard, white saturated coconut oil" isn't relevant
to the oil's biological action, but the image of "sticky varnish-like easily
oxidized unsaturated seed oils" is highly relevant to their toxicity.
The ability of some of the medium chain saturated fatl y acids 10
inhibit the liver's formation of fat very likely synergizes wilh the
pro-thyroid effect, in allowing energy to be used. rather than stored_
When fat isn't formed from carbohydrate. the sugar is avai lable for use, or
for storage as glycogen. Therefore. shifting from unsaturatcd fat s in
foods to coconut oil involves several anti-stress processes, reducing our
need for the adrenal hormones. Decreased blood sugar is a basic signal
for the release of adrenal hormones. Unsaturated oil tends to lower the
blood sugar in at least three basic ways. It damages mitochondria,
causing respiration to be uncoupled from energy production, meaning that
fuel is burned without useful effect. It suppresses the activity of the
respiratory enzyme (directly, and through its anti-thyroid actions),
decreasing the respiratory production of energy. And it tends to direct
carbohydrate into fat production, making both stress and obesity more
probable. For those of liS who use coconut oil consistently, onc of the
most noticeable changes is the ability to go for several hours without
eating, and to feel hungry without haYing symptoms of hypoglycemia.
One of the stylish ways to promote the use of unsaturated oils is
to refer to their presence in "cell membranes," and to claim that they are
essential for maintaining "membrane fluidity" As I have mentioned
above, it is the ability of the unsaturated fat s, and their breakdown
products, to interfere with enzymes and transport proteins, which
accounts for many of their toxic effects, so they definitely don't just
harmlessly form "membranes." They probably bind to all proteins, and
disrupt some of them, but for some reason their affinity for proteolytic
and respiration-related enzymes is particularly obvious_ (I think the
chemistry of this association is going to give us some important insights
into the nature of organisms_ Metchnikof's model that I have discussed
elsewhere might give us a picture of how those factors relate in growth,
physiology, and aging.) Unsaturated fats are slightly more water-soluble
182
than fully saturated fats, and so they do have a greater tendency to
concentrate at interfaces between water and fats or proteins, but there are
relatively few places where these interfaces can be usefully and hannJessly
occupied by unsaturated fats, and at a certain point, an excess becomes
harmful . We don't want "membranes" fonning where there shouldn't be
membranes. The fluidity or viscosity of cell surfaces is an extremely
complex subject, and the degree of viscosity has to be appropriate for the
function of the cell. Interestingly. in some cells, such as the cells that line
the air sacs of the lungs, cholesterol and onc of the saturated fatty acids
found in coconut oil can increase the fluidity of the cell surface.
In many cases, stressful conditions create structural disorder in
cells. These influences have been called "chaotropic," or
chaos-producing. In red blood cells, which have sometimes been wrongly
described as "hemoglobin enclosed in a cell membrane," it has been
known for a long time that lipid peroxidation of unsaturated fats weakens
the cellular structure, causing the cells to be destroyed prematurely. Lipid
peroxidation products are known to be "chaotropic," lowering the rigidity
of regions of cells considered to be membranes. But the red blood cell is
actually more like a sponge in structure, consisting of a "skeleton" of
proteins, which (if not damaged by oxidation) can hold its shape. even
when the hemoglobin has been removed . Oxidants damage the protein
structure, and it is this structural damage which in tum increases the
"fluidity" of the associated fats.
So, it is probably true that in many cases the liquid unsaturated
oils do increase "membrane fluidity ," but it is now clear that in at least
some of those cases the "fluidity" corresponds to the chaos of a damaged
cell protein structure. (N . V. Gorbunov, "Effect of structural
modification of membrane proteins on lipid-protein interactions in the
human erythrocyte membrane," Bull. F,xp. mol. & Med. 116(11),
1364-67.1993.
Although I had stopped using the unsaturated seed oils years ago,
and supposed that I wasn't heavily saturated with toxic unsaturated fat ,
when I first used coconut oil I saw an immediate response, that convinced
me my metabolism was chronically inhibited by something that was easily
alleviated by "dilution" or molecular competition. I had put a
tablespoonful of coconut oil on some rice 1 had for supper, and half an
hour later while I was reading, I noticed I was breathing more deeply than
nonnal. I saw that my skin was pink, and I found that my pulse was
faster than normal--about 98, I think. After an hour or two, my pulse and
breathing returned to nonna1 . Every day for a couple of weeks I noticed
183
the same response while I was digesting a small amount of coconut oil,
but gradually it didn't happen any more, and I increased my daily
consumption of the oil to about an ounce. I kept eating the same foods as
before (including a quart of ice cream every day), except that I added
about 200 or 250 calories per day as coconut oil. Apparently the
metabolic surges that happened at first were an indication that my body
was compensating for an anti-thyroid substance by producing more
thyroid honnone; when the coconut oil relieved the inhibit ion, I
experienced a moment of slight hyperthyroidism, but after a lime the
inhibitor became less effective, and my body adjusted by producing
slightly less thyroid hormone. But over the next few months, [ saw that
my weight was slowly and consistently decreasing. It had been steady at
185 pounds for 25 years, but over a period of six months it dropped to
about 175 pounds. I found that eating more coconut oil lowered my
weight another few pounds, and eating less caused it to increase.
The anti-obesity effect of coconut oil is clear in all of the animal
studies, and in my friends who eal it regularly. It is now hard to get it in
health food stores, since Hain stopped selling it. The Spectrum product
looks and feels a little different to me, and I suppose the particular type of
tree, region, and method of preparation can account for variations in the
consistency and composition of the product. The unmodified natural oil
is caned "76 degree melt," since that is its natural melting temperature.
One bottle from a health food store was labeled "natural coconut oil. 92%
unsaturated oil," and it had the greasy consistency of old lard. I suspect
that someone had confused palm oil (or something worse) with coconut
oil, because it should be about 96% saturated fatty acids.
Rrccnt Unsaturated Oil Research: Referrnces.

'nlC loHowing $Om.: I :<L,<!11 that discll ss th.: toxi c .:tli.'"Cl'l of
!l11&1turaK"<.I fms. some of Ih..: Ihings Ihm otler prol<!clion ag.1inst Ihem., and sollie
I, ilh :i<1lufaled fats 1 incl ude II rder.::nees on tk iss lle <If ··m..:mbranc Jlui dil y." 10 show
Ihal Iher..: b pro\"1bl: nothing. of valu..: in thaI id..:a.
I. Y. 1'. W,Ulg awl S. \.\' \\·al<ll. hoIh lirid ",d in
1'1.1..""1 ",,- Ib di,."llJi,," 1:5(3).
2 It l'a,bn,.,,,hl,,,,, . ,1 01 .. -Ftr,.... "f " 'iIh 3"l'irin <'I' ncu'.1lwl><' in Ih" TO
""."", ...""." Dn.g A k <tt,'1 lAl ....."d. J.6(3). 1n ·1 199-t. ... d.".....d> ,'0[' . nd <I.....,.)
.1. I. J'"d",1;. · ·I1,c r" di"al. with human 1l,"KJ&\,>bin. I. Spc'ctr3) I""''f'''rt;',<
ii, ,;,ihl,' rang<': Rod;a\. E,,,"i,,,", . J.l( -t)..125·339. 199-t. (Eth yl .Icohol acts a!;-'ir' .... 1,,,,, fadi""ls.)
-t. C. l. Ibnd"lI . •1 a!. ".·\"" i";', dc"",.J.."..Tld,,,tl\" n.""\lucw ..d birth dof,·<.t•• nd I""o.oa&andin E
10,·.-\, in mi,:.::.- T "f:l1ol"K" 1»<) I .
C S. J.. 1-1"" land S. S. ",Iyare. -11,) Toid 1"" m " .l1 . Ik rs phml'holipid ,"",,,p()sit i,,,, ",I/J
11 uidny ,,[" rat br.,Ul J J (lS( I ), 1995. Ol,;dny. )
6 J. \ 1. al.. ··Supplcn"·n!.!1 i.,,, " ith 1><1 0" -" "",,,,, ,n vi ,'v and Ul "ilu> <10.... no! inhibit h,' d..Tl<ily
.. 1 ( \Ia,' ac..... l PO.)
184
7 II. A "kil,,-d,I..1 "I. F. ""d li\ll)' aC1d "'...,. d," I""g:t\.""j,., off
atI" ... ....
,,,i, in ,,,,,"",,1>,: h ...,.Hahk 10)1,,'11.1""""';" <"l>I1il.'.· ,\"",;,,,,,1,,, \'.1"', Ili,,1. I
I ')On, ( 1.i,"'ki<: a .... d 1"'" '" ..", ".\ ' ' '1
j,." )
1'_ S. Tal'll'i". W. .I. I"n. ,II "I R, F l "'" t1 u.." ..'>.· "I' """," ," ,k>J lill I ,,,; ,1> '., Ih" I'" .1",1 j,., "r" "'"."
n,"-To>i, 1;,<,1, ... ,.,,1 im ..... r""li,,·6 h) ,,' ('<..-;I<.,e,,1 "",.... .. M"L Cdl Bi ...I),'"" '·0(2). 1I'J·9l>:. I 'ns.
•) T, (;lInlh ..'I", ..1 :01.. ·E n;.....I ' "'"""'0""'''''' ",,,I j"., ,., lipid ... • Cdl
11;,.,;1>"",. '.1-11: ). I ,. 145. I<J'} 5
10. C. \\". \\.d",I '. " Ik \' i.....,· "I' ,I...·
..l'
"r' ,li,1" I'Y rin
,M.,'
""I"-'fi" ...",,, I "''' "''''01 ) ti,ukl UII'" wi I:,."",i,: R(,k "I'
,i,,;d I"'n',id1li,., : R,c"" Il.adi",IU;,d . I 77.1. I
II. J. I'.. \lIa,d. ,1 aL. "1'11,,-, .. [;my :1",,1> ,1011 ,·i"uni,,·E "'ppk""-,,,., ,., lipid
loy 1>1"",,111 allJ ,,.,In,lled l,i"I." F:u,y ,·ki"" alld Lipi,"': lli"l" I (,l·I(.J.
19'/.1.
12. t.: , j) ("n.11. c1 ",.. .. ,,(" "AI,-<J,..,,,i, Y I'-n;',1 ·c"<..",,,l. ';'1\, "id
"lid ;II!rill,i" . ".1ivil\" ,., , ... ",.1,,1 ,.,;,lIli"" .. "
Lipid "le1,,!). 251)·2.<6.
I J . I), II. V I,. "Iii. "t",,, i,",I rr<' fi k "I' """''1'"'' i" I"" i.,,,, '" ."""-,,,;a I I;'11,' 1<:11 .... i, ..."
Nul' Ih.... I . .I25 •.H4 . I I'i;l, u,n,.,,· ti,;!, "II <:""i"l: l"';n"Ok ",I n,.Tc·.",-d
""',,-,,,a Ie-i" and I'" ...,
I 4. J. II. l 1"Ii and II P. y ". 'Il,,, ill ',napl' """,m I "SI" g: I'r.;,' r.,d i,"". '" ,d I),,;d ;Iy.· rr.,,", R,,,Ii,,,,
)"kd, 1!((l ). Jj ,I .I.I\l. 1 (" ... I,,,,, mOl) I,,· hy 'han " ....
St,cg,'O<\ Ih:01 l;pid " •.'ro., ida! i•• , m.>), I" a '''''i<''- I:" , 'If ii, el,,,,,
go.: in 11" id;l), <I"ri" \; tl 'e agi" r, I"'''''''''''')
E. l"h;"'lHh>. ,1 al.. (If ,.,d Il;,,,hc"'. R,.,.. C,,,,"",,n ,
2117(2). 77 ··1 19'J S, (. \ ",,,,,,,,1 al io., "f .n.",h"aic-J 1:,1 t"-.,,,l dc,,,,n ",0<1, leI ii, "Id .,,' im:l "- )
16. J. 1'. Allaflt ,1 al.. ".·:n:.:..., "I' ,">c't,;, .1 fau \' .,,';,1- and , .. lipid •• ,
h)' I""ail, ,11,,",<: 'If! d I".. Inn<: pr" /c'tl "" " " ,11,-d l, i.,I: Fall ) . \,';'1> :.,01 J.iI'W" Hi"),, 75. I (,1· I
17. A 1o.:"lIin& " "I, .. ... n,,;dily "r "';,1'<.... ",d th,,,,, ...),,· "",mho-""" :Ilk, '"'" I I\,
;m,di:tli,.,.· R"di.lt E","i,,,... 3J( . .IG.I· .l l.l. ! '>9.1. (I"'''' li,,;J "'" ,igid;,,,,-d hy
mdi'lio" hy j>cTt'x;dJ1 ' '''': ""-""hr"n,,,,< lil'iJ inl,.,.10",,; "',"",,,'" il. Iluidi!y ,,,,d....,. ,,&1\;,.,
IK A A " 01.. ·M, rI.,-dl,. ;',h;bi!,"<1 ')' 2E I "",llil';d ,,_.... ,,;tl, 1;"" inj""" ,"
fi<h r,-d "" .... Aboh ..1 ("I",. E'J'. 1-1.",. II<{Sl.
Ill. A. A N""ji. "I.. "fhl": "f I:', all'] ."tI,,,,,,,1 ,., ,u,!j"xid"", "'0""" ml-lN ,\ ;"d" ,1i•., in rJI
1;\"<"-,: J. 1-1.", 16(4). 7 ,16· ]?'H i i);,ln",' c,l l:.t ""d ,,,,i,,,.t, h,,,1 "" h,..- ;"jlll). Ii'" "il ""J
,'\1"",,,1 "us had "'\'en; Ii,,,, inj"",·. )
20. C. V. " ai.. 1"-'\)l11l>:!l"'UlCd hUr a,-i<l:o ,y,d "[Iou"",, a"n;,· 1'1:"1"'--;;'" , .... ",-,
.144(1<').11 ). \9(,. 1\194.
21 . S. C. Sahn ,",d G. C. (;ray. ""d,"" D)liA oJ.-,n,"S' and lipid I",,,,xid:.li,.,: C"n,,,, 1...1'.
113(2). 1 164. a tb","h,id \I hkt, ;, "'"" ,,,,.:0"-,' ,;mil .. h' 4"<:",'1 .... "h;d,
i. wld as am;",id"",- "ft,,, run,1;,", ""
22. S. I b,d. "(hid"ti,.. , .. I' "",,,,hi." a"d ""d ;.." as hy 1",(1.' J. . \(1. Ch,·", . .121 II),
H02·24OG.I'>94.
1.1. t.: . I..."dl","n. " ", .. ",\,,(;intla""''''h..-, 1",",,,,,,,1 1.·"I'''g "",,';,,1 in IM,;,,,I"
,,,,",,,,,-a!jc ",,'id lumor,,: Can"", R,,,,,,,rd, I'J'N. (Pn..-d"i ..>1 .. and
.igr>.fkmllly I"'ol,",gc'<! "''''i, al.)
24. J. J. ("h", 'lid Il. p, Yu. " ..\b,·,ali, ... ;" "",n,hrn",· tluidi!, In' lipid 1"',>(1,"..... "
f".., 411-118. ]'>94
25. 1. II. ("Il"i and B. P. Yu. "I' :lg<:'''''31,"<1 ah ....-.ui,.. ' "r ;m,. and lipiJ rc .. in rotl
......,,"11.·i\g,> 9.1 ·\17. 1\19·1.
16. H. J. S;p"" ,1 at. "'110" ""1al,,,)j,m "n... ia....,>lrad;"1 A I'",,;,;bk "'"",,, "I' "xid,!;,''; >I"",,,
in ("''''';''''I>,,, ..,,i, 1 I ). ) 6.17·26 4.1. ] 9'14.
27. N. \\" .. ,1 "I.. "I) N.\ lim,' :l,'w,n,ts 1i>r1\1I'..,.- llo',mO, \',,".-o'i,., ;"due,,"," In Ji,1"r:- M ill a
C<lrcinoma nlO<kL - C.Il,,,.,- 1...11 . 810(2). I 77·1 %. 1994,
2R A. ,1 al.. ·: Di,i .'), hi!fo.linol,--aI<: "il .. ,ie in og,"dy d,ol"",,-roI in Ihe 10 ,11,-.. 1 !hi, , dd-"..,;w
. "i,;,n ,,,,,,,",,1$ t<lf ",dnct;"" "f ,,'''UII <.1101<-..:],.,.,,1. S.11l1",,',..- ,,;1. """<: >-If"<JI,gly !h...
®<"1" o ils. Ih ..... prod"""" hiChc..- (j",k'O<\,.-oIlcwls in ",.,."m "'"' <:).1,.. dc"<l h' 4 n.... '!lI>.)
29. M. J. End"........ .:1 al.. 'E lf,'(1S "rr"", v .cids ';,und ;"""",,s.:J in \\"'''''''1 "h" <kwl"I1I>«: ...."·lamp'i3 '''' 11\,"
.hilny of .. d,.hd;.11 ""xiII'"
'" .. and pi;"d,1 aWeS'1;,," - S'-"'ln . J. ("I;". I"h.
b,v«>t, 54(7). 3411.H7. \\194.
]0. II, nanmmi. d .1 .• "llllerfc'TQI'·g;>nnn. and pol)"W,satu,ak-d r:lIty .cids "".,..,a"" !hc b\I,d;ns " f
lirq>o\ysal."dlari&: 10 11I''''''''''''I>>.- s: tnt J. E.\{'. 1'3tl",1.
185
II. I' ..1 aL. "r""ur.1 ,..,11 ad;,oily I» di",",,' lipid.<." ]nmu",o!. 1...'11_ 41(2-_1}.
19')4 .
.12 I L I._ ,1'1.. "ElK..., " rdi ..1 and ,'ilalllin t' ,., !)t\A U, rn:.hly·;oolal,'tI h"man
hh.J <">:11,." R...,. .•. r>:-;,.\. (i ..'I1ct . Aging J 16(1). ') I . 102. (!lieu.,. ,-itamin C ""y pnl\-id<: pr'>(c'dioll
1):-;.\ in ,"ilm k>l, it eX'IUIJ .1"" indu"" ""'aks. Cdl. lak"" atk,. cal.ing
hr,-akl:,>l had r.. U"., ""lis 'ak .." b.:fo,.c 1>r.:.H,Si. .. faSling o,...",,;g]!! lOXmS 10 c:I"'"
g.. ..'ti<;
dam"&-",)
.1,1 f U..'I'>'dl3"c,< ...1 aL dl..."<,1, of d",ary fm> in r.l1;oo. for gr,,,,-ing pig:<- 4. f .ll"",
"I' .. mH,,,, cr <>il and " ..'«"" oil Oil and !:I\ , ..1 ..,11;,.,. ,cid ",tII,'ll "fhack f.1 ;Uld hl,.oo in
pi!:J ..1,." . \rdL T;"r"nlahr (EaSl 3.j( 1). 19-.13. 19H. (Fa! in oil fOO
001:-- .1 4 d,y", " ... in Ihe £1<"'1', IK6° ., and in!h" ","ill",,',.. 0;1 fed an;",.I •. 21.\ " .. 1
,l.j J Y",hc...J, ...1 .1 .. "Elkct, "r "",..",;,1 1i,I1y acid ddi6"",":>, .., Iv"..." I;""," act;,,;ly ;n ,aI.
maim.in ..'<1 at 1I,,·nmln,·ul,alily." ("''''1'' I)iool A ( Engl.tld) 94(2). 273·276. I n'J.
""",-."",1 ;n "-'!i1in& ",,1.I><,lic rJk pn>d",xd by using ,,,C""Ui oil,,, ""ale an css...,-,t;.l f.tty
<1..,["';"'''")'. i, p,nly Ihe ....... uk of in,w."..! he:1! pr<.>ducti"" iu lI,e Ix""",, ad;po.,,", li",,,c. ' Ihe ,,"ei!#l' of !hal f31
,\.."',.... ""'-'<1 hy 28" .. "hil" it" ahi lil )' I" pr<>dtlCC heal ;',,""c.,.:.! (,<)0
.n . R. W. 0,,,,,·.,, . ,1 .1. "Direct rcf!.Uial;OO "fi,.., d1annds fall), Tt,'11d_ Ncuf<\Sci. 14.96_100. 1991,
.16 II (j , I'. •. ,1 .1 .. ' IJind;n!l <If un"'l"rok'<.l fally acid;; I" No -' .I,7-Afra'\C leading '" ,.><1
Ili''<him, lJiophys. Acta 1U24, .12_.\0. 1990.
n. (;, .\""...,. '" al.. "F........ uial IOuy ",i<J.dcf,ci",1 di,o{ PAl' Ie,...,,, ;n "nd duod<-.nnn of
tat•. ' J, Lipid (,dl 9. 145·1 B. 1994 .
.IN . J. Ral:.cl. '" .1.. "The ell".1 ,,( ",,,,.,lIi.1 f31l)" acid deficiency "" t>a ... l ""spimli.., and functi"" ,,( Ii,.....,.
m;,,,,,1,, .. d,ia in ra';..· J. Nun. 114. H5_262. 1984 .
.l9 , I' II. ('h:., .-u,d R. A I;i!!""an. 'l3min ",1.... n3; in ronirnl .lie" " by faU)' acids.'
S<.:i""" 20 I ..158·)69. 191K ''Il,;s cdt"l" cdcma was "","'<'itie. ,illce neilhe, .,,,,,ated f:,\!y , ..,0:\. nor • fat,y
.wi d ",,,'ain;,,& a .m Ve lu,d had .. >(I, dl'-"<1."
(" .1.. "E1kct.' "f di.13.)" .ll'ha. :uld g"nm,a·l"l<.,k'11ic acid> M Ii"..... fatly acids. lipid
""-'"b"h,,,,. and "",-.,·i"al in "'-1"i<. • Sh .....i. .j{ I). 11-20. "L>ict.ry GI. .. \ ",,,,,;,,,1 from "'-'P'i •. •
41 . D. .1 . "Inl1u.,,,,,' of dj,'a,,, fa\!v . cids "', in",,.,,,,..' ond COf"t'{!liano.:
"f i,,'lal,..! 'al my",;,,,,tj,,,,,. J mol ('dl (';rdj,,1 27(8). 1145·1 1995. a lr"".j I",,"'ards 8 ""''''
I"-,,l lengll""ing "'I, ... 1"..oIoa" in 'h" U· (n. \) ero"r -'<>e<1h," ,,;,11 nndl""e>,,1 f>C.,l ",I" o f ;""<1<1",,
(,"cc ""din,·. 'n,;< "",,1,,'11 ;" si!Jlir,eanl impain,k.'" of !he IWO nlCdlanical indc.w< I,"l'\;ng the load
<.k"..,,<\...'I1W of ",,",,,,,,,d;,,! s..'C fl I';.:.lc. 1169·'8
41, II. J..,n, .... ,1 al.. -1)..·wl,'P""-'" ,<lid .. ct<.. il,,'ioo or f.u)' acid dclici,-uc,' in hu",.1<l ""lolI,dial
0.:11. in 1"<11." Nail ,k.d Sc; ( 'SA 91(4). J 1995. Oleic <.k'fi'·aI;W 5.1U l...:i"'-'<atri.'11o;,
acid (20:.1 9) (5. 8.11.14.17 c i""",'!",,,,,,.,o;c. o",,,ga 1)): 20:3 "'''''&I' 9 ;ml''';'''<1 the C.2(;)
, "'Jl!'f,... i,'c eff,...1 or ( Ag"" is1-induC\.'" i"'.,-c ....'" in "'''l<.:<'!'trali<... "I' prOSlac-:-'cIiJl" PGI
2. ""d (".2 · We..e ....'<I'IC\.'i'-OOcial i"" "f C and diacylgJ)'o.:rol lewl. in li,,<.,. pla.Ill"
"k.""Ix"",,,, "f "," "n rororlUl "it ami ",m'M', .. oil d;o:1>: J. t\UI, BiOO,em 6(10). 1995. "11Ie
Icti,'al;"" "f I'KC' i•• in "itro 1\)' ditf,.."" too), • ..-ids.· 'RalS 011 ",,,,,,,,,,,t 1n3,h'dly
I"" ,.,. PK(' in her pl.",,,,, nMnh.. n"" with .liEll1 hi" . i",itie",,1 "f!he ."'i,·ily in C}10601
!h,," did ,,,,. fed ..,(lkm', .. oiL" " .. .""""'" "il r,,,,!lI.:.! in • highe, "f ,Ii.cylgl.'"wrol. in Ih"""
,,1<-,")""'' '" than did ing,'>!i"" of ",mow ... oil. ..... h,... ,,3, the I"""""i",," of f311)' acid!.- alld pi)()spI",'ipid:!
:.nd "",,,bronc nuidil)" W,"e rJts 1'o1S.- "II .........,,'" ",(u,at."" fa\!;
es,'" "ariOl" "" lipid .Ild liJ><'Pl'll.cin """"oo!;"", ill pan
44 . V. 1i.,,,I:,!\!. ,1 .1.. "r;!'I, oil ""d (,my acid dcfi,;,'11"1' !litric os;""
rot ""'croph"ll''''" ki,. ",)' Inl. .\6(
o •
1280-1286. "Bo:dl...h"," be"" :J]""" to .).IIli·infb"UlIOI'JO)·
" fl ''''.''---.
. .-\ ,\ f'arooqui. k \\"dl •. L ,\ Hort"'-b,. ·Br;:akJ.w.n or nl<'mbrane I'h""('holipid$ in Ailnein""
di"".""_.;,"'"h....lll<fl1 <If cxci1l\l<lr,. 3min" add )l.101l'he'l11 25(2-J) I ' Tll,
'cl<.'""" "f at:l.j,id<11.,c I,,,,,, !he ,.,·2 posili"" of is catalyz,,:...:1 b)' pll""('holif';>ses and lipa .......
Th""" a,,' coupled!O EA,\ ''''''l'l'''''.
lh\....,.,i"",la,i"" of !he'S<: """"'' '0<1;
n",y Il<' ;n,"o\\'.'<.1 in all" "",,,,t
h,"'k.-ootasi<. dcgada1ioo of m<,,,,br .. and thc .""""mlation of h..., fauy ."';ds.
pr<»tag.la"din •. "lid I;rid pc.... 'xido..'>, ,\o.'<!Iln",I:>I;"', of the " .."'ti .... oo ",,,,aholilcs. a.< well as abnormalili", in
sig!l.ltTans<.l"ct;oo '''''ing ,<> !IIinmlat;"" of an d may ill""!>"..! ;'1 pall,oll'",,,i,, of
!he in .... D."
46. P. H, Ch.ll and R. A. F;>!1m.n. 'T""I>i,,,[ rorIllOl;"" of $lIp..'roxidc radical. in fau y
acid-induo.:d hrnio' <1I"<1I;'1g.· J of!",'\I,od,.mi!;tIY 35. 100.\·1007. 1980.
47. T. (;u"l1,e,. ,1 .1.. ...1-< "r mag",.. i"", and iT'" "" lipid !"-'ro.• ;dolti,,,, ii, ,;uku,etI Mol. CeI!
Biodtcm. I 1995, ()'bg"",iu", prtlk'<ti against itl)Q. )
"!"f<,U!' J_ .·Po"!ll" "U pC'1 (>!:If ,'!l!'"IC'<l s .... ".o{-f) 1 ·(4 .{q "!P-'-'t!t'<0Jd
p...... np'u pp •.'!"10"!1" ··.. • ·"".""!P l""ll" 1e.,!"!P :>41 ,,",OJ;>Cj 3""1 ",,!..a.""I»-:ud
d,p.,,,!, """'1 0'1" 'c">llJO" "! p..... ='" srp' '\1l".1 )0 'p."'I' . _ 1 '(Ot, '!«,,"q
-""1 ''''1.) T -"lOS _ "'PI"ld 1!'1!'Jll! I'll< '''!p,(:, • ...,Jd ",npN<! 01 <IF'" J"
U" "!.nuol",,":ud d"p.,,,,, u'I" \1.">\'10," "! ""'.....<;I"! PlII"') "tiP" \In'.1 "'-',I JU <}'."!lJ:J. '-1" 'lI.">S."I'U:J T ' 9')
('51 ""!"" PIU "! .,npcud 1".1p.Jl'JnJ","n ),\ '.'!UI"'''''''''\,) "(ULf,t
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(',\l!P!"1l S.,,".'.PUp ',66 1 'Z\"-6 t .( I »O{ '( 'w."f"'!1[ ... "'"JI\ J" " I!p!"U
I'"" p,d'lo<flIsvljd .... )ll:>lllW·'J\ PlOJ,('I.L. ·...J",\I.:1 'S 'S ·P''''I·\ '''/I '''1 -f 'Jl<::i""fl 'S '.) -It.
',661 "(0111 '!'-'IX '1"!f1 I"-'!P"H"'-':J "'.J1"""ld
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_·..... ,t·O! ·\'1 "PI"ld _"II"" PO"'''P.'\I
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do'l:"'-'P ""1"1 "'I" ,.'I,k'." II! "''' .\llI') ....."U) 1I1II)l:1""'.' .10 _ ·to661 ·IL)!.' 'I"-'''q
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(;"",""->J<l i/"fI'o '3',!-,np "! :4,...., "'Il Ul JUP") ...r.." "'I.'"'' ""!II-"P!s<.U;>d P!'l!I W41 ».--T.r.I",
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98 1
187
,.xI"",-",! c,,,I,,"hdi"1 ."Ib" "I>ility to i>1hibit platek1 by ... _.. " r.. A N,"';, "",t J. fl'''''''r.
"Elr..'<-t "I' Oo.'S1rog... , 00.... "n wh ol< bh>.>d plMd'-1 . cti"Mioo in W.." ....'" 1,11;int ".'W 10<, du<.:
"11",. . ,,1,. lI acllIoSli . n(!» . 926.930. lW-l: ·1J' ..""a".,j k""I, of AIII' "ml .r"ctlid.",ic oci,\.indu,-,-'gram ,1l,u,yl,..,>ln>diol Platekl rek.."" <>/-
h..!Ia_lhron""'gl<>b"lin (1).1" T(1),,"" .Is.. ...."'- "Wcg:>li,., Wa,
...:d hu1 Ihi., f.,ik-d \<> rc.ch >U1i>tic.>1 .ignitic.",C\: fi,. the indi,-idual [",at" ...,\! gr""P"' " ) ....>g'-'l
domin,mc.: i, an ........',,;.1 lactor in I"",,-,,,I.n,,,,,ia. Woo ........ n-oo "I' (",Ia"l'lic) "",,,,,h,ioo,, h,,-e h..'-'1l
found 1<.> h,w <:I"... in I>r.u, N",>d ,,,,,,,,,I;, <.>flhi. worl had '" Ofi&o' in Ill" 1910. (ShUI" OIId
,md wa. b",i.:J by the I"""cr "ftl,. ,,<1"'1:'''' indmuy.
67. H. ,,,- "lnl,-'fI<'I'OO.ganllll3 "nJ lim y ncid< in,,,,,.,., Ill" hindio'g <.>f
li""polysacd...i<k ..: lnl. J. £"1'. PMlloL )6)·)61( J
MI. G. Aut_. '" aL fany ."-;d-<lcli..;" " di,{ modi fies PAF 1"",1, in and tlu<>d,.,,,,,,, of
"'l," J. l.i]>id )"1,.,ji;uOf"S Cdl Sign.Hio,l', 9. 145-1 B. 1994. or fat.
d .... r"'"-...,. from endowdn .
69. N. Auge. '" at. "Proli f,.".\i ", .. ,d of ",ildt)" lil"'l'<'«"in. ,," " ...."'1"'
"""x,uHnu""ic Bioo..il"'n J 309\Part .Il. LO I S· I020. I')'>S. "Th" prolif"'aliw d K'<..t ctl "'' >CJ\JH''......-t''
i, 0._\,'1"00.1.",...'<1 al higll "f mildly I .D I _< lor aI high o.,;J.nioo lev,,]. ) by lIl"i,
df.x:t."
70. s. " , Clinloo. al,. "'111" <:Qmbin.:d (lr..:"'" of di,,,-,,,), fa, and c"'-rug"" «, ,,,"'i,·,,!. 7.11..Ji"''-''-byll....' u(').
lire.!'! can.;...,. and pr"la<.1in nl<.1.ab" lism in ralS.." J. !'l/l ,. 1191-1204. 1995.
"Mooalily in ",.,uois wa. doub!c.,j 1»' f.<:ding • hilt> fa! ... : ", .. J>f<"S<.'>"'''' of Oi>1rogc'n may"" a J>f'-'fC<ju;,i!c
tOr s'gJlifi .."," dicta,)'
71 . 1', S. Tappia, c1 al.. " b,nu,,,,,,, " f fally :acids '" Il,,,
proo"o.i", of Illmour n<'<T\IS;' tau"" and
by ,at macropltag,,,." Mol ("dl Biodwon 143(1 ). 89.98. 1995. at 50 micro .n
fau ),
11<.;<1< "'f'pfew.'<I !'KA ad;"it),. ""'-"1'1 okic ,,-bid, incru ...'<1 it; PKC ",",h'ily ,",'" by lulOl.:ic ",:id
arId oleic acid. loo me M LA .."",d PJo.;C b y 14M ... ",I\ik EPA and DBA .... Pl"" ","'d PKC
n . R. 1..<."0" .... ,1 at. " Dewl"J'ffi""( and d,."ctc... i7<n i", of ......mi.1 fat,y .....; d do:fi,;",,<), in human ",dothdia!
edls in Proc Notl "'cad Sci l iM 9 2(4). I 147·11 Ol";c acid &:rivali""
3cid \10:3 (M'''-'P 9) (5.8.11 . 14. 17 e icosol"-"O(ae"oic. 20·S «'''-'P .1 »; 20:3 omega 9 i".,p.......'<1 th" CaW)
indicating. soprr=il'c etK>ct of it . (Agooi l'l·'mt\1OOd maca,,-,\< in coo.o::"Uati"" s of 1'1"06\alO)...iinc pciI
2 .•,,6 ,-")'"",,Iie C. 2 , w-. Nd .. <>KI in .-fad <",Ik )
73 . K hn"'Il,",i. et aI., "D issociatioo of prot"in kina .. C aai,iti"" and di a",),lgI)"C\",,1 k\'et< in li,-.,r "1. "",,
.. of ,ats on ""'-""til oi l and .,m'''''T J i,'U: J, NIM Biodlcm 6(10). 528·533. J995 , - I-"c
acti,,"I;«, or /'I,:C is aff""',--d di(f("T"CJl1 ly in "it,o It)' diff...,."" folly "Rat. on oocmUl oiL, .h.d a ",.", ..-.:Ily
lowCT Pf,;C ,,«;I·ity in pia ..... n"",lbr ..",. with sli!'t>1 hut , ;",ificant .-eductioo oflhe Ic,ivity in the C)IOMII
lIlan did I'lI\S fc'<l oi l,.. : ",.,,,,,,,,,""11 oil ,esuh ..'<1 in a C<IO'IC1rt <If di,C)·lglYC>..'T()l, in th,...,
" ... Ill .... did mgest ion of .. oi l. wh<.,.,· •• the proponi"," o f satU,Aled fauy .... anJ pho>pholipids
and """"'hrane n uidity w,"", ,;",;1., bct..-ecn f:lls difth<'fll "II sa""" likd}' that fOl<
dfe<ts on lipid antllipoprotein metabolism, in p.1t through PKC pathwa)"."
74. V. Boo\a,d. <1 al. . "Fish "il :ond fany ... defidel,C)· ,edtlO;.' nitric oxide . yulll.,;i.
by flI\ macrophages." Kidney Inc.
· •
]2 80·128(i. ]994. "DoU> ..h","c b.."<.'Il ,/1<,''''
Ie exert IJlIi ·innalluualOl)'
e OoXU. ...
75. :>'1 E Mi]kr. d.1.. "[nflu ... ", ofhorman,.. «, plaldo:t imn><>:Uula, Thrombos i. R"""",d,
"Plowlct inlntedlu!., ""Ieiu", ronD."O\tll\im and relea." ...... si",iIiCOlltly in ....om....
ingtNing lamoxifen 10 and ma-"a""tl. as ",as "latclct adhesion. in ou l
o:on\f'D.>p.;"" "Only oral <:OOIra<:qlIi,·" users had in"",.sed 5O.$l.iti>;I)' to Iggregat ing ag.."Ot"- ."plater",
ca lci um Icvds Ire d_ly related (0 the degree of plotek,,- .d1<'Sioo and aggregalioo in ";"0:
76. F. lind G, Vano:\crkra)k. of " ... 'dctr<.lpin->limu!at'-'" ,w a,;an steroid proo\"-1ioo hy ""f.
in ,dCOSl fish," Lipid. 30(6). 541·$$4. 1995. "EPA MId nll ..\ inhibited g«WiOlropin ·l'limulaled Icl'tO!;lc"l"OMc
prod"di"" in. dosc-Nlno>d nl&l'n'"...."
77. A }\ h 'ooqui , K Wells, L A HOI'T<>d<s, "llreakdov.n <If m<:mbr'''le pb<.lopholipids in ""ril"im",.
d's<:ase-involw..""'t of . ",;"0 .<id reWptcn..· Mo l Chern N"urop.llllol 2$(l ·3) I 199$. "The
", lease "f """dlioolate from the ",.2 positioo of gly<:erop/lospholipids is by ph<>Sph O!ip.1st.'S and Iipases.
These MC <:Wplod 10 f AA "f thoO$C 'eo.:p.or.; may be ;"v"l"oo in .t.-.oonal
,,"lcium b""""""..i .. degndatiUl of membrane ph""lilolipids. and tI,e 800J",ulatioo of f"", fauy ,cids,
prostag1andin .. and lipid I"-'T()xides. Accumulation of lite I11<.'I1limed .....-\abolit... as well a. ab,u:mtaliti"" in
.ii1lal 1"""""<.1;00 "",';"g 10 .tim"latioo of lipas.:s and phospholipascs, may be ;,wohed in Ill" pathogon..is or
th" ncurndeg.."Jl"",tioo in All"
188
A LOGICAL DIET
Most diets are promoted for a single purpose, such as weight loss
or heart protection, and usually they don't work even for a limited
purpose, If a diet allows you to adapt to varied activities with a minimum
of stress, it will help you to avoid many serious problems. Years ago, a
retired dentist studied healt hy people and their diets around the world,
and found that many different diets supported good health, but when they
began eating the "western" diet, based on grains, they quickly developed
all the degenerative diseases.
There are some simple biochemical reasons for avoiding grains
and beans, that I have discussed in more detail elsewhere. Plants put their
most effective poisons into their seeds to protect their progeny. These
toxins block digestive enzymes, lowering the food value of the material,
but they also poison many other physiological processes·-hormone
production, immunity, and brain development, for example.
People who are accustomed to eating wheat shaped into dozens of
foods that differ only in appearance and flavor sometimes say "there's
nothing left to eat" if they eliminate grain!;, or !;top relying on them for
their main source of calories.
If we restrict ourselves mainly to animal proteins and low·starch
fruits, we avoid the nutrient·poor foods, and still have an almost infinite
variety of very pleasant foods. These foods are generally so rich in
nutrients that a person could choose just a few of them, and be assured of
an abundance of vitamins, minerals, and proteins.
Nutritional deficiency diseases probably wouldn't have been
discovered if our diet s hadn't been based on grains. The starches in grains
aren't their only problem, but starch is uniquely suited to activate the
formation offat, and to stimulate appetite, especially an appetite for more
carbohydrate, to restore the blood glucose that has been used up in
making fat. Starch also has the ability to stimulate allergic responses, to
plug small blood vessels and to accelerate aging (according to the work
ofG. Volkheimer, and others).
There is one form of grain that is relatively harmless because of
the traditional method of processing it, and that is corn that has been
made into tortillas or other native American foods , using alkali to detoxify
it and make it more digestible. Pellagra was strongly associated with the
use of ordinary corn, but not with the traditional preparations. Tortillas
189
fried in coconut oil and salted make a pleasant snack which is less
nutritious than potato chips, but less allergenic and more digestible.
The sugars and minerals in fruits tcnd to stabilize the blood sugar,
and when they arc taken with protein foods, they allow the proteins to be
used constructively, rather than being converted into energy. This
combination minimizes the stress hormones, and promotes thyroid
function , so that energy is available for lise, rather than being stored as
fal. For example, a glass of orange juice and an egg make a good
breakfast and cherries and cheese make a good snack . Chicken and
watermelon, pineapple and ham, any combination of fruit and protein will
make a balanced meal. Milk evolved as a complete food , according to
this principle of combining sugar, protein, and minerals.
People who drink a quart of milk and a quart of orange juice
every day are much less likely to have a hormonal imbalance than people
who cat the average "well balanced" diet containing mostly vegetables,
grains. and legumes.
One vegetable has a special place in a diet to balance the
hormones, and that is the raw carrol. It is so nearly indigestiblc that ,
when it is well chewed or grated, it helps to stimulate the intestine and
reduce the reabsorption of estrogen and the absorption of bacterial toxins
In these clTects on the bowel, which improve hormonal balance, a carrot
salad resembles antibiotic therapy, except that the carrol salad can be
used every day for years without harmful side-effects. Many people find
that daily use of the raw carrot eliminates their PMS, headaches, or
allergies. The use of oil and vinegar as dressing intensifies the
bowel-cleansing effect of the salad . Coconut oil is mOTe gCITIlicidal and
thyroid promoting than olive oil , but a mixture of coconut and olive oil
improves the flavor. Lime juice. salt, cheese and meats can be used to
vary the flavor.
190
CONCLUSION
Context is everything. The idea of baJance--physiological,
honnonal, or nutritional balance, for example--requires contextual
thinking. Environmentalism is a form of contextual thinking . There are
no closed systems, anywhere. Before the second world war, there were
many influential people and institutions devoted to contextual thinking.
With the rise of overwhelming corporate/state influence in the world,
manipulative "public relations" has replaced critical thinking even, to a
great extent, in the universities.
The main channels of communication are controlled by a few
monopolies, which combine financial, weapons, pharmaceutical,
agricultural, and energy interests in ways that are creating an interlocking
set of almost rational-seeming beliefs. To orient yourself within this
system requires some attention and effort, but once you perceive that
your health and life are in the balance, it is usually possible to find the
motivation and the energy to persist in critical, evidence-based thinking.
I have looked for the best workers in many scientific fi elds, and it
seems that their discoveries fit into a meaningful picture of life. Warburg,
Shute, Biskind, Lipschutz, Selye, Szent-Gyorgyi, Barnes, Ling, Meerson,
and others have revolutionized biology and medicine, but their work has
never supported the dominant corporate view. and so it has been actively
suppressed by the forces that control science education.
The therapeutic methods that have g rown out of their discoveries
are simple, basic, inexpensive, and extremely effective.
NOTE: Some businesses have misleadingly used my name and parts of my

research to imply that I support their products. The only formulation of
progesterone that I approve is progesterone dissolved in vitamin E, and I
hold the patent on that. It is useful when applied to the skin, but oral use is
more economical. As this book explains, other solvents and additives can be
harmful. Almond oil, avocado oil, samower oil, etc., sensitize the skin to the
aging effects of the sun, and are inappropriate for use on the skin or
internally. Diosgenin, sometimes called wild yam extract, is toxic.
For informatioll on my other books, newsletters, tapes, progesterone

in vitamin E (2.850 mg. per ounce), coconut oil, etc., write to:
Raymond Peat, P.O. Box 5764, Eugene, Oregon 97405
www.efn.orgl- raypeat Tel. (541) 683-4279
,
• ......... , •
• ,.. .;,. . . . . . .
.... .... 'l,.
''11:-1>-'''',:
,..';"
•,
,
i'" . ",,"
FROM PMS TO MENOPAUSE:

.;.1
.; Fe'!,'ale in
•. .\:. (. " , #..,..", b
•
:.. : By
, Ia.. " ...... ,,,.. I
. . .f.
',_ I, -. . " . . .
'f , " . female he.8lth ';, ,
, bud,t mto' both 't medlcal ,.. education J and popular culture.
iJndenta'!ding the subject s,:ientifical!y mun. go'jog against the .. ,
-1. of both conventional medicine and alternative medicine.
......
.. "" __ - # , , , , , .
"::fr
'" . o· the roles of hormoDes _"- and ;the various
apJlrOaches. a variety of proJ:tlem
fromchildhQod to old age, are considertd in
'"
.. women
For example.
. sections focus on: ·.4> ; . _....
--d.
. .r_·
, '"
migrainehudaches
Alleviating.the"'symptoms of menopause
Losing unwanted fat with0u"t "dieting"
Regulating fertility
Protecting pregnancy _, "
Curing arthritis", ;. .
nervous disorders
.
.' hV
,
Raymond Peat ;- received bis PhD Biology from the '
University of Oregon, -specializing in physiology. He has written
"Mind and Tissue, ProgestO"Olfe in OrthomokcuMr Medicine,
Generative Energy.". and
,
NutritiOll
, for Women, besides articles in
journals. He has,
• •
taught • at the Univenlty of Oregon, Urbana
;;"College, Montana State Univenity,'National College of Naturopathic
.Medicine,
, .
Universiaad-Veracruzana, and the Univenidad Autonoma
del Estado de Mexico, and founded ·Blake College, International
. Ubiversity, He does · independent reseatth arid private endocrine
an1d . . . . i ; , or,: I
. '" 1
,
'.,
,

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,

By Raymond Peat, PhD

PART ONE: ESTROGEN IN CONTEXT

PART TWO; PROGESTERONE IN CONTEXT

PART THREE: "MYSTERIOUS" DISEASES IN CONTEXT

PART FOUR: SOME PRODUCTS IN CONTEXT

Copyright 1997 Raymond Peat, PO Box 5764 Eugene, OR 97405

Q: What are (he harmful effects of taking estrogen?

By suppressing the thyroid and st imulating the pituitary's secretion

Q: You mentioned thai estrogen causes pituitary tumors, If the

In the early 1970s. researchers at Johns Hopkins studied a group

Q: What are some of the emotional symptoms of excess estrogen?

Q: What caused your interest in estrogen?

Q: What should I do if I want to stop the pill?

Q: How can I tell if my natural estrogen level is too high?

Q: How can I get my natural estrogen level to be lower?

Adequate protein and B vitamins are essential. Vitamin A

Q : Wililowt'rill g my estrogclI have a uy harmful eITects?

There is no valid scientific evidence of its safety in any

Estrogen's contraceptive action is just one aspect of its

Estrogen is dangerous, in any amounts, unless it is balanced

Estrogen is a cumulative toxin, because it causes changes in

"Replacement" is a trick word in this context. At a European

Q: How saf(> is it for a wOnlan to take estrogen?

It simply isn't safe to take estrogen. Safety implies that adequate

Q: How saft' is estrogen in very low dost's?

[t's not safe even in low doses.

Q: Why would th e medical establishment prescribe estrogen if it's

Hundreds of millions of dollars of annual profits from estrogen

Q: Doesn't taking estrogen prevent aging and increase energy?

Because of the claims that estrogen protects the skin against

Q: Doesn', estrogen prevent osteoporosis?

No . It is said that estrogen slows the rate of bone loss, while

Q: What about laking estrogen to avoid Alzheimer's disease and

Q: Do you melln estrogen might accelcl'atc brain aging?

In animal studies, it accelerates changes in every organ

Q: My doctor said estrogen is safe if I take it with "progesterone"

Physicians often confuse the synthetic progestins with natural

Estriol is a slightly weaker variant of the stronger natural

That is reasonable, if you have access to the best information on

Many physicians prescribe c10nidine patches to prevent hot flashes

Q: How do I gel ofT eSl rogen?

Keeping estrogen's stimulating action in mind. women who want

There is no valid scientific evidence of its safety in any

Estrogen is dangerous, in any amounts, unless it is balanced

Estrogen can be produced in practically every part of t he

Estrogen's only clearly established useful functions are to

The body's normal defenses against estrogen fail with aging,

I think it will be instnlctive to consider the three steroid secreting

A note about "the female hormone." In the absence of the

NOTE AND REFERENCES:

I. L. C. Strong, Biological ofC(luecr lind Aging. Pergamon Press. 1%8.

A Better Name is Needed

If animals grow up with female traits simply because testosterone

>I<The revolving-door between the agency and the industry--the delayed

I. M, C. lJiamond. Enriching Iler.:dity: Th.: lmlXlI1l1uc<.! of Ihe En\·iromn.:nt on Ih.: of

Abdominal bloating Depression

Heart murmur Palpitations or paroxysmal