The Caffeine Roundtable

Moderated by John M. Berardi

You think "roid rage" is bad? Try taking away a habitual coffee drinker's morning java,
then see what happens! Trust me, I've seen it and it ain't pretty. It's estimated that 80% of
the world's adult population consumes caffeine in one form or another, the most common
source being coffee. It's also estimated that the average daily intake of caffeine in North
America is 300mg/day. There's no disputing the human love affair with caffeine,
especially in the form of coffee and soft drinks.

So what is it about this magic elixir that makes people go so crazy? Well, the stimulant
properties of a strong cup of coffee can't be denied, especially when the alarm clock
buzzes at 5:00 AM. and your brain's screaming "just ten more minutes, mom!" As the
coffee giant says, "The best part of waking up is Folgers in your cup." In addition, a stiff
cup of coffee before a big meeting, a big workout, or a big night out, is enough to clear
out any cerebral cobwebs, stimulate thought processes, and produce a pretty nice feel-
good high.

But let's not romanticize this topic any more than the coffee manufacturers already do.
Regardless of its social acceptance, the caffeine in coffee is still a drug, an extremely
addictive one with potent pharmaceutical actions. Therefore, just like I've done at T-mag
in the past with protein and fat, I've assembled a roundtable of smart guys to discuss
whether this chemical is a friend or a foe.

Why a whole roundtable article about caffeine? Well, in a recent Appetite For
Construction column, I placed a little unassuming discussion of the latest data on caffeine
and insulin sensitivity. Much to my surprise, the response to this article was
overwhelming! Hate mail filed in, the T-mag forum was blowin' up with arguments for
and against caffeine and coffee, and the article even started rumbles over at several
dietetics newsgroups! There's no doubt about it, people love their coffee and will use
anything in their power to justify their habits (positive or negative).

So, with all of this hubbub, Dr. Lonnie Lowery, Doug Kalman, and myself decided to
have a royal rumble over this stimulating topic.

John Berardi: To start off with I'd like to throw out a bit of information about caffeine so
that everyone is up to speed. Here's a quick crash course.

First of all, caffeine, in our circles, is known as 1,3,7 trimethylxanthine and belongs to a
group known as the methylxanthines. Some other methylxanthines with similar effects
are theobromine (3,7 dimethylxanthine) and theophylline (1,3 dimethylxanthine). While
you can continue to call it caffeine, I want to point out that the tri- and di-
methylxanthines are potent chemicals that operate through several distinct physiological
mechanisms, as you'll see below.
Mechanism number one: caffeine, by virtue of inhibiting an enzyme called
phosphodiesterase, increases cellular concentrations of a compound known as cyclic
AMP. Cyclic AMP is the substrate for phosphodiesterase, so if you inhibit the enzyme,
you get more of the substrate. More cyclic AMP means increased neural excitation
(cAMP is a second messenger for neurotransmitter receptor systems, meaning that when
a neurotransmitter binds its receptor, cAMP increases in the cell. So the more cAMP you
have to start with, the less neurotransmitter needed to initiate a cellular event/change). In
this regard, caffeine increases the sensitivity of neurons to stimuli. Therefore, when
taking caffeine, internal and external stimuli are amplified as is the response to these
stimuli.

Mechanism number two: Caffeine also inhibits chloride channel action. Chloride
channels inhibit neuronal transmission. When caffeine comes in, it disinhibits neuronal
transmission, making the nerves more likely to fire.

Mechanism number three: Caffeine antagonizes adenosine receptors. Adenosine itself

can act by binding to presynaptic terminals to inhibit neurotransmitter release. In
addition, it can bind postsynaptic receptors to prevent neurotransmitters from doing their
job. Since caffeine can block these actions of adenosine, it can promote elevated
neurotransmitter functionality.

Okay, I hope it's clear that caffeine is a pretty potent pharmacological agent with several
mechanisms of action. Just because people drink it every day and nobody's dropping over
dead immediately thereafter, it's certainly not acceptable to take its use lightly. At this
point, I'd like to get right into the debate. Let's talk caffeine, the good, the bad, and the
ugly.

First, the bad and the ugly. In reviewing the correlational or experimental data, do you
guys think that there are any negative effects of habitual caffeine or coffee consumption?
In other words, are there any grounds (pun intended) for avoiding this stuff?

Doug Kalman: Yes and no. Here are the major concerns:

First, we know that approximately ten grams of caffeine in one day can be lethal. That, of
course, is an acute problem! Since caffeine's half-life is pretty short, chronic, sub-lethal
use doesn't seem to present any toxic effects.

Another concern within the nutrition community is that caffeine might cause the leaching
of calcium from bones, thus possibly leading to or contributing towards osteoporosis.
However, the data are mixed. One line of investigation from 1994 showed that the
average female's daily intake of caffeine (300 mg) does correlate with bone loss;
however, subsequent studies demonstrated that just one glass a day of milk (8 ounces)
mitigated this problem.
Also, in pregnant and lactating women there's some data that caffeine may cause
malformations of the fetus, though the studies have only been in rats and at a dose equal
to 70 servings of caffeine daily. An association between caffeine intake and sudden infant
death syndrome (SIDS) has also been found, though it's not well proven. Most doctors
tell their pregnant patients it's okay to have one or two cups of coffee daily.

A few more concerns: In males, habitual caffeine intake may lower sperm motility,
though since Seattle doesn't have any population problems, I doubt this to be a cause of
real concern.

Also, cardiologists still debate if there's a risk for cardiac patients to have a cup of coffee
daily, but they do agree that more than that is unadvised. In terms of the diuretic effects
of caffeine, one recent study found that advising people to disregard caffeinated
beverages as part of their daily fluid intake is not substantiated. So, caffeine might not be
the strong diuretic we once thought.

JB: That was certainly thorough, Doug. I'd agree with your synopsis. I'd like to add in the
fact that recent research by Vlachopoulos and colleagues has demonstrated that 250mg of
caffeine (two 6oz cups) can acutely induce arterial stiffness and short term hypertension.
This work has been duplicated in other studies so it's not just a one-time effect, although
it may be only an acute effect. After all, the data correlating caffeine intake and
hypertension are mixed. Lonnie, anything to add?

Dr. Lonnie Lowery: Well guys, I'm neither pregnant nor lactating to my knowledge, so
I'm not too concerned about side effects. I do know that a study just hit the news
regarding caffeine causing an aberration of melatonin function. This compounds the
adrenergic effects, leading to insomnia. The suggestions were to avoid caffeine in the late
afternoon, but isn't this a no-brainer?

And regarding the benevolence of caffeine's short half-life, I partly disagree; drink
enough java and you can saturate your body's ability to metabolize the caffeine. You'll
end up with chronically elevated blood concentrations. This can be good or bad,
depending upon your point of view. Beyond these issues, attempts to link (food source)
caffeine to diseases (heart disease, cancer, osteoporosis, etc.) have generally failed.

JB: So what I'm hearing is that caffeine use should probably be avoided in cardiac
patients, in pregnant women, perhaps in women who are prone to osteoporosis and
perhaps in men trying to "free the tadpoles." If that's what you're saying, I'm in full
agreement.

However, and you knew it was coming, this roundtable was spawned by my concerns
about the effects of caffeine on insulin sensitivity and glucose disposal. How can you
ignore the potential negative effects of caffeine in this regard? Are you guys trying to rile
up ol' JB or what?

Look, there have been at least eleven human studies conducted using different
methodologies demonstrating that caffeine intake has a negative effect on glucose
disposal and acute insulin sensitivity. Let me give you a quick review of them ('scuze me
while I pull out my notes):

— In Diabetes (2002), Thong et al gave a group of healthy, habitual caffeine drinking 20-
somethings a big whack of caffeine (5mg/kg or about 350mg for a 70kg individual) after
two days of caffeine withdrawal. In this study they wanted to determine the effects of
caffeine on glucose uptake in an exercised leg vs. an unexercised leg. For you science
types, the euglycemic, hyperinsulinemic clamp technique was used and glucose uptake
was measured for 100 minutes. This measurement period occurred three hours after the
exercise and one hour after the caffeine administration. Check out the results:

As you can see, although exercise increased glucose uptake/disposal in both groups,
caffeine still blunts this effect. Talking percents, caffeine reduced glucose uptake by 55%
in the rested and 51% in the exercised leg. In addition, whole body glucose disposal was
30% lower. Muscle glycogen synthase (the enzyme that promotes the storage of carbs)
activity is also reduced.

— In Diabetes Care (2002), Keijzers et al administered caffeine to twelve healthy people

and found that caffeine decreased insulin sensitivity by 15%. The authors of this study
mentioned that the epinephrine increase seen with caffeine administration was probably
responsible for the effect. In addition, the authors hypothesized that, just like with many
of the other effects of caffeine, habitual caffeine use may not ameliorate this
phenomenon.

To corroborate the conjecture that epinephrine release is responsible for the effect of
caffeine on insulin sensitivity, several studies have been done:

— In JAP (1996), Van Soeren et al showed that in humans with impaired epinephrine
release, caffeine doesn't affect glucose disposal or insulin release.
— In JAP (2002), Thong et al showed that when 5mg/kg caffeine was administered and
epinephrine release was promoted, the insulin area under the curve was 42% greater and
whole body insulin sensitivity decreased by 25% when compared with placebo. The
researchers then used a beta-blocker, propanolol, to reduce the effect of epinephrine on
the body. When this was accomplished, the insulin resistance was abolished, completely
indicating that epinephrine caused the insulin resistance. In this study, a simple 75 gram
oral glucose tolerance test was used in conjunction with insulin and glucose measures.

— In The Journal of Clinical Investigation (1980), Deibert et al showed that epinephrine

did in fact reduce tissue sensitivity to insulin by 50%. When epinephrine was high in the
blood, insulin didn't stimulate glucose disposal or prevent hepatic glucose production.

Therefore, it's clear that it isn't necessarily the adenosine antagonism that's causing the
effect but the epinephrine release.

— In Diabetes (2001), Greer et al administered 5mg/kg of caffeine to healthy and lean

but sedentary people and saw a 25% reduction in glucose disposal and a 35% reduction in
carbohydrate storage.

DK (interrupting): Okay, I've heard enough! I think there are several issues here to
consider. First, there are rat studies that indicate caffeine does inhibit glucose uptake. But
this occurs in adipose (fat) tissue but not muscle. If you grant me that the majority of the
readership here is more muscle than they are fat, then I certainly say that caffeine's effects
on metabolically inactive adipose doesn't matter since beta-oxidation (fat burning),
glycolysis (the breakdown of carbohydrate), and other cycles that produce energy take
place in muscle cells (cytoplasm and mitochondria depending upon the cycle).

JB: That's rat research. What about the human stuff? Since skeletal muscle tissue is the
largest glucose disposal site in the whole body it must be contributing to the resistance.
After all, epinephrine, which is released with caffeine use, is well known to reduce
glucose disposal (and cause insulin resistance) in human skeletal muscle tissue!

DK: With the human stuff I have some methodological problems. One methodological
issue I have a problem with is the amount of caffeine given to the subjects. In the
Keijzers study, subjects received a loading dose of 3 mg/kg (~204 mg for a 150 pound
person) over a fifteen minute period followed by another 0.6 mg (~40 mg) per hour for
another two hours (totaling approximately 280 mg in a two hour period).

If you recall, the average caffeine intake via foods (not straight caffeine) is 300 mg per 24
hours. Without going through the whole study, the authors calculated a 15% difference in
insulin sensitivity based upon the glucose infusion rate divided by the plasma insulin only
during the last thirty minutes of the study. Thus, in my opinion, their calculated finding
may not be representative of the truth.
A better way to determine if a typical daily caffeine dose affects insulin and glucose
disposal would have been to do the study in a model of an oral glucose tolerance test,
whereas at the predetermined time points (0, 15, 30, 45, 60, 90, 120, 180, 240 minutes)
you measure the serum glucose and insulin. You do two studies, one with the OGTT
drink alone and the second with the OGTT drink plus caffeine and compare the results in
non-diabetic people. If there were a significant change or difference in the values, it
would have real world implications. As of right now, I wouldn't worry about drinking a
cup of coffee and if it's going to affect insulin levels or body fat stores for that matter.

JB: You want OGTT data? Here you go:

— In The Canadian Journal of Physiological Pharmacology (2001), Graham et al

showed that when 5mg/kg of caffeine was administered to 18 young fit males, the area
under the curve for insulin was 60% greater and the area under the curve for glucose was
24% greater in the caffeine group. These data were collected using, you guessed it, an
OGTT.

— In the European Journal of Clinical Nutrition (1998), Pizziol et al showed that 200mg
of caffeine given to 30 healthy subjects in the 20 to 30-something age range increased
glucose responses to an OGTT for the second, third, and fourth hours of the test.
Interestingly, there was no impact on insulin.

— In the Thong study mentioned earlier (the beta blocker one), they used an OGTT to
demonstrate that 42% greater insulin area under the curve and 25% reduction in whole
body insulin sensitivity with 5mg/kg caffeine.

— In the Canadian Journal of Applied Physiology (1999), Battram et al showed

increased insulin secretion but no increase in glucose area under the curve with caffeine
administration and an OGTT.

— Finally, in a yet to be published study (the work that I mentioned in my column), four
groups of normal, healthy subjects were used to evaluate the effect of caffeine and
glycemic index on insulin sensitivity (using OGTT). The first group got decaf and a low
GI breakfast. They saw a normal blood glucose and insulin response. The second group
got decaf and a high GI breakfast. They saw a bigger insulin and glucose response in the
blood.

However, when the low GI group got regular coffee with breakfast, their blood profile
was worse than that of those who got the high glycemic breakfast and decaf. Therefore
coffee/caffeine can turn a low glycemic meal into a high glycemic meal! Finally, the
group that drank coffee and had the high glycemic meal ended up looking like diabetics.

I'll admit that most of the studies use relatively high doses of caffeine (3-5mg/kg). But
remember, it wouldn't be so hard to accumulate these types of doses with the typical
coffee and cola drinking habits of many North Americans (especially the Canadians I see
every day). One 8 oz cup of coffee can contain up to 175mg of caffeine. With a five hour
half-life, two large morning coffee runs can lead to the types of blood levels of
methylxanthines indicated in the studies.

LL: Uh, I'd like to add a few things here before JB continues his tirade. To be fair, let me
first admit that I dig my morning java. A lot. My pre-workout ritual also includes it. I
think readers should know my personal feelings on this before they read my "smarty
pants" banter. It's worth it for me to brush with whitening toothpaste and deal with the
rare withdrawal headache so I can go ballistic in the gym. You'll get no apologies from
me.

Getting back to the question at hand, there are a few methodological issues I'd like to
address here. Honestly, a quick look at the literature reveals that pretty much everything
affects glucose tolerance one way or another. I'm inclined to say "insulin insensitivity? So
what?" There's a serious difference between statistical and biological significance. I
suggest that athletes don't get too concerned about screwing-up their insulin sensitivity or
glucose tolerance with caffeine.

Regardless of recent findings and "buzz" (pun intended), I've done enough oral glucose
tolerance testing to see how variable individuals are from day to day. It's huge, like 20%,
according to other researchers. And I've yet to see a caffeine-using bodybuilder with
glycosylated hemoglobin over 5.0% (desirable being less than 7.0%; normal is often
about 6.0%).

If the daily "noise" from dozens (hundreds?) of confounding variables is so high ? and
bodybuilders have low glycosylated Hb (i.e. healthy long-term blood sugar levels)
anyway ? I doubt caffeine will greatly contribute to their health or physique problems.

JB: I agree with your comments about the daily variation in glucose measures, but with
the consistent findings I've presented above, something has to be going on here. You
simply can't deny the statistically significant findings that demonstrate increased glucose
and insulin as well as decreased glucose disposal ? all of this in healthy, young subjects.

DK: Again, what about the rat data? I think what's happening is an inhibition of glucose
uptake in fat tissue but not in muscle.

LL: I'm mostly with you on that one, Doug. I'm sure many T-mag readers have heard of
"nutrient partitioning." What if something like adenosine inhibition (from caffeine)
affected tissues differently? Wait, wait? here's a nifty quote:

"Some studies have reported adenosine to increase insulin-mediated glucose metabolism

in adipose tissue and to decrease it in skeletal muscle." Keijzers, 2002
Sounds like blocking that stuff (via caffeine) isn't so bad. But overall, the research looks
pretty mixed regarding "differential sensitivity." And to be totally fair, I think that the
interplay between ingested carbohydrate and hepatic production of blood sugar and
muscle-versus-fat uptake requires techniques far beyond a blood sugar measurement or
OGTT.

JB: First, the effect I'm describing is more of an epinephrine thing than an adenosine
thing. Therefore, let's be clear. Research has established that epinephrine causes insulin
resistance, some of which occurs in the skeletal muscle. Since caffeine releases
epinephrine, there'll be some insulin resistance.

Now, if caffeine also can (and the data are equivocal) block adenosine's effects, it might
actually prevent some muscle glucose intolerance and also prevent some glucose uptake
in the fat cells. Therefore the epinephrine effects of caffeine aren't so good with respect to
insulin sensitivity and glucose disposal. The adenosine antagonism seems to be good. In
the end, the balance of the two still leads to less skeletal muscle glucose disposal and
higher blood glucose and insulin responses to an OGTT.

LL: Well, no one's going to disagree that EPI opposes the effects of insulin in general.
(Unless perhaps they've been denied their morning joe and are disagreeing with
everything!) But there's something else to discuss here. Getting back to Doug's point, I
have yet to see the "caffeine controversy" pursued in bodybuilders. The large muscle
mass they exhibit relative to their fat mass makes them an anomaly compared to everyone
else. Since fat and muscle tissues have different insulin sensitivities, as John points out,
we're left with an utterly different research population.

I think we need some repeated trials and chronic glucose intolerance data in caffeine-
using athletes. Otherwise, how can we conclude that caffeine affects them? We're not
even sure it plays a big role in the glucose intolerance that's present in about 10% of
"average" American men. And that's to say nothing of bodybuilders, per se. We're a
different population with vastly different physiologic characteristics!

DK: In the studies I've been involved with (all published in some peer-reviewed format),
we've never observed any significant changes in blood sugar values (most of these studies
have employed herbal ephedrine, caffeine and/or other thermogenic substances). Thus, in
regard to weight loss agents that include caffeine, I doubt there's a negative impact on the
insulin function.

In the general population, we surely do know that the overweight status and obesity lead
to peripheral insulin resistance which further contribute to the obesity and yet even
further contribute to Type II diabetes, heart disease and hypertension (a.k.a Syndrome X).
Thus, with respect to the overweight population, insulin resistance is something that's
well worthwhile to test for. Not all overweight people are insulin resistant. We know that
insulin resistant people respond very well to a controlled carbohydrate diet (such as 40%
carbohydrate). We also know that diets higher in the healthy fats help increase insulin
sensitivity in these individuals. The father of Syndrome X, Gerald Reaven M.D. of
Stanford University, has proven that time and time again.

In those overweight/obese people who aren't insulin resistant, the carb issue becomes one
more of quality (low glycemic, high fiber) as compared to quantity. In the mildly active
adult, exercise quite often ameliorates the insulin resistance problem. If it's still an issue,
a coupled effect of diet control and exercise is employed. Mainstream medicine isn't yet
aware of "glucose disposal agents" or "insulin sensitizing compounds" on a broad enough
scale where these can be worked into the traditional healthcare model.

JB: Good points, Doug. Before we move on I want everyone to be clear on something. I
am in no way suggesting that caffeine use or coffee drinking will cause "clinical
diabetes" or clinical insulin resistance. What I'm suggesting is that there are dozens of
factors that affect insulin sensitivity (both acute and chronic) including exercise timing
and mode, total caloric intake, macronutrient breakdown of the diet, food selection, drugs
and medications, and time of day.

While some factors may be more powerful than others, I think it's important to recognize
which factors increase insulin sensitivity and which factors decrease it. Once we know
these factors we can strive toward making good lifestyle, exercise, and dietary decisions
in favor of optimizing insulin sensitivity and glucose disposal in the muscle. Since I think
the data are relatively clear on the fact that high dose caffeine decreases insulin
sensitivity in healthy young people, we all need to be aware that coffee could present a
problem for some individuals, especially those prone to diabetes, those without a regular
exercise program, or those with poor dietary habits.

Now, I'll agree with the gist of what you're both driving at, namely that different
populations respond differently to various treatments and manipulations. That's what I
was referring to before. Indeed, the study subjects I listed in my literature assault above
weren't bodybuilders or elite athletes. In fact, some studies included sedentary subjects,
others included recreationally active individuals, and others didn't list the exercise habits
of the subjects. But all subjects were young and healthy. Since all three of us regularly
extrapolate data from "young healthies" and apply it to bodybuilders, I hope you're not
getting self-righteous on me now just to support your love of coffee!

LL: The million-dollar question is whether these data actually matter in bodybuilders
who, by all accounts, are truly unique beasts. John, you probably already know that I've
got to point out that eccentric exercise alone is enough to reduce glucose tolerance in
bodybuilders. My students and I reported on this twice last year (ASEP National
Conference, 2001, Ohio Academy of Science, 2001). But don't just take my word for it;
even Holloszy's group and Sherman, et al. (read "research studs") reported on this back in
the early nineties.
Although the intolerance is transient, the rotating body part schedule of most strength
athletes makes it a chronic situation. Despite this, they are leaner than the average
population and obviously have much greater muscle mass. I guess what I'm saying is that
exercise is such a huge modifier of physiologic function that all the data surrounding
glucose tolerance may be secondary ? at least regarding the body composition of athletes.
But as to the severity of any one factor (i.e. caffeine), who knows?

JB: Okay, now you're making some sense. Listen, since I'm the moderator and I get
ornery if people don't see things my way, if both of you are willing to admit that caffeine
does in fact increase glucose and insulin responses to a meal (as evidenced by the studies
I've listed above) and may reduce insulin sensitivity, I'm willing to change the focus and
discuss whether or not this phenomenon actually matters or if we understand enough
about insulin sensitivity to make any definitive statements about it.

LL: Before we move on ? After being involved in three recent studies related to caffeine
and blood sugar, I feel like I should point out that we saw no significant changes with
either fed, fasting, resting or exercise glucose concentrations. So at least nothing horrific
seems to be happening. Of course, we're not just talking about caffeine in these cases, so
extrapolation is difficult.

And there's something even more relevant. It has to do with the methods that are often
employed. Let's not forget that the destination (first floor: fat cells, muscle cells, and liver
cells) of circulating glucose could change and we'd never see it with simple
measurements like blood glucose or insulin levels. A finger prick or venous blood sample
is akin to sitting on the curb and counting cars drive past you on a freeway. Sure, you can
get "a number" but you'll still know nada about where they're going. This is a bummer
because ultimately the site of glucose deposition is what a bodybuilder is interested in.

JB: Yes, and the studies I mentioned didn't even focus on fasting values. They've looked
at post OGTT (i.e. meal) values. This is a very specific situation but the most applicable
one. After all, people usually have coffee with meals or with snacks. As I've said, I'm
fairly certain that fasted values will remain intact in cases where caffeine is out of the
blood by the morning. However, as I said in my last discussion of this, if the first few
meals of the day jack blood caffeine levels sky high, then the person will be "diabetic" for
some portion of the day while being seemingly "okay" in the morning. Therefore it looks
like timing is a huge issue.

The other big issue is dose. Many of the studies I've brought up used pretty high doses,
more than might be available in a thermogenic supplement or a daily cup of joe. It may
very well be that low dose caffeine intake can offer a nice stimulant effect without the
insulin resistance. That remains to be seen. So, there are certainly dose and timing issues
to consider.
Either way, I agree with both of your comments about how caffeine doesn't chronically
impair insulin sensitivity. But caffeine does increase epinephrine and free fatty acids
acutely, which causes poor glucose tolerance. Do you agree that if half of your daily
meals (the meals after your 16 oz of morning coffee) caused aberrant increases in glucose
and insulin, this would be bad for body composition, especially if those meals are higher
in carbs?

DK: Sir John, since I just finished my morning coffee and I'm feeling like I'll have
Lonnie's back up, I have a question for you. Are you stating that in an exercising or active
individual, acutely increasing free fatty acids (circulating) is bad?

JB: No, Sir Doug. And I'm glad you bring this up since it relates back to my individual
differences and timing comments listed above. Here are some scenarios that we have to
recognize.

With sedentary individuals, especially those with a traditional Western diet high in sugar
and saturated fats, elevated concentrations of circulating epinephrine and free fatty acids,
in my opinion, aren't so good since they'll negatively affect glucose tolerance and drive
insulin and glucose concentrations up after meals. And while the epinephrine may cause
free fatty acids to be lost from adipose tissue, in the absence of exercise, those free fatty
acids will probably just be taken back up and stored again, along with all the glucose
that's being driven into the fat cells. No one loses fat using caffeine supplements alone.

With exercising individuals, elevating circulating epinephrine and free fatty acids before
exercise are exactly what we're looking for since those fatty acids, which were once part
of your love handles, will be escorted into the muscle and burned up. That's why
coffee/caffeine before exercise is probably a good thing. Not only does it jack you up for
the workout but it also helps you burn up some fat.

However, there may be a negative side to pre-workout caffeine intake if it does reduce
glucose disposal. Since exercise powerfully increases insulin sensitivity, the effects of
caffeine may not put a dent in the already huge glucose uptake. However, the data above
do indicate that high dose caffeine can substantially reduce glucose uptake after exercise.
Another few studies are needed before we know what's going on here.

Now, exercising individuals may not suffer from the effects of caffeine induced insulin
resistance like their sedentary counterparts; however, I can't imagine that increased post
prandial (post meal) insulin and glucose concentrations are desirable if one wants to get
leaner or minimize fat gain while trying to gain muscle.

This last comment may be macronutrient specific, though. The effects of caffeine may be
negative when on high carbohydrate diets, causing poor glucose disposal, insulin
resistance, and fat gain. However, caffeine may be quite positive when on low
carbohydrate, high protein and fat diets.
DK: I'd postulate that there's a huge difference between we T-Men and the Al Bundy or
Fat Albert types. We certainly know that caffeine can be an ergogenic aid for very short-
term exercise and endurance events, so no negative there. Now, in the terms that you put
it (post-prandial aberrations), in the studies that we've conducted where we're giving
thermogenics (caffeine containing supplements) that are taken with meals or small
snacks, we haven't found negative changes per se in body fat levels.

In the studies where caffeine was given alone (as within coffee or in capsular form) at
worst the researchers found no change in body weight or body composition, but not a
negative change. So, the population where your theory might apply is in the sedentary or
already overweight individual.

LL: If there's one thing I've learned in umpteen years of geeking-out, it's that the human
body is incredibly adaptable. Guys who are adjusted to a high fat diet (a couple of weeks)
are going to have far fewer problems, I would think, with caffeine/coffee. They already
exhibit elevated catecholamine and fatty acid levels in their blood. It's simply a shift
toward using a different fuel.

Now, high-carb individuals may very well be different. They have chronically higher
insulin concentrations and are generally more dependent on the whole glucose-insulin
thing. There could be real problems in this case, so I guess I'm agreeing with big John in
this regard. But whether the high-carb/caffeine scenario plays a big role in the ridiculous
prevalence of obesity in this country is still speculative. It certainly seems contributory,
though.

And I may have said this, but increased fatty acids and epinephrine are "good" or "bad"
depending upon timing relative to cardio as well. I purposely drink two cups of java 60 to
90 minutes before hitting the treadmill most mornings. It not only helps me drag my sorry
keester out of bed, it serves a purpose metabolically. I want to mobilize and oxidize body
fat. By the time I'm done, 45 minutes later, I've got to believe that my "post-exercise carb
window" is still largely in effect. Then I go for the instant oatmeal. I figure that catachols
and fatty acids are going to be elevated from the cardio anyway, and I can't believe that
my morning treadmill session is inducing significant glucose intolerance.

JB: Okay, so I think we've all agreed that timing and dose of caffeine intake are crucial
factors in this debate. In addition, it's important to note that we all agree that sedentary
individuals and those prone to diabetes are most at risk for caffeine induced insulin
resistance. While we can't say conclusively whether or not caffeine intake will present
body composition problems for exercising individuals, there's no doubt that metabolism
will be altered by caffeine intake in this population.

Okay, we've focused most of this roundtable on the bad and the ugly; what about the
good?
LL: That's right, caffeine nazi, let's not forget the good stuff. Caffeine has been
repeatedly shown to preserve muscle glycogen during exercise, to improve mental focus
independent of and during exercise, to improve exercise performance, to combat fatigue,
to raise metabolic rate, to possess antioxidant properties, and it might even help prevent
Parkinson's disease and certain cancers.

JB: Agreed. While we can get metabolic increases from exercise and antioxidant effects
from scores of other vitamins and nutrients, it's probably a good idea to use caffeine
before exercise or to stay awake if you're the night watchman at Osgood Corporation.
Remember, though, the mental alertness benefits of caffeine often fade with habituation
so use it only when necessary if you desire its feel good/mental sharpness effects.

To be quite honest, in the past I was quite a coffee "pot head" as Lonnie likes to call it,
especially before training. I'd brew up a strong pot of coffee and drink 20 oz of the bitter
blend from my Superman mug. After about thirty minutes I'd head off to the gym and I
can assure you, my workouts were intense. I gave up this practice because I believe it was
causing regular headaches. However, I do miss it. Therefore even the supposed "anti-
caffeine" guy believes that there's a time and a place for coffee use (as long as it doesn't
cause you to feel like you're getting kicked in the teeth after the effects wear off).

DK: Hey guys, don't forget that it tastes good, too! From a medical standpoint, caffeine is
also used in migraine medications and certain headache treatment formulas, so coupled
with the noted benefits, it sounds like a winner to me. Too much of anything can have a
negative effect, but if you understand moderation, caffeine is a good friend.

JB: How about some concluding remarks, guys.

DK: I'd like to point out that if a reader is concerned with "insulin resistance" that he
should go have a fasting blood test done where insulin and glucose is tested. If your
fasting insulin is above 17 micro IU/ml and the glucose is normal (<126 mg/ml), you
have peripheral insulin resistance. If both the insulin and glucose are high, medication
might be indicated as well as a formal test for diabetes. As far as for us, I think that this
whole caffeine issue is really being overblown.

LL: I think "caffeine consequences" depend upon a myriad other lifestyle factors. I know
this conclusion sounds like a copout, but think about it. Exercise is an enormous factor,
so is the amount of muscle mass one carries, so is time of day (glucose tolerance sucks in
the evening anyway), and I'll bet the macronutrient profile of one's diet matters too.
Overall, I'll admit that if caffeine contributes to adiposity or retards muscle growth ? even
to a small degree ? I wouldn't want to abuse it.
Guys with a family history of diabetes or who feel they don't metabolize carbs well
should be especially wary. And John's lit review is enough to make me avoid caffeine
during creatine and carb-loading (when insulin function is important). Keeping an open
mind as data emerges is part of the game and this whole roundtable has left me a bit more
cautious. Thanks Big John, you omniscient (but slightly paranoid) stud, you.

JB: While I'm getting sick and tired of agreeing with Lonnie during these roundtables, I'll
have to do so again. I am indeed an omniscient stud! Besides that, I tend to take the data a
bit more seriously than Doug does. While caffeine may not be the new "silent killer," the
knowledge of its effects has to take its rightful place in the planning of any nutritional
scheme.

While caffeine intake certainly won't make you fat or diabetic, regardless of who you are,
it may increase your glucose and insulin responses to meals and therefore thwart the
effects of some of your low glycemic eating. But remember, dose is important. Small
doses of caffeine may not be harmful. Timing is important, too. Taken immediately
before exercise, caffeine may do some good things. As usual, more data is needed to
clarify all the specifics, but in the meantime we'll keep you on the cutting edge of
nutritional science.

About the Contributors

John M. Berardi is a scientist and PhD candidate in the area of Exercise and Nutritional
Biochemistry at the University of Western Ontario, Canada. His company Science Link:
Translating Research into Results? specializes in providing integrated training,
nutritional, and supplementation programs for high-level strength and endurance athletes.
For more information about our team or our services, please visit JohnBerardi.com.

Lonnie Lowery holds a PhD in exercise physiology, has directed laboratory operations as
an Assistant Professor of Nutrition and has taught nutritional biochemistry and research
design as graduate faculty. Lowery now co-directs ESN Consulting, lecturing in
healthcare and athletic community settings while developing educational software and
providing research consulting. He can be reached at [email protected].

Douglas Kalman works as a Director for Miami Research Associates, a pharmaceutical

and nutraceutical service organization. MRA conducts Phase II through Post Market
Surveillance trials. Their website can be found at MiamiResearch.com. Doug can be
reached at [email protected].

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