5

The Role of Food Additives

and Chemicals in Behavioral,
Learning, Activity, and Sleep
Problems in Children

JOAN BREAKEY
Consulting Dietitian, Beachmere, Australia
CONOR REILLY
Oxford Brookes University, Oxford, England
HELEN CONNELL
Queensland Health, Spring Hill, Australia

I. FEINGOLD’S HYPOTHESIS AND ITS HISTORY

In 1974 Dr. Ben Feingold, an allergist in the United States, published a book titled Why
Your Child is Hyperactive (1). The same ideas were contained in his scientific publications
(2–4). The symptoms he investigated were hyperactivity, aggression, excitability, impul-
siveness, low frustration tolerance, poor attention, clumsiness, and sleep problems. The
outcome measure was parent reports of the usefulness or otherwise of the diet.
Feingold was not the first to publish a relationship between diet and behavior. In
the 1920s behavioral or ‘‘neuropathic’’ changes due to food ‘‘allergy’’ had been described
(5–7). In 1945 Schneider (8) claimed that allergy was important in causing the ‘‘syndrome
of childhood hyperkinesis’’; Speer (9) included behavior changes in children in an ‘‘aller-
gic tension-fatigue syndrome’’ in 1954; and others also implicated diet in behavior changes
(10,11). An improvement in children with ‘‘minimal brain dysfunction’’ was reported in
1970 after allergens such as milk and chocolate were excluded (12). There were wide-
spread misconceptions about ‘‘food allergy’’ that confused the orthodox position that reac-

87

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 88 Breakey et al.

tions which definitely had an immunological basis were allergy, with a view that all types
of idiosyncratic reactions to foods or chemicals could come under the umbrella of ‘‘al-
lergy’’ (13–15). The latter view was espoused by the less orthodox clinical ecologists
who saw hyperactivity and fatigue as part of the ‘‘stimulatory and withdrawal levels of
allergic manifestations’’ (16).
Historically there were also developments in terminology describing the syndrome
involving hyperactivity (17). By 1968 new classifications, ICD-9 and DSM-111 (18,19),
introduced the term ‘‘hyperkinetic syndrome of childhood.’’ In 1983 attention was empha-
sised as the core deficit in the new name ‘‘attention deficit disorder,’’ with or without
hyperactivity (ADD or ADHD).
The Feingold diet excluded artificial colors, artificial flavors, BHA, BHT, and salicy-
lates (medicinal and natural), including apples, stone fruit, berries, almonds, cloves, tea,
grapes, oranges, tomato, chilli, cucumber, mint, and perfumes. It was derived from the
salicylate-free diet of the Kaiser–Permanente Centre used for urticaria and pruritus (20).
It used earlier work on intolerance to aspirin (21–23), with the data on salicylate in food
from much earlier studies (24). Additive exclusion had been considered since a connection
to allergic symptoms had been published from the 1940s (25–28) and in Feingold’s own
earlier publication (29).

II. EARLY STUDIES INVESTIGATING FEINGOLD’S HYPOTHESIS

Feingold’s ideas became very controversial for several reasons. He said, the ‘‘Pattern
was one of ‘turn-on’ and ‘turn-off ’ ’’ (1, p. 34); and ‘‘These children are normal. Their
environment is abnormal’’ (1, p. 74); and ‘‘The time is now overdue to look at these
chemicals, not only in relation to [hyperactivity-learning disorders] H-LD’s but in regard
to the human species as a whole’’ (1, p. 162). The discussion became polarized, with
Feingold assertively stating the problems and the food industry becoming increasingly
defensive.
Three notable double-blind studies were designed specifically to test Feingold’s hy-
pothesis. The first, led by Conners, concluded that the results ‘‘strongly suggest that the
K-P Diet reduces the perceived hyperactivity of some children’’ but was not supportive
because of the inconsistency in the results (30). The second study also concluded that
Feingold’s assertions had not been supported (31). Here parents of the preschooler group
rated their children as better on the test diet, but more formal tests did not did not show
any difference. Both groups of parents rated their school-age children as better on the test
diet but only when the diet order was the control diet followed by the Feingold Diet. The
third study utilized specially produced chocolate cookies with or without a range of artifi-
cial colors (32). These had been produced by the Nutrition Foundation in the United States
after it had suggested strategies for researching Feingold’s hypothesis in 1975 (33). Two
cookies contained 26 mg dye, the estimated daily intake. Teachers rated children as worse
on the colored cookies while on placebo medication, and parents rated children as worse
on the colored cookies while on active psychostimulant medication.
The most quoted evaluation of Feingold’s hypothesis was by the National Advisory
Committee on Hyperkinesis, chaired by Lipton, reporting to the Nutrition Foundation in
1977 (33). Its assessment was based on the three studies cited. It reported that the Feingold
hypothesis was not supported and concluded ‘‘that there are presently no data to suggest
that initiation of major changes in food manufacture or labelling is urgently needed.’’ (33,
p. 9). This report was widely publicized and it solved the public health issue in relation

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 Food Additives and Chemicals and Children 89

to effects on the whole population. Unfortunately this resolution was assumed to also apply
to clinical use of the diet with individual children, despite the identification of statistically
significant effects in some children in the studies.

III. FURTHER DOUBLE-BLIND AND CLINICAL RESEARCH

The early studies were followed by many others, in both research and clinical populations.
The gradually accumulating information altered the value of the early studies showing
the issue to be much more complex than had been anticipated. During diet implementation,
a withdrawal effect with worsening symptoms in the first week was reported (34), while
initial improvement took two to six weeks (35) and reactions took up to a week to clear
after infractions (36). An effect lasting only three hours was reported after 5 mg tartrazine
was used as a challenge (37), and after 26 mg dye, particularly in the young children (38).
This seems to contradict reports that exposure to challenge over days increased the reaction
(39,40). However, there were also reports that the reaction to different chemicals excluded
were different (39,41), and that where an effect reached significance it was in younger
children, as had been reported in the early studies.
Feingold had reported the reaction as a nonallergic all-or-nothing phenomenon. Is-
sues related to dose were not discussed. Similarly the various dyes were presumed to be
equi-potent. The earlier estimated daily dose was reevaluated, and the dose of 26 mg was
estimated as only 40% of the daily intake of dyes (42). Another researcher (43) reported
estimated intakes of 76 to 318 mg dyes/day (44). In addition it is reported that artificial
flavors are used in 10 times the dose of color in food, and in 15 times the dose in pediatric
syrups (Hulscher, 1991 personal communication). A study in 1980 (45) used 100 mg and
150 mg dye challenge and showed significant impairment with either dose.
In terms of outcome, studies reported partial responses in ADHD symptoms (40,34),
with medication still needed in some patients. Initial studies had focused on ADHD fea-
tures, but changes in other symptoms were now being reported. Physical allergic symp-
toms, ‘‘neurotic’’ symptoms, and bedwetting were reported as decreasing (35,46), and it
was noted that after diet violations in some, the behavior problems were more severe than
prior to the diet. As well, improvements in various symptoms were reported in parents
and siblings also using the diet (34).
In one study where parent assessment of the presence of dyes in cookies reached
significance the authors report that assessment of irritability and restlessness were not the
relevant hyperactive symptoms in school (42). Where parent and teacher assessment dif-
fered, each was belittled by its lack of correlation with the other, yet researchers in other
areas of psychiatry have noted that parents and teachers assess on different criteria even
on the same questionnaire (47).

IV. DEVELOPMENT OF THE DIET

Research, particularly that involving dietitians, also showed the need for changes to the
diet itself. Further food exclusions of all citrus, currants, capsicum, melon, essences, essen-
tial oils, herbs, spices, and chocolate were made (Woodhill’s diets of 1975 and 1976),
partly based on research in dermatology (48–54). A nature-identical mango flavor in un-
preserved uncolored drink was not tolerated (Breakey unpublished data 1977). Limitation
of whole foods commonly implicated in allergic reactions, such as milk, wheat, and choco-
late, were found necessary in some (34,40,55). Note that chocolate had been used to mask

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 90 Breakey et al.

dyes in research challenges. Environmental factors also producing reactions included

smells (petrol fumes, felt pens, fly sprays) (39), molds, aromatic plants (36), stress, and
infections (56). These findings were also reported by the less orthodox clinical ecologists
(57,58). It was becoming apparent that there were several ‘‘aggravating factors,’’ both
food related and environmental affecting susceptible people with individual variation in
chemicals not tolerated.

V. USEFUL DOUBLE-BLIND STUDIES OF THE 1980S

With a background of this information the research during the 1980s was even more clarify-
ing (59). In a double-blind study an initial strict oligoantigenic diet was used. It excluded
additives, most fruits and vegetables, and whole foods often implicated in allergy (60). As
well as tartrazine [150 mg/day] and benzoate, many whole foods were found to provoke
symptoms that included hyperactivity, abdominal pain, headaches, fits, and lethargy.
Another double-blind study used an additive-free diet not excluding salicylates and
a challenge of 50 mg dye. Two of eight subjects were ‘‘more irritable and restless’’ with
more sleep disturbance on the dye (61). The author argues that the inclusion of only those
who meet the strict ADHD criteria may exclude some with behavior problems which
could be helped by diet.
The much needed data on salicylate content in foods (62,63) paved the way for
a strict initial diet emphasising exclusion of salicylates, suspect additives, amines, and
monosodium glutamate (63). Additional exclusions were as follows: salicylates, excluding
pineapple, dates, rockmelon, guava, gherkin, endive, olive, champignon, radish, chicory,
and zucchini; amines, excluding all cocoa and chocolates, matured cheese, all aged foods,
vinegar, offal, yeast spreads, pork, salted fish, and bananas; natural and added monosodium
glutamate; and the preservatives sulphites, benzoates, nisin, nitrates, propionates, sorbates,
and gallates. This diet was used in double-blind research which implicated chemical intol-
erance in asthma, eczema, migraine, mouth ulcers, urticaria, irritable bowel syndrome, as
well as hyperactivity (64,65). These researchers described this as ‘‘food intolerance’’ as
no immunological mechanism was involved. Wheat and milk were investigated at small
dosage but rarely implicated.

VI. REEVALUATION OF THE EARLY STUDIES

The subsequent discoveries have shown the many limitations to the early studies. There
was no definition of the on-diet time before assessment began or washout time between
diet trials. The order effect could be explained by neglect of withdrawal in the first week
of control or test diets. The use of two diets similar enough to satisfy double-blind condi-
tions meant both were lower in additives than the normal diet. As well, the additive dose
difference between test and control diets was not great enough in the absence of accurate
salicylate data. One study was limited by its lack of exclusion of salicylates, which would
interfere with the effect of the added colors.

VII. CLINICAL TRIALS IN THE 1980S

As well as double-blind studies, this author believes it has been important that clinical trials
of dietary treatment of ADHD children occur. From 1984–1989, 516 children attending a
community child psychiatry service trialled a low additive and amine, low salicylate

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 Food Additives and Chemicals and Children 91

(LAALS) diet as part of management of behavior, learning, and hyperactivity prob-

lems. As well as perfumes, smells such as paint were investigated. A positive response
was obtained in 79.5% of children, with a normal range of behavior achieved in 54.5%.
The proportion of responders in the under 9 years old group was significantly higher
(p ⬍ 0.005). As well almost 50% benefited by limiting or excluding other foods such
as milk, wheat, and chocolate. Change occurred in behavioral, social, learning, activity,
sleep, and allergic problems. It was concluded that suspect diet substances and smells are
better thought of as aggravating the underlying predisposition in susceptible children
(66).
A second group of 112 children with ADHD symptoms was followed over 18
months. More data particularly on additive and chemical tolerance were collected, and a
questionnaire designed by Rowe (RBRI) was used to provide more detail on outcome. A
‘‘diet detective’’ approach was used. That is, patients were told that it was not possible
to predict outcome, which presenting problems may change nor the degree of change.
Other studies had not investigated interacting psychosocial issues, so clinical issues that
arose were recorded with progress notes. The sample presented with sleep problems oc-
curring in 74%, developmental problems in 65%, and allergic symptoms, such as asthma
or eczema, in 53%. Parent assessment of the value of the diet was substantiated (Fig. 1)
with 69.7% reporting benefit. The most significant finding provided by analysis of the
questionnaire was that diet was reported to change many problem areas, with the greatest
change being in irritability (see Fig. 2). This was followed by poor concentration, impul-
sivity, unreasonableness, and restlessness, with hyperactivity itself a less significant
change. Two-thirds of all responders under 6 years old improved into the normal range.
Parents consistently reported that children under 5 years had clearer reactions and that
these resolved faster. There was a positive correlation between a history of reports of
reactions to food at the first visit and a positive outcome (p ⬍ 0.005). Thirty-two percent
reported other family members benefiting from the diet.
An important part of this research involved trials of individual challenge foods rein-
troduced for 7 days to test tolerance. Only trials which were uncomplicated by other factors
were recorded (see Fig. 3). While this allowed expansion of included foods, the significant
number who did not tolerate tomato sauce and chocolate is noteworthy. Additional benefit
from limiting dairy foods occurred in 25%, but only 3.6% needed to exclude it. Sugar,
in the absence of suspect chemicals, caused reactions in less than 2%. While tolerance of

Figure 1 Reported outcome of trial of diet.

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 92 Breakey et al.

Figure 2 Diet effects for all responders.

fruit containing salicylate generally followed predictions from data on salicylate content,
this did not always occur. There was variation between varieties with the least acidic
better tolerated. Ripeness was important with salicylates decreasing with ripening (e.g.,
in bland apples), and amines increasing with ripening (e.g., in bananas). As well, smells
(perfumes, petrol, etc.), infections, inhalants (especially pollen), contact dye (face and
finger paints), and stress were identified as equally potent sources of reactions. Their ac-

Figure 3 Individual food trials and reported intolerances.

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 Food Additives and Chemicals and Children 93

knowledgment does not negate the role of dietary factors. Most patients are prepared to
adhere to a well-prepared diet if improvement is of a sufficient degree.
Clinical research shows that problems in child psychiatry are not neat and tidy.
Investigation of diet effect revealed diet interacting with many clinical issues such as
individual variation in presenting problems; family coping skills and motivation; manage-
ment of fussy, often underweight children; as well as psychodynamic factors. From this
study it is suggested that food-sensitive ADHD children are better described as hyper-
reactive than hyperactive; reacting to many aspects of the environment, of which the food
components form one part, depending on susceptibility.

VIII. A NEW VIEW OF THE DIET

The research during the 1980s allowed updating of the diet. Most fruit and vegetables
high in natural amines or glutamates are also high in salicylates (67). Overall, chemicals
implicated were added natural and artificial colors, artificial flavors, and most preserva-
tives; added and natural MSG; and natural and medicinal salicylates and amines. A diet
with these chemical exclusions formed the initial exclusion diet.
In the 1990s a second part to the initial diet became clearer. This is the role of whole
foods. Their limitation or exclusion can be based on a history of a family member having
problems with a whole food or from skin prick tests. Research which does not significantly
restrict all the chemical groups and family sensitivities will not show maximum possible
effect.
After the initial trial and challenge (or off-diet week), and washout period if deterio-
ration occurs, individual foods containing various additives, suspect chemicals, or whole
foods can be reintroduced one at a time to determine which are tolerated. Each individual

Table 1 Some Factors Contributing to Adverse Reactions: The Total Body Load
Food
Natural food chemicals: salicylates, amines,
monosodium glutamate, flavors
Additives: added natural and artificial colors and flavors, benzoates, BHA and BHT, sulphites,
nitrates, propionates
Whole foods: consider if a problem to any family member
Environment
Stress, if significant for the child or in the family
Infections: viral, bacterial, parasitic, and fungal
Inhalants: pollen, house dust mite, dander, grasses
Perfumes and smells: paint, air fresheners, glue, bubble bath
Contacts: dyes in finger paint, preservatives in creams
Excess sensory stimuli: shopping centers, crowds
Biology
Genetic susceptibility to ADD or ADHD
Genetic susceptibility to food sensitivity (allergy or food intolerance)
Age and developmental level
Temperament
Other medical problems
Note: Individual variation in susceptibility to different factors occurs. When the cumulative effect of several
factors (the total body load) exceeds the individual’s threshold, reactions are noted.

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 94 Breakey et al.

can learn doses they tolerate and so expand food intake over time. This improves compli-
ance and ensures better nutrition. With dietetic supervision of dose and form, dairy and
wheat foods can be reintroduced or increased. No screening tests have been found useful
for predicting food intolerance. A schema for diet investigation is included as ‘‘The Diet
Detective Process’’ in Appendix A, a ‘‘Diet for Suspected Food Intolerance’’ comprises
Appendix B, and an overview of factors contributing to adverse reactions (‘‘the total body
load’’) is provided in Table 1.

IX. THE ROLE OF DIET IN ADVERSE SYMPTOMS IS COMPLEX

The suspect diet substances being investigated have broadened, as have the symptoms
affected by diet. Both the dose of suspect substances and the age of child are relevant.
There is individual variation in problem profiles presented, in symptoms that change, in
amount of change, and in substances not tolerated. A review of the research from 1985
to 1995 shows that a role of diet in some ADHD children has been demonstrated (59).
However, there is much work still to be done. Various mechanisms have been proposed,
notably allergy and idiosyncrasy coexisting (60), neuropharmacological abnormality (65),
and many others (68–76). A valuable pharmacological view is provided by Neims (77).
The health of the gut may be important. Tolerance is often decreased as grain fiber is
increased. New work on probiotics in the form of degradation of some protein components
and adsorption of suspect chemicals from intestinal contents should be considered (78).
Note that most foods not tolerated are highly flavored: spices, teas, tangy fruit, to-
mato, chocolate, aged food, foods high in monosodium glutamate, and commercial sweets
and drinks. This author suggests a change in emphasis from artificial colors and preserva-
tives toward flavor to the extent that all strong aromatic natural and additive flavors be
equally emphasised suspect chemicals. Higher tolerance is related to mild, good quality
flavor. High quality foods (e.g., fine wines) and preferred smells (e.g., expensive perfumes)
are better tolerated. At the other end of the spectrum is decreased tolerance as the food
is perceived as smelling stale or musty. Perhaps this is susceptibility to very small doses
of spoilage organisms or their products. Clinically, food-sensitive people are more aware
than others of both smell and taste. They are people whose threshold for adverse reactions
seems lower than the general population, with more noticeable interaction with ‘‘the total
body load’’ of factors in the environment. On a positive note, it is of interest that few
food-sensitive people develop coronary heart disease, diabetes, or obesity.
A second suggestion is to no longer presume that salicylate is the main suspect
natural chemical. Tolerance to salicylate-containing foods varies with individuals and does
not correlate closely with analysis data. Researchers using similar methodology to Swain
report finding little salicylate in their analysis of similar foods (79,80). This does not
mean sensitivity to natural chemicals is not significant. Indeed, most of the later research
implicates natural foods as well as additives. At this time it appears wisest to clarify the
foods that are consistently causing reactions (outlined in Appendix B) and to admit that
it is not known exactly what the suspect chemicals are or why they cause reactions.
In conclusion, the research, particularly from the 1980s and 1990s, has shown diet
has a role. There are three groups of suspect substances: additives, natural chemicals, and
whole foods, with those implicated in the family given special emphasis (81). This discus-
sion has considered suspect natural substances at some length as their role is only gradually
being clarified. Artificial additive color and flavor are still the most often reported suspect
substances. Rather than susceptability being individual, as occurs in allergic reactions, it

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 Food Additives and Chemicals and Children 95

is present in a population subgroup as yet not clearly defined. A positive diet response is
more likely where there is a family history of allergic conditions, migraine, or irritable
bowel syndrome.
Further research should incorporate all of the issues raised here and should be multi-
disciplinary, preferably including psychiatry, pediatrics, allergy, food technology, neurol-
ogy, education, immunology, psychology, dietetics, molecular biology, toxicology, and
pharmacology. The latter inclusions should have a higher profile than in early work.
The picture of what could be called the side effects of foods is complex. Food
sensitivity exists and provides a challenge for all those working in related fields.

APPENDIX A: THE DIET DETECTIVE PROCESS

Use for investigation of suspected food sensitivity.

Stage 1: Screening Diet

The family detective diet. Use ‘‘The diet for suspected food sensitivity’’ plus family sus-
pect whole foods, inhalants, and chemicals. Also exclude foods causing positive skin-
prick tests. Trial diet for 4 weeks. Withdrawal effects may occur in the first 3–10 days.

Stage 2: Challenges
1. If little or no change occurred after diet trial, reintroduce all exclusions in maxi-
mum dose.
2. If noticeable change occurred, reintroduce groups of food chemicals one group
at a time.

All challenges must continue for 7 days or until a reaction is obvious if this is earlier.

Stage 3: Individualizing Diet

The aim is to finally clarify necessary exclusions and to provide foods which may be used
occasionally.

Single Food Challenges

Food challenges can be selected to provide trials of particular suspect additives or food
chemicals. Trial each food for 7 days to allow for a possible cumulative effect.
From these trials the long-term diet can show necessary exclusions, frequency of
occasional inclusions, and freely allowed items.

APPENDIX B: THE DIET FOR SUSPECTED FOOD INTOLERANCE

The diet excludes artificial and natural additive colors, flavors, some preservatives and
antioxidants, added and natural monosodium glutamate, and also natural amines and natu-
ral and medicinal salicylates. Environmental factors to also minimize are strong smells,
skin contact with children’s colored paint, and significant stress. Ensure any infection
present is treated before beginning trial.

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 96 Breakey et al.

You may use: Do not use:

Bread and cereals
All plain breads without preservative, Fruit or fancy loaves, most commercial
all flours, meals, cereals, tapioca, sago, bakery products, pasta with coloring,
rice, commercial breakfast cereals with- spaghetti in tomato sauce, cake mixes,
out coloring or flavoring, homemade custard powder, instant puddings, bread
cakes and biscuits with preservatives

Fruit
Peeled ripe pear, pawpaw, mango* (in- All other fruit, fruit juices, and dried
cluding tinned in syrup and sundried), fruit
just-ripe banana, pomegranate, peeled
nashi fruit (outer part)

Vegetables
Potatoes (peeled), lettuce, celery, cab- All other vegetables, especially tomato
bage, bamboo shoots, swede, green and tomato products, capsicum, peppers,
beans, brussels sprouts, peas, leeks, shal- gherkins, olives, minted peas
lots, chives, choko, mild carrot* and
pumpkin*, parsnip*, broccoli*, beet-
root*, marrow*, spinach*, onion*, sweet
potato*, cauliflower*, turnip*, aspara-
gus*, sweet corn*, garlic⫹

Protein foods
Plain beef, including mince, veal, Sausages, sausage mince, baked beans
lamb, chicken, pork, plain fish, lobster, in tomato sauce, luncheon sausages,
oysters, prawns, eggs, dried peas, corned beef, meat and fish pastes, com-
beans and lentils, most nuts, peanut mercial fish in batter, smoked fish or
butter*, sunflower seeds, bacon⫹, meats, almonds, water chestnuts
ham⫹

Milk products
Whole, trim & skim milk, plain yo- Commercial ice cream; fruit and fla-
ghurt, evaporated and sweetened con- vored yogurt; milk ices; matured, tasty,
densed milks, home-made ice cream, camembert, blue vein, or flavored
fresh cream, cottage, processed and cheeses; flavored milk drinks
fresh mild cheeses, plain whey milk,
plain soy milk

Fats and oils

Butter, cream, copha, oils, lard, dripping Margarines, any fat or oil containing
or ghee without preservative, butter– preservatives, olive oil, almond oil, ses-
oil blends, pale colored milk-free mar- ame and anchovy oils
garine

Drinks
Water; milk; malted milk; soda and All soft drinks, cordials, fruit juice
plain mineral waters; decaffeinated cof- drinks and juices, tea, flavored milks,
fee; diluted drinks from tinned pear, chocolate drinks, cider, wine, beer, li-
pawpaw, or mango; diluted homemade queurs
golden passionfruit# cordial

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 Food Additives and Chemicals and Children 97

You may use: Do not use:

Snacks and sweets
Sugar, golden syrup, pure maple syrup, Twisties, cheezels, flavored french fries
treacle, very bland honey*, malt syrup, or potato chips, jelly, flavored junket
plain junket tablets, plain gelatine (boil), tablets, low joule drinks, jellies, etc., all
glycerine, plain potato chips, yeast colored and flavored lollipops, ices, and
spreads* (scrape only) ice cream

Miscellaneous
Salt, pepper⫹, malt vinegar⫹, parmesan Flavor enhancer MSG, meat and
cheese⫹, garlic and onion salts⫹, home- chicken cubes, tomato and other com-
made mayonnaise mercial sauces, pickles, cider or wine
vinegar

Toothpaste, soap, and cosmetics

Unflavored white toothpaste, plain un- All mint and herbal toothpastes,
perfumed or minimally perfumed sham- room deodorizers, perfumed items,
poo, soaps, deodorant, detergents, bubble bath, paint, glues, varnish,
powders etc.
* Foods allowed during diet trial if only one serving per day (several may be included, one serving
of each).
⫹
Foods allowed if used only to flavor meals.
#
Foods allowed only as dilute flavor in drinks, not whole.
Note: To ensure sufficient vitamin C is present include four servings of fruit or vegetable daily.
Good sources include banana, potato, bean sprouts, broccoli, and mango nectar.

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