Nutrition and Diet for ADHD

Food intolerances affect the body’s stress regulation systems just as much as psychological stress or illness.
There are no specific foods that trigger ADHD. However, if an individual has a food intolerance, it can exacerbate existing ADHD (as well as other mental disorders) because it represents an additional source of stress for the body. Dietary management of an existing food intolerance therefore contributes to an improvement in ADHD symptoms. The average effect size is approximately 0.25. However, this statistical value applies to groups. If a person with ADHD has a food intolerance, avoiding that specific food has a significantly higher effect size for that person.

As early as the 1920s, food intolerances were documented as triggers of mental health disorders.¹ In the 1970s, some viewed ADHD as a consequence of an intolerance or allergy to certain foods or food additives and treated it accordingly.

If ADHD could be significantly influenced by a healthy diet, word would have gotten around long ago. Unfortunately, the effects of a dietary change on ADHD symptoms are considerably smaller than the impact of ADHD on a person’s choice of preferred diet.
A review found that diets are not a promising treatment option for ADHD.³ The effect sizes achievable through diets (alone) in terms of symptom improvement are significantly too small. For some people with ADHD—though this varies from person to person—certain substances can be identified that contribute to an increase in stress or ADHD symptoms, and eliminating these substances may help improve symptoms. As part of a comprehensive treatment plan, this approach is therefore also beneficial.
Unfortunately, it takes a great deal of effort to determine whether a person with ADHD is experiencing symptom improvement. Furthermore, only a small proportion (25 to 50 percent) of people with ADHD benefit, and the degree of improvement falls far short of that achieved with other treatment methods.

Nevertheless, there are individual effects of diet on the stress response systems and, conversely, of stress on the digestive organs. These can play a complementary role in the treatment of ADHD. However, the hope that diet alone can successfully treat existing ADHD is an illusion.

Early or prolonged stress can impair the barrier function of the intestinal mucosa and thereby contribute to chronic intestinal inflammation.⁴
During stress, the sympathetic nervous system (the activating component of the autonomic nervous system that responds early to stress) promotes the production of pro-inflammatory (inflammation-inducing) cytokines (inflammatory proteins or type 1 T-helper cytokines, e.g., tumor necrosis factor alpha, interleukin IL-1, IL-2, and IL-12, and interferon gamma), which, however, are beneficial only in the short term. If they remain active for too long (due to prolonged stress), they attack cells and tissues, which—in addition to cellular degeneration (cancer) and damage to the immune system—can lead to chronic inflammatory bowel diseases. An intestinal wall damaged by inflammatory processes limits the absorption of essential nutrients. To limit the duration of the pro-inflammatory cytokines’ effects, cortisol—released by the HPA axis (which intervenes late in response to stress)—inhibits the pro-inflammatory cytokines and promotes anti-inflammatory (anti-inflammatory) cytokines (T-helper type 2 cytokines, e.g., interleukin IL-4, IL-5, IL-6, and IL-10). TH-2 cytokines fend off extracellular pathogens (bacteria, parasites) and stimulate basophils, mast cells, and eosinophils, which, if overactive, can contribute to allergies.
A disorder in the balance of the HPA axis (hypercortisolism = too much cortisol or hypocortisolism = too little cortisol) can therefore lead to an imbalance in immune responses and promote inflammation or allergies.⁵
If these inflammations or allergies affect the digestive system, food intolerances are a likely consequence.

Furthermore, stress can alter gene expression, including that of genes responsible for producing enzymes in the digestive tract.

Gastrointestinal dysfunction was associated with certain increased ADHD symptoms in elementary school students.⁶

We are convinced that, in cases of known food intolerance, an appropriate diet could make a significant complementary contribution to the treatment of ADHD. However, diets are unsuitable as a general or sole treatment method for ADHD. The effect size of successful diets (in cases of food intolerance) is 0.25, which is so significantly lower than that of medications (up to 1.1) that treatment with diet alone is equivalent to partial non-treatment.
⇒ Effect size of various forms of ADHD treatment

1. ADHD as a Consequence of Diet / Food Intolerance¶

People who have a predisposition to a specific disorder but whose symptoms—in the absence of additional stressors—are not yet at a pathological level are considered healthy.
However, if stress on your body’s stress systems is added to the mix, the symptoms can become so intense that they cross the threshold of what is considered healthy and begin to cause problems.
For others, however, who by nature are further removed from the unhealthy level of distress, this additional stressor does not bother them. This can be described as resilience.

Once an unhealthy state has been reached, it is possible to return to a healthy state by eliminating the most recent stressor—or by eliminating other, long-standing stressors that were present at a time when there were not yet so many stressors converging that an unhealthy level was reached.

This illustration may help clarify the potential effects of various forms of treatment. Resolving a food intolerance or allergy, switching to a healthy diet, or correcting a vitamin deficiency may, in the case of a milder form of a Disorder, be just enough to move the individual out of the unhealthy stress range and bring them just below the “pathological” range. However, whether this is sufficient for the person with ADHD, or whether a more intensive treatment—one that not only brings symptoms just below the “diagnostic” threshold but reduces them more significantly into the healthy range—would be more helpful must be decided on a case-by-case basis.
In any case, severe symptoms can only be treated with medication and additional non-pharmacological therapeutic measures. However, even in these cases, eliminating an existing food intolerance is just as helpful as eliminating other stressors.

It is important to once again explicitly caution against the notion that ADHD severe enough to cause people with ADHD to regularly struggle in school or at work can be treated solely through dietary changes. The considerable effort required of the entire family often leads to a misjudgment (bias: “We’ve done so much; this simply has to help now”).
The effect size of symptom improvement resulting from the elimination of a (genuine) food intolerance is approximately 0.25 and cannot be compared to the effect size of medications (up to 1.1).
ADHD is no trivial matter. Several large-scale studies have found that untreated ADHD is associated with a reduction in life expectancy of 7 years or more. Untreated ADHD increases the risk of addiction many times over. The prevalence of ADHD in men’s prisons is about eight times higher than in the general population. ⇒ Consequences

There are various types of dietary regimens:⁷

• Elimination diets for a single suspected food
• Elimination diets for multiple foods
• Oligoantigenic diets, which limit the diet to a few foods

1.1. Foods / Dietary Supplements That Affect ADHD¶

1.1.1. Dietary Habits and ADHD¶

Children with ADHD made changes to their diet⁸

• a higher proportion of refined grain products
• a lower proportion of dairy products
• less calcium
• less vitamin B2

The composite score for diet/nutrients correlated with ADHD severity.⁸

A large study showed that ADHD is not the consequence of an unhealthy diet, but rather that an unhealthy diet is the consequence of ADHD.⁹ Another study also found that people with ADHD are more likely to choose unhealthy foods.¹⁰
A review found a significant correlation between typical dietary patterns and ADHD, with a “Western diet” showing a stronger correlation with ADHD. A “healthy” dietary pattern rich in vegetables, fruits, legumes, and fish was associated with up to a 37% reduced likelihood of ADHD. A “junk food” pattern featuring sweetened beverages and desserts, as well as the “Western” dietary pattern—featuring red meat, refined grains, processed meat, and hydrogenated fats—were associated with up to a 37% increased likelihood of ADHD-HI.¹¹ The study does not clearly distinguish between correlation and causation. Causality could only be demonstrated through specific dietary patterns and the measurement of their impact on symptoms. However, the study merely measured the typical dietary habits of people with and without ADHD. Since stress shifts dietary preferences toward easily digestible foods, the study may simply be reporting on the consequences of ADHD.
Children with ADHD who followed a Mediterranean diet had 41% fewer ADHD symptoms (1st quartile vs. 4th quartile).¹²

1.1.2. Polyunsaturated fatty acids (PUFAs)¶

Polyunsaturated fatty acids (PUFAs).
Other terms: n-3 fatty acids, n-6 fatty acids, omega-3/omega-6 fatty acids.

PUFAs are:

• Docosahexaenoic acid (DHA)
• Eicosapentaenoic acid (EPA)
• Arachidonic acid (AA)
• Alpha-linolenic acid (ALA)
• Linoleic acid (LA)

N-3 fatty acids are:

• Docosahexaenoic acid (DHA)¹³
• Eicosapentaenoic acid (EPA)¹³
• Alpha-linolenic acid (ALA)¹³
• Eicosapentaenoic acid (EPA)¹³

N-6 fatty acids are:

• Arachidonic acid (AA)¹³
• Linoleic acid (LA)¹³
• Gamma-linolenic acid (GLA)¹³

Several meta-analyses show a modest (albeit statistically significant) effect of PUFA supplementation on improving ADHD symptoms,^{1415 16} as does a recent small placebo-controlled study.¹⁷¹⁸

A study found lower levels of arachidonic acid in children with ADHD.¹⁹

Possible symptoms of a PUFA deficiency include:²⁰¹³

• Polydipsia (excessive thirst)
• Polyuria (excessive urine output)
• dry hair
• Cutaneous and follicular keratosis (fish-scale skin; white or red bumps up to the size of a pinhead, resembling goosebumps, on the upper arms, thighs, buttocks, and face)
• Dandruff

A Japanese study found significantly reduced plasma levels of polyunsaturated fatty acids in 24 people with ADHD under the age of 20²¹

• Docosahexaenoic acid (DHA)
• eicosapentaenoic acid (EPA) and
• Arachidonic acid (AA)

With regard to DHA, a 6-month placebo-controlled study involving 50 schoolchildren with ADHD found no significant improvement in ADHD symptoms.²² Nevertheless, minor improvements in behavioral problems and cognitive difficulties were reported. Other studies have sometimes confirmed an effect of DHA on ADHD, while at other times they found no benefit.²³

A diet rich in fish during pregnancy (especially in the early stages) was associated with fewer attention problems in children. In contrast, the amount of fish in the children’s diets had no effect. Fish contains many PUFAs.²⁴

A randomized study involving 75 children and adolescents—which included a 3-month placebo-controlled phase followed by an additional 3 months during which all participants received omega-3/6 supplementation—found that 26% of the participants experienced a reduction in ADHD-HI symptoms of more than 25%. In the phase that was no longer placebo-controlled, the improvement rate rose to 47% of participants after 6 months. Responders were more frequently of the inattentive subtype and had comorbid neurodevelopmental disorders. Symptom assessment was performed by the authors.²⁵

Another placebo-controlled study found behavioral improvements after 3 months of omega-3 supplementation, while no improvement in cognitive performance (attention) was observed even after 6 months.²⁶

A study of (only 18) children with ADHD suggests that omega-3 may improve heart rate variability.²⁷²⁸

Another study found that children with ADHD consumed significantly fewer foods containing omega-3 fatty acids than the control group.²⁹

A double-blind, placebo-controlled study found no difference in ADHD symptoms between children who received MPH and a placebo and those who received MPH and omega-3.³⁰

A large study of 432 children found a significantly higher omega-6-to-omega-3 ratio in the serum of children with ADHD.³¹ This correlated with a higher intake of nutrient-poor foods—such as those high in sugar and fat—and a lower intake of vegetables, fruits, and protein-rich foods compared to healthy children.
A diet high in sugar and fat has been linked to elevated inflammation markers in the PFC and liver problems, as well as to behavioral changes that are discussed in the context of ADHD.³²
It remains unclear whether dietary changes are the cause, the consequence, or a vicious cycle of ADHD.

Rats whose mothers were fed a diet low in omega-3 (DHA) during pregnancy exhibited excessive HPA axis reactivity and increased symptoms of anxiety and depression as adults.³³

A 12-week, double-blind, placebo-controlled study investigated the relationship between baseline PUFA levels and the effect of high-dose eicosapentaenoic acid (EPA, 1.2 g) in n = 92 adolescents (ages 6–18) with ADHD. Compared to the placebo group, the EPA group showed³⁴

• Improved focused attention: effect size 0.38
  • for all those treated with EPA
• Improved response time to hits: Effect size 0.89
  • only among those treated with EPA who had the lowest baseline EPA levels
• Vigilance (HRT interstimulus interval changes, HRTISIC): Effect size 0.83
  • only among those treated with EPA who had the lowest baseline EPA levels
• a smaller improvement in impulsivity (commission errors) than in the placebo group
  • for all those treated with EPA
• smaller improvements in other ADHD symptoms and emotional symptoms compared to the placebo group
  • only among those treated with EPA who had the highest baseline EPA levels
• a 1.6-fold increase in blood EPA levels
• unchanged:
  • Blood DHA level
  • hs-CRP levels
  • Plasma BDNF levels

According to a study, an 8-week course of DHA supplementation in children with ADHD is said to have resulted in a slight improvement in impulsivity.³⁵

1.1.3. Food Intolerances¶

Individual food intolerances or allergies are stressors just like illnesses, toxins, or psychological stress, and can therefore exacerbate the stress experienced by people with ADHD to the point that symptoms develop. This is not an observation specific to ADHD, but is based on more general mechanisms.³⁶

Food intolerances are not, however, the (sole) cause of schizophrenia, psychosis, or ADHD. That said, based on our understanding, food intolerances can exacerbate any form of mental disorder.
All mental disorders are “merely” the extreme forms of a corresponding predisposition. In other words: Almost all mental disorders are dimensional—that is, determined by the degree of the disorder—rather than categorical, such as pregnant/not pregnant. Mental disorders are generally accompanied by a severe imbalance in the stress regulation systems. Therefore, factors that place additional strain on these stress systems can amplify a predisposition to a mental disorder to such an extent that it reaches a disruptive (pathological) level precisely because of this final additional factor.

1.1.3.1. Elimination Diet – (Somewhat) Effective, but Difficult¶

With an elimination diet (oligoantigenic diet), the diet is initially switched for 3 weeks to low-irritant foods that are highly unlikely to trigger symptoms. Typically, the diet is restricted to rice, vegetables, and meat, with water as the only beverage. If this diet reduces symptoms after several weeks (which strongly suggests a food intolerance or allergy), one (additional) food is reintroduced into the diet every 5 days and is retained if there is no reliable recurrence of symptoms.

Egger⁴⁰ describes such a diet, which can lead to significant behavioral improvements. Egger himself describes this elimination diet (which he calls the “oligoantigenic diet”) as effective for some people with ADHD, but very challenging to implement. Other authors in the same work argue that an (oligoantigenic) elimination diet can barely be implemented in daily life.⁴¹

Several studies have found that diets lead to improvements; however, in controlled trials, they were compared to treatment with medication and psychotherapy

• Significantly fewer people with ADHD show improvement
  and also a
• a significantly smaller reduction in ADHD symptoms was observed.

For an account by a person with ADHD who has experienced the effort involved and the effects of a (presumably oligoantigenic) diet, see below.

The fact that these diets address food intolerances rather than food allergies stems from the fact that the trigger foods identified through the elimination diet did not show elevated levels of IgG and IgE antibodies in blood tests. Conversely, the substances for which IgG and IgE antibody levels were elevated were not always the same ones that exacerbated ADHD symptoms.⁴²⁴³

1.1.3.1.1. Selected Studies on Elimination Diets¶

• A meta-analysis reports an effect size ranging from 0.51 to 0.8 for the elimination diet⁴⁴, while a review reports a positive effect⁴⁵
• One of the earliest and oldest studies reports that, in 21 of 76 hyperactive children, an oligoantigenic elimination diet resulted in the complete resolution of ADHD symptoms, and in another 41, symptoms improved. 14 children (18.5%) did not benefit from it. In 28 of the children who showed improvement, eliminated foods were reintroduced into their diets (in a randomized, double-blind, placebo-controlled trial), which in each case significantly more often exacerbated or restored symptoms compared to the placebo.⁴⁶ Food colorings and preservatives were the most commonly eliminated foods, but they were never the sole triggers. This is consistent with the results of the meta-analysis by Nigg et al., which found an effect size of 0.29 for elimination diets compared to an effect size of 0.12 to 0.25 for dietary supplements.⁴⁷
• A study with a very similar design found improvements in symptoms in 59 of 78 children, though all were below the level achieved with drug treatment. Substances that had already been eliminated from the study again exacerbated symptoms in 19 of 23 participants when administered in a double-blind, masked manner. However, these findings are based solely on parental assessments.⁴⁸
• A small study of 26 people with ADHD showed that 19 children (73%) responded positively to an elimination diet, with all of them reacting to a number of foods, food colorings, and/or preservatives. A double-blind, placebo-controlled trial involving 16 children revealed significant differences between the placebo group and the exposure group. Children with allergic tendencies responded significantly more sensitively than the non-atopic group.⁴⁹
  As we understand it, allergies are typical of the ADHD-I subtype, while inflammation is more typical of ADHD-HI (with hyperactivity).
• Another study reports that an elimination diet has a positive effect on some people with ADHD. On average, 5 foods (which varied from person to person) were identified and eliminated for each person.⁵⁰⁵¹
• A relatively small study found significant improvements based on ratings from parents and teachers following an elimination diet⁵²
• Another small study, which included both assessments and objective tests, found positive results in the subjective assessments; however, these results were not confirmed by the objective tests⁵³
• A double-blind study involving 100 children demonstrated the effectiveness of an elimination diet; however, a subsequent diet based solely on IgG levels (which indicate allergies) resulted in worsening symptoms in 63% of the participants⁴³
• In a crossover, double-blind, placebo-controlled study conducted in Mannheim involving 49 children receiving inpatient treatment, the efficacy of an oligoantigenic elimination diet was compared with that of methylphenidate. While the response rate for methylphenidate (44%) was nearly twice as high as that for the elimination diet (24%), the degree of symptom improvement was nearly the same.⁵⁴
  In this regard, it should be noted that:
  • A response rate of 44% to methylphenidate is very low. A response rate of 70% is typical, although this rate can be increased to 85 to 90% by switching nonresponders to amphetamine-based medications.
  • An elimination diet is likely easier to follow in a hospital setting than in everyday life.
• A small study involving n = 10 children with ADHD found, as assessed by blinded evaluators, that 4 (up to 5) of the 10 children showed an improvement in ADHD symptoms of more than 40% on the ADHD Rating Scale IV⁵⁵
• A non-strict elimination diet was rated positively based solely on parents’ reports⁵⁶
• A small study found that, after 3.5 years, participants on an oligoantigenic diet still showed improvement compared to their ADHD status before starting the diet.⁵⁷
• Insufficient intake of certain vitamins and minerals is a risk associated with elimination diets⁵⁸
• A dietary study showed moderate to significant improvements in 12 of 23 children with hyperactivity⁵⁹
• One study used a food-restricted diet as a tool for the differential diagnosis of ADHD with hyperactivity⁶⁰
• In a follow-up study of 21 participants in an elimination diet study, parents reported after 3.5 years that improvements in ADHD symptoms had persisted over an extended period. 66.7% of the participants continued to show improvement (as indicated in the parent questionnaire), particularly in terms of impulsivity.⁶¹

One problem with evaluating diets for ADHD is that parents tend to significantly overestimate the results in parent questionnaires. Objective tests show much smaller improvements. See below for more on this.

The British National Institute for Health and Care Excellence (NICE) currently considers the risks of elimination diets to outweigh the benefits for children ages 4 to 8.⁶²

1.1.3.1.2. Records of Elimination Diets¶

    1.1.3.1.2.1. Protocol for the Dutch Elimination Diet (Few Food Diet, FFD; RED)¶

In the Netherlands, a specific, rigorous protocol is used for testing an elimination diet in children with ADHD.⁶³

• Verifying whether the family and the child meet the eligibility criteria
• Assessment of family history, family situation, and the child’s medical history; baseline assessment of the child’s behavior
• Two-week baseline period
  • The child continues to eat as usual
  • Discontinuing dietary supplements (e.g., fish oil, vitamins)
  • Continuing to take psychoactive medications
  • Parents keep a journal of their child’s daily activities, eating habits, medications, and behavior
• Repeat behavioral assessments at the end of the baseline period
• Parents receive detailed training on potential pitfalls in adhering to the FFD, based on the information from the food diary. Parents are strongly encouraged to follow the elimination diet as well (by avoiding all foods that are not permitted during the elimination diet) in order to provide the best possible support for their child. Parents receive a schematic overview of which foods are allowed, in what quantities, and on which days.
• 1 week of transitioning to an elimination diet
  • Gradually adapting the child’s diet to the expanded elimination diet
• 2-week extended elimination diet (FFD, RED)
  The following are permitted:
  • All foods in the strict FFD
  • plus small portions of certain foods:
    • Wheat (daily)
    • Lamb (daily)
    • Butter (daily)
    • Corn (twice a week)
    • Potatoes (twice a week)
    • Pear spread (twice a week)
    • Mango (twice a week)
    • Honey (twice a week)
  • if there is a relevant improvement in behavior: continuation of the extended FFD
• if there is no improvement in behavior following extended FFD:
  Gradually restrict the diet to a strict FFD for another 2 weeks
  • Rice
  • Turkey
  • Vegetables
    • Cabbage (white, green, Chinese, red)
    • Beets
    • Cauliflower
    • kale
    • rutabagas
    • Sprouts
    • Salad
  • Pear
  • Olive oil
  • Ghee (similar to clarified butter)
  • Salt
  • Rice drink with added calcium
• (relevant) behavioral improvement is observed (responder)
  • Psychiatric medications are discontinued
• no improvement in behavior is observed (non-responder)
  • further adjustments to the diet
• Repeat the behavioral assessments at the end of the FFD
• For responders, individual foods that had previously been excluded are then reintroduced into the diet.
  • If no behavioral changes occur after several days of consumption, food can be consumed again without concern
  • If there is a deterioration in behavior, the food will be permanently removed from the diet

A study reports that 60% of the 54 participating children showed behavioral improvements of 40% or more; however, only 14 of the 54 children maintained the diet for more than 6 months due to the successful behavioral improvements.⁶³

    1.1.3.1.2.2. Protocol for Egger’s Elimination Diet Study¶

The following procedure is described in Egger’s study on the elimination diet for ADHD⁴⁶:⁶⁴⁶⁵

First phase:
A 4-week, individually tailored elimination diet, typically

• two types of meat from lamb, turkey, chicken, or turkey
• two sources of carbohydrates (usually potatoes and rice)
• two types of fruit from among apples, pears, bananas, apricots, peaches, grapes, and pineapples
• Vegetables
  • Cabbage, Brussels sprouts, cauliflower, asparagus, carrots, celery, parsnips, cucumber, melon, pumpkin, onion, leek, eggplant
• Beverages
  • Fruit juices made from the fruits used, tap water, soda, spring water, mineral water, herbal tea
• Fat
  • dairy-free margarine
  • Sunflower oil
• Calcium 300 mg/day
• Vitamins
  • Multibionta 15 drops
    Theoretically, this administration of multivitamins could have led to an improvement in children with vitamin deficiencies that was not caused by food intolerances. However, this is contradicted by the fact that the dietary results in the third phase were reproduced by reintroducing the suspected foods.
• Avoiding all foods that
  • were suspected of causing behavioral problems or allergic reactions
  • for which the child had a particular preference or aversion
• Interim results: Behavioral improvement in 62 children (82%)

Phase Two:

• Every 5 to 7 days, reintroduce one food at a time that was suspected of triggering reactions

• If a reaction occurs (usually noticeable within hours to 4 days): The food was discontinued

• No reaction: The food was incorporated into the diet

• Chicken: fresh or frozen

• Oats: oatmeal, oatmeal cookies

• Beef: fresh or frozen

• Wheat: Whole wheat, pasta (egg-free)

• Rye: Rye crispbread

• Yeast: Whole-grain bread with no added milk or soy and no preservatives

• Cow’s milk: pasteurized milk, yogurt without additives

• Cheese: hard cheeses without artificial coloring

• Egg: 1 fresh egg per day, prepared however you like, during the trial period; later, a maximum of 3 eggs per week

• Fish: fresh or frozen, not canned, not smoked

• Citrus fruits: fruits or juices (without additives)

• Tomatoes: fresh or pureed (no additives)

• Pork: fresh or frozen

• Sugar: beet sugar

• Chocolate: dairy-free chocolate or cocoa powder if you are lactose intolerant

• Cereal: Wheatabix, Rice Krispies, Corn Flakes

• Tea

• Food coloring: Powdered food coloring (5 to 50 mg/day) or gummy bears (only if sugar is not a problem)

• Benzoate: corned beef, sausages, or as a powder (5 to 50 mg/day)

• Monosodium glutamate: bouillon cubes

Order of priority: based on patient needs ⁶⁵

Phase Three:

• a double-blind, placebo-controlled crossover study on the reintroduction of a suspected food allergen in children who had reacted to various foods
• The placebo and the test foods were prepared in such a way that they were indistinguishable
• Assessment of the children by parents and research team members

    1.1.3.1.2.3. Extended oligoantigenic diet¶

If the first phase of the oligoantigenic diet does not yield results, and it can be ruled out that this is due to non-compliance with the diet, a stricter oligoantigenic diet may be tried to eliminate any intolerance factors present in the initial diet:⁶⁵

• Meat: beef, pork
• Carbohydrates: Corn
• Vegetables: leafy greens, parsnips
• Fruits: pears, avocados, mangoes
• Fat: sunflower oil
• Beverages: Water
• Seasonings: Salt
• Calcium 300 mg/day
• Multivitamins: Multibionta 15 drops

    1.1.3.1.2.4. Substitution of Incompatible Foods¶

The following foods can be used as substitutes for those found to be incompatible:⁶⁵

• Cow’s milk: pasteurized goat’s milk, soy, oat drinks
• Cow’s milk cheese: goat’s milk or sheep’s milk cheese in any form
• Grains: rye, oats, corn, barley, millet
• Chicken eggs: methylcellulose (for baking), duck eggs
• Beet sugar: cane sugar, glucose, fructose, erythritol, sweeteners
• Chocolate: Carob
• Orange juice: black currant or pineapple juice

1.1.3.2. Foods That Are Often Difficult to Digest¶

1.1.3.2.1. Often Intolerable, According to Studies on Elimination Diets for ADHD¶

Studies of elimination diets report that the foods listed below frequently trigger symptoms. The percentages refer to the people with ADHD (out of fewer than 100) who were responsible for symptoms. Due to the small number of participants, the results are highly uncertain.

• Food Additives
  • 79%⁶⁶
  • 70%⁴⁸
• ’s Chocolate
  • 64%⁴⁸
  • 59%⁶⁷
  • See also “Tetrahydroisoquinolines / Tetrahydroisoquinoline (TIQ)” below
• Cow’s Milk
  • 80% (cow’s milk)⁶⁸
  • 80% (other dairy products)⁶⁸
  • 70% (casein)⁶⁸
  • 64%⁶⁷⁴⁸
• Oranges (57%)⁴⁸
• Grains and Seeds (wheat-free)
  • 55%⁶⁸
• Grapes (50%)⁶⁷
• Wheat
  • 50% (wheat)⁶⁸
  • 49%⁶⁷, (45%)⁴⁸
  • 25% (gluten)⁶⁸
• Cow’s milk cheese (45%)⁴⁸, (40%)⁶⁷
• Citrus fruits (45%)⁶⁷
• other fruits (36%)⁴⁸
• eggs
  • 45% (protein)⁶⁸
  • 40% (egg yolks)⁶⁸
  • 39%⁶⁷
  • 18%⁴⁸
• Peanuts (32%)⁶⁷
• Fruit
  • 30% ⁶⁸
• Corn (29%)⁶⁷
• Vegetables
  • 25% ⁶⁸
• Candida albicans
  • 25% ⁶⁸
• Fish
  • 23%⁶⁷
  • 10%⁶⁸
• Oats (23%)⁶⁷
• Melons (21%)⁶⁷
• “ “ tomatoes
  • 22%⁴⁸
  • 20%⁶⁷
• Meat Various types
  • 20%⁶⁸
• Pineapple (19%)⁶⁷
• Sugar (16%)⁶⁷
• Beef (16%)⁶⁷
• Beans (15%)⁶⁷
• Peas (15%)⁶⁷
• Malt (15%)⁶⁷
• Apple (13%)⁶⁷
• Pork (13%)⁶⁷
• Pears (12%)⁶⁷
• Chicken (11%)⁶⁷
• Potatoes (11%)⁶⁷
• Tea (10%)⁶⁷
• Coffee (10%)⁶⁷
• mixed nuts
  • 40%⁶⁸
  • 10%⁶⁷
• Cucumbers (9%)⁶⁷
• Bananas (8%)⁶⁷
• Peach (7%)⁶⁷
• Carrots (7%)⁶⁷
• Lamb (5%)⁶⁷
• Turkey (5%)⁶⁷
• Reis (4%)⁶⁷
• Yeast
  • 25%⁶⁸
  • 4%⁶⁷
• Apricots (3%)⁶⁷
• Onions (3%)⁶⁷

1.1.3.2.2. Sugar¶

    1.1.3.2.2.1. Fructose affects dopamine¶

A diet high in fructose reduced phasic dopamine release in the dorsolateral striatum.⁶⁹⁷⁰
Chronic fructose intake increased

• Dopamine in the hypothalamus and brainstem
• Orexin-A in the hypothalamus and brainstem
• light physical activity

Fructose makes you feel less full than glucose.⁷¹

Fructose intolerance was associated with increased ADHD symptoms, but this association was not statistically significant.⁷² A combined fructose and lactose intolerance was statistically significantly associated with increased ADHD symptoms.

    1.1.3.2.2.2. Sucrose affects dopamine¶

Sucrose is a disaccharide composed of glucose and fructose.
Sucrose has different effects on dopamine depending on the dosage form.⁷³

A single dose of sucrose increases dopamine release in the nucleus accumbens.⁷⁴

Chronic administration of a sucrose solution (7 or 21 days) to male rats

• increased the level of cumulative DA neurotransmission.⁷⁵
• did not alter dopamine⁷⁶

Intermittent glucose feeding (12 hours ad libitum, 12 hours without food) resulted in:

• Increased D1 receptor binding in the core and shell of the nucleus accumbens⁷⁷
• Decreased D2 receptor binding in the dorsal striatum^{77
  77}
• Increased opioid mu-1 receptor binding in the ACC, hippocampus, locus coeruleus, and shell of the nucleus accumbens⁷⁷
• increased dopaminergic neurotransmission in the mesocorticolimbic system⁷⁵
• Altered dopamine levels in the shell of the nucleus accumbens:
  • reduced⁷⁸
  • increased⁷⁶

    1.1.3.2.2.3. Sugar as a Food Intolerance in ADHD¶

Sugar is a potential ADHD trigger in the oligoantigenic diet (1.1.).

A diet that restricted sugar, caffeine, chocolate, food additives, artificial colors, MSG, and—for each child—foods that were potential individual allergens (such as milk), resulted in a significant improvement in behavior in 45% of the participating children, including an improvement in the sleep problems characteristic of ADHD (such as difficulty falling asleep).⁵⁶
In a parallel diary study, correlations were found between food intake and behavior in 15% of the participating children (regardless of their ADHD status).⁷⁹
In our view, these observations correlate with Egger’s findings.

A study examined urinary glucose excretion in children with and without ADHD who were on identical diets. People with ADHD were found to have unusually high levels of:⁸⁰

• Fructose (in 52.5% of people with ADHD)
• Maltose (65%)
• Galactose (75%)
• Lactose (95%).

In addition, all 40 people with ADHD were found to have

• Glycosaminoglycans (mucopolysaccharides) (at 100%) in the pathological range

The authors view this as supporting the hypothesis that ADHD is associated with abnormal carbohydrate metabolism.

A study found a correlation between sugar intake at 30 months and the risk of ADHD, sleep disorders, and anxiety. No correlation was found at 12 months of age.⁸²
It remains unclear whether this is a causal factor or a consequence of changes in food preferences resulting from a predisposition to the disorder.

(Real) sugar is said to reduce the cortisol response to stressors.⁸³ In cases of hypocortisolism (ADHD-HI: with hyperactivity), this could have consequences for sugar’s effect on stress resilience. This is likely to be particularly relevant for people with ADHD-HI and ADHD-C, who often have a reduced cortisol response to stressors (in contrast to people with ADHD-I). ⇒ The subtypes of ADHD: ADHD-HI, ADHD-I, SCT, and others

Experience has shown that a low cortisol stress response is often accompanied by a low alpha-amylase response. Alpha-amylase is an enzyme in the intestine responsible for breaking down carbohydrates into sugars. This could represent a link between stress and eating disorders or obesity and could be considered an indication of impaired glucose metabolism in the presence of a reduced cortisol stress response. Further information is needed to verify this hypothesis.

In a relatively small group of participants (n = 28), glucose administration stimulated an increase in blood adrenaline levels, which were nearly 50% lower in individuals with ADHD than in those without the condition. Plasma norepinephrine levels were also lower in individuals with ADHD than in those without the condition. These data suggest a general impairment in sympathetic activation as well as in the regulation of catecholamines (dopamine, norepinephrine, serotonin) in ADHD.⁸⁴

A diet high in sugar and fat has been linked to elevated inflammation markers in the PFC and liver problems, as well as to behavioral changes that are discussed in the context of ADHD.³²

Children and adolescents with ADHD consume sweets and fruit gummies more frequently and in greater quantities than healthy controls. It is unclear whether this is a cause or a consequence of ADHD.⁸⁵
A study of Thai medical students found that daily consumption of more than 25 g of added sugar from beverages was associated with a 1.8-fold increased risk of ADHD symptoms.⁸⁶ Here, too, it remains unclear whether sugar consumption is a cause or a consequence of ADHD.

A study comparing sugar consumption among 6- to 11-year-olds with their development of possible ADHD shows that sugar is not, in and of itself, a trigger for ADHD. No correlation was found. This supports the view that sugar is not a universal trigger for ADHD, but does not rule out the possibility that sugar intolerance may contribute to ADHD.⁸⁷ Another report reaches the same conclusion, but points out that sugar increases adrenaline synthesis.⁸⁸

    1.1.3.2.2.4. Sugar and the EEG¶

In a case study supported by us, changes in the EEG caused by sugar were observed in a person with ADHD-HI who experienced symptoms exacerbated by sugar:

• Sugar (2 chocolate bars within 5 minutes for a person weighing 90 kg) caused significant changes in the EEG of an ADHD-HI subject (with hyperactivity) during neurofeedback.
  • Beta1 rose significantly within 10 minutes.
    The thresholds for the “Theta Up / Beta Down” training had to be significantly lowered. The 85% of the target values achieved before consuming sugar had dropped to 50%. This means that the ability to relax had decreased dramatically.
  • After 20 minutes, all waveforms (theta, alpha, beta 1, beta 2, hi-beta) had decreased significantly. In relative terms, however, Beta 1 was now significantly above the SMR. Beta 1 should be below the SMR, which is why SMR training—aimed at increasing the SMR—is the first step in neurofeedback treatment for ADHD.
  • After 30 minutes, Beta1 had caught up somewhat with SMR. However, Hi-Beta was now significantly elevated.

One problem with evaluating diets for ADHD is that parents tend to significantly overestimate the results. Objective tests show much smaller improvements. More on this below in section 3.

1.1.3.2.3. Milk protein/milk casein, lactose¶

Lactose intolerance was associated with increased ADHD symptoms, which was statistically significant, particularly when combined with fructose intolerance.⁷²

A large Swedish twin study involving N = 28,058 children aged 9 and 12, respectively, found that children with ADHD had a parent-reported prevalence of lactose intolerance that was approximately 2.5 times higher:⁸⁹

• Total population: 5.9%
• Control group with no indication of a neurodevelopmental disorder (NDD; n = 22,028): approximately 5.3%
• ADHD alone (n = 377): approximately 13.0% (p < 0.001)
• any NDD (n = 1,021): approximately 10.1% (p < 0.001)
• AS alone (n = 91): approximately 7.7% (p < 0.001)
• Learning disability alone (n = 294): approximately 8.4% (not significant)

ADHD thus had the highest prevalence of lactose intolerance among the three NDDs studied. The multiple-diagnosis groups showed no further increase. However, given the small subgroups (n = 49 to 108), these values are not very reliable. Lactose intolerance was assessed solely through a single yes/no question posed to the parents, i.e., without an H₂ breath test or other diagnostic confirmation. ADHD was not clinically diagnosed but was approximated using the high cutoff score of the A-TAC telephone interview (specificity 0.93, sensitivity 0.56).

Proteins and peptides can pass directly from food into the bloodstream through the intestines.
Inhibition of certain peptidases or a genetically determined reduction in peptidase activity (= a protein intolerance that must be distinguished from an allergy) results in increased absorption of peptides from the intestine into the bloodstream. The peptides accumulate and are excreted in increased amounts in the urine (peptiduria). Elevated peptide levels in the urine therefore indicate a genetic, epigenetic, or toxic impairment of key enzymes involved in peptide cleavage. Elevated levels of bioactive peptides in the urine have been found in schizophrenia, depression, autism, and ADHD.⁹⁰

In a study of 104 children with ADHD and 36 unaffected children, not only did people with ADHD clearly differ in terms of peptide levels in their urine, but the types of peptides detected also clearly distinguished between ADHD subtypes:⁹¹

• 64 people with the ADHD-HI subtype (with hyperactivity) showed elevated levels of benzoic acid-glycoprotein-peptide complexes.
• 35 people with ADHD (all but 3 of whom met the criteria for the ADHD-I subtype without hyperactivity) showed reduced levels of uric acid complexes.
• Five people with ADHD (four of whom were hyperactive) showed reduced levels of all urinary complexes.
• Urinary peptides from people with ADHD increased serotonin uptake in blood platelets.⁹²

Unfortunately, there are barely any other studies on peptides in urine in relation to mental disorders—and none that would have refuted this hypothesis.

Proteins in the urine can be a symptom of emotional stress, among other things.⁹⁵ An analysis of the urine of 15 pet dogs and 20 shelter dogs revealed significantly elevated peptide levels in the urine of the shelter dogs.⁹⁶

If a dairy- and casein-free diet were a successful treatment for ADHD, however, this approach would likely have become widely accepted long ago. As studies on elimination diets show, the trigger foods vary greatly from person to person and therefore cannot be identified as a single group.
As part of an oligoantigenic diet, dairy products should also be tested. Dairy products (especially cow’s milk products) were often—but by no means always—eliminated from the diet.

Surprisingly, there is barely any scholarly literature on the influence of lactose intolerance on ADHD.

1.1.3.2.4. Gluten Intolerance and ADHD¶

Gluten may be a contributing factor in ADHD, but it is not “the” cause of ADHD.

Of the 67 children with ADHD who were studied, 10 were found to have gluten intolerance.³⁷ Since only 0.6 to 0.8% of the general population is affected by celiac disease, this would represent approximately 20 times the expected prevalence.
Conversely, the prevalence of ADHD among children with celiac disease was 16 percent—more than twice as high as would be expected in children without celiac disease.¹⁰³

There is evidence that the risk of serious mental disorders increases approximately fourfold in people with celiac disease.¹⁰⁴ A study of a branded gluten- and casein-free diet for ASD reportedly showed a reduction in ASD-associated gastrointestinal symptoms and improvements in antisocial behavior.¹⁰⁵ Both gluten-free and ketogenic diets can affect the gut microbiome.¹⁰⁶

A very small pilot study involving n = 6 children with ADHD who did not have serum markers for celiac disease and who followed a gluten-free diet for 4 months reported a significant reduction in digestive symptoms and headaches in all participants. ADHD symptoms improved in 3 of the children. CPT-II scores did not change significantly.¹⁰⁷

These results are not reliable due to the small number of studies and participants.
However, as part of an elimination diet (see above), wheat is often identified as a trigger food.

1.1.3.2.5. Dyes¶

Feingold’s original study findings—which suggested that a diet free of food dyes and additives could reduce ADHD symptoms such as hyperactivity—were called into question by later studies that employed more rigorous methodologies.¹⁰⁸

Food dyes may have an effect on ADHD symptoms.¹⁰⁹
A meta-analysis shows that eliminating food dyes from the diet has a weak to moderate effect on improving ADHD symptoms, particularly among people with ADHD and food intolerances.¹¹⁰¹¹¹
The authors of a meta-analysis of 24 studies on ADHD and food dyes concluded that approximately 8% of people with ADHD experience symptoms due to dietary supplements. An effect size of 0.12 to 0.25 was found, compared to an effect size of 0.29 for elimination diets.¹¹²¹¹³
Another meta-analysis of randomized, double-blind studies examining whether food dyes can trigger symptoms of hyperactivity found an effect size of 0.21. When smaller, lower-quality studies were also included, this figure rose to 0.283.¹¹⁴
The problem is that almost all studies on food coloring and ADHD rely on parental assessments, which (unless they are double-blind) introduce a significant bias toward overestimating the reduction in symptoms resulting from eliminating food coloring from the diet,¹¹⁵ especially when parents are required to monitor the diet, since following a diet involves effort that quite often leads to the expectation that this effort cannot possibly be in vain.
A meta-analysis of four studies examined blue food dyes and found that elimination diets that excluded FDA-approved blue food dyes had an effect.¹¹⁶

To determine whether the effect sizes reported represent small effects or small-to-moderate effects, one would need to know which method was used to calculate the effect sizes. See Effect size on Wikipedia.

In an elimination diet, food colorings and preservatives were the foods most commonly eliminated, but no child responded to them alone; see above.⁴⁶
A small study found that, in people with ADHD, color stimuli correlated with an increase in posterior mid-gamma power and a decrease in posterior relative alpha power on the EEG. Furthermore, a slight increase in inattention symptoms was observed.¹¹⁷

A meta-analysis discusses the findings on food dyes and autism.¹¹⁸

As of July 20, 2010, foods containing the following color additives must be labeled with the statement “may have an adverse effect on activity and attention in children”:

• E 102 (Tartrazine)
• E 104 (Chilone Yellow)
• E 110 (Yellow-Orange S)
• E 122 (Azorubine)
• E 129 (Allura Red)

Such statements always involve a significant degree of uncertainty.

Food additives (in this case: Sun Yellow, Carmoisine, Tartrazine, Ponceau 4R; Quinoline Yellow, Allura Red, Sodium Benzoate) can cause the release of histamine from circulating basophils. This process is not allergic, i.e., it does not depend on immunoglobulin E. The increased release of histamine can—in individuals who carry certain gene variants of the genes that encode histamine-degrading enzymes—exacerbate ADHD symptoms.¹¹⁹

Erythrosine is said to directly exacerbate ADHD symptoms and cause cognitive impairments, learning disabilities, and memory problems. Erythrosine is said to have an antagonistic effect on neurological development pathways and to cause a specific loss of neurotransmitter activity.¹²⁰

Tartrazine showed statistically significant results in half of all studies. (METASTUDY)¹²¹¹²² Tartrazine exhibited a concentration-dependent toxic effect. It demonstrated cytotoxicity in fibroblasts and human gastric cells, as well as mutagenic effects.¹²³

Food dyes can affect zinc levels, which are a possible factor in ADHD.¹²⁴

1.1.3.2.6. Preservatives¶

    1.1.3.2.6.1. Sodium benzoate (E 211)¶

A double-blind study of 244 children examining artificial food dyes and sodium benzoate (E 211) found a significant correlation with increased hyperactivity.¹²⁵

Another study of 267 healthy children also found that food dyes or sodium benzoate (E 211) (or both) increase hyperactive symptoms in 3- to 4-year-olds as well as in 8- to 9-year-olds.¹²⁶ The European Food and Drug Administration had this finding evaluated by a panel of experts. After making corrections to the statistical-mathematical analysis model used in the study, the 53-page report concluded that the effect, if present at all, was of minor clinical relevance.¹²⁷

Sodium benzoate can cause the release of histamine from circulating basophils. This is not an allergic reaction; that is, it does not depend on immunoglobulin E. The increased release of histamine can—in individuals who carry certain genetic variants of the genes that encode histamine-degrading enzymes—exacerbate ADHD symptoms.¹¹⁹

    1.1.3.2.6.2. Sodium nitrite (sodium nitrit)¶

There are no known direct studies on the adverse effects of sodium nitrite in relation to ADHD.

However, sodium nitrite is believed to have the potential to impair working memory.^128129130131

Sodium nitrite may interfere with the acquisition of an inhibitory avoidance response in rats and mice through a direct effect on the CNS.¹³²

Although sodium nitrite is routinely used to induce memory problems in laboratory animals as part of research into active ingredients that improve memory, there have been no studies examining the role of sodium nitrite in ADHD.

1.1.3.2.7. Flavor enhancers¶

    1.1.3.2.7.1. Monosodium glutamate (L-sodium glutamate)¶

0.4 mg/kg of monosodium glutamate (L-sodium glutamate) appears to trigger ADHD symptoms in rats.¹³³
To date, no such effect has been observed in humans.

1.1.3.2.8. High-fat diet (HFD)¶

Rodents fed a high-fat diet (HFD) for 6 weeks or longer exhibited slower dopamine reuptake¹³⁴¹³⁵ and reduced surface expression of DAT.¹³⁶
This should correlate with elevated extracellular dopamine levels.
In addition, a high-fat diet leads to reduced dopamine release¹³⁷, which is a logical consequence of reduced reuptake.
A high-fat diet (HFD) was associated with ADHD-like behavioral phenotypes and disrupted REM sleep in male mice due to dysregulation of the dopaminergic system:¹³⁸

• reduced alertness
• increased REM sleep with fragmented patterns
• reduced time spent in the central zone of the open-field test (anxiety symptoms)
• Shorter immobility time in the tail-suspension test (= increased motor activity)
• impaired visuospatial memory
• reduced preference for sucrose
• reduced mRNA levels of D1R, COMT, and DAT in the nucleus accumbens, which correlated with an increased proportion of REM sleep and more frequent REM sleep periods

This could explain why people with reduced extracellular dopamine levels—which are typical of ADHD—develop a preference for high-fat foods.

1.1.3.2.9. A Lectin-Free Diet¶

A small prospective study of 58 children with ADHD found benefits of a lectin-free diet.¹³⁹
A lectin-free diet also excludes dairy products and wheat, among other things. In the study, the diet was designed as an elimination diet, so it is unclear to what extent avoiding lectins actually provided benefits or whether the benefits stemmed from avoiding specific food intolerances. Furthermore, the diet could not be conducted as a double-blind study, so there could be significant bias on the part of the parents.

1.1.3.2.10. Mediterranean Diet vs. Western Diet¶

Western dietary habits have a negative effect on¹⁴⁰

• Integrity of the intestinal barrier
• synaptic plasticity
• Insulin resistance
• oxidative stress

A study found that following a Mediterranean diet during early pregnancy was associated with fewer mental health problems in children.¹⁴¹
The Mediterranean diet is said to have led to a slight improvement in impulsivity among children with ADHD.¹⁴²

Correlated with ADHD:

• Low adherence to a Mediterranean diet^{143144 145} was associated with a 7-fold higher incidence of ADHD diagnoses (statistically significant even after adjusting for potential confounding factors)¹⁴⁶
• less frequent consumption of fruits, vegetables, pasta, and rice¹⁴⁶¹⁴⁵
• skipping breakfast more often^146145147
• more frequent consumption of fast food¹⁴⁶
• high consumption of sugar, candy, cola drinks, and non-alcoholic beverages¹⁴⁶
• low consumption of fatty fish¹⁴⁶¹⁴⁵
• lower consumption of legumes¹⁴⁵
• increased consumption of commercially produced baked goods¹⁴⁵

In our view, a preference for rapidly digestible carbohydrates (fast food, sugar) may also be a consequence of the changes in the stress response system caused by ADHD.

A study found clear correlations between higher impulsivity scores on the BIS and:¹⁴⁸

• less sleep on the weekend
• Low adherence to a Mediterranean diet
• Internet and electronic device use >3 hours per day
• Birth weight > 2.5 kg
• delivered by cesarean section
• not breastfed
• Those who participated in sports for more than 3 days a week also scored slightly higher on the BIS

1.1.3.3. Practical and Social Challenges Associated with Diets for ADHD¶

A dietary regimen that requires such strict adherence as is necessary for an oligoantigenic diet—a threshold diet (see the patient report there)—will be feasible only in the rarest of cases during early and middle childhood. It is conceivable that a diet could be adhered to with the necessary consistency—which is, by its very nature, particularly difficult for people with ADHD—only in adolescence at the earliest and only with extreme commitment on the part of the person with ADHD.

An elimination diet is unlikely to be limited solely to eliminating foods that cause intolerance. A consistent diet likely also requires that all unknown foods be avoided (or consistently recorded, whereby trying a new food for 3 days precludes trying any other unknown foods during that time).
Even going out to eat is considerably more difficult, since it’s usually impossible to know for certain which ingredients were used to prepare the food. At best, there are only a few dishes that can be eaten without worry.
Eating at friends’ houses is difficult for the same reasons.
The significant social limitations faced by people with ADHD—which come on top of the fact that they are already “different”—and the stress they experience as a result of these additional limitations must be taken into account when considering diet as a treatment for ADHD.

1.1.3.4. Subjective Overvaluation of Dietary Therapies¶

Diets can—with considerable effort and additional social stress for people with ADHD—improve ADHD symptoms in some individuals.

The problem is that parents’ subjective assessments of their children’s performance are always far more positive than the results of objective tests.¹⁴⁹

Since assessment bias occurs even in double-blind studies, it can be assumed that parents have a significant bias (preconception) to confirm the subjectively desired outcome (that ADHD can be treated with a diet rather than with medications that are viewed skeptically).
It is also possible, however, that the parents were already enthusiastic about the slight improvements brought about by an elimination diet. Due to the study designs, parents were not allowed to know at the time of assessment the far greater benefits that could be achieved with medication and therefore had no basis for comparison. The only criterion for comparison could therefore be whether there was any improvement at all or not.
Furthermore, the enormous effort required to follow a diet for ADHD is likely to foster the expectation that this effort must pay off. It is a general psychological principle that the greater the effort expended, the more positively the results are evaluated.

It is also conceivable that the mere decision to do something for oneself through dieting—perhaps even coupled with the realization that it is beneficial—could foster a sense of self-efficacy. This could have a beneficial effect on the central psychological issue of self-esteem, even if this effect is likely to be rather small in the case of ADHD.

1.2. Foods (and dietary supplements) that may affect ADHD¶

1.2.1. Low-Density Lipoprotein¶

To avoid repetition, we have included this section under “Fatty Acids, Probiotics, and More for ADHD” in the chapter “ : Treatment—Medications for ADHD”, under the section “ : Vitamins, Minerals, and Dietary Supplements for ADHD”.

1.2.2. Saturated Fatty Acids¶

To avoid repetition, we have included this section under “Fatty Acids, Probiotics, and More for ADHD” in the chapter “ Treatment: Medications for ADHD” Under the section “ : Vitamins, Minerals, and Dietary Supplements for ADHD”.

1.2.3. Inorganic phosphorus¶

A large study of 432 children found significantly elevated serum levels of inorganic phosphorus in children with ADHD.³¹ This correlated with increased consumption of nutrient-poor foods, such as those high in sugar and fat, and reduced consumption of vegetables, fruits, and protein-rich foods.
It remains unclear whether dietary changes are a cause, a consequence, or a vicious cycle of ADHD.

1.2.4. Salt¶

High salt intake can impair cognitive function, but this effect is reversible by reducing excessive salt intake.¹⁵²

A craving for salt may be a sign of aldosterone deficiency. This could be associated with pituitary or adrenal insufficiency, which are common in ADHD-HI (with hyperactivity).
Since ADHD-I is characterized by an exaggerated endocrine stress response, an unusually strong sensation of thirst could be associated with elevated aldosterone levels in this condition.
⇒ Aldosterone In the chapter “*” ⇒ Neurological Aspects*

1.2.5. Tetrahydroisoquinolines / Tetrahydroisoquinolines (TIQ)¶

It has been reported that levels of four TIQ metabolites (which represent a different metabolic pathway from dopamine) are significantly elevated in the urine of children with ADHD.
TIQs are synthesized in the brain and are also obtained through the diet.
This raises the question of whether there is a connection to food intake in this context.¹⁵³

Chocolate (cocoa) contains significant amounts of the alkaloids salsolinol (up to 2.5 mg) (1-methyl-6,7-dihydroxy-tetrahydroisoquinoline) and salsolin (1-methyl-6-methoxy-7-hydroxy-tetrahydroisoquinoline).¹⁵⁴ However, salsolin does not appear to cross the blood-brain barrier.¹⁵⁵

Salsolinol

• is produced in the brain from dopamine and acetaldehyde or pyruvic acid
• is an endogenous neurotoxin that causes oxidative stress and mitochondrial damage by inhibiting the electron transport chain¹⁵⁶
• inhibits:¹⁵⁷¹⁵⁴
• Tyrosine hydroxylase
• DA-β-hydroxylase
• COMT
• MAO
• cAMP production
• ACTH
• Endorphins

1.2.6. Ketogenic Diet¶

A ketogenic diet is based on a breakdown of 10% carbohydrates, 20% protein, and 70% healthy fats (no trans fats). As long as you don’t make any dietary mistakes (eating too many carbohydrates), this leads to a shift in the liver’s energy metabolism toward using ketones derived from body fat.

A ketogenic diet is thought to contribute to an increase in GABA and a decrease in glutamate.¹⁵⁸
The ketogenic diet has been tested with good results in patients with epilepsy. For people with diabetes, the ketogenic diet is virtually essential, as it helps stabilize insulin levels.¹⁵⁹

Both gluten-free and ketogenic diets can affect the gut microbiome.^106160161162
A meta-analysis examined the ketogenic diet as a potential treatment for type II bipolar disorder.¹⁶³

A ketogenic diet before and during pregnancy had adverse effects on the offspring of mice.¹⁶⁴

There has been barely any research on the ketogenic diet in relation to ADHD.¹⁶⁴ Potential benefits for ADHD are being discussed.¹⁶⁵
A study in rats found that a ketogenic diet reversibly reduced the animals’ activity levels. Anxiety, however, was not reduced.¹⁶⁶ A study in dogs also found that a ketogenic diet improved certain behaviors associated with ADHD.¹⁶⁷
One study reported a slight improvement in ADHD symptoms in SHR mice (an animal model for ADHD), likely due to effects on the gut-brain axis. However, the improvement was much weaker than that achieved with MPH.¹⁶⁸ People with ADHD and comorbid epilepsy are said to have experienced benefits in terms of hyperactivity, attention, and cognitive abilities, in addition to a reduction in epileptic seizures through a ketogenic diet.¹⁶⁹ Although the author discusses dietary issues in ADHD in depth, he does not mention any benefits for people with ADHD without comorbid epilepsy.
A case study of a person with ADHD reported improvements in hyperactivity and attention following a ketogenic diet.¹⁷⁰ Another report on three case studies anecdotally describes improved attention based on parents’ reports of children with epilepsy.¹⁷¹ A case study reports the complete resolution of all symptoms of previously diagnosed severe PTSD, ADHD, severe binge eating, bipolar II disorder, depression, anxiety, and premenstrual dysphoric disorder in a 38-year-old woman.¹⁷²
We are aware of reports from some people with ADHD on the ADHD-Forum.adxs.org website stating that a ketogenic diet also improved their ADHD symptoms. One person reported no significant improvement in ADHD symptoms despite consistently following a ketogenic diet. We hypothesize that, in the cases described, the ketogenic diet resolved individual food intolerances or allergies.

Furthermore, the reduction in sugar intake associated with a ketogenic diet could be beneficial for people with ADHD.

With regard to ASD, several studies have shown improvements resulting from a ketogenic diet.^{173164174175176177178179170180181}

1.2.7. A diet rich in tyrosine / a diet that promotes tyrosine production¶

A high-protein diet (e.g., a ketogenic diet) increases tyrosine levels in the brain. Tyrosine is a precursor in dopamine synthesis. Although the rate-limiting enzyme in catecholamine synthesis is not tyrosine but tyrosine hydroxylase, an increase in tyrosine levels in the brain stimulates catecholamine production—but only in actively firing neurons.¹⁸²¹⁸³
In theory, a high-protein diet could therefore address a dopamine deficiency and alleviate ADHD symptoms if those symptoms result from problems with dopamine synthesis caused by a tyrosine deficiency. While this is likely to be rare, we believe it is conceivable that this could be one of the many mechanisms underlying ADHD and could therefore help people with ADHD.

Conversely, a diet low in tyrosine and phenylalanine (e.g., casein-free) or the intake of amino acids that compete with tyrosine and phenylalanine for transporters across the blood-brain barrier can exacerbate ADHD symptoms.

One person with ADHD reported that Vyvanse had a more consistent effect and that they experienced fewer mood swings when taking higher doses of high-quality tyrosine from the pharmacy, while inexpensive tyrosine from the dietary supplement market had less of an effect.

For more information, see Tyrosine and ADHD

1.2.8. DASH Diet¶

The DASH diet (Dietary Approaches to Stop Hypertension) includes a high proportion of fruits, vegetables, low-fat dairy products, and vitamin C, as well as a low proportion of simple sugars. A study of children ages 6 to 12 with ADHD reports a positive effect on ADHD symptoms.¹⁸⁴

1.3. Foods (and dietary supplements) with no evidence of an effect on ADHD¶

1.3.1. Intermittent fasting¶

Intermittent fasting is believed to have a potentially beneficial effect on ADHD.¹⁴⁰

1.3.2. Sweeteners¶

• Aspartame

Aspartame is suspected of inhibiting the release of dopamine, norepinephrine, and serotonin, which could lead to negative psychological consequences (particularly in cases of ADHD).¹⁸⁵
Aspartame is also marketed as the “natural” sweetener AminoSweet.

1.3.3. Exorphine (no verifiable evidence)¶

People with ADHD reported success with an exorphin-free diet.
Exorphins are atypical natural opiates found in food. They differ from endorphins in their chemical composition.

Examples of exorphins include:¹⁸⁶

• the casomorphins in cow’s and sheep’s milk
• β-casomorphin in human breast milk
  • It is unclear whether β-casomorphin reaches the infant’s brain
  • β-casomorphin injected into the brains of young rats reduces pain sensitivity in a manner typical of opioids¹⁸⁷
• Opiopeptides in wheat gluten
• Dermorphines (µ-receptor-selective)¹⁸⁸
• Deltorphins (δ-receptor-selective)¹⁸⁹

In both humans and rodents, opiate receptors are most densely concentrated in the¹⁹⁰

• Posterior horn of the spinal cord
• medial thalamus
• Brainstem
• limbic system

In contrast, cannabinoid receptors are found primarily in¹⁹¹

• Basal ganglia
• Hippocampus
• Cerebellum
• Neocortex

Opiates

• reduce sensitivity to pain by inhibiting the firing rate of the neurons responsible for pain perception¹⁹²
• inhibit the release of neurotransmitters¹⁹²
  • Adrenaline
  • Dopamine
  • Acetylcholine
  • Substance P

1.3.4. Trans fats (no verifiable evidence)¶

Trans fatty acids are produced, among other things, during the chemical hydrogenation of fats. They are found primarily in hydrogenated fats (e.g., margarine) and in foods that contain hydrogenated fats (e.g., ice cream, chocolate coatings).

According to Dr. Bod DeMario, trans fats (such as palm oil), which are frequently used in the preparation of fast food because they are inexpensive, cause a DHA deficiency.
The casein found in cow’s milk is also said to reduce DHA levels.
In cases of ADHD, elevated levels of trans fats can be detected in the blood.

This claim has not yet been verified by us. In any case, no accessible studies by DeMaria on trans fats can be found on PubMed. The only study on trans fats and ADHD that can be found on PubMed at all—¹⁹³ —is not even available as an abstract.
An American forum thread also failed to reach any meaningful conclusion regarding this hypothesis.¹⁹⁴

1.4. Foods (and dietary supplements) that have no effect on ADHD¶

1.4.1. Phosphate Intolerance (Refuted)¶

The theory of phosphate intolerance has been disproved.¹⁹⁵

Marcus¹⁹⁶ provided a detailed explanation of this:

• The legally permitted phosphate additives in food account for only 3% of total phosphorus intake. Most phosphate is found in food in its natural form.
• A reduction in phosphate intake from food is compensated for by the body through increased renal tubular reabsorption, so that the phosphate level in the blood is not reduced. Only the afternoon rise in serum phosphate levels is less pronounced; however, the fasting serum phosphate level remains unchanged.
• If phosphate were to trigger ADHD symptoms, an increased intake of phosphate should be able to cause ADHD symptoms. However, tests conducted to investigate this have not confirmed it.¹⁹⁷
• The diet, which was promoted at the time as low in phosphate, actually contained barely any less phosphate than a normal diet.

The effect of the low-phosphate diet may be due to its similarity to the oligoantigenic diet, which is still the subject of debate today.

One person with ADHD shares their story:

Note: Sugar is a potential “allergen” according to the oligoantigenic diet. The description applies to individual cases of sugar intolerance.

The requirements described for following a diet are barely adhered to by children (and especially by people with ADHD).

1.4.2. Salicylates (Feingold; refuted)¶

In the 1970s, the American Feingold proposed that salicylates and food dyes can trigger ADHD.
The theory regarding salicylates is considered outdated. Meta-analyses of controlled studies found no significant effect size.¹⁹⁸¹⁹⁹
Feingold cited several types of fruit and tomatoes in particular as foods containing salicylates.²⁰⁰
The Feingold Diet (also known as the Kaiser Permanente Diet, after the hospital where Feingold worked at the time, or the K-P Diet) consisted of:⁷¹⁹⁹

• the waiver of
  • artificial sweeteners such as aspartame, acesulfame K, saccharin, erythritol, xylitol, and neotame
  • synthetic colors and flavorings in food, medicines, and cosmetics
    • Beverages containing artificial flavors and colors
  • the preservatives
    • Butylhydroxyanisole (BHA)
      • BHA (E 320) is believed to cause severe cellular and neurological damage in the developing fetus and may lead to ADHD. Even at lower concentrations of BHA, zebrafish embryos exhibited developmental toxicity, anxiety, and memory impairments due to a decrease in AChE activity and serotonin levels, as well as altered gene expression.²⁰¹
    • Butylhydroxytoluene (BHT)
  • TBHQ (tertiary butylhydroquinone) (added to the diet later)
  • Sodium benzoate (added to the diet later)
  • Sliced sausage
  • Sausages
  • Salicylates
    • Wintergreen oil
    • Acetylsalicylic acid (ACC)
    • Foods containing natural salicylates
      • Coffee
      • Tea
      • Almonds
      • Cloves
      • Apples
      • Grapes
      • Raisins
      • currants
      • Plums
      • Prunes
      • Oranges
      • Mandarins
      • Apricots
      • Nectarines
      • Cucumbers
      • Pickles
      • Berries
      • Green bell peppers
      • Cherries
      • Peaches
      • Tomatoes
• remained permitted
  • Grapefruit
  • Pear
  • Pineapple
  • Banana
  • Beef
  • Lamb
  • Egg
  • White bread
  • certain types of grain

Many elimination diets list various types of fruit and tomatoes as triggers for symptoms.
It would be interesting to know if there are any studies that have examined the effects of salicylates on healthy people.
For information on dyes, see above.

2. Additional Nutrition-Based Treatment Approaches for ADHD¶

2.1. Desensitization of Food Intolerances¶

Although a food intolerance is not an allergy, a double-blind, placebo-controlled study by Egger—who has conducted extensive research on the elimination diets described here for ADHD—successfully demonstrated desensitization to identified food intolerances. Sixteen out of 20 participants developed a tolerance, compared to 4 out of 20 in the placebo control group.²⁰²

2.2. Probiotic treatment may influence behavior¶

In a study involving rats, probiotic treatment was shown to reduce symptoms of depression. This was accompanied by changes in pro-inflammatory cytokines, which moderate inflammation.²⁰³ Furthermore, the probiotic treatment reduced the transcription of CRH1, CRH2, and mineralocorticoid receptors in the hippocampus, whereas a high-fat diet increased it.

One study found that, of 75 children who received a probiotic (Lactobacillus rhamnosus GG, ATCC 53103) from 0 to 6 months of age, none developed ADHD or ASD by age 13, whereas in the placebo group, 17% received a diagnosis of ADHD or ASD according to ICD-10.²⁰⁴

A meta-analysis found that probiotic treatment had an effect on ADHD in only one of seven studies. That study found that probiotic treatment for mothers during pregnancy and while breastfeeding reduced the risk of ADHD in their children.²⁰⁵

2.3. Increased Intestinal Permeability in ADHD¶

A study of 40 people with ADHD and 41 people without ADHD found elevated zonulin levels in people with ADHD, which also correlated with hyperactivity²⁰⁶, suggesting that there may be a stronger association with ADHD-HI than with ADHD-I.

Zonulin is a 47-kD protein that regulates the tight junctions in the intestinal wall. The intestinal mucosa secretes zonulin in response to certain stimuli. Zonulin binds to specific receptors on the intestinal epithelial cells, which controls the opening of the interepithelial channels through the contraction of cytoskeletal proteins. An analysis of serum zonulin levels is simple and provides a reliable indication of intestinal permeability, as well as pointing to chronic inflammatory bowel diseases, such as:²⁰⁷

• Celiac disease
• Diabetes mellitus
• other autoimmune diseases
• Impaired gut flora, e.g., following antibiotic treatment

3. Basics¶

3.1. A Hearty Breakfast¶

A study found that 47% of students with ADHD and 33% of students without ADHD regularly skipped a balanced breakfast. One hour after eating a balanced breakfast, both groups showed improvements in four cognitive areas.²⁰⁸

3.2. Drink plenty of fluids¶

Even though thirst is not described as a typical ADHD symptom, increased thirst and the resulting increased water intake are commonly observed symptoms of stress.²⁰⁹ Since stress aims to raise blood pressure in order to optimally prepare the body for fight or flight, increased fluid intake is an immediately effective strategy.²¹⁰ Fluid intake significantly reduces the stress response.²¹¹

4. Further Reading¶

Further reading on the topic of nutrition and ADHD can be found at

• ADHD and Diets. Are Dietary Measures a Suitable Treatment Option for ADHD?
• Romanos, Buske-Kirschbaum, Fölster-Holst (2011): Itches and scratches – is there a link between eczema, ADHD, sleep disruption, and food hypersensitivity? Allergy 2011; 66: 1407–1409.