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Nutrition and diet for ADHD


Nutrition and diet for ADHD

As early as the 1970s, ADHD was considered by some to be the result of a food or food additive intolerance or allergy and treated accordingly.

The American Feingold1 postulated in 1975 that salicylates and colorants could trigger ADHD (see below). The German pharmacist Hertha Hafer (who incidentally also contributed to the fact that our toothpaste is fluorinated today) further developed the hypothesis into the theory of phosphate intolerance (see below). The theories on salicylates and phosphates have now been refuted. Dyes can be a co-factor that exacerbates existing ADHD, but are not “the” trigger of ADHD.

A large study showed that ADHD is not the result of unhealthy food, but that unhealthy food intake is the result of ADHD.2 Another study also found that ADHD sufferers are more likely to choose unhealthy foods.3
One review found a clear correlation between typical diet and ADHD, with a “Western diet” correlating more with ADHD. A “healthy” dietary pattern with lots of vegetables, fruit, legumes and fish correlated with up to 37% less likelihood of ADHD. A “junk food” pattern with sweetened drinks and desserts and the “Western” dietary pattern with red meat, refined grains, processed meat and hydrogenated fat correlated with an increased likelihood of ADHD-HI by up to 37%.4 The study does not clearly differentiate between correlation and causality. Causality could only be established through predetermined dietary patterns and the measurement of their effect on symptoms. However, only the typical eating habits of ADHD sufferers and non-sufferers were measured. It is known that stress shifts the dietary preference towards quickly digestible food. The study therefore possibly only reports on the consequences of ADHD.
If ADHD could be so significantly influenced by a healthy diet, word would have gotten around long ago. Unfortunately, the effects of a change in diet on ADHD symptoms are considerably smaller than the effect of ADHD on the choice of preferred diet
A review found that diets are not a promising treatment option for ADHD.5 The achievable effect strengths on symptom improvement through diets (alone) are clearly too low. For some ADHD sufferers, certain substances can be defined - depending on the individual - that contribute to an increase in stress/ADHD symptoms and whose elimination can contribute to symptom improvement. This also makes sense as part of an overall treatment.
Unfortunately, the effort required to determine whether a patient benefits from symptom improvements is high. In addition, only a small proportion (25 to 50%) of those affected benefit and the degree of improvement lags far behind that of other treatment methods.

Nevertheless, there are individual influences of food on the stress systems and, conversely, of stress on the digestive organs. These can make a complementary contribution to the treatment of ADHD. However, the hope of successfully treating existing ADHD through diet alone is an illusion.

Early or prolonged stress can impair the barrier function of the intestinal mucosa and thus promote chronic intestinal inflammation.6
During stress, the sympathetic nervous system (activating part of the autonomic nervous system that intervenes early during stress) promotes the production of pro-inflammatory cytokines (inflammatory proteins or T-helper type 1 cytokines, e.g. tumor necrosis factor alpha, interleukin IL-1, IL-2 and IL-12, interferon gamma), which are only beneficial in the short term. If they are active for too long (due to prolonged stress), they attack cells and tissue, which can lead to chronic inflammatory bowel disease in addition to the degeneration of cells (cancer) and damage to the immune system. An intestinal wall damaged by inflammatory processes restricts the absorption of vital substances. In order to limit the effect of the pro-inflammatory cytokines over time, the cortisol released by the HPA axis (intervening late in stress) has an inhibitory effect on the pro-inflammatory cytokines and promotes anti-inflammatory cytokines (T-helper type 2 cytokines, e.g. interleukin IL-4, IL-5, IL-6 and IL-10). TH-2 cytokines ward off extracellular pathogens (bacteria, parasites) and promote basophils, mast cells and eosinophils, which can promote allergies if excessive.
A disturbance in the balance of the HPA axis (hypocortisolism = too little cortisol or hypercortisolism = too much cortisol) can therefore lead to an imbalance between the immune responses and promote inflammation or allergies.7
If these inflammations or allergies affect the digestive system, food intolerances are an obvious consequence. See 1.14. and 1.18. below.

Stress can also change the expression of genes, including those responsible for the provision of enzymes in the digestive tract.

Intestinal failure correlated with certain increased ADHD symptoms in elementary school students.8

We are convinced that in cases of known food intolerance, an appropriate diet could make a relevant additional contribution to the treatment of ADHD. However, diets are unsuitable as a general or sole treatment method for ADHD. At 0.25, the effect size of successful diets (in the presence of a food intolerance) is so considerably lower than that of medication (up to 1.1) that diet treatment alone is equivalent to partial non-treatment.
Effect size of different forms of treatment for ADHD

1. ADHD as a consequence of diet / food intolerance

People who have a predisposition to a disorder, but without additional stresses and without pathological intensity, are healthy.
However, if your stress systems are under strain, the disorder can take on so much energy that it leaves the realm of the healthy and can become disruptive.
Others, however, who are further away from the unhealthy intensity of disturbance due to their disposition, do not mind the additional stressor. This can be described as resilience.

Once an unhealthy range has been reached, it can be left again by eliminating the last stressor that was added - or by eliminating other stressors that have existed for some time, but only at a time when there were not yet so many stressors that an unhealthy level was reached.

This picture may make it easier to understand the impact that different forms of treatment can have. Eliminating a food intolerance or allergy, switching to a healthy diet or eliminating vitamin deficiencies may be just enough to bring a weaker form of a disorder out of the unhealthy stress range and just below the “pathological” range. Whether this is sufficient for the person affected, however, or whether a stronger treatment that not only brings the symptoms just below the “diagnostic” level, but also reduces the symptoms more clearly into the healthy range, is not 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, the elimination of an existing food intolerance is just as helpful as the elimination of other stressors.

Once again, we must expressly warn against the idea that ADHD that is so severe that those affected regularly have difficulties at school or work can be treated with a change in diet alone. The considerable effort that has to be made by the whole family often leads to a false assessment (bias: “we have done so much, it simply has to help now”).
The effect strength of symptom improvement through the elimination of an (actually existing) food intolerance is around 0.25 and cannot be compared with the effect strength of medication (up to 1.1).
ADHD is not a triviality. Several very large studies have found an increase in premature mortality of around 1.5 percentage points with untreated ADHD. Untreated ADHD increases the risk of addiction many times over. The ADHD rate in male prisons is around 8 times higher than in the rest of the population. Consequences

1.1. Foods / dietary supplements with an influence on ADHD

1.1.1. Polyunsaturated fatty acids (PUFAs)

Polyunsaturated fatty acids = polyunsaturated fatty acids (PUFAs)
Other names: 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)9
  • Eicosapentaenoic acid (EPA)9
  • Alpha-linolenic acid (ALA)9
  • Eicosapentaenoic acid (EPA)9

N-6 fatty acids are:

  • Arachidonic acid (AA)9
  • Linoleic acid (LA)9
  • Gamma-linolenic acid (GLA)9

Several meta-analyses show a weak (albeit statistically significant) contribution of PUFA fatty acid supplementation to the improvement of ADHD symptoms,1011 12 as well as a recent small placebo-controlled study.1314

One study found lower levels of arachidonic acid in children with ADHD.15

Possible symptoms of PUFA deficiency are mentioned:169

  • Polydispia (excessive feeling of thirst)
  • Polyuria (excessive urine output)
  • Dry hair
  • Skin and follicular keratosis (chafing skin, up to pin-sized white or red pimples, similar to goose bumps, on the upper arms, thighs, buttocks, face)
  • Scaling

A Japanese study found significantly reduced blood plasma levels of polyunsaturated fatty acids in 24 ADHD sufferers under the age of 2017

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

With regard to DHA, a placebo-controlled study of 50 schoolchildren with ADHD over 6 months found no significant improvement in ADHD symptoms.18 However, small improvements in behavioral problems and cognitive difficulties were reported. Other studies sometimes confirm an effect of DHA on ADHD, sometimes they found no benefit.19

A mother’s diet rich in fish during (especially early) pregnancy correlated with fewer attention problems in the children. In contrast, the proportion of fish in the children’s diet had no influence. Fish contains many PUFAs.20

A randomized study of 75 children and adolescents, which ran for 3 months placebo-controlled and a further 3 months with omega 3/6 administration to all participants, found a reduction in ADHD-HI symptoms of more than 25 % in 26 % of the participants. In the no longer placebo-controlled part, the improvement rate increased to 47% of participants after 6 months. Responders were more often of the inattentive subtype and had comorbid neurodevelopmental disorders. Symptom assessment was performed by the authors.21

Another placebo-controlled study found improvements in behavior after 3 months of omega-3 administration, while no improvement in cognitive performance (attention) was observed even after 6 months.22

A study on (only 18) children with ADHD indicates a possible improvement in heart rate variability with omega-3.2324

Another study found that children with ADHD consumed significantly fewer foods containing omega-3 fatty acids than the comparison group.25

A double-blind placebo study found no difference in ADHD symptoms between children who received MPH and placebo and children who received MPH and omega-3.26

A large study of 432 children found a significantly higher omega-6 to omega-3 ratio in the serum of children with ADHD.27 This correlated with an increased intake of nutrient-poor foods such as foods high in sugar and fat and a lower intake of vegetables, fruit and protein-rich foods than in healthy children
A diet high in sugar and fat is associated with increased inflammation levels in the PFC and liver problems, as well as behavioral changes that are discussed in the context of ADHD.28
It remains to be seen whether the change in diet is the cause, consequence or vicious circle of ADHD.

Rats whose mothers were fed a diet low in omega-3 (DHA) during pregnancy showed increased reactivity of the HPA axis and increased anxiety and depression symptoms as adults.29

A 12-week, double-blind, placebo-controlled study investigated the relationship between baseline PUFAs levels and the effect of high-dose eicosapentaenoic acid (EPA, 1.2 g) in n = 92 adolescents (6-18 years) with ADHD. Compared to the placebo group, the EPA group showed30

  • Improved focused attention: effect size 0.38
    • In all EPA-treated patients
  • Improved hit reaction time: effect size 0.89
    • Only in the EPA-treated patients with the lowest initial EPA values
  • Vigilance (HRT interstimulus interval changes, HRTISIC): Effect size 0.83
    • Only in the EPA-treated patients with the lowest initial EPA values
  • A weaker improvement in impulsivity (commission errors) than the placebo group
    • In all EPA-treated patients
  • Less improvement in other ADHD symptoms and emotional symptoms than the placebo group
    • Only in the EPA-treated patients with the highest initial EPA values
  • Increased blood EPA value by 1.6 times
  • Unchanged:
    • Blood DHA value
    • Hs-CRP level
    • BDNF plasma levels

An 8-week course of DHA in children with ADHD is said to have brought about a slight improvement in impulsivity in one study.31

1.1.2. Food intolerances

Individual food intolerances or allergies are just as much stressors as illnesses, toxins or psychological stress and can therefore worsen the stress situation of those affected to such an extent that symptoms develop. This is not a finding specific to ADHD, but is based on more general mechanisms.32

For example, in a group of children with schizophrenia problems, dietary treatment of an existing gluten intolerance eliminated the symptoms of schizophrenia in the children affected.3334
The same was found in patients with non-affective psychosis.35

However, food intolerances are not the (singular) cause of schizophrenia, psychosis or ADHD. However, we believe that food intolerances can exacerbate any form of mental disorder.
All mental disorders are “only” the extreme forms of a corresponding predisposition. In other words: almost all mental disorders are dimensional, i.e. determined by the degree of the disorder, not categorical, such as pregnant/not pregnant. Mental disorders are generally associated with a serious imbalance in the stress regulation systems. Therefore, influences that place additional strain on the stress systems can reinforce a predisposition to a mental disorder in such a way that it reaches a disruptive (pathological) level precisely because of this last additional influence. Elimination diet - (partially) effective, but difficult

In an oligoantigenic diet, the diet is initially changed to a low-irritant and most likely non-symptomatic diet for 3 weeks. Typically, the diet is restricted to rice, vegetables and meat and water as a beverage. If this diet reduces the symptoms after several weeks (which is highly indicative of a food intolerance or allergy), a (further) food is then reintroduced into the diet every 5 days and then remains if there is no reliable return of symptoms.

Egger36 describes one such diet that can achieve significant improvements in behavior. Egger himself describes this elimination diet (which he calls an oligoantigenic diet) as effective for some sufferers, but very demanding to follow. Other authors in the same work believe that an (oligoantigenic) elimination diet can hardly be implemented in daily life.37

A number of studies have found improvements with diets, but in trials compared to drug and psychotherapeutic treatment

  • Significantly fewer people affected show an improvement
    and also a
  • Significantly weaker decrease in ADHD symptoms.

See below for the report of a person affected by the effort and effect of a (probably oligoantigenic) diet.

The fact that these diets treat food intolerances rather than food allergies is shown by the fact that the interfering substances found by means of the elimination diet did not show up in blood tests as increased IgG and IgE antibodies. Conversely, the substances for which the IgG and IgE antibodies were elevated were not always those that intensified the ADHD symptoms.3839 Individual studies on elimination diets
  • A meta-analysis reports an effect size of 0.51 to 0.8 for the elimination diet40, a review reports a positive effect41
  • One of the first and oldest studies reported that an oligoantigenic elimination diet completely eliminated ADHD symptoms in 21 of 76 hyperactive children and improved symptoms in a further 41. 14 children (18.5 %) did not benefit. In 28 of the children with improvements, eliminated foods were added back to the diet (randomized, double-blind, placebo-controlled), which significantly increased or reversed the symptoms more often than placebo.42
  • Dyes and preservatives were the most frequently eliminated foods, but were never the sole triggers. This is consistent with the results of the meta-analysis by Nigg et al. who found an effect size of 0.29 for elimination diets compared to an effect size of 0.12 to 0.25 for food supplements.43
  • A very similar study found symptom improvements in 59 of 78 children, but all below the level of drug treatment. Substances that had already been eliminated intensified the symptoms again in 19 out of 23 test subjects when administered in a double-blind, concealed manner. However, these were solely parent evaluations.44
  • A smaller study of 26 affected children showed that 19 children (73%) responded positively to an elimination diet, with all responding to a number of foods, dyes and/or preservatives. A double-blind, placebo-controlled trial in 16 children showed significant differences between placebo and exposure. Children with allergic tendencies responded significantly more sensitively than the non-atopic group.45
    As we understand it, allergies are typical in the ADHD-I subtype, while inflammation is more typical in ADHD-HI (with hyperactivity).
  • Another study reports a positive effect of an elimination diet in some ADHD sufferers. On average, 5 (individually different) foods per child were found to have been eliminated.4647
  • A fairly small study found good improvements in parent and teacher ratings as a result of an elimination diet.48
  • Another small study, which included objective tests as well as assessments, found good results in the subjective assessment, but these were not confirmed in objective tests.49
  • A double-blind study with 100 children showed good efficacy of an elimination diet, whereby a subsequent diet that selected solely according to IgG values (which mark allergies) showed symptom worsening in 63% of the participants.39
  • In a crossover/double-blind/placebo-controlled study in Mannheim, the effectiveness of an oligoantigenic elimination diet was compared with that of medication with methylphenidate in 49 hospitalized children. While the response rates for methylphenidate were almost twice as high (44%) as for the elimination diet (24%), the symptom improvements were almost the same.50
    It should be noted here:
    • A responder rate of 44% to methylphenidate is very low. The usual rate is 70 %, although this can be increased to 85 to 90 % by switching non-responders to amphetamine medication.
    • An elimination diet may be easier to follow in an inpatient hospital environment than in everyday life.
  • A non-strict elimination diet was evaluated positively in parent-only reports.51
  • A small study found that subjects on an oligoantigenic diet still showed improvement after 3.5 years compared to their ADHD status before the diet52
  • Deficiencies in certain vitamins and minerals are a risk of elimination diets.53

The problem with the evaluation of diets for ADHD is that the results are subjectively overestimated by parents in parent questionnaires. Objective tests show significantly weaker improvements. See below for more information.

The British National Institute for Health and Care Excellence (NICE) currently sees more disadvantages than advantages of elimination diets for 4 to 8-year-olds.54 Protocol of the Dutch elimination diet (Few food diet, FFD; RED)

In the Netherlands, a specific strict protocol is used for testing an elimination diet in children with ADHD.55

  • Check whether the family and child meet the participation criteria

  • Assessment of family history, family situation, medical background of the child, baseline assessment of the child’s behavior

  • Two-week baseline period

    • Child retains its usual diet
    • Discontinuation of dietary supplements (e.g. fish oil, vitamins)
    • Retention of psychoactive medication
    • Parents keep a diary of the child’s daily activities, eating habits, medication and behavior
  • Renewed behavioral measurements 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 diary. Parents are also urged to adhere to the elimination diet (omit all foods that are not permitted during the elimination diet) in order to provide optimal support for the child. Parents are given a schematic overview of which foods are allowed, in what quantities and on which days.

  • 1 week transition to elimination diet

    • Gradual adaptation of the child’s diet to the extended elimination diet
  • 2 weeks extended elimination diet (FFD, RED)
    Allowed are:

    • All foods of the strict FFD
    • Additional 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 relevant improvement in behavior: continuation of extended FFD
  • If no improvement in behavior through extended FFD
    gradual restriction of the diet to strict FFD for a further 2 weeks

    • Rice
    • Turkey
    • Vegetables
      • Cabbage (white, green, Chinese, red)
      • Turnips
      • Cauliflower
      • Kale
      • Swedes
      • Sprouts
      • Salad
    • Pear
    • Olive oil
    • Ghee (similar to clarified butter)
    • Salt
    • Rice drink with added calcium
  • (Relevant) improvement in behavior is observed (responder)

    • Psychotropic drugs are discontinued
  • No improvement in behavior is observed (non-responder)

    • Further adaptation of the diet
  • Repetition of behavioral measurements at the end of the FFD

  • In the case of responders, individual foods that had previously been excluded are then reintegrated into the diet.

    • If there is no deterioration in behavior after several days of consumption, food can be consumed again without hesitation
    • If behavior deteriorates, food is permanently banned from the diet

One study reported that 60% of the 54 participating children showed behavioral improvements of 40% or more, but only 14 of 54 children maintained the diet for more than 6 months due to successful behavioral improvement.55 Frequently incompatible foods Often intolerable according to studies on elimination diets for ADHD

Studies of elimination diets report that the following foods frequently trigger symptoms. The percentages refer to those (out of less than 100) people affected in whom the food was responsible for symptoms. Due to the small number of test subjects, the results are highly uncertain.

  • Food additives (79 %)56, (70 %)44
  • Chocolate (64 %)44, (59 %)57
    • See also below Tetrahydroisoquinoline / Tetrahydroisoquinoline (TIQ)
  • Cow’s milk (64 %)5844
  • Oranges (57 %)44
  • Grapes (50 %)58
  • Wheat (49 %)58, (45 %)44
  • Cow’s milk cheese (45 %)44, (40 %)57
  • Citrus fruits (45 %)57
  • other fruit (36 %)44
  • Eggs (39 %)57 to (18 %)44
  • Peanuts (32 %)57
  • Maize (29 %)57
  • Fish (23 %)57
  • Oats (23 %)57
  • Melons (21 %)57
  • Tomatoes (22 %)44, (20 %)57
  • Pineapple (19 %)57
  • Sugar (16 %)57
  • Beef (16 %)57
  • Beans (15 %)57
  • Peas (15 %)57
  • Malt (15 %)57
  • Apple (13 %)57
  • Pork (13 %)57
  • Pears (12 %)57
  • Chicken (11 %)57
  • Potatoes (11 %)57
  • Tea (10 %)57
  • Coffee (10 %)57
  • mixed nuts (10 %)57
  • Cucumbers (9 %)57
  • Bananas (8 %)57
  • Peach (7 %)57
  • Carrots (7 %)57
  • Lamb (5 %)57
  • Turkey (5 %)57
  • Rice (4 %)57
  • Yeast (4 %)57
  • Apricots (3 %)57
  • Onions (3 %)57 Sugar Fructose influences dopamine

A diet high in fructose reduced the phasic release of dopamine in the dorsolateral striatum.5960
Chronic fructose intake increased

  • Dopamine in the hypothalamus and brain stem
  • Orexin-A in the hypothalamus and brain stem
  • the movement activity slightly

Fructose leads to a lower feeling of satiety than glucose.61 Sucrose influences dopamine

Sucrose is a disaccharide made from glucose and fructose.
Sucrose has different effects on dopamine depending on the form in which it is presented.62

Singular sucrose administration increases the release of dopamine in the nucleus accumbens.63

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

  • increased the level of cumulative DA neurotransmission.64
  • did not change the dopamine65

Intermittent glucose feeding (12 hours ad libitum, 12 hours nothing) was effective:

  • Increase in D1 receptor binding in the nucleus and shell of the nucleus accumbens66
  • Decrease in D2 receptor binding in the dorsal striatum66
  • Increase in opioid mu-1 receptor binding in ACC, hippocampus, locus coeruleus and nucleus accumbens shell66
  • increased dopaminergic neurotransmission in the mesocorticolimbic system64
  • altered dopamine levels in the nucleus accumbens shell:
    • reduces67
    • increased65 Sugar as a food intolerance in ADHD

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

A diet that limited sugar and excluded caffeine, chocolate, food additives, artificial coloring, glutamate and foods that could potentially trigger allergies (such as milk) in the individual children resulted in a significant improvement in behavior in 45% of the participating children, including an improvement in the sleep problems phenotypical of ADHD (including a delay in falling asleep).51
In a parallel diary study, 15% of the participating children (regardless of their ADHD status) were found to have correlations between their food consumption and their behavior.68
In our view, these observations correlate with Egger’s findings.

One study tested sugar excretion in the urine of children with and without ADHD on an identical diet. The ADHD sufferers were found to have unusually high levels of:69

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

In addition, all 40 of those affected

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

The authors consider this to support the thesis that ADHD is associated with a deviant carbohydrate metabolism.

Attenuated COMT activity also reduces glucose tolerance in mice.
COMT produces the oestrogen 2-methoxyestradiol (2-ME), which is relevant for glucose tolerance. Reduced COMT activity therefore leads to reduced glucose tolerance via reduced 2-ME production.70
COMT is responsible for the degradation of dopamine. In our opinion, impaired degradation of tonic dopamine could worsen the signal-to-noise ratio of phasic dopamine.
Find out more at -&gt Dopamine degradation

One study found a correlation between sugar intake at 30 months and the risk of ADHD, sleep disorders and anxiety. No correlation was found at the age of 12 months.71
Whether this is a causal cause or a consequence of altered food preferences due to the predisposition to the disorder remains to be seen.

(Real) sugar is said to lower the cortisol response to stress triggers.72 This could result in a negative effect of sugar on stress resistance in hypocortisolism (ADHD-HI: with hyperactivity). This is likely to be particularly relevant in ADHD-HI and ADHD-C sufferers, who often have a reduced cortisol response to stressors (in contrast to ADHD-I sufferers). 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 that is responsible for breaking down carbohydrates into sugar. This could represent a link between stress and eating problems or obesity and could be seen as an indication of poorer sugar conversion with a reduced cortisol stress response. Further information is required to verify this idea.

Glucose administration stimulated an increase in adrenaline blood levels in a relatively small group of subjects (n = 28), which was almost 50 % lower in ADHD than in non-affected subjects. Plasma norepinephrine levels were also lower in those with ADHD than in those without. These data suggest a general impairment of sympathetic activation and the regulation of catecholamines (dopamine, noradrenaline, serotonin) in ADHD.73

A diet high in sugar and fat is associated with increased inflammation levels in the PFC and liver problems, as well as behavioral changes that are discussed in the context of ADHD.28

Children and adolescents with ADHD consume sweets and fruit gums more frequently and more than healthy controls. It is unclear whether this is a cause or a consequence of ADHD.74
A study of Thai medical students found that daily consumption of more than 25 g of added sugar from drinks per day was associated with a 1.8-fold risk of ADHD symptoms.75 Here, too, it is unclear whether sugar consumption is the cause or consequence of ADHD.

A study comparing the sugar consumption of 6 to 11-year-olds with their development of possible ADHD shows that sugar is not a trigger for ADHD per se. There was no correlation. This supports the view that sugar is not a universal trigger of ADHD, but does not rule out the possibility that sugar intolerance can promote ADHD.76 Another report comes to the same conclusion, but points out that sugar increases adrenaline synthesis.77 Sugar and EEG

In an individual case study that we accompanied, the changes in the EEG caused by sugar were observed in a sufferer in whom sugar caused ADHD-HI symptom intensifications:

  • Sugar (2 chocolate bars within 5 minutes at 90 kg body weight) caused significant changes in the EEG of an ADHD-HI subject (with hyperactivity) in neurofeedback.
    • Within 10 minutes, Beta1 increases considerably.
      The threshold values for theta up / beta down training had to be reduced considerably. The 85 % of the target values achieved before the sugar intake had dropped to 50 %. This means that the ability to relax had decreased drastically.
    • After 20 minutes, all values (theta, alpha, beta1, beta 2, hi-beta) were significantly reduced. Relatively speaking, however, beta 1 was now clearly above SMR. Beta1 should be below SMR, which is why SMR training, which aims to increase SMR, is the first step in neurofeedback treatment for ADHD.
    • After 30 minutes, Beta1 had caught up slightly with SMR. However, Hi-Beta was now significantly higher.

This is a single test with a single test subject. The subject was aware of the expected reaction. The exacerbation of his ADHD-HI symptoms after sugar consumption had been mirrored by several people and was consistent with his own observations. From a scientific point of view, the test result is no more than an interesting indication of possible correlations and has no probative value for transferability to other affected persons.

Another ADHD-HI sufferer told us that after consuming sugar (chocolate), he reproducibly noticed a significant increase in his ADHD-HI symptoms, in particular procrastination.

In our understanding, the observations fit the description of the effect of an oligoantigenic diet for people who are sensitive to sugar.

The problem with the evaluation of diets for ADHD is that parents subjectively overestimate the results considerably. Objective tests show significantly weaker improvements. More on this below under 3. Milk protein/milk casein, lactose

Proteins and peptides can enter the bloodstream directly from food via the intestine.

Inhibition of certain peptidases or genetically reduced peptidase activity (= protein intolerance, which must be distinguished from an allergy) causes 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 peptide cleavage enzymes. Elevated levels of bioactive peptides in urine have been found in schizophrenia, depression, autism and ADHD.78

In the study of 104 children with ADHD and 36 unaffected children, it was not only the ADHD sufferers who were clearly differentiated by peptide levels in their urine. The type of peptides found also clearly differentiated the ADHD subtype:79

  • 64 patients with the ADHD-HI subtype (with hyperactivity) showed elevated benzoic acid-glycoprotein peptide complexes.
  • 35 affected persons (who - with the exception of 3 - corresponded to the ADHD-I subtype without hyperactivity) showed reduced levels of uric acid complexes.
  • 5 patients (4 of them hyperactive) showed reduced amounts of all urinary complexes.
  • Urinary peptides from hyperactive patients increased the uptake of serotonin in blood platelets.80

Unfortunately, there are hardly any other studies on peptides in urine in mental disorders - and none that have refuted this thesis.

Another study found identical serotonin concentrations in platelets in ADHD-affected and unaffected children, and no relation to attention problems or hyperactivity, but a positive correlation to impulsive behavior.81

No significantly elevated peptide levels were found in the urine for reading/spelling difficulties (which are highly comorbid in ADHD)82

Proteins in the urine can be a symptom of emotional stress, among other things.83 An examination of the urine of 15 pet dogs and 20 shelter dogs revealed significantly increased peptide levels in the urine of the shelter dogs.84

However, if a dairy- and casein-free diet were a successful solution for ADHD, this treatment would have long since become established. As the studies on elimination diets show, the triggering foods vary greatly from individual to individual and therefore cannot be identified as a group across the board.
Dairy products should be tested as part of an oligoantigenic diet. Dairy products (especially cow’s milk products) were often, but by no means always, eliminated.

Doubtful: peptidase intake with meals

If protein intolerance is present, it is conceivable that the enzymes required to break down the proteins could be ingested artificially.

The principle is now common for lactose (milk sugar) intolerance. Lactase (which breaks down lactose) is added to dairy products during production or those affected take lactase tablets with their meals.

The following description of a study on the (alleged) effect of enzymes in autism, which at first seems impressively helpful, should definitely be read to the end of the italics.

In a study of 29 autism sufferers (17 others ended their participation prematurely for various reasons), a commercially available enzyme mixture85 from (according to the manufacturer)

  • Bromelain 230 BTU
  • Acid Fast Protease 100 SAPU
  • Lactase 330 LacU
  • Phytase 125 U
  • Galactose (as Genomeceutical) 100 mg

which was taken before each meal, showed moderate to significant symptom improvements in 13 categories in 50 to 90 % of the 29 autism sufferers who completed the test.86

In addition to the small number of test subjects, it is problematic that it is unclear whether the manufacturer of the enzyme mixture supported the study (addendum: even worse, see below) and whether the study was registered in advance, i.e. whether it would have been published even if the result had been negative. Unfortunately, it is not uncommon in the pharmaceutical industry for a large number of studies to be started, of which only those that are favorable to the manufacturer are published, while the less favorable results end up in the trash.
We do not know whether this is the case here.
Further - registered - studies by other scientists with larger numbers of test subjects and non-proprietary enzyme mixtures would provide clarity here.

  • Caso-Glutenase is not a specific enzyme, but a proprietary enzyme complex that is designed to help digest or break down casein and gluten and to be DPP-IV active.
  • Bromelain (bromelin) is said by the supplier to proteolytically break down casein.
  • Fast Acid Protease (AFP) cannot be found in the scientific literature. There is only a patent for Brodnak.87 According to the manufacturer, AFP starts breaking down proteins in the stomach, while the other enzymes (peptidases), which are (heat and) acid-sensitive per se, only become active in the small intestine. This presentation is dubious.
  • Lactase breaks down milk sugar (lactose). The quantity should be sufficient for approx. 200 ml of milk.
  • Phytase breaks down phytic acid, which is present in plants such as wheat, corn, rye, barley, beans, soybeans, etc. Phytic acid can impair the absorption of minerals such as calcium, zinc, copper, manganese, iron and magnesium by forming mineral complexes with them, which are excreted. Phytase is thus said to increase the availability of minerals and phosphate.
  • According to the manufacturer, D-galactose, a monosaccharide, is supposed to help maintain a healthy level of DPP-IV in cells “as a genomeceutical”. In our view, this is not plausible. DPP-IV inhibitors are more relevant to health anyway. We were unable to find any reports on the therapeutic purposes of administering galactose (in the stated amount of 0.1 grams). 100 grams of natural yoghurt already contains 1 gram of galactose, i.e. ten times as much.
    Publications on “genomeceuticals” are only available from Brudnak. He writes: “A genomeceutical is something that actually works on the various nucleic acids (DNA, RNA, rRNA, etc) in such a way as to change how the chromosomes in the body are working.”.88
    Genomeceutical is a registered trademark.
  • Similar enzyme complexes are also offered by other suppliers (Kirkman).89 The patent held by Brudnak was previously held by Kirkman.90
    The results are highly dubious.
  • Several enzymes described are not found in any scientific study
  • Some of the mechanisms of action described are (to put it kindly) highly dubious from a scientific point of view
  • Mark Brudnak also has a patent on an enzyme for the treatment of autism
  • Mark Brudnak publishes on the effect of enzymes for the treatment of autism
    These circumstances do not inspire any confidence.
    The model is much more reminiscent of marketing models in which media presence is generated through pseudo-scientific publications in order to promote sales of the company’s own products.
    If you now take a look at who cites the “scientific” publication mentioned at the beginning with the 29 autism sufferers (again Brudnak, without pointing out the intertwining of interests), you can understand the weight of these doubts about the scientific substance of this study.

After our in-depth research raised our doubts about the study (which Reichelt cites without comment), we have nevertheless decided to leave it here in order to explain the possible mechanisms of such dubious studies.

The intake of such enzyme complexes should always be discussed with your family doctor beforehand. has no connection whatsoever with any of the providers. The presentation is solely for the purpose of scientific discussion.

Surprisingly, there is hardly any specialist literature on the influence of lactose intolerance on ADHD. Gluten intolerance in ADHD

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

Of 67 children with ADHD examined, 10 were found to be gluten intolerant.33 Since only 0.6 to 0.8% of the entire population is affected by coeliac disease, this would be 20 times more common
Conversely, children with coeliac disease had an ADHD prevalence of 16%, which is more than twice as high as would be expected without coeliac disease.91

There is evidence that the risk of serious mental disorders increases around fourfold with coeliac disease.92 A gluten- and casein-free diet is reported to have shown reduced ASD-associated gastrointestinal symptoms and improvements in antisocial behavior in a study of a branded product in ASD.93 Both gluten-free and ketogenic diets can influence the gut microbiome.94

These results are not reliable due to the small number of studies and test subjects.
As part of an elimination diet (see above), however, wheat is often identified as a triggering food. Colorants

Feingold’s original study results, according to which a diet without colorants and food additives could reduce ADHD symptoms such as hyperactivity, were put into perspective by later, more methodologically complex studies.95

A meta-analysis shows a weak to moderate significant contribution of the exclusion of colorings from the diet to the improvement of ADHD symptoms, especially in patients with a food intolerance.1096
The authors of a meta-analysis of 24 studies on ADHD and dyes in food came to the conclusion that around 8% of ADHD sufferers have 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.9798
A further meta-analysis of randomized, double-blind studies (and thus largely free of evaluation bias) on the question of whether dyes can trigger hyperactivity symptoms found an effect size of 0.21. When small, less high-quality studies were also included, this rose to 0.283.99
It is problematic that almost all studies on dyes in ADHD are based on parent ratings, which (if not double-blind) includes a considerable bias towards an exaggeration of symptom reduction by eliminating dyes from the diet,100 especially if the parents have to monitor the diet, since a diet causes effort, which regularly leads to the expectation that this effort cannot remain without result.
A meta-analysis of 4 studies examined blue dyes and found influences of elimination diets that avoided FDA-approved blue dyes.101

In order to be able to assess whether the determined effect sizes mean small or small to medium effects, it would be necessary to know which effect size calculation method was used. See also Effect size at Wikipedia.

In an elimination diet, dyes or preservatives were the most commonly eliminated foods, but no child responded to these alone, see above.42
A small study found that in AD(HS sufferers, dyes in the EEG correlated with an increase in posterior mean gamma power and a decrease in posterior relative alpha power. A slight increase in inattention symptoms was also found.102

A meta-study discusses the results of dyes in autism.103

See also the two studies under preservatives / sodium benzoate (E 211).

Since July 20, 2010, foods containing the following colorants must be labeled with the statement “may impair activity and attention in children”:

  • E 102 (tartrazine)
  • E 104 (Chilon yellow)
  • E 110 (Yellow orange S)
  • E 122 (azorubine)
  • E 129 (Allura red)

Such information always contains a large margin of caution.

Food additives (here: Sun yellow, carmoisine, tartrazine, ponceau 4R; quinoline yellow, allura red, sodium benzoate) can cause histamine release from circulating basophils. This is not allergic, i.e. not dependent on immunoglobulin E. The increased release of histamine can increase ADHD symptoms in carriers of certain gene variants of the genes that encode histamine-degrading enzymes104 Preservatives Sodium benzoate (E 211)

A double-blind study of 244 children on artificial colors and sodium benzoate (E 211) found a significant correlation with increased hyperactivity.105

A further study of 267 healthy children also found that colorants or sodium benzoate (E 211) (or both) increase hyperactive symptoms in 3-4 year olds as well as in 8-9 year olds.106 The European Food and Drug Administration had this finding evaluated by an expert committee. After corrections to the statistical mathematical evaluation model of the investigated study, the 53-page investigation came to the conclusion that the effect, if present at all, was of little clinical relevance.107

Sodium benzoate can cause histamine release from circulating basophils. This is not allergic, i.e. not dependent on immunoglobulin E. The increased release of histamine can - in carriers of certain gene variants of the genes that code for histamine-degrading enzymes - increase ADHD symptoms104 Sodium nitrite (sodium nitrit)

No direct studies on negative effects of sodium nitrite in relation to ADHD are known.

However, sodium nitrite is said to have the potential to impair working memory.108109110111

Sodium nitrite could impair the acquisition of an inhibitory avoidance response in rats and mice through a direct effect on the CNS.112

Although sodium nitrite is systematically used to induce memory problems in laboratory animals in order to investigate compounds to improve memory performance, there is no research on sodium nitrite in ADHD. Flavor enhancer Monosodium glutamate (L-sodium glutamate)

0.4 mg / kg monosodium glutamate (L-sodium glutamate) appears to trigger ADHD symptoms in rats.113
So far, no such effect is known in humans. High fat diet

Rodents fed a high fat diet HFD for 6 weeks or longer have slower dopamine reuptake114115 and lower surface expression of DAT.116
This should correlate with an increased extracellular dopamine level.
In addition, a diet with a high fat content reduces the release of dopamine.117
High-fat diet (HFD) correlated with ADHD-like behavioral phenotypes in male mice and impaired REM sleep due to dysregulation of the dopaminergic system:118

  • reduced alertness
  • increased REM sleep with fragmented patterns
  • reduced time in the middle zone of the open-field test (anxiety symptoms)
  • shorter immobile time in the tail suspension test
  • impaired visuospatial memory
  • reduced sucrose preference
  • decreased mRNA levels of D1R, COMT and DAT in the nucleus accumbens, which correlated with increased REM sleep onset and increased REM sleep periods

This could explain why people with reduced extracellular dopamine levels, typical of ADHD, develop a preference for high-fat foods. Lectin-free diet

A small prospective study of 58 children with ADHD found benefits of a lectin-free diet.119
A lectin-free diet also avoids dairy products and wheat, among other things. In the study, the diet was designed as an omission diet, so it is unclear to what extent the avoidance of lectins really brought benefits or whether it was the benefits of avoiding individual food intolerances. In addition, the diet was not double-blind, so there could be a significant bias among parents. Practical and social problems with diets for ADHD

A food diet that requires such consistent implementation as is necessary for an oligoantigenic diet as a threshold diet (see the report of the affected person there) will only rarely be feasible in early and middle childhood. At the earliest in adolescence and only with extreme commitment on the part of the affected person is it even conceivable to adhere to the diet with the necessary consistency (which is more difficult for ADHD sufferers per se).

The restriction of an elimination diet is probably not limited to eliminating the intolerable foods. A consistent diet is also likely to require that all unknown foods are avoided (or consistently recorded, with a newly tried food excluding any other unknown foods for 3 days).
It is considerably more difficult to eat out, as it is usually not reliably known which foods have been used to prepare the food. At best, only a few dishes can be consumed without worry.
Eating with friends is difficult for the same reasons.
The considerable social restrictions of those affected, which are in addition to the already “being different” and the stress for those affected resulting from the further restrictions, must be weighed up when considering a diet as a therapy for ADHD. Subjective overvaluation of diet therapies

Diets are able to improve ADHD symptoms in individual sufferers - with considerable effort and additional social stress for those affected.

The problem is that the subjective assessments of the results by parents are always far more positive than the results of objective tests.120

Only one rather small and non-double-blind study found - compared to a control group on a waiting list - equally good improvements through an elimination diet in both parent and teacher ratings.121

Another small study, which included objective tests as well as assessments, found good results in the subjective assessment, but these were not confirmed in objective tests.49

The only study known to us that compares the effect of elimination diets and methylphenidate (and comes to equally good results for the few diet responders) is notable for its peculiarly low responder rates for methylphenidate therapy and was completed with inpatients, which naturally makes the implementation of an elimination diet extremely easy (see above under elimination diet).

Since the evaluation bias occurs even in double-blind studies, a considerable bias (default setting) of the parents can be assumed to confirm the subjectively desired result (that ADHD can be treated with a diet instead of with critically considered medication).
However, it is also conceivable that the parents were already enthusiastic about the small improvements brought about by an elimination diet. Due to the study design, the parents were not allowed to know the far better effect that could be achieved with medication at the time of the evaluation and therefore could not have a standard of comparison. The only criterion for comparison could therefore only be whether or not there was any improvement at all.
Furthermore, the enormous effort that a diet for ADHD requires is likely to encourage 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 by means of a diet - possibly even with the experience that this is good for you - enables an experience of self-efficacy. This could have a healing effect in relation to the central psychological self-esteem problem, even if this effect is likely to be rather small in ADHD.

1.1.3. High-fat food can trigger / exacerbate ADHD symptoms

In an animal study, a high-fat diet showed various ADHD-like symptoms and neurophysiological changes:122

  • reduced alertness
  • increased REM sleep with fragmented patterns
  • reduced time in the middle zone of the open-field test (= anxiety-like behavior)
  • shorter immobile time in the tail suspension test (= increased motor activity)
  • visuospatial memory impaired
  • Sucrose preference reduced
  • in the nucleus accumbens:
  • D1R reduced
  • COMT reduced
  • DAT reduced.

1.2. Food (supplements) with a possible influence on ADHD

1.2.1. Low-density lipoprotein

One study found significantly increased blood levels of total cholesterol and low-density lipoprotein (LDL) in children with ADHD, while high-density lipoprotein (HDL) and triglyceride (TG) levels did not differ from those without ADHD.123 In contrast, another study found significantly lower blood levels of total cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) in boys with ADHD (regardless of subtype).124
In adults, a large cohort study found a slightly reduced low-density lipoprotein (LDL) level.125
A KIGGS study found no differences in serum lipid parameters between ADHD (n = 1,219) and controls (n = 9,741), neither in total cholesterol, LDL, HDL, nor triglycerides, neither at baseline nor at 10-year follow-up, even when MPH intake was taken into account.126

Treatment of bipolar adults with comorbid ADHD with lisdexamfetamine (Elvanse) resulted in a significant decrease in weight, body mass index, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, but not in triglycerides or blood glucose levels.127

A study indicates a genetic change in the receptor for low-density lipoprotein in ADHD.128 The fact that lipoprotein metabolism is altered in ADHD was also the result of another small study.129

Among other things, methylphenidate reduces the low-density lipoprotein level.130

Further studies on fats and fatty acids in ADHD did not lead to a clear result.131

1.2.2. Saturated fatty acids

A large study of 432 children found significantly higher serum levels of saturated fatty acids in children with ADHD.27 This correlated with an increased intake of nutrient-poor foods such as foods high in sugar and fat and a lower intake of vegetables, fruit and protein-rich foods than healthy children. It remains to be seen whether the change in diet is a cause, a consequence or a vicious circle.

1.2.3. Inorganic phosphorus

A large study of 432 children found significantly increased serum levels of inorganic phosphorus in children with ADHD.27 This correlated with an increased intake of nutrient-poor foods such as foods high in sugar and fat and a reduced intake of vegetables, fruit and protein-rich foods.
It remains to be seen whether the change in diet is the cause, consequence or vicious circle of ADHD.

1.2.4. Salt

High salt consumption can impair cognitive abilities, but can be reversed by reducing excessive salt consumption.132

Salt cravings can be an indication of aldosterone deficiency. This could be associated with pituitary or adrenal cortical weakness, which are common in ADHD-HI (with hyperactivity).
Since ADHD-I is more likely to have an excessive endocrine stress response, a particularly high feeling of thirst could be associated with an increased aldosterone level.
Aldosterone In the chapterNeurological aspects

1.2.5. Tetrahydroisoquinolines / Tetrahydroisoquinolines (TIQ)

It has been reported that 4 metabolites of TIQ (which represent a deviant degradation pathway of dopamine) are massively elevated in the urine of children with ADHD.
TIQs are synthesized in the brain and also absorbed through food.
The question therefore arises as to whether there is a connection to food intake.133

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).134 However, salsolonil does not appear to be blood-brain compatible.135

- is formed 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 chain136
- inhibits:137134
- Tyrosine hydrolylase
- DA-β-hydroxylase
- cAMP formation
- Endorphins

1.2.6. Ketogenic diet

A ketogenic diet is based on a composition of 10 % carbohydrates, 20 % protein and 70 % good fats (no trans fats). As long as no dietary mistakes are made (too many carbohydrates), this leads to a conversion of energy metabolism in the liver to ketones from body fat.

A ketogenic diet is said to contribute to an increase in GABA and a reduction in glutamate.138
Ketogenic diets have been tested on epilepsy patients with good results. In the case of diabetes, a ketogenic diet is particularly recommended, as insulin levels are stabilized.139

Both gluten-free and ketogenic diets can influence the gut microbiome.94
A meta-study discussed the ketogenic diet as a potential treatment for type II bipolar disorder.140

Little research has been done on the ketogenic diet in relation to ADHD.
A study on rats found that a ketogenic diet reversibly reduced the animals’ activity levels. Anxiety, on the other hand, was not reduced.141 A study on dogs also found improvements in individual behaviors associated with ADHD through a ketogenic diet142
One study reported a slight improvement in ADHD symptoms in SHR (an animal model for ADHD), probably due to influences on the gut-brain axis. However, the improvement was much weaker than that of MPH.143 ADHD sufferers with comorbid epilepsy are said to have experienced benefits in terms of hyperactivity, attention and cognitive abilities in addition to an improvement in epileptic seizures with a ketogenic diet.144 Although the author deals intensively with nutritional issues in ADHD, he does not cite any benefits in ADHD without comorbid epilepsy.
We are aware of several isolated reports by sufferers from the ADHD, according to which a ketogenic diet also improved ADHD symptoms. One affected person reported no relevant improvements in ADHD symptoms from a consistent ketogenic diet. One affected person reported a more constant effect of Elvanse and fewer mood swings when taking higher doses of high-quality tyrosine from the pharmacy, while cheap tyrosine from the food supplement market had less of an effect.

Furthermore, the avoidance of sugar associated with a ketogenic diet could be beneficial for people with sugar intolerance.

1.2.7. Tyrosine-rich / tyrosine-promoting diet

Protein-rich food (e.g. ketogenic diet) increases the tyrosine level in the brain. Tyrosine is a precursor in the synthesis of dopamine. Although the rate-limiting enzyme of 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 145146
Theoretically, a protein-rich diet could therefore improve a dopamine deficiency and improve ADHD symptoms if these arise due to dopamine synthesis problems caused by tyrosine deficiency. Although this is probably only rarely the case, we believe it is conceivable that this could be one of the many pathways leading to ADHD and could therefore help those affected.

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

More on this under Tyrosine for ADHD

1.3. Food (supplements) without evidence of influence on ADHD

1.3.1. Mediterranean diet

A Mediterranean diet in early pregnancy was associated with reduced mental health problems in children in one study.147

A Mediterranean diet for children with ADHD is said to have brought about a slight improvement in impulsivity in one study.148

1.3.2. Exorphins (no evidence verifiable)

One ADHD sufferer reported success with an exorphin-free diet.
Exorphins are atypical natural opiates that are contained in food. They differ from endorphins in their different chemical composition.

Exorphins are for example:149

  • The casomorphins in bovine and sheep’s milk
  • Β-Casomorphine in human breast milk
    • Whether β-casomorphin reaches the infant’s brain is open
    • Β-casomorphine injected into the brain of young rats reduces sensitivity to pain in an opiate-typical manner150
  • Opiopeptides in wheat gluten
  • Dermorphins (µ-receptor-selective)151
  • Deltorphins (δ-receptor selective)152

In both humans and rodents, opiate receptors are most densely located in the153

  • Posterior horn of the spinal cord
  • Medial thalamus
  • Brain stem
  • Limbic system

Cannaboid receptors, on the other hand, are primarily found in154

  • Basal ganglia
  • Hippocampus
  • Cerebellum
  • Neocortex


  • Reduce sensitivity to pain by inhibiting the firing rate of the neurons responsible for pain perception155
  • Inhibit the release of the neurotransmitters155
    • Adrenalin
    • Dopamine
    • Acetylcholine
    • Substance P

1.3.3. Sweetener

  • Aspartame

Aspartame is suspected of inhibiting the release of dopamine, noradrenaline and serotonin, which could lead to negative psychological consequences (especially in ADHD).156
Aspartame is also marketed as the “natural” sweetener AminoSweet.

1.3.4. Trans fats (no evidence verifiable)

Trans fatty acids are formed during the chemical hardening of fats, among other things. They are found in particular in hardened fats (e.g. margarine) and in foods that contain hardened fats (e.g. ice cream, chocolate coating).

According to Dr. Bod DeMario, trans fats (such as palm oil), which are often used to prepare fast food due to their low cost, are said to cause a DHA deficiency.
The casein contained in cow’s milk is also said to reduce DHA.
Excessive trans fat levels in the blood can be detected in ADHD.

This statement has not yet been verified on this side. In any case, no accessible studies by DeMaria on trans fats can be found on PubMed. The only study on trans fats in ADHD that can be found on PubMed157 is also not even available as an abstract.
An American forum thread also came to no meaningful conclusion about this hypothesis.158

1.4. Food (supplements) without influence on ADHD

1.4.1. Phosphate intolerance (refuted)

The theory of phosphate intolerance has been refuted.159

Marcus37 has explained this in detail:

  • The legally permitted phosphate supplements in food only account for 3% of the total phosphorus intake. Most phosphate is contained in food in its natural form.
  • Reduced 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 increase in the afternoon phosphate serum value is lower, but the fasting phosphate serum value remains unchanged.
  • If phosphate triggers ADHD symptoms, an increased phosphate intake should be able to cause ADHD symptoms. However, corresponding tests have not been able to confirm this.160
  • The diet propagated at the time as being low in phosphate actually had hardly any reduced phosphate content compared to a normal diet.

The effect of the low-phosphate diet could be based on its proximity to the oligoantigenic diet still under discussion today.

One affected person reports:

I was an example child in one of Hertha Hafer’s books. I started the diet at 15 or 16: no wholemeal products, no cola/fanta/other soft drinks, milk max. 1 glass/day, little cheese, sausage only with milk protein instead of phosphate as an emulsifier, but ham (although I remember it was already known at the time that this was also treated with phosphate), no baked goods with baking powder (only yeast or staghorn salt), little sugar (max. one chocolate bar/day) and perhaps other things that I have since forgotten. If I ever wanted to eat something that violated the diet, I could counteract this with 3 tablets of aluminum hydroxide taken about half an hour beforehand.
Fascinatingly, the whole thing worked. After dropping linearly from 1++ when I started school to extremely at risk of failing by the 10th grade, my grades constantly improved again after the diet and it was enough for me to graduate with a 2 in front of the decimal point.
However, the diet was relentless. If there was a single slip-up, it took 3 full days of strict adherence to the diet before the symptoms disappeared again. Every misstep was punished with 3 days of full symptoms. I was pretty consistent back then, especially for my age.
In hindsight, I think that cutting down on sugar was a key factor for me. I still notice today how the inner tension typical of ADHD-HI increases with intensive sugar consumption. Drinks with aspartame instead of sugar (e.g. Diet Coke or Zero), on the other hand, do not have this effect. It is also interesting that I tolerate sugar much better if I eat something salty afterwards.
I got my adult ADHD under control very well 30 years later with MPH and neurofeedback. I no longer diet, except that I eat as little sugar as possible. With plenty of sugar (a scoop of ice cream or a large piece of sweet cake is enough), I feel like I need twice as much MPH.

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

Children (and especially those with ADHD) are unlikely to be able to seriously adhere to the dietary requirements described above.

1.4.2. Salicylates (fine gold; refuted)

In the 1970s, the American Feingold postulated that salicylates and dyes can trigger ADHD
The theory regarding salicylates is considered outdated.
Feingold named several types of fruit and tomatoes in particular as foods containing salicylate.161
Many elimination diets cite different types of fruit and tomatoes as symptom triggers.
It would be interesting to know if there are any studies that have investigated the effect of salicylates on healthy people.
For colorants see above.

2. Other nutrition-specific treatment approaches for ADHD

2.1. Desensitization of food intolerances

Although food intolerance is not an allergy, a double-blind placebo-controlled study by Egger, who has intensively researched the elimination diets for ADHD presented here, successfully demonstrated desensitization to identified food intolerances. 16 out of 20 participants developed a tolerance, compared to 4 out of 20 from the placebo control group.162

2.2. Probiotic treatment can influence behavior

In an experiment on rats, probiotic treatment showed a reduction in depression symptoms. This was associated with changes in proinflammatory cytokines, which moderate inflammation.163 Furthermore, probiotic treatment reduced the transcription of CRH1, CRH2 and mineralocorticoid receptors in the hippocampus, while a high-fat diet increased them.

A single 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, while in the placebo group 17% received an ADHD or ASD diagnosis according to ICD 10.164

A meta-study found an effect of probiotic treatment on ADHD in only one of 7 studies. This study found a reduced risk of ADHD in children as a result of probiotic treatment of mothers during pregnancy and breastfeeding.165

2.3. Increased intestinal permeability in ADHD

A study of 40 ADHD sufferers and 41 non-sufferers found elevated zonulin levels in the ADHD sufferers, which also correlated with hyperactivity,166 so there may be a higher link to ADHD-HI than to 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 contraction of cytoskeletal proteins. An analysis of the zonulin level in serum is simple and gives a reliable picture of intestinal permeability and indicates chronic inflammatory bowel diseases, e.g;167

  • Celiac disease
  • Diabetes mellitus
  • Other autoimmune diseases
  • Disturbed intestinal flora, e.g. after antibiotic therapy

3. Further literature

Further literature on the subject of nutrition and ADHD can be found at

  1. Feingold (1975): Hyperkinesis and learning disabilities linked to artificial food flavours and colors. Am J Nurs 1975; 75: 797-803, erneut abgedruckt in Journal of learning disabilities,1976, Vol 9 Nr. 9, Seite 19 ff

  2. Mian, Jansen, Nguyen, Bowling, Renders, Voortman (2019): Children’s Attention-Deficit/Hyperactivity Disorder Symptoms Predict Lower Diet Quality but Not Vice Versa: Results from Bidirectional Analyses in a Population-Based Cohort. J Nutr. 2019 Mar 27. pii: nxy273. doi: 10.1093/jn/nxy273. n = 3680

  3. Hershko, Cortese, Ert, Aronis, Maeir, Pollak (2019): Advertising Influences Food Choices of University Students With ADHD. J Atten Disord. 2019 Dec 1:1087054719886353. doi: 10.1177/1087054719886353.

  4. Shareghfarid, Sangsefidi, Salehi-Abargouei, Hosseinzadeh (2020): Empirically derived dietary patterns and food groups intake in relation with Attention Deficit/Hyperactivity Disorder (ADHD): A systematic review and meta-analysis. Clin Nutr ESPEN. 2020 Apr;36:28-35. doi: 10.1016/j.clnesp.2019.10.013. PMID: 32220366. REVIEW

  5. Cagigal, Silva, Jesus, Silva (2018): Does diet affect the symptoms of ADHD? Curr Pharm Biotechnol. 2018 Sep 25. doi: 10.2174/1389201019666180925140733. REVIEW

  6. Beitelrock (2014): Einfluss von psychosozialem Stress auf die intestinale Barriere. Dissertation

  7. Egle, Joraschky, Lampe, Seiffge-Krenke, Cierpka (2016): Sexueller Missbrauch, Misshandlung, Vernachlässigung – Erkennung, Therapie und Prävention der Folgen früher Stresserfahrungen; 4. Aufl., Schattauer, S. 443, 444

  8. Gold, Danguecan, Belza, So, de Silva, Avitzur, Wales (2019): Neurocognitive Functioning in Early School-Age Children with Intestinal Failure. J Pediatr Gastroenterol Nutr. 2019 Sep 17. doi: 10.1097/MPG.0000000000002500.

  9. Saller, Römer-Lüthi, Brignoli, Meier (2006): Mehrfach ungesättigte Fettsäuren PUFA: Ein wichtiger Bestandteil in Zellstoffwechsel und Ernährung. Schweiz. Zschr. GanzheitsMedizin 18, 384–392, 2006

  10. Sonuga-Barke, Brandeis, Cortese, Daley, Ferrin, Holtmann, Stevenson, Danckaerts, van der Oord, Döpfner, Dittmann, Simonoff, Zuddas, Banaschewski, Buitelaar, Coghill, Hollis, Konofal, Lecendreux, Wong, Sergeant, and European ADHD Guidelines Group (2013): Nonpharmacological Interventions for ADHD: Systematic Review and Meta-Analyses of Randomized Controlled Trials of Dietary and Psychological Treatments. American Journal of Psychiatry 2013 170:3, 275-289 METASTUDIE

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