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Diet and nutrition for ADHD


Diet and nutrition for ADHD

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

The American Feingold1 postulated in 1975 that salicylates and dyes could trigger ADHD (see below). The German pharmacist Hertha Hafer (who, by the way, 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 are disproven today. Dyes can be a co-factor that exacerbates existing ADHD, but are not “the” trigger of ADHD.

One 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 more often choose unhealthy foods.3
One review found a significant correlation between typical diet and ADHD, with a “Western diet” more likely to correlate with ADHD. A “healthy” dietary pattern with plenty of vegetables, fruits, legumes, and fish correlated with up to a 37% decrease in the likelihood of ADHD. A “junk food” pattern with sweetened beverages 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 neatly differentiate between correlation and causation. Causality could only come from predetermined dietary patterns and measuring their effect on symptomatology. However, only the typical eating habits of ADHD sufferers and non-affected persons were measured. It is well known that stress shifts dietary preference to fast-digesting foods. Therefore, the study may only report on consequences of ADHD.
If ADHD could be influenced so significantly with a healthy diet, word would have spread long ago. Regrettably, the effects of dietary change on ADHD symptoms are considerably smaller than the effect of ADHD on the choice of preferred diet
One review found that dieting for ADHD is not a promising treatment option for ADHD.5 The achievable effect sizes on symptom improvement through diets (alone) are clearly too low. For a part of ADHD sufferers - individually different - certain substances can be defined that contribute to an increase of stress/ADHD symptoms in them and whose elimination can contribute to symptom improvement. As an element of an overall treatment, this then also makes sense.
Unfortunately, the effort required to determine whether a sufferer benefits from symptom improvements is high. Moreover, only a small proportion (25-50%) of sufferers benefit, and the degree of improvement lags far behind that of other treatments.

Nevertheless, there are individual influences of food on the stress systems and vice versa of stress on the digestive organs. These can make a complementary contribution to the treatment of ADHD. The hope of successfully treating an existing ADHD through nutrition alone, however, 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 proinflammatory (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, however, only beneficial in the short term. If they are active for too long (due to prolonged stress), they attack cells and tissues, which, in addition to degeneration of cells (cancer) and damage to the immune system, can lead to chronic inflammatory bowel disease. An intestinal wall damaged by inflammatory processes restricts the absorption of vital substances. To temporally limit the effect of proinflammatory cytokines, cortisol released by the HPA axis (intervening late during stress) has an inhibitory effect on proinflammatory 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 repel extracellular pathogens (bacteria, parasites) and promote basophils, mast cells, and eosinophils, which can promote allergies if they are excessive.
Thus, a disturbance in the balance of the HPA axis (hypocortisolism = too little cortisol or hypercortisolism = too much cortisol) can lead to an imbalance between 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.

Further, stress can alter the expression of genes, including those responsible for providing enzymes in the digestive tract.

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

In our opinion, in cases of a known food intolerance, an appropriate diet could form a thoroughly relevant 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 the presence of food intolerance) is with 0.25 so significantly below that of medication (up to 1.1) that a sole diet treatment corresponds to a partial non-treatment.
Effect size of different forms of treatment for ADHD

1. ADHD as a dietary consequence / food intolerance

People who have a predisposition to a disorder, but who have it at a level of intensity that is not yet pathological without additional stresses, are healthy.
However, if a strain on the stress systems occurs in your case, the disturbance pattern can become so energetic that it leaves the realm of the healthy and can become disturbing.
Others, however, who are further away from the unhealthy intensity of disturbance by disposition, do not mind the additional stressor. This can be called resilience.

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

With this picture, it may become more understandable what influences different forms of treatment can have. The elimination of a food intolerance or an allergy, the change to a healthy diet or the elimination of vitamin deficiencies may possibly be just sufficient for a weaker form of a disorder to leave the unhealthy stress range again and to lead it just below the “pathological” range. Whether this is sufficient for the affected person or whether a stronger treatment, which 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 in each individual case.
Strong disturbance manifestations are in any case only treatable with medication and additional non-drug therapeutic measures. However, even in these cases, the elimination of an existing food intolerance is just as helpful a support as the elimination of other stressors.

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

1.1. Food / dietary supplements with influence on ADHD

1.1.1. Polyunsaturated fatty acids (PUFAs)

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 (although statistically significant) contribution of PUFA fatty acid supplementation to ADHD symptom improvement,1011 12 as does a recent small placebo-controlled trial.1314

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

Possible symptoms of PUFA deficiency include:169

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

A Japanese study found significantly decreased blood plasma levels of polyunsaturated fatty acids in 24 ADHD sufferers under 20 years of age17

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

With respect to DHA, a placebo-controlled study over 6 months in 50 school-aged children with ADHD found no significant improvement in ADHD symptoms.18 Nevertheless, small improvements in behavioral problems and cognitive difficulties were reported. Other studies sometimes confirmed an effect of DHA in ADHD, and at other times found no benefit.19

A diet rich in fish for the mother during (especially early) pregnancy correlated with lower 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 that ran for 3 months placebo-controlled and another 3 months with omega 3/6 administration to all participants found a reduction in ADHD-HI symptoms of with more than 25% in 26% of participants. In the no longer placebo-controlled portion, the rate of improvement increased to 47% of participants at 6 months. Responders were more often of the inattentive subtype and had comorbid neurodevelopmental disorders. Symptom ratings were made by the authors.21

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

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

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

A double-blind placebo study found no difference in ADHD symptomatology between children receiving MPH and placebo and children receiving MPH and omega-3.26

A large study of 432 children found a significantly increased serum omega-6 to omega-3 ratio in children with ADHD.27 This correlated with an increased intake of nutrient-poor foods such as high-sugar and high-fat foods and a decreased intake of vegetables, fruits and protein-rich foods than in healthy children
A diet high in sugar and fat has been associated with increased levels of inflammation in the PFC and liver problems, as well as behavioral changes discussed in the context of ADHD.28
It is an open question whether the altered diet is the cause, consequence, or vicious cycle 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 examined 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 with the placebo group, the EPA group showed30

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

An 8-week course of DHA in children with ADHD was reported to have produced 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 diseases, toxins or psychological stress and can therefore worsen the stress situation of affected individuals to such an extent that symptoms develop. This is not an ADHD-specific finding, 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 schizophrenia symptoms in the children affected.3334
The same was found in sufferers with non-affective psychosis.35

Food intolerances are nevertheless not the (singular) cause of schizophrenia, psychoses or ADHD. However, food intolerances can, in our understanding, 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 accompanied by a serious imbalance in stress regulatory systems. Therefore, influences that put additional stress on the stress systems can reinforce a predisposition to a mental disorder in such a way that it is precisely this last additional influence that causes it to reach a disturbing (pathological) level. Elimination diet - (conditionally) 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. Provided this diet reduces symptoms after several weeks (which is highly suggestive of food intolerance or allergy), one (more) food is then reintroduced into the diet every 5 days and remains if there has been reliably no symptom return.

Egger36 describes such a diet with which behavioral improvements can be achieved to an appreciable extent. Egger himself describes this elimination diet (which he calls an oligoantigenic diet) as effective for some sufferers, but very demanding to implement. Other authors in the same work believe that an (oligoantigenic) elimination diet can hardly be implemented in daily life.37

Quite a few studies have found improvements with diets, however, in reviews through testing compared to drug and psychotherapeutic treatment

  • Significantly fewer sufferers show improvement
    and also a
  • Significantly weaker decrease in ADHD symptoms was detectable.

For the report of a sufferer of the effort and effect of a (in the result probably oligoantigenic) diet see below.

The fact that these diets treat food intolerances rather than food allergies is evident from the fact that the interfering substances found by means of the elimination diet were not conspicuous in blood tests by elevated IgG and IgE antibodies. Conversely, the substances for which IgG and IgE antibodies were elevated were not always those that increased ADHD symptoms.3839 Individual studies on elimination diets
  • A meta-analysis reported an effect size of 0.51 to 0.8 for the elimination diet40
  • One of the first and oldest studies reported that an oligoantigen elimination diet produced complete elimination of ADHD symptoms in 21 of 76 hyperactive children and improvements in symptoms in another 41. fourteen 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), each of which significantly increased or decreased symptoms more often than placebo.41
  • Coloring agents and preservatives were the most frequently eliminated foods, but 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 versus an effect size of 0.12 to 0.25 for dietary supplements.42
  • 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, when administered in a double-blind masked fashion, increased symptoms again in 19 of 23 subjects. However, these are only parent ratings.43
  • A smaller study of 26 affected children showed that 19 children (73%) responded positively to an elimination diet, with all responding to quite a few foods, dyes, and/or preservatives. A double-blind, placebo-controlled review in 16 children showed significant differences between placebo and exposure. Children with allergic tendencies responded significantly more sensitively than the non-atopic group.44
    Our understanding is that allergies are typical in ADHD-I subtype, whereas inflammation is more typical in ADHD-HI (with hyperactivity).
  • Another study reported a positive effect of an elimination diet in some of the ADHD sufferers. On average, 5 (individually different) foods were found to be eliminated per child.4546
  • A fairly small study found good improvements with an elimination diet in parent and teacher ratings.47
  • Another small study that included objective tests in addition to assessments found good results in subjective assessment, but these were not confirmed in objective tests.48
  • A double-blind study of 100 children demonstrated good efficacy of an elimination diet, with a subsequent diet that selected for IgG levels alone (which mark allergies) showing symptom exacerbations in 63% of participants.39
  • In 49 hospitalized children, a crossover/double-blind/placebo-controlled study in Mannheim compared the efficacy of an oligoantigen elimination diet with that of medication with methylphenidate. While the responder rates for methylphenidate were almost twice as high (44%) as for elimination diet (24%), the symptom improvements were almost equal.49
    In this regard, it should be noted:
    • A responder rate of 44% to methylphenidate is very low. The usual rate is 70%, although this can be increased to 85-90% by switching nonresponders to amphetamine medication.
    • An elimination diet is likely to be easier to adhere to in an inpatient hospital setting than in everyday life.
  • A nonstrict elimination diet was positively evaluated in parent-only reports.50
  • A small study found subjects on an oligoantigenic diet still improved from pre-diet ADHD status after 3.5 years51
  • Deficiencies in certain vitamins and minerals are a risk of elimination diets.52

Problematic in the evaluation of diets in ADHD is that the results are subjectively significantly overestimated by parents in parent questionnaires. Objective tests show much weaker improvements. For more on this, see below.

The UK’s National Institute for Health and Care Excellence (NICE) currently sees more disadvantages than advantages to elimination diets in 4- to 8-year-olds.53 Dutch elimination diet protocol (Few food diet, FFD; RED)

In the Netherlands, a specific strict protocol is used for testing an elimination diet in children with ADHD.54

  • Verification that the family and child meet the participation criteria

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

  • Two-week baseline period

    • Child retains his usual diet
    • Discontinuation of nutritional supplements (e.g. fish oil, vitamins)
    • Retention of psychoactive medications
    • Parents keep diary of child’s daily activities, eating habits, medications and behavior
  • Renewed behavioral measurements at the end of the baseline period

  • Parents receive detailed training on possible pitfalls in adhering to the FFD, based on the information provided by the diary. Parents are urged to also follow the elimination diet (omit all foods that are not allowed during elimination diet) to optimally support the child. Parents are provided with a schematic overview of which foods are allowed in which 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
    • Additionally 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 behavioral improvement: continuation of extended FFD
  • If no behavioral improvement from extended FFD
    gradual restriction of diet to strict FFD for then 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)

    • Psychotropic drugs are discontinued
  • No improvement in behavior is observed (nonresponder)

    • Further adjustment of the diet
  • Repeat behavioral measurements at the end of the FFD

  • In 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 behavioral deterioration results, food is permanently banned from 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 because of successful behavioral improvement.54 Frequently incompatible foods Often incompatible according to studies on elimination diets for ADHD

Studies of elimination diets report the following foods frequently triggering symptoms. Percentages are for those (out of less than 100) subjects in whom the food was responsible for symptoms. Because of the small number of subjects, the results are highly uncertain.

  • Food additives (79%)55, (70%)43
  • Chocolate (64%)43, (59%)56
    • See also below Tetrahydroisoquinoline / Tetrahydroisoquinoline (TIQ)
  • Cow’s milk (64 %)5743
  • Oranges (57%)43
  • Grapes (50%)57
  • Wheat (49%)57, (45%)43
  • Cow’s milk cheese (45%)43, (40%)56
  • Citrus (45%)56
  • other fruit (36 %)43
  • Eggs (39%)56 to (18%)43
  • Peanuts (32 %)56
  • Corn (29 %)56
  • Fish (23 %)56
  • Oats (23 %)56
  • Melons (21%)56
  • Tomatoes (22%)43, (20%)56
  • Pineapple (19%)56
  • Sugar (16 %)56
  • Beef (16 %)56
  • Beans (15%)56
  • Peas (15%)56
  • Malt (15 %)56
  • Apple (13 %)56
  • Pork (13 %)56
  • Pears (12 %)56
  • Chicken (11 %)56
  • Potatoes (11 %)56
  • Tea (10 %)56
  • Coffee (10 %)56
  • mixed nuts (10 %)56
  • Cucumbers (9%)56
  • Bananas (8%)56
  • Peach (7%)56
  • Carrots (7%)56
  • Lamb (5%)56
  • Turkey (5%)56
  • Rice (4 %)56
  • Yeast (4 %)56
  • Apricots (3%)56
  • Onions (3 %)56 Sugar 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 colors, glutamate, and, for each child individually, potentially allergenic foods (such as milk) produced significant behavioral improvement in 45% of the participating children, including improvement in sleep problems phenotypic of ADHD (including delay in falling asleep).50
In a parallel diary study, 15% of participating children (regardless of ADHD status) were found to have associations between their food consumption and behavior.58
In our view, these observations correlate with Egger’s results.

One study tested urinary sugar excretion in children with and without ADHD on identical diets. The ADHD sufferers were found to have unusually elevated levels of:59

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

In addition, all 40 affected persons were found to be

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

The authors consider this to support the hypothesis that ADHD is associated with aberrant carbohydrate metabolism.

Attenuated COMT activity simultaneously decreases glucose tolerance in mice.
COMT produces the estrogen 2-methoxyestradiol (2-ME), which is relevant for glucose tolerance. Reduced COMT activity therefore leads to reduced glucose tolerance via reduced 2-ME production.60
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.
Read more at -&gt Dopamine degradation

One study found a correlation between sugar intake at 30 months and risk for ADHD, sleep disorders and anxiety. No correlation was found at 12 months of age.61
Whether this is a causal cause or a consequence of altered food preferences due to the disorder predisposition is an open question.

(Real) sugar is thought to lower the cortisol response to stress triggers.62 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 shows 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 sugar. This could be a link between stress and eating problems or obesity and could be seen as an indication of poorer sugar conversion in the presence of a reduced cortisol stress response. More information is needed to verify this idea.

Glucose administration stimulated an increase in blood epinephrine levels in a fairly small group of subjects (n = 28), which were almost 50% lower in ADHD than in unaffected subjects. Plasma norepinephrine levels were also lower in ADHD than in unaffected subjects. These data suggest a general impairment in sympathetic activation as well as regulation of catecholamines (dopamine, norepinephrine, serotonin) in ADHD.63

A diet high in sugar and fat has been associated with increased levels of inflammation in the PFC and liver problems, as well as behavioral changes 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 consequence of ADHD.64

That sugar is not per se a trigger of ADHD is shown by a study that compared the sugar consumption of 6- to 11-year-olds with their development of possible ADHD. No correlation was found. This supports the view that sugar is not a universal trigger of ADHD, but does not rule out the possibility that sugar intolerance may promote ADHD.65 Another report comes to the same conclusion, but points out that sugar increases adrenaline synthesis.66 Sugar and EEG

In a single-case study that we supervised, the changes in EEG caused by sugar were observed in an affected person in whom sugar caused ADHD-HI symptom intensifications:

  • Sugar (2 candy 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 increased significantly.
      The threshold values during theta up / beta down training had to be reduced considerably. The 85% of target values reached before 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 well above SMR. Beta1 should be below SMR, so SMR training aimed at increasing SMR is the first step of neurofeedback treatment of ADHD.
    • After 30 minutes, Beta1 had caught up somewhat with SMR. Hi-Beta was now significantly higher.

This is a single test with a single subject. The subject knew about the expected reaction. The aggravation of his ADHD-HI symptoms after sugar consumption had been mirrored to him by quite a few persons and coincided with his own observation. 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 reported to us that after sugar consumption (chocolate) he reproducibly noticed a considerable increase in his ADHD-HI symptoms, in particular procrastination.

We understand that the observations fit the description of the effect of oligoantigenic diet for individuals who are sensitive to sugar.

Problematic in the evaluation of diets for ADHD is that the results are subjectively significantly overestimated by parents. Objective tests show much 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 (= a protein intolerance, which is to 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 urinary peptide levels therefore indicate genetic, epigenetic, or toxic impairment of key enzymes involved in peptide cleavage. Elevated levels of bioactive peptides in urine have been found in schizophrenia, depression, autism, and ADHD.67

In the study of 104 children with ADHD and 36 unaffected children, not only did the ADHD sufferers clearly differ according to peptide levels in the urine. The type of peptides found also clearly differentiated the ADHD subtype:68

  • Sixty-four sufferers with the ADHD-HI subtype (with hyperactivity) showed elevated benzoic acid-glycoprotein-peptide complexes.
  • 35 affected individuals (all but 3 of whom corresponded to the ADHD-I subtype without hyperactivity) showed reduced levels of uric acid complexes.
  • 5 affected individuals (4 of whom were hyperactive) showed reduced amounts of all urinary complexes.
  • Urinary peptides of hyperactive sufferers increased the uptake of serotonin in platelets.69

Unfortunately, there are hardly any other studies on peptides in urine in mental disorders - not even any 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.70

No significantly elevated urinary peptide levels were found for dyslexia (which is comorbid in ADHD)71

Proteins (proteins) in urine can be a symptom of emotional stress, among other things.72 An examination of the urine of 15 pet dogs and 20 shelter dogs revealed significantly elevated peptide levels in the urine of the shelter dogs.73

However, if a dairy- and casein-free diet were a successful solution for ADHD, this treatment should have become established long ago. As the studies on elimination diets show, the triggering foods are highly individual and therefore cannot be identified as a group across the board.
In the context of an oligoantigenic diet, dairy products are also to be tested. 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 would be conceivable to artificially ingest the enzymes required to break down the proteins.

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

The following account of what at first appears to be an impressively helpful study on the (claimed) effect of enzymes in autism should definitely be read to the end of the italicized section.

In a study of 29 autism sufferers (17 others terminated participation prematurely for various reasons), a purchasable enzyme mixture74 produced (according to the manufacturer)

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

taken before each meal, showed moderate to significant symptom improvements in 13 categories in 50% to 90% of the 29 autism sufferers who took the test.75

In addition to the small number of 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 had been registered beforehand, i.e. whether it would also have been published if the result had been negative. Unfortunately, it is not uncommon in the pharmaceutical industry that a large number of studies are started, of which only those that are favorable to the manufacturer are published, while the less favorable results end up in the wastepaper basket.
We do not know whether this is the case here.
Further - registered - studies by other scientists with larger numbers of subjects and non-manufacturer-specific enzyme mixtures would provide clarity here.

  • Caso-Glutenase is not a specific enzyme, but a trademarked enzyme complex that is said to help digest or break down casein and gluten, as well as being DPP-IV active.
  • According to the supplier, bromelain (bromelin) proteolytically breaks down casein.
  • Fast Acid Protease (AFP) is not found in the scientific literature. There is only a patent for Brodnak.76 According to the manufacturer, AFP starts protein degradation already in the stomach, while the other enzymes (peptidases), which are per se (heat- and) acid-sensitive, become effective only in the small intestine. The presentation is dubious.
  • Lactase breaks down milk sugar (lactose). The amount should be sufficient for about 200 ml of milk.
  • Phytase degrades phytic acid, which is present in plants such as wheat, corn, rye, barley, beans, soybean, etc.. Phytic acid can interfere with the absorption of minerals such as calcium, zinc, copper, manganese, iron, and magnesium by forming mineral complexes with them that are excreted. Phytase is thus thought to increase the availability of minerals and phosphate.
  • D-galactose, a simple sugar, is said by the manufacturer to “act as a genomeceutical” to help maintain healthy levels of DPP-IV in cells. This is not plausible in our view. In any case, DPP-IV inhibitors are more relevant from a health perspective. We could not find reports on therapeutic purposes of the administration of galactose (in the named amount of 0.1 gram). 100 grams of natural yogurt already contains 1 gram of galactose, i.e. ten times that amount.
    Publications about “genomeceutical” 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”.77
    Genomeceutical is a registered trademark.
  • Similar enzyme complexes are also offered by other suppliers (Kirkman).78 The patent held by Brudnak was formerly held by Kirkman.79
    The results are highly dubious.
  • Several enzymes described are not found in any scientific study
  • Some of the described mechanisms of action are (to put it kindly) scientifically highly doubtful
  • Mark Brudnak has at the same time 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 rather reminiscent of marketing models in which a media presence is generated by sham scientific publications in order to promote the sale of one’s own products.
    If one now still looks at who leads the “scientific” publication mentioned at the beginning with the 29 autism sufferers (again Brudnak, and without pointing out the intertwining of interests), it becomes comprehensible what weight these doubts have about the scientific substance of this investigation.

After our more in-depth research has raised our doubts about the study (cited by Reichelt without comment), we have nevertheless decided to leave this account here in order to explain the possible mechanisms of such dubious studies.

It is essential to discuss the intake of such enzyme complexes with the family doctor beforehand. is not affiliated with any of the providers in any way. It is presented solely for the purpose of scientific discussion.

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

Gluten can be a factor in ADHD, but 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 celiac disease, this would be about 20 times more common
Conversely, children with celiac disease had an ADHD prevalence of 16%, more than twice the prevalence expected without celiac disease.80

There is evidence that the risk of serious mental disorders increases approximately fourfold in celiac disease.81 A gluten- and casein-free diet reportedly showed reduced ASD-associated gastrointestinal symptoms and improvements in antisocial behavior in a study of a brand-name ASD.82 Both gluten-free and ketogenic diets may affect the gut microbiome.83

These results are not robust due to the small number of studies and subjects.
However, in the context of an elimination diet (see above), wheat is often identified as the triggering food. Dyes

Feingold’s original study results, according to which a diet without dyes and food additives could reduce ADHD symptoms such as hyperactivity, were put into perspective by later, methodologically more complex studies.84

A meta-analysis shows a weak to moderate significant contribution of dietary dye exclusion to ADHD symptom improvement, especially in those with food intolerance.1085
The authors of a meta-analysis of 24 studies on ADHD and dyes in food concluded that about 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.8687
Another meta-analysis of randomized, double-blind (and thus largely removed from assessment bias) studies on whether dyes can trigger hyperactivity symptoms found an effect size of 0.21. When smaller, lower-quality studies were also added, this increased to 0.283.88
It is problematic that almost all studies on dyes in ADHD are based on parent ratings, which (if not double-blind) implies a considerable bias towards an exaggeration of symptom reduction by eliminating dyes from the diet,89 especially if the parents have to monitor the diet, since a diet causes effort, which quite regularly leads to the expectation that this effort cannot remain fruitless.
A meta-analysis of 4 studies examined blue dyes and found influences of elimination diets that avoided FDA-approved blue dyes.90

In order to be able to judge whether the calculated effect sizes mean small or small to medium effects, one would need to know which effect size calculation method was used. See for this Effect size at Wikipedia.

On an elimination diet, dyes or preservatives were the most commonly eliminated foods, but no child responded to these alone, see above.41
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. Further, a small increase in inattention symptoms was found.91

A meta-study discusses findings on dyes in autism.92

See also the two studies under Preservatives / Sodium benzoate (E 211).

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

  • E 102 (tartrazine)
  • E 104 (chilon yellow)
  • E 110 (yellow orange S)
  • E 122 (azorubine)
  • E 129 (allura red)

Such indications always include a large margin of caution. 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.93

Another study of 267 healthy children also found that dyes or sodium benzoate (E 211) (or both) increased hyperactive symptoms in 3-4 year olds as in 8-9 year olds.94 The European Food and Drug Administration had this finding evaluated by a panel of experts. After corrections to the statistical mathematical evaluation model of the study under investigation, the 53-page review concluded that the effect, if present at all, was of little clinical relevance.95 Sodium nitrite (sodium nitrit)

There are no known direct studies on sodium nitrite regarding negative effects in relation to ADHD.

However, sodium nitrite is said to be potentially capable of impairing working memory.96979899

Sodium nitrite could affect the acquisition of an inhibitory avoidance response in rats and mice through a direct effect on the CNS.100

Although sodium nitrite is systematically used to cause memory problems in experimental animals to explore agents to improve memory performance, there is no study related to sodium nitrite in ADHD. Flavor enhancer Monosodium glutamate (L-sodium glutamate)

0.4 mg / kg monosodium glutamate (L-sodium glutamate) appears to induce ADHD symptoms in rats.101
So far, no such effect is known in humans. Practical and social problems with diets for ADHD

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

The restriction of an elimination diet is unlikely to be limited to eliminating the intolerable foods alone. In addition, a consistent diet probably further requires that all unknown foods be avoided (or consistently recorded, with a new food tried for 3 days precluding the trying of any other unknown foods).
Going out to eat already is considerably more difficult, since it is usually not likely to be reliably known which foods have been used for preparation. At best, only a few dishes can be consumed without worry.
Eating at a friend’s house is more difficult for the same reasons.
The significant social limitations of those affected, in addition to the already “being different,” and the stress for those affected resulting from the further limitations, must be weighed when considering diet as a therapy for ADHD. Subjective overestimation of dietary therapies

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

The problem is that subjective assessments of the results by parents are always far more positive than the results of objective tests.102

Only one fairly small and non-double-blind study found equally good improvements with an elimination diet in both parent and teacher ratings - compared to a wait-list control group.103

Another small study that included objective tests in addition to assessments found good results in subjective assessment but did not find confirmation in objective tests.48

The only study known to us that compares the effect of elimination diet and methylphenidate (and arrives at equally good results for the few diet responders) is conspicuous 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).

Because assessment bias occurs even in double-blind studies, a substantial bias (preconception) of parents to confirm the subjectively desired outcome (that ADHD could be treated by diet rather than critically considered medication) can be assumed.
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 designs, the parents were not allowed to know the much better effect that could be achieved by medication at the time of evaluation and therefore could not have a comparison criterion. The only criterion for comparison could therefore only be whether or not there was any improvement at all.
Furthermore, the enormous effort required for a diet in ADHD is likely to promote an expectation that this effort must pay off. It is a general psychological principle that the greater the effort expended, the more positively results are evaluated.

It is also conceivable that the decision alone to do something for oneself by means of a diet - possibly even with the experience that this does good - 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.

1.2. Food (supplement) with possible influence on ADHD

1.2.1. Low-density lipoprotein

In ADHD-affected children, one study found significantly elevated blood levels of total cholesterol and low-density lipoprotein (LDL), while high-density lipoprotein (HDL) and triglyceride (TG) levels did not differ from unaffected individuals.104 In contrast, another study found significantly decreased blood levels of total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) in boys with ADHD (regardless of subtype).105
In adults, a large cohort study found slightly reduced low-density lipoprotein (LDL) levels.106

Treatment of bipolar adults with comorbid ADHD with lisdexamfetamine (Elvanse) produced significant decreases in weight, body mass index, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, but not triglyceroids or blood glucose levels.107

A study suggests a genetic alteration of the receptor for low-density lipoprotein in ADHD.108 The fact that lipoprotein metabolism is altered in ADHD was also the result of another small study.109

Methylphenidate reduces low-density lipoprotein levels, among other things.110

Further studies on fats and fatty acids in ADHD did not lead to clear results.111

1.2.2. Saturated fatty acids

A large study of 432 children found significantly higher serum levels of saturated fat in children with ADHD.27 This correlated with an increased intake of nutrient-poor foods such as high-sugar and high-fat foods and a decreased intake of vegetables, fruits and protein-rich foods than healthy children. It is an open question whether the altered diet is a cause, consequence, or vicious cycle.

1.2.3. Inorganic phosphorus

A large study of 432 children found significantly elevated serum levels of inorganic phosphorus in children with ADHD.27 This correlated with an increased intake of nutrient-poor foods such as high-sugar and high-fat foods and a decreased intake of vegetables, fruits and protein-rich foods.
It is an open question whether the altered diet is the cause, consequence, or vicious cycle of ADHD.

1.2.4. Salt

High salt consumption can impair cognitive abilities, but is reversible by reducing excessive salt consumption.112

Salt starvation may be an indication of aldosterone deficiency. This could be associated with pituitary or adrenal insufficiency, which are common in ADHD-HI (with hyperactivity).
Since ADHD-I is more likely to have an exaggerated endocrine stress response, a particularly high sense of thirst could be associated with elevated aldosterone levels in this case.
Aldosterone In chapterNeurological aspects

1.2.5. Tetrahydroisoquinolines / Tetrahydroisoquinolines (TIQ)

It was reported that 4 metabolites of TIQ (representing an aberrant degradation pathway of dopamine) were massively elevated in urine in children with ADHD.
TIQ are synthesized in the brain and also absorbed through food.
The question therefore arises as to whether there is a relationship to food intake here.113

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).114 However, salsolonil does not appear to be blood-brain mobile.115

- 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 chain116
- inhibits:117114
- Tyrosine hydrolylase
- DA-β-hydroxylase
- cAMP education
- Endorphins

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

1.3.1. Ketogenic diet

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

Ketogenic diet is thought to contribute to GABA increase and glutamate decrease.118
Ketogenic diet has been tested in epilepsy patients with good success. In diabetes, ketogenic diet is just required, because the insulin level is very much verse.119 ADHD sufferers with comorbid epilepsy are reported to experience benefits in hyperactivity, attention, and cognitive abilities in addition to improvement in epileptic seizures with ketogenic diet.120 Although the author discusses nutritional issues in ADHD intensively, he does not name any benefits in ADHD without comorbid epilepsy.

Both gluten-free and ketogenic diets can affect the gut microbiome.83
One metastudy discussed ketogenic diets as a potential treatment for type II bipolar disorder.121

In relation to ADHD, ketogenic nutrition has hardly been researched. In principle, the elimination of sugar associated with a ketogenic diet could be beneficial for sufferers with sugar intolerance. One study in rats found that ketogenic diets reversibly decreased the animals’ activity levels. Anxiety, on the other hand, was not reduced.122 Another study in dogs also found improvements in individual ADHD-related behaviors with a ketogenic diet.123
In one individual case known to us, a consistent ketogenic diet did not produce any relevant improvements in ADHD symptoms.

1.3.2. Mediterranean diet

A Mediterranean diet in early pregnancy was associated with reduced mental health problems in children in one study.124

A Mediterranean diet in children with ADHD was reported to have slightly improved impulsivity in one study.125

1.3.3. Exorphins (no evidence verifiable)

An ADHD sufferer reported success on an exorphin-free diet.
Exorphins are atypical natural opiates found in food. They differ from endorphins by a different chemical composition.

Exorphins are for example:126

  • The casomorphins in bovine and ovine 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 opiate-like pain sensitivity127
  • Opiopeptides in wheat gluten
  • Dermorphins (µ-receptor selective)128
  • Deltorphins (δ-receptor selective)129

Opiate receptors in both humans and rodents are most densely located in the130

  • Posterior horn of the spinal cord
  • Medial thalamus
  • Brainstem
  • Limbic system

In contrast, cannaboid receptors are found primarily in131

  • Basal Ganglia
  • Hippocampus
  • Cerebellum
  • Neocortex


  • Reduce pain sensitivity by inhibiting the firing rate of the neurons responsible for pain perception132
  • Inhibit the release of the neurotransmitters132
    • Adrenalin
    • Dopamine
    • Acetylcholine
    • Substance P

1.3.4. Sweetener

  • Aspartame

Aspartame is suspected of inhibiting the release of dopamine, norepinephrine, and serotonin, which (especially in ADHD) could lead to negative psychological consequences.133
Aspartame is also marketed as the “natural” sweetener AminoSweet.

1.3.5. Trans fats (no evidence verifiable)

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

According to Dr. Bod DeMario, trans fats (such as palm oil), which are commonly used to prepare fast food because they are inexpensive, are thought to cause DHA deficiency.
The casein (casein) found in cow’s milk is also thought to reduce DHA.
In ADHD, excessive trans fat levels are detectable in the blood.

This statement could not be verified on this side so far. In any case, no studies by DeMaria on trans fats can be found on PubMed. The only study on trans fats in ADHD that can be found at all at PubMed134 is also not even available as an abstract.
An American forum thread also came to no meaningful conclusion on this hypothesis.135

1.4. Food (supplement) without influence on ADHD

1.4.1. Phosphate incompatibility (refuted)

The thesis of phosphate intolerance has been disproved.136

Marcus37 has justified this in detail:

  • The legally permissible phosphate supplements in food comprise only 3% of the total phosphorus intake. Most phosphate is found in natural form in foods.
  • Reduced dietary phosphate intake is compensated by the body through increased renal tubular reabsorption, so that the blood phosphate level is not reduced. Only the increase in the afternoon serum phosphate value is lower, but the fasting serum phosphate value remains unchanged.
  • If phosphate were to trigger ADHD symptoms, an increased phosphate intake should be able to cause ADHD symptoms. However, corresponding tests could not confirm this.137
  • The diet that was promoted at the time as low in phosphates actually showed hardly any reduction in phosphate levels compared with a normal diet.

The effect of the low-phosphate diet could be based on its proximity to the oligoantigenic diet, which is still discussed 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 whole grain products, no cola / Fanta / other sodas, milk max. 1 glass / day, little cheese, sausage only with milk protein instead of phosphate as an emulsifier, but ham (although to my recollection it was already known at that time that this was also treated with phosphate), no pastries with baking powder (only yeast or deer horn salt), little sugar (max one candy 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 it with 3 tablets of aluminum hydroxide taken about half an hour before.
Fascinatingly, the whole thing worked. After I had dropped linearly from 1++ when I started school to the 10th grade to being extremely at risk of transferring, my grades consistently improved again after the diet and it was enough for an Abi with a 2 before the decimal point.
However, the diet was relentless. In the case of a single slip, it took 3 full days of strict dietary adherence for the symptoms to disappear again. Any misstep was punished with 3 days of full symptoms. I was pretty consistent back then, even more so for my age.
In retrospect, I think that sugar reduction was a major key for me. I still notice today how the ADHD-HI-typical inner tension grows with intensive sugar consumption. Drinks with aspartame instead of sugar (e.g. Cola light or Zero), on the other hand, do not have this effect. It is also interesting that I tolerate sugar much better when I eat something salty afterwards.
I have managed my adult ADHD very well 30 years later with MPH and neurofeedback. I no longer diet, except that I eat as little sugar as possible. When I eat a lot of sugar (a scoop of ice cream or a big 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 covers for the individual case of sugar intolerance.

It is unlikely that children (and especially ADHD sufferers) will be able to seriously adhere to the requirements described when following a diet.

1.4.2. Salicylates (fine gold; refuted)

American Feingold postulated in the 1970s that salicylates and dyes can trigger ADHD
The theory regarding salicylates is considered outdated.
Feingold named several types of fruit and tomatoes as foods containing salicylates.138
Many elimination diets cite different fruits and tomatoes as symptom triggers.
It would be interesting to know if there is any work that has studied the effect of salicylates on healthy people.
For dyes, 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 extensively researched elimination diets for ADHD presented here, successfully demonstrated desensitization to identified food intolerances. 16 of 20 participants developed tolerance, compared to 4 of 20 from the placebo control group.139

2.2. Probiotic treatment can influence behavior

In an experiment in rats, probiotic treatment showed a reduction in depression symptoms. This was associated with changes in proinflammatory cytokines that moderate inflammation.140 Further, probiotic treatment decreased 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 13 years of age, while 17% in the placebo group received an ICD 10 diagnosis of ADHD or ASD.141

A metastudy found an effect of probiotic treatment on ADHD in only one of 7 studies. This study found a reduced risk of ADHD in children due to probiotic treatment of mothers during pregnancy and breastfeeding.142

2.3. Increased intestinal permeability in ADHD

A study of 40 ADHD sufferers and 41 nonafflicted found elevated zonulin levels in the ADHD sufferers, which at the same time correlated with hyperactivity,143 so there may be a higher association with ADHD-HI than with ADHD-I.

Zonulin is a 47 KD protein that regulates tight junctions in the intestinal wall. The intestinal mucosa secretes zonulin in response to specific stimuli. Zonulin binds to specific receptors on intestinal epithelial cells, which controls the opening of interepithelial channels by contraction of cytoskeletal proteins. Analysis of serum zonulin levels is simple and provides a reliable picture of intestinal permeability and indicates chronic inflammatory bowel diseases, such as;144

  • 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 METASTUDY

  11. Firth, Teasdale, Allott, Siskind, Marx, Cotter, Veronese, Schuch, Smith, Solmi, Carvalho, Vancampfort, Berk, Stubbs, Sarris (2019): The efficacy and safety of nutrient supplements in the treatment of mental disorders: a meta-review of meta-analyses of randomized controlled trials. World Psychiatry. 2019 Oct;18(3):308-324. doi: 10.1002/wps.20672. n = 10,951 METASTUDY

  12. Bozzatello, Rocca, Mantelli, Bellino (2019): Polyunsaturated Fatty Acids: What is Their Role in Treatment of Psychiatric Disorders? Int J Mol Sci. 2019 Oct 23;20(21). pii: E5257. doi: 10.3390/ijms20215257.

  13. Döpfner, Dose, Breuer, Heintz, Schiffhauer, Banaschewski (2019): Efficacy of Omega-3/Omega-6 Fatty Acids in Preschool Children at Risk of ADHD: A Randomized Placebo-Controlled Trial. J Atten Disord. 2019 Nov 2:1087054719883023. doi: 10.1177/1087054719883023. n = 40

  14. Lange (2020): Micronutrients and Diets in the Treatment of Attention-Deficit/Hyperactivity Disorder: Chances and Pitfalls. Front Psychiatry. 2020 Feb 26;11:102. doi: 10.3389/fpsyt.2020.00102. PMID: 32174856; PMCID: PMC7055526. REVIEW

  15. Grazioli, Crippa, Mauri, Piazza, Bacchetta, Salandi, Trabattoni, Agostoni, Molteni, Nobile (2019): Association Between Fatty Acids Profile and Cerebral Blood Flow: An Exploratory fNIRS Study on Children with and without ADHD. Nutrients. 2019 Oct 10;11(10). pii: E2414. doi: 10.3390/nu11102414.

  16. Scassellati, Bonvicini, Faraone, Gennarelli, (2012): Biomarkers and Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Meta-Analyses; JOURNAL OF THE AMERICAN ACADEMY OF CHILD & ADOLESCENT PSYCHIATRY VOLUME 51 NUMBER 10 OCTOBER 2012, Seite 1003, S. 1012 METASTUDY

  17. Yonezawa, Nonaka, Iwakura, Kusano, Funamoto, Kanchi, Yamaguchi, Kusumoto, Imamura, Ozawa (2018): Investigation into the plasma concentration of ω3 polyunsaturated fatty acids in Japanese attention-deficit hyperactivity disorder patients. J Neural Transm (Vienna). 2018 Jun 20. doi: 10.1007/s00702-018-1895-z.; n = 24

  18. Crippa, Tesei, Sangiorgio, Salandi, Trabattoni, Grazioli, Agostoni, Molteni, Nobile (2018): Behavioral and cognitive effects of docosahexaenoic acid in drug-naïve children with attention-deficit/hyperactivity disorder: a randomized, placebo-controlled clinical trial. Eur Child Adolesc Psychiatry. 2018 Sep 24. doi: 10.1007/s00787-018-1223-z.

  19. Mallick, Basak, Duttaroy (2019): Docosahexaenoic acid,22:6n-3: its roles in the structure and function of the brain. Int J Dev Neurosci. 2019 Oct 17. pii: S0736-5748(19)30214-X. doi: 10.1016/j.ijdevneu.2019.10.004.

  20. Julvez, Fernández-Barrés S1, Gignac, López-Vicente, Bustamante, Garcia-Esteban, Vioque, Llop, Ballester, Fernández-Somoano, Tardón, Vrijheid, Tonne, Ibarluzea, Irazabal, Sebastian-Galles, Burgaleta, Romaguera, Sunyer (2019): Maternal seafood consumption during pregnancy and child attention outcomes: a cohort study with gene effect modification by PUFA-related genes. Int J Epidemiol. 2019 Oct 2. pii: dyz197. doi: 10.1093/ije/dyz197.

  21. Johnson, Ostlund, Fransson, Kadesjö, Gillberg (2008): Omega-3/omega-6 fatty acids for attention deficit hyperactivity disorder: a randomized placebo-controlled trial in children and adolescents. J Atten Disord. 2009 Mar;12(5):394-401. doi: 10.1177/1087054708316261.

  22. Rodríguez, García, Areces, Fernández, García-Noriega, Domingo (2019): Supplementation with high-content docosahexaenoic acid triglyceride in attention-deficit hyperactivity disorder: a randomized double-blind placebo-controlled trial. Neuropsychiatr Dis Treat. 2019 May 8;15:1193-1209. doi: 10.2147/NDT.S206020. n = 66

  23. Buchhorn, Koenig, Jarczok, Eichholz, Willaschek, Thayer, Kaess (2017): A case series on the potential effect of omega-3-fatty acid supplementation on 24-h heart rate variability and its circadian variation in children with attention deficit (hyperactivity) disorder. Atten Defic Hyperact Disord. 2018 Jun;10(2):135-139. doi: 10.1007/s12402-017-0240-y.

  24. Buchhorn, Baumann, Willaschek (2019): Alleviation of arrhythmia burden in children with frequent idiopathic premature ventricular contractions by omega-3-fatty acid supplementation. Int J Cardiol. 2019 Sep 15;291:52-56. doi: 10.1016/j.ijcard.2019.05.054.

  25. Fuentes-Albero, Martínez-Martínez, Cauli (2019): Omega-3 Long-Chain Polyunsaturated Fatty Acids Intake in Children with Attention Deficit and Hyperactivity Disorder. Brain Sci. 2019 May 23;9(5). pii: E120. doi: 10.3390/brainsci9050120. n = 135

  26. Mohammadzadeh, Baghi, Yousefi, Yousefzamani (2019): On the effect of omega-3 supplementation with methylphenidate as an alternative therapy to reduce Attention Deficit Hyperactivity Disorder (ADHD) in children. Korean J Pediatr. 2019 May 20. doi: 10.3345/kjp.2018.06982. n = 66

  27. Wang, Yu, Fu, Yeh, Hsu, Yang, Yang, Huang, Wei, Chen, Chiang, Pan (2019): Dietary Profiles, Nutritional Biochemistry Status, and Attention-Deficit/Hyperactivity Disorder: Path Analysis for a Case-Control Study. J Clin Med. 2019 May 18;8(5). pii: E709. doi: 10.3390/jcm8050709. n = 432

  28. Veniaminova, Oplatchikova, Bettendorff, Kotenkova, Lysko, Vasilevskaya, Kalueff, Fedulova, Umriukhin, Lesch, Anthony, Strekalova (2019): Prefrontal cortex inflammation and liver pathologies accompany cognitive and motor deficits following Western diet consumption in non-obese female mice. Life Sci. 2019 Dec 13;241:117163. doi: 10.1016/j.lfs.2019.117163.

  29. Chen, Su (2013): Exposure to a maternal n-3 fatty acid-deficient diet during brain development provokes excessive hypothalamic-pituitary-adrenal axis responses to stress and behavioral indices of depression and anxiety in male rat offspring later in life. J Nutr Biochem. 2013 Jan;24(1):70-80. doi: 10.1016/j.jnutbio.2012.02.006.

  30. Chang, Su, Mondelli, Satyanarayanan, Yang, Chiang, Chen, Pariante (2019): High-dose eicosapentaenoic acid (EPA) improves attention and vigilance in children and adolescents with attention deficit hyperactivity disorder (ADHD) and low endogenous EPA levels. Transl Psychiatry. 2019 Nov 20;9(1):303. doi: 10.1038/s41398-019-0633-0.

  31. San Mauro Martin, Sanz Rojo, González Cosano, Conty de la Campa, Garicano Vilar, Blumenfeld Olivares (2019):Impulsiveness in children with attention-deficit/hyperactivity disorder after an 8-week intervention with the Mediterranean diet and/or omega-3 fatty acids: A randomised clinical trial. Article in English, Spanish - Neurologia. 2019 Dec 26. pii: S0213-4853(19)30132-X. doi: 10.1016/j.nrl.2019.09.007. n = 60

  32. de Theije, Bavelaar, Lopes da Silva, Korte, Olivier, Garssen, Kraneveld (2014): Food allergy and food-based therapies in neurodevelopmental disorders. Pediatr Allergy Immunol. 2014 May;25(3):218-26. doi: 10.1111/pai.12149.

  33. Niederhofer (2011): Association of Attention-Deficit/Hyperactivity Disorder and Celiac Disease: A Brief Report; Prim Care Companion CNS Disord. 2011; 13(3): PCC.10br01104; doi: 10.4088/PCC.10br01104; PMCID: PMC3184556, n = 67

  34. ähnlich: Okusaga, Yolken, Langenberg, Sleemi, Kelly, Vaswani, Giegling, Hartmann, Konte, Friedl, Mohyuddin, Groer, Rujescu, Postolache (2013): Elevated gliadin antibody levels in individuals with schizophrenia. World J Biol Psychiatry. 2013 Sep;14(7):509-15. doi: 10.3109/15622975.2012.747699.

  35. Lachance, McKenzie (2013): Biomarkers of gluten sensitivity in patients with non-affective psychosis: a meta-analysis. Schizophr Res. 2014 Feb;152(2-3):521-7. doi: 10.1016/j.schres.2013.12.001.

  36. Egger: Möglichkeiten von Diätbehandlungen bei hyperkinetischen Störungen, Seite 117 ff, in Steinhausen (Hrsg.) (2000): Hyperkinetische Störungen bei Kindern, Jugendlichen und Erwachsenen, 2. Aufl., Kohlhammer

  37. Marcus: Wirksamkeit und Durchführbarkeit von Diäten zur Beeinflussung expansiven Verhaltens im Kindesalter; S. 102 ff in Steinhausen, (Hrsg.) (2000): Hyperkinetische Störungen bei Kindern, Jugendlichen und Erwachsenen, 2. Aufl., Kohlhammer

  38. nach Deutschlandfunk, Diät gegen ADHS; Nahrungsumstellung hilft bei Aufmerksamkeitsstörung, Beitrag vom 06.04.2011

  39. Pelsser, Frankena, Toorman (2011): Effects of a restricted elimination diet on the behaviour of children with attention-deficit hyperactivity disorder (INCA study): a randomised controlled trial. Lancet 2011; 377: 494–503, n = 100

  40. Pelsser, Frankena, Toorman, Rodrigues Pereira (2017): Diet and ADHD, Reviewing the Evidence: A Systematic Review of Meta-Analyses of Double-Blind Placebo-Controlled Trials Evaluating the Efficacy of Diet Interventions on the Behavior of Children with ADHD. PLoS One. 2017 Jan 25;12(1):e0169277. doi: 10.1371/journal.pone.0169277. PMID: 28121994; PMCID: PMC5266211. METASTUDY

  41. Egger, Carter, Graham, Gumley, Soothill (1985): Controlled trial of oligoantigenic treatment in the hyperkinetic syndrome. Lancet 1985; 1: 540–555.

  42. Nigg, Lewis, Edinger, Falk (2012): Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives. J Am Acad Child Adolesc Psychiatry. 2012 Jan;51(1):86-97.e8. doi:10.1016/j.jaac.2011.10.015.

  43. Carter, Urbanowicz, Hemsley, Mantilla, Strobel, Graham, Taylor (1993): Effects of a few food diet in attention deficit disorder. Arch Dis Child 1993; 69: 564–568.

  44. Boris M, Mandel FS. Foods and additives are common causes of the attention deficit hyperactive disorder in children. Ann Allergy 1994; 72: 462–468.



  47. Pelsser LM, Frankena K, Toorman J et al. A randomised controlled trial into the effects of food on ADHD. Eur Child Adolesc Psychiatry 2009; 18: 12–19. n = 27

  48. Schulte-Körne, Deimel, Gutenbrunner, Hennighausen, Blank, Rieger, Remschmidt (1996): Effect of an oligo-antigen diet on the behavior of hyperkinetic children; (PMID:9459674); Zeitschrift fur Kinder- und Jugendpsychiatrie und Psychotherapie [01 Sep 1996, 24(3):176-183], n= 21

  49. Schmidt MH, Möcks P, Lay B et al. Does oligoantigenic diet influence hyperactive/conduct-disordered children—a controlled trial. Eur Child Adolesc Psychiatry 1997; 6: 88–95.

  50. Kaplan, McNicol, Conte, Moghadam (1989): Dietary Replacement in Preschool-Aged Hyperactive Boys; Pediatrics 1989;83;7

  51. Walz G, Blazynski N, Frey L, Schneider-Momm K, Clement HW, Rauh R, Schulz E, Biscaldi M, Clement C, Fleischhaker C (2022): Long-Term Effects of an Oligoantigenic Diet in Children with Attention-Deficit/Hyperactivity Disorder (ADHD) on Core Symptomatology. Nutrients. 2022 Dec 1;14(23):5111. doi: 10.3390/nu14235111. PMID: 36501141. n = 21

  52. Pinto S, Correia-de-Sá T, Sampaio-Maia B, Vasconcelos C, Moreira P, Ferreira-Gomes J (2022): Eating Patterns and Dietary Interventions in ADHD: A Narrative Review. Nutrients. 2022 Oct 16;14(20):4332. doi: 10.3390/nu14204332. PMID: 36297016; PMCID: PMC9608000. REVIEW

  53. NICE: Attention deficit hyperactivity disorder: diagnosis and management; Clinical guideline [CG72] Published date: September 2008 Last updated: February 2016

  54. Pelsser, Frankena, Toorman, Rodrigues Pereira (2020): Retrospective Outcome Monitoring of ADHD and Nutrition (ROMAN): The Effectiveness of the Few-Foods Diet in General Practice. Front Psychiatry. 2020 Mar 12;11:96. doi: 10.3389/fpsyt.2020.00096. PMID: 32226397; PMCID: PMC7081264.

  55. Egger, Carter, Graham, Gumley, Soothill (1985): Controlled trial of oligoantigenic treatment in the hyperkinetic syndrome. Lancet 1985; 1: 540–555., zitiert nach Egger, Möglichkeiten von Diätbehandlungen bei hyperkinetischen Störungen (2000) in: Steinhausen (Herausgeber): Hyperkinetische Störungen bei Kindern, Jugendlichen und Erwachsenen, Seite 122

  56. Egger, Carter, Graham, Gumley, Soothill (1985): Controlled trial of oligoantigenic treatment in the hyperkinetic syndrome. Lancet 1985; 1: 540–555., zitiert nach Egger, Möglichkeiten von Diätbehandlungen bei hyperkinetischen Störungen (2000) in: Steinhausen (Herausgeber): Hyperkinetische Störungen bei Kindern, Jugendlichen und Erwachsenen, Kohlhammer, Seite 122

  57. Egger, Carter, Graham, Gumley, Soothill (1985): Controlled trial of oligoantigenic treatment in the hyperkinetic syndrome. Lancet 1985; 1: 540–555., zitiert nach Egger, Möglichkeiten von Diätbehandlungen bei hyperkinetischen Störungen (2000) in: Steinhausen (Herausgeber): hyperkinetische Störungen bei Kindern, Jugendlichen und Erwachsenen, Kohlhammer, Seite 122

  58. Kaplan, McNicol, Conte, Moghadam (1989): Overall Nutrient Intake of Preschool Hyperactive and Normal Boys; 4Journal of Abnormal Child Psychology, Vol. 17, No. 2, 1989

  59. Endreffy, Bjørklund, Urbina, Chirumbolo, Doşa, Dicső (2020): High Levels of Glycosaminoglycans in the Urines of Children with Attention-Deficit/Hyperactivity Disorder (ADHD). J Mol Neurosci. 2020 Jul;70(7):1018-1025. doi: 10.1007/s12031-020-01496-w. PMID: 32128665. n = 74

  60. Kanasaki, Srivastava, Yang, Xu, Kudoh, Kitada, Ueki, Kim, Li, Takeda, Kanasaki, Koya (2017): Deficiency in catechol-o-methyltransferase is linked to a disruption of glucose homeostasis in mice. Scientific Reports Volume 7, Article number: 7927 2017

  61. Voltas N, Jardí C, Hernández-Martínez C, Arija V, Canals J (2022): Association between free sugars intake and early psychopathological problems. J Child Health Care. 2022 Oct 25:13674935221135106. doi: 10.1177/13674935221135106. PMID: 36282888. n = 86

  62. Yvonne Ulrich-Lai (Universität in Cincinnati) et al.: Beitrag auf dem Jahrestreffen der Gesellschaft für Neurowissenschaften, Washington, zitiert aus Bild der Wissenschaft, 16.11.2005

  63. Girardi, Shaywitz, Shaywitz, Marchione, Fleischman, Jones, Tamborlane (21995): Blunted catecholamine responses after glucose ingestion in children with attention deficit disorder. Pediatr Res. 1995 Oct;38(4):539-42.

  64. Wolff, Reimelt, Ehrlich, Hölling, Mogwitz, Roessner (2018): On the positive association between candy and fruit gum consumption and hyperactivity in children and adolescents with ADHD. Z Kinder Jugendpsychiatr Psychother. 2018 Aug 22:1-11. doi: 10.1024/1422-4917/a000609.

  65. Del-Ponte, Anselmi, Assunção, Tovo-Rodrigues, Munhoz, Matijasevich, Rohde, Santos (2018): Sugar consumption and attention-deficit/hyperactivity disorder (ADHD): A birth cohort study.; J Affect Disord. 2018 Sep 17;243:290-296. doi: 10.1016/j.jad.2018.09.051.

  66. Paglia, Friuli, Colombo, Paglia (2019): The effect of added sugars on children’s health outcomes: Obesity, Obstructive Sleep Apnea Syndrome (OSAS), Attention-Deficit/Hyperactivity Disorder (ADHD) and Chronic Diseases. Eur J Paediatr Dent. 2019 Jun;20(2):127-132. doi: 10.23804/ejpd.2019.20.02.09.

  67. Reichelt (ca. 2003): Die Gehirn-Darm-Achse bei neurologischen und psychiatrischen Störungen

  68. Hole, Lingjaerde, Møskrid, Bøsler, Saelid, Diderichsen, Jøsrgen, Ruud, Reichelt (1988): Attention Deficit Disorders: A Study of Peptide-Containing Urinary Complexes; Journal of Developmental & Behavioral Pediatrics 9: 205-212

  69. siehe auch Liu, Reichelt (2001): A serotonin uptake-stimulating tetra-peptide found in urines from ADHD children; World J Biol Psychiatry. 2001 Jul;2(3):144-8.

  70. Hercigonja Novkovic, Rudan, Pivac, Nedic, Muck-Seler (2009): Platelet Serotonin Concentration in Children with Attention-Deficit/Hyperactivity Disorder); Neuropsychobiology 2009;59:17–22; DOI:10.1159/000202825; n = 114

  71. Knivsberg (1997): Urine patterns, peptide levels and IgA/IgG antibodies to food proteins in children with dyslexia; Pediatric Rehabilitation Volume 1, 1997 – Issue 1; Pages 25-33.; die Erwiderung von Stanley konnten wir auch nicht als Abstracts einsehen; Stanley als Erwiderung auf Knivsberg (1997): Urine peptide patterns in dyslexia; Pediatric Rehabilitation, 1: 25-33, 1997.


  73. Persönlicher Bericht einer Systemischen Therapeutin über eine von ihr erstellte Studienarbeit

  74. EnzymAid Multi-Enzyme Complex Capsules

  75. Brudnak, Rimland, Kerry, Dailey, Taylor, Stayton, Waickman, Waickman, Pangborn, Buchholz (2002) Enzyme-based therapy for autism spectrum disorders – Is it worth another look? Medical Hypotheses58(5), 422±428. doi: 10.1054/mehy.2001.1513; n = 29

  76. und

  77. Recherche geneceutical in Google Scholar, 01.11.2017

  78. Kirkman EnZym-Complete/DPP-IV


  80. Coburn, Rose, Sady, Parker, Suslovic, Weisbrod, Kerzner, Streisand, Kahn (2019): Mental Health Disorders and Psychosocial Distress in Pediatric Celiac Disease. J Pediatr Gastroenterol Nutr. 2019 Dec 24. doi: 10.1097/MPG.0000000000002605.

  81. Hallert, Derefeldt (1982): Psychic disturbances in adult coeliac disease: I. clinical observations. Scand J Gastroenterol. 1982;17(1):17–19. n = 42

  82. Grimaldi, Gibson, Vulevic, Giallourou, Castro-Mejía, Hansen, Gibson, Nielsen, Costabile (2019): A prebiotic intervention study in children with autism spectrum disorders (ASDs). Microbiome. 2018 Aug 2;6(1):133. doi: 10.1186/s40168-018-0523-3. – Vorsicht – Untersuchung eines Markenprodukts

  83. Reddel, Putignani, Del Chierico (2019): The Impact of Low-FODMAPs, Gluten-Free, and Ketogenic Diets on Gut Microbiota Modulation in Pathological Conditions. Nutrients. 2019 Feb 12;11(2). pii: E373. doi: 10.3390/nu11020373.

  84. Kanarek (2011): Artificial food dyes and attention deficit hyperactivity disorder. Nutr Rev. 2011 Jul;69(7):385-91. doi: 10.1111/j.1753-4887.2011.00385.x. PMID: 21729092.


  86. Nigg, Lewis, Edinger, Falk (2012): Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives. J Am Acad Child Adolesc Psychiatry. 2012 Jan;51(1):86-97.e8. doi: 10.1016/j.jaac.2011.10.015. METASTUDY

  87. Nigg, Holton (2014): Restriction and elimination diets in ADHD treatment. Child Adolesc Psychiatr Clin N Am. 2014 Oct;23(4):937-53. doi: 10.1016/j.chc.2014.05.010. PMID: 25220094; PMCID: PMC4322780. REVIEW

  88. Schab, Trinh (2004): Do artificial food colors promote hyperactivity in children with hyperactive syndromes? A meta-analysis of double-blind placebo-controlled trials; J Dev Behav Pediatr 2004;25:423–434.

  89. Shrestha, Lautenschleger, Soares (2020): Non-pharmacologic management of attention-deficit/hyperactivity disorder in children and adolescents: a review. Transl Pediatr. 2020 Feb;9(Suppl 1):S114-S124. doi: 10.21037/tp.2019.10.01. PMID: 32206589; PMCID: PMC7082245. REVIEW

  90. Rambler RM, Rinehart E, Boehmler W, Gait P, Moore J, Schlenker M, Kashyap R (2022): A Review of the Association of Blue Food Coloring With Attention Deficit Hyperactivity Disorder Symptoms in Children. Cureus. 2022 Sep 16;14(9):e29241. doi: 10.7759/cureus.29241. PMID: 36262950; PMCID: PMC9573786.

  91. Kirkland, Langan, Holton (2020): Artificial food coloring affects EEG power and ADHD symptoms in college students with ADHD: a pilot study. Nutr Neurosci. 2020 Mar 1:1-10. doi: 10.1080/1028415X.2020.1730614. PMID: 32116139. n = 29

  92. Bakthavachalu, Kannan, Qoronfleh (2020): Food Color and Autism: A Meta-Analysis. Adv Neurobiol. 2020;24:481-504. doi: 10.1007/978-3-030-30402-7_15. PMID: 32006369.

  93. Bateman, Warner, Hutchinson, Dean, Rowlandson, Gant, Grundy, Fitzgerald, Stevenson (2004): The effects of a double blind, placebo controlled, artificial food colourings and benzoate preservative challenge on hyperactivity in a general population sample of preschool children. Arch Dis Child 2004; 89: 506–511.

  94. McCann, Barrett, Cooper, Crumpler, Dalen, Grimshaw, Kitchin, Lok, Porteous, Prince, Sonuga-Barke, Warner, Stevenson (2007): Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial. Lancet 2007; 370: 1560–1567., n = 267

  95. Scientific Opinion of the Panel on Food Additives, Flavourings, Processing Aids and Food Contact Materials (AFC) on a request from the Commission on the results of the study by McCann et al. (2007) on the effect of some colours and sodium benzoate on children’s behaviour. The EFSA Journal (200x) 660, 1-53.

  96. Hu, Fan, Hu (2015): [Effect of sodium nitrite on phosphorylation of cytoskeletal proteins and spatial learning and memory in rats].[Article in Chinese] Sheng Li Xue Bao. 2015 Oct 25;67(5):479-86.

  97. Biradar, Joshi, Tarak (2013): Cerebroprotective effect of isolated harmine alkaloids extracts of seeds of Peganum harmala L. on sodium nitrite-induced hypoxia and ethanol-induced neurodegeneration in young mice. Pak J Biol Sci. 2013 Dec 1;16(23):1687-97.

  98. Chen, Huang, Zhao (2001): [Clinical and experimental study on treatment of childhood hyperkinetic syndrome with yizhidan]. [Article in Chinese]. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2001 Jan;21(1):19-21.

  99. Wang, Li, Li (1995): [Clinical and experimental studies on tiaoshen liquor for infantile hyperkinetic syndrome].[Article in Chinese]; Zhongguo Zhong Xi Yi Jie He Za Zhi. 1995 Jun;15(6):337-40.

  100. Martinez, Jensen, Vasquez, Lacob, McGaugh, Purdy (1979): Acquisition deficits induced by sodium nitrite in rats and mice. Psychopharmacology (Berl). 1979 Feb 28;60(3):221-8.

  101. Abu-Elfotuh K, Abdel-Sattar SA, Abbas AN, Mahran YF, Alshanwani AR, Hamdan AME, Atwa AM, Reda E, Ahmed YM, Zaghlool SS, El-Din MN (2022): The protective effect of thymoquinone or/and thymol against monosodium glutamate-induced attention-deficit/hyperactivity disorder (ADHD)-like behavior in rats: Modulation of Nrf2/HO-1, TLR4/NF-κB/NLRP3/caspase-1 and Wnt/β-Catenin signaling pathways in rat model. Biomed Pharmacother. 2022 Nov;155:113799. doi: 10.1016/j.biopha.2022.113799. PMID: 36271575.

  102. Rothenberger in Steinhausen, Rothenberger, Döpfner (2010): Handbuch ADHS, Kohlhammer, Seite 188

  103. Pelsser, Frankena, Toorman, Savelkoul, Pereira, Buitelaar (2009): A randomised controlled trial into the effects of food on ADHD. Eur Child Adolesc Psychiatry. 2009;18(1):12-19. doi:10.1007/s00787-008-0695-7, n = 27

  104. Ugur, Uneri, Goker, Sekmen, Aydemir, Solmaz (2018): The assessment of serum lipid profiles of children with attention deficit hyperactivity disorder. .Psychiatry Res. 2018 Apr 7;264:231-235. doi: 10.1016/j.psychres.2018.04.006. n = 176

  105. Avcil (2018): Association between altered lipid profiles and attention deficit hyperactivity disorder in boys, Nordic Journal of Psychiatry, 72:5, 361-366, DOI: 10.1080/08039488.2018.1465591

  106. Pinho, Wang, Becker, Rothenberger, Outeiro, Herrmann-Lingen, Meyer (2018): Attention-deficit/hyperactivity disorder is associated with reduced levels of serum low-density lipoprotein cholesterol in adolescents. Data from the population-based German KiGGS study., World J Biol Psychiatry. 2018 Jan 11:1-9. doi: 10.1080/15622975.2017.1417636. n = 6898

  107. McIntyre, Alsuwaidan, Soczynska, Szpindel, Bilkey, Almagor, Woldeyohannes, Powell, Cha, Gallaugher, Kennedy (2013): The effect of lisdexamfetamine dimesylate on body weight, metabolic parameters, and attention deficit hyperactivity disorder symptomatology in adults with bipolar I/II disorder. Hum Psychopharmacol. 2013 Sep;28(5):421-7. doi: 10.1002/hup.2325. n = 45

  108. Yamamoto, Okuzaki, Yamanishi, Xu, Watanabe, Yoshid, Yamashita, Goto, Nishiguchi, Shimada, Nojima, Yasunaga, Okamura, Matsunaga, Yamanishi (2013): Genetic analysis of genes causing hypertension and stroke in spontaneously hypertensive rats. Int J Mol Med. 2013 May;31(5):1057-65. doi: 10.3892/ijmm.2013.1304.

  109. Irmisch, Thom, Reis, Hässler, Weirich (2011): Modified magnesium and lipoproteins in children with attention deficit hyperactivity disorder (ADHD). World J Biol Psychiatry. 2011 Sep;12 Suppl 1:63-5. doi: 10.3109/15622975.2011.600292. n = 20

  110. Charach, Kaysar, Grosskopf, Rabinovich, Weintraub (2009): Methylphenidate has positive hypocholesterolemic and hypotriglyceridemic effects: new data. J Clin Pharmacol. 2009 Jul;49(7):848-51. doi: 10.1177/0091270009336736. n = 42

  111. Irmisch, Richter, Thome, Sheldrick, Wandschneider (2013): Altered serum mono- and polyunsaturated fatty acid levels in adults with ADHD. Atten Defic Hyperact Disord. 2013 Sep;5(3):303-11. doi: 10.1007/s12402-013-0107-9.

  112. Faraco, Brea, Garcia-Bonilla, Wang, Racchumi, Chang, Buendia, Santisteban, Segarra, Koizumi, Sugiyama, Murphy, Voss, Anrather, Iadecola (2018): Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response; Nature Neuroscience (2018); doi:10.1038/s41593-017-0059-z

  113. Steinhausen, Rothenberger, Döpfner (2010): Handbuch ADHS, Seite 76

  114. Ebermann, Elmadfa (2008): Lehrbuch Lebensmittelchemie und Ernährung; Springer-Verlag, 08.09.2008 – 739 Seiten, Seite 500

  115. Thümen, Behnecke, Qadri, Bäuml, Thümen, Behnecke, Qadri, Bäuml, Moser (2002):. N-methyl-norsalsolinol, a putative dopaminergic neurotoxin, passes through the blood-brain barrier in vivo. Neuroreport. 2002 Jan 21;13(1):25-8. doi: 10.1097/00001756-200201210-00010. PMID: 11924888.

  116. Meiser, Weindl, Hiller (2013): Complexity of dopamine metabolism. Cell Commun Signal. 2013 May 17;11(1):34. doi: 10.1186/1478-811X-11-34. PMID: 23683503; PMCID: PMC3693914. REVIEW

  117. Napolitano, Manini, d’Ischia (2011): Oxidation chemistry of catecholamines and neuronal degeneration: an update. Curr Med Chem. 2011;18(12):1832-45. doi: 10.2174/092986711795496863. PMID: 21466469.

  118. Kovács, D’Agostino, Diamond, Kindy, Rogers, Ari (2019): Therapeutic Potential of Exogenous Ketone Supplement Induced Ketosis in the Treatment of Psychiatric Disorders: Review of Current Literature. Front Psychiatry. 2019 May 23;10:363. doi: 10.3389/fpsyt.2019.00363. eCollection 2019. REVIEW

  119. Paoli, Rubini, Volek, Grimaldi (2013): Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets; Eur J Clin Nutr. 2013 Aug; 67(8): 789–796; doi: 10.1038/ejcn.2013.116; PMCID: PMC3826507 REVIEW

  120. Millichap (2011): Attention Deficit Hyperactivity Disorder Handbook. A Physician’s Guide to ADHD, Seite 150

  121. Campbell, Campbell (2019): Ketosis and bipolar disorder: controlled analytic study of online reports. BJPsych Open. 2019 Jul 4;5(4):e58. doi: 10.1192/bjo.2019.49. 141 Fundstellen mit n = 274 Probanden

  122. Murphy, Burnham (2006): The ketogenic diet causes a reversible decrease in activity level in Long-Evans rats. Exp Neurol. 2006 Sep;201(1):84-9.

  123. Packer, Law, Davies, Zanghi, Pan, Volk (2016): Effects of a ketogenic diet on ADHD-like behavior in dogs with idiopathic epilepsy. Epilepsy Behav. 2016 Feb;55:62-8. doi: 10.1016/j.yebeh.2015.11.014.

  124. House, Mendez, Maguire, Gonzalez-Nahm, Huang, Daniels, Murphy, Fuemmeler, Wright, Hoyo (2018): Periconceptional Maternal Mediterranean Diet Is Associated With Favorable Offspring Behaviors and Altered CpG Methylation of Imprinted Genes. Front Cell Dev Biol. 2018 Sep 7;6:107. doi: 10.3389/fcell.2018.00107. eCollection 2018. n = 325

  125. San Mauro Martin, Sanz Rojo, González Cosano, Conty de la Campa, Garicano Vilar, Blumenfeld Olivares (2019):Impulsiveness in children with attention-deficit/hyperactivity disorder after an 8-week intervention with the Mediterranean diet and/or omega-3 fatty acids: A randomised clinical trial. Article in English, Spanish Neurologia. 2019 Dec 26. pii: S0213-4853(19)30132-X. doi: 10.1016/j.nrl.2019.09.007. n = 60

  126. Baldauf (2004): Opiatmodulation der Monoamine im Vorderhirn des Haushuhnkükens (Gallus gallus domesticus): Eine mögliche Rolle in der emotionalen Regulation? Dissertation. Seite 7

  127. Eliot (2001): Was geht da drinnen vor? Die Gehirnentwicklung in den ersten 5 Lebensjahren. Seite 261

  128. Amiche, Sagan, Mor, Delfour, Nicolas (1988): Characterisation of the receptor binding profile of [3H]-dermorphine in the rat brain. Int J Pept Protein Res. 32: 506-511

  129. Erspamer, Melchiorri, Falconieri-Espamer, Negri, Corsi, Severini, Barra, Simmaco, Kreil (1989): Deltorphine: A familiy of naturally occuring peptides with high affinity and selectivity for δ opioid binding sites. Proc Natl Acad Sci. USA 86: 5188-5192

  130. Snyder, Pasternak (2003): Historical review: Opioid receptors. TRENDS in Pharmacol Sci. 24: 198-205 REVIEW

  131. Nahas, Sutin, Harvey, Agurell (1999): Marihuana and Medicine. Springer.

  132. Strand (1999): Endogenous Opiate Neuropeptides: Endorphins, Enkephalins, Dynorphins, TyrMIF-1, and Nociceptin, in: Neuropeptides, MIT Press Cambridge

  133. Choudhary, Lee (2017): Neurophysiological symptoms and aspartame: What is the connection? Nutr Neurosci. 2017 Feb 15:1-11. doi: 10.1080/1028415X.2017.1288340.

  134. Kim, Nam, Kim, Lee, Shim, Lee (2012): Relationship between attention-deficit/hyperactivity disorder and trans fatty acids intake in female adolescents. Acta Paediatr. 2012 Sep;101(9):e431-3. doi: 10.1111/j.1651-2227.2012.02726.x.


  136. Damals: Hafer (1986): Die heimliche Droge – Nahrungsphosphat, Kriminalistik Verlag, 4. Auflage 1986, mit umfangreicher Diätanleitung, sowie Hafer (1978): Nahrungsphosphat als Ursache für Verhaltensstörungen und Jugendkriminalität. Kriminalistik Verlag, Heidelberg

  137. Walther (1982): Nahrungsphosphat und Verhaltensstörungen im Kindesalter – Ergebnisse einer kontrollierten Verhaltensstudie, S. 111 ff.; Doppelblindstudie, n = 35; in: Steinhausen: Das konzentrationsgestörte und hyperaktive Kind, Kohlhammer

  138. 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

  139. Egger, Stolla, McEwen (1992): Controlled trial of hyposensitisation in children with food-induced hyperkinetic syndrome, The Lancet, Volume 339, Issue 8802, 1992, Pages 1150-1153, ISSN 0140-6736,

  140. Abildgaard, Elfving, Hokland, Wegener, Lund (2017): Probiotic treatment reduces depressive-like behaviour in rats independently of diet. Psychoneuroendocrinology. 2017 May;79:40-48. doi: 10.1016/j.psyneuen.2017.02.014.

  141. Pärtty, Kalliomäki, Wacklin, Salminen, Isolauri (2015): A possible link between early probiotic intervention and the risk of neuropsychiatric disorders later in childhood: a randomized trial. Pediatr Res. 2015 Jun;77(6):823-8. doi: 10.1038/pr.2015.51.

  142. Rianda, Agustina, Setiawan, Manikam (2019): Effect of probiotic supplementation on cognitive function in children and adolescents: a systematic review of randomised trials. Benef Microbes. 2019 Dec 9;10(8):873-882. doi: 10.3920/BM2019.0068. PMID: 31965841. REVIEW

  143. Özyurt, Öztürk, Appak, Arslan, Baran, Karakoyun, Tufan, Pekcanlar (2018): Increased zonulin is associated with hyperactivity and social dysfunctions in children with attention deficit hyperactivity disorder. Compr Psychiatry. 2018 Nov;87:138-142. doi: 10.1016/j.comppsych.2018.10.006. n = 81


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