Feed your brain, treat ADHD naturally.
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental and behavioral disorder that is characterized by poor concentration and hyperactivity (1).
The diagnosis for ADHD uses a subjective criteria from the Diagnostic and Statistical Manual of Mental Disorders (DSM). It includes symptoms on perceived difficulties in the areas of attention, hyperactivity, and impulsivity.
Aside from the subjective DSM criteria, the cutoff between normality and abnormality is to a large extent based on performance of a child in a particular family, school, and community environment such as cognitive and behavioral ratings from teachers and parents.
Thus, understanding this phenomenon can save on healthcare costs and provide safe and life-long treatment for ADHD.
The mechanisms behind ADHD
Up to this date, there is no single universally accepted explanation for the pathophysiology of ADHD. Studies hypothesize that alterations in the brain, such as brain volume, reduced functional capacities of certain central nervous system, and abnormalities in the brain neurotransmitters (messengers) dopamine and norepinephrine, are associated with the development of ADHD(2).
For example, a meta-analysis by Valera(3) showed decreased volumes in various parts of the brain which are involved in concentration, impulse control, inhibition, and motor activity.
Similarly, when brain scans of twins were compared(4), twins with ADHD were found to have abnormally smaller center of the brain (caudate) compared to the unaffected twins.
On the other hand, a study by Zang(5) found decreased activity in the prefrontal cortex, and this is the brain part that is responsible for inhibiting irrelevant motor actions. This may explain distractibility and motor hyperactivity found in ADHD(2).
Finally, Bush(6) found hypoactivity in the part of the brain that plays a central role in focus and attention.
Another hypothesis for ADHD pathophysiology is disturbances in neurotransmitter systems such as catecholamine, dopamine and norepinephrine. Genetic factor may play a role, as supported by evidences showing genetic variations of genes DRD4, DRD5, DAT, DBH,5-HTT, HTR1B, and SNAP-25, which are involved in regulation of neurotransmitters that are associated with increased rates of ADHD(2).
Due to these mechanisms, the most common medication therapy for ADHD are stimulants, such as methylphenidate (Ritalin) and amphetamine, which block the reuptake of both dopamine and norepinephrine and inhibit monoamine oxidase, an enzyme that plays a role in metabolizing catecholamines(2). The amphetamines also facilitate the release of dopamine and norepinephrine.
Profits in ADHD
According to the Centers for Disease Control and Prevention, 15 % of high school-age children was diagnosed with ADHD in 2012, and that the number of children on medication for the disorder had soared from 600,000 in 1990 to 3.5 million in 2012, making $9 billion in profits that is more than five times the $1.7 billion a decade before(8).
This led to a controversy on why the medical industry authorized the diagnosis for ADHD and critics suspect that their real motive is to promote overreliance to pharmaceutical drugs for its treatment (8).
In the attempt to provide evidences on alternative approaches for ADHD, scientists studied the effects of diet modifications to improve symptoms in children with ADHD (9). This is supported by studies showing that dietary patterns of children with ADHD consists of mostly junk foods that are low in vitamins and minerals and essential fatty acids needed for normal brain function (10).
The following are dietary approaches to correct nutrient imbalance and intolerance in ADHD:
1. Polyunsaturated fatty acid supplements (pufa) diets
It is well established that proper metabolism of certain long-chain polyunsaturated fatty acids (LC-PUFAs), particularly arachidonic acid (AA) and docosahexaenoic acid (DHA) are critical for normal brain development. Low levels of PUFA were reported in ADHD children, which is believed to be due to genetically disturbances in fatty acid metabolism. Millichap(12) showed that supplementation of 300 to 600mg/day of omega-3 and 30 to 60mg/day of omega- 6 fatty acids for 2 or 3 months showed improved school grades and lessening of symptoms of ADHD, without occurrence of adverse effects. Moreover, Joshi(13) demonstrated that supplementation of flaxseed oil (n-3) significantly improved hyperactivity symptoms of ADHD.
2. Additive and salicylate-free (Feingold) diet
In 1973 Feingold published his study, claiming that 50% of treated children improved after elimination of all food colorings and naturally occurring salicylates (including fruits). This is still quite popular but focuses mainly on the elimination of artificial colors, flavors, sweeteners, and certain preservatives, with most natural salicylates eventually added back to the diet(14).
Meta analysis of previous studies shows inconsistent results with elimination of synthetic food dyes and preservatives(16). Two previously described studies from the United Kingdom, researchers found that the adverse effects of food dyes on symptoms of ADHD were moderated partly by histamine degradation gene (HNMT) polymorphisms. Further indirect support of this as a plausible idea comes from research demonstrating that:
1) there are histamine receptors in the brain
2) food additives can trigger histamine release
3) HNMT polymorphisms can impair histamine clearance.
Additionally, drugs used in the treatment of ADHD, such as methylphenidate and atomoxetine, affect the histamine system(15).
3. Oligoantigenic (hypoallergenic/elimination) diet
An oligoantigenic diet eliminates most known sensitizing food antigens or allergens which includes cow’s milk, cheese, wheat cereals, egg, chocolate, nuts, and citrus fruits(14).
The effectiveness of the diet is demonstrated by a larger randomized controlled trial in an unselected group of 100 children with ADHD in Netherlands. This study consisted of an open-label phase (phase 1; 5 weeks of a restricted elimination diet or healthy control diet) followed by a double-blind crossover, challenge phase (phase 2). They found that the lowered immunoglobulin (Ig) G levels achieved from elimination diet resulted to an increase (improvement) of 20.8 points on the ADHD rating scale(12).
Also, a case report by Ritz et al(18) on a 5 year old child showed that feeding with an elimination diet accompanied with nutrition supplements resulted to reduction in IgG food antibody responses that is accompanied by a drastic improvement in the patient’s behavior.
4. Ketogenic diet
In 1921, the ketogenic diet which is a high fat and low carbohydrate diet was introduced as a diet treatment for Epilepsy(14).
Mutual interconnections exists between ADHD and epilepsy which include co-morbidity between both diseases; ADHD as a risk factor for epilepsy; and epilepsy as a risk factor for ADHD have been repeatedly described.
It is reported that up to 28–39% of epileptic patients have hyperactivity impulsivity, while up to 30% of ADHD children reveal subclinical epileptiform EEG activity. Moreover, up to 80% of ADHD children with subclinical epileptiform EEG abnormalities (frontal theta frequency excess and interhemispheric hyper-coherence) ineffectively treated with Ritalin are successfully treated with antiepileptic drugs. Thus, it is speculated that this diet would work for ADHD.
5. Mega vitamins
a. Vitamin B6
Neurotransmitters such as serotonin, dopamine, norepinephrine, and epinephrine are chemical messengers in the brain that affects concentration, behavior, and mood.
A series of chemical reactions produces neurotransmitters, one of which uses the amino acid tryptophan as a raw material. However, tryptophan has to be metabolized through a pathway that involves a series of steps most of which will not take place without enough vitamin B6 for the reason that B6 comprises the co-enzyme called Pyridoxal phoshate (PLP). Co-enzymes are the "assistants or helpers" that assists the reactions. And as you can see in this diagram, PLP is mostly involved in assisting reactions to convert tryptophan to its metabolites.
The kynurenine pathway decribes the breakdown of the amino acid Tryptophan into by-products. Dolina et al(17) compared the levels of kynurenine pathway by-products (metabolites) between healthy subjects(controls), untreated ADHD subjects, and ADHD subjects treated with ritalin. The data obtained have shown that tryptophan degradation by PLP- dependent reactions in the Kynurenine pathway is completely disordered in untreated ADHD patients and to some extent corrected in patients treated with Ritalin.
As you can see in the diagram, untreated ADHD patients have high levels of tryptophan, indicating it is not metabolized (broken down). Consequently, the by-products of tryptophan degradation by PLP-depended reactions such as indole, kynurenic acid, anthranilic acid are decreased. While the toxic Hydroxy-kynurenin is increased because tryptophan has nowhere to go but in that pathway. The sharp increase in the hydroxy-kynurenin results to toxic effect in the brain and is one of the major factors why b6 deficiency leads to ADHD.
Since vitamin B6 disorders were found to be the root cause of biochemical disturbances inherent in ADHD, the authors suggests multi-year pyridoxine treatment of up to 100 mg /day in children of 4–8 years; 200 mg/day in adolescents as a replacement therapy for ADHD. Their trial found that it takes several weeks of such treatment to normalize the pattern of behavior in ADHD. However, 1 to 2 months holding of treatment restores ADHD symptoms.
b. Zinc
Low zinc levels were reported in serum, red cells, hair, urine, and nails of children affected with ADHD and two placebo-controlled trials with zinc supplementation report significant benefit. In addition, zinc supplements also enhanced the benefit from d-amphetamine, a drug that has a similar effect with Ritalin in keeping sufficient levels of norepinephrine and dopamine in the brain.
A number of mechanisms exist behind zinc's effect on ADHD. First, it is a cofactor for metabolism of neurotransmitters and fatty acids and also regulates dopamine metabolism involved in ADHD (12). Also, as seen in the diagram, B6 and zinc are essential for enzymes involved in neurotransmitter metabolism. While B6 is the co-factor in PLP-dependent reactions, Zinc plays an equally important role because the molecules of enzymes in neurotransmitter reactions are binded by zinc fingers that hold them together.
c. Iron
Behavioral and mood symptoms of Iron deficiency are similar to ADHD. This is supported by studies showing that children with ADHD have significantly lower serum ferritin levels than in those not diagnosed with ADHD (19).
Also, similar to B6, iron is also a co-factor or "helpers" of enzymes that converts the amino acid Tyrosine into neurotransmitter dopamine, which is a chemical messenger to the brain. Low levels of dopamine can affect mood and behavior.
To test whether iron supplementation will work on symptoms of ADHD, A randomized controlled trial by Konofal(19) randomized children with ADHD to receive placebo or iron pills for 12 weeks. They found that iron supplementation (80 mg/day) appeared to improve ADHD symptoms only in children with low serum ferritin levels.
Take home message:
Based on the findings, it appears that the etiology of ADHD are food sensitivities and allergies, as well as nutritional imbalances that can be corrected by dietary approaches. Nutritional therapies are safe for long-term use and do not pose serious side effects. Thus, by properly assessing the patient for food allergies and intolerance, and using accurate measurements of nutritional biomarkers, people with ADHD can benefit from restricting food allergens in combination with appropriate nutritional supplements rather than relying on life-long prescription medications, which is clearly a profit-making business in the medical industry.
References:
1. Carolina, N., & Carolina, S. (2011). 21 Attention Deficit Hyperactivity Disorder, 299–306. doi:10.1016/B978-1-4377-3463-8.00021-7
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3. Valera EM, Faraone SV, Murray KE, et al. Meta-analysis of structural imaging findings in attention-deficit/hyperactivity disorder. Biol Psychiatry 2006
4. Castellanos, F. X., Sharp, W. S., Gottesman, R. F., Greenstein, D. K., Giedd, J. N., & Rapoport, J. L. (2003). Anatomic brain abnormalities in monozygotic twins discordant for attention deficit hyperactivity disorder. The American Journal of Psychiatry, 160(9), 1693–6. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/
5. Zang, Y.-F., He, Y., Zhu, C.-Z., Cao, Q.-J., Sui, M.-Q., Liang, M., … Wang, Y.-F. (2007). Altered baseline brain activity in children with ADHD revealed by resting-state functional MRI. Brain & Development, 29(2), 83–91. doi:10.1016/j.braindev.2006.07.002
6. Bush, G., Frazier, J. a, Rauch, S. L., Seidman, L. J., Whalen, P. J., Jenike, M. a, … Biederman, J. (1999). Anterior cingulate cortex dysfunction in attention-deficit/hyperactivity disorder revealed by fMRI and the Counting Stroop. Biological Psychiatry, 45(12), 1542–52. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10376114
7. National Collaborating Centre for Mental Health. The NICE guideline on diagnosis and management of ADHD in children, young people and adults – National Clinical Practice Guideline Number 72. The British Psychological Society and The Royal College of Psychiatrists, 2009.
8. Shwarz, A. (2013, December 14) The Selling of Attention Deficit Disorder. The New York Times. Retrieved from http://www.nytimes.com/2013/12/15/health/the-selling-of-attention-deficit-disorder.html?ref=todayspaper&_r=1&smid=fb-share&
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10. Wiles, N. J., Northstone, K., Emmett, P., & Lewis, G. (2009). Europe PMC Funders Group “ Junk food ” diet and childhood behavioural problems : Results from the ALSPAC cohort, 63(4), 491–498. doi:10.1038/sj.ejcn.1602967.
11. Hurt, E. a., & Arnold, L. E. (2014). An Integrated Dietary/Nutritional Approach to Attention-Deficit/Hyperactivity Disorder. Child and Adolescent Psychiatric Clinics of North America. doi:10.1016/j.chc.2014.06.002
12. Millichap, J. G., & Yee, M. M. (2012). The Diet Factor in Attention-De fi cit / Hyperactivity Disorder abstract. doi:10.1542/peds.2011-2199
13. Joshi, K., Lad, S., Kale, M., Patwardhan, B., Mahadik, S. P., Patni, B., … Pandit, A. (2006). Supplementation with flax oil and vitamin C improves the outcome of Attention Deficit Hyperactivity Disorder (ADHD). Prostaglandins, Leukotrienes, and Essential Fatty Acids, 74(1), 17–21. doi:10.1016/j.plefa.2005.10.001
14. Newmark, S. C. (2009). Nutritional intervention in ADHD. Explore (New York, N.Y.), 5(3), 171–4. doi:10.1016/j.explore.2009.03.006
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16. Nigg, J. T., Lewis, K., Edinger, T., & Falk, M. (2012). Meta-analysis of attention-deficit/hyperactivity disorder or attention-deficit/hyperactivity disorder symptoms, restriction diet, and synthetic food color additives. Journal of the American Academy of Child and Adolescent Psychiatry, 51(1), 86–97.e8. doi:10.1016/j.jaac.2011.10.015
17. Dolina, S., Margalit, D., Malitsky, S., & Rabinkov, a. (2014). Attention-deficit hyperactivity disorder (ADHD) as a pyridoxine-dependent condition: urinary diagnostic biomarkers. Medical Hypotheses, 82(1), 111–6. doi:10.1016/j.mehy.2013.11.018
18. Ritz, B.W., Lord, R.S. (2005). Case study : the effectiveness of a dietary sensitivity in adhd, 11(3), 72–75.
19. Konofal, E., Lecendreux, M., Deron, J., Marchand, M., Cortese, S., Zaïm, M., … Arnulf, I. (2008). Effects of iron supplementation on attention deficit hyperactivity disorder in children. Pediatric Neurology, 38(1), 20–6. doi:10.1016/j.pediatrneurol.2007.08.014
