Title: Diet and ADHD
Key words: ADD, frontal lobe, dopamine, catecholamines, gut permeability, elimination diets, zinc deficiency, autism, casein, gluten, gut flora, opioids, adrenal function, omega-3
Date: Jan 2001
Category: 13. Specific conditions
Author: Kate Neil (NS3)
Diet and ADHD
Recent research supports the long-held belief that ADHD has an underlying neurological basis1. This biologically based behavioural disability has a pervasive negative impact on a wide-range of adaptive functioning2. Frontal lobe functions are executive in nature and are involved in developing plans, organising resources, controlling motor behaviour and inhibiting attentional focus on distractor or irrelevant stimuli2.
Support for frontal lobe involvement comes from positron emission tomographic (PET) scan studies which finds reduced utilisation of glucose in the brain, particularly the frontal area, and specifically the posterior-medial orbital areas1,3. Researchers have found, through regional cerebral blood flow comparisons of dysphasic, ADD, and control children, that ADD children show decreased metabolic activity in the frontal lobes and basal ganglia, with increased metabolic activity in the primary sensory and sensorimotor regions1.
Recent research using advanced neuroimaging morphological procedures show that children do not have the normal right-greater-than left asymmetry of the caudate1,2. Consistent with this finding, computerised quantitative electronencephalographic analysis shows significantly greater slow-wave (theta) activity and significantly less fast-wave (beta) activity predominantly in the frontal regions in boys1,2. This would indicate possible decreased cortical arousal in those areas of the brain frequently associated with executive control and language1.
More recent studies have shown that the dopamine transporter is defective4. This might provide a genetic basis for ADD as the dopamine transporter gene has now been identified3. Researchers have generally accepted that the catecholamines (dopamine, norepinephrine) are implicated in ADD and appear to affect a wide variety of behaviours, including attention, inhibition and response of the motor system, and motivation2.*
ADD/ADHD may have several different causes5. Twin studies/adopted children support this position5. Other suspected causes include: complications in pregnancy/birth, illness, lead poisoning, injury, prenatal drug exposure5 nutrient deficiencies, faulty enzyme systems, endocrine dysfunction, increased permeability of the gut and blood/brain barriers6. Reactions to food colourings/preservatives are implicated, as is food allergy7.
Atopic children with ADHD respond well to elimination diets7,8,9, though consideration should be given to the disrupting effects of long-term exclusion on family life6,7,8. As allergy is not always life-long, permanent removal is not always necessary8. Double-blind controlled provocation studies can help confirm the diagnosis of food intolerance8. Exposure to food antigens may result in mucosal oedema, poor digestive and absorptive functioning leading to numerous nutritional insufficiencies10 including zinc. It would seem prudent for the family to rotate foods and adopt a low-sugar diet, high in natural, fresh, unprocessed foods without food additives and to provide suitable alternatives to offending foods7.
Reducing/avoiding salicylates and additives can be helpful as they are weak inhibitors of the conversion of EFAs to prostaglandins7. This lends support for Feigngold’s approach. Studies show that artificial food colours reduce digestive enzyme activity11.
Dietary strategies similar to autism may help, as parallels exist between these conditions7. Opioids from incomplete breakdown of proteins (casein and gluten particularly) may profoundly affect the central nervous system CNS due to increased permeability of the gut and blood/brain barrier7. Diets that support a healthy gut flora should minimise the uptake of opioids across the intestinal membrane12. Many hyperactives suffer from imbalanced gut flora7.
Reducing intake of foods that inhibit phenolsulphotransferase-P may be helpful in some sufferers. Low P-form give rise to raised levels of catecholamines in the CNS13,14.* Adrenaline and noradrenaline’s response to a glucose load also seems lower than normal in ADHD, suggesting impaired adrenal function7.
The functioning of neurotransmitters is profoundly influenced by the lipid environment15. Consistent research supports a case for omega-3 fatty acid deficiency in a sub-set of sufferers. Identifying the subset that would benefit from supplementation of this fatty-acid would prove fruitful15. Dietary deficiency is common and often overwhelmed by omega-6 fatty acids frequently from un-healthful sources.
A functional medicine approach to ADHD involves defining, quantifying and treating the antecedents, triggers and mediators contributing to each individual’s condition10.