Food intolerance and the few-foods(or oligoantigenic)diet in children with attention-deficit hyperactivity disorder

The hypothesis that some children with attention-deficit hyperactivity disorder(ADHD)may show sensitivity or allergic reactions to various food items has led to the development of the the few-foods(or oligoantigenic)diet.The rationale of the diet is to eliminate certain foods from the diet in order to exclude potential allergens contained either naturally in food or in artificial ingredients with allergenic properties.The oligoantigenic diet attempts to identify individual foods to which a person might be sensitive.First,ADHD symptoms are monitored while multiple foods are excluded from the diet.Subsequently,if symptoms remit,foods are re-introduced,while observing the individual for the return of symptoms.An advantage of the oligoantigenic diet is that it can be tailored to the individual.A growing body of evidence suggests that behavioral symptoms of subgroups of children with ADHD may benefit from the elimination of certain foods.The effect sizes of an oligoantigenic diet regarding improvement of ADHD symptoms have been found to be medium to large.Available evidence suggests that the investigation of the role of food hypersensitivities in ADHD is a promising avenue worthy of further exploration.Further large-scale,randomized controlled studies including assessment of long-term outcome are therefore warranted.

Diet and medical foods in Parkinson’s disease

Parkinson’s disease (PD) is a slowly progressive neurodegenerative disorder with motor and non-motorsigns, which begins long before the diagnosis can be made. Pharmacotherapy with dopaminergic drugsis the mainstay of PD therapy. There is no currently available cure or disease-modifying treatment. Dietand various foods have been proposed as possible risk factors for PD. Nutritional supplementation withomega-3 fatty acids, vitamin D, B vitamins, and coenzyme Q may have potential in the management ofPD. In addition, several strategies could possibly lead to the development of medical foods in PD. Forexample, ketogenic diets may have effects complementary to pharmacotherapy. Gut microbial dysbiosisand altered microbial metabolites found in PD may lead to chronic low-grade inflammation in gut andbrain. Interventions targeting gut microbiota, such as the supplementation of probiotics, may providenovel approaches to PD in regard to both symptomatic treatment and disease modification. High qualityrandomized controlled trials need to be conducted in order to evaluate whether these food-basedstrategies have symptomatic efficacy or the potential to delay the progression of PD.

Tea and depression

The available evidence,which derives from studies investigating mechanistic effects of tea,research on animal models as well as epidemiological studies and intervention trials in humans,suggests that compounds contained in tea may have the potential to aid in the prevention of depression or in its treatment as an addition to established therapies.A wide range of potentially antidepressive biological activities of tea components have been reported.However,the mechanisms of tea phytochemicals possibly capable of decreasing the risk of depressive symptoms are complex,multifaceted and not well understood.Potent pharmacological effects on circumscribed neurobiological systems may be produced not by individual tea components but rather by the synergistic action of various compounds on multiple pathophysiological mechanisms involved in depression.While epidemiological studies have generally demonstrated beneficial effects of tea consumption on mood and depressive symptoms,cross-sectional studies are unable to prove a cause-effect relationship.If positive effects on mood could be firmly established,tea drinking could support mental health.However,the moderate antidepressive effects observed in healthy people are not necessarily indicative of possible clinical effects in major depressive disorder.Randomized controlled intervention studies are needed to establish a causal relationship between bioactive compounds in tea and depression.

Green tea, epigallocatechin gallate and the prevention of Alzheimer’s disease: clinical evidence

Given its increasing global prevalence,Alzheimer’s disease(AD)has become a major public health challenge worldwide.The symptomatic treatments available for AD have shown no significant efficacy,and no disease-modifying interventions are capable of slowing the progression of the disorder.The potential of lifestyle-related factors,including diet,is increasingly recognized as an important consideration in the primary prevention of AD.Numerous mechanisms potentially underlying neuroprotective effects of bioactive components contained in tea,such as(-)-epigallocatechin-3-gallate,as well as their preventive efficacy against AD,have been elucidated in preclinical studies.However,in contrast to the abundance of mechanistic findings in animals,clinical results demonstrating efficacy in humans are scarce.While epidemiological studies have provided some evidence indicating that green tea consumption is associated with a reduced risk of age-related cognitive decline and AD,a causal relationship cannot be established on the basis of these observations.The clinical evidence regarding preventive or therapeutic effects of green tea and its bioactive components is unsatisfactory.A role of green tea in the prevention of AD cannot be recommended until well-designed,randomized,placebo-controlled clinical trials using standardized formulations confirm the purported beneficial effects of green tea.

Medical foods in Alzheimer’s disease

Alzheimer’s disease(AD)is the most prevalent cause of dementia worldwide.Treatments achieving a marked improvement in symptoms or preventing or delaying the progression of the disease are not available.Various diet-related risk factors for AD have been identified.Evidence for a protective effect of the Mediterranean diet on AD risk is inconclusive.Medical foods are designed to meet specific dietary needs for certain diseases.Improvements in symptomatology and regional brain atrophy in AD have been claimed for several medical foods,for example,those providing ketone bodies as alternative energy supply to neurons,those containing precursors believed to improve synaptic function,and those addressing oxidative stress related to memory loss.Many methodological shortcomings render the interpretation of the available findings of medical food trials in AD difficult.Optimal results of medical foods in AD may be expected when administered in presymptomatic or early stages of the disease.This requires the reliable identification of minimal neuropathological changes related to AD.The outcome measures currently used may not be able to detect subtle changes in cognition and function in early AD.Large-scale clinical studies using valid,sensitive,and reliable assessment tools are needed to establish the efficacy of medical foods in AD.

Ketogenic diets and Alzheimer’s disease

Alzheimer’s disease(AD)is a progressive neurodegenerative disorder characterized by decline in cognitive functions and associated with the neuropathological hallmarks of amyloid-peptide plaques and neurofibrillary tangles.Cerebral glucose uptake and metabolism deteriorate in AD and this hypometabolism precedes the onset of clinical signs in AD.The early decline in brain glucose metabolism in AD has become a potential target for therapeutic intervention.This has led to investigations assessing the supplementation of the normal glucose supply with ketone bodies which are produced by the body during glucose deprivation and can be metabolized by the brain when glucose utilization is impaired.The present review provides a synopsis of preclinical studies and clinical trials assessing the efficacy of ketogenic diets in the treatment of AD.Both the direct administration of ketone bodies and the use of high-fat,low-carbohydrate ketogenic diets have been shown to be efficacious in animal models of AD and clinical trials with AD patients.The mechanism underlying the efficacy of ketogenic diets remains unclear,but some evidence points to the normalization of aberrant energy metabolism.At present there is only limited evidence of the usefulness of ketogenic diets in AD.However,this dietary approach seems to be promising and deserves further clinical investigations.