Dietary Sensitivities and ADHD Symptoms: Thirty-five Years of Research

Department of Foods & Nutrition, Purdue University, 700 State Street (G-46), West Lafayette, IN 47907, USA.
Clinical Pediatrics (Impact Factor: 1.15). 12/2010; 50(4):279-93. DOI: 10.1177/0009922810384728
Source: PubMed


Artificial food colors (AFCs) have not been established as the main cause of attention-deficit hyperactivity disorder (ADHD), but accumulated evidence suggests that a subgroup shows significant symptom improvement when consuming an AFC-free diet and reacts with ADHD-type symptoms on challenge with AFCs. Of children with suspected sensitivities, 65% to 89% reacted when challenged with at least 100 mg of AFC. Oligoantigenic diet studies suggested that some children in addition to being sensitive to AFCs are also sensitive to common nonsalicylate foods (milk, chocolate, soy, eggs, wheat, corn, legumes) as well as salicylate-containing grapes, tomatoes, and orange. Some studies found "cosensitivity" to be more the rule than the exception. Recently, 2 large studies demonstrated behavioral sensitivity to AFCs and benzoate in children both with and without ADHD. A trial elimination diet is appropriate for children who have not responded satisfactorily to conventional treatment or whose parents wish to pursue a dietary investigation.

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    • "Although the contribution to behavioural disturbances is still controversial [9], evidence suggests that AFD consumption increases the risk of behavioural change in children [10]–[13]. Earlier reports indicated that children with ADHD may show above-average sensitivity to AFDs [14], while other findings suggested that AFDs may affect healthy populations as well [15]. In particular, previous studies showed that AFD consumption results in increased motor activity [15]–[16]. "
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    ABSTRACT: The consumption of artificial food dye (AFD) during childhood and adolescence has been linked to behavioural changes, such as hyperactivity. It is possible that the vulnerability to AFDs is modified by prenatal stress. Common consequences of prenatal stress include hyperactivity, thus potentially leading to synergistic actions with AFDs. Here, we investigated the compounding effect of multigenerational prenatal stress (MPS) and AFD consumption on the development of hyperactivity and anxiety-related behaviours across the lifespan in male rats. MPS treatment involved a family history of four consecutive generations of prenatal stress (F4 generation). AFD treatment included a 4%-concentration of FD&C Red 40, FD&C Yellow 5, FD&C Yellow 6, and FD&C Blue 1 in the drinking water from postnatal days 22 to 50 to resemble juvenile and adolescent dietary exposure. Using several exploration tasks, animals were tested in motor activity and anxiety-like behaviours from adolescence to 13 months of age. MPS resulted in hyperactivity both early (50 days) and later in life (13 months), with normalized activity patterns at reproductive age. AFD consumption resulted in hyperactivity during consumption, which subsided following termination of treatment. Notably, both MPS and AFD promoted risk-taking behaviour in young adults (3 months). There were few synergistic effects between MPS and AFD in this study. The findings suggest that AFDs exert the most noticeable effects at the time of exposure. MPS, however, results in a characteristic lifespan profile of behavioural changes, indicating that development and aging represent particularly vulnerable periods in life during which a family history of prenatal stress may precipitate.
    PLoS ONE 06/2014; 9(6):e92132. DOI:10.1371/journal.pone.0092132 · 3.23 Impact Factor
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    • "Corn is found in a wide variety of packaged foods, such as cereals, candies, jams, syrups, sauces, snack foods, canned fruits, prepared meats and beverages. Though not considered a common food allergen corn allergy is increasingly being discussed between doctors across the world [1] [2]. Treatment for corn allergy includes strict avoidance of corn ingredients. "
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    • "This ques‑ tion, in fact, is the theme of many reports in environmental health. The more significant paradox about the passage above by the FDA Food Advisory Committee (2011b) is its view that an effect size of 0.18 [in the range of many of the pub‑ lished studies (see Schab and Trinh 2004; Stevens et al. 2011)] can be considered trivial. Effect size is often used to gauge the impor‑ tance or strength of a finding; therefore, how it applies to McCann et al. (2007)—and its interpretation—is worth examining with a more familiar example. "
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    ABSTRACT: The proposition that synthetic food colors can induce adverse behavioral effects in children was first enunciated in 1975 by Feingold [Why Your Child Is Hyperactive. New York:Random House (1975)], who asserted that elevated sensitivity to food additives underlies the signs of hyperactivity observed in some children. Although the evidence suggested that some unknown proportion of children did respond to synthetic food colors, the U.S. Food and Drug Administration (FDA) interpreted the evidence as inconclusive. A study published in 2007 [McCann et al. 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 370:1560-1567 (2007)] drew renewed attention to the hypothesis because of the study's size and scope. It led the FDA to review the evidence, hold a public hearing, and seek the advice of its Food Advisory Committee. In preparation for the hearing, the FDA reviewed the available evidence and concluded that it did not warrant further agency action. In this commentary I examine the basis of the FDA's position, the elements of the review that led to its decision and that of the Food Advisory Committee, and the reasons that this is an environmental health issue. The FDA review confined itself, in essence, to the clinical diagnosis of hyperactivity, as did the charge to the committee, rather than asking the broader environmental question of behavioral effects in the general population; it failed to recognize the significance of vulnerable subpopulations; and it misinterpreted the meaning of effect size as a criterion of risk. The FDA's response would have benefited from adopting the viewpoints and perspectives common to environmental health research. At the same time, the food color debate offers a lesson to environmental health researchers; namely, too narrow a focus on a single outcome or criterion can be misleading.
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