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Research
Food Hypersensitivity & Bisphenol

Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
June 30, 2009

In 2007, Ohshima and colleagues reported that levels of a plastics chemical known as bisphenol A (BPA) were inversely correlated with oral tolerance which - when suboptimal - is associated with food hypersensitivities and autoimmunity (1).

Background

Allergies to various foods are increasing in the U.S. and elsewhere (2). More than 60% among >2500 autism parents reported improvements when their autistic child is on a gluten-free or casein-free diet (3). Bisphenol A has become common in breast milk, cord blood, and bodies of humans (eg, 4-8) and may be etiologically significant in some and perhaps many cases of food hypersensitivity (1). As cited below, other BPA effects may be relevant to autism.

First, a technical but important aside: BPA was found to alter function of immune cells labeled with surface markers known as CD4 and CD25 (1). These cells participate in immunological anergy and, when functioning properly, minimize or prevent autoimmunity and induce appropriate oral tolerance to food antigens (1, 9-11).

Caveat and counter-caveat: The Ohshima et al findings occurred in a murine model wherein BPA levels were substantially higher than average levels found in humans (1). However, the findings may pertain to humans with impaired detoxification. For instance, glutathione participates in neutralization and detoxification of BPA (eg, 12-13). Many humans have one or more polymorphisms which diminish effectiveness or availability of glutathione (eg, 14-15). And weak alleles in GSH-related pathways are increasingly described in autism (eg, 16-17).  Furthermore, BPA detoxification includes glucuronidation, which can be affected by polymorphisms (eg, 18) and BPA-detoxification is affected by androgens (19-21). Lower levels of GSH, suboptimal utilization of GSH, weak alleles of genes participating in glucuronidation, and elevated androgens are factors suggesting relevance of BPA's role in food hypersensitivities among infants and children with impaired ability to detoxify BPA.

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Gluten Encephalopathy with Psychiatric Onset
Nicola Poloni, Simone Vender, Emilio Bolla, Paola Bortolaso, Chiara Costantini and Camilla Callegari

Department of Clinical Medicine-Psychiatry, University of Insubria, Via O. Rossi 9, 21100 Varese, Italy

Clinical Practice and Epidemiology in Mental Health 2009, 5:16doi:10.1186/1745-0179-5-16


The electronic version of this article is the complete one and can be found online at:http://www.cpementalhealth.com/content/5/1/16
Received:    7 July 2008
Accepted:    26 June 2009
Published:    26 June 2009

© 2009 Poloni et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract

Many cases of coeliac disease, a gastrointestinal autoimmune disorder caused by sensitivity to gluten, can remain in a subclinical stage or undiagnosed. In a significant proportion of cases (10–15%) gluten intolerance can be associated with central or peripheral nervous system and psychiatric disorders.

A 38-year-old man was admitted as to our department an inpatient for worsening anxiety symptoms and behavioural alterations. After the addition of second generation antipsychotic to the therapeutic regimen, the patient presented neuromotor impairment with high fever, sopor, leukocytosis, raised rhabdomyolysis-related indicators. Neuroleptic malignant syndrome was strongly suspected. After worsening of his neuropsychiatric conditions, with the onset of a frontal cognitive deficit, bradykinesia and difficulty walking, dysphagia, anorexia and hypoferraemic anaemia, SPET revealed a reduction of cerebral perfusion and ENeG results were compatible with a mainly motor polyneuropathy. Extensive laboratory investigations gave positive results for anti-gliadin antibodies, and an appropriate diet led to a progressive remission of the encephalopathy.

Introduction

Coeliac disease is an inflammatory disease of the upper small intestine resulting from gluten ingestion [1]. The diagnosis is based on: a clinical picture suggesting malabsorption of nutrients, serology for anti-gliadin, anti-endomysial and anti-transglutaminase antibodies, sometimes a biopsy of the intestinal mucosa, and resolution of the lesions following the institution of a gluten-free diet [1]. Many cases of coeliac disease long remain in a subclinical stage [2], or undiagnosed because of poor awareness of the condition among primary care physicians [1]. In a significant proportion of cases (10–15%) gluten intolerance can be associated with central or peripheral nervous system disorders, such as cerebellar ataxia, myoclonus, epilepsy, ophthalmoplegia, dementia, multifocal leukoencephalopathy, peripheral neuropathies and myopathies [3] and with psychiatric disorders such as anxiety, depression, psychotic symptoms and personality disorders [4]. These manifestations are sometimes the presenting symptoms of the disease [4-6]. The physiopathological mechanisms underlying these associations are still not known, even though genetic causes [6] and autoimmune factors [7,8] have been hypothesised.

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