Archive February 2016

Gluten Sensitivity and Neurological Disorders – From Gut to Brain!

Gluten sensitivity (GS) may be defined as a state of heightened immunological responsiveness in genetically susceptible people. This definition does not imply bowel involvement. The authors, all affiliated with the Department of Neurology at The Royal Hallamshire Hospital, Sheffield, UK, suggest that regarding GS as principally a disease of the small bowel is a historical misconception. They state that GS can be primarily, and at times exclusively a neurological disease, and that IgG antigliadin antibody should be part of the routine investigation of all patients with neurological dysfunction of obscure aetiology, particularly patients with ataxia and peripheral neuropathy. Statistical evidence showed that patients with neurological disease of unknown aetiology were found to have a much higher prevalence of circulating antigliadin antibodies (57%) in their blood than either healthy controls (12%) or those with neurological disorders of known aetiology (5%). More celiac disease (CD) specific serological markers such as anti-endomysium and transglutaminase antibodies may have helped in diagnosing CD, but their sensitivity as markers of other manifestation of GS (where the bowel is not affected) is low. Early diagnosis and removal of the trigger factor by the introduction of a gluten-free diet may be the most promising therapeutic intervention.

Hadjivassiliou M, et al. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry 2002 72:560-563. Published by


Gluten Sensitivity- A Significant Clinical Challenge:

Besides celiac disease (CD) and wheat allergy, the most studied forms of gluten-related disorders characterized by an immune response (autoimmune in CD and IgE-mediated in wheat allergy), non-celiac gluten sensitivity (NCGS) apparently is not driven by an aberrant immune response. NCGS is characterized by a heterogeneous clinical picture with intestinal and extra-intestinal symptoms arising after gluten ingestion and rapidly improving after its withdrawal from the diet. The pathogenesis of NCGS is largely unknown, but factors such as the stimulation of the innate immune system, direct cytotoxic effects of gluten, and the synergy with other wheat molecules are suspects and any one, or any combination of any and all may all play a role. Diagnostic procedures remain problematic due to the absence of efficient diagnostic markers; therefor, diagnosis is based on the symptomatic response to a gluten free diet and the recurrence of symptoms after gluten reintroduction. While the timing of gluten reintroduction in evaluating NCGS is challenging, once the determination is made, the withdrawal of gluten from the diet appears to be the correct patient management approach for those with NCGS.

Eli L, Roncoroni L, Bardella MT. Non-celiac gluten sensitivity: Time for sifting the grain. Wordl J Gastroentero. 2015 Jul 21;21(27):8221-6.


B12 Deficiency Associated With Autism, Schizophrenia and Aging!

Researchers from Northeastern, Harvard, Nova Southeastern and Boston Universities discovered that vitamin B12 levels in the brain are much lower in those with autism or schizophrenia compared to their peers at similar ages, and the elderly. Researchers measured levels of cobalamin in postmortem human frontal cortex samples from 19 weeks fetal development through age 80 among 12 individuals with autism, 9 with schizophrenia, and 43 controls. Total cobalamin was significantly lower in controls older than 60, indicating a more that 10-fold age-dependent decline in methylcobalamin levels. Methylcobalamin and adenosylcobalamin levels were more that 3-fold lower in those with autism or schizophrenia, compared with controls. Lower methylcobalamin was associated with decreased methionine synthase activity and increased levels of substrate homocysteine in those with autism. The findings are particularly significant because the differences found in brain B12 with aging, autism and schizophrenia are not seen in the blood, where B12 levels are usually measured. Researchers concluded that B12 levels, especially methylcobalamin, in human frontal cortex decrease with age, which plays a crucial role in regulating all methylation reactions, including those providing epigenetic regulation of gene expression. The vitamin deficits in autistic and schizophrenic subjects suggests that impaired methylation may be a critical pathological component of these brain disorders, as well as other neurological and neuropsychiatric conditions.

Zhang Y, et al. Decreased Brain Levels of Vitamin B12 in Aging, Autism and Schizophrenia. PLOS ONE, 2016; 11(1): e0146797 DOI: 10.1371/journal.pone.0146797


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