Autism in Oman: Nutritional deficiencies in vitamin B12 and folate associated with gender-specific abnormalities in serum thiol levels.
Lead Presenter: Nathaniel Hodgson
Currently 1 in 110 children in the U.S. will develop autism, with the rate being 4-fold higher for males than females. Environmental factors (xenobiotics) appear to be largely responsible for increasing autism rates. The synthesis of glutathione (GSH) by sulfur metabolism plays a central role in the detoxification of many xenobiotics. Several studies have reported significantly lower plasma levels of GSH, in association with oxidative stress in autistic subjects. The folate and vitamin B12-dependent enzyme methionine synthase is a key redox switch, whose activity determines the balance between methylation activity and GSH synthesis through the re-routing of sulfur metabolites. We studied 20 male and 20 female autistic children in Oman, and examined their dietary intake and serum levels of folate and vitamin B12. We then measured serum levels of sulfur metabolites, including cysteine, cysteine, cystathionine, reduced and oxidized GSH, homocysteine, homocysteine, methionine, S-adenosylhomocysteine (SAH) and S-adenosylmethionine (SAM). Our results show differences in thiol metabolism and oxidative stress in Omani autistic children, similar to the findings of other studies. However, the presence of low B12 and folate levels indicates that the oxidative stress was largely due to a nutritional deficiency, which is not the case for autism in the U.S. Thus, a common metabolic abnormality (oxidative stress) is associated with autism of different origins. Further, our data shows gender specific differences in thiol metabolite levels among autistic subjects, with males showing a greater deficit in GSH and a higher level of oxidative stress.