A recent paper adds to the roll-call of a potential homocysteine-autism link. The paper by Amanat Ali and colleagues* is here (open-access) and reports on a case-control study of fasting plasma homocysteine levels in a small group of children with autism from the Sultanate of Oman. I noted that the paper lists Richard Deth (pronounced Deeth) as a co-author who some readers will know from his work on oxidative stress and methylation. As an aside, there was also a particularly interesting IMFAR poster from Deth and colleagues a couple of years back on how dietary-derived opiates might link into homocysteine and glutathione findings in autism (sorry its only an abstract).
I digress. Back to the paper in question:
- Forty Omani children with autism, aged between 3-5 years old were compared against 40 age- and sex-matched controls for levels of fasting plasma homocysteine, folate and vitamin B12. Immunoassays were the preferred choice of analysis.
- Mean levels of homocysteine were significantly higher in the children with autism over controls; indeed over double the average amount detected in controls. At the same time folate and vitamin B12 levels were significantly lower on average than controls; indeed levels were generally reported as being below the 'deficient' cut-off values described by other authors. I wonder if the folate findings might hark back to the reported folate receptor autoantibodies story?
There's not too much more to say about this paper aside from the fact that it seems to be reporting trends roughly in line with what other authors have previously said. The fact that this study relied on Omani children would tend to suggest that the previous homocysteine findings, limited as they are at the moment, might pass across different ethnicities which is interesting bearing in mind the genetic and environmental differences compared say with Europe or the US. If I was to be a nit-picker I might question the small participant group and could perhaps question the accuracy of immunoassays over other more direct separative analytical technologies particularly when teasing out homocysteine and its dimer homocystine. I don't however want to distract from the main findings which whilst still preliminary, are nevertheless important.
I will keep coming back to homocysteine and its buddy compounds in the methionine cycle and beyond (e.g. methylmalonic acid) as and when they crop up on the research radar.
To end a spot of Strauss to bring back some memories of a space odyssey or a seemingly distant New Years day (Das Neujahrskonzert der Wiener Philharmoniker).
* Ali A. et al. Hyperhomocysteinemia among Omani autistic children: a case-control study. Acta Biochmica Polonica. December 2011
The Folate-Methylation-Transulfuration cycle complex is the central link between genetics and environment. Dysfunction in these interrelated pathways create scenarios for altered biochemistry in all of us. I see it daily in my patients with autism and work hard at correcting it. - Dr. MikeReplyDelete
Thanks Dr Mike.ReplyDelete
It certainly does appear from the evidence that disruption of this wonderful cycle of compounds shows more than a passing relationship to at least some cases of autism.