B12 in Autism

B12 levels

Then the quantity found in serum has not been adequately repeated such that we can see repeated information coming from the scientific results.

 

B12 is present as a vitamin in the diet that requires cobalt in very small amounts to be present.  It is best absorbed from the terminal areas of the ileum. 

 

 

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Cobalamin

 

 

Serum levels found in autism

 

This has not  been measured and published by many groups, despite the method being fully available by many medical groups throughout the world.  The suggestion is that it is not so much a low level of B12 but rather of the methylated product of it.  This also has no adequate data. 

 

Paşca SP, Nemeş B, Vlase L, Gagyi CE, Dronca E, Miu AC, Dronca M. High levels of homocysteine and low serum paraoxonase 1 arylesterase activity in children with autism. Life Sci. 2006 Apr 4;78(19):2244-8. Epub 2005 Nov 17. (This measured also the B12 levels and found them to be low or low normal).

 

 

Methylcobalamin used as a potential treatment

 

The consideration has been that there has been inadequate methylation capacity and that the addition of the methyl format of vitamin B12 may actually cause this to be modified.  The work by James indicated that many changes were seen in the oxidative stress pathways (and the formation of compounds to prevent it) should this be given as a treatment.  Can I recommend going through this article to try to understand the change seen in the oxidative, transsulphuration and methylation pathways:

 

 

James SJ, Cutler P, Melnyk S, Jernigan S, Janak L, Gaylor DW, Neubrander JA. Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism. Am J Clin Nutr. 2004 Dec;80(6):1611-7.

(“The addition of injectible methylcobalamin to the protocol (intervention 2) was based on empirical observations of clinical improvement in speech and cognition (by JAN) and the possibility that it might enhance methionine synthase activity under conditions of oxidative stress by replacing oxidized inactive coenzyme B-12 [cob(II)alamin] or by posttranslational upregulation of methionine synthase, or both.  One month after the addition of methylcobalamin, the methionine concentrations were within the control range”)

 

Deth R, Muratore C, Benzecry J, Power-Charnitsky VA, Waly M. How environmental and genetic factors combine to cause autism: A redox/methylation hypothesis. Neurotoxicology. 2008 Jan;29(1):190-201. Epub 2007 Oct 13. Review. 

 

 

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