Researchers at UC Davis published a survey  in Epidemiology purportedly reporting on the effect of prenatal vitamins and their ability to preclude births of children with autism.  Drs. Schmidt (2), Hansen, Hartiala, Allayee, Hooman, Tancredi, Tassone, and Hertz-Picciotto (UC Davis) reported that women who took prenatal vitamins BEFORE pregnancy (and during pregnancy) were ½ as likely to have a child with autism; those that had high risk mutations were associated with a 7 fold reduction.

The researchers examined 707 families who had 2 to 5 y old children (over the years 2003-2009).   Of the children, 278 were normal, 288 had autism, and 141 had autism spectrum disorder (ASD).  The mothers were asked whether they took vitamins, when they took them,  and what kind.  The critical data piece was that if a mother started taking vitamins during the second month of pregnancy or later (in other words, once they really knew they were pregnant), the vitamins had no effect as to whether the child manifested autism.  Only if the mother took vitamins 1 month prior to pregnancy or perhaps as late as the first month manifested the protective effect.

The two gene mutations that were most likely associated wit autism were the MTFHR (methylenetetrahydrofolate reductase) and COMT (catechol-O-methyltransferase).  MTHFR mutations affected folic acid metabolism and augmented the level of homocysteine. COMT is involved with the degradation of catecholamines such as dopamine, epinephrine, and norepinephrine (adds a methyl group).

The problem as I see it is the ability of someone to recall when they began taking vitamins accurately some 2 to 5 years after the fact.  Moreover, it is not likely that many women would take prenatal vitamins before knowing they were pregnant.  But, if a woman knows she is a carrier to the two genes that are most likely to lead to a child with autism, it would certainly behoove them to take prenatal vitamins while they are trying to conceive.  And, until additional studies are done, I certainly would recommend same.  In so doing, they can reduce the risk of a child with autism by some 7 times, given the data in this study.

In another study, Dr. Geschwind of UCLA assembled a team (including researchers from the University of Toronto (who did the RNA testing) and Kings College (who did tissue extraction and replication) that examined the temporal and frontal lobes of 19 subjects suffering from autism and 17 normal subjects.

As published in Nature, they found that subjects with autism did not have different genes expressed between the lobes.  Those without ASD did have different characteristics.  While the cause for autism will differ among subjects, the gene and protein interactions surprisingly manifested similar patterns.  There was virtually no difference between frontal and temporal lobe gene and protein interactions.  A total of 209 genes communicated and operated similarly in the lower functions of the brain, while 235 genes associated with immune (and inflammatory) responses were also similar.  This is presumably related to incomplete or defective brain development.

Since this was a rather small study, additional effort needs to be expended to determine if these results are common, and what can be done to improve the treatment and development of patients with ASD.

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