![]() | |
Pregnant women are encouraged to take folic acid before and during pregnancy. |
I just read a bit of interesting research that suggests the
addition of folic acid to the American diet through fortifying our foods has
prevented “natural selection” from occurring and allowing children with a
predisposition to autism to be born (Rogers, 2008). Rogers (2008) hypothesizes that maternal
folate nutritional status through a fortified diet or supplemented before and
during pregnancy with folic acid has reduced the incidence of infants born with
open neural tube defects (e.g., spina bifida), but questions whether the
improved folate status masked adverse biological effects associated with
limited methylation (the body’s way of detoxifying itself) and prevented
fetuses with a common polymorphism (mutation) from being miscarried. This polymorphism is commonly referred to as
MTHFR (MethyleneTetraHydroFolate Reductase), and the most common mutations are
C677T and A1298C.
![]() |
A greatly simplified diagram of the methylation cycle. |
Rogers’ hypothesis agrees with an earlier study that
concluded combined MTHFR mutations are likely to carry a selective disadvantage
and contribute to decreased fetal viability (Isotalo, Wells & Donnelly,
2000). MTHFR plays an important role in
folate metabolism and assists in the conversion of homocysteine into methionine,
which are amino acids in the methylation cycle.
MTHFR polymorphisms are known to cause hyperhomocysteinemia (elevated
levels of homocysteine), which occurs when the body is unable to methylate
homocysteine properly. Neural Tube
Defects (NTDs), stillbirths and recurrent miscarriages have all been associated
with hyperhomocysteinemia, so this seems to be a plausible theory. Elevated levels of homocysteine and oxidative
stress are characteristic of autism spectrum disorders.
Ryan is homozygous (meaning he got one copy of the gene from
me and one from my husband), which means his methylation status is severely
compromised. Although MTHFR is not an uncommon
polymorphism among the general population, research has shown it occurs at
higher prevalence in individuals with autism spectrum disorders.
![]() |
Homozygous and Heterozygous |
The vast majority of cases of idiopathic autism do not
exhibit genetic anomalies and epigenetics may be important in the etiology of
autism (Goin et al, 2009). Epigenetics
refers to changes in gene status without changes to the DNA sequence. Methylation status is a type of epigenetic
change. Not every gene in our bodies is
active at all times, but are “switched on and off”. DNA methylation can “turn off” certain genes
by tagging them with a methyl group. Research by James et al (2004) suggests
that autism has an association with metabolic anomalies that contribute to
hypomethylation (low methylation status) of DNA and found children with
regressive autism had metabolic profiles consistent with impaired DNA
methylation capacity.
In two independent National Institutes of Health
(NIH)-funded studies, Reif et al (2008) studied adverse events (AE) following
Vaccinia (small pox) vaccination in populations and concluded in both studies
that MTHFR polymorphisms were associated with AEs. I could find no studies that examined the occurrence
of AEs in populations with MTHFR polymorphisms with other vaccination types. However, it seems possible if the prevalence
of AEs following small pox vaccination is higher among individuals with MTHFR
polymorphisms, this population could be susceptible to AEs caused by other vaccines.
The cause of autism is still unknown, but it is generally
accepted that it occurs where there is a genetic predisposition to
environmental insults. Perhaps MTHFR
with its effect on methylation status is one such genetic marker that could
help identify vulnerable populations.
References
Guo, T., Chen, H., Liu, B., Ji, W., Yang, C. (2012).
Methylenetetrahydrofolate Reductase Polymorphisms. Genetic Testing and Molecular Biomarkers, Vol. 16(8), 968 – 973.
Isotalo, P. A., Wells, G. A., and Donnelly, J. G.
(2000). Neonatal and Fetal MTHFR Genetic
Polymorphisms: An Examination of C677T and A1298C Mutations. Am. J.
Hum. Genet. 67: 986 – 990.
James, S.J., Cutler, P., Melnyk, S., Jernigan, S., Janak,
L., et al. (2004). Metabolic Biomarkers
of increased Oxidative Stress and Impaired Methylation Capacity in Children
with Autism. Am J. Clin Nutr, 80; 1611 – 1617.
Park, JW., Ro, MJ., Pyun, JA. and Kwack, KB. (2014). MTHFR
1298A>C is a risk factor for autism spectrum disorder in the Korean
population. Psychiatry Research, Vol. 215; 258 – 259.
Reif, D.M., McKinney, B.A., Motsinger-Reif, A. A., Chanock,
S.J., Edwards, K.M., Rock, M.T., et al. (2008). Genetic Basis for Adverse
Events after Small Pox Vaccination. J Infect Dis 2009; 198: 16 – 22.
Rogers, E.J. (2008). Has enhanced folate status during
pregnancy altered natural selection and possibly Autism prevalence? A closer
look at a possible link. Med Hypotheses 2008; 71: 406 – 410.
This comment has been removed by the author.
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