http://mthfr.net/folic-acid-fortification-increase-in-mthfr-and-rise-in-autism/2012/05/11/
If we sit back and evaluate the dates when folic acid fortification began and the fast rise of autism – do they correlate?
“In Spain, the prevalence of the MTHFR 677TT genotype has reportedly approximately doubled in the population since the introduction in 1982 of folic acid supplements for women in early pregnancy”…
“Folic acid fortification and supplement use might be “a genetic time bomb.” The first premise of this dramatic claim, that folic acid use increases the proportion of children born with the T allele of MTHFR, is as yet poorly documented and is clearly in urgent need of further study.
Studies of the MTHFR genotype frequencies in children before and after fortification should be carried out in countries planning fortification of food with folic acid. Thus, saving fetuses that have a genetic constitution that favors abortion or nonsurvival could lead to children being born with genotypes that favor increased disease during life”"[
1]
Folic acid fortification started heavily in 1992.[
2]
Autism began to quickly rise in 1993.
In the early 1990s, autism diagnoses began to soar. In the 10 years between 1993 and 2003, the number of American schoolchildren with autism diagnoses increased by over 800%. In 2006, the CDC noted a slight decrease in the number of new cases diagnosed.[
3]
Autism began to rise at the same time folic acid fortification began.
Is the rise of autism due to an increased survival rate of babies with MTHFR defects?
...I cannot summarize their study better than they, so here is their conclusion:
It is hypothesized here that the enhancement of maternal folate status before and during pregnancy in the last 15 years has altered natural selection by increasing survival rates during pregnancy of infants possessing the MTHFR C677T polymorphism, via reduction in hyperhomocysteinemia associated with this genotype and thereby miscarriage rates. This also points directly to an increased rate of births of infants with higher postnatal requirements for folic acid needed for normal methylation during this critical neurodevelopmental period. If these numbers have increased then so have the absolute number of infants that after birth fail to maintain the higher folate status experienced in utero thus leading to an increased number of cases of developmental disorders such as Autism. Detection of the C677T polymorphism as well as other methionine cycle enzymes related to folate metabolism and methylation at birth as part of newborn screening programs could determine which newborns need be monitored and maintained on diets or supplements that ensure adequate folate status during this critical postnatal neurodevelopment period.
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