Has enhanced folate status during pregnancy altered natural selection and possibly Autism prevalence? A closer look at a possible link
Abstract
The inverse association between maternal folate status and incidence of infants born with neural tube defects (NTD's) was recognized over twenty years ago and led the US health agencies in the early 1990s to recommend that women of childbearing age consume 400 microg of folic acid each day. The FDA followed by mandating that certain foods be fortified with folic acid and this has resulted in a significant enhancement of maternal folate status to levels that are often difficult to otherwise achieve naturally. At least one study indicates that this has decreased the incidence of NTD's. However, this same time period directly coincides with what many feel is the apparent beginning and continuous increase in the prevalence of Autism and related Autism Spectrum Disorders (ASD's) in the US. Are these similar time frames of changes in maternal folate status and possible Autism prevalence a random event or has improved maternal (and fetal) folate status during pregnancy played a role? It is not only plausible but highly likely. A particular polymorphic form to a key enzyme required to activate folate for methylation in neurodevelopment, 5-methylenetetrahydrofolate reductase (MTHFR), demonstrates reduced activity under low or normal folate levels but normal activity under conditions of higher folate nutritional status. A consequence of the presence of the polymorphic form of this enzyme during normal or reduced folate status are higher plasma homocysteine levels than noncarriers and the combination of these factors have been shown in several studies to result in an increase rate of miscarriage via thrombotic events. However, the incidence of hyperhomocysteinemia in the presence of the polymorphism is reduced under the common condition of enhanced folate status and thereby masks the latent adverse effects of the presence of this enzyme form during pregnancy. Of great importance is that this polymorphism, although common in the normal population, is found in significantly higher frequency in Autisic individuals. 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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Prenatal exposure to folic acid has also been associated with the risk of autism.
“Furthermore, prenatal exposure to folic acid (known to decrease the risk of neural tube defects) has also been associated with the risk of autism (64).”
From Gene × Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms (2014) · cites this paper as [64]
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- Authors
- Rogers, E. J.
- Affiliations
- University of Massachusetts Lowell (US)
- Corresponding author
- Rogers, Eugene J.
- Venue
- Medical Hypotheses
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 71
- Issue
- 3
- Pages
- 406-410
- ISSN
- 0306-9877 (ISSN-L)
- OpenAlex
- W1996217325
- Cited by
- 75
- References
- 13
- Citations by year
- 2026: 1 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 5 · 2018: 1 · 2017: 7 · 2016: 5 · 2015: 8 · 2014: 9 · 2013: 3 · 2012: 9
- FWCI
- 3.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Medical Hypotheses (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Folate and B Vitamins Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Pharmacological Effects and Toxicity Studies
- Keywords
- maternal folate status, autism spectrum disorder, autism prevalence, MTHFR C677T polymorphism, natural selection, folic acid supplementation, neural tube defects, hyperhomocysteinemia, miscarriage, brain development, prenatal folate supplementation
- MeSH terms
- Autistic Disorder, Female, Folic Acid, Homocysteine, Humans, Neural Tube Defects, Polymorphism, Genetic, Pregnancy, Selection, Genetic, Methylenetetrahydrofolate Reductase (NADPH2)
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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