Folate is a water-soluble B vitamin that facilitates the transfer of carbon atoms in the synthesis of nucleic acids and amino acids. The word folate is derived from folium meaning leaf. The name is a reminder that green leafy plants like spinach and lettuce are a rich source of folate. Other sources include okra, asparagus, organ meat (liver, kidney) and tomato juice. These food sources account for 20% of our folate levels the rest being produced by intestinal microorganisms.
Folate is commonly used in the treatment for reduced amount red blood cells in a condition called megaloblastic anemia. Mixed results have been found when using folate in the treatment of depression, as a cognitive enhancer or as a way of lowering the risk for cancer (e.g., colonorectal, pancreatic).
Deficiencies of folate are seen primarily in people with poor diets, alcohol dependence, pregnancy, digestive problems, and individuals with kidney or liver disease. Low folate levels are manifested by soreness and shallow ulcerations in the tongue and oral mucosa, and changes in fingernail pigmentation. When testing folate levels the physician takes into account the age of the patient, whether the levels were taken from red blood cells (reflecting long-term folate intake) or plasma (reflecting short-term folate intake), and the possible intake of vitamin or dietary supplements.
Folate supplementation during pregnancy decreases the risk of acquiring major malformations of the nervous system (i.e., being born with a split open spinal cord or lacking most of the brain) by 50-70%. However, according to some authors, very high levels of folate in pregnant women may increase the risk for autism. High folate levels in pregnant women may be due to excessive supplementation. However, cells need vitamin B12 in order to metabolize folate. If vitamin B12 levels are low folate may accumulate and build up in the blood.
The results of studies linking autism to folate levels may be arguable and open to criticism depending on whether some confounds have been taken into account including prescription of vitamins, food intake and/or nutrient supplementation in children with autism, and how the folate levels were measured. When many of these confounds are taken into account the medical literature leads to inconsistent conclusions (Castro et al, 2014, DeVilbiss et al. 2015). Indeed, feeding behaviors in autistic individuals differ significantly from those of controls and may expose them to inadequate calcium, sodium, iron, vitamin C intake and folate (Castro et al, 2016). Some studies have even claimed that folate supplementation during pregnancy may actually decrease the risk for autism spectrum disorder in the offspring and possibly more so if the mother is taking anticonvulsants for seizures (Anderson, 2016).
References
Anderson P. Folic acid linked to less autism in kids of women with epilepsy. Medscape Medical News, June 9, 2016 (http://www.medscape.com/viewarticle/864563)
Castro K, Kelin LD, Baronio D, Gottfried C, Riesgo R, Perry IS. Folic acid and autism: What do we know? Nutr Neurosci [Epub ahead of time] PMID: 25087906
Castro K, Faccioli LS, Baronio D, Gottfried C, Perry IS, Riesgo R. Feeding behavior and dietary intake of male children and adolescents with Autism Spectrum Disorder: a case-control study. Int J Dev Neurosci [Epub ahead of print] PMID: 27432261
DeVibiss EA, Gardner RM, Newsschaffer CJ, Lee BK. Maternal folate as a risk factor for autism spectrum disorders: a review of existing literature. Br J Nutr 114(5):663-72, 2015.
Cortical Chauvinism 
There is also a high incidence of polymorphisms (aka variations) for the Methylenetetrahydrofolate reductase (MTHFR) gene in the general population, and some, but not all, researchers have linked these polymorphisms in MTHFR to Autism. The MTHFR gene is in the folate metabolism pathway that produces 5 methylenetetrahydrofolate (5-MTHF). For example, the C677T polymorphism in the MTHFR gene results in a fragile form of the enzyme and can lead to a deficiency in the enzymatic product of folate called 5-MTHF. When someone has both copies of their MTHFR gene with the weaker «T» version, or alllele, of the MTHFR gene, the lack of 5MTHF can further lead to a build up of homocysteine in the body, since 5MTHF is a cofactor in the reconversion of homocysteine to methionine. Homocyteine build up can be dangerous, and is thought to lead to an increased risk of blood clots, and neural tube defects. This C677T polymorphism, which is present on both chromosomes (homozygous) of 10% of the North American population (and is more common in Hispanic individuals, and less common in African Americans), has been observed to occur more frequently in individuals with autism in some, but not all studies. It has also been linked to schizophrenia and depression. Since it is a very common variant, if it does have an effect on ASD risk, it might be of low effect size. However, a low effect size for one gene polymorphism, may still shed light on the etiology of a disorder as a whole. There is precedence for this in thinking about ADHD and the DRD4 dopamine receptor variant. the DRD4 48 bp VNTR allele has repeatedly been linked to ADHD in many, but not all studies, and metanalysis shows that it has a low effect size. However, few medical professionals doubt the involvement of dopamine in attention tasks or response inhibition, nor the utility of drugs that increase dopamine at the synaptic level as valid treatments for ADHD. In an analogous manner, MTHFR polymorphisms may be informing us to the risks for ASDs in affected individuals, or in children born from mothers with polymorphisms.
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