Source: Genetic Lifehacks
An interesting study came out this year in the Journal of Clinical Psychiatry. The study, Correlation of Clinical Response With Homocysteine Reduction During Therapy With Reduced B Vitamins in Patients With MDD Who Are Positive for MTHFR C677T or A1298C Polymorphism: A Randomized, Double-Bind, Placebo-Controlled Study, is available in full on the journal’s website.
The study included 330 adults with major depressive disorder who had either MTHFR C667T or A1298C polymorphisms. (Check your status on these SNPS) While the study report focuses on the marked reduction in homocysteine levels in the vitamin-treated group, it also reports very impressive reduction in depression scores.
The vitamin treated group were taking high doses of three forms of folate (1mg folic acid, 2.5 mg folinic acid, and 7mg of l-methylfolate), magnesium, zinc, phosphotidylserine, and iron, along with microgram doses of the active forms of thiamine, B6, adenosyl-B12, NADH, and TMG. Please see the study for the specific types of each of these vitamins and minerals.
The results of the 8 week trial showed that the vitamin treated group had an average reduction in homocysteine levels from 9.6 at baseline to 7.2 umol/L while the placebo group had a slight increase.
The study included a MADRS (Montgomery-Asberg Depression Rating Scale) score at baseline and after 8 weeks. The vitamin treated group saw a decrease from an average score of 27 at baseline to 15 after 8 weeks, while the placebo group only saw a 1.3 point drop.
Again, I encourage you all to read through the study for yourselves, but to me, it seems to show a significant improvement for those with MTHFR polymorphisms and major depressive disorder.
Other recent studies on MTHFR, methylfolate, homocysteine, and depression:
1) Effectiveness of add-on l-methylfolate therapy in a complex psychiatric illness with MTHFR C677T genetic polymorphism.
2) Association between MTHFR C677T polymorphism and depression: a meta-analysis in the Chinese population.
3) Homocysteine excess: delineating the possible mechanism of neurotoxicity and depression
4) MTHFR: Genetic variants, expression analysis and COMT interaction in major depressive disorder
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