Strategic Supplementation for Methylation Processes (Part 2 of 3)
Knowing what the research demonstrates (as presented in Part 1 of this blog post series), those individuals with polymorphisms that alter their ability to methylate and who are experiencing related symptoms may benefit from supplementation of folate or folic acid, vitamin B6 and vitamin B12.
Using methylated (active) versions of these vitamins can help bypass inefficiency occurring. Ensuring adequate levels of helper molecules (‘cofactors’) for methylation processes is of importance. Some cofactors to consider include methionine (an amino acid), vitamin B6 and magnesium (necessary for the metabolism of homocysteine - an amino acid), in conjunction with the overall methylation processes.[i]
Supplementing with methylcobalamin and methylfolate (methylated forms of vitamins B12 and B9) may be prudent for those presenting with hypomethylation (sub-optimal methylation) symptoms. C677T heterozygotes and homozygotes have ~65% and 30%, respectively, of the enzyme activity as compared to those who do not possess a genetic abnormality.[ii]
Two different studies demonstrated that using 5-methyltetrahydrofolate (5-MTHF – an active, tissue-ready form of folate), had similar effects on homocysteine levels as did folic acid. Considering that 5-MTHF bypasses the methylation processes (which is impaired in MTHFR individuals), this may be a better option.[iii]
Additionally, due to the fact that so many of the B-complex vitamins influence one other, I would suggest a B-complex that includes L-5-MTHF, pyridoxal 5’-phosphate and methylcobalamin, monitoring and adjusting, as needed.
Ideally, this would be done through whole food consumption of protein sources and a wide variety of plant foods, but those with genetic predispositions may require additional supplementation of these nutrients. While I’m certainly a believer in the ‘Food First’ approach, I know, firsthand (I carry the homozygous MTHFR C677>TT genotype), that in some cases, therapeutic supplementation is necessary when working towards correcting nutritional deficiencies.
[i] Oberg, E., Givant, C., Fisk, B., Parikh, C., & Bradley, R. (2015). Epigenetics in Clinical Practice: Characterizing Patient and Provider Experiences with MTHFR Polymorphisms and Methylfolate. J
[ii] Oberg, E., Givant, C., Fisk, B., Parikh, C., & Bradley, R. (2015). Epigenetics in Clinical Practice: Characterizing Patient and Provider Experiences with MTHFR Polymorphisms and Methylfolate. J
[iii] Henderson, A. M., Aleliunas, R. E., Loh, S. P., Khor, G. L., Harvey-Leeson, S., Glier, M. B., & ... Devlin, A. M. (2018). l-5-Methyltetrahydrofolate Supplementation Increases Blood Folate Concentrations to a Greater Extent than Folic Acid Supplementation in Malaysian Women. The Journal Of Nutrition, 148(6), 885-890. doi:10.1093/jn/nxy057
Sicińska, E., Brzozowska, A., Roszkowski, W., & Finglas, P.M. (2017). Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer’s Disease. The New England Journal of Medicine, 346(7): 64-73 https://doi-org.uws.idm.oclc.org/10.1080/09637486.2017.1320536