enzyme

MTHFR (Methylenetetrahydrofolate reductase)

MTHFR is an enzyme encoded by the MTHFR gene; it catalyzes the conversion of homocysteine to methionine (Fig. 48.3). High levels of homocysteine (hyperhomocysteinemia), often resulting from MTHFR gene polymorphisms and/or low intake of cofactors such as folate, vitamin B6, and vitamin B12, can themselves determine MTHFR dysfunction. Hyperhomocysteinemia is potentially an independent risk factor for myocardial infarction, hypertension, stroke, and glaucoma. The MTHFR C677T mutation is the polymorphism mostly associated with CVD. It may occur in the heterozygous (CT) and homozygous genotype (TT). The 677C→T variant encodes a thermolabile enzyme with reduced activity. Homocysteine levels are higher in individuals carrying the TT and the CT genotypes. Those individuals undergo significant homocysteine reduction after a Mediterranean diet intake. However, a large-scale prospective study enrolling 24,968 participants and examining healthy white American women for 10 years did not confirm the effect of the Mediterranean diet on the incidence of CVD (de Lorgeril and Salen, 2011). In fact, although the TT genotype determined higher homocysteine levels and higher intakes of folate and B vitamins reduce such homocysteine levels, neither the MTHFR 677C→T mutation nor the intake of folate or B vitamins significantly affected the incidence of CVD. However, a metaanalysis on cardiovascular outcomes related to the MTHFR C677T polymorphism showed that populations carrying the TT genotype experienced a higher incidence of stroke in response to low folate intake.

Ref:
Rosalinda Madonna, Raffaele De Caterina, Chapter 48 - The Nutrigenetics of Cardiovascular Disease, Editor(s): Raffaele DE Caterina, J. Alfredo Martinez, Martin Kohlmeier, Principles of Nutrigenetics and Nutrigenomics, Academic Press, 2020, Pages 355-360, ISBN 9780128045725, https://doi.org/10.1016/B978-0-12-804572-5.00048-3. (https://www.sciencedirect.com/science/article/pii/B9780128045725000483)

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Added on Feb 5, 2022 by Barbara Van De Keer
Edited on Oct 22, 2022 by Barbara Van De Keer

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