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. 2019 Dec 16;43(6):779–786. doi: 10.1007/s40618-019-01163-x

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© The Author(s) 2019

Open AccessThis article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/.

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Fig. 1 — Rationale for homocysteine removal by the administration of a full array of activated micronutrients. The one carbon cycle is regulated by the availability of its substrates; accordingly, a wider availability of each substrate may enhance its performance. Blue background substrates: Folates, B12, chelated zinc, Vit. B2 and Vit. B3 feed homocysteine re-methylation by the folate pathway; Folates in the form of methylfolate escape possible genetic defects in the activity of DHFR and MTHFR; B12 in the form of methylcobalamin escapes possible genetic defects in the activity of MTRR. Red background substrates: Betaine and chelated zinc feed homocysteine re-methylation by the betaine pathway; Pre-formed betaine escapes possible genetic defects in the activity of CHDH and provide an excess of substrate for the BHMT reaction. Green background substrates: Vit. B6, chelated zinc and cysteines feed homocysteine transsulfuration to glutathione (GSH); Excess of cysteines downstream to CBS reaction ensure GSH production even in case of genetic defects of CBS. Key enzymes subject to genetic variability: DHFR DiHydroFolate reductase, MTHFR methylenetetrahydrofolate reductase, MTR methionine reductase (methionine synthase), MTRR methionine synthase reductase, CBS cystathionine beta synthase