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Session: Nutrient-Gene Interactions/Precision Nutrition (Poster Theater Flash Session 5)

(PTFS05-06-24) Effect of Methylfolate, Pyridoxal-5'-phosphate, and Methylcobalamin Supplementation on Homocysteine and LDL-C Levels in Patients With MTHFR, MTR, and MTRR Polymorphisms

Sunday, June 30, 2024
10:20 AM – 10:24 AM CT
Location:  Hall F1 (The Hub) - Poster Theater
Objectives: Exploring the link between genetic polymorphisms in folate metabolism genes (MTHFR, MTR, MTRR) and cardiovascular disease (CVD), this study evaluates the effect of B vitamin supplements (methylfolate, pyridoxal-5’-phosphate, and methylcobalamin) on homocysteine and lipid levels, potentially guiding personalized CVD risk management.

Methods: In a randomized, double-blind, placebo-controlled trial, 54 patients aged 40-75 with elevated homocysteine and moderate LDL-C levels were divided based on MTHFR, MTR, and MTRR genetic polymorphisms. Over six months, they received either a combination of methylfolate, P5P, and methylcobalamin or a placebo.

Results: At 6-month follow-up, the treatment group demonstrated a significant reduction in homocysteine levels by 30.0% (95% CI: -39.7% to -20.3%) and LDL-C by 7.5% (95% CI: -10.3% to -4.7%), compared to the placebo (p < 0.01 for all)

In the subgroup analysis, homozygous minor allele carriers showed a more significant reduction in homocysteine levels (48.3%, 95% CI: -62.3% to -34.3%, p< 0.01) compared to mixed allele carriers (18.6%, 95% CI: -25.6% to -11.6%, p< 0.01), with a notable intergroup difference (29.7%, 95% CI: -50.7% to -8.7%, p< 0.01). LDL-C levels decreased by 11.8% in homozygous carriers (95% CI: -15.8% to -7.8%, p< 0.01) and 4.8% in mixed allele carriers (95% CI: -6.8% to -2.8%, p< 0.01), with a significant between-group difference (7.0%, 95% CI: -13.0% to -1.0%, p< 0.01).

Conclusions: Methylfolate, P5P, and methylcobalamin supplementation tailored to genetic profiles effectively reduced homocysteine and LDL-C levels in patients with specific MTHFR, MTR, and MTRR polymorphisms, particularly with homozygous minor allele polymorphisms.

Funding Sources: The authors declare that this study received funding from S.Lab (SOLOWAYS), LLC. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this abstract or the decision to submit it for publication.