Effect of Methylfolate, Pyridoxal-5'-Phosphate, and Methylcobalamin (SolowaysTM) Supplementation on Homocysteine and Low-Density Lipoprotein Cholesterol Levels in Patients with Methylenetetrahydrofolate Reductase, Methionine Synthase, and Methionine Synthase Reductase Polymorphisms: A Randomized Controlled Trial.

Exploring the link between genetic polymorphisms in folate metabolism genes (MTHFR, MTR, and 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. 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. At the 6 months 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). 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.

The Impact of Glucomannan, Inulin, and Psyllium Supplementation (SolowaysTM) on Weight Loss in Adults with FTO, LEP, LEPR, and MC4R Polymorphisms: A Randomized, Double-Blind, Placebo-Controlled Trial.

This study aimed to determine the impact of a fiber supplement on body weight and composition in individuals with obesity with specific genetic polymorphisms. It involved 112 adults with obesity, each with at least one minor allele in the FTO, LEP, LEPR, or MC4R polymorphism. Participants were randomized to receive either a fiber supplement (glucomannan, inulin, and psyllium) or a placebo for 180 days. The experimental group showed significant reductions in body weight (treatment difference: -4.9%; 95% CI: -6.9% to -2.9%; p < 0.01) and BMI (treatment difference: -1.4 kg/m2; 95% CI: -1.7 to -1.2; p < 0.01) compared to placebo. Further significant decreases in fat mass (treatment difference: -13.0%; 95% CI: -14.4 to -11.7; p < 0.01) and visceral fat rating (treatment difference: -1.3; 95% CI: -1.6 to -1.0; p < 0.01) were noted. Homozygous minor allele carriers experienced greater decreases in body weight (treatment difference: -3.2%; 95% CI: -4.9% to -1.6%; p < 0.01) and BMI (treatment difference: -1.2 kg/m2; 95% CI: -2.0 to -0.4; p < 0.01) compared to heterozygous allele carriers. These carriers also had a more significant reduction in fat mass (treatment difference: -9.8%; 95% CI: -10.6 to -9.1; p < 0.01) and visceral fat rating (treatment difference: -0.9; 95% CI: -1.3 to -0.5; p < 0.01). A high incidence of gastrointestinal events was reported in the experimental group (74.6%), unlike the placebo group, which reported no side effects. Dietary supplementation with glucomannan, inulin, and psyllium effectively promotes weight loss and improves body composition in individuals with obesity, particularly those with specific genetic polymorphisms.

Evaluating the Impact of Omega-3 Fatty Acid (SolowaysTM) Supplementation on Lipid Profiles in Adults with PPARG Polymorphisms: A Randomized, Double-Blind, Placebo-Controlled Trial.

Emerging evidence suggests that PPARG gene polymorphisms may influence lipid metabolism and cardiovascular risk, with omega-3 fatty acids proposed to modulate these effects. This study aims to assess the effects of fish oil supplementation on cardiovascular markers among adults with PPARG gene polymorphisms in a randomized, double-blind, placebo-controlled trial. A cohort of 102 patients with LDL-C 70-190 mg/dL was randomized to receive either 2000 mg of omega-3 fatty acids or a placebo daily for 90 days. In the omega-3 group with PPARG polymorphisms, LDL-C was reduced by 15.4% (95% CI: -19.8% to -11.0%), compared with a 2.6% decrease in the placebo group (95% CI: -4.1% to -1.1%; p < 0.01). In the omega-3 group without PPARG polymorphisms, LDL-C was reduced by 3.7% (95% CI: -6.9% to -0.6%), not significantly different from the placebo group's reduction of 2.9% (95% CI: -5.1% to -0.8%; p = 0.28). The reduction in LDL-C was notably 11.7% greater in those with PPARG polymorphisms than in those without (95% CI: -19.3% to -4.0%; p < 0.01). Triglycerides decreased by 21.3% in omega-3 recipients with PPARG polymorphisms (95% CI: -26.5% to -16.2%; p < 0.01), with no significant changes in HDL-C, total cholesterol, or hsCRP levels in any groups. Minor allele frequencies and baseline characteristics were comparable, ensuring a balanced genetic representation. Omega-3 fatty acids significantly reduce LDL-C and triglycerides in carriers of PPARG polymorphisms, underlining the potential for genetic-driven personalization of cardiovascular interventions.