Methylation status marker — elevation reflects B-vitamin (B12, folate, B6) sufficiency and overall methylation capacity.
Homocysteine is an amino acid intermediate in methionine metabolism. Elevation reflects insufficient B12, folate, or B6 — the cofactors required to remethylate homocysteine back to methionine or convert it to cysteine. Persistently elevated homocysteine associates with cardiovascular disease, cognitive decline, and bone fracture risk.
While the causal link to CV events is debated (homocysteine-lowering trials with B-vitamins haven't reliably reduced CV events), elevated homocysteine remains a useful read on methylation health — relevant for B-vitamin sufficiency, MTHFR status, and overall metabolic resilience.
Homocysteine is influenced by: B12 status, folate status, B6 status, MTHFR genotype (677TT raises modestly), kidney function (rises with declining eGFR), alcohol intake, smoking, hypothyroidism, and pharmacologic agents — methotrexate raises; metformin can lower B12 → raise homocysteine; some anticonvulsants raise; B-vitamin supplementation lowers reliably.
Pair with B12, folate (RBC folate ideally), and creatinine for full context. If elevated, methylated B-vitamins (methylcobalamin + L-methylfolate) typically lower it within 4–8 weeks. MTHFR variants warrant the methylated forms specifically. Long-term metformin use can drive B12 deficiency that raises homocysteine — monitor on GLP-1 + metformin combos.
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Start tracking →Informational only — not medical advice. Reference ranges vary by lab and individual context. Work with a licensed provider to interpret your specific results.