Methylation & Detox

Key enzyme for converting folate to its active methylfolate form

Second MTHFR variant affecting enzyme activity in the regulatory domain

Folate transporter — how well folate gets into your cells

Folate processing enzyme — reduced stability increases choline need

B12 recycling enzyme — regenerates active B12 for the methylation cycle

Methionine synthase — uses B12 to convert homocysteine to methionine

Vitamin D receptor — affects how well vitamin D activates cellular processes

Vitamin D activation — converts D3 to 25(OH)D in the liver

Phosphatidylcholine production — affects dietary choline requirements

Dopamine/catecholamine breakdown — affects stress response and methyl donor tolerance

Common synonymous variant in the CBS gene associated with reduced cardiovascular disease risk and enhanced response to folate supplementation

A synonymous variant in CBS affecting homocysteine metabolism and associated with modest changes in transsulfuration pathway activity

Intronic variant in betaine-homocysteine methyltransferase gene associated with selenium levels but no known disease risk

Alters one-carbon metabolism and folate distribution; influences cancer risk, folate levels, and cardiovascular disease in combination with MTHFR variants

Regulatory variant affecting S-adenosylhomocysteine hydrolase expression, influencing methylation cycle balance and SAH clearance

Histamine breakdown in gut - reduced activity means dietary histamine accumulates

DAO structural variant affecting enzyme activity and histamine degradation

DAO structural variant near the catalytic domain affecting histamine degradation

Histamine breakdown in blood and tissues - uses methyl groups from SAM

HNMT structural variant - reduces enzyme stability and histamine clearance in tissues

Nitric oxide production - reduced activity increases cardiovascular risk and oxidative stress

NOS3 expression - controls how much eNOS enzyme is produced for nitric oxide synthesis

Phase II detoxification - acetylation of aromatic amines and certain medications

Slow acetylator variant affecting Phase II detoxification capacity

NAT2 acetylation speed tag SNP - marks rapid vs slow acetylator haplotypes

Lactase persistence - ability to digest lactose (milk sugar) in adulthood

Primary mitochondrial antioxidant enzyme - variant reduces superoxide detoxification in mitochondria

Selenium-dependent antioxidant enzyme that neutralizes hydrogen peroxide; the Leu variant reduces enzyme activity and responsiveness to selenium

Phase II detoxification enzyme that conjugates glutathione to carcinogens, drugs, and oxidative stress products; this variant alters the active site geometry, changing substrate specificity

Second functional variant in glutathione S-transferase Pi 1, reducing enzyme activity to ~80% of normal and defining key GSTP1 haplotypes that affect detoxification capacity and cancer susceptibility

Tag SNP proxy for GSTM1 gene deletion status — the most common pharmacogenomic variant worldwide, eliminating a Phase II detoxification enzyme that conjugates glutathione to environmental carcinogens

Phase II detoxification enzyme that reduces quinones and recycles CoQ10 to its active ubiquinol form; variant causes near-complete loss of enzyme activity

Phase I detoxification enzyme that activates polycyclic aromatic hydrocarbons and metabolizes estrogens; the Val variant increases catalytic activity, producing more reactive intermediates

Phase I detoxification enzyme that hydroxylates estradiol to potentially genotoxic 4-hydroxyestradiol and activates environmental procarcinogens including PAHs

Catalase promoter variant affecting hydrogen peroxide clearance and antioxidants defense capacity

Complete deletion of the GSTT1 gene eliminating glutathione conjugation capacity for industrial solvents and certain carcinogens