Acetaminophen in doses above 2g/day (saturates sulfation and glucuronidation, depletes glutathione catastrophically) R Alcohol (depletes glutathione, NAD+, SAM-e, and directly damages hepatocytes) R Charcoal-grilled meats (heterocyclic amines that undergo bioactivation via sulfation and acetylation, generating DNA-reactive intermediates) R Chronic NSAID use (competes for glucuronidation and amino acid conjugation pathways) Excess fructose (depletes ATP and drives uric acid production, impairing energy-dependent conjugation) R Glyphosate residues on non-organic produce (disrupts glycine metabolism and chelates manganese) R High-dose turmeric or quercetin without cycling (both inhibit SULT1A1 and can paradoxically impair sulfation at high sustained doses) R Processed foods with benzoate preservatives (benzoic acid consumes glycine through conjugation, depleting the glycine pool for other Phase II reactions) R Proton pump inhibitors chronically (reduce magnesium absorption, impair glucuronidation) R Testing These tests can help identify which conjugation pathways are impaired and what is contributing to the dysfunction
MOTS-c and epithalon sit further out on the timeline
As methionine, ingested as protein in the diet, is the only source of homocysteine, it would be expected that food intake would cause increased concentrations of homocysteine in plasma
Papp KA, Menter MA, Abe M, et al
We suggest regular checks of: Serum B12 levels Methylmalonic acid (MMA) levels Complete Blood Count (CBC) These tests help doctors see if B12 is working right and adjust treatment as needed
