Homocysteine !

Homocysteine forms when methionine donates methyl groups. If it builds up, it damages vessels and favours thrombosis.

Updated 2026-11-01

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Key facts

It comes from S-adenosylhomocysteine after each methylation made by SAM.
Two fates: back to methionine (methionine synthase, with B12 and 5-methyl-THF) or on to cysteine (cystathionine β-synthase, with B6).
It rises with B12, folate or B6 deficiency, kidney failure and homocystinuria.
It is not part of proteins.

It has one more carbon than cysteine in the side chain, which ends in a thiol group (–SH).

High homocysteine with high methylmalonic acid points to B12 deficiency; with normal methylmalonic acid, to folate deficiency.
Hyperhomocysteinaemia is linked to atherosclerosis and to arterial and venous thrombosis.
Classic homocystinuria (CBS) gives lens dislocation, a marfanoid habitus and thrombosis.

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Which two vitamins does remethylation of homocysteine to methionine need?

B12 (methylcobalamin) and folate as 5-methyltetrahydrofolate.

How does methylmalonic acid separate B12 deficiency from folate deficiency?

Both raise homocysteine, but only B12 deficiency raises methylmalonic acid.

Which B6 enzyme sends homocysteine towards cysteine?

Cystathionine β-synthase, which joins it to serine to make cystathionine.

Molecules are shown in their neutral form, as the databases deposit them; in the cell the acids and phosphates are ionised.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: L-Homocysteine (CID 91552) (PubChem, NCBI, 2026) · Public domain; Homocysteine Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); Sulfur amino acid metabolism (Reactome, 2026).

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Representative model, for educational purposes only.