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A raised homocysteine is usually not a heart finding but a vitamin finding — and B12 belongs measured before folate is taken.
Also known as: hyperhomocysteinemia · elevated homocysteine
Open in the tool — with search and all the links →This compilation is for information and replaces neither medical diagnosis nor treatment. If you have symptoms, see a doctor.
Homocysteine is an intermediate in protein metabolism. The body normally breaks it down promptly — for that it needs vitamin B12, folate and vitamin B6. If one of them is short, the substance builds up, and that is exactly what the value measures. It is therefore less an illness than an indicator: a raised homocysteine means in the great majority of cases that one of these three vitamins is running low — and that is the real piece of information. Other reasons for a high value are declining kidney function, an underactive thyroid, smoking and several medicines, among them metformin, stomach protectants, methotrexate and levodopa. The gene variant MTHFR is often mentioned here; it is very common and on its own usually without consequence — it explains a high value only together with short vitamins. Under B12 and folate the value falls reliably. What that fall achieves at the heart and vessels is still judged differently; the tangible gain lies elsewhere: a high value almost always uncovers a real B12 or folate deficiency, and that matters for blood and nerves in its own right. Two tests therefore belong alongside it before anything is taken.
This is the most important order in the whole dossier. Folate puts the blood count right even when B12 is what is truly missing — and then the only visible clue falls away while the nerves go on taking damage.
B12, folate and B6 work at the same place. Filling only one often merely shifts the imbalance.
If the eGFR falls, homocysteine rises by itself. Then the value is not the problem but what drives it.
An underactive thyroid lifts the value along and is easily missed, because it otherwise announces itself little. One TSH is enough.
Folate sits in spinach, salad, broccoli, lentils and chickpeas. It is heat-sensitive, so briefly cooked brings more than long boiled.
The value responds slowly. A single measurement says little; only the second shows whether the gap has closed.
Folic acid, B12 and B6 lower homocysteine reliably — by about a quarter to a third within four to eight weeks. What they did not achieve in large trials is a fall in heart attack and stroke; for stroke, reviews showed a small effect. So the value can be lowered without that answering everything — one of the clearer cases where a number and an outcome part company.
A value above 15 µmol/l counts as raised; above 30 as moderate, above 100 as severe. The blood sample must be processed within an hour, because the value rises in standing blood — a tube processed too late is the most common cause of a falsely high value. On B vitamins the value falls within four to eight weeks by about a quarter to a third. About one in ten people carries a gene variant that raises it slightly.
Red cells that are too large are the classic companion. They point to B12 or folate — which of the two, only the measurement decides.
If that is added, it is almost always about B12 and not about the homocysteine value itself. It is the sign not to wait on.
Metformin and stomach protectants reduce B12 uptake over time, methotrexate acts on folate metabolism. That is no reason to stop, but one to check the value.
Very many people carry this gene variant. On its own it rarely explains anything; it becomes visible only together with low folate. A test as a rule changes nothing about what is done.
In that situation the value is often measured along. It is then one of several pieces and not the explanation by itself.
The value itself. It varies with kidney function and rises with age, so it is always read together with the creatinine.
The most important of the three. It belongs before any folate is taken, because folate alone can tidy the blood count while a B12 deficiency quietly continues at the nerves.
The second building block. The serum value shifts with the last meal; folate inside the red cells is steadier.
The kidney helps break homocysteine down. Some raised values are explained by that alone — and then the kidney is the actual finding.
An underactive thyroid raises the homocysteine value, and treating it lowers it again. That is one of the few points in this matter that can be cleanly fixed.
Metformin lowers the B12 level over years, and homocysteine rises with it. Anyone on metformin has B12 measured regularly — that is the practical consequence of this value.
Homocysteine is broken down with these three vitamins. If one is missing, the value rises. Leafy greens and pulses supply folate, animal foods B12; with a proven deficiency supplementation is targeted.
The vitamins reliably lower homocysteine by 20–30 %. Whether that means fewer heart attacks could not be shown by large trials. Both belong in the same sentence.
Folate, B12 and B6 reliably lower homocysteine by 20–30 %. Whether fewer heart attacks and strokes follow could not be shown by large trials — the value falls, the event remains.
A B12 deficiency is one of the most common causes of raised homocysteine and is often missed — especially on metformin and with a plant-based diet.