Lab result explainedMetabolic panelLast updated November 8, 2026

Homocysteine blood test: what high homocysteine means and how to lower it

Homocysteine · Homocysteine (often ordered with vitamin B12, folate and methylmalonic acid) · reported in µmol/L (micromoles per litre); some labs report mg/L (1 mg/L = 7.4 µmol/L)

Homocysteine is a sulfur-containing amino acid that your body makes when it breaks down methionine from dietary protein. It is normally recycled quickly back to methionine or converted to cysteine, and both routes depend on B vitamins: folate and vitamin B12 for the recycling pathway, vitamin B6 for the conversion pathway, and riboflavin (B2) as a cofactor for the MTHFR enzyme. A normal fasting level is roughly 5 to 15 micromoles per litre (µmol/L), and many researchers consider under 10 optimal. When the B vitamins are short, or the kidneys cannot clear it, homocysteine builds up in the blood.

People search for homocysteine for two main reasons. The first is that a high level is a sensitive sign of folate or vitamin B12 deficiency, often before the blood count changes, and it is used alongside methylmalonic acid to confirm a borderline B12 result. The second is cardiovascular risk: observational studies consistently show that higher homocysteine goes with more heart attacks, strokes, blood clots and dementia. The twist, and the reason this test is less fashionable than it was, is that lowering homocysteine with B vitamins in large randomised trials did not reduce heart attacks, although it did reduce stroke modestly, by about 10 to 25 percent.

The common MTHFR C677T gene variant, carried in its double (TT) form by about 10 percent of people of European descent and more in Hispanic populations, slows folate metabolism and raises homocysteine by around 20 to 25 percent, but only when folate intake is low. Severe elevations above 100 µmol/L are rare and come from inherited enzyme deficiencies (homocystinuria) that are picked up on newborn screening. For most adults, a mildly high homocysteine is a prompt to check B12, folate, kidney and thyroid function and to look at diet, smoking and coffee, rather than a diagnosis in itself.

Homocysteine at a glance

What it is: an amino acid formed from methionine; cleared by folate- and B12-dependent remethylation and B6-dependent transsulfuration, and by the kidneys.
Normal: about 5–15 µmol/L fasting (some labs 4–12); under 10 is considered optimal. Levels rise with age and are slightly higher in men.
Mild elevation 15–30 µmol/L: most often low folate or B12, kidney impairment, hypothyroidism, smoking, heavy coffee, or the MTHFR TT variant with a low-folate diet.
Intermediate 30–100 µmol/L: moderate to severe B12 deficiency, advanced kidney disease, or certain drugs. Over 100 µmol/L: inherited homocystinuria.
Folic acid (0.4–1 mg), B12 and B6 lower homocysteine by about 25 percent within 6 weeks; riboflavin helps in people with the MTHFR TT genotype.
Large trials show that lowering homocysteine reduces stroke by about 10–25 percent but does not reduce heart attacks; it is not a substitute for treating cholesterol and blood pressure.

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What Homocysteine measures

Methionine from food is activated to S-adenosylmethionine, the body's main methyl donor for DNA, neurotransmitters and cell membranes. After it donates its methyl group it becomes homocysteine. Homocysteine then has two exits. In remethylation, the enzyme methionine synthase uses vitamin B12 and 5-methyltetrahydrofolate (made from folate by MTHFR, which needs riboflavin) to turn it back into methionine; the liver and kidney can also use betaine from choline. In transsulfuration, cystathionine beta-synthase uses vitamin B6 to convert it to cystathionine and then cysteine. Block either exit and homocysteine spills into the blood.

The test measures total plasma homocysteine, which includes the free amino acid and the larger fraction bound to proteins and to itself, by immunoassay or liquid chromatography. Fasting for 8 to 12 hours is usually requested because a protein meal raises it by 10 to 15 percent for several hours. Sample handling matters more than for most tests: red blood cells keep releasing homocysteine after the draw, raising the result by about 10 percent per hour at room temperature, so the tube must be kept on ice and separated within an hour. A mildly high result from a sample that sat on a bench is a common artefact.

Homocysteine is about 70 percent cleared by the kidneys through metabolism rather than filtration, so it rises as kidney function falls; nearly everyone on dialysis has a level of 20 to 40 µmol/L. Levels are 1 to 2 µmol/L higher in men than women, rise with age, fall by 30 to 50 percent during pregnancy, and are raised by smoking, heavy coffee drinking, hypothyroidism, psoriasis and a range of drugs. Homocysteine is also a functional marker: in B12 deficiency both homocysteine and methylmalonic acid rise, whereas in folate deficiency only homocysteine rises, which helps separate the two.

Normal range for Homocysteine

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (µmol/L (micromoles per litre); some labs report mg/L (1 mg/L = 7.4 µmol/L))	Notes
Adults, typical fasting reference range	5–15 µmol/L	Some labs quote 4–12 or up to 13.5 (women) and 15 (men). Use the printed range.
Optimal (lowest observed vascular risk)	Below 10 µmol/L	Cohort studies show risk rising steadily above about 10; most well-nourished adults in countries with folic acid fortification sit at 7–10.
Mild hyperhomocysteinemia	15–30 µmol/L	Low folate or B12 intake, early kidney impairment, hypothyroidism, MTHFR TT genotype, smoking, heavy coffee, alcohol, some drugs.
Intermediate hyperhomocysteinemia	30–100 µmol/L	Significant B12 deficiency (pernicious anemia), advanced chronic kidney disease or dialysis, methotrexate, nitrous oxide exposure, or heterozygous homocystinuria.
Severe hyperhomocysteinemia	Above 100 µmol/L	Classical homocystinuria (cystathionine beta-synthase deficiency) or severe untreated B12 deficiency; needs specialist metabolic care.
Children	About 3–10 µmol/L	Lower than adults; rises through puberty, more in boys.
Pregnancy	About 3–8 µmol/L (30–50 percent below non-pregnant)	Hemodilution and higher kidney clearance; a level above 10 in pregnancy is considered raised and is associated with preeclampsia and placental complications.
Older adults (over 65)	Often 10–18 µmol/L	Partly falling kidney function and B12 absorption; still worth checking B12 and folate rather than accepting as normal.

High homocysteine

A high homocysteine most often means one of the B vitamins that clear it is in short supply, or that the kidneys are not clearing it well. In fortified countries like the United States, folate deficiency has become uncommon and vitamin B12 deficiency is now the leading nutritional cause, particularly in people over 60, vegans and vegetarians, people on metformin or long-term acid suppressants, and anyone with pernicious anemia, celiac disease or previous stomach or bowel surgery. A high homocysteine with a high methylmalonic acid confirms B12 deficiency even when the serum B12 is in the low-normal range (200 to 350 pg/mL).

The second message is about vascular risk. In a pooled analysis of 30 observational studies, a 25 percent lower homocysteine (about 3 µmol/L) was associated with 11 percent less coronary heart disease and 19 percent less stroke, and high levels are also linked to venous blood clots, cognitive decline, osteoporotic fracture and pregnancy complications. However, randomised trials of B vitamins that successfully lowered homocysteine by 25 to 30 percent did not reduce heart attacks or cardiovascular death, which suggests that for the heart, homocysteine is largely a marker of other problems (kidney function, diet, smoking) rather than a direct cause. For stroke the trials are more encouraging: B-vitamin treatment reduced stroke by about 10 percent overall and by 21 percent in a large Chinese trial in people without folic acid fortification.

Very high levels tell a different story. Values above 30 µmol/L in an adult usually reflect significant B12 deficiency, advanced kidney disease or a drug effect, and values above 100 point to an inherited disorder of methionine metabolism. In homocystinuria, untreated high homocysteine causes dislocated lenses, a tall thin build, osteoporosis, learning difficulties and, most dangerously, blood clots in young adulthood, and treatment with B6, folate, B12, betaine and a low-methionine diet dramatically lowers the clot risk.

Common causes

Vitamin B12 deficiency
The leading nutritional cause in the US. Pernicious anemia, vegan diets, metformin, proton-pump inhibitors, gastric bypass, Crohn's disease and ageing gut all reduce B12 absorption. Homocysteine typically rises to 15–50 µmol/L, alongside a raised methylmalonic acid, often before the MCV or hemoglobin change.
Folate deficiency or low folate intake
Still common where flour is not fortified, and in people with alcohol dependence, poor diets, celiac disease or on methotrexate, phenytoin or sulfasalazine. Folate deficiency raises homocysteine but not methylmalonic acid.
MTHFR C677T variant (TT genotype)
About 10 percent of white and 15 to 20 percent of Hispanic Americans carry two copies. The enzyme works at about 30 percent efficiency and is less stable without riboflavin. Homocysteine runs 20 to 25 percent higher than in CC carriers, but only when folate status is low; with adequate folate the difference nearly disappears. Routine MTHFR testing is not recommended by the American College of Medical Genetics.
Chronic kidney disease
Homocysteine rises steadily as eGFR falls below about 60 mL/min and is 2 to 4 times normal in dialysis patients. B vitamins lower it only partially in kidney failure and did not improve outcomes in dialysis trials.
Hypothyroidism
Low thyroid hormone slows homocysteine clearance and reduces kidney function; levels fall back into the normal range within months of starting levothyroxine. Hyperthyroidism lowers homocysteine.
Medications
Methotrexate and other antifolates, phenytoin, carbamazepine, metformin (via B12), nitrous oxide anesthesia (inactivates B12), fibrates, niacin, levodopa, cyclosporine and some oral contraceptives each raise homocysteine, typically by 10 to 30 percent.
Smoking, heavy coffee and alcohol
Smokers run about 1 to 2 µmol/L higher; drinking more than 4 cups of coffee a day raises homocysteine by around 1 to 2 µmol/L (the effect is from coffee compounds, not caffeine alone, and filtered coffee is lower); heavy alcohol use raises it by impairing folate and B6 metabolism.
Vitamin B6 deficiency
Less common on its own, but raises homocysteine after meals more than fasting; seen with alcohol dependence, kidney disease, isoniazid, oral contraceptives and inflammatory conditions that consume B6.
Inherited homocystinuria
Cystathionine beta-synthase deficiency affects about 1 in 100,000 to 300,000 births and produces levels over 100 µmol/L; MTHFR deficiency (severe, not the common variant) and cobalamin metabolism disorders are rarer. Most are now detected by newborn screening for methionine.
Sample handling artefact
Blood left at room temperature before separation gains about 1 µmol/L (roughly 10 percent) per hour as red cells release homocysteine. A mildly raised result that does not fit should be repeated with the sample placed on ice.

Symptoms that can go with it

Usually none; a mildly raised homocysteine is found on blood testing rather than suspected from symptoms
Fatigue, pale skin, breathlessness and a sore tongue if folate or B12 deficiency is the cause
Numbness, tingling or burning in the feet and hands, unsteady walking, and memory or mood changes with B12 deficiency
Swelling, pain and warmth in one leg, or sudden breathlessness and chest pain, with a venous clot (homocysteine is a modest clot risk factor)
In inherited homocystinuria: dislocated eye lenses, severe short-sightedness, a tall thin build, chest or spine deformities, learning difficulties and early blood clots
Recurrent miscarriage, preeclampsia or placental problems in pregnancy are associated with high homocysteine

Low homocysteine

A low homocysteine (below about 5 µmol/L) is not a cause for concern in itself and is usually a sign of generous B-vitamin intake, a plant-rich diet, pregnancy, or being young. There is no lower threshold linked with harm in population studies, and people taking a daily multivitamin or B-complex often sit at 5 to 7 µmol/L.

A handful of situations produce very low values. People with Down syndrome have lower homocysteine because the cystathionine beta-synthase gene is on chromosome 21 and is over-expressed. High-dose B-vitamin supplements, hyperthyroidism, and some rare sulfur amino acid disorders also lower it. A very low homocysteine with symptoms such as weakness or pain has occasionally been linked in small studies with low cysteine and glutathione production, but this is not an established clinical problem and is not something to treat.

Common causes

High B-vitamin intake or supplementation
Folic acid, B12 and B6 in a multivitamin or fortified foods push homocysteine toward the bottom of the range; levels of 4 to 6 µmol/L are common in supplement users.
Pregnancy
Homocysteine falls 30 to 50 percent from the first trimester, through hemodilution, higher kidney clearance and fetal uptake; a pregnancy value of 4 µmol/L is normal.
Down syndrome
Over-expression of cystathionine beta-synthase on chromosome 21 speeds conversion of homocysteine to cystathionine, so levels run below those of other people.
Hyperthyroidism
Raised thyroid hormone increases kidney clearance and metabolism of homocysteine; levels normalise once the thyroid is treated.
Younger age and female sex
Children and premenopausal women have lower values than men and older adults; a result of 5 µmol/L in a young woman is typical.

Symptoms that can go with it

None; a low homocysteine does not produce symptoms
If you take high-dose B vitamins and have symptoms, the symptoms need another explanation

Read it alongside

Vitamin B12 — the most important companion test; a high homocysteine with a low or low-normal B12 (under 350 pg/mL) strongly suggests deficiency.
Methylmalonic acid (MMA) — rises only in B12 deficiency, not folate deficiency, so homocysteine plus MMA separates the two.
Folate (serum or red cell) — low folate raises homocysteine on its own; red cell folate reflects the previous 3 months.
Creatinine and eGFR — kidney function is one of the strongest determinants of homocysteine; a level of 20 µmol/L with an eGFR of 40 may be fully explained.
TSH — hypothyroidism raises homocysteine and is easy to miss.
CBC with MCV — a high MCV (over 100 fL) with a high homocysteine points to B12 or folate deficiency, though the MCV is often normal early on.
LDL cholesterol, blood pressure, A1C and hs-CRP — the established cardiovascular risk factors that homocysteine should be read alongside, not instead of.
Lipoprotein(a) and antiphospholipid antibodies — when homocysteine is checked as part of a work-up for unexplained blood clots or early vascular disease.

What usually happens next

A homocysteine above 15 µmol/L is usually followed by vitamin B12, folate, methylmalonic acid, creatinine and TSH to find the cause; most mild elevations are explained by one of these.
If B12 or folate is low, the deficiency is treated and homocysteine is rechecked after 6 to 8 weeks; it typically falls by 25 to 50 percent and often normalises.
If the cause is kidney disease, hypothyroidism or a medication, the homocysteine is managed by treating the underlying issue; B vitamins may still be given but outcomes evidence is weak in kidney failure.
Ask whether the sample was processed promptly and whether you were fasting; if either is uncertain, a repeat is reasonable before investigating further.
A homocysteine above 30 µmol/L that is not explained by B12 deficiency, kidney disease or drugs, or any level above 100, warrants referral to a metabolic specialist and consideration of genetic testing for homocystinuria, particularly with a personal or family history of early blood clots or lens dislocation.
For cardiovascular purposes, treat homocysteine as a risk marker: make sure LDL cholesterol, blood pressure, glucose and smoking are addressed, since those interventions have proven benefit.

Diet, lifestyle and natural levers with evidence

What can move Homocysteine once the cause is known. Nothing here replaces finding the cause.

Folate from food or folic acid

Strong evidence

Folic acid is the most effective single agent. A meta-analysis of 25 randomised trials by the Homocysteine Lowering Trialists' Collaboration found that 0.8 mg a day lowered homocysteine by about 23 percent, with little further benefit above that dose; 0.2 mg gave about 13 percent and 0.4 mg about 20 percent. The reduction is largest in people with high baseline homocysteine and low folate. Food sources (leafy greens, legumes, liver, fortified grains) work too; US flour fortification lowered population homocysteine by about 7 percent and halved the prevalence of levels above 13 µmol/L.

Folic acid can correct the anemia of B12 deficiency while nerve damage continues, so B12 should be checked or given alongside. Doses above 1 mg a day are prescription-only in the US and are not more effective for homocysteine.

Vitamin B12

Strong evidence

Adding B12 (0.4 mg a day in trials, often 0.5 to 1 mg in supplements) to folic acid lowers homocysteine by a further 7 percent in the general population, and far more in people who are B12-deficient, where levels can fall from 40 to under 12 µmol/L within weeks of injections or high-dose oral B12. Oral doses of 1,000 micrograms a day correct deficiency in most people, including many with pernicious anemia, because about 1 percent is absorbed passively.

Nitrous oxide inactivates B12 and can precipitate severe deficiency in people with marginal stores; mention B12 deficiency before any procedure using it.

Vitamin B6

Moderate evidence

B6 has little effect on fasting homocysteine in trials (about 1 to 3 percent lower with 10 to 50 mg a day) but lowers the rise after a protein meal or methionine load by around 20 percent, and it is essential in homocystinuria, where about half of patients respond to high-dose pyridoxine. Most trials used it as part of a folate-B12-B6 combination (typically 2.5 mg folic acid, 50 mg B6, 1 mg B12 in HOPE-2), which lowered homocysteine by about 3 µmol/L.

Chronic intakes above 100 mg a day (and sometimes less over years) cause peripheral nerve damage; the US upper limit is 100 mg a day.

Riboflavin (vitamin B2), particularly for the MTHFR TT genotype

Moderate evidence

Riboflavin is the cofactor that stabilises the MTHFR enzyme, and the variant enzyme in people with the TT genotype loses it easily. In a randomised trial, 1.6 mg a day of riboflavin for 12 weeks lowered homocysteine by 22 percent in TT carriers with low riboflavin status, with no effect in CC carriers. The same group later showed the same dose lowered blood pressure by 5 to 13 mmHg systolic in TT carriers with hypertension in three trials. Riboflavin is found in dairy, eggs, meat and fortified cereals and is non-toxic at these doses.

Betaine (trimethylglycine) and dietary choline

Moderate evidence

Betaine donates a methyl group to homocysteine in the liver through an alternative, folate-independent pathway. In randomised trials, 6 g a day of betaine lowered fasting homocysteine by 10 to 20 percent and blunted the post-methionine rise by up to 50 percent; lower doses of 1.5 to 3 g give smaller reductions, and dietary choline and betaine intake (eggs, beets, spinach, wheat germ, shellfish) are inversely associated with homocysteine in cohort studies. Betaine is the standard add-on treatment in homocystinuria that does not respond to B6.

Doses of 6 g a day raise LDL cholesterol by around 5 to 10 percent and can cause nausea or diarrhea; the effect on long-term outcomes is untested outside homocystinuria.

Less coffee, no smoking and moderate alcohol

Moderate evidence

In a randomised crossover trial, drinking 1 litre of unfiltered coffee a day for 2 weeks raised homocysteine by about 10 percent (around 1 µmol/L) compared with abstaining, and observational studies show a dose-response with heavy intake; filtered coffee has a smaller effect. Smokers' homocysteine runs 1 to 2 µmol/L above non-smokers' and falls after quitting. Heavy alcohol raises homocysteine by depleting folate and B6, whereas light drinking has little effect. These are modest levers but they add up and carry independent vascular benefits.

When to see a clinician promptly

A homocysteine above 100 µmol/L, or any level above 30 µmol/L without an obvious explanation, particularly in a young person or with a family history of early blood clots, dislocated lenses or stroke: possible inherited homocystinuria.
A high homocysteine with symptoms of B12 deficiency, especially numbness, tingling, unsteady walking, memory change or vision change: nerve damage from B12 deficiency can become permanent if treatment is delayed.
Sudden swelling and pain in one leg, sudden breathlessness, chest pain, or sudden weakness, numbness, speech or vision loss: possible clot or stroke, which are emergencies regardless of the homocysteine value.
A high homocysteine in pregnancy or when planning pregnancy, because of the links to neural tube defects, preeclampsia and miscarriage and the importance of folate and B12 before conception.
A high homocysteine with a falling eGFR, or a new high value after starting methotrexate, phenytoin, metformin or another interacting drug.
A high homocysteine that does not fall after 2 to 3 months of appropriate B-vitamin treatment, which suggests a cause other than deficiency.

Frequently asked questions

What is a normal homocysteine level?

Most US labs give a fasting reference range of about 5 to 15 µmol/L, with some using 4 to 12 or sex-specific upper limits of 13.5 for women and 15 for men. Cohort studies show vascular risk rising steadily above about 10 µmol/L, so many clinicians regard under 10 as optimal, 10 to 15 as high-normal, 15 to 30 as mildly raised, 30 to 100 as intermediate and over 100 as severe. Levels rise with age and are a little higher in men.

Is a homocysteine of 12, 15 or 20 high?

A homocysteine of 12 µmol/L is within most reference ranges but above the 'optimal' 10; it is worth checking B12 and folate, especially if you are over 60, vegetarian or on metformin. A level of 15 is at the upper limit and usually prompts the same tests plus kidney function and TSH. A level of 20 is mildly raised and nearly always has a findable cause: B12 or folate deficiency, kidney impairment, hypothyroidism, smoking, heavy coffee, or a medication. None of these values indicates an inherited disorder.

How do I lower homocysteine naturally?

Folate is the biggest lever: 0.4 to 0.8 mg of folic acid a day, or a diet rich in leafy greens, beans and fortified grains, lowers homocysteine by about 20 to 25 percent within 6 weeks. Adding vitamin B12 (especially if you are over 60, vegan or on metformin) lowers it further, B6 helps mainly after meals, and riboflavin helps people with the MTHFR TT variant. Cutting back from heavy coffee intake, stopping smoking and limiting alcohol each take off another 1 to 2 µmol/L. Betaine from beets, spinach and wheat germ works through a separate pathway.

Does high homocysteine cause heart attacks?

Probably not directly. People with higher homocysteine do have more heart disease, but in randomised trials involving more than 37,000 people, lowering homocysteine by 25 to 30 percent with folic acid, B12 and B6 for up to 7 years did not reduce heart attacks or cardiovascular deaths. The same trials did show a modest reduction in stroke, about 10 percent overall and 21 percent in a large Chinese trial of folic acid in people not exposed to fortified flour. The current view is that homocysteine marks vascular risk, mainly from kidney function, B-vitamin status and lifestyle, more than it causes it, so cholesterol, blood pressure, glucose and smoking remain the priorities.

What is the connection between homocysteine and vitamin B12?

Vitamin B12 is the cofactor for methionine synthase, the enzyme that recycles homocysteine back to methionine, so when B12 is low, homocysteine accumulates. Homocysteine rises early in B12 deficiency, often before anemia or a high MCV appear, which is why it is used with methylmalonic acid to confirm deficiency when the serum B12 is borderline (200 to 350 pg/mL). If both homocysteine and methylmalonic acid are high, B12 deficiency is very likely; if only homocysteine is high, folate deficiency is more likely.

Should I get tested for MTHFR if my homocysteine is high?

Usually not. The American College of Medical Genetics and other bodies recommend against routine MTHFR testing because the result does not change management: whether or not you carry the C677T variant, the treatment for high homocysteine is adequate folate (with B12 and riboflavin), and with adequate folate the variant has almost no effect on homocysteine. If you want to act on a possible MTHFR variant, eating folate-rich foods or taking 0.4 mg of folic acid or methylfolate and ensuring good riboflavin and B12 intake covers it. Testing is reasonable only if homocysteine stays high despite correcting vitamins and other causes.

Do I need to fast for a homocysteine test?

Yes, ideally for 8 to 12 hours, because a protein-rich meal raises homocysteine by 10 to 15 percent for several hours. Also avoid taking B-vitamin supplements on the morning of the test if you want a baseline value, and tell the lab if you are on methotrexate, anticonvulsants or metformin. The sample should be placed on ice and separated within an hour; if your result is unexpectedly high, ask whether the sample was processed promptly.

Is high homocysteine linked to dementia or Alzheimer's disease?

Higher homocysteine is associated with faster brain shrinkage and roughly a 1.5 to 2-fold higher risk of dementia in cohort studies, and B12 or folate deficiency can cause reversible cognitive impairment. In the VITACOG trial, B vitamins slowed brain atrophy by about 30 percent in older people with mild cognitive impairment and homocysteine above 11 µmol/L, but larger trials in people with normal cognition showed no benefit on memory. Correcting a deficiency is clearly worthwhile; taking B vitamins to prevent dementia in people with normal levels is not supported.

References

Homocysteine test. MedlinePlus, US National Library of Medicine (2023)View source
Folate: fact sheet for health professionals. NIH Office of Dietary Supplements (2022)View source
Vitamin B12: fact sheet for health professionals. NIH Office of Dietary Supplements (2024)View source
Homocysteine Studies Collaboration. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA (2002)
Homocysteine Lowering Trialists' Collaboration. Dose-dependent effects of folic acid on blood concentrations of homocysteine: a meta-analysis of the randomized trials. American Journal of Clinical Nutrition (2005)
Lonn E, Yusuf S, Arnold MJ, et al.. Homocysteine lowering with folic acid and B vitamins in vascular disease (HOPE-2). New England Journal of Medicine (2006)
Clarke R, Halsey J, Lewington S, et al.. Effects of lowering homocysteine levels with B vitamins on cardiovascular disease, cancer, and cause-specific mortality: meta-analysis of 8 randomized trials involving 37,485 individuals. Archives of Internal Medicine (2010)
Huo Y, Li J, Qin X, et al.. Efficacy of folic acid therapy in primary prevention of stroke among adults with hypertension in China: the CSPPT randomized clinical trial. JAMA (2015)
Li Y, Huang T, Zheng Y, Muka T, Troup J, Hu FB. Folic acid supplementation and the risk of cardiovascular diseases: a meta-analysis of randomized controlled trials. Journal of the American Heart Association (2016)
McNulty H, Dowey le RC, Strain JJ, et al.. Riboflavin lowers homocysteine in individuals homozygous for the MTHFR 677C→T polymorphism. Circulation (2006)
Olthof MR, van Vliet T, Boelsma E, Verhoef P. Low dose betaine supplementation leads to immediate and long term lowering of plasma homocysteine in healthy men and women. Journal of Nutrition (2003)
Hickey SE, Curry CJ, Toriello HV. ACMG practice guideline: lack of evidence for MTHFR polymorphism testing. Genetics in Medicine (2013)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.