Homocysteine
Homocysteine reflects folate and vitamin B12 status. Published upper limits run from 10 to about 15 µmol/L by source, sex and age. Cohorts link higher levels to more heart disease, stroke and dementia. In trials, B vitamins lowered homocysteine about 25% without reducing heart attacks or deaths, with slightly fewer strokes and no effect on cognitive function.
- Status
- A blood test ordered by a clinician and also sold direct to consumers by some US laboratories.
- Measures
- The total concentration in plasma or serum of homocysteine, a sulfur-containing product of methionine metabolism whose level reflects the functional status of folate, vitamin B12 and vitamin B6 [1][2].
- Also called
- total homocysteine, plasma homocysteine, serum homocysteine, homocysteine total, tHcy, Hcy, homocyst(e)ine
- Tested for
- heart disease risk, stroke risk, dementia risk, vitamin B12 or folate deficiency, MTHFR gene variants, blood clots, homocystinuria
Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on
Linked in research1
Reported risks0
No risks sourced yet.
Reference ranges
Each range is the one its source published, in µmol/L. Where sources differ, each is shown.
Third US National Health and Nutrition Examination Survey, 1999, men, definition of a high result
Male participants aged 12 and older · [3]
| Range | What the source calls it |
|---|---|
| below 11.4 µmol/L | No name given |
| 11.4 or above µmol/L | "high" |
The survey defined a high concentration as one above the 95th percentile of its reference sample of vitamin-replete men aged 20 to 39, and reports the figure as at least 11.4 µmol/L. The survey defined reference ranges as the 5th to 95th percentiles among participants who were replete in folate and vitamin B12 and had normal creatinine. Samples were serum, collected from 1991 to 1994 [3]. About two thirds of high results were associated with low vitamin concentrations. The survey reports that upper reference limits rose with age, so this single cut point sits below its own upper limit of 15.3 for men aged 60 and older [3].
Third US National Health and Nutrition Examination Survey, 1999, women, definition of a high result
Female participants aged 12 and older · [3]
| Range | What the source calls it |
|---|---|
| below 10.4 µmol/L | No name given |
| 10.4 or above µmol/L | "high" |
The survey defined a high concentration as one above the 95th percentile of its reference sample of vitamin-replete women aged 20 to 39, and reports the figure as at least 10.4 µmol/L. The survey defined reference ranges as the 5th to 95th percentiles among participants who were replete in folate and vitamin B12 and had normal creatinine. Samples were serum, collected from 1991 to 1994 [3]. Its upper reference limit for women aged 60 and older is higher, at 11.6 [3].
Third US National Health and Nutrition Examination Survey, 1999, men aged 60 and older
Men aged 60 and older · [3]
| Range | What the source calls it |
|---|---|
| below 5.9 µmol/L | No name given |
| 5.9 to 15.3 µmol/L | "reference range" |
| above 15.3 µmol/L | No name given |
The survey defined reference ranges as the 5th to 95th percentiles among participants who were replete in folate and vitamin B12 and had normal creatinine. Samples were serum, collected from 1991 to 1994 [3]. The survey gives no term for results outside the range [3].
Third US National Health and Nutrition Examination Survey, 1999, women aged 60 and older
Women aged 60 and older · [3]
| Range | What the source calls it |
|---|---|
| below 4.9 µmol/L | No name given |
| 4.9 to 11.6 µmol/L | "reference range" |
| above 11.6 µmol/L | No name given |
The survey defined reference ranges as the 5th to 95th percentiles among participants who were replete in folate and vitamin B12 and had normal creatinine. Samples were serum, collected from 1991 to 1994 [3]. The survey gives no term for results outside the range [3].
Third US National Health and Nutrition Examination Survey, 1999, boys and young men aged 12 to 19
Male participants aged 12 to 19 · [3]
| Range | What the source calls it |
|---|---|
| below 4.3 µmol/L | No name given |
| 4.3 to 9.9 µmol/L | "reference range" |
| above 9.9 µmol/L | No name given |
The survey defined reference ranges as the 5th to 95th percentiles among participants who were replete in folate and vitamin B12 and had normal creatinine. Samples were serum, collected from 1991 to 1994 [3]. The age band runs to 19, so it includes some young adults [3].
Third US National Health and Nutrition Examination Survey, 1999, girls and young women aged 12 to 19
Female participants aged 12 to 19 · [3]
| Range | What the source calls it |
|---|---|
| below 3.3 µmol/L | No name given |
| 3.3 to 7.2 µmol/L | "reference range" |
| above 7.2 µmol/L | No name given |
The survey defined reference ranges as the 5th to 95th percentiles among participants who were replete in folate and vitamin B12 and had normal creatinine. Samples were serum, collected from 1991 to 1994 [3]. The age band runs to 19, so it includes some young adults [3].
German, Austrian and Swiss Homocysteine Society (DACH-LIGA Homocystein) consensus, 2003
Adults, in the setting of cardiovascular and thrombotic disease risk · [1]
| Range | What the source calls it |
|---|---|
| below 10 µmol/L | "target" |
| 10 to 12 µmol/L | No name given |
| above 12 µmol/L | "moderate hyperhomocysteinemia" |
The consensus sets a target plasma level below 10 µmol/L and describes levels above 12 µmol/L as elevated, calling them moderate hyperhomocysteinemia. Its published summary gives no term for results from 10 to 12, which are above its target, and reports that risk rises from about 10 µmol/L with no specific threshold. Only that summary was read for this page, so any higher grades the full paper defines are not shown. The consensus predates the large trials of lowering homocysteine and states that their results were needed before screening and treatment could be advised for the apparently healthy general population [1].
International consensus statement on homocysteine and dementia, 2018
Older adults, for risk of cognitive decline and dementia · [2]
| Range | What the source calls it |
|---|---|
| 11 or below µmol/L | No name given |
| above 11 µmol/L | "moderately raised" |
The statement describes plasma total homocysteine above 11 µmol/L as moderately raised and common in the elderly. It also notes that a value above 13 µmol/L was used in a cost model and for recruiting one trial, that a threshold between 10 and 11 may prove more appropriate, and that 10 to 13 µmol/L is well within the normal range found in the elderly. It is a statement by a group of researchers in the field, set for cognitive outcomes [2].
Smith and Refsum review, 2021
Adults · [4]
| Range | What the source calls it |
|---|---|
| 10 or below µmol/L | "probably safe" |
| 11 or above µmol/L | "may justify intervention" |
The conclusion of two authors' review of the literature, not a guideline. They state the two values as whole numbers, 10 or below and 11 or above, and name nothing between them. The labels are the authors' own words [4].
What has been shown to move it
Shown to lower it5
Homocysteine
Shown to lower homocysteine in adults with high levels, kidney disease or type 2 diabetes. In kidney disease, cardiovascular events did not fall.
The numbers and sources
- Effect
- In 36 RCTs of adults with high homocysteine, folic acid alone lowered homocysteine (SMD -0.99, 95% CI -1.15 to -0.83, I² 90%), with the largest effects at 5 to 15 mg a day and after 6 months or more [12]. In 14 RCTs in chronic kidney disease, folate-based supplements lowered homocysteine by 8.09 µmol/L (95% CI -11.54 to -4.63, I² 98%), while cardiovascular events (RR 0.88, 95% CI 0.68 to 1.13), all-cause mortality and cardiovascular mortality did not change [13]. In 29 studies in type 2 diabetes, folic acid with B12 lowered homocysteine (SMD -2.77, 95% CI -3.23 to -2.30) [14].
- Population
- Adults with high homocysteine [12]; 8,625 adults with chronic kidney disease in 37 studies [13]; adults with type 2 diabetes [14].
- Sources
- [12], [13], [14]
- Caveats
- Heterogeneity was high in all three. The high-homocysteine review found substantial risk of bias and likely overestimation from small-study effects and publication bias, and no included trial reported adjudicated heart attacks, strokes or cardiovascular deaths [12]. The type 2 diabetes estimate is about three times the size of the other review's and combined folic acid with B12 [14]. Lower homocysteine did not translate into fewer cardiovascular events in kidney disease [13].
Homocysteine
Shown to lower homocysteine about 1.2 to 1.3 μmol/L at 4 g a day or more in healthy adults. Heart disease was not measured.
The numbers and sources
- Effect
- Across 5 RCTs of at least 4 g a day for 6 to 24 weeks, betaine lowered plasma homocysteine by 1.23 μmol/L (95% CI -1.61 to -0.85) [1]. A later meta-analysis found a fall of 1.30 μmol/L (95% CI -1.61 to -0.98) [2].
- Population
- Healthy adults in 5 RCTs [1]; RCTs pooled up to February 2021 [2].
- Sources
- [1], [2]
- Caveats
- The two reviews overlap in trials. Neither measured heart disease or death.
Memory and cognitive aging
Not shown to change memory or thinking across 11 trials. One trial in older adults with mild cognitive impairment found slower brain shrinkage.
The numbers and sources
- Effect
- Across 11 trials, B vitamins lowered homocysteine by 26% to 28% and did not change memory, speed, executive function or global cognition (z score difference 0.00, 95% CI -0.05 to 0.06) [3]. In one trial in mild cognitive impairment, brain atrophy was 0.76% a year on B vitamins and 1.08% on placebo (P = 0.001) [4].
- Population
- 22,000 participants in 11 trials, mean 2.3 to 5 years [3]; 168 people over 70 with mild cognitive impairment who completed MRI scans, 24 months [4].
- Sources
- [3], [4]
- Caveats
- The atrophy trial measured brain volume, not cognition. Its effect was concentrated in people with homocysteine above 13 µmol/L [4].
Methylfolate in place of folic acid
Shown to raise blood folate and lower unmetabolized folic acid more than folic acid in women of childbearing age. These are blood markers, not health outcomes.
The numbers and sources
- Effect
- Over 24 weeks, 113 µg a day of L-methylfolate lowered homocysteine 14.6% and 100 µg of folic acid 9.3% against placebo. Red blood cell folate rose 23% and 31% [8]. A 2025 meta-analysis of 11 RCTs in women of childbearing age found that active folate, compared with folic acid, raised plasma folate (p 0.04) and red blood cell folate (p 0.01) and lowered unmetabolized folic acid (p below 0.0001), with no difference in homocysteine or B12. In women with a history of adverse pregnancy outcomes, it was linked to higher later pregnancy rates and fewer adverse outcomes [9]. A 2026 systematic review found that 5-MTHF in place of folic acid reduced unmetabolized folic acid in 3 trials (SMD 0.99, 95% CI 0.20 to 1.79, GRADE low), and showed no difference in homocysteine [10]. A 2024 review reported a lack of clinical studies testing methylfolate for preventing neural tube defects [11].
- Population
- 167 healthy volunteers [8]; women of childbearing age in 11 RCTs [9]; trials and observational studies in two reviews [10][11].
- Sources
- [8], [9], [10], [11]
- Caveats
- Most results are blood markers, not health outcomes. The 2025 meta-analysis notes low study quality and short treatment [9]. The 2026 review found the two trials of red blood cell folate pointed in opposite directions, and found no evidence that unmetabolized folic acid causes harm on its own. Its authors disclosed ties to a company developing a folinic acid drug [10]. [11] is a narrative review funded by ITF Research Pharma.
Correcting B12 deficiency by mouth instead of injection
Shown to raise blood B12 by mouth about as well as injection in people with B12 deficiency. One small trial in children favored injection.
Across 16 studies, serum B12 rose by a pooled 402.6 pg/mL (95% CI 293.6 to 511.5) and homocysteine fell by 4.83 µmol/L, with no significant difference between oral, sublingual and intramuscular routes (p = 0.270) and no dose relationship.
The numbers and sources
- Effect
- In two trials using 1,000 µg a day by mouth, blood B12 levels showed no clinically relevant difference from intramuscular injection. One trial using 2,000 µg a day by mouth found blood B12 680 pg/mL higher than injection (95% CI 392.7 to 967.3) [1]. Across 16 studies, serum B12 rose by a pooled 402.6 pg/mL (95% CI 293.6 to 511.5) and homocysteine fell by 4.83 µmol/L, with no significant difference between oral, sublingual and intramuscular routes (p = 0.270) and no dose relationship [2]. A 2026 review of 13 studies in adults found that all three routes raised serum B12, several with comparable or larger rises by mouth [3]. In a 2026 trial, hemoglobin recovery at 28 days did not differ by route after adjustment, comparing B12 given in the nose, into a vein or into muscle [4].
- Population
- 3 RCTs, 153 people with B12 deficiency, mean ages 38.6 to 72, treated for 3 to 4 months [1]; 16 RCTs and observational studies with 6,098 participants [2]; 13 studies of adults with an indication for replacement in 10 countries [3]; 153 adults with B12 deficiency anemia [4].
- Sources
- [1], [2], [3], [4]
- Caveats
- The Cochrane review rated its evidence low quality, and no trial reported symptoms of deficiency, quality of life or acceptability [1]. The 2025 meta-analysis pooled RCTs with observational studies, heterogeneity was above 80% in most comparisons, and it found signs of publication bias [2]. The 2026 review did not pool, judged every trial at some risk of bias, and was funded by Myralis Indústria Farmacêutica [3]. In children with deficiency anemia, the only trial, at high risk of bias, found larger rises in B12 and hemoglobin with injection [5]. Graded B rather than A because the 2025 meta-analysis mixed in observational studies and the 2026 review did not pool.
Tested, and not shown to change it1
B12 status on a vegan diet
One small trial found a multinutrient with B12 raised blood B12 markers in healthy vegan adults over 4 months.
Methylmalonic acid and homocysteine did not differ between groups.
The numbers and sources
- Effect
- After 4 months, a multinutrient supplement with 82 µg of B12 a day raised serum B12, holotranscobalamin and a combined B12 status indicator against placebo. Methylmalonic acid and homocysteine did not differ between groups [10].
- Population
- 72 healthy vegan adults aged 19 to 57 in Germany [10].
- Sources
- [10]
- Caveats
- One small trial of a supplement with several nutrients, measuring blood markers only [10].
How it compares with the reference method
Matched the reference method1
Variation within one person
Small studies found homocysteine fairly stable within a person, with a within-person standard deviation of about 0.9 µmol/L over a year in older adults.
The numbers and sources
- Compared with
- The same person's repeat measurements
- Effect
- In 20 healthy people sampled weekly for 4 weeks the reliability coefficient was 0.94, and over 30 months it was 0.65, or 0.82 with one outlier excluded. The authors concluded that a single measurement characterizes a person's average concentration reasonably well [16]. In 96 older adults measured over 1 year, mean homocysteine was 10.4 µmol/L, the standard deviation between people was 2.5 µmol/L and within a person 0.93 µmol/L, a reliability coefficient of 0.88, with little seasonal variation [17].
- Population
- 20 healthy participants [16]. 96 adults aged 65 to 74 [17].
- Sources
- [16], [17]
- Caveats
- Two small studies from the 1990s. A within-person standard deviation near 1 µmol/L is as large as the gap between some published cut points.
Mixed results2
Agreement between laboratories and methods
Limited evidence: one study of 14 laboratories found results varied about 9% between laboratories, and in another two immunoassays read within 4% of reference methods.
The numbers and sources
- Compared with
- Gas chromatography-mass spectrometry and HPLC methods
- Effect
- Across 14 laboratories using 8 types of method, the mean variation among laboratories was 9.3% for plasma samples and the variation between runs within a laboratory was 5.6%. Some methods read systematically higher or lower than gas chromatography-mass spectrometry, and variation among laboratories using one method could exceed variation among methods [14]. In a six-center European evaluation, two immunoassays showed bias of -2% to 3% and 2% to 4% against HPLC and gas chromatography-mass spectrometry, with within-laboratory imprecision below 5% and below 9% [15].
- Population
- 14 laboratories in an international study [14]. Six centers in four countries [15].
- Sources
- [14], [15]
- Caveats
- Both studies date from 1999 and 2000, so current assays may differ. With published cut points only 1 to 2 µmol/L apart, a 9% difference can move a result across one.
Homocysteine as a test of folate or vitamin B12 status
Limited evidence: in one US survey about two thirds of high homocysteine results went with low vitamin levels, and WHO describes the test as not specific.
The numbers and sources
- Compared with
- Serum folate and vitamin B12 concentrations
- Effect
- In a US national survey, approximately two thirds of high homocysteine concentrations were associated with low serum vitamin concentrations [3]. WHO and FAO list total plasma homocysteine of 12 to 16 µmol/L as a cut-off when it is used as an indicator of vitamin B12 status. They describe it as a predictor of B12 status that also rises with inadequate folate, and as not specific because it is also increased by deficiencies of vitamins B2 and B6 and influenced by sex, race and renal insufficiency [18].
- Population
- 3,563 male and 4,523 female participants aged 12 and older [3].
- Sources
- [3], [18]
- Caveats
- One cross-sectional survey from 1991 to 1994 [3]. WHO and FAO print a range of 12 to 16, not a single cut point, so it is not shown as a band above [18].
What studies tie it to
Linked in research1
Dementia in cohorts
Linked to more dementia at higher levels, 35% higher odds for each 5 µmol/L across 8 pooled cohorts.
The numbers and sources
- Effect
- In a meta-analysis of 8 cohort studies, each 5 µmol/L higher serum homocysteine had an odds ratio for new dementia of 1.35 (95% CI 1.02 to 1.79), or 1.50 (95% CI 1.13 to 2.00) after adjustment for regression dilution [10]. In the Framingham Study, each standard deviation higher log homocysteine had a relative risk of dementia of 1.4 (95% CI 1.1 to 1.9), and a level above 14 µmol/L nearly doubled the risk of Alzheimer's disease [11]. A consensus statement reports relative risks from 1.15 to 2.5 across clinical studies [2].
- Population
- 8,669 participants in 8 cohorts, mean ages 47 to 81, median study duration 5 years [10]. 1,092 people without dementia, mean age 76, 111 cases over a median 8 years [11].
- Sources
- [10], [11], [2]
- Caveats
- Observational. The meta-analysis authors state that the results do not provide evidence of cause and effect [10].
Mixed results3
Heart disease and stroke in cohorts and genetic studies
Mixed results: cohorts linked 25% lower homocysteine to 11% less heart disease and 19% less stroke, while large genetic datasets found little or no effect on heart disease.
The numbers and sources
- Effect
- In a meta-analysis of individual data, a 25% lower usual homocysteine level (about 3 µmol/L) was associated in the prospective studies with an 11% lower risk of ischemic heart disease (OR 0.89, 95% CI 0.83 to 0.96) and a 19% lower risk of stroke (OR 0.81, 95% CI 0.69 to 0.95), after adjustment for known risk factors. Associations were stronger in retrospective studies, where blood was drawn after disease onset [5]. In 19 unpublished genetic datasets, people with the MTHFR variant that raises homocysteine by about 20% had no excess of coronary heart disease (OR 1.02, 95% CI 0.98 to 1.07). In 86 published studies of the same variant the odds ratio was 1.15 (95% CI 1.09 to 1.21), a discrepancy the authors attribute to publication bias or methodological problems [6].
- Population
- 30 prospective or retrospective studies with 5,073 ischemic heart disease events and 1,113 stroke events [5]. 48,175 coronary heart disease cases and 67,961 controls in the unpublished datasets, and 28,617 cases and 41,857 controls in the published ones [6].
- Sources
- [5], [6]
- Caveats
- The cohort authors conclude that raised homocysteine is at most a modest independent predictor in healthy populations [5]. The genetic datasets did not measure homocysteine itself and tested heart disease, not stroke [6].
Stroke in trials that lowered homocysteine
Mixed results: a Cochrane review found 10% fewer strokes with homocysteine-lowering B vitamins, while a pooled analysis of 8 trials found no significant effect.
The numbers and sources
- Effect
- A Cochrane review found a small reduction in stroke with homocysteine-lowering B vitamins against placebo (4.3% against 5.1%, RR 0.90, 95% CI 0.82 to 0.99, 10 trials) [8]. An individual-data meta-analysis of 8 trials found a rate ratio for stroke of 0.96 (95% CI 0.87 to 1.06) [7]. In a Chinese trial in adults with hypertension, adding folic acid 0.8 mg to enalapril lowered first stroke (HR 0.79, 95% CI 0.68 to 0.93) over a median 4.5 years, with no difference in heart attack or death from any cause [9].
- Population
- 44,224 participants in the 10 trials with stroke data [8]. 37,485 participants in 8 trials [7]. 20,702 adults with hypertension and no history of stroke or heart attack [9].
- Sources
- [8], [7], [9]
- Caveats
- The Cochrane authors calculate that about 143 people would need treatment with folic acid plus enalapril for 5.4 years to prevent 1 stroke, and note that this evidence came from one very large trial [8].
Cognitive decline and brain shrinkage in trials that lowered homocysteine
Mixed results: pooled trials found no effect of homocysteine-lowering B vitamins on cognitive function, while one trial in mild cognitive impairment found slower brain shrinkage.
The numbers and sources
- Effect
- In a meta-analysis of 11 trials, B vitamins lowered homocysteine by 26% to 28% and had no significant effect on individual cognitive domains or on global cognitive function (z score difference -0.01, 95% CI -0.03 to 0.02). The authors calculate that a 25% reduction in homocysteine equated to 0.02 years of cognitive aging per year (95% CI -0.10 to 0.13) [12]. In a 2-year trial in people over 70 with mild cognitive impairment, the yearly rate of brain atrophy was 0.76% (95% CI 0.63 to 0.90) with folic acid, vitamin B12 and vitamin B6 and 1.08% (95% CI 0.94 to 1.22) with placebo. Among participants whose homocysteine was above 13 µmol/L, the rate was 53% lower with treatment [13].
- Population
- 22,000 participants in 11 trials, treated for a mean of 2.3 to 5 years [12]. 271 people randomized, 168 of whom completed the brain scans [13].
- Sources
- [12], [13]
- Caveats
- The single trial measured brain volume on scans as its main outcome, in one center [13]. In 7 of the 11 pooled trials, cognitive tests were available only at the end of treatment [12].
Checked, no link found1
Heart attack and death in trials that lowered homocysteine
Not shown to fall when homocysteine is lowered: B vitamins cut homocysteine about 25%, and heart attacks and deaths did not differ from placebo across pooled trials.
The numbers and sources
- Effect
- In a meta-analysis of individual data from 8 placebo-controlled trials, folic acid lowered homocysteine by an average of 25% and had no significant effect on major vascular events (rate ratio 1.01, 95% CI 0.97 to 1.05) or major coronary events (1.03, 95% CI 0.97 to 1.10), overall or in any subgroup studied. Nor did it change overall cancer incidence (1.05, 95% CI 0.98 to 1.13) or death from any cause (1.02, 95% CI 0.97 to 1.08) [7]. A Cochrane review of 15 trials found no difference from placebo in heart attack (RR 1.02, 95% CI 0.95 to 1.10, 12 trials) or death from any cause (RR 1.01, 95% CI 0.96 to 1.06, 11 trials), and judged that further trials were unlikely to change the finding [8].
- Population
- 37,485 people at increased cardiovascular risk in 8 trials, median follow-up 5 years, 9,326 major vascular events [7]. 71,422 participants in 15 trials with follow-up of 1 to 7.3 years [8].
- Sources
- [7], [8]
- Caveats
- The pooled trials ran for a median of 5 years in people at increased risk of cardiovascular disease, so they say little about longer treatment or lower-risk people [7].
Sources
- Stanger O, Herrmann W, Pietrzik K, et al. DACH-LIGA Homocystein (German, Austrian and Swiss Homocysteine Society): Consensus Paper on the Rational Clinical Use of Homocysteine, Folic Acid and B-Vitamins in Cardiovascular and Thrombotic Diseases: Guidelines and Recommendations. Clinical Chemistry and Laboratory Medicine. 2003. https://doi.org/10.1515/CCLM.2003.214
- Smith AD, Refsum H, Bottiglieri T, et al. Homocysteine and Dementia: An International Consensus Statement. Journal of Alzheimer's Disease. 2018. https://doi.org/10.3233/JAD-171042
- Selhub J, Jacques PF, Rosenberg IH, et al. Serum Total Homocysteine Concentrations in the Third National Health and Nutrition Examination Survey (1991-1994): Population Reference Ranges and Contribution of Vitamin Status to High Serum Concentrations. Annals of Internal Medicine. 1999. https://doi.org/10.7326/0003-4819-131-5-199909070-00003
- Smith AD, Refsum H. Homocysteine, from disease biomarker to disease prevention. Journal of Internal Medicine. 2021. https://doi.org/10.1111/joim.13279
- Homocysteine Studies Collaboration. Homocysteine and Risk of Ischemic Heart Disease and Stroke: A Meta-analysis. JAMA. 2002. https://doi.org/10.1001/jama.288.16.2015
- Clarke R, Bennett DA, Parish S, et al. Homocysteine and Coronary Heart Disease: Meta-analysis of MTHFR Case-Control Studies, Avoiding Publication Bias. PLoS Medicine. 2012. https://doi.org/10.1371/journal.pmed.1001177
- 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. https://doi.org/10.1001/archinternmed.2010.348
- Martí-Carvajal AJ, Solà I, Lathyris D, Dayer M. Homocysteine-lowering interventions for preventing cardiovascular events. Cochrane Database of Systematic Reviews. 2017. https://doi.org/10.1002/14651858.CD006612.pub5
- 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. https://doi.org/10.1001/jama.2015.2274
- Wald DS, Kasturiratne A, Simmonds M. Serum homocysteine and dementia: Meta-analysis of eight cohort studies including 8669 participants. Alzheimer's & Dementia. 2011. https://doi.org/10.1016/j.jalz.2010.08.234
- Seshadri S, Beiser A, Selhub J, et al. Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease. New England Journal of Medicine. 2002. https://doi.org/10.1056/NEJMoa011613
- Clarke R, Bennett D, Parish S, et al. Effects of homocysteine lowering with B vitamins on cognitive aging: meta-analysis of 11 trials with cognitive data on 22,000 individuals. The American Journal of Clinical Nutrition. 2014. https://doi.org/10.3945/ajcn.113.076349
- Smith AD, Smith SM, de Jager CA, et al. Homocysteine-Lowering by B Vitamins Slows the Rate of Accelerated Brain Atrophy in Mild Cognitive Impairment: A Randomized Controlled Trial. PLoS ONE. 2010. https://doi.org/10.1371/journal.pone.0012244
- Pfeiffer CM, Huff DL, Smith SJ, Miller DT, Gunter EW. Comparison of Plasma Total Homocysteine Measurements in 14 Laboratories: An International Study. Clinical Chemistry. 1999. https://doi.org/10.1093/clinchem/45.8.1261
- Nexo E, Engbaek F, Ueland PM, et al. Evaluation of Novel Assays in Clinical Chemistry: Quantification of Plasma Total Homocysteine. Clinical Chemistry. 2000. https://doi.org/10.1093/clinchem/46.8.1150
- Garg UC, Zheng ZJ, Folsom AR, et al. Short-term and long-term variability of plasma homocysteine measurement. Clinical Chemistry. 1997. https://doi.org/10.1093/clinchem/43.1.141
- Clarke R, Woodhouse P, Ulvik A, et al. Variability and determinants of total homocysteine concentrations in plasma in an elderly population. Clinical Chemistry. 1998. https://doi.org/10.1093/clinchem/44.1.102
- Allen L, de Benoist B, Dary O, Hurrell R, eds. Guidelines on food fortification with micronutrients. Geneva: World Health Organization and Food and Agriculture Organization of the United Nations, 2006. ISBN 92-4-159401-2. https://iris.who.int/handle/10665/43412