Vitamin B12 is a water-soluble vitamin. The term vitamin B12 includes the free vitamin (cyanocobalamin) and two coenzymes methylcobalamin and 5-deoxyadenosylcobalamin.
Vitamin B12 is released from dietary proteins by pepsin and HCl in the stomach. It is bound by R-protein and then the complex travels to the small intestine; in the duodenum, R-protein is hydrolyzed and free vitamin B12 is released. Free vitamin B12 is bound by a second protein called the intrinsic factor which is required for absorption of the vitamin in the ileum.
At low levels of intake (0.1 mcg), approximately 80% of consumed vitamin B12 is absorbed by humans with healthy digestive systems. At higher intakes, absorption of vitamin B12 rapidly drops to approximately 3%.
Unlike other water-soluble vitamins, vitamin B12 is stored in the human body. The body stores between 5 and 12 mg of vitamin B12, primarily in the liver and kidneys, and excesses are excreted by way of kidney or in bile.
Plasma vitamin B12 tends to decrease with age. Estimates are that 10 to 30 percent of adults over the age of 50 years have reduced production of hydrochloric acid in the stomach. This often undiagnosed effect of aging compromises the ability to absorb food-bound vitamin B12. The RDAs for men and women 51 years old and older advise that most of the intake of this vitamin be of crystalline vitamin B12, either as a dietary supplement or in fortified foods, as absorption is not affected by atrophic gastritis. 1
Vitamin B12 is essential for two types of enzymatic reactions in humans; methyl group transfer and transfer of a hydrogen atom from one carbon to an adjacent carbon atom.
Vitamin B12 participates in three essential enzymatic reactions in the human body. Methionine synthetase requires methylcobalamin for conversion of homocysteine to methionine. Methylmalonyl CoA mutase requires 5’-deoxyadenosylcobalamin to convert L-methylmalonyl CoA to succinyl CoA. Leucine aminomutase requires 5’-deoxyadenosylcobalamin to isomerize L-leucine and beta-leucine
Males 9 to 13 years 14 to 18 years 19 to 30 years 31 to 50 years 51 to 70 years >70 years Females 9 to 13 years 14 to 18 years 19 to 30 years 31 to 50 years 51 to 70 years >70 years
1.8 2.4 2.4 2.4 2.4** 2.4**
1.8 2.4 2.4 2.4 2.4** 2.4**
ND ND ND ND ND ND
ND ND ND ND ND ND
Pregnancy <= 18 years 19 to 50 years
Lactation <= 18 years 19 to 50 years
*Values for infants are Adequate Intake (AI), others are RDA. ND=Not determinable due to lack of data of adverse effects in this age group and concern with regard to lack of ability to handle excess amounts.
**It is advisable for most of this amount to be obtained by consuming foods fortified with B12 or a B12-containing supplement.
Vitamin B12 deficiencies manifest primarily as anemia and neurologic changes, although a deficiency of this vitamin inhibits DNA synthesis, which affects growth and repair of all cells.
Pernicious anemia is a form of megaloblastic anemia caused by either inadequate vitamin B12 intake or reduced gastric secretion of intrinsic factor, which inhibits absorption.
The hematologic effects of vitamin B12 deficiency are indistinguishable from those of folate deficiency. These include pallor of skin, tiredness, syncope, headache, shortness of breath, and palpitations. Hematologic complications are completely reversed by treatment with vitamin B12.
Neurologic changes due to vitamin B12 deficiency can occur in the absence of any hematologic abnormalities. Depending on the duration of symptoms, neurologic complications of vitamin B12 deficiency may or may not be reversible following treatment.
According to the 2005-2006 National Health and Nutrition Education Survey (NHANES), the average vitamin B12 intake from food for adults 20 and over was 5.64 mcg.2 Vitamin B12 is found only in foods of animal origin or in fermented foods where bacteria produce the vitamin. Organ meats are the best sources of vitamin B12 (liver, kidney, heart, and pancreas), followed by clams, oysters, extra-lean beef, seafood, eggs, milk and yogurt, chicken, cheese, and miso (a fermented soybean product). For people who lack intrinsic factor, it has been found that a 1,000 mcg daily oral dose can substitute adequately for parenteral therapy.
Atrophic gastritis with decreased pepsin production is prevalent in the elderly. Consequently, absorption of food-bound vitamin B12 is lower in older than in younger, healthier people. For this reason, the RDAs advise that adults 51 years and older consume foods with vitamin B12 or a B12-containing supplement.
Alcohol reduces the absorption of dietary cobalamin. In addition, it can interfere with storage of vitamin B12 in the body. Daily vitamin B12 supplements could prevent deficiency for people who consume excessive alcohol.
Since the primary sources of vitamin B12 in the diet are animal products, vegetarians have a high risk of developing B12 deficiency. Therefore, supplements are recommended for vegetarians to prevent deficiency.3
Smoking tobacco can reduce storage of vitamin B12 in tissues. Supplements could benefit those who choose to use tobacco.
Metformin may diminish the absorption of vitamin B12. Reduced serum levels of vitamin B12 occur in up to 30% of patients taking metformin chronically.7
Absorption of vitamin B12 from the gastrointestinal tract may be decreased by aminoglycoside antibiotics, such as gentamicin, tobramycin, and amikacin. The concurrent administration of chloramphenicol, an antibiotic agent, and vitamin B12 may decrease the hematopoietic response to vitamin B12 in vitamin B12-deficient patients. Serum vitamin B12 concentrations of these patients should be monitored, and other antibiotics should be considered.
Phenytoin and Phenobarbital have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluid levels in some patients. It's also suggested that reduced vitamin B12 levels may contribute to the neuropsychiatric side effects of these drugs.
Colchicine, an antiinflammatory medication for the treatment of gout, has been reported to reduce absorption of vitamin B12 if taken more than two weeks. Both colchicine and vitamin B12 deficiency are reported to cause neuropathies, but it remains unclear whether neuropathies caused by colchicine could be due to vitamin B12 depletion. Neomycin-induced malabsorption of vitamin B12 may be increased by concurrent administration of colchicine. Vitamin B12 supplementation may be beneficial during long-term colchicine therapy.
Predinisone, an anti-inflammatory agent, has been shown to increase the absorption of vitamin B12 and secretion of intrinsic factor in the stomach in a few patients with pernicious anemia, but not in patients with partial or total gastrectomy. The clinical importance of these findings is unknown. It is advisable to consult with a physician or pharmacist about vitamin use before beginning therapy.
Chemotherapeutic drugs such as methotrexate, antiparasitic agents such as pyrimethamine, and other anti-infective medications invalidate blood assays for vitamin B12, giving false-positive test results for intrinsic factor antibodies that are present in blood in 50% of the patients with pernicious anemia.
Bile acid sequestrants such as cholestyramine and colestipol decrease the enterohepatic reabsorption of vitamin B12. Concentrations of vitamin B12 usually remain in the normal range with these medications. However, multivitamin-mineral supplements may be advisable.
Chronic use of salicylates has been shown to reduce blood concentrations of vitamin B12. Antituberculosis drugs such as isoniazids (INH) are structurally similar to salicylates and may decrease absorption of vitamin B12. People should consider using daily multivitamin/mineral supplements during therapy.
Proton pump inhibitors (PPIs) such as lansoprazole, used to treat ulcers, may interfere with the absorption of vitamin B12 from food, but not from supplemental vitamin B12, due to PPI-induced low stomach acidity. It is advisable to take vitamin B12 supplementation to prevent this problem. There is some evidence that cranberry juice may increase the vitamin's absorption possibly because the juice is somewhat acidic.
Cimetidine, an H2 blocker used to treat ulcers, given 4 times daily (1,000 mg total) reduces absorption of dietary vitamin B12, but not supplemental vitamin B12, in some peptic patients. It is advisable to take vitamin B12 supplementation to decrease malabsorption.
Zidovudine, an antiviral agent used to treat HIV infection, may deplete concentrations of vitamin B12. It is advisable to take vitamin B12 supplementation.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Effects of homocysteine-lowering with folic acid plus vitamin B12 vs placebo on mortality and major morbidity in myocardial infarction survivors: a randomized trial.
A double-blind, placebo-controlled, randomized clinical investigated the effects of long-term homocysteine lowering with folic acid and vitamin B12 on vascular and non-vascular outcomes in myocardial infarction survivors. 12,064 myocardial infarction survivors were enrolled in this study in the United Kingdom. Participants were randomly assigned to receive 2 mg folic acid plus 1 mg vitamin B12 daily or a placebo for the duration of the trial. The combined vitamin supplement lowered homocysteine by a mean of 3.8 micromol/L (28%). During 6.7 years of follow-up, major vascular events occurred in 1,537 of 6,033 people receiving vitamin supplements (25.5%) and in 1,493 of 6,031 people in the placebo group (24.8%) (relative risk [RR] 1.04, 95% confidence interval [95% CI] 0.97 to 1.12, P=0.28). Vitamin supplementation and lowering of homocysteine produced no change in major coronary events (vitamins, 1,229 [20.4%], vs. placebo, 1,185 [19.6%]; RR, 1.05; 95% CI, 0.97-1.13), stroke (vitamins, 269 [4.5%], vs. placebo, 265 [4.4%]; RR, 1.02; 95% CI, 0.86-1.21), or non-coronary revascularizations (vitamins, 178 [3.0%], vs. placebo, 152 [2.5%]; RR, 1.18; 95% CI, 0.95-1.46). Additionally, there were no differences in deaths attributed to vascular causes (vitamins, 578 [9.6%], vs. placebo, 559 [9.3%]) or non-vascular causes (vitamins, 405 [6.7%], vs. placebo, 392 [6.5%]) or in the incidence of any cancer (vitamins, 678 [11.2%], vs. placebo, 639 [10.6%]).8
Lowering homocysteine in patients with ischemic stroke to prevent recurrent stroke, myocardial infarction, and death: the Vitamin Intervention for Stroke Prevention (VISP) randomized controlled trial.
The Vitamin Intervention for Stroke Prevention Trial (VISP) evaluated the efficacy of vitamins B6,, B12, and folic acid for reducing risk of stroke, myocardial infarction, and death for patients with ischemic stroke. Participants (3,680 adults) were randomly assigned to receive daily supplements of vitamin B6 (25 mg), vitamin B12 (0.4 mg), and folic acid (2.5 mg) or vitamin B6 (0.200 mg), vitamin B12 (0.006 mg), and folic acid (0.020 mg) daily for two years. Supplements were found to lower homocysteine levels but no changes in risk for stroke, myocardial infarction, or death were found. A subgroup of participants (2,155 patients with an average age of 66 years) was more likely to benefit from vitamin therapy. For this subgroup, risk for the combined endpoint of stroke, coronary disease, or death was reduced by 21% (unadjusted P=0.049). The subgroup was selected by excluding those likely to have B12 malabsorption, receiving parenteral B12 and other supplements, and those with renal failure. It was concluded that in the era of food folate fortification, response to vitamin therapy to lower homocysteine was largely dependent on initial vitamin B12 status. The authors concluded that certain subgroups may require higher doses of vitamin B12 or other therapies.9,10
Vitamin B12, homocysteine and carotid plaque in the era of folic acid fortification of enriched cereal grain products.
This study evaluated the role of B12 as an important determinant of homocysteine levels in the era of folic acid fortification. The researchers measured total carotid plaque area by ultrasound and determined homocysteine and serum B12 levels in 421 people with vascular disease. Seventeen percent of participants were found to have vitamin B12 deficiency. The mean area of carotid plaque was found to be significantly larger among the group of patients whose B12 levels were below the median (1.36 (standard deviation [SD] 1.27) cm,sup>2 vs. 1.09 (SD 1.0) cm2; p=0.016). These results indicate that vitamin B12 deficiency was evident in people with vascular disease and that this deficiency was correlated with carotid plaque size for these participants. Further studies are required to investigate this correlation.11
Homocysteine lowering and cardiovascular events after acute myocardial infarction.
The Norwegian Vitamin Trial (NORVIT) evaluated the efficacy of homocysteine-lowering treatment with B vitamins for secondary prevention in patients with a history of acute myocardial infarction (MI). A total of 3,749 men and women were randomly assigned to receive folic acid (0.8 mg), vitamin B12 (0.4 mg), and vitamin B6 (40 mg), folic acid and vitamin B12, vitamin B6 alone, or placebo. Patients were seen at a 2 month follow-up visit and at a final visit after 2 to 3.5 years. Despite a substantial reduction in plasma total homocysteine, intervention with B vitamins did not lower the risk of recurrent cardiovascular disease or death after an acute MI. In the group receiving folic acid, vitamin B12, and vitamin B6, there was a trend toward an increased rate of events (relative risk, 1.22; 95 percent confidence interval, 1.00 to 1.50; P=0.05). Researchers concluded that B vitamin intervention not be recommended after acute MI.12
Homocysteine lowering with folic acid and B vitamins in vascular disease.
The Heart Outcomes Prevention Evaluation (HOPE) 2 trial evaluated whether therapy with homocysteine-lowering B vitamins reduced the risk for major vascular events in a high risk population. A total of 5,522 patients aged 55 years or older with vascular disease or diabetes participated in the trial. Participants randomly assigned to consume a daily supplement with a B vitamin combination (2.5 mg folic acid, 50 mg vitamin B6, 1 mg vitamin B12) or a placebo for an average of 5 years. The results showed that daily administration of the B vitamin combination significantly lowered homocysteine but had no beneficial effects on major vascular events in a high risk population with vascular disease.13
Homocysteine-lowering therapy and stroke risk, severity, and disability: additional findings from the HOPE 2 trial.
An analysis of data from the Heart Outcomes Prevention Evaluation (HOPE) 2 trial evaluated stroke risk and B vitamin supplementation. Five-thousand-five-hundred-twenty-two adults with cardiovascular disease participated in the trial. Participants were randomly assigned to receive a daily B vitamin supplement (containing 2.5 mg folic acid, 50 mg vitamin B6, 1 mg vitamin B12) or a placebo. During a mean five-year follow-up period, 258 participants suffered a stroke (4.7%). The geometric mean homocysteine concentration decreased by 2.2 micromol/L in the B vitamin supplemented group and by 0.8 micromol/L in the placebo group. The stroke incidence rate was 0.88 per 100 person-years in the B vitamin group versus 1.15 per 100 person-years in the placebo group (hazard ratio (HR) 0.75, 95% confidence interval (CI) 0.59-0.97). B vitamin supplementation decreased risk of nonfatal stroke (HR 0.72, 95% CI 0.54-0.95). No changes were found in neurological deficit at 24 hours (P=0.45) or functional dependence at 7 days (OR 0.95, 95% CI 0.57-1.56). These results suggest a modest risk reduction for stroke incidence but not severity. 14
Homocysteine and Vitamin B12 Status Relate to Bone Turnover Markers, Broadband Ultrasound Attenuation, and Fractures in Healthy Elderly People.
The relationship of homocysteine and vitamin B12 with bone turnover markers, broadband ultrasound attenuation (BUA), and fracture incidence was studied in 1,267 people participating in the Longitudinal Aging Study Amsterdam. Fourteen percent of male participants and 9% of female participants had elevated homocysteine levels and low vitamin B12 concentrations. For women with low vitamin B12 and high homocysteine levels, BUA was decreased, increased serum osteocalcin, and increased urinary excretion of deoxypyridinoline (DPD) with competitive IA and corrected for creatinine (Cr) concentration. Male participants did not show these changes. Twenty-eight men experienced a fracture during the trial; the RR for fractures (95% CI) for those with elevated homocysteine or low vitamin B12 concentrations was 3.8 (1.2-11.6). Forty-three women had a fracture during the trial; the RR for fracture was 2.8 (1.3-5.7) for those with elevated homocysteine or low vitamin B12. These results suggest that elevated homocysteine and low vitamin B12 levels were significantly associated with low BUA, high markers of bone turnover, and increased risk of fracture.15
Low serum vitamin B-12 levels are associated with increased hip bone loss in older women: a prospective study.
To investigate the relationship between serum vitamin B12 and bone loss in women, a subset of participants in the original Study of Osteoporotic Fractures were included in a new study. Of the original 9,704 white women aged at least 65 years, non-estrogen using women who had serum samples taken at baseline and continued for both follow up points were included, a total of 83 women. Two years after baseline, BMD of the hip was measured, with repeat measurements of both calcaneal and hip BMD after 5.9 and 3.5 years of follow-up respectively. Vitamin B12 assays were performed from serum samples. Women in the lowest quintile of vitamin B12 levels experienced an annual change of -1.6% (95% confidence interval, -2.4% to -0.8%) in total hip BMD. Women in higher quintiles experienced an annual change of with -0.2% (-0.5% to 0.2%). Researchers concluded that low serum vitamin B12 levels were associated with increased rates of hip, but not calcaneal, bone loss in older women.16
Relation between homocysteine and B-vitamin status indicators and bone mineral density in older Americans.
This study explored the association between homocysteine, B-vitamin status and bone health. Researchers collected data from 1,553 men and women aged 55 years and older who underwent DEXA scans of the hip as participants in phase 2 of the third U.S. National Health and Nutrition Examination Survey. Serum vitamin B12 concentration was related to bone mineral density (BMD) in a dose-response fashion up to a concentration of 200 pmol/L. Participants with homocysteine concentrations higher than 20 micromol/L had significantly lower BMD than those with homocysteine concentrations lower than 20 micromol/L. The OR (95% CI) for osteoporosis/osteopenia was 2.0 (1.0 to 3.9) for a serum vitamin B12 concentration below the 25th percentile. After adjusting for various other risk factors, it was found that bone mineral density (BMD) decreased and osteoporosis increased significantly with increasing serum MMA. These findings suggest elevated homocysteine and low vitamin B12 status are associated with BMD in older Americans.17
Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease
This case-control study examined the link between Alzheimer’s progression and blood levels of total homocysteine, folate, and vitamin B12. Included were 164 patients with a clinical diagnosis of dementia of Alzheimer type, including 76 patients with histologically confirmed Alzheimer’s disease, and 108 control subjects. Elevated serum homocysteine levels and low folic acid and vitamin B12 concentrations were found in participants with dementia of Alzheimer type and in confirmed Alzheimer’s disease compared to controls. The odds ratio was 4.5 (95% confidence interval, 2.2-9.2) for confirmed AD associated with a tHcy level in the top third compared with the bottom third of the control distribution, after adjustment for age, sex, social class, cigarette smoking, and apolipoprotein E epsilon4. Radiological evidence of disease progression in people with dementia of Alzheimer type during three years of follow-up was greater among those with higher baseline tHcy levels. The results of the study demonstrate that elevated serum homocysteine and low concentrations of folic acid and vitamin B12 are associated with Alzheimer’s disease.18
Predictive value of folate, vitamin B12 and homocysteine levels in late-life depression.
A cross-sectional prospective study investigated the relationship between folic acid, vitamin B12, homocysteine, and depression in a group of older Korean adults. At baseline, 732 participants over the age of 65 years were enrolled in the study; 631 were not depressed at baseline while 101 were found to be depressed using the Geriatric Mental State schedule. Participants were followed for two to three years. Low folate and low vitamin B12 levels and elevated homocysteine at baseline were associated with an increased risk for depression at follow-up. Depression at baseline was associated with a decline in vitamin B12 and an increase in homocysteine at follow-up. These results suggest that vitamin B12, folate, and homocysteine are important factors to consider with age-related depression.19
A prospective study on folate, B12, and pyridoxal 5’-phosphate (B6) and breast cancer.
A nested, case-control, prospective study evaluated the incidence of breast cancer and prediagnostic serum concentrations of folate, vitamin B12, and vitamin B6 in 195 women with breast cancer and 195 matched controls. Samples were collected during two time periods. Average vitamin B12 levels were lower among women with breast cancer than the matched controls with statistically significant differences in a subgroup of postmenopausal women (1974 cohort, 413 versus 482 pg/ml, P=0.03; 1989 cohort, 406 versus 452 pg/ml, P=0.02). For women who were postmenopausal at the beginning of the trial, women in the lowest quintile of vitamin B12, were at increased risk for breast cancer than those in the higher four quintiles (lowest versus highest quintile: 1974 cohort, matched odds ratio=4.00 (95% confidence interval=1.05-15.20); 1989 cohort, matched odds ratio=2.25 (95% confidence interval=0.86-5.91)). These results suggest that vitamin B12 status may be an important factor to consider in relation to breast cancer development. 20
Neural-tube defects (NTD) are associated with low concentrations of cobalamin (vitamin B12) in amniotic fluid.
Both genetic and environmental factors are implicated in the pathogenesis of neural tube defects (NTDs), including maternal folate deficiency, maternal cobalamin deficiency, and hyperhomocysteinemia. A pilot case-control study investigated the associations between folate deficiency, vitamin B12 levels, homocysteine concentrations, and NTDs. Amniotic fluid samples were collected and analyzed from 16 NTD pregnancies and 64 matched controls. Only low concentrations of vitamin B12 were identified in the NTD samples compared to the normal controls. The ratios of vitamin B12 to intermediates related to methionine synthase, which may be implicated in the development of NTDs. The vitamin B12:folate ratio for NTD versus controls was 48 versus 126 (P<0.001). The ratio of methionine:(folate x tHcy) was 1.4 versus 2.7 (P<0.001) for NTD versus controls. These findings suggest vitamin B12 status to be an independent risk factor for NTDs. 21
Age-related hearing loss, vitamin B-12, and folate in elderly women.
Researchers evaluated whether age-related hearing loss was associated with poor vitamin B12 and folate status. Fifty-five women aged 60 to 71 years participated in the study; eleven were found to have impaired hearing. Those with impaired hearing had 38% lower serum vitamin B12 compared to women with normal hearing (236 compared with 380 pmol/L, respectively, P=0.008). Red cell folate was also 31% lower for women with impaired hearing compared to those with normal hearing (425 compared with 619 nmol/L, respectively, P=0.02). These findings suggest that inadequate dietary intake of vitamin B12 and folic acid may increase risk of hearing loss for women. 22
The effect of folate and cobalamin on osteoarthritic hands.
A two month double-blinded, crossover study evaluated the effects of folate and vitamin B12 supplements in 26 people diagnosed with osteoarthritis of the hands. After a ten day washout period, participants were randomly assigned to consume 6.4 mg folic acid, 6.4 mg folic acid plus 0.02 mg vitamin B12, or a placebo for two months. Mean grip strength was significantly higher for participants consuming folic acid plus vitamin B12. Results suggest that daily use of a combination of folic acid, vitamin B12, and acetaminophen as needed, is comparable to NSAID treatment and was superior to NSAID for side effects and cost. 23
Effect of B-vitamin therapy on progression of diabetic nephropathy: a randomized controlled trial.
The Diabetic Intervention with Vitamins to Improve Nephropathy (DIVINe) study investigated the efficacy of B vitamin supplements for improvement of diabetic nephropathy. This multi-center, randomized, double-blind, placebo-controlled study enrolled 238 participants with type 1 or type 2 diabetes mellitus and a diagnosis of diabetic nephropathy. Participants were randomized to receive a combination supplement containing 2.5 mg folic acid, 25 mg vitamin B6, and 1 mg vitamin B12 or a placebo. As expected, plasma total homocysteine decreased by a mean (SE) of 2.2 (0.4) micromol/L in the B-vitamin group compared with a mean (SE) increase of 2.6 (0.4) micromol/L in the placebo group (mean difference, -4.8; 95% CI, -6.1 to -3.7; P<0.001, in favor of B vitamins). After a mean follow-up of 31.9 +/- 14.4 months, radionuclide GFR decreased by a mean (SE) of 16.5 (1.7) mL/min/1.73 m2 in the B-vitamin group compared with 10.7 (1.7) mL/min/1.73 m2 in the placebo group (mean difference, -5.8; 95% confidence interval [CI], -10.6 to -1.1; P=0.02). There was no difference in requirement of dialysis (hazard ratio [HR], 1.1; 95% CI, 0.4-2.6; P=0.88). Vascular events (myocardial infarction, stroke, revascularization, and all cause mortality) occurred more frequently in the B-vitamin supplemented group (HR, 2.0; 95% CI, 1.0-4.0; P=0.04). This study suggests that high-dose B-vitamin supplementation has benefits for diabetic nephropathy. 24
Folic acid, pyridoxine, and cyanocobalamin combination treatment and age-related macular degeneration in women: the Women's Antioxidant and Folic Acid Cardiovascular Study.
A randomized, double-blind, placebo-controlled trial investigated B vitamin supplementation and the risk of age-related macular degeneration (AMD). Five-thousand-five female health care professionals over the age of 40 years with cardiovascular disease or at high risk for cardiovascular disease participated in the trial. Participants were free of AMD at the beginning of the trial. Participants were randomized to receive B vitamins (2.5 mg folic acid, 50 mg vitamin B6, and 1 mg vitamin B12) or a placebo daily. The trial lasted an average of 7.3 years including treatment and follow-up. At the end of the trial, there were 55 cases of AMD in the B vitamin group and 82 in the placebo group (relative risk, 0.66; 95% confidence interval, 0.47-0.93 [P=0.02]). There were 26 cases of visually significant AMD in the B vitamin group and 44 in the placebo group (RR, 0.59; 95% CI, 0.36-0.95 [P=0.03]). These results suggest that B vitamins may help reduce risk for AMD. Further studies are needed to clarify and support these results. 25
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