Health benefits of Vitamin B12 and its role in human nutrition boost energy
Cardiovascular disease is the most standard reason for death in industrialized countries, like the United States, and is on the rise in developing countries. Risks for cardiovascular disease include elevated low-density lipoprotein (LDL) levels, hypertension, low high-density lipoprotein (HDL) levels, obesity, and diabetes.
Elevated homocysteine levels are also identified as an independent risk factor for coronary disease. Homocysteine is a sulfur-containing amino acid based on methionine that is normally present in blood. Elevated homocysteine levels are believed to promote thrombogenesis, impair endothelial vasomotor function, promote lipid peroxidation, and induce vascular smooth muscle proliferation. Evidence from retrospective, cross-sectional, and prospective studies links elevated homocysteine levels with heart disease and stroke.
Vitamin B12, folate, and vitamin B6 take part in homocysteine metabolism. In the presence of insufficient vitamin B12, homocysteine levels can rise because of inadequate function of methionine synthase . Is a result of several randomized controlled trials indicate that mixtures of vitamin B12 and folic acid supplements without or with vitamin B6 decrease homocysteine levels in individuals with vascular disease or diabetes and in young adult women. In another study, older men and ladies who took a multivitamin/multimineral supplement for 2 months experienced a significant reduction in homocysteine levels.
Evidence supports a job for folic acid and vitamin B12 supplements in reducing homocysteine levels, but is a result of several large prospective research has not shown these supplements decrease the risk of coronary disease. In the Women’s Antioxidant and Folate Cardiovascular Study, women at high-risk of cardiovascular disease who took daily supplements containing 1 mg vitamin B12, 2.5 mg folate, and 50 mg vitamin B6 for 7.3 years did not have a reduced chance of major cardiovascular events, despite lowered homocysteine levels.
One’s heart Outcomes Prevention Evaluation (HOPE) 2 trial, including 5,522 patients over the age of 54 years with vascular disease or diabetes, discovered that daily treatment with 2.5 mg folate, 50 mg vitamin B6, and 1 mg vitamin B12 for typically 5 years reduced homocysteine levels and the chance of stroke but didn’t reduce the risk of major cardiovascular events. Within the Western Norway B Vitamin Intervention Trial, including 3,096 patients undergoing coronary angiography, daily supplements of 0.4 mg vitamin B12 and 0.8 mg folate with or without 40 mg vitamin B6 for 12 months reduced homocysteine levels by 30% but didn’t affect total mortality or even the risk of major cardiovascular events during 38 months of follow-up. The Norwegian Vitamin (NORVIT) trial  and the Vitamin Intervention for Stroke Prevention trial had similar results.
The American Heart Association has figured the available evidence is inadequate to aid a role for B vitamins in lessening cardiovascular risk.
Dementia and cognitive function
Scientific study has long been interested in the possibility connection between vitamin B12 deficiency and dementia. An insufficiency in vitamin B12 causes an amount of homocysteine in the blood  and might decrease amounts of substances needed to metabolize neurotransmitters. Observational research has shown positive associations between elevated homocysteine levels and the incidence of both Alzheimer’s and dementia. Low vitamin B12 status has additionally been positively associated with cognitive decline.
Despite evidence that vitamin B12 lowers homocysteine levels and correlations between low vitamin B12 levels and cognitive decline, studies have not shown that vitamin B12 comes with an independent effect on cognition. In a single randomized, double-blind, placebo-controlled trial, 195 subjects aged 70 years or older without any or moderate cognitive impairment received 1,000 mcg vitamin B12, 1,000 mcg vitamin B12 plus 400 mcg folate, or placebo for 24 weeks. Treatment with vitamin B12 plus folic acid reduced homocysteine concentrations by 36%, but neither vitamin B12 treatment nor vitamin B12 plus folate treatment improved cognitive function.
Women at high-risk of cardiovascular disease who took part in the Women’s Antioxidant and Folate Cardiovascular Study were randomly allotted to receive daily supplements containing 1 mg vitamin B12, 2.5 mg folate and 50 mg vitamin B6, or placebo. Following a mean of 1.24 months, B-vitamin supplementation did not affect mean cognitive vary from baseline compared with placebo. However, inside a subset of women with low baseline dietary intake of B vitamins, supplementation significantly slowed the speed of cognitive decline. Inside a trial conducted through the Alzheimer’s Disease Cooperative Study consortium that included people with mild-to-moderate Alzheimer’s disease, daily supplements of just one mg vitamin B12, 5 mg folate, and 25 mg vitamin B6 for 1 . 5 years did not slow cognitive decline in contrast to placebo. Another study found similar leads to 142 individuals at risk of dementia who received supplements of two mg folic acid and 1 mg vitamin B12 for 3 months.
The authors of two Cochrane reviews and an organized review of randomized trials from the effects of B vitamins on cognitive function figured insufficient evidence can be obtained to show whether vitamin B12 alone or perhaps in combination with vitamin B6 or folate has an effect on cognitive function or dementia. Additional large numerous studies of vitamin B12 supplementation are essential to assess whether vitamin B12 includes a direct effect on cognitive function and dementia.
Energy and endurance
Because of its role in energy metabolism, vitamin B12 is often promoted as an energy enhancer and an athletic performance and endurance booster. These claims derive from the fact that correcting the megaloblastic anemia brought on by vitamin B12 deficiency should enhance the associated symptoms of fatigue and weakness. However, vitamin B12 supplementation seems to have no beneficial impact on performance in the absence of a nutritional deficit.