Vitamin B12
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Lower Blood Pressure |
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Lowers Homocysteine |
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Protect Against Alzheimer's and Dementia |
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Ward Off Depression |
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Prevent Neural Tube Defects |
What Is It?
Vitamin B12 is a water-soluble vitamin. Water-soluble vitamins dissolve in water. After the body uses these vitamins, leftover amounts leave the body through the urine. Typically, water-soluble vitamins can not be stored by the body. Vitamin B12 is special, because the body can store it for years in the liver. Because of this, a vitamin B12 deficiency is very rare.
Vitamin B12, like the other B vitamins, is important for metabolism . It helps in the formation of red blood cells and in the maintenance of the central nervous system .
Medline Plus
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Health Benefits
Heart Disease
Taken as part of a vitamin B-complex supplement, vitamin B6 may help protect against heart disease and a host of other disorders. For example, in concert with folic acid and vitamin B12 , it aids the body in processing homocysteine, an amino acid like compound that, at elevated levels, increases the risk for heart disease and other vascular disorders.
Wholehealthmd.com
The amount of homocysteine in the blood is regulated by at least three vitamins: folate (folic acid), vitamin B12 , and vitamin B6. Analysis of the results of 12 homocysteine-lowering trials showed folic acid supplementation (500mcg - 5 mg/day) had the greatest lowering effect on blood homocysteine levels (25% decrease); co-supplementation with folic acid and vitamin B12 (mean 0.5 mg/day or 500 mcg/day) provided an additional 7% reduction (32% decrease) in blood homocysteine concentrations. The results of a sequential supplementation trial in 53 men and women indicated that after folic acid supplementation, vitamin B12 became the major determinant of plasma homocysteine levels. Some evidence indicates that vitamin B 12 deficiency is a major cause of elevated homocysteine levels in people over the age of 60. Two studies found blood methylmalonic acid (MMA) levels to be elevated in more than 60% of elderly individuals with elevated homocysteine levels. An elevated MMA level in conjunction with elevated homocysteine, in the absence of impaired kidney function, suggests either a vitamin B12 deficiency or a combined B12 and folate deficiency. Thus, it is important to evaluate vitamin B12 status as well as kidney function in older individuals with elevated homocysteine levels prior to initiating homocysteine-lowering therapy.
Linus Pauling Institute
Even moderately elevated levels of homocysteine in the blood have been associated with increased risk for cardiovascular disease, including heart disease and stroke. During protein digestion, amino acids, including methionine, are released. Homocysteine is an intermediate in the metabolism of methionine. Healthy individuals utilize two different pathways to metabolize homocysteine. One pathway converts homocysteine back to methionine and is dependent on folic acid and vitamin B12. The other pathway converts homocysteine to the amino acid cysteine and requires two vitamin B6 (PLP)-dependent enzymes. Thus, the amount of homocysteine in the blood is regulated by at least three vitamins: folic acid, vitamin B12 , and vitamin B6. Several large observational studies have demonstrated an association between low vitamin B6 intake or status with increased blood homocysteine levels and increased risk of cardiovascular diseases. A large prospective study found the risk of heart disease in women who consumed, on average, 4.6 mg of vitamin B 6 daily was only 67% of the risk in women who consumed an average of 1.1 mg daily .
Linus Pauling Institute
Although oral B12 did not reduce homocysteine in every case, when it did, the results were dramatic. Some of the people in the study had homocysteine levels as high as 175 micromoles per liter (the optimal safe range for homocysteine is under 6). In the case of one patient, 2,000 micrograms of oral B12 for four months reduced their homocysteine from 113.4 micromoles per liter to 8.2. Injected B12 also significantly reduced homocysteine - the main difference being that the injected version worked faster.
Interestingly, some of the patients did not respond to supplemental vitamin B12. It was discovered that they were also deficient in folate (folic acid), and until folate was replaced, their homocysteine remained elevated. Vitamin B12 and folate work synergistically in the chemical reactions that recycle homocysteine back to methionine in the methylation cycle.
Life Extension
Alzheimer's and Dementia
B12-deficiency can cause a dementia that looks exactly like Alzheimer's disease. And the connection between Alzheimer's disease itself is characterized by brain deficiencies of both vitamin B12 and the methylating factor, S-adenosylmethionine (SAMe). A new study from Germany correlates B12 deficiency in Alzheimer's patients with two personality changes—irritability and disturbed behavior. n B12 deficiency and mental illness has been documented repeatedly. According to the latest research, as much as 30% of hospitalized mental patients may be deficient in the vitamin. And what's disturbing is that studies repeatedly show that the deficiency is frequently missed by standard blood tests. For example, a recent study from Germany shows that out of 67 hemodialysis patients who were B12-deficient by the measurement of methylmalonic acid (it goes up when B12 goes down), only two of them were deficient by a standard blood test. Looking at the data, one can't help but wonder how many people with B12 deficiency get treated for mental illness when what they should get is a vitamin!
Life Extension
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Depression
Observational studies have found as many as 30% of patients hospitalized for depression are deficient in vitamin B12. A cross-sectional study of 700 community-living, physically disabled women over the age of 65 found that vitamin B12 deficient women were twice as likely to be severely depressed as non-deficient women. A population-based study in 3,884 elderly men and women with depressive disorders found that those with vitamin B12 deficiency were almost 70% more likely to experience depression than those with normal vitamin B 12 status. The reasons for the relationship between vitamin B12 deficiency and depression are not clear but may involve S-adenosylmethionine (SAMe). Vitamin B12 and folate are required for the synthesis of SAMe, a methyl group donor essential for the metabolism of neurotransmitters whose bioavailability has been related to depression. This hypothesis is supported by several studies that have shown supplementation with SAMe improves depressive symptoms. Because few studies have examined the relationship of vitamin B12 status and the development of depression over time, it cannot yet be determined if vitamin B12 deficiency plays a causal role in depression. However, due to the high prevalence of vitamin B12 deficiency in older individuals, it may be beneficial to screen for vitamin B12 deficiency as part of a medical evaluation for depression.
Linus Pauling Institute
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Neural tube defects
Neural tube defects (NTD) may result in anencephaly or spina bifida , devastating and sometimes fatal birth defects. The defects occur between the 21st and 27th days after conception, a time when many women do not realize they are pregnant. Randomized controlled trials have demonstrated 60% to 100% reductions in NTD cases when women consumed folic acid supplements in addition to a varied diet during the month before and the month after conception. Increasing evidence indicates that the homocysteine -lowering effect of folic acid plays a critical role in lowering the risk of NTD. Homocysteine may accumulate in the blood when there is inadequate folate and/or vitamin B12 for effective functioning of the methionine synthase enzyme . Decreased vitamin B12 levels in the blood and amniotic fluid of pregnant women have been associated with an increased risk of NTD, suggesting that adequate vitamin B12 intake in addition to folic acid may be beneficial in the prevention of NTD.
Linus Pauling Institute
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