B12 and folate relationship with god

Vitamin Bfolate interrelationships.

Jun 21, Intake of folate, vitamin B12, B6, and methionine were measured using a PC risk in relation to high plasma folate levels, while dietary folate [4] .. J. B. Mason, “Folate, cancer risk, and the Greek god, Proteus: a tale of two. You need to take in a well-balanced mix of nutrients to maintain optimal health, and sometimes understanding the interactions between the essential vitamins. B12 deficiency can cause depression, fatigue, and other serious problems. are any influence/ correlation between the antidepressant to b12? im feeling very Finally, if severely deficient, cut out alcohol (if you drink), and, I swear to god.

Sang-Woon Choi, MD of Tufts University points out that serum levels of folate are a poor indicator of levels in tissues and that it may well be that there is a correlation between folate levels in breast tissue and breast cancer risk.

Vitamin B12-folate interrelationships.

Choi speculates that a vitamin B12 deficiency may lead to breast cancer because it could result in less folate being available to ensure proper DNA replication and repair. A prospective study of folate, B12, and pyridoxal 5'-phosphate B6 and breast cancer.

Several studies have shown that anywhere from 5 to 15 per cent of elderly people suffer from a vitamin B12 deficiency. Although the only formally recognized disorder linked to a cobalamin deficiency is megaloblastic anaemia, it is now becoming clear that many neurological and psychiatric symptoms may also be caused by a vitamin B12 deficiency. Ataxia shaky movements and unsteady gaitmuscle weakness, spasticity, incontinence, hypotension, vision problems, dementia, psychoses, and mood disturbances are but a few of the disorders which have recently been linked to possible vitamin B12 deficiencies.

Delva points out that these disorders may occur at vitamin B12 levels just slightly lower than normal and considerably above the levels normally associated with anaemia. She also cautions that the blood level of cobalamin is an unreliable indicator of deficiency and that tissue levels of the vitamin may be quite low even though the blood levels are normal. The best test of cobalamin deficiency involves measuring the blood levels of homocysteine and methylmalonic acid.

If the level of these two precursors to the metabolic reactions controlled by cobalamin are high then the vitamin B12 level is low. Vitamin B12 deficiencies may be treated by injections of the vitamin or by oral supplementation. Oral supplementation is just as effective as injections in most people and a lot less expensive. Cobalamin has no known toxic effects. Vitamin B12 replacement - To B12 or not to B12? Canadian Family Physician, Vol. Swedish researchers have discovered that many older people are deficient in vitamin B Their study involved men and women aged 75 years or older.

Analysis of blood serum showed that 11 per cent of the participants were deficient in cobalamin vitamin B The researchers point out that a vitamin B deficiency has been linked to neuropsychiatric disorders such as memory loss and dementia. The researchers discovered several cases of gastritis inflammation of the lining of the stomach and two cases of celiac disease among patients with low serum values of cobalamin.

They conclude that routine screening for a vitamin B deficiency is justified in the case of older people. The patient, an year-old man, had developed progressive memory loss and lethargy over a two-year period. Although his serum level of vitamin B was within the currently accepted range, the doctors decided to proceed with vitamin B therapy. The patient received an intramuscular injection of micrograms of vitamin B for three consecutive days, then micrograms weekly for a month, and then one injection every month.

By the fifth injection his mental status had vastly improved and his lethargy had completely vanished. The doctors conclude that the levels of serum vitamin B concentrations currently considered normal in the United States may be too low and should be reassessed. The doctors suggest that a trial of vitamin B therapy is warranted in patients with borderline cobalamin serum levels as it is effective and inexpensive. Eggersten, Robert, et al. Prevalence and diagnosis of cobalamin deficiency in older people.

It is becoming increasingly clear that a vitamin B deficiency can have serious consequences, particularly in elderly people. A vitamin B deficiency can be misdiagnosed as Alzheimer's disease, amyotrophic lateral sclerosis Lou Gehrig's diseasespinal cord compression, or alcoholic or diabetic peripheral neuropathy.

A vitamin B deficiency is also associated with elevated homocysteine levels that in turn have been linked to a significantly increased risk for atherosclerosis and heart disease. The elderly are at special risk for being deficient in vitamin B and, as researchers at the Philadelphia Veterans Affairs Medical Centre report, so are people who have had stomach surgery for peptic ulcers and similar conditions. The study involved 61 patients with a mean age of 63 years who had undergone gastric surgery as far back as 30 years ago and controls.

The researchers found that 31 per cent of the surgery group had a vitamin B deficiency as compared to 2 per cent among the controls. The presence of a deficiency was established through measurements of the levels of vitamin B, total homocysteine, and methylmalonic acid in the blood.

The deficiencies were corrected by daily injections of micrograms of vitamin B for five days followed by monthly injections.

The researchers recommend that physicians ensure that those of their patients who had gastric surgery, no matter how long ago, be checked periodically for a vitamin B deficiency. If one is found, the patients should be given lifelong vitamin B therapy periodic intramuscular injections.

Elevated methylmalonic acid and total homocysteine levels show high prevalence of vitamin B deficiency after gastric surgery. Annals of Internal Medicine, Vol. Researchers at Columbia University have confirmed that elderly people often suffer from a lack of vitamin B12 cobalamin. The deficiency is usually only discovered when patients develop megaloblastic anaemia. However, before this stage is reached, cobalamin-deficient individuals may develop neuropsychiatric damage and show signs of disorientation and confusion.

The researchers evaluated men and women aged 67 to 96 years and compared their cobalamin and folate status to that of healthy, younger control subjects. They found that There was no significant difference in folate status between the two groups. The researchers also found that people who took oral supplements containing vitamin B12 and folate 6 micrograms and micrograms per day respectively were much less likely to suffer from a deficiency than were people who did not supplement.

They point out that as people age they become less and less able to absorb vitamin B12 from food and therefore are likely to develop a deficiency. As gastric atrophy progresses vitamin B12 status can only be maintained by taking high oral doses of cobalamin micrograms daily or by routine intramuscular injections providing 1 mg per month. The researchers also point out that a vitamin B12 deficiency leads to an accumulation of homocysteine in the blood. An increased serum concentration of homocysteine and its derivatives is now recognized as a major risk factor in heart disease and stroke.

Lindenbaum, John, et al. Prevalence of cobalamin deficiency in the Framingham elderly population. Vitamin B deficiency in elderly individuals: An international team of researchers have confirmed that elderly people often suffer from a deficiency of vitamins B-6, B and folic acid. Their investigation involved 99 healthy young people aged64 healthy elderly subjects agedand elderly hospitalized patients aged The researchers measured the blood concentrations of the vitamins in all subjects as well as the concentration of certain metabolic products that tend to build up if a vitamin deficiency is present.

Recent experiments have shown that weekly injections of vitamin B, B-6, and folate are highly effective in normalizing the elevated metabolite concentrations in elderly people.

Joosten, Etienne, et al. Metabolic evidence that deficiencies of vitamin B cobalaminfolate, and vitamin B-6 occur commonly in elderly people.

Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic

Vitamin B12 deficiency is fairly common among older people and can cause anemia, pain and depression. Supplementation with cobalamin may reverse the deficiency, however, the ideal dose when given orally is yet to be determined. A team from the University of Wageningen undertook a study in which participants were given either 2. These doses cover the full range from recommended dietary allowance in the Netherlands to the normal dose used in injections for B12 deficiency.

The participants were aged 70 to 94, with an average age of They were all mildly deficient in vitamin B12, with serum concentrations of to picomoles per liter. Their levels of methylmalonic acid MMA, a marker for vitamin B12 deficiency were above 0. All of the participants received each of the experimental doses for 16 weeks, in a random order. Compliance with the medication was very high, at 98 per cent. Overall, levels of MMA and serum vitamin B12 improved with increasing doses of cobalamin.

Elevated MMA was significantly reduced after 8 weeks, and remained so after 16 weeks. The percentages of participants whose MMA reduced to below 0. The researchers explain that a major knowledge gap existed over the lowest oral cobalamin dose required to normalize elevated MMA. They state that in this study, a daily dose of ug was the lowest dose to give per cent of the maximum reduction in MMA. These doses led to an average reduction in MMA of 33 per cent.

However, they add that diagnosing vitamin B12 deficiency is complicated due to the limitations of current techniques. The authors conclude that the lowest dose needed to normalize vitamin B12 deficiency is more than times higher than the recommended dietary allowance.

They add that the relevance of treating vitamin B12 deficiency in older people could be substantial, were further trials able to show benefits to cognitive functioning and depression. Oral cyanocobalamin supplementation in older people with vitamin B12 deficiency. This deficiency is mostly related to an inability to absorb cobalamin bound to food. Several experiments have shown that this problem does not affect people's ability to absorb free or synthetic cobalamin.

A lack of vitamin-B12 can lead to megaloblastic anemia and, if untreated, to irreversible neurological damage that may mimic Alzheimer's disease. It is not clear, however, whether smaller amounts, such as the 25 mcg or so found in multivitamins, are sufficient to correct a deficiency. A team of researchers from the universities of Washington and Colorado has just released a study designed to determine just how much oral cobalamin supplementation is required to reverse a deficiency.

Rajan, S, et al. Response of elevated methylmalonic acid to three dose levels of oral cobalamin in older adults. These include deficiencies in vitamin C, coenzyme Q10, magnesium, zinc, sodium, l-tryptophan, l-carnitine, essential fatty acids, and various B vitamins.

He points out that there is some evidence that the deficiencies are caused by the disease itself rather than by an inadequate diet. He suggests that the deficiencies not only contribute to the symptoms of CFS but also impair the healing process. Although the results of supplementation trials involving CFS patients have been inconclusive so far Dr. Werbach nevertheless recommends that CFS patients be given large doses of certain supplements for at least a trial period to see if their symptoms improve.

Nutritional strategies for treating chronic fatigue syndrome. Alternative Medicine Review, Vol. It is common medical dogma that patients suffering from pernicious anaemia are unable to absorb sufficient vitamin B from their diet and therefore require intramuscular injections of the vitamin on a regular basis. Recent research is questioning this assumption. Elia of the Dunn Clinical Nutrition Centre persuasively outlines the reasons why oral supplementation is at least as effective as intramuscular injections.

Elia points out that vitamin B is absorbed from the intestine via two different routes. One involves intrinsic factor and is estimated to lead to absorption of about 60 per cent of the amount of vitamin B ingested in the diet. The other does not need intrinsic factor which is absent in pernicious anaemia patients and only leads to absorption of about 1 per cent of the ingested amount.

The body needs about He points out that mild vitamin B deficiency, which can lead to abnormalities in cognitive function and increased risk of cardiovascular disease, affects per cent of all elderly people in the United States where the average daily vitamin B intake is about six micrograms - well above the RDA.

Oral or parenteral therapy for B12 deficiency. Pernicious anaemia can be treated with intramuscular injections of cobalamin vitamin B The problem, according to Dr.

Lederle performed a survey among Minneapolis internists in and again in In none of the respondents used oral cobalamin in the treatment of pernicious anaemia. A subsequent survey in showed that 19 per cent of the internists responding were now using oral cobalamin.

However, even in71 per cent of the internists still held the incorrect view that sufficient quantities of cobalamin cannot be absorbed from oral supplements 91 per cent of the internists held this view in Lederle concludes that the majority of Minneapolis interns are still unaware of the oral treatment option. Oral cobalamin for pernicious anemia: Older people are often found to have a vitamin B deficiency even though they do not suffer from pernicious anaemia.

The body's ability to absorb vitamin B from food decreases markedly with age probably because of a lack of stomach acid. The conventional way of correcting a vitamin B deficiency has been through intramuscular injection of the vitamin. Now researchers at the Universities of Brussels and Antwerp report that oral administration of free vitamin B- 12 is effective in normalizing low vitamin B levels.

Their experiment involved 94 patients without pernicious anaemia with a mean age of 84 years who through repeated tests had been found to have an average vitamin B level in serum of After 10 days 69 per cent of the patients had normal vitamin B levels The researchers conclude that older patients with a vitamin B deficiency unrelated to pernicious anaemia can be successfully treated with orally administered vitamin B Normalization of low vitamin B serum levels in older people by oral treatment.

Adenosylcobalamin is an important coenzyme, which is involved in the metabolism of branched-chain amino acids, cholesterol, methionine, and odd-chain fatty acids. It is synthesized in the cell nucleus from vitamin B cyanocobalamin. Now researchers at the University of Arkansas have found that the synthesis of adenosylcobalamin is impaired if the cell membranes have been subjected to peroxidative free radical attack.

They also found, through experiments with cell cultures, that vitamin E effectively prevents the peroxidation and thereby allows the enzyme synthesis to proceed unhindered. Alpha-tocopherol protects against a reduction in adenosylcobalamin in oxidatively stressed human cells. Journal of Nutrition, Vol. Deficiency of vitamin B12 is common among older people.

As this vitamin is crucial for brain and nervous system functioning, researchers have proposed that supplementation may have beneficial effects on cognitive function in this group.

However, randomized trial results have so far been inconclusive. Researchers from Wageningen University carried out a large study with a long duration and rigorous cognitive tests. They investigated the effects of daily oral supplementation with vitamin B12 at a high dose 1,ug on adults aged 70 years or above with a mild deficiency. High-dose vitamin B12 supplements are considered to be safe and no upper safety level has been set in the US or Europe.

Among the group of participants, some were given ug folic acid alongside the vitamin B12, and others a placebo. Compliance was very high, with a mean of 99 per cent. After 24 weeks, vitamin B12 status and cognitive function were assessed. Vitamin B12 supplementation reversed deficiency, and those taking folic acid showed raised folic acid levels in their red blood cells. Both supplementation groups had lower homocysteine levels, which is beneficial in terms of heart disease risk.

Homocysteine was lowered to a greater extent in the combined supplement group, as expected based on knowledge of how the two nutrients interact.

However, neither supplement was linked to better results than placebo on tests of cognitive performance which covered attention, construction, sensomotor speed, memory, and executive function.

Folate and vitamin B biomarkers in NHANES: history of their measurement and use

Participants in all three groups showed improved memory, but the researchers concluded that the supplementation regimes used in this study did not lead to improved cognitive function. This may be because a longer course of vitamin B12 is necessary to repair any existing cognitive damage. Despite the results, the authors write, these findings cannot exclude beneficial effects on cognitive function from longer-term vitamin B12 supplementation.

Individuals who have had mild cognitive impairment for less than six months may also be more likely to respond to treatment with vitamin B Effect of oral vitamin B with or without folic acid on cognitive function in older people with mild vitamin B deficiency: Two years ago researchers at the Massachusetts General Hospital reported that the antibiotic clioquinol inhibited and even reduced the build-up of amyloid plaques in the brain of mice engineered to developed Alzheimer-like deposits.

Now researchers at the Harvard Medical School and the University of Melbourne are about to release the results of a phase II trial involving the use of clioquinol in human Alzheimer's patients.

So far the findings are extremely promising. Clioquinol treatment slowed down the disease and significantly reduced the accumulation of beta-amyloid plaques, a cardinal feature of Alzheimer's.

Ashley Bush of the Harvard Medical School believes that Alzheimer's disease begins when iron, copper and zinc accumulates in the brain and turns beta-amyloid into a rogue enzyme that catalyses the production of hydrogen peroxide which then attacks and destroys brain cells.

In the process beta-amyloid forms into the long chain of insoluble plaque so characteristic of Alzheimer's. Bush believes that clioquinol works by removing chelating? This, in turn, stops the formation of hydrogen peroxide and thus the destruction of brain cells and also prevents the beta-amyloid particles from clumping together. There is some concern that clioquinol depletes vitamin-B12 in the body so vitamin B12 supplementation is a must when taking clioquinol.

An antibiotic to treat Alzheimer's? You must remember this… New Scientist, August 3,p. Vitamin B12 deficiency is associated with the development of megaloblastic anemia, mental dysfunction, and dementia resembling Alzheimer's disease. Vitamin-B12 cobalamin is a very important cofactor in several biochemical reactions including the conversion of homocysteine to methionine and the synthesis of SAMe S-adenosylmethionine.

These reactions are believed to be crucial in maintaining neurological health. Researchers at the University of Milan now report that a vitamin B12 deficiency is associated with higher levels of the inflammatory cytokine, tumour necrosis factor-alpha TNF-alpha and reduced levels of epidermal growth factor EGF. It is believed that high levels of TNF-alpha speed up the progression of Alzheimer's disease thus explaining the association between low vitamin B12 levels and Alzheimer's.

Vitamin B12 deficiency is widespread among older people. Taking a 1 mg sublingual B12 tablet daily could prevent a lot of future health problems.

Vitamin B12 deficiency, tumor necrosis factor-alpha and epidermal growth factor: Some studies have found a correlation between low vitamin B12 levels and the development of Alzheimer's disease AD and dementia; other studies have found no such correlation.

Researchers at the Karolinska Institute now provide convincing evidence that a deficiency of either vitamin B12 or folic acid folate is associated with an increased risk of AD and dementia. Their study involved non-demented people aged 75 years and older who were not supplementing with vitamin B12 or folate. The participants were tested at baseline to determine mental status and had blood samples drawn for analysis of vitamin-B12 and folate levels.

Only subjects who showed no signs of dementia was included in the follow-up group. Three years later 77 of the participants had developed dementia; of these 59 were diagnosed with AD. Compared with participants with normal levels of vitamin B12 and folate the participants with low levels of at least one of the vitamins had a 2.

These risk estimates were obtained after adjusting for other risk factors such as age, sex, and educational attainment. The researchers speculate that homocysteine, a known neurotoxin, may be involved in the development of AD and that vitamin B12 and folic acid help prevent this effect by reducing homocysteine levels in the body.

Wang, H-X, et al. Vitamin B12 and folate in relation to the development of Alzheimer's disease. Suspicion has been growing that a lack of vitamin B12 is somehow implicated in the development of Alzheimer's disease. Now researchers in the United Kingdom have confirmed this suspicion. They evaluated members of a family with a genetic predisposition towards Alzheimer's disease.

They found that four out of six 67 per cent of family members with confirmed Alzheimer's disease had abnormally low vitamin B12 levels in their blood.

This compares to only one out of 12 8 per cent among the family members who were at equal genetic risk for developing Alzheimer's disease but did not. The researchers speculate that a vitamin B12 deficiency could result in impaired methylation reactions in the central nervous system - a characteristic feature in Alzheimer's disease.

They also consider the possibility that the genetic predisposition to Alzheimer's disease may actually be related to a genetic impairment in the ability to absorb vitamin B Vitamin B12 deficiency in itself often causes disorientation and confusion and thus mimics some of the prominent symptoms of Alzheimer's disease.

Familial Alzheimer's disease and vitamin B12 deficiency. Age and Ageing, Vol. Since it has been mandatory to fortify grain-based foods with folic acid in the United States. Recent reports indicate that this measure has resulted in a 19 per cent decrease in the incidence of neural tube defects. A similar fortification program is being considered in the UK. Irish researchers now suggest that the fortification protocol should include not only folic acid, but also vitamin B They point out that folic acid supplementation also lowers the level of homocysteine, a potent risk factor for heart and vascular disease.

However, a recent trial carried out by the Dublin researchers clearly showed that as blood levels of folic acid increased through supplementation, blood levels of vitamin-B12 became the limiting factor. In other words, additional folic acid as well as additional vitamin B12 is required in order to attain the maximum reduction in homocysteine levels. Four to five hundred micrograms per day of folic acid were found to increase folic acid levels by 80 to per cent and lower homocysteine levels by about 30 per cent in both men and women.

Both folate and homocysteine levels tended to revert to their pre-supplementation levels after 10 weeks of no supplementation; this shows that continuous supplementation is necessary in order to keep homocysteine levels under control.

Importance of both folic acid and vitamin B12 in reduction of risk of vascular disease. High blood levels of the amino acid homocysteine have been associated with an increased risk of atherosclerosis. Homocysteine is formed in the body from methionine an amino acid found in proteins in a process that can be blocked by folic acid and vitamins B6 and B High homocysteine levels can induce endothelial dysfunction a narrowing of the arterieswhich in turn is believed to be a precursor of atherosclerosis.

Researchers at the National Taiwan University Hospital now report that homocysteine-induced endothelial dysfunction can be avoided or very significantly ameliorated by supplementing with folic acid and vitamins B6 and B The study involved two men and fourteen women between the ages of 41 and 55 years.

At the start of the study all participants had their blood levels of homocysteine and their blood flow through the brachial artery measured after a hour overnight fast. They were then given an oral methionine-loading test to simulate the intake of a high protein meal. The experiment was repeated, but this time 5 mg of folic acid was given together with the methionine; the results were similar to those obtained in the first experiment indicating that folic acid does not act immediately as an "antidote" to a high intake of methionine.

The participants were then given 5 mg of folic acid, mg of vitamin B6, and 0. At the end of the five weeks their average homocysteine level had decreased to 5. The methionine-loading test was repeated. The researchers conclude that short-term five weeks administration of folic acid and vitamins B6 and B12 will reduce post-methionine load homocysteine levels and eliminate or ameliorate endothelial dysfunction an early manifestation of atherosclerosis. Chao, Chia-Lun, et al. Effect of short-term vitamin folic acid, vitamins B6 and B12 administration on endothelial dysfunction induced by post-methionine load hyperhomocysteinemia.

In addition to higher dietary intakes, methionine can also be regenerated if more circulating 5-Methyl THF is available to remethylate homocysteine to methionine, which may be the case when folate intake is high. Together, our findings suggest that the driver in the one-carbon metabolism pathway in diseased PC tissues may be methionine and not folate and that previous inconsistent findings in relation to folate intake or in circulation and higher PC risk could be attributed to cohorts in which methionine metabolism is impaired [ 546 ], though of course this is purely speculative and future larger studies are needed to confirm our findings.

AC variants also reduce enzyme activity but to a lesser extent [ 54 ]. In our study, higher intakes of methionine reported by PC cases may further diminish MTHFR function, which would diminish availability of 5-methyl THF to remethylate homocysteine into methionine, which in turn may cause homocysteine accumulation, an effect that has been associated with adenocarcinomas of the breast and ovary [ 5657 ].

Associations between PC risk and higher intakes of folate, vitamin B6, and vitamin B12 were not evident. Although we cannot rule out the possibility that our null associations could have been due to a limited sample size, confirming these findings in a larger study will be important.

Our findings showed that higher intakes of vitamin B12, a cofactor in the reaction of methionine synthase to regenerate methionine from homocysteine [ 59 ], was unrelated to PC risk in contrast to a prior study, which showed increased overall PC risk [ 8 ].

Together, our results could indicate that methionine metabolism may be impaired in older men who develop PC, and that consuming higher intakes of methionine may aggravate this impairment. Future research is needed to understand the underlying mechanism for these associations, while more studies are needed to determine whether the effect of high dietary methionine would cause methylation alterations [ 44 ].

The main limitation of this study is the small sample size and consequent inability to adequately evaluate the role of common variants in the MTHFR, which limited our ability for stratified analyses by PC grade. Also, the small sample size leads to concerns about type I errors for our significant findings and type II errors for our null observations. Another limitation is that dietary intake does not account for metabolized nutrients, and circulating levels of nutrients involved in the one-carbon metabolism pathway were not measured and neither were the upstream markers for homocysteine levels.

However, this study provides early data in support of the provocative hypothesis that excessive intake of one carbon cycle nutrients [ 2930 ] may be associated with increased PC risk. Conclusion In summary, our results suggest that higher intakes of methionine, presumably through higher protein consumption, is associated with increased PC risk, regardless of grade of lesion, but only in men carrying the polymorphism MTHFR AC.

These findings remain preliminary and hypothesis generating. Larger studies are required to validate these findings. View at Google Scholar C.

Adams, Nutritive Value of American Foods, vol.