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Vitamin B12 (Cyanocobalamine) - When, How, and Why to Supplement

Sources and Functions of Physiology

Source: Liver, kidneys, muscle meat, eggs, cheese, milk and fish are excellent sources of vitamin B12. It is not found in plant foods or in yeast. Fermented foods like soy sauce, soy sauce, and miso, and soy-rich foods are also sources of these vitamins.

Biochemistry: Vitamin B12 is water soluble. Cobalamine contains cobalt elements surrounded by porphyrins such as rings. The forms of coenzyme cobalamin are 5 'deoxyadenosylcobalamine and methylcobalamine. Four types of cobalamin play a role in human metabolism, including cyanocobalamin (a form known as B12), methylcobalamin (a major form of serum), and adenosylcobalamin (a major form of storage in the liver). Cobalamin acts as a coenzyme in two known human metabolic pathways: demethylation of folate derivatives required for thymidylate synthesis, and folic acid conjugation into folate-active polymeric forms. Cobalamin deficiency can cause folate deficiency to function by trapping folate in this pathway and limiting its growth. Cobalamin is essential for the regeneration of tetrahydrofolate required in the synthesis of purine and thymidine. Vitamin B12 is essential for growth, blood cell formation, nutrient metabolism, thyroid function, and myelin formation. It prevents the accumulation of methyl monoacetic acid, and thus, prevents the production and incorporation of abnormal fatty acids into nerve cell membranes. This may account for some of the neurological manifestations associated with deficiency. It may play a role in the metabolism of homocysteine ​​and therefore, control atherosclerosis.

At-risk population: Vitamin B12 deficiency is usually caused by anemia (PA). The main defect in PA is gastric atrophy and there is no intrinsic factor, which is important for B12 absorption. Gastric mucosa disorders, intestinal infections, secondary to gastrectomy, total ileal disease, or resection and genetic defects in absorption and transport mechanisms can lead to development of deficiency. Strict vegetarianism over a long period of time and worm attack are other risk factors. One study showed that vegans have B12 intake under the RNI; and 35% of long-term vegetarians and vegans have serum vitamin B12 concentrations below the reference range. Cigarettes also affect vitamin B12 status. Univariate analysis showed low plasma, red blood cells (RBCs), and bucca mucosa with vitamin B12 concentration in smokers compared with cigarette smokers.

Signs and Symptoms of Deficiency: The major drawback of B12 deficiency is the decline in quality, especially fast-growing cells such as RBCs. Infants with severe deficiencies present with anemia and neurological problems, such as degeneration, poor muscle control, sweating, and abnormal electroencephalogram. In adults, it is characterized by megaloblastic anemia and subsequently the development of neuropsychiatric symptoms. Neurological symptoms include numbness in the hands and feet, parasthesias, decreased sensation, and ataxia. CNS symptoms can occur without anemia and are irreversible. Bad growth, pain, smooth tongue, spleenomegaly, thrombocytopenia, and leucopenia are also seen.

Vitamin B12 toxicity: No signs of vitamin B12 poisoning, it seems. There are some rarely reported side effects that may be associated with vitamins, but these side effects are not necessarily dose related. Possible side effects include: diarrhea, blood clots in the legs, swelling around the body. These are symptoms of allergic reactions: nausea or rash, itching, swelling of the mouth, mouth, or throat, nausea or difficulty breathing.

Vitamin B12 is generally considered to be a non-toxic substance. Even taking it at high doses does not seem to increase the risk for toxicity

Increased levels of Vitamin B12 can occur in polycythemia vera. Polycythemia vera is a condition in which the blood volume occupied by red blood cells increases. Diagnosis is characterized by an absolute increase in red blood cells and in whole blood, although it is not uncommon for white blood cells and platelets to increase. Bone marrow tests can be done. However, it does not work in determining the final diagnosis. Laboratory studies confirm the diagnosis by showing an increase in RBC mass and normal arterial oxygen saturation associated with splenomegaly (spleen enlargement) or two of the following: thrombocytosis, leukocytosis, high levels of alkaline phosphatase leukocytes, or elevated serum B12 serum or B12 capacity.

Suggestions: RDA in μg (mcg)

  • Babies born to 6 months - 0.3mcg

  • Baby 6 mos to 1 year - 0.5mcg

  • Children 1 to 3 years - 0.7mcg

  • Kids 4 to 6 years - 1.0mcg

  • Kids 7 to 10 - 1.4mcg

  • Men from 11yr to 14 years old - 2.0mcg

  • Young women ages 11 to 14 - 2.0mcg

  • Young men aged 15 to 18 - 2.0mcg

  • Young women 15 to 18 years - 2.0mcg

  • Male adults 19 to 50 years - 2.0mcg

  • Adults 19 to 50 years old - 2.0mcg

  • 51 year old male added - 2.0mcg

  • 51 year old female added - 2.0mcg

  • Pregnant women - 2.2mcg

  • Breastfeeding (first 6 months) - 2.6mcg

  • Breastfeeding Mother (2 months 6) - 2.6mg

Cyanocobalamin B12

Food Source Size / Number # mcg / meal

Liver (boiled beef) 3.5 oz 71 mcg

Liver (boiled beef) 3.5 oz 36.50 mcg

Eggs (boiled) 1 egg 0.56 mcg

Cheddar cheese 3.5 oz 0.83 mcg

Monterey cheese 3.5 oz 0.23 mcg

Milk 2% 8 fl oz 0.89 mcg

3 oz clams (4 large or 9 small) 42.05 mcg

Tuna (canned in water) 3 oz 2.54 mcg

Homocysteine ​​Literature:

Total levels of homocysteine ​​(tHcy) in serum are associated with pregnancy complications, neural tube defects, mental disorders, and cognitive impairment in the elderly. In addition, more than 80 clinical and epidemiological studies provide ample evidence that high levels of tHcy are common cardiovascular risk factors. The effect of vitamin B12 on tHcy levels was modest with a maximum of 10 to 15% reduction. However, low levels of B12 serum may prevent optimal response to folic acid. There is also concern that folic acid supplementation may simply correct the hematological findings associated with B12 deficiency, but may affect the neurological sequelae of B12 deficiency.

Cognitive deficiency in parents

Vitamin B12 deficiency is found in up to 15% of the elderly. It is documented by high methylmalonic acid with or without total homocysteine ​​concentration plus low or low vitamin B12 combination. The clinical signs and symptoms of vitamin B12 are less sensitive in older subjects, and comorbidities in these subjects respond to therapies that are difficult to interpret. Obvious megaloblastic anemia and myelopathy or neuropathy are rare in strict vitamin subjects. Many elderly subjects with hyperhomocysteinemia have vitamin B12 deficiency that is not diagnosed with high serum methylmalonic acid concentration. Therefore, elderly subjects should not receive folic acid supplements before their vitamin B12status is diagnosed. The study results show the potential use of serum MMA and Hcys in identifying vitamin and subclinical or tissue deficiencies. Clinicians need to know about the risks of vitamin B12 deficiency in parents and screening algorithms when using serum metabolites. A large amount of vitamin B12 can be effectively used to lower the value of serum methylmalonic acid in parents. However, the most common dose of vitamin B12in in multivitamin preparations is too low for this purpose. The traditional treatment for malignant anemia in the United States is vitamin B12 injection. However, several studies in subjects with pernicious anemia have shown that oral doses of 300-1000 mg are effective in increasing serum vitamin B12concentrations and preventing clinical abnormalities. It is possible that similar doses of vitamin B12 (100-1000 mg) may be effective in older subjects with less complete malabsorption.

Undiagnosed anemia is a common finding in older people, especially among black and white women. Findings from a study by Carmel show that nearly 800,000 elderly people in the United States suffer from undiagnosed and untreated anemia and, thus, are at risk for cobalamin deficiency if exposed to large amounts of folate. This number does not include parents with cobalamin deficiency caused by other disorders or an unknown number of young people with unknown anemia and other possible causes.

Low levels of cobalamin are common in older people. Although only a minority of these people display clinically clear symptoms or signs, metabolic data clearly show a lack of cobalamin cells in most cases. Evidence suggests that this is not a normal physiological expression of the aging process. On the other hand, parents appear to be at greater risk for mild and premature cobalamin deficiency. Classical disorders such as malignant anemia are the cause of this deficiency in only a small proportion of the elderly. A more common problem is the malabsorption of food-cobalamin, which usually arises from atopic gastritis and hypochloric acid, but other mechanisms appear to be involved in some patients. One study showed no significant differences in the absorption of free cobalamin or protein binding between healthy adults and healthy adults, and no change in the absorption of cobalamin in subjects identified as mild to moderate atrophic gastritis. Therefore, the low prevalence of cobalamin levels in the elderly cannot be explained by the mild and moderate process of atrophic gastritis. Decreased absorption should not be seen as a natural consequence of aging. According to the American Journal of Clinical Nutrition, the partial nature of this form of malabsorption results in slower progressive cobalamin penetration than the complete malabsorption caused by intrinsic absorption-mediated absorption disorders. Decreased deterioration is the most likely cause and this explains why low pre-clinical levels are most often associated with malabsorption of food-cobalamin rather than with malignant anemia.

The effect of hypochlorothrosia and the consumption of acidic drinks on the absorption of vitamin B12 bound protein has been investigated in elderly subjects. Omeprazole causes hypoklorhidria and thus, vitamin B12 protein-bound malabsorption, and acidic beverages increase the absorption of protein-bound vitamin B12. Omeprazole therapy significantly reduces the absorption of cyanocobalamin in a dose-dependent manner. Patients taking cimetidine should also take vitamin B12 supplements. About 10-20% of the elderly lack cobalamine. There was a lack of cobalamin deficiency (14.5%) as indicated by the increase in serum methylmalonic acid and homocysteine ​​in addition to low or low normal cobalamin serum levels in elderly patients. Serum cobalamin levels were not sensitive to examination because the number of patients was similar to the normal cobalamin serum levels of 201-300 pg / mL compared to patients with low levels of cobalamin (<or = 200 pg / mL) having high metabolites. falls with cobalamin treatment. Recent studies suggest that the lower limit of normal range for Cbl levels should be increased to 300 pg / mL.

Hearing impairment is one of the four most common chronic conditions in the elderly. Houston et. al., in their recent article, suggested that vitamin B12 and poor vitamin status may be associated with age-related hearing impairment.

Data show that serum cobalamin levels decrease in normal aging. This association exists only in uninitiated groups, but not unidentified groups. In one study, a lower concentration of cobalamin was observed in Alzheimer's patients living in their own home compared to those who were diagnosed with AD, which may be related to, but not fully explained, eating habits. Patients with AD living in their own homes are at risk for cobalamin deficiency, and monitoring serum cobalamin concentrations may be helpful in this group. A small study in 22 elderly patients with low serum cobalamin showed that vitamin B12 may be useful in the treatment of Alzheimer's. A study in 50 Chinese subjects suggested that cobalamin deficiency does not always cause cognitive impairment in older people. In another study, replacement of vitamin B12 did not cause dementia.

As it becomes clear that most of the low concentration of cobalamin in the elderly is not a common artifact or expression of aging, it does represent a mild clinical condition (and sometimes clinically light one), and as it becomes clear that in one half of cases The absorption of cobalamin is affected in one way or another, the normal dismissal of patients with low cobalamin concentration should be reviewed. The broad spectrum of choices can be summed up, although nothing has changed the general consensus that symptoms should be treated promptly. Options include the following:

1. Do nothing about the concentration of cobalamin unless they become clinically significant. These supporting arguments include the number of patients involved, the cost, doubts about medical intervention for biochemical changes, the fact that only a small minority of affected patients are symptomatic, the possibility that any progress is slow, and the fact that studies have shown no adverse effects, even after years of delayed treatment. The counter arguments are that the absence of a clear symptom is not necessarily the same as the condition of well-being, that the underlying gastric disorders are half the people who show that cobalamin deficiency will persist and may progress, preventing at least as much merit as medicine, and preclinical carbohydrate deficiency can be a serious underlying sentinel, such as anemia that damages premyelopathic or celiac disease.

2. Automatically treat all patients with low concentration of cobalamin. The arguments that support this hypothesis are a cheap way to ensure that no one may benefit from treatment, that detailed work may not be practical or effective given the expense and limited availability of newer tests, and that the test is non-toxic and will not harm them that may not be necessary. The arguments for this approach are the failure to identify serious underlying diseases that may cause some patients, failure to identify in some need for more complex treatment or attention to complications, and the possibility that the number and possible oral route The therapeutic cobalamin approach as defined may prove inadequate for some patients. Keep in mind that cobalamin deficiency, although less frequent in unused individuals, is still present in elderly patients taking cobalamin supplements. Therefore, although cobalamin supplements may work well in people with diet-induced malabsorption, they have never been established and may be more complex than assumed. One can ask whether cobalamin pills taken with food bind to food proteins and fail to be absorbed by someone with malabsorption of food-cobalamin. In addition, not all patients with unwanted anemia (estimated to be present in 2% of all parents and 10-20% of those with low carbohydrate concentrations) will absorb sufficient cobalamin from the pill, especially if the dose is <100 mg. taken, or if taken carelessly, in addition to regular routine.

3. Give cobalamin supplements to all parents, regardless of their concentration. The arguments in favor of this, other than those mentioned in the preceding options, are that such rating problems can benefit from the same broad solution, that it saves on the cost of extensive cobalamine testing (which in any case can give a false normal and false results are abnormal), and they may have potential benefits for patients with early stages of negative balance. These counter counters are the recommended supplements of the population that tend to lead to higher consumption by the richer, health conscious, and functioning more, and tend to be ignored by the poor and the disadvantaged.

4. Continue the traditional medical approach to assessment and individual therapy. The arguments for this approach are based on the goals to be commended for making a specific diagnosis; identify possible diseases; addressing prognostic issues; treating those who need it with a specialized, specialized therapeutic approach; and avoid the treatment of people who don't need it. His arguments are costly and costly to millions of people, and uncertainty about what constitutes an optimal diagnostic assessment, given that standard clinical trials such as blood tests and Schilling tests provide negative results in most cases.

The choices that will be made between these options and their variations can only reflect personal philosophy and bias. To the concerns mentioned, it may add uncertainty about the potential adverse effects created by changes in folate status and other changes. Unsafe exposure to nitrous oxide, an inhalant widely used during surgery, may be a common and less recognized clinical risk factor for older people with marginal cobalamin status. All of these issues need to be carefully considered when adopting an optimal approach to the common problems of moderate and premature aging in older adults.

Development of HIV disease

In a study conducted on HIV positive men, participants with low serum vitamin B12 concentrations (<120 pmol / L) had significantly lower AIDS times than those with adequate vitamin B12 concentration (median free time AIDS = 4 vs 8 y, respectively, P = 0.004). In a cross-sectional study, Remacha et. al. found that HIV-1-infected patients with low vitamin B12 concentrations had hemoglobin, leukocytes, CD4 + lymphocytes and CD4 + / CD8 + lymphocytes from patients with HIV-1 with normal serum vitamin B12 concentrations. Ninety percent of patients with low serum B12 concentration have AIDS compared to only 66% of patients with adequate vitamin B12 concentration. Similar results have been noted in other studies. Another study showed that subjects who were associated with low CD4 lymphocytes, low vitamin B12 serum levels, anemia, or low neutrophils were more likely to have hematological toxic effects when treated with AZT. Low serum concentrations of vitamin B6 and folate were not associated with AIDS progression or decreased CD4 + lymphocyte counts. Therefore, the concentration of vitamin B12 Serum appears to be an early and independent cause of HIV-1. The efficacy of vitamin B12 replacement therapy in the development of slow disease, however, remains unknown and should be the focus of further research.

Breast cancer

Menopausal women with a low median B12 concentration were found to be at higher risk for breast cancer development when compared to controls. In the same study, an increased risk of breast cancer was observed among women in the lower five of vitamin B12 distribution compared with women in the higher fours, indicating a threshold effect for B12. However, it cannot be excluded that unknown protective factors for breast cancer associated with higher B12 concentrations may result in protective associations between vitamin B12 and breast cancer. The mechanism underlying the relationship between B12 and breast cancer may be explained by the role of B12 as a co-substrate in the synthesis of methionine, in which the methyl group is transferred from methyl tetrahydrofolate to homocysteine. Thus, low concentration of B12 may lead to reduced synthesis of the methyl de novo group, leading to DNA hypomethylation, which may play a role in carcinogenesis. Through the availability of unstructured tetrahydrofolate, which is involved in the reaction producing thymidilate and purine, a lower concentration of B12 may also lead to a reduction in DNA synthesis and, therefore, impair DNA repair mechanisms.

Male Infertility:

Vitamin B12 deficiency can lead to decreased sperm count and reduced sperm motility. Therefore, it has been suggested that B12 supplementation may increase fertility in men who are deficient in these vitamins.

Diabetic Neuropathy:

In a double-blind study, patients with diabetic neuropathy receiving methylcobalamin showed statistically significant improvement in somatic and autonomic symptoms with regression of diabetic neuropathy symptoms. Studies of motor and sensory nerve conduction showed no statistically significant improvement after 4 months. The drug is tolerant to the patient and has no side effects. In another study, intrathecal injection of methylcobalamine (2,500 micrograms in 10 ml saline) in patients with symptomatic diabetic neuropathy showed an increase in paresthesia, arthritis, and weight gain. The flow velocity of the peroneal motor nerve does not change significantly. Methylcobalamin does not cause side effects regarding subjective symptoms or spinal fluid characteristics. Therefore, these findings indicate that high concentrations of methylcobalamin in spinal fluid are very effective and safe in the treatment of diabetic neuropathy symptoms.

Multiple sclerosis:

One dose of methyl vitamin B12 (60 mg daily for 6 months) is given to 6 patients with chronic progressive MS, a disease that usually has a morbid prognosis and widespread demilelination in the central nervous system. Although motor impairments do not improve clinically, abnormalities in both visual and brain hearing may increase more frequently during therapy than during the pre-treatment period. Therefore, it is suggested that large dose of methyl vitamin B12 therapy may be useful in addition to immunosuppressive treatment for chronic progressive MS. Another study showed that serum cobalamin deficiency is not uncommon in multiple sclerosis.


Vitamin B12 is essential for the synthesis of purine and thymidine. It is also essential for growth, blood cell formation, nutrient metabolism, thyroid function, and myelin formation. It helps maintain the integrity of the nerve cell membrane and is also required in the production of mood that affects a substance called SAM (S-adenosyl methionine). Cobalamin deficiency can produce functional folate deficiency by trapping folate in the metabolic pathway and limiting its growth, and also works with folate in lowering plasma homocysteine ​​levels, which is a risk factor for coronary artery disease.

Several claims have been made regarding the conditions under which Vitamin B12 may support: Malignant anemia, Crohn's disease, Vitiligo, Tinnitus, Atherosclerosis, High Cholesterol, Diabetes, Osteoporosis, Retinopathy, HIV Support, Wood (herpes zoster / postherpetic neuralgia, Hepatitis, asthma, and infertility in men.

Strong evidence supports that Vitamin B12 has a modest effect in reducing tHcy and optimizing its response to folic acid. There is also concern that folic acid supplementation may simply correct the hematological findings associated with B12 deficiency, but may affect the neurological sequelae of B12 deficiency. Total levels of homocysteine ​​(tHcy) in serum are associated with pregnancy complications, neural tube defects, mental disorders, and cognitive impairment in the elderly. Vitamin B12 may have protective effects against breast cancer risk. Low concentrations of B12 have been shown to be associated with increased risk of breast cancer, which may be due to low concentrations of B12 which may lead to reduced synthesis of the methyl de novo group leading to DNA hypomethylation, which may play a role in carcinogenesis. Serum vitamin B12 concentration seems to be an early and independent cause of HIV-1 disease, although the efficacy of vitamin B12 replacement therapy in slowing disease progression remains unknown. The role of B12 in the reduction of homocysteine ​​is further discussed in the section on Homocysteine. Clinicians should be aware of the possibility of cobalamin deficiency in the context of neuropsychiatric illness.

Vitamin B12 deficiency is common in older people, most of whom are not diagnosed with high levels of serum monoamine acidic acid. Although the high prevalence of low cobalamin in the elderly may not be well explained by the process of aging or mild to moderate atropic gastritis, unknown non-diagnosed anemia and malabsorption of cobalamin are very common in the elderly. Patients with Alzheimer's disease who live in their own homes are also at risk for cobalamin deficiency. Vitamin B12 and poor folate status may be associated with age-related hearing loss. Therefore, in one half of cases, absorption of cobalamin is disrupted in one way or another, and normal dismissal of patients with low cobalamin concentration should be re-examined.

In general populations exposed to deficiencies, such as patients with malignant anemia and those with gastric mucosa disorders, intestinal infections, gastrectomy, ilium or resection, and genetic defects in absorption and transport mechanisms, should be supplemented. Strict vegetarians and smokers should consume sufficient amounts in their diet to prevent the development of hematological and neurological symptoms of B12 deficiency. Delays in diagnosing and treating vitamin B12 deficiency can lead to permanent neurological damage.

Our recommendation for adults is 800 μg / d. This amount is available from about 1.4 boiled eggs, 1 serving of cheddar cheese, 8 fl oz milk with 2% fat and 1/100 liver meal (boiled beef). Patients with toxic anemia have traditionally been treated with vitamin B12 injection, while oral doses of 300-1000 μg / d have been shown to be equally effective in increasing serum vitamin B12 concentration and preventing clinical abnormalities. A dose of 100-1000 μg / d may be effective in older patients. Anyone supplemented with more than 1000 μg / d of folic acid can be evaluated early to avoid potential problems.


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