Vitamin B12 can be found in the liver, kidney, muscle meats, eggs, cheese, milk, and fish. It is absent from yeast and plant-based diets. Other significant sources include fortified foods like soymilk and fermented foods like soy sauce, tempeh, and miso.
Vitamin B12, from a chemical perspective, is water-soluble. The cobalt in cobalamine is bound in a porphyrin-like ring. Cobalamine exists in two coenzyme forms: methylcobalamin and 5′-deoxyadenosylcobalamine. Cyanocobalamin, or B12, is one of four forms of cobalamin involved in human metabolism. Methylcobalamin is the most abundant form in the blood, and adenosylcobalamin is the most excellent form in the liver. Demethylation of the folate derivative required for thymidylate production and conjugation of folic acid into the active polymer forms of folate are two recognized routes of human metabolism in which cobalamin works as a coenzyme. Cobalamin insufficiency may cause a functional folate shortage by
preventing folate regeneration. Regenerating tetrahydrofolate, which is required for purine and thymidine synthesis, requires cobalamin. Myelin creation, healthy thyroid function, new cell formation in the red blood cells, and overall growth and development depend on vitamin B12. The methylmalonic acid buildup is inhibited, and aberrant fatty acids are not produced or incorporated into the membrane of nerve cells. This could explain why some neurological symptoms are seen in deficiency. It may play a part in homocysteine metabolism and, by extension, regulate atherosclerosis.
Pernicious anemia (PA) is the most common cause of vitamin B12 deficiency in at-risk populations. PA’s primary defects are the lack of intrinsic factors necessary for B12 absorption and stomach atrophy. Genetic problems in the absorption and transport systems, as well as disorders of the gastric mucosa, intestinal infections, malabsorption due to gastrectomy, complete ileal disease or resection, and other causes, can lead to a deficient status. Other risk factors include long-term strict vegetarianism and tapeworm infection. 35% of long-term vegetarians and vegans had serum vitamin B12 concentrations below the reference range, while the research found that vegans had B12 intakes below the RNI. Vitamin B12 levels are impacted by smoking as well. Univariate analysis shows cigarette smokers have lower levels of vitamin B12 in their plasma, red blood cells (RBCs), and buccal mucosa than nonsmokers.
Deficiency symptoms include a delay in cell division, which is especially noticeable in rapidly replicating cells like immature RBC. Flaccidity, poor muscle control, jerking, and aberrant electroencephalogram are neurological symptoms in infants with severe deficiency. Megaloblastic anemia and the emergence of neuropsychiatric disorders in adulthood are its hallmarks. Parasthesias diminished vibration sensation, and ataxia are all neurological signs. In the absence of anemia, CNS symptoms are permanent. Symptoms include lack of development, a painful, smooth tongue, splenomegaly, low platelet counts, and low white blood cell counts.
No symptoms of vitamin B12 toxicity have been seen. Some infrequent adverse events have been linked to the vitamin, however, they are not always dose-dependent. Diarrhea, blood clots in the legs, and a generalized feeling of swelling are some of the potential adverse reactions. Hives, a rash, itching, lips, mouth, or throat swelling, wheezing, or any other difficulties breathing are all symptoms of an allergic reaction.
Vitamin B12 is widely regarded as being safe for human consumption. High-dose intravenous administration does not appear to increase toxicity.
Polycythemia vera is associated with high levels of vitamin B12. Red blood cell volume increases in polycythemia vera as a percentage of total blood volume. Increases in white blood cells and platelets are not uncommon, but an absolute rise in red blood cells and the total blood volume are diagnostic. An analysis of bone marrow samples may be performed. However, it cannot be used to make an accurate diagnosis. Thrombocytosis, leukocytosis, an elevated leukocyte alkaline phosphatase level, or a high serum vitamin B12 or unbound B12-binding capacity, along with normal arterial oxygen saturation and splenomegaly (enlarged spleen), are all diagnostic of this condition.
Ages 0-6 months: 0.3 mg
6-month to 1-year-old infants: 0.5mcg
1–3-year-old children: 0.7 mcg
Kids aged 4 to 6: 1mcg
7-10-year-old kids: 1.4mcg
Young men aged 11 to 14: 2.0mcg
Females 11–14 years old: 2.0mcg
Teenage boys (15-18): 2.0mcg
Female adolescents 15–18 years old: 2.0mcg
Males aged 19-50 years: 2.0mcg
Females aged 19-50: 2.0mcg
Males over the age of 51: 2.0mcg
Women aged 51 and up: 2.0 mcg
Women Who Are Expecting: 2.2 mcg
Nursing Mothers (Initial Six Months): 2.6mcg
Second-Semester Breast-Feeding Mothers (2.6mg)
B-12 cyanocobalamin
Food Origin Amount Served Number of Micrograms per Serving
Beef liver (braised), 3.5 ounces; 71 micrograms
3.5 ounces of braised veal liver (36.5 micrograms)
Eggs (boiled): 0.56 micrograms per egg
3.5 oz of Cheddar Cheese, 0.83 mcg
Cheese, Monterey, 3.5 oz., 0.23 mcg
8 ounces of 2% milk has 0.89 micrograms of caffeine.
3 ounces of uncooked clams (4 large or nine small): 42.05 micrograms
Three ounces of tuna (2.54 mcg) canned in water
Pregnancy difficulties, neural tube defects, mental disorders, and cognitive impairment in the elderly are all linked to total serum homocysteine (tHcy) levels. Moreover, a high tHcy level is a prevalent cardiovascular risk factor, supported by over 80 clinical and epidemiological investigations. Even at its highest, vitamin B12 only lowers tHcy by about 10–15%. In contrast, folic acid may not work as well if your serum B12 level is low. It is also possible that correcting the hematological results of B12 insufficiency with folic acid therapy alone could lead to the onset of the neurological sequelae of B12 deficiency.
Up to 15% of the senior population may be deficient in vitamin B12. As evidence, high levels of methylmalonic acid coexist with low or low-normal levels of vitamin B12 and high levels of total homocysteine. Detection of vitamin B12 insufficiency through clinical signs and symptoms is less reliable in the elderly, and co-morbidities further complicate the interpretation of therapy responses. Megaloblastic anemia, myelopathy, and neuropathy are uncommon in the elderly because of a lack of vitamin B12. Serum methylmalonic acid levels often increase in older people with hyperhomocysteinemia due to untreated vitamin B12 deficiency. Therefore, unless their vitamin B12 status is established, the elderly should not use folic acid
supplements. Serum MMA and Hcys were found to have the potential to be beneficial in detecting vitamin B12 insufficiency at the subclinical or tissue level. The risk of vitamin B12 insufficiency in the elderly and the current screening algorithms based on serum metabolites should be familiar to clinicians. Massive doses of oral vitamin B12 treatment may reduce serum methylmalonic acid levels in the elderly. Most multivitamins, however, don’t contain nearly enough vitamin B12 to serve this function. In the United States, pernicious anemia is treated with vitamin B12 injections. Oral dosages of 300–1000 mg of vitamin B12 have been shown to increase serum vitamin B12 concentrations and prevent clinical abnormalities in various investigations of people with pernicious anemia. In senior people with less complete malabsorption, it is possible that equivalent doses of vitamin B12 (100-1000 mg) would be beneficial.
In the elderly, pernicious anemia is common, especially among women of color. Carmel found that about 800,000 elderly Americans have undiagnosed and untreated pernicious anemia, putting them at risk for hidden cobalamin deficiency if they were to be given significant doses of folate. The number of younger persons with undiagnosed pernicious anemia and other types of poverty is still unknown. It does not account for the elderly with cobalamin insufficiency caused by other conditions.
The elderly often have inadequate levels of cobalamin. Metabolic data reveal a cellular shortage of cobalamin in most cases, even if only a minority of such people exhibit clinically evident symptoms or indications. This does not appear to be a natural physiological consequence of becoming older. Instead, there seems to be a higher prevalence of preclinical cobalamin insufficiency among the elderly. Only a tiny percentage of the aged population has this insufficiency due to classical illnesses such as pernicious anemia. Food-cobalamin malabsorption is a more common issue,
typically caused by atrophic gastritis and hypochlorhydria, although other processes appear to be at play in some instances. Free and protein-bound cobalamin absorption was similar in healthy middle-aged and older individuals and subjects with mild to moderate atrophic gastritis, according to a single study. Therefore, neither aging nor mild to moderate atrophic gastritis can account for the high prevalence of low cobalamin levels in the elderly. The decline in absorption is not an inevitable part of becoming older. Research published in the American Journal of Clinical Nutrition found that the gradual loss of cobalamin stores caused by this malabsorption was slower than that caused by the interruption of intrinsic factor-mediated absorption. Mild pre-clinical low levels are linked more commonly with food-cobalamin malabsorption than with pernicious anemia, likely because of the slowed progression of depletion.
Protein-bound vitamin B12 absorption was studied in the context of hypochlorhydria and the use of acidic beverages in the elderly. Protein-bound vitamin B12 malabsorption is induced by omeprazole, which is counteracted by drinking an acidic liquid. Treatment with omeprazole immediately and dose-dependently reduced cyanocobalamin absorption. Cimetidine users who are also deficient in vitamin B12 may benefit from a supplement. Cobalamine deficiency affects the elderly at a rate of about 10%-20%. Cobalamin deficiency, as measured by low or low normal serum cobalamin levels and elevations in serum methylmalonic acid and homocysteine, was prevalent among elderly outpatients (14.5%). Patients with low cobalamin levels ( or = 200 pg/mL) and those with low normal serum cobalamin levels (201-300 pg/mL) exhibited identical numbers of patients with considerably elevated metabolites, which reduced with cobalamin treatment, making the serum cobalamin level insensitive for screening. According to the second study, a Cbl level of 300 pg/mL should be considered normal.
Hearing loss is one of the four most common chronic illnesses in the senior population. What’s up, Houston et al. al., in their recent article, hypothesized that low vitamin B12 and folate levels are linked to hearing loss in the elderly.
Serum cobalamin levels appear to decline with age. The group suffering from dementia does not share this correlation. A lower cobalamin concentration was found in people with Alzheimer’s disease who were still living at home compared to those who were in an institutional setting. This difference may be related to but does not fully explain, differences in dietary choices. Patients with Alzheimer’s who live independently are at risk for cobalamin insufficiency; therefore, tracking their serum cobalamin levels could be helpful. There is preliminary evidence that vitamin B12 can aid in treating Alzheimer’s disease, based on a small trial including 22 elderly people with low serum cobalamin. Cobalamin insufficiency was not consistently associated with cognitive decline in an older population, according to research of 50 Chinese participants. Another study found that supplementing with vitamin B12 did not reduce the rate of dementia deterioration.
As it becomes more apparent that in half of the cases, cobalamin absorption is impaired in one way or another, the typical dismissal of patients with low cobalamin concentrations should be re-examined. Most low cobalamin concentrations in the elderly are neither artifacts nor everyday expressions of aging but represent a mild clinical deficiency state (and occasionally a clinically overt one). Though many strategies are possible, there is widespread agreement that symptomatic insufficiency should always be treated immediately. The following are some of the possibilities:
1. Except in extreme cases, cobalamin levels should not be regulated. Proponents point to the sheer number of patients, the associated costs, skepticism of medical intervention for biochemical changes, the fact that only a subset of affected patients experiences symptoms, the likelihood that any progression is prolonged, and the fact that studies have shown no ill effects, even after many years of withholding treatment. Some counterarguments include the following: preclinical cobalamin deficiency may be a sentinel of underlying severe diseases like pernicious anemia in its pre-myelopathic stage or celiac disease; the absence of overt symptoms does not necessarily equal a state of well-being; the underlying gastric disturbance is present in half of the affected individuals, suggesting that the cobalamin deficiency will persist and probably progress; prevention has at least as much merit as a cure.
2. All patients who have low cobalamin levels should be given treatment immediately. Reasons in favor of this theory include the fact that administering cobalamin is not toxic and will not harm those who might receive it unnecessarily, that it is a cheap, efficient way to ensure that no one who might benefit goes untreated and that a detailed work-up may be neither practical nor effective due to its expense and the limited availability of many of the newer tests. Arguments against this method include the possibility that the amount and, presumably, the oral route of cobalamin therapy that such an approach dictates may prove inadequate to some patients and the failure to identify underlying severe diseases that may have caused the deficiency in some patients. Cobalamin deficiency was identified in older patients receiving cobalamin supplements, albeit at a lower rate than in those not taking the supplement. Therefore, it has never been shown and may be more complex than believed that cobalamin supplements will work adequately for those with food-cobalamin malabsorption. A person with food-cobalamin malabsorption may wonder if taking a cobalamin supplement at mealtime may cause the vitamin to be bound to the protein in their food and not absorbed. However, not all patients with pernicious anemia (estimated to affect 2% of all elderly and 10%-20% of those with low cobalamin concentrations) will absorb enough cobalamin from a pill, especially if doses of 100 mg are taken, or if it is taken haphazardly, as is familiar with routine supplements.
3. All older people should take cobalamin supplements regardless of their cobalamin levels. In addition to the reasons stated for the first choice, this one has the potential to help patients in the earliest stages of negative balance, reduce the cost of widespread cobalamin testing (which may provide falsely normal and falsely abnormal results), and eliminates the need for general cobalamin testing. One could argue that the poor and the disabled are less likely to take supplements when suggested for the entire population, whereas the wealthy and the health-conscious are more likely to take them.
4. Maintain the standard medical practice of treating each patient individually. Its focus on accurate diagnosis highlights the merits of this strategy, the detection of treatable underlying diseases, the resolution of prognostic concerns, the provision of individualized therapeutic care for those in need, and the avoidance of unnecessary care for those who do not. The standard clinical tests that are now used, such as blood counts and Schilling tests, typically yield negative results, which is an argument against it, as is the uncertainty of what constitutes good diagnostic evaluation.
Only one’s values and preferences may inform a decision among various alternatives at this stage. Add to those worries the unknown potential for harmful effects brought on by changes in folate status and other factors. An additional, potentially underappreciated source of clinical risk for the elderly with suboptimal cobalamin status is unprotected exposure to nitrous oxide, a commonly utilized inhalant during surgery. Mild, preclinical cobalamin insufficiency is a prevalent disease in the elderly, and all of these factors must be carefully examined when developing the best solution.
HIV-positive men with inadequate vitamin B12 levels (serum concentration 120 pmol/L) had a lower median survival time than those with high levels (median AIDS-free duration = 8 years vs. four years, P = 0.004). The researchers Remacha et al. reduced serum vitamin B12 levels in HIV-1 infected individuals were associated with decreased hemoglobin, leukocytes, CD4+ lymphocytes, and CD4+/CD8+ lymphocyte counts compared to HIV-1 infected patients with normal serum vitamin B12 levels. Among those with insufficient levels of vitamin B12 in their blood, 90% had AIDS, but only 66% of those with normal levels did. Identical findings were found in parallel research. Another study found that AZT’s hematologic toxic effects were more common in people with low CD4 lymphocyte counts, low blood vitamin B12 levels, anemia, or low neutrophil counts. Neither the development of AIDS nor a decrease in CD4+ lymphocyte count was linked to low serum concentrations of vitamin B6 and folate. Therefore, vitamin B12 levels in the blood are an independent and early indicator of HIV-1 disease development. Further study is needed to determine whether or not vitamin B12 replacement therapy helps halt illness development.
Lower median B12 concentrations in postmenopausal women were associated with an increased incidence of breast cancer compared with controls. A threshold effect for vitamin B12 may explain why women in the lowest fifth of the distribution had a higher risk of breast cancer than women in the other four higher fifths of the distribution, as found in the same study. Vitamin B12 has been linked to a lower risk of breast cancer. However, this beneficial association could have been caused by other factors associated with greater B12 levels. Methionine synthesis, which requires transferring a methyl group from methyl tetrahydrofolate to homocysteine, may shed light on the pathways between B12 and breast cancer. DNA hypomethylation, which may play a role in carcinogenesis, may result from insufficient B12, which may lead to decreased production of de novo methyl groups. Lower B12 levels may contribute to decreased DNA synthesis and worse DNA repair mechanisms by reducing the availability of unsubstituted tetrahydrofolate, which is involved in processes creating thymidylate and purines.
Low levels of vitamin B12 have been linked to decreased sperm counts and motility. Therefore, it is hypothesized that men deficient in B12 would see an improvement in fertility if they take B12 supplements.
Patients with diabetic neuropathy treated with methylcobalamin improved statistically in somatic and autonomic symptoms, with reversal of diabetic neuropathy symptoms, in a double-blind research. After four months, there was still no statistically significant improvement in motor and sensory nerve conduction tests. Patients reported no adverse effects while taking the medicine. Patients with symptomatic diabetic neuropathy had relief from paresthesia, burning sensations, and heaviness after receiving an intrathecal injection of methylcobalamin (2,500 micrograms in 10 ml of saline). There was little to no variation in the mean peroneal motor-nerve conduction velocity. No subjective complaints or changes in spinal fluid features were associated with methylcobalamin. These results imply that treating diabetic neuropathy symptoms with a high concentration of methylcobalamin in spinal fluid is both practical and safe.
Six patients with chronic progressive multiple sclerosis, characterized by a dismal outlook and systemic demyelination, were given an extremely high dose of methyl vitamin B12 (60 mg daily for six months). Despite no clinical improvement in motor impairment, medication was associated with more significant improvement in visual and brainstem auditory evoked potential abnormalities than before treatment. Another study found that serum cobalamin deficiency is unusual in MS, suggesting that high-dose methyl vitamin B12 therapy may be effective as an adjuvant to immunosuppressive treatment for chronic progressive MS.
Purine and thymidine synthesis require vitamin B12. It depends on myelin formation, thyroid health, cell division, nutrition metabolism, and growth. It’s necessary to synthesize SAM (S-adenosyl methionine), a chemical that regulates mood and aids in maintaining the membranes surrounding nerve cells. In addition to working with folate to reduce plasma homocysteine levels, an independent risk factor for coronary artery disease, cobalamin shortage may cause functional folate insufficiency by trapping folate in metabolic pathways and inhibiting its regeneration.
Vitamin B12 has been touted as a possible treatment for a wide range of medical issues, including but not limited to pernicious anemia, Crohn’s disease, vitiligo, tinnitus, atherosclerosis, high cholesterol, diabetes, osteoporosis, retinopathy, HIV support, shingles (herpes zoster/postherpetic neuralgia), hepatitis, asthma, and male infertility.
Total homocysteine (tHcy) in the serum is linked to pregnancy complications, neural tube defects, mental disorders, and cognitive impairment, and evidence suggests that vitamin B12 has a modest effect in lowering the tHcy and optimizes the response to folic acid. There is also concern that folic acid supplementation alone may correct the hematological findings associated with B12 deficiency but may precipitate the
neurological sequelae of B12 deficiency. The chance of developing breast cancer may be reduced by taking vitamin B12. Evidence suggests that a lack of vitamin B12 raises the possibility of developing breast cancer; this may be because people with depleted B12 levels produce less de novo methyl groups, resulting in DNA hypomethylation and perhaps contributing to carcinogenesis. Although the efficacy of vitamin B12 replacement therapy in delaying the progression of HIV-1 disease is unknown, serum vitamin B12 concentrations appear to be an early and independent indication of disease progression. The Homocysteine section elaborates on the importance of vitamin B12 in reducing homocysteine levels. Clinicians treating patients with neuropsychiatric disorders should be on the lookout for cobalamin insufficiency.
Most people over 60 have increased serum methylmalonic acid levels and are undiagnosed with vitamin B12 insufficiency. Undiagnosed pernicious anemia and food-cobalamin malabsorption are common in the elderly, even though the significant incidence of low cobalamin levels in older persons cannot be explained by either the aging process or mild to severe atrophic gastritis. Cobalamin deficiency is also more common in those with Alzheimer’s who live alone. Age-related hearing loss may be linked to low vitamin B12 and folate levels. The customary dismissal of patients with low cobalamin concentrations should thus be re-examined, as in half of the instances, cobalamin absorption is impeded in one way or another.
Patients with pernicious anemia, those with gastric mucosa problems, intestinal infections, gastrectomy, ileal illness, or resection, and those with genetic deficiencies in absorption and transport mechanisms are all at risk of being deficient and should be supplemented. To avoid the hematological and neurological signs of B12 insufficiency, strict vegetarians and smokers should receive enough of it in their diets. Permanent nerve damage can occur if vitamin B12 deficiency isn’t diagnosed and treated in time.
We suggest that people aim for 800 micrograms each day. This quantity can be obtained by eating about 1.4 hard-boiled eggs, 1 ounce of cheddar cheese, eight fluid ounces of milk containing 2% fat, and 0.1 ounces of beef liver (braised). Though vitamin B12 injections have been the standard of care for patients with pernicious anemia, oral dosages of 300–1000 g/d be similarly efficient in increasing serum vitamin B12 concentrations and preventing clinical abnormalities. The elderly may benefit from doses between 100 and 1000 g daily. Anyone using more than 1000 micrograms per day of folic acid as a supplement should be checked out first to ensure there aren’t any issues.
Read also: Tips On How To Talk To Your Doctor About Infecundity Testing.
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