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Vitamin B12 has the largest and most complex chemical structure of all the vitamins. It is unique among vitamins in that it contains a metal ion, cobalt. For this reason cobalamin is the term used to refer to compounds having vitamin B12 activity. Methylcobalamin and 5-deoxyadenosyl cobalamin are the forms of vitamin B12 used in the human body (1). The form of cobalamin used in most supplements, cyanocobalamin, is readily converted to 5-deoxyadenosyl and methylcobalamin in the body. In mammals, cobalamin is a cofactor for only two enzymes, methionine synthase and L-methylmalonyl-CoA mutase (2).
Cofactor for methionine synthase
Methylcobalamin is required for the function of the folate-dependent enzyme, methionine synthase. This enzyme is required for the synthesis of the amino acid, methionine, from homocysteine. Methionine in turn is required for the synthesis of S-adenosylmethionine, a methyl group donor used in many biological methylation reactions, including the methylation of a number of sites within DNA and RNA (3). Methylation of DNA may be important in cancer prevention. Inadequate function of methionine synthase can lead to an accumulation of homocysteine, which has been associated with increased risk of cardiovascular diseases (diagram).
Cofactor for L-methylmalonyl-CoA mutase
5-Deoxyadenosylcobalamin is required by the enzyme that catalyzes the conversion of L-methylmalonyl-CoA to succinyl-CoA. This biochemical reaction plays an important role in the production of energy from fats and proteins. Succinyl CoA is also required for the synthesis of hemoglobin, the oxygen carrying pigment in red blood cells (3).
Vitamin B12 deficiency is estimated to affect 10%-15% of individuals over the age of 60 (4). Absorption of vitamin B12 from food requires normal function of the stomach, pancreas, and small intestine. Stomach acid and enzymes free vitamin B12 from food, allowing it to bind to other proteins called R proteins (3). In the alkaline environment of the small intestine, R proteins are degraded by pancreatic enzymes, freeing vitamin B12 to bind to intrinsic factor (IF), a protein secreted by specialized cells in the stomach. Receptors on the surface of the small intestine take up the IF-B12 complex only in the presence of calcium, which is supplied by the pancreas (5). Vitamin B12 can also be absorbed by passive diffusion, but this process is very inefficient—only about 1% absorption of the vitamin B12 dose is absorbed passively (2).
Causes of vitamin B12 deficiency
The most common causes of vitamin B12 deficiency are: 1) an autoimmune condition known as pernicious anemia and 2) food-bound vitamin B12 malabsorption. Although both causes become more common with increasing age, they are separate conditions (4).
Pernicious anemia has been estimated to be present in approximately 2% of individuals over 60 (6). Although anemia is often a symptom, the condition is actually the end stage of an autoimmune inflammation of the stomach, resulting in destruction of stomach cells by one's own antibodies. Progressive destruction of the cells that line the stomach causes decreased secretion of acid and enzymes required to release food-bound vitamin B12. Antibodies to intrinsic factor (IF) bind to IF preventing formation of the IF-B12 complex, further inhibiting vitamin B12 absorption. If the body's vitamin B12 stores are adequate prior to the onset of pernicious anemia, it may take years for symptoms of deficiency to develop. About 20% of the relatives of pernicious anemia patients also have pernicious anemia, suggesting a genetic predisposition. Treatment of pernicious anemia generally requires injections of vitamin B12 to bypass intestinal absorption. High-dose oral supplementation is another treatment option, because consuming 1,000 mcg (1 mg)/day of vitamin B12 orally should result in the absorption of about 10 mcg/day (1% of dose) by passive diffusion (4). In fact, high-dose oral therapy is considered to be as effective as intramuscular injection (7-10).
Food-bound vitamin B12 malabsorption
Food-bound vitamin B12 malabsorption is defined as an impaired ability to absorb food or protein-bound vitamin B12, although the free form is fully absorbable (11). In the elderly, food-bound vitamin B12 malabsorption is thought to result mainly from atrophic gastritis, a chronic inflammation of the lining of the stomach that ultimately results in the loss of glands in the stomach (atrophy) and decreased stomach acid production. Because stomach acid is required for the release of vitamin B12 from the proteins in food, vitamin B12 absorption is diminished. Decreased stomach acid production also provides an environment conducive to the overgrowth of anaerobic bacteria in the stomach, which further interferes with vitamin B12 absorption (3). Because vitamin B12 in supplements is not bound to protein, and because intrinsic factor (IF) is still available, the absorption of supplemental vitamin B12 is not reduced as it is in pernicious anemia. Thus, individuals with food-bound vitamin B12 malabsorption do not have an increased requirement for vitamin B12; they simply need it in the crystalline form found in fortified foods and dietary supplements.
Atrophic gastritis is thought to affect 10%-30% of people over 60 years of age, and the condition is frequently associated with infection by the bacteria, Heliobacter pylori. H. pylori infection induces chronic inflammation of the stomach, which may progress to peptic ulcer disease, atrophic gastritis, and/or gastric cancer in some individuals. The relationship of H. pylori infection to atrophic gastritis, gastric cancer, and vitamin B12 deficiency is presently an area of active research (4).
Other causes of vitamin B12 deficiency
Other causes of vitamin B12 deficiency include surgical resection of the stomach or portions of the small intestine where receptors for the IF-B12 complex are located. Conditions affecting the small intestine, such as malabsorption syndromes (celiac disease and tropical sprue), may also result in vitamin B12 deficiency. Because the pancreas provides critical enzymes as well as calcium required for vitamin B12 absorption, pancreatic insufficiency may contribute to B12 deficiency. Since vitamin B12 is found only in foods of animal origin, a strict vegetarian (vegan) diet has resulted in cases of vitamin B12 deficiency. Alcoholics may experience reduced intestinal absorption of vitamin B12 (2). Individuals with acquired immunodeficiency syndrome (AIDS) appear to be at increased risk of deficiency, possibly related to a failure of the IF-B12 receptor to take up the IF-B12 complex (3). Long-term use of acid-reducing drugs has also been implicated in vitamin B12 deficiency (see Drug interactions).
Symptoms of vitamin B12 deficiency
Vitamin B12 deficiency results in impairment of the activities of B12-requiring enzymes. Impaired activity of methionine synthase may result in elevated homocysteine levels, while impaired activity of L-methylmalonyl-CoA mutase results in increased levels of a metabolite of methylmalonyl-CoA called methylmalonic acid (MMA). Individuals with mild vitamin B12 deficiency may not experience symptoms, although blood levels of homocysteine and/or MMA may be elevated (12).
Diminished activity of methionine synthase in vitamin B12 deficiency inhibits the regeneration of tetrahydrofolate (THF) and traps folate in a form that is not usable by the body (diagram), resulting in symptoms of folate deficiency even in the presence of adequate folate levels. Thus, in both folate and vitamin B12 deficiencies, folate is unavailable to participate in DNA synthesis. This impairment of DNA synthesis affects the rapidly dividing cells of the bone marrow earlier than other cells, resulting in the production of large, immature, hemoglobin-poor red blood cells. The resulting anemia is known as megaloblastic anemia and is the symptom for which the disease, pernicious anemia, was named (3). Supplementation with folic acid will provide enough usable folate to restore normal red blood cell formation. However, if vitamin B12 deficiency is the cause, it will persist despite the resolution of the anemia. Thus, megaloblastic anemia should not be treated with folic acid until the underlying cause has been determined (5).
The neurologic symptoms of vitamin B12 deficiency include numbness and tingling of the arms and, more commonly, the legs, difficulty walking, memory loss, disorientation, and dementia with or without mood changes. Although the progression of neurologic complications is generally gradual, such symptoms are not always reversible with treatment of vitamin B12 deficiency, especially if they have been present for a long time. Neurologic complications are not always associated with megaloblastic anemia and are the only clinical symptom of vitamin B12 deficiency in about 25% of cases (6). Although vitamin B12 deficiency is known to damage the myelin sheath covering cranial, spinal, and peripheral nerves, the biochemical processes leading to neurological damage in B12 deficiency are not well understood (3).
Tongue soreness, appetite loss, and constipation have also been associated with vitamin B12 deficiency. The origins of these symptoms are unclear, but they may be related to the stomach inflammation underlying some cases of B12 deficiency, or to the increased vulnerability of rapidly dividing gastrointestinal cells to impaired DNA synthesis (6).
The current RDA was revised by the Food and Nutrition Board (FNB) of the Institute of Medicine in 1998. Because of the increased risk of food-bound vitamin B12 malabsorption in older adults, the FNB recommended that adults over 50 years of age get most of the RDA from fortified food or vitamin B12-containing supplements (6).
|Recommended Dietary Allowance (RDA) for Vitamin B12|
|Life Stage||Age||Males (mcg/day)||Females (mcg/day)|
|Infants||0-6 months||0.4 (AI)||0.4 (AI)|
|Infants||7-12 months||0.5 (AI)||0.5 (AI)|
|Adults||51 years and older||2.4*||2.4*|
*Vitamin B12 intake should be from supplements or fortified foods due to the age-related increase in food bound malabsorption.
The results of more than 80 studies indicate that even moderately elevated levels of homocysteine in the blood increase the risk of cardiovascular diseases (13), though the mechanism by which homocysteine increases the disease risk remains the subject of a great deal of research. The amount of homocysteine in the blood is regulated by at least three vitamins: folate, vitamin B12, and vitamin B6 (diagram). Analysis of the results of 12 homocysteine-lowering trials showed folic acid supplementation (0.5-5 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 (14). 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 (15). Some evidence indicates that vitamin B12 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 (16). 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. For more information regarding homocysteine and cardiovascular diseases, see the article on folic acid.
Although increased intake of folic acid and vitamin B12 has been found to decrease homocysteine levels, it is not presently known whether increasing intake of these vitamins will translate to reductions in risk for cardiovascular diseases. However, several randomized placebo-controlled trials are presently being conducted to determine whether homocysteine lowering through folic acid and other B vitamin supplementation reduces the incidence of cardiovascular diseases. A meta-analysis of data from four of the ongoing trials shows that B vitamin supplementation had no significant effect on risk of coronary heart disease or stroke, but only about 14,000 participants were included in analysis and thus any conclusions are limited (17). Nevertheless, the completion of ongoing clinical trials should help to answer whether or not supplemental B vitamins lower risk for cardiovascular diseases.
Folate is required for synthesis of DNA, and there is evidence that decreased availability of folate results in strands of DNA that are more susceptible to damage. Deficiency of vitamin B12 traps folate in a form that is unusable by the body for DNA synthesis. Both vitamin B12 and folate deficiencies result in a diminished capacity for methylation reactions (diagram). Thus, vitamin B12 deficiency may lead to an elevated rate of DNA damage and altered methylation of DNA, both of which are important risk factors for cancer. A recent series of studies in young adults and older men indicated that increased levels of homocysteine and decreased levels of vitamin B12 in the blood were associated with a biomarker of chromosome breakage in white blood cells. In a double-blind, placebo-controlled study, the same biomarker of chromosome breakage was minimized in young adults who were supplemented with 700 mcg of folic acid and 7 mcg of vitamin B12 daily in cereal for two months (18).
A case-control study compared prediagnostic levels of serum folate, vitamin B6, and vitamin B12 in 195 women later diagnosed with breast cancer and 195 age-matched women who were not diagnosed with breast cancer (19). Among women who were postmenopausal at the time of blood donation, the association between blood levels of vitamin B12 and breast cancer suggested a threshold effect. The risk of breast cancer was more than doubled in women with serum vitamin B12 levels in the lowest quintile (1/5) compared to women in the four highest quintiles. The investigators found no relationship between breast cancer and serum levels of vitamin B6, folate, or homocysteine. A case-control study in Mexican women (475 cases and 1,391 controls) reported that breast cancer risk for women in the highest quartile (1/4) of vitamin B12 intake was 68% lower than those in the lowest quartile (20). Stratification of the data revealed that the inverse association between dietary vitamin B12 intake and breast cancer risk was stronger in postmenopausal women compared to premenopausal women, though both associations were statistically significant. Because these studies were observational, it cannot be determined whether decreased serum levels of vitamin B12 or low dietary vitamin B12 intakes were a cause or a result of breast cancer. Previously, there has been little evidence to suggest a relationship between vitamin B12 status and breast cancer risk. However, high dietary folate intakes have been associated with reduced risk for breast cancer in several studies, and some studies have reported that vitamin B12 intake may modify this association (21, 22).
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 (23). 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 (24). 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.
Individuals with Alzheimer's disease often have low blood levels of vitamin B12. One study found lower vitamin B12 levels in the cerebrospinal fluid of patients with Alzheimer's disease than in patients with other types of dementia, though blood levels of vitamin B12 did not differ (25). The reason for the association of low vitamin B12 status with Alzheimer's disease is not clear. Vitamin B12 deficiency, like folate deficiency, may lead to decreased synthesis of methionine and S-adenosylmethionine, thereby adversely affecting methylation reactions. Methylation reactions are essential for the metabolism of components of the myelin sheath of nerve cells as well as neurotransmitters. Also, moderately increased homocysteine levels as well as decreased folate and vitamin B12 levels have been associated with Alzheimer's disease and vascular dementia.
Some but not all studies have associated elevated homocysteine concentrations or decreased serum levels of vitamin B12 with an increased risk of Alzheimer's disease. A case-control
study of 164 patients with dementia of Alzheimer's type included 76
cases in which the diagnosis of Alzheimer's disease was confirmed by examination
of brain cells after death (26).
Compared to 108 control subjects without evidence of dementia, subjects
with dementia of Alzheimer's type and confirmed Alzheimer's disease had
higher blood homocysteine
levels and lower blood levels of folate and vitamin B12. Measures of
general nutritional status indicated that the association of increased
homocysteine levels and diminished vitamin B12 status with
Alzheimer's disease was not due to dementia-related malnutrition (26). In another study, low
serum vitamin B12
(≤ 150 pmol/L) or folate (≤ 10 nmol/L) levels were associated with
a doubling of the risk of developing Alzheimer's disease in 370 elderly
men and women followed over three years (27).
In a sample of 1,092 men and women without dementia followed for an average
of ten years, those with higher plasma
homocysteine levels at baseline had a significantly higher risk of developing
Alzheimer's disease and other types of dementia (28).
Specifically, those with plasma homocysteine levels greater than 14 micromol/L had nearly
double the risk of developing Alzheimer's disease. A study in 650 elderly men and women reported that the risk of elevated plasma homocysteine levels was significantly higher in those with lower cognitive function scores (29). A prospective study in 816 elderly men and women reported that those with elevated homocysteine levels
(> 15 micromol/L) had a significantly higher risk of developing Alzheimer's disease or dementia, but vitamin B12 status was not related to risk of Alzheimer's disease or dementia in this study (30). Similarly, another prospective study in 965 older adults found that vitamin B12 status was not related to the risk of Alzheimer's disease (31). Further, a prospective study in 1,041 older adults, followed for a median of 3.9 years, found that vitamin B12 dietary intake was not associated with risk of developing Alzheimer's disease (32).
B vitamin supplementation is commonly used to treat hyperhomocysteinemia. A recent randomized, double-blind, placebo-controlled clinical trial in 253 older individuals with plasma homocysteine concentrations equal to or greater than 13 micromol/L found that daily B vitamin supplementation (1 mg folic acid, 0.5 mg vitamin B12, and 10 mg vitamin B6) for two years did not affect measures of cognitive performance despite an average 4.36 micromol/L reduction in plasma homocysteine concentrations (33). Another randomized, double-blind, placebo-controlled study in 195 elderly adults reported that oral vitamin B12 supplementation (1 mg daily) for six months had no effect on measures of cognitive function (34). Several of the homocysteine-lowering trials primarily focused on assessing cardiovascular disease risk will also assess measures of cognitive function (35). Thus, the findings of these ongoing trials may provide insight into whether long-term B vitamin supplementation is protective against dementia.
Observational studies have found as many as 30% of patients hospitalized for depression are deficient in vitamin B12 (36). 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 (37). 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 B12 status (38). 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 (39-42). 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.
Only bacteria can synthesize vitamin B12. Vitamin B12 is present in animal products such as meat, poultry, fish (including shellfish), and to a lesser extent milk, but it is not generally present in plant products or yeast (1). Fresh pasteurized milk contains 0.9 mcg per cup and is an important source of vitamin B12 for some vegetarians (6). Those vegetarians who eat no animal products need supplemental vitamin B12 to meet their requirements. Also, individuals over the age of 50 should obtain their vitamin B12 in supplements or fortified foods like fortified cereal because of the increased likelihood of food-bound vitamin B12 malabsorption.
Most people do not have a problem obtaining the RDA of 2.4 mcg/day of vitamin B12 in food. In the United States, the average intake of vitamin B12 is about 4.5 mcg/day for young adult men, and 3 mcg/day for young adult women. In a sample of adults over the age of 60, men were found to have an average dietary intake of 3.4 mcg/day and women had an average dietary intake of 2.6 mcg/day (6). Some foods with substantial amounts of vitamin B12 are listed in the table below along with their vitamin B12 content in micrograms (mcg). For more information on the nutrient content of specific foods, search the USDA food composition database.
|Food||Serving||Vitamin B12 (mcg)|
|Clams (steamed)||3 ounces||84.0|
|Mussels (steamed)||3 ounces||20.4|
|Crab (steamed)||3 ounces||8.8|
|Salmon (baked)||3 ounces*||2.4|
|Rockfish (baked)||3 ounces||1.0|
|Beef (cooked)||3 ounces||2.1|
|Chicken (roasted)||3 ounces||0.3|
|Turkey (roasted)||3 ounces||0.3|
|Egg (poached)||1 large||0.6|
|Milk (skim)||8 ounces||0.9|
|Brie (cheese)||1 ounce||0.5|
*A three-ounce serving of meat or fish is about the size of a deck of cards.
Cyanocobalamin is the principal form of vitamin B12 used in supplements but methylcobalamin is also available as a supplement. Cyanocobalamin is available by prescription in an injectable form and as a nasal gel for the treatment of pernicious anemia. Over-the-counter preparations containing cyanocobalamin include multivitamin, vitamin B-complex, and vitamin B12 supplements (43).
No toxic or adverse effects have been associated with large intakes of vitamin B12 from food or supplements in healthy people. Doses as high as 1 mg (1000 mcg) daily by mouth or 1 mg monthly by intramuscular (IM) injection have been used to treat pernicious anemia without significant side effects. When high doses of vitamin B12 are given orally, only a small percentage can be absorbed, which may explain the low toxicity. Because of the low toxicity of vitamin B12, no tolerable upper intake level (UL) was set by the Food and Nutrition Board in 1998 when the RDA was revised (6).
A number of drugs reduce the absorption of vitamin B12. Proton pump inhibitors (e.g., omeprazole and lansoprazole), used for therapy of Zollinger-Ellison syndrome and gastroesophageal reflux disease (GERD), markedly decrease stomach acid secretion required for the release of vitamin B12 from food but not from supplements. Long-term use of proton pump inhibitors has been found to decrease blood vitamin B12 levels. However, vitamin B12 deficiency does not generally develop until after at least three years of continuous therapy (44). Another class of gastric acid inhibitors known as H2-receptor antagonists (e.g., Tagamet, Pepsid, Zantac), often used to treat peptic ulcer disease, has also been found to decrease the absorption of vitamin B12 from food. Because inhibition of gastric acid secretion is not as prolonged as with proton pump inhibitors H2-receptor antagonists have not been found to cause overt vitamin B12 deficiency even after long-term use (45). Individuals taking drugs that inhibit gastric acid secretion should consider taking vitamin B12 in the form of a supplement because gastric acid is not required for its absorption. Other drugs found to inhibit vitamin B12 absorption from food include cholestyramine (a bile acid-binding resin used in the treatment of high cholesterol), chloramphenicol and neomycin (antibiotics), and colchicine (anti-gout medicine). Metformin, a medication for individuals with type 2 (non-insulin dependent) diabetes, decreases vitamin B12 absorption by tying up free calcium required for absorption of the IF-B12 complex. This effect is correctable by drinking milk or taking calcium carbonate tablets along with food or supplements (5). Previous reports that megadoses of vitamin C destroy vitamin B12 have not been supported (46) and may have been an artifact of the assay used to measure vitamin B12 levels (6).
Nitrous oxide, a commonly used anesthetic, inhibits both of the vitamin B12- dependent enzymes and can produce many of the clinical features of vitamin B12 deficiency, such as megaloblastic anemia or neuropathy. Because nitrous oxide is commonly used for surgery in the elderly, some experts feel vitamin B12 deficiency should be ruled out prior to its use (4, 12).
Large doses of folic acid given to an individual with an undiagnosed vitamin B12 deficiency could correct megaloblastic anemia without correcting the underlying vitamin B12 deficiency, leaving the individual at risk of developing irreversible neurologic damage (6). For this reason the Food and Nutrition Board of the Institute of Medicine advises that all adults limit their intake of folic acid (supplements and fortification) to 1000 mcg (1 mg) daily.
A varied diet should provide enough vitamin B12 to prevent deficiency in most individuals 50 years of age and younger. Individuals over the age of 50, strict vegetarians, and women planning to become pregnant should take a multivitamin supplement daily or eat a fortified breakfast cereal, which would ensure a daily intake of 6 to 30 mcg of vitamin B12 in a form that is easily absorbed. Higher doses of vitamin B12 supplements are recommended for patients taking medications that interfere with its absorption (see Drug interactions).
Older adults (> 50 years)
Because vitamin B12 malabsorption and vitamin B12 deficiency are more common in older adults, the Linus Pauling Institute recommends that adults older than 50 years take 100 to 400 mcg/day of supplemental vitamin B12.
Written in March 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in August 2007 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in August 2007 by:
Jeffrey Blumberg, Ph.D., F.A.C.N., F.A.S.N.
Professor, Friedman School of Nutrition Science and Policy
Jean Mayer USDA Human Nutrition Research Center on Aging
Copyright 2000-2014 Linus Pauling Institute
The Linus Pauling Institute Micronutrient Information Center provides scientific information on the health aspects of dietary factors and supplements, foods, and beverages for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
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