Vitamin B
Vitamin B Complex
Vitamin B Complex
Benefit of B complex for skin, hair and nails
Urine will be yellow colored.
What Are The Richest Sources Of B Vitamins?
Here we have collated the top 10 foods that contain most of the B-complex vitamins.
B Vitamins
You’re probably familiar with Vitamin B6 and B12, but did you know there are actually eight B vitamins?
- B1 (thiamin)
- B2 (riboflavin)
- B3 (niacin)
- B5 (pantothenic acid)
- B6 (pyridoxine)
- B7 (biotin)
- B9 (folate [folic acid])
- B12 (cobalamin)
These vitamins help a variety of enzymes do their jobs, ranging from releasing energy from carbohydrates and fat to breaking down amino acids and transporting oxygen and energy-containing nutrients around the body.
B1 Thiamine
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Thiamine, also known as thiamin and vitamin B1, is a vitamin, an essential micronutrient for humans and animals.[3][4] It is found in food and commercially synthesized to be a dietary supplement or medication.[1][5] Phosphorylated forms of thiamine are required for some metabolic reactions, including the breakdown of glucose and amino acids.[1]
Food sources of thiamine include whole grains, legumes, and some meats and fish.[1][6] Grain processing removes much of the vitamin content, so in many countries cereals and flours are enriched with thiamine.[1] Supplements and medications are available to treat and prevent thiamine deficiency and disorders that result from it include beriberi and Wernicke encephalopathy. They are also used to treat maple syrup urine disease and Leigh syndrome. Supplements and medications are typically taken by mouth, but may also be given by intravenous or intramuscular injection.[7]
Thiamine supplements are generally well tolerated. Allergic reactions, including anaphylaxis, may occur when repeated doses are given by injection.[7][8] Thiamine is on the World Health Organization's List of Essential Medicines.[9] It is available as a generic medication, and in some countries as a non-prescription dietary supplement.[7]
Deficiency[edit]
Well-known disorders caused by thiamine deficiency include beriberi, Wernicke–Korsakoff syndrome, optic neuropathy, Leigh's disease, African seasonal ataxia (or Nigerian seasonal ataxia), and central pontine myelinolysis.[13] Symptoms include malaise, weight loss, irritability and confusion.[10][14][15]
In Western countries, chronic alcoholism is a risk factor for deficiency. Also at risk are older adults, persons with HIV/AIDS or diabetes, and those who have had bariatric surgery.[1] Varying degrees of thiamine insufficiency have been associated with the long-term use of diuretics.
Medical uses[edit]
During pregnancy, thiamine is sent to the fetus via the placenta. Pregnant women have a greater requirement for the vitamin than other adults, especially during the third trimester. Pregnant women with hyperemesis gravidarum are at an increased risk of thiamine deficiency due to losses when vomiting.[25] In lactating women, thiamine is delivered in breast milk even if it results in thiamine deficiency in the mother.[4][26]
Thiamine is important not only for mitochondrial membrane development, but also for synaptic membrane function.[27] It has also been suggested that a deficiency hinders brain development in infants and may be a cause of sudden infant death syndrome.[20]
Dietary recommendations[edit]
| US National Academy of Medicine | |
| Age group | RDA (mg/day) |
|---|---|
| Infants 0–6 months | 0.2* |
| Infants 6–12 months | 0.3* |
| 1–3 years | 0.5 |
| 4–8 years | 0.6 |
| 9–13 years | 0.9 |
| Females 14–18 years | 1.0 |
| Males 14+ years | 1.2 |
| Females 19+ years | 1.1 |
| Pregnant/lactating females 14–50 | 1.4 |
| * Adequate intake for infants, as an RDA has yet to be established[4] | |
| European Food Safety Authority | |
| Age group | Adequate intake (mg/MJ)[28] |
| All persons 7 months+ | 0.1 |
| Neither the US National Academy of Medicine nor the European Food Safety Authority have determined the tolerable upper intake level for thiamine[4] | |
The US National Academy of Medicine updated the Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for thiamine in 1998. The EARs for thiamine for women and men aged 14 and over are 0.9 mg/day and 1.1 mg/day, respectively; the RDAs are 1.1 and 1.2 mg/day, respectively. RDAs are higher than EARs to provide adequate intake levels for individuals with higher than average requirements. The RDA during pregnancy and for lactating females is 1.4 mg/day. For infants up to the age of 12 months, the Adequate Intake (AI) is 0.2–0.3 mg/day and for children aged 1–13 years the RDA increases with age from 0.5 to 0.9 mg/day.[4]
The European Food Safety Authority (EFSA) refers to the collective set of information as Dietary Reference Values, with Population Reference Intakes (PRIs) instead of RDAs, and Average Requirements instead of EARs. For women (including those pregnant or lactating), men and children the PRI is 0.1 mg thiamine per megajoule (MJ) of energy in their diet. As the conversion is 1 MJ = 239 kcal, an adult consuming 2390 kilocalories ought to be consuming 1.0 mg thiamine. This is slightly lower than the US RDA.[29]
Neither the National Academy of Medicine nor EFSA have set an upper intake level for thiamine, as there is no human data for adverse effects from high doses.[4][28]
Safety[edit]
Thiamine is generally well tolerated and non-toxic when administered orally.[7] There are rare reports of adverse side effects when thiamine is given intravenously, including allergic reactions, nausea, lethargy, and impaired coordination.[28][3]
Sources[edit]
Thiamine is found in a wide variety of processed and whole foods,[18] including lentils, peas, whole grains, pork, and nuts.[6][32] A typical daily prenatal vitamin product contains around 1.5 mg of thiamine.[33]
Food fortification[edit]
Some countries require or recommend fortification of grain foods such as wheat, rice or maize (corn) because processing lowers vitamin content.[34] As of February 2022, 59 countries, mostly in North and Sub-Saharan Africa, require food fortification of wheat, rice or maize with thiamine or thiamine mononitrate. The amounts stipulated range from 2.0 to 10.0 mg/kg.[35] An additional 18 countries have a voluntary fortification program. For example, the Indian government recommends 3.5 mg/kg for "maida" (white) and "atta" (whole wheat) flour.[36]
Absorption, metabolism and excretion[edit]
In the upper small intestine, thiamine phosphate esters present in food are hydrolyzed by alkaline phosphatase enzymes. At low concentrations, the absorption process is carrier-mediated. At higher concentrations, absorption also occurs via passive diffusion.[3] Active transport can be inhibited by alcohol consumption or by folate deficiency.[10]
The majority of thiamine in serum is bound to proteins, mainly albumin. Approximately 90% of total thiamine in blood is in erythrocytes. A specific binding protein called thiamine-binding protein has been identified in rat serum and is believed to be a hormone-regulated carrier protein important for tissue distribution of thiamine.[14] Uptake of thiamine by cells of the blood and other tissues occurs via active transport and passive diffusion.[10] Two members of the family of transporter proteins encoded by the genes SLC19A2 and SLC19A3 are capable of thiamine transport.[20] In some tissues, thiamine uptake and secretion appear to be mediated by a Na+-dependent transporter and a transcellular proton gradient.[14]
Human storage of thiamine is about 25 to 30 mg, with the greatest concentrations in skeletal muscle, heart, brain, liver, and kidneys. ThMP and free (unphosphorylated) thiamine are present in plasma, milk, cerebrospinal fluid, and, it is presumed, all extracellular fluid. Unlike the highly phosphorylated forms of thiamine, ThMP and free thiamine are capable of crossing cell membranes. Calcium and magnesium have been shown to affect the distribution of thiamine in the body and magnesium deficiency has been shown to aggravate thiamine deficiency.[20] Thiamine contents in human tissues are less than those of other species.[14][55]
Thiamine and its metabolites (2-methyl-4-amino-5-pyrimidine carboxylic acid, 4-methyl-thiazole-5-acetic acid, and others) are excreted principally in the urine.[3]
Interference[edit]
The bioavailability of thiamine in foods can be interfered with in a variety of ways. Sulfites, added to foods as a preservative,[56] will attack thiamine at the methylene bridge, cleaving the pyrimidine ring from the thiazole ring. The rate of this reaction is increased under acidic conditions.[14] Thiamine is degraded by thermolabile thiaminases present in some species of fish, shellfish and other foods.[10] The pupae of an African silk worm, Anaphe venata, is a traditional food in Nigeria. Consumption leads to thiamine deficiency.[57] Older literature reported that in Thailand, consumption of fermented, uncooked fish caused thiamine deficiency, but either abstaining from eating the fish or heating it first reversed the deficiency.[58] In ruminants, intestinal bacteria synthesize thiamine and thiaminases. The bacterial thiaminases are cell surface enzymes that must dissociate from the cell membrane before being activated; the dissociation can occur in ruminants under acidotic conditions. In dairy cows, over-feeding with grain causes subacute ruminal acidosis and increased ruminal bacteria thiaminase release, resulting in thiamine deficiency.[59]
From reports on two small studies conducted in Thailand, chewing slices of areca nut wrapped in betel leaves and chewing tea leaves reduced food thiamine bioavailability by a mechanism that may involve tannins.[58][60]
Bariatric surgery for weight loss is known to interfere with vitamin absorption.[61] A meta-analysis reported that 27% of people who underwent bariatric surgeries experience vitamin B1 deficiency.[62]
History[edit]
Thiamine was the first of the water-soluble vitamins to be isolated.[63] The earliest observations in humans and in chickens had shown that diets of primarily polished white rice caused beriberi, but did not attribute it to the absence of a previously unknown essential nutrient.[64][65]
In 1884, Takaki Kanehiro, a surgeon general in the Imperial Japanese Navy, rejected the previous germ theory for beriberi and suggested instead that the disease was due to insufficiencies in the diet.[64] Switching diets on a navy ship, he discovered that replacing a diet of white rice only with one also containing barley, meat, milk, bread, and vegetables, nearly eliminated beriberi on a nine-month sea voyage. However, Takaki had added many foods to the successful diet and he incorrectly attributed the benefit to increased protein intake, as vitamins were unknown at the time. The Navy was not convinced of the need for such an expensive program of dietary improvement, and many men continued to die of beriberi, even during the Russo-Japanese war of 1904–5. Not until 1905, after the anti-beriberi factor had been discovered in rice bran (removed by polishing into white rice) and in barley bran, was Takaki's experiment rewarded. He was made a baron in the Japanese peerage system, after which he was affectionately called "Barley Baron".[64]
The specific connection to grain was made in 1897 by Christiaan Eijkman, a military doctor in the Dutch East Indies, who discovered that fowl fed on a diet of cooked, polished rice developed paralysis that could be reversed by discontinuing rice polishing.[65] He attributed beriberi to the high levels of starch in rice being toxic. He believed that the toxicity was countered in a compound present in the rice polishings.[66] An associate, Gerrit Grijns, correctly interpreted the connection between excessive consumption of polished rice and beriberi in 1901: He concluded that rice contains an essential nutrient in the outer layers of the grain that is removed by polishing.[67] Eijkman was eventually awarded the Nobel Prize in Physiology and Medicine in 1929, because his observations led to the discovery of vitamins.
In 1910, a Japanese agricultural chemist of Tokyo Imperial University, Umetaro Suzuki, isolated a water-soluble thiamine compound from rice bran, which he named aberic acid. (He later renamed it Orizanin.) He described the compound as not only an anti-beriberi factor, but also as being essential to human nutrition; however, this finding failed to gain publicity outside of Japan, because a claim that the compound was a new finding was omitted in translation of his publication from Japanese to German.[63] In 1911 a Polish biochemist Casimir Funk isolated the antineuritic substance from rice bran (the modern thiamine) that he called a "vitamine" (on account of its containing an amino group).[68][69] However, Funk did not completely characterize its chemical structure. Dutch chemists, Barend Coenraad Petrus Jansen and his closest collaborator Willem Frederik Donath, went on to isolate and crystallize the active agent in 1926,[70] whose structure was determined by Robert Runnels Williams, in 1934. Thiamine was named by the Williams team as a portmanteau of "thio" (meaning sulfur-containing) and "vitamin". The term "vitamin" coming indirectly, by way of Funk, from the amine group of thiamine itself (although by this time, vitamins were known to not always be amines, for example, vitamin C). Thiamine was also synthesized by the Williams group in 1936.[71]
Sir Rudolph Peters, in Oxford, used pigeons to understand how thiamine deficiency results in the pathological-physiological symptoms of beriberi. Pigeons fed exclusively on polished rice developed opisthotonos, a condition characterized by head retraction. If not treated, the animals died after a few days. Administration of thiamine after opisthotonos was observed led to a complete cure within 30 minutes. As no morphological modifications were seen in the brain of the pigeons before and after treatment with thiamine, Peters introduced the concept of a biochemical-induced injury.[72] In 1937, Lohmann and Schuster showed that the diphosphorylated thiamine derivative, TPP, was a cofactor required for the oxidative decarboxylation of pyruvate.[73]
Folate (Folic Acid) – Vitamin B9
Folate is the natural form of vitamin B9, water-soluble and naturally found in many foods. It is also added to foods and sold as a supplement in the form of folic acid; this form is actually better absorbed than that from food sources—85% vs. 50%, respectively. Folate helps to form DNA and RNA and is involved in protein metabolism. It plays a key role in breaking down homocysteine, an amino acid that can exert harmful effects in the body if it is present in high amounts. Folate is also needed to produce healthy red blood cells and is critical during periods of rapid growth, such as during pregnancy and fetal development.
Recommended Amounts
RDA: The Recommended Dietary Allowance for folate is listed as micrograms (mcg) of dietary folate equivalents (DFE). Men and women ages 19 years and older should aim for 400 mcg DFE. Pregnant and lactating women require 600 mcg DFE and 500 mcg DFE, respectively. People who regularly drink alcohol should aim for at least 600 mcg DFE of folate daily since alcohol can impair its absorption.
UL: A Tolerable Upper Intake Level (UL) is the maximum daily dose unlikely to cause adverse side effects in the general population. The UL for adults for folic acid from fortified food or supplements (not including folate from food) is set at 1,000 mcg a day.
Folate and Health
Food Sources
A wide variety of foods naturally contain folate, but the form that is added to foods and supplements, folic acid, is better absorbed. In January 1998, the U.S. Food and Drug Administration required food manufacturers to add folic acid to foods commonly eaten, including breads, cereals, pasta, rice, and other grain products, to reduce the risk of neural tube defects. This program has helped to increase the average folic acid intake by about 100 mcg/day. [38,39] Good sources of folate include:
- Dark green leafy vegetables (turnip greens, spinach, romaine lettuce, asparagus, Brussels sprouts, broccoli)
- Beans
- Peanuts
- Sunflower seeds
- Fresh fruits, fruit juices
- Whole grains
- Liver
- Aquatic foods
- Eggs
- Fortified foods and supplements
Signs of Deficiency and Toxicity
Deficiency
A folate deficiency is rare because it is found in a wide range of foods. However, the following conditions may put people at increased risk:
- Alcoholism. Alcohol interferes with the absorption of folate and speeds the rate that folate breaks down and is excreted from the body. People with alcoholism also tend to eat poor-quality diets low in folate-containing foods.
- Pregnancy. The need for folate increases during pregnancy as it plays a role in the development of cells in the fetus.
- Intestinal surgeries or digestive disorders that cause malabsorption. Celiac disease and inflammatory bowel disease can decrease the absorption of folate. Surgeries involving the digestive organs or that reduce the normal level of stomach acid may also interfere with absorption.
- Genetic variants. People carrying a variant of the gene MTHFR cannot convert folate to its active form to be used by the body.
Signs of deficiency can include: megaloblastic anemia (a condition arising from a lack of folate in the diet or poor absorption that produces less red blood cells, and larger in size than normal); weakness, fatigue; irregular heartbeat; shortness of breath; difficulty concentrating; hair loss; pale skin; mouth sores.
Toxicity
It is extremely rare to reach a toxic level when eating folate from food sources.
However, an upper limit for folic acid is set at 1,000 mcg daily because studies have shown that taking higher amounts can mask a vitamin B12 deficiency. This deficiency occurs most often in older adults or those eating a vegan diet in whom a B12 deficiency is more common. Both folate and B12 are involved in making red blood cells, and a shortage of either can result in anemia. A person taking high-dosage supplements of folic acid may be able to correct the anemia and feel better, but the B12 deficiency still exists. In this case, if high folate intake continues to “hide” the symptoms of B12 deficiency for a long time, a slow but irreversible damage to the brain and nervous system may occur. If you choose to use a folic acid supplement, stick with the lower range available of 400 mcg a day or less, as you will likely obtain additional folic acid from fortified foods like cereals and breads, as well as natural folate in food.
Overall, the evidence suggests that the amount of folic acid in a typical multivitamin does not cause any harm—and may help prevent some diseases, especially among people who do not get enough folate in their diets, and among individuals who drink alcohol.
Did You Know
Folate is also referred to as vitamin B9. Despite the number, there are only eight B vitamins in total.
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| Vit B6 |
Vitamin B6, or pyridoxine, is a water-soluble vitamin found naturally in many foods, as well as added to foods and supplements. Pyridoxal 5’ phosphate (PLP) is the active coenzyme form and most common measure of B6 blood levels in the body. PLP is a coenzyme that assists more than 100 enzymes to perform various functions, including the breakdown of proteins, carbohydrates, and fats; maintaining normal levels of homocysteine (since high levels can cause heart problems); and supporting immune function and brain health.
Recommended Amounts
RDA: The Recommended Dietary Allowance (RDA) for men ages 14-50 years is 1.3 mg daily; 51+ years, 1.7 mg. The RDA for women ages 14-18 years is 1.2 mg; 19-50 years, 1.3 mg; and 51+ years, 1.5 mg. For pregnancy and lactation, the amount increases to 1.9 mg mcg and 2.0 mg, respectively. [1]
UL: A Tolerable Upper Intake Level (UL) is the maximum daily dose unlikely to cause adverse side effects in the general population. The UL for adults 19 years and older is 100 mg daily, with slightly lesser amounts in children and teenagers. This amount can only be achieved by taking supplements. Even higher amounts of vitamin B6 supplements are sometimes prescribed for medical reasons, but under the supervision of a physician as excess vitamin B6 can cause toxicity. [1,2]
Vitamin B6 and Health
Vitamin B6 has been widely studied for its role in disease prevention. The vitamin in supplement form shows the most promise for the treatment of pregnancy-induced nausea, but such use should only occur under the supervision of a physician. Adequate blood levels of B6 may be associated with lower risk of cancers, compared to low blood levels. However, the use of separate B6 supplements (apart from the RDA amounts in typical multivitamin preparations) is inconclusive and not recommended.
Food Sources
Vitamin B6 is found in a variety of animal and plant foods.
- Beef liver
- Tuna
- Salmon
- Fortified cereals
- Chickpeas
- Poultry
- Some vegetables and fruits, especially dark leafy greens, bananas, papayas, oranges, and cantaloupe
Signs of Deficiency and Toxicity
Deficiency
A vitamin B6 deficiency most often occurs when other B vitamins in the body are low, particularly vitamin B12 and folic acid. A mild deficiency may have no symptoms, but a more severe or prolonged deficiency can exhibit the following:
- Microcytic anemia
- Skin conditions
- Depression
- Confusion
- Lowered immunity
Certain conditions can increase the risk of developing a deficiency by interfering with the absorption of vitamin B6:
- Kidney disease
- Autoimmune intestinal disorders like celiac disease, ulcerative colitis, and Crohn’s disease
- Autoimmune inflammatory disorders such as rheumatoid arthritis
- Alcoholism
Toxicity
It is quite unlikely to reach a toxic level of vitamin B6 from food sources alone. Vitamin B6 is a water-soluble vitamin so that unused amounts will exit the body through the urine. [2] However, a toxic level can occur from long-term very high dose supplementation of greater than 1,000 mg daily. [1] Symptoms usually subside after stopping the high dosage. Symptoms include:
- Neuropathy in feet and hands
- Ataxia (loss of control of body movements)
- Nausea
Vit B12
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| Vit B12 |
Vitamin B12, or cobalamin, is naturally found in animal foods. It can also be added to foods or supplements. Vitamin B12 is needed to form red blood cells and DNA. It is also a key player in the function and development of brain and nerve cells.
Vitamin B12 binds to the protein in the foods we eat. In the stomach, hydrochloric acid and enzymes unbind vitamin B12 into its free form. From there, vitamin B12 combines with a protein called intrinsic factor so that it can be absorbed further down in the small intestine.
Supplements and fortified foods contain B12 in its free form, so they may be more easily absorbed. There is a variety of vitamin B12 supplements available. Although there are claims that certain forms—like sublingual tablets or liquids placed under the tongue to be absorbed through the tissues of the mouth—have better absorption than traditional tablets, studies have not shown an important difference. Vitamin B12 tablets are available in high dosages far above the recommended dietary allowance, but these high amounts are not necessarily the amount that will be absorbed because an adequate amount of intrinsic factor is also needed. In cases of severe vitamin B12 deficiency due to inadequate intrinsic factor (pernicious anemia), doctors may prescribe B12 injections in the muscle.
Recommended Amounts
RDA: The Recommended Dietary Allowance for men and women ages 14 years and older is 2.4 micrograms (mcg) daily. For pregnancy and lactation, the amount increases to 2.6 mcg and 2.8 mcg daily, respectively. [1]
UL: A Tolerable Upper Intake Level (UL) is the maximum daily dose unlikely to cause adverse side effects in the general population. No upper limit has been set for vitamin B12, as there is no established toxic level. However, some evidence suggests that supplements of 25 mcg per day or higher may increase the risk of bone fractures. [2]
Vitamin B12 and Health
Food Sources
- Fish, shellfish
- Liver
- Red meat
- Eggs
- Poultry
- Dairy products such as milk, cheese, and yogurt
- Fortified nutritional yeast
- Fortified breakfast cereals
- Enriched soy or rice milk
Signs of Deficiency and Toxicity
Deficiency
Measuring vitamin B12 in the blood is actually not the best way to determine whether someone is deficient, as some people with a deficiency can show normal B12 blood levels. Blood levels of methylmalonic acid, a protein breakdown product, and homocysteine are better markers that capture actual vitamin B12 activity. These values increase with a vitamin B12 deficiency. It is estimated that up to 15% of the general population has a vitamin B12 deficiency. [1]
Factors that may cause vitamin B12 deficiency:
- Avoiding animal products. People who do not eat meat, fish, poultry, or dairy are at risk of becoming deficient in vitamin B12, since it is only found naturally in animal products. Studies have shown that vegetarians have low vitamin B blood levels. [5] For this reason, those who follow a vegetarian or vegan diet should include B12-fortified foods or a B12 supplement in their diets. This is particularly important for pregnant women, as the fetus requires adequate vitamin B12 for neurologic development and deficiency can lead to permanent neurological damage.
- Lack of intrinsic factor. Pernicious anemia is an autoimmune disease that attacks and potentially destroys gut cells so that intrinsic factor is not present, which is crucial for vitamin B12 to be absorbed. If vitamin B12 deficiency ensues, other types of anemia and neurological damage may result. Even the use of a high-dose B12 supplement will not solve the problem, as intrinsic factor is not available to absorb it.
- Inadequate stomach acid or medications that cause decreased stomach acid. A much more common cause of B12 deficiency, especially in older people, is a lack of stomach acid, because stomach acid is needed to liberate vitamin B12 from food. An estimated 10-30% of adults over the age of 50 have difficulty absorbing vitamin B12 from food. [1] People who regularly take medications that suppress stomach acid for conditions like gastroesophageal reflux disease (GERD) or peptic ulcer disease—such as proton-pump inhibitors, H2 blockers, or other antacids—may have difficulty absorbing vitamin B12 from food. These drugs can slow the release or decrease production of stomach acid. In theory this can prevent the vitamin from being released into its free usable form in the stomach; however, research has not shown an increased prevalence of a deficiency in people using these medications. Anyone using these medications for an extended time and who are at risk for a vitamin B12 deficiency for other reasons should be monitored closely by their physician. They may also choose to use fortified foods or supplements with vitamin B12, as these forms are typically absorbed well, and do not require stomach acid.
- Intestinal surgeries or digestive disorders that cause malabsorption. Surgeries that affect the stomach where intrinsic factor is made, or the ileum (the last portion of the small intestine) where vitamin B12 is absorbed, can increase the risk of a deficiency. Certain diseases including Crohn’s and celiac disease that negatively impact the digestive tract also increase the risk of deficiency.
- Medications that interfere with absorption. Long-term use of metformin, a drug commonly prescribed for type 2 diabetes, is strongly associated with vitamin B12 deficiency and lower folic acid levels as it can block absorption, which may lead to increased homocysteine levels and risk for cardiovascular disease. [6] Proton pump inhibitors and histamine blockers prescribed to reduce stomach acid are also associated with lower vitamin B12 levels.
Signs of deficiency may include:
- Megaloblastic anemia—a condition of larger than normal sized red blood cells and a smaller than normal amount; this occurs because there is not enough vitamin B12 in the diet or poor absorption
- Pernicious anemia—a type of megaloblastic anemia caused by a lack of intrinsic factor so that vitamin B12 is not absorbed
- Fatigue, weakness
- Nerve damage with numbness, tingling in the hands and legs
- Memory loss, confusion
- Dementia
- Depression
- Seizures
Toxicity
Vitamin B12 is a water-soluble vitamin, so any unused amount will exit the body through the urine. Generally, up to 1000 mcg a day of an oral tablet to treat a deficiency is considered safe. The Institute of Medicine states “no adverse effects have been associated with excess vitamin B12 intake from food and supplements in healthy individuals.” [1] However, it is important not to start a high-dosage supplement of any kind without first checking with your doctor.
Did You Know?
- A B vitamin complex supplement is often touted to boost energy levels and mood. People who have a B vitamin deficiency may feel a rise in energy levels after using the supplement because the vitamin is directly involved in making healthy blood cells and can correct anemia if present. However, there is no evidence of benefit if people without a deficiency take extra B vitamins.
- People who eat a vegan diet are often told to include Brewer’s or nutritional yeast for its B12 content. However, yeast does not naturally contain this vitamin and will only be present if fortified with it. Be aware that certain brands, but not all, contain B12.
- Nori (purple laver), the dried edible seaweed used to make sushi rolls, is sometimes promoted as a plant source of vitamin B12. It does contain small amounts of active vitamin B12, but the amount varies among types of seaweed, with some containing none. Therefore is not considered a reliable food source.
Related
Spotlight on Three of the Bs: Folate, Vitamin B6, and Vitamin B12
One of the advances that changed the way we look at vitamins was the discovery that too little folate is linked to birth defects such as spina bifida and anencephaly.
Folate (Folic Acid) – Vitamin B9
Another line of research about folate and two other B vitamins, vitamin B6 and vitamin B12, explores their roles in reducing some types of cancer and heart disease.
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