Recommended Nutrient Intakes for Vitamin and Minerals

Vitamin B

There are actually a whole group of B vitamins.

Many of the B vitamins serve as coenzymes to the enzymes which release energy from carbohydrate, fat and protein. Other B vitamins assist the metabolism of amino acids and help cells to multiply

Thiamin - Vitamin B1

Function

Thiamin is involved in the metabolism of carbohydrates.

Recommended Intakes

Table 2: Recommended intake of thiamine (mg/day)

Food Sources

There are no foods rich in thiamine. The best sources are wheatgerm, whole wheat and products, yeast and yeast extracts, pulses, nuts, pork, duck, oatmeal, fortified breakfast cereals, and other meats.

Deficiency

People who fail to reach energy needs risk deficiency. Also individuals who derive most of their energy from low nutrients sources such as alcohol risk vitamin B1 deficiency. In addition alcohol increases the excretion of thiamin, putting alcoholics at an even greater risk of deficiency.

Wernicke-Korsakoff syndrome is one of 2 major vitamin B1 deficiency diseases. It is usually seen in people who have been drinking alcohol heavily for some weeks and eaten very little. It may also be seen in people on a prolonged fast or with persistent vomiting. Clinical signs of deficiency include, a state of quiet confusion, lowered consciousness, inco-ordination, and paralysis of one or more external movements of the eyes. These clinical manifestations of thiamin deficiency are usually reversed with thiamin injections. However, if treatment is delayed, the memory may never recover. The memory disorder resulting from Wernicke-encephalopathy is called Korsakoff's psychosis. There is an inability to retain new information.

The other major disease resulting from thiamin deficiency is beri beri. This disease was first observed in East Asia when the custom of polishing rice became widespread. Rices provided 80% of the energy intake of people in that area, and rice hulls were their principle source of thiamin. In Western countries occasional cases are seen in alcoholics. Because thiamin participates in nerve processes, paralysis sets in when it is lacking. The symptoms of beri beri include damage to the nervous system as well as to the heart and other muscles. Deficiency symptoms include, edema, enlarged heart, abnormal heart rhythms, heart failure, degeneration, wasting, weakness, painful calf muscles, low morale, difficulty walking, loss of ankle and knee jerk reflexes, mental confusion, and paralysis.

It is not clear why one person develops Wernicke-Korsakoff syndrome and another develops beri beri, and why the two diseases seldom coincide. One suggestion has been that the cardiac disease may occur in people who use their muscles for heavy work while encephalopathy is the first manifestation in inactive people.

Riboflavin - Vitamin B2

Function

Riboflavin helps enzymes to facilitate the release of energy from nutrients in all body cells.

Recommended Intakes

Table 3: Recommended intake of Riboflavin (mg/day)

Food Sources

Riboflavin is present in most foods although the best sources include milk, milk products, eggs, liver, kidney, yeast extracts and fortified breakfast cereals. Dairy products contribute significantly to riboflavin intake in Western diets.

Deficiency

The clinical deficiencies include, angular stomatitis, cheilosis, atrophy of the tongue papillae, nasolabial dyssebacea and anaemia. These are very minor, probably due to the body's ability to conserve riboflavin.

Riboflavin deficiency (ariboflavinosis) is most commonly seen along-side other nutrient deficiencies.

Toxicity

The toxicity of riboflavin is very low. The gastrointestinal tract cannot absorb more than about 20-25mg of riboflavin in a single dose.

Niacin

Niacin is the name that describes 2 chemical structures: nicotinic acid and nicotinamide.

Function

Nicotinamide is part of the coenzymes nicotinamide-adenine dinucleotide (NAD) and nicotinamide-adenine-dinucleotide phosphate (NADP). NAD and NADP participate in numerous metabolic activities. They are central in energy-transfer reactions, especially the metabolism of glucose, fat and alcohol.

Recommended Intakes

Niacin is unique in that the body can make it from the amino acid tryptophan. To make 1mg of niacin requires approximately 60mg of dietary tryptophan. In most conditions tryptophan supplies about half the body's niacin.

Table 4: Recommended intake of Niacin (mg niacin equivalents (NE)/day)

Food Sources

Good sources of preformed niacin include liver and kidney, other meat, poultry, fish, brewers yeast and yeast extracts, peanuts, bran, pulses, wholemeal wheat. There is also some niacin in coffee. Other foods which are rich in protein provide tryptophan.

Deficiency

The disease caused by niacin deficiency is called pellagra (the name means "sour skin" in Italian). Symptoms include diarrhoea, dermatitis, dementia, and eventually death. There is inflammation of the skin where it is exposed to sunlight, resembling severe sunburn. The tongue is also likely to be inflamed (glossitis).

In the early 1900s pellagra was widespread in the U.S. South, where people subsisted on a low protein diet centred on corn. This diet supplied neither enough niacin nor tryptophan. At least 70% of the niacin in corn is unavailable. In pre-Columbian America the ground maize was steeped in warm lime water (calcium hydroxide), which liberates the niacin, making it biologically available.

Toxicity

Large doses of niacin exhibit a pharmacological-like effect on the nervous system, and on blood lipids and blood glucose. When niacin in the form of nicotinic acid is taken in does 10x the RDA or more, it dilates the capillaries and causes a tingling sensation caused by histamine release. This can be painful and is know as "niacin flush".

At does of 3g/day (100xRDA) its inhibit lipolysis in adipose tissue and lowers plasma cholesterol and triglycerides. Such therapy needs to be monitored because of its adverse side effects including liver damage and peptic ulcers for example.

Pharmacological doses of nicotinamide are being used in a large international study to prevent diabetes (IDDM).

Biotin

Function

Biotin plays an important role in metabolism as a coenzyme that carries carbon dioxide. This role is critical in the Citric Acid Cycle. The biotin coenzyme also serves key roles in gluconeogenesis (synthesis of glucose), fatty acid synthesis, and the breakdown of various fatty acids and amino acids. Thus, biotin is important for the metabolism of carbohydrate, fat and protein.

Recommended Intakes

Biotin is needed in very small amounts. Recommendations for daily intakes have not been established. Instead, "estimated safe and adequate intakes" have been set. For adults this is estimated at 30-100mg/day.

Food Sources

Biotin is widespread in foods (including egg yolks) and so eating a variety of foods protects against deficiencies. Biotin is also synthesised in by bacteria in the large intestine which appears to supplement dietary intake.

Deficiency

Biotin deficiency is very rare because biotin is found in a wide range of foods. Deficiency can be produced when humans eat large amounts of uncooked egg white (i.e. more than 12 raw egg whites daily). Egg white contains avidin which binds to biotin in the gut, preventing absorption. Avidin is destroyed by heating. Biotin deficiency (sometimes known as eggwhite injury) impairs lipid and energy metabolism. In human cases biotin deficiency has been associated with scaly dermatitis (altered fatty acid metabolism may contribute to this condition), glossitis, anorexia, depression, and hypercholesterolaemia (high blood cholesterol levels).

Pantothenic Acid

Function

Pantothenic acid is involved in over 100 different steps in the synthesis of lipids, neurotransmitters, steroid hormones, and haemoglobin. It serves as part of coenzyme A which is the compound involved in several different pathways including the Citric Acid Cycle. Coenzyme A helps shuttle acetate (as acetyl CoA) and other small molecules along pathways in glucose, fatty acid, and energy metabolism.

Recommended Intakes

No RDA exists for pantothenic acid. Instead estimated and safe intakes are set. For adults this is 4-7mg/day.

Food Sources

Pantothenic acid is widespread in foods. Meat, fish, poultry, wholegrain cereals and legumes are particularly good sources. Pantothenic acid loss during food preparation can be substantial because it is readily destroyed by heat.

Deficiency

Pantothenic acid deficiency is rare because it is widespread in foods and typical diets seem to provide adequate amounts. Any dietary deficiency in humans is usually associated with other nutrient deficiencies.

Individuals given an antagonist to pantothenic acid developed a deficiency with symptoms of depression, fatigue, insomnia, vomiting, muscle weakness, and a burning sensation in the feet. Changes in glucose tolerance, an increase in insulin sensitivity, postural hypotension, and decreased antibody production were also noted.

Vitamin B₆

Vitamin B₆ occurs in three forms - pyridoxal, pyridoxine, and pyridoxamine. All three can be converted to the coenzyme PLP.

Function

PLP is the major coenzyme form in the body. It functions in practically all reactions involved in amino acid metabolism. PLP is also involved in carbohydrate metabolism. It is associated with the enzyme glycogen phosphorylase which releases glucose from glycogen stores.

Recommended Intakes

Table 5: Recommended intake of vitamin B6 (mg/d)

Food Sources

Meats, fish, and poultry (red), potatoes, and a few other vegetables (green) and fruits (purple) offer vitamin B₆.

Foods lose vitamin B₆ when heated.

Deficiency

The symptoms of deficiency include general weakness, sleeplessness, peripheral neuropathy, personality changes, dermatitis, cheilosis and glossitis, anaemia, and impaired immunity. Deficiency on its own is rare.

There are a number of inborn errors in amino acid metabolism that respond to supranutritional doses of pyridoxine.

Vitamin B6 deficiency is common in chronic alcoholics, who may have impaired absorption.

Toxicity

Vitamin B₆ toxicity was first reported in women taking supplements of very high doses of pyridoxine (2000-6000mg/day) for premenstrual syndrome. These women developed peripheral neuropathy and lost sensation in their feet. Intakes in supplements of 200mg/day (100xRDA) have been associated with neuropathy.

Folate

Folate is used as the generic name for compounds chemically related to pteroyl glutamic acid, folic acid. Folic acid is the primary vitamin form  from a chemical point of view, and is the pharmaceutical form  because of its stability. But it is rare in foods and in the body. Most folates are in the form, tetrahydrofolate (THF)

Functions

Tetrahydrofolate plays an essential role in 1-caron transfers in the body. This action helps convert vitamin B₁₂ to one of its coenzyme forms and helps synthesise the DNA required for rapidly growing cells.

Recommended Intakes

Table 6: Recommended intake of folate (mg/d)

Food Sources

Leafy green vegetables and legumes are the best sources of folate. It also occurs in other foods including liver, kidney, beetroot, bran, peanuts, yeast extract, avocadoes, bananas, wholemeal bread, eggs, and some fish. There is a little folate in beer and tea. In many countries breakfast cereals and some breads are fortified with folic acid.

Folate is destroyed in foods by prolonged boiling.

Deficiency

Folate deficiency impairs cell division and protein synthesis - processes critical to growing tissues. In folate deficiency the replacement of red blood cells and gastrointestinal (GI) cells falters. Thus the first symptoms of folate deficiency are anaemia and GI tract deterioration.

The anaemia of folate deficiency is characterised by large, immature red blood cells. Without folate, DNA synthesis slows and cells lose their ability to divide. As a result the immature blood cells are enlarged and oval-shaped. They cannot carry oxygen or travel through the capillaries as efficiently as normal red blood cells.

Folate deficiencies may develop from inadequate intake or may result from impaired absorption, or an unusual metabolic need for the vitamin. Metabolic needs increase whenever cell multiplication must speed up (e.g. in pregnancies involving twins or triplets, in cancer, in skin destroying diseases such as chicken pox and measles, in burns, blood loss and GI tract damage).

Toxicity

The main concern is that if someone with vitamin B12 deficiency (pernicious anaemia) is treated with a fairly high (supranutritional) dose of folic acid (5mg/day) the anaemia may improve but the biochemical basis for the neurological symptoms of vitamin B12 deficiency is not corrected.

Folate and Neural Tube Defects

Several research studies have looked at the role of folate in preventing neural tube defects. The neural tube is the embryonic tissue from which the central nervous system develops. The defects commonly arise in the first weeks of pregnancy. They cause serious disability and infant mortality. Recent research suggests that taking folic acid supplements before and during the first trimester of pregnancy can reduce the risk of neural tube defects. For this reason, it is recommended that women of child-bearing age should consume 400 micrograms of folate daily. Many women typically have intakes of around 200 micrograms. For this reason, and because most pregnancies are unplanned, many government organizations are investigating the proposal to fortify a staple foods (perhaps flour) with folic acid. Controversy surrounds the safety of fortification. For example, high folate intakes complicate the diagnosis of vitamin B12 deficiency.  Also folates role in neural tube defects remains unclear. Most women whose babies develop neural tube defects are not deficient in folate. Researchers speculate that folate deficiency must act on an underlying nutrient-sensitive genetic defect to yield a defective newborn.

Vitamin B₁₂

Vitamin B₁₂ and folate are closely related. Each depends on the other for activation. Vitamin B12 removes a methyl group to activate the folate coenzyme and folate donates a methyl group to activate the vitamin B12 coenzyme.

Vitamin B12 is also known as cobalamin. It is a red compound made up of a corrinoid ring. It had a complex structure which can only be synthesised by bacteria. There are a range of naturally occurring corrinoids but not all have vitamin B12 activity.

After B12 is ingested, it is released from the proteins to which it was attached by hydrochloric acid and the enzyme pepsin in the body. The vitamin then binds with an "intrinsic factor" for absorption from  the intestine.

Function

The coenzymes forms of B12 are methylcobalamin and deoxyadenosylocbalamin, and are used in new cell synthesis. B12 helps maintain nerve cells, reforms the folate coenzyme, and helps to breakdown some fatty acids and amino acids. It can also reduce high levels of homocysteine (homocysteinaemia) which may increase the risk for vascular disease.

Recommended Intakes

Table 7: Recommended Intakes for Vitamin B12 (mg/day)

Food Sources

Since vitamin B12 is synthesised by microorganisms, it is found in bacterially fermented foods, or meat and offal from ruminant animals in which the vitamin is synthesised by ruminal bacteria.

Therefore B12 is found almost exclusively in foods derived from animals. The richest source of the vitamin is liver. Other sources include shellfish, fish, meat, eggs, milk, cheese and yoghurt.

Not all corrinoids exhibit vitamin B12 activity. For example, in spirulina, a type of algae often promoted as a source of B12 for vegetarians, 80% of the corrinoids do not have vitamin B12 activity.

Deficiency

People who stop eating foods containing B12 may take up to 20 years to develop deficiencies because the body recycles much of its B12, reabsorbing it over and over again. Even when the body fails to absorb vitamin B12, deficiency may take up to 3 years to develop because the body conserves its supply.

Most B12 deficiencies reflect poor absorption. Inadequate absorption usually occurs because of either a lack of hydrochloric acid or intrinsic factor.

Many people, especially as they age develop atrophic gastritis, where there is inadequate hydrochloric acid. Consequently B12 is not released from dietary proteins and so vitamin B12 status diminishes.

Some people inherit a defective gene for the intrinsic factor and therefore develop deficiency symptoms. Some cases where the stomach has been damaged and cannot produce enough intrinsic factor, B12 has to be injected to bypass the need for intestinal absorption. Vitamin B12 deficiency caused by lack of intrinsic factor is known as pernicious anaemia.

Because vitamin B12 is required to convert folate to its active form, one of the deficiency symptoms of B12 is the anaemia of folate. This anaemia is characterised by large immature red blood cells. Either folate or B12 will clear up this anaemia, but if folate is given when B12 is needed, the results are disastrous, with devastating neurological symptoms. B12 maintain the sheath that surrounds and protects nerve fibres and promotes their normal growth. So if folate is administered when B12 is deficient, the blood symptoms of B12 deficiency disappear but the nerve symptoms progress. Therefore folate "masks" a B12 deficiency. Vitamin B12 deficiency causes a creeping paralysis of nerves and muscles, which begins at the extremities and works inward and up the spine. Early detection and correction is necessary to prevent permanent nerve damage and paralysis.