Vitamin A can be obtained in two forms:
• preformed retinol (retinyl esters) found in animal derived foods
• carotenoids which are mainly plant derived (beta carotene being the most abundant carotenoid), some of which can be converted to retinol in the body; 6mg of beta carotene is equivalent to 1mg of retinol.
The total vitamin A content of the diet (from both animal and plant sources) is normally expressed as retinol equivalents (RE).
Vitamin A is essential to the normal structure and function of the skin and mucous membranes such as in the eyes, lungs and digestive system. Therefore, it is vital for vision, embryonic development, growth and cellular differentiation, and the immune system.
Vitamin A deficiency is a serious public health problem worldwide,. It can lead to night blindness (impaired adaptation to low-intensity light) and an eye condition called xerophthalmia (dryness of the conjunctiva and cornea) and eventually total blindness. Marginal deficiency contributes to childhood susceptibility to infection, and therefore morbidity and mortality, in both developing and developed countries. Vitamin A deficiency is common in many developing countries especially among young children.
In the UK, frank deficiency is rare but low intakes are relatively common. For example, depending on age and sex between 6% and 20% of children have intakes that are unlikely to be adequate (below the Lower Reference Nutrient intake, LRNI). In adults, intakes tend to be higher although 16% of men aged 19-24 have intakes below the LRNI. In the UK, supplements containing 233µg of vitamin A are recommended for infants and young children from age 1 to 5 years (from 6 months for infants that receive breast milk as their main drink).
Excess retinol during pregnancy can increase the risk of birth defects. As a precautionary measure, women who are pregnant, or who might become pregnant, are advised not to consume high dose vitamin A supplements (>2800-3300 μg/day). Liver and liver products may contain a large amount of vitamin A, so these should also be avoided in pregnancy.
Large amounts of retinol can also cause liver and bone damage. To prevent adverse effects on bones, intakes above 1500 µgrams of retinol equivalents from food or supplements should be avoided. The Food Standards Agency advises that, as a precaution, regular consumers of liver (once a week or more) should not increase their intake of liver or take supplements containing retinol (for example, cod liver oil).
Liver, whole milk, cheese, butter, margarine and many reduced fat spreads are dietary sources of retinol. Carrots, dark green leafy vegetables and orange-coloured fruits, e.g. mangoes and apricots are dietary sources of carotenoids. In the UK, the law states that margarine must be fortified with vitamin A (and vitamin D). Vitamin A is also often voluntarily added to reduced fat spreads, as is vitamin D.
Dietary vitamin D exists as either ergocalciferol (vitamin D2) or cholecalciferol (vitamin D3). Ergocalciferol (D2) is derived from the UV irradiation of the plant sterol ergosterol, which is widely distributed in plants and fungi. (D3 ) is formed from the action of UV irradiation on 7-dehydrocholesterol in the skin of animals including humans.
Dietary sources are relatively insignificant, compared with the synthesis in the skin from exposure to sunlight or ultraviolet rays, because there are not many rich food sources of vitamin D.
Vitamin D is not classically a vitamin but a pro-hormone, acting as a precursor to one of the hormones involved in calcium homeostasis. Cholecalciferol is metabolised to the active steroid hormone 1,25-dihydroxyvitamin D3 in the liver and kidney. In this form it works as a hormone regulating the amount of calcium absorbed in the intestine. It is also essential for the absorption of phosphorus and for normal bone mineralisation. Vitamin D is also involved in the regulation of cell proliferation and differentiation. Vitamin D is also an activator of insulin-like growth factor (IGF-1) and, associated with this, poor vitamin D status is linked to sarcopenia (age related loss of skeletal muscle) which affects up to 25% of those over the age of 65 years and more than half of those over 85.
Deficiency of vitamin D results in poor calcification of the skeleton and hence skeletal deformity in children (rickets) and it leads to pain and bone fragility in adults (osteomalacia). Osteoporosis is not due to vitamin D deficiency but vitamin D may be beneficial in treatment. In the UK some groups of people such as Asian, black, older, institutionalised and housebound people and those who habitually cover the skin are vulnerable to vitamin D deficiency as a result of limited exposure to sunlight. Poor vitamin D status and rickets in children used to be commonplace in the UK but fortification and supplementation policies following the Second World War made rickets a thing of the past. However, in recent years, cases are again being reported, particularly in some ethnic minority groups from the Middle East and Indian subcontinent. Poor vitamin D status (a blood level of 25hydroxyitaminD below 25nmol/L – judged to be sufficient to prevent rickets) is also commonplace in the white population of the UK, emphasising the importance of balancing the need for sun exposure with the use of sun screen. For example, 36% of men and 38% of women aged 65-84 and living in institutions had low status in the NDNS for this age group. Amongst other age groups, the worst statistics were for young adults aged 19-24 years; 24% males and 28% of females. As sunlight is the major source, status tends to be lower in the winter/ spring than summer/autumn. Many young women enter pregnancy with poor stores of the vitamin.
It is recommended that pregnant and lactating women and people aged 65 years and over take vitamin D supplements (10µg per day). For other ‘at risk’ groups, for example ethnic groups that have limited sun exposure because of their style of dress, supplements may also be necessary. Infants are recommended to receive supplements containing 7.5µg of vitamin D; and these are available under the Healthy Start Scheme.
Excessive dietary vitamin D intake may lead to hypercalaemia (high calcium level in the blood), and some infants are especially sensitive to hypercalcaemia resulting from vitamin D toxicity. It is thought that skin synthesis is self-regulating.
Oily fish, eggs, fortified cereals and margarine are the main dietary sources of vitamin D. In the UK, the law states that margarine must be fortified with vitamin D (and vitamin A). Vitamin D is also often voluntarily added to reduced fat spreads, as is vitamin A. Human milk contains low levels of vitamin D, but infant formula is fortified with 0.001-0.0025 mg/100kcal.
Most vitamin D is obtained through the action of sunlight on our skin during the summer months. The latitude and strength of the sun in the UK means that the skin can only make vitamin D between 11am and 3pm, during the months of April to October.
Vitamin E is a group of eight lipid-soluble compounds synthesised by plants, tocopherols and tocotrienols. Alpha-tocopherol accounts for 90% of the vitamin E in human tissues. Vitamin E acts as an antioxidant and is required to protect cells against oxidative damage from free radicals, for example oxidation of the lipids in cell membranes. Vitamin E content in food is expressed in terms of mg equivalents based on the biological activities of the tocopherols present.
Existence of dietary vitamin E deficiency is not considered to be a problem even in people consuming a relatively poor diet. Deficiency only occurs in people with severe fat malabsorption and rare genetic disorders.
Vitamin E has very low toxicity and humans appear to be able to tolerate high levels of the vitamin without untoward effects (e.g. between 540-970 mg/day). However, at very high doses vitamin E may have negative effects on other fat-soluble vitamins; it exacerbates the effects of vitamin K deficiency and interferes with the absorption of vitamin A.
Foods containing large amount of polyunsaturated fatty acids will generally contain large amounts of vitamin E, therefore the richest sources of vitamin E are vegetable oils, nuts and seeds. Since vegetable oils are the richest source, deficiency is rare.
Vitamin K is required for the synthesis of several of proteins required for normal blood clotting and bone structure. Vitamin K is synthesised by bacteria in the large bowel and is also present in both plant and animal foods.
Deficiency is rare as vitamin K is widely available from the diet and is also provided by gut bacteria. Thus, deficiency is generally secondary to conditions such as malabsorption or impaired gut synthesis. However, there is growing interest in the role of vitamin K in optimising bone health. Newborn babies up to six weeks old have low levels of vitamin K, which puts them at risk of potentially fatal ‘haemorrhage disease of the newborn’, and is known as vitamin K deficiency bleeding in infancy. Therefore, is it usual to give all newborn infants prophylactic vitamin K.
Few toxic reactions to Vitamin K have been identified.
Dietary vitamin K is obtained from green leafy vegetables, dairy products and meat.
Water soluble vitamins
The B vitamins
Thiamin (vitamin B1)
Thiamin is a co-enzyme for several central energy-yielding metabolic pathways, and therefore is required to release energy from carbohydrate. As a result thiamin requirement is related to the amount of energy consumed. Thiamin is also involved in the normal function of the nervous system and other excitable tissues, such as skeletal muscles and the heart.
Deficiency of thiamin causes the peripheral nervous system disease beri-beri. This became a public health issue in the Far East in the nineteenth century with the introduction of highly milled (polished) rice. While beriberi is now rare, it remains a problem in some parts of the world where rice is the staple food. A different condition due to thiamin deficiency, affecting the central nervous system rather than the peripheral is sometimes seen in alcoholics and people with HIV, known as Wernicke-Korsakoff syndrome. This is caused by a combination of low intake and impairment of absorption and utilisation of the vitamin.
There is no evidence of any toxic effect of high doses of thiamin as the body excretes any excess.
Whole grains, nuts, meat (especially pork), fruit and vegetables and fortified breakfast cereals are sources of thiamin in the diet. In the UK, white and brown bread flour are fortified with thiamin by law (and also with calcium, iron and niacin).
Riboflavin (vitamin B2)
Riboflavin functions as a coenzyme in a wide variety of reactions that take place in the body. Riboflavin is required to release energy from protein, carbohydrate and fat. It is also involved in the transport and metabolism of iron in the body and is needed for the normal structure and function of mucous membranes and the skin.
According to UK surveys, intakes of riboflavin are low in a number of population subgroups, in particular teenage girls (over 20% have intakes below the LRNI), young women (15% of 19-24 year olds below the LRNI) and women over 65 years living at home (10% of those 65-84, 15% of those over 85 years with intakes below the LRNI). A low status of riboflavin is also common but there is no clear deficiency disease because there is very efficient conservation and reutilisation of riboflavin in tissues; therefore deficiency is never fatal. Deficiency is characterised by dryness and cracking of the skin around the mouth and nose and a painful tongue that is red and dry (magenta tongue).
No toxic or adverse reactions to riboflavin in humans have been reported. The body excretes excess riboflavin in urine.
Milk, eggs, fortified breakfast cereals, liver, legumes, mushrooms and green vegetables are all sources of riboflavin.
Niacin (nicotinic acid)
Niacin is required for the release of energy from food (it is the precursor to the coezymes NAD and NADP which are fundamental to key reactions in carbohydrate metabolism). As a result niacin requirement is related to the amount of energy consumed. Niacin is also required for the normal function of the skin and mucous membranes and for normal functioning of the nervous system.
Niacin can be synthesised from the essential amino acid tryptophan to meet daily requirements and dietary intake is only necessary when tryptophan metabolism is disturbed or intake of this amino acid is inadequate.
Deficiency of niacin results in the disease pellagra. It is characterized by sun-sensitive skin producing effects similar to severe sunburn. Advanced pellagra also results in dementia and if untreated is fatal. Pellagra is now rare but was a major public health problem in the early part of the last century up until the 1980s in some parts of the world. It was usually seen in communities where maize forms the staple diet as maize contains little tryptophan and the niacin that is present is in an unavailable form.
Reports of niacin/nicotinic acid toxicity in humans have been observed from its use as a treatment of hyperlipidaemia (high blood lipid levels). Adverse effects are dose related and generally subside with a reduction in dose or the cessation of treatment. Acute toxic symptoms include flushing, itching of the skin, nausea and gastrointestinal disturbances.
Meat, wheat and maize flour, eggs, dairy products and yeast are all dietary sources of niacin.
Vitamin B6 (Pyridoxine)
Vitamin B6 comprises 3 forms (vitamers): pyridoxine, pyridoxal and pyridoxamine, and has a central role in the metabolism of amino acids. It is involved in breaking down glycogen and has a role in the modification of steroid hormone action. It is also essential for the formation of red blood cells and the metabolism and transport of iron. Together with folate and vitamin B12, vitamin B6 is required for maintenance of normal blood homocysteine levels. Raised homocysteine is a risk factor for cardiovascular disease.
Deficiency of vitamin B6 is rare because it is widely distributed in foods and is synthesised by the body’s gut flora. Deficiency may only occur as a complication of disease or prolonged administration of certain drugs.
Long-term intake of high dose vitamin B6 from supplements (typically >200mg/day) has been reported to result in sensory nerve damage.
Poultry, white fish, milk, eggs, whole grains, soya beans, peanuts and some vegetables are sources of vitamin B6.
Vitamin B12 (Cyanocobalamin)
Vitamin B12 serves as a cofactor for enzymes involved in the normal function of the nervous system, the formation of red blood cells and for the metabolism of folate. It is also involved in energy production. Together with folate and vitamin B6, vitamin B12 is required for maintenance of normal blood homocysteine levels. Raised homocysteine is a risk factor for cardiovascular disease.
Dietary deficiency is rare in younger people and only occurs among strict vegans. It is more common in older people as a result of impaired absorption, usually due to chronic inflammation of the stomach lining (atrophic gastritis) or lack of intrinsic factor (the substance required for vitamin B12 absorption). Deficiency results in the development of pernicious anaemia, in which red blood cells are enlarged (megaloblastic), and peripheral neurological damage develops.
There are few reports of any adverse effects of high intakes of vitamin B12.
Vitamin B12 is found in almost all foods of animal origin. Green plants provide none but it can be synthesized by some algae and bacteria, although the bioavailability of such forms has been disputed. Meat, fish, milk, cheese, eggs, yeast extract and fortified breakfast cereals are all dietary sources.
The term folate describes a group of derivatives of pteryl glutamic acid. Folic acid is the synthetic form of folate. It is used in supplements and for food fortification.
Folate functions together with vitamin B12 to form healthy red blood cells. It is also required for normal cell division, the normal structure of the nervous system and specifically in the development of the neural tube (which develops into the spinal cord and skull) in the embryo.
There is conclusive evidence that supplements of 400μg/day of folic acid taken before conception and during the first 12 weeks of pregnancy prevent the majority of neural tube defects (e.g. spina bifida) in babies. It is recommended that all women of childbearing age who are planning a pregnancy take a daily supplement as it is difficult to achieve 400μg/day from diet alone.
Together with vitamins B6 and B12, folate is involved with the maintenance of normal blood homocysteine levels. The amino acid homocysteine is an intermediate in folate metabolism and evidence suggests that raised blood homocysteine (hyperhomocysteinemia) is an independent risk factor for cardiovascular disease. High intakes of folate have been found to lower the blood concentration of homocysteine in people genetically at risk of hyperhomocysteinemia and, as a result it has been proposed that folic acid supplementation might reduce the risk of cardiovascular disease. However, a recent meta-analysis of a number of large trials failed to demonstrate an effect of folic acid on either coronary heart disease or stroke risk.
Deficiency results in megaloblastic anaemia and may be due to poor diet or increased requirement, for example in pregnancy, from prolonged drug use or malabsorption. Megaloblastic anaemia is characterized by the release of immature red blood cell precursors into the circulation due to impairment of the normal process of maturation in the bone marrow. There may also be a low white cell and platelet count in the blood. Deficiency is often accompanied by insomnia, depression, forgetfulness and irritability.
Few adverse effects have been reported although high intakes may mask vitamin B12 deficiency and excessive intakes can cause complications if taken with certain drugs, for example anticonvulsants used in the treatment of epilepsy.
Green leafy vegetables, brown rice, peas, oranges, bananas and fortified breakfast cereals are sources of folate.
In various parts of the world folic acid is added by law to flour and bread e.g. USA, Canada and Chile. The UK is yet to commit to this fortification, largely because of concerns that high intakes of folic acid mask vitamin B12 deficiency in older people who are particularly susceptible, and some concerns regarding the relationship between folic acid and cancer. In 2005 the Scientific Advisory Committee on Nutrition (SACN) reviewed the research to underpin potential folic acid fortification in the UK and recommended that ‘mandatory fortification’ with folic acid should be implemented. Their conclusions were considered by the Food Standards Agency’s Board and it was agreed by the Board that mandatory fortification should go ahead. But before the recommendations were finalized, it was agreed to wait for the findings of ongoing trials investigating the relationship between folic acid and cancer. These trials have now finished and have been considered by SACN: an outcome is awaited.
Vitamin C (ascorbic acid)
Vitamin C has antioxidant properties, potentially protecting cells from oxidative damage caused by free radicals. Vitamin C is also involved in the synthesis of collagen which is required for the normal structure and function of connective tissues such as skin, cartilage and bones. It is therefore an important nutrient for the healing process. It is also involved in the normal structure and function of blood vessels and neurological function. Vitamin C also increases the absorption of non-haem iron (iron from plant sources) in the gut.
Severe deficiency of vitamin C leads to scurvy. Signs of deficiency do not manifest until previously adequately nourished individuals have been deprived of vitamin C for 4-6 months. Deficiency is associated with fatigue, weakness, aching joints and muscles. Most of the other symptoms of scurvy are due to impaired collagen synthesis and are characterized by bleeding gums, poor wound healing and damage to bone and other tissues.
Acute high doses of vitamin C are occasionally associated with diarrhoea and intestinal discomfort. A significant number of people take high dose (1000mg) vitamin C supplements (the RNI for adults is 40mg/day); however there is no evidence that this either confers any benefit or presents negative health consequences.
Fresh fruits especially citrus fruits and berries; green vegetables, peppers and tomatoes are all sources of vitamin C. It is also found in potatoes (especially new potatoes).
The bioavailability and absorption of vitamins
The bioavailability of a vitamin (i.e. how readily it can be absorbed and used by the body) may be influenced by a variety of factors. The proportion of a vitamin absorbed from the diet following consumption can vary, and will depend upon the individual person’s needs, their ability to absorb nutrients, the amount available to them and other components of the diet. For example, vitamin C can enhance the absorption of non-haem iron when foods or drink containing both vitamin C and non-haem iron are consumed in the same meal. Some vitamins, e.g. vitamin C and riboflavin, are labile and susceptible to damage by heat, light, oxygen, enzymes and minerals and these losses may occur during food processing, preparation and storage.
Although most people are able to meet their requirements for vitamins by eating a varied diet, there are certain groups of the population who have higher than normal requirements for some nutrients, e.g. ill people, those taking certain drugs and pregnant women. Such people need to ensure they eat foods rich in particular vitamins and sometimes supplements are advised. Infants and young children are recommended to have supplements of vitamins A, C and D up to age 5 years. Vitamin D supplements are also recommended for older people and pregnant and lactating women. Some women may require additional iron if menstrual losses are high and folic acid is advised for women planning a pregnancy and for pregnant women in the first 12 weeks of pregnancy.
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