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Vitamins, Minerals and Supplements: Part Three

Posted on: Wednesday, 30 November 2005, 06:00 CST

By Thompson, June

DIETARY SUPPLEMENTS

Vitamins and minerals are organic food substances essential to the normal functioning of the body. They are only required in small amounts but cannot be synthesised by humans and must be ingested in the diet. In the third of an occasional series on vitamins, minerals and supplements, JUNE THOMPSON gives an overview of the role that water-soluble vitamins play in the health of the individual, including their functions and the potential impact of any deficiency

As previously discussed,1,2 there are two types of vitamins: fat- soluble and water-soluble. Fat-soluble vitamins are stored in the body, primarily the liver, and include vitamins A, D, E and K. Water- soluble vitamins, which include the B vitamins and vitamin C, are not stored by the body and need ongoing replacement.

The B vitamins are an interrelated group of nutrients that occur together in foods and are known as the B-complex. They consist of thiamin (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5) (see Community Practitioner 2005; 78, 10: 366-368), and pyridoxine (B6), cobalamin (B12), biotin and folk acid (folate). Pyridoxine (B6), cobalamin (B12) and biotin will be discussed in this article.

Reference Nutrient Intake

Dietary Reference Values (DRVs) for energy and nutrients were most recently set for the UK in 1991.3 They define the range of estimated dietary requirements in different groups of individuals. DRVs include the Reference Nutrient Intake (RNI) - the amount of a nutrient that is enough for almost every individual, even someone who has high needs for the nutrient in the distribution of individual requirements. The RNI for the B vitamins will be included in this article.

Pyridoxine (vitamin B6)

Pyridoxine is a water-soluble vitamin that exists in three forms, Pyridoxine, pyridoxal and pyridoxamine, all of which are normally present in foods. Pyridoxine is necessary for the synthesis and breakdown of amino acids, the building blocks of protein, the metabolism of fatty acids for normal nerve function and the formation of red blood cells. It also helps keep the skin healthy. Pyridoxine is an approved treatment for sideroblastic anaemias4,5 and pyridoxine-dependent errors of metabolism. Pyridoxine has also been claimed to alleviate the symptoms of a range of conditions including premenstrual syndrome, sickness during pregnancy, carpal tunnel syndrome and neuropathies.4 Adequate vitamin B6 levels are important for the conversion of homocysteine into cysteine.6 Vitamin B6 may also inhibit sickling of erythrocytes in sickle-cell anaemia (SCA).5

Sources

Pyridoxamine and pyridoxal are found in animal products, and Pyridoxine in animals and plants.4 Pyridoxine is found in chicken (4.2 mg/kg), fish, liver, kidney, pork, eggs (1.1 mg/kg), milk, wheatgerm (11.5 mg/kg) and brewer's yeast (25 mg/kg). Other sources include brown rice (5.5 mg/kg), soybeans (6.3 mg/kg), oats, whole- wheat grains, peanuts and walnuts (7.3 mg/kg).4 Long-term storage, canning, roasting or stewing of meat and food-processing techniques can destroy pyridoxine. Boiling reduces the pyridoxine content of food because of losses into the water. Pyridoxine is present in a number of food supplements, generally at doses of up to 10 mg/day, but some single-dose food supplements may contain 50-150 mg. Single nutrient products (recommended maximum daily doses of 10-100 mg) are available without the supervision of a pharmacist.4

Reference Nutrient Intake

Recommended intakes of pyridoxine are based on protein intake. In the UK, the RNI is set at 15 g/g protein for adults. This is equivalent to approximately 1.4-1.2 mg/day in the UK for males and females respectively.4 Pregnant and lactating women and older people, who have low vitamin B6 levels, can usually increase their intake through a high-protein diet. Dietary Reference Values (DRVs) for formula-fed infants are based on the Vitamin B6 concentration in breastmilk.7

Deficiency symptoms

Pyridoxine deficiency is unusual in humans.4,5 Clinical pyridoxine deficiency manifests itself as peripheral neuropathy, glossitis, and sideroblastic anaemia.4,5,8 Children who had been given milk in which the pyridoxine had been destroyed by overheating displayed various symptoms, including: weakness, irritability, nervousness, susceptibility to noise, weight loss and insomnia.4 Pyridoxine deficiency also contributes to hyperhomocysteinaemia.4,6,8 Rarely, pyridoxine dependency, an autosomal recessive disorder, may occur where much higher tissue levels of pyridoxal phosphate are necessary for the enzyme to have any significant activity. The condition results in seizures of prenatal or neonatal onset and treatment with large doses of pyridoxine is necessary to prevent severe mental retardation or death.4

Biotin, which is found in egg yolk, has been claimed to be beneficial in the treatment of brittle nails, hyperinsulinaemia and impaired glucose tolerance and in sternocostoclavicular hyperostosis

Cobalamin (B12)

Cobalamin (B12) with folic acid is necessary for the synthesis of DNA (deoxyribonucleic acid). It is involved in the formation and regeneration of red blood cells, thus helping to prevent anaemia; is necessary for carbohydrate, fat and protein metabolism; maintains a healthy nervous system; promotes growth in children and increases energy needed for calcium absorption.4 Unlike other watersoluble vitamins, B12 can be stored in the body (liver). Results of studies in humans have suggested that large doses of vitamin B12 may influence biological rhythms and thus may be beneficial in the treatment of sleep disorders. Vitamin B12 has also been reported to increase light sensitivity by affecting melatonin secretion. In combination with folic acid, it may be beneficial in certain disorders, such as idiopathic osteoarthritis and vitiligo.4

To be absorbed, vitamin B12 requires intrinsic factor (IF), a protein produced in the stomach and secreted by the gastric parietal cells, to ensure adequate absorption by the ileum at normal dietary intake levels.4,9 Intrinsic factor maybe lacking because, for example, abnormal antibodies produced by an overactive immune system attack and destroy the stomach cells that produce intrinsic factor - an autoimmune reaction. Pernicious anaemia, a more severe autoimmune form of gastric atrophy, is characterised by an autoimmune attack against gastric parietal cells and/or intrinsic factor.8,9

Sources

Because cobalamin originates from bacteria, fungi and algae, and is synthesised by intestinal bacteria, its natural food source is exclusively animal protein.4,8 Plants contain no vitamin B12 beyond that derived from microbial contamination.4 Major dietary sources of vitamin B12 include meat, particularly liver and fish (such as salmon and tuna), and dairy products.4,9 Vitamin B12 is distributed into the liver, bone marrow and virtually all other tissues, including the placenta and breast milk of nursing mothers.4

Reference Nutrient Intake

The RNI for vitamin B12 in adults in the UK is 0.0015 mg/day.3 No increment is required during pregnancy but there is a recommended increment of 0.0005 mg/day for breastfeeding mothers.4 There are insufficient data from studies in humans and animals to set a safe upper level for vitamin B12. It is generally accepted that ingested cobalamin has a very low toxicity in humans.4

Deficiency symptoms

Dietary deficiency is rare in younger people living in the community4 but develops over years and is due to inadequate absorption and poor dietary intake.9 Inadequate absorption is seen with gastric disease, pernicious anaemia and ileal loss from disease or removal.9 Poor oral intake is most often seen in alcoholics and the elderly.4,9 Individuals adhering to vegan diets may also be at risk.4,8,9 Deficiency is also associated with elevated plasma homocysteine with a presumed increased risk of cardiovascular disease,4,8,9 and with neurological disease and megaloblastic anaemia.9

A study to investigate B vitamins and homocysteine as a risk factor for offspring with spina bifida found marginal maternal vitamin B12 status increases the risk of offspring with spina bifida.10 Higher vitamin B12 levels have been significantly associated with a better outcome in patients with a major depressive illness.11 Serum vitamin B12 concentrations progressively decline during pregnancy, which may be independent of dietary intakes and may not represent decreased maternal stores or deficiency at the biochemical level.12

Biotin

Also known as vitamin H, biotin plays an important biochemical role in every living cell and is used as cofactor of enzymes involved in carboxylation reactions. In humans there are five biotin- dependent carboxylases. These enzymes catalyse key reactions in gluconeogenesis (glycogen manufacture), fatty acid metabolism and amino acid catabolism. Thus, biotin plays an essential role in maintaining metabolic homeostasis.8,13 Biotin also plays an important role in regulating gene transcription4,8 and aids in the utilisation of protein, folic acid, pantothenic acid, and vitamin B12.

Sources

Biotin is widely distributed in natural foodstuffs, but at very low levels compared to other water-soluble vitamins. Foods relatively rich in biotin include egg yolk, liver, kidney, muscle and organ meats, and some vegetables, such as cauliflower. Liver contains approximately 1 mg/kg biotin, whereas fruits and most other meats contain approximately 0.01 mg/kg biotin. Biotin, \usually either in the form of crystalline D-biotin or brewer's yeast, is included in many dietary supplements, infant milk formulas and baby foods, as well as various dietetic products.4 It is synthesised by bacteria in the colon.

Reference Nutrient Intake

Due to insufficient data there are no set requirements but intakes of between 10 and 200 pg/day are considered both safe and adequate.7

Deficiency symptoms

Biotin deficiency can occur in people who consume large amounts of uncooked egg white as avidin, a glycoprotein present in raw egg white, binds tightly to dietary biotin and prevents its absorption.4,8 Once cooked, avidin no longer binds to biotin. Deficiency can also occur in sufferers from inherent or acquired biotin malabsorption, haemodialysis patients, and individuals receiving some forms of long-term anticonvulsant therapy.4 Biotin concentrations are significantly lower in pregnancy than in the non- pregnant, non-lactating state and decrease progressively throughout pregnancy.12

There is evidence of accelerated biotin metabolism in women who smoke which results in marginal biotin deficiency. This is of concern because marginal biotin deficiency is teratogenic in mammals.14 Signs of biotin deficiency include a fine scaly desquamating dermatitis and characteristic skin rash frequently observed around the eyes, nose and mouth, hair loss, conjunctivitis and ataxia.4 Biotin-deficient infants show signs of hypotonia, lethargy, developmental delay and withdrawn behaviour, all of which are characteristic of a biotin deficiency-related neurological disorder.4 'Egg white injury' may be associated with glossitis, anorexia, nausea, hallucinations, depression and somnolence.4

Biotin has been claimed to be beneficial in the treatment of brittle nails, hyperinsulinaemia and impaired glucose tolerance and in sternocostoclavicular hyperostosis.4 Biotin supplements are also indicated in the management of inborn biotin-associated enzyme abnormalities such as the biotin-responsive multiple carboxylase deficiencies.4 These are autosomal recessively inherited disorders of metabolism in which biotindependent carboxylases show diminished activity. This results in an accumulation of organic acids in the urine.15 The clinical picture involves the nervous system, skin, respiratory system, digestive system and immune system. The disorder has a good prognosis if biotin therapy is introduced early. If not, it can result in irreversible damage to the central nervous system and early death from metabolic acidosis." Biotin deficiency has been shown to cause abnormal foetal development in animals.4

Community practitioner 2005; 78, 11:407-408

The next part of this series will look at the role offolate and the B vitamins in the prevention of elevated homocysteine levels, which is considered an independent risk factor for cardiovascular disease, stroke and Alzheimer's disease

References

1 Thompson J. Vitamins, minerals and supplements. Community Practitioner 2005; 78, 1:24-26.

2 Thompson J. Vitamins, minerals and supplements: part two. Community Practitioner2005; 78, 10: 366-368.

3 Department of Health. Report on health social subjects 41. Dietary reference values for food energy and nutrients for the United Kingdom. Report of the Panel on Dietary Reference Values of the Committee on Medical Aspects of Food Policy. London: HMSO, 1991,

4 The Food Standards Agency. Safe upper levels for vitamins and minerals: report of the expert group on vitamins and minerals. London: Food Standards Agency, May 2003.

5 Fishman SM et al. The role of vitamins in the prevention and control of anaemia. Public Health Nutrition 2000; 3, 2: 125-150.

6 Zhang Shumin M. Role of vitamins in the risk, prevention, and treatment of breast cancer. Current Opinion in Obstetrics and Gynecology 2004; 16, 1: 19-25.

7 Department of Health. Dietary reference values - a guide. London: HMSO, 1991.

8 Halsted CH. Absorption of water-soluble vitamins [Small intestine]. Current Opinion in Gastroenterology 2003; 19,2: 113- 117.

9 Sharma N et al. Vitamin supplementation: what the gastroenterologist needs to know. Journal of Clinical Gastroenterology 2004; 38, 10: 844-854.

10 Groenen PM. Marginal maternal vitamin B12 status increases the risk of offspring with spina binda. American Journal of Obstetrics and Gynecology 2004; 191, 1: 11-17.

11 Hintikka Jukka et al. High vitamin B12 level and good treatment outcome may be associated in major depressive disorder. BMC Psychiatry 2003; 3:17.

12 Ladipo Oladapo A. Nutrition in pregnancy: mineral and vitamin supplements. American Journal of Clinical Nutrition 2000; 72, 1: 280S-290S.

13 Pacheco-Alvarez D et al. Biotin in metabolism and its relationship to human disease. Archives of Medical Research 2002; 33, 5: 439-447.

14 Sealey WM et al. Smoking accelerates biotin catabolism in women. American Journal of Clinical Nutrition 2004; 80, 4: 932-935.

15 Seymonds K et al. Dermatological signs of biotin deficiency leading to the diagnosis of multiple carboxylase deficiency. Pediatric Dermatology 2004; 21, 3:231-235.

June Thompson

Part time health visitor and freelance journalist

Copyright TG Scott & Son Ltd. Nov 2005

Source: Community Practitioner

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