Three other trace minerals for which there are DRVs in the UK are copper, iodine, and selenium. Copper is considered in detail elsewhere in this volume and will not be discussed further here. In this section, the roles of iodine and selenium will be reviewed briefly.
The non-metallic element iodine is an essential nutrient that, apparently, has a single function in the body as a component of the thyroid hormones thyroxine (T4) and triiodotyronine (T3). These hormones are necessary for a range of body processes, the most important of which are the control of metabolic rate, cellular metabolism, growth and neural development. Production of T4 and T3 is controlled by tissue demands which are mediated by the secretions of the pituitary gland and by the supply of iodine in the diet.
Deficiency of iodine can result in a number of diseases, ranging from severe cretinism with mental retardation to barely visible enlargement of the thyroid gland. Goitre is the name given to enlargement of the gland that occurs as the body attempts to compensate for a reduction of its supply of iodine by increasing the size of the gland. The amount of enlargement is related to the degree of iodine deficiency. The condition is widespread throughout the world, with up to a billion people affected (Hetzel and Mano, 1989). It occurs especially in poorer remote areas where the soil is depleted of iodine and the general diet is limited and lacks useful sources of the mineral. Goitre was once endemic in parts of the UK and other European countries, before the introduction of iodised salt and an improvement in the general diet.
Seafood is the major natural source of iodine in the diet. Fish, crustaceans and seaweeds are rich in the element. Milk is another good, though adventitious, source of dietary iodine as a result of the use of iodine-containing chemicals to sterilise dairy equipment. This practice has now ceased in many countries, with the result that dairy products are decreasing in value as a source of the nutrient. Cereals, vegetables and meat are generally poor sources. Iodised salt (sodium chloride) was introduced in many countries in the mid-twentieth century to combat endemic goitre and its use led to a significant improvement in the iodine nutritional status. Today, a reduction in the availability of iodised salt, coupled with an overall decrease in consumption of table and cooking salt, has resulted in a fall in iodine intakes. There is some concern that as a result, goitre may return to countries where it was once endemic (Solca et al, 1999).
The RNI for iodine in the UK is 140 mg/day for adults, close to the US RDI of 150 mg. These levels are easily achieved by consumption of a normal diet. Higher intakes of more than 1 mg/day may cause toxicity. This can be the result of excessive use of iodine supplements or, in certain cases, even of natural iodine-rich foods (such as certain seaweeds that can contain more than 4mg/kg of iodine). Paradoxically, high intakes of iodine depress thyroid function and produce goitre in certain individuals. Because some people, especially the elderly, may be sensitive to high iodine intakes, a Safe Limit of not more than 1 mg/day is recommended in the UK.
The metalloid selenium, although one of the rarest of the elements, is an essential trace nutrient for humans and all animals, but not for plants. Its essentiality was only recognised in the 1970s when the enzyme glutathione peroxidase was shown to be a selenoprotein (Rotruck et al, 1973). Previously the element had been known only for its toxicity (Reilly, 1996a).
Selenium, in the form of the unique amino acid selenocysteine, is the co-factor in several important functional metalloproteins. At physiological pH, the selenium in the selenocysteine is almost totally ionised and is an extremely efficient redox catalyst. At least 30 selenoproteins have been shown to occur in mammalian cells. Several of these have been fully characterised and their functions determined in human tissues. One group, the glutathione peroxidases, plays a role in intracellular antioxidant systems. Selenium is also an essential cofactor in the iodothyronine deiodinases, which are enzymes involved in thyroid hormone metabolism. Another important selenoenzyme is thioredoxin reductase which helps to control cell growth and division. Several other selenoproteins, including selenoprotein P and selenoprotein W, also occur in human tissues where they appear to have antioxidant and redox roles (Arthur and Beckett, 1994).
Selenium deficiency is associated with several diseases of major economic importance in farm animals. In humans chronic low intake of dietary selenium is responsible for Keshan disease, a sometimes fatal cardiomyopathy which occurs especially in children and young women, as well as for Kashin-Beck disease, a chronic osteoarthropathy, which also affects mainly children. These diseases are found in parts of China and other areas of Central Asia where soil levels of selenium are very low. Several other selenium-responsive conditions occur in humans, including cardiomyopathies and muscular problems in patients on total parenteral nutrition (TPN) if there is inadequate selenium in the fluid. Normal function of the thyroid gland is also dependent on an adequate supply of the element (Arthur et al, 1999). There is evidence that selenium deficiency can cause a wide range of other problems including immunodeficiency (Beck, 1999), increased susceptibility to various forms of cancer and to coronary arterial disease.
Selenium has been added relatively recently to the dietary recommendations in some countries as evidence establishing its important role in human health has become officially accepted. The UK RNI of 60 mg/day for adult females and 75 mg/day for adult males, is higher than the current US Dietary Reference Intake of 55 mg/day for adults (Institute of Medicine, Food and Nutrition Board, 2000). It is believed, however, by some health experts that these intakes are insufficient to meet human needs since they do not take into consideration the element's critically important protective role against oxidative damage.
Selenium is widely distributed, but normally at levels of less than 1 mg/kg, in most foods. The richest sources are organ meat, such as liver (0.05-1.33mg/kg), muscle meat (0.06-0.42mg/kg) and fish (0.05-0.54mg/kg). Though cereals contain only 0.01-0.31 mg/kg, cereal products make a major contribution to intake because of the relatively large amount of such foods consumed in most diets. Another good source of the element is nuts, particularly Brazil nuts which are the richest food source of the element known (Reilly, 1999). Vegetables, fruit and dairy products are poor sources.
Levels of selenium in plant foods, and in animals that feed on them, reflect levels in soils on which they grow. Soil concentrations are subject to considerable regional variations, and consequently levels in different foods can show a wide range. This has important consequences for dietary intakes in some countries. Thus, in the US where much of the food-producing regions have selenium-rich soils, the average intake of the element is 62-216 mg/day. In parts of China, where the soil is severely depleted, intakes are as low as 3-22 mg/day. In the UK, where, as in other European countries, soil levels are relatively low, average selenium intake is about 40 mg/day.
There is concern among some nutritionists about the possible adverse health effects of low selenium intakes and steps have been taken in some countries to protect the population against them. In Finland the law requires that selenium be added to all fertilisers and, as a result, the selenium status of the population has been more than doubled in recent years. In New Zealand the law permits but does not require farmers to use selenium-enriched top dressings on grazing land, to combat selenium deficiency in farm animals. Self-medication with selenium dietary supplements is widely practised by individuals, and is actively promoted by the pharmaceutical industry and the media in many countries (Reilly, 1996b).
Selenium toxicity, or selenosis, has been well documented in farm animals. It has also occurred in humans in some parts of China where very high levels occur in the soil. There have also been reports of selenosis in individuals who consume excessive amounts of selenium supplements. There is some debate about the levels of intake that will cause toxicity. Residents of some high soil areas appear to have no symptoms of selenium toxicity, although they consume as much as 700 mg/day. According to the Environmental Protection Agency in the US, a daily intake of 5 mg/kg body weight (350 mg for a 70 kg adult) is not toxic. In the UK the recommended maximum safe selenium daily intake from all sources for adults in 6 mg/kg body weight or 450 mg for an adult male (Department of Health, 1991).
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