Title: Selenium Status in the UK

Key words: Glutathione peroxidase, immune system, cancer, thyroid disease, cardiovascular disease, infertility, abortions, miscarriages

Date: July 2000

Category: 3. Micronutrients

Type: Article

Author: Dr van Rhijn


Selenium Status in the UK



The populations in parts of Europe, New Zealand, Eastern USA and the UK are consuming less selenium (Se) than is generally recommended. The 1991 COMA report gives a reference nutrient intake of 1m g/Kg/Day (approx. 75 m g/day) for adults, yet recent figures show the average dietary intake in the UK is about half this amount1. This is due to the decrease in consumption of imported Canadian wheat, grown in soil which has naturally higher concentrations of Se than in Europe2. Nutritional Se deficiency disease, due to low soil Se content, is well recognized in British livestock. Se has multiple biochemical metabolic functions in the body and this brief discussion will look at the nutritional importance of Se in disease prevention and consequences of inadequate intake.

UK Selenium Status

A review of human blood selenium concentrations, worldwide, reveals very large differences in the apparent dietary status of individuals in different areas. A Scottish study, looking at dietary selenium intake and indices of Se status in apparently healthy individuals (between 40 and 60 yrs), found low average reported Se intake (43m g/d) as well as low levels of plasma Se, suggesting that the Se status of certain Scottish individuals may be compromised3. A study in north-west England confirmed that a substantial proportion of both healthy volunteers (25%) and medical patients (50%) have low Se nutritional status, with serum Se values below those required for full expression of Se-dependent enzyme activity4.

Further UK studies found low mean serum Se (50.8 m g/L)5 in third trimester healthy pregnant women, and similarly low levels (47 m g/L)6 in pregnant women at delivery, both towards the lower end of the expected range at this stage of pregnancy (28-190 m g/L). Plasma and serum, concentrations of Se and the activity levels of Se dependent enzymes glutathione peroxidase7, 8, 9 in erythrocytes or even selenoprotein-P in plasma10, are reliable indexes of Se status in terms of bioavailability and function.

Antioxidant Effect

Selenium is an integral co-factor of the glutathione peroxidases (GSHPx)11 isoenzymes, which protect against oxidative damage in the body. This attribute accounts for the majority of selenium's health benefits. The mechanism by which this is achieved is by reduction of H2O2 lipid and free phospholipids hydroperoxides12 by using the GSH as the hydrogen donor [H202 + 2GSH ® 2H20 + GSSG].

Research has shown that the most potent selenium compound, selenodiglutathione (SDG), a natural metabolite of selenite, does not induce oxidative stress. It is also part of thioredoxin reductase, which is a reducing enzyme (-S-S- bonds in proteins) with peroxidase activity and helps to regulate the intracellular redox state.

Selenoprotein P is an abundant extracellular selenoprotein that may also act as an antioxidant defence system13, by quenching the extremely reactive peroxynitrite free radical. Selenoprotein W is a muscle protein containing selenocysteine. Selenium is an essential element of the glutathione synthase enzyme, and a cofactor for the production of superoxide dismutase (SOD). The removal of phospholipid hydroperoxides by GSHPx reduces the risk of inflammation, blood clotting and accumulation of LDL in artery walls, thus reducing the effects of CHD.

Immunological Effects

Selenium is an essential nutrient, required for optimal growth of mammalian cells. It also affects various immune functions. Se enhances the capacity of lymphocytes to proliferate and differentiate into cytotoxic effector cells. Se supplementation increased the tumor cytotoxicity of mice cytotoxic lymphocytes, lymphokine activated killer cells and macrophages, and human cytotoxic lymphocytes and natural killer (NK) cells14 by enhancing functional IL-2R/cell and proliferation and clonal expansion of cytotoxic precursor cells15. Harmless coxsackie viruses can become virulent in a Se-deficient host.

A lack of dietary Se is associated with various clinical conditions, such as myopathy16. The best known is Keshan’s disease, a cardiomyopathy (coxsackievirus B317) endemic in areas of China18. Although supplementation and general dietary improvements have reduced the incidence of Keshan’s disease significantly19, research suggests the involvement of Vitamin E deficiency as well. Experimental evidence suggests that Vitamin E and Se (via GSHPx) have a protective role in numerous viral infections (HIV20, 21) by stimulating the immune response and inhibiting HIV replication22. Se administration reduced mortality in chronic and recurrent pancreatitis.

Higher intakes of Se than currently recommendedhad a substantial protective effect on the risk of total cancer incidence in US adults, especially advanced prostate cancer23, as well as lung and colorectal cancers24. These intakes led to higher plasma levels than is currently believed necessary to optimise selenium-containing enzyme activity in the body. There is also associative epidemiological evidence of a protective role for Se in liver25, bladder, stomach, thyroid and breast cancer and it may act pharmacologically26 in a chemo-preventative role in cancer27.

Other Health Benefits

The human thyroid gland has the highest selenium content (per gram of tissue) of all the organs. The selenocysteine-containing proteins, respectively enzymes that are functionally expressed in the thyroid (mainly in thyrocytes to protect against oxidative damage) are the three forms of glutathione peroxidases (cGPx, pGPx, and PH-GPx), thioredoxin reductase, selenoprotein P 28 and iodothyronine 5’-deiodinase (IDI). Research confirmed that the latter, required for converting thyroxin (T4) to the more metabolically active triiodothyronine (T3), is a Se-containing protein29, 30. Coexistence of iodine and Se deficiency may potentiate the myxedematous form of endemic cretinism, resulting in adverse effects on growth, development (neuromuscular and intellectual impairment) and neonatal survival31.

Epidemiological evidence for its protective role in cardiovascular disease is equivocal32, 33, 34. Low serum Se may be a risk factor in pancreatitis35, and Se deficiency has been linked in conditions such as muscular dystrophy, malaria, asthma, thrombosis, rheumatoid arthritis, ulcerative colitis, adolescent osteoarthopathy (Kashin-Beck disease)36, nail changes and impaired tyrosine & melanin production. Supplementation with 100 m g/day of Se significantly decreased anxiety, depression37 and tiredness.

Se is important in reproduction, and deficiency results in infertility38, abortions39 (although not recurrent40) and placenta retention and infants from selenium-deficient mothers suffer from muscular weakness41. Se supplementation in subfertile men with low selenium status can improve sperm motility (incorporated in sperm mitochondrial capsule protein) and the chance of successful conception, highlighting the inadequate provision of this essential element in the Scottish diet42. Se is also required for normal testosterone production43.


Deficiency of the antioxidant activities of Se and Se dependent enzymes may be relevant to geographical differences in morbidity from a wide range of human disease states due to the subsequent diminished protective role in various degenerative conditions and viral infections. The reduced Se status in the UK gives rise for concern and fortification of flour or adding Se to fertilisers should be considered as public health measures, as already implemented for animals.


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