Selenium deficiency


Selenium deficiency is relatively rare in healthy well-nourished individuals. Few cases in humans have been reported.

Signs and symptoms

Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency also contributes to Kashin-Beck disease. The primary symptom of Keshan disease is myocardial necrosis, leading to weakening of the heart. Kashin-Beck disease results in atrophy, degeneration and necrosis of cartilage tissue. Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases.
Selenium is also necessary for the conversion of the thyroid hormone thyroxine into its more active counterpart triiodothyronine, and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage.

Causes

It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, those who have had gastrointestinal bypass surgery, and also in persons of advanced age.
People dependent on food grown from selenium-deficient soil may be at risk for deficiency. Increased risk for developing various diseases has also been noted, even when certain individuals lack optimal amounts of selenium, but not enough to be classified as deficient.
For some time now, it has been reported in medical literature that a pattern of side-effects possibly associated with cholesterol-lowering drugs may resemble the pathology of selenium deficiency.

Diagnosis

Epidemiology and prevention

These diseases are most common in certain parts of China where the intake is low because the soil is extremely deficient in selenium. Studies in Jiangsu Province of China have indicated a reduction in the prevalence of these diseases by taking selenium supplements. In Finland, selenium salts are added to chemical fertilizers, as a way to increase selenium in soils. Dietary supplements may utilize sodium selenite, L-selenomethionine or selenium-enriched yeast.

In non-human animals

In some regions, selenium deficiency in some animal species is common unless supplementation is carried out. Selenium deficiency is responsible for many of the cases of WMD, evidenced at slaughter or during necropsy by whitish appearance of striated muscle tissue due to bleaching by peroxides and hydroperoxides. Although this degenerative disease can occur in foals, pigs and other animal species, ruminants are particularly susceptible. In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain. Sheep are more susceptible than cattle to WMD, and goats are more susceptible than sheep. Because of selenium's role in certain peroxidases and because of the antioxidant role of vitamin E, a low level of Se can be somewhat compensated by a high level of vitamin E. Some studies have indicated that about 0.12 or 0.23 mg Se per kg of dry matter intake may be sufficient for avoiding Se deficiency in sheep in some circumstances. However, somewhat higher Se intake may be required for avoidance of WMD where certain legumes are consumed. The cyanogenic glycosides in some white clover varieties may influence the Se requirement, presumably because of cyanide from the aglycone released by glucosidase activity in the rumen and inactivation of glutathione peroxidases by the effect of absorbed cyanide on the glutathione moiety.
In areas where selenium deficiency in livestock is a concern, selenium may be supplemented in feed. In some countries, e.g. the US and Canada, such supplementation is regulated. Neonate ruminants at risk of WMD may be administered both Se and vitamin E by injection; some of the WMD myopathies respond only to Se, some only to vitamin E, and some to either.