Selenium is a trace element that is required for many essential biochemical functions in the body. This includes its antioxidant role in several redox reactions, such as those involving glutathione peroxidase. These functions are part of maintaining a normal metabolic status, immune regulation, and inflammation.
Image Credit: Danijela Maksimovic / Shutterstock
Selenium is an essential component of the important enzyme iodothyronine deiodinase responsible for converting thyroxine or T4 to its active form, triiodothyronine, or T3. The thyroid hormone regulates a number of essential metabolic activities in the body. The recommended daily allowances of selenium are 0.070 mg/d for men, 0.055 mg/d for women, and 8.7 × 10-4 mg/kg/d for infants.
The first recognition of selenium deficiency's pathologic effects occurred in the identification of liver necrosis in laboratory animals raised on a diet that contained brewer’s yeast as a source of protein. This was abolished by the feeding of baker’s yeast instead. The scientist Schwarz found, after careful investigation, that the factor which helped to prevent liver necrosis was selenium. This was followed by identifying exudative diathesis in chickens and the occurrence of white muscle disease in livestock.
The important antioxidant and anti-inflammatory roles of selenium in the body lead to the association of selenium deficiency with an increased tendency to succumb to metabolic or inflammatory challenges, leading to illness development. One striking example is the occurrence of Keshan disease in selenium-deficient areas of China.
Disease conditions associated with selenium deficiency
Keshan disease is cardiomyopathy characterized by abnormalities in the ECG, cardiomegaly, and eventually cardiac failure. The essential pathological feature of the disease is the presence of multiple necrotic areas in the myocardium. It is usually seen in children and in women of reproductive age. It seems to be linked to stress, such as viral infections, in people who are selenium deficient. This syndrome has been successfully controlled with the government-introduced supplementation of selenium in the affected areas.
Another disease that has traditionally been linked to selenium deficiency is Kashin-Beck disease, a disfiguring form of arthritis resulting from cartilage atrophy, breakdown, and death, usually occurring in children between 5 and 13 years of age, seen in some parts of China, Tibet, and Siberia. The incidence of this condition has also been brought down by supplementation of selenium.
Again, it is suspected that selenium deficiency predisposes to a higher risk of cretinism by aggravating the effects of iodine deficiency. Male infertility has also been thought to have some links to low levels of selenium in the body.
Causes of selenium deficiency
Selenium deficiency is most often found in the following situations:
Plants grown in selenium-poor soils are often deficient in selenium content. This is especially a cause of selenium deficiency when the population is predominantly vegetarian.
Some regions of China are noted for their low soil selenium content. The people there, who subsist chiefly on vegetables, have the doubtful distinction of having the lowest selenium intakes in the world.
Long-term hemodialysis is associated with a significantly lower range of selenium in the blood because the procedure drains some selenium from the filtered blood. Other reasons include the strict dietary restrictions enforced on these patients and attendant nausea and vomiting of uremia.
The fall in selenium levels in this group has several explanations, including:
- a reduced dietary intake,
- poor absorption from the gut due to chronic and intractable diarrhea, and
- other malabsorption issues.
Research has found some association between selenium deficiency in these patients and a higher incidence of cardiomyopathy, death, vertical transmission of the virus, and earlier age at death of their offspring.
Again, supplementation of selenium has been found to improve the clinical course, reduce hospital admission rate, limit the increase in the viral load, and a corresponding increase in the number of CD4 cells, which are the primary viral targets. This association with reduced viremia has not been proven to exist in pregnant women, though early infant death is reduced.