Selenium for certain diseases

Selenium and diseases

Selenium and arthritis

Research on low-selenium areas of China also provided the first indication that some types of arthritis may respond to selenium supplementation when the trace element is low in the blood serum.

The Kashin-Beck disease (endemic osteoarthritis deformans) is an endemic osteoarthropathy which is a degenerative joint disease that starts bone during the first or second decade of life (31). If it is treated, this condition progresses to generalized osteoarthritis affecting the elbows, knees and ankles with joint ankylosis.

In an uncontrolled therapeutic trial, over 80% of subjects treated with sodium selenite and vitamin E showed some improvement in his condition, but the response was limited to children in the early stages of the disease (32). In a controlled trial, were orally administered doses of selenium, ranging between 1 and 2 mg of sodium selenite with 15 mg of vitamin E, for children up to age 13. Improvement was noted in 82% of children after one year (33).

Patients on a regimen of total parenteral nutrition (TPN) frequently suffer from a deficiency in selenium which is due to the absence of an intake of this mineral. and a resulting common consequence is pain in the joints and muscles. These disappear when administered 100 ug of selenium, usually in the form of seleno-methionine supplement (34).

Low concentrations of selenium in blood serum and red blood cells have been reported in studies conducted on patients crossed affected by rheumatoid arthritis and juvenile chronic arthritis.

There is a relationship between the level of selenium and activity and severity of disease. There is also a low activity of glutathione peroxidase in serum and red blood cells and white blood of patients with rheumatoid arthritis, which can be remedied by dietary supplementation with selenium (35). In these same patients. Serum selenium fluctuated with the disease activity, since, at lower levels of selenium was more pronounced symptoms and manifestations of the disease. Selenium supplementation in these circumstances was estimated, therefore, optional warranty.

The selenium level in other diseases

Selenium and Crohn's disease

Patients with Crohn's Disease tend to have reduced levels of selenium and glutathione peroxidase in the blood plasma and red blood cells in the length of intestine when they have been removed is more than 200 inches (5 m approximately). This deficiency of selenium is probably involved with surgical removal of part of the absorption capacity. These patients must measure up the plasma selenium level and if low, supplementation with the trace element is warranted (36). The selenium status of these patients reflects a level of generally low selenium blood of all patients suffering from gastrointestinal disease.

Selenium and chronic pancreatitis

It has been found that selenium in the blood concentrations are significantly lower in patients with chronic pancreatitis in healthy controls (37). As the activity of the enzyme glutathione peroxidase correlates with selenium concentration (Selenium is an essential part of this enzyme), the activity is also significantly lower in patients with this disease. The most plausible explanation of the reduction of the activity of glutathione peroxidase is the elevation of lipid peroxides observed in chronic pancreatitis. Selenium deficiency is probably a combination of low dietary intakes, more reduction in mineral absorption. Acute pancreatitis affect the levels of selenium in blood. These findings reflect the importance of maintaining levels of selenium in platelets of those with this chronic disease because selenium deficiency is likely to increase the chances of thrombosis.

Selenium and alcoholism

The selenium level was investigated in nine alcoholic subjects while intoxicated, by taking a series of blood and urine samples during hospitalization for alcohol detoxification. We also determined the selenium content of different alcoholic beverages and samples of hospital diets.

The average plasma selenium level and average selenium excretion him were both significantly lower (p <0.01) in alcoholic subjects than in control subjects at the time of admission. In addition, the daily dietary intake of selenium before hospitalization was estimated as less than the margin of safety recommended as suitable in most alcoholics. The selenium content of different alcoholic beverages was determined to be very low (between 0.1 and 0.8 (tg/d1). These data suggest that selenium depletion is occurring in alcoholics, and should, in all probability, to the low dietary intake. selenium depletion in this group of patients was corrected by suspending ethanol intake and with an adequate dietary intake of selenium without additional supplementation (33).

Selenium and malaria

Selenium deficiency may also have positive effects. The malaria parasite apparently oxidants generated inside infected red blood cells, thus making less affected cells capable of preventing or repairing damage to the oxidizer (39). Therefore, it was assumed that the generator of free oxygen radicals may be useful in treating malaria. This did not happen. Selenium deficiency (or deficiencies of vitamins B2, C and E) were found to attenuate the development of malaria parasites in the experimental subjects due to premature lysis of red blood cells (40). In fact, when some African villages were malnourished nourished properly, there was a resurgence of latent infections of malaria. Low levels of selenium are found to be a protection against the Somali nomads malaria parasite (41).

Selenium and immune response

There have been numerous reports of selenium deficiency in patients after undergoing total parenteral nutrition (TPN) long. Symptoms of selenium deficiency include anomalies observed in the growth and appearance of hair and nails, muscle diseases of varying degrees of severity and signs of liver damage (42), but little is known immune about the level of such patients. Information is lacking on this point, given the recognized role of selenium in maintaining the immune response. and the evidence found in animal experiments, indicating suppression of antibody response of prostaglandin biosynthesis of lymphocytes, which are the natural destructive cells, and the activity of macrophages, and possibly other immune system functions, before Tina selenium deficiency (43).

An article by Peretz and his team (44) describes the effects of selenium on immune parameters in patients on home TPN. Selenium supplementation in this study had no effect on the apparent cell groups or on the production of interferon. The lack of response is of interest in view of the results obtained in animal experiments, indicating a deletion of the T helper lymphocyte type in selenium deficiency. This could mean that a depressed partner type T lymphocytes in humans occurs only in the most severe degree of selenium deficiency.

In contrast with the results of Peretz and his team, another study on selenium supplementation in normal human subjects elevations sheds type suppressor T lymphocytes (45). This may reflect an effect on the chemical form of selenium supplied, which in this case was a sodium selcnito instead of L-(+)-seleniornetionina. In vitro investigations have shown that the induction of antibody production by lymphocytes mitogenetic is affected by the chemical form of selenium added to the medium. Peretz and his team used L-(+)-selenomethionine because this compound represents a normal nutritional selenium.

Selenium in the form of selenomethionine is better retained than selenite, but can not be immediately effective because it must first be converted into a physiologically active compound. Selenite administration can provide a quicker effects observable because this form of selenium is immediately incorporated in the common metabolic background interchangeably selenium selenite. However, selenite could not work in all compartments to which comes the selenium-methionine. Although generally selenite is added to the TPN solutions, L-(+) selenomethionine could be preferable for some patients, especially those requiring long term TPN treatment.

All this raises the question of the dosage of selenium in TPN patients. Peretz and his team point out correctly that 50 ug / day are not enough, because they allow the replenishment of depleted selenium body stores. To this end, suggest a dose of supplemental selenium in amounts ranging from 200 to 900 ug / day (46).

Selenium and thyroid

Thyroxine (T4), which is the main product of the thyroid hormone is converted by desiodinación (with loss of an iodine atom) in tri-iodothyronine (T3), more biologically active. This conversion may also take place in the liver, kidney and muscle by the action of a type I deiodinase. Some time ago it is known that in some areas endemically deficient iodine, iodine supplementation simply do not cure the problems associated with iodine deficiency. The reasons are ignored, and different theories emerged, among them the state has resistance to iodine. Recently, however, has been that the deiodinases contain selenium, without which they can not function. Therefore, in the seleniaI deficiency states, these enzymes can reduce the iodine to convert T4 to T3 and, consequently loses much of the activity of tri-iodothyronine and symptoms appear in iodine deficiency (47).

The countries in which associations between the thyroid gland, iodine and selenium have been identified, finding weaknesses in both elements are found in Africa, Asia and Latin America. Suffice selenium deficiency resulting only adversely affected functions of the thyroid gland. The importance of selenium is also reflected in the first findings of the fact that this failure is due to a blockade of the function of the control system of feedback to the thyroid gland (48).

How secure is selenium?

Selenium is not as toxic as once thought, according to a study by Flodin (49). It has been found that the vitamin E and selenium are complementary in animal experiments. Higher intakes of selenium are less toxic in animals with adequate levels of vitamin E that have deficiencies in vitamin E (50). Still have not found sensitive biochemical indicators for detecting selenium poisoning (51).

The level of dietary selenium exposure necessary to cause chronic poisoning in humans is not known with certainty, but approximately 5 mg / day of selenium from foods produced changes in fingernails and hair loss in a seleniferous of China (52).

Chinese investigators also report that, in an individual who had consumed 1 mg selenium per day in the form of sodium selenite, for over 2 years, thickening was observed, but with increased fragility, nails, plus a smell of garlic skin excretions. In the United States, 13 people developed selenium poisoning after taking a dietary supplement manufactured incorrectly containing 27.3 mg of selenium per tablet. Symptoms are brought nausea, abdominal pain, diarrhea, hair and nail changes, peripheral neuropathy, fatigue and irritability (53).

Women who consumed the highest dose of selenium (2.387 g in a period of 2 ½ months) experienced hair loss, softening and falling fingernails, nausea and vomiting, with scents of sour milk, and increased fatigue (54). Lower intakes they can cause toxicity problems. It finds evidence of impaired homeostasis selenium intakes above 750 ug (55), and there were problems early on nails in adults with intakes of 900 ug per day. For these reasons, the UK authorities have recommended as maximum safe selenium intake for adult males, whatever the source, 450 ug per day.

Source: Dr Leonard Mervyn - Lamberts

References
31. Sokoloff, L. Endentic forms of osteoarthritis. Clin.Pharin.Dis. II. p.187-202. 1985.
32. LIN, Q. Chinese Medicine ed. H. WU, MTP Dam. Lancasternlarton, 2, p.259-263, 1984.
33. L1ANG, S. The prophylactic and curing effect of Selenioni in combattin ... 1 Kashin-Beck's disease. Newsletter of Endemic Diseases, Prevention and Cure. Moment of Endetnic Disease, Shaanxi Province, p.5-12, 1985.
34. BROWN, M. R. and others. Proximal muscle weakness and selenium deficiency associated with long-term parenteral nutrition. Am.J.Clin.Nutr., 43, p.549-54. 1986.
35. TARP, V. and others. Selenium in Rheumatoid Arthritis. A Historical Prospective Approach. J. Trace Elern. Electrolytes Health Dis., 3, p.93-95, 1989
36. RANNEM, J. and others. Selenium status in patients with Crohn's Disease, Am.J.Clin.Nutr., 56, p.933-7, 1992.
37. VEHARA, S. and others. Clinical Signiticance of Selenium Level in Chronic Pancreatitis, J.Clin.11iochem.Nutr., 5, p.201-207, 1988.
38. Dutta, S. K. and others. Selenium and Acute Alcoholism, Am.J.Clin.Nutr., 38. p.713-I8, 1983.
39. Etkin. N.L. and Eaton, J. W. Malaria-induced erythrocyte oxidant sensitivity. in Erythrocyte Structure and Function, ed. G.J. BREWER, pub. by Liss, New York. p.219-34, 1975.
40. Thurnham, D.1. Nutrient deficiencies and malaria: a curse or a blessing? Proc. Int.Congr.Nutr 13th. ed T.G. T A Y - LOR, N.K. JENK1NS, L1BBY Pub, London, p.I29-31, 1986.
41. MURRAY, M. J. and MURRAY, A.B. The effect of selenium deficiency and repletion on host resistance to infection. In Trace elements in man and animal, ed. C.F. MILLS and others, pub by UK Commonwealth Agriculture] Bureaux, Slough, UK., P.244-47. 1985.
42, Kiel. C.L. and Ganther, H.E. Selenium deficiency in total parenteral nutrition, Am.J.Clin.Nutr., 37, p.319, 1983.
43. KOLLER, L.D. and others. Immune Responses in Rats Supplemented with Selenium, Clin. Exp.Immunol., 63, p.570. 1982.
44. Peretz T.P. and others. Nutrition, 7 (3), p.223-11. 1991.
45. HEREZFERD, A. and others. Proc. Element Int.Trace 6th Symp .. 3. Leipzig, Germany, Karl Marx University Press, p.915, 1989.
46. VON STOCKHAUSEN, H.II. Selenium in total parenteral nutrition, Biol.Trace Elein.Res., 15, p.147, 1988.
47. Burk, R.F. Recent developments in trace element metabolism and funetion: newer roles of selenium in nutrition. J.Nutr .. 119. p.1051-4, 1989.
48. BECUkETT. G.J. and others. Effects of selenium and iodine cotnbined, thyroid hormone deficiency on metabolism in rats. Arn.J.CITILNutr .. 57, p.2405-35, 1993.
49. Flodin, N.W. Pharmacology of micronutrients: Selenium. Alan R. Liss (pub) New York, p.269-84, 1988.
50. Levander, A.O. Selenium; Biochemical actions, interactions. and some hurnan health implications. Man R. Liss (pub) New York, p.345-68, 1982.
51. National Research Council. Selenium, Recommended dietary allowances. 10 'edition, National Academy Press, Washington, DC. p.217-24, 1989.
52. YANG, G.S. and others. Endemic selenium intoxication of humans in China. Am.J.Clin.Nutr., 37, p.872-81, 1983.
53. HELZLSOVER, K.R. and others. Acute selenium intoxication in the United States, Fed.Proc., 44. p.1670-4, 1985.
54. JENSEN, R. W. and others. Selenium intoxication in New York. Morb.Mortal.Week.Rep., 33, p.157-8, 1984.
55. YANG. G. and others. Snidies of safe maximal daily dietary intake in a seleniferous The area in China. Part II. Relation Between The intake and the manifestation of clinical signs and Certain Biochemical Alterations in blood and urine. ElentElectrolytes J.Trace Health Dis., 3, p.123-30. 1989.

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