| Study Finds Selenium Affects Survival in HIV/AIDS
Miami, Florida, September 30, 1997
Scientists at the University of Miami School of Medicine, Center for Disease Prevention, reported today in the Journal of AIDS that deficiency of selenium, an essential trace element for maintaining a healthy immune system, has a profound effect on survival in HIV infected men and women. The researchers, led by Dr. Marianna K. Baum, found that HIV-1 infected patients with selenium deficiency, were 19.9 times more likely to die of HIV related causes than those with adequate selenium levels.
The dramatic results of this NIH funded study in 125 HIV infected men and women, published on September 30 of the Journal of Acquired Immune Deficiency Syndrome, demonstrate that selenium plays a critical role in HIV-1 disease. The researchers also found that while other nutrients (vitamins A, B12, and zinc) affect survival, these nutrients produce a substantially lower risk for mortality. In fact, when the nutrients were examined together, SELENIUM had the strongest impact upon mortality.
The authors suggest that the striking relationship between selenium deficiency and mortality could be related to selenium¹s antioxidant function and/or action in gene regulation which may affect HIV replication. As proposed in a report of Dr. Will Taylor, the University of Georgia, published in the same issue of the Journal of AIDS, selenium as part of selenoproteins, could have an important role in regulating HIV expression. He has proposed a novel viral mechanism that contributes to a decline in selenium levels accelerating disease progression, while adequate selenium would be expected to prevent HIV replication, and thus, delay the course of disease progression.
Based on this research, Dr. Baum's team is developing a study to determine whether selenium treatment can slow disease progression and improve survival over time in HIV infected men and women. The study has been approved and is under consideration for funding by NIH institutes, including the National Institute on Drug Abuse and the Fogarty International Center
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Low selenium tied to lung cancer risk NEW YORK, Nov 19 (Reuters Health)
Low blood levels of the trace element selenium may be linked to an increased risk of lung cancer, according to a study in the American Journal of Epidemiology.
Selenium affects the immune system, inhibits cell proliferation, and may have other anti-carcinogenic effects, findings from previous studies have suggested.
In the new study, Dr. Paul Knekt of the National Public Health Institute in Helsinki, Finland, and colleagues compared the long-term selenium intake of 95 volunteers with lung cancer to that of 190 cancer-free volunteers of similar ages.
The researchers calculated the volunteers' long-term selenium intake by analyzing the selenium content of two samples of their blood. All had given blood roughly 30 years and 20 years earlier. On both occasions, all of the volunteers were healthy.
On average, the volunteers had relatively low selenium intake by analyzing the selenium content of two samples of their blood — between 53.2 and 57.8 micrograms per liter — roughly 60% of levels usually seen in other western countries, the researchers explain.
Volunteers with selenium levels in the highest third, however, had a almost a 60% lower risk of developing lung cancer than those with levels in the lowest third, Knekt's team reports. Among volunteers with low vitamin E levels, those with selenium levels in the highest third ran a 76% lower risk of lung cancer than those with levels in the lowest third, according to the researchers.
And among volunteers who smoked, those who had the highest selenium levels had an 84% reduction in the lung cancer risk compared to those with the lowest levels of the mineral, they write.
The findings confirm those of some — but not all — previous studies investigating the relationship between selenium intake and cancer risk. While a number of studies have suggested that the micronutrient lowers risk of lung cancer, others have found no evidence of any anticarcinogenic effect.
It is possible that different studies have come to different conclusions because of differences among the populations they have included, Knekt and colleagues speculate.
Since all of the volunteers in their study had relatively low selenium levels in their blood, it is possible that the mineral "may exert its protective effect only when the basic level is low," they write. In light of the fact that the decrease in risk associated with higher selenium intake was more pronounced among those with low vitamin E levels than among those with higher vitamin E levels, another possibility is that selenium lowers risk only in people with low vitamin E intake, they speculate.
"In conclusion, the results that suggest that different methodological issues may conceal the association between selenium status and lung cancer occurrences in observational studies, and that low selenium status in some circumstances may be a risk factor in causing lung cancer," the researchers write.
The recommended daily allowances for selenium are 70 micrograms for men and 55 micrograms for women. Foods with relatively high selenium content include fish, particularly tuna, asparagus, Brazil nuts, meat, poultry, and bread.
SOURCE: American Journal of Epidemiology 1998; 148:975-982. Copywright 1998 Reuters Ltd.
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New Discoveries Expand Our Knowledge About Selenium's Importance by Richard A. Passwater, Ph. D.
A lot has happened since the last time I reviewed the health benefits of selenium in this column. Unfortunately for them, the average person still hasn't even heard of the trace mineral selenium. Fortunately, most nutritionally oriented health food advocates are aware of much about selenium. This review will cover many of the important findings since "Selenium Update" and "Selenium As Food and Medicine."
Background:
Selenium is an essential trace element for humans and other animals. Selenium was named after the moon goddess, Selene, by the Swedish chemist Jons Jakob Berzelius in 1817. Dr. Klaus Schwarz established selenium as an essential nutrient for animals in 1957, but the first selenium function in humans wasn't discovered until 1973. [1] Dr. John Rotruck and his colleagues at the University of Wisconsin demonstrated that selenium was incorporated into molecules of an enzyme called glutathione peroxidase (GPX). This vital enzyme protects red blood cells, cell membranes and sub-cellular components against undesirable reactions with soluble peroxides.
The discovery of GPX opened the door to our understanding of how selenium is protective against cancer, heart disease, arthritis and accelerated aging. Now more scientific excitement is being generated with the recent finding that selenium is also a vital component of other mammalian enzymes.
Phospholipid Hydroperoxide Glutathione Peroxidase (PHGPX) protects membranes against peroxides already bound to membrane surfaces. [2] PHGPX blocks formation of the extremely harmful alkoxyl radical and inhibits peroxidative chain branching. This activity is even of more importance in the prevention of cancer, heart disease and accelerated aging.
Now addition pathways in which selenium is involved in health are being uncovered. Selenium is a component of the enzyme that is needed to produce the most active thyroid hormone. ***Sub-optimal amounts of selenium impair thyroid hormone*** function and thus affects many body functions.
Biochemists are now studying several other selenium proteins and have classified them into four main categories. [3]
Cancer:
First there were animal studies that showed that selenium protected against chemicals and ultraviolet energy that cause cancer. [4-7] These laboratory findings were also supported by epidemiological studies (population surveys), and now large scale clinical studies are being sponsored by the U. S. government. [8-15]
Heart Disease:
Epidemiological studies have shown that persons with low-selenium diets have two-to-three times greater risk of heart disease than those eating selenium rich diets. [16] In a clinical study, patients with blockage of all three coronary arteries had low blood selenium levels, while those with high blood selenium levels were healthy and free of coronary heart disease. [17] Strikingly, those with one diseased coronary artery had the next highest blood selenium levels, and those with two blocked coronary arteries had the second lowest blood selenium levels.
Clearly, the antioxidant protection of the selenium-containing enzymes, GPX and PHGPX, protect the arteries and cholesterol-carrying lipoproteins against the damage that leads to heart disease.
Arthritis:
Arthritic inflammation is produced by certain hormone-like compounds called prostaglandins. Selenium is involved in controlling these specific prostaglandins by controlling the free-radical damage that stimulates their production.
Norwegian physicians had noted that arthritis patients tended to have low blood selenium levels. When their arthritis ***patients were given selenium supplements, they dramatically** improved. [18] A Danish study has confirmed the Norwegian study. [19]
Hypothyroidism:
Selenium is a component of the enzyme that is needed to produce the thyroid hormone triiodothyronine (T3). T3 is the preponderant metabolic thyroid hormone. The selenium-containing enzyme, iodothyronine deiodinase, converts the prohormone thyroxine (T4) into T3. [20] This explains the observation that selenium deficiency impairs thyroid hormone function. Impaired thyroid hormone function is called hypothyroidism and affects many body functions.
Other Areas of Study:
The role of selenium in possibly slowing the aging process has been under laboratory study for more than 25 years, but there are no known plans for clinical studies at this time. [21-3] Studies also indicate that selenium protects against cataracts and skin damage, and is important to prostate function. A patent has even been applied for that claims selenium significantly helps Alzheimer's patients. [24] Several books describe the many beneficial roles of selenium in health. [23, 25-6]
Forms of Selenium Supplements:
The most efficacious and safest forms to supplement our diet with selenium is not the inorganic salt form, but the organic forms, selenium yeast and selenomethionine.
Selenium Yeast:
Selenium yeast is produced when selenium is naturally incorporated into the protein of growing yeast under optimum conditions. The resultant yeast has a high concentration of the selenium-containing proteins, selenomethionine and selenocysteine. Products that are created by mixing yeast with inorganic selenium are still merely inorganic selenium products.
Beneficial nutritional brewer's yeast (Saccharomyces cerevisiae) does not contribute to yeast infections such as Candida albicans. Food yeasts are not infectious. Nutritional yeasts are not live yeast cells. If they were, live yeast cells would actually compete with one another and nutritional yeasts would actually suppress Candida albicans yeast growth. However, selenium yeast is carefully dried after it is grown. This kills the yeast and it can no longer grow or multiply. Brewer's yeast has been a staple of the health food industry since its inception. The famous health teachers all advocated brewer's yeast in one form or another because it is rich in the B-complex vitamins and other nutrients that were not available as purified nutrients in the past. Brewer's yeast still may contain nutrients that we have yet to discover.
Selenium yeast was found to out-perform inorganic selenium in increasing the amount of selenium in the milk of lactating mothers and the blood of their infants. The researchers concluded, "Selenium yeast was safe and more effective than selenite." [27]
In another test, 150 micrograms daily of selenium as selenium yeast was effective in raising blood selenium levels of healthy adults, whereas the same amount of inorganic yeast failed to raise blood selenium levels. [28] Dr. Gerhard Schrauzer of the University of California-San Diego concludes "since a ten-fold lower oral dosage of organic selenium produced a two-fold greater increase in selenium levels in the blood, organically-bound selenium is at least twenty-fold more effective in providing the body with the trace element." [29]
Selenomethionine:
Selenomethionine is a purified selenium-containing amino acid. There is no yeast in selenomethionine. Selenomethionine is a naturally occurring component of food. Selenomethionine is ***similar to the essential amino acid methionine but with an atom of selenium instead of an atom of sulfur.
The form of selenomethionine that the body can use is L-selenomethionine. L-selenomethionine is better absorbed and better incorporated into body components than any other known form of selenium. Experiments comparing inorganic selenium with DL-selenomethionine found that DL-selenomethionine was not as effective as the inorganic selenium [45].
D-selenomethionine is degraded to inorganic selenium and returned to the inorganic selenium body pool, and thus is only one-fifth as bioavailable as L-selenomethionine. [31]
I have been using various forms of selenium in my animal studies for thirty years and find that the selenium-containing amino acids (selenomethionine and selenocysteine) and the methylated selenides are far superior to the inorganic forms of selenium (selenite and selenate) in terms of overall health, longevity and freedom from cancer.
In studies in New Zealand, it was found that selenomethionine was at least 75 percent bioavailable, compared to 59 percent for sodium selenite. Blood selenium levels rose more quickly and didn't plateau as early with selenomethionine than with sodium selenite. [30-32] In a Finnish study, again selenomethionine raised blood selenium levels higher and remained in the blood longer than inorganic selenium. [33]
In a later Finnish study, it was found that as much as 3,500 micrograms of inorganic selenium had to be given to raise their blood selenium levels to match that of typical Americans. The long-term safety of such a high dose of inorganic selenium is not known.
In 1984, a MIT study determined that organic forms of selenium are able to increase the body pool size about 70 percent more effectively than inorganic selenite. [34]
Dr. P. Whanger of Oregon State University has spent several years studying the effectiveness of several forms of selenium supplements. He has published several papers on this subject through the years utilizing various laboratory animals and human clinical trials. His latest research was published in the MArch issue of the American Journal of Clinical Nutrition. Some of his ***findings include, "The selenium concentrations in all blood*** fractions increased at a faster rate (two- to three- fold) in women taking selenomethionine than in those taking selenate...About 95 percent of the selenium was associated with hemoglobin in women taking selenomethionine - interestingly, most of the GPX activity was also associated with hemoglobin...This suggests that selenium increases in these fractions only when selenomethionine is supplied and that the increase is restricted ***to hemoglobin." [35]
Selenoproteins and selenium transport:
We now know that several selenium-containing proteins exist, so selenium is essential in more ways than we knew in 1973. Earlier I discussed two new enzymes, PHGPX and iodothyronine deiodinase. Enzymes are proteins. But there are many other selenium-containing proteins, including muscle proteins and other selenium-containing enzymes. Dr. Roger Sunde of the University of Missouri-Columbia has classified selenoproteins into four distinct groups. [3] Table 1 lists the proteins of the selenium ion-specific selenoproteins, the selenomethionine-specific proteins, the selenocysteine-specific proteins and the selenium binding proteins.
Selenomethionine can furnish the required form of selenium for all four, whereas inorganic selenium has to be converted into selenomethionine or selenocysteine to be incorporated into two of the classes of selenoproteins. Notice in figure 1 that selenomethionine is incorporated directly into the selenomethionine-specific proteins. Selenomethionine can also be converted in the body into selenocysteine to form the selenocysteine-specific proteins. Also, selenomethionine can be catabolized into selenium ions to form the selenium ion-specific selenoproteins. It is easier for selenomethionine to provide selenium ions than it is for inorganic selenium to be converted into selenomethionine. The transport protein for selenium ions is selenoprotein-P.
Inorganic selenium:
As discussed earlier, inorganic selenium forms (selenate and selenite) are not as well absorbed as organic selenium-containing amino acids (selenomethionine and selenocysteine). However, inorganic selenium dissolved in the drinking water of laboratory animals has been effective in preventing various cancers. However, this is not how humans normally get most of their selenium; it is in their food, nottheir water.
Inorganic selenium, at low doses, is better than no selenium at all. However, larger doses of inorganic selenium has an oxidative effect that increases undesirable lipofuscin production. [36] The selenium in inorganic selenite is in the plus four valance state which is very oxidative. The selenium of selenomethionine is in the minus two valance state. The lipofuscin accumulation in the liver can be accounted for by the fact that in order for selenium to go from the inorganic plus four valance state to the plus minus valance state, six electrons must be obtained from liver cells. The safety of inorganic selenium is about one-third that of selenomethionine. [37]
Inorganic sources of selenium do not find their way to muscle protein to an appreciable extent. If laboratory animals are fed selenomethionine, selenium soon increases in all organs, muscles, GPX and hemoglobin. When inorganic selenium is fed to animals, it accumulates in the liver, kidneys and GPX. Inorganic selenium reacts spontaneously with sulphydryl groups to form selenotrisulfides. This can severely disrupt the structure of proteins.
Inorganic selenium reacts with the sulfhydryl groups of glutathione to form selenopersulfide and free selenide. Inorganic selenium, due to its free-radical promoting oxidative nature, is mutagenic and has caused cataracts at high doses in mice. [44] In contrast, selenium-containing amino acids are stable, less toxic, and do not have mutagenic or oxidizing activity.
Synergism With Vitamins C and E:
Vitamin C increases the absorption of selenomethionine and organic selenium-containing yeasts. Two differing reports exist concerning vitamin C and inorganic selenite. [38,39] One report shows that vitamin C inhibits inorganic selenium absorption, while the other shows that vitamin C enhances inorganic selenium absorption. The confusion may result from the fact that if vitamin C mixes with inorganic selenium in the food, the inorganic selenium is reduced to insoluble and biologically inert metallic selenium.
Vitamin E is a partner with selenium in protecting body components against oxidative free radicals. Both vitamin E and selenium have their own specific modes of stopping free radicals, plus they have common modes. The two are "synergistic" which means that the activity of both together is greater than the sums of the activity of each by itself. It's a case of nutritionally adding one plus one and getting more than three. Vitamin E and selenium are a powerful combination and the body needs both together.
Daily intake and safety:
In 1980, the National Academy of Sciences stated that a safe and effective range for selenium intake is 50 to 200 micrograms. In 1989, a daily RDA of 75 micrograms for men and 55 micrograms for women was established. The FDA has not as yet *** set a USRDA for selenium. Conventional supplementation practices are to add 50 to 200 micrograms of selenium to the daily diet.
In my three-part 1986 series on selenium safety, I discussed that many natural diets contained more than 600 micrograms of selenium daily. [40-42] In Northern Greenland, many residents consume about 1,300 micrograms of selenium daily. And, in China, some residents were found who took 1,000 micrograms of selenium daily when they found out that it protected them from certain selenium-deficiency diseases (including Keshan disease) endemic to their area. They developed thickened fingernails and a garlic-like breath. Now we have a report that a woman took 2,400,000 micrograms of selenium daily for seventy-five days with only mild and reversible side effects. [43] This is 12,000 times the recommended upper limit for supplementation for healthy people.
Keep in mind that everything -- even oxygen and water -- is toxic at some level. It is the dose that makes the poison. The amount of selenium supplement that is safe and effective is the old recommended daily range of 50 to 200 micrograms daily. Yet, we continue to read the foolishness that the cancer-protecting dose is toxic. That nonsense is a disservice to everyone.
Conclusion:
We still have more to learn about selenium than we already know, but it is clear that selenium is extremely important to our health. It's a shame that more people don't know about selenium. In a future article on selenium, I will interview Dr. Gerhard Schrauzer of the University of California-San Diego. Perhaps Dr. Schrauzer's provocative comments will help to get the public interested in protecting their health with selenium.
REFERENCES:
1. Rotruck, J. T., et al., Science 179:588-90 (1973)
2. Ursini, F., et al., Biochim. Biophys. Acta 839:62-70 (1985)
3. Sunde, Roger A., Molecular Biology of Selenoproteins, in Annual Review of Nutrition (1990), eds. Olson, Robert E., et al., Annual Reviews, Inc., Palo Alto, Ca. (1990).
4. Passwater, Richard A., Amer. Lab. 5(6) 10-22 (1973)
5. .... Advan. in Cancer Res. 29:419 (1979)
6. .... Prevent. Med. 9:362 (1980)
7. .... Cancer Res 41:4386 (1981)
8. .... Arch. Environ. Health 31:231 (1976)
9. .... Bioinorg. Chem. 7:23 (1977)
10. .... Lancet II 130 (1983)
11. .... Amer. J. Epidem. 120:342 (1984)
12. .... Nutr. Cancer 6:13 (1985)
13. .... Fed. Proceed. 44:2584 (1985)
14. .... Brit. Med. J. 290:417 (1985)
15. .... Biolog. Tr. Element Res. 7:21 (1985)
16. .... Lancet II 175 (1982)
17. .... Clin. Chem. 30:1171 (1984)
18. Aaseth, J., et al.; Selenium in Biology and Medicine (May, 1980)
19. Tarp, U., et al., Scandinavian J. Rheumatol. 7:237-40 (1985)
20. Berry, Maria J., et al., Nature 349:438-40 (Jan 31, 1991)
21. Passwater, Richard A., Amer. Lab. 3(4) 36-40 (1971)
22. Passwater, Richard A., Amer. Lab. 3(5) 21-6 (1971)
23. Passwater, Richard A., The New Supernutrition, Pocket Books, NY (1991)
24. Birkmayer, J., Eur. Pat. Appl. EP 345,247 (Dec. 6, 1989).
25. Passwater, Richard A., Selenium as Food and Medicine, Keats Publ., New Canaan, CT (1980)
26. Passwater, Richard A., Selenium Update, Keats Publ., New Canaan, CT (1987)
27. Kumpulainen, J., et al., Amer. J. Clin. Nutr. 42 829-35 (1985)
28. Schrauzer, G., Trace Substances in Environmental Health 13:64 (1979)
29. Schrauzer, G., Bioinorganic Chem. 8:303-18 (1978)
30. Thomson, C. D., et al., Br. J. Nutr. 39:579-87 (1978)
31. Thomson, C. D., et al., Amer. J. Clin. Nutr. 36:24-31 (1982)
32. Robinson, M. F., et al., Br. J. Nutr. 39:589-600 (1978)
33. Levander, O. A., et al., Fed. Proc. 42:927 (March 1983)
34. Janghorbani, M., et al., Amer. J. Clin. Nutr. 40:208-18 (1984)
35. Butler, J. A., et al., Amer. J. Clin. Nutr. 53:748-54 (1991)
36. Foo Pan and Traver, H. Arch. Biochem. Biophys. 119:429-34 (1967)
37. Csallany, A. S. and Menken, B. Z., J. Amer. Coll. Toxic. 5(1) 79-85 (1986)
38. Clark, L. C. and Combs, G. F., J. Nutr. 116:170 (Jan. 1986)
39. Mutanen, M. and Mykkanen, H. M., Human Nutrition; Clinical Nutrition 39C 221-226 (1985)
40. 39.
41. Selenium: Old Horror Tales Disproved, Whole Foods 9(11) 11-12 (Nov. 1986).
42. Selenium: The Upper Limit of Safety, Whole Foods 9(10) 11-14 (Oct. 1986).
43. Selenium Safety, Part I, Whole Foods 9(9) 7-11 (Sep. 1986). Here's Health p6 (April 1990)
44. Whiting, R. F. In: Selenium in Biology and Medicine, Spallholz, J. E., Martin, J. L. and Ganther, H. E., Eds. AVI Publishing, Westport, p325 (1981)
45. Thompson, H. J., et al., Cancer Res. 44(7) 2803-06 (July 1984)
All rights, including electronic and print media, to this article are copyrighted by Richard A. Passwater, Ph.D. and Whole Foods magazine (WFC Inc.).
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Is Selenium Deficiency Behind Ebola, AIDS and Other Deadly Infections? by Jack Challem
The latest Ebola epidemic in Zaire may be over, but it's probably only a matter of time before this supergerm returns-and still others emerge. The reason: Ebola and other deadly viruses, including the human immunodeficiency virus 1 (HIV-1), might be stimulated by deficiencies in the mineral selenium. And Zaire-where the Ebola and HIV-1 viruses first appeared-may be a viral "hot zone" because of low selenium levels in the soil and widespread selenium deficiencies among people living off that land.
Too strange to be true? To the contrary, a similar connection has been established in China, where a common virus mutates into a dangerous form when it infects people deficient in selenium. Selenium, an essential mineral, functions as an antioxidant and a component of another antioxidant, glutathione peroxidase. Deficiencies of either substance impair the body's immune system and ability to fight infections. But if recent research is any indication, the role of selenium in disease prevention may be much more profound than previously imagined.
Admittedly, there's no neat, well-documented association between selenium deficiency and the Ebola virus, but the evidence strongly suggests one. "It is certainly intriguing that a number of viruses have emerged from these regions in Africa, which appear to be selenium deficient," said E. Will Taylor, Ph.D., a viral researcher at the University of Georgia, Athens.
Selenium and Viral Mutations So far, there are three pieces to the selenium-virus puzzle. The first comes from the recent dramatic discovery that a selenium deficiency in a person or animal triggers a mutation in the coxsackievirus. The common form of this virus is generally benign, causing symptoms no more serious than a common cold or sore throat. The coxsackievirus mutation, however, attacks heart tissue, causing Keshan disease (a type of cardiomyopathy) and heart failure.
In China, Keshan disease is known to be associated with selenium deficiency. But because of the seasonal nature of Keshan disease, researchers suspected that an infectious microorganism was also involved. That's when they turned up the coxsackievirus, which also infects an estimated 20 million Americans annually.
The plot twisted last year when Melinda Beck, Ph.D., a virologist at the University of North Carolina, and Orville Levander, Ph.D., a nutritional chemist at the USDA's Agricultural Research Service, described how a run-of-the-mill coxsackievirus mutated into the deadly, rapidly reproducing strain when an infected person or animal was deficient in selenium or vitamin E. The coxsackievirus in animals eating a selenium-rich diet did not mutate. However, the mutated virus could infect and be deadly to a person or animal eating adequate selenium.
(Journal of Medical Virology, 1994;43:66-70 and Journal of Nutrition, 1994;124:345-58.)
Their research took on greater significance this past May, when Beck and Levander described the specific genetic changes that occurred in this coxsackievirus mutation. By comparing the genetic structure of the benign "parent" coxsackievirus to that of its virulent descendants, Beck and Levander identified six specific changes in the genetic structure of the virulent coxsackievirus strain. Although it's not yet clear whether one or all of these genetic changes triggered the more aggressive virus, the genetic evidence provides the scientific proof needed to link a host's selenium deficiency with a more dangerous form of the coxsackievirus. (Nature Medicine, May 1995;1:433-6.)
The coxsackievirus infection is made worse because selenium deficiency weakens the host's immunity, preventing the virus from being effectively challenged by T-cell lymphocytes or antibodies. As a result, the mutated virus can reproduce faster than it would in a relatively healthy person. In addition, the lack of selenium prevents the quenching of mutation-causing free radicals, so when the virus reproduces, it also mutates at a faster rate.
Although Beck and Levander studied only one virus, the implications are profound. They have already begun looking at whether other "host" nutritional deficiencies cause viral mutations as well. According to Beck, this propensity to mutate in a selenium-deficient animal or person might explain why new influenza strains regularly emerge from China, where selenium deficient soils are common. The flu virus originates in Chinese ducks, jumps to pigs, and then infects people.
"The importance of this finding is not limited to nutritionally deprived populations," the researchers said in a statement released by the USDA Agricultural Research Service. "In theory, it would take only one selenium-deficient person or animal to produce a new family of virus mutants."
Selenium and HIV
The second piece of the Ebola-selenium puzzle comes from Taylor at the University of Georgia, Athens. Last year, he theorized that several little-known genes in HIV control the formation of selenocysteines, proteins with a voracious appetite for selenium.
When the virus depletes all of the selenium in an HIV-infected cell, it reproduces and begins attacking other cells in search of more selenium. The more selenium the virus uses, the less that's available for the body's immune system. Eventually, immunity becomes so weak that AIDS patients become vulnerable to life-threatening "opportunistic" infections.
(Journal of Medicinal Chemistry, Aug. 19, 1994;37:2637-54.)
If the theory is correct, supplemental selenium would do two things, Taylor said in an interview. First, it would provide what the HIV virus needs so it wouldn't spread throughout, creating a biochemical stalemate of sorts. Second, it would help keep the person's overall immune system functioning, so it could resist the secondary infections that usually kill HIV patients.
Genetic evidence and clinical studies using selenium in the treatment of AIDS suggest that the theory is true. In one ongoing study, Juliane Sacher, M.D., of Frankfurt, Germany, reported that selenium-upplemented AIDS patients gain weight, have a general feeling of well-being, and sometimes benefit from increases in protective CD4 T-cells. (Chemico-Biological Interactions, 1994; 91:199-205.)Another study has found that selenium inhibits the growth of HIV-1 in the test tube. (Taylor EW, Antiviral Research, 1995;26:A271-86.)
The Selenium-Ebola Link
The third piece of the Ebola-selenium puzzle comes from a recent paper Taylor has submitted for publication. In it, he draws on his earlier work and that of Beck and Levander to build a compelling argument that Ebola also contains genes dependent on selenium. Like HIV, when selenium levels in Ebola-infected cells drop, or are low to begin with, the virus reproduces and "escapes" in search of cells with more selenium-spreading the infection throughout the body.
The difference is that the genes in the Zaire strain of Ebola genes appear to need 10 times more selenium than does HIV, and Ebola's greater dependence on selenium may partly account for the speed with which it kills. Seventy-five percent of the people infected with Ebola die within three weeks.
Again, compounding the infection, normal immune defenses against to the virus would be handicapped if the host-an animal or person-were deficient in selenium. "This raises the possibility that selenium deficiency in host populations may actually foster viral replication, possibly triggering outbreaks and perhaps even facilitating the emergence of more virulent viral strains," explained Taylor.
It's all very speculative, he admits. But the widespread soil deficiency of selenium in Zaire, documented by a number of researchers, would set the stage for vital mutation and a highly susceptible population, much the way it does in China.
But there's still another aspect, Taylor points out. Sulfur dioxide, a byproduct of the burning of fossil fuels, reacts with selenium compounds in the soil, making the mineral more difficult to absorb by plants. "It has long been suspected that fossil fuel burning and acid rain may be contributing to a gradual decrease of selenium in the food chain," Taylor said. "Thus, the deforestation of jungles and rain forests-exactly what is being done in Zaire and elsewhere-may also contribute to the emergence of new viral diseases.
This article originally appeared in the Natural Foods Merchandiser, published by New Hope Communications. The information provided by Jack Challem and The Nutrition Reporter™ newsletter is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your physician.
Copyright 1994 by Jack Challem, The Nutrition Reporter™ All rights reserved. Used with permission. For subscription information visit The Nutrition Reporter website.
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