Life Extension Magazine
|LE Magazine May 2001 |
|Studies from throughout the world that can help you live longer|
Table Of Contents
- Selenium, vitamin E and rheumatoid arthritis
Full source: EPIDEMIOLOGY, 2000, Vol 11, Iss 4, pp 402-405
A study investigated whether antioxidants could protect against rheumatoid arthritis in 18,709 adult men and women who had neither arthritis nor a history of it in 1973-1978. By 1989, 122 had developed rheumatoid arthritis. The results showed that when the level of selenium was low, the later occurrence of rheumatoid factor-negative was high, and vice versa. The average risk was 84% for rheumatoid factor-negative. But this was not true for rheumatoid factor-positive rheumatoid arthritis (4% risk). During the first 10 years of follow-up, the average risk for rheumatoid arthritis for the highest compared with the lowest tertile of blood vitamin E was 56%. Therefore, low selenium status may be a risk factor for rheumatoid factor-negative rheumatoid arthritis, and low vitamin E status may be a risk factor for rheumatoid arthritis.
- Diet and overall survival in the very old
Full source: EPIDEMIOLOGY, 2000, Vol 11, Iss 4, pp 440-445
A 5-year study among 162 self-sufficient residents in a public home for the elderly evaluated the association between the consumption of specific food groups and nutrients (using a food-frequency questionnaire), with overall five-year survival. Those who ate citrus fruit at least two times per week had half the risk of dying than that of individuals who consumed citrus fruit less than once a week (48%). High levels of intake of vitamin C, vitamin B2 and linoleic acid were associated with 50% to 60% decreases in mortality risk. High consumption of meat was associated with a higher risk of mortality (average risk was 9.72 out of 35.1) among those with chronic diseases. Thus, frequent consumption of citrus fruit, milk and yogurt; low consumption of meat; and high intake of vitamin C, vitamin B2 and linoleic acid are associated with longevity.
- Alpha-lipoic acid protects antioxidant capacity of COQ10
Full source: Journal of Biosciences, 1998, Vol 53, Iss 3-4, pp 250-253
COQ10 (ubiquinone) and alpha-lipoic acid are natural constituents which are involved in mitochondrial energy metabolism. Through their bioenergetic activities they are graded to a reduced form and require re-cycling. COQ10 was found to interfere with lipid peroxidation of liposomal membranes and then become degraded by oxidation. The efficiency of the antioxidative capacity of the COQ10 was found to be diminished through prooxidant activities of the antioxidant-derived metabolites. Thus, the antioxidative derived reaction products of COQ10 in turn promoted lipid peroxidation. Lipoic acid, however, was found to totally recycle COQ10 to the antioxidant active form. This study demonstrates that lipoic acid recycles COQ10 to the antioxidative-active form of COQ10.
- DHEA replacement in the healthy elderly
Full source: JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM, 2000, Vol 85, Iss 9, pp 3208-3217
DHEA (dehydroepiandrosterone; 50 and 25 mg) and placebo tablets were given daily to 24 healthy aging men and women (avg. age 67.8) for eight days. At the start, the blood levels of DHEA(S) were relatively low. With the reestablishment of "younger" levels, four important results were obtained. 1) Blood DHEA had an apparent terminal half-life of more than 20 hours, the same order of magnitude as that of blood DHEAS. 2) The conversion of DHEAS to DHEA was significantly greater in women than in men. 3) There was no accumulation of steroids. 4) There was no transformation to androgen (male hormones) and estrogen; the limited increased estradiol in aged women could be predicted to be beneficial. These results suggested that daily oral administration of DHEA (25/50 mg) is safe in elderly subjects. The 50-mg dose was chosen for a 1 year trial of daily oral administration of DHEA in 60- to 80-yr-old individuals.
- Antioxidant supplements: Effects on disease and aging
Full source: JOURNAL OF THE AMERICAN AGING ASSOCIATION, 2000, Vol 23, Iss 1, pp 25-31
Ingestion of antioxidant supplements by the United States (US) population has increased steadily since the mid-1950's. Experimental animal studies have demonstrated that antioxidant supplements lower the incidence of a wide variety of diseases and increase life span. Antioxidants are associated with similar changes in man. Changes since the mid-1950's in the US population include: 1) ingestion of antioxidant supplements has increased from 1%, or less, to 40% to 50% today, 2) disproportionate increases in the percentage of older individuals as average life expectancy rose, 3) declining chronic disability in the elderly since 1982, 4) declining cancer mortality since 1991, and 5) the decline in the rate of reported cardiovascular disease beginning in the 1950's which significantly increased further in 1965. The last four changes suggest that the rate of increase in physiological age with time has been slowed. This can be attributed to decreases in the rate of accumulation of free radical-induced aging changes by the joint action of antioxidant supplements/dietary measures, and improvements in conventional measures which increase average life expectancy, e.g., better medical care, nutrition, housing, accident prevention. The contribution by antioxidants to decreases in physiological age is seemingly small compared to that of conventional measures. However, it will grow relative to conventional measures as the amount and duration of supplement use increases and improvements in conventional measures raise average life expectancy closer to 85 years and beyond.
- Melatonin prevents gallstones
Full source: HEPATOLOGY, 2000, Vol 32, Iss 3, pp 455-460
Free radical stress has been implicated in the start of gallstone formation. A study examined the oxidative stress changes during gallstone formation and investigated whether melatonin could act as a preventive agent in guinea pigs. Stone and/or sludge developed in vessel-constricted guinea pigs without melatonin. Total antioxidant activity in bile of guinea pigs at day 14 after bile duct vessel constriction (ligation) reduced to one third of the level in sham-operated controls. In addition, the bile of ligated guinea pigs had increased pH, bile salts and malondialdehyde (a marker of stress), compared to sham controls. However, pretreatment of guinea pigs with melatonin at a dose of 1,000 mu g/kg significantly decreased the incidence of gallstone formation at day 14 after vessel constriction, as compared to no pretreatment (0/7 vs. 8/10). Melatonin also reverted the constriction-induced changes in bile salts, pH, malondialdehyde and total antioxidant activity to normal control levels. This shows that free radicals play a role in the bile duct ligation-induced pigment gallstone formation. Thus, antioxidants should prove useful in preventing pigment gallstone formation in humans.
- Melatonin suppresses fat, leptin and blood insulin
Full source: Endocrinology, 1999, Vol 140, Iss 2, pp 1009-1012
Human and rat pineal melatonin secretion decline with aging, but fat and blood insulin levels increase. Melatonin modulates fat metabolism in some mammals. This study investigated the effects of daily melatonin supplementation on male rats, starting at middle age (10 months) and continuing into old age (22 months). The dosage produced nighttime blood melatonin levels in middle-aged rats which were 15-fold higher than in young rats. However, blood melatonin levels in middle-aged rats receiving a 10-fold lower dosage were not significantly different from young or middle-aged controls. In this case, fat, blood insulin and leptin levels were all significantly increased at middle age when compared to young rats. All were restored within 10 weeks to youthful (four month) levels in response to both high and low dosages of melatonin. Continued treatment until old age maintained suppression of fat levels. Since increased fat is associated with increased insulin resistance, diabetes and cardiovascular disease, the results suggest that melatonin supplementation may prevent disease, or provide therapy for some prominent pathologies associated with aging.
- Melatonin plus interleukin-2 and cancer immunotherapy
Full source: International Journal of Immunotherapy, 1998, Vol 14, Iss 3, pp 169-174
The pineal gland plays a fundamental role in the neuroendocrine regulation of antitumor immunity. The pineal hormone, melatonin, has been found to amplify the effectiveness of interleukin (IL)-2 anticancer immunotherapy. This study describes the three year survival rate obtained with IL-2 plus melatonin in a group of untreatable solid tumor patients, compared to use of IL-2 alone. The study included 120 advanced cancer patients with a life expectancy of less than six months, suffering from lung cancer or gastrointestinal tract abnormal tissue growths. Patients received a) supportive care only, b) IL-2 alone or c) IL-2 plus 20-40 mg/day of melatonin. Tumor regression was significantly higher in patients treated with IL-2 and melatonin with respect to that seen in both groups of patients treated with supportive care or IL-2 alone. Accordingly, the percentage of three year survival was significantly higher in patients treated with IL-2 and melatonin. These results confirm that IL-2 and melatonin may be considered a new effective therapy of advanced human abnormal growths, capable of prolonging the survival time in patients for whom no standard therapy is available, and for growths which are generally resistant to IL-2 alone.
- DHEA and aging
Full source: Steroids, 1998, Vol 63, Iss 5-6, pp 322-328
Human adrenals secrete large amounts of dehydroepiandrosterone (DHEA) and its sulfate (DHEA-S). They are converted into potent androgens and estrogens in peripheral tissues, which provides autonomous control to tissues that can adjust the formation and metabolism of active sex steroids according to local requirements. Rapid progress in this area has recently been made in knowledge of the structure of most of the genes that encode the enzymes responsible for the transformation of these inactive precursor steroids into androgens and/or estrogens. It is estimated that 30% to 50% of total androgens in men are synthesized from inactive adrenal precursors while, in women, peripheral estrogen formation is even more important, the best estimate being 75% before menopause and 100% after menopause. The marked reduction in the formation of DHEA-S by the adrenals during aging, especially before the age of 50 years, results in a dramatic fall in the formation of active sex steroids. This is a situation that is thought to be associated with a long series of age-related decreases such as insulin resistance, obesity, osteoporosis, cardiovascular diseases, loss of muscle mass, cancer and other diseases. This study showed a series of medically important beneficial effects of DHEA administered for 12 months to post-menopausal women. Most interestingly, the bone mineral density significantly increased. This relatively rapid change was associated with an increase in plasma osteocalcin, an indicator of bone formation. Conversely, there was decrease in bone resorption. There was also estrogenic stimulation of vaginal cells which occurred in the absence of any sign of stimulatory effect on the endometrium. This is potentially of major interest for the prevention and management of menopause. In addition, the inhibitory effect of DHEA on the growth of human breast cancer grafts in mice supports the beneficial use of DHEA as hormone replacement therapy in women.
- Green tea inhibits breast cancer cell growth
Full source: BIOCHEMICAL PHARMACOLOGY, 2000, Vol 60, Iss 7, pp 937-946
Green tea preferentially inhibited the growth of human breast cancer cells compared with growth of normal breast cells. Inhibited cancer cells became smaller, and cell death was accompanied by a condensed and fragmented appearance of the DNA, suggestive of apoptosis (programmed cell death). The normal breast cells recovered from treatment, whereas growth of breast cancer cells was inhibited by green tea at concentrations as low as 1 mu M given twice per day. At dosages of 50 mu M, the cancer cells and did not recover at all.
- Green tea vs. liver tumors
Full source: CARCINOGENESIS, 2000, Vol 21, Iss 9, pp 1671-1676
Treatment to increase the activity of gap junctional intercellular communication (GJIC) is important in preventing tumor promotion. A study explored the potential preventive effects of green tea against the cancer promoting action of a carcinogen in mouse liver cancer development. They examined whether drinking green tea prevents the lowered activity of GJIC inhibition in the liver caused by the carcinogen. Mice were given a green tea for 1 week and then the carcinogen in the diet for the following two weeks, along with green tea treatment. The result showed that a dose-related decrease of GJIC in the liver cells was evident in the mice treated with the carcinogen alone, and was associated with a reduction in plaques in the plasma membrane and an increase in cell proliferation index. However, drinking green tea significantly protected mice against the reduction in GJIC, the reduction in plaques and the elevation of the cell proliferation index. Thus, green tea might act as an anti-promoter against liver cancer development by its ability to prevent the decrease of GJIC activity.
- DHEA and melatonin vs. anthrax toxin production
Full source: CELL BIOLOGY AND TOXICOLOGY, 2000, Vol 16, Iss 3, pp 165-174
Low levels of the lethal toxin from anthrax bacteria are known to induce release of cytokines (proteins) such as tumor necrosis factor alpha (TNF-alpha). A study investigated the effect of dehydroepiandrosterone (DHEA) or melatonin on production of lethal toxin-induced TNF-alpha in macrophages (immune cells). Results showed that treatment with DHEA significantly inhibited the TNF-alpha production caused by anthrax lethal toxin. Exposure of melatonin to anthrax lethal toxin-treated macrophages also decreased the release of TNF-alpha to outside the cell as compared to the control group. The results suggest that DHEA and melatonin may have a therapeutic role in reducing the increased cytokine production caused by the lethal anthrax toxin.
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