 | April 11, 2008 | | | | An article published online on April 7, 2008 in the Proceedings of the National Academy of Sciences reported that human cells grown in a magnesium deficient environment undergo accelerated senescence (aging). Studies have indicated that increased cellular senescence can lead to tissue damage and promote the development of diseases associated with aging. Aging-related diseases, including cardiovascular disease, hypertension, diabetes, osteoporosis, and some cancers have all been linked with magnesium inadequacy, a condition that is estimated to affect half of the population in the United States. David W. Killilea and Bruce N. Ames, PhD of Children’s Hospital Oakland Research Institute in California cultured human fibroblasts, which are cells that provide a structural framework for many tissues, in magnesium deficient media to which magnesium was added to provide 13 percent, 50 percent or 100 percent of the magnesium level in normal human serum. Although there was no decrease in cell viability, cells in the reduced magnesium media appeared to undergo accelerated senescence. An increased loss of population doublings was shown to be associated with decreased magnesium exposure, as well as an increase in beta-galactosidase activity, which is a senescence-associated biomarker. The deficient cells also underwent an increased loss of telomere length compared with cells cultured in normal magnesium conditions. Telomeres are DNA sequences that cap the ends of chromosomes, which shrink with age. Telomere malfunction has been associated with aging and the development of cancer. According to the authors, the mechanism supporting magnesium deficiency’s effect on cellular senescence may involve an increase in oxidative stress levels which damages telomeres. Supplemental antioxidant vitamins C and E, as well as niacinamide have all been shown to slow telomere shortening in human cell cultures. “The long-term consequence of inadequate magnesium availability in human fibroblast cultures was accelerated cellular senescence,” Drs Killilea and Ames conclude, “which may be a mechanism through which chronic magnesium inadequacy could promote or exacerbate age-related disease.” | |  |  | | Multiple studies recommend that people who have high blood pressure (or who are at risk of developing it) maintain an adequate intake of magnesium (Touyz RM et al 2004). In recent years, researchers in Japan have been focusing on the benefits of magnesium because magnesium intake has diminished in Japan as the traditional Japanese diet of seafood and vegetables is being replaced by a diet high in fat and animal products (Kumeda Y et al 2005). Researchers have found that: - Magnesium is necessary for the activity of chemicals that lower cholesterol in the body, which contributes to its ability to fight atherosclerosis and endothelial dysfunction (Inoue I 2005).
- Women taking magnesium supplements have a significantly lower risk of developing metabolic syndrome (Song Y et al 2005).
- A diet low in magnesium is associated with a potassium deficiency, which alters the balance of sodium and potassium in favor of sodium. Also, a low magnesium level is associated with high intracellular calcium levels, which contributes to vasoconstriction and high blood pressure (Rosanoff A 2005). The author of this study recommended long-term, adequate intake of magnesium to ensure a healthy balance of potassium to sodium and of magnesium to calcium.
For people who are taking diuretics or have kidney problems, retaining an adequate amount of magnesium in the body is more difficult. Most Americans get far less magnesium from their diets than they need, so supplementation is a good option. There is some evidence that magnesium improves insulin sensitivity, which decreases the risk of developing high blood pressure (Guerrero-Romero F et al 2004). Another study showed that taking magnesium along with beta blockers significantly reduced blood pressure compared to taking beta blockers alone (Wirell MP et al 1994). | Events: The Prostate Cancer Conference 2008
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September 6-7, 2008 The Prostate Cancer Conference 2008 is the 10th major conference devoted to prostate cancer, planned and/or produced by members of The Prostate Cancer Research Institute. As in the past, this conference will provide insight for patients, caregivers and medical professionals. The conference faculty is composed of physicians and scientists who are experts in prostate cancer. http://www.prostate-cancer.org/events/conf2008/index.html | |  |   | | Internally produced antioxidants—including the enzymes superoxide dismutase (SOD) and catalase—are the body's primary defense against free radical assault, offering up to thousands of times more protection against certain dangerous free radicals than dietary antioxidants. The body's supply of youthful antioxidant enzymes such as SOD rapidly decreases with age. Fortunately SODzyme™ with GliSODin® and Wolfberry combines three advanced SOD catalysts to replenish the body's supply of SOD, vastly enhancing its natural antioxidant defenses. | | | 5-Loxin®  | | Scientific studies show that, along with normal aging, excess arachidonic acid ignites a biochemical cascade that increases levels of the 5-lipoxygenase (5-LOX) enzyme, which can induce undesirable effects in cells throughout the body. This cascade culminates in the excess accumulation of leukotriene B4, a proinflammatory compound that attacks the joints, the arterial wall, and other tissues. In India, extracts from the Boswellia plant have been used for centuries as anti-inflammatory agents. Recent human studies have confirmed that a specific Boswellia extract known as AKBA (3-O-acetyl-11 keto-ß-boswellic acid) selectively inhibits 5-LOX. Unlike other boswellic acids that only partially inhibit 5-LOX,2,3 AKBA binds directly to 5-LOX, effectively suppressing its pro-inflammatory activity. | | | |  | | Life Extension Update | | What's Hot | | Life Extension magazine | |
