Life Extension Magazine®

Issue: Sep 1998

Vascular Disease & Atherosclerosis

Studies from throughout the world that can help you live longer, including how genistein-soy diets and vitamin C can improve your health.




LEF Magazine September, 1998


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Table Of Contents


    Genistein, vascular disease and atherosclerosis
  1. S. Kapiotis, M. Hermann, I. Held, C. Seelos, H. Ehringer, B.M.K. Gmeiner Arteriosclerosis Thrombosis and Vascular Biology, 1997, Vol 17, Iss 11, pp 2868-2874

    There is now growing evidence that the oxidative modification of LDL plays a potential role in atherosclerosis. In this study, genistein, a compound derived from soy with a flavonoid chemical structure, has been evaluated for its ability to act as an LDL antioxidant and a vascular cell protective agent against oxidized LDL. Results showed that genistein was able to inhibit the oxidation of LDL in the presence of copper ions or superoxide/nitric oxide radicals. Human endothelial cell-mediated LDL oxidation was also inhibited in the presence of genistein. In addition to its antioxidative potential during LDL oxidating processes, genistein effectively protected vascular cells from damage by oxidized lipoproteins. Genistein was found to block upregulation of two tyrosine-phosphorylated proteins in endothelial cells induced by oxidized LDL. These findings support the suggested and documented beneficial action of soy in preventing chronic vascular diseases and early atherogenic events.



    Genistein inhibits bone loss
  2. M. Yamaguchi, Y.H. Gao, Biochemical Pharmacology, 1998, Vol 55, Iss 1, pp 71-76

    This study investigated the effect of genistein on bone resorption (assimilation) in vitro. Bone tissues were obtained from elderly female rats. The bone-resorbing factors parathyroid hormone (PTH), prostaglandin (PGE), and lipopolysaccharide caused a significant decrease in bone calcium content. However, the decrease in bone calcium content induced by these bone-resorbing factors was inhibited completely by genistein. In addition, this isoflavonoid completely inhibited the PTH or PGE-induced increase in medium glucose consumption and lactic acid production by bone tissues. Also, genistein blocked both PTH-increased acid phosphatase and decreased alkaline phosphatase activities of bone tissues. On the other hand, Tamoxifen, an anti-estrogen reagent, clearly prevented the inhibitory effect of genistein on PTH-stimulated bone resorption. These findings indicate that genistein has a direct inhibitory effect on bone resorption in tissue culture.



    Vitamin C in mammals
  3. W. Ficek. Biochemical Archives, 1997, Vol 13, Iss 4, pp 207-213

    Vitamin C (ascorbic acid) is an essential component of every living cell. In mammals that cannot synthesize vitamin C, intake is of paramount importance to various stages of physiological processes. Vitamin C (a) has a beneficial effect on collagen synthesis, which is essential to cell growth and regeneration, (b) facilitates the healing of wounds via cell regeneration, (c) lowers the cholesterol level by increasing the elimination of cholesterol from the intestines via bile, thus preventing ischemic heart disease, (d) enhances the absorption of iron in the digestive tract and influences the production of erythrocytes, (e) prevents scurvy, and (f) absorbs free radicals, which are responsible for many diseases, including neoplastic and heart diseases as well as the aging of cells and the body.



    Vitamin C vs. newborn malformation
  4. Diabetologia, 1997, Vol 40, Iss 12, pp 1416-1424

    An excess of reactive oxygen species (free radicals) has been associated with the increased rate of congenital malformations in experimental diabetic pregnancy. Studies have shown that antioxidants can protect the embryonic development in a diabetic environment. The capacity of vitamin C as an antioxidative agent and dietary supplement in diabetic pregnancy was investigated. Vitamin C treatment reduced the rates of late resorptions and malformations in the diabetic groups in proportion to the dose administered. Vitamin C treatment caused accumulation of ascorbic acid in the placenta, and in maternal and fetal liver. Vitamin C supplementation yielded increased alpha- tocopherol concentration in the placenta and caused a reduction of the high concentrations of thiobarbituric acid reactive substances in the serum of pregnant diabetic rats. Thus, vitamin C treatment reduced the rates of congenital malformations and late resorptions, thereby supporting the proposition that free radicals are involved in the embryonic dysmorphogenesis (abnormal development of tissue) of diabetic pregnancy.



    Diminished GH secretion in aging humans
  5. J.D. Veldhuis, A. Iranmanesh, A. Weltman, Endocrine, 1997, Vol 7, Iss 1, pp 41-48

    Remarkable decreases in growth hormone (GH) secretion accompany healthy aging. There are concurrent changes in body composition (with increased fat), physiological declines in estrogen and androgen concentrations, differences in gender responses to aging, and alterations not only in the quantity of GH secreted, but also in the orderliness or regularity of the GH release process. In addition, physical fitness or aerobic capacity also positively modulates GH secretion. Variables such as altered sleep patterns and nutritional state may contribute to overall regulation of the GH axis in aging. Studies suggest partial growth hormone-releasing hormone (GHRH) deficiency in healthy older individuals, presumptively combined with somatostatin excess, and disruption of the moment-to-moment pattern of coordinated and orderly GH release. The full article reviews these selected facets of recent experimental evaluation of human GH insulin-like growth factor-I in aging humans.



    Sunscreen ingredients cause DNA damage
  6. R. Dunford, A. Salinaro, L.Z. Cai, N. Serpone, S. Horikoshi, H. Hidaka, J. Knowland FEBS Letters, 1997, Vol 418, Iss 1-2, pp 87-90

    Titanium dioxide (TiO2) is a safe sunscreen because it reflects and scatters UVB and UVA in sunlight. However, TiO2 absorbs about 70 percent of incident UV, and in aqueous environments this leads to the generation of hydroxyl radicals that can initiate oxidation. The full study shows that all the sunscreen TiO2 samples tested cause the photo-oxidation of a representative organic substrate (phenol)and that sunlight-illuminated TiO2 causes DNA damage both in vitro and in human cells.



    Ginkgo extract prevents mitochondrial aging
  7. J. Sastre, A. Millan, J.G. delaAsuncion, R. Pla, G. Juan, F.V. Pallardo, E. O'Connor, J.A. Martin, M.T. DroyLefaix, J. Vina, Free Radical Biology and Medicine, 1998, Vol 24, Iss 2, pp 298-304

    This study found that mitochondrial DNA from the brains and livers of older rats exhibited oxidative damage that was significantly higher than that found in mitochondrial DNA from young rats. Mitochondrial glutathione is also more oxidized in old than in young rats, and peroxide formation in mitochondria from old animals was higher than in those from young ones. According to morphological parameters (size and complexity), there are two populations of mitochondria. One is large, highly complex mitochondria, and the other population is smaller and less complex. Brains and livers from old animals had a higher proportion of the large highly complex mitochondria than from young animals. Treatment with the Ginkgo biloba extract partially prevented these morphological changes as well as the indices of oxidative damage observed in brain and liver mitochondria from old animals.




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