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Life Extension Magazine

LE Magazine June 2001

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Studies from throughout the world that can help you live longer

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June 2001 Table of Contents

  1. Vitamin E succinate promotes breast cancer tumor dormancy
  2. Silymarin exhibits anti-cancer effects
  3. Anti-tumor effects of soybean on the breast tumors
  4. Melatonin + Interleukin (IL-2) prolongs cancer survival
  5. Effect of selenium combination therapy on cancer
  6. Vitamin E supplementation improves LDL oxidation
  7. Vitamin A may help prevent breast cancer
  8. Infections may lead to heart attacks
  9. Fat, not calcium responsible for heart attacks
  10. Eating whole grains may protect against disease
  11. Effect of alcohol on nutrients
  12. Curcumin, genistein, quercetin and cisplatin and oral cancer
  13. Tumor size after surgery predicts recurrence
  14. Physical activity and mortality in men with heart disease
  15. Antiatherogenic action of vitamin C and E
  16. Caloric restriction of monkeys lowers free radical damage
  17. Effect of NAC on free radical stress and brain lesions
  18. Generation of free radicals after exhaustive exercise

1. Vitamin E succinate promotes breast cancer tumor dormancy

Vitamin E succinate (VES) is the most potent anti-tumor form of vitamin E in culture. A study investigated the effect of VES on the growth of human breast cancer cells in the body. The results showed that VES decreased cancer cell viability and increased human breast cancer cell death. VES was found to inhibit vascular endothelial growth factor (VEGF) gene activity in breast cancer cells. Thus, VES inhibits the growth of breast cancer cells in culture and in the body. This is the first report of VES inhibition of established tumor growth in the body. The mechanism of VES's effects in the body may involve inhibition of tumor angiogenesis (development of blood vessels) since VES inhibits VEGF gene activity.

JOURNAL OF SURGICAL RESEARCH, 2000, Vol 93, Iss 1, pp 163-170


2. Silymarin exhibits anti-cancer effects

Silymarin, a naturally occurring flavanoid antioxidant, exhibits anti-cancer effects against several cancers. A study assessed its potential as an anti-angiogenic agent with human umbilical vein cells (HUVC), prostate, and breast cancer cells. When HUVC were treated for 48 hours, cells that stuck together decreased by 50 and 90% at 50 and 100 mu g/ml doses, respectively. A 5 to 6 hour exposure of prostate and breast cancer cells to silymarin resulted in a dose-dependent decrease in the epithelial growth factor (protein) level in as early as 1 hour without any visible change in cell structure. This indicates a rapid inhibitory action of silymarin on the secretion of this primary angiogenic protein by cancer epithelial cells. Thus, the results show that silymarin possesses an anti-angiogenic ability that may critically contribute to its cancer chemopreventive efficacy.

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2000, Vol 276, Iss 1, pp 371-378


3. Anti-tumor effects of soybean on the breast tumors

Soybeans are reported to have cancer inhibitory effects, probably due to their isoflavones. Soybean hypocotyls are embryo buds of soybeans and contain a higher amount of isoflavones and other factors than soybeans themselves. The effects of soy protein isolate (SPI), 1.5% and 5% soybean hypocotyls as diets on the development of induced tumors were examined in 120 female rats for 6 weeks. Results showed that tumor development of the SPI diet group and the hypocotyl diet groups was less than that of the milk protein (control) diet group. Tumors were detected in 9 out of 24 rats in the control diet group, 5 of 20 in SPI diet group, 6 out of 24 in the 1.5% hypocotyl diet group and 6 out of 23 in the 5% hypocotyl diet group. However, the formation of tumors was significantly less rapid in the SPI diet group and the hypocotyl diet groups than the milk group. No difference in tumor promotion was observed between the SPI diet group and the soybean hypocotyl diet groups. The results show that dietary soybeans and soybean hypocotyls are capable of suppressing tumor promotion.

ANTICANCER RESEARCH, 2000, Vol 20, Iss 3A, pp 1439-1444


4. Melatonin + Interleukin (IL-2) prolongs cancer survival

Interleukin-2 (IL-2) has proven to be able to generate an effective anticancer immunity against both solid and blood malignancies. A study of 12 individuals evaluated the efficacy and tolerability of a combination of low-dose IL-2 plus the pineal hormone melatonin (MLT) in advanced malignancies of the blood, including non-Hodgkin's lymphoma, Hodgkin's disease, multiple myeloma, acute and chronic leukemia which did not respond to previous standard therapies. IL-2 was given for six days per week for four weeks. Melatonin was given orally at 20 mg/day. Cancer was stabilized and did not progress in 8 out of 12 (67%) individuals, with an average duration of 21 months and was well tolerated. The results show that the combined administration of low-dose IL-2 plus melatonin may prolong the survival time in untreatable advanced blood cell malignancies. The results were comparable to those previously reported using a more toxic immunotherapy, consisting of high-dose IL-2 alone.

ANTICANCER RESEARCH, 2000, Vol 20, Iss 3B, pp 2103-2105


5. Effect of selenium combination therapy on cancer

A study examined the additive or synergistic effect of selenium alone and in combination with standard anti-cancer drugs, Adriamycin (Doxorubicin) and Taxol, on various tumor cells after 72 hours. Results demonstrated that breast, lung, small intestine, colon and liver cells showed an increase in apoptosis (cell death). In contrast, prostate and colon were not significantly affected by selenium alone. However, the addition of Adriamycin or Taxol in combination with selenium caused small but significant inhibition of prostate cancer cells as well as further inhibition of breast, lung, small intestine and liver cells. Thus, selenium has a significant anti-cancer effect on breast, lung, liver and small intestinal tumor cells. Supplementation with selenium enhanced the chemotherapeutic effect of Taxol and Doxorubicin in these cells beyond that seen with the chemotherapeutic drugs used alone.

ANTICANCER RESEARCH, 2000, Vol 20, Iss 3A, pp 1391-1414


6. Vitamin E supplementation improves LDL oxidation

Vitamin E as an antioxidant vitamin reduces the susceptibility of low-density lipoprotein (LDL) cholesterol to oxidation and may have antiatherosclerotic (arterial plaque buildup) effects. A study tested the hypothesis that six months of 400 mg vitamin E supplementation favorably affects early functional changes in atherosclerotic process in men with hypercholesterolemia (excess of blood cholesterol). After the intervention period, the dilation of the veins in the arm increased significantly in the vitamin E group while it did not change in the placebo group. Thus, six months of oral vitamin E supplementation results in improvement in vasodilatation in men with hypercholesterolemia.

PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 2000, Vol 440, Iss 5, Suppl. S, pp R126-R128


7. Vitamin A may help prevent breast cancer

A gene that is believed to stop tumors from growing has been found to be switched off in several types of tumors, including breast cancer. A new treatment that includes a form of vitamin A may help prevent or treat cancer by reactivating the gene that suppresses the tumor. A study looked at the effects of a retinoid on breast cancer cells. Retinoids, derivatives or analogs of vitamin A, being of similar structure, are thought to interact with this gene, Researchers hypothesized that the tumor-suppressing gene was deactivated by a process called methylation. Methylation is the process of putting a methyl group (one carbon atom and three hydrogen atoms), on proteins, enzymes, chemicals, DNA or amino acids like homocysteine. When a methyl group is transferred from folic acid to homocysteine, the homocysteine is converted to the essential amino acid, methionine. When a methyl group is transferred from TMG to homocysteine, the homocysteine is similarly converted to methionine (and TMG is converted to dimethylglycine). This process of methylation results in lower homocysteine and an increase in methionine. Methylation helps regulate the switching on and off of genes, which is one of the most crucial regulators of health and life itself. Researchers then treated several types of breast cancer cells with a substance that reverses this process, a demethylating agent. Then the cells were exposed to the retinoid. The results showed that in several of the 16 varieties of breast cancer cells tested, the tumor suppressor gene was reactivated. In other breast cancer cells, where the gene was already activated before the treatment, the activity increased. In other types of cells, the activation of the gene either did not increase or did not occur at all, according to the report. In another experiment, they found that the activation of the gene was linked with cancer, and the genes were switched off in six of the eight tumors studied. Later-stage tumors were more likely to have the gene switched off as well. Drugs that reverse the methylation process have been beneficial in animals with cancer.

Journal of the National Cancer Institute 2000; 92:780-781, 826


8. Infections may lead to heart attacks

A recent five year study of 826 men and women (40 to 79) provides strong evidence that chronic bacterial infection is a risk factor for atherosclerosis. Only bacterial infections, such as lung and urinary tract infections, as well as gum disease, not infections caused by viruses like cytomegalovirus, the herpes zoster virus, or hepatitis B or C, increased the risk of artery disease. Results showed that people with chronic bacterial infections were 2.78 times more likely (41%) to develop new plaques in carotid arteries (large arteries in the neck, delivering blood to the brain). This build-up of plaque (fat) can increase the risk of stroke, and is a sign that heart arteries may be clogged. Those with infections who also had high levels of inflammation tended to have a greater risk of atherosclerosis, as well. However, not all infections were linked to an increased risk of atherosclerosis. Infections were more common in heavy smokers and drinkers, older people and individuals of low socioeconomic status. The researchers suspected that bacterial infections might trigger the immune system to turn against itself (autoimmune response), which may damage vessels, and make it easier for fatty deposits to accumulate. The use of antibiotics to fight chronic infections, and hopefully prevent atherosclerosis is being tested in clinical trials. In the meantime, taking steps to reduce the risk of developing chronic infections include improving oral health, eating a healthy diet and not smoking.

Circulation 2001; 103:1064-1070


9. Fat, not calcium responsible for heart attacks

A study showed that people whose arteries are clogged with inflamed fatty plaque may be more susceptible to heart attack than those whose arteries are coated with calcium-containing plaque, because the fatty plaque is more likely to rupture and cause the formation of blood clots, which can cause heart attack and stroke. The plaques without any calcium deposits are not detectable by angiograms or CAT scans, but they are the most common cause of sudden death from a heart attack. They do not cause symptoms, such as angina, until they rupture, and then it is too late. They cannot be treated by coronary bypass procedures. While calcification may suggest a more extensive form of heart disease, it is less likely to lead to heart attack. Researchers added that it is important to identify the unstable lesions before they rupture. Several promising methods of doing this are magnetic resonance imaging (MRI) or catheter-based techniques. Thus, treatments aimed at reducing the build-up of cholesterol in the arteries may be more useful than drugs that try to reduce amounts of plaque that contain calcium deposits.

Circulation 2001; 103


10. Eating whole grains may protect against disease

Eating whole grain bread may promote longevity and protect against certain diseases, study findings suggest. Similar findings among Americans have prompted the United States Department of Agriculture to recommend that Americans “eat a variety of grains daily, especially whole grains.” In the study of nearly 34,000 Norwegian adults, those who ate the highest amounts of whole grain had a 23% reduced risk of death from heart disease, and a 21% reduced risk of death from cancer compared with people who ate little or no whole grains. “This study bolsters the whole idea that the whole grain might be good for you,” lead study author Dr. David Jacobs Jr., of the University of Minnesota in Minneapolis, told Reuters Health. Study participants reported eating anywhere from one slice of whole grain bread made with 5% whole grain flour per day, to nine slices made with 60% whole grain flour per day, Jacobs and his colleagues report in the February issue of the European Journal of Clinical Nutrition. However, people who eat a lot of whole grain products tend to lead healthier lifestyles in general. Some other factors associated with such a lifestyle may be responsible for the dip in mortality risk seen in whole grain eaters, the report indicates. The researchers did take into account the fact that whole grain eaters tend to be non-smokers, are less likely have high cholesterol and high blood pressure, and are more likely to consume less fat than those who eat less whole grain bread. However, they did not take into account fruit and vegetable intake, which may be partly responsible for the lower death risk seen in the whole grain eaters. “`The people who eat (whole grains) tend to have healthier lifestyles in general, so their diet is generally higher in fruits and vegetables and lower in red meat,” Jacobs said. “We find then that part of the benefit of the whole grain is the other things that people do with it, but part of it seems to be related to the whole grain itself.” Consumers interested in increasing their intake of whole grains should note that not all breads labeled “multi-grain” will fit the bill, Jacobs warns. “Those multi-grain breads are notorious for being lots of different kinds of refined grain, but all of them are mostly starch,” he said. There is therefore less nutritional value in these breads than if the grains were non-refined. If you really want to eat a whole grain bread, “rolled” oats, “cracked” wheat, or “steel cut” wheat or oats should be the first ingredient listed on the label, Jacobs said.

European Journal of Clinical Nutrition 2001;55:137-143.


11. Effect of alcohol on nutrients

Despite an adequate diet, alcohol can contribute to the entire group of liver diseases, mainly by generating free radicals through its metabolism. The activation of nutrients is hindered, causing changes in nutritional requirements. For example, a process impaired by liver disease is the activation of methionine (one of the essential amino acids) to S-adenosylmethionine (SAMe). So, in the presence of significant liver disease, SAMe (rather than methionine) must be supplemented. In primate studies, It weakened lesions in the mitochondria (energy producer of cell) and replenished glutathione (endogenous antioxidant). Mortality was significantly reduced in those with Child A or B cirrhosis of the liver. In addition, phosphatidylcholine depletion results from alcoholic liver disease, with serious consequences for the integrity of cell membranes. This process can be offset by polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated phosphatidylcholines made up of dilinoleoylphosphatidylcholine (DLPC), which has high bioavailability. PPC (and DLPC) opposes major toxic effects of alcohol, reduces free radical stress, and increases collagen activity, which in primates prevents septal fibrosis and cirrhosis.

ANNUAL REVIEW OF NUTRITION, 2000, Vol 20, pp 395-+


12. Curcumin, genistein, quercetin and cisplatin and oral cancer

Evidence indicates that plant derived flavonoids and other phenolic antioxidants protect against heart disease and cancer. A study evaluated the potency of three different plant phenolics: curcumin, genistein and quercetin in comparison with that of cisplatin (a cancer inhibitory drug) on growth and proliferation of human oral squamous cancer cells. Cisplatin and curcumin induced significant dose-dependent inhibition in both cell growth as well as cell proliferation. Genistein and quercetin had two-phase effect, depending on their concentrations, on cell growth as well as cell proliferation. It was concluded that curcumin is considerably more potent than genistein and quercetin, but cisplatin is five fold more potent than curcumin in inhibition of growth and DNA synthesis in oral cancer cells.

ANTICANCER RESEARCH, 2000, Vol 20, Iss 3A, pp 1733-1738


13. Tumor size after surgery predicts recurrence

Visual estimate of the percentage of cancer development is an independent predictor of prostate cancer recurrence after radical prostatectomy but remains somewhat controversial. Many pathologists do not report these measurements routinely. A study looked at the association between the visual estimate of the percentage of cancer in prostate tissue from radical prostatectomy specimens and prostate cancer recurrence rates in those who underwent radical prostatectomy. Of the 595 patients, 46 (8%) had evidence of tumor recurrence. The average percentage of cancer in the prostatectomy specimen was 11.3% in the group who did not have disease recurrence and 23.8% in the group of who did experience disease recurrence. The percentage of cancer, preoperative prostate specific antigen (PSA) levels, tumor differentiation (Gleason grade), and pathologic stage all were significant predictors of disease recurrence. The tumor stage, the Gleason score, and the percentage of cancer development were independent predictors of disease recurrence. For each 5% increase in the percentage of cancer development in the surgical specimen, there was an 11% incremental increase in the chance of tumor recurrence. Thus, the visual estimate of the percentage of cancer development in prostate tissue specimens from those who undergo radical prostatectomy is a practical, simple, and inexpensive method that provides important prognostic information after radical prostatectomy.

CANCER, 2000, Vol 89, Iss 6, pp 1308-1314


14. Physical activity and mortality in men with heart disease

A study addresses the relations between physical activity, types of physical activity, and changes in physical activity and all-cause mortality in men with established coronary heart disease (CHD). In 1992, 12 to 14 years after the initial screening (Q1) of 7,735 men (age 40-59), 5,934 (91% of available survivors (avg. age 63) provided further information on physical activity (Q92) and were followed up for 5 years; 963 had CHD (heart attack or angina). After exclusions, there were 772 men with established CHD, 131 of whom died of all causes. The lowest risks for all-cause and cardiovascular mortality were seen in light and moderate activity groups. Recreational activity of greater than or equal to 4 hours per weekend, moderate or heavy gardening, and regular walking (greater than 40 min/day) were all associated with a significant reduction in all-cause mortality. Non-sporting activity was more beneficial than sporting activities. Men sedentary at Q1 who began at least light activity by Q92 showed a 42% lower mortality rate on follow-up than those who remained sedentary. Thus, light or moderate activity in men with established CHD is associated with a significantly lower risk of all-cause mortality. Regular walking and moderate or heavy gardening were sufficient to achieve this benefit.

CIRCULATION, 2000, Vol 102, Iss 12, pp 1358-1363


15. Antiatherogenic action of vitamin C and E

The premise that oxidative stress, among several other factors, plays an important role in atherogenesis implies that the development and progression of atherosclerosis can be inhibited by antioxidants. The antioxidants vitamin C and vitamin E may protect against atherosclerosis by several mechanisms including 1) inhibition of LDL oxidation and 2) inhibition of leukocyte (immune cell) adhesion to the endothelium (cells that line the body cavities) and vascular endothelial dysfunction. Overall, vitamin C appears to be more effective than vitamin E in lessening these pathophysiological processes, most likely because of its abilities to effectively scavenge a wide range of free radicals and to regenerate vitamin E. In contrast, vitamin E can act as either an antioxidant or a pro-oxidant to inhibit or facilitate, respectively, lipid peroxidation in LDL. However, this pro-oxidant activity of vitamin E is prevented by vitamin C acting as a co-antioxidant. Therefore, an optimum vitamin C intake may help protect against atherosclerosis, and vitamin E may only be effective in combination with vitamin C.

CIRCULATION RESEARCH, 2000, Vol 87, Iss 5, pp 349-354


16. Caloric restriction of monkeys lowers free radical damage

Caloric restriction (CR) in animals slows down several age-dependent physiological and biochemical changes in skeletal muscle, including increased levels of free radical damage to lipids, DNA and proteins. In primates from 2 to 34 years old, a 4-fold increase in levels of HNE-modified proteins (measure of free radical damage) was observed in monkey skeletal muscle. Carbonyl radical levels increased 2-fold with aging. Comparing 17-23 year olds fed normally to that of age-matched monkeys subjected to caloric restriction for 10 years, levels of HNE-modified proteins, protein carbonyls, and nitrotyrosine in skeletal muscle from the CR group were significantly less than control group values. There was an accumulation of lipid peroxidation-derived aldehydes, such as malondialdehyde (a stress marker), and protein carbonyls were measured and confirmed the data. The study is the first to quantify structurally and localize the age-dependent accumulation of free radical damage in the skeletal muscle of mammals, and to demonstrate that caloric restriction lowers free radical damage in primates.

FASEB JOURNAL, 2000, Vol 14, Iss 12, pp 1825-1836


17. Effect of NAC on free radical stress and brain lesions

In rodents with brain toxicity artificially caused, there was an increase in oxidative stress in both the corpus striatum (mass of gray and white substance) and cortical synaptosomes as well as lesions in the striatum. Treatment of rats with N-acetylcysteine (NAC), a known glutathione precursor, before brain toxicity was administered protected against free radical damage. NAC treatments before toxic administration significantly reduced the size of striatal lesions. This suggests that free radical damage causes striatal lesion formation and that antioxidant treatment may be a useful therapeutic strategy against neurotoxicity and perhaps against Huntington's Disease as well.

JOURNAL OF NEUROCHEMISTRY, 2000, Vol 75, Iss 4, pp 1709-1715


18. Generation of free radicals after exhaustive exercise

A study compared biomarkers of free radical stress: lipid peroxidation, protein oxidation and total antioxidants in blood after exhaustive aerobic (AE) and non-aerobic isometric exercise (IE) in 12 participants. Results showed oxidative stress increased 14-fold with aerobic exercise compared with 2-fold with isometric exercise. Protein carbonyls increased 67% before AE, to 1 hour after AE, and 12% before and immediately after IE. The levels returned to the starting point 1 hour after IE. Lipid hydroperoxides increased 36% above rest during IE compared with 24% during AE. Free radical absorbance capacity increased 25% prior to and after AE, compared with 9%. Lipid hydroperoxides, protein carbonyls, and total antioxidants increased after both IE and AE. Greater oxygen consumption was ruled out as a mass action effect and the sole mechanism for exercise-induced free radical stress due to the different metabolic demands of aerobic and isometric exercise. Thus, evidence showed free radical stress after both exhaustive aerobic and isometric exercise.

MEDICINE AND SCIENCE IN SPORTS AND EXERCISE, 2000, Vol 32, Iss 9, pp 1576-1581



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