Life Extension Magazine®

Issue: Oct 1998

Life Extension Magazine October 1998

Studies from around the world that can help you live longer, including controlling iron absorption and boosting cardiac output.

Scientifically reviewed by: Dr. Gary Gonzalez, MD, in January 2021. Written by: Life Extension Editorial Staff.

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Medical Updates succinctly review studies that are of importance to those seeking an extended lifespan. The complete scientific abstracts for these studies are available as a special service to Life Extension Foundation members. If you read here about new studies you want to learn more about or want to show to your doctor, send a self-addressed, stamped envelope to the: Life Extension Foundation, P.O. Box 229120, Hollywood, Fla., 33022, USA.

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Table Of Contents

    Controlling iron absorption
  1. Full Source:The American Journal of Clinical Nutrition (1998; 68:3-4)

    Iron is a catalyst for the generation of free radical activity that has been identified as an underlying cause of cancer, atherosclerosis, liver cirrhosis, neurologic disease and other aging-related disorders. Many people have too much iron in their bodies. If a blood test reveals your serum iron level to be over 100 micrograms per deciliter, it would be desirable to lower iron to under the 100 mark. A practical way of lowering iron is to interfere with its absorption from food. One study showed that if 300 mg of calcium is taken with a meal, the amount of iron absorbed would be reduced by 40%. That's a simple and inexpensive way to reduce iron in the blood. This is especially important for hepatitis C patients who suffer liver cell damage when the hepatitis virus interacts with iron. In order to obtain 300 mg of calcium, it is necessary to take a calcium supplement that supplies 300 mg of elemental calcium. Three capsules of Mineral Formula for Women provides over 300 elemental milligrams of calcium. According to the published studies, the maximum amount of calcium that will inhibit iron absorption is 300 mg with each meal. Amounts of calcium greater than 300 mg do not cause any additional interference with iron absorption. On the other hand, if you are iron-deficient, avoid taking calcium with meals since the calcium will block iron absorption. In cases of iron deficiency, take calcium at night, but not with foods high in fiber.

    Boosting cardiac output
  2. Full source: The American Journal of Clinical Nutrition (1998;68:3-4)

    Those suffering from congestive heart failure or cardiomyopathy are advised to consume nutrients that enhance the energy output of heart muscle cells. Clinical studies show a benefit when patients take 100 to 300 mg a day of coenzyme Q10, 2,000 mg a day of carnitine, and 3,000 mg a day of taurine. Other studies show that fish oil improves cardiac mechanical function. In one study, fish oil or corn oil was tested on 234 healthy humans for seven weeks. Echocardiography showed improved left ventricular function in the fish oil group but not in the corn oil group. Other hemodynamic measurements indicated that fish oils have cardioprotective effects beyond lowering triglyceride levels and preventing abnormal arterial blood clot formation (thrombosis). In order to obtain the cardiac cell energy-enhancing effects shown in the most recent study, it would be necessary to take between six and 10 capsules of a supplement called Mega EPA, which contains 2.33 times more of the essential fatty acids EPA and DHA than conventional fish oil supplements. With conventional fish oil capsules, many more capsules would be required.

    NAC inhibits nitric oxide induction
  3. Full source:K. Pahan, F.G. Sheikh, A.M.S. Namboodiri, I. Singh, Free Radical Biology and Medicine, 1998, Vol 24, Iss 1, pp 39-48

    This study underscores the importance of N-acetylcysteine (NAC), a potent antioxidant, in inhibiting the induction of nitric oxide (NO) caused by lipopolysaccharides (molecules in which lipids and polysaccharides are linked) and cytokines (proteins that regulate the intensity and duration of immune responses and are involved in cell-to-cell communication). The production of NO was induced to different degrees by interleukin-1 beta, interferon-gamma, and tumor necrosis factor alone or in combinations. NAC, when added two hours earlier along with these stimuli, potentially blocked the increase in NO production in macrophages, astrocytes and glial cells. The degree of inhibition decreased progressively with the increase in time interval when NAC was added after the addition of the lipopolysaccharides. Besides blocking NO, NAC also blocked the production of tumor necrosis factor in rat peritoneal macrophages activated with endotoxin. These results suggest that expression of oxide synthase activity and tumor necrosis factor in macrophages does involve oxygen radicals, and that NAC may control the various harmful effects of cytokines released by activated macrophages and glial cells.

    NAC reduces lung injury
  4. Full source: C.J. Davreux, I. Soric, A.B. Nathens, R.W.G. Watson, I.D.. McGilvray, Z.E. Suntres, P.N. Shek, O.D. Rotstein, Shock, 1997, Vol 8, Iss 6, pp 432-438

    The development of the adult respiratory distress syndrome (ARDS) in critically ill patients is associated with significant morbidity and mortality. The pulmonary dysfunction in ARDS is largely secondary to neutrophil-mediated oxidant injury. This study examined the effect of the antioxidant N-acetylcysteine (NAC) on a rodent model of lung injury. NAC administration significantly reduced increases in lung permeability and reduced the LPS-dependent increase in lipid peroxidation caused by the endotoxin lipopolysaccharide (LPS). Neutrophil activation was significantly downregulated by NAC. Importantly, NAC administration up to two hours after endotoxin challenge was still able to significantly ameliorate LPS-induced lung injury. These data suggest that the reduction of acute lung injury by NAC in this rodent model is related to free radical scavenging and inhibition of the neutrophil oxidative burst, rather than by an effect on inflammatory cell migration.

    Curcumin inhibits kidney cell injury
  5. Full source: H.H.P. Cohly, A. Taylor, M.F. Angel, A.K. Salahudeen, Free Radical Biology and Medicine, 1998, Vol 24, Iss 1, pp 49-54

    Cell injury by oxidative stress is an important mechanism for renal (kidney) epithelial cell destruction. Curcumin has been shown to possess potent antioxidant properties. This study observed the protective effect of curcumin and its constituents on hydrogen peroxide-induced injury. Curcumin gave as much protection as did vitamin E in inhibition of lipid peroxidation. These findings support evidence that curcumin provides protection against oxidative stress in a kidney cell line.

    Antioxidant compounds in broccoli
  6. Full source: G.W. Plumb, K.R. Price, M.J.C. Rhodes, G. Williamson, Free Radical Research, 1997, Vol 27, Iss 4, pp 429-435

    This study examined the antioxidant activity of the major phenolic compounds in broccoli: quercetin, kaempferol, and four hydroxycinnamic acid esters. The antioxidant capacity and inhibition of iron/ascorbate-induced lipid peroxidation of phosphatidylcholine vesicles were measured. Quercetin was a potent inhibitor of lipid peroxidation. The hydroxycinnamic acid esters were highly effective at preventing lipid damage. The six compounds analyzed demonstrate the antioxidant activity of the major phenolics in broccoli.

    Pycnogenol enhances antioxidant defenses
  7. Full source: Z.H. Wei, Q.L. Peng, B.H.S. Lau, Redox Report, 1997, Vol 3, Iss 4, pp 219-224

    Reactive oxygen species (ROS), or free radicals such as hydrogen peroxide (H2O2), superoxide anion (O2-), and hydroxyl radical (OH) have been implicated in mediating various pathological events such as cancer, atherosclerosis, diabetes, ischemia, inflammatory diseases, and the aging process. Glutathione and antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) play important roles in scavenging ROS and preventing cell injury. Pycnogenol has been shown to protect endothelial cells against oxidant-induced injury. This study determined the effects of pycnogenol on cellular metabolism of H2O2 and superoxide anion O2-, and on glutathione-dependent and independent antioxidant enzymes in bovine pulmonary artery endothelial cells (PAEC). Oxidative stress was triggered by H2O2. Pycnogenol caused a concentration-dependent enhancement of H2O2 and O2- clearance. It increased intracellular glutathione content and the activities of glutathione peroxidase and glutathione disulfide reductase. It also increased the activities of SOD and CAT. The results suggest that pycnogenol promotes a protective antioxidant state by upregulating important enzymatic and nonenzymatic oxidant scavenging systems.

    Dietary fish oil increases survival
  8. Full Source:S. Bjornsson, I. Hardardottir, E. Gunnarsson, A. Haraldsson, Scandinavian Journal of Infectious Diseases, 1997, Vol 29, Iss 5, pp 491-493

    The effect of dietary fish-oil supplementation on the survival of mice after a pneumonia infection was investigated. Thirty mice in each group were fed a fish-oil enriched diet, olive-oil enriched diet, or standard chow diet. After 6 weeks, the mice were injected intramuscularly with pneumonia. After 120 hours, the survival of the mice fed the fish-oil enriched diet was 40 percent, while the survival for mice fed the standard or olive-oil enriched diets was 20 percent and 25 percent respectively. Survival over 120 hours was significantly improved for mice fed a fish-oil enriched diet, compared with the survival curves for mice fed the other two diets. The study was repeated by comparing the survival of mice fed a fish-oil enriched diet with those given a corn-oil enriched diet. After 120 hours the survival curve for mice fed the fish-oil enriched diet was significantly better, compared with the survival curve for mice given the corn-oil enriched diet. A fish-oil enriched diet, therefore, increases survival in mice following Klebsiella pneumoniae infection, whether compared with a standard diet, olive-oil enriched diet or corn-oil enriched diet.

    Smoking, dementia, and Alzheimer's disease
  9. Lancet, June 20, 1998

    Alzheimer's disease is widespread. Memory loss is one of the first symptoms of the di sease. In the final stages of the illness, sufferers may not recognize the faces and names of their closest friends and relatives. Although there is no cure for Alzheimer's disease, drugs can reduce some of the symptoms. Previous studies suggested a protective effect of smoking on Alzheimer's disease, but the results of this study challenge this finding. In a population-based follow-up study of 6,870 people aged 55 years and older, it was found that smoking doubled the risk of dementia and Alzheimer's disease. The onset of the illness also occurred about four years earlier in smokers. Smoking not only increases the chances of getting the most common form of senile dementia, but it could also bring it on at a younger age. The researchers examined whether age, sex, and the apolipoprotein (APO) genotype modified this risk. There are five families of apolipoproteins, designated A-E. Only one form of the gene (APO-E4) had an effect on risk; carriers of this form of the gene were not at increased risk of dementia, which suggests an interaction between the APO-E4 genotype and smoking in the cause of Alzheimer's disease. Smokers who carry the gene were no more likely to develop the disease than were non-smokers. The researchers are not sure why APO-E4 protects smokers, but they think the nicotine in cigarettes may alter brain chemistry to counterbalance the effects of Alzheimer's disease.

    From the Foundation:
    Diet, exercise, dietary supplements, and lifestyle can significantly lower the risk for Alzheimer's disease. For example, those in Japan who follow the traditional Japanese diet and lifestyle have a very low rate of Alzheimer's disease, but when these people immigrate to the U.S. and assume the Westernized diet and lifestyle, their Alzheimer's disease rate increases to that of other U.S. citizens. This fact, in itself, is very strong evidence that we do have control over the risks for Alzheimer's disease.

    Mammography benefits women under 50
  10. Cancer 1998; 82:2221-2226

    A breast cancer study that compared tumor detection and survival rates in younger and older women provides evidence that women under age 50 should get regular mammograms. According to the study, clinical breast exams alone may not detect growing tumors early enough. Researchers have disagreed on the benefits of mammography for younger women. While the technique has clearly improved breast cancer survival rates for women over 50, the benefits are not as clear for younger women, whose denser breast tissue makes the scans less effective at locating small tumors. This study compared the tumor sizes and survival rates of women whose tumors were first found by a mammogram with those women whose tumors were initially located by a conventional breast exam. Of 869 women, 37% had been diagnosed with breast cancer by a mammogram, and 63% had their tumors detected by a doctor during a breast exam. The researchers at the University of Chicago compared the average size of the tumors in women younger than and older than 50. Tumor size is important, since the likelihood of successfully treating cancer and preventing recurrence is much higher if the tumor is detected early on, while it is still small. For women whose tumors were detected by mammography, they found that women (of all ages) were first diagnosed when their tumors were about 1 centimeter in size. However, for women whose tumors were first found by clinical exam, there was a substantial difference in tumor size between younger and older women. The average size of clinically detected tumors for women over 50 was 1.5 cm. For women under 50, average tumor size at detection was 2 cm, indicating that "if left to grow to the size necessary for clinical detectability, the tumors are larger and more aggressive in younger women." These results translate into comparable 5-year survival rates. There was no difference in survival rates between younger and older women whose tumors had been detected by mammogram. For patients with clinically detected tumors, though, women under age 50 had a 77% 5-year survival rate, much lower than the older women's 87% survival rate. They suggest that from an individual young woman's perspective, the benefits of mammography are stronger than the drawbacks.

    Mammograms detect tumors much earlier in younger women, and the damage is much more dramatic if they aren't detected. The lead researcher said that, based on this research, she would recommend her own patients have a yearly mammogram after age 40, which is also the policy of the American Cancer Society.

    RNA fights brain tumors in rats
  11. Nature Biotechnology 1998; 16:556-560

    By using a genetically engineered small portion of RNA, researchers have found a way to inhibit the growth of aggressive brain tumor cells in rats. Such aggressive brain tumors, known as malignant gliomas, are the third leading cause of death from cancers in people aged 15 to 34. These tumors often fail to respond to radiation or chemotherapy, and scientists have been searching for new ways to fight the cancer. The genetically engineered RNA molecule, known as a ribozyme, attacked the production of an enzyme that spurs the growth of the glioma cells. RNA is key to translating genetic information into a functioning enzyme. The ribozyme however, binds to and destroys the RNA, effectively halting the production of Cthe enzyme, known as PKC alpha. Researchers injected glioma cells into rats, a process that causes tumors to form. The tumors were then injected with either an inactive substance, or the modified ribozyme. Twenty days after treatment, rats which received the inactive substance had tumors that weighed an average of 14 grams, while rats which received the modified ribozyme had tumors that shrunk to an average of 0.25 grams. Similar ribozymes have been used in past studies to treat rat tumors, but the ribozymes could be degraded by enzymes found in the body, and thus were limited as a potential treatment.