Life Extension Magazine®

April 1999 Medical Updates

Studies from around the world that can help you live longer.

Scientifically reviewed by: Dr. Gary Gonzalez, MD, in October 2024. Written by: Life Extension Editorial Staff.

Click here to access the complete Medical Update Archives.

Click here to access the Complete Scientific Abstracts Online.



April 1999
Table Of Contents
 
  1. DHEA significantly inhibits breast tumor growth
  2. Tomatoes prevent digestive-tract cancers
  3. Melatonin activates immune system in cancer patients
  4. Melatonin and coronary heart disease
  5. Mixed carotenoids prevent oxidative damage
  6. Melatonin may prevent/treat chronic tonsilitis
  7. Antioxidant defenses during physical exercise
  8. Selenium may help prevent atherosclerosis
  9. Selenium vs. Diabetes
  10. Selenium supplementation increases glutathione and limits arrhythmias
  11. Soy protein suppresses bone loss
  12. Dietary zinc modifies onset/severity of spontaneous diabetes
  13. Cured and broiled meat consumption cause brain tumors and leukemia in children. Vitamins reduce the risk
  14. Mitochondrial dysfunction in Parkinson disease
  15. Cellular immune responses to vitamin C supplementation in ageing humans assessed by the in vitro leucocyte migration inhibition test
  16. Could diet reduce the risk of developing Alzheimer's disease?
  17. CLA reduces arachidonic acid and prostaglandin synthesis
  18. Vitamin D3 vs. early prostate cancer
  19. Doxycycline inhibits prostate cancer cell growth
  20. Aspirin protects against heart disease

  1. DHEA significantly inhibits breast tumor growth

    Full source: Journal of the National Cancer Institute, 1998 Vol 90, Iss 10, pp 772-778

    In the mammary gland, androgens (male hormones) are formed from the precursor steroid dehydroepiandrosterone (DHEA). Clinical evidence indicates that androgens have inhibitory effects on breast cancer. Estrogens, on the other hand, stimulate the development and growth of breast cancer. This study looked at the effect of DHEA alone or in combination with a pure anti-estrogen (EM-800) on the growth of human breast cancer. Mice received either a) estrone (E-1) (an estrogenic hormone) alone, b) estrone (E-1) and EM-800, c) DHEA alone or d) DHEA in combination with EM-800. The results showed a 9.4-fold increase in tumor size in 9.5 months in mice receiving E-1 alone. Administration of EM-800 in E-1-supplemented mice led to inhibitions of up to 94% in tumor size. DHEA independently suppressed the growth of E-1-stimulated tumors by up to 80%. Administration of DHEA at the defined doses did not alter the inhibitory effect of EM-800.



  2. Tomatoes prevent digestive-tract cancers

    Full source: Proceedings of the Society for Experimental Biology and Medicine, 1998, Vol 218, Iss 2, pp 125-128

    Tomatoes have been estimated as the second most important source of vitamin C, after oranges, in an Italian population. The relationship between tomato intake and the risk of digestive tract cancers was studied using data from studies conducted in Italy between 1983 and 1992 of histologically confirmed incident cases of cancer. Allowance was made for age, sex, study center, education, smoking, alcohol drinking, and total calorie intake. There was a consistent pattern of protection for all sites. The was a 35% risk reduction for cancer of the oral cavity, pharynx, and esophagus, 57% for stomach, 61% for colon, and 48% for rectum. Previous studies have confirmed that tomato intake is significantly protective on colorectal cancer risk, even after allowance for measures of body mass index, calorie intake, and physical activity. This study confirms the Foundation's stand since 1985 on lycopene in tomatoes as a cancer preventative.



  3. Melatonin activates immune system in cancer patients

    Full source: Anticancer Research, 1998, Vol 18, Iss 2B, pp 1329-1332

    The neuroendocrine system modulates the immune response through neuropeptides and neurohormones. In this study, the pineal gland demonstrated anti-cancer properties, which include the action of its principal hormone, melatonin (MLT) on the immune system through the release of cytokines by activated T-cells and monocytes. (Cytokines are proteins such as interferon and interleukin, which regulate the intensity and duration of immune responses). Thirty-one patients with advanced solid tumors (7 gastric, 9 enteric, 8 renal, 5 bladder, 2 prostate) who either failed to respond to hemotherapy and radiotherapy or showed insignificant responses were therefore shifted to MLT therapy (10 mg/day orally for 3 months). Results showed significant differences in cytokine circulating levels before and after MLT administration. After 3 months of therapy, there were no adverse reactions to MLT. Twelve patients (39%) achieved disease stabilization with no further growth either of the primary tumor or of secondaries. They also experienced an improvement in their general well being, associated with a significant decrease of Interleukin-6 circulating levels. These findings are consistent with the hypothesis that melatonin modulates immune function in cancer patients by activating the cytokine system which exerts growth-inhibitory properties over a wide range of tumor cell types. By stimulating the cytotoxic activity of macrophages and monocytes, melatonin plays a critical role in host defense against the progression of cancer.



  4. Melatonin and coronary heart disease

    Full source: Biological Rhythm Research, 1998, Vol 29, Iss 2, pp 121-128

    Cortisol and melatonin have well known circadian rhythms, coupled to the solar day. Melatonin is secreted by the pineal gland throughout the night but not during the day. Patients with coronary heart disease (CHD) have significant depressed nocturnal melatonin secretion compared to healthy individuals. Nineteen patients with documented CHD (mean age 53) participated in this study. It was found that: a) melatonin serum concentrations at night were significantly depressed (68%) in patients with coronary heart disease in comparison to the control group, b) Cortisol values at night were significantly raised (71%) in patients with coronary heart disease in comparison to the control group. The results of this study indicate that people with coronary heart disease have atypical secretory patterns of nocturnal cortisol and melatonin secretion.



  5. Mixed carotenoids prevent oxidative damage

    Full source: FEBS Letters, 1998, Vol 427, Iss 2, pp 305-308

    Antioxidant activity of carotenoids in multilamellar liposomes were ranked by inhibition of formation of free radicals as follows: lycopene, alpha-tocopherol, alpha-carotene, beta-cryptoxanthin, zeaxanthin = beta-carotene, lutein. Mixtures of carotenoids were more effective than the single compounds. This synergistic effect was most pronounced when lycopene or lutein was present. The superior protection of mixtures may be related to specific positioning of different carotenoids in membranes. This points out the need to take supplements that provide mixed carotenoids including alpha carotene, lutein, and lycopene.



  6. Melatonin may prevent/treat chronic tonsilitis

    Full source: Neuroscience Letters, 1998, Vol 247, Iss 2-3, pp 131-134

    Tonsils have a privileged situation in the immune system in that they are in touch with the environment. Melatonin is a hormone that is influenced by the circadian environmental variations of dark-light and is a modulator of the immune system. Thirty-five children with recurrent acute tonsillitis were submitted for tonsillectomy. After a culture was taken, the B-lymphocyte decreased but were restored in the presence of melatonin and even increased above the values of the control. This process was specific for B cells and there was no occurrence for T lymphocytes or natural killer cells. Melatonin is found in the crossroads of the interaction of the microorganisms, pollens, or inert substances with the tonsillar lymphocytes in the production of the immune defenses. Further study is needed on melatonin's possible therapeutic role in tonsillar pathology.



  7. Antioxidant defenses during physical exercise

    Full source: Nutrition, 1998, Vol 14, Iss 5, pp 448-451

    Physical exercise is known to induce oxidative stress leading to the generation of free radicals. This increased generation of free radicals might lead to lipid peroxidation and tissue damage, more so under deficient/impaired antioxidant states. This study reports the role of vitamin E and selenium (Se) during exercise-induced oxidative stress in the pulmonary tissue. Vitamin E and/or Se deficiency in rats resulted in generation of free radicals in the lung tissue, indicating the onset of oxidative stress. When these animals were subjected to a single bout of exhaustive exercise, there was an additional increase in the generation of oxy-free radicals, which might eventually lead to tissue damage. However, there was no such evidence recorded in the lung tissue of vitamin E-and Se-supplemented animals, when subjected to a similar exercise program, suggesting that protection is offered by vitamin E and Se in combating oxidative stress. This confirms the need for antioxidants in the bodies of those who exercise.



  8. Selenium may help prevent atherosclerosis

    Full Source: General Physiology and Biophysics, 1998, Vol 17, Iss 1, pp 71-78

    This study compared results of three rat fed diets: (I) High fat diet (HFD), (II) HFD + selenium supplemented and (III) Controls. After three months of treatment, there were significant increases in serum cholesterol and triglycerides in HFD fed group as compared to control. However, in Se supplemented group, the levels of serum cholesterol and triglycerides were significantly less as compared to group I. Selenium-dependent glutathione peroxidase (GSH-Px) activity in the liver and the aorta increased significantly in HFD fed animals and also showed additional significant increase on the selenium supplemented group. Malonyldialdehyde (MDA) concentrations in serum, liver and aorta and the activity of nitric oxide synthase (NOS) in plasma showed significant increases in HFD fed group. However, supplementation of selenium led to a significant reduction in these levels. The important finding here is that selenium supplementation modulates the sequences that favor pathogenesis of atherosclerosis.



  9. Selenium vs. Diabetes

    Full Source: Biomedicine & Pharmacotherapy, 1998, Vol 52, Iss 2, pp 89-95

    The effect of oral administration of sodium selenite on diabetic mice was studied on the following parameters: levels of blood glucose, lipid peroxidation, glutathione (GSH), glutathione peroxidase (GPx), glutathione S-transferase (GST) activities, and blood selenium levels. Diabetes caused hyperglycemia (280% increase) with a significant increase in the malondialdehyde levels (89% in liver and 83% in blood) and GST activity (55%). There were marked decreases in GSH levels (approximately 73% in blood and 79% in liver) in the 5th week as compared to normal control animals. Treatment with sodium selenite changed these parameters to near control values in almost all cases. The results suggest that selenium plays a role in reducing the oxidative stress associated with diabetes.



  10. Selenium supplementation increases glutathione and limits arrhythmias

    Full Source: Journal of Trace Elements in Medicine and Biology, 1998 Vol 12, Iss 1, pp 28-38

    Oxygen free radicals have been implicated as a possible cause of reperfusion-arrhythmias (RA). However, the use of diverse exogenous oxyradical scavengers designed to reduce RA has given contradictory results. The aim of this study was to determine whether enhancing the activity of the main enzyme involved in peroxide elimination in cardiac cells, glutathione peroxidase, might limit RA in heart preparations by increasing their antioxidant status. Fifteen rats received a selenium-enriched diet for ten weeks (1.5 mg Se/kg diet). Control animals received a standard diet containing 0.05 mg Se/kg diet. The incidence of early ventricular arrhythmias was investigated after regional ischemia was induced by constriction of left coronary artery. Selenium-supplementation significantly increased the global selenium status of the animals. In the isolated heart preparations, the selenium supplementation induced a significant reduction of the severity of RA. This was shown by the limitation of the incidence of both ventricular tachycardia (control = 91% vs. selenium = 36%, and irreversible ventricular fibrillation (control = 45% vs. selenium 0%. These effects were associated with a significant increase in cardiac mitochondrial and glutathione peroxidase activities in the heart.

    These results illustrate the potential protective effect of selenium against ischemia-reperfusion injury and suggest that peroxides might play an essential role in the genesis of some aspects of the reperfusion syndrome.



  11. Soy protein suppresses bone loss

    Full Source: Journal of Nutritional Science and Vitaminology, 1998 Vol 44, Iss 2, pp 257-268

    This study was designed to investigate the modulatory effect of dietary soybean protein on the skeleton of rats with postmenopausal osteoporosis and ovaries removed. The four experimental groups were: a) Soy group, b) Estrogen group (fed casein diet and injected with estrogen, c) Casein group (fed casein diet), and d) Sham group (sham-operated and fed casein diet). Rats in the Soy, Sham, and Estrogen groups had significantly higher (p < 0.05) femur and tibia ash and calcium content than those in the Casein group. Serum total and bone-type alkaline phosphatase levels were both significantly lower in the Estrogen and Sham groups in relation to the Soy and Casein groups. Unlike estrogen, soy protein diet did not have any effect on the uterus. This study demonstrates that a 22% soybean protein diet could be just as effective as daily estrogen administration in suppressing bone loss.



  12. Dietary zinc modifies onset/severity of spontaneous diabetes

    Full Source: Molecular Genetics and Metabolism, 1998, Vol 63, Iss 3, pp 205-213

    Diabetes-prone rats were fed diets containing either 1000 ppm (HZ), 50 ppm (NZ), or 1 ppm zinc (LZ) starting at 30 days of age. Non-diabetes-prone rats were fed NZ and designated as controls (NORM). At 90 days of age HZ rats had a lower incidence of diabetes (19%) than NZ (53%) or LZ (44%) animals. By age 100 days, for the HZ group, there was a 60% reduction in the number of expected overt diabetic rats. HZ animals also had higher concentrations of both pancreatic and serum insulin and exhibited lower serum glucose and triglycerides. Immunohistochemistry of HZ rats was clearly different from NZ rats and showed evidence of nearly normal pancreatic endocrine activity. The data indicates that dietary treatment of genetically predisposed rodents with zinc appears to be an effective approach for delaying or preventing the onset of diabetes. This finding may suggest further experimental studies regarding dietary means for preservation of pancreatic function.



  13. Cured and broiled meat consumption cause brain tumors and leukemia in children. Vitamins reduce the risk

    Full Source: Cancer Causes and Control 1994, 5, 141-148

    The study consisted of 234 cancer cases (including 56 acute lymphocytic leukemia, 45 brain tumors) and 206 controls. Five meat groups (ham, bacon, or sausage; hot dogs; hamburgers; bologna, pastrami, corned beef, salami, or lunch meats; charcoal broiled foods) were assessed. The results showed that consumption of hot dogs by the mother during pregnancy of one or more times per week was associated with childhood brain tumors was 230%. Among children, eating hamburgers one or more times per week was associated with risk of lymphocytic leukemia was 200%, and eating hot dogs one or more times per week was associated with brain tumors 210%. Among children, the combination of no vitamins and eating meats was associated more strongly with both lymphocytic leukemia and brain cancer than either no vitamins or meat consumption alone, producing 200%-700%. The results linking hot dogs and brain tumors (replicating an earlier study) and the apparent synergism between no vitamins and meat consumption suggests an adverse effect of dietary nitrites and nitrosames.



  14. Mitochondrial dysfunction in Parkinson disease

    Full Source: American Journal of Human Genetics, 1998, Vol 62, Iss 4, pp 758-762

    Disordered mitochondrial metabolism may play an important role in a number of neurodegenerative disorders with unknown causes. The question of mitochondrial dysfunction is particularly attractive in the case of Parkinson disease, since it was recognized in the 1980s that the parkinsonism-inducing compound methyl-4-phenyl-1,2,3,6-tetrahydropyridine is also a mitochondrial toxin. Although occasionally inherited, the vast majority of the time such diseases of unknown cause appear sporadically.

    Because of unique features of mitochondria, mitochondrial inheritance can allow for the apparent sporadic nature of these diseases. This shows the importance of taking COQ10, which plays a role in maintaining mitochondrial energy production.



  15. Cellular immune responses to vitamin C supplementation in ageing humans assessed by the in vitro leucocyte migration inhibition test

    Full Source: Medical Science Research, 1998 Vol 26, Iss 4, pp 227-230

    Aging is associated with greater susceptibility to progressive senescence of the immune system. We have determined the effect of dietary supplementation with vitamin C (200mg/day for 30, 60 and 90 days) on immune responses in young (20 to 30 years old) and older people (above 60 years old). The leucocyte count, neutrophils, lymphocytes, absolute neutrophil and lymphocyte numbers and leucocyte ascorbic acid were significantly lower, whereas leucocyte migration inhibition was significantly higher, in older individuals than in young ones. Supplementation with vitamin C enhanced immunocompetent cells and the ascorbic acid concentration in leucocytes, and suppressed leucocyte migration in older individuals.



  16. Could diet reduce the risk of developing Alzheimer's disease?

    Full Source: Medical Hypotheses, 1998, Vol 50, Iss 4, pp 335-337

    Researchers have recently reported a possible inverse relationship between taking steroids or non-steroidal anti-inflammatory drugs, or both, and the development of Alzheimer's disease. In this article it is hypothesized that the reduction in the human body of the amount of available arachidonic acid, the precursor of inflammatory eicosanoids, by dietary methods might offer a path to prevention of Alzheimer's disease without resorting to drugs having potentially harmful side effects, and without inhibiting the production of highly important, non-inflammatory eicosanoids. Perilla, flax and fish oil also reduce the amount of available of arachidonic acid. Aspirin should also be considered daily for prevention of thrombosis, inflammatory vascular wall injury and prevention of Alzheimer's.



  17. CLA reduces arachidonic acid and prostaglandin synthesis

    Full Source: Cancer Letters, 1998, Vol 127, Iss 1-2, pp 15-22

    Dietary conjugated linoleic acid (CLA) is associated with decreased 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced tumor promotion in mouse skin. CLA also decreases prostaglandin E synthesis PGE(2) and ornithine decarboxylase activity in cells compared with linoleic acid (LA) and arachidonic acid (AA). In this study, when LA and CLA were added to keratinocyte cell cultures, the amounts of each of these cellular fatty acids increased significantly in a dose-dependent manner. LA treatment was associated with increased cellular AA. However, when cultures were treated with CLA, the AA and PGE(2) content of keratinocytes was reduced significantly. CLA was more potent than LA at decreasing the level of arachidonic acid incorporated into cellular phosphatidylcholine. These results will provide insight into the anti-promoter mechanisms of CLA.



  18. Vitamin D3 vs. early prostate cancer

    Full Source: Journal of Urology, 1998, Vol 159, Iss 6, pp 2035-2039

    Substantial experimental and epidemiological data indicate that vitamin D3 (calcitriol) has potent antiproliferative effects on human prostate cancer cells. This study tried to determine whether calcitriol therapy is safe and efficacious for early recurrent prostate cancer. After primary treatment with radiation or surgery, recurrence of cancer was indicated by rising serum PSA levels. Seven subjects then completed calcitriol therapy in 6 to 15 months. The rate of PSA rise during versus before calcitriol therapy significantly decreased in 6 of 7 patients. This pilot study provides preliminary evidence that calcitriol effectively slows the rate of PSA rise in select cases, although dose dependent calciuric side effects limit its clinical usefulness. The development of calcitriol analogues with decreased calcemic side effects is promising, since such analogues may be even more effective for treating prostate cancer.



  19. Doxycycline inhibits prostate cancer cell growth

    Full Source: Cancer Letters, 1998, Vol 127, Iss 1-2, pp 37-41

    Prostate cancer is the most common form of cancer in older men and the major cause of death from prostate cancer is metastatic disease. The "matrix metalloproteinases" (MMPs) play a significant role in the growth, invasion and metastasis of many tumors, including those of the prostate. Doxycycline, a synthetic tetracycline, inhibits MMPs and cell proliferation and induces apoptosis in several cancer cell lines including inhibition of tumor size and regrowth after resection in metastatic breast cancer. In this study, significant inhibition of cell growth occurred after exposure to doxycycline, while cell growth was normal in untreated cells. Radioisotope incorporation into proteins was reduced by doxycycline. DNA fragmentation, consistent with apoptosis, was demonstrated in cells treated with doxycycline. This shows that doxycycline may have potential utility in the management of prostate cancer.



  20. Aspirin protects against heart disease

    Full Source: Circulation Research, 1998, Vol 82, Iss 9, pp 1016-1020

    Aspirin has recently been shown to increase endothelial cell resistance to oxidative damage, However, the mechanism underlying aspirin-induced cell protection is still unknown. This study investigated the effect of aspirin on ferritin, a protective protein that seizes free iron, the main catalyst of oxygen radical formation. Aspirin administration at low antithrombotic concentrations induced the synthesis of ferritin protein up to 5-fold over starting levels. Aspirin-induced cell protection from hydrogen peroxide toxicity was copied by exogenous apoferritin (with an iron-free content), demonstrating the antioxidant function of newly synthesized ferritin under these conditions. Ferritin induction by aspirin was unusual in that other nonsteroidal anti-inflammatory drugs such as salicylic acid, indomethacin, or diclofenac failed to alter ferritin protein levels. The results suggest induction of ferritin as a novel mechanism by which aspirin may prevent endothelial injury in cardiovascular disease, e.g., during atherogenesis.