Cardiovascular Dangers of Iron
- The American Journal of Epidemiology (1998;147:161-166) confirms the cardiovascular dangers of iron. This study showed that women over age 60 were 1.4 times more likely to have heart disease for each 50 mg increase in iron intake per month. Men over age 60 were 3.5 times more likely to have heart disease for each 50 mg of iron intake per month. The study involved 329 patients with heart disease who were compared with 570 people the same age who were admitted to the hospital for minor diseases or conditions unrelated to diet.
Most multi-vitamin/mineral supplements on the market today contain at least 9 mg of iron per daily dose. That means that people who use these supplements are adding 270 mg of iron to their body every month. Based on the results of this new study, these people may be increasing their risk of heart disease more than 8-fold.
In 1983, the Life Extension Foundation first warned its members to avoid supplements containing iron. There was significant evidence then to indicate that excess iron in the body would act as a catalyst for free radical generation that would increase the incidences of heart attack, cancer and other age-related diseases. This evidence has grown greatly over the years, yet most supplement companies have still not gotten the message. That's one of many reasons why membership in the Life Extension Foundation could save your life.
Curcumin vs. Atherosclerosis
- It has been shown that curcumin and related phenolic compounds have a powerful antioxidant action. Previous research has shown significant decreases in the levels of lipid peroxides in the blood of both mice and human subjects administered curcumin. This study shows that a daily intake of 20 mg of the phenolic antioxidant curcumin for 60 days decreases the high levels of peroxidation of both HDL and LDL cholesterol in 30 healthy volunteers ranging in age from 40 to 90 years. The effect was quite striking in the persons with high baseline values of peroxidized compounds in these lipoproteins. In view of current concepts on the atherogenic role played by peroxidized HDL, and especially by peroxidized LDL, this study suggests that curcumin, because of its high antioxidant activity and lack of toxicity, might be a useful complement to standard hypo-lipidemic drugs in the prevention and treatment of atherosclerosis.
Age, 1997, Vol 20, Iss 3, pp 165-168
Curcumin Lowers Cholesterol
- Two daily grams of curcumin administered to 33 subjects before and after a 60-day period reduced total cholesterol by up to 12.5%, triglycerides up to 34%, and LDL cholesterol up to 17% within 15 days. This lowering of fat concentration was accompanied by decreased blood lipid peroxidation. The antioxidant properties of curcumin are thus useful for the prevention of coronary heart disease.
Medical Science Research, 1997, Vol 25, Iss 10, pp 695-698
Glutathione, Oxidative Stress and Aging
- The free radical theory of aging proposes that the impairment in physiological performance associated with aging is caused by the detrimental effects of oxygen free radicals. Free radicals are involved in many diseases of aging, including cancer, diabetes or atherosclerosis. The involvement of glutathione in aging has been known since the early seventies. Several studies have reported that reduced glutathione is decreased in cells from old animals, but oxidized glutathione tends to be increased. Glutathione is one of the main nonprotein antioxidants in cells. Mitochondrial glutathione plays a key role in the protection against free radical damage associated with aging. Oxidative damage to mitochondrial DNA is directly related to oxidation of mitochondrial glutathione. In fact, aging is associated with oxidative damage to proteins, nucleic acids, and lipids. These molecular lesions may be responsible for the low physiological performance of aged cells.
Age, 1996, Vol 19, Iss 4, pp 129-139
Tretinoin/Retinol vs. Bladder Cancer
- Tretinoin or Retinol was found to enhance the proliferation and cytotoxicity of lymphokine-activated killer cells from patients with bladder cancer. Lymphokines are protein mediators postulated to be released by sensitized lymphocytes on contact with antigens, and believed to play a role in macrophage activation, lymphocyte transformation, and cell-mediated immunity.
Acta Pharmacologica Sinica, 1997, Vol 18, Iss 6, pp 522-524
Vitamin D3 and Cancer
- The principal cause of death from most forms of cancer is metastatic disease (transfer of disease from one organ or part of the body to another not directly connected with it). Cancer cells appear to grow quickly out of the control of the normal host regulatory mechanisms. Many factors contribute to this unrestrained proliferation, including, 1) degradation of the extracellular matrix surrounding cancer cells; 2) angiogenesis (development of new blood vessels), permitting easy access of the cells to the bloodstream; and, 3) decrease or loss of programmed cell death, or apoptosis, an important mechanism for removal of abnormal or senescent cells. In this study, vitamin D3 strikingly inhibited cancer cell proliferation and induced apoptosis in human breast, prostate and osteosarcoma cancer cell lines.
Cancer Letters, 1997, Vol 120, Iss 1, pp 65-69
N-acetyl-L-cysteine Protects Against Gastritis
- Several studies have suggested that oxidative damage may contribute to gastritis. This damage is counteracted by various scavengers including glutathione (produced by the body), which may help defend the mucous tissue lining the digestive tract. The effects of N-acetyl-L-cysteine (NAC), a glutathione precursor, were assessed in 18 patients who had been confirmed with chronic atrophic gastritis but no peptic ulcer. After treatment with 1 gram and 2 grams of NAC, 72% of patients showed improvement, irrespective of NAC dose, and 28% showed no change. Histologically, immune system infiltration was significantly reduced in patients who received 2 grams of NAC. The results suggest that in patients with gastritis and non-ulcer dyspepsia, NAC is fairly well tolerated and apparently leads to endoscopic, symptomatic, and to some extent histologic improvement, unrelated to changes in mucosal glutathione levels.
Current Therapeutic Research - Clinical and Experimental, 1997, Vol 58, Iss 10, pp 724-733
DHEA Acts As Antioxidant
- Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. DHEA has been found to have antioxidant properties. When administered to rats, DHEA pretreatment protected tissues against lipid peroxidation induced by dextrose. The results of this study indicate that the in vivo administration of DHEA increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia. This helps to confirm DHEA's role in mitigating diabetic complications.
Journal of Endocrinology, 1997, Vol 155, Iss 2, pp 233-240
Fish Oil Suppresses Tumor Growth
- Tumor-bearing mice that were fed fish oil, which is rich in omega-3 fatty acids, had a significantly slower growth of primary tumors, lower mortality rate, and lower metastatic spread, in contrast with mice fed soybean oil rich in omega-6 fatty acids. This trend was also observed in mice fed first with soybean oil and after tumor inoculation transferred to the fish oil diet. Indomethacin (an anti-inflammatory nonsteroidal drug) significantly reduced the metastasis growth in the soybean oil-fed group, but exerted only a small effect in the fish oil-fed counterpart. This suggests that omega-6 fatty acids support the process of tumor growth, and that the long chain polyunsaturated fatty acids of fish oil, which are sensitive to oxidation, could act as targets for membrane perforation and eventual elimination of the proliferating tumor cells.
Journal of Nutritional Biochemistry, 1997, Vol 8, Iss 11, pp 619-622
Fish Oil and Insulin Resistance
- In type II diabetic patients, several pathologic changes including insulin resistance and hypertension can be detected. Fish oils containing omega-3 fatty acids have a beneficial effect in preventing atherosclerotic diseases. Compared with control rats on a normal diet, rats on a fructose-rich diet consistently developed hypertriglyceridemia (excess of triglycerides in the blood), fasting hyperinsulinemia (increased insulin levels in the blood), fasting hyperglycemia (insulin resistance syndrome), and systolic hypertension within 3 weeks. Glucose uptake from the blood stimulated by insulin was significantly reduced. However, rats fed the same high fructose diet but supplemented with fish oil had a lessening of all of these metabolic defects and a normalized insulin sensitivity and blood pressure.
This study suggests that dietary high fructose induced hypertriglyceridemia and insulin resistance and induced hypertension was not associated with blood abnormalities at all, but probably caused by other undefined pathologic changes that can be prevented by dietary omega fatty acids.
Metabolism-Clinical and Experimental, 1997, Vol 46, Iss 11, pp 1252-1258