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High cholesterol levels increase prostate tumor growth
Researchers at Children's Hospital Boston led by Michael Freeman, PhD, who is the program director of the hospital’s Urological Diseases Research Center, injected human prostate cancer cells into mice and elevated their cholesterol by dietary means. They observed that the outer cell membranes experienced an accumulation of cholesterol, particularly in lipid rafts, which are cholesterol structures that aggregate and disaggregate like icebergs. This accumulation was found to activate a cell-survival pathway known as Akt, which is believed to be a prostate cancer pathway, allowing the tumor cells to resist apoptosis, or programmed cell death.
Although having high cholesterol was not linked to the risk of developing new cancers in the animals, after six weeks tumor incidence in mice receiving injected cancer cells more than doubled and tumors were much larger.
In another experiment, the cholesterol-reducing drug simvastain was added to cells in vitro. Simvastain was found to inhibit the Akt pathway, increase programmed cell death and arrest the growth of tumors. Adding cholesterol to the cell membranes halted the drug’s benefit.
Dr Freeman stated, "Our study opens up a new paradigm in thinking about how cancer might be controlled pharmacologically by manipulating cholesterol. Our data support the notion that cholesterol-lowering drugs -- which are widely used and fairly safe -- might be effective in prevention of prostate cancer, or as an adjunctive therapy."
The slower tumor growth associated with the low-fat diet occurred even after the formation of measurable tumors when the diets were changed from 40% fat to 21% fat. Serum PSA levels also were highest in the 40.5 kcal% fat group and lowest in another group fed only 2.3 kcal% fat.
Measures to prevent PC must be a routine part of the counsel that general practitioners and internists give their patients. Selenium intake of at least 200 mcg a day should be a consideration in the prevention of PC. Low plasma selenium is associated with a four- to fivefold increased risk of PC. In addition, levels of plasma selenium also decrease with age, resulting in middle-aged to older men being at a higher risk for low selenium levels. Ideally, baseline levels of selenium should be obtained before beginning routine selenium supplementation. It would make sense to begin such a micronutrient and mineral assessment at age 25 and perhaps every 10 years thereafter.
Research studies have shown that vitamin E reduces growth rates of PCs resulting from a high fat diet. Tumor growth rates were highest in the animals fed a 40.5%-kcal fat diet (the typical American diet). Tumors in animals fed 40.5%-kcal fat plus vitamin E were the same as those fed a 21.2%- kcal fat diet (an ideal fat level).
As an essential cofactor of glutathione peroxidase, selenium is an important antioxidant. It is also involved with iodine metabolism, DNA repair, immune function, and the detoxification of heavy metals. High doses of vitamin C (over 1 gram) may reduce the absorption of selenium. This mineral is best taken one hour before or 20 minutes after taking vitamin C supplements. Vitamin E has been added because it works synergistically with selenium.
Just one softgel capsule of Life Extension Super Booster provides important nutrients such as gamma-tocopherol that are lacking in multinutrient formulas. The latest version of Super Booster provides sesame lignans to enhance the dissemination of gamma-tocopherol to cells throughout the body.
In human and animal studies, administration of sesame lignans increases tissue and serum levels of gamma and alpha-tocopherol. This is critical because gamma-tocopherol, but not alpha-tocopherol, quenches reactive nitrogen species, such as the dangerous peroxynitrite radical.
The effects of selenium in boosting glutathione are well established. Even the FDA says that some scientific evidence suggests that consumption of selenium may reduce the risk of certain forms of cancer.
Eric R. Braverman, MD, one of the foremost integrative medical experts, will be visiting South Florida and conducting individual screening and diagnostic procedures at the Life Extension Medical Center, located at 1100 West Commercial Boulevard in Fort Lauderdale.
Dr. Braverman will be utilizing the Brain Electrical Activity Mapping (BEAM) machines that measure the speed and strength of neurotransmissions via electrical activity. These tests, known as brain mapping, allow early diagnosis of such degenerative conditions that can affect all aspects of our metabolism, immune system, cognitive functions, hormone balance, and cellular integrity. With the results of these tests, early intervention through integrative medicine can mean the difference between optimal longevity and rapid decline.
Mini Mental Status exams done by neurologists and Wechlser Memory Scales do not pick up the brain's age. Only P300 testing or brain processing speed and other studies of brain quickness identify the brain's age. Here is what researchers say about BEAM:
“Braverman and Blum have conducted an excellent study assessing event related potential in a large clinical and control population. They found that P300 latency, an objective measure of brain function, accurately predicts memory impairment. At a time when the US population is aging the electrophysiological findings bode well as a valuable prognostic tool for brain impairment." - Ernest P. Noble, PhD, MD, Former Director of NIAAA (division of NIH), Professor of Psychiatry, UCLA
"This study provides a potential avenue to earlier diagnosis of Alzheimer's disease and further insights into how the early stages of the disease impair cognition. The use of quantitative EEG measures is a promising technique to access memory and other cognitive functions." - Orrin Devinsky, MD, Professor of Neurology, Neurosurgery and Psychiatry, NYU School of Medicine and Director of the Comprehensive Epilepsy Center at the NYU School of Medicine.
"It's a better cornerstone than anything available today for Alzheimer's early detection." - John Polich, PhD, Associate Professor of Neuropharmacology at The Scripps Research Institute, La Jolla , CA.
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