Men should not stop using Avodart because of heart attack fears! Life Extension’s Rebuttle

Life Extension’s rebuttal by William Faloon in reference to published clinical study in Thursday’s New England Journal of Medicine on Avodart and increased risk for sudden myocardial infarction.

I suspect none of the study participants where using testosterone creams, even though they were ALL likely to be testosterone deficient. You will soon read the findings of an internal study we did on Life Extension Foundation members that found 86% of men have less than optimal testosterone levels.

The significance of this is that testosterone deficiency predisposes a man to heart failure. By taking a drug like Avodart when in a testosterone deficient state, the heart muscle will be robbed completely of this vital anabolic hormone. That may be why this study showed higher heart failure rates in the Avodart group.

 Those with prostate cancer often intentionally suppress their testosterone levels and have to be extra vigilant in protecting against heart attack. Log on to http://www.lef.org/magazine/mag2009/mag2009_05.htm for information on how to protect against multiple risk factors underlying coronary atherosclerosis.

 Aging men (without prostate cancer) should do whatever is necessary to maintain free testosterone blood levels of 20-25 pg/mL, while keeping DHT blood levels at the very low end of the reference range.

This provides the heart, brain and other vital parts their testosterone requirements while protecting the prostate gland against the adverse effects of excess DHT.

 The Avodart study exposes the flaws in so many of these single agent trials. We know, for example, that 25-hydroxyvitamin D serum levels strongly predict prostate cancer risk. If this potent confounding factor was not accounted for, then the results shown with Avodart have little meaning.

If, for example the placebo group’s median 25-hydoxyvitamin D level was 35 ng/mL, and the Avodart group was only 25 ng/mL, this would skew the results in a way to show Avodart less effective than it may really be. Dietary intakes of cruciferous vegetables would have an equally significant confounding effect.

 Bill Faloon

Resveratrol May Reverse Arterial Aging

Resveratrol

“Atherosclerosis is reversible” is not a phrase we expected to hear from mainstream medical researchers until very recently—since these are the precise opening words of a remarkable editorial about resveratrol that appeared in a recent issue of the prestigious New England Journal of Medicine. Just as astonishingly, the editorial was written by a renowned immunologist, Linda K. Curtiss, PhD, of the Scripps Research Institute in La Jolla, California. The fact that an immunologist is writing about cardiovascular disease in a trend-setting medical journal speaks volumes about how far we have come in our understanding of chronic diseases and their relationships with inflammation, which is an immune system phenomenon. What truly sets Dr. Curtiss’s article apart, though, is her description of a dramatic new phenomenon mediated by the grape polyphenol resveratrol.

Curtiss’s excitement comes from work done by Cleveland Clinic cell biologist Young-Mi Park, MD, who was exploring the role of oxidant stress and inflammation on the pathogenesis, or disease-causing mechanisms, of atherosclerosis. Knowing that fat-laden inflammatory cells called foam-cell macrophages trigger inflammation when they become trapped beneath the lining of blood vessels, Park’s team sought to understand why the cells become trapped, and how they could be freed from their “endothelial bondage,” thereby reversing the inflammatory process.

The most natural approach to take, Park’s group decided, was simply to test known antioxidants’ ability to prevent the foam cells from migrating into the endothelial lining in the first place, and their ability to release any cells that were already present. Specifically, they studied how oxidized low-density lipoprotein (LDL) promotes foam-cell formation and impairs migration. To do this they blocked LDL oxidation with several potent antioxidants. They found that oxidized LDL actually triggered production of a sort of cellular “glue” in the form of filaments of actin, one of the proteins also found in muscle tissue. The actin filaments were entangling the foam cells, preventing their natural migration out of the endothelial lining, leading to progressive inflammatory changes.

Park’s group chose resveratrol as one of the two antioxidants to test—another testimony to the respect that mainstream researchers are according this remarkable molecule (the other was N-acetylcysteine, also an antioxidant available in supplement form). Resveratrol treatment of the foam cells inhibited production of reactive oxygen species by greater than 90%, an important first step in breaking the cycle. Even more impressively, resveratrol supplements partially restored the foam cells’ ability to move out of the entangling actin filaments, and migrate away from the endothelial lining!

This brings us back to Dr. Curtiss’s astounding initial observation that atherosclerosis is a reversible condition—through the use of powerful antioxidants such as resveratrol, we can now understand how oxidized LDL contributes to invasion of endothelium by inflammatory cells, and how prevention or reversal of LDL oxidation promotes mobilization of inflammatory cells and their emigration away from vessel linings.

As Dr. Park concluded, “[these studies] also provide additional mechanistic support for the atheroprotective effect of antioxidants.” Resveratrol is already well-known as a cardiovascular protective supplement—the work of Park and others is now showing us that resveratrol must also be considered a valuable cardiovascular therapeutic supplement, one that can literally “turn back the clock” on chronic vascular diseases of aging!

Vitamin D deficiency: emerging cardiovascular disease risk factor

emerging cardiovascular disease risk factor

A review published in the December 9, 2008 issue of the Journal of the American College of Cardiology describes the involvement of deficient vitamin D levels in common risk factors for cardiovascular disease (including high blood pressure, diabetes, and obesity) and in cardiovascular events.

Vitamin D deficiency is estimated to affect up to half of all adults and 30 percent of children in the United States. While the vitamin’s role in bone health has long been known, a flurry of recent studies have uncovered associations between deficient levels of the vitamin and a number of diseases, including cardiovascular disease. In their review, Michael F. Holick, MD, PhD and colleagues note that insufficient levels of vitamin D activate the renin-angiotensin-aldosterone system, which can lead to hypertension and thickening of the heart and blood vessel walls. Altered hormone levels related to a deficiency of vitamin D (which is also a hormone) increase the risk of diabetes, which is a well known risk factor for the development of cardiovascular disease. In 15,088 subjects from the NHANES III national cohort registry, higher vitamin D levels were related to a lower risk of diabetes as well as hypertension, high triglycerides, and obesity. And among Framingham Heart Study participants who had levels of vitamin D of less than 15 nanograms per milliliter upon enrollment, the risk of subsequent cardiovascular events was twice as great as the risk experienced by those with higher levels of the vitamin.

Chronic vitamin D deficiency is associated with secondary hyperparathyroidism, which increases the risk of inflammation and cardiovascular events. Elevated parathyroid levels were associated with an increased risk of death among older individuals compared to those with normal levels over the course of follow-up in a recent observational study.

“We are outside less than we used to be, and older adults and people who are overweight or obese are less efficient at making vitamin D in response to sunlight,” stated review coauthor James H. O’Keefe, MD, who is a cardiologist and director of Preventive Cardiology at the Mid America Heart Institute in Kansas City, Missouri. The authors’ strategy for restoring vitamin D to optimal levels in cardiovascular disease patients includes initial treatment with 50,000 international units (IU) vitamin D2 or D3 weekly for 8 to 12 weeks followed by maintenance with 1,000 to 2,000 IU daily. They also suggest limited sun exposure as a means of increasing vitamin D. They observe that supplementation with vitamin D is safe and that such effects as elevated calcium levels and kidney stone development have only rarely been observed among individuals who consume 20,000 IU per day or more.

“Vitamin D deficiency is an unrecognized, emerging cardiovascular risk factor, which should be screened for and treated,” stated Dr O’Keefe. “Vitamin D is easy to assess, and supplementation is simple, safe and inexpensive.”

“Restoring vitamin D levels to normal is important in maintaining good musculoskeletal health, and it may also improve heart health and prognosis,” Dr. O’Keefe concluded. “We need large randomized controlled trials to determine whether or not vitamin D supplementation can actually reduce future heart disease and deaths.”