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January 8, 2008

Framingham researchers find heart disease linked to vitamin D deficiency

Life Extension Update Exclusive

A report published in the January 8, 2007 issue of Circulation: A Journal of the American Heart Association revealed the discovery of Framingham Heart Study researchers that having deficient levels of vitamin D is associated with double the risk of experiencing a cardiovascular event, including heart attack, heart failure or stroke, within a five year period compared to individuals with normal levels.

For the current study, Harvard Medical School assistant professor of medicine Thomas J. Wang, MD and colleagues evaluated data from 1,739 offspring of Framingham Heart Study participants. The subjects, whose average age was 59 and who had no evidence of cardiovascular disease upon enrollment, were tested for serum vitamin D levels and followed for an average of 5.4 years, during which they received periodic physical examinations and lab assessments of cardiovascular risk factors.

Evaluation of vitamin D concentrations found that only 10 percent of the participants had optimal levels of over 30 nanograms per milliliter. Twenty-eight percent were found to have levels that were less than half the optimal level, and 9 percent had concentrations lower than 10 ng/mL. Analysis of the data determined that having deficient blood levels of vitamin D at below 15 nanograms per milliliter doubled the risk of having a cardiovascular event over follow up, compared to those with normal levels. After adjustment for conventional cardiovascular risk factors, the risk remained 62 percent higher than that experienced by non-deficient individuals.

In a separate analysis of 688 of the participants, hypertension was found to double event risk among vitamin D deficient individuals after adjustment for traditional cardiovascular risk factors. “Vitamin D deficiency is associated with increased cardiovascular risk, above and beyond established cardiovascular risk factors,” Dr Wang stated. “The higher risk associated with vitamin D deficiency was particularly evident among individuals with high blood pressure.”

“Low levels of vitamin D are highly prevalent in the United States, especially in areas without much sunshine,” he observed. “Twenty to 30 percent of the population in many areas has moderate to severe vitamin D deficiency.”

“A growing body of evidence suggests that low levels of vitamin D may adversely affect the cardiovascular system,” he continued. “Vitamin D receptors have a broad tissue distribution that includes vascular smooth muscle and endothelium, the inner lining of the body’s vessels. Our data raise the possibility that treating vitamin D deficiency, via supplementation or lifestyle measures, could reduce cardiovascular risk.”

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Health Concern Life Extension Highlight

Coronary artery disease

The cause and progression of atherosclerosis are intimately related to the health of the inner arterial wall. Arteries are composed of three layers. The outer layer is mostly connective tissue and provides structure to the layers beneath. The middle layer is smooth muscle; it contracts and dilates to control blood flow and maintain blood pressure. The inner lining consists of a thin layer of endothelial cells (the endothelium) that provides a smooth, protective surface. Endothelial cells prevent toxic, blood-borne substances from penetrating the smooth muscle of the artery. They also respond to changes in blood pressure and release substances into the cells of the smooth muscle that help change the muscle tone of the artery. Furthermore, endothelial cells secrete chemicals that provoke a protective response in the artery after an injury. This protective response includes signaling smooth muscle cells and white blood cells to congregate at the site of an injury.

The cause and progression of atherosclerosis are intimately related to the health of the inner arterial wall. Arteries are composed of three layers. The outer layer is mostly connective tissue and provides structure to the layers beneath. The middle layer is smooth muscle; it contracts and dilates to control blood flow and maintain blood pressure. The inner lining consists of a thin layer of endothelial cells (the endothelium) that provides a smooth, protective surface. Endothelial cells prevent toxic, blood-borne substances from penetrating the smooth muscle of the artery. They also respond to changes in blood pressure and release substances into the cells of the smooth muscle that help change the muscle tone of the artery. Furthermore, endothelial cells secrete chemicals that provoke a protective response in the artery after an injury. This protective response includes signaling smooth muscle cells and white blood cells to congregate at the site of an injury.

As we age, however, the endothelium becomes leaky, allowing lipids and toxins to penetrate the endothelial layer and enter the smooth muscle cells. As a result, smooth muscle cells gather at the site of the injury, and the artery loses some flexibility. In response, the endothelium signals white blood cells to congregate along the cell wall. These white blood cells produce pro-inflammatory substances, such as leukotrienes and prostaglandins, as well as damaging free radicals that attack the endothelium (Touyz RM 2005). Toxins soon begin to penetrate into the arterial wall, where lipids such as LDL, cholesterol, and triglycerides accumulate and become oxidized.

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