Diabetics deficient in vitamin D can't process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. New research has identified a mechanism linking low vitamin D levels to heart disease risk, and may lead to ways to fix the problem, simply by increasing levels of vitamin D.
Vitamin D inhibits the uptake of cholesterol by cells called macrophages. When people are deficient in vitamin D, the macrophage cells absorb more cholesterol, and can't get rid of it. The macrophages get clogged with cholesterol and become what scientists call foam cells, which are one of the earliest markers of atherosclerosis.Macrophages are dispatched by the immune system in response to inflammation and often are activated by diseases such as diabetes.
In an article scheduled to appear in the Annals of Epidemiology, epidemiologist Cedric Garland, DrPH and his associates at the University of California San Diego's Moores Cancer Center propose that cancer, rather than commencing with genetic mutations, is initially caused by a reduction in the of ability of cells to stick together.
Research has shown that inadequate vitamin D can result in a loss of stickiness between cells as well as a loss of differentiation, which causes cells to revert to a stem cell-like state. Additionally, extracellular calcium ions are necessary for intercellular adherence.
"The first event in cancer is loss of communication among cells due to, among other things, low vitamin D and calcium levels," explained Dr Garland, who is a professor of family and preventive medicine at the UC San Diego School of Medicine "In this new model, we propose that this loss may play a key role in cancer by disrupting the communication between cells that is essential to healthy cell turnover, allowing more aggressive cancer cells to take over."
Accessed 02 June 2009
Background: Excessive kyphosis may be associated with earlier mortality, but previous studies have not controlled for clinically silent vertebral fractures, which are a known mortality risk factor.
Objective: To determine whether hyperkyphosis predicts increased mortality independent of vertebral fractures.
Design: Prospective cohort study.
Setting: Four clinical centers in Baltimore County, Maryland; Portland, Oregon; Minneapolis, Minnesota; and the Monongahela Valley, Pennsylvania.
Patients: 610 women, age 67 to 93 years, from a cohort of 9704 women recruited from community-based listings between 1986 and 1988.
Measurements: Kyphosis was measured by using a flexicurve. Prevalent radiographic vertebral fractures at baseline were defined by morphometry, and mortality was assessed during an average follow-up of 13.5 years.
Results: In age-adjusted models, each SD increase in kyphosis carried a 1.14-fold increased risk for death (95% CI, 1.02 to 1.27; P = 0.023). After adjustment for age and other predictors of mortality, including such osteoporosis-related factors as low bone density, moderate and severe prevalent vertebral fractures, and number of prevalent vertebral fractures, women with greater kyphosis were at increased risk for earlier death (relative hazard per SD increase, 1.15 [CI, 1.01 to 1.30]; P = 0.029). On stratification by prevalent vertebral fracture status, only women with prevalent fractures were at increased mortality risk from hyperkyphosis, independent of age, self-reported health, smoking, spine bone mineral density, number of vertebral fractures, and severe vertebral fractures (relative hazard per SD increase, 1.58 [CI, 1.06 to 2.35]; P = 0.024).
Limitation: The study population included only white women.
Conclusion: In older women with vertebral fractures, hyperkyphosis predicts an increased risk for death, independent of underlying spinal osteoporosis and the extent and severity of vertebral fractures.
Primary Funding Source: National Institute of Arthritis and Musculoskeletal and Skin Diseases and National Institute on Aging.
Take home message: Have your spine adjusted by a chiropractor regularly.
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