Insufficient levels of vitamin D puts elderly at increased risk of dying from heart disease

A new study by researchers at the University of Colorado Denver and Massachusetts General Hospital (MGH) shows vitamin D plays a vital role in reducing the risk of death associated with older age. The research, just published in the Journal of the American Geriatrics Society, evaluated the association between vitamin D levels in the blood and the death rates of those 65 and older. The study found that older adults with insufficient levels of vitamin D die from heart disease at greater rates that those with adequate levels of the vitamin.

"It's likely that more than one-third of older adults now have vitamin D levels associated with higher risks of death and few have levels associated with optimum survival," said Adit Ginde, MD, MPH, an assistant professor at the University of Colorado Denver School of Medicine's Division of Emergency Medicine and lead author on the study. "Given the aging population and the simplicity of increasing a person's level of vitamin D, a small improvement in death rates could have a substantial impact on public health."

Older adults are at high risk for vitamin D deficiency because their skin has less exposure to the sun due to more limited outdoor activities as well as reduced ability to make vitamin D.

The study analyzed data from the Third National Health and Nutrition Examination Survey conducted by the National Center for Health Statistics. The research team analyzed vitamin D in blood samples of more than 3,400 participants that were selected to be representative of the 24 million older adults in the United States. Compared to those with optimal vitamin D status, those with low vitamin D levels were 3 times more likely to die from heart disease and 2.5 times more likely to die from any cause.

Dr. Ginde says the findings suggest that current daily recommendations of vitamin D may not be enough for older adults to maintain optimal health. The research team has applied for research funding from the National Institutes of Health to perform a large, population-based clinical trial of vitamin D supplementation in older adults to see if it can improve survival and reduce the incidence of heart disease.

"Confirmation of these results in large randomized trials is critically important for advancing public health," says Carlos Camargo, MD, DrPH, of the MGH Department of Emergency Medicine, the senior author of the study and an associate professor of medicine at Harvard Medical School.

The study looking at elderly death rates is the second of two studies by the same team of researchers on vitamin D and general health. The first study, published in Archives of Internal Medicine earlier this year, identified vitamin D as playing a significant role in boosting the immune system and warding off colds and flu.

"Vitamin D has health effects that go beyond strong bones," says Ginde. "It's likely that it makes a vital contribution to good health."

Faculty at the University of Colorado Denver's School of Medicine work to advance science and improve care. These faculty members include physicians, educators and scientists at University of Colorado Hospital, The Children's Hospital, Denver Health, National Jewish Health, and the Denver Veterans Affairs Medical Center. Degrees offered by the UC Denver School of Medicine include doctor of medicine, doctor of physical therapy, and masters of physician assistant studies. The School is located on the University of Colorado's Anschutz Medical Campus, one of four campuses in the University of Colorado system. For additional news and information, please visit the UC Denver newsroom online (http://ucdenver.edu/about/newsroom/Pages/Newsroom.aspx).

Massachusetts General Hospital, established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of $550 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, systems biology, transplantation biology and photomedicine. For more information, visit http://www.massgeneral.org.

There is also reason to surmise that vitamin D can be curative of shingles and, by extension, also of many cases of chronic fatigue syndrome.

From PubMed:

While the underlying pathophysiology of herpes zoster infection has been well characterised, many of the mechanisms relating to the subsequent development of post herpetic neuralgia (PHN) remain uncertain. The dorsal horn atrophy and reduction in skin innervation seen in PHN patients does not adequately explain many clinical features or the efficacy of a number of topical treatments. In the central nervous system the glia, their receptors and their secreted signalling factors are now known to have a major influence on neural function. In the peripheral nervous system, schwann cell activation in response to infection and trauma releases a number of neuroexcitatory substances. Activation of the nervi nervorum in the peripheral nervous system also leads to the release of calcitonin gene related peptide, substance P and nitric oxide. Schwann cell and/or nervi nervorum activation could be an additional mechanism of pain generation in PHN. Such a paradigm shift would mean that drugs useful in the treatment of glial cell activation such as naloxone, naltrexone, minocycline, pentoxifyllline, propentofylline, AV411 (ibudilast) and interleukin 10 could be useful in PHN. These drugs could be used systemically or even topically. High dose topical vitamin D would appear to offer particular promise because vitamin D has the ability to both reduce glial inflammation and reduce nitric oxide production.

Med Hypotheses, 2009 Jul 25, "Post herpetic neuralgia, schwann cell activation and vitamin D," Bartley J., The Auckland Regional Pain Service, FRACS, 10 Owens Rd., Epsom, Auckland 1023, New Zealand.

This article posits that infection of the peripheral ganglia causes at least some cases of Chronic Fatigue Syndrome (CFS), with a neurotropic herpesvirus, particularly varicella-zoster virus (VZV), as the most likely cause of the infection. Virtually all CFS symptoms could be produced by an infection of the peripheral ganglia, with infection of the autonomic ganglia causing fatigue, postural hypotension, and sleep disturbances, and infection of the sensory ganglia causing sensory symptoms such as chronic pain. Furthermore, infections of the peripheral ganglia are known to cause long-term nerve dysfunction, which would help explain the chronic course of CFS. Herpesviruses have long been suspected as the cause of CFS; this theory has recently been supported by studies showing that administering antiherpes agents causes substantial improvement in some CFS patients. VZV is known to frequently reactivate in the peripheral ganglia of previously healthy adults and cause sudden, debilitating illness, making it a likely candidate as a cause of CFS. Moreover, many of the symptoms of CFS overlap with those of herpes zoster (shingles), with the exception that painful rash is not one of the symptoms of CFS. A model is therefore proposed in which CFS is one of the many manifestations of zoster sine herpete; that is, herpes zoster without rash. Furthermore, re-exposure to VZV in the form of chickenpox has become less common in the past few decades; without such re-exposure, immunity to VZV drops, which could explain the increased incidence of CFS. Co-infection with multiple herpesviruses is a possibility, as some CFS patients show signs of infection with other herpesviruses including Epstein-Barr, Cytomegalovirus, and HHV6. These three herpesviruses can attack immune cells, and may therefore promote neurotropic herpesvirus reactivation in the ganglia. The possibility of VZV as the causal agent in CFS has previously received almost no attention; the possibility that CFS involves infection of the peripheral ganglia has likewise been largely overlooked. This suggests that the search for a viral cause of CFS has been far from exhaustive. Several antiherpes drugs are available, as is a vaccine for VZV; more research into such agents as possible treatments for CFS is urgently needed.

Med Hypotheses, 2009 Jun 9, "Does varicella-zoster virus infection of the peripheral ganglia cause Chronic Fatigue Syndrome?" Shapiro JS., 3424 Platt Road, Ann Arbor, MI 48108, USA.

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