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Chronic fatigue syndrome increases heart disease risk

 

 

 

Doctor With Heat in Palm of HandA new study sheds light on the underlying mechanisms explaining the increased risk of early death due to heart failure in chronic fatigue syndrome patients seen in earlier research.

The work conducted at the Maes Clinics in Antwerp, Belgium, proposes various mechanisms associated with chronic low-level inflammation and both oxidative and nitrosative stress may explain the apparent link between chronic fatigue syndrome (ME/CFS) and an increased risk of cardiovascular disease (CVD), including heart failure.

Dr. Micheal Maes, Director of the the Maes Clinics, and colleagues sought answers in the medical literature to explain why ME/CFS patients seem to have an increased risk of cardiovascular disease. A study published in 2006 found the average age of death from heart failure was significantly lower in ME/CFS patients than the general US population at just under 59 years, compared to just over 81.

This was not the first sign that the heart is involved in ME/CFS either. Work by Dr. Arnold Peckerman, PhD, an American cardiopulmonary physiologist, published in 2003, revealed that people suffering from ME/CFS have reduced blood volume, reduced blood pressure, and reduced blood flow to organs and tissues. In Peckerman's study the severity of these problems in individual patients was strongly associated with their level of disability (learn more - The Heart of the Matter: CFS & Cardiac Issues by Dr. Paul Cheney, MD.).

By reviewing the research on ME/CFS and CVD, Maes and colleagues found a number of factors that could contribute to ME/CFS patients having an increased risk of CVD and of early death from heart failure. It is well established that CVD is an inflammatory disease and research suggests that chronic low-level inflammation plays a major role in ME/CFS.

Factors known to be, or thought to be, involved in triggering and perpetuating ME/CFS include viral and bacterial infections, increased intestinal permeability (leaky gut syndrome) and associated absorption of bacteria, partially digested food particles and other 'antigens', and psychological stress. All of these factors trigger a response in the immune system. The Belgian researchers report that the immune systems of ME/CFS patients chronically produce elevated levels of inflammatory molecules including nuclear factor kappa B, tumour necrosis factor alpha, and COX-2. All of which they say could contribute to increased risk for CVD. Decreased levels of omega-3 polyunsaturated fatty acids (PUFAs) and increased levels of omega-6 PUFAs and saturated fat were also found. This represents an increased risk for both inflammatory processes and CVD.

In addition, increased levels of oxidative and nitrosative stress and decreased antioxidant levels are present in both ME/CFS and CVD. What this means is that both groups of patients have elevated levels of highly reactive chemicals known as 'free radicals' which can damage the cells, tissues, and organs of the body if there are not sufficient levels of antioxidants present to neutralise them. Maes and colleagues report that ME/CFS patients have reduced levels of a variety of important antioxidants including coenzyme Q10, zinc (required by the antioxidant enzyme 'superoxide dismutase'), and the adrenal hormone dehydroepiandrosterone sulphate (DHEA-S). High oxidative and nitrosative stress and low antioxidant status contributes to damage to artery walls and the development of heart disease. Low levels of coenzyme Q10 particularly are also associated with poor heart function as it is required for the production of energy within the cells; the heart muscle having a huge requirement for energy.

Maes and colleagues conclude that "ME/CFS is a multisystemic metabolic-inflammatory disorder" and that alterations in the inflammatory, oxidative and nitrosative (IO&NS) pathways may increase the risk for cardiovascular disorders.

Source: Maes M and Twisk FN (2009) Why myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) may kill you: disorders in the inflammatory and oxidative and nitrosative stress (IO&NS) pathways may explain cardiovascular disorders in ME/CFS NEuro Endocrinolology Letters 30(6): [Epub ahead of print]


 

 

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