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With a mouse model, Lerner has shown that raised myocardial viral titers accompany physical exertion in the host. He shows that when an infectious cardiomyopathy is present, overactivity causes necrosis of cardiac tissue and disease progression. Government researchers, in contrast, routinely state that CFS is a disease of underactivity and that a couch-potato lifestyle is the cause of symptoms. While governemnt researchers advocate exercise, Lerner advises resting the heart in order to "do no harm" and to prevent necrosis of cardiac tissue.
Lerner and colleagues have also documented abnormal ejection fractions in CFS, another finding which backs up CFS patients' claim that disease progression occurs with exercise. An ejection fraction is the fraction of blood within the left ventricle that is ejected with the contraction -- when it goes down, the blood is not dispelling. Some patients had reduced ejection fractions at rest while others had an ejection fraction that decreased during exercise from 51% to 36%. In a normal subject, an ejection fraction will rise during exercise. They note that a stationary or falling ejection fraction is abnormal. Their work cites studies showing that declining ejection fractions are not seen in normal persons leading a sedentary life. Deconditioning and a sedentary lifestyle in normal subjects are not causes of decreased or falling left ventricular ejection fractions. On the contrary, these cardia abnormalities are likely virally induced: in some of the CMV patients, ejection fractions reverted to normal after anti-viral therapy with ganciclovir.
Interestingly, these researchers offer an alternative theoretical framework to the important Johns Hopkins finding of Rowe et al. that CFS patients have an abnormal response to upright tilt. Lerner and colleagues deny that the basis is induced by cardiomyopthy itself.
When a theory comes along that explains more of the data than others have, I think the research community needs to take a serious look at that theory -- the thesis of Lerner and colleagues explains a myria of phenomena that others, and other theories, have simply failed to explain. for example, if CFS is indeed an infectious cardiomyopathy in which raised myocardial viral titers follow physical exertion, then we can understand more fully not only why patients relapse with exertion, but also why only physically active persons acquire the disease to begin with (and why bedridden patients in one hospital outbreak completely escaped contracting the disease). The thesis also explains why stress is a major aggravant in the disorder: Stress activates herpes viruses, and stress aggravates heart conditions. If CFS is an EBV or CMV herpes infection og the heart, then obviously stress will be doubly harmful in the condition. As mentioned above, the thesis also explains why some EBV or CMV seropositive individuals are healthy while others are sick. The infectious cardiomyopothy theory is also consistent with Robert Suhadolnik's recent finding that CFS entails an abnormality in an antiviral lymphocyte enzyme system, the 2-5A pathway, which suggests the presence of chronic viral infection.
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