ME Advocacy Blog post extract, 14 June 2016: Circulatory Impairment in Myalgic Encephalomyelitis: A Preliminary Thesis, by Maryann Spurgin, Ph.D.
Here is my proposal:
For many years, I have followed and collated research on Myalgic Encephalomyelitis (ME), in particular on the circulatory impairment of which Dr. A. Melvin Ramsay spoke and of which there are many recently discovered facets. Despite lack of research on circulatory impairment in ME in the 1950’s, Dr. A. Melvin Ramsay astutely observed it clinically as one of the three essential components of ME, noting pale, cold skin as a sign.
Sixty years later, the research behind these observations is now extensive, although some of that research was published under the name “CFS”; yet it applies to patients with ME or those with ME who are misdiagnosed with “CFS,” itself a govt construct that, as noted above, has impeded consistent findings. My view is that “CFS” is a government construct.
There are people with everything from MS to fibromyalgia to depression to ME who are diagnosed with “CFS.” So there are not two separate diseases, ME and “CFS”; rather, those diagnosed with “CFS” have something else in need of diagnosis, whether ME or another disease. Much of the research on ME was done under the name “CFS.”
I have spent 22 years studying circulatory impairment in ME by reading published research on its many facets, beginning over 20 years ago with Dr. L.O. Simpson’s work on impaired capillary blood flow [1], the haematological/ hemorheological flow problems that impede delivery of oxygen and nutrients to organs and tissues and impede removal of lactic acid, toxins and metabolic waste due to poorly deformable Red Blood Cells.
Much later, in the 1990’s, Dr. David Bell’s and the late Dr. David Streeten’s joint work on low blood volume (hypovolemia) in ME was published [2, 3]. Dr. Streeten was a world-renowned endocrinologist whose area of specialization was blood pressure and orthostatic disorders.
The third aspect of circulatory impairment is cardiac:
The late Dr. A. Martin Lerner pioneered it, with his hypothesis that the disease is a viral cardiomyopathy. He found on biopsies virally infected cardiac myocytes in the disease, published in the 1990’s [4-6]. He argued that the disease is at its root a viral cardiomyopathy.
Importantly, there was also NIH grant-funded research by Drs Benjamin Natelson and Arnold Peckerman on abnormal impedance cardiography and other cardiac abnormalities in ME patients [7]. These important studies influenced researcher/clinician Dr. Paul Cheney, who found and illuminated problems with cardiac diastolic dysfunction in the disease (diastolic problems not caused by volume depletion but by a pathology in the heart itself), following his own experience with heart failure and his subsequent heart transplant.
This extensive body of research shows that, without identifying the root cause of ME, disorders of microcirculation and macrocirculation are well established pathophysiological findings [8-11], and that combined circulation problems can conspire to create havoc in the heart and other organs of the body.
I have thought a lot about circulatory problems over many years, and how these impairments come together to create the intolerable symptomatology of ME that could lead someone to be so impaired as to not be able to swallow, and could lead the Institute of Medicine to declare that organ failure, even death, can occur from the slightest exertion and/or sensory overload.
This happens, I believe, when one or more or all of the following three conditions hold:
- Metabolic demand exceeds the capacity for cardiac output. Studies have shown that if the level of exertion or metabolic demand on the heart exceeds the capacity of the heart to pump blood by even 1%, the organism dies. Rest and limiting demands on a heart whose output is reduced by disease is crucial to survival.
- An impaired RBC/capillary delivery system is present (My own theory is that this impairment may be a defense mechanism to slow metabolic demand in order to protect the heart); And…
- When low blood volume is present.
One of these impairments alone could cause havoc, but the three of these pathophysiologies together could lead to extreme multisystem involvement and death. In a patient who is already volume depleted, poor diastolic filling from still another, cardiac problem could be doubly dangerous, yet this is exactly what Dr. Cheney has found.
Although this research does not hypothesize a cause, and circulation problems are likely the result of some underlying (likely viral) cause, this particular aspect of the pathophysiology, I believe, is crucial to a biological understanding of ME, and to explaining why ME patients relapse and can die from exertion. Mitochondrial problems that are not primary mitochondrial disease but are an epiphenomenon of the (unknown) cause or causes likely also play a role, especially in cardiac and brain dysfunction (see the home page of my website that discusses mitochondrial epiphenomena and the references I provided on the site).
