Etiology, Exercise and CFS
By Suzanne Vernon, Phd
Hot off the press from the journal Psychosomatic Medicine is a paper by Samuel B. Harvey, Michael Wadsworth, Simon Wessely and Matthew Hotopf entitled “Etiology of Chronic Fatigue Syndrome: Testing Popular Hypotheses Using a National Birth Cohort Study.” Despite the psychological spin they put on the results, the findings in this paper validate what many in the patient community describe regarding activity levels prior to the onset of illness: “I was a runner. . . ”; “I loved to hike. . . ”; “until I got CFS.” This is an important publication because of that validation. This paper also reminds us of the importance and possible impact of events that happen across the lifespan.
Let’s first break down the title so that we understand what the study attempts to do. Etiology is the study of causation. Even though many investigators have searched for the cause of CFS, it has proven to be elusive. There have been many explanations as to why scientists haven’t pinned down a cause, but the most likely one is that CFS is a complex, chronic disease resulting from a combination of gene-environment interactions.
Chronic diseases like CFS are tough to study let alone to identify a cause because—as the name chronic implies and the definition insists upon—the disease occurs over time. The term birth cohort refers to a group of people enrolled in a study from birth and followed for a certain period to evaluate any number of issues across the lifespan.
Three of this study’s investigators are from the Institute of Psychiatry at King’s College London and the other, Professor Michael Wadsworth, is the retired director of the Department of Epidemiology and Public Health at University College London. This is the department that operated the National Survey of Health and Development, a British national birth cohort survey established in 1946, originally to investigate how lifespan health matters might affect fertility and obstetric issues.
In this study, the investigators aimed to test a set of hypotheses about the cause of CFS. They examined whether there were increased rates of allergy and asthma (referred to as atopic illness), decreased levels of physical exercise and/or increased childhood illnesses in people with CFS. Since this is a birth cohort, each hypothesis tapped into information from various ages. For example, childhood illness was evaluated between the ages of 6 to 15 years. A history of atopic illness was taken when the study subjects were 36 and 43 years old. Information on physical activity was gathered across the lifespan up to 53 years of age. While there is a great deal of data on this cohort, only information relevant to the above hypotheses was analyzed. (You can read more about this cohort and the kinds of information collected at http://ije.oxfordjournals.org/cgi/reprint/35/1/49.pdf.)
The first step was to determine how many people in this cohort self-reported a diagnosis of CFS. Of 2,983 participants, 10 men and 24 women (1%) reported a diagnosis of CFS with fatigue symptoms starting between 41 and 53 years of age. When investigators looked at rates of childhood illnesses that resulted in school absence or hospitalization in these 34 people with CFS, they were no different from the rest. There were also no differences in the rates of atopic illness. And rather than finding decreased levels of physical exercise, the authors were surprised to find that the 34 people with CFS had higher than average levels of exercise throughout childhood and a lower body mass index prior to their CFS diagnosis. Interestingly, these same folks reported continued exercise even after they began to experience early symptoms of fatigue.
So does this study identify the cause of CFS as being exercise? No. However, it did a reasonable job of decreasing the possible importance of atopic illness, lifetime inactivity or exercise phobia as causes of CFS.
The authors also did a good job of acknowledging some of the strengths and weaknesses of the study. But the greatest weakness of this study (which was not acknowledged) is using a national birth cohort that was designed to study something else. Since this particular British national birth cohort was designed to study fertility and obstetric issues, the information collected is particularly relevant to these two health questions. So some potentially CFS-relevant information may be missing. For example, the information on childhood illness is limited, and there’s no information on illnesses—in particular infectious disease episodes—after age 15.
The information that was not collected from this national birth cohort isn’t the fault of the authors. But rather than interpreting that the drive to be physically active is a personality trait that predisposes people to CFS, what might these researchers have found if they had the information and inclination to approach their investigation from a gene-environment perspective? There is sufficient evidence in the literature that points to genetic vulnerability for CFS. There’s also extensive evidence documenting environmental events, such as infectious mononucleosis, that can trigger CFS. Now we see a possible connection to body mass and lifetime activity. So what happens to active individuals who get the “flu” and return to that same lifestyle after they feel they’ve recovered? It’s time for investigators to step out of their comfort zone and step up to the task of connecting these tantalizing bits of disparate information to get to the cause(s) of CFS.
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