Posted to misc.fitness.aerobic by Larry DeLuca, EdM, CSCS under the subject Blair, ACSM, and obesity on 1999/05/13

[Pet worldviews, single studies, and Stephen Blair.]

Blair is not the only researcher who has suggested the rejection of the "Fit or Fat" theory, nor is he attempting to do so on the results of a single study. The idea is not a very new one, at least in exercise physiology circles.

In 1995, ACSM removed "obesity" from its list of risk factors for cardio- vascular disease. In their _Guidelines for Exercise Testing and Prescription, 5th Edition_, it was explained that in reviewing large amounts of study data collected in a variety of areas over many years that obesity *by itself* was a very poor marker of disease risk, and that *more specific markers* (like hypertension, hypercholesterolemia, physical inactivity, etc.) were much better predictors of disease risk.

AHA flip-flops back and forth on obesity as an independent risk factor. I don't know what their current status on it is, though last I heard they were planning on re-adding it to their list of risk factors.

The upshot of all of this is that no matter who you talk to, it's very clear that certain risk factors (like hypertension) are much more firmly established than others (like obesity). Part of what's brought about the change in thinking about obesity is that the assumption that obese people are a homogenous population has been shattered. Obese people who have high levels of cardiovascular fitness, normal blood lipid profiles, and are normotensive, etc., etc., are certainly not the majority, but they now exist in large enough numbers that it is becoming possible to tease out the primary effects of obesity from the secondary effects of a sedentary lifestyle due to (or contributed to by) obesity.

Part of the reason that I think Blair's work is exciting (and not that surprising) is that we have been through such cycles of refinement of thought many times as we have learned more about a given physiological problem. For example, the link between cholesterol and heart disease was understood long before we understood cholesterol metabolism well enough to differentiate between HDL and LDL, and before we appreciated the significance of saturated fat intake on blood cholesterol levels, or the impact of exercise on HDL. These refinements in our understanding have led us to new ways of looking at disease, and have had a profound influence upon the interventions we offer.

Similarly, we have gone through a complete metamorphosis on the lower bound of physical activity necessary for health benefits. Given the public's overall low participation in exercise programming of the traditional variety, much research effort has been expended to figure out just how low the "dose" of exercise can be to achieve some sort of treatment "response." The answers have been quite surprising, and have dramatically altered our notions of what the lower bound is. People would have scoffed at "Exercise Lite" 10 years ago because we didn't appreciate the fact that health benefits could be realized from physical activity at low to moderate levels even in the absence of improvements in traditional markers of fitness (i.e., VO2max).

Blair's work (and that of the others upon which he builds) strongly suggest that we are on the verge of a major refinement in our understanding of the impact of obesity on health. It does not suggest for a moment that there is no reason to lose excess body fat, nor does it claim (as some would suggest) that obesity is not associated with other disorders (such as hypertension and hypercholesterolemia) that may have an impact on CVD risk.

What it *does* say is that we can't just stop at "obesity" and assign someone a risk factor for heart disease. We need to look more closely, asking questions about blood pressure, blood lipids, family/personal history, activity level, etc., before we can assess someone's CVD risk, obese or not.

larry...

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