Wednesday, October 22, 2014
Regular readers may recall my previous attempts at finding an etiological framework for defining obesity subtypes.
This idea is by no means new.
Here is what Stunkard had to say about the need to differentiate different types of obesity:
“In the ambition to explain all instances of obesity, it has frequently been assumed, albeit implicitly, that obesity is a single disease with a single etiology. In the sense that the production of obesity requires at least a temporary disorder in the regulation of energy balance, obese persons do have something in common. But any physiological regulation is apt to require a complex piece of apparatus, and one as precise and vital as that controlling energy balance must contain a good many parts which could go awry. There seems to be no reason to assign all the possible disorders of all the possible parts to a single etiological agent.”
“Such considerations have persuaded investigators in several fields of research to consider obesity to be a symptom of multiple etiology… For’ if one did not feel obliged to find common features in every case of obesity, but could restrict one’s efforts to members of subgroups of obese persons, it should increase the likelihood of discovering common and distinctive psychological features…if there are indeed different types of obesity, it would be preferable to select samples by criteria which might be more closely related to differences in etiology.”
Unfortunately, over 50 years after this paper was published, we are still doing obesity research with BMI as the sole “defining variable” of this phenotype.
Imagine if we were to do studies in cancer research, where we included participants with any kind of cancer.
Or infectious disease research, in which we included participants with any kind of fever.
Or cadiac research, in anyone with heart disease.
You get the idea.