AS A POINT of departure for this summary I wish to present an outline of mechanisms for the development of obesity. With minor changes, it is one recently proposed by Van Itallie and is based on the concept that there exist multiple etiologic factors— genetic, traumatic and environmental—in the development of obesity.
The fact that there are two main categories—1) regulatory, i.e., with no primary metabolic abnormality, and 2) metabolic—does not imply that patients with obesity obey some law higher than that of the conservation of energy. Studies by Newburgh and his co-workers established this for all patients beyond argument from wishful nonbelievers. Mayer has stressed, however, that Newburgh's work should not serve as a rigid, at times puritanical, obstacle to consideration of the problems of individual patients, a point of view inherent in Newburgh's listing of different "proximate causes to which some persons respond (in part) by overeating."
Patients with a regulatory disorder may develop obesity as a result of increased caloric intake or decreased caloric output or frequently both. Under increased caloric intake, we have two categories, "organic" and "functional." We have put quotes about both headings because this common form of categorization implies a sharp division in our thinking and sometimes interferes with our therapeutic approach to patients; most of us still feel more comfortable with a patient whose complaints are organic rather than so-called functional. We think of nephrosis and galactosemia as organic diseases but, in the present state of our knowledge, have to fall back on calling the increased glomerular permeability of the former and the enzymatic defect of the latter, lesions in chemical anatomy. Perhaps advances in electronmicroscopy and histochemistry will ultimately make use of this term more literal.
- Copyright © 1957 by the American Academy of Pediatrics