We may consider it as established that in most obese people the amount of energy consumed pro kilo of protoplasm is altogether normal, and that there is no "retardation of the metabolism." Overfeeding alone, that is, a disproportion between the food intake and the energy output, is the cause of the increase in the fat layers. Obese individuals and frequently, too, physicians, when the first regulations directed towards the reduction of obesity fail to produce immediate results, are very much inclined to attribute the obesity and the lack of success in its treatment not to the habits of life of the patients, but rather to some perversion of their metabolism. The deeper, however, one attempts to gain an insight into the peculiarities of each case, the more frequently will one become convinced that it is unnecessary to conjure up unknown factors, for wrong habits of life alone generally suffice to explain the pathogenesis of the obesity. Nevertheless, there are actually cases in which occasionally an exact and conscientious calculation of the diet demonstrates that these patients not only consume an ordinary normal amount of food, but actually eat less than normal, while at the same time their muscular activity is rather above than below the normal average; and, notwithstanding all this, such individuals become obese; so that here one is actually forced to the assumption that less caloric energy is developed per kilogramme of protoplasm than is normal. In such rare instances one may then actually speak of a "retardation of the metabolism" in the old and venerable sense. Experimental investigations in regard to the amount of oxygen consumed in such obese individuals rather bear out this contention.

Formerly I was inclined to look for the cause of this reduced caloric energy development exclusively in a particular inherited or acquired endogenous constitution of the protoplasm. In numerous cases this explanation is probably the correct one. Of recent years, however, attention has been directed to influences emanating from the thyroid gland. The internal secretion of the thyroid to a large extent governs the intensity of the oxydation processes. We know by very exact investigations that in Basedow's disease (hyperthyroidism) the intensity of oxydation processes (the consumption of energy) is increased by 25 to 50%, whereas in myxedema (hypothyroidism) it may be reduced by 20 to 30%. These are extreme conditions, and between the two poles are undoubtedly many intermediary stages. Slight perversions of the internal thyroid function, upward or downward, will hardly stigmatize individuals inflicted in this way as cases of Basedow's disease or of myxedema in the clinical sense. Nevertheless, the energy development in such cases is changed, sometimes more, sometimes less. The ordinary calculations in regard to the maintenance diet are not only upset, but the patients consume more, or less, than an average normal individual would consume under the same external conditions; so that while they are taking the same amount of food as an average individual, they, nevertheless, emaciate or grow obese (see Vol. VIII).

Hypothyroidism seems to be not infrequently the cause of retarded metabolism. In part a primary insufficiency of the thyroid gland must be incriminated, and in part a secondary insufficiency of an otherwise healthy thyroid, the function of the latter becoming depressed by chemical influences emanating from other glands (so-called chemical correlation). Such remote effects may originate from the following organs: pancreas, sexual glands, hypophysis, suprarenals, thymus. The clinical and experimental experience we have acquired so far justifies this statement. At the same time a great deal of work remains to be done in order to thoroughly clear these problems.

Considerations of this kind are not only of theoretical interest, but they are of the greatest practical importance. We should always make the attempt to treat etiologically and not only symptomatically. If, therefore, we are confronted with a case of obesity that has developed on the basis of primary or secondary hypofunction of the thyroid, then reduction of the amount of food or increase of the muscular labor would merely constitute symptomatic treatment, whereas the same measures employed in obesity, due to overfeeding or in obesity due to lack of exercise, would possess the dignity of etiologic treatment. In thyreogenous obesity the administration of thyroid preparations more closely approximates an etiologic plan of therapy, and incidentally, as we will have occasion to show, produces fairly good results, whereas the same treatment in the forms of obesity discussed previously and characterized as obesity from overfeeding would be merely symptomatic.