At one time it was thought that this mechanism might be concerned with the sex glands. Such a connection was suggested by the fact that many juvenile obese patients show an under-development of the sex organs. The middle-age spread in men and the tendency of many women to put on weight in the menopause seemed to indicate a causal connection between diminishing sex function and overweight. Yet, when highly active sex hormones became available, it was found that their administration had no effect whatsoever on obesity. The sex glands could therefore not be the seat of the disorder.
The Thyroid Gland
When it was discovered that the thyroid gland controls the rate at which body-fuel is consumed, it was thought that by administering thyroid gland to obese patients their abnormal fat deposits could be burned up more rapidly. This too proved to be entirely disappointing, because as we now know, these abnormal deposits take no part in the body’s energy-turnover – they are inaccessibly locked away. Thyroid medication merely forces the body to consume its normal fat reserves, which are already depleted in obese patients, and then to break down structurally essential fat without touching the abnormal deposits. In this way a patient may be brought to the brink of starvation in spite of having a hundred pounds of fat to spare. Thus any weight loss brought about by thyroid medication is always at the expense of fat of which the body is in dire need.
While the majority of obese patients have a perfectly normal thyroid gland and some even have an overactive thyroid, one also occasionally sees a case with a real thyroid deficiency. In such cases, treatment with thyroid brings about a small loss of weight, but this is not due to the loss of any abnormal fat. It is entirely the result of the elimination of a mucoid substance, called myxedema, which the body accumulates when there is a marked primary thyroid deficiency. Moreover, patients suffering only from a severe lack of thyroid hormone never become obese in the true sense. Possibly also the observation that normal persons – though not the obese – lose weight rapidly when their thyroid becomes overactive may have contributed to the false notion that thyroid deficiency and obesity are connected. Much misunderstanding about the supposed role of the thyroid gland in obesity is still met with, and it is now really high time that thyroid preparations be once and for all struck off the list of remedies for obesity. This is particularly so because giving thyroid gland to an obese patient whose thyroid is either normal or overactive, besides being useless, is decidedly dangerous.
The Pituitary Gland
The next gland to be falsely incriminated was the anterior lobe of the pituitary, or hypophysis. This most important gland lies well protected in a bony capsule at the base of the skull. It has a vast number of functions in the body, among which is the regulation of all the other important endocrine glands. The fact that various signs of anterior pituitary deficiency are often associated with obesity raised the hope that the seat of the disorder might be in this gland. But although a large number of pituitary hormones have been isolated and many extracts of the gland prepared, not a single one or any combination of such factors proved to be of any value in the treatment of obesity. Quite recently, however, a fat-mobilizing factor has been found in pituitary glands, but it is still too early to say whether this factor is destined to play a role in the treatment of obesity.
Recently, a long series of brilliant discoveries concerning the working of the adrenal or suprarenal glands, small bodies which sit atop the kidneys, have created tremendous interest. This interest also turned to the problem of obesity when it was discovered that a condition which in some respects resembles a severe case of obesity – the so called Cushing’s Syndrome – was caused by a glandular new-growth of the adrenals or by their excessive stimulation with ACTH, which is the pituitary hormone governing the activity of the outer rind or cortex of the adrenals.
When we learned that an abnormal stimulation of the adrenal cortex could produce signs that resemble true obesity, this knowledge furnished no practical means of treating obesity by decreasing the activity of the adrenal cortex. There is no evidence to suggest that in obesity there is any excess of adrenocortical activity; in fact, all the evidence points to the contrary. There seems to be rather a lack of adrenocortical function and a decrease in the secretion of ACTH from the anterior pituitary lobe.3
So here again our search for the mechanism which produces obesity led us into a blind alley. Recently, many students of obesity have reverted to the nihilistic attitude that obesity is caused simply by overeating and that it can only be cured by under eating.