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The second way in which obesity can become established is the lowering of a previously normal fat-banking capacity owing to some other diencephalic disorder.
It seems to be a general rule that when one of the many diencephalic centers is particularly overtaxed; it tries to increase its capacity at the expense of other centers. In the menopause and after castration the hormones previously produced in the sex-glands no longer circulate in the body.
In the presence of normally functioning sex-glands their hormones act as a brake on the secretion of the sexgland stimulating hormones of the anterior pituitary. When this brake is removed the anterior pituitary enormously increases its output of these sex-gland stimulating hormones, though they are now no longer effective. In the absence of any response from the non-functioning or missing sex glands, there is nothing to stop the anterior pituitary from producing more and more of these hormones. This situation causes an excessive strain on the diencephalic center which controls the function of the anterior pituitary. In order to cope with this additional burden the center appears to draw more and more energy away from other centers, such as those concerned with emotional stability, the blood circulation (hot flushes) and other autonomous nervous regulations, particularly also from the not so vitally important fat-bank.
The so called stable type of diabetes involves the diencephalic blood sugar regulating center the diencephalon tries to meet this abnormal load by switching energy destined for the fat bank over to the sugar-regulating center, with the result that the fat-banking capacity is reduced to the point at which it is forced to establish a fixed deposit and thus initiate the disorder we call obesity. In this case one would have to consider the diabetes the primary cause of the obesity, but it is also possible that the process is reversed in the sense that a deficient or overworked fat-center draws energy from the sugar-center, in which case the obesity would be the cause of that type of diabetes in which the pancreas is not primarily involved. Finally, it is conceivable that in Cushing's syndrome those symptoms which resemble obesity are entirely due to the withdrawal of energy from the diencephalic fat-bank in order to make it available to the highly disturbed center which governs the anterior pituitary adrenocortical system.
Whether obesity is caused by a marked inherited deficiency of the fat-center or by some entirely different diencephalic regulatory disorder, its insurgence obviously has nothing to do with overeating and in either case obesity is certain to develop regardless of dietary restrictions. In these cases any enforced food deficit is made up from essential fat reserves and normal structural fat, much to the disadvantage of the patient's general health.
