1) The Inherited Factor
Assuming that there is a limit to the diencephalon’s fat banking capacity, it follows that there are three basic ways in which obesity can become manifest. The first is that the fat-banking capacity is abnormally low from birth. Such a congenitally low diencephalic capacity would then represent the
inherited factor in obesity. When this abnormal trait is markedly present, obesity will develop at an early age in spite of normal feeding; this could explain why among brothers and sisters eating the same food at the same table some become obese and others do not.
(2) Other Diencephalic Disorders
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 sex-gland 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 heavily 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.
3) The Exhaustion of the Fat-bank
But there is still a third way in which obesity can become established, and that is when a presumably normal fat-center is suddenly — the emphasis is on suddenly — called upon to deal with an enormous influx of food far in excess of momentary requirements. At first glance it does seem that here we have a straight-forward case of overeating being responsible for obesity, but on further analysis it soon becomes clear that the relation of cause and effect is not so simple. In the first place we are merely assuming that the capacity of the fat center is normal while it is possible and even probable that only persons who have some inherited trait in this direction can become obese merely by overeating.
Secondly, in many of these cases the amount of food eaten remains the same and it is only the consumption of fuel which is suddenly decreased, as when an athlete is confined to bed for many weeks with a broken bone or when a man leading a highly active life is suddenly tied to his desk in an office and to television at home. Similarly, when a person, grown up in a cold climate, is transferred to a tropical country and continues to eat as before, he may develop obesity because in the heat far less fuel is required to maintain the normal body temperature.
When a person suffers a long period of privation, be it due to chronic illness, poverty, famine or the exigencies of war, his diencephalic regulations adjust themselves to some extent to the low food intake. When then suddenly these conditions change and he is free to eat all the food he wants, this is liable to overwhelm his fat-regulating center. During the last war about 6000 grossly underfed Polish refugees who had spent harrowing years in Russia were transferred to a camp in India where they were well housed, given normal British army rations and some cash to buy a few extras. Within about three months, 85% were suffering from obesity.
In a person eating coarse and unrefined food, the digestion is slow and only a little nourishment at a time is assimilated from the intestinal tract. When such a person is suddenly able to obtain highly refined foods such as sugar, white flour, butter and oil these are so rapidly digested and assimilated that the rush of incoming fuel which occurs at every meal may eventually overpower the diecenphalic regulatory mechanisms and thus lead to obesity. This is commonly seen in the poor man who suddenly becomes rich enough to buy the more expensive refined foods, though his total caloric intake remains the same or is even less than before.