As a basis for our discussion we postulate that obesity in all its many forms is due to an abnormal functioning of some part of the body and that every ounce of abnormally accumulated fat is always the result of the same disorder of certain regulatory mechanisms. Persons suffering from this particular disorder will get fat regardless of whether they eat excessively, normally or less than normal. A person who is free of the disorder will never get fat, even if he frequently overeats.

Those in whom the disorder is severe will accumulate fat very rapidly, those in whom it is moderate will gradually increase in weight and those in whom it is mild may be able to keep their excess weight stationary for long periods.  In all these cases a loss of weight brought about by dieting, treatments with thyroid, appetite-reducing drugs, laxatives, violent exercise, massage, baths, etc., is only temporary and will be rapidly regained as soon as the reducing regimen is relaxed. The reason is simply that none of these measures corrects the basic disorder.

While there are great variations in the severity of obesity, we shall consider all the different forms in both sexes and at all ages as always being due to the same disorder. Variations in form would then be partly a matter of degree, partly an inherited bodily constitution and partly the result of a secondary involvement of endocrine glands such as the pituitary, the thyroid, the adrenals or the sex glands. On the other hand, we postulate that no deficiency of any of these glands can ever directly produce the common disorder known as obesity.

If this reasoning is correct, it follows that a treatment aimed at curing the disorder must be equally effective in both sexes, at all ages and in all forms of obesity. Unless this is so, we are entitled to harbor grave doubts as to whether a given treatment corrects the underlying disorder. Moreover, any claim that the disorder has been corrected must be substantiated by the ability of the client to eat normally of any food he pleases without regaining abnormal fat after treatment. Only if these conditions are fulfilled can we legitimately speak of curing obesity rather than of reducing weight.

Our problem thus presents itself as an enquiry into the localization and the nature of the disorder which leads to obesity. The history of this enquiry is a long series of high hopes and bitter disappointments.

There was a time, not so long ago, when obesity was considered a sign of health and prosperity in man and of beauty, amorousness and fecundity in women. This attitude probably dates back to Neolithic times, about 8000 years ago; when for the first time in the history of culture, man began to own property, domestic animals, arable land, houses, pottery and metal tools. Before that, with the possible exception of some races such as the Hottentots, obesity was almost non-existent, as it still is in all wild animals and most primitive races.

Today obesity is extremely common among all civilized races, because a disposition to the disorder can be inherited. Wherever abnormal fat was regarded as an asset, sexual selection tended to propagate the trait. It is only in very recent times that manifest obesity has lost some of its allure, though the cult of the outsize bust – always a sign of latent obesity – shows that the trend still lingers on.

In the early Neolithic times another change took place which may well account for the fact that today nearly all inherited dispositions sooner or later develop into manifest obesity. This change was the institution of regular meals. In pre-Neolithic times, man ate only when he was hungry and only as much as he required to still the pangs of hunger. Moreover, much of his food was raw and all of it was unrefined. He roasted his meat, but he did not boil it, as he had no pots, and what little he may have grubbed from the Earth and picked from the trees, he ate as he went along.

The whole structure of man””s omnivorous digestive tract is, like that of an ape, rat or pig, adjusted to the continual nibbling of tidbits. It is not suited to occasional gorging as is, for instance, the intestine of the carnivorous cat family. Thus the institution of regular meals placed a great burden on modern man””s ability to cope with large quantities of food suddenly pouring into his system from the intestinal tract.

The institution of regular meals meant that man had to eat more than his body required at the moment of eating so as to tide him over until the next meal. Food rendered easily digestible suddenly flooded his body with nourishment of which he was in no need at the moment. Somehow, somewhere this surplus had to be stored.

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 clients 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 clients their abnormal fat deposits could be burned up more rapidly. These abnormal deposits take no part in the body””s energy-turnover – they are inaccessibly locked away therefore any weight loss brought about by thyroid medication is always at the expense of fat of which the body is in dire need.

The Pituitary Gland

The next gland to be falsely incriminated was the anterior lobe of the pituitary, or hypophysis. 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.

The Adrenals

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.

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]

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.

The Diencephalon or Hypothalamus

For those of us who refused to be discouraged there remained one slight hope. Buried deep down in the massive human brain there is a part which we have in common with all vertebrate animals the so-called diencephalon. It is a very primitive part of the brain and has in man been almost smothered by the huge masses of nervous tissue with which we think reason and voluntarily move our body. The diencephalon is the part from which the central nervous system controls all the automatic animal functions of the body, such as breathing, the heart beat, digestion, sleep, sex, the urinary system, the autonomous or vegetative nervous system and via the pituitary the whole interplay of the endocrine glands.

It was therefore not unreasonable to suppose that the complex operation of storing and issuing fuel to the body might also be controlled by the diencephalon. It has long been known that the content of sugar – another form of fuel – in the blood depends on a certain nervous center in the diencephalon. When this center is destroyed in laboratory animals, they develop a condition rather similar to human stable diabetes. It has also long been known that the destruction of another diencephalic center produces a voracious appetite and a rapid gain in weight in animals which never get fat spontaneously.

Assuming that in man such a center controlling the movement of fat does exist, its function would have to be much like that of a bank. When the body assimilates from the intestinal tract more fuel than it needs at the moment, this surplus is deposited in what may be compared with a current account. Out of this account it can always be withdrawn as required. All normal fat reserves are in such a current account, and it is probable that a diencephalic center manages the deposits and withdrawals.

When now, for reasons which will be discussed later, the deposits grow rapidly while small withdrawals become more frequent, a point may be reached which goes beyond the diencephalon”s banking capacity. Just as a banker might suggest to a wealthy client that instead of accumulating a large and unmanageable current account he should invest his surplus capital, the body appears to establish a fixed deposit into which all surplus funds go but from which they can no longer be withdrawn by the procedure used in a current account. In this way the diencephalic “fat-bank” frees itself from all work which goes beyond its normal banking capacity. The onset of obesity dates from the moment the diencephalon adopts this labor-saving ruse. Once a fixed deposit has been established the normal fat reserves are held at a minimum, while every available surplus is locked away in the fixed deposit and is therefore taken out of normal circulation.

(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 client”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 diencephalic 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.

Much has been written about the psychological aspects of obesity. Among its many functions the diencephalon is also the seat of our primitive animal instincts, and just as in an emergency it can switch energy from one center to another, so it seems to be able to transfer pressure from one instinct to another. Thus, a lonely and unhappy person deprived of all emotional comfort and of all instinct gratification except the stilling of hunger and thirst can use these as outlets for pent up instinct pressure and so develop obesity. Yet once that has happened, no amount of psychotherapy or analysis, happiness, company or the gratification of other instincts will correct the condition.

Compulsive Eating

Most obese clients do not suffer from compulsive eating; they suffer genuine hunger – real, gnawing, torturing hunger – which has nothing whatever to do with compulsive eating. Compulsive eating does occur in some obese clients. It comes on in attacks and is never associated with real hunger, a fact which is readily admitted by the clients. They only feel a feral desire to stuff.

A careful enquiry into what may have brought on an attack almost invariably reveals that it is preceded by a strong unresolved sex-stimulation, the higher centers of the brain having blocked primitive diencephalic instinct gratification. The pressure is then let off through another primitive channel, which is oral gratification. Clients suffering from real compulsive eating are comparatively rare. In my practice they constitute about 1-2%.

Reluctance to Lose Weight

Some clients are deeply attached to their fat and cannot bear the thought of losing it. If they are intelligent, popular and successful in spite of their weight, this is a source of pride. Some overweight girls look upon their weight as a safeguard against erotic involvements, of which they are afraid. They fear that, after weight loss, people will like them on account of their figure rather than be attracted by their intelligence or character only.  Some have a feeling that reducing means giving up an almost cherished and intimate part of them. An affectionate attachment to abnormal fat is usually seen in clients who became obese in childhood, but this is not necessarily so.

There are a large number of ways in which obesity can be initiated, though the disorder itself is always due to the same mechanism, an inadequacy of the diencephalic fat-center and the laying down of abnormally fixed fat deposits in abnormal places. This means that once obesity has become established, it can no more be cured by eliminating those factors which brought it on than a fire can be extinguished by removing the cause of the conflagration

Weight alone is not a satisfactory criterion by which to judge whether a person is suffering from the disorder we call obesity or not. Every nutritional counselor is familiar with the sylphlike lady who enters the consulting room and declares emphatically that she is getting horribly fat and wishes to reduce. Many an honest and sympathetic nutritional counselor at once concludes that they are dealing with a “nut.” In my experience the lady is nearly always right and the counselor wrong. When such a client is carefully examined one finds many signs of potential obesity, which is just about to become manifest as overweight. The client distinctly feels that something is wrong with her, that a subtle change is taking place in her body, and this alarms her.
There are a number of signs and symptoms which are characteristic of obesity.

Signs and symptoms of obesity

The bodily signs may be divided into such as have developed before puberty, indicating a strong inherited factor, and those which develop at the onset of manifest disorder. Early signs are a disproportionately large size of the two upper front teeth, the first incisor, or a dimple on both sides of the sacral bone just above the buttocks. When the arms are outstretched with the palms upward, the forearms appear sharply angled outward from the upper arms. The same applies to the lower extremities. The client cannot bring his feet together without the knees overlapping; he is, in fact, knock-kneed.

The beginning accumulation of abnormal fat shows as a little pad just below the nape of the neck, colloquially known as the Duchess” Hump. There is a triangular fatty bulge in front of the armpit when the arm is held against the body. When the skin is stretched by fat rapidly accumulating under it, it may split in the lower layers. When large and fresh, such tears are purple, but later they are transformed into white scar-tissue. Such striation, as it is called, commonly occurs on the abdomen of women during pregnancy, but in obesity it is frequently found on the breasts, the hips and occasionally on the shoulders. In many cases striation is so fine that the small white lines are only just visible. They are always a sure sign of obesity, and though this may be slight at the time of examination such clients can usually remember a period in their childhood when they were excessively chubby.

Another typical sign is a pad of fat on the insides of the knees, a spot where normal fat reserves are never stored. There may be a fold of skin over the pubic area and another fold may stretch round both sides of the chest, where a loose roll of fat can be picked up between two fingers. In the male an excessive accumulation of fat in the breasts is always indicative, while in the female the breast is usually, but not necessarily, large. Obviously excessive fat on the abdomen, the hips, thighs, upper arms, chin and shoulders are characteristic, and it is important to remember that any number of these signs may be present in persons whose weight is statistically normal; particularly if they are dieting on their own with iron determination.

Common clinical symptoms which are indicative only in their association and in the frame of the whole clinical picture are: frequent headaches, rheumatic pains without detectable bony abnormality; a feeling of laziness and lethargy, often both physical and mental and frequently associated with insomnia, the clients saying that all they want is to rest; the frightening feeling of being famished and sometimes weak with hunger two to three hours after a hearty meal and an irresistible yearning for sweets and starchy food which often overcomes the client quite suddenly and is sometimes substituted by a desire for alcohol; constipation and a spastic or irritable colon are unusually common among the obese, and so are menstrual disorders.

Returning once more to our sylphlike lady, we can say that a combination of some of these symptoms with a few of the typical bodily signs is sufficient evidence to take her case seriously. A human figure, male or female, can only be judged in the nude, we will however not ask you to strip and will provide assistance in measuring if you desire; any opinion by us based on the dressed appearance can be quite fantastically wide off the mark so you will be asked to be objective concerning your self.

The Lady Whose Fat Was All in One Place

One of our clients weighed in at 116lbs, obviously not obese in terms of pounds. Her issue was the placement of those pounds. Most of her complaint was her hips. We started the HCG + diet protocol and at the mid point she weighed in at 1lb lighter but had lost 7 inches in her hips. By the end of the 30 day protocol she had lost an additional pound and an additional 5 inches in her hips.

Fat but not Obese

While a person who is statistically underweight may still be suffering from the disorder which causes obesity, it is also possible for a person to be statistically overweight without suffering from obesity. For such persons weight is no problem, as they can gain or lose at will and experience no difficulty in reducing their caloric intake. They are masters of their weight, which the obese are not. Moreover, their excess fat shows no preference for certain typical regions of the body, as does the fat in all cases of obesity. Thus, the decision whether a borderline case is really suffering from obesity or not cannot be made merely by consulting weight tables.