weight Gain/Loss

[Guest guest]

I can't find the post where we were talking about people having

difficulty losing and keeping weight off. I posted this link and

part of the paper by the original doctor who found that people with

damage to the hypothalmus gland had this problem. And how to tell if

it would apply to you.

Dr. A.T.W. Simeons Manuscript, " Pounds and Inches "

From hcgdietinfo.com

FOREWORD - Introduction by Dr. Simeons

This book discusses a new interpretation of the nature of obesity,

and while it does not advocate yet another fancy slimming diet it

does describe a method of treatment which has grown out of

theoretical considerations based on clinical observation.

What I have to say is, in essence, the views distilled out of forty

years of grappling with the fundamental problems of obesity, its

causes, its symptoms, and its very nature. In these many years of

specialized work, thousands of cases have passed through my hands and

were carefully studied. Every new theory, every new method, every

promising lead was considered, experimentally screened and critically

evaluated as soon as it became known. But invariably the results were

disappointing and lacking in uniformity.

I felt that we were merely nibbling at the fringe of a great problem,

as, indeed, do most serious students of overweight. We have grown

pretty sure that the tendency to accumulate abnormal fat is a very

definite metabolic disorder, much as is, for instance, diabetes. Yet

the localization and the nature of this disorder remained a mystery.

Every new approach seemed to lead into a blind alley, and though

patients were told that they are fat because they eat too much, we

believed that this is neither the whole truth nor the last word in

the matter.

Refusing to be side-tracked by an all too facile interpretation of

obesity, I have always held that overeating is the result of the

disorder, not its cause, and that we can make little headway until we

can build for ourselves some sort of theoretical structure with which

to explain the condition. Whether such a structure represents the

truth is not important at this moment. What it must do is to give us

an intellectually satisfying interpretation of what is happening in

the obese body. It must also be able to withstand the onslaught of

all hitherto known clinical facts and furnish a hard background

against which the results of treatment can be accurately assessed.

To me this requirement seems basic, and it has always been the center

of my interest. In dealing with obese patients it became a habit to

register and order every clinical experience as if it were an odd

looking piece of a jig-saw puzzle. And then, as in a jig saw puzzle,

little clusters of fragments began to form, though they seemed to fit

in nowhere. As the years passed these clusters grew bigger and

started to amalgamate until, about sixteen years ago, a complete

picture became dimly discernible. This picture was, and still is,

dotted with gaps for which I cannot find the pieces, but I do now

feel that a theoretical structure is visible as a whole.

With mounting experience, more and more facts seemed to fit snugly

into the new framework, and then, when a treatment based on such

speculations showed consistently satisfactory results, I was sure

that some practical advance had been made, regardless of whether the

theoretical interpretation of these results is correct or not.

The clinical results of the new treatment have been published in

scientific journal and these reports have been generally well

received by the profession, but the very nature of a scientific

article does not permit the full presentation of new theoretical

concepts nor is there room to discuss the finer points of technique

and the reasons for observing them.

During the 16 years that have elapsed since I first published my

findings, I have had many hundreds of inquiries from research

institutes, doctors and patients. Hitherto I could only refer those

interested to my scientific papers, though I realized that these did

not contain sufficient information to enable doctors to conduct the

new treatment satisfactorily. Those who tried were obliged to gain

their own experience through the many trials and errors which I have

long since overcome.

Doctors from all over the world have come to Italy to study the

method, first hand in my clinic in the Salvator Mutidi International

Hospital in Rome. For some of them the time they could spare has been

too short to get a full grasp of the technique, and in any case the

number of those whom I have been able to meet personally is small

compared with the many requests for further detailed information

which keep coming in. I have tried to keep up with these demands by

correspondence, but the volume of this work has become unmanageable

and that is one excuse for writing this book.

In dealing with a disorder in which the patient must take an active

part in the treatment, it is, I believe, essential that he or she

have an understanding of what is being done and why. Only then can

there be intelligent cooperation between physician and patient. In

order to avoid writing two books, one for the physician and another

for the patient - a prospect which would probably have resulted in no

book at all - I have tried to meet the requirements of both in a

single book. This is a rather difficult enterprise in which I may not

have succeeded. The expert will grumble about long-windedness while

the lay-reader may occasionally have to look up an unfamiliar word in

the glossary provided for him.

To make the text more readable I shall be unashamedly authoritative

and avoid all the hedging and tentativeness with which it is

customarily to express new scientific concepts grown out of clinical

experience and not as yet confirmed by clear-cut laboratory

experiments. Thus, when I make what reads like a factual statement,

the professional reader may have to translate into: clinical

experience seems to suggest that such and such an observation might

be tentatively explained by such and such a working hypothesis,

requiring a vast amount of further research before the hypothesis can

be considered a valid theory. If we can from the outset establish

this as a mutually accepted convention, I hope to avoid being accused

of speculative exuberance.

Obesity a Disorder

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 chanisms. 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, or baths 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 patient 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.

The History of Obesity

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.

The Significance of Regular Meals

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 on1y as much as he required too 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, particularly of food rendered rapidly, 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.

Three Kinds of Fat

In the human body we can distinguish three kinds of fat. The first is

the structural fat which fills the gaps between various organs, a

sort of packing material. Structural fat also performs such important

functions as bedding the kidneys in soft elastic tissue, protecting

the coronary arteries and keeping the skin smooth and taut. It also

provides the springy cushion of hard fat under the bones of the feet,

without which we would be unable to walk.

The second type of fat is a normal reserve of fuel upon which the

body can freely draw when the nutritional income from the intestinal

tract is insufficient to meet the demand. Such normal reserves are

localized all over the body. Fat is a substance which packs the

highest caloric value into the smallest space so that normal reserves

of fuel for muscular activity and the maintenance of body temperature

can be most economically stored in this form. Both these types of

fat, structural and reserve, are normal, and even if the body stocks

them to capacity this can never be called obesity.

But there is a third type of fat which is entirely abnormal. It is

the accumulation of such fat, and of such fat only, from which the

overweight patient suffers. This abnormal fat is also a potential

reserve of fuel, but unlike the normal reserves it is not available

to the body in a nutritional emergency. It is, so to speak, locked

away in a fixed deposit and is not kept in a current account, as are

the normal reserves.

When an obese patient tries to reduce by starving himself, he will

first lose his normal fat reserves. When these are exhausted he

begins to burn up structural fat, and only as a last resort will the

body yield its abnormal reserves, though by that time the patient

usually feels so weak and hungry that the diet is abandoned. It is

just for this reason that obese patients complain that when they diet

they lose the wrong fat. They feel famished and tired and their face

becomes drawn and haggard, but their belly, hips, thighs and upper

arms show little improvement. The fat they have come to detest stays

on and the fat they need to cover their bones gets less and less.

Their skin wrinkles and they look old and miserable. And that is one

of the most frustrating and depressing experiences a human being can

have.

Injustice to the Obese

When then obese patients are accused of cheating, gluttony, lack of

will power, greed and sexual complexes, the strong become indignant

and decide that modern medicine is a fraud and its representatives

fools, while the weak just give up the struggle in despair. In either

case the result is the same: a further gain in weight, resignation to

an abominable fate and the resolution at least to live tolerably the

short span allotted to them - a fig for doctors and insurance

companies.

Obese patients only feel physically well as long as they are

stationary or gaining weight. They may feel guilty, owing to the

lethargy and indolence always associated with obesity. They may feel

ashamed of what they have been led to believe is a lack of control.

They may feel horrified by the appearance of their nude body and the

tightness of their clothes. But they have a primitive feeling of

animal content which turns to misery and suffering as soon as they

make a resolute attempt to reduce. For this there are sound reasons.

In the first place, more caloric energy is required to keep a large

body at a certain temperature than to heat a small body. Secondly

the muscular effort of moving a heavy body is greater than in the

case of a light body. The muscular effort consumes calories which

must be provided by food. Thus, all other factors being equal, a fat

person requires more food than a lean one. One might therefore reason

that if a fat person eats only the additional food his body requires

he should be able to keep his weight stationary. Yet every physician

who has studied obese patients under rigorously controlled conditions

knows that this is not true. Many obese patients actually gain weight

on a diet which is calorically deficient for their basic needs. There

must thus be some other mechanism at work.

Glandular Theories

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. 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.

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. 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.

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.

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.

The Fat- bank

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 diericephalic " 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.

Three Basic Causes of Obesity

(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

diericephalic 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.

(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 (with emphasis 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 the 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 WWII 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.

Three Basic Causes Of Obesity

Psychological Aspects

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

No end of injustice is done to obese patients by accusing them of

compulsive eating, which is a form of diverted sex gratification.

Most obese patients do not suffer from compulsive eating; they suffer

genuine hunger - real, gnawing, torturing hunger - which has nothing

whatever to do with compulsive eating. Even their sudden desire for

sweets is merely the result of the experience that sweets, pastries

and alcohol will most rapidly of all foods allay the pangs of hunger.

This has nothing to do with diverted instincts.

On the other hand, compulsive eating does occur in some obese

patients, particularly in girls in their late teens or early

twenties. Fortunately from the obese patients' greater need for food,

it comes on in attacks and is never associated with real hunger, a

fact which is readily admitted by the patients. They only feel a

feral desire to stuff. Two pounds of chocolates may be devoured in a

few minutes; cold, greasy food from the refrigerator, stale bread,

leftovers on stacked plates, almost anything edible is crammed down

with terrifying speed and ferocity.

I have occasionally been able to watch such an attack without the

patient's knowledge, and it is a frightening, ugly spectacle to

behold, even if one does realize that mechanisms entirely beyond the

patient's control are at work. A careful enquiry into what may have

brought on such 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. In my experience the only thing

that will cure this condition is uninhibited sex, a therapeutic

procedure which is hardly ever feasible, for if it were, the patient

would have adopted it without professional prompting, nor would this

in any way correct the associated obesity. It would only raise new

and often greater problems if used as a therapeutic measure.

Patients suffering from real compulsive eating are comparatively

rare. In my practice they constitute about 1-2%. Treating them for

obesity is a heartrending job. They do perfectly well between

attacks, but a single bout occurring while under treatment may annul

several weeks of therapy. Little wonder that such patients become

discouraged. In these cases I have found that psychotherapy may make

the patient fully understand the mechanism, but it does nothing to

stop it. Perhaps society's growing sexual permissiveness will make

compulsive eating even rarer.

Whether a patient is really suffering from compulsive eating or not

is hard to decide before treatment because many obese patients think

that their desire for food (to them unmotivated) is due to compulsive

eating, while all the time it is merely a greater need for food. The

only way to find out is to treat such patients. Those that suffer

from real compulsive eating continue to have such attacks, while

those who are not compulsive eaters never get an attack during

treatment.

Reluctance to Lose Weight

Some patients 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 handicap, this is a source of pride. Some fat girls

look upon their condition as a safeguard against erotic involvements,

of which they are afraid. They work out a pattern of life in which

their obesity plays a determining role and then become reluctant to

upset this pattern and face a new kind of life which will be entirely

different after their figure has become normal and often very

attractive. They fear that people will like them - or be jealous - 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. In

many of these cases psychotherapy can be helpful, as it enables these

patients to sec the whole situation in the full light of

consciousness. An affectionate attachment to abnormal fat is usually

seen in patients who became obese in childhood, but this is not

necessarily so.

In all other cases the best psychotherapy can do in the usual

treatment of obesity is to render the burden of hunger and never-

ending dietary restrictions slightly more tolerable. Patients who

have successfully established an erotic transfer to their

psychiatrist are often better able to bear their suffering as a

secret labor of love.

There are thus 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. Thus

a discussion of the various ways in which obesity can become

established is useful from a preventative point of view, but it has

no bearing on the treatment of the established condition. The

elimination of factors which are clearly hastening the course of the

disorder may slow down its progress or even halt it, but they can

never correct it.

Not by Weight alone

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 physician 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

physician at once concludes that he is dealing with a " nut. " If he is

busy he will give her short shrift, but if he has time he will weigh

her and show her tables to prove that she is actually underweight.

I have never yet seen or heard of such a lady being convinced by

either procedure. The reason is that in my experience the lady is

nearly always right and the doctor wrong. When such a patient is

carefully examined one finds many signs of potential obesity, which

is just about to become manifest as overweight. The patient

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. In manifest obesity many and often all these signs and

symptoms are present. In latent or just beginning cases some are

always found, and it should be a rule that if two or more of the

bodily signs are present, the case must be regarded as one that needs

immediate help.

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 patient 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 many 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

patients 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 patients

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 patient 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; any

opinion based on the dressed appearance can be quite fantastically

wide off the mark, and I feel myself driven to the conclusion that

apart from frankly psychotic patients such as cases of anorexia

nervosa; a morbid weight fixation does not exist. I have yet to see a

patient who continues to complain after the figure has been rendered

normal by adequate treatment.

The Emaciated Lady

I remember the case of a lady who was escorted into my consulting

room while I was telephoning. She sat down in front of my desk, and

when I looked up to greet her I saw the typical picture of advanced

emaciation. Her dry skin hung loosely over the bones of her face, her

neck was scrawny and collarbones and ribs stuck out from deep

hollows. I immediately thought of cancer and decided to which of my

colleagues at the hospital I would refer her. Indeed, I felt a little

annoyed that my assistant had not explained to her that her case did

not fall under my specialty. In answer to my query as to what I could

do for her, she replied that she wanted to reduce. I tried to hide my

surprise, but she must have noted a fleeting expression, for she

smiled and said " I know that you think I'm mad, but just wait. " With

that she rose and came round to my side of the desk. Jutting out from

a tiny waist she had enormous hips and thighs.

By using a technique which will presently be described, the abnormal

fat on her hips was transferred to the rest of her body which had

been emaciated by months of very severe dieting. At the end of a

treatment lasting five weeks, she, a small woman, had lost 8 inches

round her hips, while her face looked fresh and florid, the ribs were

no longer visible and her weight was the same to the ounce as it had

been at the first consultation.

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.

The Treatment Of Obesity

If obesity is always due to one very specific diencephalic

deficiency, it follows that the only way to cure it is to correct

this deficiency. At first this seemed an utterly hopeless

undertaking. The greatest obstacle was that one could hardly hope to

correct an inherited trait localized deep inside the brain, and while

we did possess a number of drugs whose point of action was believed

to be in the diencephalons, none of them had the slightest effect on

the fat-center. There was not even a pointer showing a direction in

which pharmacological research could move to find a drug that had

such a specific action. The closest approach wee the appetite-

reducing drugs - the amphetamines----- but these cured nothing.

A Curious Observation

Mulling over this depressing situation, I remembered a rather curious

observation made many years ago in India. At that time we knew very

little about the function of the diencephalon, and my interest

centered round the pituitary gland. Proehlich had described cases of

extreme obesity and sexual underdevelopment in youths suffering from

a new growth of the anterior pituitary lobe, producing what then

became known as Froehlich's disease. However, it was very soon

discovered that the identical syndrome, though running a less

fulminating course, was quite common in patients whose pituitary

gland was perfectly normal. These are the so-called " fat boys " with

long, slender hands, breasts any flat-chested maiden would be proud

to posses, large hips, buttocks and thighs with striation, knock-

knees and underdeveloped genitals, often with undescended testicles.

It also became known that in these cases the sex organs could he

developed by giving the patients injections of a substance extracted

from the urine of pregnant women, it having been shown that when this

substance was injected into sexually immature rats it made them

precociously mature. The amount of substance which produced this

effect in one rat was called one International Unit, and the purified

extract was accordingly called " Human Chorionic Gonadotrophin "

whereby chorionic signifies that it is produced in the placenta and

gonadotropin that its action is sex gland directed.

The usual way of treating " fat boys " with underdeveloped genitals is

to inject several hundred international Units twice a week. Human

Chorionic Gonadotrophin which we shall henceforth simply call hCG is

expensive and as " fat boys " are fairly common among Indians I tried

to establish the smallest effective dose. In the course of this study

three interesting things emerged. The first was that when fresh

pregnancy-urine from the female ward was given in quantities of about

300 cc. by retention enema, as good results could be obtained as by

injecting the pure substance. The second was that small daily doses

appeared to be just as effective as much larger ones given twice a

week. Thirdly, and that is the observation that concerns us here,

when such patients were given small daily doses they seemed to lose

their ravenous appetite though they neither gained nor lost weight.

Strangely enough however, their shape did change. Though they were

not restricted in diet, there was a distinct decrease in the

circumference of their hips.

Fat on the Move

Remembering this, it occurred to me that the change in shape could

only be explained by a movement of fat away from abnormal deposits on

the hips, and if that were so there was just a chance that while such

fat was in transition it might be available to the body as fuel. This

was easy to find out, as in that case, fat on the move would be able

to replace food. It should then he possible to keep a " fat boy " on a

severely restricted diet without a feeling of hunger, in spite of a

rapid loss of weight. When I tried this in typical cases of

Froehlich's syndrome, I found that as long as such patients were

given small daily doses of hCG they could comfortably go about their

usual occupations on a diet of only 500 Calories daily and lose an

average of about one pound per day. It was also perfectly evident

that only abnormal fat was being consumed, as there were no signs of

any depletion of normal fat. Their skin remained fresh and turgid,

and gradually their figures became entirely normal. The daily

administration of hCG appeared to have no side-effects other than

beneficial ones.

From this point it was a small step to try the same method in all

other forms of obesity. It took a few hundred cases to establish

beyond reasonable doubt that the mechanism operates in exactly the

same way and seemingly without exception in every case of obesity. I

found that, though most patients were treated in the outpatients

department, gross dietary errors rarely occurred. On the contrary,

most patients complained that the two meals of 250 calories each were

more than they could manage, as they continually had a feeling of

just having had a large meal.

Pregnancy and Obesity

Once this trail was opened, further observations seemed to fall into

line. It is well known that during pregnancy an obese woman can very

easily lose weight. She can drastically reduce her diet without

feeling hunger or discomfort and lose weight without in any way

harming the child in her womb. It is also surprising to what extent a

woman can suffer from pregnancy-vomiting without coming to any real

harm.

Pregnancy is an obese woman's one great chance to reduce her excess

weight. That she so rarely makes use of this opportunity is due to

the erroneous notion, usually fostered by her elder relations, that

she now has " two mouths to feed " and must " keep up her strength for

the coming event. All modern obstetricians know that this is

nonsense and that the more superfluous fat is lost the less difficult

will be the confinement, though some still hesitate to prescribe a

diet sufficiently low in calories to bring about a drastic reduction.

A woman may gain weight during pregnancy, but she never becomes obese

in the strict sense of the word. Under the influence of the hCG which

circulates in enormous quantities in her body during pregnancy, her

diencephalic banking capacity seems to be unlimited, and abnormal

fixed deposits are never formed. At confinement she is suddenly

deprived of hCG, and her diencephalic fat-center reverts to its

normal capacity. It is only then that the abnormally accumulated fat

is locked away again in a fixed deposit. From that moment on she is

again suffering from obesity and is subject to all its consequences.

Pregnancy seems to be the only normal human condition in which the

dicncephalic fat banking capacity is unlimited. It is only during

pregnancy that fixed fat deposits can be transferred back into the

normal current account and freely drawn upon to make up for any

nutritional deficit. During pregnancy, every ounce of reserve fat is

placed at the disposal of the growing fetus. Were this not so, an

obese woman, whose normal reserves are already depleted, would have

the greatest difficulties in bringing her pregnancy to full term.

There is considerable evidence to suggest that it is the hCG produced

in large quantities in the placenta which brings about this

diencephalic change.

Though we may be able to increase the dieneephalic fat banking

capacity by injecting hCG, this does not in itself affect the weight,

just as transferring monetary funds from a fixed deposit into a

current account does not make a man any poorer; to become poorer it

is also necessary that he freely spends the money which thus becomes

available. In pregnancy the needs of the growing embryo take care of

this to some extent, but in the treatment of obesity there is no

embryo, and so a very severe dietary restriction must take its place

for the duration of treatment.

Only when the fat which is in transit under the effect of hCG is

actually consumed can more fat be withdrawn from the fixed deposits.

In pregnancy it would be most undesirable if the fetus were offered

ample food only when there is a high influx from the intestinal

tract. Ideal nutritional conditions for the fetus can only be

achieved when the mother's blood is continually saturated with food,

regardless of whether she eats or not, as otherwise a period of

starvation might hamper the steady growth of the embryo. It seems

that hCG brings about this continual saturation of the blood, which

is the reason why obese patients under treatment with hCG never feel

hungry in spite of their drastically reduced food intake.

The Nature of Human Chorionic Gonadotropin

hCG is never found in the human body except during pregnancy and in

those rare cases in which a residue of placental tissue continues to

grow in the womb in what is known as a chorionic epithelioma. It is

never found in the male. The human type of chorionic gonadotrophin is

found only during the pregnancy of women and the great apes. It is

produced in enormous quantities, so that during certain phases of her

pregnancy a woman may excrete as much as one million International

Units per day in her urine - enough to render a million infantile

rats precociously mature. Other mammals make use of a different

hormone, which can be extracted from their blood serum but not from

their urine. Their placenta differs in this and other respects from

that of man and the great apes. This animal chorionic gonadotrophin

is much less rapidly broken down in the human body than hCG, and it

is also less suitable for the treatment of obesity.

As often happens in medicine, much confusion has been caused by

giving hCG its name before its true mode of action was understood. It

has been explained that gonadotrophin literally means a sex-gland

directed substance or hormone, and this is quite misleading. It dates

from the early days when it was first found that hCG is able to

render infantile sex glands mature, whereby it was entirely

overlooked that it has no stimulating effect whatsoever on normally

developed and normally functioning sex-glands. No amount of hCG is

ever able to increase a normal sex function. It can only improve an

abnormal one and in the young hasten the onset of puberty. However,

this is no direct effect. hCG acts exclusively at a diencephalic

level and there brings about a considerable increase in the

functional capacity of all those centers which are working at maximum

capacity.

The Real Gonadotrophins

Two hormones known in the female as follicle stimulating hormone

(FSH) and corpus luteum stimulating hormone (LSH) are secreted by the

anterior lobe of the pituitary gland. These hormones are real

gonadotropilins because they directly govern the function of the

ovaries. The anterior pituitary is in turn governed by the

diencephalon, and so when there is an ovarian deficiency the

diencephalic center concerned is hard put to correct matters by

increasing the secretion from the anterior pituitary of FSH or LSH,

as the case may be. When sexual deficiency is clinically present,

this is a sign that the diencephalic center concerned is unable, in

spite of maximal exertion, to cope with the demand for anterior

pituitary stimulation. When then the administration of hCG increases

the functional capacity of the diencephalon, all demands can be fully

satisfied and the sex deficiency is corrected.

That this is the true mechanism underlying the presumed gonadotrophic

action of hCG is confirmed by the fact that when the pituitary gland

of infantile rats is removed before they are given hCG, the latter

has no effect on their sex-glands. hCG cannot therefore have a direct

sex gland stimulating action like that of the anterior pituitary

gonadotrophins, as FSH and LSH are justly called. The latter are

entirely different substances from that which can be extracted from

pregnancy urine and which, unfortunately, is called chorionic

gonadotrophin. It would be no more clumsy, and certainly far more

appropriate, if hCG were henceforth called chorionic

dienccphalotrophin.

hCG no Sex Hormone