Have you tried diet
after diet, only to lose weight and gain it back? If you
have been reading my site, then you know that I always want to
know why. So with obesity, I wanted to know why so many
people are so overweight. Not for a minute was I
convinced that overeating was the cause. In fact,
sometimes it is apparent that overeating is a symptom of
something deeper. For years, I researched. For my
clients and for me. When my clients asked me
how to lose weight, I honestly told them that I did not
know. Now I know and so should
you.
Dr. Simeons was an Italian
doctor who treated the elite, the stars, quietly, discreetly,
for five decades. What he learned through his medical
observations that prompted him to develop the protocol was
pregnant women in third world countries whom were food
deprived, yet delivered babies with a healthy
weight. Pregnant women (and men at certain times)
manufacture the hormone HCG (do not confuse this with
HGH).
When this natural hormone is administered
in low doses, it stimulates the body to release about 2,000
calories of fat daily. Combined with a very specific,
strict diet, the patient loses between .5 and 1 pound daily of
abnormal fat stores. This is different than other diets,
where normal fat stores are lost first, then the abnormal fat
stores. The body is contoured as the weight is lost
and the skin shrinks.
With obesity,
the hypothalmus gland is malfunctioning and sometimes the
thyroid also; however, it is the hypothalmus gland that
is the culprit. This gland is sometimes called the
Master Gland, as it regulates all other glands in the
body. The HCG hormone takes the endocrine gland off
line, so that it can rest and heal, while releasing excess
abnormal fat stores. The bodies weight is set at a lower
set weight.
Beyond the protocol to lose the
abnormal fat stores, it is necessary to address the cause of
the malfunctioning hypothalmus gland. We know that
food manufactures put chemicals in foods to stimulate
appetite, stimulate food cravings, stimulate weight
gain. (Not sure about that? Rent SuperSize Me, the
movie, sit back and learn more.) How are these chemical
additives affecting the body. It is clear to me that
these chemicals are affecting the entire Endocrine
System.
We know that manmade chemicals are
stored in the body. In the fat cells, in the glands, in
organs, in the nerves, in the tissue. All over.
Sure, the body eliminates what it can, but what it cannot, it
stores. As fat is being released with the protocol, so
are those toxins that are stored in the fat cells.
We also know that those whom are suffering from
obesity almost always have an overgrowth of Candida yeast
fungi in the digestive tract and sometimes throughout the
body.
Detoxification is imperative for long term
success and to manage the rapid dumping of fat and
toxins.
DETOXIFICATION AND RESTORATION, A
WHOLE BODY APPROACH
Not
all that long ago, the world was much less toxic. Today, every bit of
food we eat, air we breathe, and water we drink delivers a
hefty dose of toxins to our system. Our bodies were not
designed to manage the amount of toxins that it is presented,
and this contributes to the malfunction of the digestive
tract, hypothalamus (including the entire endocrine system)
and immune system. As an experienced health care professional,
specializing in detoxification, I have been using extensively
(for myself and hundreds of clients) the following method with
outstanding, thorough effects:
Natural Cellular Defense liquid
zeolites: This one product will remove all heavy metals,
herbicides, pesticides, volatile organic compounds and other
chemicals from the body. The delivery system is tasteless and odorless
drops. Because it
is biochemistry, it works every single time. 10-15 drops, three to
four times a day for one to two months. To maintain and
continue to seek further improvements, consider a maintenance
amount of 3 drops, three times daily.
Agarigold: This is also drops and
they taste similar to soy sauce. This is the most
potent immune support / beta glucan product on the
market. It
stimulates the body to manufacture Natural Killer cells. NK cells identify and
eradicate virus, bacteria, parasites, fungi, cancer and other
pathogens. Just six drops a
day.
FermPlus: This is the only probiotic in the world that will recolonize
the digestive tract with good bacteria (because it grows), and
that is the key to getting rid of Candida yeast fungi
overgrowth once and forever. If a probiotic does
not grow once inside the gut, it is not doing it’s job to
renourish, replenish and re-establish the microflora. No or little
microflora = overgrowth of Candida yeast fungi; therefore,
re-establishing the microflora removes the cause of an
overgrowth of Candida! The microflora
(good bacteria) has many functions, such as cleaning the colon
lining, synthesizing vitamins, eradicating parasites, keeping
Candida yeast fungi in check, eradicating parasites and much
more. A healthy
colon eliminates the need for colonics and other colon
cleansers, as well as many stand alone vitamins.
Candida
G: If you are looking for
solutions to your sugar cravings, Candida G is the
answer. While
this great probiotic will lower the Candida yeast fungi
population, it will not renourish your microflora, which is
the cause of an overgrowth of Candida yeast fungi. FermPlus has the
ability to address sugar cravings alone; although, some wish
to utilize Candida G as well, to accelerate the process, or as
an introduction before FermPlus. When it comes to the
HCG protocol, during the adminstration of HCG hormone,
FermPlus cannot be utilized, however, Candida G is suitable at
this time.
And now I proudly
present the brilliant DR. SIMEONS
MANUSCRIPT:
Pounds & Inches
A NEW APPROACH TO
OBESITY
BY: A.T.W. SIMEONS,
M.D.
SALVATOR
MUNDI
INTERNATIONAL
HOSPITAL
00152 -
ROME
VIALE MURA
GIANICOLENSI, 77
FOREWORD
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.