POUNDS & INCHES A NEW APPROACH TO OBESITY The Original HCG Diet Manuscript as written by DR. A.T.W. SIMEONS
SALVATOR MUNDI INTERNATIONAL HOSPITAL 00152 ROME VIALE MURA GIANICOLENSI, 77
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Dr. Simeons Manuscript- Forward -1 The Nature of Obesity 2 The History of Obesity 3 The Significance of Regular Meals 4 Three Kinds of Fat 5 Injustice to the Obese 6 Glandular Theories 7 The Hypothalamus 8 The Fat Bank 9 The Three Basics of Obesity 10 Psychological Aspects 11 Compulsive Eating 12 Reluctance to Lose Weight 13 Not by Weight Alone 14 Signs and Symptoms of Obesity 15 The Emaciated Lady 16 Fat but Not Obese 17 The Treatment of Obesity 18 A Curious Observation 19 Fat on the Move 20 Pregnancy and Obesity 21 The Nature of Human Chorionic Gonadotropin -22 The Real Gonadotrophins -23 HCG no Sex Hormone 24 Importance and Potency of HCG-25 Complicating Disorders-26 Diabetes-27 Rheumatism-28 Cholesterol-29 Gout-30 Blood Pressure-31 Peptic Ulcer-32 Psoriasis, Fingernails, Hair, Varicose Ulcers 33 The Pregnant Male -34 Technique Warning History Taking -35 Duration of Treatment 36 Immunity to hCG -37 Menstruation -38 Further Courses 39 Conditions that must be accepted before treatment -40 Examining the Patient -41 Gain before Loss -42 Starting Treatment -43 The Diet 44 Making up the calories 45 Vegetarians 46 Faulty Dieting -47 vitamins and anemia- 48 The First Days of Treatment 49 Fluctuations in weight loss -50 Interruptions of Weight Loss and The Plateau 51 Menstrual Interruption -52 Dietary Errors 53 Water 54 Constipation 55 Investigating Dietary Errors -56 Liars and Fools -57 Cosmetics -58 The Voice for singers -59 Other Reasons for a Gain 60 Appetite-reducing Drugs-61 Unforeseen Interruptions of Treatment -62 Muscular Fatigue -63 Massage -64 Blood Sugar 65 The Ratio of Pounds to Inches 66 Preparing the Solution 67 Injecting 68 fibroids and gallstones -69 The Heart and Coronary Occlusion 70 Teeth and Vitamins -71 Alcohol 72 Tuberculosis 73 The Painful Heel 74 The Skeptical Patient 75 Concluding a Course -76 Skipping a Meal -77 Losing more Weight -78 Trouble After Treatment -79 Beware of Over-enthusiasm -80 Protein deficiency -81 Relapses 82 Plan of a Normal Course -83 CONCLUSION -84 GLOSSARY -85 Literary References to the Use of Chorionic Gonadotropin In Obesity -86
SALVATOR MUNDI INTERNATIONAL HOSPITAL
00152 ROME VIALE MURA GIANICOLENSI, 77
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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 an essence of 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 when then 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 journaland 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 Mundi 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 customary 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.
THE NATURE OF OBESITY
As a basis for our discussion we postulate that obesity in all its many forms is due to an abnormal functioning of some part of the body and that every ounce of abnormally accumulated fat is always the result of the same disorder of certain regulatory mechanisms. Persons suffering from this particular disorder will get fat regardless of whether they eat excessively, normally or less than normal. A person who is free of the disorder will never get fat, even if he frequently overeats.
Those in whom the disorder is severe will accumulate fat very rapidly, those in whom it is moderate will gradually increase in weight and those in whom it is mild may be able to keep their excess weight stationary for long periods. In all these cases a loss of weight brought about by dieting, treatments with thyroid, appetite-reducing drugs, laxatives, violent exercise, massage, baths, etc., is only temporary and will be rapidly regained as soon as the reducing regimen is relaxed. The reason is simply that none of these measures corrects the basic disorder.
While there are great variations in the severity of obesity, we shall consider all the different forms in both sexes and at all ages as always being due to the same disorder. Variations in form would then be partly a matter of degree, partly an inherited bodily constitution and partly the result of a secondary involvement of endocrine glands such as the pituitary, the thyroid, the adrenals or the sex glands. On the other hand, we postulate that no deficiency of any of these glands can ever directly produce the common disorder known as obesity.
If this reasoning is correct, it follows that a treatment aimed at curing the disorder must be equally effective in both sexes, at all ages and in all forms of obesity. Unless this is so, we are entitled to harbor grave doubts as to whether a given treatment corrects the underlying disorder. Moreover, any claim that the disorder has been corrected must be substantiated by the ability of the 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 to still the pangs of hunger. Moreover, much of his food was raw and all of it was unrefined. He roasted his meat, but he did not boil it, as he had no pots, and what little he may have grubbed from the Earth and picked from the trees, he ate as he went along.
The whole structure of mans 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 assimilable, placed a great burden on modern mans 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.
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 bodys 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, or hypophysis. 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 anyvalue 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.
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 Cushings 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.
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 diencephalons banking capacity. Just as a banker might suggest to a wealthy client that instead of accumulating a large and unmanageable current account he should invest his surplus capital, the body appears to establish a fixed deposit into which all surplus funds go but from which they can no longer be withdrawn by the procedure used in a current account. In this way the diencephalic fat-bank frees itself from all work which goes beyond its normal banking capacity. The onset of obesity dates from the moment the diencephalon adopts this labor-saving ruse. Once a fixed deposit has been established the normal fat reserves are held at a minimum, while every available surplus is locked away in the fixed deposit and is therefore taken out of normal circulation.
THREE BASIC CAUSES OF OBESITY:
(1)The Inherited Factor
Assuming that there is a limit to the diencephalons fat banking capacity, it follows that there are three basic ways in which obesity can become manifest. The first is that the fat-banking capacity is abnormally low from birth. Such a congenitally low diencephalic capacity would then represent the
inherited factor in obesity. When this abnormal trait is markedly present, obesity will develop at an early age in spite of normal feeding; this could explain why among brothers and sisters eating the same food at the same table some become obese and others do not.
(2)Other Diencephalic Disorders
The second way in which obesity can become established is the lowering of a previously normal fat-banking capacity owing to some other diencephalic disorder. It seems to be a general rule that when one of the many diencephalic centers is particularly overtaxed; it tries to increase its capacity at the expense of other centers.
In the menopause and after castration the hormones previously produced in the sex-glands no longer circulate in the body. In the presence of normally functioning sex-glands their hormones act as a brake on the secretion of the sex-gland stimulating hormones of the anterior pituitary. When this brake is removed the anterior pituitary enormously increases its output of these sex-gland stimulating hormones, though they are now no longer effective. In the absence of any response from the non-functioning or missing sex glands, there is nothing to stop the anterior pituitary from producing more and more of these hormones. This situation causes an excessive strain on the diencephalic center which controls the function of the anterior pituitary. In order to cope with this additional burden the center appears to draw more and more energy away from other centers, such as those concerned with emotional stability, the blood circulation (hot flushes) and other autonomous nervous regulations, particularly also from the not so vitally important fat-bank.
The so-called stable type of diabetes heavily involves the diencephalic blood sugar regulating center. The diencephalon tries to meet this abnormal load by switching energy destined for the fat bank over to the sugar-regulating center, with the result that the fat-banking capacity is reduced to the point at which it is forced to establish a fixed deposit and thus initiate the disorder we call obesity. In this case one would have to consider the diabetes the primary cause of the obesity, but it is also possible that the process is reversed in the sense that a deficient or overworked fat-center draws energy from the sugar-center, in which case the obesity would be the cause of that type of diabetes in which the pancreas is not primarily involved. Finally, it is conceivable that in Cushings 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 patients general health.
3)The Exhaustion of the Fat-bank
But there is still a third way in which obesity can become established, and that is when a presumably normal fat-center is suddenly the emphasis is on suddenly called upon to deal with an enormous influx of food far in excess of momentary requirements. At first glance it does seem that here we have a straight-forward case of overeating being responsible for obesity, but on further analysis it soon becomes clear that the relation of cause and effect is not so simple. In the first place we are merely assuming that the capacity of the fat center is normal while it is possible and even probable that only persons who have some inherited trait in this direction can become obese merely by overeating.
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