by JEAN MAYER
MOST of us can clearly remember the time when manufacturers of foods and bottlers of beverages advertised that the consumption of their products led you to feel pleasantly satiated. They felt that you liked the idea of receiving full value for your money. Bread built you up eight ways; beer had body as well as purity and flavor. Now that has all been changed. These days, beers are “light and “non-caloric”; soft drinks are “less filling”; bread is “non-fattening”; and preserves are “lo-cal.” You are assured that you can eat and drink with the full confidence that you will not unwittingly absorb calories. This change of emphasis has taken place because of the widespread recognition of the prevalence of obesity and of its association with many of the degenerative diseases, in particular diabetes and heart and liver ailments.
The general view is that lack of self-restraint, voluntary self-delusion, and a wantonly hedonistic philosophy have led you to gluttony. Obesity, it is flatly stated, comes from eating too much and that is all there is to it. Any attempt to search for causes deeper than self-indulgence can only give support to patients already seeking every possible means to evade their own responsibility.
You may object and say that if a farmer wants to produce fat animals he appears to select obese strains of cattle or geese. You may recall that the type of pigs bred for lard is different from the type of hogs bred for chops or ham. You also seem to remember that our farmer implants estrogen pellets in his capons and that he castrates his cattle — practices based on the known effects of hormones. And, finally, you are aware that our husbander of fat animals prevents them from running around.
All this, you will be told when you impiously refer to it, is indeed so. But men, you will be admonished, are different. Alcoholism is not explained, but simply redefined, when you assert, that it is due to habitual overdrinking. But obesity, peculiarly enough, is explained by declaring that it is due to overeating!
Let us agree at the outset that fat does not materialize out of thin air. We can rest assured that for excessive amounts of fat to accumulate in bulging deposits we do have to eat more than we expend. But the real problem is: Why do we eat too much? And this leads us immediately to other questions: Why do we want to eat, anyway? Why do we stop eating?
In attempting to answer these questions, one is driven to a discussion of such terms as appetite, hunger, satiety, and regulation of food intake. “Appetite” may, perhaps, be defined as the fairly pleasurable group of sensations and perceptions which make the individual desire food. “Hunger,” in man, has a more intense connotation. “Hunger feeling” is the decidedly unpleasant sensation of being in dire need of food. “Hunger behavior” is the unrest and apparent anxiety which accompany prolonged deprivation of food; hunger gastric contractions become increasingly painful as deprivation continues. “Regulation of food intake,” on the other hand, is not necessarily associated with psychologic or behavior characteristics. It is the mechanism which ensures that the energy needs of the body are satisfactorily covered by the food which is consumed.
Appetite, hunger, and the short-term regulation are affected by a number of well-known factors. Gastric distention, sudden temperature changes, a sudden call for violent exercise, the action of certain appetite-depressing drugs, or fear, rage, or grief will momentarily decrease, if not eliminate, hunger and appetite and disturb the regulation of food intake. But it stands to reason that the normal functioning of the organism, so dependent on its fuel, could not long persist if there were not another and deeper mechanism controlling intake of food.
For a brief period some physiologists thought that such a mechanism had been found. After Walter Cannon at Harvard, soon followed by Anton Carlson in Chicago, had shown that localized sensations of hunger pain coincided with waves of contractions of the empty stomach, Carlson suggested that a low blood sugar might be at the root of the stomach contractions and, hence, of the feelings of hunger. This theory was rapidly abandoned as a result of the findings of Sir Charles Sherrington in Cambridge and later of Morton Grossman in Chicago. These two showed that total denervation of the stomach did not prevent the occurrence of hunger feelings or decrease their intensity, but simply made the pain more diffuse. Thus, Crossman observed that those of the patients who previously had specifically referred hunger to the pit of the stomach would, after section of the vagus nerves (which abolishes gastric contractions) or of the splanchnic nerves (which eliminates awareness of contractions), say simply that they felt hungry all over.
An important advance in the study of hunger was the demonstration by Hanson and his co-workers in Chicago that destruction of two symmetrical centers in the midbrain of rats caused those animals to overeat and, eventually, to become grossly obese. Actually, “hypothalamic hyperphagia,” the overeating resulting from lesions of this area of the midbrain, had been identified as a clinical entity for at least thirty years. But its experimental reproduction had an important effect in reminding physiologists that there must be a somatic basis for the hunger mechanism. The work of Fanson was confirmed and extended at Yale by John Brobeck and his colleagues. In particular, Brobeck and an Indian associate, Bal K. Anand, showed that destruction of an additional pair of centers caused rats to stop eating. “Hypothalamic hyperphagia” had been studied in animal species other than rats; it has been reproduced in dogs, monkeys, cats, and sheep. Last year, my co-workers and I succeeded in destroying the proper area in the midbrain of the mouse and in producing hypothalamic obese mice. Other investigations disclosed that other parts of the brain were also involved in intake regulation. Destruction or disconnection of certain areas of the frontal lobes, which has been done in psychotic patients and in experimental animals, also causes overeating. The next problem was to try to find out how these nervous centers are informed of the needs of the body.
The search for this missing link has been actively pursued in my laboratory in the Nutrition Department of the Harvard School of Public Health, thanks to the generous support of a number of agencies, especially the United States Public Health Service and the Nutrition Foundation. In the course of the last few years and on the basis of a large number of experiments on animals and on human volunteers, we have elaborated what we call the “glucostatic” scheme of regulation of food intake. This theory, which hits been confirmed by other studies independent of ours, postulates that satiety occurs as a result of the active utilization of sugar by “glucoreceptors” situated in the midbrain. Decreased blood sugar levels would increase the desire for food. So would decreased utilization of sugar in the body, as in diabetes.
While a number of difficulties remain, it would appear that the “glucostatic theory” is at least a useful research tool. Whether it is eventually retained or not, it illustrates the complexity of regulation of food intake. The mechanism appears subject to all the vagaries of the metabolism of sugars and, because of their interrelationship with sugar metabolism, of other body constituents its well; to possible disturbances of receptor centers in the midbrain; and to the hazards of central integration, of subconscious awareness and of conscious interpretation and decision. Little wonder that the mechanism can go wrong, and in a multiplicity of ways! And, most certainly, all of us know the infinite variety of factors which can decrease one’s appetite. What about the causes of abnormal increase?
As FAR as obesity is concerned, there are three kinds of causative factors: genetic, traumatic, and environmental. Both constitutional and extrinsic factors play a part. Accordingly, while environmental conditions — such as availability of food must obviously be favorable, “genetic” obesity is that which is clearly inherited in a recognizable pattern. Examples derived from animal husbandry have already been mentioned. In the laboratory several other examples are known. In the mouse there are both a Mendelian dominant form of obesity, called “yellow” obesity because of its association with coat color, and a recessive type. The latter, first observed by Miss Margaret Dickie at the Jackson Memorial Laboratory, has been intensively studied at Harvard. We have called it the “obese hyperglycemic syndrome” because of its association with diabetes in the mice afflicted with it. One of the peculiarities of these animals is that their high blood sugar occurs in spite of a high insulin content in the pancreas.
Other forms of hereditary obesity in experimental animals are beginning to be studied. In man such studies are still in their infancy because of the slowness of production of successive generations, the impossibility of applying the methods of enforced marriages (and incestuous marriages at, that) which are used to “inbreed” animal strains, and the difficulty of distinguishing between genetic obesity patterns and familial or other cultural traditions influencing the amount and kinds of food eaten. Slowly, however, observations show that a number of genes may predispose to obesity in man as well as in other animals.
One example of traumatic factors causing overeating has already been presented: surgical intervention in the midbrain leading to “hypothalamic hyperphagia.” Injection of a single dose of the chemical gold thioglucose causes obesity in mice. A pituitary tumor which first appeared in mice exposed to the initial Los Alamos explosion and which can he injected into other mice also causes obesity in these animals. Castration and hormonal treatments used to fatten domestic animals fall into this “traumatic” category of obesity.
So do the cases of psychogenic obesity reported by psychiatrists in some patients following emotional trauma. Among such cases, sudden real or imagined insecurity appears to be a frequent factor. A case history may show a striking parallel between the advent (or removal) of an important element of insecurity in the life of the subject and the beginning (or cessation) of a period of overeating.
Finally, the environment is of conspicuous importance. It determines availability of food. In this connection the phenomenally abundant food supply in the United States today is eminently favorable to the development of obesity. On the other hand, the type of food consumed and the spacing of meals are probably less important than has often been maintained. Given sufficient supply, people seem to become fat quite as successfully on macaroni as on lard, on meats and poultry as on rice. While the idea that a large breakfast will prevent obesity is widespread, it can be noted that Frenchmen, who generally reduce their morning meal to the strict minimum of a cup of coffee, become no more obese than do Americans who have cereal plus bacon and eggs. (This does not mean, however, that a good breakfast is not a pleasant and perhaps even a useful thing, though it may be overrated as a reducing aid.)
In our studies in Boston of food choices of obese women and high school girls compared with normalweight controls of the same height, age, and economic environment, we could find no consistent qualitative difference between obese and thin subjects. Even the constant nibbling so often venomously ascribed to obese women appeared to be characteristic of all women who lived at home, whether obese or not, and particularly if they took care of small children and ate only one “formal” meal a day. The only consistent difference between the obese and the non-obese is that the former tended to consume a large proportion of their calories in the evening.
While the importance of the nature (not the quantity) of the diet has probably been overstated, the importance of another environmental factor, physical activity, has been overwhelmingly underrated. Temperature is another frequently neglected environmental factor. Modern heating techniques and the prevalence of indoor life under contemporary conditions have eliminated another traditional means of expending energy; we are kept, warm by gadgets rather than by burning our fat.
WE HAVE classified types of obesity by their origin. We can distinguish them also by the mechanism of their development. There are two different types of experimental “constitutional” obesity. In one type there is something basically wrong in the way in which the organism handles its fat. The obese hyperglycemic syndrome of the mouse is an example in point; labeling foodstuffs with radioactive tracers demonstrated to us that these mice make too much fat even when they are not allowed to overeat. When starved, they jettison protein as well as fat. Chemically speaking, they are still obese when reduced to normal non-obese weight or when made underweight. Too much of them, percentagewise, is still fat.
By contrast, their litter mates made obese by gold thioglucose treatment or by hypothalamic injury are metabolically normal; they make excessive fat only in the measure in which they are permitted to overeat; when underfed, they lose only their fat; they can be brought down to normal body composition as well as to normal weight. The lesion in this case is not fundamentally in the way in which the body handles its foodstuffs, but in the amount that it has to consume to feel satiety. We have called this latter form of constitutional obesity “regulatory,” because the error is in the regulator, in contrast with the “metabolic” form, in which the regulator works but the metabolism is tilted toward synthesis of excessive fat.
Work done recently at Michigan State College on obese human patients suggests that the two types of reactions to underfeeding may be found also in man.
Knowing that the immediate cause of obesity is overeating is not enough, regrettably, for effective action. This unpleasant truth is well underlined by a recent study conducted by Dr. Martha Trulson and her co-workers at Harvard. The results of a one-year, a two-year, and a three-year follow-up of two weight-reduction regimens were compared. One involved individual instruction in the outpatient nutrition clinic of one of the most advanced teaching hospitals in Boston. The other was a matter of group psychotherapy, conducted by a psychiatrist and a psychologist with graduate students in psychology, teachers, and a minister helping to lead the discussions. For a control group, a random sample of obese patients was used.
The striking and tremendously discouraging result was that, particularly over the longer periods (two or three years), there was practically no difference between the weight reductions obtained and held by the various groups; none of the groups did very well. At the end of the two-year period, the clinic group comprised a slightly higher proportion of patients who had gained weight. The other two groups were bitterly similar to their starting points two years before.
One could multiply examples. The story of the treatment of obesity is full of instances of shortterm success and long-term failure. You can fast some of these obese patients some of the time, a very few of them all of the time, but you cannot starve all of them all of the time.
It’s simple enough. They get hungry. Hunger is one of the strongest motivators of human behavior. When the obese patient resorts to the derided formula, “But, Doctor, I eat like a bird,” he may not be lying, as is usually inferred, but may merely be conscious of satisfying his disordered appetite on the light side. It is the excessively thin patients who are usually conscious of “stuffing" themselves, possibly because their appetite is too easily satisfied.
Until such time as we truly understand hunger and can, therefore, learn to control it, it is all too probable that we shall continue to be faced with the recurrent and general failure of weight-control programs.
IN THE meantime, what can we do? Not knowing enough about the mechanics of food intake to evolve a formula to decrease appetite, we can either increase energy expenditure or, painfully, decrease food intake, or do both. Exercise does consume considerable food energy and does not necessarily lead to an increased appetite. Dieting, without an increase in energy expenditure, usually means that the dieter is going to be hungry part of the lime, unless the overeating was purely a social or traditional affair. A successful diet is one on which the patient will not only lose weight but will also stay reduced.
There are on the market a number of diets, all associated with tales of triumph. The best-known is the low calorie, relatively high protein, and moderate fat diet popularized in particular by the Michigan State College and the Cornell groups. It is an easily prepared diet which will not strike its users as outlandish, a circumstance which may or may not be helpful. Low calorie, high protein, and low fat diets have been devised in other clinical centers. These rely heavily on skim milk, cottage cheese, and lean meat, as a rule. The Pennington diet, a novel one, is very high in protein and very high in fat, with the large amount of fat supposedly corresponding to an inability of obese individuals to use sugar properly. The theoretical basis for the diet is unproved, but Dr. Pennington has claimed great success with it. He considers that its satiety value is such that its users automatically cut down their calorie intake to the point where they lose weight and lose weight rapidly. A similar result is claimed for the Rockefeller Hospital or Dole diet. This is extremely low in protein; again lack of appetite is claimed to follow, and it is contended that patients using it lose weight.
There are also what academic people refer to as “fad” diets; for example, the boiled eggs and grapefruit diet (fundamentally a high protein, low calorie diet) and the banana diet (a low protein diet). The very multiplicity of diets, while proving that hope is eternal, is all too clear a proof of the eventual failure of dietary treatment. Yet each of them is presented as a “good" reducing diet presumably for all forms of obesity.
It would appear that an experimental approach might often prove to be the most reasonable, starting out with, say, the Michigan diet and experimenting with other diets if it is found to be unendurable after a serious try. This same experimental approach can be used as far as the spacing of meals is concerned. Some individuals feel happier, and should presumably diet more successfully accordingly, if some of the calories planned for meals are consumed instead in small snacks between meals. This practice breaks the long intervals between the regular meals and brings the dieter to the table at the standard mealtimes without a ravenous appetite. Other individuals keep thin by eating one or two meals a day. It may be useful to remember, too, our findings (which have been confirmed independently by several other investigators) that extra calories are generally consumed in the evening. If sleeplessness does not result, the first step in dieting could be the elimination of evening snacks.
A word should be said here as to who should reduce. An obvious answer could be: Everybody who is too fat should reduce. This is the position of most of the agencies engaged in mass health education campaigns. But there are reasons to think that weight reduction should be an individual prescription. Among psychiatrists who have made outstanding studies of obesity, Hilde Bruch of Columbia, Albert Stunkard of Cornell, and Erich Lindemann of Harvard have emphasized that in some cases overeating cannot be eliminated without precipitating much more serious mental or emotional disorders, including overt psychosis.
Dr. Bruch particularly warns against being too forceful with children who have been steadily obese from early childhood. Declaring that success in reducing these children is doubtful anyway, she points to a real danger of initiating neurosis. Dr. Stunkard suggests the following criteria as a good guide to who can be reduced safely: The patient has a history of fluctuating weight rather than a persisting state of obesity; he has, at times, lost weight on his own; he can stand the first week of reducing diet without developing either anxiety or excessive discomfort. Where responses to all such criteria are negative, Dr. Stunkard is doubtful of success and, in fact, anticipates possible trouble.
What about reducing pills and drugs? Most nutritionists agree that they represent a gigantic fraud on the American public. Not that appropriate drugs, acting selectively to correct malfunctioning regulatory mechanisms or deep metabolic errors, cannot eventually be found, but merely that they have not yet been found. Present-day preparations are either ineffective after a few days or they are effective because they are non-specific poisons and therefore eventually dangerous. Thyroid pills, when given to patients who actually suffer from hypothyroidism, are safe and effective. When given to the great majority of patients, they superimpose a danger state of hyperthyroidism on the much more benign obesity in order to eliminate excess fat. Badgering one’s physician into prescribing thyroid pills is emphatically not a good idea.
Victims should recognize that obesity is an undesirable condition which entails definite risk, and they should obtain professional help. Families should not, on the other hand, hound the sufferers by constant reminders and invidious comments; this is particularly important where the afflicted person is a young child or even an adolescent. Therapeutists should bear in mind that if they fail to help their patient it matters very little that they were right in some lordly way all the time and the patient was wrong, deceitful, and weak-willed. The failure is that of the therapeutists. And, for the long pull, we may hope that research in this fascinating and important area of hunger, appetite, and regulation of food intake will continue to be encouraged so that someday we may practice effectively instead of preaching unconvincingly.