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Obesity in Children
OBESITY IN CHILDREN NATHAN
B.
TALBOT,
M.D.
CLINICIANS dealing with children see a great many patients who are overweight for their height. Of the children who are seen in the outpatient and in-patient departments of the Massachusetts General Hospital, approximately one in ten fall into this group. Definition of Obesity.-Though most overweight patients are obese, a careful examination sometimes shows that the extra weight is due to a well. developed musculature rather than to an excessive accumulation of adipose tissue. Such muscular individuals, though "overweight," do not properly come under the classification of obesity. In fact, if obesity is defined as an accumulation of subcutaneous fat which is excessive with relation to the underlying musculature and bones, then certain children may be obese without being significantly overweight for their height.!' Generally speaking, however, most persons who weigh 20 per cent or more than the normal for their height and age are obese.
CAUSES OF OBESITY
Fundamental Causes.-The evidence now available clearly establishes the fact that obesity is due to an intake of 'calories which exceeds the caloric requirements for energy metabolism, physical activity and growth (protein anabolism).2, 3 Thus, in the development of adiposity, the two important variables are the caJoJ;ic. intake and the caloric expenditure. A relative increase in the di~t or a relative decrease in the energy metabolism, physical activity and/or rate of protein anabolism (growth) will tend to yield a surplus of calories which may be stored as body fat. Most obesity is due to overeating rather than to a diminished energy expenditure on a normal dietary intake. Not uncommonly patients or their parents will cling tenaciously to the thesis that the quantity of food eaten is not large. However, when this is the case, it is almost always possible to elicit a history of dietary excess at some earlier date. In other words, once a patient has eaten too much and become fat"he will tend to remain so if he is eating a maintenance diet. He will not lose weight until such titne as he eats fewer calories than he is expending. I
.... From the Department of Pediatrics, Harvard Medical School and the Children's Medical Service, Massachusetts General Hospi~~J, Boston. The observations and points of view recorded here were based upon studies supported by the Commonwealth Fund of Ne",· York and the Permanent Charity Fund of Boston. * Assistant Professor of Pediatrics, Harvard Medical School; Assistant Physician, Massachusetts Memorial Hospital. 1217
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NATHAN B. TALBOT
Contributing Causes.-A· number of different factors may induce overeating. Among these are personality problems,4,5 organic lesions of the brain (especially of the hypothalamus)3 andi hypoglycemia. 3 On the other hand, physical inertia,· hypometabolism and decreased ·protein anabolism (slow growth), may .be responsible for·· a decrease in the energy requirements. -... Of these factors, the personality ones are by far'themost impor~ant in the. maj'ority of obese boys and gi!ls. Some chi~dren tend to nibble at food to help relieve themselves of worry, unhappiness or boredom. Others have become accustomed to tables heavily lp,den wi~h nutritious foods and. to seeing their parents, brothers. or sisters take gluttonous servings. Sometimes parents erroneously assume ~hat ·a large appetite per se ensures good health and therefore urge their children to eat too much. Similarly, parents may not be aware of the normal.decilne in appetite which may occur at about two years of age when the rapid growth of infancy subsides. Attempts to prevent such a normal decline in appetite has led to the development of adiposity in acquiescent children. In the resistant child the- same treatment may result in anorexia and leanness. The mechanism by which organic brain lesions stimulate the appetite is not clear. For reasons beyond metabolic definition, a reasonable meal ~oes not "satisfy." Hypoglycemia secondary to hyperinsulinism induces hunger in some people, but fails to do so in others. It is rarely a factor in childhood adiposity. Hypothyroidism (decreased energy metabolism, growth and physical activity) is seldom noted in association with obesity in children. CLINICAL TYPES OF OBESITY IN CHILDREN
While the degree of adiposity is referable to the caloric balance, tJ1e distribution of accumulated adipose tissue may be influenced by endogenous factors. .Simple Obesity.-Over 95 per cent of all fat children fall into this group. The only thing wrong with these children is that for personality or environmental reasons they have eaten too much. Studies have revealed that the majority of these children are only children or the youngest child and that many of them are unwanted. In·many families the rehltionship of the .parents is unhappy. Food may have taken on exaggerated importance and may become a substitute for love, security and satisfaction.4, 5 A careful survey of the history almost always reveals a. period or periods of dietary excess. There is no history suggestive of serious intracranial disease. They are free from symptoms of hypothyroidism. In. other words, they are healthy. children. On physical examination fat boys and girls wtih uncomplicated obesity are usually found to be of average or slightly taller than average stature. 6 They are of normal intelligence; quite a few stand in the
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Fig. 173.-This 5 year old boy is presented as an example of simple obesity. He was of normal weight at 1 year (11.8 kg.). From that time on he gained at a steady and very excessive rate so that by the age of. 5 years he· weighed 44 kg. or about 21 kg. more· than he should weigh. During this period of rapid weight gain he also grew rapidly, attaining a height of 125 em. at the age of 5 (normal 105 to 116 cm~). He is fond of bread, potatoes, cakes, cookies, puddings, candy bars and the like. Other members of the family also have hearty 'appetites, for a brother of 13 years weighs 80 kg. ( 175 pounds), a sister of 11 years weighs 48 kg. (105 pounds) and his father who'is 170 em. (5 feet 8 inches) tall weights 100 kg. (220 pounds). He is- of normal intelligence and is free from symptoms of increased intracranial pressure. There is nothing in the history to suggest hypothyroidism: Aside from the excessive accumulation of subcutaneous tissue and tallness in stature, physical examination is not remarkable. The blood pressure is 120/80. Roehtgenograrns of the skull show a normal sella turcica and fail to reveal any abnormalities. Roentgenograms of the hand, and wrist show that his skeletal development corresponds to the average normal for his chronologie age. The urinary 17-ketosteroid output is 0.6 mg. per day, a normal value. By the simple ~xpedient of reducing his intake of starchy foods to one-half piece of bread or its equivalent per meal three times a day, he is losing weight at the ' rate of about OS kg. (1, pound) per month.
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NATHAN B. TALBOT
top third of their class at school. Some of these children are found to be only moderately plump while others are extremely fat (see Figs. 173 and 174). The exc~ss ~dipose tissue though generally distributed often accumulates especially in the region of the b~easts, hips and lower abdomen. Though the breast regions may thus appear enlarged, palpation usually fails·::,to .:rev~al any true marf.lmary gland de~elopment
A
B
Fig. 174.-A, Extreme example of simple obesity in a boy of 6 years weighing 65 kg. and measuring 126 em. and \\J~ith genu varum probably secondary to excess weight bearing. During a period of 8 months on a caloric intake of from -1000 to 5eo calories per day,. he lost 29 kg. B,. The administration of thyroid had essentially no effect' upon the rate of weight loss. During this period the -genu varum was corrected by bilateral osteotomies.
except in' adolescent girls. A transient and ~pparently pp.ysiologic development of.'the mammary tissues is noted in a small number of normal adolescent -boys. _ The eyes, extraocu,lar movements, visual fields -and eyegrounds- are . normal. While the ch'est and heart are normal, the blood pressure may be slightly elevated. In this respect it is _helpful to remember that the
OBESITY IN CHILDREN
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use of a blood pressure cuff which is' too small for the patient's arm will result in an overestimation of the blood. pressure. The abdomen is free from abnormal masses. The genitalia in boys often appear to be 'small because they are embedded in a thick pad of pubic fat. By pressing the fat aside, this .erroneous impression can be dispelled. In ·this connection, it is noteworthy that in normal boys the genitalia. -remain of essentially infantile size until approximately 11 to 12 years of age. 7 Not until that ,time do the testes secrete ~nough male hormone to "stimulate any significant development of .the masculine secondary sex characteristics. Moreover, some normal boys develop one or two· years later than the average. For these reas6ns boysneed::not necessarily be considered hypogonad ev~n if genitaLgrowth.is oelayed to the thirteenth or fourt~enth year. Sexual development.js~moderately acpelerated in some of these children. 6 The skin is s1l\i)oth,. warm, moi~t and of normal color. Apparently as a consequence Qt~·stretching of the skin, striae over the hip regions ·are occasionally s~.In contrast to the striae of Cushing's syndrome which arepurple,t~e~e are pinkish white. There is no pathologic hirsutism. The extremj~~~,~'are normal. Roentgenograms· of the skull are uniforml~~J:~fnormal appearance. X-ray films of the hand and wrist reveal that t~.:'·skeletal development either corresponds 'to the normal fOf the chtf'Jogic age (according to Todd's standard Atlas of Skeletal Matu"::;ct'1 P)" or· is slightly advanced. 6 Likewise, the urinary excretion of.~i;~~~ketosteroids is either normal for the patient's age, or if the patient is~exceedingly obese, may be. slightly elevated. 8 As a rule, "physiologic. ages" as measured by genital development, the skeletal development and·· the 17-ketosteroid excretion, respectively, correspoI).d closely to .each, other. ' There has been considerable debate concerning the basal metabolism of such children. The present ccnsensusis· that their basal metabolic rate 'corresponds closely to the normal and' tends, if anything, to be elevated. 2 , 9. This becomes clear .when the metabolic rate .is computed with due consideration for the fact that in;fobesity an abQormally large proportion of the' body weight is compo~edof relatively inert fat. . Obes,ity in Association with Mental Retardationa.ndjor Other Bodily ·Defects.-In contrast to the preceding group are children w'ho in addition to being obese have"one or Plore of, tlle following defects: J;etinal degeneration or retinitis pigmentosa-, mental retardation, polydactylism, ;syndactyli~m, hypogonadism, microphthalmus, enlargement .of the parietal foramens of the skull or a related disorder. lo , ll.Many of thes~ def~cts appear to be hereditary familial deviations~ On th~ other hand, it is of interest that somewhat similar congenital defects 'have been;observed in th~ offspring of. mothers who. received a nutritionally inade;;" quate diet12, 13' orwho contracted German measles during pregnancy..14 When. the hereditary familial defects~retinitis pigmentosa, ob'esjty, hypogon~dism, mental retardation a:nd polydactylism-happen to occur
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NATHAN B. TALBOT
in one individual, the resultant combination is sometimes called the Laurence-Moon-Biedl syndrome. Like normal children, tQese patients are fat because they have eaten relatively too much. It is postulated without much factual basis that these excessive appetite may be due to a hypothalamic lesion.
Obesity in Association with an Expanding Intracranial 'Lesion (Frohlich's Syndrome).-This is a rare condition usually due to a craniopharyn-
gio,ma or suprasellar cyst. 15 Children sqffering from this disease present
Fig. 175.-0besity in a 9 year old boy with a sliprasellercyst. Note the strabismus.
such· typical symptoms and signs of an expanding lesion in· the region of the optic chiasm as headache, vomiting, disturbances of vision (bitemporal hemia'nopsia) or of ·.extraocular movements, optic atrophy, separation of.. the cranial sutures and· increased spinal fluid pressure (Fig. 17.5). Roentgenograms of the skull may. reveal erosion of the sella turcica.:.or an area of calcification in the neighborQood thereof. These expa,l.1ding .lesions apparently influence the appetite in much the' same manner that experimentally produced hypothalamic ·lesions
OBESIT'Y IN CHILDREN
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do. They may also interfere\vith the function of the anterior and/or posterior pituitary gland either directly by causing pressure atrophy of the gland or indirectly by interfering with normal neurohypophyseal regulatory mechanisms. When the anterior pituitary function is impaired, various disturbances in growth and development may be noted. Interference with the production of the growth hormone results in dwarfism. Failure to produce the thyroid-stimulating hormone results in hypothyroidism which leads to retardation in growth and in skeletal maturation. When there is failure to produce the anterior pituitary gonad-stimulating hormones, the gonads themselves remain infantile and little or no secondary sexual development occurs. Finally, lack 'of the anteri~r pituitary adrenal-cortical stimulating hormone results in atrophy of adrenal cortices a~d the development of Addison's disease. In a given patient there may be a complete or only partial impairment in the production of anyone or more of these anterior pituitary hormones. Hence, patients with destructive lesions in the region of ,the hypothalamus or the pituitary may .present a variety of clinical pictu'res. In fact, certain lesions which affect the hypothalamus but leave the anterior pituitary intact sometimes lead' to precocious growth and development. Hypothalamic stimulation of the anterior pituitary is believed to be responsible for such precocity. In so far as hypothalamic lesions stimulate polyphagia, they may be considered as factors predisposing to obesity. There is no evidence that they induce adiposity by' other mechanisms. Similarly, it is fair to say that there is no such thing as '1>ituitary" obesity. Many patients with destructive lesions of the pituitary actually suffer a marked loss of appetite and as a consequence become cachectic (Simmonds' cachexia). Though the foregoing types of intracranial lesion have received much publicity, other intracranial conditions such' as internal hydrocephalus, brain tumors, xanthomatosis, pinealoma, syphilis, poro'ncephaly and postencephalitic changes likewise may lead to obesity and to disturb,ances in obesity and development. Obesity in Association with Hypoglycemia.-Hypoglycemia resulting from hyperinsulinism or from glycogen disease induces overeating in some individuals. Such conditions as these are but rarely encountered in pediatric practice. 'An abnormally low fasting blood' sugar value is suggestive of hyperinsulinism. Hepatomegaly, ketonuria and hypoglycemia are suggestive .of glycogen 'storage disease. 16 Patients with this condition show very little elevation of the blood sugar concentration following the administration of adrenaline Obesity in Association with Hypothyroidism.-It is unusual to discover hypothyroidism in an obese child. This' is explained by the fact that hypothyroidism tends to cause a diminution in appetite as well as a decrease in the total energy metabolism, physical activity and growth.
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NATHAN B. TALBOT
The most characteristic symptoms' of thyroid lack in children are easy fatigability, both phy~ical and mental, constipation, sensi~ivity to cold weather and slowness in statural growth. On examination almost all hyopthyroid children are found to be of dwarfed stature. Mental deficiency is not a consistent finding. The skin is pale, coarse; cool and dry. There is often a subtle appearance of puffiness around the face due to local accumulations of myxedema fluid. Accumulations of, myxedema fluid in other localities may also give rise to ,a pudgy appearance. Roentgenograms 'of the hand and wrist reveal a retardation in the skeletal development. In children this diminution in bone growth is associated wIth a lowered serum phosphatase value (less than 4.5 Bodansky units per'100cc,,)17 An elevation in the serum cholesteI:'ol concentration above 250 mg. per 100 cc. is also suggestive. However, in many hypothyroid. children who. have never received thyroid medication, this value is either normal or low rather than elevated. On the other hand, when such hypothyroid children are given adequate doses of thyroid (1 to 2 grains of 'U.S.P. thyroid daily) for a month or longer and then their medication is discontinued, they develop hypercholesterolemia within the next one to three months. Children with normal thyroid function do not do SO.18 The basal metabolic rate is mucl! less reliable as an index of hypothyroidism in children than in adults. Possibly the best index of thyroid' function is the concentration of protein-bound (thyroid hormone) iodine in the plasma or serum. This should receive increasing attention as more laboratories become equipped, to make the determination. . Obesity a"s Effected by Other Enclocrine Disturbances.-Certain steroid hormones of the adrenal cortex and possibly of the sex glands may e'xert a striking influence upon the distribution of body fat. The outstanding example is Cushing's syndrome (Fig. 176), a (rare condition which is thought to be due to an excess of those adrenal cortical hormoneS which accel~rate gluconeogenesis from protein. 19 This condition may occur at anyage. 20 ,.21 The youngest recorded patient was only eleven weeks old. The incidence is considerably .greater in girls than in boys. The obesity is often, not always:, of, the "buffalo" type. That is, there is a marked accumulation of fat about the head and neck, while the extremities are relatively lean. Muscular, weakness is a characteristic finding. The cheeks in the characteristic patient are plethoric in appearance. There are purplish striae in the skin over ,the hips, abdomen aRd thighs; acne is common especially in older girl patients. There is often generalized' hirsutism. The genitalia may be precociously developed. Hypertension is an outstanding finding. This is reflected by the plethoric '~ppearance already mentioned and may also be manifested by cardiac enlargement and occasionally by cerebral hemorrhages. When the disease is due to an adrenal cortical carcinoma, an abdominal tumor may be palpable.
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Intravenous pyelograms may be helpful in revealing such tumors. There is a decreased tolerance for sugar and a tendency to insulin :resistance. 19 In some patients there is a marked increase in the urinary excretion of 17-ketosteroids; in others, the values are essentially. normal. 19 ,22 Osteoporosis of the spine especially is a notable sign. The skeletal development. tends to be normal for age and sex.
Fig. 176.-Cushing's syndrome in' a 12 year old girl. (Courtesy of Dr. F. Albright. 20 ) I
Though not so clear-cut, there is also some. evidence to suggest that the testicular male hormones favor a distribution of fat in the upper segment of the body while the ovarian female hormones' cause the fat to be distributed in the lower body segment. Most preadolescent children show a fairly even 'distributi~n of fat when they become obese. Hypogonadism per se does not cause obesity.3 Obesity, on the other hand, occasionally retards the onset of adolescence. In this respect it is of interest that simple weight reduction by dietary means often results in prompt adolescent development in children with simple obesity.
1226
NATHAN B. TALBOT COMMENTS ON THE CLINICAL STUDY OF OBESE CHILDREN
In view of the fact that obesity, though not a metabolic or endocrine disease per se, may be a sign of some important associated condition, it is desirable to emphasize certain. parts of the history and physical examination of fat children. Thus, in the history, symptoms of intracranial disease, physical inactivity. hypometabolism, mental deficiency or family maladjustments may be helpful. In the physical examination, signs of increased intracranial pressure, abnormal eyegrounds, a marked hypertension, an abdominal tumor, skeletal anomalies, a "buffalo" distribution of fat, muscular weakness or shortness of stature may lead to a specific diagnosis. The value of a careful examination of these patients is well exemplified by one patient who superficially appeared to be a typical example of simple obesity. However, routine examination of the eyegrounds revealed unmistakable papilledema. That child was subsequently found to have a brain tumor. Roentgenograms of the skull occasionally reveal abnormalities not previously evident. Roentgenograms of the hand and wrist permit an estimation of the skeletal development which is helpful when deviations in the rate of maturation are suspected. Fasting blood sugar determinations as well as glucose and glucose-insulin tolerance tests 23 may be helpful occasionally. Likewise, in the patient suspected of having adrenal cortical disease, a urinary 17-ketosteroid measurement can be diagnostic. Determinations of the basal metabolic rate are seldom helpful and often lead to an erroneous diagnosis of hypothyroidism. Other means for establishing a diagnosis of this disease have been discussed above. TREATMENT OF CHILDHOOD OBESITY
General Considerations.-One of the first considerations in treatment is the question, is it worth while to attempt to reduce the body weight of all fat children? The answer depends partly upon the type and degree of . obesity. Because children are growing individuals, it sometimes suffices merely to prevent further gains in weight. A quantity of fat which was moderately excessive for a small child will be normal for the same child when he is a few inches taller. On the other hand, a markedly excessive accumulation of fat may interfere with the physical efficiency of a child to such an extent that participation in normal childhood pursuits is greatly impeded. Furthermore, as mentioned earlier, adiposity per se occasionally retards adolescent development, an occurrence which may cause considerable concern to patients and their parents. .. . As indicated in the introduction, any person will lose weight when the caloric intake is consistently less than the caloric output. In general, it is more profitable to produce such a caloric deficit through
OBESITY IN CHII.DRRN
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reducing the caloric intake (underfeeding) than by increasing the caloric expenditures with the aid of exercise and/or medications. It requires a considerable amount of exercise to increase the total caloric output significantly. Thus, even for an adult man weighing 70 kilograms an hour's walk on a level road at a rate of about 3 miles per hour requires only 160 calories or 17 gm. of fat. 24 Vigorous exercise tends to stimulate a voracious appetite. After underfeeding is instituted there may be a one or two week interval before a loss of body weight occurs. This is explained by the fact that while the patient loses fat during this period, he retains an equal weight of water. 2 Sooner or later there is a spontaneous diuresis with the loss of one or more kilograms of weight during the course of a few days. Thereafter weight loss is steady. How can one induce a child to eat less? In younger children whose diet is completely under the control of their elders, this may not present too great a problem. In the older and more independent child, success depends largely upon gaining the interest and cooperation of the patient. Without these, attempts at therapy are usually a failure. In other words, the problem is a psychological one. Frequently the primary fault lies chiefly with parents who need advice on the management of children. On the other hand, the child often needs to develop pride in his appearance, a feeling of self-confidence and an ap·petite for something more important than food. Dietary Therapy.-Regimen A.-This regimen permits eating any reasonable quantities of protein and other relatively low caloric foods while forbidding the eating of certain high caloric items. 1. Eat no candy, cakes, cookies, jams or sugar and no desserts to which such ingredients or flour have been added in any considerable amount. 2. Eat not more than one-half piece of bread (any type) a meal or its equivalent in rice, macaroni, spaghetti, potato or other starchy food. 3. Drink 2 to 3 glasses of skimmed milk a day. 4. Except for these instructions, eat as desired at mealtimes of lean meats, fish, colored vegetables, salads, fresh fruits. Use vinegar or mineral oil dressing. Use ordinary common sense in not stuffing on any particular diet. 5. Plan to eat three reasonable meals a day. The individual who eats no breakfast, a small lunch and a huge dinner tends to gain more weight than the person who eats the same amount of food divided equally between three meals.
In favor of this regimen is its simplicity and the fact that individuals on it are less tempted to eat the forbidden because they feel starved. While it suffices in many instances at least to prevent further weight gairis it is ineffective in others. When a ffioce precise adjustment of the caloric intake is desired, diets similar to those of Regimen B may be prescribed. Regimen B.-It is appropriate to offer a diet calorically equal to the basal energy· metabolism. For practical purposes this may be predicted roughly from the ideal weight for the patient's height as follows:
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NATHAN B. TALBOT
Height, cnl. 73 115 137 150 160 170
Ideal Body 'Veight, kg.
Basal Heat Production, Calories per d ay 25
10
550 870 1100 1250 1400 1550
20 30 40
50
60
Provided ·the mineral, nitrogen and vitamin requirements are met, patients suffer no damage from such underfeeding so long as excess body fat remains. Sample diets· follow: 1. 750 cals., P 53 gm., F 20 gm., CHO 90 gm.
Breakfast a. Orange juice, ¥2 cup. b. Toast, lh slice, or cereal, ~ cup. c. Butter or oleolnargarine, 12 sqyare. Noon a. Clear soup (broth, bouillon or consomme) ad lib. b. One egg or lean meat, fish, fowl or cottage cheese, 2 oz. or 5 tablespoons or a piece about lhx2x3 inches. c. Vegetables, 2 servings (1;2 cup each) raw or cooked without sauces. d. Fruit, lh cup or equivalent. e. Skim milk, lh cup. Night Same as at noon, but add lh slice bread and square butter. 2. 1000 cals., P 68 gm., F 30 gm., CHO 115 gm. Add to regimen 1, 1 cup skim milk, 1 slice bread, 1 egg, 12 square butter. 3. 1200 cals., P 70 gm., F 51 gm., CHO 115 gm. Substitute 2~ cups whole milk for the skim milk of regimen 2.
*
The following suggestions as to the choice of foods may be helpful. Vegetables: A serving of potatoes, kidney, lima, navy or soup beans and of corn shall be considered as :JA instead of lh cup. Lettuce and celery may be used ad lib. All other vegetables equal ~~ cup. Fruits: No sweetened fruit is to be used. Unsweetened canned fruits can be purchased. A serving of banana is lh a small banana. Meats, etc.: All visible fat is removed. Ham, pork, bacon, wieners and picnic meats not allowed. -Obviously fat fish, such as those packed in oil and such as mackerel, shall not be used. All cheese except cottage cheese is prohibited. Method of Preparation.: Cook all foods without fat unless that allowed for the meal is used. Broiling, steaming or boiling is the method of choice for cooking meats. No flour gravies or sauces are allowed. At least one vegetable a day should be served raw. Other Foods: Prohibited!
Other Therapy.-Benzedrine sulfate (amphetamine sulfate) may be helpful in controlling the appetite. It should be given one-half hour before meals. The recommended adult dose for chronic medication is usually 10 mg. repeated three or four times daily. An appropriate fraction of this dose may be given to children. Since occasional patients • We are indebted to Miss S. Wells, dietitian in charge at the Metabolic Ward of the Massachusetts General Hospital, for these diets.
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are sensitive to the drug and develop cerebral symptoms, the initial dose should be small. A tendency to increased appetite has been noted after discontinuation of the drug and the effect may be only temporary.26 Thyroid therapy is disappointing except in the rare obese child who is suffering from hypothyroidism. The administration of this hormone to euthyroid fat children often results in an increased appetite-a reaction which, unless carefully controlled, is clearly undersirable. In sizeable doses it also tends to cause such symptoms· and signs of thyrotoxicosis as nervousness, excitability, tachycardia, sweating, tremors, diarrhea and even demineralization of the skeleton and protein depletion. Obesity is not ordinarily an indication for sex hormone (testosterone, estrogen, etc.) or anterior-pituitary-like (chorionic gonadotropin) therapy. As mentioned above, most fat children mature sexually in a normal manner. In some this process is expedited by simple dietary weight reduction. A discussion of the therapy of significant hypogonadism and of Cushing's syndrome is beyond the scope of this article. BIBLIOGRAPHY
1. Talbot, N. B.: Measurement of Obesity by the Creatinine Coefficient. Am. ]. Dis. Child., 55:42, 1938. 2. Newburgh, L. H.: Obesity: I. Energy Metabolism. Physiol. Rev., 24:18, 1944. 3. Conn, ]. W.: Obesity: II. Etiological Aspects. Physiol. Rev., 24.:31, 1944. 4. (a) Bruch, H.: Obesity in Childhood: III. Physiologic and Psychologic Aspects of the Food Intake of Obese Children. Am. J. Dis. Child., 59: 739, 1940. (b) Bruch, H. and Touraine, G.: Obesity in Childhood: V. The Family Frame of Obese Children. Psychosomatic Med., 2:141, 1940. ,5. Bronstein, I. P., Wexler, S., Brown, A. W. and Halpern, L. J.: Obesity in Childhood. Psychologic Studies. Am. ]. Dis. Child., 63:238, 1942. 6. Bruch, II.: Obesity in Childhood: I. Physical Growth and Development of Obese Children. Am. J. Dis. Child., 58:457, 1939. 7. Schonfeld, W. A.: Primary and Secondary Sexual Characteristics. Study of their Development in Males from Birth through Maturity, with Biometric Study of Penis and Testes. Am. J. Dis. Child., 65:535, 1943. 8. Talbot, N. B., Butler, A. M., Berman, R. A., Rodriguez, P. M. and MacLachlan, E. A.: Excretion of 17-Ketosteroids by Normal and by Abnormal Children. Am. J. Dis. Child., 6'>:364, 1943. 9. Talbot, N. B. and Worcester, J.: The Basal Metabolism of Obese Children. }. Pediat., 16:146, 1940. 10. ';Varkany, J., Frauenberger, G. S. and Mitchell, A. G.: Heredo-familial Deviations: I. The Laurence-Moon-Biedl Syndrome. Am. J. Dis. Child., 53: 455, 1937. J~. Warkany, J. and Weaver, T. S.: Heredofamilial Deviations: II. Enlarged Parietal Foramens Combined with Obesity, Hypogenitalism, Microphthalmos and Mental Retardation. Am. J. Dis. Child., 60:1147, 1940. I~. Warkany, J., Nelson, R. C. and Schraffenberger, E.: Congenital Malformations Induced in Rats by Maternal Nutritional Deficiency: Use of Varied Diets and of Different Str~ins of Rats. Am. J. Dis. Child., 64:860, 1942. 0
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J.: Effect of Maternal Rachitogenic Diet on Skeletal Development of Young Rat. Am. J. Dis. Child., 66:511, 1943. Erickson, C. A.: Rubella Early in Pregnancy Causing Congenital Malformations of Eyes and Heart. J. Pediat., 25':281, 1944. Bruch, H. The Frohlich Syndrome: Report of the Original Case. Am. J. Dis. Child., 58:1282, 1938. Van Creveld, S.: Glycogen Disease. Medicine, 18.:1, 1939. Talbot, N. B., Hoeflel, G., Shwachman, H. and Tuohy, E. L.: Serunl Phosphatase as an Aid in the Diagnosis of Cretinism and Juvenile Hypothyroidism. Am. J. Dis. Child., 62:273, 1941. Wilkins, L. and Fleischmann, W.: Hypothyroidism in Childhood: III. The Effect of Withdrawal of Thyroid Therapy upon the Serum Cholesterol. Relationship of Cholesterol, Basal Metabolic Rate, Weight and Clinical Symptoms. J. Clin. Endocrinol., 1.:19, 1941. Albright, F.: Cushing's Syndrome. The Harvey Lecture Series, 38:123, 19421943. Marks, T. M., Thomas, ]. M. and Warkany, J.: Adrenocortical Obesity in Children. Am. J. Dis. Child., 60:923, 1940. Farber, J. E., Gustina, F. J. and Postoloff, A. V.: Cushing's Syndrome in Children. Am. J. Dis. Child., 65':593, 1943. Talbot, N. B. and Butler, A. M.: Urinary 17-Ketosteroid Assays in Clinical Medicine. J. Clin. Endocrinol., 2:724, 1942. Fraser, R., Albright, F. and Smith, P. H.: Carbohydrate Metabolism: The Value of the Glucose Tolerance Test, the Insulin T olerance Test and the Glucose-Insulin Tolerance Test in the Diagnosis of Endocrinologic Disorders of Glucose Metabolism. J. Clin. Endocrinol., 1:297, 1941. Lusk, G.: The Science of Nutrition, 4th ed. Philadelphia and London, W. B. Saunders Co., 1928. Talbot, F. B.: Basal Metabolism of Children. In Practice of Pediatrics, Chapter 22, Volume I, Edited by J. Brennernann, Hagerstown, Md., W. F. Prior Co., Inc., 1944. Kunstadter, R. H.: Experience with Benzedrine Sulfate in the ManageInent of Obesity in Children. ]. Pediat., 17:490, 1940.
13. Warkany,
14. 15. 16.
17. 18.
19.
20. 21. 22. 23.
24. 25. 26.
NATHAN B. TALBOT
B.
TALBOT,
M.D.
CLINICIANS dealing with children see a great many patients who are overweight for their height. Of the children who are seen in the outpatient and in-patient departments of the Massachusetts General Hospital, approximately one in ten fall into this group. Definition of Obesity.-Though most overweight patients are obese, a careful examination sometimes shows that the extra weight is due to a well. developed musculature rather than to an excessive accumulation of adipose tissue. Such muscular individuals, though "overweight," do not properly come under the classification of obesity. In fact, if obesity is defined as an accumulation of subcutaneous fat which is excessive with relation to the underlying musculature and bones, then certain children may be obese without being significantly overweight for their height.!' Generally speaking, however, most persons who weigh 20 per cent or more than the normal for their height and age are obese.
CAUSES OF OBESITY
Fundamental Causes.-The evidence now available clearly establishes the fact that obesity is due to an intake of 'calories which exceeds the caloric requirements for energy metabolism, physical activity and growth (protein anabolism).2, 3 Thus, in the development of adiposity, the two important variables are the caJoJ;ic. intake and the caloric expenditure. A relative increase in the di~t or a relative decrease in the energy metabolism, physical activity and/or rate of protein anabolism (growth) will tend to yield a surplus of calories which may be stored as body fat. Most obesity is due to overeating rather than to a diminished energy expenditure on a normal dietary intake. Not uncommonly patients or their parents will cling tenaciously to the thesis that the quantity of food eaten is not large. However, when this is the case, it is almost always possible to elicit a history of dietary excess at some earlier date. In other words, once a patient has eaten too much and become fat"he will tend to remain so if he is eating a maintenance diet. He will not lose weight until such titne as he eats fewer calories than he is expending. I
.... From the Department of Pediatrics, Harvard Medical School and the Children's Medical Service, Massachusetts General Hospi~~J, Boston. The observations and points of view recorded here were based upon studies supported by the Commonwealth Fund of Ne",· York and the Permanent Charity Fund of Boston. * Assistant Professor of Pediatrics, Harvard Medical School; Assistant Physician, Massachusetts Memorial Hospital. 1217
1218
NATHAN B. TALBOT
Contributing Causes.-A· number of different factors may induce overeating. Among these are personality problems,4,5 organic lesions of the brain (especially of the hypothalamus)3 andi hypoglycemia. 3 On the other hand, physical inertia,· hypometabolism and decreased ·protein anabolism (slow growth), may .be responsible for·· a decrease in the energy requirements. -... Of these factors, the personality ones are by far'themost impor~ant in the. maj'ority of obese boys and gi!ls. Some chi~dren tend to nibble at food to help relieve themselves of worry, unhappiness or boredom. Others have become accustomed to tables heavily lp,den wi~h nutritious foods and. to seeing their parents, brothers. or sisters take gluttonous servings. Sometimes parents erroneously assume ~hat ·a large appetite per se ensures good health and therefore urge their children to eat too much. Similarly, parents may not be aware of the normal.decilne in appetite which may occur at about two years of age when the rapid growth of infancy subsides. Attempts to prevent such a normal decline in appetite has led to the development of adiposity in acquiescent children. In the resistant child the- same treatment may result in anorexia and leanness. The mechanism by which organic brain lesions stimulate the appetite is not clear. For reasons beyond metabolic definition, a reasonable meal ~oes not "satisfy." Hypoglycemia secondary to hyperinsulinism induces hunger in some people, but fails to do so in others. It is rarely a factor in childhood adiposity. Hypothyroidism (decreased energy metabolism, growth and physical activity) is seldom noted in association with obesity in children. CLINICAL TYPES OF OBESITY IN CHILDREN
While the degree of adiposity is referable to the caloric balance, tJ1e distribution of accumulated adipose tissue may be influenced by endogenous factors. .Simple Obesity.-Over 95 per cent of all fat children fall into this group. The only thing wrong with these children is that for personality or environmental reasons they have eaten too much. Studies have revealed that the majority of these children are only children or the youngest child and that many of them are unwanted. In·many families the rehltionship of the .parents is unhappy. Food may have taken on exaggerated importance and may become a substitute for love, security and satisfaction.4, 5 A careful survey of the history almost always reveals a. period or periods of dietary excess. There is no history suggestive of serious intracranial disease. They are free from symptoms of hypothyroidism. In. other words, they are healthy. children. On physical examination fat boys and girls wtih uncomplicated obesity are usually found to be of average or slightly taller than average stature. 6 They are of normal intelligence; quite a few stand in the
OBESITY IN CHILDREN
1219
Fig. 173.-This 5 year old boy is presented as an example of simple obesity. He was of normal weight at 1 year (11.8 kg.). From that time on he gained at a steady and very excessive rate so that by the age of. 5 years he· weighed 44 kg. or about 21 kg. more· than he should weigh. During this period of rapid weight gain he also grew rapidly, attaining a height of 125 em. at the age of 5 (normal 105 to 116 cm~). He is fond of bread, potatoes, cakes, cookies, puddings, candy bars and the like. Other members of the family also have hearty 'appetites, for a brother of 13 years weighs 80 kg. ( 175 pounds), a sister of 11 years weighs 48 kg. (105 pounds) and his father who'is 170 em. (5 feet 8 inches) tall weights 100 kg. (220 pounds). He is- of normal intelligence and is free from symptoms of increased intracranial pressure. There is nothing in the history to suggest hypothyroidism: Aside from the excessive accumulation of subcutaneous tissue and tallness in stature, physical examination is not remarkable. The blood pressure is 120/80. Roehtgenograrns of the skull show a normal sella turcica and fail to reveal any abnormalities. Roentgenograms of the hand, and wrist show that his skeletal development corresponds to the average normal for his chronologie age. The urinary 17-ketosteroid output is 0.6 mg. per day, a normal value. By the simple ~xpedient of reducing his intake of starchy foods to one-half piece of bread or its equivalent per meal three times a day, he is losing weight at the ' rate of about OS kg. (1, pound) per month.
1220
NATHAN B. TALBOT
top third of their class at school. Some of these children are found to be only moderately plump while others are extremely fat (see Figs. 173 and 174). The exc~ss ~dipose tissue though generally distributed often accumulates especially in the region of the b~easts, hips and lower abdomen. Though the breast regions may thus appear enlarged, palpation usually fails·::,to .:rev~al any true marf.lmary gland de~elopment
A
B
Fig. 174.-A, Extreme example of simple obesity in a boy of 6 years weighing 65 kg. and measuring 126 em. and \\J~ith genu varum probably secondary to excess weight bearing. During a period of 8 months on a caloric intake of from -1000 to 5eo calories per day,. he lost 29 kg. B,. The administration of thyroid had essentially no effect' upon the rate of weight loss. During this period the -genu varum was corrected by bilateral osteotomies.
except in' adolescent girls. A transient and ~pparently pp.ysiologic development of.'the mammary tissues is noted in a small number of normal adolescent -boys. _ The eyes, extraocu,lar movements, visual fields -and eyegrounds- are . normal. While the ch'est and heart are normal, the blood pressure may be slightly elevated. In this respect it is _helpful to remember that the
OBESITY IN CHILDREN
1221
use of a blood pressure cuff which is' too small for the patient's arm will result in an overestimation of the blood. pressure. The abdomen is free from abnormal masses. The genitalia in boys often appear to be 'small because they are embedded in a thick pad of pubic fat. By pressing the fat aside, this .erroneous impression can be dispelled. In ·this connection, it is noteworthy that in normal boys the genitalia. -remain of essentially infantile size until approximately 11 to 12 years of age. 7 Not until that ,time do the testes secrete ~nough male hormone to "stimulate any significant development of .the masculine secondary sex characteristics. Moreover, some normal boys develop one or two· years later than the average. For these reas6ns boysneed::not necessarily be considered hypogonad ev~n if genitaLgrowth.is oelayed to the thirteenth or fourt~enth year. Sexual development.js~moderately acpelerated in some of these children. 6 The skin is s1l\i)oth,. warm, moi~t and of normal color. Apparently as a consequence Qt~·stretching of the skin, striae over the hip regions ·are occasionally s~.In contrast to the striae of Cushing's syndrome which arepurple,t~e~e are pinkish white. There is no pathologic hirsutism. The extremj~~~,~'are normal. Roentgenograms· of the skull are uniforml~~J:~fnormal appearance. X-ray films of the hand and wrist reveal that t~.:'·skeletal development either corresponds 'to the normal fOf the chtf'Jogic age (according to Todd's standard Atlas of Skeletal Matu"::;ct'1 P)" or· is slightly advanced. 6 Likewise, the urinary excretion of.~i;~~~ketosteroids is either normal for the patient's age, or if the patient is~exceedingly obese, may be. slightly elevated. 8 As a rule, "physiologic. ages" as measured by genital development, the skeletal development and·· the 17-ketosteroid excretion, respectively, correspoI).d closely to .each, other. ' There has been considerable debate concerning the basal metabolism of such children. The present ccnsensusis· that their basal metabolic rate 'corresponds closely to the normal and' tends, if anything, to be elevated. 2 , 9. This becomes clear .when the metabolic rate .is computed with due consideration for the fact that in;fobesity an abQormally large proportion of the' body weight is compo~edof relatively inert fat. . Obes,ity in Association with Mental Retardationa.ndjor Other Bodily ·Defects.-In contrast to the preceding group are children w'ho in addition to being obese have"one or Plore of, tlle following defects: J;etinal degeneration or retinitis pigmentosa-, mental retardation, polydactylism, ;syndactyli~m, hypogonadism, microphthalmus, enlargement .of the parietal foramens of the skull or a related disorder. lo , ll.Many of thes~ def~cts appear to be hereditary familial deviations~ On th~ other hand, it is of interest that somewhat similar congenital defects 'have been;observed in th~ offspring of. mothers who. received a nutritionally inade;;" quate diet12, 13' orwho contracted German measles during pregnancy..14 When. the hereditary familial defects~retinitis pigmentosa, ob'esjty, hypogon~dism, mental retardation a:nd polydactylism-happen to occur
1222
NATHAN B. TALBOT
in one individual, the resultant combination is sometimes called the Laurence-Moon-Biedl syndrome. Like normal children, tQese patients are fat because they have eaten relatively too much. It is postulated without much factual basis that these excessive appetite may be due to a hypothalamic lesion.
Obesity in Association with an Expanding Intracranial 'Lesion (Frohlich's Syndrome).-This is a rare condition usually due to a craniopharyn-
gio,ma or suprasellar cyst. 15 Children sqffering from this disease present
Fig. 175.-0besity in a 9 year old boy with a sliprasellercyst. Note the strabismus.
such· typical symptoms and signs of an expanding lesion in· the region of the optic chiasm as headache, vomiting, disturbances of vision (bitemporal hemia'nopsia) or of ·.extraocular movements, optic atrophy, separation of.. the cranial sutures and· increased spinal fluid pressure (Fig. 17.5). Roentgenograms of the skull may. reveal erosion of the sella turcica.:.or an area of calcification in the neighborQood thereof. These expa,l.1ding .lesions apparently influence the appetite in much the' same manner that experimentally produced hypothalamic ·lesions
OBESIT'Y IN CHILDREN
1223
do. They may also interfere\vith the function of the anterior and/or posterior pituitary gland either directly by causing pressure atrophy of the gland or indirectly by interfering with normal neurohypophyseal regulatory mechanisms. When the anterior pituitary function is impaired, various disturbances in growth and development may be noted. Interference with the production of the growth hormone results in dwarfism. Failure to produce the thyroid-stimulating hormone results in hypothyroidism which leads to retardation in growth and in skeletal maturation. When there is failure to produce the anterior pituitary gonad-stimulating hormones, the gonads themselves remain infantile and little or no secondary sexual development occurs. Finally, lack 'of the anteri~r pituitary adrenal-cortical stimulating hormone results in atrophy of adrenal cortices a~d the development of Addison's disease. In a given patient there may be a complete or only partial impairment in the production of anyone or more of these anterior pituitary hormones. Hence, patients with destructive lesions in the region of ,the hypothalamus or the pituitary may .present a variety of clinical pictu'res. In fact, certain lesions which affect the hypothalamus but leave the anterior pituitary intact sometimes lead' to precocious growth and development. Hypothalamic stimulation of the anterior pituitary is believed to be responsible for such precocity. In so far as hypothalamic lesions stimulate polyphagia, they may be considered as factors predisposing to obesity. There is no evidence that they induce adiposity by' other mechanisms. Similarly, it is fair to say that there is no such thing as '1>ituitary" obesity. Many patients with destructive lesions of the pituitary actually suffer a marked loss of appetite and as a consequence become cachectic (Simmonds' cachexia). Though the foregoing types of intracranial lesion have received much publicity, other intracranial conditions such' as internal hydrocephalus, brain tumors, xanthomatosis, pinealoma, syphilis, poro'ncephaly and postencephalitic changes likewise may lead to obesity and to disturb,ances in obesity and development. Obesity in Association with Hypoglycemia.-Hypoglycemia resulting from hyperinsulinism or from glycogen disease induces overeating in some individuals. Such conditions as these are but rarely encountered in pediatric practice. 'An abnormally low fasting blood' sugar value is suggestive of hyperinsulinism. Hepatomegaly, ketonuria and hypoglycemia are suggestive .of glycogen 'storage disease. 16 Patients with this condition show very little elevation of the blood sugar concentration following the administration of adrenaline Obesity in Association with Hypothyroidism.-It is unusual to discover hypothyroidism in an obese child. This' is explained by the fact that hypothyroidism tends to cause a diminution in appetite as well as a decrease in the total energy metabolism, physical activity and growth.
1224
NATHAN B. TALBOT
The most characteristic symptoms' of thyroid lack in children are easy fatigability, both phy~ical and mental, constipation, sensi~ivity to cold weather and slowness in statural growth. On examination almost all hyopthyroid children are found to be of dwarfed stature. Mental deficiency is not a consistent finding. The skin is pale, coarse; cool and dry. There is often a subtle appearance of puffiness around the face due to local accumulations of myxedema fluid. Accumulations of, myxedema fluid in other localities may also give rise to ,a pudgy appearance. Roentgenograms 'of the hand and wrist reveal a retardation in the skeletal development. In children this diminution in bone growth is associated wIth a lowered serum phosphatase value (less than 4.5 Bodansky units per'100cc,,)17 An elevation in the serum cholesteI:'ol concentration above 250 mg. per 100 cc. is also suggestive. However, in many hypothyroid. children who. have never received thyroid medication, this value is either normal or low rather than elevated. On the other hand, when such hypothyroid children are given adequate doses of thyroid (1 to 2 grains of 'U.S.P. thyroid daily) for a month or longer and then their medication is discontinued, they develop hypercholesterolemia within the next one to three months. Children with normal thyroid function do not do SO.18 The basal metabolic rate is mucl! less reliable as an index of hypothyroidism in children than in adults. Possibly the best index of thyroid' function is the concentration of protein-bound (thyroid hormone) iodine in the plasma or serum. This should receive increasing attention as more laboratories become equipped, to make the determination. . Obesity a"s Effected by Other Enclocrine Disturbances.-Certain steroid hormones of the adrenal cortex and possibly of the sex glands may e'xert a striking influence upon the distribution of body fat. The outstanding example is Cushing's syndrome (Fig. 176), a (rare condition which is thought to be due to an excess of those adrenal cortical hormoneS which accel~rate gluconeogenesis from protein. 19 This condition may occur at anyage. 20 ,.21 The youngest recorded patient was only eleven weeks old. The incidence is considerably .greater in girls than in boys. The obesity is often, not always:, of, the "buffalo" type. That is, there is a marked accumulation of fat about the head and neck, while the extremities are relatively lean. Muscular, weakness is a characteristic finding. The cheeks in the characteristic patient are plethoric in appearance. There are purplish striae in the skin over ,the hips, abdomen aRd thighs; acne is common especially in older girl patients. There is often generalized' hirsutism. The genitalia may be precociously developed. Hypertension is an outstanding finding. This is reflected by the plethoric '~ppearance already mentioned and may also be manifested by cardiac enlargement and occasionally by cerebral hemorrhages. When the disease is due to an adrenal cortical carcinoma, an abdominal tumor may be palpable.
OBESITY IN CHILDREN
1225
Intravenous pyelograms may be helpful in revealing such tumors. There is a decreased tolerance for sugar and a tendency to insulin :resistance. 19 In some patients there is a marked increase in the urinary excretion of 17-ketosteroids; in others, the values are essentially. normal. 19 ,22 Osteoporosis of the spine especially is a notable sign. The skeletal development. tends to be normal for age and sex.
Fig. 176.-Cushing's syndrome in' a 12 year old girl. (Courtesy of Dr. F. Albright. 20 ) I
Though not so clear-cut, there is also some. evidence to suggest that the testicular male hormones favor a distribution of fat in the upper segment of the body while the ovarian female hormones' cause the fat to be distributed in the lower body segment. Most preadolescent children show a fairly even 'distributi~n of fat when they become obese. Hypogonadism per se does not cause obesity.3 Obesity, on the other hand, occasionally retards the onset of adolescence. In this respect it is of interest that simple weight reduction by dietary means often results in prompt adolescent development in children with simple obesity.
1226
NATHAN B. TALBOT COMMENTS ON THE CLINICAL STUDY OF OBESE CHILDREN
In view of the fact that obesity, though not a metabolic or endocrine disease per se, may be a sign of some important associated condition, it is desirable to emphasize certain. parts of the history and physical examination of fat children. Thus, in the history, symptoms of intracranial disease, physical inactivity. hypometabolism, mental deficiency or family maladjustments may be helpful. In the physical examination, signs of increased intracranial pressure, abnormal eyegrounds, a marked hypertension, an abdominal tumor, skeletal anomalies, a "buffalo" distribution of fat, muscular weakness or shortness of stature may lead to a specific diagnosis. The value of a careful examination of these patients is well exemplified by one patient who superficially appeared to be a typical example of simple obesity. However, routine examination of the eyegrounds revealed unmistakable papilledema. That child was subsequently found to have a brain tumor. Roentgenograms of the skull occasionally reveal abnormalities not previously evident. Roentgenograms of the hand and wrist permit an estimation of the skeletal development which is helpful when deviations in the rate of maturation are suspected. Fasting blood sugar determinations as well as glucose and glucose-insulin tolerance tests 23 may be helpful occasionally. Likewise, in the patient suspected of having adrenal cortical disease, a urinary 17-ketosteroid measurement can be diagnostic. Determinations of the basal metabolic rate are seldom helpful and often lead to an erroneous diagnosis of hypothyroidism. Other means for establishing a diagnosis of this disease have been discussed above. TREATMENT OF CHILDHOOD OBESITY
General Considerations.-One of the first considerations in treatment is the question, is it worth while to attempt to reduce the body weight of all fat children? The answer depends partly upon the type and degree of . obesity. Because children are growing individuals, it sometimes suffices merely to prevent further gains in weight. A quantity of fat which was moderately excessive for a small child will be normal for the same child when he is a few inches taller. On the other hand, a markedly excessive accumulation of fat may interfere with the physical efficiency of a child to such an extent that participation in normal childhood pursuits is greatly impeded. Furthermore, as mentioned earlier, adiposity per se occasionally retards adolescent development, an occurrence which may cause considerable concern to patients and their parents. .. . As indicated in the introduction, any person will lose weight when the caloric intake is consistently less than the caloric output. In general, it is more profitable to produce such a caloric deficit through
OBESITY IN CHII.DRRN
1227
reducing the caloric intake (underfeeding) than by increasing the caloric expenditures with the aid of exercise and/or medications. It requires a considerable amount of exercise to increase the total caloric output significantly. Thus, even for an adult man weighing 70 kilograms an hour's walk on a level road at a rate of about 3 miles per hour requires only 160 calories or 17 gm. of fat. 24 Vigorous exercise tends to stimulate a voracious appetite. After underfeeding is instituted there may be a one or two week interval before a loss of body weight occurs. This is explained by the fact that while the patient loses fat during this period, he retains an equal weight of water. 2 Sooner or later there is a spontaneous diuresis with the loss of one or more kilograms of weight during the course of a few days. Thereafter weight loss is steady. How can one induce a child to eat less? In younger children whose diet is completely under the control of their elders, this may not present too great a problem. In the older and more independent child, success depends largely upon gaining the interest and cooperation of the patient. Without these, attempts at therapy are usually a failure. In other words, the problem is a psychological one. Frequently the primary fault lies chiefly with parents who need advice on the management of children. On the other hand, the child often needs to develop pride in his appearance, a feeling of self-confidence and an ap·petite for something more important than food. Dietary Therapy.-Regimen A.-This regimen permits eating any reasonable quantities of protein and other relatively low caloric foods while forbidding the eating of certain high caloric items. 1. Eat no candy, cakes, cookies, jams or sugar and no desserts to which such ingredients or flour have been added in any considerable amount. 2. Eat not more than one-half piece of bread (any type) a meal or its equivalent in rice, macaroni, spaghetti, potato or other starchy food. 3. Drink 2 to 3 glasses of skimmed milk a day. 4. Except for these instructions, eat as desired at mealtimes of lean meats, fish, colored vegetables, salads, fresh fruits. Use vinegar or mineral oil dressing. Use ordinary common sense in not stuffing on any particular diet. 5. Plan to eat three reasonable meals a day. The individual who eats no breakfast, a small lunch and a huge dinner tends to gain more weight than the person who eats the same amount of food divided equally between three meals.
In favor of this regimen is its simplicity and the fact that individuals on it are less tempted to eat the forbidden because they feel starved. While it suffices in many instances at least to prevent further weight gairis it is ineffective in others. When a ffioce precise adjustment of the caloric intake is desired, diets similar to those of Regimen B may be prescribed. Regimen B.-It is appropriate to offer a diet calorically equal to the basal energy· metabolism. For practical purposes this may be predicted roughly from the ideal weight for the patient's height as follows:
1228
NATHAN B. TALBOT
Height, cnl. 73 115 137 150 160 170
Ideal Body 'Veight, kg.
Basal Heat Production, Calories per d ay 25
10
550 870 1100 1250 1400 1550
20 30 40
50
60
Provided ·the mineral, nitrogen and vitamin requirements are met, patients suffer no damage from such underfeeding so long as excess body fat remains. Sample diets· follow: 1. 750 cals., P 53 gm., F 20 gm., CHO 90 gm.
Breakfast a. Orange juice, ¥2 cup. b. Toast, lh slice, or cereal, ~ cup. c. Butter or oleolnargarine, 12 sqyare. Noon a. Clear soup (broth, bouillon or consomme) ad lib. b. One egg or lean meat, fish, fowl or cottage cheese, 2 oz. or 5 tablespoons or a piece about lhx2x3 inches. c. Vegetables, 2 servings (1;2 cup each) raw or cooked without sauces. d. Fruit, lh cup or equivalent. e. Skim milk, lh cup. Night Same as at noon, but add lh slice bread and square butter. 2. 1000 cals., P 68 gm., F 30 gm., CHO 115 gm. Add to regimen 1, 1 cup skim milk, 1 slice bread, 1 egg, 12 square butter. 3. 1200 cals., P 70 gm., F 51 gm., CHO 115 gm. Substitute 2~ cups whole milk for the skim milk of regimen 2.
*
The following suggestions as to the choice of foods may be helpful. Vegetables: A serving of potatoes, kidney, lima, navy or soup beans and of corn shall be considered as :JA instead of lh cup. Lettuce and celery may be used ad lib. All other vegetables equal ~~ cup. Fruits: No sweetened fruit is to be used. Unsweetened canned fruits can be purchased. A serving of banana is lh a small banana. Meats, etc.: All visible fat is removed. Ham, pork, bacon, wieners and picnic meats not allowed. -Obviously fat fish, such as those packed in oil and such as mackerel, shall not be used. All cheese except cottage cheese is prohibited. Method of Preparation.: Cook all foods without fat unless that allowed for the meal is used. Broiling, steaming or boiling is the method of choice for cooking meats. No flour gravies or sauces are allowed. At least one vegetable a day should be served raw. Other Foods: Prohibited!
Other Therapy.-Benzedrine sulfate (amphetamine sulfate) may be helpful in controlling the appetite. It should be given one-half hour before meals. The recommended adult dose for chronic medication is usually 10 mg. repeated three or four times daily. An appropriate fraction of this dose may be given to children. Since occasional patients • We are indebted to Miss S. Wells, dietitian in charge at the Metabolic Ward of the Massachusetts General Hospital, for these diets.
OBESITY IN CHILDREN
1229
are sensitive to the drug and develop cerebral symptoms, the initial dose should be small. A tendency to increased appetite has been noted after discontinuation of the drug and the effect may be only temporary.26 Thyroid therapy is disappointing except in the rare obese child who is suffering from hypothyroidism. The administration of this hormone to euthyroid fat children often results in an increased appetite-a reaction which, unless carefully controlled, is clearly undersirable. In sizeable doses it also tends to cause such symptoms· and signs of thyrotoxicosis as nervousness, excitability, tachycardia, sweating, tremors, diarrhea and even demineralization of the skeleton and protein depletion. Obesity is not ordinarily an indication for sex hormone (testosterone, estrogen, etc.) or anterior-pituitary-like (chorionic gonadotropin) therapy. As mentioned above, most fat children mature sexually in a normal manner. In some this process is expedited by simple dietary weight reduction. A discussion of the therapy of significant hypogonadism and of Cushing's syndrome is beyond the scope of this article. BIBLIOGRAPHY
1. Talbot, N. B.: Measurement of Obesity by the Creatinine Coefficient. Am. ]. Dis. Child., 55:42, 1938. 2. Newburgh, L. H.: Obesity: I. Energy Metabolism. Physiol. Rev., 24:18, 1944. 3. Conn, ]. W.: Obesity: II. Etiological Aspects. Physiol. Rev., 24.:31, 1944. 4. (a) Bruch, H.: Obesity in Childhood: III. Physiologic and Psychologic Aspects of the Food Intake of Obese Children. Am. J. Dis. Child., 59: 739, 1940. (b) Bruch, H. and Touraine, G.: Obesity in Childhood: V. The Family Frame of Obese Children. Psychosomatic Med., 2:141, 1940. ,5. Bronstein, I. P., Wexler, S., Brown, A. W. and Halpern, L. J.: Obesity in Childhood. Psychologic Studies. Am. ]. Dis. Child., 63:238, 1942. 6. Bruch, II.: Obesity in Childhood: I. Physical Growth and Development of Obese Children. Am. J. Dis. Child., 58:457, 1939. 7. Schonfeld, W. A.: Primary and Secondary Sexual Characteristics. Study of their Development in Males from Birth through Maturity, with Biometric Study of Penis and Testes. Am. J. Dis. Child., 65:535, 1943. 8. Talbot, N. B., Butler, A. M., Berman, R. A., Rodriguez, P. M. and MacLachlan, E. A.: Excretion of 17-Ketosteroids by Normal and by Abnormal Children. Am. J. Dis. Child., 6'>:364, 1943. 9. Talbot, N. B. and Worcester, J.: The Basal Metabolism of Obese Children. }. Pediat., 16:146, 1940. 10. ';Varkany, J., Frauenberger, G. S. and Mitchell, A. G.: Heredo-familial Deviations: I. The Laurence-Moon-Biedl Syndrome. Am. J. Dis. Child., 53: 455, 1937. J~. Warkany, J. and Weaver, T. S.: Heredofamilial Deviations: II. Enlarged Parietal Foramens Combined with Obesity, Hypogenitalism, Microphthalmos and Mental Retardation. Am. J. Dis. Child., 60:1147, 1940. I~. Warkany, J., Nelson, R. C. and Schraffenberger, E.: Congenital Malformations Induced in Rats by Maternal Nutritional Deficiency: Use of Varied Diets and of Different Str~ins of Rats. Am. J. Dis. Child., 64:860, 1942. 0
1230
J.: Effect of Maternal Rachitogenic Diet on Skeletal Development of Young Rat. Am. J. Dis. Child., 66:511, 1943. Erickson, C. A.: Rubella Early in Pregnancy Causing Congenital Malformations of Eyes and Heart. J. Pediat., 25':281, 1944. Bruch, H. The Frohlich Syndrome: Report of the Original Case. Am. J. Dis. Child., 58:1282, 1938. Van Creveld, S.: Glycogen Disease. Medicine, 18.:1, 1939. Talbot, N. B., Hoeflel, G., Shwachman, H. and Tuohy, E. L.: Serunl Phosphatase as an Aid in the Diagnosis of Cretinism and Juvenile Hypothyroidism. Am. J. Dis. Child., 62:273, 1941. Wilkins, L. and Fleischmann, W.: Hypothyroidism in Childhood: III. The Effect of Withdrawal of Thyroid Therapy upon the Serum Cholesterol. Relationship of Cholesterol, Basal Metabolic Rate, Weight and Clinical Symptoms. J. Clin. Endocrinol., 1.:19, 1941. Albright, F.: Cushing's Syndrome. The Harvey Lecture Series, 38:123, 19421943. Marks, T. M., Thomas, ]. M. and Warkany, J.: Adrenocortical Obesity in Children. Am. J. Dis. Child., 60:923, 1940. Farber, J. E., Gustina, F. J. and Postoloff, A. V.: Cushing's Syndrome in Children. Am. J. Dis. Child., 65':593, 1943. Talbot, N. B. and Butler, A. M.: Urinary 17-Ketosteroid Assays in Clinical Medicine. J. Clin. Endocrinol., 2:724, 1942. Fraser, R., Albright, F. and Smith, P. H.: Carbohydrate Metabolism: The Value of the Glucose Tolerance Test, the Insulin T olerance Test and the Glucose-Insulin Tolerance Test in the Diagnosis of Endocrinologic Disorders of Glucose Metabolism. J. Clin. Endocrinol., 1:297, 1941. Lusk, G.: The Science of Nutrition, 4th ed. Philadelphia and London, W. B. Saunders Co., 1928. Talbot, F. B.: Basal Metabolism of Children. In Practice of Pediatrics, Chapter 22, Volume I, Edited by J. Brennernann, Hagerstown, Md., W. F. Prior Co., Inc., 1944. Kunstadter, R. H.: Experience with Benzedrine Sulfate in the ManageInent of Obesity in Children. ]. Pediat., 17:490, 1940.
13. Warkany,
14. 15. 16.
17. 18.
19.
20. 21. 22. 23.
24. 25. 26.
NATHAN B. TALBOT