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The Effect of Early Feeding on the Development of Obesity

ELLEN S. P A R H A M , PD, R D

Early influences associated with adult obesity include overfeeding leading to f a t cell hyperplasia, inactivity, and faulty mechanisms of control of food intake. T h e first year of life is critical for the intiation of these influences; thus w e need t o reevaluate some of the approaches to infant feeding. Excessive weight gains in infants must be taken seriously. Th i s article reviews related literature and makes recommendations for preventing early obesity.

I I

HYPERPLASIA

‘,? “\

I OVER-RELIANCE I I ON FOOD

1 1‘ 1 UNDERACTIVITY

OF CONTROL OF \ I FOOD INTAKE 1

SEDENTARY APPROACH 1 TO LIFE 1

Figure 1. Early Influences Contributingto the Development of Certain Character- istics Associated With Adult Obesity

For centuries man has sensed that the foundations of adult health were laid early in life. However, due to the difficulties of longitudinal studies and the lack of techniques for study- ing subtle influences and multifactorial situations, we have had to content ourselves with short-term criteria of good health and nutrition. W e had to be satisfied if the infant was free of disease, “thriving,” and achieving “normal” increments in weight, height, and general development.

Recently, however, new techniques, particularly in the study of growth at the cellular level, have permitted new understanding of the role of nutrition in the overall process of growth, de-

velopment, and maintenance. This paper concerns the influence of early feeding on later obesity and several current theories regarding this re- lationship.

Some Basic Facts About Obesity Obesity is due to a calorie intake

that exceeds calorie expenditure, i.e., overeating. Those who go no further than this simplistic view would treat obesity by merely informing the per- sons that they overeat and educating them about the relative caloric value of foods. The fallacy of this approach can be seen by drawing an analogy to alcoholism. Although alcoholism is due to overdrinking, we would not

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attempt to treat the alcoholic by tell- ing him he drinks too much and point- ing out the alcohol content of various beverages. In obesity, as in alcoholism, we must discover why the individual consumes more than he can handle. In both conditions, the best treat- ment is prevention.

Possible mechanisms of obesity are outlined in Figure 1 and Table 1.1.2

Obesity is not a single disease, but a symptom common to several diseases with differing etiologies. Environment and heredity affect obesity. The mech- anism of genetic influence has not been found but could lie in hormonal or enzymatic action and, possibly, fa t cell hyperplasia.

Furthermore, an individual may quite likely be influenced by several mechanisms. A child may have a hereditary predisposition to obesity coupled with a family pattern of meet- ing psychological needs through food. This may be complicated by the middle-class 20th century tendencies toward passive activities such as tele- vision viewing, spectator sports, auto- mobiles as transportation, etc.

Baby Fat is Not Outgrown Obesity during infancy and child-

hood should not be lightly dismissed as baby fat. The majority of the 10 to 39% of American school children who are overweight or obese will likely be obese adults. The overweight child has a slim chance of outgrowing his pr0blem.~*4 When relative weights of 174 adults were compared to their weights 20 years previously, only an approximate 20% who were over- weight children were normal weight as adults. Of those who were normal weight as children, 82% were normal weight as adult^.^

Figure 1 shows early influences which may contribute to the develop- ment of adult obesity, such as fa t cell hyperplasia, inactivity, and faulty mechanisms of control of food in- rake.

Fat Cell Hyperplasia Hyperplasia is tissue growth in-

Table 1. Types of Obesity According to Mechanism

I . Regulatory obesity (no primary metabolic abnormality) A. Increased caloric intake

1. “Organic”-injury or damage to control mechanisms (rare) 2. “Functional”

a. Neurotic overeating: psychological influences b. Non-neurotic overeating: social and cultural influences, reliance on

external clues to hunger 8. Decreased caloric output

1. “Organic”-inability to exercise, example: crippling arthritis 2. “Functional”-social and cultural, psychological influences toward

sedentary life style 11. Metabolic

A. Neurological (rare) 6. Hormonal: abnormalities reported, may be effect rather than cause of

C. Enzymatic: possibly the site of genetic influences

intake (?)

obesity

I 11. Fat cell hyperplasia-may influence metabolism and/or regulation of food

Modified after Gordanl and Van ltallie and Campbell.*

volving increases in the number of cells; it is normal a t certain stages of development and within certain limits. After hyperplasia, the rate of cell division slows (transition stage). Then the tissue grows by increasing cell size (hypertrophy). Effects of nutri- tion during hyperplasia appear ir- reversible. For example, undernutri- tion appears to prohibit achievement of normal numbers of brain cellss

Obese adults may have any com- bination of hyperplasia and hyper- trophy of their fat cells. Studies suggest that fat cell hyperplasia is as- sociated with overfeeding very early in life. Of two groups comparable in degree of obesity, Hirsch found the hyperplasic group had many more fat cells than normal, but the cells were normal in size. The hypertrophic group had fewer fat cells, but the cells were enlarged. Most of the hyperplasic subjects were obese be- fore 2 years of age.‘

Loss of 100 pounds reduced the fat cell size to below normal but did not affect cell number in 63% of sub- jects studied by Hirsch. Before diet- ing, the mean number of fat cells of the subjects was about twice that of normal controls. In 37% of the sub- jects, weight loss decreased cell size

to about half the size of fat cells of the controls and appeared to reduce the number of fa t cells. However, this “decrease” in cell number may have been artificial because it is dif- ficult to adequately fix and count such small cells7

Normally, the number of cells in- creases through 14 years of age. Obese subjects seem to undergo active hy- perplasia in the first year followed by a long transition stage through early adolescence.* There may be a second stage of hyperplasia in early ado- lescense. Hypertrophy continues throughout life. Hirsch states that most adipose cells are formed late in gestation; some cells are added in the first year of life, some in early adoles- cence. He feels that nutrition in- fluences adult fat cell numbers most during these stages.$

Some individuals may have a genetic predisposition that causes them to be born with abnormally large numbers of fa t cells. However, studies of genetically obese mice have shown that increased body fat seems largely due to hypertrophy rather than hy- perpla~ia.9~~0 Thus, environmental factors, including intrauterine and in- fant nutrition, are responsible for the increase of fat cells observed in early

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onset 0besity.O In 221 children studied from the

first 6 months of life through 6 or 7 years of age, weight gain in infancy was found to be a better predictor of overweight than birthweight or par- ents’ weight. The incidence of fat- ness at followup .was 20.3% among children who were above the 90th percentile as infants and 6.9% among those whose infancy weight was about the 50th percentile or lower. The re- lationship of birthweight to later weight was not clear. There was no significant difference between breast- and artificially-fed babies with regard to later obesity.ll

According to the health histories of 1S8 obese girls, they were already significantly heavier at 1 year of age than a control group of normal girls. There was no difference in the birth- weights of the groups. Apparently, among these children, the mechanisms of obesity were activated after birth, before 1 year of age.

Fat cell number and size are signifi- cant factors in body metab0lism.12’~~ Increased numbers of fat cells may cause metabolic conditions that in- crease hunger or decrease satiety.

Development of Hunger and Satiety Response

Most people experience internal and external signals of hunger. Internal clues include stomach symptoms, headache, tiredness, etc. Some ex- ternal clues that prompt us to eat are awareness of the hour, sight or smell of food, and social situations.

Although the obese experience stomach contractions, they do not al- ways associate the sensation with hunger.le Deprived of environmental clues to prompt food intake, they seem to have little desire to eat. Hashim and Van Itallie observed obese and normal weight adults caused to rely on a “feeding machine” for total food intake. This machine pro- vides liquid nourishment which is sucked through a tube. The subject eats as much as he wants, but cannot visually monitor his food intake, and

must rely on body sensations to de- termine how much to eat. Under these circumstances, the normal weight sub- ject consumed quantities approximat- ing his usual calorie intake. Typically, the obese subject’s intake dropped to just a few hundred calories.l?

Obese individuals are insensitive to internal clues to hunger and rely largely on external signals, according to Schachter.18 External clues derive from the environment, not from the individual’s own needs, and depen- dence on such clues can result in greatly distorted food intake.

Wooley suggests that normal weight subjects also exhibit distorted food intake behavior when they cannot ac- curately monitor their intake. She found that both obese and normal sub- jects ate less and felt fuller when given beverages which appeared to be high calorie (but were not) than when given beverages that appeared to be low calorie.19

Young babies seem very sensitive to internal clues to hunger. When a baby is hungry, only food will satisfy, and when satisfied, he is uninterested in food. The infant is soon influenced to conform to a schedule and respond less to his body signals and more to the environmental signals. As the in- fant grows into a preschool child, his growth slows down and his appe- tite wanes. However, his mother’s ex- pectations for food consumption do not decrease. Children are encouraged to eat the quantities determined as “enough” by mother, not the amounts their bodies signal.

Other Factors Social attitudes toward exercise and

activity and reliance on food to as- suage personal and social problems also predispose to obesity.

Even in the first months of life, amount of physical activity apparently is a major factor in the development of obesity. Mayer found that fat and thin babies did not differ in calorie intake, but did differ in degree of activity; the thinner babies were more active.20 Obese teenage girls actually

eat less than their slender peers; the major difference is that the obese are less active. Exercise seems essential to trigger normal mechanisms of con- trol of food intake in animalsZ1 and humans22

Were the Old Practices Better? Because the increased incidence of

childhood obesity coincides with in- creased use of bottle feeding and early introduction of semisolid foods, we must question whether these prac- tices contribute to the problem. Breast- feeding is believed to result in leaner babies. Harfouche states that breast- and bottle-fed infants had equal weight gains from birth to 4 m0nths.~3 During these months, nitrogen re- tention was higher in breastfed in- fants, suggesting that weight gains represented more lean tissue than in the bottle-fed babies. From the fourth month, the bottle-fed infants gained more rapidly. On the other hand, Eid found no significant difference in incidence of obesity in children who had been fed by the two methods.ll

Certainly an infant may consume too many calories from excessive quantities of breast or cow’s milk. The tendency toward leaner babies when breastfed is possibly due to one of the following: 1) the breastfed in- fant, rather than his mother, decides how much he should take; 2) the breastfed baby usually has to suck harder for his milk, thus burning more calories and possibly becoming discouraged when somewhat satisfied; 3) a breastfed baby who is weaned directly to a cup will not be given a bottle for a pacifier, a practice which results in alarmingly high milk in- take in some infants and children. All of these factors can be compensated for in a careful program of bottle feeding.

Although early introduction of semisolid foods is of questionable value, there is no strong evidence to implicate it in infant obesity. Even when introduced early, these foods may not be consumed in any sig- nificant quantity for several months.

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Particularly in the last 6 months of the first year, these foods contribute important quantities of iron, vitamin C, and vitamin A.

Recommendations How are we going to cope with

this ever-increasing problem of early onset obesity? I would make the following recommendations:

1. Screen for probable causes. Look for a family history of obesity and unusually rapid weight gain during the first 6 months. Especially note in- fants whose weight is above the 95th percentile on standard charts and those who have crossed percentile lines during the first year.

2. Take infant obesity seriously and convince the family of your concern. However, avoid making the family feel that the infant is abnormal or somehow “bad.” Extreme family anxiety only adds to the problem. Offer constructive suggestions.

3. Encourage practices which pro- mote greater physical activity in in- fants. These may include maderate visual and auditory stimulation, play periods in little or no clothing, and avoiding long times in confining ap- paratuses such as infant carriers or high chairs.

4. Encourage breastfeeding in in- terested mothers. Otherwise instruct the mother on how to avoid over- feeding.

5. Do not recommend wholesale “reducing diets” for infants. Infancy is the period for hyperplasia for all tissue and health depends on adequate food intake. Reduced calorie formulas can be tricky and need careful super- vision by the physician.

6. Help mothers develop feeding practices that encourage the infant to rely on his own internal clues to hunger and satiety. As far as practical, let the infant determine the feeding schedule. Never use food as a sub- stitute for attention.

7. Watch for further developments as nutritional science grapples with the question of how early feeding affects adult obesity.

References I. Gordan, H. H.: “A Summary of

Some Clinical Aspects of Obesity.” Pediatrics 20:556559, 1957

2. Van Itallie, T. B., and R. C. Campbell: “Multidisciplinary Approach to the Problem of Obesity.” J . A m Diet Assoc 65:385-390, 1972

Juvenile Obesity.” Arch Dis Child 3. Mullins, A. G.: “The Prognosis in

33:307-314, 1958 4. Heald, F. P., and R. J.

Hollander: “The Relationship Between Obesity in Adolescence and Early Growth.” J . Pediatr 67:35-38, 1965

“Relationship of Excess Weight in Children and Adults.” Public Health Rep 75:263-273, 1960

6. Winick, M., and P. Rosso: “The Effect of Severe Early Malnutrition on Cellular Growth of Human Brain.” Pediatr Res 3:181-184, 1969

“Cellularity Obese and Non-Obese Human Adipose Tissue.” Fed Proc 29:15161521, 1970

8. Brook, C. G. D., J. K. Lloyd, and 0. H. Wolf: “Relation Between Age of Onset of Obesity and Size and Number of Fat Cells.” Br Med J

5. Abraham, S., and M. Nordsieck:

7. Hirsch, J., and J. L. Knittle:

2:25-27, 1972 9. Hirsch, J: “Can W e Modify the

Number of Adipose Cells?” Postgrad Med 51 :83-86,1972

10. Johnson, P. R., and J. Hirsch: “Cellularity of Adipose Depots in Six Strains of Genetically Obese Mice.” J Lipid Res 13:2-11, 1972

11. Eid, E. E.: “Follow-Up Study of Physical Growth of Children Who Had Excessive Weight Gain in First Six Months of Life.” Br Med J 2:74-76, 1970

12. Smith, U.: “Effect of Cell Size on Lipid Synthesis by Human Adipose Tissue in Vitro.” J. Lipid Res 12:65-69, 1971

13. Salans, L. B., J. L. Knittle, and J. Hirsch: “The Role of Adipose Cell Size and Adipose Tissue Insulin Sensitivity in the Carbohydrate Intolerance of Human Obesity.” J Clin Invest 47:153-165, 1968

14. Zinder, O., and B. Shapiro: “Effect of Cell Size on Epinephrene- and ACTH-Induced Fatty Acid Release from Isolated Fat Cells.” J Lipid Res 12:91-95, 1971

IS. Bjarntorp and L. Sjostrom: “Fat Cell Size and Number in Adipose Tissue in Relation to Metabolism.” Ismel J Med 8:320-324, 1972

16. Skunkard, A., and C. Koch: “The Interpretation of Gastric Motility.

I. Apparent Bias in the Reports of Hunger by Obese Persons.” Arch Gen Psych 11:74-89, 1964

17. Hashim, S. A., and T. B. Van Itallie: “Studies in Normal and Obese Subjects with a Monitored Food Dispensing Device.” Ann N Y Acad Sci 131:654-656, 1965

18. Schachter, S.: “Obesity and Eating.” Science 1613751-756, 1968

19. Wooley, S. C.: “Physiologic Versus Cognitative Factors in Short Term Food Regulation in the Obese and Nonobese.” Psychosom Med 34:6243,1972

20. Mayer, J.: “The Fat Baby.” Postgrad Med 44:277-278, 1972

21. Mayer, J., N. B. Marshall, J. J. Vitale, J. H. Christensen, M. B. Mashayekhi, and F. J. Stare: ‘‘Exercise, Food Intake and Body Weight in Normal Rats and Genetically Obese Rats.” A m J pbysioi 177:s44-54a, 1954

22. Mayer, J., P. Royn, and K. P. Mitra: “Relation Between Caloric Intake, Body Weight, and Physical Work.” A m J Clin Nutr 4:169-175, 1956

23. Harfouche, J. K.: “The Importance of Breast-Feeding.’’ J Trop Ped 135-175, Sept 1970

Address reprint requests to Ellen S. Parham, PhD, 508 South 7th Street, DeKalb, IL 60115.

The author is Associate Professor of Dietetics, Nutrition and Food Science at Northern Illinois Uni- versity at DeKalb. She holds a PhD in hurr?an nutrition from the Uni- versity of Tennessee, Knoxville, and a BS from Virginia Poly- technic Institute in Blacksburg. She is a Registered Dietitian with the American Dietetic Association. Doctor Pmhmn has published ar- ticles on early nutrition, lactose intolerance, and cyclamates in var- ious health periodicals. She is a member of the Society for Nu- trition Education, the American Home Economics Association, llli- nois Association for Maternal and Child Health, Phi Kappa Phi, and Phi Sigma.

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