The Effect of Early Feeding on the Development of Obesity

Download The Effect of Early Feeding on the Development of Obesity

Post on 20-Jul-2016




1 download

Embed Size (px)


  • - 0 0 continuing education

    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


    ,? \





    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

    May/June 1974 JOGN Nursing 58

  • 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 (?)


    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

    MayJJune 1974 JOGN Nursing 59

  • 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 subjects 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 individuals own needs, and depen- dence on such clues can result in greatly distorted food intak


View more >