|Activity, Energy Expenditure and Energy Requirements of Infants and Children (International Dietary Energy Consultative Group - IDECG, 1989, 412 pages)|
|The desirable upper limits of energy intake in childhood: Short- and long-term consequences|
The fat cell hypothesis of obesity (HIRSCH and KNITTLE, 1970) became extremely popular and led to the routine classification of patients in the United States as having either hypercellular or normocellular obesity. With the heavier adults usually having a longstanding history of obesity, often stemming from childhood, it was soon considered that the hypercellular grossly obese adults had been reprogrammed to generate new adipocytes and that this excessive proliferation occurred in childhood (KNITTLE, 1972). This concept was amplified by the observation that those obese children with an estimated high fat cell number had become obese in infancy (BROOK, LLOYD and WOLF, 1972). Infancy might then be a critical period for adipocyte development analogous to other critical periods of development.
Despite DAUNCEY and GAIRDNER's (1975) finding that the expansion of fat cells within the first year of life was ample for accommodating fat deposition without the need to invoke further replication of adipocytes, the enthusiasm for the hypercellular theory of obesity remained untouched until we showed from extensive studies of adipocytes in different depots that the true number of adipocytes in the body had been substantially underestimated. Once the numerous small adipocytes of the omentum and abdominal mesentery began to fill, the method of calculating total adipocyte numbers would imply spuriously that there had been an absolute increase in adipocytes (JUNG et al., 1978; GURR et al., 1982).
Since then, there has been very little work on the hypothesis, but it should be recognized that criticism of the hypercellular theory of obesity does not signify that early feeding does not affect adult adiposity.