For many years the study of growth has rested mainly on the application of anthropometric techniques and the measurement of height and weight. A few years ago Tanner9 correctly pointed out that studies on body composition were mainly related to body weight and, therefore, added little to the thinking. A more penetrating approach to the study of growth was recommended.2
The present approach,11 documented in part here, has been to apply biochemical and physiological techniques for the measurement of body cell mass, cell size, cell number and, to some extent, cell function. Body function and heat production as well as maturational age have been of concern. These studies have been made in the same children at tile same time. It is anticipated that inspection of these three dimensions of growth, size, function, and maturational age should help to elucidate problems related to growth retardation.
In the clinic it is possible to predict cell-extracellular mass of children by applying equations based on relationships between body composition and height and weight.
We began by presenting information on growth of muscle and the differences between the sexes with the progress of time and with respect to size and number of cells. Increments in growth rate of the male at adolescence were found. Such differences in cell growth must be related to some extent to the restrictive action of estrogens on cell multiplication in the female and to the stimulating action of androgens in the male. Growth hormone is an important hormone for the multiplication of cells, while insulin is of importance to protein synthesis. Both hormones are needed for growth. Thyroid hormone appears to play a secondary role but is important to protein synthesis especially in early postnatal life. The energy requirement for normal growth is only slightly above the basal state and the visceral cell mass is the most direct standard of reference for heat production. Restriction of nutrition can either retard growth in the size of cells, in the number of cells, or both.
Current studies58 show that ingestion of protein and calories incite the secretion of growth hormone and insulin in specific patterns and at appropriate times. Growth hormone has been labelled the "feasting" hormone and insulin tile "feasting" hormone.59 Thus, the subtle relationship between nutrition and cell growth becomes apparent.
Of concern is the possibility that overnutrition early in life may program excess secretion of hormones such as insulin or growth hormone. Overnutrition is a major problem in the affluent society, while conservative nutrition is compatible with longevity.6 Hirsch, et al.60 informs us that growth of adipose tissue is mainly by cell number increase–as we have seen for muscle. Again, a steady state of cell number is reached for fat cells. But, obese subjects have an excess of fat cells which do not disappear with time and diet. Such cells become increasingly insensitive to insulin as they enlarge.61
One might view the passing parade of life and growth and observe the relation of the intracellular phase to body weight from infancy to senility (Fig. 12). Here we see the upward increase of cell mass with respect to time and body weight increase. The adult data are taken from F. D. Moore.62 Clearly, with senility we can suspect that more and more of the body weight is extracellular or connective tissue and less and less of the weight is soft tissue or oxidizing protoplasm. Data on body potassium are even more remarkable in this demonstration.11 It is difficult to say with Browning:
Grow old along with me!
The best is yet to be....
Nevertheless, it is possible that with increased information and research the understanding of these stages of cell growth will be achieved and, no doubt, the departure from the steady state of cell population which occurs at the autumn of our existence– when cancer, and cardiovascular disease supervene–will be understood.63 However, the problems of aging can only be exposed after the physiology of growth is understood.
Differential Metabolic Sensitivity of Insulin-like-response- and mTORC1-Dependent Overgrowth in Drosophila Fat Cells