222 GROWTH PRINCIPLES AND THEORY 2 



Apart from humans, lull data as required for such analysis are available almost 

 only for the small laboratory animals. Even here wide discrepancies in empirical 

 growth data exist. For example, there is a large discussion as to what is to be 

 considered the "typical" growth curve of the rat (L. Zucker et al., 1941a, b; 

 T. F. Zucker et al., 1941, 1942; Dunn, Murphy and Rockland, 1947; Murphy and 

 Dunn, 1948; Mayer, 1948). The classical data of Donaldson (1924) (used in Fig. 

 26) are not considered to be satisfactory because increased growth rate and change 

 of the shape of the growth curve can be obtained by use of improved laboratory 

 diets. Thus, each of the mentioned groups of investigators proposed a different 

 empirical ecjuation for the growth of the rat which, however, does not fit data of 

 other observers. These controversial observations and calculations show that the 

 growth curve of rats can be widely modified by different diets. In addition the 

 more basic problem mentioned on p. 138 arises as to whether "optimaF' growth is 

 identical with "normal" growth. If Donaldson's data presumably represent a 

 "suboptimal" course of growth, it has to be considered, on the other hand, whether 

 a synthetic diet yielding maximum weight increase, does not lead to "super- 

 normal" growth, particularly with respect to deposition of fat. 



Thus, even more than in the cases discussed hitherto, quantitative analysis of 

 growth in mammals must be considered as provisional. The presence of a pre- 

 pubertal and postpubertal growth cycle, and the overall classification of mamma- 

 lian growth as belonging to the First Type may be considered as well established. 

 However, the growth formulas used can only be considered as a crude first approxi- 

 mation. This is not changed by the fact that they fit the data well and even 

 better than more complicated formulas. 



Based upon the growth theory discussed, the following deductions were derived 

 from mathematical analysis of growth in mammals (Bertalanffy, 1938, 1942a): 



I. Protein turnover takes place at a much faster rate than presupposed 

 in classical physiology; 2. There is a synthesis and re-synthesis of amino acids 

 and proteins from ammonia and nitrogen-free chains; 3. Under a diet low 

 in protein, nitrogen is retained from catabolized organic compounds and is 

 used for regeneration of protein. This explains the protein-sparing effect of 

 carbohydrates, that is, the fact that under a diet rich in carbohydrates, the 

 organism needs less protein than would correspond to the nitrogen excretion in 

 starvation. 



Qualitatively, these deductions proved to be excellent predictions, later con- 

 firmed by isotope experiments (Sprinson and Rittenberg, 1949a, b). The isotope 

 method has demonstrated the rapid protein turnover, the regeneration of proteins 

 from the metabolic pool, and the utilization of ammonia for protein synthesis 

 under a low-protein diet. 



Quantitatively, however, it has to be considered that equating the growth- 

 inhibiting factors contained in the constant x with manifest protein turnover is a 

 crude oversimplification. This simplification is confirmed, as a first approximation, 

 in simple growth curves and when metabolic processes, differentiation, changes in 

 chemical composition {e.g. content of dry substance, protein-fat ratio) are rela- 

 tively slow (Table 11, p. 200). However, these complicating factors cannot be 

 overlooked, but there is no way at present to quantify them. Beside manifest 



