270 PHYSIOLOGIC GENETICS 



It is generally agreed that hormones do not initiate biochemical reactions per- 

 formed by cells, but that they can govern the rates at which these reactions take place. 

 If, for instance, a hormonal deficiency is induced by surgical or pharmaceutical 

 methods, cells retain a modicum of their inherent ability to perform their highly 

 specialized tasks; but now these tasks are performed slowly, inadequately, and in- 

 efficiently. If the level of the missing hormone is raised by exogenous administration 

 of the hormone, the rate of reactions can be raised in proportion to the amount of 

 hormone injected. It is assumed that the genetically determined rates of hormone 

 secretion similarly set the rates at which the inherent cellular reaction take place. 



All cells within a body come in contact with all endogenous hormones which are 

 carried by the common blood stream bathing the cells. However, in spite of this general 

 distribution via the blood stream, hormones react only with their specific, genetically 

 conditioned end organs. The biochemical reasons for this ability of the different 

 cells to discriminate between hormones and to respond only to their own specific 

 trophic substances remains largely unknown, although it is presumed to be a matter of 

 activation of mechanisms which are permissive of optimal intracellular interaction 

 between enzymatic systems and substrates. Examples of such specialized activation of 

 end organs are plentiful. Gonadotrophic hormone, for instance, is a specialized 

 growth hormone which increases the metabolic activity of the gonads but has no 

 such effect on somatic cells or on the cells of other glands. Conversely, somatotrophic 

 hormone is a growth hormone which stimulates growth of somatic cells but has no 

 effect on the metabolic activity of gonads. 



This apparent autonomy of hormonal systems should not lead to the conclusion 

 that the efficiency of any one hormone-end-organ reaction is independent of other 

 endocrine interactions in the body. While there is a specific trophic hormone for al- 

 most every reproductive event and almost every end organ, optimal responses are 

 possible only in euhormonal internal environments. For example, only gonadotrophic 

 hormone can stimulate growth of gonads, but optimal growth of gonads can be achieved 

 only in an endocrine environment in which all other glands (thyroids, adrenals, and so 

 forth) are functioning at a satisfactory level. For this reason it is necessary to distinguish 

 between primary, secondary and, occasionally, tertiary deficiencies. For instance, 

 lowered fertility or even sterility of animals may be erroneously attributed to a deficiency 

 of gonadotrophic hormone, while in reality it may be due to the inability of a normal 

 level of gonadotrophic hormone to produce optimal gonadal responses because of a 

 deficiency of hormones other than gonadotrophins. 



Since hormones govern rates of reactions it can be presumed, and in some cases 

 demonstrated, that genes or genie complexes determine the rates at which hormones 

 are secreted. Rates of hormonal secretion are frequently the only phenotypic ex- 

 pressions which can be measured and used as a guide to the genotypic differences known 

 to exist. Estimates of rate of hormonal secretion can be obtained in a variety of ways. 



In some instances the relationship between genotype and endocrine phenotype 

 is simple, as in cases in which only one hormone is known to be involved and in which 



