Nearly a century ago, Darwin described the fact that well-nourished domestic animals are more fertile than animals receiving a poor diet (Darwin, 1896).Since that time, scores of research articles have testified to the importance of nutritional factors in the regulation of reproduction in virtually every mammalian species, including man.In Western societies over the last 300 years, we have witnessed a dramatic decline in the age of puberty onset, a phenomenon associated with improved diet and socio-economic conditions.Studies by Kennedy & Mitra (1963) in the early 1960s established that the age of puberty onset in the rat is more closely correlated with the animal's body-weight than chronological age.This relation was soon shown to apply to human beings as well.On the basis of epidemiological information, showing an association between body-weight and the onset of menarche in girls, Frisch & Revelle (1970) proposed that a 'critical body-weight' was determinative in controlling the onset of puberty.Further investigation, again based on epidemiological information, led to the suggestion of a 'minimum percentage of body fat' as a possible signal to puberty onset (Frisch & MacArthur, I 974).Excitement and controversy swelled around these findings (Wilen & Naftolin, 1977;Penny et al. 1978;Glass & Swerdloff, 1980); the findings were not in question, only the inference that body composition per se could somehow trigger the awakening of the reproductive system at the time of puberty.Others, finding exceptions to the rule, were won to become dissatisfied with the body-composition theory and argued that 'basal metabolic rate' was more likely to serve as a physiological link between the body's energy-regulating components and the reproductive system (Crawford & Osler, 1975).It remains unchallenged that all these variables-body size, body fat and metabolic rate-are somehow associated with the activity of the reproductive axis; however, despite these labours and our collective wisdom, we are left with only descriptive associations--no mechanisms to explain how the body 'knows' its metabolic rate or how big and fat it may be.Some light has been shed on this problem by studying the effect of metabolic stresses on the reproductive system.For example, in the case of gevere weight loss in the adult human, caused by anorexia nervosa, gonadotrophin secretion is markedly reduced owing to an inhibition of gonadotrophin-releasing hormone (GnRH) secretion (Boyar et al. 1974).When these patients recover during
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Robert A. Steiner (1987) studied this question.
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