Body Fat, Puberty and Fertility

Summary 1. The high percentage of fat, about 26–28% in the mature human female, may influence reproductive ability directly through two mechanisms: ( a ) fat converts androgens to oestrogens; ( b ) relative fatness influences the direction of metabolism of oestrogen to the most potent or least potent forms. The relative degree of fatness thus is directly related to both the quantity of circulating oestrogen and the biological effectiveness of the oestrogen. This is a neat mechanism for relating rates of growth, nutrition and energy outputs to the energy requirements for reproduction. Fat is the most labile body tissue; it therefore reflects environmental changes more rapidly than other tissues of the body. 2. The slow maturation of the hypothalamus and pituitary up to menarche, or first oestrus, is accompanied by a slow maturation of the body, which changes not only in size but in the relative proportion of bone, muscle, and fat. Evidence is presented that a particular threshold ratio of fat to lean mass is normally necessary for puberty and the maintenance of female reproductive ability in the human and in the rat. The synchronizing mechanisms may be metabolic, relating food intake to core temperature and/or fat storage. 3. Undernutrition and weight loss in the range of 10–15 % of normal weight for height delays menarche and causes amenorrhoea. Ballet dancers and athletes also have delayed menarche and amenorrhoea. The cessation of reproduction in both groups can be considered adaptive. Refeeding and/or cessation of intense activity results in the initiation or resumption of menstrual cycles after varying periods of time. A necessary threshold weight for height can be predicted from a fatness index. 4. Differences in the natural fertility of historical and contemporary populations may be explained by a direct effect of food intake and energy outputs on fecundity. 5. The late maturing fat ‐ ‘sex fat’ ‐ may have a special role in reproduction.