Science, Nutrition, Fat, and Policy: Tests of the Critical-Fat Hypothesis [and Comments and Reply]

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Abstract
Supplementation of the diets of pregnant and nursing mothers in underdeveloped countries is sometimes criticized because more food for these women is seen as producing more body fat, shortened postpartum amenorrhea, and increased fertility. We argue that the link between body fat and shortened postpartum amenorrhea is based on a hypothesis that has not been corroborated. The critical-fat hypothesis is that menarche, maintenance of menstrual cycles, and the delay of menstruation after pregnancy are all determined by "critical" (causal) fat levels. Data refute the menarche-fat link outright. Evidence for the link between menstrual-cycle maintenance and fat is clouded by outside variables such as physical or emotional stress. Of special importance to postpartum amenorrhea is type and duration of lactation, with frequent, on-demand nursing of an unsupplemented infant being associated with longer amenorrhea. The nutrition-fat-fertility link, therefore, is uncorroborated and may be on the way to refutation. Considerable benefit can come from maternal diet-supplementation programs, and their curtailment on the basis of an uncorroborated hypothesis is both poor science and poor policy.

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