This alternative hypothesis may also tell us something profound about the relationship between nutrition and fertility. That shouldn’t be surprising, because reproductive biologists, as we discussed earlier (see Chapter 21), have long considered the availability of food to be the most important environmental factor in fertility and reproduction. By this hypothesis, the critical variable in fertility is not body fat, as is commonly believed, but the immediate availability of metabolic fuels. This was suggested in the late 1980s, when the reproductive biologists George Wade and Jill Schneider described their research on hamsters, which were chosen because of their clockwork four-day estrous cycles. The experiments were remarkably consistent. These animals will go into heat whether they are fat or lean, and they will continue to cycle, as long as they can eat as much food as they want. If both fatty-acid and glucose oxidation are inhibited, however, and they’re not allowed to increase their food intake in response, their estrous cycles stop. They’ll remain infertile, whether they are gaining or losing weight at the time. These animals are responding to the general availability of metabolic fuels. The same observation has been made about pigs, sheep, and cattle. Monkeys will shut down their secretion of the hormone that triggers ovulation if they go twenty-four hours without food, but they’ll re-establish secretion immediately upon eating. The more the monkeys are allowed to eat, the more hormone they’ll secrete.

If it is true that fertility is determined by the availability of metabolic fuels, as Wade and Schneider explained, then “it would be expected that ovulatory cycles would be inhibited by treatments that direct circulating metabolic fuels away from oxidation and into storage in adipose tissue.” This is what insulin does, of course, and, indeed, infusing insulin into animals will shut down their reproductive cycles. In hamsters, insulin infusion “totally blocks” estrous cycles, unless the animals are allowed to increase their normal food intake substantially to compensate. This hypothesis can also explain the infertility associated with obesity in both humans and lab animals. If “an excessive portion of available calories” is locked away in fat tissue, then the animal will act as if it’s starving. In such a situation, Wade and Schneider said, “there will be insufficient calories to support both the reproductive and the other physiological processes essential for survival” reproductive activity shuts down until more food is available to compensate.

This metabolic-fuel hypothesis of fertility has escaped the attention of clinicians. The clear implication is that a woman struggling with infertility or amenorrhea (the suppression of menstruation) will benefit more from a diet that lowers insulin but still provides considerable calories—a low-carbohydrate, high-fat diet—and thus repartitions the fuel consumed so that more is available for oxidation and less is placed in storage.