Impact of sleep duration on food intake regulation: Different mechanisms by sex?

In this issue of the journal, Broussard and colleagues (1) report findings of elevated ghrelin concentrations after a period of severe sleep restriction in healthy young men. This increase in the food intake-stimulating hormone would explain the greater caloric intake of these men under sleep-restricted conditions relative to their normal sleep duration. Increased food intake, of similar order of magnitude as those reported by Broussard et al., has been observed by others (2, 3) and it is readily accepted that energy intake is increased by approximately 300 kcal/d when sleep is curtailed by 2.5–4 h/night. However, controversy exists with respect to the effects of sleep restriction on regulators of food intake. A recent meta-analysis concluded no effect of sleep restriction on ghrelin, with high heterogeneity among studies (4). Our own interpretation of the findings in this field is similar (5, 6). One source of heterogeneity may be sex. The paucity of studies enrolling sufficient participants of both sexes is striking in sleep research. In fact, most studies enroll men only or too few participants to perform sex-specific analyses. It is further noteworthy that studies enrolling exclusively males, including the report by Broussard et al. (1), report significant effects of sleep restriction on ghrelin concentrations whereas those including women do not. Could it be that sleep restriction affects different food intake regulators in men and women? This is very likely since the end result, increased food intake due to sleep restriction, occurs in both sexes yet ghrelin seems to be elevated only in men.

We have proposed the possibility of 2 separate mechanisms, one affecting appetite in men, and one affecting satiety in women, to explain the effects of sleep restriction on food intake. Results by Broussard et al. (1) seem to lend support to our hypothesis: the appetite-stimulating hormone ghrelin was increased with sleep restriction whereas the satiety-promoting hormone pancreatic polypeptide was largely unchanged. In a similar sleep restriction study conducted by our group, ghrelin was increased in men, whereas glucagon-like peptide 1, a satiety-signaling hormone, was reduced in women as a result of sleep restriction (7).

Other factors related to the design of studies assessing the hormonal controls of food intake with sleep restriction may be responsible for between-study differences. One such factor may be the state of energy balance in which participants are maintained during the controlled feeding component of the study (6). Controlled feeding vs ad libitum feeding conditions is another probable explanatory factor. However, the potential sex difference hypothesis needs further exploration and future studies should enroll adequate numbers of both men and women to perform sex-specific analyses. Excluding women from sleep restriction studies is not justified. Further, additional information on other regulators of food intake, such as pancreatic polypeptide and glucagon-like peptide 1, but also cholecystokinin, peptide YY, and glucose-dependent insulinotropic polypeptide, to name a few, is needed. Maybe then can we have more definitive answers on the hormonal mechanisms underlying the increase in food intake resulting from sleep restriction.