Two factors intrinsic to health are diet and sleep. These two behaviors may well influence one another. Indeed, that insufficient sleep adversely impacts dietary intakes is well documented. On the other hand, diet may influence sleep via melatonin and its biosynthesis from tryptophan. Experimental data exist indicating that provision of specific foods rich in tryptophan or melatonin can improve sleep quality. Whole diets rich in fruits, vegetables, legumes, and other sources of dietary tryptophan and melatonin have been shown to predict favorable sleep outcomes. Although clinical trials are needed to confirm a causal impact of dietary patterns on sleep and elucidate underlying mechanisms, available data illustrate a cyclical relation between these lifestyle factors. We recommend adopting a healthful diet to improve sleep, which may further promote sustained favorable dietary practices.

Background: Poor sleep increases cardiovascular disease risk, and diet likely contributes to this relationship. However, there are limited epidemiological data on the relationship between measures of sleep quality and habitual dietary patterns. This study examined these associations in a diverse sample of women. Methods and Results: Baseline data from 495 participants in the AHA Go Red for Women prospective cohort study (age: 20–76 years; 61% racial/ethnic minority) were examined. Sleep quality and sleep‐onset latency were measured using the Pittsburgh Sleep Quality Index ( PSQI ) and insomnia using the Insomnia Severity Index. The validated Block Brief Food Frequency Questionnaire was used to assess diet quantity and quality. Linear regression models adjusted for confounding variables tested relationships between sleep and diet variables. Results showed that higher PSQI scores, indicative of poorer sleep quality, were associated with lower unsaturated fat intake (β=−0.14, P 60 minutes had higher intakes of food by weight (β=235.2, P< 0.01) and energy (β=426, P <0.01), and lower intakes of whole grains (β=−0.37, P =0.01) than women with sleep‐onset latency ≤15 minutes. Greater insomnia severity was associated with higher food weight (β=9.4, P =0.02) and energy (β=17, P =0.01) consumed and lower total (β=−0.15, P =0.01) and unsaturated fat intakes (β=−0.11, P <0.01). Conclusions: Poor sleep quality was associated with greater food intake and lower‐quality diet, which can increase cardiovascular disease risk. Future studies should test whether promoting sleep quality could augment efforts to improve cardiometabolic health in women.

A sleepless night may feel awful in its aftermath, but sleep’s revitalizing powers are substantial, perpetuating the idea that convalescent sleep is a consequence-free physiological reset. Although recent studies have shown that catch-up sleep insufficiently neutralizes the negative effects of sleep debt, the mechanisms that control prolonged effects of sleep disruption are not understood. Here, we show that sleep interruption restructures the epigenome of hematopoietic stem and progenitor cells (HSPCs) and increases their proliferation, thus reducing hematopoietic clonal diversity through accelerated genetic drift. Sleep fragmentation exerts a lasting influence on the HSPC epigenome, skewing commitment toward a myeloid fate and priming cells for exaggerated inflammatory bursts. Combining hematopoietic clonal tracking with mathematical modeling, we infer that sleep preserves clonal diversity by limiting neutral drift. In humans, sleep restriction alters the HSPC epigenome and activates hematopoiesis. These findings show that sleep slows decay of the hematopoietic system by calibrating the hematopoietic epigenome, constraining inflammatory output, and maintaining clonal diversity.

Although short-term studies have found that serving larger portions of food increases intake in preschool children, it is unknown whether this portion size effect persists over a longer period or whether energy intake is moderated through self-regulation. We tested whether the portion size effect is sustained in preschool children across 5 consecutive days, a period thought to be sufficient for regulatory systems to respond to the overconsumption of energy. With the use of a crossover design, over 2 periods we served the same 5 daily menus to 46 children aged 3–5 y in their childcare centers. In 1 period, all foods and milk were served in baseline portions, and in the other period, all portions were increased by 50%. The served items were weighed to determine intake. Increasing the portion size of all foods and milk by 50% increased daily consumption: weighed intake increased by a mean ± SEM of 143 ± 21 g/d (16%) and energy intake increased by 167 ± 22 kcal/d (18%; both P < 0.0001). The trajectories of intake by weight and energy across the 5-day period were linear and the slopes did not differ between portion conditions (both P > 0.13), indicating that there were sustained increases in intake from larger portions without compensatory changes over time. Children differed in their response to increased portions: those with higher weight status, lower ratings for satiety responsiveness, or higher ratings for food responsiveness had greater increases in intake from larger portions (all P < 0.03). This demonstration that preschool children failed to adjust their intake during prolonged exposure to larger portions challenges the suggestion that their self-regulatory behavior is sufficient to counter perturbations in energy intake. Furthermore, overconsumption from large portions may play a role in the development of overweight and obesity, as the magnitude of the effect was greater in children of higher weight status. This trial was registered at www.clinicaltrials.gov as NCT02963987.