The central hypothesis of the current study was that sleep quality and social well-being would interact in predicting inflammation in a national sample of middle-aged men and women. The results provide support for this hypothesis. The association between subjective sleep quality and inflammation was significantly weaker in male participants with higher scores on the positive relations with others scale. Positive relations with others also moderated the association of objectively assessed sleep efficiency and IL-6. We previously reported that positive relations with others moderated the relationship between sleep efficiency, assessed using the Nightcap system, and IL-6 in older women.25
We observed the same pattern of results in the current study in additional analyses of women over the age of 60, although the results were not statistically significant (data not shown). In sum, the current results extend our earlier work to a national sample, and they suggest that across a 50-year age range, social engagement may buffer against the proinflammatory effects of poor sleep (and good sleep may compensate for low levels of social engagement), particularly in men.
As expected, poorer subjective sleep quality, as measured by the PSQI, predicted higher levels of both IL-6 and E-selectin in men and women. A number of studies have reported links between poor subjective sleep quality and higher circulating levels of inflammatory proteins,13,45,46
but to the best of our knowledge, this study is the first to document this association in a national sample with broad demographic representation. These associations were also independent of an array of health status and health behavior measures, including factors that are strongly linked to inflammation, such as obesity.47,48
Subjective sleep quality is thus an important independent predictor of biological processes related to age-related disease.
In the subsample that provided actigraphy data, longer sleep durations, shorter latencies to fall asleep, and greater sleep efficiency all predicted lower levels of IL-6 in women, but not in men, in bivariate analyses; greater sleep efficiency was also associated with lower levels of E-selectin in women. In multivariate analyses, however, only sleep efficiency continued to predict IL-6 and E-selectin after adjustments for demographic characteristics, and those associations were eliminated by further adjustment for health status and health behavior. Age is the most likely factor to account for the sleep duration and sleep latency results. IL-6 in particular rises with age,1
and older adults typically sleep less than younger adults.49
Age thus represents a likely confound for these associations. With regard to sleep efficiency, obesity was the strongest predictor of both IL-6 and E-selectin among the health status variables, and as it is strongly linked to disturbed sleep, particularly due to increased risk of sleep apnea,50
obesity is the most likely mediator of the association between sleep efficiency and inflammation. It is worth noting that the relationship between sleep efficiency and inflammation was the most robust of the actigraphic measures. This is consistent with the research on sleep and loneliness, which centers on differences in sleep quality without differences in sleep quantity,24
and with other lines of work examining the links among social factors, sleep, and health more broadly.51
We also found in bivariate analyses that greater subjective sleep quality, greater sleep efficiency, and reduced sleep latency in men were all associated with greater social engagement. These complement earlier studies reporting poorer sleep in young and older adults with higher levels of loneliness,21–23
and suggest that the link between sleep and social contact may involve not merely the presence or absence of loneliness but also the presence or absence of high levels of social engagement. There is rising interest in the positive end of the spectrum of psychological functioning, including flourishing, and the extent to which positive functioning is an independent predictor of mental and physical health above and beyond the lack of negative functioning.52
Nevertheless, this relationship was not a central focus of the current study, and the extent to which these associations are explained by other factors, such as demographic characteristics of health-related variables, remains to be determined.
There were marked gender differences in sleep quality and inflammation in the MIDUS sample, and this is consistent with a number of earlier studies. Women typically have a greater number of subjective sleep complaints than men, but when sleep quality is assessed objectively using polysomnography or actigraphy, women are often found to sleep better than men.49,53–55
Indeed, while women had significantly higher PSQI scores in the current study, indicating greater sleep pathology, actigraphic assessments showed that compared to men, women took less time to fall asleep, slept longer, and slept for a greater proportion of the night. Men in this sample also had higher levels of E-selectin than women, and this is consistent with other studies.27,56
Inter estingly, while bivariate analyses showed that better subjective and objective sleep quality was more likely to predict lower levels of IL-6 and E-selectin in women, the moderating effect of social engagement on the link between sleep quality and inflammation was apparent only in men. The reasons for this pattern of results are not clear. In some instances, links between psychosocial factors and health are stronger in women.46
On the other hand, there is scant literature on interactive associations among psychological and behavioral factors in predicting inflammation. The current results are similar to those from an earlier study in which exposure to chronic discrimination was linked to higher levels of E-selectin in men from the MIDUS study in spite of the fact that women reported greater exposure to discriminatory treatment.35
Interpretation of these results should be tempered by several limitations of the study. First and foremost, these analyses are cross-sectional, so it is not possible to determine the causal association among the key variables. This is particularly relevant for the link between sleep and inflammation, as inflammatory proteins such as IL-6 are known to impair sleep57
and increase fatigue.58,59
In addition, while this sample was racially diverse, much of that diversity comes from a regional sample of African Americans, and there may be differences between this sample and those from other regions of the country. Finally, inflammatory proteins were only assessed once, which, given variability in their levels within individuals, might produce inaccurate estimates of each person's circulating levels. Nevertheless, such variability would be expected to reduce the likelihood of detecting associations, meaning that the strength of the relationships observed may be underestimated.
In spite of these limitations, the present study adds to the literature on links between sleep and inflammation, social engagement and inflammation, and social engagement and sleep. It also extends our earlier work on interactive associations between sleep and social engagement to a national sample of middle-aged and older adults. These findings underscore the importance of considering the ways in which factors in multiple domains of experience within the same individual interact to affect biological processes related to health. They also highlight the role of positive psychological functioning in the maintenance of advantageous profiles of biological risk as well as the ways in which positive functioning may compensate for the presence of other risk factors.