This study is the first to document changes in adiponectin, an anti-atherogenic endocrine marker, in response to sleep restriction in healthy adults between 22–45 years of age. While no systematic changes in adiponectin levels were observed in the total sample or for men of either race/ethnicity, there was a significant sex by race/ethnicity interaction in which Caucasian women were found to have a decrease in adiponectin levels in response to sleep restriction and African American women demonstrated an increase. These results partially supported our hypothesis that sleep restriction would result in a decrease in adiponectin, particularly among Caucasian participants. We found no significant main effect of sleep restriction on adiponectin levels among N=41 healthy men, which is consistent with the report by Shea and colleagues [27
]. A novel finding in our investigation was that both Caucasian and African American women demonstrated reliable adiponectin responses to sleep restriction, albeit it opposite directions.
The underlying basis of the differential adiponectin responses we observed for sex and racial/ethnic groups is unclear. There is also evidence of sex differences in relationships between both sleep duration and quality with inflammation, with stronger associations among women [11
]. In the current study, however, there was a sex by race/ethnicity interaction, such that Caucasian women were observed to have a decrease after sleep restriction in adiponectin, a beneficial anti-inflammatory marker, while African American women were observed to have an increase. While menstrual phase was not aligned for study participation in women, there was no significant effect of self-reported menstrual phase on change in adiponectin level (p
> .05), suggesting that this factor was not a significant contributor to the study results. No additional post-hoc comparisons examining relationships between change in adiponectin and other potential variables of interest (e.g., changes in leptin [35
], a proxy for childhood socioeconomic status [parental education], depression scores) were significant.
We know of no other evidence for a differential vulnerability to the effects of sleep restriction based on race/ethnicity (e.g., on cognitive performance measures, sleepiness ratings). With respect to amount of habitual sleep duration, two recent studies have shown that African Americans are more likely to report both short and long sleep durations compared to Caucasians [36
]; however, given the 6.5–8.5h habitual sleep duration eligibility requirement for the current study, it is unlikely that there was a systematic race/ethnicity-based difference in the magnitude of sleep restriction imposed on participants by this protocol. Race/ethnicity-based differences in some sleep-related variables have been documented, however [e.g., nocturnal dips in blood pressure], and recent evidence suggests that psychosocial factors (e.g., education, marital status, social support) may mediate this relationship [38
]. These studies raise the possibility of a third-variable (e.g., psychosocial factors) that may also be mediating at least part of the observed relationships relative to sex and race/ethnicity in the current study.
Data regarding the relative secretion of adiponectin from subcutaneous and visceral adipose tissue are currently limited [41
]. African American women have been reported to have significantly higher subcutaneous and total fat levels than any other sex-race/ethnicity group, with both African American and Caucasian women having higher levels of visceral fat than men [42
]. However, in several studies adjusting for body mass index (or using populations with similar BMIs), African Americans have been observed to have less total fat mass [43
] and less intra-abdominal visceral adipose tissue compared to Caucasians [44
]. Together, these studies suggest that the distribution of adipose tissue, as well as the relative production of adiponectin from these tissue sources, may play a role in the interaction between sex and race/ethnicity in adiponectin response to sleep restriction.
The significant decrease in adiponectin levels in response to sleep restriction among Caucasian women is consistent with other evidence suggesting an inflammation-increasing response to sleep restriction [29
] and adds to the growing evidence that short sleep durations are associated with risk for obesity and cardiovascular disease [1
], at least among some segments of the population. While there may be an underlying genetic basis for the observed differential adiponectin responses between racial/ethnic groups among women (e.g., in adipose fat distribution), it is also possible that there may be differences in behavioral responses to sleep restriction (e.g., in rates of food consumption, or food consumption preferences) between groups, which may in turn contribute to the different adiponectin levels observed among women in response to sleep restriction.
The direction of the findings, suggesting a protective or beneficial response of increased adiponectin among African American women in response to sleep restriction, does not parallel epidemiological findings that risks for heart disease and stroke are higher among African American compared to Caucasian women [51
]. However, paradoxical relationships between adiponectin and cardiovascular disease have been observed; among individuals with extant coronary artery disease a positive (rather than the predicted negative) relationship between adiponectin levels and future cardiac events has been reported [21
]. As such, it may be that adiponectin levels serve as a counter-regulatory factor following a physiological challenge [21
] and if so, sleep restriction may also trigger a similarly physiologically protective response. Moreover, the severity (acuity/chronicity) of sleep loss and the extent to which it is voluntary versus involuntary, are two among likely many factors that contributor to cardiovascular disease risk, including those that have a more direct effect, such as diet or levels of C-reactive protein [52
It is a limitation of the current study that exact energy intake and expenditures (i.e., food consumption and physical activity) were not assessed, as it is possible that these factors contributed to the observed systematic sex-based variance in the data. There is mixed evidence about whether food consumption and preferences change with sleep restriction [53
], and whether shifts in food intake (e.g., increased consumption of sodium-rich foods) affect adiponectin levels in humans [55
]; as such, quantifying food intake and examining effects on adiponectin levels will be an important area to explore in future studies. Another methodological limitation was the use of a single blood draw per sampling day. Although adiponectin has not been observed to have a circadian rhythm [27
], the methodology utilized in the current study may not have adequately captured any potential changes in adiponectin over a 24h period in response to sleep restriction. Lastly, while a relatively large sample was enrolled in the current study, participants were restricted to healthy adults, limiting the generalizations that can be made regarding the effects of sleep restriction on adiponectin levels across a more representative population-based sample, or one at greater immediate risk for cardiovascular disease.