Our findings show that sleep continuity and sleep quality are associated with increased levels of CRP, but not IL-6 or TNF-α. No association was found between sleep duration and any of the inflammatory markers. These findings complement existing data (Friedman et al., 2005
; Liukkonen et al., 2007
; McDade et al., 2006
; Okun and Coussons-Read, 2007
; Suarez, 2008
). They are also interesting and thought provoking given the evidence that inflammation, and in particular chronic, low-grade inflammation, is a risk factor for future medical disease, especially those that are more prevalent in women, such as preeclampsia, polycystic ovarian syndrome, cardiovascular disease and Type 2 diabetes (Benderly et al., 2007
; Freeman et al., 2004
; Pradhan et al., 2001
; Vgontzas et al., 2006
). Persistent poor sleep, likely originating in young adulthood, and continuing into middle adulthood, may increase chronic, low-grade inflammation and the risk for inflammatory-related illnesses later in life. This relationship needs further examination in young women.
We did not corroborate the relationship between sleep duration and inflammation. This may reflect differences in methodologies as previous studies evaluated experimentally induced sleep restriction (Irwin et al., 2006
; Meier-Ewert et al., 2004
; Vgontzas et al., 2004
). Women in this study naturalistically slept an average of 7½ (range 6–9½) h per night over the course of 2-weeks. These values and the variability (standard deviations) are well within expected ranges for young adult women (Baker and Driver, 2004
; Tworoger et al., 2005
). Women with restricted sleep periods, possibly due to family or career obligations, may exhibit similar inflammatory responses to those observed in laboratory settings.
A modulating factor of interest is oral contraceptive (OC) use. OC have immunomodulatory effects (Cauci et al., 2008
; Giraldo et al., 2008
; Salkeld et al., 2001
). However, in agreement with a recent report (Giraldo et al., 2008
), we found no difference in IL-6 or TNF-α between OC users and non-users. We did observe a differential effect of OC use on CRP which is consistent with a report by Cauci et al. (Cauci et al., 2008
). The menstrual phase was also examined since inflammatory markers fluctuate during the menstrual cycle (O’brien et al., 2007
). There was no affect of menstrual phase on any of the inflammatory markers which may be due to the small sample.
Even though our preliminary findings are interesting, we acknowledge certain limitations. We did not screen out for sleep disorders, assess current infections or ascertain BMI at enrollment. All of which can influence inflammatory markers (Vgontzas et al., 2000
). Solely relying on subjective indices of sleep does not allow for a complete evaluation between two physiological processes. However, there is sufficient evidence that the subjective experience (i.e. sleep quality) is as important to alterations in inflammatory markers as physiologic measures (i.e. polysomnography) (Opp, 2006
). Another limitation is the one blood sample collected at the convenience of the participant. Having such variability in collection times, in addition to the fact that cytokines levels are lowest during the day (Vgontzas et al., 2005
), may partially explain why we found no relationship between sleep quality and IL-6 or TNF-α. Levels may have been too low to detect. In fact, our average IL-6 level (.54 pg/ml) was substantially lower than levels reported by Mills et al. (1.58 pg/ml for women) (Mills et al., 2007
Finally, we recognize that the demographics of our sample limits the generalizability of the findings. Given that children are a source of sleep disruptions (Lee, 1992
) and only 21% of our sample had children at home, we cannot extend these findings to all women. Future studies need to assess naturalistic sleep patterns in a representative cohort of women concomitantly with multiple blood draws in order to examine the relationship between poor sleep quality and continuity and chronic, low-grade inflammation.
In summary, we found that young, healthy women who have poor sleep continuity and quality have higher levels of CRP than women with few sleep complaints. We speculate that these increased, low levels of inflammation may contribute to increased disease risk in otherwise healthy women. Understanding this relationship among women may be especially important given that gender is an important factor in inflammation (O’connor et al., 2007
) and inflammation plays a role in several diseases that commonly afflict women, including polycystic ovary syndrome (PCOS) (Vgontzas et al., 2006
) and preeclampsia (Qiu et al., 2004
). Future work should longitudinally evaluate how these relationships may affect development of chronic disease in apparently healthy young women.