Sleep depth and fatigue: role of cellular inflammatory activation.

Individuals with underlying inflammation present with a high prevalence of non-specific co-morbid symptoms including sleep disturbance and fatigue. However, the association between cellular expression of proinflammatory cytokines, alterations of sleep depth and daytime fatigue has not been concurrently examined. In healthy adults (24-61 years old), evening levels of monocyte intracellular proinflammatory cytokine production were assessed prior to evaluation of polysomnographic sleep and measures of fatigue the following day. Stimulated monocyte production of interleukin-6 (IL-6), but not tumor necrosis factor α (TNF-α), was negatively associated with slow wave sleep (ΔR²=.17, p=.029). In contrast, stimulated monocyte production of IL-6 was positively associated with rapid-eye movement (REM) sleep duration during the first sleep cycle (ΔR²=.26, p<.01). Moreover, evening stimulated production of IL-6 was associated with fatigue the following day (ΔR²=.17, p=.05). Mediation analyses showed that slow wave sleep, but not REM sleep duration, mediated the relationship between evening levels of IL-6 production and daytime fatigue. These results indicate that increases in stimulated monocyte production of IL-6 may be associated with decreases in slow wave sleep and increases in REM sleep duration. Relative loss of slow wave sleep may be one pathway through which cellular inflammation leads to daytime fatigue.

Autonomic and cardiovascular function in HIV spectrum disease: early indications of cardiac pathophysiology.

Autonomic dysfunction in persons with acquired immune deficiency syndrome (AIDS) has been reported previously but its incidence in early stage HIV infection and its relation to cardiovascular function have not been fully examined. The present study evaluated cardiovascular and autonomic function in 55 HIV-seronegative, and 52 HIV-asymptomatic and 31 HIV-symptomatic seropositive men. Measures of hemodynamic and autonomic function were obtained at rest and during a standardized battery of autonomic tests. Results were compared across groups while controlling for age, body mass, and physical activity. Analyses indicated that measures of autonomic function did not differ among groups. However, at rest, both HIV seropositive groups exhibited diminished stroke volume and elevated diastolic blood pressure, albeit within normotensive levels. In addition, the ability to sustain a blood pressure response during prolonged challenge and the relationship between stroke volume and baroreceptor/vagal responsiveness were disrupted in the HIV-symptomatic group. Therefore, in the pre-AIDS stages of infection, autonomic functioning appeared intact; yet alterations in baroreceptor/vagal function associated with depressed myocardial function may be an early warning signal reflecting cardiovascular pathological processes potentially exacerbated by HIV spectrum disease.

Aberrant parasympathetic and hemodynamic function distinguishes a subgroup of psychologically distressed individuals with asymptomatic type-I diabetes mellitus.

In a previous study, a subgroup of asymptomatic insulin-dependent diabetic individuals (termed IDDM-2) were identified on the basis of diminished parasympathetic cardiac input and elevated heart rate at rest. When compared to another group of asymptomatic IDDM participants (termed IDDM-1), and a nondiabetic healthy control group, the IDDM-2 group displayed elevated blood pressure, supported by elevated total peripheral resistance. Measures of psychological regulation were also taken in this study, and form the basis of this article, which examined whether these IDDM-2 patients differed from the other two groups on these measures. The possible role of glycemic control, IDDM duration, and number of somatic complaints among group differences in psychological regulation was also examined. The IDDM-2 group reported increased psychological distress, as reflected by increased dysphoric or depressive symptoms, trait anxiety, perceived stress, and cynical hostility, as well as decreased optimism and interpersonal, but not family, social support. Glycemic control did not account for any of the group differences in psychological regulation. However, group differences in dysphoria and anxiety were accounted for by differences in somatic complaints, whereas differences in interpersonal social support were accounted for by IDDM duration. Moreover, none of the variables investigated accounted for the diminished optimism of the IDDM-2 group. Therefore, in individuals with IDDM, who would otherwise be considered, after medical examination, as no different from other asymptomatic IDDM individuals, the combination of diminished parasympathetic cardiac input and elevated heart rate was associated with aberrant alterations of both hemodynamic and psychological functioning; the increased psychological distress in these individuals may be influenced, in part, by increased diabetes duration and number of somatic symptoms.

Blood pressure morning surge and hostility.

This study examined the effects of hostility on blood pressure (BP) during the early morning hours before awakening and several hours afterward. Our objective was to determine whether the pattern of BP change and the slope of the morning BP surge were related to hostility. The subjects were 32 patients with a history of Stage 1 hypertension. The morning surge in BP was derived from ambulatory BP monitoring of sleeping and waking hours, which were averaged per subject and centered around the wake-up hour. The periods used were 3 h before and 3 h after awakening. Only systolic blood pressure (SBP) is being reported on in this paper as this is the primary measure found relevant to the morning surge phenomenon. Hostility was assessed by the Buss-Durkee Hostility Inventory (total score). The results revealed significant differences between low and high hostility subjects for overall levels of sleep SBP: 120 +/- 11.4 mm Hg for low hostility and 131.3 +/- 14.9 mm Hg for high hostility subjects (P = .02). Low hostility subjects showed a steep rise in SBP from sleeping to waking while high hostility subjects had almost reached their post-sleep level of SBP in the hours immediately before waking up (P = .03). These data indicate that individual differences in hostility are related to different patterns of BP during sleep and the early morning hours, a period of the day that has been associated with an increased risk of cardiovascular incidents. The data also suggest the need for further study of the significance of hostility and other personality traits and the relationship of these traits to the mechanisms of the morning surge and the risk of cardiovascular events.