Measures of adiposity predict interleukin-6 responses to repeated psychosocial stress

Abstract

Objective Overweight and obese individuals, who comprise approximately two-thirds of the U.S. population, are at increased risk for developing a range of diseases. This increased risk may be due in part to maladaptive stress responses within this group, including heightened low-grade inflammation and HPA axis non-habituation. In this study we tested the relationship between adiposity, plasma interleukin-6 (IL-6) and HPA axis responses to repeated stress. Methods Sixty-seven healthy participants were exposed to the Trier Social Stress Test (TSST) on two consecutive days. We collected saliva for cortisol measurements at baseline and at 1, 10, 30, 60 and 120 minutes post-TSST, and blood for plasma IL-6 measurements at baseline and 30 and 120 minutes post-TSST. Results Stress exposure induced significant increases of cortisol and IL-6 on both days (cortisol: F=38, p<0.001; IL-6: F=90.8; p<0.001), and repeated exposure was related with cortisol habituation (F=8.2; p<0.001) and IL-6 sensitization (F=5.2; p=0.022). BMI and body fat were related with higher cortisol responses to repeated stress (BMI: beta=0.34; p=0.014; body fat: beta=0.29; p=0.045), and with higher IL-6 responses to repeated stress (BMI: beta=0.27, p=0.044; body fat: beta=0.37; p=0.006). Conclusions Taken together, individuals with higher measures of adiposity showed less efficient HPA axis habituation as well as sensitization of IL-6 responses to repeated acute stress. These findings point to maladaptive stress response patterns in overweight humans, which, through exposure to higher levels of inflammatory mediators, might partially explain diseases related with overweight and/or obesity.

Post-menopausal Women Exhibit Greater Interleukin-6 Responses to Mental Stress Than Older Men

“…Consistent with most previous reports, baseline IL-6 levels were associated with older age, greater adiposity levels, and higher depressive symptoms score and inversely with socioeconomic position and frequency of physical activity [9,10,13]. We observed an increase (31 %) in circulating levels of IL-6 in response Values are means (SD) or N (%)…”

“…An adiposity component was computed using participants' BMI, waist circumference, and fat mass [10,13]. Mood symptoms were assessed with the Center for Epidemiologic Study Depression (CES-D) Scale [25], and scores were dichotomized into <16 or ≥16 (no/little risk and at risk for depression) [26].…”

“…Interestingly, there appear to be robust individual differences in the magnitude and pattern of inflammatory stress responses [8,9]. In addition, inflammatory responses do not seem to habituate to repeated exposure to acute stress; in other words, inflammatory responses sensitize [10,11]. This suggests that over time, continued exposure to stressinduced inflammatory responses to psychosocial stress may up-regulate low-grade, peripheral inflammation.…”

Role of inflammatory cytokines in depression: Focus on interleukin-1β

“…Furthermore, it has been stated that the three pro-inflammatory cytokines, IL-6, TNF and IL-1β are implicated in the pathophysiology of depressive illness (21). IL-6 has been proposed to be central in the systemic consequences of psychological stress, mediating with stress through the hypothalamic-pituitary-adrenal (HPA) axis and catecholamines leading to insulin resistance, coagulation abnormalities and endothelial dysfunction (22)(23)(24). Similarly, depression has been associated with systemic diseases involving induction of a pro-inflammatory state or upregulation of inflammatory markers.…”

The Relationship between Stress and Severe Obesity: A Case-Control Study

“…Prentice [21] suggested that eating after stress can worsen health status, particularly in individuals with dysfunctional eating patterns. McInnis et al [22] explained obesity in terms of cellular disturbances. Maladaptive stress triggers a compensatory mechanism that could explain obesity and overweight.…”