Post-menopausal women exhibit greater interleukin-6 responses to mental stress than older men

Background Acute stress triggers innate immune responses and elevation in circulating cytokines including interleukin-6 (IL-6). The effect of sex on IL-6 responses remains unclear due to important limitations of previous studies. Purpose The purpose of this study was to examine sex differences in IL-6 responses to mental stress in a healthy, older (post-menopausal) sample accounting for several moderating factors. Methods Five hundred six participants (62.9 ± 5.60 years, 55 % male) underwent 10 min of mental stress consisting of mirror tracing and Stroop task. Blood was sampled at baseline, after stress, and 45 and 75 min post-stress, and assayed using a high sensitivity kit. IL-6 reactivity was computed as the mean difference between baseline and 45 min and between baseline and 75 min post-stress. Main effects and interactions were examined using ANCOVA models. Results There was a main effect of time for the IL-6 response (F 3,1512 = 201.57, p = <.0001) and a sex by time interaction (F 3,1512 = 17.07, p = <.001). In multivariate adjusted analyses, IL-6 reactivity was significantly greater in females at 45 min (M = 0.37 ± 0.04 vs. 0.20 ± 0.03 pg/mL, p = .01) and at 75 min (M = 0.57 ± 0.05 vs. 0.31 ± 0.05 pg/mL, p = .004) post-stress compared to males. Results were independent of age, adiposity, socioeconomic position, depression, smoking and alcohol consumption, physical activity, statin use, testing time, task appraisals, hormone replacement, and baseline IL-6. Other significant predictors of IL-6 reactivity were lower household wealth, afternoon testing, and baseline IL-6. Conclusions Healthy, post-menopausal females exhibit substantially greater IL-6 responses to acute stress. Inflammatory responses if sustained over time may have clinical implications for the development and maintenance of inflammatory-related conditions prevalent in older women

The effect of experimentally induced sedentariness on mood and psychobiological responses to mental stress.

Background Evidence suggests a link between sedentary behaviours and depressive symptoms. Mechanisms underlying this relationship are not understood, but inflammatory processes may be involved. Autonomic and inflammatory responses to stress may be heightened in sedentary individuals contributing to risk, but no study has experimentally investigated this. Aim To examine the effect of sedentary time on mood and stress responses using an experimental design. Method Forty-three individuals were assigned to a free-living sedentary condition and to a control condition (usual activity) in a cross-over, randomised fashion and were tested in a psychophysiology laboratory after spending 2 weeks in each condition. Participants completed mood questionnaires (General Health Questionnaire and Profile of Mood States) and wore a motion sensor for 4 weeks. Results Sedentary time increased by an average of 32 min/day (P = 0.01) during the experimental condition compared with control. Being sedentary resulted in increases in negative mood independent of changes in moderate to vigorous physical activity (ΔGHQ = 6.23, ΔPOMS = 2.80). Mood disturbances were associated with greater stress-induced inflammatory interleukin-6 (IL-6) responses (β = 0.37). Conclusion Two weeks of exposure to greater free-living sedentary time resulted in mood disturbances independent of reduction in physical activity. Stress-induced IL-6 responses were associated with changes in mood

Decreased reaction time variability is associated with greater cardiovascular responses to acute stress

Cardiovascular (CV) responses to mental stress are prospectively associated with poor CV outcomes. The association between CV responses to mental stress and reaction times (RTs) in aging individuals may be important but warrants further investigation. The present study assessed RTs to examine associations with CV responses to mental stress in healthy, older individuals using robust regression techniques. Participants were 262 men and women (mean age = 63.3 ± 5.5 years) from the Whitehall II cohort who completed a RT task (Stroop) and underwent acute mental stress (mirror tracing) to elicit CV responses. Blood pressure, heart rate, and heart rate variability were measured at baseline, during acute stress, and through a 75-min recovery. RT measures were generated from an ex-Gaussian distribution that yielded three predictors: mu-RT, sigma-RT, and tau-RT, the mean, standard deviation, and mean of the exponential component of the normal distribution, respectively. Decreased intraindividual RT variability was marginally associated with greater systolic (B = −.009, SE = .005, p = .09) and diastolic (B = −.004, SE = .002, p = .08) blood pressure reactivity. Decreased intraindividual RT variability was associated with impaired systolic blood pressure recovery (B = −.007, SE = .003, p = .03) and impaired vagal tone (B = −.0047, SE = .0024, p = .045). Study findings offer tentative support for an association between RTs and CV responses. Despite small effect sizes and associations not consistent across predictors, these data may point to a link between intrinsic neuronal plasticity and CV responses

Effect of short-term weight loss on mental stress-induced cardiovascular and pro-inflammatory responses in women

Epidemiologic evidence links psychosocial stress with obesity but experimental studies examining the mechanisms that mediates the effect of stress on adiposity are scarce. The aim of this study was to investigate whether changes in adiposity following minimal weight loss affect heightened stress responses in women, and examine the role of the adipokine leptin in driving inflammatory responses. Twenty-three overweight or obese, but otherwise healthy, women (M age ¼ 30.41 ± 8.0 years; BMI ¼ 31.9 ± 4.1 kg/m2 ) completed standardized acute mental stress before and after a 9-week calorie restriction program designed to modify adiposity levels. Cardiovascular (blood pressure and heart rate) and inflammatory cytokines (leptin and interleukin-6; IL-6) responses to mental stress were assessed several times between baseline and a 45-min post-stress recovery period. There were modest changes in adiposity measures while the adipokine leptin was markedly reduced (27%) after the intervention. Blood pressure reactivity was attenuated (3.38 ± 1.39 mmHg) and heart rate recovery was improved (2.07 ± 0.96 Bpm) after weight loss. Blood pressure responses were inversely associated with changes in waist to hip ratio post intervention. Decreased levels of circulating leptin following weight loss were inversely associated with the IL-6 inflammatory response to stress (r ¼ 0.47). We offered preliminary evidence suggesting that modest changes in adiposity following a brief caloric restriction program may yield beneficial effect on cardiovascular stress responses. In addition, reductions in basal leptin activity might be important in blunting pro-inflammatory responses. Large randomized trials of the effect of adiposity on autonomic responses are thus warranted

The progression of CAC over 3 years follow up (n = 466).

<p>Filled bars designate CAC scores at follow up. Coronary artery calcification scores of 100–400, 400–999, and ≥1000 predict up to 4-, 7-, and 11-fold increases in future CVD risk, respectively, compared with patients with no detectable CAC. There was a significant increase in log Agatston score between baseline and follow up (2.25 vs 2.65, p<0.001), and 38.2% had progression of CAC as defined by an increase in >10 Agatston units.</p

Risk factors for relative CAC changes over follow up (N = 466).

<p>*Effect estimates are adjusted for age and sex.</p>†<p>per SD increase.</p><p>BP – Blood pressure; HbA1c - glycated haemoglobin; AUC - Area under the curve.</p

Characteristics of the study population at baseline in relation to CAC progression (N = 466).

<p>*CAC progression defined as an increase >10 Agatston units between baseline and follow up.</p><p>Values are means ± SD.</p

Risk factors for CAC progression of >10 Agatston units (N = 466).

<p>*Effect estimates are mutually adjusted for all presented variables and follow up time.</p>†<p>per SD increase.</p