Eating After Acute Psychosocial Stress in Healthy Men and Women: Sex Differences and Endocrine Mechanisms.

CONTEXT: Overweight and obesity have become a major health burden with a higher prevalence of obesity in women than in men. Mental stress has been discussed to play a role in this context. OBJECTIVE: We investigated endocrine mechanisms underlying eating after acute psychosocial stress and potential sex differences therein. METHODS: A total of 32 male and 31 female healthy participants underwent the Trier Social Stress Test before they tasted ice cream in a bogus taste test 15 minutes after stress. We repeatedly assessed the stress hormone cortisol and the satiety hormone cholecystokinin (CCK) in saliva as well as perceived hunger before and up to 1 hour after stress. RESULTS: Lower immediate total cortisol stress reactivity predicted higher hunger (Ps ≤ .004), but was not associated with food intake (Ps ≥ .90) or total CCK release (Ps ≥ .84). As compared to men, women ate less after stress (Ps < .001) and had consistently lower levels of hunger (Ps ≤ .024) and cortisol (Ps ≤ .008) as well as a lower immediate total cortisol stress reactivity (Ps = .002). Further, they differed in the kinetics of CCK over the total experimental procedure (Ps ≤ .011), in immediate reaction to stress (Ps ≤ .038), and after eating (Ps ≤ .072), with women's CCK levels continuously decreasing while men's CCK levels were reactive. CONCLUSION: We found evidence for lower immediate total cortisol stress reactivity relating to higher perceived hunger, with lower cortisol levels in women. Unlike in men, CCK levels in women were not reactive to acute stress and eating and decreased continuously. Our results may suggest a higher risk for stress-induced eating in women.

Lower diurnal HPA-axis activity in male hypertensive and coronary heart disease patients predicts future CHD risk.

Background: Coronary heart disease (CHD) and its major risk factor hypertension have both been associated with altered activity of the hypothalamus-pituitary-adrenal (HPA)-axis but the biological mechanisms underlying prospective associations with adverse disease outcomes are unclear. We investigated diurnal HPA-axis activity in CHD-patients, hypertensive (HT) and healthy normotensive men (NT) and tested for prospective associations with biological CHD risk factors. Methods: Eighty-three male CHD-patients, 54 HT and 54 NT men repeatedly measured salivary cortisol over two consecutive days. Prospective CHD risk was assessed by changes between baseline and follow-up in the prothrombotic factors D-dimer and fibrinogen, the pro-inflammatory measures interleukin (IL)-6, tumor necrosis factor-alpha (TNF-α), and acute phase protein C-reactive protein (CRP), as well as blood lipids in terms of total cholesterol (tChol)/high-density-lipoprotein cholesterol (HDL)-ratio. We aggregated coagulation and inflammatory measures to respective indices. Results: The groups differed in repeated daytime cortisol (dayCort) secretion (p=.005,η2 p=.03,f=0.18) and cortisol awakening response (CAR) (p=.006,η2 p=.03,f=0.18), with similarly lower overall dayCort and CAR in CHD-patients and HT, as compared to NT. The groups differed further in cortisol at awakening (p=.015,η2 p=.04,f=0.20) with highest levels in HT (p´s≤.050), and in diurnal slope between waking and evening cortisol (p=.033,η2 p=.04,f=0.20) with steepest slopes in HT (p´s≤.039), although in part not independent of confounders. Lower aggregated dayCort and CAR in terms of area-under-the-curve (AUC) independently predicted increases in future overall CHD risk (AUCdayCort: p=.021,η2 p=.10,f=0.33;AUCCAR: p=.028,η2 p=.09,f=0.31) 3.00 ± 0.06(SEM) years later, with risk prediction most pronounced in fibrinogen (AUCdayCort: p=.017,ΔR 2= 0.12;AUCCAR: p=.082). Conclusion: We found evidence for an HPA-axis hypoactivity in CHD and HT with lower diurnal HPA-axis activity predicting increases in cardiovascular risk as evidenced by increases in circulating levels of biomarkers of atherothrombotic risk. Down-regulation of basal HPA-axis activity may contribute to the pathogenesis of atherosclerosis and thrombosis in CHD via effects on coagulation.

Do Hypertensive Men Spy With an Angry Little Eye? Anger Recognition in Men With Essential Hypertension - Cross-sectional and Prospective Findings.

BACKGROUND: Higher trait anger has inconsistently been associated with hypertension and hypertension development, but social context in terms of recognition of other persons' anger has been neglected in this context. PURPOSE: Here, we investigated anger recognition of facial affect and trait anger in essential hypertensive and normotensive men in addition to prospective associations with blood pressure (BP) increases. METHODS: Baseline assessment comprised a total of 145 participants including 57 essential hypertensive and 65 normotensive men who were otherwise healthy and medication-free. Seventy-two eligible participants additionally completed follow-up assessment 3.1 (±0.08 SEM) years later to analyze BP changes over time. We assessed emotion recognition of facial affect with a paradigm displaying mixed facial affect of two morphed basic emotions including anger, fear, sadness, and happiness. Trait anger was assessed with the Spielberger trait anger scale. RESULTS: Cross-sectionally, we found that with increasing BP, hypertensive men overrated anger displayed in facial expressions of mixed emotions as compared to normotensive men (ps ≤ .019) while there were no differences in trait anger (p = .16). Prospectively, the interaction between mean anger recognition and trait anger independently predicted BP increases from baseline to follow-up (ps ≤ .043), in that overrating displayed anger predicted future BP increases only if trait anger was high. CONCLUSIONS: Our findings indicate an anger recognition bias in men with essential hypertension and that overrating displayed anger in combination with higher trait anger seems to predict future BP increases. This might be of clinical relevance for the development and progression of hypertension and cardiovascular disease.

Acute Stress-Induced Blood Lipid Reactivity in Hypertensive and Normotensive Men and Prospective Associations with Future Cardiovascular Risk.

Hyperreactivity to stress may be one explanation for the increased risk of cardiovascular disease (CVD) in individuals with essential hypertension. We investigated blood lipid reactivity to the Montreal Imaging Stress Task (MIST), a psychosocial stressor, in hypertensive and normotensive men and tested for prospective associations with biological risk factors. Fifty-six otherwise healthy and medication-free hypertensive and normotensive men underwent the MIST. We repeatedly measured cortisol and blood lipid profiles (total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG)) immediately before and up to 1 h after stress. Lipid levels were corrected for stress hemoconcentration. Thirty-five participants completed follow-up assessment 2.9 ± 0.12 (SEM) years later. CVD risk was assessed by prospective changes in TC/HDL-C ratio, IL-6, D-dimer, and HbA1c from baseline to follow-up. The MIST induced significant changes in all parameters except TC (p-values ≤ 0.043). Compared with normotensives, hypertensives had higher TC/HDL-C-ratio and TG (p-values ≤ 0.049) stress responses. Blood lipid stress reactivity predicted future cardiovascular risk (p = 0.036) with increases in HbA1c (ß = 0.34, p = 0.046), IL-6 (ß = 0.31, p = 0.075), and D-dimer (ß = 0.33, p = 0.050). Our results suggest that the greater blood lipid reactivity to psychosocial stress in hypertensives, the greater their future biological CVD risk. This points to lipid stress reactivity as a potential mechanism through which stress might increase CVD risk in essential hypertension.

Acute Stress Improves Concentration Performance.

Acute stress can have both detrimental and beneficial effects on cognitive processing, but effects on concentration performance remain unclear. Here, we investigate the effects of acute psychosocial stress on concentration performance and possible underlying physiological and psychological mechanisms. The study sample comprised 47 healthy male participants who were randomly assigned either to a psychosocial stress situation (Trier Social Stress Test) or a neutral control task. Concentration performance was assessed using the d2 Test of Attention before and 30 min after the stress or control task. Salivary cortisol and alpha-amylase were repeatedly measured before and up to 1 hr after stress. We repeatedly assessed state anxiety using the State-Trait Anxiety Inventory and anticipatory cognitive stress appraisal using the Primary Appraisal Secondary Appraisal questionnaire. The stress group showed a significantly stronger improvement of concentration performance compared to the control group (p = .042). Concentration performance improvement was predicted by increased state anxiety (p = .020) and lower cortisol (stress) changes (p = .043). Neither changes in alpha-amylase nor cognitive stress appraisal did relate to concentration performance. Our results show improved concentration performance after acute psychosocial stress induction that was predicted by higher state anxiety increases and lower cortisol increases. This points to a potential modulating role of specific psycho-emotional and physiological factors with opposite effects.