Relationship between cortisol, life events and metabolic syndrome in men

Abstract

Psychological factors and stressful life events (LE) are considered to play a role in the onset of the metabolic syndrome (MS). We tested the association between LE and cortisol, a marker of chronic stress, with the risk of developing MS and their interaction. From a total number of 2906 men who completed a screening for the early detection of prostate cancer, 149 healthy men (mean ± SD age, 58.6 ± 7.7 years) were included in this study. Participants were assessed by the Holmes and Rahe questionnaire about their experience of LE during the previous 1-5 years. MS was diagnosed according to National Cholesterol Education Program-Adult Treatment Panel III (ATP-III) and International Diabetes Federation (IDF) criteria. Serum cortisol was measured at 08:00-09:00 h. Participants with MS (IDF criteria) reported significantly more past LE (p = 0.009) and greater summed weight of LE (p = 0.049) than those without MS. Furthermore, LE interacted with cortisol in relation to MS: in men with increased serum cortisol levels ( ≥ 13.7 μg/dl), number of LE significantly predicted MS-status (relative risk (RR) = 1.16, p = 0.03), whereas in men with low cortisol, LE were unrelated to MS (p = 0.52). We conclude that LE were significantly more prevalent in men with the MS than without the MS, according to IDF criteria, independent of the effects of age and body mass index, especially in men with increased serum cortisol levels.

Stressful life events and incident metabolic syndrome: the Hoorn study

“…To date, such an association was only observed in cross-sectional studies (Fabre et al, 2013;Horri et al, 2010;Vogelzangs et al, 2007), in which similar effect sizes were observed, ranging from 4 to 9% increased risk. We also observed that the association between the number of stressful life events and metabolic syndrome factors was strongest for waist circumference, which is also in line with previous cross-sectional studies (Fabre et al, 2013;Pyykkonen et al, 2010;Vogelzangs et al, 2007). Moreover, our findings (at least partly) support the ''Bjorntorp hypothesis'', which states that the increased activation of the HPA axis due to stress, results in the increased cortisol levels to upturn visceral fat storage (Bjorntorp, 1996).…”

“…Over the past 20 years, several studies have investigated the association between chronic stress and prevalent or incident metabolic syndrome (Bergmann et al, 2014;Di Castelnuovo et al, 2013;Fabre et al, 2013;Frisman & Kristenson, 2009;Goldbacher & Matthews, 2007;Hjemdahl, 2002;Horri et al, 2010;Lee et al, 2014;Puustinen et al, 2011;Pyykkonen et al, 2010;Raikkonen et al, 2007;Troxel et al, 2005;Vitaliano et al, 2002;Vogelzangs et al, 2007;Whisman & Uebelacker, 2012;Yamamoto et al, 2011). A recent meta-analysis of the only four prospective studies (Bergmann et al, 2014) that used objective stress measurements, showed that persons who experienced stressful life events had an on average two times higher probability of developing the metabolic syndrome at follow-up (Lee et al, 2014;Raikkonen et al, 2007;Troxel et al, 2005;Vitaliano et al, 2002).…”

Optimization of stress response through the nuclear receptor-mediated cortisol signalling network

“…Biological systems are routinely exposed to external challenge, such as the stress response where each challenge causes a transient spike in blood cortisol, activating catecholamine production in the brain and glucose mobilization in the liver, forming the classical fight or flight response3. It is clear that prolonged or repeated stress is associated with the development of pathophysiology456; for example, high stress police work is associated positively with the development of metabolic syndrome78. As such, it is both an important biological question, and challenging modelling scenario, to understand how these metabolic networks function efficiently, balancing both the pharmacodynamic (physiological effect of the challenge on the biological system) and pharmacokinetic (metabolic response to the challenge, leading to a return to homoeostasis) responses to stress: This ensures an efficient fight or flight response, while minimizing the overstimulation associated with increased morbidity.…”

Gene‐environment interaction between the brain‐derived neurotrophic factor Val66Met polymorphism, psychosocial stress and dietary intake in early psychosis

“…25 Previous studies include the use of this scale to explore the relationship between life events and subclinical psychotic symptoms in the general population 26 or metabolic abnormalities in healthy individuals. 27 The 14-item Perceived Stress Scale (PSS) 28 was used to explore the psychological repercussion of stress. This instrument is a self-report scale that assesses the perception of stressful experiences over the previous month.…”