Cardiovascular stress responsivity, body mass and abdominal adiposity

Steptoe, Andrew; Wardle, Jane

doi:10.1038/sj.ijo.0803011

Cited by 92 publications

(97 citation statements)

References 40 publications

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“…46 Consistent with previous results, we found a positive association between impaired post-stress recovery of diastolic BP and adiposity. 15 There was also a positive relationship at all time points between leptin levels and heart rate, independent of baseline heart rate and BMI. Chronic leptin infusion has been shown to stimulate sympathetic outflow to thermogenic and non-thermogenic organs of rodents, and to increase heart rate and arterial BP in animals.…”

Section: Discussionmentioning

confidence: 81%

“…Supporting this, a more recent analysis of middle-aged people from the Whitehall II cohort found that impaired cardiovascular recovery following an acute laboratory stressor, manifest as prolonged elevations in systolic BP and cardiac index, was longitudinally associated with central adiposity in men, predicting a 3-year increase in waist-hip ratio. 15 Several factors may contribute to individual variation in responsiveness to stress including genetic predisposition, gender, early life and current events. 5 Notably, chronic stress exposure has been associated with a dysregulated HPA and/ or SNS response, and there is growing evidence for an association between chronic stress and abdominal adiposity.…”

Section: Introductionmentioning

confidence: 99%

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Stress-induced cytokine responses and central adiposity in young women

et al. 2007

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Background: Evidence suggests that people who are more responsive to psychological stress are at an increased risk of developing obesity. However, the biological mechanisms underlying this phenomenon are poorly understood. The cytokines leptin, interleukin-1 receptor antagonist (IL-1Ra) and interleukin-6 (IL-6) play a key role in fat metabolism and abnormal circulating levels of these proteins have been reported in obese people and in individuals subject to stress. Objective: This study investigated whether cytokine responses to acute mental stress are associated with adiposity in healthy young women. Design and Subjects: A laboratory study of 67 women, aged 18-25 years, recruited from University College London. Measurements: Height, weight and waist circumference were measured and body fat mass was estimated by bioelectrical impedance body composition analysis. Laboratory mental stress testing was carried out and blood pressure and heart rate were recorded at baseline, during two moderately challenging tasks (Stroop and speech) and during recovery 40-45 min post-stress. Blood samples taken at baseline, immediately post-stress and 45 min post-stress, were used for assessment of circulating cytokines. Saliva samples taken throughout the session were assessed for cortisol. Results: Women who had larger cytokine responses to stress were more abdominally obese than women with smaller cytokine stress responses. Specifically, there was a positive correlation between waist circumference and stress-induced increases in plasma levels of leptin (r ¼ 0.35, Po0.05) and IL-1Ra responses (r ¼ 0.29, Po0.05). There was also a significant positive correlation between prolonged diastolic blood pressure responses to stress and measures of total and abdominal obesity (r ¼ 0.28-0.33, Po0.05). Conclusion: Increased cytokine production could be a mechanism linking stress and abdominal obesity.

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Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Stress-induced cytokine responses and central adiposity in young women

et al. 2007

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“…Delayed poststress BP and heart rate variability recovery is more common in adults with a lower SES (31), and it has been associated with social isolation, poor mental health, and impaired hemostatic responses to stress (32). It also predicts future increases in BP and abdominal adiposity (33,34). Sustained reductions in heart rate variability following stress may have adverse effects on cardiovascular disease risk (35).…”

Section: Discussionmentioning

confidence: 99%

Shorter telomeres with high telomerase activity are associated with raised allostatic load and impoverished psychosocial resources

Zalli

Carvalho

Lin

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

159

118

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Recent work has linked psychological stress with premature cellular aging as indexed by reduced leukocyte telomere length. The combination of shorter telomeres with high telomerase activity (TA) may be indicative of active cell stress. We hypothesized that older individuals characterized by shorter telomeres with high TA in unstimulated leukocytes would show signs of high allostatic load and low levels of protective psychosocial resources. We studied 333 healthy men and women aged 54-76 y who underwent laboratory testing in which we measured cardiovascular, neuroendocrine, and inflammatory responses to standardized mental stress tasks. The tasks elicited prompt increases in blood pressure (BP), heart rate, cortisol, and mediators of inflammation and reductions in heart rate variability, returning toward baseline levels following stress. However, men having shorter telomeres with high TA showed blunted poststress recovery in systolic BP, heart rate variability, and monocyte chemoattractant protein-1, together with reduced responsivity in diastolic BP, heart rate, and cortisol, in comparison to men with longer telomeres or men with shorter telomeres and low TA. Shorter telomeres with high TA were also associated with reduced social support, lower optimism, higher hostility, and greater early life adversity. These effects were independent of age, socioeconomic status, and body mass index. We did not observe differences among older women. Our findings suggest that active cell stress is associated with impaired physiological stress responses and impoverished psychosocial resources, reflecting an integration of cellular, systemic, and psychological stress processes potentially relevant to health in older men. cellular senescence | allostasis | psychological distress T elomeres are nucleoprotein structures composed of tandem hexanucleotide repeats of the sequence TTAGGG that cap the ends of eukaryotic chromosomes, protecting them from end-to-end fusion and degradation during cell division. Human telomeric DNA naturally shortens with age during somatic cell divisions and as a result of oxidative attack (1, 2). At critical shortness, telomeres exhibit impaired function, leading to genomic instability, apoptosis, and cell senescence, often with altered transcriptional programming and mitochondrial dysfunction (1). Telomere attrition represents one of the hallmarks of aging (3). In humans, Mendelian singlegene mutations that directly compromise telomere maintenance cause premature mortality and onset of a spectrum of diseases overlapping with the age-related diseases common in the population (4). In addition, genome-wide association studies show that certain combinations of SNPs at genetic loci encoding known telomere-maintenance factors are associated with increased relative risks for pulmonary and coronary diseases (5). Shorter telomere length (TL) in white blood cells is linked and, in some cases, anticipates aging-related morbidity and mortality from conditions with immune system involvement, such as infectious disease...

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“…Reactivity and recovery regression models were adjusted for baseline levels of the relevant measure. Covariates also included age and BMI which are established predictors of basal blood pressure and cardiovascular stress reactivity (Matthews and Stoney, 1988;Steptoe and Wardle, 2005a). To control for negative affect, the negative affective items from the POMS were subsequently added as a covariate to each model.…”

Section: Discussionmentioning

confidence: 99%