Psychosocial stress is associated with risk of obesity although little is known about stress-induced biological mechanisms of obesity. We examined the potential mediating role of inflammatory processes. Data were collected from a nationally representative sample of 7540 individuals (54% women, mean age 46.8+/-15.4 years), from the Scottish Health Surveys. We calculated risk estimates of obesity for increasing numbers of psychosocial stressors (based on social position, education, psychological distress and marital/partner discord) using logistic regression analyses. Obesity was assessed using body mass index and central obesity using waist circumference. Potential mediators included inflammatory markers (C-reactive protein and fibrinogen) and health behaviours (physical activity, smoking, alcohol, and dietary intake). The unadjusted odds ratio of obesity for three or more psychosocial stressors was 1.81 (95% CI, 1.39-2.36, p<0.001). In multivariate analyses that adjusted for age, gender, health behaviours and inflammatory markers the association between psychosocial stress and obesity was attenuated but remained significant (1.49, 1.11-2.00, p<0.001). Inflammatory markers independently accounted for approximately 25% of the association between stress and obesity. We found similar associations in separate analyses of psychosocial stress and central obesity, although results were confounded by overall obesity. In summary, inflammatory processes appear to be an important intermediate pathway in the association between psychosocial stress and obesity.
"Stress is well established as a serious health problem in industrialized human societies, since it favors several major pathologies such as cardiovascular failure (Manni et al., 2008; Wirtz et al., 2008), cancer (Quick et al., 2008) and depression (Chaplin et al., 2008). Other emerging deleterious effects of stress include feeding disorders and body weight (BW) dysregulations (Harris et al., 2002; Hamer and Stamatakis, 2008). In animals, many studies reported that different paradigms of stress produce a significant reduction in food intake (FI), unless access to food is given after the stress period. "
[Show abstract][Hide abstract] ABSTRACT: We studied the long term effects of a single exposure to immobilization stress (IS) (1 h) on the expression of anorexigenic (Pro-opiomelanocortin: POMC and cocaine amphetamine related transcript: CART) and orexigenic (neuropeptide Y:NPY, Agouti related peptide: AgRP) factors in hypothalamus and dorso vagal complex (DVC). We showed, by using RT-PCR that in the hypothalamus, that the mRNAs of POMC and CART were up-regulated at the end of IS and up to 24 h. This up regulation persists until 48–72 h after IS for CART only. In the DVC, their expressions peak significantly at 24 h post stress and decline afterwards; CART mRNA is down regulated after 48 h post stress. NPY and AgRP mRNAs show a gradual increase just after the end of IS. The up regulation is significant only at 24 h after stress for AgRP but remains significantly higher for NPY compared to controls. In DVC, the mRNAs of the two factors show generally a similar post stress pattern. A significant increase jut after the end of IS of rats which persists up to 24 h after is firstly noticed. The levels tend then to reach the basal levels although, they were slightly but significantly higher up to 72 h after stress for mRNA NPY. The comparison between the expression profiles of anorexigenic and the two orexigenic peptides investigated shows the presence of a parallelism between that of POMC and AgRP and that of CART and NPY when each brain region (hypothalamus and DVC) is considered separately. It seems that any surge in the expression of each anorexigenic factor stimulates the expression of those of corresponding and appropriated orexigenic one. These last reactions from orexigenic peptides tend to attenuate the anorexigenic effects of CART and POMC and by consequent to abolish the anorexia state generated by stress.
"High levels of depression have been shown to be related to a range of chronic diseases from type 2 diabetes  to Alzheimer's . A consistent finding is a link between stress, anxiety, and depression and increased inflammatory markers, which can be associated with  or independent of body weight . "
[Show abstract][Hide abstract] ABSTRACT: The obesity epidemic and associated chronic diseases are often attributed to modern lifestyles. The term "lifestyle" however, ignores broader social, economic, and environmental determinants while inadvertently "blaming the victim." Seen more eclectically, lifestyle encompasses distal, medial, and proximal determinants. Hence any analysis of causality should include all these levels. The term "anthropogens," or "…man-made environments, their by-products and/or lifestyles encouraged by these, some of which may be detrimental to human health" provides a monocausal focus for chronic diseases similar to that which the germ theory afforded infectious diseases. Anthropogens have in common an ability to induce a form of chronic, low-level systemic inflammation ("metaflammation"). A review of anthropogens, based on inducers with a metaflammatory association, is conducted here, together with the evidence for each in connection with a number of chronic diseases. This suggests a broader view of lifestyle and a focus on determinants, rather than obesity and lifestyle per se as the specific causes of modern chronic disease. Under such an analysis, obesity is seen more as "a canary in a mineshaft" signaling problems in the broader environment, suggesting that population obesity management should be focused more upstream if chronic diseases are to be better managed.
"Psychosocial stressors such as parental divorce
[48,49], poor mental health of parents
[50,51] or of children themselves
[52,53], are often associated with negative health outcomes
[54-56], but appear to act as moderators rather than mediators of weight-loss. To our knowledge, the ANS response to acute (experimental) stress
 has not been evaluated as a potential predictor of weight-loss and weight-loss maintenance in children and adolescents. "
[Show abstract][Hide abstract] ABSTRACT: Obesity in adults and children is increasing worldwide at alarming rates. Obese children and adolescents are likely to become obese adults with increased risk of a number of comorbidities. In addition to preventing the development of obesity at young age, it is necessary to individualize the therapy of already obese children and adolescents in order to increase the likelihood of weight loss and maintenance. Therefore, the aim of this study is to identify predictors which play a significant role in successful weight loss and weight loss maintenance in children and adolescents.
Over a one year period, 60 obese children and adolescents between 9 to 17 years of age shall be recruited at an inpatient children rehabilitation facility in Germany. They will be investigated twice within a few days following admission and prior to discharge. The study will be an integrated component of an established inpatient weight-loss and in part psychosomatic therapy. The collected data can be grouped into four clusters: 1) demographic, sociometric and psychometric data, 2) objective and subjective parameters of body condition, 3) autonomic nervous system regulated functions and 4) objective and subjective parameters for eating behavior. Primary outcome is the change of the body mass index standard deviation score (BMI-SDS). In order to evaluate the data appropriately, all examinations will be also conducted in a normal-weight reference group, matched for age and gender.
For some of the collected parameters the time span between measures may be too short. Therefore, a 6 months, 1 year and 2 year follow-up will be performed for evaluating the different predictors and their influence in regard to a successful intervention. Further middle- and long-term follow-up studies are planned.
The study protocol was approved by the Ethics Committee of the University Hospital Tübingen, Germany. This study is registered at the German Clinical Trials Register (DRKS) with the clinical trial number DRKS00005122.
Journal of Eating Disorders 03/2014; 2(1):7. DOI:10.1186/2050-2974-2-7
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