Obesity and type 2 diabetes continue to be major public health burdens with type 2 diabetes rising in epidemic proportions. Since known risk factors do not explain all of the variance in the population, it is important to identify novel risk factors that can lead to development of new preventive measures. Chronic psychological stress and depression are associated with type 2 diabetes but the mechanism remains unclear. Neuroendocrine changes induced by these stressors, specifically activation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS), might provide a unifying explanation. The objectives of this review are (1) to summarize the metabolic impact of HPA axis and SNS dysfunction induced by depression and stress, (2) to summarize the relation of neuroendocrine parameters to risk factors for diabetes, (3) to discuss the limitations of assessing neuroendocrine function in population-based and intervention studies, and (4) to summarize the evidence of the impact of stress reduction, by cognitive behavior therapy (CBT), on neuroendocrine factors and on outcomes in diabetes and obesity.
"Pathophysiology is defined as the study of mechanisms of disease, that is, how changes in normal physiology can cause diseases . Some literatures have in general terms sought to describe the pathophysiology underlying the comorbidity between type 2 diabetes and depression    ; however, to our best knowledge, no previous review has addressed possible direction specific pathophysiological mechanisms for why we observe comorbidity between type 2 diabetes and depression. This review therefore aims to give an overview over possible pathophysiological mechanisms for each of the directions of the association between type 2 diabetes and depression, with special emphasis on stress-theory. "
[Show abstract][Hide abstract] ABSTRACT: Type 2 diabetes and depression are regarded as comorbid conditions, and three possible directions of the association between the diseases can underlie this observation of comorbidity. First, common etiology can increase a person's risk of both diseases; second, persons with type 2 diabetes have increased prevalence or risk of future development of depression; or third, persons with depression have increased prevalence or risk of development of type 2 diabetes. This review gives an overview over possible pathophysiological mechanisms for each of the directions of the association between type 2 diabetes and depression and further discusses epigenetics as an additional, direction independent approach. We argue that unspecific pathophysiological mechanisms involved in the stress response might, at least to some extent, explain each of the directions of the association between type 2 diabetes and depression, while changes in brain structure and function among persons with diabetes and possible increased risk of development of type 2 diabetes after use of antidepressant agents could represent more disease specific mechanisms underlying the comorbidity.
International Journal of Endocrinology 10/2015; 2015(443):164760. DOI:10.1155/2015/164760 · 1.95 Impact Factor
"This buffering effect might even attenuate some of the physiological load associated with chronically high blood sugar. This may take place through reduced chronic activation of stress-responsive pathways such as the hypothalamic-pituitary-adrenal axis, via effects on the regulation of inflammation and the adaptive immune response (Golden, 2007; Segerstrom and Miller, 2004). Women do sometimes report satisfaction related to these roles, and other scholars have noted how families evaluate the merits or demerits of wives based on the quality of family care that those wives provide (Cohen, 2000; Dern e, 1995). "
"Activation of the hypothalamic–pituitary axis due to stress results in excess secretion of cortisol, leading to increases in blood glucose levels and, eventually, insulin resistance (Black, 2006; Golden, 2007). Additionally, activation of the sympathetic nervous system and the subsequent release of epinephrine and norepinephrine can lead to abdominal obesity and insulin resistance (Black, 2006; Golden, 2007). PTSD is also associated with unhealthy behaviors such as poor diet and physical inactivity, which are risk factors for diabetes (Dedert et al., 2010; Pietrzak et al., 2011). "
[Show abstract][Hide abstract] ABSTRACT: Objective
To explore the temporal relationship between 9/11-related posttraumatic stress disorder (PTSD) and new-onset diabetes in World Trade Center (WTC) survivors up to 11 years after the attack in 2001.
Three waves of surveys (conducted from 2003 to 2012) from the WTC Health Registry cohort collected data on physical and mental health status, sociodemographic characteristics, and 9/11-related exposures. Diabetes was defined as self-reported, physician-diagnosed diabetes reported after enrollment. After excluding prevalent cases, there were 36,899 eligible adult enrollees. Logistic regression and generalized multilevel growth models were used to assess the association between PTSD measured at enrollment and subsequent diabetes.
We identified 2143 cases of diabetes. After adjustment, we observed a significant association between PTSD and diabetes in the logistic model [adjusted odds ratio (AOR) 1.28, 95% confidence interval (CI) 1.14–1.44]. Results from the growth model were similar (AOR 1.37, 95% CI 1.23–1.52).
This exploratory study found that PTSD, a common 9/11-related health outcome, was a risk factor for self-reported diabetes. Clinicians treating survivors of both the WTC attacks and other disasters should be aware that diabetes may be a long-term consequence.
Preventive Medicine 09/2014; 66. DOI:10.1016/j.ypmed.2014.05.016 · 3.09 Impact Factor
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