A review of the evidence for a neuroendocrine link between stress, depression and diabetes mellitus.
ABSTRACT 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.
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ABSTRACT: Background: Depression is one of the most common psychological states in type 2 diabetes that contributes to adverse health outcomes. This study aimed to investigate the risk factors for the incidence of depression in type 2 diabetic patients. Materials and Methods: In this descriptive cross-sectional study, 254 type 2 diabetic patients were selected through convenience sampling among diabetes outpatient clinics of Tehran university of medical sciences and also Iranian diabetes society during 2010-11. Data were collected using demographic and disease characteristic questionnaire, patient health questionnaire, social support scale and diabetes self-management scale (DSMS) and then analyzed using Chi square, t-test and binary logistic regression. Results: Increased pain and functional disability (OR=11.725), decreased social support (OR=3.086), decreased performance for diabetes self-care (OR=4.088), longer duration of diabetes (OR=1.328), diabetes complications (OR=2.324), the need for insulin therapy (OR=2.431), HbA1c>9% (OR=21.575), BMI>25kg/m 2 (OR=2.251) and major life events (OR=14.043) were significantly different between the diabetic patients with and without depression (P=0.001). There was no significant difference in age, sex and socio-economic status between the two groups. The regression model correctly was fitted in 95.3% of the cases. Conclusion: Pain and functional disability, poor social support, weaker diabetes self-care, longer duration of diabetes, diabetes complications, the need for insulin therapy, HbA1c>9%, BMI>25kg/m 2 and the experience of major life events all together contribute to the incidence of depression in type 2 diabetic patients. The results of the study have implications for the prevention of depression in diabetic patients.
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ABSTRACT: It has recently become clear that obstructive sleep apnea (OSA) is an independent risk factor for the development of metabolic syndrome, a disorder of defective energy storage and use. Several mechanisms have been proposed to explain this finding, drawing upon the characteristics that define OSA. In particular, intermittent hypoxia, sleep fragmentation, elevated sympathetic tone, and oxidative stress – all consequences of OSA – have been implicated in the progression of poor metabolic outcomes in OSA. In this review we examine the evidence to support each of these disease manifestations of OSA as a unique risk for metabolic dysfunction. Tissue hypoxia and sleep fragmentation are each directly connected to insulin resistance and hypertension, and each of these also may increase sympathetic tone, resulting in defective glucose homeostasis, excessive lipolysis, and elevated blood pressure. Oxidative stress further worsens insulin resistance and in turn, metabolic dysfunction also increases oxidative stress. However, despite many studies linking each of these individual components of OSA to the development of metabolic syndrome, there are very few reports that actually provide a coherent narrative about the mechanism underlying metabolic dysfunction in OSA.Sleep and Biological Rhythms 10/2014; 13(1). DOI:10.1111/sbr.12078 · 1.05 Impact Factor