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Background: Obesity and depression both individually contribute to the risk of Type II Diabetes (T2DM). The extent to which obesity can be set-off by depression is unknown.Methods: In a sample of 9340 participants followed for 15.4 years (79,372 person-years) from the prospective MONICA/KORA population-based cohort conducted in Southern Germany, we investigated the impact of obesity, defined as Body Mass Index (BMI) _a 30, and depression on the incidence of T2DM using Cox Proportional Hazards Regression.Results: The relative risk of T2DM was over 6 fold higher among obese participants in comparison to normal weight participants (HR 6.05; 95% CI 4.82 to 7.59; p

Summary Context Preliminary evidence points to aldosterone being not only prominently involved in the systemic regulation of the blood pressure but also to play a role in the pathophysiology of depression. Objective We evaluated whether the combination of hypertension and depressed symptomatology is useful to screen for individuals suffering an activation of the renin–angiotensin–aldosterone system (RAAS). Design We conducted a cross-sectional analysis in participants from the Cooperative Health Research in the Region of Augsburg (KORA) F4 Study conducted between 2006 and 2008 in Southern Germany. A total of 1805 participants of the F4 study were included in the study. Methods The association between aldosterone and renin levels and the different combinations of hypertension and depressed symptomatology was examined in four different models of multiple linear regression adjusted for age, sex, creatinine levels, potassium levels, body mass index (BMI) and behavioural risk factors. Results Individuals suffering both, depressed symptomatology and hypertension exhibited highly significantly increased aldosterone levels ( p p = 0.08) compared to individuals with no depressed symptomatology and no hypertension. No significant activation of the RAAS was seen in only depressed or only hypertensive individuals. Conclusions The finding of highly significantly increased aldosterone levels and increased renin levels in individuals suffering both, depressed symptomatology and hypertension provides further evidence for the involvement of the RAAS in the pathogenesis of depressed symptomatology. These findings have important implications for future research concerning the pathophysiological pathways that link depression and cardiovascular disease.

Objective During an acute myocardial infarction, patients often use denial as a coping mechanism which may provide positive mood regulating effects but may also prolong prehospital delay time (PHD). However, empirical evidences are still sparse. Methods This cross-sectional study included 533 ST-elevated myocardial infarction (STEMI) patients from the Munich Examination of Delay in Patients Experiencing Acute Myocardial Infarction (MEDEA) study. Data on sociodemographic, clinical and psycho-behavioral characteristics were collected at bedside. The outcome was assessed using the Cardiac Denial of Impact Scale (CDIS) with the median split as cutoff point. A total of 206 (41.8%) STEMI patients were thus classified as deniers. Results Deniers were less likely to suffer from major depression (p=0.04), anxiety (p=0.01) and suboptimal well-being (p=0.01) compared to non-deniers during the last six months prior to STEMI. During STEMI, they were less likely to perceive severe pain strength (p=0.04) and racing heart (p=0.02). Male deniers were also less likely to perceive shortness of breath (p=0.03) and vomiting (p=0.01). Denial was not associated with overall delay time. However, in the time window of 3 to 24h, denial accounted for roughly 40min extra delay (356 vs. 316.5min p=0.02 n=196). Conclusions Denial not only contributes to less suffering from acute heart related symptoms and negative affectivity but also leads to a clinically significant delay in the prevalent group.

The renin-angiotensin-aldosterone-system (RAAS) is one of the most important systems involved in the pathogenesis of cardiovascular diseases. Its role in stress response has been generally neglected, although the progression of cardiovascular disease is considerably increased in the presence of stress and especially in the presence of depression risk. With the present analysis we aimed to evaluate whether the activity of the RAAS correlates with depressive symptomatology and with chronic stress. Moreover, we aimed to analyse whether stress response is altered in the presence of depressed symptomatology. We chose "living alone" to be our paradigm of chronic stress.Aldosterone and renin levels were assessed in 1743 (829 men, 914 women) from the population-based KORA study (Cooperative Health Research in the Region of Augsburg). The relationship between aldosterone, renin levels and the different combinations of living alone and depressive symptomatology was examined in three different multiple linear regression models adjusted for age, sex, creatinine levels, potassium levels, body mass index (BMI) and bio-behavioural factors. Neither "living alone" nor depressive symptomatology alone were associated with an activation of the RAAS, but the combination of living alone and depressive symptomatology yielded a highly significant increase in the aldosterone (p0.01) and renin level (p=0.03).Our findings show that depressive symptomatology is associated with a hyper-responsiveness to chronic stress. Under the condition of chronic stress depressed individuals have an activated RAAS. Activation of the RAAS might explain the known increased risk of negative cardiovascular disease outcomes in this group.

Despite the fact that mitochondrial dysfunctions are increasingly recognized as key components in stress-related mental disorders, very little is known about the association between posttraumatic stress disorder (PTSD) and mitochondrial variants. To identify susceptibility mitochondrial genes for PTSD, we analyzed a total number of 978 mitochondrial single-nucleotide polymorphisms (mtSNPs) in a sample of 1238 individuals participating in the KORA (Cooperative Health Research in the Region of Augsburg) study. Participants were classified with 'no PTSD', 'partial PTSD' or 'full PTSD' by applying the Posttraumatic Diagnostic Scale and the Impact of Event Scale. To assess PTSD-mtSNP association while taking heteroplasmy into account, we used the raw signal intensity values measured on the microarray and applied linear regression. Significant associations were obtained between full versus no PTSD and two mtSNPs; mt8414CT (β=-0.954±0.06, Padjusted=0.037) located in adenosine triphosphate (ATP) synthase subunit 8 (MT-ATP8) and mt12501GA (β=-1.782±0.40, Padjusted=0.015) located in the NADH dehydrogenase subunits 5 (MT-ND5). Heteroplasmy for the two variants towards a larger number of the respective minor alleles increases the risk of having PTSD. NADH dehydrogenase and ATP synthase are both linked to the regulation of reactive oxygen species. Our results highlight the important role of the mitochondrial genome among the factors that contribute to the risk of PTSD. Mitochondrial genetic variants may be more important than has previously been assumed, leading to further insights regarding effects of existing medications, or even to the development of innovative treatments. As this is the first mitochondrial genome-wide association study for PTSDs, further analyses are needed to follow up on the present findings.

Objective: To assess whether alexithymia is a risk factor for exacerbation in spasmodic torticollis (ST). Methods: ST patients (2×10) with high vs. low alexithymia scores (mean score on the 20-item Toronto Alexithymia Scale [TAS-20]=69.2 vs. 28.7) were compared on physiological, motor and subjective responses to a cognitive and an emotional laboratory stressor. Changes in sustained abnormal head/shoulder positions and maximum range of motion (ROM) of the cervical spine were kinematically quantified. Skin conductance level (SCL), nonspecific skin conductance fluctuations (NS.SCF), heart rate (HR) and skin temperature (T) were measured. Results: High alexithymia had no effect on the abnormal head posture or movements, but high-alexithymic ST patients showed generally increased levels of autonomic arousal (more NS.SCF, higher SCL; analysis of variance [ANOVA]: P =.016 and P =.051, respectively) under all experimental conditions. When ST symptom severity (TSUI-score) was partialled out, these group differences were somewhat reduced (analysis of covariance [ANCOVA]: P =.052 and P =.143). Conclusions: High alexithymia did not lead to increased abnormal head movements to stressors, but may result in a subtle increase in tonic level of sympathetic activity.

Objective: Biobehavioral mechanisms relating the Distressed (Type D) personality to cardiovascular disease are only beginning to be understood. Studies have suggested a number of biological mechanisms, but also behavioral mechanisms seem to play a role. The purpose of this review was to provide an overview of the current state of affairs onmechanisms that may explain the link between Type D personality and cardiovascular disease incidence and progression. Methods: A systematic search of the literature was performed in Pubmed and PsychInfo. Studies were selected that assessed biobehavioral mechanisms associated with Type D personality in healthy, at risk, or cardiovascular patient samples. Result: In heart failure patients, Type D personality has been related to autonomic dysfunction, increased levels of inflammation, increased anemia, renal dysfunction and elevated oxidative stress. In patients with acute coronary syndrome, cortisol levels were elevated. Type D personality was also associated with an increased risk of cardiac arrhythmia and acute myocardial stunning. Behavioral factors include poor adherence to treatment and poor health behaviours, including physical inactivity and smoking. However, these mechanisms may differ depending on age and the stage of the disease, as mortality effects of Type D also decline in older patients and in patients with severe heart disease i.e. heart failure. Conclusions: Type D seems to be associated with dysfunction of major biological regulatory systems as well as adverse health behaviours. Future studies should focus on the interrelations between biological and behavioral factors to elucidate their combined pathophysiological effects, and to guide the development of effective intervention strategies.

ObjectiveTo examine whether depression or social isolation or the combination of both is associated with high leptin levels.Research methods and proceduresIn this cross-sectional study, the study population comprised 1229 subjects. Social network was assessed according to the Social Network Index initially designed for the Alameda study. Depression was assessed using the DEEX scale. Four categories were built: “socially integrated, not depressed”, “socially integrated, depressed”, “socially isolated, not depressed”, “socially isolated, depressed”. Serum leptin concentrations were assessed.Logistic regression was performed in men and women separately to investigate the influence of the three different categories “socially integrated, depressed”, “socially isolated, not depressed” and “socially isolated, depressed” in comparison with the reference category “socially integrated, not depressed”. The probability belonging to the upper 30% of leptin values was modelled. Four models were adjusted for BMI, age, lifestyle factors, psychosomatic complaints and metabolic variables.ResultsIn men, but not in women a significant effect could be seen. The combination of depressed state and social isolation was associated with a four fold increased risk of belonging to the group with the 30% highest leptin levels in men, whereas in women odds ratios did not reach significance.DiscussionMen, who were socially isolated and depressed, had an increased risk for high leptin levels. Therefore the combination of social isolation and depression, which is known to be associated with the worst outcome in cardiovascular disease, may have the potential to increase leptin levels in men.