6 research outputs found

    Longitudinal Relationship of Depressive and Anxiety Symptoms With Dyslipidemia and Abdominal Obesity

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    <p>Objective: Previous research indicates that patients with severe symptoms of depression or anxiety are prone toward the development of dyslipidemia and abdominal obesity. We sought to study these associations longitudinally. Methods: Among 2126 Netherlands Study of Depression and Anxiety participants, we studied whether severity of depressive (Inventory of Depressive Symptoms) or anxiety (Beck Anxiety Inventory) symptoms at baseline was associated with changes in lipids (i.e., total, high-density lipoprotein [HDL] or low-density lipoprotein cholesterol, and triglycerides) or waist circumference during a 2-year follow-up period. We also examined whether changes in severity of symptoms were associated with changes in lipid or waist circumference levels over these 2 years. Multivariate linear regression analyses were adjusted for age, sex, education, and tobacco consumption. Results: Baseline symptoms of depression or anxiety predicted a decrease in HDL cholesterol (adjusted beta = -.062 [p = .003] and beta = -.050 [p = .02], respectively) and an increase in waist circumference (adjusted beta = .060 [p = .01] and beta = .053 [p = .02], respectively) for 2 years. Reduction of symptoms of depression or anxiety over time did not coincide with an amelioration of lipid or waist circumference values. Conclusions: People with initially severe symptoms of depression or anxiety showed a subsequent decrease in HDL cholesterol levels and an increase in abdominal obesity over time, independent of a potential reduction in symptom severity in this period. Therefore, such people are at elongated and increasing risk for dyslipidemia and obesity, predisposing them to cardiovascular disease.</p>

    The impact of stress systems and lifestyle on dyslipidemia and obesity in anxiety and depression

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    <p>Background: Dyslipidemia and obesity have been observed in persons with severe anxiety or depression, and in tricyclic antidepressant (TCA) users. This likely contributes to the higher risk of cardiovascular disease (CVD) in anxiety and depressive disorders. We aimed to elucidate whether biological stress systems or lifestyle factors underlie these associations. If so, they may be useful targets for CVD prevention and intervention.</p><p>Methods: Within 2850 Netherlands Study of Depression and Anxiety (NESDA) participants, we evaluated the explaining impact of biological stress systems (i.e., the hypothalamic-pituitary- adrenal [HPA] axis, autonomic nervous system [ANS] and inflammation) and lifestyle factors (i.e., tobacco and alcohol use, and physical activity) on adverse associations of anxiety and depression severity and TCA use with high and low-density lipoprotein cholesterol, triglycerides, body mass index and waist circumference. Through linear regression analyses, percentual change (%Delta) in beta was determined and considered significant when %Delta > 10.</p><p>Results: The inflammatory marker C-reactive protein had the most consistent impact (explaining 14-53% of the associations of anxiety and depression severity and TCA use with lipid and obesity levels), followed by tobacco use (explaining 34-43% of the associations with lipids). The ANS mediated all associations with TCA use (explaining 32-61%). The HPA axis measures did not explain any of the associations.</p><p>Conclusions: Increased dyslipidemia and (abdominal) obesity risk in patients with more severe anxiety disorders and depression may be partly explained by chronic low-grade inflammation and smoking. TCAs may increase metabolic risk through enhanced sympathetic and decreased parasympathetic ANS activity. That the HPA axis had no impact in our sample may reflect the possibility that the HPA axis only plays a role in acute stress situations rather than under basal conditions. (C) 2012 Elsevier Ltd. All rights reserved.</p>

    Assessment of biopsychosocial complexity and health care needs: Measurement properties of the INTERMED self-assessment version

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    Objective: The INTERMED Self-Assessment questionnaire (IMSA) was developed as an alternative to the observer-rated INTERMED (IM) to assess biopsychosocial complexity and health care needs. We studied feasibility, reliability, and validity of the IMSAwithin a large and heterogeneous international sample of adult hospital inpatients and outpatients as well as its predictive value for health care use (HCU) and quality of life (QoL). Methods: A total of 850 participants aged 17 to 90 years from five countries completed the IMSA and were evaluated with the IM. The following measurement properties were determined: feasibility by percentages of missing values; reliability by Cronbach a; interrater agreement by intraclass correlation coefficients; convergent validity of IMSA scores with mental health (Short Form 36 emotional well-being subscale and Hospital Anxiety and Depression Scale), medical health (Cumulative Illness Rating Scale) and QoL (Euroqol-5D) by Spearman rank correlations; and predictive validity of IMSA scores with HCU and QoL by (generalized) linear mixed models. Results: Feasibility, face validity, and reliability (Cronbach a = 0.80) were satisfactory. Intraclass correlation coefficient between IMSA and IM total scores was.78 (95% CI =.75-.81). Correlations of the IMSAwith the Short Form 36, Hospital Anxiety and Depression Scale, Cumulative Illness Rating Scale, and Euroqol-5D (convergent validity) were-.65,.15,.28, and-.59, respectively. The IMSA significantly predicted QoL and also HCU (emergency department visits, hospitalization, outpatient visits, and diagnostic examinations) after 3-and 6-month follow-up. Results were comparable between hospital sites, inpatients and outpatients, as well as age groups. Conclusions: The IMSA is a generic and time-efficient method to assess biopsychosocial complexity and to provide guidance for multidisciplinary care trajectories in adult patients, with good reliability and validity across different cultures

    Increased Sympathetic and Decreased Parasympathetic Activity Rather Than Changes in Hypothalamic-Pituitary-Adrenal Axis Activity Is Associated with Metabolic Abnormalities

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    Context: Stress is suggested to lead to metabolic dysregulations as clustered in the metabolic syndrome, but the underlying biological mechanisms are not yet well understood. Objective: We examined the relationship between two main str systems, the autonomic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis, with the metabolic syndrome and its components. Design: Thedesignwasbaseline data (yr 2004-2007) of a prospective cohort: the Netherlands Study of Depression and Anxiety (NESDA). Setting: The study comprised general community, primary care, andspecialized mental health care. Participants: This study included 1883 participants aged 18-65 yr. Main Outcome Measures: Autonomic nervous system measures included heart rate, respiratory sinus arrhythmia (RSA; high RSA reflecting high parasympathetic activity), and preejection period (PEP; high PEP reflecting low sympathetic activity). HPA axis measures included the cortisol awakening response, evening cortisol, and a 0.5 mg dexamethasone suppression test as measured in saliva. Metabolic syndrome was based on the updated Adult Treatment Panel III criteria and included high waist circumference, serum triglycerides, blood pressure, serum glucose, and low high-density lipoprotein cholesterol. Results: RSA and PEP were both independently negatively associated with the presence of the metabolic syndrome, the number of metabolic dysregulations as well as all individual components except high-density lipoprotein cholesterol (all P <0.02). Heart rate was positively related to the metabolic syndrome, the number of metabolic dysregulations, and all individual components (all P <0.001). HPA axis measures were not related to metabolic syndrome or its components. Conclusion: Our findings suggest that increased sympathetic and decreased parasympathetic nervous system activity is associated with metabolic syndrome, whereas HPA axis activity is not. (J Clin Endocrinol Metab 95: 2458-2466, 2010
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