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Title: Basal autonomic activity, stress reactivity, and increases in metabolic syndrome components over time
Author(s): MX Hu, F Lamers, SA Hiles, BW Penninx and JCN de Geus
Journal: Psychoneuroendocrinology
Year: 2016
Month: September
Volume: 71
Pages: 119-26
DOI: 10.1016/j.psyneuen.2016.05.018
File URL: /vuams-pubs/Hu_2016__2_.pdf
Abstract: CONTEXT: Basal autonomic nervous system (ANS) functioning has been linked to the metabolic syndrome (MetS), but the role of ANS reactivity in response to stress remains unclear. OBJECTIVE: To examine cross-sectionally and longitudinally to what extent ANS basal level and stress reactivity are related to MetS. DESIGN: 2-year and 6-year data from a prospective cohort: the Netherlands Study of Depression and Anxiety. SETTING: Participants were recruited from the general community, primary care, and mental health care organizations. PARTICIPANTS: 1922 respondents (mean age=43.7years). MAIN OUTCOME MEASURES: Indicators of ANS functioning were heart rate (HR), respiratory sinus arrhythmia (RSA) and pre-ejection period (PEP). ANS stress reactivity was measured during a cognitively challenging stressor and a personal-emotional stressor. MetS components included triglycerides, high-density lipoprotein cholesterol, blood pressure, glucose and waist circumference. RESULTS: Cross-sectional analyses indicated that higher basal HR, lower basal values of RSA and PEP, and higher RSA reactivity during cognitive challenge were related to less favorable values of almost all individual MetS components. Longitudinal analyses showed that higher basal HR and shorter basal PEP predicted 4-year increase in many MetS abnormalities. Higher RSA stress reactivity during cognitive challenge predicted 4-year increase in number of MetS components. CONCLUSION: Higher basal sympathetic, lower basal parasympathetic activity, and increased parasympathetic withdrawal during stress are associated with multiple MetS components, and higher basal sympathetic activity predicts an increase in metabolic abnormalities over time. These findings support a role for ANS dysregulation in the risk for MetS and, consequently, the development of cardiovascular disease.

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