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.

Objectives 
It remains unclear whether depressive and anxiety disorders are associated with hyporeactivity or hyperreactivity of the autonomic nervous system (ANS) and whether deviant reactivity occurs in all types of stressors. This study compared ANS reactivity in people with current or remitted depression/anxiety with reactivity in healthy controls during two stress conditions.
Methods 
From the Netherlands Study of Depression and Anxiety, data of 804 individuals with current depression/anxiety, 913 individuals with remitted depression/anxiety, and 466 healthy controls (mean age = 44.1 years; 66.4% female) were available. Two conditions were used to evoke stress: a) an n-back task, a cognitively challenging stressor, and 2) a psychiatric interview, evoking personal-emotional stress related to the occurrence of symptoms of depression/anxiety. Indicators of ANS activity were heart rate (HR), root mean square of differences between successive interbeat intervals (RMSSD), respiratory sinus arrhythmia (RSA), and preejection period.
Results 
As compared with controls, participants with psychopathology had significant hyporeactivity of HR (controls = 4.1 ± 4.2 beats/min; remitted = 3.5 ± 3.5 beats/min; current psychopathology = 3.1 ± 3.4 beats/min), RMSSD (controls = −6.2 ± 14.5 milliseconds; remitted = −5.4 ± 17.8 milliseconds; current psychopathology = −3.5 ± 15.4 milliseconds), and RSA (controls = −9.3 ± 17.0 milliseconds; remitted = −7.4 ± 16.5 milliseconds; current psychopathology = −6.9 ± 15.0 milliseconds) during the n-back task. In contrast, during the psychiatric interview, they showed significant hyperreactivity of HR (controls = 2.7 ± 3.4 beats/min; remitted = 3.5 ± 3.4 beats/min; current psychopathology = 4.0 ± 3.3 beats/min), RMSSD (controls = −3.4 ± 12.2 milliseconds; remitted = −4.1 ± 12.1 milliseconds; current psychopathology = −5.6 ± 11.8 milliseconds), and RSA (controls = −3.8 ± 8.1 milliseconds; remitted = −4.3 ± 7.9 milliseconds; current psychopathology = −5.0 ± 7.9 milliseconds). The lack of group differences in preejection period reactivity suggests that the found effects were driven by altered cardiac vagal reactivity in depression/anxiety.
Conclusions 
The direction of altered ANS reactivity in depressed/anxious patients is dependent on the type of stressor, and only the more ecologically valid stressors may evoke hyperreactivity in these patients.

Objectives
This study determined temporal stability of ambulatory measured cardiac autonomic activity for different time periods and investigated potential drivers of changes in this activity.
Methods
Data was drawn from baseline (n=2379), 2-year (n=2245), and 6-year (n=1876) follow-up from the Netherlands Study of Depression and Anxiety. Cardiac autonomic activity was measured with heart rate (HR), respiratory sinus arrhythmia (RSA) and pre-ejection period (PEP). Autonomic temporal stability was determined across 2, 4, and 6year intervals. We subsequently examined the association between sociodemographics, lifestyle, mental health, cardiometabolic health, and the use of antidepressant and cardiac medication with change in cardiac autonomic activity.
Results
Over 2years, stability was good for HR (ICC=0.703), excellent for RSA (ICC=0.792) and moderate for PEP (ICC=0.576). Stability decreased for a 4- (HR ICC=0.688, RSA ICC=0.652 and PEP ICC=0.387) and 6-year interval (HR ICC=0.633, RSA ICC=0.654 and PEP ICC=0.355). The most important determinants for increase in HR were (increase in) smoking, increase in body mass index (BMI) and (starting) the use of antidepressants. Beta-blocking/antiarrhythmic drug use led to a decrease in HR. Decrease in RSA was associated with age, smoking and (starting) antidepressant use. Decrease in PEP was associated with age and (increase in) BMI.
Conclusions
Cardiac autonomic measures were rather stable over 2years, but stability decreased with increasing time span. Determinants contributing to cardiac autonomic deterioration were older age, (increase in) smoking and BMI, and (starting) the use of antidepressants. (Starting) the use of cardiac medication improved autonomic function.

Background
Antidepressant medication and running therapy are both effective treatments for patients with depressive and anxiety disorders. However, they may work through different pathophysiological mechanisms and could differ in their impact on physical health. This study examined effects of antidepressants versus running therapy on both mental and physical health.
Methods
According to a partially randomized patient preference design, 141 patients with depression and/or anxiety disorder were randomized or offered preferred 16-week treatment: antidepressant medication (escitalopram or sertraline) or group-based running therapy ≥2 per week. Baseline (T0) and post-treatment assessment at week 16 (T16) included mental (diagnosis status and symptom severity) and physical health indicators (metabolic and immune indicators, heart rate (variability), weight, lung function, hand grip strength, fitness).
Results
Of the 141 participants (mean age 38.2 years; 58.2 % female), 45 participants received antidepressant medication and 96 underwent running therapy. Intention-to-treat analyses showed that remission rates at T16 were comparable (antidepressants: 44.8 %; running: 43.3 %; p = .881). However, the groups differed significantly on various changes in physical health: weight (d = 0.57; p = .001), waist circumference (d = 0.44; p = .011), systolic (d = 0.45; p = .011) and diastolic (d = 0.53; p = .002) blood pressure, heart rate (d = 0.36; p = .033) and heart rate variability (d = 0.48; p = .006).
Limitations
A minority of the participants was willing to be randomized; the running therapy was larger due to greater preference for this intervention.
Conclusions
While the interventions had comparable effects on mental health, running therapy outperformed antidepressants on physical health, due to both larger improvements in the running therapy group as well as larger deterioration in the antidepressant group.
Trial registration
Trialregister.nl Number of identification: NTR3460.

Objectives: Cardiac repolarization may be affected by psychiatric disorders and/or antidepressant use, but evidence for this is inconclusive. This study examined the relationship between depressive and anxiety disorder and use of antidepressants with T-wave amplitude (TWA) and QT-interval.Methods: Data was obtained from the Netherlands Study of Depression and Anxiety (n = 1,383). Depression/anxiety was diagnosed with the DSM-IV based Composite International Diagnostic Interview. The use of tricyclic antidepressants (TCAs), selective serotonin and noradrenalin reuptake inhibitors (SNRIs), and selective serotonin reuptake inhibitors (SSRIs) was established. T-wave amplitude and QT-interval corrected for heart rate (QTc) were obtained from an ECG measured in a type II axis configuration.Results: Compared to controls, persons with depression or anxiety disorders did not show a significantly different TWA (p = 0.58; Cohen’s d = 0.046) or QTc (p = 0.48; Cohen’s d = −0.057). In spite of known sympathomimetic effects, TCA use (p = 0.26; Cohen’s d = −0.162) and SNRI use (p = 0.70; Cohen’s d = −0.055) were not significantly associated with a lower TWA. TCA use (p = 0.12; Cohen’s d = 0.225) and SNRI use (p = 0.11; Cohen’s d = 0.227) were also not significantly associated with a prolonged QTc.Conclusion: We did not find evidence that either depressive/anxiety disorder or antidepressant use is associated with abnormalities in TWA or QTc. Earlier found sympathomimetic effects of TCAs and SNRIs are not evident in these measures of cardiac repolarization.