The relation between fetal growth retardation and cardiovascular and metabolic diseases in later life has been demonstrated in many studies. However, debate exists around the potential independent role of postnatal growth acceleration. Furthermore, it is unknown whether a potential effect of growth acceleration on cardiovascular and metabolic function is confined to certain timeframes.

Diagnosis and treatment of children affected by disruptions of attachment (out of home placement, multiple changes of primary caregiver) is an area of considerable controversy. The possible contribution of psychobiological theories is discussed in three parts. The first part relates the attachment theoretical perspective to major psychobiological theories on the developmental associations of parent-child relationships and emotional response. The second part reviews studies of autonomic reactivity and HPA-axis activity with foster children, showing that foster children show more reactivity within physiological systems facilitating fight or flight behaviours rather than social engagement, especially foster children with atypical attachment behaviour. The third part is focused on treatment of children suffering from the consequences of disrupted attachment, based on a psychotherapy study with psychophysiological outcome measures. Implications are discussed for theory, diagnosis, and intervention.

Autonomic underarousal, indicated by low heart rate (HR) and skin conductance level (SCL), is related to childhood aggression. However, results are inconsistent in preschoolers. We assessed HR, SCL, heart rate reactivity and skin conductance reactivity in four-year-old children. Comparisons were made between children with a high level and with a low level of aggressive behavior according to the Child Behavior Checklist 1½–5 as well as between children who were diagnosed with Oppositional Defiant Disorder or Conduct Disorder (ODD/CD) and children with a low level of aggression. Preschool children with a high level of aggressive behavior showed lower SCL and SCR and children with ODD/CD showed lower SCL. In contrast, we did not find lower HR and HRR in preschool children with a high level of aggressive behavior or ODD/CD. Thus, results suggest that decreased SCL, but not HR, is a characteristic of preschool children with aggressive behavior or ODD/CD.

Objective
The idea that distinct psychosocial factors may underlie specific patterns of neuroendocrine stress responses has been a topic of recurrent debate. We examined a recent contribution to this debate, the Social Self Preservation Theory, which predicts that stressors involving social evaluative threat (SET) characteristically activate the hypothalamic-pituitary-adrenal (HPA) axis.

Methods
Sixty-one healthy university students (31 females) performed a challenging speech task in one of three conditions that aimed to impose increasing levels of SET: performing the task alone (no social evaluation), with 1 evaluating observer, or with 4 evaluating observers. Indices of sympathetic (pre-ejection period) and parasympathetic (heart rate variability) cardiac drive were obtained by impedance- and electrocardiography. Salivary cortisol was used to index HPA activity. Questionnaires assessed affective responses.

Results
Affective responses (shame/embarrassment, anxiety, negative affect, and self-esteem), cortisol, heart rate, sympathetic, and parasympathetic activation all differentiated evaluative from non-evaluative task conditions (p<.001). The largest effect-sizes were observed for cardiac autonomic responses. Physiological reactivity increased in parallel with increasing audience size (p<.001). A rise in cortisol was predicted by sympathetic activation during the task (p<.001), but not by affective responses. Conclusion It would appear that SET determines the magnitude, rather than the pattern, of physiological activation. This potential to broadly perturb multiple physiological systems may help explain why social stress has been associated with a range of health outcomes. We propose a threshold-activation model as a physiological explanation for why engaging stressors, such as those involving social evaluation or uncontrollability, may appear to selectively induce cortisol release.

Background
Hostility and anger have been attributed as psychosocial risk factors for coronary heart disease. Heightened cardiovascular reactivity (CVR), and poor recovery, to provocative stressors are thought to hasten this risk.
Purpose
To examine the relationship between hostility and anger inhibition (AI), and the moderating situational influences of harassment and evaluation, in predicting CVR and recovery to mental arithmetic (MA) stress using a multiple regression approach.
Methods
48 male undergraduate students engaged in the following 3 minute tasks during recording of the electrocardiogram, impedance cardiography, and blood pressure: baseline, MA, and evaluation. Hostility and AI were assessed with the Cook-Medley Hostility Scale and the Speilberger Anger In subscale, respectively.
Results
An interaction between hostility and AI showed high diastolic blood pressure reactivity to the MA task among hostile anger inhibitors. Harassment did not modify this effect. However, harasser evaluation predicted prolonged systolic blood pressure (SBP) responding among men scoring high in AI, and facilitated SBP recovery among those scoring low on AI.
Conclusions
The findings highlight the interactive influences of AI and hostility in predicting CVR to stress and underscore the importance of recovery assessments in understanding the potentially pathogenic associations of these constructs.

Objective: 
To determine whether patients with different types of anxiety disorder (panic disorder, social phobia, generalized anxiety disorder) have higher heart rate and lower heart rate variability compared with healthy controls in a sample that was sufficiently powered to examine the confounding effects of lifestyle and antidepressants.
Methods: 
The standard deviation of the normal-to-normal intervals (SDNN), heart rate (HR), and respiratory sinus arrhythmia (RSA) were measured in 2059 subjects (mean age = 41.7 years, 66.8% female) participating in The Netherlands Study of Depression and Anxiety (NESDA). Based on the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) and Composite International Diagnostic Interview (CIDI), NESDA participants were classified as healthy controls (n = 616), subjects with an anxiety diagnosis earlier in life (n = 420), and subjects with current anxiety diagnosis (n = 1059).
Results: 
Current anxious subjects had a significantly lower SDNN and RSA compared with controls. RSA was also significantly lower in remitted anxious subjects compared with controls. These associations were similar across the three different types of anxiety disorders. Adjustment for lifestyle had little impact. However, additional adjustment for antidepressant use reduced all significant associations between anxiety and HRV to nonsignificant. Anxious subjects who used a tricyclic antidepressant, a selective serotonin reuptake inhibitor, or another antidepressant showed significantly lower mean SDNN and RSA compared with controls (effect sizes = 0.20–0.80 for SDNN and 0.42–0.79 for RSA). Nonmedicated anxious subjects did not differ from controls in mean SDNN and RSA.
Conclusion: 
This study shows that anxiety disorders are associated with significantly lower HR variability, but the association seems to be driven by the effects of antidepressants.
ANOVA = analysis of variance;
ANS = autonomic nervous system;
ATC = anatomical therapeutic chemical;
BAI = Beck Anxiety Inventory;
BMI = body mass index;
CIDI = Composite International Diagnostic Interview;
CVD = cardiovascular disease;
dZ = changes in thorax impedance;
ECG = electrocardiogram;
GAD = generalized anxiety disorder;
HR = heart rate;
HRV = heart rate variability;
IBI = inter-beat-interval;
MDD = major depressive disorder;
MET = multiple of one’s resting metabolic rate times minutes of physical activity;
NESDA = The Netherlands Study of Depression and Anxiety;
PD = panic disorder;
pv = peak-valley;
PNS = parasympathetic nervous system;
RR = respiratory rate;
RSA = respiratory sinus arrhythmia;
SDNN = standard deviation of the normal-to-normal interval;
SNS = sympathetic nervous system;
SP = social phobia;
VU-AMS = Vrije Universiteit Ambulatory Monitoring System;
SSRI = selective serotonin reuptake inhibitor;
TCA = tricyclic antidepressant.

The relationships between road and rail traffic noise with pre-ejection period (PEP) and with respiratory sinus arrhythmia (RSA) during sleep, as indices of cardiac sympathetic and parasympathetic nervous system tone, were investigated in the field (36 subjects, with 188 and 192 valid subject nights for PEP and RSA, respectively). Two analyses were conducted. The first analysis investigated the overall relationships across the entire sleep period. A second analysis investigated differences in the relationships between the first and second halves of the sleep period. Separate multilevel linear regression models for PEP and RSA were employed. Potential covariates for each model were selected from the same pool of variables, which included: gender, age, body-mass index, education level, traffic noise source type, intake of medication, caffeine, alcohol and cigarette smoke, and hindrance during sleep due to the ambulatory recordings. RSA models were adjusted for respiration rate. Mean indoor traffic noise exposure was negatively related to mean RSA during the sleep period, specifically during the second half of the sleep period. Both respiration rate and age were negatively associated with RSA. No significant relationships were observed for PEP. The results indicate that higher indoor traffic noise exposure levels may lead to cardiac parasympathetic withdrawal during sleep, specifically during the second half of the sleep period. No effect of indoor traffic noise on cardiac sympathetic tone was observed.

The present study compared blood pressure levels between subjects with clinical anxiety and depressive disorders with healthy controls. Cross-sectional data were obtained in a large cohort study, the Netherlands Study of Depression and Anxiety (N=2981). Participants were classified as controls (N=590) or currently or remittedly depressed or anxious subjects (N=2028), of which 1384 were not and 644 were using antidepressants. Regression analyses calculated the contributions of anxiety and depressive disorders and antidepressant use to diastolic and systolic blood pressures, after controlling for multiple covariates. Heart rate and heart rate variability measures were subsequently added to test whether effects of anxiety/depression or medication were mediated by vagal control over the heart. Higher mean diastolic blood pressure was found among the current anxious subjects (β=0.932; P=0.03), although anxiety was not significantly related to hypertension risk. Remitted and current depressed subjects had a lower mean systolic blood pressure (β=−1.74, P=0.04 and β=−2.35, P=0.004, respectively) and were significantly less likely to have isolated systolic hypertension than controls. Users of tricyclic antidepressants had higher mean systolic and diastolic blood pressures and were more likely to have hypertension stage 1 (odds ratio: 1.90; 95% CI: 0.94 to 3.84; P=0.07) and stage 2 (odds ratio: 3.19; 95% CI: 1.35 to 7.59; P=0.008). Users of noradrenergic and serotonergic working antidepressants were more likely to have hypertension stage 1. This study shows that depressive disorder is associated with low systolic blood pressure and less hypertension, whereas the use of certain antidepressants is associated with both high diastolic and systolic blood pressures and hypertension.