Socially explosive minds: the triple imbalance hypothesis of reactive aggression.

The psychobiological basis of reactive aggression, a condition characterized by uncontrolled outbursts of socially violent behavior, is unclear. Nonetheless, several theoretical models have been proposed that may have complementary views about the psychobiological mechanisms involved. In this review, we attempt to unite these models and theorize further on the basis of recent data from psychological and neuroscientific research to propose a comprehensive neuro-evolutionary framework: The Triple Imbalance Hypothesis (TIH) of reactive aggression. According to this model, reactive aggression is essentially subcortically motivated by an imbalance in the levels of the steroid hormones cortisol and testosterone (Subcortical Imbalance Hypothesis). This imbalance not only sets a primal predisposition for social aggression, but also down-regulates cortical-subcortical communication (Cortical-Subcortical Imbalance Hypothesis), hence diminishing control by cortical regions that regulate socially aggressive inclinations. However, these bottom-up hormonally mediated imbalances can drive both instrumental and reactive social aggression. The TIH suggests that reactive aggression is differentiated from proactive aggression by low brain serotonergic function and that reactive aggression is associated with left-sided frontal brain asymmetry (Cortical Imbalance Hypothesis), especially observed when the individual is socially threatened or provoked. This triple biobehavioral imbalance mirrors an evolutionary relapse into violently aggressive motivational drives that are adaptive among many reptilian and mammalian species, but may have become socially maladaptive in modern humans.

Should neonates sleep alone?

BACKGROUND: Maternal-neonate separation (MNS) in mammals is a model for studying the effects of stress on the development and function of physiological systems. In contrast, for humans, MNS is a Western norm and standard medical practice. However, the physiological impact of this is unknown. The physiological stress-response is orchestrated by the autonomic nervous system and heart rate variability (HRV) is a means of quantifying autonomic nervous system activity. Heart rate variability is influenced by level of arousal, which can be accurately quantified during sleep. Sleep is also essential for optimal early brain development. METHODS: To investigate the impact of MNS in humans, we measured HRV in 16 2-day-old full-term neonates sleeping in skin-to-skin contact with their mothers and sleeping alone, for 1 hour in each place, before discharge from hospital. Infant behavior was observed continuously and manually recorded according to a validated scale. Cardiac interbeat intervals and continuous electrocardiogram were recorded using two independent devices. Heart rate variability (taken only from sleep states to control for level of arousal) was analyzed in the frequency domain using a wavelet method. RESULTS: Results show a 176% increase in autonomic activity and an 86% decrease in quiet sleep duration during MNS compared with skin-to-skin contact. CONCLUSIONS: Maternal-neonate separation is associated with a dramatic increase in HRV power, possibly indicative of central anxious autonomic arousal. Maternal-neonate separation also had a profoundly negative impact on quiet sleep duration. Maternal separation may be a stressor the human neonate is not well-evolved to cope with and may not be benign.

Guilt and pride are heartfelt, but not equally so.

We examined the cardiovascular physiology of guilt and pride to elucidate physiological substrates underpinning the behavioral motivations of these moral emotions. Although both emotions motivate prosocial behavior, guilt typically inhibits ongoing behavior, whereas pride reinforces current behavior. To succeed in eliciting real emotions, we used a novel social interaction task. We found dissociable sympathetic activation during guilt and pride; specifically, Guilt participants experienced prolonged cardiac sympathetic arousal as measured by preejection period (PEP), whereas Pride participants experienced transient non-cardiac somatic arousal and a shift to low frequency (LF) power in the cardiac spectrogram. This dissociation supports their distinctive motivational functions. Higher self-reported Behavioral Inhibition System (BIS) sensitivity was furthermore uniquely associated with guilt, supporting its function as a punishment cue.

Gray's BIS/BAS dimensions in non-comorbid, non-medicated social anxiety disorder.

Gray's behavioural inhibition and behavioural activation (BIS/BAS) neural systems model has led to research on approach and withdrawal as the two most fundamental dimensions of affective behaviour, and their role in psychopathology. Although Gray proposed the BIS as the neurological basis of anxiety, there are no reports examining approach and withdrawal predispositions in social anxiety disorder. Here we report approach and withdrawal predispositions in a group of 23 non-medicated individuals with social anxiety disorder (SAD) without co-morbid depression and in 48 normal controls. Results show increased BIS and decreased BAS fun-seeking in SAD subjects thereby underscoring Gray's dimensional model.

Behavioral inhibition: a neurobiological perspective.

Behavioral inhibition (BI) during early childhood has been associated with subsequent development of anxiety disorders. However, understanding of the neuroanatomical substrates of BI in humans generally has not kept pace with that of anxiety disorders. Recent interpretations and implementations of Gray's and Kagan's concepts of BI are examined from the perspective of current neurobiological models. Particular attention is given to evidence pointing to conceptual and operational limitations of self-report scales purported to measure trait BI in adults, and especially to inconsistent correlations between such behavioral inhibition system (BIS) scores and amygdala and autonomic responses to fear- or startle-inducing stimuli. Evidence showing a dissociation of both BI and trait anxiety from the amygdala is considered. Possible reasons for the poor association between BIS and trait anxiety self-report scale scores and predicted physiological outputs of the BIS are identified. Reasons to distinguish between the neural bases of BI as against trait anxiety also are discussed. The need to critically examine the role of the amygdala in BI and trait anxiety, as well as to consider other brain areas that appear to be involved in subserving these emotional traits, is emphasized.

Rapid, simple, and accurate method for measurement of VFA and carbonate alkalinity in anaerobic reactors.

This paper presents a new simple, rapid, and accurate method suitable for on-site measurement of volatile fatty acids (VFA) and carbonate alkalinity in anaerobic reactors. This titrimetric method involves eight pH observations, and typically, the full procedure takes approximately 15 min. An important feature of the method is a built-in quality control mechanism allowing the user a rapid means of assessing the reliability of the experimental procedure. To evaluate the accuracy of the method, both laboratory-made waters and industrial UASB effluent were tested. High accuracy for both VFA and carbonate alkalinity measurements (error within 2% and 1%, respectively) plus good repetition (average standard deviation of 6.7% and 1.45%, respectively) was obtained. The method takes into account the effects of the phosphate, ammonium, and sulfide weak acid subsystems. Appraisal of the effect of an input error in these subsystems revealed that VFA measurement is fairly insensitive to phosphate and ammonium concentrations. It is, however, sensitive to H2S loss during titration where the sulfide concentration is higher than approximately 10 mg/Las S. With regard to the carbonate alkalinity measurement, error in concentration of either phosphate or sulfide or H2S loss might result in a significant error. Short guidelines for correct execution of the method are given in an appendix.