Reactivity to 35% carbon dioxide in bulimia nervosa and panic disorder.

The inhalation of 35% carbon dioxide (CO2) induces panic and anxiety in people with panic disorder (PD) and in people with various other psychiatric disorders. The anxiogenic effect of CO2 in people with eating disorders has received sparse attention despite the fact that PD and bulimia nervosa (BN) have several common psychological and neurobiological features. This study compared CO2-reactivity across three groups of participants: females with BN, females with PD, and female controls without known risk factors for enhanced CO2-reactivity (e.g., social anxiety disorder, first degree relatives with PD). Reactivity was measured by self-reported ratings of panic symptomatology and subjective anxiety, analyzed as both continuous variables (change from room-air to CO2) and dichotomous variables (positive versus negative responses to CO2). Analyses of each outcome measure demonstrated that CO2-reactivity was similar across the BN and PD groups, and reactivity within each of these two groups was significantly stronger than that in the control group. This is the first study to demonstrate CO2-hyperreactivity in individuals with BN, supporting the hypothesis that reactivity to this biological paradigm is not specific to PD. Further research would benefit from examining transdiagnostic mechanisms in CO2-hyperreactivity, such as anxiety sensitivity, which may account for this study's results.

The insomnia and suicide link: toward an enhanced understanding of this relationship.

Despite current knowledge of risk factors for suicidal behaviors, suicide remains a leading cause of death worldwide. This suggests a strong need to identify and understand additional risk factors. A number of recent studies have identified insomnia as a modifiable, independent suicide risk factor. Although a link between insomnia and suicide is emerging, further research is required in order to understand the nature of the relationship. Accordingly, this paper presents an overview of the insomnia and suicide literature to-date, and a discussion of two major limitations within this literature that hinder its progress. First, the classification and assessment of insomnia and suicide-related thoughts and behaviors are inconsistent across studies; and second, there is a lack of empirical studies focused on investigating mediators of the insomnia and suicide relationship. Suggestions are offered within this paper for future studies to address these issues and facilitate new developments in this important research area. Following these suggested lines of research will ultimately inform whether insomnia treatments, particularly cognitive-behavioral therapy for insomnia, can be used to target suicide risk prevention and intervention.

The 35% carbon dioxide test in stress and panic research: overview of effects and integration of findings.

The carbon dioxide test--a vital capacity breath of air containing 35% carbon dioxide (CO(2))--provokes panic attacks in many individuals with panic disorder (PD). It has thus been extensively used as an experimental model of panic and less frequently as a clinical method of provoking symptoms for interoceptive exposure treatment. Recently, stress researchers have suggested another use for the CO(2) test: that of an acute physiological stressor indexing the human stress response. The purpose of this review is to synthesize findings about the effects of the CO(2) test from both the panic and stress literatures in order to advance understanding about this increasingly popular test. Both panic and stress researchers have examined the fleeting effects of the CO(2) test, finding that the test engenders transient breathlessness, dizziness, and minor anxiety in most participants and panic attacks in those with or at risk for PD. Physiological measurements after the test indicate a brief homeostatic disruption in many bodily systems, including increased respiration, systolic blood pressure, and noradrenaline, and decreased heart rate. Most studies indicate increased cortisol. Possible benefits of integrating findings from the panic and stress research lines, given their common use of the CO(2) test, are discussed.

Prepulse inhibition deficits in schizophrenia are modified by smoking status.

BACKGROUND: Schizophrenia is associated with high rates of cigarette smoking and deficits in sensorimotor gating, as measured by prepulse inhibition (PPI) of the startle response. However, the relationship between PPI deficits and smoking status is unclear. We examined whether smoking status modifies PPI deficits in schizophrenia. METHODS: We studied PPI as a function of smoking status and schizophrenia diagnosis in four groups using a cross-sectional design: Smokers with schizophrenia (SS; n=14), non-smokers with schizophrenia (SNS; n=15), control smokers (CS; n=11), and control non-smokers (CNS; n=10). PPI in smokers was recorded under conditions of smoking satiation, and smoking status was verified biochemically. RESULTS: The Diagnosis x Smoking Status x Prepulse Interval interaction was significant (F(11,140)=5.01, p<0.001). At all prepulse to pulse intervals (PPTPIs; 30, 60 and 120 ms), we found that SNS had reductions (~50%; p<0.01) in PPI compared to CNS. However, when SS were compared to CS under conditions of smoking satiation, SS had comparable levels of PPI to CS, and significantly higher levels of PPI than SNS. CONCLUSIONS: Our findings suggest that PPI deficits are present in nonsmokers with schizophrenia, and may be modified by smoking status. Acute smoking in schizophrenia is associated with an elevation of PPI to the levels in non-psychiatric control smokers. These findings have significant implications for understanding vulnerability to tobacco dependence in schizophrenia, which may lead to the development of more effective treatments for PPI deficits and tobacco dependence in this population.