Testing a hierarchical model of anxiety and depression in adolescents: a tri-level model.

The present study examined the structural relationships among anxiety and depressive symptoms in a sample of high school juniors. The best-fitting structural representation was a tri-level hierarchical arrangement with a broad general factor (general distress), two factors of intermediate breadth (anxious-misery and fears), and five conceptually meaningful, narrow group factors. In accord with the integrative hierarchical model of anxiety and depression, the results supported a structure with a symptom factor central to major depression, and other symptom factors specific to particular anxiety disorders. These group factors displayed significant, unique associations with clinician severity ratings (CSRs) for their respective DSM diagnoses. The hierarchical arrangement demonstrated temporal invariance over a one-year period and configural and partial metric invariance in females and males. Implications for DSM classification and arrangement of anxiety and depressive disorders are discussed as is how present findings help bridge existing research conducted at symptom and diagnostic levels.

Acute HPA axis response to naltrexone differs in female vs. male smokers.

BACKGROUND: Both opioid antagonist administration and cigarette smoking acutely increase hypothalamic-pituitary-adrenal (HPA) axis activity as measured by adrenocorticotropic hormone (ACTH) and cortisol levels. However, male and female smokers may differ in their response to the opioid antagonist naltrexone, which may be partially mediated by sex differences in HPA axis function. Smokers, as a group, have frequently been shown to have HPA axis dysfunction, which may have relevance to the course and maintenance of nicotine dependence. The purpose of this study was to examine possible sex differences in HPA axis function by comparing stress-hormone response to naltrexone within healthy male and female smokers. Additionally, exploratory analyses compared the combined effects of naltrexone and cigarette smoking on hormonal responsivity between the sexes. METHOD: Thirty-eight healthy smokers (22 men) were tested in two separate morning sessions after 12h of smoking abstinence. For women, self-reports of menstrual cycle information were obtained prior to each session (date of last menstruation, cycle length, reproductive phase, etc.). Each participant received 50mg naltrexone or placebo capsule (in random order) and plasma levels of ACTH and cortisol were assessed at regular intervals for several hours. A subgroup of 12 participants underwent a similar, additional session in which they smoked a single cigarette three hours after naltrexone administration. RESULTS: Naltrexone significantly increased ACTH and cortisol levels in women, but not men (DrugxSexxTime, p<0.05). A post hoc analysis suggested that women at an estimated 'high estrogen' phase had a greater cortisol response (DrugxEstrogen level, p<0.05) than those at an estimated 'low estrogen' phase. Exploratory analyses showed that smoking a single cigarette potentiated naltrexone-induced increases in ACTH (p<0.05) and cortisol (p<0.01) in all participants. CONCLUSION: The findings support the hypothesis that women are more sensitive to opioid antagonism at the level of the HPA axis. Although further studies are needed to examine mechanisms underlying these responses, both results may have clinical implications for the use of naltrexone as a treatment for nicotine dependence.

Subtypes of panic attacks: a critical review of the empirical literature.

BACKGROUND: Panic disorder is a heterogeneous disorder, comprising a variety of somatic, physiological, and cognitive symptoms during repeated panic attacks. As a result, considerable data have examined whether panic attacks may be classified into distinct diagnostic or functional subtypes. The aim of this study is to evaluate the existing literature regarding the validity of panic attack subtypes. METHODS: This review focuses on data published since 2000, with the publication of DSM-IV-TR, augmented by replicated data published since 1980, with the publication of DSM-III and subsequently DSM-IV. Published reports evaluating empirical evidence for the validity of panic attack subtypes are reviewed. RESULTS: Five sets of panic symptoms (respiratory, nocturnal, nonfearful, cognitive, and vestibular) have been shown to cluster together at varying degrees of consistency. However, none of these potential subtypes have been associated with sufficient and reliable external validation criteria indicative of functional differences. This apparent lack of findings may be related to methodological inconsistencies or limitations across the reviewed studies. CONCLUSIONS: Although at present the data do not warrant the utility of subtyping, further research aimed at patent gaps in the literature, including clearer operationalization of symptom subtypes, greater use of biological challenge paradigms and physiological and other more objective measures of fear and anxiety, and exploration of subtyping based on biological factors such as genetics, may support the future designation of panic attack subtypes and their ultimate clinical utility.

Tobacco chippers show robust increases in smoking urge after alcohol consumption.

OBJECTIVE AND RATIONALE: Heavy social drinkers often engage in occasional cigarette smoking, especially in the context of consuming large quantities of alcohol. The current study assessed alcohol's effects on smoking urge as a function of alcohol dose and time course in tobacco chippers with heavy social drinking patterns. METHOD: The study assessed 39 chippers who underwent three separate evening sessions. Each subject received a placebo (1% volume alcohol as a taste mask), a low alcohol dose (two to three drinks equivalent), and a high alcohol dose (four to five drinks equivalent) in random order. No smoking was permitted during the sessions and the participants were abstinent from smoking for at least 3 h before arrival. Throughout the session, cigarette craving was assessed by the Brief Questionnaire of Smoking Urges and alcohol response was assessed by the Biphasic Alcohol Effects Scale (BAES). RESULTS: The results showed that alcohol significantly increased cigarette craving in a dose-dependent manner (p<0.001). At the high alcohol dose, craving was heightened during the rising portion of the blood alcohol curve (BAC). There was a strong relationship between BAC and craving for positive reinforcement and this relationship was partially mediated by BAES stimulation, but not sedation. CONCLUSIONS: The findings show that alcohol directly increases smoking urge in chipper smokers. Tobacco chippers may crave cigarettes more during heavier than during lighter drinking bouts, and this effect appears to be driven by heightened stimulation levels rather than as a means to offset alcohol's sedative effects.

Alcohol dose-dependent increases in smoking urge in light smokers.

BACKGROUND: The current study assessed dose-dependent effects of alcohol compared with placebo on ratings of urge to smoke in light smokers. METHODS: Sixteen nonalcoholic social drinker-smokers were tested individually in three separate early evening sessions where they received a placebo (with 1% ethanol as a taste mask), a low-dose (0.4 g/kg) alcoholic beverage, or high-dose (0.8 g/kg) alcoholic beverage administered in random order. Participants refrained from smoking 2 hr before and throughout the entire early evening experimental sessions. Two subfactors of the Brief Questionnaire of Smoking Urges, BQSU; (factor 1, urge to smoke for stimulation; factor 2, urge to smoke to relieve negative mood and withdrawal) were assessed at baseline and again at rising and declining portions of the blood alcohol curve. RESULTS: Both the high and low doses of alcohol significantly increased BQSU factor 1 scores during the rising and declining blood alcohol concentration (BAC) limbs (p < 0.05). Comparisons across doses during both limbs revealed that the high dose significantly increased factor 1 smoking urge compared with the low dose and placebo beverage (p < 0.05, high > low = placebo). Alcohol tended to increase factor 2 scores throughout the BAC curve, but levels were not as increased as factor 1 scores. Finally, there was no significant association between participants' smoking levels and smoking urge ratings during the high- and low-dose sessions. CONCLUSIONS: The results support a dose-dependent alcohol-induced increase in smoking urge in cigarette-deprived light smokers. These smoking urge increases were apparent during the rising limb of the BAC and maintained throughout the declining limb. Smoking urge increases were greater for positive reinforcing effects than for negative reinforcing effects.

Naltrexone attenuates acute cigarette smoking behavior.

This within-subjects, placebo-controlled laboratory study was designed to examine the effects of naltrexone on cigarette response in 44 chronic smokers (23 male, 21 female). Each participant received either 50-mg oral naltrexone or identical placebo during the morning of the session after maintaining overnight abstinence. Subsequently, the participant was administered a smoking cue (holding lit cigarette) to examine craving and associated features of smoking, and instructed to smoke a cigarette 1 h later. This was followed by a smoking interval in which participants could choose to smoke up to four more cigarettes over a 2-h period. Subjective measures (withdrawal, craving, affect, and side effects) and smoking behavior were assessed throughout the session. Naltrexone significantly reduced the total number of choice cigarettes smoked and expired carbon monoxide levels (Ps<.05). Naltrexone significantly increased total side effects, especially for sedation (P<.01). Further, naltrexone significantly increased overall negative affect, and decreased positive affect 1 h after smoking the first cigarette (Ps<.05). However, naltrexone did not affect acute withdrawal or smoking urges. Despite mixed findings, women reported more overall naltrexone-induced withdrawal (P<.05) and side effects (P<.08) compared to men. Although the exact mechanism is unknown, the findings support an opioid antagonist attenuation of smoking behavior.