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INCE THE EARLY 1990S, STUDIES have reported prevalences of major depression between 17% and 27% in hospitalized patients with coronary artery disease (CAD). 1 Most have also demonstrated that depression has a negative cardiac prognostic impact. 2,3 Only 1 large randomized trial, the Enhancing Recovery in Coronary Heart Disease (ENRICHD) study, 4 has tried to determine whether treating depression could improve cardiac prognosis in CAD patients. Although ENRICHD demonstrated that a combination of short-term individual cognitive behavior therapy (CBT) and a selective serotonin reuptake inhibitor (SSRI), when needed, was significantly better than usual care at reducing depressive symptoms over 6 months in depressed or socially iso-For editorial comment see p 411.

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Cholecystokinin-tetrapeptide (CCK-4) and placebo were injected to 11 panic disorder patients. CCK-4 induced a panic attack identical to spontaneous panic attacks in all patients; placebo did not induce any attacks. The role of CCK-4 in anxiety disorders is discussed.

There is evidence for the role of the cholecystokinin (CCK) neurotransmitter system in the neurobiology of panic disorder (PD). 1 The CCK receptor agonist, CCKtetrapeptide (CCK-4) fulfills criteria for a panicogenic agent 1 and there is evidence that PD might be associated with an abnormal function of the CCK system. For example, PD patients show an enhanced sensitivity to CCK-4, and exhibit lower CSF and lymphocyte CCK concentration as compared to healthy controls (reviewed by Bradwejn et al. 2 ). Also, untreated PD patients display an increased CCK-4-induced intracellular Ca 2+ mobilization in T cells relative to treated PD, depression and schizophrenia. 3 The CCK receptors have been classified into two subtypes: CCK-A and CCK-B. We report here a study of polymorphisms in the CCK pre-pro hormone gene (CCK), CCK-AR, and CCK-BR in DSM-IV panic patients (n = 99) vs controls matched for gender and ethnicity. The CCK polymorphism revealed no association with PD. We identified a new polymorphism for the CCK-A receptor gene, and tested it in our sample, with negative results. A single nucleotide polymorphism has been found in the coding region of the CCK-B receptor gene 4 (CCK-BR) and D Collier (personal communication) identified a highly polymorphic dinucleotide (CT) n microsatellite in the 5Ј regulatory region. For the CCK-B receptor gene polymorphism, PD patients showed a significant association. Our genetic dissection of the CCK system thus far suggests that the CCK-B receptor gene variation may contribute to the neurobiology of panic disorder.Non-significant P-values were obtained for the CCK peptide gene (genotype: P = 0.915; allele: P = 0.87) and CCK-A gene (genotype: P = 0.502; allele: P = 0.58) markers. The CCK-B polymorphism showed a significant P-value for association with panic disorder, using our a priori design of grouping alleles into four categories ( 2 = 13.8, 3 d.f., P = 0.004). An analysis using all alleles (see Table 1) was also significant ( 2 = 26.0, 15 d.f., P = 0.038). Simulations using the Monte Carlo method 5 supported this positive association. Panic patients showed an excess of alleles 6 and 7, with odds ratios of 2.3 (95% CI 1.3-3.9) and 1.7 (95% CI 1.0-2.7), respectively. For these two risk alleles, the sum chisquare is 12.38, 2 d.f., P-value 0.002.Our study showed no evidence that panic disorder is associated with the cholecystokinin pre-pro-hormone gene polymorphism, results that are contradictory to the recent study by Wang and colleagues 6 who reported significant findings in two populations. We also developed and examined a DNA polymorphism for CCK-AR (see Methods) and found negative results. We did find evidence supporting an association between PD and CCK-BR, suggesting a role for this gene as a modifying factor in conferring susceptibility to the disorder. In view of the location of the marker in the promoter region, variation in gene expression may cause dysregulation of the CCK system, which could result in a risk factor for panic attacks.A limitation of this study is the use o...

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This study evaluated the validity of the interpersonal model of binge-eating disorder (BED) psychopathology in a clinical sample of women with BED. Data from a cross-sectional sample of 255 women with BED were examined for the direct effects of interpersonal problems on BED symptoms and psychopathology, and indirect effects mediated by negative affect. Structural equation modelling analyses demonstrated that higher levels of interpersonal problems were associated with greater negative affect, and greater negative affect was associated with higher frequency of BED symptoms and psychopathology. There was a significant indirect effect of interpersonal problems on BED symptoms and psychopathology mediated through negative affect. Interpersonal problems may lead to greater BED symptoms and psychopathology, and this relationship may be partially explained by elevated negative affect. The results of the study are the first to provide support for the interpersonal model of BED symptoms and psychopathology in a clinical sample of women.