| 1. |
- Viktorin, Alexander, et al.
(författare)
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The risk of switch to mania in patients with bipolar disorder during treatment with antidepressants alone and in combination with a mood stabilizer
- 2014
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Ingår i: The American Journal of Psychiatry. - Stockholm : Karolinska Institutet, Dept of Medical Epidemiology and Biostatistics. - 0002-9556 .- 0002-953X .- 1535-7228.
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Tidskriftsartikel (refereegranskat)abstract
- Objective: This study examined the risk of antidepressant-induced manic switch in patients with bipolar disorder treated either with antidepressant monotherapy or with an antidepressant in conjunction with a mood stabilizer. Method: Using Swedish national registries, the authors identified 3,240 patients with bipolar disorder who started treatment with an antidepressant and had no antidepressant treatment during the previous year. Patients were categorized into those receiving antidepressant monotherapy and those receiving an antidepressant plus a mood stabilizer. A within-individual design was used to control for confounding by disorder severity, genetic makeup, and early environmental factors. Cox regression analyses conditioned on individual were used to compare the rate of mania 0–3 months and 3–9 months after the start of antidepressant treatment with a preceding non-treatment period. Results: Nearly 35% of the patients were treated with antidepressant monotherapy. The increased risk of treatment-emergent mania was confined to patients on antidepressant monotherapy (hazard ratio=2.83, 95% CI=1.12, 7.19). Among patients treated with a concurrent mood stabilizer, no acute change in risk of mania was observed during the 3 months after the start of antidepressant treatment (hazard ratio=0.79, 95% CI=0.54, 1.15), and a decreased risk was observed during the period 3–9 months after treatment initiation (hazard ratio=0.63, 95% CI=0.42, 0.93). Conclusions: In this national registry study, antidepressant monotherapy was associated with an increased risk of mania. However, no risk of mania was seen in patients receiving an antidepressant while treated with a mood stabilizer. The results highlight the importance of avoiding antidepressant monotherapy in the treatment of bipolar disorder.
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| 2. |
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| 3. |
- Bulik, CM, et al.
(författare)
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The changing "weightscape" of bulimia nervosa
- 2012
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Ingår i: The American journal of psychiatry. - : American Psychiatric Association Publishing. - 1535-7228 .- 0002-953X. ; 169:10, s. 1031-1036
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Tidskriftsartikel (refereegranskat)
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| 4. |
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| 5. |
- Crump, Casey, et al.
(författare)
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Comorbidities and Mortality in Persons With Schizophrenia: A Swedish National Cohort Study
- 2013
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 1535-7228 .- 0002-953X. ; 170:3, s. 324-333
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Schizophrenia is associated with premature mortality, but the specific causes and pathways are unclear. The authors used outpatient and inpatient data for a national population to examine the association between schizophrenia and mortality and comorbidities. Method: This was a national cohort study of 6,097,834 Swedish adults, including 8,277 with schizophrenia, followed for 7 years (2003-2009) for mortality and comorbidities diagnosed in any outpatient or inpatient setting nationwide. Results: On average, men with schizophrenia died 15 years earlier, and women 12 years earlier, than the rest of the population, and this was not accounted for by unnatural deaths. The leading causes were ischemic heart disease and cancer. Despite having twice as many health care system contacts, schizophrenia patients had no increased risk of nonfatal ischemic heart disease or cancer diagnoses, but they had an elevated mortality from ischemic heart disease (adjusted hazard ratio for women, 3.33 [95% CI=2.73-4.05]; for men, 2.20 [95%, CI=1.83-2.65]) and cancer (adjusted hazard ratio for women, 1.71 [95% CI=1.38-2.10; for men, 1.44 [95% CI=1.15-1.80]). Among all people who died from ischemic heart disease or cancer, schizophrenia patients Were less likely than others to have been diagnosed previously with these conditions (for ischemic heart disease, 26.3% compared with 43.7%; for cancer, 73.9% compared with 82.3%). The association between schizophrenia and mortality was stronger among women and the employed. Lack of antipsychotic treatment was also associated with elevated mortality.. Conclusions: Schizophrenia patients had markedly premature mortality, and the leading causes were ischemic heart disease and cancer, which appeared to be under-diagnosed. Preventive interventions should prioritize primary health care tailored to this population, including more effective risk modification and screening for cardiovascular disease and cancer. (Am J Psychiatty 2013; 170:324-333)
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| 6. |
- Cuijpers, Pim, et al.
(författare)
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Interpersonal Psychotherapy for Depression: A Meta-Analysis
- 2011
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Ingår i: AMERICAN JOURNAL OF PSYCHIATRY. - : American Psychiatric Association. - 0002-953X .- 1535-7228. ; 168:6, s. 581-592
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Forskningsöversikt (refereegranskat)abstract
- Objective: Interpersonal psychotherapy (IPT), a structured and time-limited therapy, has been studied in many controlled trials. Numerous practice guidelines have recommended IPT as a treatment of choice for unipolar depressive disorders. The authors conducted a meta-analysis to integrate research on the effects of IPT. Method: The authors searched bibliographical databases for randomized controlled trials comparing IPT with no treatment, usual care, other psychological treatments, and pharmacotherapy as well as studies comparing combination treatment using pharmacotherapy and IPT. Maintenance studies were also included. Results: Thirty-eight studies including 4,356 patients met all inclusion criteria. The overall effect size (Cohens d) of the 16 studies that compared IPT and a control group was 0.63 (95% confidence interval [CI]=0.36 to 0.90), corresponding to a number needed to treat of 2.91. Ten studies comparing IPT and other psychological treatments showed a nonsignificant differential effect size of 0.04 (95% CI=-0.14 to 0.21; number needed to treat=45.45) favoring IPT. Pharmacotherapy (after removal of one outlier) was more effective than IPT (d=-0.19, 95% CI=-0.38 to -0.01; number needed to treat=9.43), and combination treatment was not more effective than IPT alone, although the paucity of studies precluded drawing definite conclusions. Combination maintenance treatment with pharmacotherapy and IPT was more effective in preventing relapse than pharmacotherapy alone (odds ratio=0.37; 95% CI=0.19 to 0.73; number needed to treat=7.63). Conclusions: There is no doubt that IPT efficaciously treats depression, both as an independent treatment and in combination with pharmacotherapy. IPT deserves its place in treatment guidelines as one of the most empirically validated treatments for depression.
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| 7. |
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| 8. |
- Dong, Li, et al.
(författare)
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Effects of the Circadian Rhythm Gene Period 1 (Per1) on Psychosocial Stress-Induced Alcohol Drinking
- 2011
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 0002-953X .- 1535-7228. ; 168:10, s. 1090-1098
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Circadian and stress-response systems mediate environmental changes that affect alcohol drinking. Psychosocial stress is an environmental risk factor for alcohol abuse. Circadian rhythm gene period 1(Per1) is targeted by stress hormones and is transcriptionally activated in corticotropin releasing factor-expressing cells. The authors hypothesized that Per1 is involved in integrating stress response and circadian rhythmicity and explored its relevance to alcohol drinking. Method: In mice, the effects of stress on ethanol intake in mPer1-mutant and wild-type mice were assessed. In humans, single nucleotide polymorphisms (SNPs) in hPer1 were tested for association with alcohol drinking behavior in 273 adolescents and an adult case-control sample of 1,006 alcohol-dependent patients and 1,178 comparison subjects. In vitro experiments were conducted to measure genotype-specific expression and transcription factor binding to hPer1. Results: The mPer1-mutant mice showed enhanced alcohol consumption in response to social defeat stress relative to their wild-type littermates. An association with the frequency of heavy drinking in adolescents with the hPer1 promoter SNP rs3027172 and with psychosocial adversity was found. There was significant interaction between the rs3027172 genotype and psychosocial adversity on this drinking measure. In a confirmatory analysis, association of hPer1 rs3027172 with alcohol dependence was shown. Cortisol-induced transcriptional activation of hPer1 was reduced in human B-lymphoblastoid cells carrying the risk genotype of rs3027172. Binding affinity of the transcription factor Snail1 to the risk allele of the hPer1 SNP rs3027172 was also reduced. Conclusions: The findings indicate that the hPer1 gene regulates alcohol drinking behavior during stressful conditions and provide evidence for underlying neurobiological mechanisms.
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| 9. |
- Epperson, C Neill, et al.
(författare)
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Premenstrual dysphoric disorder: evidence for a new category for DSM-5.
- 2012
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Ingår i: The American journal of psychiatry. - : American Psychiatric Association Publishing. - 1535-7228 .- 0002-953X. ; 169:5, s. 465-75
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Tidskriftsartikel (refereegranskat)abstract
- Premenstrual dysphoric disorder, which affects 2%–5% of premenopausal women, was included in Appendix B of DSMIV, "Criterion Sets and Axes Provided for Further Study." Since then, aided by the inclusion of specific and rigorous criteria in DSM-IV, there has been an explosion of research on the epidemiology, phenomenology, pathogenesis, and treatment of the disorder. In 2009, the Mood Disorders Work Group for DSM-5 convened a group of experts to examine the literature on premenstrual dysphoric disorder and provide recommendations regarding the appropriate criteria and placement for the disorder in DSM-5. Based on thorough review and lengthy discussion, the work group proposed that the information on the diagnosis, treatment, and validation of the disorder has matured sufficiently for it to qualify as a full category in DSM-5. A move to the position of category, rather than a criterion set in need of further study, will provide greater legitimacy for the disorder and encourage the growth of evidence-based research, ultimately leading to new treatments.
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| 10. |
- Gold, Rinat, et al.
(författare)
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Auditory Emotion Recognition Impairments in Schizophrenia : Relationship to Acoustic Features and Cognition
- 2012
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 0002-953X .- 1535-7228. ; 169:4, s. 424-432
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Schizophrenia is associated with deficits in the ability to perceive emotion based on tone of voice. The basis for this deficit remains unclear, however, and relevant assessment batteries remain limited. The authors evaluated performance in schizophrenia on a novel voice emotion recognition battery with well-characterized physical features, relative to impairments in more general emotional and cognitive functioning. Method: The authors studied a primary sample of 92 patients and 73 comparison subjects. Stimuli were characterized according to both intended emotion and acoustic features (e.g., pitch, intensity) that contributed to the emotional percept. Parallel measures of visual emotion-recognition, pitch perception, general cognition, and overall outcome were obtained. More limited measures were obtained in an independent replication sample of 36 patients, 31 age-matched comparison subjects, and 188 general comparison subjects. Results: Patients showed statistically significant large-effect-size deficits in voice emotion recognition (d=1.1) and were preferentially impaired in recognition of emotion based on pitch features but not intensity features. Emotion recognition deficits were significantly correlated with pitch perception impairments both across (r=0.56) and within (r=0.47) groups. Path analysis showed both sensory-specific and general cognitive contributions to auditory emotion recognition deficits in schizophrenia. Similar patterns of results were observed in the replication sample. Conclusions: The results demonstrate that patients with schizophrenia show a significant deficit in the ability to recognize emotion based on tone of voice and that this deficit is related to impairment in detecting the underlying acoustic features, such as change in pitch, required for auditory emotion recognition. This study provides tools for, and highlights the need for, greater attention to physical features of stimuli used in studying social cognition in neuropsychiatric disorders.
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| 11. |
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| 12. |
- Higier, Rachel G, et al.
(författare)
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Enhanced neurocognitive functioning and positive temperament in twins discordant for bipolar disorder
- 2014
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 0002-953X .- 1535-7228. ; 171:11, s. 1191-1198
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Based on evidence linking creativity and bipolar disorder, a model has been proposed whereby factors influencing liability to bipolar disorder confer certain traits with positive effects on reproductive fitness. The authors tested this model by examining key traits known to be associated with evolutionary fitness, namely, temperament and neurocognition, in individuals carrying liability for bipolar disorder. Schizophrenia probands and their co-twins were included as psychiatric controls.METHOD: Twin pairs discordant for bipolar disorder and schizophrenia and control pairs were identified through the Swedish Twin Registry. The authors administered a neuropsychological test battery and temperament questionnaires to samples of bipolar probands, bipolar co-twins, schizophrenia probands, schizophrenia co-twins, and controls. Multivariate mixed-model analyses of variance were conducted to compare groups on temperament and neurocognitive scores.RESULTS: Bipolar co-twins showed elevated scores on a "positivity" temperament scale compared with controls and bipolar probands, while bipolar probands scored higher on a "negativity" scale compared with their co-twins and controls, who did not differ. Additionally, bipolar co-twins showed superior performance compared with controls on tests of verbal learning and fluency, while bipolar probands showed performance decrements across all neurocognitive domains. In contrast, schizophrenia co-twins showed attenuated impairments in positivity and overall neurocognitive functioning relative to their ill proband counterparts.CONCLUSIONS: These findings suggest that supra-normal levels of sociability and verbal functioning may be associated with liability for bipolar disorder. These effects were specific to liability for bipolar disorder and did not apply to schizophrenia. Such benefits may provide a partial explanation for the persistence of bipolar illness in the population.
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| 13. |
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| 14. |
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| 15. |
- Kendler, Kenneth S., et al.
(författare)
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Genetic and Family and Community Environmental Effects on Drug Abuse in Adolescence: A Swedish National Twin and Sibling Study
- 2014
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 1535-7228 .- 0002-953X. ; 171:2, s. 209-217
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Using Swedish nationwide registry data, the authors investigated genetic and environmental risk factors in the etiology of drug abuse by twin sibling modeling. The authors followed up with epidemiological analyses to identify shared environmental influences on drug abuse. Method: Drug abuse was defined using public medical, legal, or pharmacy records. Twin and sibling pairs were obtained from the national twin and genealogical registers. Information about sibling pair residence within the same household, small residential area, or municipality was obtained from Statistics Sweden. The authors predicted concordance for drug abuse by years of co-residence until the older sibling turned 21 and risk for future drug abuse in adolescents living with parental figures as a function of family-level socioeconomic status and neighborhood social deprivation. Results: The best twin sibling fit model predicted substantial heritability for drug abuse in males (55%) and females (73%), with environmental factors shared by siblings operating only in males and accounting for 23% of the variance in liability. For each year of living in the same household, the probability of sibling concordance for drug abuse increased 2%-5%. When not residing in the same household, concordance was predicted from residence in the same small residential area or municipality. Risk for drug abuse was predicted both by family socioeconomic status and neighborhood social deprivation. Controlling for family socioeconomic status, each year of living in a high social deprivation neighborhood increased the risk for drug abuse by 2%. Conclusions: Using objective registry data, the authors found that drug abuse is highly heritable. A substantial proportion of the shared environmental effect on drug abuse comes from community-wide rather than household-level influences. Genetic effects demonstrated in twin studies have led to molecular analyses to elucidate biological pathways. In a parallel manner, environmental effects can be followed up by epidemiological studies to clarify social mechanisms.
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| 16. |
- Kossowsky, J., et al.
(författare)
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The separation anxiety hypothesis of panic disorder revisited : A meta-analysis
- 2013
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association. - 0002-953X .- 1535-7228. ; 170:7, s. 768-781
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Evidence suggests that childhood separation anxiety disorder may be associated with a heightened risk for the development of other disorders in adulthood. The authors conducted a metaanalysis to examine the relationship between childhood separation anxiety disorder and future psychopathology. Method: PubMed, PsycINFO, and Embase were searched for studies published through December 2011. Case-control, prospective, and retrospective cohort studies comparing children with and without separation anxiety disorder with regard to future panic disorder, major depressive disorder, any anxiety disorder, and substance use disorders were included in the analysis. Effects were summarized as pooled odds ratios in a random-effects model. Results: Twenty-five studies met all inclusion criteria (14,855 participants). A metaanalysis of 20 studies indicated that children with separation anxiety disorder weremore likely to develop panic disorder later on (odds ratio=3.45; 95% CI=2.37-5.03). Five studies suggested that a childhood diagnosis of separation anxiety disorder increases the risk of future anxiety (odds ratio=2.19; 95% CI=1.40-3.42). After adjusting for publication bias, the results of 14 studies indicated that childhood separation anxiety disorder does not increase the risk of future depression (odds ratio=1.06; 95% CI=0.78- 1.45). Five studies indicated that childhood separation anxiety disorder does not increase the risk of substance use disorders (odds ratio=1.27; 95% CI=0.80-2.03). Of the subgroup analyses performed, differences in comparison groups and sample type significantly affected odds ratio sizes. Conclusions: A childhood diagnosis of separation anxiety disorder significantly increases the risk of panic disorder and any anxiety disorder. These results support a developmental psychopathology conceptualization of anxiety disorders.
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| 17. |
- Lichtenstein, Paul, et al.
(författare)
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The genetics of autism spectrum disorders and related neuropsychiatric disorders in childhood.
- 2010
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 0002-953X .- 1535-7228. ; 167:11, s. 1357-1363
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Autism spectrum disorders are considered to be among the most heritable mental disorders, a notion based on surprisingly sparse data from small clinical studies. Population-based studies of the heritability of other neuro-psychiatric disorders and comorbidities among them have also been sparse. The authors sought to address both of these issues. Method: Parents of all Swedish 9- and 12-year-old twin pairs born between 1992 and 2000 (N=10,895) were interviewed regarding autism spectrum disorders and associated conditions (response rate, 80%). Concordance rates and structural equation modeling were used for evaluating causes for familial aggregation and overlap between conditions. Results: Monozygotic twins had higher concordance rates than dizygotic twins for autism spectrum disorders, attention defcit hyperactivity disorder (ADHD), developmental coordination disorder, and tic disorder. Genetic effects accounted for 80% (95% CI=29-91) of the variation in liability for autism spectrum disorders, 79% (95% CI=61-88) for ADHD, 70% (95% CI=35-83) for developmental coordination disorder, and 56% (95% CI=37-68) for tic disorder. Among monozygotic co-twins of children with autism spectrum disorders, the probability of having a diagnosis of ADHD was 44%, compared with 15% for dizygotic co-twins. Differences in cross-disorder effects between monozygotic and dizygotic twins were observed for most other comorbidities, and substantial proportions of the genetic variance for autism spectrum disorders was shared with each of the other disorders. Conclusions: Different neuropsychiatric disorders seem to have a common genetic etiology, suggesting caution in the use of diagnostic entities and proband status in efforts to uncover genes predisposing to autism spectrum disorders.
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| 18. |
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| 19. |
- Pomara, Nunzio, et al.
(författare)
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Lower CSF amyloid beta peptides and higher F2-isoprostanes in cognitively intact elderly individuals with major depressive disorder.
- 2012
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Ingår i: The American journal of psychiatry. - : American Psychiatric Association Publishing. - 1535-7228 .- 0002-953X. ; 169:5, s. 523-30
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Tidskriftsartikel (refereegranskat)abstract
- Major depressive disorder is common in the elderly, and symptoms are often not responsive to conventional antidepressant treatment, especially in the long term. Soluble oligomeric and aggregated forms of amyloid beta peptides, especially amyloid beta 42, impair neuronal and synaptic function. Amyloid beta 42 is the main component of plaques and is implicated in Alzheimer's disease. Amyloid beta peptides also induce a depressive state in rodents and disrupt major neurotransmitter systems linked to depression. The authors assessed whether major depression was associated with CSF levels of amyloid beta, tau protein, and F2-isoprostanes in elderly individuals with major depressive disorder and age-matched nondepressed comparison subjects.
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| 20. |
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| 21. |
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| 22. |
- Wicks, S., et al.
(författare)
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Social Risk or Genetic Liability for Psychosis? A Study of Children Born in Sweden and Reared by Adoptive Parents
- 2010
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Ingår i: American Journal of Psychiatry. - : American Psychiatric Association Publishing. - 0002-953X .- 1535-7228. ; 167, s. 1240-1246
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Recent studies suggest a role for social factors during childhood in the later development of schizophrenia. Since social conditions in childhood are closely related to parental psychiatric illness, there is a need to disentangle how genes and social environmental factors interact. Method: A total of 13,163 children born in Sweden between 1955 and 1984 and reared in Swedish adoptive families were linked to the National Patient Register until 2006 regarding admissions for non-affective psychoses, including schizophrenia. Hazard ratios for nonaffective psychoses were estimated in relation to three indicators of socioeconomic position in childhood (household data of the rearing family obtained via linkage to the National Censuses of 1960–1985) and in relation to indicator of genetic liability (biological parental inpatient care for psychosis). In addition, the total Swedish-born population was investigated. Results: Increased risks for nonaffective psychosis were found among adoptees (without biological parental history of psychosis) reared in families with disadvantaged socioeconomic position, which consisted of adoptive parental unemployment (hazard ratio=2.0), single-parent household (hazard ratio=1.2), and living in apartments (hazard ratio=1.3). The risk was also increased among persons with genetic liability for psychosis alone (hazard ratio=4.7). Among those exposed to both genetic liability and a disadvantaged socioeconomic situation in childhood, the risk was considerably higher (hazard ratio=15.0, 10.3, and 5.7 for parental unemployment, single-parent household, and apartment living, respectively). Analyses in the larger population supported these results. Conclusions: The results indicate that children reared in families with a disadvantaged socioeconomic position have an increased risk for psychosis. There was also some support for an interaction effect, suggesting that social disadvantage increases this risk more in children with genetic liability for psychosis.
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| 23. |
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