Faculty Opinions recommendation of A twin study of depression and migraine: evidence for a shared genetic vulnerability.

SynopsisIn a population based sample of 2163 personally interviewed female twins, substantial comorbidity was observed between DSM-III-R defined major depression (MD) and 4 subtypes of phobia: agoraphobia, social phobia, animal phobia and situational phobia. However, the level of comorbidity of MD with agoraphobia was much greater than that found with the other phobic subtypes. We conducted bivariate twin analyses to decompose the genetic and environmental sources of comorbidity between MD and the phobias. Our results suggest that a modest proportion of the genetic vulnerability to MD also influences the risk for all phobic subtypes, with the possible exception of situational phobias. Furthermore, the magnitude of comorbidity resulting from this shared genetic vulnerability is similar across the phobic subtypes. By contrast, the non-familial environmental experiences which predispose to depression substantially increase the vulnerability to agoraphobia, have a modest impact on the risk for social and situational phobias and no effect on the risk for animal phobias. The increased comorbidity between MD and agoraphobia results, nearly entirely, from individual-specific environmental risk factors for MD which also increase the risk for agoraphobia but not for other phobias.

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No evidence of associations between genetic liability for schizophrenia and development of cannabis use disorder

Psychological Medicine ◽

10.1017/s0033291719003362 ◽

2019 ◽

pp. 1-6 ◽

Cited By ~ 2

Author(s):

Carsten Hjorthøj ◽

Md Jamal Uddin ◽

Theresa Wimberley ◽

Søren Dalsgaard ◽

David M. Hougaard ◽

...

Keyword(s):

Standard Deviation ◽

Psychiatric Disorders ◽

Strong Predictor ◽

Autism Spectrum ◽

Cannabis Use ◽

Risk Scores ◽

Cannabis Use Disorder ◽

Standard Deviation Increase ◽

Genetic Vulnerability ◽

Shared Genetic

Abstract Background Cannabis use and cannabis use disorder (CUD) is increased in patients with schizophrenia. It is important to establish if this is explained by non-causal factors, such as shared genetic vulnerability. We aimed to investigate whether the polygenic risk scores (PRS) for schizophrenia and other psychiatric disorders would predict CUD in controls, patients with schizophrenia, and patients with other psychiatric disorders. Methods We linked nationwide Danish registers and genetic information obtained from dried neonatal bloodspots in an observational analysis. We included people with schizophrenia, other psychiatric disorders, and controls. The exposures of interest were the PRS for schizophrenia, attention-deficit hyperactivity disorder (ADHD) autism spectrum disorder, and anorexia nervosa. The main outcome of interest was the diagnosis of CUD. Results The study included 88 637 individuals. PRS for schizophrenia did not predict CUD in controls [hazard ratio (HR) = 1.16, 95% CI 0.95–1.43 per standard-deviation increase in PRS, or HR = 1.47, 95% CI 0.72–3.00 comparing highest v. remaining decile], but PRS for ADHD did (HR = 1.27, 95% CI 1.08–1.50 per standard-deviation increase, or HR = 2.02, 95% CI 1.27–3.22 for the highest decile of PRS). Among cases with schizophrenia, the PRS for schizophrenia was associated with CUD. While CUD was a strong predictor of schizophrenia (HR = 4.91, 95% CI 4.36–5.53), the inclusion of various PRS did not appreciably alter this association. Conclusion The PRS for schizophrenia was not associated with CUD in controls or patients with other psychiatric disorders than schizophrenia. This speaks against the hypothesis that shared genetic vulnerability would explain the association between cannabis and schizophrenia.

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Tobacco smoking and schizophrenia: re-examining the evidence

BJPsych Advances ◽

10.1192/bja.2019.33 ◽

2019 ◽

Vol 25 (6) ◽

pp. 363-372

Author(s):

Amila Isuru ◽

Mahesh Rajasuriya

Keyword(s):

Risk Factor ◽

Nicotine Dependence ◽

Tobacco Smoking ◽

Mental Illnesses ◽

The Self ◽

List Type ◽

Self Medication ◽

Genetic Vulnerability ◽

Shared Genetic

SUMMARYTobacco smoking among people with mental illnesses can be explained by biological, psychological and social factors. The prevalence of smoking in people diagnosed with schizophrenia is higher than in people with other mental disorders and in the general population. This article explores three current hypotheses that explain this higher prevalence of smoking in schizophrenia. The first, the self-medication hypothesis, is increasingly countered by a growing body of evidence indicating that smokers experience more severe symptoms of schizophrenia. Numerous researchers have already identified smoking as a possible risk factor for the development of schizophrenia, which is the second hypothesis. The third hypothesis (shared genetic vulnerability) identifies certain genes that confer vulnerability for both schizophrenia and nicotine dependence. Understanding the reasons behind the higher prevalence of smoking among people with schizophrenia is vital in planning effective primary, secondary and tertiary smoking prevention for these individuals.LEARNING OBJECTIVESAt the end of this article, readers will be able to: •understand the self-medication hypothesis in relation to tobacco smoking by people with schizophrenia•understand the role of tobacco smoking as a possible risk factor for causation of schizophrenia•understand the role of shared genetic vulnerability in the causation of both schizophrenia and nicotine dependence.

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