Although the ICD and DSM differentiate between different psychiatric disorders, these often share symptoms, risk factors, and treatments. This was a population-based, case–control, sibling study examining familial clustering of all psychiatric disorders and low IQ, using data from the Israel Draft-Board Registry on all Jewish adolescents assessed between 1998 and 2014.

We identified all cases with autism spectrum disorder (ASD, N = 2128), severe intellectual disability (ID, N = 9572), attention-deficit hyperactive disorder (ADHD) (N = 3272), psychotic (N = 7902), mood (N = 9704), anxiety (N = 10 606), personality (N = 24 816), or substance/alcohol abuse (N = 791) disorders, and low IQ (⩾2 SDs below the population mean, N = 31 186). Non-CNS control disorders were adolescents with Type-1 diabetes (N = 2427), hernia (N = 29 558) or hematological malignancies (N = 931). Each case was matched with 10 age-matched controls selected at random from the Draft-Board Registry, with replacement, and for each case and matched controls, we ascertained all full siblings. The main outcome measure was the relative recurrence risk (RRR) of the sibling of a case having the same (within-disorder RRR) or a different (across-disorder RRR) disorder.

Within-disorder RRRs were increased for all diagnostic categories, ranging from 11.53 [95% confidence interval (CI): 9.23–14.40] for ASD to 2.93 (95% CI: 2.80–3.07) for personality disorders. The median across-disorder RRR between any pair of psychiatric disorders was 2.16 (95% CI: 1.45–2.43); the median RRR between low IQ and any psychiatric disorder was 1.37 (95% CI: 0.93–1.98). There was no consistent increase in across-disorder RRRs between the non-CNS disorders and psychiatric disorders and/or low IQ.

These large population-based study findings suggest shared etiologies among most psychiatric disorders, and low IQ.

Personality disorders are prevalent in 6–10% of the population, but their risk for cause-specific mortality is unclear. The aim of the study was to assess the association between personality disorders diagnosed in late adolescence and all-cause as well as cause-specific (cardiovascular-related, external-related) mortality.

We performed a longitudinal study on a historical prospective cohort based on nationwide screening prior to recruitment to the Israeli army. The study participants were 16–19-year-old persons who attended the army screening (medical and cognitive, including screening for psychiatric disorders) between 1967 and 2006. Participants were followed from 1967 till 2011.

The study included 2 051 606 subjects, of whom 1 229 252 (59.9%) were men and 822 354 (40.1%) were women, mean age 17.36 years. There were 55 508 (4.5%) men and 8237 (1.0%) women diagnosed with personality disorders. The adjusted hazard ratio (HRs) for coronary, stroke, cardiovascular, external-related causes and all-cause mortality among men with personality disorders were 1.34 (1.03–1.74), 1.82 (1.20–2.76), 1.45 (1.23–1.71), 1.41 (1.30–1.53) and 1.44 (1.36–1.51), respectively. The absolute rate difference for all-cause mortality was 56.07 and 13.19 per 105 person-years among men and women, respectively. Among women with personality disorders, the adjusted HRs for external-related causes and all-cause mortality were 2.74 (1.87–4.00) and 2.01 (1.56–2.58). Associations were already evident within 10 years of follow-up.

Personality disorder in late adolescence is associated with increased risk of cardiovascular, external- and all-cause mortality. Increased cardiovascular mortality is evident before the age of 40 years and may point to the importance of lifestyle education already in youth.

The association between incarceration and psychiatric disorders has been noted. Yet, existing studies are cross-sectional or examine the risk of recidivism, which has limited the predictive validity of psychiatric disorders as a risk factor for incarceration. To overcome this limitation, this study used a prospective cohort to examine whether psychiatric diagnoses in early adulthood predicted incarceration throughout a 30-year follow-up. It tested the association between psychiatric diagnoses with future incarcerations, their number and durations, controlling for education and ethnic status.

This study merged data from three sources in Israel: a prospective 10-year birth cohort study of young adults aged 25–34, conducted in the 1980s (N = 4914) that included a psychiatric interview; data from the Prison Service, including the cause, number and duration of incarcerations; and from the Vital Statistics Registry on death records.

Multivariate analysis showed that substance-use disorders, antisocial personality and lower levels of education predicted future incarceration, their number and maximum duration. The remainder diagnoses were not significantly associated with future incarceration.

Results limited the prediction of future incarcerations to persons diagnosed with substance use and antisocial personality, and do not support an independent predictive association between additional psychiatric diagnoses and future incarceration.

Previous studies reported an association between advanced paternal age at birth and increased risk for schizophrenia and bipolar disorder. While some hypothesize that this association is caused by de-novo mutations in paternal spermatozoa, others cite factors associated with psycho-social characteristics of fathers who have children at a late age. This study aims to test these hypotheses.

A historical-prospective, population-based cohort study, performed by linking the Israeli Draft Board Registry and the Israeli National Psychiatric Hospitalization Registry (N = 916 439; 4488 with schizophrenia, 883 with bipolar disorder). Odds ratios (OR) and two-sided 95% confidence intervals (CI) were calculated by logistic regression models, using paternal age as predictor and risk for later hospitalizations for schizophrenia or bipolar disorder as outcome measure. Models were first fitted unadjusted, then adjusted for paternal age at birth of the first child.

In the unadjusted model, offspring of fathers aged 45 and above at birth had increased risk of schizophrenia (OR = 1.71, 95% CI 1.49–1.99) and bipolar disorder (OR = 1.63, 95% CI 1.16–2.24). However, taking into account paternal age at birth of first child, advanced paternal age was no longer associated with increased risk of schizophrenia (OR = 0.60, 95% CI 0.48–0.79) or bipolar disorder (OR = 1.03, 95% CI 0.56–1.90).

Controlling for paternal age at birth of the first offspring, advanced paternal age does not predict increased risk for schizophrenia or bipolar disorder. These data indicate that the association between advanced paternal age and having an offspring with schizophrenia and bipolar disorder is likely due to psychos-social factors, or common genetic variation associated with delayed initial fatherhood.

Being a current psychiatric in-patient is one of the strongest statistical risk factors for suicide. It is usually assumed that this strong association is not causal but is a result of the combination of the selection of high-risk patients for admission and the imperfect protection from suicide afforded by psychiatric wards. Logically, a third factor, which is causal, might play a role in the association. It has recently been suggested that adverse experiences in psychiatric units such as trauma, stigma and loss of social role might precipitate some in-patient suicides.

To consider whether there is a causal association between psychiatric hospitalisation and suicide.

We used the framework of Austin Bradford Hill's criteria for assessing causality in epidemiology to consider the possibility that psychiatric hospitalisation might causally contribute to the extent and variation in in-patient suicide rates.

The association between psychiatric hospitalisation and suicide clearly meets five of the nine Hill's criteria (strength of association, consistency, plausibility, coherence and analogy) and partially meets three of the remaining four criteria (gradient of exposure, temporality and experimental evidence).

Admission to hospital itself might play a causal role in a proportion of in-patient suicides. The safety of being in hospital with respect to suicide could be examined with a large-scale randomised controlled trial (RCT). In the absence of an RCT, the possibility of a causal role provides further impetus to calls to make care in the community more available and psychiatric hospitals more acceptable to patients.

Previous work suggests that the association between urbanicity and schizophrenia may be greatest in those with pre-existing vulnerability.

To test for synergism in risk of schizophrenia between population density and a combined exposure of poor premorbid social and cognitive functioning.

For 371 603 adolescent males examined by the Israeli Draft Board on social and cognitive functioning, data on population density of place of residence and later hospitalisation for schizophrenia were obtained from population-based registries.

There was an interaction between population density (five levels) and poor premorbid social and cognitive functioning (interaction χ2=4.6, P=0.032). The adjusted increase in cumulative incidence associated with one unit change in population density was 0.10% in the vulnerable group (95% CI 0.019–0.18, P=0.015), nine times larger than that in the non-vulnerable group (0.011%, 95% CI 0.0017–0.020, P=0.021).

Risk of schizophrenia may increase when people with a genetic liability to the disorder, expressed as poor social and cognitive functioning, need to cope with city life.

The extent of premorbid changes associated with the onset of schizophrenia are debated.

The study examined cognitive and behavioural functioning prior to, and after, first hospitalisation for schizophrenia.

Data from the Israeli Draft Board Register of intelligence, social functioning and behaviour testing for all Israeli males aged 16–17 was linked with data from the National Psychiatric Hospitalisation Case Register. This identified 692 men who had been admitted to hospital for schizophrenia. Cases and non-cases matched on age and school were compared, as were cases aggregated by the time that had elapsed between testing and first admission to hospital.

Cases performed worse than non-cases on all measures. On Social Functioning and on Raven's Progressive Matrices–R, differences between cases and non-cases were progressively greater for cases admitted closer to the time of testing. These differences were greatest for persons tested after first psychiatric hospitalisation.

The results confirm premorbid deficits associated with schizophrenia and support the hypothesis that decline is progressive.