It is unclear if psychiatric morbidity among parents bereaved of a child is related to major loss in general or if the cause of death matters. Whether such a link is consistent with a causal explanation also remains uncertain.

We identified 3 114 564 parents through linkage of Swedish nationwide registers. Risk of psychiatric hospitalization was assessed with log-linear Poisson regression and family-based analyses were used to explore familial confounding.

A total of 3284 suicides and 14 095 any-cause deaths were identified in offspring between 12 and 25 years of age. Parents exposed to offspring suicide had considerably higher risk of subsequent psychiatric hospitalization than unexposed parents [relative risk (RR) 1.90, 95% confidence interval (CI) 1.72–2.09], higher than parents exposed to offspring non-suicide death relative to controls (RR 1.18, 95% CI 1.11–1.26). We found no risk increase among stepfathers differentially exposed to biologically unrelated stepchildren's death or suicide, and the relative risk was notably lower among full siblings differentially exposed to offspring death or suicide.

Parental psychiatric hospitalization following offspring death was primarily found in offspring suicide. Familial (e.g. shared genetic) effects seemed important, judging from both lack of psychiatric hospitalization in bereaved stepfathers and attenuated risk when bereaved parents were contrasted to their non-bereaved siblings. We conclude that offspring suicide does not ‘cause’ psychiatric hospitalization in bereaved parents.

Little is known about suicide risk among offspring of parents hospitalized for schizophrenia and the mechanisms behind this association.

We applied a nested case–control design based on linkage of Swedish population-based registers. Among 12- to 30-year-old offspring, we identified 68 318 offspring with suicidal behavior (attempted and completed suicide) and their parents. Five healthy control–parent pairs were matched to each suicidal case–parent pair and conditional logistic regression used to obtain odds ratios (ORs). Further, to disentangle familial confounding from causal environmental mechanisms, we compared the population-based suicide risk with the risk found within full-cousins and half-cousins differentially exposed to parental schizophrenia.

Offspring of parents with schizophrenia had significantly increased suicide risk after accounting for socio-economic status, parental suicidal behavior and offspring mental illness [OR 1.68, 95% confidence interval (CI) 1.53–1.85]. Suicide risks in offspring of schizophrenic mothers and fathers were similar in magnitude; so were risks across different developmental periods. Importantly, offspring suicide risk remained essentially unchanged across genetically different relationships; offspring of siblings discordant for schizophrenia had equivalent risk increases within full-cousins (OR 1.96, 95% CI 1.66–2.31) and half-cousins (OR 1.69, 95% CI 1.17–2.44).

Parental schizophrenia was associated with increased risk of offspring suicidal behavior, independent of gender of the schizophrenic parent, and persisting into adulthood. The suicide risk in offspring remained at a similar level when comparing genetically different relationships, which suggests that at least part of the association is due to environmental mechanisms. These findings should inspire increased attention to suicidal ideation and prevention efforts in offspring of parents with schizophrenia.

Research suggests that suicidal behaviour is aggregated in families. However, due to methodological limitations, including small sample sizes, the strength and pattern of this aggregation remains uncertain.

We examined the familial clustering of completed suicide in a Swedish total population sample. We linked the Cause of Death and Multi-Generation Registers and compared suicide rates among relatives of all 83 951 suicide decedents from 1952–2003 with those among relatives of population controls.

Patterns of familial aggregation of suicide among relatives to suicide decedents suggested genetic influences on suicide risk; the risk among full siblings (odds ratio 3.1, 95% confidence interval 2.8–3.5, 50% genetic similarity) was higher than that for maternal half-siblings (1.7, 1.1–2.7, 25% genetic similarity), despite similar environmental exposure. Further, monozygotic twins (100% genetic similarity) had a higher risk than dizygotic twins (50% genetic similarity) and cousins (12.5% genetic similarity) had higher suicide risk than controls. Shared (familial) environmental influences were also indicated; siblings to suicide decedents had a higher risk than offspring (both 50% genetically identical but siblings having a more shared environment, 3.1, 2.8–3.5 v. 2.0, 1.9–2.2), and maternal half-siblings had a higher risk than paternal half-siblings (both 50% genetically identical but the former with a more shared environment). Although comparisons of twins and half-siblings had overlapping confidence intervals, they were supported by sensitivity analyses, also including suicide attempts.

Familial clustering of suicide is primarily influenced by genetic and also shared environmental factors. The family history of suicide should be considered when assessing suicide risk in clinical settings or designing and administering preventive interventions.

Etiological theory and prior research with small or selected samples suggest that interpersonal violence clusters in families. However, the strength and pattern of this aggregation remains mostly unknown.

We investigated all convictions for violent crime in Sweden 1973–2004 among more than 12.5 million individuals in the nationwide Multi-Generation Register, and compared rates of violent convictions among relatives of violent individuals with relatives of matched, non-violent controls, using a nested case–control design.

We found strong familial aggregation of interpersonal violence among first-degree relatives [e.g. odds ratio (OR)sibling 4.3, 95% confidence interval (CI) 4.2–4.3], lower for more distant relatives (e.g. ORcousin 1.9, 95% CI 1.9–1.9). Risk patterns across biological and adoptive relations provided evidence for both genetic and environmental influences on the development of violent behavior. Familial risks were stronger among women, in higher socio-economic strata, and for early onset interpersonal violence. There were crime-specific effects (e.g. ORsibling for arson 22.4, 95% CI 12.2–41.2), suggesting both general and subtype-specific familial risk factors for violent behavior.

The observed familiality should be accounted for in criminological research, applied violence risk assessment, and prevention efforts.