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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.
Attention deficit hyperactivity disorder (ADHD) frequently persists into adulthood. Family and twin studies delineate a disorder with strong genetic influences among children and adolescents based on parent- and teacher-reported data but little is known about the genetic and environmental contribution to DSM-IV ADHD symptoms in adulthood. We therefore aimed to investigate the impact of genetic and environmental influences on the inattentive and hyperactive–impulsive symptoms of ADHD in adults.
Twin methods were applied to self-reported assessments of ADHD symptoms from a large population-based Swedish twin study that included data from 15 198 Swedish male and female twins aged 20 to 46 years.
The broad heritability [i.e. A + D, where A is an additive genetic factor and D (dominance) a non-additive genetic factor] was 37% (A = 11%, D = 26%) for inattention and 38% (A = 18%, D = 20%) for hyperactivity–impulsivity. The results also indicate that 52% of the phenotypic correlation between inattention and hyperactivity–impulsivity (r = 0.43) was explained by genetic influences whereas the remaining part of the covariance was explained by non-shared environmental influences. These results were replicated across age strata.
Our findings of moderate broad heritability estimates are consistent with previous literature on self-rated ADHD symptoms in older children, adolescents and adults and retrospective reports of self-rated childhood ADHD by adults but differ from studies of younger children with informant ratings. Future research needs to clarify whether our data indicate a true decrease in the heritability of ADHD in adults compared to children, or whether this relates to the use of self-ratings in contrast to informant data.
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.
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