| 1. |
- Beckley, Amber L., et al.
(författare)
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Association of height and violent criminality : results from a Swedish total population study
- 2014
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 43:3, s. 835-842
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Tidskriftsartikel (refereegranskat)abstract
- Background: Violent criminality is at least moderately heritable, but the mechanisms behind this remain largely unexplained. Height, a highly heritable trait, may be involved but no study has estimated the effect of height on crime while simultaneously accounting for important demographic, biological and other heritable confounders. Methods: We linked nationwide, longitudinal registers for 760 000 men who underwent mandatory military conscription from 1980 through 1992 in Sweden, to assess the association between height and being convicted of a violent crime. We used Cox proportional hazard modelling and controlled for three types of potential confounders: physical characteristics, childhood demographics and general cognitive ability (intelligence). Results: In unadjusted analyses, height had a moderate negative relationship to violent crime; the shortest of men were twice as likely to be convicted of a violent crime as the tallest. However, when simultaneously controlling for all measured confounders, height was weakly and positively related to violent crime. Intelligence had the individually strongest mitigating effect on the height-crime relationship. Conclusions: Although shorter stature was associated with increased risk of violent offending, our analyses strongly suggested that this relationship was explained by intelligence and other confounding factors. Hence, it is unlikely that height, a highly heritable physical characteristic, accounts for much of the unexplained heritability of violent criminality.
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| 2. |
- Chang, Zheng, et al.
(författare)
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Maternal age at childbirth and risk for ADHD in offspring : a population-based cohort study
- 2014
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Ingår i: International Journal of Epidemiology. - Oxford, United Kingdom : Oxford University Press. - 0300-5771 .- 1464-3685. ; 43:6, s. 1815-1824
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Tidskriftsartikel (refereegranskat)abstract
- Background: Women who give birth at younger ages (e.g. teenage mothers) are more likely to have children who exhibit behaviour problems, such as attention-deficit/hyperactivity disorder (ADHD). However, it is not clear whether young maternal age is causally associated with poor offspring outcomes or confounded by familial factors.Methods: The association between early maternal age at childbirth and offspring ADHD was studied using data from Swedish national registers. The sample included all children born in Sweden between 1988 and 2003 (N = 1 495 543), including 30 674 children with ADHD. We used sibling- and cousin-comparisons to control for unmeasured genetic and environmental confounding. Further, we used a children-of-siblings model to quantify the genetic and environmental contribution to the association between maternal age and offspring ADHD.Results: Maternal age at first birth (MAFB) was associated with offspring ADHD. Teenage childbirth (<20 years) was associated with 78% increased risk of ADHD. The association attenuated in cousin-comparison, suggesting unmeasured familial confounding. The children-of-siblings model indicated that the association between MAFB and ADHD was mainly explained by genetic confounding.Conclusions: All children born to mothers who bore their first child early in their reproductive lives were at increased risk of ADHD. The association was mainly explained by genetic factors transmitted from mothers to their offspring that contribute to both age at childbirth and ADHD in offspring. Our results highlight the importance of using family-based designs to understand how early life circumstances affect child development.
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| 3. |
- D'Onofrio, Brian M., et al.
(författare)
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Paternal age at childbearing and offspring psychiatric and academic morbidity
- 2014
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Ingår i: JAMA psychiatry. - Chicago, United States : American Medical Association. - 2168-6238 .- 2168-622X. ; 71:4, s. 432-438
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Tidskriftsartikel (refereegranskat)abstract
- Importance: Advancing paternal age is associated with increased genetic mutations during spermatogenesis, which research suggests may cause psychiatric morbidity in the offspring. The effects of advancing paternal age at childbearing on offspring morbidity remain unclear, however, because of inconsistent epidemiologic findings and the inability of previous studies to rigorously rule out confounding factors.Objective: To examine the associations between advancing paternal age at childbearing and numerous indexes of offspring morbidity.Design, setting and participants: We performed a population-based cohort study of all individuals born in Sweden in 1973-2001 (N = 2,615,081), with subsets of the data used to predict childhood or adolescent morbidity. We estimated the risk of psychiatric and academic morbidity associated with advancing paternal age using several quasi-experimental designs, including the comparison of differentially exposed siblings, cousins, and first-born cousins.Exposure: Paternal age at childbearing.Main outcomes and measures: Psychiatric (autism, attention-deficit/hyperactivity disorder, psychosis, bipolar disorder, suicide attempt, and substance use problem) and academic (failing grades and low educational attainment) morbidity.Results: In the study population, advancing paternal age was associated with increased risk of some psychiatric disorders (eg, autism, psychosis, and bipolar disorders) but decreased risk of the other indexes of morbidity. In contrast, the sibling-comparison analyses indicated that advancing paternal age had a dose-response relationship with every index of morbidity, with the magnitude of the associations being as large or larger than the estimates in the entire population. Compared with offspring born to fathers 20 to 24 years old, offspring of fathers 45 years and older were at heightened risk of autism (hazard ratio [HR] = 3.45; 95% CI, 1.62-7.33), attention-deficit/hyperactivity disorder (HR = 13.13; 95% CI, 6.85-25.16), psychosis (HR = 2.07; 95% CI, 1.35-3.20), bipolar disorder (HR = 24.70; 95% CI, 12.12-50.31), suicide attempts (HR = 2.72; 95% CI, 2.08-3.56), substance use problems (HR = 2.44; 95% CI, 1.98-2.99), failing a grade (odds ratio [OR] = 1.59; 95% CI, 1.37-1.85), and low educational attainment (OR = 1.70; 95% CI, 1.50-1.93) in within-sibling comparisons. Additional analyses using several quasi-experimental designs obtained commensurate results, further strengthening the internal and external validity of the findings.Conclusions and relevance: Advancing paternal age is associated with increased risk of psychiatric and academic morbidity, with the magnitude of the risks being as large or larger than previous estimates. These findings are consistent with the hypothesis that new genetic mutations that occur during spermatogenesis are causally related to offspring morbidity.
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| 4. |
- Kuja-Halkola, Ralf, et al.
(författare)
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Maternal smoking during pregnancy and adverse outcomes in offspring : genetic and environmental sources of covariance
- 2014
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Ingår i: Behavior Genetics. - : Springer. - 0001-8244 .- 1573-3297. ; 44:5, s. 456-467
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Tidskriftsartikel (refereegranskat)abstract
- Maternal smoking during pregnancy (SDP) has been associated with several psychiatric outcomes in the offspring; studies have questioned whether the associations are causal, however. We analyzed all children born in Sweden between 1983 and 2009 to investigate the effect of SDP on multiple indicators of adverse outcomes in three areas: pregnancy outcomes (birth weight, preterm birth and being born small for gestational age), long-term cognitive abilities (low academic achievement and general cognitive ability) and externalizing behaviors (criminal conviction, violent criminal conviction and drug misuse). SDP was associated with all outcomes. Within-family analyses of the pregnancy outcomes were consistent with a causal interpretation as the associations persisted when siblings discordant for SDP were compared. For the cognitive and externalizing outcomes, the results were not consistent with causal effects; when comparing differentially exposed siblings none of the associations remained significant. In quantitative genetic models genetic factors explained the majority of the associations between SDP and cognitive and externalizing outcomes. The results suggest that the associations between SDP in mothers and cognition and externalizing behaviors in their offspring is primarily due to genetic effects that influence the behaviors in both generations.
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| 5. |
- Kuja-Halkola, Ralf
(författare)
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Twin and family studies on the development of cognitive and externalizing problems
- 2014
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Cognitive and externalizing problems are responsible for much personal suffering, as well as large monetary costs for society. Intervention and prevention efforts have often failed in reduction of unwanted behaviors, perhaps due to lack of understanding of the development of these complex traits. Studies on risk factors often treat the associations naively by not considering potential unmeasured common causes of the risk factor and the outcome. These common causes may be shared within families; i.e., the association is subject to familial confounding. Analyses informed of family belonging can help to further the knowledge regarding causality. Therefore, in this thesis, I used existing, and developed novel, methodologies to assess familial confounding. Models to adjust for familial confounding, as well as models identifying sources of familial confounding, were implemented. Further, I developed a genetically sensitive longitudinal design with multiple raters and time-points. In study I, advancing paternal age was associated with offspring violent offending. Advancing paternal age was found to increase the incidence of violent criminal convictions among re-offending offspring when siblings were compared; a result congruent with causal inference. Contrary, and congruent with non-causal inference, advancing paternal age did not increase the probability to ever be convicted a violent criminal offence. Study II identified an association between maternal smoking during pregnancy (SDP) and offspring stress coping in late adolescence. However, the association did not persist when exposure-discordant siblings were compared. This result is compatible with anon-causal interpretation, and suggests that the association is due to familial confounding; other factors shared between siblings accounts for the association. In a quantitative genetic analysis these factors were found to be of genetic origin. Study III continued the investigation of SDP, this time as a risk factor for cognitive outcomes (general cognitive ability and poor academic achievement), externalizing outcomes (criminal convictions, violent criminal convictions, and drug misuse), and pregnancy related outcomes (birth weight, preterm birth, and born small for gestational age). SDP was associated with all outcomes, but within-sibling analyses found that the association persisted only for pregnancy related outcomes, and disappeared for cognitive and externalizing outcomes. Quantitative genetic analyses found that genetics accounted for the majority of the association between SDP and cognitive and externalizing outcomes. In study IV externalizing traits in mid-childhood were found to predict ADHD-like traits in adolescence when pre-existing associations were adjusted for. Further, ADHD- like traits in late adolescence predicted externalizing behavior in young adult age. The two traits were correlated in mid-childhood (age 8-9), and become even more correlated through early (age 13-14) and late (age 16-17) adolescence and young adult age (age 19-20). Stable and new factors accounted for approximately half of the correlation between the traits each, throughout development. Genetic variation explained two thirds of the correlations. In conclusion, advancing paternal age might increase the rate of violent offending among violent re-offenders. SDP does not seem to be causing offspring cognitive and externalizing problems in adolescence and adulthood; the observed associations are better explained by shared genetic factors. Externalizing behavior predicts ADHD early in development, and ADHD predicts externalizing behavior late in development. And, although new sources of covariance arise throughout development, ADHD-like and externalizing traits become even more correlated from childhood to young adulthood.
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| 6. |
- Mosing, Miriam A, et al.
(författare)
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Practice does not make perfect : no causal effect of music practice on music ability
- 2014
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Ingår i: Psychological Science. - : Sage Publications. - 0956-7976 .- 1467-9280. ; 25:9, s. 1795-1803
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Tidskriftsartikel (refereegranskat)abstract
- The relative importance of nature and nurture for various forms of expertise has been intensely debated. Music proficiency is viewed as a general model for expertise, and associations between deliberate practice and music proficiency have been interpreted as supporting the prevailing idea that long-term deliberate practice inevitably results in increased music ability. Here, we examined the associations (rs = .18–.36) between music practice and music ability (rhythm, melody, and pitch discrimination) in 10,500 Swedish twins. We found that music practice was substantially heritable (40%−70%). Associations between music practice and music ability were predominantly genetic, and, contrary to the causal hypothesis, nonshared environmental influences did not contribute. There was no difference in ability within monozygotic twin pairs differing in their amount of practice, so that when genetic predisposition was controlled for, more practice was no longer associated with better music skills. These findings suggest that music practice may not causally influence music ability and that genetic variation among individuals affects both ability and inclination to practice.
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| 7. |
- Sandin, Sven, et al.
(författare)
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The familial risk of autism
- 2014
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Ingår i: Journal of the American Medical Association (JAMA). - Chicago, USA : American Medical Association. - 0098-7484 .- 1538-3598. ; 311:17, s. 1770-1777
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Tidskriftsartikel (refereegranskat)abstract
- Importance: Autism spectrum disorder (ASD) aggregates in families, but the individual risk and to what extent this is caused by genetic factors or shared or nonshared environmental factors remains unresolved.Objective: To provide estimates of familial aggregation and heritability of ASD.Design, setting and participants: A population-based cohort including 2,049,973 Swedish children born 1982 through 2006. We identified 37,570 twin pairs, 2,642,064 full sibling pairs, 432,281 maternal and 445,531 paternal half sibling pairs, and 5,799,875 cousin pairs. Diagnoses of ASD to December 31, 2009 were ascertained.Main outcomes and measures: The relative recurrence risk (RRR) measures familial aggregation of disease. The RRR is the relative risk of autism in a participant with a sibling or cousin who has the diagnosis (exposed) compared with the risk in a participant with no diagnosed family member (unexposed). We calculated RRR for both ASD and autistic disorder adjusting for age, birth year, sex, parental psychiatric history, and parental age. We estimated how much of the probability of developing ASD can be related to genetic (additive and dominant) and environmental (shared and nonshared) factors.Results: In the sample, 14,516 children were diagnosed with ASD, of whom 5689 had autistic disorder. The RRR and rate per 100,000 person-years for ASD among monozygotic twins was estimated to be 153.0 (95% CI, 56.7-412.8; rate, 6274 for exposed vs 27 for unexposed ); for dizygotic twins, 8.2 (95% CI, 3.7-18.1; rate, 805 for exposed vs 55 for unexposed); for full siblings, 10.3 (95% CI, 9.4-11.3; rate, 829 for exposed vs 49 for unexposed); for maternal half siblings, 3.3 (95% CI, 2.6-4.2; rate, 492 for exposed vs 94 for unexposed); for paternal half siblings, 2.9 (95% CI, 2.2-3.7; rate, 371 for exposed vs 85 for unexposed); and for cousins, 2.0 (95% CI, 1.8-2.2; rate, 155 for exposed vs 49 for unexposed). The RRR pattern was similar for autistic disorder but of slightly higher magnitude.We found support for a disease etiology including only additive genetic and nonshared environmental effects. The ASD heritability was estimated to be 0.50 (95% CI, 0.45-0.56) and the autistic disorder heritability was estimated to 0.54 (95% CI, 0.44-0.64).Conclusions and relevance: Among children born in Sweden, the individual risk of ASD and autistic disorder increased with increasing genetic relatedness. Heritability of ASD and autistic disorder were estimated to be approximately 50%. These findings may inform the counseling of families with affected children.
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