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  • 1
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  European Journal of Public Health Vol. 32, No. 6 ( 2022-11-29), p. 933-938
    In: European Journal of Public Health, Oxford University Press (OUP), Vol. 32, No. 6 ( 2022-11-29), p. 933-938
    Abstract: Parental substance abuse (SA) of alcohol and drugs is associated with offspring mortality, including sudden infant death syndrome (SIDS), in infancy, but research on cause-specific mortality and mortality in later childhood is scarce. Methods Using population-based register data on all births in Sweden in 1973–2013 (N = 4.2 million) and Cox regressions, we examined the associations of mother’s and father’s SA registered between 2 years before and 12 years after the child birth with offspring all-cause and cause-specific mortality in infancy and childhood. Results Parental SA was associated with increased offspring all-cause and natural-cause mortality in infancy, but not in the neonatal period, and with external-cause mortality in ages 1–9. Risk of SIDS was 130–280% higher in infants with parental SA compared to infants with no parental SA. Adjusting for parental socioeconomic and immigrant status and severe psychiatric disorders, paternal SA was associated with 66% higher mortality due to communicable diseases and infections in infancy, and both maternal and paternal SA were associated with 40–174% higher mortality due to accidents in infancy and in ages 1–9. The associations between parental SA and offspring mortality were similar for male and female offspring. Conclusions Child mortality is rare in contemporary Sweden, and parental SA has variable associations with elevated offspring mortality throughout the first 10 years of life, excluding the neonatal period, which is indicative of insufficient recognition of children at risk. Preventive measures should be long-term and targeted to both parental and offspring behaviour.
    Type of Medium: Online Resource
    ISSN: 1101-1262 , 1464-360X
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2033525-8
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  • 2
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 182, No. 5 ( 2020-05), p. 473-480
    Abstract: Co-aggregation of autoimmune diseases is common, suggesting partly shared etiologies. Genetic factors are believed to be important, but objective measures of environmental vs heritable influences on co-aggregation are absent. With a novel approach to twin studies, we aimed at estimating heritability and genetic overlap in seven organ-specific autoimmune diseases. Design Prospective twin cohort study. Methods We used a cohort of 110 814 twins to examine co-aggregation and heritability of Hashimoto’s thyroiditis, atrophic gastritis, celiac disease, Graves’ disease, type 1 diabetes, vitiligo and Addison’s disease. Hazard ratios (HR) were calculated for twins developing the same or different disease as compared to their co-twin. The differences between monozygotic and dizygotic twin pairs were used to estimate the genetic influence on co-aggregation. Heritability for individual disorders was calculated using structural equational modeling adjusting for censoring and truncation of data. Results Co-aggregation was more pronounced in monozygotic twins (median HR: 3.2, range: 2.2–9.2) than in dizygotic twins (median HR: 2.4, range: 1.1–10.0). Heritability was moderate for atrophic gastritis (0.38, 95% CI: 0.23–0.53) but high for all other diseases, ranging from 0.60 (95% CI: 0.49–0.71) for Graves’ disease to 0.97 (95% CI: 0.91–1.00) for Addison’s disease. Conclusions Overall, co-aggregation was more pronounced in monozygotic than in dizygotic twins, suggesting that disease overlap is largely attributable to genetic factors. Co-aggregation was common, and twins faced up to a ten-fold risk of developing diseases not present in their co-twin. Our results validate and refine previous heritability estimates based on smaller twin cohorts.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 1485160-X
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  • 3
    In: Schizophrenia Bulletin, Oxford University Press (OUP), Vol. 43, No. suppl_1 ( 2017-03-01), p. S8-S9
    Type of Medium: Online Resource
    ISSN: 0586-7614 , 1745-1701
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2017
    detail.hit.zdb_id: 2180196-4
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2020
    In:  Social Cognitive and Affective Neuroscience Vol. 15, No. 4 ( 2020-06-23), p. 423-436
    In: Social Cognitive and Affective Neuroscience, Oxford University Press (OUP), Vol. 15, No. 4 ( 2020-06-23), p. 423-436
    Abstract: A female advantage in social cognition (SoC) might contribute to women’s underrepresentation in autism spectrum disorder (ASD). The latter could be underpinned by sex differences in social brain structure. This study investigated the relationship between structural social brain networks and SoC in females and males in relation to ASD and autistic traits in twins. We used a co-twin design in 77 twin pairs (39 female) aged 12.5 to 31.0 years. Twin pairs were discordant or concordant for ASD or autistic traits, discordant or concordant for other neurodevelopmental disorders or concordant for neurotypical development. They underwent structural magnetic resonance imaging and were assessed for SoC using the naturalistic Movie for the Assessment of Social Cognition. Autistic traits predicted reduced SoC capacities predominantly in male twins, despite a comparable extent of autistic traits in each sex, although the association between SoC and autistic traits did not differ significantly between the sexes. Consistently, within-pair associations between SoC and social brain structure revealed that lower SoC ability was associated with increased cortical thickness of several brain regions, particularly in males. Our findings confirm the notion that sex differences in SoC in association with ASD are underpinned by sex differences in brain structure.
    Type of Medium: Online Resource
    ISSN: 1749-5016 , 1749-5024
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2236933-8
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  • 5
    In: Nephrology Dialysis Transplantation, Oxford University Press (OUP), Vol. 33, No. suppl_1 ( 2018-05-01), p. i45-i45
    Type of Medium: Online Resource
    ISSN: 0931-0509 , 1460-2385
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 1465709-0
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  • 6
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2019
    In:  International Journal of Epidemiology Vol. 48, No. 3 ( 2019-06-01), p. 926-933
    In: International Journal of Epidemiology, Oxford University Press (OUP), Vol. 48, No. 3 ( 2019-06-01), p. 926-933
    Abstract: Smoking and use of Swedish smokeless tobacco (snus) are associated with increased risk of type 2 diabetes (T2D). Our aim was to estimate the unique and shared genetic components of these traits and to what extent the association is explained by shared genetic factors. Methods We used twins of the Swedish Twin Registry who responded to a questionnaire between 1998 and 2006 (n = 40 247) and were followed until 2015 in the National Prescription and Patient Registries. We estimated hazard ratios (HRs) and odds ratios (ORs) for the association between smoking/snus use and T2D (n = 2130) and used structural equation models to estimate genetic and environmental variance components and genetic correlations. Results Current smokers [HR 1.69, 95% confidence interval (CI), 1.49–1.92] and snus users (HR 1.19, 95% CI 1.01–1.41) had an increased risk of T2D. In within-pair analyses of monozygotic twins, corresponding ORs were 1.36, 95% CI 0.75–2.46 (smoking) and 1.54, 95% CI 0.80–2.99 (snus). Heritability was 43% (95% CI 36–51) for ever smoking, 58% (95% CI 44– 70) for ever snus use and 66% (95% CI 59–72) for T2D. The genetic correlation with T2D was 18% (95% CI 1–35) for smoking and –6% (95% CI –24 to 4) for snus use, indicating that only a small fraction of the genetic influence is shared. Conclusions We could confirm that consumers of snus and cigarettes are at increased risk of T2D. Both snus use and smoking have strong genetic components, which appears to be attributable primarily to genes that are distinct from those promoting T2D.
    Type of Medium: Online Resource
    ISSN: 0300-5771 , 1464-3685
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1494592-7
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  • 7
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2014
    In:  Brain Vol. 137, No. 7 ( 2014-07), p. e288-e288
    In: Brain, Oxford University Press (OUP), Vol. 137, No. 7 ( 2014-07), p. e288-e288
    Type of Medium: Online Resource
    ISSN: 1460-2156 , 0006-8950
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
    detail.hit.zdb_id: 1474117-9
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  European Journal of Endocrinology Vol. 186, No. 6 ( 2022-06-01), p. 677-685
    In: European Journal of Endocrinology, Oxford University Press (OUP), Vol. 186, No. 6 ( 2022-06-01), p. 677-685
    Abstract: Type 1 diabetes and Hashimoto’s thyroiditis frequently cluster in individuals and in families, indicating shared origins. The objective of this study was to investigate familial co-aggregation of these diseases and to quantify shared genetic and environmental factors. Design This study is a twin cohort study. Methods National health registers were used to identify cases among 110 814 Swedish twins. Co-aggregation was calculated as risk ratios for type 1 diabetes among co-twins of individuals with Hashimoto’s thyroiditis, and vice-versa. Variance explained by genetics (i.e. heritability), and the proportions thereof shared between the diseases, was estimated by contrasting associations in monozygotic and dizygotic twins using structural equation models. Results Individuals with one disease were at a high risk for the other disease (adjusted risk ratio: 11.4 (95% CI: 8.5–15.3)). Co-aggregation was more common in monozygotic than in dizygotic pairs, with adjusted risk ratios of 7.0 (95% CI: 3.2–15.1) and 1.7 (95% CI: 0.7–4.1), respectively. Genetic effects shared across diseases accounted for 11% of the variance for type 1 diabetes and 9% of the variance for Hashimoto’s thyroiditis, while environmental factors unique to individual twins, but shared across diseases, accounted for 10% of the variance for type 1 diabetes and 18% of the variance for Hashimoto’s thyroiditis. Conclusions Both genes and environment unique to individual twins contribute to considerable etiologic overlap between type 1 diabetes and Hashimoto’s thyroiditis. These findings add to the current knowledge on the mechanisms behind autoimmune disease clustering and could guide future research aimed at identifying pathophysiological mechanisms and intervention targets.
    Type of Medium: Online Resource
    ISSN: 0804-4643 , 1479-683X
    RVK:
    Language: Unknown
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1485160-X
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  • 9
    In: International Journal of Epidemiology, Oxford University Press (OUP), Vol. 51, No. 3 ( 2022-06-13), p. 898-909
    Abstract: Attention-deficit/hyperactivity disorder (ADHD) has been associated with several autoimmune diseases (AD), both within individuals and across relatives, implying common underlying genetic or environmental factors in line with studies indicating that immunological mechanisms are key to brain development. To further elucidate the relationship between ADHD and autoimmunity we performed a population-wide familial co-aggregation study. Methods We linked Swedish national registries, defined a birth cohort with their biological relatives and identified individuals diagnosed with ADHD and/or 13 ADs. The cohort included 5 178 225 individuals born between 1960 and 2010, of whom 118 927 (2.30%) had been diagnosed with ADHD. We then investigated the associations between ADHD and ADs within individuals and across relatives, with logistic regression and structural equation modelling. Results Within individuals, ADHD was associated with a diagnosis of any of the 13 investigated ADs (adjusted odds ratio (OR) =1.34, 95% confidence interval (CI) = 1.30-1.38) as well as several specific ADs. Familial co-aggregation was observed. For example, ADHD was associated with any of the 13 ADs in mothers (OR = 1.29, 95% CI = 1.26–1.32), fathers (OR = 1.14, 95% CI = 1.11–1.18), full siblings (OR = 1.19, 95% CI = 1.15–1.22), aunts (OR = 1.12, 95% CI = 1.10–1.15), uncles (OR = 1.07, 95% CI = 1.05–1.10) and cousins (OR = 1.04, 95% CI = 1.03–1.06). Still, the absolute risks of AD among those with ADHD were low. The genetic correlation between ADHD and a diagnosis of any of the investigated ADs was 0.13 (95% CI = 0.09–0.17) and the environmental correlation was 0.02 (95% CI = -0.03–0.06). Conclusions We found that ADHD and ADs co-aggregate among biological relatives, indicating that the relationship between ADHD and autoimmune diseases may in part be explained by shared genetic risk factors. The patterns of familial co-aggregation of ADHD and ADs do not readily support a role of maternal immune activation in the aetiology of ADHD. The findings have implications for aetiological models of ADHD. However, screening for autoimmunity among individuals with ADHD is not warranted.
    Type of Medium: Online Resource
    ISSN: 0300-5771 , 1464-3685
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1494592-7
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  • 10
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2019
    In:  Cerebral Cortex Vol. 29, No. 3 ( 2019-03-01), p. 1342-1350
    In: Cerebral Cortex, Oxford University Press (OUP), Vol. 29, No. 3 ( 2019-03-01), p. 1342-1350
    Type of Medium: Online Resource
    ISSN: 1047-3211 , 1460-2199
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1483485-6
    SSG: 12
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