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| 2. |
- Edwards, A. C., et al.
(författare)
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Geographic proximity is associated with transmission of suicidal behaviour among siblings
- 2019
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Ingår i: Acta Psychiatrica Scandinavica. - : Wiley. - 0001-690X .- 1600-0447. ; 140:1, s. 30-38
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Tidskriftsartikel (refereegranskat)abstract
- Objective: The aim of this study was to clarify the role of ‘contagion’, or social transmission, in risk of suicidal behaviour (SB) among siblings. Methods: We followed Swedish sibling pairs until one of them (S1; N = 111,848) was registered for a suicide attempt or completion. We tested the effect of geographic proximity between siblings on risk of a first SB registration of S1's sibling (S2). To control for familial confounding, we conducted complementary analyses of sibling trios (N = 701), comparing risk in different siblings as a function of their respective proximity to S1. Results: The best-fitting model across sibling pairs included an effect of distance between siblings (HR = 0.96, 95% CI = 0.93–0.99). Hazard ratios declined quickly up to 25 km and largely stabilized beyond 150 km. Across all pairs, a larger age difference between siblings was associated with reduced SB risk (HR = 0.96 95% CI = 0.93–0.98). Findings were consistent within the sibling trios. Conclusions: Consistent with the concept of suicide contagion, risk of suicidal behaviour subsequent to a sibling's suicide completion or attempt is higher as a function of sibling closeness. These findings are robust to potentially confounding familial factors.
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| 3. |
- Kendler, K. S., et al.
(författare)
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Social and economic consequences of alcohol use disorder : a longitudinal cohort and co-relative analysis
- 2017
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Ingår i: Psychological Medicine. - 0033-2917. ; 47:5, s. 925-935
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Tidskriftsartikel (refereegranskat)abstract
- Background: Although alcohol use disorder (AUD) is associated with future risk for psychosocial dysfunction, the degree to which this arises from a direct causal effect of AUD on functioning v. from correlated risk factors (also known as confounders) is less clearly established. Method: AUD was assessed from Swedish medical, criminal and pharmacy registries. In a large general population cohort, using Cox proportional hazard and regression models, we predicted from the onset of AUD four outcomes: early retirement, unemployment, social assistance, and individual income. We then examined the degree to which these associations were attenuated by relevant confounders as well as by the use of discordant cousin, half-sibling, full-sibling, and monozygotic twin pairs. Results: In males, AUD most strongly predicted social assistance [hazard ratio (HR) 8.27, 95% confidence interval (CI) 7.96–8.59], followed by early retirement (HR 5.63, 95% CI 5.53–5.72) and unemployment (HR 2.75, 95% CI 2.65–2.85). For income at age 50, AUD was associated with a decrease in income of 0.24 s.d.s (95% CI −0.25 to −0.23). Results were similar in females. Modest to moderate attenuation of these associations was seen in both sexes after the addition of relevant covariates. These associations were reduced but remained robust in discordant co-relative pairs, including monozygotic twins. Conclusions: Our results suggest that AUD has a causal impact on a range of measures reflective of psychosocial dysfunction. These findings provide strong support for the drift hypothesis. However, some of the associations between AUD and dysfunction appear to be non-causal and result from shared risk factors, many of which are likely familial.
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| 5. |
- Kendler, K. S., et al.
(författare)
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A developmental model for alcohol use disorders in Swedish men
- 2016
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Ingår i: Psychological Medicine. - 0033-2917. ; 46:13, s. 2759-2770
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Tidskriftsartikel (refereegranskat)abstract
- Background: Alcohol use disorder (AUD) is a classic multifactorial syndrome and it is critical to understand the diversity of the relevant risk factors and how they inter-relate over development. Method: We examined 21 risk factors for AUD in four developmental tiers reflecting (i) birth, (ii) childhood and early adolescence, (iii) late adolescence, and (iv) early adulthood in 47 414 Swedish men of whom 3907 (8.2%) were registered for AUD at or after age 25 with a mean length of follow-up of 33.9 (6.6) years. Structural equational model fitting was performed using Mplus. Results: The best-fitting model provided a good fit to the data and explained 23.4% of the variance in AUD. The five strongest predictors were: externalizing behaviors, criminal behavior, father's alcohol consumption, genetic risk, and low educational attainment. Two developmentally early familial/genetic risk factors had substantial direct paths to AUD: father's alcohol consumption and genetic liability. Other broad developmental pathways to risk for AUD were evident: externalizing, psychosocial and internalizing. Overall, the externalizing pathway to AUD was the strongest. However, these pathways were substantially interwoven over time such that risk factors from one domain were commonly predicted by and/or predicted risk factors from the other broad domains of risk. Conclusion: AUD in men is an etiologically complex syndrome influenced by familial-genetic, psychosocial, internalizing, and especially externalizing risk factors that act and interact over development and have complicated mediational pathways.
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| 6. |
- Kendler, K. S., et al.
(författare)
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The role of marriage in criminal recidivism : a longitudinal and co-relative analysis
- 2017
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Ingår i: Epidemiology and Psychiatric Sciences. - 2045-7960. ; 26:6, s. 655-663
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Tidskriftsartikel (refereegranskat)abstract
- Aims.: Marriage is associated with a reduced rate of criminal recidivism, but the underlying mechanisms have only partly been elucidated. We seek to clarify the nature of the association between marriage and recidivism and how that relationship may be moderated as a function of gender, deviance of spouse, a history of violence and familial risk. Method.: We utilise a longitudinal cohort design consisting of Swedish men (n = 239 328) and women (n = 72 280), born between 1958 and 1986, who were convicted of at least one crime before age 20 and were not married prior to age 20. The analyses used Cox regression with marriage as a time-dependent covariate. We also perform co-relative analyses in sibling and first cousin pairs. Results.: Marriage after a first crime substantially reduces risk of recidivism in both males (hazard ratio (HR) with key covariates and 95% confidence intervals 0.55, 0.53–0.57) and females (HR = 0.38, 0.34–0.42), although the effect is stronger in females. Marriage to a deviant spouse increases recidivism rates in males. In males, a history of violent criminality and high familial risk, respectively, decrease and increase sensitivity to the protective effect of marriage on recidivism. Consistent with a causal effect of marriage on recidivism, marriage was associated with a decline in risk for criminal relapse comparable with that in the population in both male–male sibling pairs (raw HR = 0.53, 0.45–0.62) and cousin pairs (HR = 0.55, 0.47, 0.65) concordant for prior convictions. Conclusions.: The protective effect of marriage on risk for criminal recidivism is likely largely causal and is of importance in both males and females. Those at high familial risk for criminal behaviour are more sensitive to the protective effects of marriage.
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| 7. |
- Chattopadhyay, S., et al.
(författare)
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Influence of family history on risk of second primary cancers and survival in patients with squamous cell skin cancer
- 2020
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Ingår i: British Journal of Dermatology. - : Oxford University Press (OUP). - 0007-0963 .- 1365-2133. ; 183:3, s. 488-494
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Tidskriftsartikel (refereegranskat)abstract
- Background: Patients with squamous cell skin cancer (SCC) have an excellent prognosis but second primary cancers (SPCs) weaken survival prospects. Family history is a known risk factor for cancer but whether it is a risk factor for SPC in patients with SCC is not known. Objectives: To quantify the risk of family history on SPCs in patients with SCC and estimate survival probabilities of patients with SPCs depending on family history. Methods: With 13 945 histologically verified SCCs, relative risks (RRs) were estimated for family history using a generalized regression model. For survival analysis, hazard ratios (HRs) were assessed using a multivariable Cox proportional-hazards model. Results: Family history of invasive SCC increased risk of second invasive SCC [RR = 42·92, 95% confidence interval (CI) 33·69–50·32] compared with risk without family history (RR 19·12, 95% CI 17·88–21·08). Family history of any nonskin cancer in invasive SCC increased risk of the same cancers to be diagnosed as SPC (RRFH = 1·48, 95% CI 1·35–1·61 vs. RRno FH = 1·40, 95% CI 1·32–1·48); significant increases were observed for seven different nonskin cancers. Most results were replicated for in situ SCC. SPC was deleterious for survival irrespective of family history; HR for patients with SPC was 4·28 (95% CI 3·83–4·72) vs. those without SPC (1·04). Conclusions: Family history of nonskin cancer was associated with approximately a doubling of risk for SPCs in patients with SCC. SPC increases the death rate in patients with SCC 3–4 times, irrespective of family history. Taking family history into account at SCC diagnosis may help prevention or early detection of SPCs. What's already known about this topic? Second primary cancers (SPCs) are frequently diagnosed in patients with invasive and in situ squamous cell carcinoma (SCC); some epidemiological studies suggest a link to immune dysfunction. Family history of cancer is a risk factor for practically all first primary cancers but whether it also influences risk of SPCs in patients with SCC is not known. The possible influence of family history on survival in patients with SCC remains to be established.
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| 8. |
- Friberg, Danielle, et al.
(författare)
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Sibling risk of pediatric obstructive sleep apnea syndrome and adenotonsillar hypertrophy.
- 2009
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Ingår i: Sleep. - : Oxford University Press (OUP). - 0161-8105 .- 1550-9109. ; 32:8, s. 1077-1083
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Tidskriftsartikel (refereegranskat)abstract
- Objectives:To estimate sibling risk of hospitalization for children with sleep disordered breathing (SDB), diagnosed with (1) obstructive sleep apnea syndrome (OSAS), or (2) adenotonsillar hypertrophy in the total Swedish population.Design, Setting, and Participants:Using the MigMed database at the Karolinska Institute, we divided the population of Sweden aged 0–18 years into sibling groups based on a shared mother and father and presence of a primary hospital diagnosis of OSAS or adenotonsillar hypertrophy for each individual born between 1978 and 1986, during the follow-up period 1997–2004. Individuals with at least one affected sibling were identified and the incidence rates were computed, using standardized incidence ratios (SIRs) with 95% confidence intervals (CIs). Reference groups were boys and girls with unaffected siblings of 2 or more.Results:After accounting for socioeconomic status, age, and geographic region, boys with at least one sibling with OSAS had an increased risk of having OSAS (SIR, 33.2; 95% CI, 16.5–64.8), and in girls the SIR was 40.5 (19.4–81.4). For hypertrophy of the tonsils or hypertrophy of the adenoids and tonsils the corresponding SIRs were 4.53 (3.0–6.8) for boys and 4.94 (3.3–7.4) for girls.Conclusions:The study indicate an increased sibling risk of sleep disordered breathing in children, which may be due to heritable genes and/or shared environment such as increased awareness among family members or referring doctors. Caregivers should ask parents if siblings have similar symptoms, and thus offer them early treatment.
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| 9. |
- Hemminki, K., et al.
(författare)
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Familial association between type 1 diabetes and other autoimmune and related diseases
- 2009
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Ingår i: Diabetologia. - : Springer Science and Business Media LLC. - 1432-0428 .- 0012-186X. ; 52:9, s. 1820-1828
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Tidskriftsartikel (refereegranskat)abstract
- In the era of genome-wide association studies, familial risks are used to estimate disease heritability and success in gene identification. We wanted to estimate associations between type 1 diabetes mellitus and 33 autoimmune and related diseases in parents, offspring, singleton siblings and twins. The availability of a Multigeneration Register in Sweden provides reliable access to families throughout the last century. The diseases in individual family members were obtained through linkage to the Hospital Discharge Register. Standardised incidence ratios (SIRs) were calculated as relative risks of contracting type 1 diabetes in family members of affected patients compared with those lacking affected family members. Among a total of 450,899 patients, 21,168 were diagnosed with type 1 diabetes. Familial cases amounted to 10.3% of all type 1 diabetes patients. SIR for type 1 diabetes was 8.23 in offspring of affected parents, 11.92 in singleton siblings, 39.22 in multiplex families and 21.88 in twins; the calculated risk for monozygotic twins was 32.33. Type 1 diabetes in offspring was associated with 13 diseases in parents, including Addison's disease (SIR 2.41), asthma (1.38), coeliac disease (2.73), Graves' disease/hyperthyroidism (1.86), Hashimoto disease/hypothyroidism (2.35), pernicious anaemia (3.09), primary biliary cirrhosis (3.63), rheumatoid arthritis (2.12), sarcoidosis (1.62), systemic lupus erythematosus (2.04), ulcerative colitis (1.23) and Wegener's granulomatosis (2.12). The concordant familial risks for type 1 diabetes were high and the calculated risk for multiplex families and monozygotic twins may be explained by epistatic gene x gene or gene x environment interactions. Familial associations with several autoimmune and related diseases suggest genetic sharing and challenge to gene identification.
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| 10. |
- Hemminki, K., et al.
(författare)
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Familial associations of lymphoma and myeloma with autoimmune diseases
- 2017
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Ingår i: Blood Cancer Journal. - : Springer Science and Business Media LLC. - 2044-5385. ; 7:1
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Tidskriftsartikel (refereegranskat)abstract
- Many B-cell neoplasms are associated with autoimmune diseases (AIDs) but most evidence is based on a personal rather than a family history of AIDs. Here we calculated risks for non-Hodgkin lymphoma (NHL), Hodgkin lymphoma (HL) and multiple myeloma (MM) when family members were diagnosed with any of 44 different AIDs, or, independently, risk for AIDs when family members were diagnosed with a neoplasm. A total of 64 418 neoplasms and 531 155 AIDs were identified from Swedish nationwide health care records. NHL was associated with a family history of five AIDs, all increasing the risk, HL was associated with one AID increasing and three AIDs decreasing the risk while MM had no association. A family history of NHL was associated with eight, HL with seven and MM with seven different AIDs, nine increasing and 13 decreasing the risk. The present family data on B-cell neoplasms and AIDs show an approximately equal number of associations for risk increase and risk decrease, suggesting that inherited genes or geneenvironment interactions may increase the risk or be protective. These results differed from published data on personal history of AID, which only report increased risks, often vastly higher and for different AIDs compared with the present data.
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