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51.
  • Kendler, Kenneth S., et al. (författare)
  • Parent-offspring transmission of drug abuse and alcohol use disorder : Application of the multiple parenting relationships design
  • 2019
  • Ingår i: American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics. - : Wiley. - 1552-4841 .- 1552-485X. ; 180:4, s. 249-257
  • Tidskriftsartikel (refereegranskat)abstract
    • With complete genealogical and cohabitation information, new genetic-epidemiological designs can be developed to clarify causes of parent-offspring transmission. We propose the Multiple Parenting Relationships (MPR) Design and apply it to drug abuse (DA) and alcohol use disorder (AUD). Using national Swedish registries, we identified four kinds of informative parents with multiple children with whom they had different genetic and/or rearing relationships. These types had children for whom they provided: (a) genes (G) plus rearing (R), G only and R only; (b) G + R and G only; (c) G only and R only; and (d) G + R and R only. We identified DA and AUD cases from national registries in over 475,000 informative parent-offspring pairs. Controlling for parental resemblance for DA or AUD, all estimates were statistically homogeneous across family types. The weighted average tetrachoric correlation (SE) for DA for G + R, R only and G only relationships were, respectively, +0.21 (0.01), +0.10 (0.02), and +0.16 (0.02). Parallel results for AUD were +0.16 (0.01), +0.04 (0.02), and +0.14 (0.01). Analyses within families with affected parents showed significantly higher disorder risks in offspring with a G + R versus an R only relationship. The MPR design is complementary to other methods, especially adoption and triparental designs, in clarifying the sources of cross-generational transmission. Consistent with results from these other designs applied to the Swedish population, we find that for DA and AUD, parent-offspring resemblance was strongest for G + R relationships, intermediate for G only relationships and weakest but significant for R only relationships.
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52.
  • Kendler, Kenneth S., et al. (författare)
  • The actions and interactions of family genetic risk scores for alcohol use disorder and major depression on the risk for these two disorders
  • 2022
  • Ingår i: American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics. - : Wiley. - 1552-4841 .- 1552-485X. ; 189:5, s. 128-138
  • Tidskriftsartikel (refereegranskat)abstract
    • We know little about how genetic risk factors for two disorders jointly act and interact in predisposing to illness. Therefore, in the Swedish population, born 1970–1990 (n = 2,116,082) and followed through 2015, we examine, using additive Cox models, the impact of the family genetic risk scores (FGRS) for alcohol use disorder (AUD) and major depression (MD), their interaction with each other and with the relevant comorbid disorder on risk for AUD and MD. FGRS scores are constructed using rates of illness in first-fourth degree relatives. FGRS for AUD and MD interacted in predicting of both disorders and one FRGS (e.g., for AUD) interacted with the phenotype of MD to predict that disorder (e.g., AUD). These FGRS interactions were not substantially attenuated by adding interactions with the disorders. These results replicated across sexes. In predicting risk for a given disorder, we rarely consider genetic liabilities for other disorders. But such effects were here significant and interactive. Furthermore, the primary disorder genetic risk interacts with comorbid disorders. The pathways to risk for disorders from their and other disorders' genetic liability may be more complex than commonly considered.
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53.
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54.
  • Klar, Joakim, et al. (författare)
  • A Meniere's disease gene linked to chromosome 12p12.3.
  • 2006
  • Ingår i: American Journal of Medical Genetics Part B. - : Wiley. - 1552-4841 .- 1552-485X. ; 141B:5, s. 463-467
  • Tidskriftsartikel (refereegranskat)abstract
    • Meniere's disease (MD) is characterized by spontaneous attacks of vertigo, fluctuating sensorineural hearing loss, tinnitus, and aural fullness. The majority of patients with MD appear sporadic but 5%–13% of the cases have a family history for the disease. The cause of both the sporadic and inherited forms of MD remains unclear despite a number of candidate genes defined from their association with hearing loss. We have performed a genome wide linkage scan on a large Swedish family segregating MD in five generations. Five candidate regions with a lod score of >1 were identified. Two additional families with autosomal dominant MD were analyzed for linkage to these regions and a cumulative Zmax of 3.46 was obtained for a single region on chromosome 12p. In two of the three families, a shared haplotype was found to extend over 1.7 Mb which suggests a common ancestral origin. Within this region, a single recombination event restricts the candidate region to 463 kb.
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55.
  • Konneker, T, et al. (författare)
  • A searchable database of genetic evidence for psychiatric disorders
  • 2008
  • Ingår i: American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics. - : Wiley. - 1552-485X. ; 147B:6, s. 671-675
  • Tidskriftsartikel (refereegranskat)
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56.
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57.
  • Lavebratt, C, et al. (författare)
  • PER2 variantion is associated with depression vulnerability
  • 2010
  • Ingår i: American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics. - : Wiley. - 1552-485X. ; 153B:2, s. 570-581
  • Tidskriftsartikel (refereegranskat)
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58.
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59.
  • Li, Lin, 1989-, et al. (författare)
  • Attention-deficit/hyperactivity disorder symptoms and dietary habits in adulthood : A large population-based twin study in Sweden
  • 2020
  • Ingår i: American Journal of Medical Genetics Part B. - : John Wiley & Sons. - 1552-4841 .- 1552-485X. ; 183:8, s. 475-485
  • Tidskriftsartikel (refereegranskat)abstract
    • Associations between adult attention-deficit/hyperactivity disorder (ADHD) symptoms and dietary habits have not been well established and the underlying mechanisms remain unclear. We explored these associations using a Swedish population-based twin study with 17,999 individuals aged 20-47 years. We estimated correlations between inattention and hyperactivity/impulsivity with dietary habits and fitted twin models to determine the genetic and environmental contributions. Dietary habits were defined as (a) consumption of food groups, (b) consumption of food items rich in particular macronutrients, and (c) healthy and unhealthy dietary patterns. At the phenotypic level, inattention was positively correlated with seafood, high-fat, high-sugar, high-protein food consumptions, and unhealthy dietary pattern, with correlation coefficients ranging from 0.03 (95%CI: 0.01, 0.05) to 0.13 (95% CI: 0.11, 0.15). Inattention was negatively correlated with fruits, vegetables consumptions and healthy dietary pattern, with correlation coefficients ranging from -0.06 (95%CI: -0.08, -0.04) to -0.07 (95%CI: -0.09, -0.05). Hyperactivity/impulsivity and dietary habits showed similar but weaker patterns compared to inattention. All associations remained stable across age, sex and socioeconomic status. Nonshared environmental effects contributed substantially to the correlations of inattention (56-60%) and hyperactivity/impulsivity (63-80%) with dietary habits. The highest and lowest genetic correlations were between inattention and high-sugar food (rA = .16, 95% CI: 0.07, 0.25), and between hyperactivity/impulsivity and unhealthy dietary pattern (rA = .05, 95% CI: -0.05, 0.14), respectively. We found phenotypic and etiological overlap between ADHD and dietary habits, although these associations were weak. Our findings contribute to a better understanding of common etiological pathways between ADHD symptoms and various dietary habits.
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