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- Taylor, M. J., et al.
(författare)
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Is There a Female Protective Effect Against Attention-Deficit/Hyperactivity Disorder? Evidence From Two Representative Twin Samples
- 2016
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Ingår i: Journal of the American Academy of Child and Adolescent Psychiatry. - Stockholm : Elsevier BV. - 0890-8567 .- 1527-5418. ; 55:6, s. 504-512
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Attention-deficit/hyperactivity disorder (ADHD) is more frequent in males than in females. The "female protective effect" posits that females undergo greater exposure to etiological factors than males in order to develop ADHD, leading to the prediction that relatives of females with ADHD will display more ADHD behaviors. We thus tested whether cotwins of females displaying extreme ADHD traits would display more ADHD traits than cotwins of males displaying extreme ADHD traits. Method: Parents of approximately 7,000 pairs of nonidentical twins in Sweden, and approximately 4,000 pairs of twins in England and Wales, completed dimensional assessments of ADHD traits. Probands were selected on the basis of scoring within the highest 10% of the distribution in each sample. Dimensional scores of cotwins of probands, as well as the categorical recurrence rate, were investigated by proband sex. Results: Cotwins of female probands displayed higher mean ADHD trait scores (mean = 0.62-0.79) than cotwins of male probands (mean = 0.38-0.55) in both samples. This trend was significant in the Swedish sample (p <.01) and when the 2 samples were merged into a single, larger sample (p <.001). When the samples were merged, there was also a significant association between proband sex and cotwin's categorical status, with more cotwins of female probands also being probands than cotwins of male probands. Conclusion: These findings support a female protective effect against ADHD behaviors, suggesting that females require greater exposure to genetic and environmental factors associated with ADHD in order to develop the condition.
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| 2. |
- Taylor, M. J., et al.
(författare)
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Examining the Association Between Autistic Traits and Atypical Sensory Reactivity: A Twin Study
- 2018
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Ingår i: Journal of the American Academy of Child and Adolescent Psychiatry. - : Elsevier BV. - 0890-8567 .- 1527-5418. ; 57:2, s. 96-102
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Atypical responses to sensory stimuli are common features of autism spectrum disorders (ASD). Consequently, atypical sensory reactivity (SR) is now a diagnostic feature of ASD. Quantitative genetic research on ASD has overlooked these symptoms, however. We therefore investigated the association between autistic traits and SR using twin methods. Method: Autistic traits and SR were assessed by 2 separate scales in 12,419 Swedish twin pairs (n = 3,586 monozygotic [MZ], n = 8,833 dizygotic [DZ]) when the twins were 9 or 12 years of age. The classic twin design estimated the degree to which etiological factors associated with autistic traits were also associated with SR, and the degree to which such shared factors explained the covariance between these phenotypes. DeFries Fulker analysis estimated the genetic correlation between screening diagnoses of ASD, defined broadly and strictly, and SR. Results: Autistic traits and SR were both highly heritable (62%-75% and 66%-71%, respectively). There was a moderate phenotypic correlation between autistic traits and SR (r = 0.47). Genetic influences on these phenotypes correlated moderately (genetic correlation = 0.60). These overlapping genetic factors explained most of the correlation between autistic traits and SR. Genetic correlations with SR increased for broad ASD (genetic correlation = 0.72) and strict ASD (genetic correlation = 0.80). Conclusion: The genetic overlap observed between autistic traits and SR lends quantitative genetic support to the notion that ASD and SR are strongly linked. Stich symptoms may thus comprise part of the ASD genotype, as well as phenotype. Associations persisted across all definitions of ASD, indicating a genetic link between the broader ASD phenotype and SR.
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