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FältnamnIndikatorerMetadata
00004949naa a2200601 4500
001oai:gup.ub.gu.se/314041
003SwePub
008240528s2022 | |||||||||||000 ||eng|
009oai:DiVA.org:oru-97655
009oai:prod.swepub.kib.ki.se:148853894
024a https://gup.ub.gu.se/publication/3140412 URI
024a https://doi.org/10.1038/s41398-022-01833-02 DOI
024a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-976552 URI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1488538942 URI
040 a (SwePub)gud (SwePub)orud (SwePub)ki
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Carlsson, T.u Karolinska Institutet4 aut
2451 0a Association of cumulative early medical factors with autism and autistic symptoms in a population-based twin sample
264 c 2022-02-22
264 1b Springer Science and Business Media LLC,c 2022
520 a Although highly heritable, environment also contributes to the etiology of autism spectrum disorder (ASD), with several specific environmental factors previously suggested. A registry-linked population-based twin cohort of 15,701 pairs (586 individuals with an ASD diagnosis), was established within the Child and Adolescent Twin Study in Sweden. Participants were evaluated for autistic symptoms at age 9 using the Autism-Tics, ADHD and other Comorbidities parental interview. A series of binary cut-offs indicated whether participants scored over various ASD symptom percentiles. Three early medical factors previously associated with ASD, beyond familial confounding (low birth weight, congenital malformations and perinatal hypoxia), were summed up creating an individual cumulative exposure load. A series of unconditional logistic regressions between all individuals and conditional regressions within twin pairs were performed for each outcome and exposure level. Between all individuals increasing cumulative early exposure loads were associated with increasing risk of ASD diagnosis (OR 3.33 (95%CI 1.79-6.20) for three exposures) and autistic symptoms (ranging from OR 2.12 (1.57-2.86) for three exposures at the 55th symptom percentile cut-off to OR 3.39 (2.2-5.24) at the 95th). Within twin pairs, the association between three exposures and an ASD diagnosis remained similar, but not statistically significant (OR 2.39 (0.62-9.24)). Having a higher load of early cumulative exposure was consistently associated with autistic symptoms after adjusting for familial confounding and sex (OR 3.45 (1.66-7.15) to OR 7.36 (1.99-27.18)). This study gives support to the cumulative stress hypothesis of ASD, and the dimensional model regarding environmental exposures, after adjustment for familial confounding.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Psykiatri0 (SwePub)302152 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Psychiatry0 (SwePub)302152 hsv//eng
653 a spectrum disorder
653 a antidepressant use
653 a risk
653 a pregnancy
653 a children
653 a birth
653 a age
653 a heritability
653 a adaptation
653 a pollutant
653 a Psychiatry
700a Rosenqvist, M.u Karolinska Institutet4 aut
700a Butwicka, A.u Karolinska Institutet4 aut
700a Larsson, Henrik,d 1975-u Örebro universitet,Institutionen för medicinska vetenskaper,Department of Medical Epidemiology & Biostatistics, Karolinska Institutet, Stockholm, Sweden4 aut0 (Swepub:oru)hiln
700a Lundström, Sebastianu Gothenburg University,Göteborgs universitet,Centrum för etik, juridik och mental hälsa,Gillbergcentrum,Centre for Ethics, Law, and Mental Health,Gillberg Neuropsychiatry Centre,Gillberg Neuropsychiatry Centre, University of Gothenburg, Gothenburg, Sweden; Centre for Ethics, Law, and Mental Health, University of Gothenburg, Gothenburg, Sweden4 aut0 (Swepub:gu)xluseb
700a Pan, P. Y.u Karolinska Institutet, Stockholm, Sweden; Stockholm Health Care Services, Region Stockholm, Stockholm, Sweden4 aut
700a Remnelius, K. L.u Karolinska Institutet4 aut
700a Taylor, M. J.u Karolinska Institutet4 aut
700a Bolte, S.u Karolinska Institutet4 aut
710a Karolinska Institutetb Institutionen för medicinska vetenskaper4 org
773t Translational Psychiatryd : Springer Science and Business Media LLCg 12:1q 12:1x 2158-3188
856u https://www.nature.com/articles/s41398-022-01833-0.pdf
856u https://doi.org/10.1038/s41398-022-01833-0y Fulltext
8564 8u https://gup.ub.gu.se/publication/314041
8564 8u https://doi.org/10.1038/s41398-022-01833-0
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-97655
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:148853894

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