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Sökning: onr:"swepub:oai:DiVA.org:oru-95111" > FAMILIAL LIABILITY ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00004771naa a2200421 4500
001oai:DiVA.org:oru-95111
003SwePub
008211021s2021 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:147818492
024a https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-951112 URI
024a https://doi.org/10.1016/j.euroneuro.2021.08.0362 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1478184922 URI
040 a (SwePub)orud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a vet2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Leone, Maricau Karolinska Institutet, Solna, Sweden4 aut
2451 0a FAMILIAL LIABILITY FOR ENDOCRINE-METABOLIC DISORDERS AND DEPRESSION
264 1b Elsevier,c 2021
338 a print2 rdacarrier
520 a Background: Endocrine-metabolic disorders are common in individuals with depression. Better understanding of the underlying factors contributing to their concomitant occurrence is needed. This study investigates the familial co-aggregation of depression and endocrine-metabolic disorders and estimates the contribution of genetic and environmental risk factors to their co-occurrence.Methods: We conducted a population-based cohort study using Swedish national data. A total of 2,263,311 individuals born between 1973 and 1996 were included and followed up until death, emigration, or December 31, 2013, whichever occurred first. Each participant was linked to their biological parents, allowing identification of full-, maternal half-, and paternal half-siblings. We investigated clinical diagnoses of depression and endocrine-metabolic disorders diagnosed at any point during the follow-up period, grouping the latter into autoimmune disorders (i.e., hypothyroidism, Graves’ disease, and type 1 diabetes) and non-autoimmune disorders (i.e., type 2 diabetes, obesity, and polycystic ovarian syndrome). Logistic regression and Cox proportional hazards regression were used to estimate the association between endocrine-metabolic disorders and depression within the same individual and across siblings. Quantitative genetic modeling was performed to investigate the relative contribution of genetic and environmental influences.Results: Individuals diagnosed with endocrine-metabolic disorders had significantly higher risk of depression, with odds ratios ranging from 1.43 [95% CI, 1.30-1.57] for Graves’ disease to 2.44 [2.37-2.50] for obesity. Overall, increased risks extended to full- and half-siblings. Quantitative genetic modeling showed that shared genetic factors explained the phenotypic correlations between endocrine-metabolic disorders and depression to different extents (ranging from 36% for autoimmune hypothyroidism, to 74% for obesity), except for type 1 diabetes, for which the association was mainly explained by non-shared environmental factors (84%).Discussion: Endocrine-metabolic disorders and depression co-occur in individuals and display familial co-aggregation. Shared genetic risk factors explained much of this relationship, but unique environmental influences also contributed significantly. These findings expand the current knowledge of the etiological sources of comorbidity between somatic and psychiatric disorders, which could guide future research aiming at identifying the pathophysiological mechanisms and potentially intervention targets.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
700a Kuja-Halkola, Ralfu Karolinska Institutet, Solna, Sweden4 aut
700a Skov, Jakobu Karolinska Institutet, Solna, Sweden4 aut
700a Zhang, Ruyueu Karolinska Institutet, Solna, Sweden4 aut
700a Liu, Shengxinu Karolinska Institutet, Solna, Sweden4 aut
700a Butwicka, Agnieszkau Karolinska Institutet, Solna, Sweden4 aut
700a Larsson, Henrik,d 1975-u Örebro universitet,Institutionen för medicinska vetenskaper4 aut0 (Swepub:oru)hiln
700a Leval, Amyu Janssen Pharmaceutical, RWE and Epidemiology, Beerse, Belgium4 aut
700a Bergen, Sarahu Karolinska Institutet, Solna, Sweden4 aut
710a Karolinska Institutet, Solna, Swedenb Institutionen för medicinska vetenskaper4 org
773t European Neuropsychopharmacologyd : Elsevierg 51, s. e112-e112q 51<e112-e112x 0924-977Xx 1873-7862
856u https://doi.org/10.1016/j.euroneuro.2021.08.036
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-95111
8564 8u https://doi.org/10.1016/j.euroneuro.2021.08.036
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:147818492

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