Reproductive stoppage in autism spectrum disorder in a population of 2.5 million individuals / Ralf KUJA-HALKOLA in Molecular Autism, 10 (2019)  

Public ISBD [article]  inMolecular Autism > 10 (2019) . - 45 p. Titre : Reproductive stoppage in autism spectrum disorder in a population of 2.5 million individuals Type de document : texte imprimé Auteurs : Ralf KUJA-HALKOLA, Auteur ; Henrik LARSSON, Auteur ; Sebastian LUNDSTROM, Auteur ; Sven SANDIN, Auteur ; Azadeh CHIZARIFARD, Auteur ; Sven BÖLTE, Auteur ; Paul LICHTENSTEIN, Auteur ; Emma FRANS, Auteur Article en page(s) : 45 p. Langues : Anglais (eng) Mots-clés : Autism  Autism spectrum disorder  Fecundity  Reproduction  Reproductive stoppage Index. décimale : PER Périodiques Résumé : Background: It has been suggested that parents of children with autism spectrum disorder (ASD) curtail their reproduction, a phenomenon known as reproductive stoppage. To investigate the presence of reproductive stoppage, we followed the reproduction in mothers of children with or without an ASD diagnosis using Swedish population-based registries. Methods: We followed all families with first child born in 1987 or later. In total 2,521,103 children, nested within 1,270,017 mothers, were included. Exposure was presence of ASD diagnosis in earlier born siblings, and outcome was considered as (1) inter-pregnancy interval and (2) number of subsequent children. Results: Analyses of inter-pregnancy intervals showed that the association differed across birth orders, with a lower rate of second children when first child had ASD diagnosis, but an increased rate of third and higher birth orders in families where a previous child had an ASD diagnosis. When all birth orders were simultaneously considered, families with a child with an ASD diagnosis were less likely to have another child (hazard ratio (HR), 0.79; 95% confidence interval [95% CI], 0.78-0.80). However, when adjusted for birth order, the association was close to null (HR, 0.97; 95% CI, 0.96-0.99), and after additional adjustments (maternal age, birth period, sex, paternal age, and maternal education), the association disappeared (HR, 1.00; 95% CI, 0.99-1.02). In analyses of subsequent children, after adjustment for covariates, families with an ASD diagnosis had 4% more subsequent children (rate ratio, 1.04; 95% CI, 1.03-1.05). Limitations: The study was undertaken in a country with largely tax-funded healthcare; results may not generalize to other societies. Following the current dominating umbrella concept of ASD, we did not differentiate between the ASD sub-diagnoses; it is possible that reproductive patterns can be dependent on ASD subtypes and the severity and composition of ASD phenotypes and comorbidities. Conclusions: This study does not support a universal reproductive stoppage effect in ASD families, when birth order and other factors are considered. Therefore, proper attention to birth order and other factors may alleviate potential bias in familial aggregation studies of ASD. En ligne : http://dx.doi.org/10.1186/s13229-019-0300-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=414 [article] Reproductive stoppage in autism spectrum disorder in a population of 2.5 million individuals [texte imprimé] / Ralf KUJA-HALKOLA, Auteur ; Henrik LARSSON, Auteur ; Sebastian LUNDSTROM, Auteur ; Sven SANDIN, Auteur ; Azadeh CHIZARIFARD, Auteur ; Sven BÖLTE, Auteur ; Paul LICHTENSTEIN, Auteur ; Emma FRANS, Auteur . - 45 p. Langues : Anglais (eng) in Molecular Autism > 10 (2019) . - 45 p. Mots-clés : Autism  Autism spectrum disorder  Fecundity  Reproduction  Reproductive stoppage Index. décimale : PER Périodiques Résumé : Background: It has been suggested that parents of children with autism spectrum disorder (ASD) curtail their reproduction, a phenomenon known as reproductive stoppage. To investigate the presence of reproductive stoppage, we followed the reproduction in mothers of children with or without an ASD diagnosis using Swedish population-based registries. Methods: We followed all families with first child born in 1987 or later. In total 2,521,103 children, nested within 1,270,017 mothers, were included. Exposure was presence of ASD diagnosis in earlier born siblings, and outcome was considered as (1) inter-pregnancy interval and (2) number of subsequent children. Results: Analyses of inter-pregnancy intervals showed that the association differed across birth orders, with a lower rate of second children when first child had ASD diagnosis, but an increased rate of third and higher birth orders in families where a previous child had an ASD diagnosis. When all birth orders were simultaneously considered, families with a child with an ASD diagnosis were less likely to have another child (hazard ratio (HR), 0.79; 95% confidence interval [95% CI], 0.78-0.80). However, when adjusted for birth order, the association was close to null (HR, 0.97; 95% CI, 0.96-0.99), and after additional adjustments (maternal age, birth period, sex, paternal age, and maternal education), the association disappeared (HR, 1.00; 95% CI, 0.99-1.02). In analyses of subsequent children, after adjustment for covariates, families with an ASD diagnosis had 4% more subsequent children (rate ratio, 1.04; 95% CI, 1.03-1.05). Limitations: The study was undertaken in a country with largely tax-funded healthcare; results may not generalize to other societies. Following the current dominating umbrella concept of ASD, we did not differentiate between the ASD sub-diagnoses; it is possible that reproductive patterns can be dependent on ASD subtypes and the severity and composition of ASD phenotypes and comorbidities. Conclusions: This study does not support a universal reproductive stoppage effect in ASD families, when birth order and other factors are considered. Therefore, proper attention to birth order and other factors may alleviate potential bias in familial aggregation studies of ASD. En ligne : http://dx.doi.org/10.1186/s13229-019-0300-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=414

Shared familial risk factors between autism spectrum disorder and obesity - a register-based familial coaggregation cohort study / Richard AHLBERG in Journal of Child Psychology and Psychiatry, 63-8 (August 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-8 (August 2022) . - p.890-899 Titre : Shared familial risk factors between autism spectrum disorder and obesity - a register-based familial coaggregation cohort study Type de document : texte imprimé Auteurs : Richard AHLBERG, Auteur ; Miguel GARCIA-ARGIBAY, Auteur ; Tatja HIRVIKOSKI, Auteur ; Marcus BOMAN, Auteur ; Qi CHEN, Auteur ; Mark J. TAYLOR, Auteur ; Emma FRANS, Auteur ; Sven BÖLTE, Auteur ; Henrik LARSSON, Auteur Article en page(s) : p.890-899 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/etiology/genetics  Cohort Studies  Female  Genetic Predisposition to Disease  Humans  Intellectual Disability/complications  Male  Obesity/epidemiology/genetics  Registries  Risk Factors  Sweden/epidemiology  Autism  family factors  obesity Index. décimale : PER Périodiques Résumé : BACKGROUND: Meta-analyses suggest an association between autism spectrum disorder (ASD) and obesity, but the factors underlying this association remain unclear. This study investigated the association between ASD and obesity stratified on intellectual disability (ID). In addition, in order to gain insight into possible shared etiological factors, the potential role of shared familial liability was examined. METHOD: We studied a cohort of 3,141,696 individuals by linking several Swedish nationwide registers. We identified 35,461 individuals with ASD and 61,784 individuals with obesity. Logistic regression models were used to estimate the association between ASD and obesity separately by ID and sex and by adjusting for parental education, psychiatric comorbidity, and psychotropic medication. Potential shared familial etiologic factors were examined by comparing the risk of obesity in full siblings, maternal and paternal half-siblings, and full- and half-cousins of individuals with ASD to the risk of obesity in relatives of individuals without ASD. RESULTS: Individuals with ASD+ID (OR=3.76 [95% CI, 3.38-4.19]) and ASD-ID (OR=3.40 [95% CI, 3.23-3.58]) had an increased risk for obesity compared with individuals without ASD. The associations remained statistically significant when adjusting for parental education, psychiatric comorbidity, and medication. Sex-stratified analyses indicated a higher relative risk for males compared with females, with statistically significant interaction effects for ASD-ID, but not for ASD+ID in the fully adjusted model. First-degree relatives of individuals with ASD+ID and ASD-ID had an increased risk of obesity compared with first-degree relatives of individuals without ASD. The obesity risk was similar in second-degree relatives of individuals with ASD+ID but was lower for and ASD-ID. Full cousins of individuals with ASD+ID had a higher risk compared with half-cousins of individuals with ASD+ID). A similar difference in the obesity risk between full cousins and half-cousins was observed for ASD-ID. CONCLUSIONS: Individuals with ASD and their relatives are at increased risk for obesity. The risk might be somewhat higher for males than females. This warrants further studies examining potential common pleiotropic genetic factors and shared family-wide environmental factors for ASD and obesity. Such research might aid in identifying specific risks and underlying mechanisms in common between ASD and obesity. En ligne : http://dx.doi.org/10.1111/jcpp.13538 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 [article] Shared familial risk factors between autism spectrum disorder and obesity - a register-based familial coaggregation cohort study [texte imprimé] / Richard AHLBERG, Auteur ; Miguel GARCIA-ARGIBAY, Auteur ; Tatja HIRVIKOSKI, Auteur ; Marcus BOMAN, Auteur ; Qi CHEN, Auteur ; Mark J. TAYLOR, Auteur ; Emma FRANS, Auteur ; Sven BÖLTE, Auteur ; Henrik LARSSON, Auteur . - p.890-899. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-8 (August 2022) . - p.890-899 Mots-clés : Autism Spectrum Disorder/etiology/genetics  Cohort Studies  Female  Genetic Predisposition to Disease  Humans  Intellectual Disability/complications  Male  Obesity/epidemiology/genetics  Registries  Risk Factors  Sweden/epidemiology  Autism  family factors  obesity Index. décimale : PER Périodiques Résumé : BACKGROUND: Meta-analyses suggest an association between autism spectrum disorder (ASD) and obesity, but the factors underlying this association remain unclear. This study investigated the association between ASD and obesity stratified on intellectual disability (ID). In addition, in order to gain insight into possible shared etiological factors, the potential role of shared familial liability was examined. METHOD: We studied a cohort of 3,141,696 individuals by linking several Swedish nationwide registers. We identified 35,461 individuals with ASD and 61,784 individuals with obesity. Logistic regression models were used to estimate the association between ASD and obesity separately by ID and sex and by adjusting for parental education, psychiatric comorbidity, and psychotropic medication. Potential shared familial etiologic factors were examined by comparing the risk of obesity in full siblings, maternal and paternal half-siblings, and full- and half-cousins of individuals with ASD to the risk of obesity in relatives of individuals without ASD. RESULTS: Individuals with ASD+ID (OR=3.76 [95% CI, 3.38-4.19]) and ASD-ID (OR=3.40 [95% CI, 3.23-3.58]) had an increased risk for obesity compared with individuals without ASD. The associations remained statistically significant when adjusting for parental education, psychiatric comorbidity, and medication. Sex-stratified analyses indicated a higher relative risk for males compared with females, with statistically significant interaction effects for ASD-ID, but not for ASD+ID in the fully adjusted model. First-degree relatives of individuals with ASD+ID and ASD-ID had an increased risk of obesity compared with first-degree relatives of individuals without ASD. The obesity risk was similar in second-degree relatives of individuals with ASD+ID but was lower for and ASD-ID. Full cousins of individuals with ASD+ID had a higher risk compared with half-cousins of individuals with ASD+ID). A similar difference in the obesity risk between full cousins and half-cousins was observed for ASD-ID. CONCLUSIONS: Individuals with ASD and their relatives are at increased risk for obesity. The risk might be somewhat higher for males than females. This warrants further studies examining potential common pleiotropic genetic factors and shared family-wide environmental factors for ASD and obesity. Such research might aid in identifying specific risks and underlying mechanisms in common between ASD and obesity. En ligne : http://dx.doi.org/10.1111/jcpp.13538 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486

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