Age effects on autism heritability and etiological stability of autistic traits / Agnieszka BUTWICKA ; Ebba DU RIETZ ; Aleksandra KANINA ; Mina A. ROSENQVIST ; Henrik LARSSON ; Paul LICHTENSTEIN ; Mark J. TAYLOR in Journal of Child Psychology and Psychiatry, 65-9 (September 2024)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 65-9 (September 2024) . - p.1135-1144 Titre : Age effects on autism heritability and etiological stability of autistic traits Type de document : Texte imprimé et/ou numérique Auteurs : Agnieszka BUTWICKA, Auteur ; Ebba DU RIETZ, Auteur ; Aleksandra KANINA, Auteur ; Mina A. ROSENQVIST, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Mark J. TAYLOR, Auteur Article en page(s) : p.1135-1144 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Background Autism and autistic traits onset in childhood but persist into adulthood. Little is known about how genetic and environmental factors influence autism and autistic traits into adulthood. We aimed to determine age effects on the heritability of clinically diagnosed autism and the etiological stability of autistic traits from childhood to adulthood using twin methods. Methods From 23,849 twin pairs in the Swedish Twin Register born between 1959 and 2010, we identified 485 individuals (1.01%, 31.5% female) with a clinical autism diagnosis. We estimated and compared the relative contribution of genetic, shared, and nonshared environmental influences to autism in childhood and adulthood. We further used multivariate twin analysis with four measurement points among 1,348 twin pairs in the longitudinal Twin Study of Child and Adolescent Development to assess the phenotypic and etiological stability of autistic traits - measured with three scales from the Child Behavior Checklist - from childhood to adulthood. Results Autism heritability was comparable from childhood, (96% [95% CI, 76-99%]) to adulthood (87% [67-96%]). Autistic traits were moderately stable (phenotypic correlation = 0.35-0.61) from childhood to adulthood, and their heritability varied between 52 and 71%. We observed stable as well as newly emerging genetic influences on autistic traits from ages 8-9 to 19-20, and unique nonshared environmental influences at each age. Conclusions Genetic factors are important for autism and autistic traits in adulthood and separate genetic studies in adults are warranted. En ligne : https://doi.org/10.1111/jcpp.13949 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=534 [article] Age effects on autism heritability and etiological stability of autistic traits [Texte imprimé et/ou numérique] / Agnieszka BUTWICKA, Auteur ; Ebba DU RIETZ, Auteur ; Aleksandra KANINA, Auteur ; Mina A. ROSENQVIST, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Mark J. TAYLOR, Auteur . - p.1135-1144. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 65-9 (September 2024) . - p.1135-1144 Index. décimale : PER Périodiques Résumé : Background Autism and autistic traits onset in childhood but persist into adulthood. Little is known about how genetic and environmental factors influence autism and autistic traits into adulthood. We aimed to determine age effects on the heritability of clinically diagnosed autism and the etiological stability of autistic traits from childhood to adulthood using twin methods. Methods From 23,849 twin pairs in the Swedish Twin Register born between 1959 and 2010, we identified 485 individuals (1.01%, 31.5% female) with a clinical autism diagnosis. We estimated and compared the relative contribution of genetic, shared, and nonshared environmental influences to autism in childhood and adulthood. We further used multivariate twin analysis with four measurement points among 1,348 twin pairs in the longitudinal Twin Study of Child and Adolescent Development to assess the phenotypic and etiological stability of autistic traits - measured with three scales from the Child Behavior Checklist - from childhood to adulthood. Results Autism heritability was comparable from childhood, (96% [95% CI, 76-99%]) to adulthood (87% [67-96%]). Autistic traits were moderately stable (phenotypic correlation = 0.35-0.61) from childhood to adulthood, and their heritability varied between 52 and 71%. We observed stable as well as newly emerging genetic influences on autistic traits from ages 8-9 to 19-20, and unique nonshared environmental influences at each age. Conclusions Genetic factors are important for autism and autistic traits in adulthood and separate genetic studies in adults are warranted. En ligne : https://doi.org/10.1111/jcpp.13949 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=534

Etiological links between autism and difficulties in initiating and maintaining sleep: a familial co-aggregation and twin study / M. J. TAYLOR in Journal of Child Psychology and Psychiatry, 63-3 (March 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-3 (March 2022) . - p.315-323 Titre : Etiological links between autism and difficulties in initiating and maintaining sleep: a familial co-aggregation and twin study Type de document : Texte imprimé et/ou numérique Auteurs : M. J. TAYLOR, Auteur ; H. LARSSON, Auteur ; S. LUNDSTRÖM, Auteur ; P. LICHTENSTEIN, Auteur ; Agnieszka BUTWICKA, Auteur Article en page(s) : p.315-323 Langues : Anglais (eng) Mots-clés : Autism  comorbidity  genetics  sleep  twin study Index. décimale : PER Périodiques Résumé : BACKGROUND: Difficulties initiating and maintaining sleep (DIMS) are frequent features of autism, yet little is known about why these conditions co-occur. One possibility is that they share etiological factors, yet this hypothesis remains to be tested using quantitative genetic designs. We thus investigated etiological links between autism and DIMS using familial co-aggregation and twin methods. METHODS: Twins, siblings, half-siblings, and cousins of 50,097 individuals with autism were identified from Swedish population registries. Their risk of DIMS, defined through diagnoses of insomnia and/or melatonin prescriptions, was then estimated. Twin analyses conducted on 15,279 child and adolescent twin pairs investigated etiological links between DIMS and ASD. RESULTS: 22.8% of autistic individuals had DIMS. Monozygotic co-twins of individuals with autism were most at risk of DIMS compared to the reference group (OR?=?6.6 [2.5-17.4]), followed by dizygotic co-twins (OR?=?2.6 [1.5-4.5]) and full siblings (OR?=?2.5 [2.4-2.6]). Half-siblings and cousins of individuals with autism were least likely to have DIMS relative to the reference group (OR range?=?1.3-1.5). Twin analyses estimated a correlation of 0.57 (0.53-0.61) between autism and DIMS, with a genetic correlation of 0.62 (0.60-0.68). These overlapping genetic factors explained 94% of the covariance between these conditions. Autistic traits also showed genetic overlap with DIMS. CONCLUSIONS: Our results suggest that shared genetic mechanisms underlie autism and DIMS, which may lead them to co-occur. Untangling the etiological overlap between these conditions has potential to assist in understanding the etiology of each condition, as well as their associated outcomes. En ligne : http://dx.doi.org/10.1111/jcpp.13473 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457 [article] Etiological links between autism and difficulties in initiating and maintaining sleep: a familial co-aggregation and twin study [Texte imprimé et/ou numérique] / M. J. TAYLOR, Auteur ; H. LARSSON, Auteur ; S. LUNDSTRÖM, Auteur ; P. LICHTENSTEIN, Auteur ; Agnieszka BUTWICKA, Auteur . - p.315-323. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-3 (March 2022) . - p.315-323 Mots-clés : Autism  comorbidity  genetics  sleep  twin study Index. décimale : PER Périodiques Résumé : BACKGROUND: Difficulties initiating and maintaining sleep (DIMS) are frequent features of autism, yet little is known about why these conditions co-occur. One possibility is that they share etiological factors, yet this hypothesis remains to be tested using quantitative genetic designs. We thus investigated etiological links between autism and DIMS using familial co-aggregation and twin methods. METHODS: Twins, siblings, half-siblings, and cousins of 50,097 individuals with autism were identified from Swedish population registries. Their risk of DIMS, defined through diagnoses of insomnia and/or melatonin prescriptions, was then estimated. Twin analyses conducted on 15,279 child and adolescent twin pairs investigated etiological links between DIMS and ASD. RESULTS: 22.8% of autistic individuals had DIMS. Monozygotic co-twins of individuals with autism were most at risk of DIMS compared to the reference group (OR?=?6.6 [2.5-17.4]), followed by dizygotic co-twins (OR?=?2.6 [1.5-4.5]) and full siblings (OR?=?2.5 [2.4-2.6]). Half-siblings and cousins of individuals with autism were least likely to have DIMS relative to the reference group (OR range?=?1.3-1.5). Twin analyses estimated a correlation of 0.57 (0.53-0.61) between autism and DIMS, with a genetic correlation of 0.62 (0.60-0.68). These overlapping genetic factors explained 94% of the covariance between these conditions. Autistic traits also showed genetic overlap with DIMS. CONCLUSIONS: Our results suggest that shared genetic mechanisms underlie autism and DIMS, which may lead them to co-occur. Untangling the etiological overlap between these conditions has potential to assist in understanding the etiology of each condition, as well as their associated outcomes. En ligne : http://dx.doi.org/10.1111/jcpp.13473 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=457

Familial and genetic associations between autism spectrum disorder and other neurodevelopmental and psychiatric disorders / L. GHIRARDI in Journal of Child Psychology and Psychiatry, 62-11 (November 2021)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 62-11 (November 2021) . - p.1274-1284 Titre : Familial and genetic associations between autism spectrum disorder and other neurodevelopmental and psychiatric disorders Type de document : Texte imprimé et/ou numérique Auteurs : L. GHIRARDI, Auteur ; R. KUJA-HALKOLA, Auteur ; Agnieszka BUTWICKA, Auteur ; J. MARTIN, Auteur ; H. LARSSON, Auteur ; B. M. D'ONOFRIO, Auteur ; P. LICHTENSTEIN, Auteur ; M. J. TAYLOR, Auteur Article en page(s) : p.1274-1284 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/epidemiology/genetics  Cohort Studies  Comorbidity  Humans  Intellectual Disability/epidemiology/genetics  Neurodevelopmental Disorders/epidemiology/genetics  Autism spectrum disorder  family based study  genetic association  neurodevelopmental disorders Index. décimale : PER Périodiques Résumé : BACKGROUND: Familial and genetic associations between autism spectrum disorder (ASD) and other neurodevelopmental and psychiatric disorders have been reported, sometimes with conflicting results. We estimated familial and genetic associations between ASD and nine disorder groups, and explored differences in these associations for ASD in the context of intellectual disability, epilepsy, chromosomal abnormalities, and congenital malformations. METHODS: Individuals born between 1985 and 2009 living in Sweden on their seventh birthday were linked to their biological parents in order to identify different types of relatives. We retrieved information on all the disorders considered from the National Patient Register. Logistic regression was used to estimate the familial association between ASD and other neurodevelopmental and psychiatric disorders in the different groups of relatives. Structural equation modeling was used to estimate phenotypic (r(p) ) and genetic associations (r(g) ), as well as the contribution of genetic influences to r(p) . RESULTS: The study included 2,398,608 individuals. Among relatives of individuals diagnosed with ASD, there was an increased risk of the disorders considered, compared to relatives of individuals who were not diagnosed with ASD. Stronger associations were detected for ASD without any additional diagnosis of intellectual disability, epilepsy, chromosomal abnormalities, and congenital malformations. The strongest genetic correlation was estimated between ASD and other neurodevelopmental disorders (r(g)  = 0.73; 95% CI = 0.66-0.79). Moderate genetic correlations were estimated for anxiety disorders (r(g)  = 0.47; 95% CI = 0.33-0.61), depression (r(g)  = 0.52; 95% CI = 0.37-0.66), and intentional self-harm (r(g)  = 0.54; 95% CI = 0.36-0.71). CONCLUSIONS: ASD shows familial and genetic association not only with other neurodevelopmental disorders, but also with other psychiatric disorders, such as anxiety, depression, and intentional self-harm. Family history of ASD comorbid with intellectual disability, epilepsy, congenital malformations, or chromosomal abnormalities is less related to other psychiatric disorders, potentially suggesting a different etiology for this subgroup of patients. En ligne : http://dx.doi.org/10.1111/jcpp.13508 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456 [article] Familial and genetic associations between autism spectrum disorder and other neurodevelopmental and psychiatric disorders [Texte imprimé et/ou numérique] / L. GHIRARDI, Auteur ; R. KUJA-HALKOLA, Auteur ; Agnieszka BUTWICKA, Auteur ; J. MARTIN, Auteur ; H. LARSSON, Auteur ; B. M. D'ONOFRIO, Auteur ; P. LICHTENSTEIN, Auteur ; M. J. TAYLOR, Auteur . - p.1274-1284. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 62-11 (November 2021) . - p.1274-1284 Mots-clés : Autism Spectrum Disorder/epidemiology/genetics  Cohort Studies  Comorbidity  Humans  Intellectual Disability/epidemiology/genetics  Neurodevelopmental Disorders/epidemiology/genetics  Autism spectrum disorder  family based study  genetic association  neurodevelopmental disorders Index. décimale : PER Périodiques Résumé : BACKGROUND: Familial and genetic associations between autism spectrum disorder (ASD) and other neurodevelopmental and psychiatric disorders have been reported, sometimes with conflicting results. We estimated familial and genetic associations between ASD and nine disorder groups, and explored differences in these associations for ASD in the context of intellectual disability, epilepsy, chromosomal abnormalities, and congenital malformations. METHODS: Individuals born between 1985 and 2009 living in Sweden on their seventh birthday were linked to their biological parents in order to identify different types of relatives. We retrieved information on all the disorders considered from the National Patient Register. Logistic regression was used to estimate the familial association between ASD and other neurodevelopmental and psychiatric disorders in the different groups of relatives. Structural equation modeling was used to estimate phenotypic (r(p) ) and genetic associations (r(g) ), as well as the contribution of genetic influences to r(p) . RESULTS: The study included 2,398,608 individuals. Among relatives of individuals diagnosed with ASD, there was an increased risk of the disorders considered, compared to relatives of individuals who were not diagnosed with ASD. Stronger associations were detected for ASD without any additional diagnosis of intellectual disability, epilepsy, chromosomal abnormalities, and congenital malformations. The strongest genetic correlation was estimated between ASD and other neurodevelopmental disorders (r(g)  = 0.73; 95% CI = 0.66-0.79). Moderate genetic correlations were estimated for anxiety disorders (r(g)  = 0.47; 95% CI = 0.33-0.61), depression (r(g)  = 0.52; 95% CI = 0.37-0.66), and intentional self-harm (r(g)  = 0.54; 95% CI = 0.36-0.71). CONCLUSIONS: ASD shows familial and genetic association not only with other neurodevelopmental disorders, but also with other psychiatric disorders, such as anxiety, depression, and intentional self-harm. Family history of ASD comorbid with intellectual disability, epilepsy, congenital malformations, or chromosomal abnormalities is less related to other psychiatric disorders, potentially suggesting a different etiology for this subgroup of patients. En ligne : http://dx.doi.org/10.1111/jcpp.13508 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=456

Familial risk and heritability of intellectual disability: a population-based cohort study in Sweden / Paul LICHTENSTEIN in Journal of Child Psychology and Psychiatry, 63-9 (September 2022)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1092-1102 Titre : Familial risk and heritability of intellectual disability: a population-based cohort study in Sweden Type de document : Texte imprimé et/ou numérique Auteurs : Paul LICHTENSTEIN, Auteur ; Magnus TIDEMAN, Auteur ; Patrick F. SULLIVAN, Auteur ; Eva SERLACHIUS, Auteur ; Henrik LARSSON, Auteur ; Ralf KUJA-HALKOLA, Auteur ; Agnieszka BUTWICKA, Auteur Article en page(s) : p.1092-1102 Langues : Anglais (eng) Mots-clés : Child  Cohort Studies  Genetic Predisposition to Disease  Humans  Intellectual Disability/epidemiology/genetics  Male  Registries  Risk Factors  Sweden/epidemiology  Intellectual disability  family factors  genetics  siblings  twins Index. décimale : PER Périodiques Résumé : BACKGROUND: Intellectual disability (ID) aggregates in families, but factors affecting individual risk and heritability estimates remain unknown. METHODS: A population-based family cohort study of 4,165,785 individuals born 1973-2013 in Sweden, including 37,787 ID individuals and their relatives. The relative risks (RR) of ID with 95% confidence intervals (95% CI) were obtained from stratified Cox proportional-hazards models. Relatives of ID individuals were compared to relatives of unaffected individuals. Structural equation modeling was used to estimate heritability. RESULTS: Relatives of ID individuals were at increased risk of ID compared to individuals with unaffected relatives. The RR of ID among relatives increased proportionally to the degree of genetic relatedness with ID probands; 256.70(95% CI 161.30-408.53) for monozygotic twins, 16.47(13.32-20.38) for parents, 14.88(12.19-18.16) for children, 7.04(4.67-10.61) for dizygotic twins, 8.38(7.97-8.83) for full siblings, 4.56(4.02-5.16) for maternal, 2.90(2.49-3.37) for paternal half-siblings, 3.03(2.61-3.50) for nephews/nieces, 2.84(2.45-3.29) for uncles/aunts, and 2.04(1.91-2.20) for cousins. Lower RRs were observed for siblings of probands with chromosomal abnormalities (RR 5.53, 4.74-6.46) and more severe ID (mild RR 9.15, 8.55-9.78, moderate RR 8.13, 7.28-9.08, severe RR 6.80, 5.74-8.07, and profound RR 5.88, 4.52-7.65). Male sex of relative and maternal line of relationship with proband was related to higher risk (RR 1.33, 1.25-1.41 for brothers vs. sisters and RR 1.49, 1.34-1.68 for maternal vs. paternal half-siblings). ID was substantially heritable with 0.95(95% CI 0.93-0.98) of the variance in liability attributed to genetic influences. CONCLUSIONS: The risk estimates will benefit researchers, clinicians, families in understanding the risk of ID in the family and the whole population. The higher risk of ID related to male sex and maternal linage will be of value for planning and interpreting etiological studies in ID. En ligne : http://dx.doi.org/10.1111/jcpp.13560 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 [article] Familial risk and heritability of intellectual disability: a population-based cohort study in Sweden [Texte imprimé et/ou numérique] / Paul LICHTENSTEIN, Auteur ; Magnus TIDEMAN, Auteur ; Patrick F. SULLIVAN, Auteur ; Eva SERLACHIUS, Auteur ; Henrik LARSSON, Auteur ; Ralf KUJA-HALKOLA, Auteur ; Agnieszka BUTWICKA, Auteur . - p.1092-1102. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1092-1102 Mots-clés : Child  Cohort Studies  Genetic Predisposition to Disease  Humans  Intellectual Disability/epidemiology/genetics  Male  Registries  Risk Factors  Sweden/epidemiology  Intellectual disability  family factors  genetics  siblings  twins Index. décimale : PER Périodiques Résumé : BACKGROUND: Intellectual disability (ID) aggregates in families, but factors affecting individual risk and heritability estimates remain unknown. METHODS: A population-based family cohort study of 4,165,785 individuals born 1973-2013 in Sweden, including 37,787 ID individuals and their relatives. The relative risks (RR) of ID with 95% confidence intervals (95% CI) were obtained from stratified Cox proportional-hazards models. Relatives of ID individuals were compared to relatives of unaffected individuals. Structural equation modeling was used to estimate heritability. RESULTS: Relatives of ID individuals were at increased risk of ID compared to individuals with unaffected relatives. The RR of ID among relatives increased proportionally to the degree of genetic relatedness with ID probands; 256.70(95% CI 161.30-408.53) for monozygotic twins, 16.47(13.32-20.38) for parents, 14.88(12.19-18.16) for children, 7.04(4.67-10.61) for dizygotic twins, 8.38(7.97-8.83) for full siblings, 4.56(4.02-5.16) for maternal, 2.90(2.49-3.37) for paternal half-siblings, 3.03(2.61-3.50) for nephews/nieces, 2.84(2.45-3.29) for uncles/aunts, and 2.04(1.91-2.20) for cousins. Lower RRs were observed for siblings of probands with chromosomal abnormalities (RR 5.53, 4.74-6.46) and more severe ID (mild RR 9.15, 8.55-9.78, moderate RR 8.13, 7.28-9.08, severe RR 6.80, 5.74-8.07, and profound RR 5.88, 4.52-7.65). Male sex of relative and maternal line of relationship with proband was related to higher risk (RR 1.33, 1.25-1.41 for brothers vs. sisters and RR 1.49, 1.34-1.68 for maternal vs. paternal half-siblings). ID was substantially heritable with 0.95(95% CI 0.93-0.98) of the variance in liability attributed to genetic influences. CONCLUSIONS: The risk estimates will benefit researchers, clinicians, families in understanding the risk of ID in the family and the whole population. The higher risk of ID related to male sex and maternal linage will be of value for planning and interpreting etiological studies in ID. En ligne : http://dx.doi.org/10.1111/jcpp.13560 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486

Hypospadias and increased risk for neurodevelopmental disorders / Agnieszka BUTWICKA in Journal of Child Psychology and Psychiatry, 56-2 (February 2015)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 56-2 (February 2015) . - p.155-161 Titre : Hypospadias and increased risk for neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique Auteurs : Agnieszka BUTWICKA, Auteur ; Paul LICHTENSTEIN, Auteur ; Mikael LANDÉN, Auteur ; Anna S. NORDENVALL, Auteur ; Anna NORDENSTRÖM, Auteur ; Agneta NORDENSKJÖLD, Auteur ; Louise FRISÉN, Auteur Article en page(s) : p.155-161 Langues : Anglais (eng) Mots-clés : Hormones  ADHD  autism spectrum disorder  ICD  intellectual disability Index. décimale : PER Périodiques Résumé : Background Hypospadias (aberrant opening of the urethra on the underside of the penis) occurs in 1 per 300 newborn boys. It has been previously unknown whether this common malformation is associated with increased psychiatric morbidity later in life. Studies of individuals with hypospadias also provide an opportunity to examine whether difference in androgen signaling is related to neurodevelopmental disorders. To elucidate the mechanisms behind a possible association, we also studied psychiatric outcomes among brothers of the hypospadias patients. Methods Registry study within a national cohort of all 9,262 males with hypospadias and their 4,936 healthy brothers born in Sweden between 1973 and 2009. Patients with hypospadias and their brothers were matched with controls by year of birth and county. The following outcomes were evaluated (1) any psychiatric (2) psychotic, (3) mood, (4) anxiety, (5) eating, and (6) personality disorders, (7) substance misuse, (8) attention-deficit hyperactivity disorder (ADHD), (9) autism spectrum disorders (ASD), (10) intellectual disability, and (11) other behavioral/emotional disorders with onset in childhood. Results Patients with hypospadias were more likely to be diagnosed with intellectual disability (OR 3.2; 95% CI 2.8–3.8), ASD (1.4; 1.2–1.7), ADHD (1.5; 1.3–1.9), and behavioral/emotional disorders (1.4; 1.2–1.6) compared with the controls. Brothers of patients with hypospadias had an increased risk of ASD (1.6; 1.3–2.1) and other behavioral/emotional disorders with onset in childhood (1.2; 0.9–1.5) in comparison to siblings of healthy individuals. A slightly higher, although not statistically significant, risk was found for intellectual disability (1.3; 1.0–1.9). No relation between other psychiatric diagnosis and hypospadias was found. Conclusions This is the first study to identify an increased risk for neurodevelopmental disorders in patients with hypospadias, as well as an increased risk for ASD in their brothers, suggesting a common familial (genetic and/or environmental) liability. En ligne : http://dx.doi.org/10.1111/jcpp.12290 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=259 [article] Hypospadias and increased risk for neurodevelopmental disorders [Texte imprimé et/ou numérique] / Agnieszka BUTWICKA, Auteur ; Paul LICHTENSTEIN, Auteur ; Mikael LANDÉN, Auteur ; Anna S. NORDENVALL, Auteur ; Anna NORDENSTRÖM, Auteur ; Agneta NORDENSKJÖLD, Auteur ; Louise FRISÉN, Auteur . - p.155-161. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 56-2 (February 2015) . - p.155-161 Mots-clés : Hormones  ADHD  autism spectrum disorder  ICD  intellectual disability Index. décimale : PER Périodiques Résumé : Background Hypospadias (aberrant opening of the urethra on the underside of the penis) occurs in 1 per 300 newborn boys. It has been previously unknown whether this common malformation is associated with increased psychiatric morbidity later in life. Studies of individuals with hypospadias also provide an opportunity to examine whether difference in androgen signaling is related to neurodevelopmental disorders. To elucidate the mechanisms behind a possible association, we also studied psychiatric outcomes among brothers of the hypospadias patients. Methods Registry study within a national cohort of all 9,262 males with hypospadias and their 4,936 healthy brothers born in Sweden between 1973 and 2009. Patients with hypospadias and their brothers were matched with controls by year of birth and county. The following outcomes were evaluated (1) any psychiatric (2) psychotic, (3) mood, (4) anxiety, (5) eating, and (6) personality disorders, (7) substance misuse, (8) attention-deficit hyperactivity disorder (ADHD), (9) autism spectrum disorders (ASD), (10) intellectual disability, and (11) other behavioral/emotional disorders with onset in childhood. Results Patients with hypospadias were more likely to be diagnosed with intellectual disability (OR 3.2; 95% CI 2.8–3.8), ASD (1.4; 1.2–1.7), ADHD (1.5; 1.3–1.9), and behavioral/emotional disorders (1.4; 1.2–1.6) compared with the controls. Brothers of patients with hypospadias had an increased risk of ASD (1.6; 1.3–2.1) and other behavioral/emotional disorders with onset in childhood (1.2; 0.9–1.5) in comparison to siblings of healthy individuals. A slightly higher, although not statistically significant, risk was found for intellectual disability (1.3; 1.0–1.9). No relation between other psychiatric diagnosis and hypospadias was found. Conclusions This is the first study to identify an increased risk for neurodevelopmental disorders in patients with hypospadias, as well as an increased risk for ASD in their brothers, suggesting a common familial (genetic and/or environmental) liability. En ligne : http://dx.doi.org/10.1111/jcpp.12290 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=259

Increased Risk for Substance Use-Related Problems in Autism Spectrum Disorders: A Population-Based Cohort Study / Agnieszka BUTWICKA in Journal of Autism and Developmental Disorders, 47-1 (January 2017)  

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Melatonin use and the risk of self-harm and unintentional injuries in youths with and without psychiatric disorders / Marica LEONE in Journal of Child Psychology and Psychiatry, 64-7 (July 2023)  

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A twin study of genetic and environmental contributions to attention-deficit/hyperactivity disorder over time / Mark J. TAYLOR in Journal of Child Psychology and Psychiatry, 64-11 (November 2023)  

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