Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Résultat de la recherche
4 recherche sur le mot-clé 'Sweden/epidemiology'
Affiner la recherche Générer le flux rss de la recherche
Partager le résultat de cette recherche Faire une suggestion
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)
[article]
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
in Journal of Child Psychology and Psychiatry > 63-9 (September 2022) . - p.1092-1102[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 Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden / R. M. GARDNER in Autism Research, 14-9 (September 2021)
[article]
Titre : Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden Type de document : Texte imprimé et/ou numérique Auteurs : R. M. GARDNER, Auteur ; I. SAMUELSSON, Auteur ; E. G. SEVERANCE, Auteur ; H. SJÖQVIST, Auteur ; R. H. YOLKEN, Auteur ; C. DALMAN, Auteur ; H. KARLSSON, Auteur Article en page(s) : p.2002-2016 Langues : Anglais (eng) Mots-clés : Attention Deficit Disorder with Hyperactivity Autism Spectrum Disorder/epidemiology Case-Control Studies Female Gliadin Humans Pregnancy Sweden/epidemiology attention deficit hyperactivity disorder autism spectrum disorder gliadin gluten-sensitivity intellectual disability Index. décimale : PER Périodiques Résumé : While individuals diagnosed with autism spectrum disorders (ASD) have higher levels of antibodies directed towards gliadin, a component of wheat gluten, no study has examined anti-gliadin antibodies (AGA) in etiologically relevant periods before diagnosis. The objective of this study was to investigate if maternal levels of AGA, during pregnancy and at the time of birth, are associated with ASD in offspring. We analyzed AGA in archived neonatal dried blood spots (NDBS) for 921 ASD cases and 1090 controls, and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations with ASD diagnoses as a group and considering common comorbidities (intellectual disability [ID] and attention-deficit/hyperactivity disorder). We compared 206 cases to their unaffected siblings to examine the potential for confounding by shared familial factors. Odds of ASD tended to be lower among those with the highest levels (?90th percentile) of AGA compared to those with low levels (<80th percentile; OR 0.78, 95% CI 0.56-1.09, measured in NDBS). This pattern was more apparent for ASD with comorbid ID when measured in NDBS (0.51, 0.30-0.87), with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of AGA were similarly associated with lower odds of ASD in the sibling comparison. In summary, we found little association between maternal antibodies raised against components of gluten and risk of ASD in general. Exposure to high levels of AGA in the pre- and perinatal periods may be protective in terms of risk for ASD with ID. LAY SUMMARY: There is a debate among both scientists and community members as to whether an immune reaction to gluten exposure could be considered a cause of autism. We examined antibodies that are directed against gliadin, a part of gluten, in samples collected from pregnant mothers and their newborn babies. We did not see any major differences in the antibody level among those children diagnosed with ASD or their mothers compared to children who were not diagnosed with ASD. High levels of the antibodies were in fact associated with a somewhat lower risk of ASD with co-occurring intellectual disabilities, though we cannot tell from this study why that might be the case. En ligne : http://dx.doi.org/10.1002/aur.2567 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450
in Autism Research > 14-9 (September 2021) . - p.2002-2016[article] Maternal antibodies to gliadin and autism spectrum disorders in offspring-A population-based case-control study in Sweden [Texte imprimé et/ou numérique] / R. M. GARDNER, Auteur ; I. SAMUELSSON, Auteur ; E. G. SEVERANCE, Auteur ; H. SJÖQVIST, Auteur ; R. H. YOLKEN, Auteur ; C. DALMAN, Auteur ; H. KARLSSON, Auteur . - p.2002-2016.
Langues : Anglais (eng)
in Autism Research > 14-9 (September 2021) . - p.2002-2016
Mots-clés : Attention Deficit Disorder with Hyperactivity Autism Spectrum Disorder/epidemiology Case-Control Studies Female Gliadin Humans Pregnancy Sweden/epidemiology attention deficit hyperactivity disorder autism spectrum disorder gliadin gluten-sensitivity intellectual disability Index. décimale : PER Périodiques Résumé : While individuals diagnosed with autism spectrum disorders (ASD) have higher levels of antibodies directed towards gliadin, a component of wheat gluten, no study has examined anti-gliadin antibodies (AGA) in etiologically relevant periods before diagnosis. The objective of this study was to investigate if maternal levels of AGA, during pregnancy and at the time of birth, are associated with ASD in offspring. We analyzed AGA in archived neonatal dried blood spots (NDBS) for 921 ASD cases and 1090 controls, and in paired maternal sera collected earlier in pregnancy for a subset of 547 cases and 428 controls. We examined associations with ASD diagnoses as a group and considering common comorbidities (intellectual disability [ID] and attention-deficit/hyperactivity disorder). We compared 206 cases to their unaffected siblings to examine the potential for confounding by shared familial factors. Odds of ASD tended to be lower among those with the highest levels (?90th percentile) of AGA compared to those with low levels (<80th percentile; OR 0.78, 95% CI 0.56-1.09, measured in NDBS). This pattern was more apparent for ASD with comorbid ID when measured in NDBS (0.51, 0.30-0.87), with a similar trend in maternal sera (0.55, 0.24-1.29). High levels of AGA were similarly associated with lower odds of ASD in the sibling comparison. In summary, we found little association between maternal antibodies raised against components of gluten and risk of ASD in general. Exposure to high levels of AGA in the pre- and perinatal periods may be protective in terms of risk for ASD with ID. LAY SUMMARY: There is a debate among both scientists and community members as to whether an immune reaction to gluten exposure could be considered a cause of autism. We examined antibodies that are directed against gliadin, a part of gluten, in samples collected from pregnant mothers and their newborn babies. We did not see any major differences in the antibody level among those children diagnosed with ASD or their mothers compared to children who were not diagnosed with ASD. High levels of the antibodies were in fact associated with a somewhat lower risk of ASD with co-occurring intellectual disabilities, though we cannot tell from this study why that might be the case. En ligne : http://dx.doi.org/10.1002/aur.2567 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=450 Effect of co-twin gender on neurodevelopmental symptoms: a twin register study / J. M. ERIKSSON in Molecular Autism, 7 (2016)
[article]
Titre : Effect of co-twin gender on neurodevelopmental symptoms: a twin register study Type de document : Texte imprimé et/ou numérique Auteurs : J. M. ERIKSSON, Auteur ; S. LUNDSTRÖM, Auteur ; P. LICHTENSTEIN, Auteur ; Susanne BEJEROT, Auteur ; E. ERIKSSON, Auteur Article en page(s) : 8p. Langues : Anglais (eng) Mots-clés : Attention Deficit Disorder with Hyperactivity/genetics/physiopathology Autism Spectrum Disorder/genetics/physiopathology Child Comorbidity Diseases in Twins Female Follow-Up Studies Gender Identity Humans Interview, Psychological Male Neurodevelopmental Disorders/genetics/physiopathology Parents Pregnancy Prenatal Exposure Delayed Effects Sex Characteristics Stereotyped Behavior Sweden/epidemiology Testosterone/physiology Tic Disorders/genetics/physiopathology Twins, Dizygotic/psychology Asperger syndrome Attention-deficit hyperactivity disorders Autistic disorder Symptom assessment Twin study Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental disorders thought to have both genetic and environmental causes. It has been hypothesized that exposure to elevated levels of prenatal testosterone is associated with elevated traits of ASD and ADHD. Assuming that testosterone levels from a dizygotic male twin fetus may lead to enhanced testosterone exposure of its co-twins, we aimed to test the prenatal testosterone hypothesis by comparing same-sex with opposite-sex dizygotic twins with respect to neurodevelopmental symptoms. METHODS: Neuropsychiatric traits were assessed in a population-based twin cohort from the Child and Adolescent Twin Study in Sweden (CATSS). Parental interviews were conducted for 16,312 dizygotic twins, 9 and 12 years old, with the Autism-Tics, ADHD, and other Comorbidities inventory (A-TAC). RESULTS: Girls with a female co-twin had an increased risk of reaching the cut-off score for ADHD compared with girls with a male co-twin. Both boys and girls with a female co-twin displayed a larger number of traits related to attention deficit and repetitive and stereotyped behaviors than those with a male twin. In girls, this also extended to social interaction and the combined measures for ASD and ADHD, however, with small effect sizes. CONCLUSIONS: Our results are reverse to what would have been expected from the prenatal testosterone hypothesis but consistent with a previous study of ASD and ADHD traits in dizygotic twins. The seemingly protective effect for girls of having a twin brother may be an effect of parent report bias, but may also be an unexpected effect of sharing the intrauterine environment with a male co-twin. En ligne : http://dx.doi.org/10.1186/s13229-016-0074-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328
in Molecular Autism > 7 (2016) . - 8p.[article] Effect of co-twin gender on neurodevelopmental symptoms: a twin register study [Texte imprimé et/ou numérique] / J. M. ERIKSSON, Auteur ; S. LUNDSTRÖM, Auteur ; P. LICHTENSTEIN, Auteur ; Susanne BEJEROT, Auteur ; E. ERIKSSON, Auteur . - 8p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 8p.
Mots-clés : Attention Deficit Disorder with Hyperactivity/genetics/physiopathology Autism Spectrum Disorder/genetics/physiopathology Child Comorbidity Diseases in Twins Female Follow-Up Studies Gender Identity Humans Interview, Psychological Male Neurodevelopmental Disorders/genetics/physiopathology Parents Pregnancy Prenatal Exposure Delayed Effects Sex Characteristics Stereotyped Behavior Sweden/epidemiology Testosterone/physiology Tic Disorders/genetics/physiopathology Twins, Dizygotic/psychology Asperger syndrome Attention-deficit hyperactivity disorders Autistic disorder Symptom assessment Twin study Index. décimale : PER Périodiques Résumé : BACKGROUND: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental disorders thought to have both genetic and environmental causes. It has been hypothesized that exposure to elevated levels of prenatal testosterone is associated with elevated traits of ASD and ADHD. Assuming that testosterone levels from a dizygotic male twin fetus may lead to enhanced testosterone exposure of its co-twins, we aimed to test the prenatal testosterone hypothesis by comparing same-sex with opposite-sex dizygotic twins with respect to neurodevelopmental symptoms. METHODS: Neuropsychiatric traits were assessed in a population-based twin cohort from the Child and Adolescent Twin Study in Sweden (CATSS). Parental interviews were conducted for 16,312 dizygotic twins, 9 and 12 years old, with the Autism-Tics, ADHD, and other Comorbidities inventory (A-TAC). RESULTS: Girls with a female co-twin had an increased risk of reaching the cut-off score for ADHD compared with girls with a male co-twin. Both boys and girls with a female co-twin displayed a larger number of traits related to attention deficit and repetitive and stereotyped behaviors than those with a male twin. In girls, this also extended to social interaction and the combined measures for ASD and ADHD, however, with small effect sizes. CONCLUSIONS: Our results are reverse to what would have been expected from the prenatal testosterone hypothesis but consistent with a previous study of ASD and ADHD traits in dizygotic twins. The seemingly protective effect for girls of having a twin brother may be an effect of parent report bias, but may also be an unexpected effect of sharing the intrauterine environment with a male co-twin. En ligne : http://dx.doi.org/10.1186/s13229-016-0074-z Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328 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)
[article]
Titre : Shared familial risk factors between autism spectrum disorder and obesity - a register-based familial coaggregation cohort study Type de document : Texte imprimé et/ou numérique 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
in Journal of Child Psychology and Psychiatry > 63-8 (August 2022) . - p.890-899[article] Shared familial risk factors between autism spectrum disorder and obesity - a register-based familial coaggregation cohort study [Texte imprimé et/ou numérique] / 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