Childhood and adolescence outcomes in offspring to parents with bipolar disorder: the impact of lifetime parental comorbidity, parental sex, and bipolar subtype / Mengping ZHOU ; Marcus BOMAN ; Arvid SJÖLANDER ; Henrik LARSSON ; Brian M. D'ONOFRIO ; Erik PETTERSSON ; Paul LICHTENSTEIN ; Mikael LANDÉN in Journal of Child Psychology and Psychiatry, 65-10 (October 2024)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 65-10 (October 2024) . - p.1355-1368 Titre : Childhood and adolescence outcomes in offspring to parents with bipolar disorder: the impact of lifetime parental comorbidity, parental sex, and bipolar subtype Type de document : Texte imprimé et/ou numérique Auteurs : Mengping ZHOU, Auteur ; Marcus BOMAN, Auteur ; Arvid SJÖLANDER, Auteur ; Henrik LARSSON, Auteur ; Brian M. D'ONOFRIO, Auteur ; Erik PETTERSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Mikael LANDÉN, Auteur Article en page(s) : p.1355-1368 Langues : Anglais (eng) Mots-clés : Bipolar disorder  adolescence  epidemiology  suicidal behavior  parent-child relationships Index. décimale : PER Périodiques Résumé : Background Offspring of parents with bipolar disorder have increased risks of their own psychopathology. However, a large-scale survey of psychiatric, somatic, and adverse social outcomes up to adulthood, which could aid in prioritizing and tailoring prevention, is lacking. It also remains to clarify how risks are modified by other parental factors. Methods Swedish population registers were linked to compare offspring having (N?=?24,788) and not having (N?=?247,880) a parent with bipolar disorder with respect to psychiatric diagnoses and psychotropic medication, birth-related and somatic conditions, social outcomes, accidents, suicide attempts, and mortality. Individuals were followed until age 18. We estimated the influence of lifetime parental psychiatric comorbidity, bipolar disorder subtype, and sex on outcomes. Results Children of parents with bipolar disorder had 2?3 times higher risks of all psychiatric diagnoses, except for bipolar disorder, for which the risk was 11-fold. Significantly increased risks were also found for several somatic conditions, low school grades, criminal behavior, victimization, accidents, and suicidal behavior. Adjusting for lifetime parental psychiatric comorbidity attenuated most associations. Offspring of a parent with bipolar disorder type 2 had statistically significantly higher risks of attention deficit hyperactivity disorder, respiratory tract conditions, and accidents compared with offspring of a parent with bipolar disorder type 1. Offspring of mothers with bipolar disorder had higher risks of several psychiatric diagnoses, respiratory tract conditions, low school grades, and accidents compared with offspring of fathers with bipolar disorder. Having two parents with bipolar disorder entailed the highest risks of psychiatric outcomes in offspring. Conclusions Early intervention and family support are particularly warranted for the offspring of a parent with bipolar disorder in the presence of lifetime parental psychiatric comorbidity, when the parent has bipolar disorder type 2, or when the mother or both parents have bipolar disorder. En ligne : https://doi.org/10.1111/jcpp.13982 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=535 [article] Childhood and adolescence outcomes in offspring to parents with bipolar disorder: the impact of lifetime parental comorbidity, parental sex, and bipolar subtype [Texte imprimé et/ou numérique] / Mengping ZHOU, Auteur ; Marcus BOMAN, Auteur ; Arvid SJÖLANDER, Auteur ; Henrik LARSSON, Auteur ; Brian M. D'ONOFRIO, Auteur ; Erik PETTERSSON, Auteur ; Paul LICHTENSTEIN, Auteur ; Mikael LANDÉN, Auteur . - p.1355-1368. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 65-10 (October 2024) . - p.1355-1368 Mots-clés : Bipolar disorder  adolescence  epidemiology  suicidal behavior  parent-child relationships Index. décimale : PER Périodiques Résumé : Background Offspring of parents with bipolar disorder have increased risks of their own psychopathology. However, a large-scale survey of psychiatric, somatic, and adverse social outcomes up to adulthood, which could aid in prioritizing and tailoring prevention, is lacking. It also remains to clarify how risks are modified by other parental factors. Methods Swedish population registers were linked to compare offspring having (N?=?24,788) and not having (N?=?247,880) a parent with bipolar disorder with respect to psychiatric diagnoses and psychotropic medication, birth-related and somatic conditions, social outcomes, accidents, suicide attempts, and mortality. Individuals were followed until age 18. We estimated the influence of lifetime parental psychiatric comorbidity, bipolar disorder subtype, and sex on outcomes. Results Children of parents with bipolar disorder had 2?3 times higher risks of all psychiatric diagnoses, except for bipolar disorder, for which the risk was 11-fold. Significantly increased risks were also found for several somatic conditions, low school grades, criminal behavior, victimization, accidents, and suicidal behavior. Adjusting for lifetime parental psychiatric comorbidity attenuated most associations. Offspring of a parent with bipolar disorder type 2 had statistically significantly higher risks of attention deficit hyperactivity disorder, respiratory tract conditions, and accidents compared with offspring of a parent with bipolar disorder type 1. Offspring of mothers with bipolar disorder had higher risks of several psychiatric diagnoses, respiratory tract conditions, low school grades, and accidents compared with offspring of fathers with bipolar disorder. Having two parents with bipolar disorder entailed the highest risks of psychiatric outcomes in offspring. Conclusions Early intervention and family support are particularly warranted for the offspring of a parent with bipolar disorder in the presence of lifetime parental psychiatric comorbidity, when the parent has bipolar disorder type 2, or when the mother or both parents have bipolar disorder. En ligne : https://doi.org/10.1111/jcpp.13982 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=535

Relative immaturity and ADHD: findings from nationwide registers, parent- and self-reports / Linda HALLDNER in Journal of Child Psychology and Psychiatry, 55-8 (August 2014)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 55-8 (August 2014) . - p.897-904 Titre : Relative immaturity and ADHD: findings from nationwide registers, parent- and self-reports Type de document : Texte imprimé et/ou numérique Auteurs : Linda HALLDNER, Auteur ; Annika TILLANDER, Auteur ; Cecilia LUNDHOLM, Auteur ; Marcus BOMAN, Auteur ; Niklas LANGSTROM, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur Article en page(s) : p.897-904 Langues : Anglais (eng) Mots-clés : ADHD  child development  pharmacotherapy  epidemiological studies Index. décimale : PER Périodiques Résumé : Background We addressed if immaturity relative to peers reflected in birth month increases the likelihood of ADHD diagnosis and treatment. Methods We linked nationwide Patient and Prescribed Drug Registers and used prospective cohort and nested case–control designs to study 6–69 year-old individuals in Sweden from July 2005 to December 2009 (Cohort 1). Cohort 1 included 56,263 individuals diagnosed with ADHD or ever used prescribed ADHD-specific medication. Complementary population-representative cohorts provided DSM-IV ADHD symptom ratings; parent-reported for 10,760 9-year-old twins born 1995–2000 from the CATSS study (Cohort 2) and self-reported for 6,970 adult twins age 20–47 years born 1959–1970 from the STAGE study (Cohort 3). We calculated odds ratios (OR:s) for ADHD across age for individuals born in November/December compared to January/February (Cohort 1). ADHD symptoms in Cohorts 2 and 3 were studied as a function of calendar birth month. Results ADHD diagnoses and medication treatment were both significantly more common in individuals born in November/December versus January/February; peaking at ages 6 (OR: 1.8; 95% CI: 1.5–2.2) and 7 years (OR: 1.6; 95% CI: 1.3–1.8) in the Patient and Prescribed Drug Registers, respectively. We found no corresponding differences in parent- or self-reported ADHD symptoms by calendar birth month. Conclusion Relative immaturity compared to class mates might contribute to ADHD diagnosis and pharmacotherapy despite absence of parallel findings in reported ADHD symptom loads by relative immaturity. Increased clinical awareness of this phenomenon may be warranted to decrease risk for imprecise diagnostics and treatment. We speculate that flexibility regarding age at school start according to individual maturity could reduce developmentally inappropriate demands on children and improve the precision of ADHD diagnostic practice and pharmacological treatment. En ligne : http://dx.doi.org/10.1111/jcpp.12229 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=237 [article] Relative immaturity and ADHD: findings from nationwide registers, parent- and self-reports [Texte imprimé et/ou numérique] / Linda HALLDNER, Auteur ; Annika TILLANDER, Auteur ; Cecilia LUNDHOLM, Auteur ; Marcus BOMAN, Auteur ; Niklas LANGSTROM, Auteur ; Henrik LARSSON, Auteur ; Paul LICHTENSTEIN, Auteur . - p.897-904. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 55-8 (August 2014) . - p.897-904 Mots-clés : ADHD  child development  pharmacotherapy  epidemiological studies Index. décimale : PER Périodiques Résumé : Background We addressed if immaturity relative to peers reflected in birth month increases the likelihood of ADHD diagnosis and treatment. Methods We linked nationwide Patient and Prescribed Drug Registers and used prospective cohort and nested case–control designs to study 6–69 year-old individuals in Sweden from July 2005 to December 2009 (Cohort 1). Cohort 1 included 56,263 individuals diagnosed with ADHD or ever used prescribed ADHD-specific medication. Complementary population-representative cohorts provided DSM-IV ADHD symptom ratings; parent-reported for 10,760 9-year-old twins born 1995–2000 from the CATSS study (Cohort 2) and self-reported for 6,970 adult twins age 20–47 years born 1959–1970 from the STAGE study (Cohort 3). We calculated odds ratios (OR:s) for ADHD across age for individuals born in November/December compared to January/February (Cohort 1). ADHD symptoms in Cohorts 2 and 3 were studied as a function of calendar birth month. Results ADHD diagnoses and medication treatment were both significantly more common in individuals born in November/December versus January/February; peaking at ages 6 (OR: 1.8; 95% CI: 1.5–2.2) and 7 years (OR: 1.6; 95% CI: 1.3–1.8) in the Patient and Prescribed Drug Registers, respectively. We found no corresponding differences in parent- or self-reported ADHD symptoms by calendar birth month. Conclusion Relative immaturity compared to class mates might contribute to ADHD diagnosis and pharmacotherapy despite absence of parallel findings in reported ADHD symptom loads by relative immaturity. Increased clinical awareness of this phenomenon may be warranted to decrease risk for imprecise diagnostics and treatment. We speculate that flexibility regarding age at school start according to individual maturity could reduce developmentally inappropriate demands on children and improve the precision of ADHD diagnostic practice and pharmacological treatment. En ligne : http://dx.doi.org/10.1111/jcpp.12229 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=237

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 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 [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

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