ABSTRACT
La exposición prenatal al alcohol es causa de alteraciones somáticas, cognitivas y conductuales que se agrupan bajo el término de trastorno del espectro alcohólico fetal (TEAF). La evolución a largo plazo de los sujetos afectados a menudo es desfavorable, especialmente a nivel académico y adaptativo social. En el perfil neuropsicológico es característica la disfunción ejecutiva a menudo asociada a trastornos de la conducta que evolucionan en muchos casos hacia la delincuencia a partir de la adolescencia y en la edad adulta. Se han descrito también déficits de las habilidades sociales y la empatía. La exposición prenatal al alcohol constituye la causa más frecuente de trastorno del neurodesarrollo adquirido y prevenible.
Prenatal exposure to alcohol is the cause of cognitive and behavioural disorders grouped under the term fetal alcohol spectrum disorders (FASD). The long-term evolution of subjects with FASD is often unfavourable, especially in social and academic fields. Executive dysfunction is a hallmark deficit for children with FASD with increased rates of externalizing behaviours, such as aggressiveness and frequently delinquency in adolescence and adulthood. Deficits in social skills, empathy and communication ability are frequent observed among FASD. Prenatal exposure to alcohol is the most frequent cause of acquired and preventable neurodevelopmental disorder.
Subject(s)
Humans , Animals , Female , Pregnancy , Developmental Disabilities/diagnosis , Fetal Alcohol Spectrum Disorders/diagnosis , Prognosis , Social Behavior Disorders/etiology , Chick Embryo , Developmental Disabilities/complications , Developmental Disabilities/physiopathology , Uncertainty , Diagnostic Errors , Fetal Alcohol Spectrum Disorders/physiopathologyABSTRACT
Prenatal exposure to alcohol is the cause of cognitive and behavioural disorders grouped under the term fetal alcohol spectrum disorders (FASD). The long-term evolution of subjects with FASD is often unfavourable, especially in social and academic fields. Executive dysfunction is a hallmark deficit for children with FASD with increased rates of externalizing behaviours, such as aggressiveness and frequently delinquency in adolescence and adulthood. Deficits in social skills, empathy and communication ability are frequent observed among FASD. Prenatal exposure to alcohol is the most frequent cause of acquired and preventable neurodevelopmental disorder.
La exposición prenatal al alcohol es causa de alteraciones somáticas, cognitivas y conductuales que se agrupan bajo el término de trastorno del espectro alcohólico fetal (TEAF). La evolución a largo plazo de los sujetos afectados a menudo es desfavorable, especialmente a nivel académico y adaptativo social. En el perfil neuropsicológico es característica la disfunción ejecutiva a menudo asociada a trastornos de la conducta que evolucionan en muchos casos hacia la delincuencia a partir de la adolescencia y en la edad adulta. Se han descrito también déficits de las habilidades sociales y la empatía. La exposición prenatal al alcohol constituye la causa más frecuente de trastorno del neurodesarrollo adquirido y prevenible.
Subject(s)
Developmental Disabilities/diagnosis , Fetal Alcohol Spectrum Disorders/diagnosis , Animals , Chick Embryo , Developmental Disabilities/complications , Developmental Disabilities/physiopathology , Diagnostic Errors , Female , Fetal Alcohol Spectrum Disorders/physiopathology , Humans , Pregnancy , Prognosis , Social Behavior Disorders/etiology , UncertaintyABSTRACT
OBJECTIVE: To investigate the prospective associations between early childhood lead exposure and subsequent risk of attention deficit hyperactivity disorder (ADHD) in childhood and its potential effect modifiers. STUDY DESIGN: We analyzed data from 1479 mother-infant pairs (299 ADHD, 1180 neurotypical) in the Boston Birth Cohort. The child's first blood lead measurement and physician-diagnosed ADHD was obtained from electronic medical records. Graphic plots and multiple logistic regression were used to examine dose-response associations between lead exposure and ADHD and potential effect modifiers, adjusting for pertinent covariables. RESULTS: We found that 8.9% of the children in the Boston Birth Cohort had elevated lead levels (5-10 µg/dL) in early childhood, which was associated with a 66% increased risk of ADHD (OR, 1.66; 95% CI, 1.08-2.56). Among boys, the association was significantly stronger (OR, 2.49; 95% CI, 1.46-4.26); in girls, the association was largely attenuated (P value for sex-lead interaction = .017). The OR of ADHD associated with elevated lead levels among boys was reduced by one-half if mothers had adequate high-density lipoprotein levels compared with low high-density lipoprotein, or if mothers had low stress compared with high stress during pregnancy. CONCLUSIONS: Elevated early childhood blood lead levels increased the risk of ADHD. Boys were more vulnerable than girls at a given lead level. This risk of ADHD in boys was reduced by one-half if the mother had adequate high-density lipoprotein levels or low stress. These findings shed new light on the sex difference in ADHD and point to opportunities for early risk assessment and primary prevention of ADHD.