4 research outputs found
Association Between Childhood to Adolescent Attention Deficit/Hyperactivity Disorder Symptom Trajectories and Late Adolescent Disordered Eating
Purpose Disordered eating is more prevalent among adolescents with attention deficit/hyperactivity disorder. Both inattention and hyperactivity/impulsivity symptoms show strong associations with disordered eating, but few investigations of these associations have been longitudinal. Thus, we examined the effect of childhood to adolescent inattention and hyperactivity/impulsivity symptom trajectories on late adolescent disordered eating. Methods We used growth mixture modeling to identify distinct inattention and hyperactivity/impulsivity symptom trajectories (called “classes”) across three time points (ages 8–9, 13–14, and 16–17 years) in the Swedish Twin study of CHild and Adolescent Development. The resulting classes were used to predict Eating Disorder Inventory-2 Bulimia, Drive for Thinness, and Body Dissatisfaction subscales at age 16–17 years, with adjustment for sex and body mass index at age 16–17 years. Results The combined inattention and hyperactivity/impulsivity symptom trajectory classes included: a “low symptom” class characterized by low inattention and hyperactivity/impulsivity throughout childhood/adolescence; a “predominantly inattention” class characterized by elevated inattention, but not hyperactivity/impulsivity, throughout childhood/adolescence; a “predominantly hyp/imp” class characterized by elevated hyperactivity/impulsivity, but not inattention, throughout childhood/adolescence; and a “both inattention and hyp/imp” class characterized by elevated inattention and hyperactivity/impulsivity throughout childhood/adolescence. After adjusting for sex and body mass index or sex and anxiety/depression symptoms, the “both inattention and hyp/imp” (vs. “low symptom”) class predicted significantly higher Eating Disorder Inventory-2 subscale scores during late adolescence. Conclusions Increased vigilance for disordered eating among children who have both inattention and hyperactivity/impulsivity symptoms throughout childhood and adolescence could aid in early identification of eating disorders
Paternal age at childbirth and eating disorders in offspring
Background. Advanced paternal age at childbirth is associated with psychiatric disorders in offspring, including schizophrenia,
bipolar disorder and autism. However, few studies have investigated paternal age’s relationship with eating
disorders in offspring. In a large, population-based cohort, we examined the association between paternal age and offspring
eating disorders, and whether that association remains after adjustment for potential confounders (e.g. parental
education level) that may be related to late/early selection into fatherhood and to eating disorder incidence.
Method. Data for 2 276 809 individuals born in Sweden 1979–2001 were extracted from Swedish population and healthcare
registers. The authors used Cox proportional hazards models to examine the effect of paternal age on the first incidence
of healthcare-recorded anorexia nervosa (AN) and all eating disorders (AED) occurring 1987–2009. Models were
adjusted for sex, birth order, maternal age at childbirth, and maternal and paternal covariates including country of birth,
highest education level, and lifetime psychiatric and criminal history.
Results. Even after adjustment for covariates including maternal age, advanced paternal age was associated with
increased risk, and younger paternal age with decreased risk, of AN and AED. For example, the fully adjusted hazard
ratio for the 45+ years (v. the 25–29 years) paternal age category was 1.32 [95% confidence interval (CI) 1.14–1.53] for AN
and 1.26 (95% CI 1.13–1.40) for AED.
Conclusions. In this large, population-based cohort, paternal age at childbirth was positively associated with eating disorders
in offspring, even after adjustment for potential confounders. Future research should further explore potential
explanations for the association, including de novo mutations in the paternal germline.NonePublishe