Duration of breast feeding and attention-deficit/hyperactivity disorder in United States preschool-aged children.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by difficulties sustaining attention and controlling hyperactivity and impulsive behavior. Population-based studies concerning the association between breast-feeding duration and ADHD among preschool-aged children in the United States (U.S.) have been sparse. AIMS: To determine whether there is an association between the duration of breast feeding and ADHD in U.S. children aged 2-5 years. METHODS AND PROCEDURES: We used nationally representative data from the 2016, 2017, and 2018 National Survey of Children's Health (NSCH) to examine the association between breast-feeding duration and ADHD in U.S. preschool-aged children. Sample characteristics were compared using Rao-Scott chi-square test, and adjusted prevalence odds ratios and 95 % confidence intervals were estimated using unconditional logistic regression. OUTCOMES AND RESULTS: Of the 20,453 children eligible for our study, 1.5 % had received a diagnosis of ADHD and 77.5 % were reported to have been fed human milk as infants. Prevalence odds of ADHD were 57 % lower among children fed human milk for 6-12 months compared to children never fed human milk after controlling for potential confounders. Among children with durations of breast feeding lasting less than 6 months or lasting 12 months or longer, prevalence odds of ADHD were not significantly lower than the comparison group, children who were never fed human milk, after controlling for potential confounders. CONCLUSIONS AND IMPLICATIONS: We noted an inverse association between breast feeding durations of 6-12 months and parent-reported diagnosis of ADHD in preschool-aged children in the U.S. Future studies should use longitudinal designs to examine ADHD and duration of breast-feeding measures.

Developmental mechanisms in the prodrome to psychosis.

Psychotic disorders continue to be among the most disabling and scientifically challenging of all mental illnesses. Accumulating research findings suggest that the etiologic processes underlying the development of these disorders are more complex than had previously been assumed. At the same time, this complexity has revealed a wider range of potential options for preventive intervention, both psychosocial and biological. In part, these opportunities result from our increased understanding of the dynamic and multifaceted nature of the neurodevelopmental mechanisms involved in the disease process, as well as the evidence that many of these entail processes that are malleable. In this article, we review the burgeoning research literature on the prodrome to psychosis, based on studies of individuals who meet clinical high risk criteria. This literature has examined a range of factors, including cognitive, genetic, psychosocial, and neurobiological. We then turn to a discussion of some contemporary models of the etiology of psychosis that emphasize the prodromal period. These models encompass the origins of vulnerability in fetal development, as well as postnatal stress, the immune response, and neuromaturational processes in adolescent brain development that appear to go awry during the prodrome to psychosis. Then, informed by these neurodevelopmental models of etiology, we turn to the application of new research paradigms that will address critical issues in future investigations. It is expected that these studies will play a major role in setting the stage for clinical trials aimed at preventive intervention.

The development of psychotic disorders in adolescence: a potential role for hormones.

This article is part of a Special Issue "Puberty and Adolescence". The notion that adolescence is characterized by dramatic changes in behavior, and often by emotional upheaval, is widespread and longstanding in popular western culture. In recent decades, this notion has gained increasing support from empirical research showing that the peri- and post-pubertal developmental stages are associated with a significant rise in the rate of psychiatric symptoms and syndromes. As a result, interest in adolescent development has burgeoned among researchers focused on the origins of schizophrenia and other psychotic disorders. Two factors have fueled this trend: 1) increasing evidence from longitudinal research that adolescence is the modal period for the emergence of "prodromal" manifestations, or precursors of psychotic symptoms, and 2) the rapidly accumulating scientific findings on brain structural and functional changes occurring during adolescence and young adulthood. Further, gonadal and adrenal hormones are beginning to play a more prominent role in conceptualizations of adolescent brain development, as well as in the origins of psychiatric symptoms during this period (Walker and Bollini, 2002; Walker et al., 2008). In this paper, we begin by providing an overview of the nature and course of psychotic disorders during adolescence/young adulthood. We then turn to the role of hormones in modulating normal brain development, and the potential role they might play in the abnormal brain changes that characterize youth at clinical high-risk (CHR) for psychosis. The activational and organizational effects of hormones are explored, with a focus on how hormone-induced changes might be linked with neuropathological processes in the emergence of psychosis.

The prodrome and clinical risk for psychotic disorders.

The psychosis prodrome offers great promise for identifying neural mechanisms involved in psychotic disorders and offers an opportunity to implement empirical interventions to delay, and ultimately ameliorate, illness onset. This article summarizes the literature on individuals in the putatively prodromal phase of psychosis/deemed at clinical high risk (CHR) for psychosis onset. Standardized measurement and manifestation of the CHR syndromes are discussed, followed by empirical findings that highlight the psychological deficits and biological abnormalities seen in CHR syndromes and psychotic disorders. Current controversies surrounding the diagnosis of CHR syndromes and issues related to the treatment of CHR individuals are also presented.

Longitudinal changes in cortisol secretion and conversion to psychosis in at-risk youth.

Elevations in hypothalamic-pituitary-adrenal (HPA) axis activity have been implicated in the origins and exacerbation of mental disorders. Several lines of investigation suggest HPA activity, indexed by increased cortisol, is elevated in patients with schizophrenia and other psychotic disorders. This study examined the relation of cortisol levels and longitudinal changes with psychotic outcomes in at-risk adolescents. Participants were 56 adolescents who met risk criteria for psychosis, namely, schizotypal personality disorder (n = 5), prodromal symptom criteria based on the Structured Interview for Prodromal Symptoms (n = 17), or both (n = 34). Of these, 14 subsequently met DSM-IV criteria for an Axis I psychotic disorder (schizophrenia, schizoaffective disorder, or mood disorder with psychotic features). Participants were assessed at baseline and then followed longitudinally. Salivary cortisol was sampled multiple times at initial assessment, interim follow-up, and 1-year follow-up. Area under the curve (AUC) was computed from the repeated cortisol measures. The findings indicate that at-risk subjects who subsequently developed psychosis showed significantly higher cortisol at the first follow-up, a trend at the 1-year follow-up, and a significantly larger AUC when compared to those who did not convert. A similar pattern of group differences emerged from analyses excluding those who may have converted prior to the 1-year follow-up. These findings converge with previous reports on HPA activity in psychosis, as well as theoretical assumptions concerning the effects of cortisol elevations on brain systems involved in psychotic symptoms. Future research with larger samples is needed to confirm and extend these results.

Catechol-O-methyltransferase modulation of cortisol secretion in psychiatrically at-risk and healthy adolescents.

OBJECTIVE: Recent research implicates the catechol-O-methyltransferase (COMT) ValMet polymorphism in stress sensitivity, through modulation of hypothalamic-pituitary-adrenal (HPA) function. In healthy samples, Met homozygosity has been associated with greater HPA activity (i.e., cortisol) and stress sensitivity, though findings are mixed among clinical samples. To date, there are no reports examining baseline or longitudinal changes in HPA activity as a function of COMT genotype in youth. This study tested the hypothesis that COMT genotype would be associated with cortisol secretion in normal and at-risk adolescents; specifically, that COMT genotype would be linked in a dose-response manner such that Met homozygotes would have the highest salivary cortisol levels, followed by heterozygotes, then Val homozygotes. In addition, this study examined the relation of COMT genotype with longitudinal changes in cortisol. METHODS: This study examined the association of COMT with salivary cortisol across a 1-year period in healthy and at-risk adolescents with Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision Axis II diagnoses. RESULTS: Results indicated higher cortisol levels for Met homozygotes (compared with heterozygotes and Val homozygotes) at the 1-year follow-up, and increased mean cortisol levels across a 1-year period among Met carriers, suggesting that COMT associates with differences in cortisol secretion during adolescence. CONCLUSION: Findings are discussed with respect to COMT genotype as a potential genetic indicator of psychiatric risk that modulates developmental changes in HPA activity.

Childhood and current autistic features in adolescents with schizotypal personality disorder.

The diagnostic boundaries between autistic- and schizophrenia-spectrum disorders have varied over the years, and some overlap in diagnostic criteria persists. The present study examined childhood and current signs of autistic disorder (AD) in adolescents with schizotypal personality disorder (SPD) or other personality disorders, as well as healthy controls. A structured interview was administered to rate participants' current symptoms. Participants' guardians were interviewed with the Autism Diagnostic Inventory-Revised (ADI-R), a clinical assessment of childhood and current autistic signs. Compared to both the other personality-disordered and healthy groups, adolescents with SPD were rated as having significantly more impairment on childhood and current social functioning, and having more unusual interests and behaviors. For the entire sample, impaired childhood social functioning and unusual interests and behaviors were associated with higher negative symptom scores. Current impairments in social functioning, unusual interests and behaviors, and communication were also linked with greater negative symptoms. However, neither childhood nor current autistic features significantly predicted later conversion to an Axis I psychotic disorder over the course of three years of follow-up. The findings indicate that past and current autistic signs are more common in adolescents with SPD, but neither current nor childhood autistic features are linked with conversion to psychosis.