Showing papers by "Stephen V. Faraone published in 2006"
TL;DR: Efforts are needed to increase the detection and treatment of adult ADHD and research is needed to determine whether effective treatment would reduce the onset, persistence, and severity of disorders that co-occur with adult ADHD.
Abstract: Objective: Despite growing interest in adult attention deficit hyperactivity disorder (ADHD), little is known about its prevalence or correlates. Method: A screen for adult ADHD was included in a probability subsample (N=3,199) of 18–44-year-old respondents in the National Comorbidity Survey Replication, a nationally representative household survey that used a lay-administered diagnostic interview to assess a wide range of DSM-IV disorders. Blinded clinical follow-up interviews of adult ADHD were carried out with 154 respondents, oversampling those with positive screen results. Multiple imputation was used to estimate prevalence and correlates of clinician-assessed adult ADHD. Results: The estimated prevalence of current adult ADHD was 4.4%. Significant correlates included being male, previously married, unemployed, and non-Hispanic white. Adult ADHD was highly comorbid with many other DSM-IV disorders assessed in the survey and was associated with substantial role impairment. The majority of cases were u...
3,280 citations
TL;DR: By their young adult years, ADHD youth were at high risk for a wide range of adverse psychiatric outcomes including markedly elevated rates of antisocial, addictive, mood and anxiety disorders.
Abstract: Background Our objective was to estimate the lifetime prevalence of psychopathology in a sample of youth with and without attention deficit hyperactivity disorder (ADHD) through young adulthood using contemporaneous diagnostic and analytic techniques. Method We conducted a case-control, 10-year prospective study of ADHD youth. At baseline, we assessed consecutively referred male, Caucasian children with (n=140) and without (n=120) DSM-III-R ADHD, aged 6-18 years, ascertained from psychiatric and pediatric sources to allow for generalizability of results. At the 10-year follow-up, 112 (80%) and 105 (88%) of the ADHD and control children, respectively, were reassessed (mean age 22 years). We created the following categories of psychiatric disorders: Major Psychopathology (mood disorders and psychosis), Anxiety Disorders, Antisocial Disorders (conduct, oppositional-defiant, and antisocial personality disorder), Developmental Disorders (elimination, language, and tics disorder), and Substance Dependence Disorders (alcohol, drug, and nicotine dependence), as measured by blinded structured diagnostic interview. Results The lifetime prevalence for all categories of psychopathology were significantly greater in ADHD young adults compared to controls, with hazard ratios and 95% confidence intervals of 6.1 (3.5-10.7), 2.2 (1.5-3.2), 5.9 (3.9-8.8), 2.5 (1.7-3.6), and 2.0 (1.3-3.0), respectively, for the categories described above. Conclusions By their young adult years, ADHD youth were at high risk for a wide range of adverse psychiatric outcomes including markedly elevated rates of antisocial, addictive, mood and anxiety disorders. These prospective findings provide further evidence for the high morbidity associated with ADHD across the life-cycle and stress the importance of early recognition of this disorder for prevention and intervention strategies.
778 citations
TL;DR: The total insula volumes, and the left aINS(lbl) in particular, were significantly volumetrically smaller in schizophrenia compared to controls, and significantly correlated with bizarre behavior.
572 citations
King's College London1, Trinity College, Dublin2, Radboud University Nijmegen3, Memorial Hospital of South Bend4, University of Göttingen5, Ghent University6, Shaare Zedek Medical Center7, University of Valencia8, University Medical Center Groningen9, University of Zurich10, VU University Amsterdam11, University of Southampton12, State University of New York Upstate Medical University13
TL;DR: In this article, the authors examined 1038 single-nucleotide polymorphisms (SNPs) spanning 51 candidate genes involved in the regulation of neurotransmitter pathways, particularly dopamine, norepinephrine and serotonin pathways, in addition to circadian rhythm genes.
Abstract: Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental disorder, starting in early childhood and persisting into adulthood in the majority of cases. Family and twin studies have demonstrated the importance of genetic factors and candidate gene association studies have identified several loci that exert small but significant effects on ADHD. To provide further clarification of reported associations and identify novel associated genes, we examined 1038 single-nucleotide polymorphisms (SNPs) spanning 51 candidate genes involved in the regulation of neurotransmitter pathways, particularly dopamine, norepinephrine and serotonin pathways, in addition to circadian rhythm genes. Analysis used within family tests of association in a sample of 776 DSM-IV ADHD combined type cases ascertained for the International Multi-centre ADHD Gene project. We found nominal significance with one or more SNPs in 18 genes, including the two most replicated findings in the literature: DRD4 and DAT1. Gene-wide tests, adjusted for the number of SNPs analysed in each gene, identified associations with TPH2, ARRB2, SYP, DAT1, ADRB2, HES1, MAOA and PNMT. Further studies will be needed to confirm or refute the observed associations and their generalisability to other samples.
532 citations
TL;DR: Adults who reported having received a diagnosis of ADHD in the community had significant impairment in multiple domains of functioning compared with age- and gender-matched controls without this diagnosis, highly consistent with findings derived from carefully diagnosed referred samples.
Abstract: OBJECTIVE The objective of this study was to evaluate functional impairments in a nonreferred sample of adults identifying themselves as having been diagnosed with attention-deficit/hyperactivity disorder (ADHD) by a clinician in their community. METHOD We completed a survey in April and May 2003 of a community sample of 500 adults who reported having received a diagnosis of ADHD in the community and 501 gender- and age-matched comparisons from a national sample representative of the U.S. population. RESULTS Adults with self-reports of diagnosed ADHD in the community were significantly less likely to have graduated high school (83% vs. 93% of controls; p < or = .001) or obtain a college degree (19% vs. 26%; p < .01), were less likely to be currently employed (52% vs. 72%; p < or = .001), and had significantly more mean job changes over 10 years (5.4 vs. 3.4 jobs; p < or = .001). They also were significantly more likely to have been arrested (37% vs. 18% of controls; p < or = .001) or divorced (28% vs. 15%; p < or = .001) and were significantly less satisfied (p < or = .001) with their family, social, and professional lives. CONCLUSION Adults who reported having received a diagnosis of ADHD in the community had significant impairment in multiple domains of functioning compared with age- and gender-matched controls without this diagnosis, highly consistent with findings derived from carefully diagnosed referred samples.
531 citations
TL;DR: The pilot Adult ADHD Self-Report Scale symptom checklist is a reliable and valid scale for evaluating ADHD for adults and shows a high internal consistency and high concurrent validity with the rater-administered ADHD RS.
Abstract: Background. The goal of this study was to validate the pilot Adult ADHD Self-Report Scale (pilot ASRS) versus standard clinician ratings on the ADHD Rating Scale (ADHD RS).Method. Sixty adult ADHD patients took the self-administered ADHD RS and then raters administered the standard ADHD RS. Internal consistency of symptom scores was assessed by Cronbach's alpha. Agreement of raters was established by intra-class correlation coefficients (ICCs) between scales.Results. Internal consistency was high for both patient and rater-administered versions (Cronbach's alpha 0.88, 0.89, respectively). The ICC between scales for total scores was also high (0.84); ICCs for subset symptom scores were also high (both 0.83). There was acceptable agreement for individual items (% agreement: 43%–72%) and significant kappa coefficients for all items (p < 0.001).Conclusions. The pilot Adult ADHD Self-Report Scale symptom checklist is a reliable and valid scale for evaluating ADHD for adults and shows a high internal consistenc...
530 citations
TL;DR: It is suggested that MB-COMT over-expression due to promoter hypomethylation and/or hyperactive allele of COMT may increase dopamine degradation in the frontal lobe providing a molecular basis for the shared symptoms of schizophrenia and bipolar disorder.
Abstract: The variability in phenotypic presentations and the lack of consistency of genetic associations in mental illnesses remain a major challenge in molecular psychiatry. Recently, it has become increasingly clear that altered promoter DNA methylation could play a critical role in mediating differential regulation of genes and in facilitating short-term adaptation in response to the environment. Here, we report the investigation of the differential activity of membrane-bound catechol-O-methyltransferase (MB-COMT) due to altered promoter methylation and the nature of the contribution of COMT Val158Met polymorphism as risk factors for schizophrenia and bipolar disorder by analyzing 115 post-mortem brain samples from the frontal lobe. These studies are the first to reveal that the MB-COMT promoter DNA is frequently hypomethylated in schizophrenia and bipolar disorder patients, compared with the controls (methylation rate: 26 and 29 versus 60%; P = 0.004 and 0.008, respectively), particularly in the left frontal lobes (methylation rate: 29 and 30 versus 81%; P = 0.003 and 0.002, respectively). Quantitative gene-expression analyses showed a corresponding increase in transcript levels of MB-COMT in schizophrenia and bipolar disorder patients compared with the controls (P = 0.02) with an accompanying inverse correlation between MB-COMT and DRD1 expression. Furthermore, there was a tendency for the enrichment of the Val allele of the COMT Val158Met polymorphism with MB-COMT hypomethylation in the patients. These findings suggest that MB-COMT over-expression due to promoter hypomethylation and/or hyperactive allele of COMT may increase dopamine degradation in the frontal lobe providing a molecular basis for the shared symptoms of schizophrenia and bipolar disorder.
441 citations
TL;DR: The data support the idea that adults with ADHD have a valid disorder with persistent biological features, with volume differences in brain regions in areas involved in attention and executive control.
357 citations
University of Göttingen1, University of Dundee2, University of London3, University of Cagliari4, King's College London5, Katholieke Universiteit Leuven6, University of Cologne7, State University of New York Upstate Medical University8, University of Amsterdam9, University of Zurich10, University of Southampton11
TL;DR: A systematic review of published and unpublished data on the use of long-acting medications in ADHD and hyperkinetic disorder is reported, giving effect sizes and numbers-to-treat for extended-release stimulant preparations and atomoxetine (ATX).
Abstract: A systematic review of published and unpublished data on the use of long-acting medications in ADHD and hyperkinetic disorder is reported, giving effect sizes and numbers-to-treat for extended-release stimulant preparations and atomoxetine (ATX). A panel of experts from several European countries used the review to make recommendations about the use of these drugs in practice, and conclusions are reported: (1) Long-acting preparations should be available and used; (2) They should not replace short-acting drugs (which will be the initial treatment for many children for reasons of cost and flexibility of dosing). Individual clinical choice is needed. (3) Both ATX and extended-release preparations of stimulants should be available. The choice will depend upon the circumstances, and detailed recommendations are made.
351 citations
TL;DR: The data about the clinical features of probands and the pattern of transmission of ADHD among relatives found little evidence for the validity of subthreshold ADHD among such subjects, who reported a lifetime history of some symptoms that never met DSM-IV's threshold for diagnosis.
Abstract: Objective: Diagnosing attention deficit hyperactivity disorder (ADHD) in adults is difficult when diagnosticians cannot establish an onset before the DSM-IV criterion of age 7 or if the number of symptoms recalled does not achieve DSM’s diagnosis threshold. Method: The authors addressed the validity of DSM-IV’s age-at-onset and symptom threshold criteria by comparing four groups of adults: 127 subjects with full ADHD who met all DSM-IV criteria for childhood-onset ADHD, 79 subjects with late-onset ADHD who met all criteria except the age-at-onset criterion, 41 subjects with subthreshold ADHD who did not meet full symptom criteria for ADHD, and 123 subjects without ADHD who did not meet any criteria. The authors hypothesized that subjects with late-onset and subthreshold ADHD would show patterns of psychiatric comorbidity, functional impairment, and familial transmission similar to those seen in subjects with full ADHD. Results: Subjects with late-onset and full ADHD had similar patterns of psychiatric com...
304 citations
01 Oct 2006
TL;DR: The validity of DSM-IV's age-at-onset and symptom threshold criteria by comparing four groups of adults: 127 subjects with full ADHD, 79 subjects with late onset ADHD, 41 subjects with sub-threshold ADHD, and 123 subjects without ADHD who did not meet any criteria as discussed by the authors.
Abstract: Objective
Diagnosing attention deficit hyperactivity disorder (ADHD) in adults is difficult when diagnosticians cannot establish an onset before the DSM-IV criterion of age 7 or if the number of symptoms recalled does not achieve DSM’s diagnosis threshold.
Method
The authors addressed the validity of DSM-IV’s age-at-onset and symptom threshold criteria by comparing four groups of adults: 127 subjects with full ADHD who met all DSM-IV criteria for childhood-onset ADHD, 79 subjects with late-onset ADHD who met all criteria except the age-at-onset criterion, 41 subjects with subthreshold ADHD who did not meet full symptom criteria for ADHD, and 123 subjects without ADHD who did not meet any criteria. The authors hypothesized that subjects with late-onset and subthreshold ADHD would show patterns of psychiatric comorbidity, functional impairment, and familial transmission similar to those seen in subjects with full ADHD.
Result
Subjects with late-onset and full ADHD had similar patterns of psychiatric comorbidity, functional impairment, and familial transmission. Most children with late onset of ADHD (83%) were younger than 12. Subthreshold ADHD was milder and showed a different pattern of familial transmission than the other forms of ADHD.
Conclusions
The data about the clinical features of probands and the pattern of transmission of ADHD among relatives found little evidence for the validity of subthreshold ADHD among such subjects, who reported a lifetime history of some symptoms that never met DSM-IV’s threshold for diagnosis. In contrast, the results suggested that late-onset adult ADHD is valid and that DSM-IV’s age-at-onset criterion is too stringent.
Journal Article•
TL;DR: In this article, the authors compared drugs used to treat attention-deficit/hyperactivity disorder (ADHD) using direct comparative trials, and found that comparisons among drugs are hindered by the absence of direct comparative trial data.
Abstract: Objective
Medications used to treat attention-deficit/hyperactivity disorder (ADHD) have been well researched, but comparisons among drugs are hindered by the absence of direct comparative trials.
Journal Article•
TL;DR: Investigating ADHD's impact on individual employment and income, and the costs of ADHD on workforce productivity for the US population found decreased individual income among adults with ADHD contributes to substantial loss in US workforce productivity.
Abstract: Readers are encouraged to respond to George Lundberg, MD, Editor of MedGenMed, for the editor's eyes only or for possible publication via email: ten.epacsdem@grebdnulg
TL;DR: Psychometrically defined deficits of executive functioning may help identify a subgroup of adults with ADHD at high risk for occupational and academic underachievement and more efforts are needed to identify cost-effective approaches to screen individuals with ADHD for deficits ofexecutive functioning.
Abstract: Objective: The association between deficits in executive functioning and functional outcomes was examined among adults with attention deficit hyperactivity disorder (ADHD). Method: Subjects were adults who did (N=213) and did not (N=145) meet DSMIV criteria for ADHD. The authors defined having deficits in executive functioning as having at least two measures of executive functioning with scores 1.5 standard deviations below those of matched comparison subjects. Results: Significantly more adults with ADHD had deficits of executive functioning than comparison subjects. Deficits of executive functioning were associated with lower academic achievement, irrespective of ADHD status. Subjects with ADHD with deficits of executive functioning had a significantly lower socioeconomic status and a significant functional morbidity beyond the diagnosis of ADHD alone. Conclusions: Psychometrically defined deficits of executive functioning may help identify a subgroup of adults with ADHD at high risk for occupational and academic underachievement. More efforts are needed to identify cost-effective approaches to screen individuals with ADHD for deficits of executive functioning.
TL;DR: In this article, the authors correlated measures reflecting each construct in four separate, large-scale ADHD research samples and found that the correlation between symptoms and impairment accounted for less than 10% of variance.
Abstract: Diagnosing ADHD based primarily on symptom reports assumes that the number/frequency of symptoms is tied closely to the impairment imposed on an individual's functioning. That presumed linkage encourages diagnosis more by Diagnostic and Statistical Manual of Mental Disorders (4th ed.) style symptom lists than well-defined, psychometrically sound assessments of impairment. The current study correlated measures reflecting each construct in four separate, large-scale ADHD research samples. Average correlation between symptoms and impairment accounted for less than 10% of variance. Symptoms never predicted more than 25% of the variance in impairment. When an ADHD group was formed according to a measure of current symptoms, the sample size shrunk by 77% when a criterion-based measure of impairment was added. The partial unlinking of symptoms and impairment has implications for decisions about the diagnostic process, research criteria for participant inclusion, prevalence estimates, gender ratios, evaluation of treatment effects, service delivery, and many other issues.
Journal Article•
TL;DR: The relevance and implications of genetic associations with ADHD for clinical practice and future research are discussed.
Abstract: A growing body of behavioral and molecular genetics literature has indicated that the development of attention-deficit/hyperactivity disorder (ADHD) may be attributed to both genetic and environmental factors. Family, twin, and adoption studies provide compelling evidence that genes play a strong role in mediating susceptibility to ADHD. Molecular genetic studies suggest that the genetic architecture of ADHD is complex, while the handful of genome-wide scans conducted thus far is not conclusive. In contrast, the many candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder. For the 8 genes for which the same variant has been studied in 3 or more case-control or family-based studies, 7 show statistically significant evidence of association with ADHD based on pooled odds ratios across studies: the dopamine D 4 receptor gene (DRD4), the dopamine D 5 receptor gene (DRD5), the dopamine transporter gene (DAT), the dopamine β-hydroxylase gene (DBH), the serotonin transporter gene (5-HTT), the serotonin receptor 1B gene (HTR1B), and the synaptosomal-associated protein 25 gene (SNAP25). Recent pharmacoge-netic studies have correlated treatment nonresponse with particular gene markers, while preclinical studies have increased our understanding of gene expression paradigms and potential analogs for human trials. This literature review discusses the relevance and implications of genetic associations with ADHD for clinical practice and future research.
Journal Article•
TL;DR: A growing body of behavioral and molecular genetics literature has indicated that the development of attention-deficit/hyperactivity disorder (ADHD) may be attributed to both genetic and environmental factors.
Abstract: A growing body of behavioral and molecular genetics literature has indicated that the development of attention-deficit/hyperactivity disorder (ADHD) may be attributed to both genetic and environmental factors Family, twin, and adoption studies provide compelling evidence that genes play a strong role in mediating susceptibility to ADHD Molecular genetic studies suggest that the genetic architecture of ADHD is complex, while the handful of genome-wide scans conducted thus far is not conclusive In contrast, the many candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder For the 8 genes for which the same variant has been studied in 3 or more case-control or family-based studies, 7 show statistically significant evidence of association with ADHD based on pooled odds ratios across studies: the dopamine D 4 receptor gene (DRD4), the dopamine D 5 receptor gene (DRD5), the dopamine transporter gene (DAT), the dopamine β-hydroxylase gene (DBH), the serotonin transporter gene (5-HTT), the serotonin receptor 1B gene (HTR1B), and the synaptosomal-associated protein 25 gene (SNAP25) Recent pharmacoge-netic studies have correlated treatment nonresponse with particular gene markers, while preclinical studies have increased our understanding of gene expression paradigms and potential analogs for human trials This literature review discusses the relevance and implications of genetic associations with ADHD for clinical practice and future research
TL;DR: A review of past and current literature finds that the symptoms of ADHD are not sex specific, but that identification of girls with ADHD is hampered by parental and teacher bias, and confusion.
Abstract: Attention-deficit hyperactivity disorder (ADHD) in girls is a topic of growing research and clinical interest. For many years, girls with ADHD have been ignored and overshadowed by hyperkinetic and impulsive boys, but they are now attracting interest in an effort to understand the similarities and differences in the prevalence, symptoms, familial risk, comorbidities and treatment of ADHD in the two sexes. A review of past and current literature finds that the symptoms of ADHD are not sex specific, but that identification of girls with ADHD is hampered by parental and teacher bias, and confusion. Girls are more likely to be inattentive without being hyperactive or impulsive, compared with boys. Girls and boys share the same familial risk patterns, as well as similar, although not identical, comorbidity or impairment patterns. The risk of non-treatment is as great in girls as it is in boys; up to 70–80% of identified children will have persistent symptoms and impairment that extends into adolescence and adulthood. Treatment modalities are equally effective in girls and boys. Stimulants, non-stimulants and behavioural modalities are the mainstays of effective treatment.
TL;DR: These prospective follow-up findings documenting high morbidity associated with ADHD extend to females previously reported findings in male samples and underscore the importance of early recognition and intervention efforts for youth with ADHD of both genders.
TL;DR: These results extend the gateway hypothesis to an ADHD sample and provide evidence that this effect may be particularly robust in ADHD youth, and underscore the already pressing need to prevent smoking in ADHD children.
TL;DR: MAS XR is safe and effective in adults with ADHD and controlled ADHD symptoms for up to 12 hours, suggesting a 12-hour duration of effect.
Abstract: Introduction Attention-deficit/hyperactivity disorder (ADHD) is a serious neurobehavioral disorder of childhood onset that often persists into adolescence and adulthood. Functional impairments, underachievement, and difficult interpersonal relationships illustrate the need for effective treatment of ADHD through adulthood. Method This prospective, multisite, randomized, double-blind, placebo-controlled, parallel-group, dose-escalation study was conducted to assess the efficacy, safety, and duration of action of mixed amphetamine salts extended-release (MAS XR) in adults with ADHD, combined type. Adults > or =18 years of age were given placebo or MAS XR 20, 40, or 60 mg/day for 4 weeks. The main outcome measures were the ADHD Rating Scale and Conners' Adult ADHD Rating Scale Short Version Self-Report (CAARS-S-S). Results Two hundred fifty-five subjects were randomly assigned to treatment with MAS XR or placebo. MAS XR treatment was associated with statistically and clinically significant ADHD symptom reduction at endpoint; mean ADHD Rating Scale scores were 18.5 for the 20-mg group (P=.001), 18.4 for the 40-mg group (P 32 at baseline) had significantly greater symptom reduction with the highest MAS XR dose (60 mg/day), however, this dose-response relationship was determined by post-hoc analysis. The mean MAS XR effect size was 0.8. Statistically significant (P Conclusion These results suggest that MAS XR is safe and effective in adults with ADHD and controlled ADHD symptoms for up to 12 hours.
TL;DR: The International Multi-centre ADHD Gene (IMAGE) project exemplifies current collaborative research efforts on the genetics of ADHD as discussed by the authors, which is well placed to take advantage of the resources that are emerging following sequencing of the human genome and the development of international resources for whole genome association analysis.
Abstract: The genetic mechanisms involved in attention deficit hyperactivity disorder (ADHD) are being studied with considerable success by several centres worldwide. These studies confirm prior hypotheses about the role of genetic variation within genes involved in the regulation of dopamine, norepinephrine and serotonin neurotransmission in susceptibility to ADHD. Despite the importance of these findings, uncertainties remain due to the very small effects sizes that are observed. We discuss possible reasons for why the true strength of the associations may have been underestimated in research to date, considering the effects of linkage disequilibrium, allelic heterogeneity, population differences and gene by environment interactions. With the identification of genes associated with ADHD, the goal of ADHD genetics is now shifting from gene discovery towards gene functionality – the study of intermediate phenotypes ('endophenotypes'). We discuss methodological issues relating to quantitative genetic data from twin and family studies on candidate endophenotypes and how such data can inform attempts to link molecular genetic data to cognitive, affective and motivational processes in ADHD. The International Multi-centre ADHD Gene (IMAGE) project exemplifies current collaborative research efforts on the genetics of ADHD. This European multi-site project is well placed to take advantage of the resources that are emerging following the sequencing of the human genome and the development of international resources for whole genome association analysis. As a result of IMAGE and other molecular genetic investigations of ADHD, we envisage a rapid increase in the number of identified genetic variants and the promise of identifying novel gene systems that we are not currently investigating, opening further doors in the study of gene functionality.
TL;DR: Dimensional analyses showed significantly higher inattentive scores in subjects whose mothers smoked>or=10 cigarettes per day than in others after adjusting for confounding factors, and previous findings documenting the association between prenatal exposure to nicotine and broadly defined ADHD in clinical samples were expanded.
Abstract: Objective Few previous studies assessed specifically attention-deficit/hyperactivity disorder, predominantly inattentive subtype (ADHD-I) in nonreferred samples. This study investigated the association between ADHD-I and prenatal exposure to nicotine. Method In a case-control study performed between September 2002 and April 2005, we assessed a nonreferred Brazilian sample of 100 children and adolescents with ADHD-I and 100 non-ADHD controls (6-18 years old). Cases and controls, matched by gender and age, were screened using teacher reports in the Swanson, Nolan, and Pelham-IV (SNAP-IV) scale. They were systematically evaluated through structured diagnostic interviews. Prenatal exposure to nicotine and potential confounding factors were evaluated by direct interview with mothers. Results Adjusting for confounding factors (maternal ADHD, oppositional defiant disorder, birth weight, and alcohol use during pregnancy), children whose mothers smoked ≥10 cigarettes per day during pregnancy presented a significantly higher odds ratio for ADHD-I than children who were not exposed to nicotine during pregnancy (odds ratio 3.44; 95% confidence interval 1.17-10.06). Dimensional analyses showed significantly higher inattentive scores in subjects whose mothers smoked ≥10 cigarettes per day than in others after adjusting for confounding factors (p = .002). Conclusions In a nonreferred sample, the authors expanded to ADHD-I previous findings documenting the association between prenatal exposure to nicotine and broadly defined ADHD in clinical samples.
TL;DR: Data support a physiological difference (an exaggerated fMRI response) in DLPFC in adolescents at genetic risk for schizophrenia, independent of psychosis.
TL;DR: The results showing similar neuropsychological underpinning in subjects with late-onset ADHD suggest that the DSM-IV age at onset criterion may be too stringent, and suggest that ADHD subjects who failed to ever meet the psychiatric threshold for diagnosis have a milder form of the disorder.
TL;DR: The effects of prolonged OROS MPH therapy on growth were clinically insignificant and limited to slight decreases in weight during the first months of therapy, thus of questionable utility for limiting potential effects of treatment on growth.
Abstract: Objective To investigate whether prolonged therapy with a long-acting stimulant affects growth in children with attention-deficit/hyperactivity disorder (ADHD). Method One hundred seventy-eight children ages 6 to 13 years received OROS methylphenidate (OROS MPH, CONCERTA) for at least 21 months. Height and weight were measured monthly during the first year and every 3 months thereafter. Results At baseline, subjects were approximately the expected height for their age and somewhat heavier than expected. Subjects gained height steadily throughout the study and were on average 0.23 cm less than expected at month 21. Weight did not increase and BMI decreased slightly in the first 4 months. Thereafter, weight Z score and BMI Z score remained relatively constant and children were on average 1.23 kg less than expected at month 21. Previous stimulant therapy tended to be associated with a smaller decrease in Z score during the study compared with no previous stimulant therapy. Drug holidays did not significantly affect growth. Conclusions The effects of prolonged OROS MPH therapy on growth were clinically insignificant and limited to slight decreases in weight during the first months of therapy. Drug holidays did not reduce any impact on growth and are thus of questionable utility for limiting potential effects of treatment on growth. J. Am. Acad. Child Adolesc. Psychiatry , 2006;45(5):000-000.
TL;DR: In a general population sample, LCA identifies a CBCL-JBD phenotype latent class that is associated with high rates of suicidality, is highly heritable, and speaks to the comorbidity between attention problems, aggressive behavior, and anxious/depression in children.
TL;DR: Variation in the HTR1B gene may primarily affect the inattentive subtype of ADHD.
TL;DR: It is concluded that the variable responsiveness of individuals to atomoxetine cannot be largely accounted for by differences in broad-spectrum psychopathology or neuropsychological indicators of attentional capacity.
Abstract: Objective The objective of this study was to determine if measures of broad clinical psychopathology or neuropsychological performance could aid in the prediction of therapeutic response to the highly selective norepinephrine transporter inhibitor, atomoxetine, among adults with attention-deficit/hyperactivity disorder (ADHD). Method We analyzed data from 2 double-blind, placebo-controlled, parallel design studies of adult patients (Study I, N = 280; Study II, N = 256) with DSM-IV-defined ADHD who were recruited by referral and advertising. Subjects were randomly assigned to 10 weeks of treatment with atomoxetine or placebo and were assessed with Conners' Adult ADHD Rating Scales (CAARS), the General Well-Being Schedule (GWB), the Sheehan Disability Scale, the Stroop Color-Word Test (SCWT), and the Structured Clinical Interview for DSM-IV (SCID) before and after treatment. Results Therapeutic improvement on atomoxetine as evidenced by reduced CAARS scores was reliably predicted by the presence of a lifetime comorbid diagnosis of depression or post-traumatic stress disorder at baseline, while improvement on subscales of the GWB and Sheehan Disability Scale were predicted by these and other SCID endorsements, such as alcohol and substance use, as well as demographics such as age and gender. In light of the exploratory nature of this work and the many comparisons that were examined in the corresponding regression models, these findings should be regarded as tentative pending replication and extension in another dataset. Conclusion From these findings, we conclude that the variable responsiveness of individuals to atomoxetine cannot be largely accounted for by differences in broad-spectrum psychopathology or neuropsychological indicators of attentional capacity.
TL;DR: In this article, the authors identify aspects of personality, psychopathology and social development that differentiate high-risk and control individuals, and find that higher risk individuals have more physical anhedonia, less positive involvement with peers and more problems with peers, siblings and opposite gender.
Abstract: Background Evaluation of individuals at high genetic risk of schizophrenia is a powerful method for identifying precursors of the illness.
Aims To identify aspects of personality, psychopathology and social development that differentiate high-risk and control individuals.
Method Adolescent and young-adult first-degree relatives ( n =35) of people with schizophrenia or schizoaffective disorder and a control group ( n =55) were compared on 36 measures at baseline of a longitudinal study. Measures differentiating high-risk and control participants were related to four genetic loading indices.
Results High-risk participants older than 17 years showed more physical anhedonia, less positive involvement with peers and more problems with peers, siblings and the opposite gender. Older high-risk individuals also were less cooperative, less self-directed and less reward-dependent. Problems with peers and the opposite gender, as well as reward dependence, were related linearly to genetic loading.
Conclusions Alterations in personality traits and social development are present in high-risk individuals, and may be markers for genetic liability toward the illness.