Stephen V Faraone

State University of New York Upstate Medical University, Syracuse, New York, United States

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Publications (929)4633.77 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: While pediatric mania and depression can be distinguished from each other, differentiating between unipolar major depressive disorder (unipolar MDD) and bipolar major depression (bipolar MDD) poses unique clinical and therapeutic challenges. Our aim was to examine the current body of knowledge on whether unipolar MDD and bipolar MDD in youth could be distinguished from one another in terms of clinical features and correlates.
    Journal of Affective Disorders 05/2015; 176. DOI:10.1016/j.jad.2015.01.037 · 3.71 Impact Factor
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    ABSTRACT: Discovering the genetic basis of early-onset psychiatric disorders has been the aim of intensive research during the last decade. We will first selectively summarize results of genetic research in child and adolescent psychiatry by using examples from different disorders and discuss methodological issues, emerging questions and future directions. In the second part of this review, we will focus on how to link genetic causes of disorders with physiological pathways, discuss the impact of genetic findings on diagnostic systems, prevention and therapeutic interventions. Finally we will highlight some ethical aspects connected to genetic research in child and adolescent psychiatry. Advances in molecular genetic methods have led to insights into the genetic architecture of psychiatric disorders, but not yet provided definite pathways to pathophysiology. If replicated, promising findings from genetic studies might in some cases lead to personalized treatments. On the one hand, knowledge of the genetic basis of disorders may influence diagnostic categories. On the other hand, models also suggest studying the genetic architecture of psychiatric disorders across diagnoses and clinical groups.
    European Child & Adolescent Psychiatry 04/2015; DOI:10.1007/s00787-015-0702-8 · 3.55 Impact Factor
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    ABSTRACT: Individuals with attention deficit/hyperactivity disorder (ADHD) are at increased risk of developing substance use disorders (SUDs) and nicotine dependence. The co-occurrence of ADHD and SUDs/nicotine dependence may in part be mediated by shared genetic liability. Several neurobiological pathways have been implicated in both ADHD and SUDs, including dopamine and serotonin pathways. We hypothesized that variations in dopamine and serotonin neurotransmission genes were involved in the genetic liability to develop SUDs/nicotine dependence in ADHD. The current study included participants with ADHD (n = 280) who were originally part of the Dutch International Multicenter ADHD Genetics study. Participants were aged 5-15 years and attending outpatient clinics at enrollment in the study. Diagnoses of ADHD, SUDs, nicotine dependence, age of first nicotine and substance use, and alcohol use severity were based on semi-structured interviews and questionnaires. Genetic risk scores were created for both serotonergic and dopaminergic risk genes previously shown to be associated with ADHD and SUDs and/or nicotine dependence. The serotonin genetic risk score significantly predicted alcohol use severity. No significant serotonin × dopamine risk score or effect of stimulant medication was found. The current study adds to the literature by providing insight into genetic underpinnings of the co-morbidity of ADHD and SUDs. While the focus of the literature so far has been mostly on dopamine, our study suggests that serotonin may also play a role in the relationship between these disorders. © 2015 Society for the Study of Addiction.
    Addiction Biology 04/2015; DOI:10.1111/adb.12230 · 5.93 Impact Factor
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    ABSTRACT: The prevalence of ADHD among patients with substance use disorder (SUD) is substantial. This study addressed the following research questions: Are early developmental, temperamental and educational problems overrepresented among SUD patients with ADHD compared to SUD patients without ADHD? Do this comorbid group receive early help for their ADHD, and are there signs of self-medicating with illicit central stimulants?
    03/2015; 131. DOI:10.1016/j.abrep.2015.03.001
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a heritable neurodevelopmental disorder. It has been linked to reductions in total brain volume and subcortical abnormalities. However, owing to heterogeneity within and between studies and limited sample sizes, findings on the neuroanatomical substrates of ADHD have shown considerable variability. Moreover, it remains unclear whether neuroanatomical alterations linked to ADHD are also present in the unaffected siblings of those with ADHD. To examine whether ADHD is linked to alterations in whole-brain and subcortical volumes and to study familial underpinnings of brain volumetric alterations in ADHD. In this cross-sectional study, we included participants from the large and carefully phenotyped Dutch NeuroIMAGE sample (collected from September 2009-December 2012) consisting of 307 participants with ADHD, 169 of their unaffected siblings, and 196 typically developing control individuals (mean age, 17.21 years; age range, 8-30 years). Whole-brain volumes (total brain and gray and white matter volumes) and volumes of subcortical regions (nucleus accumbens, amygdala, caudate nucleus, globus pallidus, hippocampus, putamen, thalamus, and brainstem) were derived from structural magnetic resonance imaging scans using automated tissue segmentation. Regression analyses revealed that relative to control individuals, participants with ADHD had a 2.5% smaller total brain (β = -31.92; 95% CI, -52.69 to -11.16; P = .0027) and a 3% smaller total gray matter volume (β = -22.51; 95% CI, -35.07 to -9.96; P = .0005), while total white matter volume was unaltered (β = -10.10; 95% CI, -20.73 to 0.53; P = .06). Unaffected siblings had total brain and total gray matter volumes intermediate to participants with ADHD and control individuals. Significant age-by-diagnosis interactions showed that older age was linked to smaller caudate (P < .001) and putamen (P = .01) volumes (both corrected for total brain volume) in control individuals, whereas age was unrelated to these volumes in participants with ADHD and their unaffected siblings. Attention-deficit/hyperactivity disorder was not significantly related to the other subcortical volumes. Global differences in gray matter volume may be due to alterations in the general mechanisms underlying normal brain development in ADHD. The age-by-diagnosis interaction in the caudate and putamen supports the relevance of different brain developmental trajectories in participants with ADHD vs control individuals and supports the role of subcortical basal ganglia alterations in the pathophysiology of ADHD. Alterations in total gray matter and caudate and putamen volumes in unaffected siblings suggest that these volumes are linked to familial risk for ADHD.
    JAMA Psychiatry 03/2015; DOI:10.1001/jamapsychiatry.2014.3162 · 12.01 Impact Factor
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    ABSTRACT: In view of ICD-11 revision, we evaluate whether the 18 DSM-IV diagnostic items retained by DSM-5 could be further improved (i) in predicting ADHD 'caseness' and 'impairment' and (ii) discriminating ADHD without CD (ADHD - CD) cases from ADHD with CD (ADHD + CD) cases. In a multi-centre study sample consisting of 1497 ADHD probands and 291 unaffected subjects, 18 diagnostic items were examined for redundancy; then each item was evaluated for association with caseness, impairment and CD status using Classical Test Theory, Item-Response Theory and logistic regression methods. First, all 18 DSM-IV items contributed significantly and independently to the clinical diagnosis of ADHD. Second, not all the DSM-IV items carried equal weighting. "Often loses things", "forgetfulness" and "difficulty sustaining attention" mark severity for Inattentiveness (IA) items and "often unduly noisy", "exhibits a persistent pattern of restlessness", "leaves seat in class" and "often blurts out answers" for Hyperactivity/Impulsivity (HI) items. "Easily distracted", "inattentive to careless mistakes", "often interrupts" and "often fidgets" are associated with milder presentations. In the IA domain, "distracted" yields most information in the low-severity range of the latent trait, "careless" in the mid-severity range and "loses" in the high-severity range. In the HI domains, "interrupts" yields most information in the low-severity range and "motor" in the high-severity range. Third, all 18 items predicted impairment. Fourth, specific ADHD items are associated with ADHD + CD status. The DSM-IV diagnostic items were valid and not redundant; however, some carried more weight than others. All items were associated with impairment.
    European Child & Adolescent Psychiatry 03/2015; DOI:10.1007/s00787-015-0683-7 · 3.55 Impact Factor
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a heritable neuropsychiatric disorder associated with abnormal reward processing. Limited and inconsistent data exist about the neural mechanisms underlying this abnormality. Furthermore, it is not known whether reward processing is abnormal in unaffected siblings of participants with ADHD. We used event-related functional magnetic resonance imaging (fMRI) to investigate brain responses during reward anticipation and receipt with an adapted monetary incentive delay task in a large sample of adolescents and young adults with ADHD (n = 150), their unaffected siblings (n = 92), and control participants (n = 108), all of the same age. Participants with ADHD showed, relative to control participants, increased responses in the anterior cingulate, anterior frontal cortex, and cerebellum during reward anticipation, and in the orbitofrontal, occipital cortex and ventral striatum. Responses of unaffected siblings were increased in these regions as well, except for the cerebellum during anticipation and ventral striatum during receipt. ADHD in adolescents and young adults is associated with enhanced neural responses in frontostriatal circuitry to anticipation and receipt of reward. The findings support models emphasizing aberrant reward processing in ADHD, and suggest that processing of reward is subject to familial influences. Future studies using standard monetary incentive delay task parameters are needed to replicate our findings. Copyright © 2015 American Academy of Child and Adolescent Psychiatry. Published by Elsevier Inc. All rights reserved.
    Journal of the American Academy of Child and Adolescent Psychiatry 03/2015; 54(5). DOI:10.1016/j.jaac.2015.02.012 · 6.35 Impact Factor
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    ABSTRACT: Brain white matter (WM) tracts, playing a vital role in the communication between brain regions, undergo important maturational changes during adolescence and young adulthood, a critical period for the development of nicotine dependence. Attention-deficit/hyperactivity disorder (ADHD) is associated with increased smoking and widespread WM abnormalities, suggesting that the developing ADHD brain might be especially vulnerable to effects of smoking. This study aims to investigate the effect of smoking on (WM) microstructure in adolescents and young adults with and without ADHD. Diffusion tensor imaging was performed in an extensively phenotyped sample of nonsmokers (n = 95, 50.5% ADHD), irregular smokers (n = 41, 58.5% ADHD), and regular smokers (n = 50, 82.5% ADHD), aged 14-24 years. A whole-brain voxelwise approach investigated associations of smoking, ADHD and their interaction, with WM microstructure as measured by fractional anisotropy (FA) and mean diffusivity (MD). Widespread alterations in FA and MD were found for regular smokers compared to irregular and nonsmokers, mainly located in the corpus callosum and WM tracts surrounding the basal ganglia. Several regions overlapped with regions of altered FA for ADHD versus controls, albeit in different directions. Irregular and nonsmokers did not differ, and ADHD and smoking did not interact. Results implicate that smoking and ADHD have independent effects on WM microstructure, and possibly do not share underlying mechanisms. Two mechanisms may play a role in the current results. First, smoking may cause alterations in WM microstructure in the maturing brain. Second, pre-existing WM microstructure differences possibly reflect a risk factor for development of a smoking addiction. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 03/2015; 36(3). DOI:10.1002/hbm.22695 · 6.92 Impact Factor
  • Stephen V Faraone
    The Lancet 02/2015; DOI:10.1016/S0140-6736(14)61822-5 · 39.21 Impact Factor
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) often persists into adulthood, but it remains unclear which childhood factors predict future outcome.
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    ABSTRACT: Objective: Dysfunctional response inhibition is a key executive function impairment in attention deficit hyperactivity disorder (ADHD). Still, behavioral response inhibition measures do not consistently differentiate affected from unaffected individuals. The authors therefore investigated neural correlates of response inhibition and the familial nature of these neural correlates. Methods: Functional MRI measurements of neural activation during the stop-signal task and behavioral measures of response inhibition were obtained in adolescents and young adults with ADHD (N=185), their unaffected siblings (N=111), and healthy comparison subjects (N=124). Results: Stop-signal task reaction times were longer and error rates were higher in participants with ADHD, but not in their unaffected siblings, while reaction time variability was higher in both groups than in comparison subjects. Relative to comparison subjects, participants with ADHD and unaffected siblings had neural hypoactivation in frontal-striatal and frontal-parietal networks, whereby activation in inferior frontal and temporal/parietal nodes in unaffected siblings was intermediate between levels of participants with ADHD and comparison subjects. Furthermore, neural activation in inferior frontal nodes correlated with stop-signal reaction times, and activation in both inferior frontal and temporal/parietal nodes correlated with ADHD severity. Conclusions: Neural activation alterations in ADHD are more robust than behavioral response inhibition deficits and explain variance in response inhibition and ADHD severity. Although only affected participants with ADHD have deficient response inhibition, hypoactivation in inferior frontal and temporal-parietal nodes in unaffected siblings supports the familial nature of the underlying neural process. Activation deficits in these nodes may be useful as endophenotypes that extend beyond the affected individuals in the family.
    American Journal of Psychiatry 01/2015; DOI:10.1176/appi.ajp.2014.13121635 · 13.56 Impact Factor
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    ABSTRACT: Introduction Response inhibition is one of the executive functions impaired in attention-deficit/hyperactivity disorder (ADHD). Increasing evidence indicates that altered functional and structural neural connectivity are part of the neurobiological basis of ADHD. Here, we investigated if adolescents with ADHD show altered functional connectivity during response inhibition compared to their unaffected siblings and healthy controls. Methods Response inhibition was assessed using the stop signal paradigm. Functional connectivity was assessed using psycho-physiological interaction analyses applied to BOLD time courses from seed regions within inferior- and superior frontal nodes of the response inhibition network. Resulting networks were compared between adolescents with ADHD (N = 185), their unaffected siblings (N = 111), and controls (N = 125). Results Control subjects showed stronger functional connectivity than the other two groups within the response inhibition network, while subjects with ADHD showed relatively stronger connectivity between default mode network (DMN) nodes. Stronger connectivity within the response inhibition network was correlated with lower ADHD severity, while stronger connectivity with the DMN was correlated with increased ADHD severity. Siblings showed connectivity patterns similar to controls during successful inhibition and to ADHD subjects during failed inhibition. Additionally, siblings showed decreased connectivity with the primary motor areas as compared to both participants with ADHD and controls. Discussion Subjects with ADHD fail to integrate activation within the response inhibition network and to inhibit connectivity with task-irrelevant regions. Unaffected siblings show similar alterations only during failed stop trials, as well as unique suppression of motor areas, suggesting compensatory strategies. These findings support the role of altered functional connectivity in understanding the neurobiology and familial transmission of ADHD.
    01/2015; 35. DOI:10.1016/j.nicl.2015.01.004
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    ABSTRACT: BackgroundA developmental improvement of symptoms in Attention-Deficit/Hyperactivity Disorder (ADHD) is frequently reported, but the underlying neurobiological substrate has not been identified. The aim of this study was to determine whether white matter microstructure is related to developmental improvement of ADHD symptoms.MethodsA cross-sectional Magnetic Resonance Imaging (MRI) analysis was embedded in a prospective follow-up of an adolescent cohort of ADHD and control subjects (NeuroIMAGE). Mean age at baseline was 11.9 years, mean interval of follow-up was 5.9 years. About 75.3% of the original cohort was retained successfully. Data of 101 participants with ADHD combined type at baseline and 40 healthy controls were analysed. ADHD symptoms were measured with semistructured, investigator-based interviews and Conners' questionnaires, on the basis of DSM-IV criteria. Fractional anisotropy (FA) and mean diffusivity (MD) indices of white matter microstructure were measured using whole brain diffusion tensor imaging at follow-up only. In a dimensional analysis FA and MD were related to change in ADHD symptoms. To link this analysis to DSM-IV diagnoses, a post hoc categorical group analysis was conducted comparing participants with persistent (n = 59) versus remittent (n = 42) ADHD and controls.ResultsOver time, participants with ADHD showed improvement mainly in hyperactive/impulsive symptoms. This improvement was associated with lower FA and higher MD values in the left corticospinal tract at follow-up. Findings of the dimensional and the categorical analysis strongly converged. Changes in inattentive symptoms over time were minimal and not related to white matter microstructure.Conclusions The corticospinal tract is important in the control of voluntary movements, suggesting the importance of the motor system in the persistence of hyperactive/impulsive symptoms.
    Journal of Child Psychology and Psychiatry 01/2015; DOI:10.1111/jcpp.12379 · 5.67 Impact Factor
  • Stephen V Faraone, Paul G Hammerness, Timothy E Wilens
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    ABSTRACT: Children with ADHD frequently manifest behavioral difficulties in the morning prior to school. We sought to assess the reliability and validity of the Before-School Functioning Questionnaire (BSFQ) as a measure of morning behaviors impaired by ADHD. We used pre-treatment data from a randomized crossover study of 6- to 12-year-old participants comparing the methylphenidate transdermal delivery system (MTS) with a placebo transdermal system (PTS) for a total of 4 weeks. The BSFQ investigator-rated scale shows very good internal homogeneity (Cronbach's α = .91), good test-retest reliability (r = .60), good concurrent validity (r range = .42-.86), and a strong treatment effect (effect size = -.93). The self-rated BSFQ showed lower levels of reliability and validity. The investigator-rated BSFQ should be used in future trials of ADHD medications aimed at assessing efficacy in the morning before school. © 2015 SAGE Publications.
    Journal of Attention Disorders 01/2015; DOI:10.1177/1087054714564623 · 2.40 Impact Factor
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    ABSTRACT: Borderline personality disorder (BPD) and substance use disorders (SUDs) often co-occur, partly because they share risk factors. In this international multicenter study, risk factors for BPD were examined for SUD patients. In total, 1,205 patients were comprehensively examined by standardized interviews and questionnaires on psychiatric diagnosis and risk factors, and it was found that 1,033 (85.7%) had SUDs without BPD (SUD) and 172 (14.3%) had SUD with BPD (SUD + BPD). SUD + BPD patients were significantly younger, more often females and more often diagnosed with comorbid adult attention deficit/hyperactivity disorder. SUD + BPD patients did not differ from SUD patients on most risk factors typical for SUD such as maternal use of drugs during pregnancy or parents having any SUD. However, SUD + BPD patients did have a higher risk of having experienced emotional and physical abuse, neglect, or family violence in childhood compared to SUD patients, suggesting that child abuse and family violence are BPD-specific risk factors in patients with SUDs. © 2015 S. Karger AG, Basel.
    European Addiction Research 01/2015; 21(4):188-94. DOI:10.1159/000371724 · 2.07 Impact Factor
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    ABSTRACT: Benzodiazepines are widely prescribed for patients with bipolar disorders in clinical practice, but very little is known about the subtypes of patients with bipolar disorder or aspects of bipolar illness that contribute most to benzodiazepine use. We examined the prevalence of and factors associated with benzodiazepine use among 482 patients with bipolar I or II disorder enrolled in the Bipolar CHOICE study. Eighty-one subjects were prescribed benzodiazepines at study entry and were considered benzodiazepine users. Stepwise logistic regression was used to model baseline benzodiazepine use versus nonuse, using entry and exit criteria of P < 0.1. In bivariate analyses, benzodiazepine users were prescribed a significantly higher number of other psychotropic medications and were more likely to be prescribed lamotrigine or antidepressants as compared with benzodiazepine nonusers. Benzodiazepine users were more likely to have a diagnosis of bipolar I disorder and comorbid anxiety disorder, but not comorbid alcohol or substance use disorders. Benzodiazepine users also had experienced more anxiety and depressive symptoms and suicidality, but not irritability or manic symptoms, than did benzodiazepine nonusers. In the multivariate model, anxiety symptom level (regardless of diagnosis), lamotrigine use, number of concomitant psychotropic medications, college education, and high household income predicted benzodiazepine use. Benzodiazepine use in patients with bipolar disorders is associated with greater illness complexity as indicated by a higher number of concomitant psychotropic medications and higher anxiety symptom burden, regardless of a comorbid anxiety disorder diagnosis. Demographic factors were also important determinants of benzodiazepine use, which may be related to access to care and insurance coverage for benzodiazepines.
    Journal of Clinical Psychopharmacology 12/2014; 35(1). DOI:10.1097/JCP.0000000000000257 · 3.76 Impact Factor
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    ABSTRACT: Background Individuals with panic disorder (PD) exhibit a hypersensitivity to inhaled carbon dioxide (CO2), possibly reflecting a lowered threshold for sensing signals of suffocation. Animal studies have shown that CO2-mediated fear behavior depends on chemosensing of acidosis in the amygdala via the acid sensing ion channel ASIC1a. We examined whether the human ortholog of the ASIC1a gene, ACCN2, is associated with the presence of PD and with amygdala structure and function. Methods We conducted a case-control analysis (N=414 PD cases, 846 healthy controls) of ACCN2single nucleotide polymorphisms (SNPs) and PD. We then tested whether variants showing significant association with PD are also associated with amygdala volume (n=1,048) and/or task-evoked reactivity to emotional stimuli (n=103) in healthy individuals. Results Two SNPs at the ACCN2 locus showed evidence of association with PD: rs685012 (OR=1.32, gene-wise corrected p=0.011) and rs10875995 (OR=1.26, gene-wise corrected p=0.046). The association appeared to be stronger when early-onset (age ≤ 20) PD cases and when cases with prominent respiratory symptoms were compared to controls. The PD risk allele at rs10875995 was associated with increased amygdala volume (p=0.035), as well as task-evoked amygdala reactivity to fearful and angry faces (p=0.0048). Conclusions Genetic variation at ACCN2 appears to be associated with PD and with amygdala phenotypes that have been linked to anxiety proneness. These results support the possibility that modulation of acid-sensing ion channels may have therapeutic potential for PD.
    Biological psychiatry 12/2014; DOI:10.1016/j.biopsych.2013.12.018 · 9.47 Impact Factor
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    ABSTRACT: PMID: 24571924 Introduction The Lifetime Impairment Survey, conducted in Europe, assessed impairment and symptoms of attention-deficit/hyperactivity disorder (ADHD) in childhood, and experiences of ADHD diagnosis and treatment, as recalled by adults. Adults with ADHD and without ADHD (control group) were invited to participate in an internet-based survey and report on their childhood experiences. History of ADHD diagnosis was self-reported. Groups were compared using impairment and symptom scales. Overall, 588 adults with ADHD and 736 without ADHD participated. Mean (standard deviation [SD]) age at diagnosis of ADHD was 20.0 (12.6) years (median 18.0) following consultation with 3.8 (5.1) doctors (median 2) over 44.6 (69.3) months (median 17.0). A total of 64.1% (377/588) of adults with ADHD reported frustration or difficulties during the diagnostic process. The ADHD group had a higher mean (SD) score versus control for general (3.3 [1.2] vs 2.1 [1.2]; p < 0.001) and school impairment (2.8 [0.7] vs 2.3 [0.6]; p < 0.001) but not home impairment (2.1 [0.5] for both groups). Discussion The survey demonstrated that ADHD had a negative impact on all aspects of childhood investigated, as recalled by adults. These data provide insights into childhood impairments and identify areas for improvement in the management and treatment of ADHD.
    CNS spectrums 12/2014; DOI:10.1017/S1092852914000078 · 1.30 Impact Factor
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    ABSTRACT: This study examined whether exposure to maternal smoking during pregnancy in children with and without ADHD is associated with smoking in offspring and whether this association is selective to ADHD children. Ninety-six exposed and 400 unexposed participants were derived from two longitudinal studies of boys and girls with and without ADHD. Maternal smoking during pregnancy was defined by interviews with participants' mothers. A significant association was observed between exposure to maternal smoking in pregnancy and cigarette smoking in offspring (p = .02). Exposed offspring were also more likely to have higher rates of major depression (p = .04), bipolar disorder (p = .04), and conduct disorder (p = .04), and lower IQ (p = .01), lower Global Assessment of Functioning (GAF) score (p = .02), and more impaired Social Adjustment Inventory for Children and Adolescents (SAICA) scores versus unexposed offspring, adjusting for social class. Maternal smoking during pregnancy was found to increase the risk for smoking and a wide range of adverse psychiatric, cognitive, and functional outcomes in youth. © 2014 SAGE Publications.
    Journal of Attention Disorders 11/2014; DOI:10.1177/1087054714557357 · 2.40 Impact Factor

Publication Stats

49k Citations
4,633.77 Total Impact Points


  • 2005–2015
    • State University of New York Upstate Medical University
      • • Department of Neuroscience and Physiology
      • • Department of Psychiatry and Behavioral Sciences
      Syracuse, New York, United States
    • New York University
      New York City, New York, United States
    • Western Psychiatric Institute and Clinic
      Pittsburgh, Pennsylvania, United States
    • University of California, San Diego
      • Department of Psychiatry
      San Diego, CA, United States
  • 2014
    • Duke University Medical Center
      • Department of Medicine
      Durham, North Carolina, United States
  • 2008–2014
    • King's College London
      • MRC Social, Genetic and Developmental Psychiatry Centre
      Londinium, England, United Kingdom
    • CUNY Graduate Center
      New York, New York, United States
  • 2004–2014
    • Trinity College Dublin
      • • Department of Psychiatry
      • • Department of Genetics
      Dublin, Leinster, Ireland
    • Peking University
      • Institute of Mental Health
      Beijing, Beijing Shi, China
  • 2013
    • VU University Amsterdam
      • Department of Clinical Neuropsychology
      Amsterdam, North Holland, Netherlands
  • 1991–2013
    • Massachusetts General Hospital
      • Department of Psychiatry
      Boston, Massachusetts, United States
  • 1987–2013
    • Harvard University
      • Social Neuroscience and Psychopathology Laboratory
      Cambridge, Massachusetts, United States
    • Alpert Medical School - Brown University
      Providence, Rhode Island, United States
  • 2012
    • Cardiff University
      • Department of Psychological Medicine and Neurology
      Cardiff, WLS, United Kingdom
    • University of Bergen
      • Department of Biomedicine
      Bergen, Hordaland, Norway
    • Ghent University
      • Department of Experimental Clinical and Health Psychology
      Gand, Flanders, Belgium
  • 2011–2012
    • National Cheng Kung University
      • Institute of Clinical Medicine
      Tainan, Taiwan, Taiwan
    • University of Nebraska Medical Center
      Omaha, Nebraska, United States
    • University of Cambridge
      • Department of Psychiatry
      Cambridge, England, United Kingdom
    • Hôpital Universitaire Robert Debré
      Lutetia Parisorum, Île-de-France, France
    • Chang Jung Christian University
      臺南市, Taiwan, Taiwan
  • 1985–2011
    • Harvard Medical School
      • • Department of Psychiatry
      • • Commonwealth Research Center
      Boston, Massachusetts, United States
  • 2009
    • University of California, Los Angeles
      Los Angeles, California, United States
  • 2007
    • Syracuse VA Medical Center
      Syracuse, New York, United States
    • Michigan State University
      • Department of Psychology
      East Lansing, MI, United States
  • 2006–2007
    • Beth Israel Deaconess Medical Center
      • Department of Psychiatry
      Boston, MA, United States
    • National Taiwan University Hospital
      • Department of Psychiatry
      Taipei, Taipei, Taiwan
    • University of Vermont
      • Department of Psychiatry
      Burlington, Vermont, United States
  • 2003
    • University of Utah
      • Department of Psychiatry
      Salt Lake City, Utah, United States
    • Yale University
      • Department of Psychiatry
      New Haven, Connecticut, United States
    • California State University, Sacramento
      Sacramento, California, United States
  • 2002
    • Tulane University
      New Orleans, Louisiana, United States
    • University of Pennsylvania
      • Department of Psychiatry
      Filadelfia, Pennsylvania, United States
    • University of Haifa
      • Department of Psychology
      H̱efa, Haifa, Israel
    • Tufts University
      • Department of Pediatrics
      Бостон, Georgia, United States
  • 1989–2002
    • Boston University
      • Department of Psychology
      Boston, Massachusetts, United States
  • 2001
    • University of Washington Seattle
      • Department of Psychiatry and Behavioral Sciences
      Seattle, WA, United States
  • 2000
    • University of California, Davis
      • School of Medicine
      Davis, CA, United States
  • 1995
    • Beverly Hospital, Boston MA
      BVY, Massachusetts, United States