Douglas L. Noordsy, MD, is Clinical Professor and Associate Chair of Clinical Integration & Coordination, Director of Sports Psychiatry, and psychiatrist on the INSPIRE Early Psychosis Clinic in the Department of Psychiatry & Behavioral Sciences at Stanford University School of Medicine. Dr. Noordsy was previously Professor of Psychiatry, Director of Psychosis Services and Investigator in the Psychopharmacology Research Group at the Geisel School of Medicine at Dartmouth. His research interests include medication and psychosocial treatments for individuals with psychotic disorders, including those with co-occurring substance use disorders; methods to facilitate recovery and promote achievement of optimal outcomes for people with schizophrenia and bipolar disorder; rehabilitation and recovery interventions (including cognitive behavioral therapy and physical exercise); and methods to prevent progression of early psychotic disorders. He is particularly interested in the role of physical exercise for prevention of progression of early psychosis and for potentiating learning in CBTp and supported employment and education. Dr. Noordsy is a member of the Schizophrenia International Research Society, the International Early Psychosis Association, and is a fellow of the American Psychiatric Association. He is a member of the editorial boards for Community Mental Health Journal, Clinical Schizophrenia & Related Psychosis, and Schizophrenia Bulletin. Dr. Noordsy was recognized with the Exemplary Psychiatrist Award from the National Alliance on Mental Illness in 2001.

Clinical Focus

  • Psychiatry
  • Early psychosis
  • Sports Psychiatry
  • Lifestyle medicine

Academic Appointments

  • Clinical Professor, Psychiatry and Behavioral Sciences

Administrative Appointments

  • Associate Chair of Clinical Integration and Coordination, Psychiatry & Behavioral Sciences (2016 - Present)
  • Director of Sports Psychiatry, Psychiatry & Behavioral Sciences (2015 - Present)

Professional Education

  • Board Certification: Psychiatry, American Board of Psychiatry and Neurology (1990)
  • Residency:Darmouth-Hitchcock Medical Center (1989) NH
  • M.D., Washington University School of Medicine, Medicine (1985)
  • B.S. magna cum laude, St. Lawrence University, Chemistry (1981)

2017-18 Courses

All Publications

  • Therapeutic Potential of Physical Exercise in Early Psychosis. The American journal of psychiatry Noordsy, D. L., Burgess, J. D., Hardy, K. V., Yudofsky, L. M., Ballon, J. S. 2018; 175 (3): 209–14

    View details for DOI 10.1176/appi.ajp.2017.17060716

    View details for PubMedID 29490501

  • An RCT Evaluating the Effects of Skills Training and Medication Type on Work Outcomes Among Patients With Schizophrenia PSYCHIATRIC SERVICES Glynn, S. M., Marder, S. R., Noordsy, D. L., O'Keefe, C., Becker, D. R., Drake, R. E., Sugar, C. A. 2017; 68 (3): 271-277
  • Risperidone versus olanzapine among patients with schizophrenia participating in supported employment: Eighteen-month outcomes Journal of Psychiatric Research Noordsy, D. L., Glynn, S. M., Sugar, C. A., O'Keefe, C. D., Marder, S. R. 2017
  • Genetic Correlation Profile of Schizophrenia Mirrors Epidemiological Results and Suggests Link Between Polygenic and Rare Variant (22q11.2) Cases of Schizophrenia. Schizophrenia bulletin Duncan, L. E., Shen, H., Ballon, J. S., Hardy, K. V., Noordsy, D. L., Levinson, D. F. 2017


    New methods in genetics research, such as linkage disequilibrium score regression (LDSR), quantify overlap in the common genetic variants that influence diverse phenotypes. It is becoming clear that genetic effects often cut across traditional diagnostic boundaries. Here, we introduce genetic correlation analysis (using LDSR) to a nongeneticist audience and report transdisciplinary discoveries about schizophrenia. This analytical study design used publically available genome wide association study (GWAS) data from approximately 1.5 million individuals. Genetic correlations between schizophrenia and 172 medical, psychiatric, personality, and metabolomic phenotypes were calculated using LDSR, as implemented in LDHub in order to identify known and new genetic correlations. Consistent with previous research, the strongest genetic correlation was with bipolar disorder. Positive genetic correlations were also found between schizophrenia and all other psychiatric phenotypes tested, the personality traits of neuroticism and openness to experience, and cigarette smoking. Novel results were found with medical phenotypes: schizophrenia was negatively genetically correlated with serum citrate, positively correlated with inflammatory bowel disease, and negatively correlated with BMI, hip, and waist circumference. The serum citrate finding provides a potential link between rare cases of schizophrenia (strongly influenced by 22q11.2 deletions) and more typical cases of schizophrenia (with polygenic influences). Overall, these genetic correlation findings match epidemiological findings, suggesting that common variant genetic effects are part of the scaffolding underlying phenotypic comorbidity. The "genetic correlation profile" is a succinct report of shared genetic effects, is easily updated with new information (eg, from future GWAS), and should become part of basic disease knowledge about schizophrenia.

    View details for DOI 10.1093/schbul/sbx174

    View details for PubMedID 29294133

  • Ethical Issues in the Care of People with Schizophrenia Focus: The Journal of Lifelong Learning in Psychiatry Noordsy, D. L. 2016; 14 (3): 349-353
  • Long-Acting Injectable vs Oral Risperidone for Schizophrenia and Co-Occurring Alcohol Use Disorder: A Randomized Trial JOURNAL OF CLINICAL PSYCHIATRY Green, A. I., Brunette, M. F., Dawson, R., Buckley, P., Wallace, A. E., Hafez, H., Herz, M., Narasimhan, M., Noordsy, D. L., O'Keefe, C., Sommi, R. W., Steinbook, R. M., Weeks, M. 2015; 76 (10): 1359-1365


    Alcohol use disorders worsen the course of schizophrenia. Although the atypical antipsychotic clozapine appears to decrease alcohol use in schizophrenia, risperidone does not. We have proposed that risperidone's relatively potent dopamine D2 receptor blockade may partly underlie its lack of effect on alcohol use. Since long-acting injectable (LAI) risperidone both results in lower average steady-state plasma concentrations than oral risperidone (with lower D2 receptor occupancy) and encourages adherence, it may be more likely to decrease heavy alcohol use (days per week of drinking 5 or more drinks per day) than oral risperidone.Ninety-five patients with DSM-IV-TR diagnoses of schizophrenia and alcohol use disorder were randomized to 6 months of oral or LAI risperidone between 2005 and 2008. Explanatory (efficacy) analyses were carried out to evaluate the potential benefits of LAI under suitably controlled conditions (in contrast to real-world settings), with intent-to-treat analyses being secondary.Explanatory analyses showed that heavy drinking in the oral group worsened over time (P = .024) and that there was a statistical trend toward significance in the difference between the changes in heavy drinking days in the oral and LAI groups (P = .054). Furthermore, the 2 groups differed in the mean number of drinking days per week (P = .035). The intent-to-treat analyses showed no difference in heavy drinking but did show a difference in average drinking days per week similar to that obtained from the explanatory analyses (P = .018). Neither explanatory nor intent-to-treat analyses showed any between-group differences in alcohol use as measured by intensity or the Alcohol Use Scale. The plasma concentrations of the active metabolite 9-hydroxyrisperidone were significantly lower in patients taking LAI (P < .05), despite their significantly (overall) better treatment adherence (P < .005).For the population considered here, schizophrenia patients with alcohol use disorder appear to continue drinking some alcohol while taking either form of risperidone. Nonetheless, our data suggest that injectable risperidone may be a better choice than the oral form for these dual diagnosis identifier: NCT00130923.

    View details for DOI 10.4088/JCP.13m08838

    View details for Web of Science ID 000368347900022

    View details for PubMedID 26302441

  • Low-Dose Quetiapine Induced or Worsened Mania in the Context of Possible Undertreatment JOURNAL OF THE AMERICAN BOARD OF FAMILY MEDICINE Millard, H. Y., Wilson, B. A., Noordsy, D. L. 2015; 28 (1): 154-158


    Bipolar disorder is a mental illness with a lifetime prevalence of 2% and has a dramatic impact on quality of life. Mania is a distinct period of abnormal and sustained elevated, expansive, or irritable mood and increase in goal-directed activity or energy that lasts at least 1 week and is present for most of each day. Quetiapine is an atypical antipsychotic approved for the treatment of bipolar depression and mania. For the treatment of acute mania, a dose of 600 to 800 mg/day is recommended. There has been concern of potential induction or worsening of hypomanic or manic symptoms at low doses via the ratio of 5HT2A/D2 receptor antagonism, which at lower doses favors greater 5HT2A receptor blockade and thus increases dopamine concentrations. This article describes a case report of hypomania worsening to mania with psychotic features in a drug-naïve patient who was started on low-dose quetiapine. This case adds to the existing literature of case reports indicating that low-dose quetiapine may be associated with induction or worsening of hypomanic/manic symptoms, while acknowledging the difficulty of suggesting a causal relationship.

    View details for DOI 10.3122/jabfm.2015.01.140105

    View details for Web of Science ID 000347880900024

    View details for PubMedID 25567837

  • Pharmacotherapy of Co-Occurring Schizophrenia and Substance Use Disorders. Current addiction reports Akerman, S. C., Brunette, M. F., Noordsy, D. L., Green, A. I. 2014; 1 (4): 251-260


    Substance use disorders, common in patients with schizophrenia, can lead to poor outcomes. Here we review the literature on the use of antipsychotics in patients with co-occurring schizophrenia and substance use disorder as well as evidence for the use of adjunctive pharmacological treatments targeting substance use in these patients. We also discuss a neurobiological formulation suggesting that the cooccurrence of these disorders may be related to a dysfunction in the dopamine mediated brain reward circuitry. Typical antipsychotics do not appear to decrease substance use in this population. Randomized, controlled trials provide some support for use of the atypical antipsychotic clozapine for co-occurring cannabis use disorder, naltrexone and disulfiram for alcohol use disorder, and also nicotine replacement therapy, sustained-release bupropion and varenicline for tobacco use disorder. Nonetheless, data regarding treatment in patients with these co-occurring disorders are still limited, and many studies reported to date have been either underpowered or did not include a control condition. Further research is needed to evaluate optimal pharmacotherapeutic strategies for this population.

    View details for PubMedID 27226947

    View details for PubMedCentralID PMC4877030

  • Neuroleptic Malignant Syndrome During Multiple Antipsychotic Therapy COMMUNITY MENTAL HEALTH JOURNAL McDermott, M., Noordsy, D. L., Traum, M. 2013; 49 (1): 45-46

    View details for DOI 10.1007/s10597-011-9452-3

    View details for Web of Science ID 000313654900006

    View details for PubMedID 22038421

  • A Randomized Trial of Clozapine Versus Other Antipsychotics for Cannabis Use Disorder in Patients With Schizophrenia JOURNAL OF DUAL DIAGNOSIS Brunette, M. F., Dawson, R., O'Keefe, C. D., Narasimhan, M., Noordsy, D. L., Wojcik, J., Green, A. I. 2011; 7 (1-2): 50-63


    Cannabis use disorder is the most common co-occurring drug use disorder in people with schizophrenia and is associated with poor outcomes. We launched a randomized controlled trial to assess the impact of clozapine compared with treatment as usual on cannabis use in patients with schizophrenia and co-occurring cannabis use disorder.Thirty-one patients with schizophrenia and co-occurring cannabis use disorder were randomly assigned to switch to clozapine or to stay on their current antipsychotic and were then followed weekly for 12 weeks. Blinded raters assessed participants weekly with the Timeline Follow-back for substance use and the expanded Brief Psychiatric Rating Scale for symptoms. Longitudinal random effects models were used to investigate the time-varying differences in cannabis use and other outcomes between the treatment as usual and clozapine groups.The two groups differed in average intensity of cannabis use by approximately 4.5 joints/week, with lesser use in the clozapine group (t = -1.77; df = 28.5; p=.086; effect size ~ 0.6). Symptoms and functioning were not different between the two groups.Clozapine may reduce cannabis use among patients with schizophrenia and co-occurring cannabis use disorder. Further controlled trials are warranted.

    View details for DOI 10.1080/15504263.2011.570118

    View details for Web of Science ID 000290671900006

    View details for PubMedID 25914610

    View details for PubMedCentralID PMC4407140

  • Treatment of catatonic schizophrenia with lorazepam and aripiprazole SCHIZOPHRENIA RESEARCH Cummings, T. S., Noordsy, D. L. 2009; 112 (1-3): 194-195

    View details for DOI 10.1016/j.schres.2009.04.009

    View details for Web of Science ID 000268153900029

    View details for PubMedID 19411162

  • Six-month outcomes for patients who switched to olanzapine treatment PSYCHIATRIC SERVICES Noordsy, D. L., O'Keefe, C., Mueser, K. T., Xie, H. Y. 2001; 52 (4): 501-507


    This study evaluated the outcomes of patients in a community mental health center who switched from treatment with another antipsychotic to olanzapine treatment. It also sought to determine whether simultaneous access to case management and psychosocial rehabilitation and olanzapine leads to enhanced functional improvement.Six-month outcomes for a consecutive series of 104 patients who switched from a conventional antipsychotic medication to olanzapine were evaluated. Forty-nine patients in the same treatment program who continued to take conventional antipsychotics were also monitored as a reference group. Outcomes of the group receiving olanzapine were compared with their own baseline status and with outcomes of the reference group.At six months, patients in the olanzapine group demonstrated significant improvement over baseline across multiple measures of symptoms and psychosocial function. Compared with the reference group, the olanzapine group was more symptomatic at baseline and demonstrated significantly greater improvement at follow-up on the Brief Psychiatric Rating Scale and all subscales; Mini Psychiatric Rating Scale negative symptom, disorganization, anxiety, depression, and medication side effects items; and Clinical Global Improvement scale and Case Manager's Rating Scale-Plus illness factors. There was a trend toward superior improvement in psychosocial functioning among patients in the olanzapine group that achieved significance when patients in acute relapse at baseline were excluded.Olanzapine is effective in managing markedly to severely ill patients with psychotic disorders in a community mental health center. Simultaneous treatment with olanzapine, case management, and psychosocial rehabilitation leads to enhanced functional improvement among nonrelapsing patients.

    View details for Web of Science ID 000167877100014

    View details for PubMedID 11274497