Psychiatric Annals

CME Article 

Health Disparities in Black Patients with Severe Mental Illness and the Role of Structural Racism

Uzoamaka Asonye, MD; Nicholas Apping, MD; Leonardo V. Lopez, MD; Dennis M. Popeo, MD


Black patients with severe mental illness (SMI) experience health disparities when compared to White patients. These disparities include differences in the availability of culturally appropriate, affordable care; a disproportionate diagnosis of psychotic illnesses; differential and inequitable access to certain medications and treatments; and a decreased likelihood of being referred to higher-quality, evidence-based after-care programming. These disparities are not due to Black people being “sicker,” but instead are due to implicit bias and structural racism. In this article, we describe the health disparities that Black patients with SMI suffer in access to mental health care, diagnosis, treatment, and aftercare. We discuss the origins of these disparities and some ways that each of us can combat them in our day-to-day practice. [Psychiatr Ann. 2020;50(11):483–488.]


Black patients with severe mental illness (SMI) experience health disparities when compared to White patients. These disparities include differences in the availability of culturally appropriate, affordable care; a disproportionate diagnosis of psychotic illnesses; differential and inequitable access to certain medications and treatments; and a decreased likelihood of being referred to higher-quality, evidence-based after-care programming. These disparities are not due to Black people being “sicker,” but instead are due to implicit bias and structural racism. In this article, we describe the health disparities that Black patients with SMI suffer in access to mental health care, diagnosis, treatment, and aftercare. We discuss the origins of these disparities and some ways that each of us can combat them in our day-to-day practice. [Psychiatr Ann. 2020;50(11):483–488.]

A health disparity is the difference in the burden of disease experienced by one group compared to another. There are multiple factors that can cause these disparities including race, ethnicity, sex, gender identity, age, and socioeconomic status.1 Psychiatry is not immune from health disparities that disproportionately affect the morbidity and mortality of some groups. For instance, African Americans are 3 to 5 times more likely to receive a diagnosis of schizophrenia than White patients, and those African Americans that are diagnosed with schizophrenia achieve a worse functional outcome than their White counterparts.2 Mental illness itself can cause health disparities, especially in those who suffer from severe disorders.

Serious mental illness (SMI) is defined as a mental disorder that results in a serious impairment that substantially interferes with or limits one or more major life activities.3 Patients with these illnesses suffer from decreased ability to work and to form meaningful interpersonal relationships. They have more medical illnesses, receive worse medical care, and die on average 25 years earlier than the general population.3

The intersection of the variables of race and SMI can multiply their effect to increase health disparities. The differences in outcomes between African American and White patients illustrate this point. These disparities are not fully explained by underlying biological differences related to susceptibility to psychosis or by illness severity.4 Instead they may be a result of a complex set of factors. This article discusses the literature that characterizes these racial disparities and explores the role that implicit bias, racism, and racialization play in sustaining the disparity in mental health care. We present the disparities in the framework of a typical inpatient psychiatric admission, from barriers to appropriate preventive care, diagnosis, treatment, and aftercare. Although the constructs of race and ethnicity are distinct, they are not typically distinguished in the literature. Therefore, in this article, we use the terms Black and African American interchangeably.


The barriers to receiving mental health care for Black patients are like the barriers to receive any health care. Systemic racism has significantly contributed5 to the wealth gap, a lack of insurance coverage, and underfunded and otherwise limited options for care in areas that are majority Black.6 It can be an onerous process to receive care, and that care is often not culturally appropriate and given by practitioners who are not culturally or structurally competent.6 The disproportionate rates of Black patients with SMI who are incarcerated and experiencing homelessness also affects access to care. They disproportionately are usually relegated to safety-net care, or receive care in the prison system, both of which are inadequate to keep up with the demand for care.7

Beliefs and attitudes of patients also play a role in accessing care. A qualitative study of 34 Black patients with SMI attempted to describe these beliefs.8 The participants indicated that stigma surrounding mental illness was a serious concern. This stigma extended to hesitation to confide in typical support systems like family and religious community for fear of shunning, which fuels denial of mental health problems. Participants reported suspicions of the medical community and medications, and sometimes reported not receiving enough information about diagnosis and treatment. Finally, some participants described that believing in mental health care and therapy were inherent to White people, and that Black people should possess the strength to solve their own problems.8

Finally, since many patients with SMI will have contact with the legal system, sometimes as their introduction to the mental health system, it must be noted that more Black people with SMI are killed during police interactions than White people with SMI.9


Evidence consistently shows that African Americans are disproportionately diagnosed with psychotic disorders at a rate that is 3 to 4 times higher than White Americans despite there being no evidence of an increase in prevalence among African Americans in large epidemiologic studies.4 After controlling for clinical characteristics and demographics, African Americans remain 3 times more likely to receive a diagnosis of schizophrenia or schizoaffective affective disorder.4 A study conducted by Neighbors et al.10 shows that these disparities persist even when semi-structured in-person clinical interviews are used, but do not persist when assessors are blinded to the race of the participant. Conclusions based on a literature review conducted by Garb11 reveal that African Americans are more likely to be diagnosed with schizophrenia even when measures of psychopathology do not justify the diagnosis. African Americans with affective disorders are at higher risk of being misdiagnosed for schizophrenia because their affective symptoms are underappreciated, although when structured clinical interviews are performed, this effect disappears.12 Unfortunately, these findings extend to Black adolescents, who are also assigned a diagnosis of psychotic disorder at greater rates than White adolescents.13

There remains no clear explanation for the overrepresentation of African Americans in psychotic disorders. Although a review of the ontological history of diagnostic classification proves illuminating, Metzl14 hypothesizes a chronological narrative and the sociopolitical context for understanding how schizophrenia transformed into a disease more commonly diagnosed in African Americans. In the first iteration of the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1952, mental disorders were described as a series of reactions that were due to the interaction of a person's personality with their environment; thus, schizophrenia reflected an emotional disharmony that resulted in regressive behavior and unpredictable streams of thought.15 Then, schizophrenia was a disease of middle-class White women who were viewed as spoiled children, but in the 1960s, the disease shifted to one of “hostile” Black men.14 This change has been posited to be connected to two events in the era: (1) a political climate that challenged white supremacy through riots and protests and (2) revisions to the diagnostic criteria of schizophrenia. The DSM-II attempted to narrow the definition of psychotic disorders and represent them as distinct illnesses rather than “reactions,” and included the subtype of paranoid schizophrenia, which was characterized by persecutory delusions and hostility.16 The era of DSM-II was marked by the assassinations of Dr. Martin Luther King, Jr., in 1968 and Malcolm X in 1965, along with the growing prominence of the Black Panther Party organization, and Black people who used civil disobedience as their perceived rational and justifiable response to racism.15 Metzl14 argues that the new criteria of schizophrenia reflected smoldering White fear related to the rise of Black political movements, and the flames of this fear were stoked by pharmaceutical companies who capitalized on these anxieties. Using racist tropes, they promoted the message that social problems broached by “angry” Black men could be treated, at the clinical level, with antipsychotic medications. One obvious example is an ad from the makers of haloperidol that appeared in an issue of Archives of General Psychiatry in 1974.16 The ad read “Assaultive and belligerent?” Cooperation begins with HALDOL,” which was juxtaposed against the likeness of a stereotypical “angry Black man.” Although the intention of DSM writers was not to codify racism, the unintentional effects were clear—schizophrenia became a racialized disease and thus pathologized Black protestors.14 Today, there is no apparent racial bias embedded within the diagnostic criteria of schizophrenia; however, as evidenced by our clinical practice, relics of our collective history remain.


There are substantial differences in the pharmacologic treatment received by White and African American patients diagnosed with schizophrenia. African American patients are approximately 1.5 to 2 times as likely to receive first-generation antipsychotics (FGAs) as White patients; the risk rises when only high-potency FGAs are considered and is particularly accentuated among young Black men.17 Not surprisingly, African American patients consequently develop tardive dyskinesia (TD) at higher rates than do White patients.18 Development of TD in African American patients appears to be related to the use of high-dose, long-acting formulations of FGAs.19 Indeed, African American patients are prescribed long-acting antipsychotics 90% more frequently than are White patients, a difference that cannot be fully accounted for by differences in adherence.20 Insofar as the literature does suggest that African American patients are less adherent to medications than White patients, the question must be raised as to why such a disparity would exist, and as to what strategies to encourage adherence are being used with White patients.

By contrast, African American patients have consistently been shown to receive second-generation antipsychotics (SGA) and clozapine, a drug developed during the first generation of antipsychotic development but typically classified along with SGAs as “atypical,” at lower rates than White patients.18 SGAs have fewer extra-pyramidal side-effects than FGAs, particularly high-potency FGAs, and are generally thought to be more tolerable and possibly to reduce relapse risk as a result, so it is troubling that African American patients are as much as 6 times less likely to receive SGAs.21 Clozapine has superior efficacy to other antipsychotics in both treatment-responsive and treatment-resistant patients and is the only medication with a US Food and Drug Administration indication for the prevention of suicide, but Black patients are at least 30% less likely to receive clozapine than are White patients.22 Although underuse of clozapine among African American patients may be partially explained by inappropriate discontinuation due to benign ethnic neutropenia, this is not sufficient to explain the entirety of the difference, and in and of itself suggests a failure to appreciate impediments to care that are unique to the African American population.23

Electroconvulsive therapy (ECT) is one of the most effective treatments for the population of patients with SMI with mood and psychotic disorders, but it is not delivered in an equitable manner.24 In the 1980s and 1990s, this disparity was blamed on structural racism; Black people were more likely than White people to be treated at lower quality hospitals where ECT was not available.25 Although the availability of ECT to the Black community has changed, the equity has not. The hospitalizations of over 680,000 elderly patients for moderate to severe depression in the US from 2002 to 2015 were reviewed and showed that although Black and White people were admitted to hospitals that offered ECT at similar rates, Black people were one-half as likely to receive that treatment than White people.25 The overdiagnosis of schizophrenia in the Black population may play a role in this disparity.2 Black and White patients have comparable outcomes from ECT, even though Black patients who receive ECT tend to be more severely ill than White patients—suggesting that Black patients may be deprived of beneficial treatment until they are sicker.25

Aftercare Services

Aftercare services are a form of tertiary prevention for patients with SMI aimed to decrease hospitalizations and emergency visits, and to increase outpatient engagement. Eack and Newhill2 observed 925 patients with SMI for 1 year posthospitalization and found African American patients to have less improvement in psychotic symptoms, to be less likely to return to work, and to have less improvement in global functioning when compared to White patients with SMI.2 The authors suggested that improvement in access to psychosocial interventions after discharge would improve outcomes.2

Although not an all-encompassing list of available services, for this article, we discuss Assertive Community Treatment (ACT) and family inclusion. ACT teams are multidisciplinary behavioral health teams who provide comprehensive health care and psychosocial support to people who have SMI. ACT teams, like other areas of mental health care, rely heavily on the therapeutic alliance developed between the patient and care team. An article by Maura and Weisman de Mamani26 surmised the racial disparities within these psychosocial interventions are in part due to cultural differences between providers and patients, and lack of cross-cultural competence among providers. This point is further supported by Larrison et al.27 who investigated 62 mental health professionals and 551 of their patients to look for physician-mediated factors leading to disparities. Although outcomes varied considerably, clinician experiences and relationships with people from racial/ethnic and cultural groups was a statistically significant predictor of differences in Black versus White patient outcomes.27 With ACT team initiation representing a transitional point in the care of a patient, this creates a new point of increased vulnerability. Horvitz-Lennon et al.28 reported a prospective observational study of 6,829 African American, Latinx, and White patients with SMI receiving ACT services and found throughout the study period that Black patients had a lower probability of using ACT team services and had lower intensity of engagement with services at treatment initiation than White patients.26 Although African Americans were found to use services more intensely at the 3- and 12-month mark than White patients,28 one must consider how dangerous delays can be in our populations with the highest risks.

Family psychoeducation and involvement in treatment has demonstrated protective effects in decreasing the number of hospitalizations and increasing medication adherence in populations with SMI, which may be of increased significance for racial minority groups, as they are more likely to live with family members.26 Early family involvement is of particular importance to prevent progression of first-episode psychosis (FEP) to SMI. FEP treatment involves coordinated-specialty-care (CSC), recovery-oriented programs aimed at preventing progression to SMI through early and collaborative pharmacological, psychological, and psychosocial interventions, including family involvement. Oluwoye et al.29 explored racial disparities of patients enrolled in the RAISE-ETP (Recovery After an Initial Schizophrenia Episode–Early Treatment Program) trial. Overall, rates of family involvement were low in both community and CSC populations (8% vs 31%, respectively); however, non-Latinx Black participants were even less likely to receive family psychoeducation (odds ratio = 0.53; P = .009) when compared to non-Latinx White participants within the CSC subgroup.28 This finding predicts a future widening of outcome disparities among Black patients with SMI with a continuation of racial stigma toward the disease within society.


Disparities in the care of Black patients with SMI affect all aspects of mental health care: access, diagnosis, and treatment with medications and psychosocial interventions. We believe that both implicit bias and structural/institutional racism have substantially contributed to these disparities. Institutional racism is a system of policies and practices in which public and private entities reinforce inequity between races, whereas structural racism encompasses institutional racism and other societal, ideological, and process-based systems to again reinforce inequity.30 This is best described by Gee and Ford31 as an iceberg, with the portion above the surface as obvious, public displays of racism—using racial epithets or flying a Confederate flag. They describe institutional and structural racism, which are more insidious and widespread, as the portion of the iceberg hiding under the surface of the water.31 This hidden menace serves to further marginalize people who are vulnerable and feeds into mistrust.

While we have come to the point where an advertisement for an antipsychotic medication that pairs an image of a Black face with negative aspects of mental illness would be deemed unacceptable for inclusion in a mainstream, academic psychiatry journal, we have not come to the point where the treatment of Black patients with SMI is equitable. As psychiatrists, we have the unique opportunity to combat racism and promote equity. We are trained to acknowledge and understand the unconscious mind and its heuristics that can lead to bias, as well as to recognize and change maladaptive thoughts and behaviors. Reading this article and the other articles in this issue32–34 is an important first step. As the great novelist and essayist James Baldwin wrote, “not everything that is faced can be changed, but nothing can be changed until it is faced.”

We must not allow ourselves to automatically rule out treatment modalities or outpatient services without fully examining our thought processes for bias. We should add questions about social determinants of health to evaluation processes and to our formulations. Our profession allows us the opportunity to work with diverse populations and colleagues; we need to embrace this, as building these relationships will assist in curbing our biases. We must commit to continuing to educate ourselves, our colleagues, and our trainees about health care disparities in general and those that specifically affect our Black patients. Finally, we must work to understand and change the effects of systematic racism in psychiatry and also in society as a whole. Leaders in our field must think carefully about recommendations and policies with an eye toward promoting equity and limiting inequity. We must be able to look back at the unintended consequences of policies that caused inequity and have the courage to change them. Melting the iceberg of racism will be difficult and will take a concerted effort, but such an effort is necessary to improve the care of all of our patients.


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Uzoamaka Asonye, MD, is a Resident in Psychiatry. Nicholas Apping, MD, is a Resident in Psychiatry. Leonardo V. Lopez, MD, is an Associate Professor of Psychiatry. Dennis M. Popeo, MD, is an Associate Professor of Psychiatry. All authors are affiliated with the Department of Psychiatry, NYU Grossman School of Medicine.

Address correspondence to Dennis M. Popeo, MD, Bellevue Hospital Center, 462 First Avenue, Room 12S-23C, New York, NY 10016; email:

Disclosure: The authors have no relevant financial relationships to disclose.


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