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Conceptualizing the Influence of Social and Structural Determinants of Neurobiology and Mental Health: Why and How Biological Psychiatry Can Do Better at Addressing the Consequences of Inequity

Open AccessPublished:June 16, 2022DOI:https://doi.org/10.1016/j.bpsc.2022.06.004

      Abstract

      Psychiatry and allied disciplines have recognized the potency of structural and social determinants of mental health, yet there has been scant attention given to the roles of neurobiology in the links between structural and social determinants and mental health. In this article, we make the case for why greater attention must be given to structural and social determinants of biological psychiatry by researchers, practitioners, and policy-makers. After defining these terms and theoretical frameworks for considering their relevance in biological psychiatry, we review empirical research with marginalized and minoritized racial, ethnic, gender, sexual, and economic communities that reveals the ways in which structural and social determinants affect neurobiological functioning with implications for mental health. We give particular emphasis to developmental science and developmentally informed research, because structural and social determinants influence neurobiological adaptation and maturation across the lifespan. We conclude with recommendations for advancing research, practice, and policy that connect biological psychiatry with structural and social determinants of health. Foremost among these is diversifying the ranks of biological psychiatry, from classrooms through laboratories, hospitals, and community health centers. Transforming and advancing the understanding of the structural and social determinants of neurobiology and mental health is most likely to come through transforming the discipline itself.

      Keywords

      Disparities and inequities in mental health across diverse marginalized and minoritized communities are well documented (
      American Psychiatric Association
      Disparities in mental health status and mental health care.
      ,
      • Shim R.
      • Koplan C.
      • Langheim F.J.P.
      • Manseau M.W.
      • Powers R.A.
      • Compton M.T.
      The social determinants of mental health: An overview and call to action.
      ). Recognition of structural and social determinants of mental health is increasing (
      • Bradley R.H.
      • Corwyn R.F.
      Socioeconomic status and child development.
      ,
      World Health Organization and Calouste Gulbenkian Foundation
      Social Determinants of Mental Health.
      ). Many theories posit that the development and functioning of the brain and peripheral biological systems play key roles in the links between inequities and worse mental health across the lifespan (
      • Harnett N.G.
      Neurobiological consequences of racial disparities and environmental risks: A critical gap in understanding psychiatric disorders.
      ,
      • Hertzman C.
      • Boyce T.
      How experience gets under the skin to create gradients in developmental health.
      ). Yet, until recently, the roles that neurobiology plays in the developmental processes linking structural and social determinants with mental health have received relatively little attention.
      We present arguments and evidence in support of committing greater attention to structural and social determinants of biological psychiatry. First, we provide a brief overview of theoretical frameworks linking structural and social determinants with mental health via neurobiology, which cohere around a developmental perspective on health. Second, in our role as developmental scientists, this perspective is reflected in our review of relevant research examining structural and social determinants in relation to brain structure and function, diurnal and acutely reactive hypothalamic-pituitary-adrenal (HPA) axis functioning, and tonic (baseline) and phasic (reactive) aspects of the autonomic nervous system (ANS) and immune (inflammatory) system. Third, the article concludes with suggestions for translating these perspectives and empirical findings into actions for advancing research, training, practice, and policy in biological psychiatry and allied disciplines.

      Definitions and Perspectives

      Interpretations of structural and social determinants vary, and our perspective is informed by multiple sources (

      National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on Community-Based Solutions to Promote Health Equity in the United States. (2017): Communities in Action: Pathways to Health Equity. Weinstein NJ, Geller A, Negussie Y, Baciu A, editors. Washington, DC: National Academies Press.

      ,
      • Carger E.
      • Westen D.
      Robert Wood Johnson Foundation
      A New Way to Talk About the Social Determinants of Health.
      ,
      World Health Organization (WHO)
      Closing the Gap in a Generation: Health Equity Through Action on the Social Determinants of Health.
      ). Consideration of this topic requires acknowledgment of the current and historically perpetuated geographic, political, economic, and societal conditions into which one is born and within which one lives. These conditions variably constrain or provide access to opportunities that promote healthy biopsychosocial adjustment. Collectively, one’s life conditions are seen as the roots of one’s health, including neurobiological and mental health (
      • Campion J.
      • Bhugra D.
      • Bailey S.
      • Marmot M.
      Inequality and mental disorders: Opportunities for action.
      ,
      • Ramsay S.E.
      • Morris R.W.
      • Whincup P.H.
      • Subramanian S.V.
      • Papacosta A.O.
      • Lennon L.T.
      • Wannamethee S.G.
      The influence of neighbourhood-level socioeconomic deprivation on cardiovascular disease mortality in older age: Longitudinal multilevel analyses from a cohort of older British men.
      ,
      • Ziol-Guest K.M.
      • Duncan G.J.
      • Kalil A.
      • Boyce W.T.
      Early childhood poverty, immune-mediated disease processes, and adult productivity.
      ), and these conditions vary across racial, ethnic, national, gender, sexual, economic, and other individual and community characteristics. Recognizing that variability exists in individuals’ life conditions necessitates also recognizing that lives begin on an uneven playing field for healthy development.
      Structural and social determinants are overlapping and interdependent constructs. Whether a measure or phenomenon is understood as operating at the structural or social level, or both simultaneously, can depend on how narrow or broad a lens one brings to that understanding. Acknowledging others may use the terms differently, or apply additional distinctions (i.e., institutional, systemic) (

      National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on Community-Based Solutions to Promote Health Equity in the United States. (2017): Communities in Action: Pathways to Health Equity. Weinstein NJ, Geller A, Negussie Y, Baciu A, editors. Washington, DC: National Academies Press.

      ), we define structural determinants as encompassing the political, economic, and social policies, practices, and values that function at national and local levels to affect the availability of resources, civil rights and protections, and overall cultural climate within which people live. When these determinants reinforce power structures that disadvantage some groups and place them in subordinate and underresourced positions relative to more dominant groups, such as the gender wage gap, redlining and neighborhood segregation, and voter suppression, the disadvantaged individuals and groups are structurally minoritized (

      National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on Community-Based Solutions to Promote Health Equity in the United States. (2017): Communities in Action: Pathways to Health Equity. Weinstein NJ, Geller A, Negussie Y, Baciu A, editors. Washington, DC: National Academies Press.

      ,
      World Health Organization (WHO)
      Closing the Gap in a Generation: Health Equity Through Action on the Social Determinants of Health.
      ,
      • Hatzenbuehler M.L.
      • Link B.G.
      Introduction to the special issue on structural stigma and health.
      ,
      • Hatzenbuehler M.L.
      • Phelan J.C.
      • Link B.G.
      Stigma as a fundamental cause of population health inequalities.
      ). Social determinants include people’s daily lived experiences resulting from these structural conditions, such as personal material resources, education and employment, neighborhood resources, health care access, and inclusive versus discriminatory treatment by others. More neurobiological research has focused on social than structural determinants (
      • Hatzenbuehler M.L.
      • Link B.G.
      Introduction to the special issue on structural stigma and health.
      ), although the latter may be the primary drivers of national and global health inequities (
      World Health Organization and Calouste Gulbenkian Foundation
      Social Determinants of Mental Health.
      ,
      World Health Organization (WHO)
      Closing the Gap in a Generation: Health Equity Through Action on the Social Determinants of Health.
      ).
      Several theoretical models position structural and social determinants as contributors to neurobiology and mental health. McEwen’s (
      • McEwen B.S.
      Stress, adaptation, and disease. Allostasis and allostatic load.
      ,
      • McEwen B.S.
      • Stellar E.
      Stress and the individual. Mechanisms leading to disease.
      ) model of allostatic load (AL) posits that prolonged stress system activation due to chronically aversive life conditions eventually disrupts the ability of stress systems to flexibly modulate activity in response to daily challenges (
      • Sterling P.
      • Eyer J.
      Allostasis: A new paradigm to explain arousal pathology.
      ), thereby eroding healthy functioning. The stress sensitization hypothesis contends that varying exposures to chronic or severe stressors in early-life primes biological stress systems for exaggerated reactivity in adolescence and adulthood (
      • Levine S.
      Developmental determinants of sensitivity and resistance to stress.
      ), which Hostinar et al. (
      • Hostinar C.E.
      • Swartz J.R.
      • Alen N.V.
      • Guyer A.E.
      • Hastings P.D.
      The role of stress phenotypes in understanding childhood adversity as a transdiagnostic risk factor for psychopathology. J Psychopathology and Clinical Science.
      ) extended to distinguish multiple biopsychological repertoires of acute stress responses that may underlie resilience versus distinct psychopathologies. Meyer (
      • Meyer I.H.
      Prejudice, social stress, and mental health in lesbian, gay, and bisexual populations: Conceptual issues and research evidence.
      ), Myers (
      • Myers H.F.
      Ethnicity- and socio-economic status-related stresses in context: An integrative review and conceptual model.
      ), and others have proposed minority stress models that apply these views directly to the experiences and development of marginalized populations. Informed by an intersectional perspective on the synergistic consequences of having multiple identity characteristics (
      • Crenshaw K.
      Demarginalizing the intersection of race and sex: A Black feminist critique of antidiscrimination doctrine, feminist theory and antiracist politics.
      ), such as being racially marginalized and devalued for being transgender, minority stress models posit that both direct experiences of discrimination and lack of resources (social determinants) and overarching life conditions that maintain disadvantage, marginalization, and disempowerment (structural determinants) are neurotoxic, undermining mental health through their biological effects (
      • Parra L.A.
      • Hastings P.D.
      Integrating the neurobiology of minority stress with an intersectionality framework for LGBTQ-Latinx populations.
      ,
      • Parra L.A.
      • Hastings P.D.
      Challenges to identity integration indirectly link experiences of heterosexist and racist discrimination to lower waking salivary cortisol in sexually diverse Latinx emerging adults.
      ).
      These models of biological embedding, or “stress getting under the skin” (
      • Taylor S.E.
      • Repetti R.L.
      • Seeman T.
      Health psychology: What is an unhealthy environment and how does it get under the skin?.
      ), implicitly or explicitly reflect a lifespan developmental perspective. Structural and social determinants are relatively severe, chronic, and stable—often, multigenerational—conditions. These may influence developing neurobiological systems underlying mental health throughout the lifespan. This perspective pertains even when considering adult populations, and research indicates that adverse social and economic conditions in the first 2 decades of life predict mental and physical health disparities in adulthood and older age (
      • Cohen S.
      • Janicki-Deverts D.
      • Chen E.
      • Matthews K.A.
      Childhood socioeconomic status and adult health.
      ,
      • Gruenewald T.L.
      • Karlamangla A.S.
      • Hu P.
      • Stein-Merkin S.
      • Crandall C.
      • Koretz B.
      • Seeman T.E.
      History of socioeconomic disadvantage and allostatic load in later life.
      ). In this review, we consider the evidence that structural and social determinants affect neurobiological maturation, and affect mental health through neurobiology, with particular focus on the first 2 decades of life.

      Evidence for Relations Between Social and Structural Determinants and Neurobiology

      Of the social determinants, most research has focused on either household economic resources or individuals’ experiences of discrimination. Considering economics and the brain first, being raised in poverty is associated with structural and functional changes including reduced hippocampal volume, altered prefrontal cortex (PFC) activity to emotional and cognitive tasks, and reduced connectivity between the PFC and the amygdala (
      • Brito N.H.
      • Noble K.G.
      Socioeconomic status and structural brain development.
      ,
      • Liberzon I.
      • Ma S.T.
      • Okada G.
      • Ho S.S.
      • Swain J.E.
      • Evans G.W.
      Childhood poverty and recruitment of adult emotion regulatory neurocircuitry.
      ,
      • Page M.E.
      • Conger K.
      • Guyer A.E.
      • Hastings P.D.
      • Thompson R.
      Children and the intergenerational transmission of poverty: Research frontiers and policy implications.
      ), potentially attributable to experiencing more stressors at home (
      • Luby J.
      • Belden A.
      • Botteron K.
      • Marrus N.
      • Harms M.P.
      • Babb C.
      • et al.
      The effects of poverty on childhood brain development: The mediating effect of caregiving and stressful life events.
      ). Childhood poverty continues to leave a mark on the brain in adulthood. Men who were raised in highly disadvantaged neighborhoods showed less differentiation in structural brain networks (
      • Krishnadas R.
      • McLean J.
      • Batty G.D.
      • Burns H.
      • Deans K.A.
      • Ford I.
      • et al.
      Socioeconomic deprivation and cortical morphology: Psychological, social, and biological determinants of ill health study.
      ), and middle-aged individuals from lower socioeconomic status (SES) backgrounds have been found to have lower resting-state connectivity and reduced cortical thickness (
      • Chan M.Y.
      • Na J.
      • Agres P.F.
      • Savalia N.K.
      • Park D.C.
      • Wig G.S.
      Socioeconomic status moderates age-related differences in the brain’s functional network organization and anatomy across the adult lifespan.
      ), which are neural indices of less functionality and organizational efficiency. Conversely, increasing economic resources for impoverished children promotes healthier brain development. The Baby’s First Years randomized controlled trial of monthly cash transfers to low-income new mothers showed that financial support to families enhanced infants’ electroencephalography power in high-frequency bands associated with better cognitive, language, and social-emotional functioning (
      • Troller-Renfree S.V.
      • Costanzo M.A.
      • Duncan G.J.
      • Magnuson K.
      • Gennetian L.A.
      • Yoshikawa H.
      • et al.
      The impact of a poverty reduction intervention on infant brain activity.
      ). For U.S. Mexican–origin adolescents living in poverty, increasing family income from age 10 to 16 years predicted stronger resting-state functional connectivity between the posterior cingulate gyrus and insula and the right inferior frontal gyrus, which are regions of the default mode network that support social cognition (
      • Weissman D.G.
      • Conger R.D.
      • Robins R.W.
      • Hastings P.D.
      • Guyer A.E.
      Income change alters default mode network connectivity for adolescents in poverty.
      ); income changes were not associated with connectivity for youths living in more financially secure families.
      Economic hardship is linked with altered stress responses, including both reduced (hypocortisolism) (
      • Badanes L.S.
      • Watamura S.E.
      • Hankin B.L.
      Hypocortisolism as a potential marker of allostatic load in children: Associations with family risk and internalizing disorders.
      ) and exaggerated (hypercortisolism) (
      • Lupien S.J.
      • King S.
      • Meaney M.J.
      • McEwen B.S.
      Can poverty get under your skin? Basal cortisol levels and cognitive function in children from low and high socioeconomic status.
      ) diurnal and acute HPA activity, which can incur myriad physical and mental health problems (
      • McEwen B.S.
      Stress, adaptation, and disease. Allostasis and allostatic load.
      ,
      • McEwen B.S.
      • Stellar E.
      Stress and the individual. Mechanisms leading to disease.
      ,
      • Guerry J.D.
      • Hastings P.D.
      In search of HPA axis dysregulation in child and adolescent depression.
      ). Diurnal hypercortisolism is more prevalent in infants and younger children living in poverty (
      • Perrone L.
      • Frost A.
      • Kuzava S.
      • Nissim G.
      • Vaccaro S.
      • Rodriguez M.
      • et al.
      Indicators of deprivation predict diurnal cortisol regulation during infancy.
      ), whereas hypocortisolism emerges after more time spent in poverty (
      • Blair C.
      • Raver C.C.
      • Granger D.
      • Mills-Koonce R.
      • Hibel L.
      Family Life Project Key Investigators
      Allostasis and allostatic load in the context of poverty in early childhood.
      ,
      • Ursache A.
      • Noble K.G.
      • Blair C.
      Socioeconomic status, subjective social status, and perceived stress: Associations with stress physiology and executive functioning.
      ), potentially reflecting the cumulative toll of AL. Exemplifying early emerging stress activation, Fernald and Gunnar (
      • Fernald L.C.H.
      • Gunnar M.R.
      Poverty-alleviation program participation and salivary cortisol in very low-income children.
      ) reported that hypercortisolism in preschool-aged children living in low-income families in rural Mexico was alleviated through a cash-transfer program, compared with children in families who were not enrolled in the program. Exemplifying the suppressive effect of more chronically endured poverty, U.S. Mexican–origin adolescents who lived in deep poverty from age 10 to 16 years evinced HPA hyporeactivity (decreasing cortisol) following a social exclusion task, whereas youths who had not experienced poverty evinced cortisol increases from before to after the social challenge (
      • Johnson L.E.
      • Parra L.A.
      • Ugarte E.
      • Weissman D.G.
      • Han S.G.
      • Robins R.W.
      • et al.
      Patterns of poverty across adolescence predict salivary cortisol stress responses in Mexican-origin youths.
      ).
      Childhood poverty predicts elevated tonic and reactive cardiovascular activity, especially blood pressure (
      • Ziol-Guest K.M.
      • Duncan G.J.
      • Kalil A.
      • Boyce W.T.
      Early childhood poverty, immune-mediated disease processes, and adult productivity.
      ,
      • Evans G.W.
      • Exner-Cortens D.
      • Kim P.
      • Bartholomew D.
      Childhood poverty and blood pressure reactivity to and recovery from an acute stressor in late adolescence: The mediating role of family conflict.
      ), in adolescence and adulthood. Effects are less consistent in preadolescent children (
      • Alkon A.
      • Boyce W.T.
      • Tran L.
      • Harley K.G.
      • Neuhaus J.
      • Eskenazi B.
      Prenatal adversities and Latino children’s autonomic nervous system reactivity trajectories from 6 months to 5 years of age.
      ,
      • Blair C.
      • Berry D.
      • Mills-Koonce R.
      • Granger D.
      FLP Investigators
      Cumulative effects of early poverty on cortisol in young children: Moderation by autonomic nervous system activity.
      ,
      • Stülb K.
      • Messerli-Bürgy N.
      • Kakebeeke T.H.
      • Arhab A.
      • Zysset A.E.
      • Leeger-Aschmann C.S.
      • et al.
      Age-adapted stress task in preschoolers does not lead to uniform stress responses.
      ), suggesting that ANS effects emerge over prolonged exposure to poverty or that adolescence may be a sensitive period for the effects of poverty on cardiovascular health (
      • Page M.E.
      • Conger K.
      • Guyer A.E.
      • Hastings P.D.
      • Thompson R.
      Children and the intergenerational transmission of poverty: Research frontiers and policy implications.
      ). Similarly, SES in childhood and adolescence is inversely associated with chronic inflammation, both concurrently and into adulthood (
      • Gimeno D.
      • Ferrie J.E.
      • Elovainio M.
      • Pulkki-Raback L.
      • Keltikangas-Jarvinen L.
      • Eklund C.
      • et al.
      When do social inequalities in C-reactive protein start? A life course perspective from conception to adulthood in the Cardiovascular Risk in Young Finns Study.
      ,
      • Surachman A.
      • Jenkins A.I.C.
      • Santos A.R.
      • Almeida D.M.
      Socioeconomic status trajectories across the life course, daily discrimination, and inflammation among Black and White adults.
      ,
      • Tabassum F.
      • Kumari M.
      • Rumley A.
      • Lowe G.
      • Power C.
      • Strachan D.P.
      Effects of socioeconomic position on inflammatory and hemostatic markers: A life-course analysis in the 1958 British birth cohort.
      ,
      • Chen E.
      • Hanson M.D.
      • Paterson L.Q.
      • Griffin M.J.
      • Walker H.A.
      • Miller G.E.
      Socioeconomic status and inflammatory processes in childhood asthma: The role of psychological stress.
      ). These associations hold after accounting for changes in occupation and education over time (
      • Loucks E.B.
      • Pilote L.
      • Lynch J.W.
      • Richard H.
      • Almeida N.D.
      • Benjamin E.J.
      • Murabito J.M.
      Life course socioeconomic position is associated with inflammatory markers: The Framingham Offspring Study.
      ) and appear to magnify with age (
      • Lam P.H.
      • Chiang J.J.
      • Chen E.
      • Miller G.E.
      Race, socioeconomic status, and low-grade inflammatory biomarkers across the lifecourse: A pooled analysis of seven studies.
      ). Studies of AL involving activity across multiple systems (i.e., HPA, ANS, immune) are consistent; children raised in poverty have increased AL in late adolescence (
      • Brody G.H.
      • Yu T.
      • Chen E.
      • Miller G.E.
      • Kogan S.M.
      • Beach S.R.H.
      Is resilience only skin deep?: Rural African Americans’ socioeconomic status-related risk and competence in preadolescence and psychological adjustment and allostatic load at age 19.
      ,
      • Evans G.W.
      • Kim P.
      Childhood poverty and young adults’ allostatic load: The mediating role of childhood cumulative risk exposure.
      ) and adulthood (
      • Gruenewald T.L.
      • Karlamangla A.S.
      • Hu P.
      • Stein-Merkin S.
      • Crandall C.
      • Koretz B.
      • Seeman T.E.
      History of socioeconomic disadvantage and allostatic load in later life.
      ).
      Similarly to poverty, experiences of discrimination that target persons based on their nonmajority social status constitute severe and pervasive sources of social stress that affect numerous biological systems (
      • Berger M.
      • Sarnyai Z.
      “More than skin deep”: Stress neurobiology and mental-health consequences of racial discrimination.
      ). Interpreting acute negative treatment as racial/ethnic discrimination evokes elevated anterior cingulate cortex (ACC) activity associated with emotion regulation in both Black adults in the United States (
      • Masten C.L.
      • Telzer E.H.
      • Eisenberger N.I.
      An fMRI Investigation of attributing negative social treatment to racial discrimination.
      ) and Turkish adults in Germany (
      • Akdeniz C.
      • Tost H.
      • Streit F.
      • Haddad L.
      • Wüst S.
      • Schäfer A.
      • et al.
      Neuroimaging evidence for a role of neural social stress processing in ethnic minority-associated environmental risk [published correction appears in JAMA Psychiatry 2014;71:888].
      ), potentially reflective of stress and coping efforts. Experiencing more chronic racial discrimination predicts reduced total brain volume in Black youths with depressive symptoms (
      • Meyer C.S.
      • Schreiner P.J.
      • Lim K.
      • Battapady H.
      • Launer L.J.
      Depressive symptomatology, racial discrimination experience, and brain tissue volumes observed on magnetic resonance imaging.
      ), disrupted white matter microstructure in Black women with trauma histories (
      • Fani N.
      • Harnett N.
      • Carter S.
      • Bradley B.
      • Ressler K.
      Effects of racial discrimination on white matter microarchitecture in trauma-exposed Black American women.
      ), and increased activation and connectivity of multiple regions involved in vigilance, arousal, and emotion regulation in Black adults with trauma histories (
      • Fani N.
      • Carter S.E.
      • Harnett N.G.
      • Ressler K.J.
      • Bradley B.
      Association of racial discrimination with neural response to threat in Black women in the US exposed to trauma.
      ,
      • Webb E.K.
      • Bird C.M.
      • deRoon-Cassini T.A.
      • Weis C.N.
      • Huggins A.A.
      • Fitzgerald J.M.
      • et al.
      Racial discrimination and resting-state functional connectivity of salience network nodes in trauma-exposed Black adults in the United States.
      ). Such findings reveal the cumulative toll of racial discrimination on brain health.
      Numerous studies indicate that marginalized individuals evince flatter diurnal cortisol slopes, especially for those who have experienced more discrimination (
      • Parra L.A.
      • Hastings P.D.
      Integrating the neurobiology of minority stress with an intersectionality framework for LGBTQ-Latinx populations.
      ,
      • Busse D.
      • Yim I.S.
      • Campos B.
      • Marshburn C.K.
      Discrimination and the HPA axis: Current evidence and future directions.
      ), manifested as both hypocortisolism (
      • Huynh V.W.
      • Guan S.-S.A.
      • Almeida D.M.
      • McCreath H.
      • Fuligni A.J.
      Everyday discrimination and diurnal cortisol during adolescence.
      ,
      • Kaholokula J.K.
      • Grandinetti A.
      • Keller S.
      • Nacapoy A.H.
      • Kingi T.K.
      • Mau M.K.
      Association between perceived racism and physiological stress indices in Native Hawaiians.
      ) and hypercortisolism (
      • Zeiders K.H.
      • Doane L.D.
      • Roosa M.W.
      Perceived discrimination and diurnal cortisol: Examining relations among Mexican American adolescents.
      ,
      • Zeiders K.H.
      • Hoyt L.T.
      • Adam E.K.
      Associations between self-reported discrimination and diurnal cortisol rhythms among young adults: The moderating role of racial-ethnic minority status.
      ). Hypercortisolism also is evidenced by increased hair cortisol concentrations in adults who experienced more discrimination (
      • Lehrer H.M.
      • Goosby B.J.
      • Dubois S.K.
      • Laudenslager M.L.
      • Steinhardt M.A.
      Race moderates the association of perceived everyday discrimination and hair cortisol concentration.
      ). Racial discrimination experiences in early adolescence, but not early adulthood, predicted diurnal hypocortisolism in Black adults 20 years later (
      • Adam E.K.
      • Heissel J.A.
      • Zeiders K.H.
      • Richeson J.A.
      • Ross E.C.
      • Ehrlich K.B.
      • et al.
      Developmental histories of perceived racial discrimination and diurnal cortisol profiles in adulthood: A 20-year prospective study.
      ); pubertal maturation and identity formation processes may make early adolescence a particularly sensitive period for the neurotoxic effects of discrimination. Yet, Black mothers’ experiences of discrimination predicted their infants’ elevated acute cortisol reactivity at 12 months (
      • Dismukes A.
      • Shirtcliff E.
      • Jones C.W.
      • Zeanah C.
      • Theall K.
      • Drury S.
      The development of the cortisol response to dyadic stressors in Black and White infants.
      ), indicating that discrimination has effects across the lifespan, and again suggesting that stressful life contexts may initially increase HPA activity, before tonically suppressing it after chronic exposure.
      Sexual and gender identity discrimination is associated with disrupted adrenocortical functioning in lesbian, gay, bisexual, transgender, and queer (LGBTQ+) youths and adults. Sexual or gender minority status disclosure may increase discrimination exposure (
      • Pachankis J.E.
      The psychological implications of concealing a stigma: A cognitive-affective-behavioral model.
      ), and being “out” has been associated with elevated cortisol and distress (
      • DuBois L.Z.
      • Powers S.
      • Everett B.G.
      • Juster R.P.
      Stigma and diurnal cortisol among transitioning transgender men.
      ,
      • Huebner D.M.
      • Davis M.C.
      Gay and bisexual men who disclose their sexual orientations in the workplace have higher workday levels of salivary cortisol and negative affect.
      ). Conversely, those who are not “out” may perceive greater risk with disclosing (
      • Juster R.P.
      • Smith N.G.
      • Ouellet É.
      • Sindi S.
      • Lupien S.J.
      Sexual orientation and disclosure in relation to psychiatric symptoms, diurnal cortisol, and allostatic load.
      ). Unlike other marginalized identity characteristics, family members typically do not share the sexual or gender identity of LGBTQ+ individuals. Lack of family support predicted stronger HPA reactivity in LGB young adults (
      • Burton C.L.
      • Bonanno G.A.
      • Hatzenbuehler M.L.
      Familial social support predicts a reduced cortisol response to stress in sexual minority young adults.
      ). Identifying with multiple minoritized characteristics can carry biological burdens (
      • Parra L.A.
      • Hastings P.D.
      Integrating the neurobiology of minority stress with an intersectionality framework for LGBTQ-Latinx populations.
      ,
      • Cook S.H.
      • Juster R.P.
      • Calebs B.J.
      • Heinze J.
      • Miller A.L.
      Cortisol profiles differ by race/ethnicity among young sexual minority men.
      ). LGBTQ+ Latinx young adults who experienced both heterosexist and racist discrimination were challenged in forming an integrated intersectional identity, which in turn predicted hypocortisolism (
      • Parra L.A.
      • Hastings P.D.
      Challenges to identity integration indirectly link experiences of heterosexist and racist discrimination to lower waking salivary cortisol in sexually diverse Latinx emerging adults.
      ).
      Across adolescence and adulthood, discrimination is associated with activity of the cardiovascular and immune systems (
      • Surachman A.
      • Jenkins A.I.C.
      • Santos A.R.
      • Almeida D.M.
      Socioeconomic status trajectories across the life course, daily discrimination, and inflammation among Black and White adults.
      ,
      • Berger M.
      • Sarnyai Z.
      “More than skin deep”: Stress neurobiology and mental-health consequences of racial discrimination.
      ,
      • Lockwood K.G.
      • Marsland A.L.
      • Matthews K.A.
      • Gianaros P.J.
      Perceived discrimination and cardiovascular health disparities: A multisystem review and health neuroscience perspective.
      ). As evidence of discrimination’s cumulative effect, African American adults’ experiences of discrimination predicted greater chronic inflammation only for those who also had experienced higher levels of discrimination 18 years earlier, in preadolescence (
      • Simons R.L.
      • Woodring D.
      • Simons L.G.
      • Sutton T.E.
      • Lei M.K.
      • Beach S.R.H.
      • et al.
      Youth adversities amplify the association between adult stressors and chronic inflammation in a domain specific manner: Nuancing the early life sensitivity model.
      ). This “double-hit model” again indicates that early adolescence may be a susceptible period for the pernicious neurobiological effects of discrimination against core identity characteristics. Indeed, meta-analyses have shown that from adolescence through late adulthood, chronic inflammation increased more in racially minoritized and impoverished than in majority and economically secure groups (
      • Lam P.H.
      • Chiang J.J.
      • Chen E.
      • Miller G.E.
      Race, socioeconomic status, and low-grade inflammatory biomarkers across the lifecourse: A pooled analysis of seven studies.
      ). Inflammatory markers also were elevated in LGBTQ+ individuals versus heterosexual and cisgender individuals (
      • Diamond L.M.
      • Dehlin A.J.
      • Alley J.
      Systemic inflammation as a driver of health disparities among sexually diverse and gender-diverse individuals.
      ), possibly exacerbated by lack of family support (
      • Wood E.P.
      • Cook S.H.
      Father support is protective against the negative effects of perceived discrimination on CRP among sexual minorities but not heterosexuals.
      ) and discrimination experiences for those who are “out” (
      • Doyle D.M.
      • Molix L.
      Disparities in social health by sexual orientation and the etiologic role of self-reported discrimination.
      ).
      Fewer studies have directly addressed links between structural determinants and neurobiology. Unequal prevalence of ethnic and racial minority groups across neighborhoods, often the intentional result of policy decisions pertaining to zoning, mortgages, and highway construction (

      National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on Community-Based Solutions to Promote Health Equity in the United States. (2017): Communities in Action: Pathways to Health Equity. Weinstein NJ, Geller A, Negussie Y, Baciu A, editors. Washington, DC: National Academies Press.

      ), during early adulthood predicted Black participants’ reduced brain volume in middle adulthood (
      • Zeki Al Hazzouri A.
      • Jawadekar N.
      • Kezios K.
      • Caunca M.R.
      • Elfassy T.
      • Calonico S.
      • et al.
      Racial residential segregation in young adulthood and brain integrity in middle age: Can we learn from small samples?.
      ) and was concurrently linked to increased inflammation and AL in adults (
      • Bellatorre A.
      • Finch B.K.
      • Phuong Do D.
      • Bird C.E.
      • Beck A.N.
      Contextual predictors of cumulative biological risk: Segregation and allostatic load.
      ). This latter finding was true for all racial/ethnic groups, over and above SES; hence, neighborhood segregation takes a biological toll on both advantaged majority group members and less advantaged and marginalized peoples. Structural racism quantified at the state level (e.g., racial differences in incarceration rates) predicted reduced hippocampal volume for Black and Latinx, but not White, preadolescents living in states with greater structural racial/ethnic stigma, independent of personal experiences of discrimination (
      • Hatzenbuehler M.L.
      • Weissman D.G.
      • McKetta S.
      • Lattanner M.R.
      • Ford J.V.
      • Barch D.M.
      • McLaughlin K.A.
      Smaller hippocampal volume among Black and Latinx youth living in high-stigma contexts.
      ); a similar effect was noted for girls, but not boys, living in states with more structural gender stigma. Analogously, LGB young adults who had spent their adolescence living in counties and states that were more stigmatizing of LGBTQ+ people had hyporeactive cortisol responses to an acute stressor, relative to LGB individuals who had been raised in less stigmatizing environments (
      • Hatzenbuehler M.L.
      • McLaughlin K.A.
      Structural stigma and hypothalamic–pituitary–adrenocortical axis reactivity in lesbian, gay, and bisexual young adults.
      ). Similarly, beyond individual characteristics and state-level poverty, state-level structural racism predicted elevated prevalence of myocardial infarction for Black adults living in more versus less racist states; a weaker opposite tendency was noted for White adults (
      • Lukachko A.
      • Hatzenbuehler M.L.
      • Keyes K.M.
      Structural racism and myocardial infarction in the United States.
      ).
      As noted previously, chronic structural stressors may suppress HPA axis activity, whereas acute structural stressors may have the opposite effect. We found that young adults in California evinced diurnal hypercortisolism immediately following the 2016 Pulse Nightclub Massacre in Florida, which gradually declined over the subsequent 2 months (
      • Parra L.A.
      • Helm J.L.
      • Hastings P.D.
      Adrenocortical responses of emerging adults in California in the two months following the Pulse Night Club massacre: Evidence for distal stress responses.
      ). This could be seen as indicative of peripheral biological impacts from structural determinants related to lax gun control laws and strong beliefs in gun ownership rights that contribute to the U.S. public health crisis of mass gun violence (
      • DeFoster R.
      • Swalve N.
      Guns, culture or mental health? Framing mass shootings as a public health crisis.
      ,
      • Gelzhiser J.A.
      International student perceptions of American gun culture and school shootings: A public health examination.
      ,
      • Malina D.
      • Morrissey S.
      • Campion E.W.
      • Hamel M.B.
      • Drazen J.M.
      Rooting out gun violence.
      ). This stress activation response was equally evident in those who shared or did not share identity characteristics with the majority of the 49 victims of the massacre (LGBTQ+, Latinx, male), paralleling evidence of elevated distress symptoms in the general Florida population following the massacre (
      • Ben-Ezra M.
      • Hamama-Raz Y.
      • Mahat-Shamir M.
      • Pitcho-Prelorentzos S.
      • Kaniasty K.
      Shattering core beliefs: Psychological reactions to mass shooting in Orlando.
      ). Again, such findings suggest that structural inequities may undermine the well-being of all people, not only the marginalized people who are most directly disadvantaged by those inequities.
      SES is a multifaceted construct that can demarcate exposure to various determinants (
      • Conger R.D.
      • Conger K.J.
      Understanding the processes through which economic hardship influences families and children.
      ), including where families live. Disparities between neighborhoods prospectively predict the prevalence of psychiatric disorders (
      • O’Donoghue B.
      • Roche E.
      • Lane A.
      Neighbourhood level social deprivation and the risk of psychotic disorders: A systematic review.
      ,
      • Hastings P.D.
      • Serbin L.A.
      • Bukowski W.
      • Helm J.L.
      • Stack D.M.
      • Dickson D.J.
      • et al.
      Predicting psychosis-spectrum diagnoses in adulthood from social behaviors and neighborhood contexts in childhood.
      ,
      • Cohen-Cline H.
      • Beresford S.A.A.
      • Barrington W.E.
      • Matsueda R.L.
      • Wakefield J.
      • Duncan G.E.
      Associations between neighbourhood characteristics and depression: A twin study.
      ,
      • Dowdall N.
      • Ward C.L.
      • Lund C.
      The association between neighbourhood-level deprivation and depression: Evidence from the South African National Income Dynamics Study.
      ). Whether neighborhood-level measures should be considered structural or social determinants is debatable. Local crime rates, median household value, and unemployment affect individuals’ daily experiences (social) and are the products of municipal, state, and national laws, policies, and practices (structural) (

      National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on Community-Based Solutions to Promote Health Equity in the United States. (2017): Communities in Action: Pathways to Health Equity. Weinstein NJ, Geller A, Negussie Y, Baciu A, editors. Washington, DC: National Academies Press.

      ). Neighborhood characteristics have been associated with the neurobiology underlying mental health. Independent of family economic resources, living in neighborhoods with greater poverty, deterioration, and crime during childhood (
      • Gard A.M.
      • Maxwell A.M.
      • Shaw D.S.
      • Mitchell C.
      • Brooks-Gunn J.
      • McLanahan S.S.
      • et al.
      Beyond family-level adversities: Exploring the developmental timing of neighborhood disadvantage effects on the brain.
      ,
      • Rakesh D.
      • Seguin C.
      • Zalesky A.
      • Cropley V.
      • Whittle S.
      Associations between neighborhood disadvantage, resting-state functional connectivity, and behavior in the adolescent brain cognitive development study: The moderating role of positive family and school environments.
      ) or adolescence (
      • Cará V.M.
      • Esper N.B.
      • de Azeredo L.A.
      • Iochpe V.
      • Dalfovo N.P.
      • Santos R.C.
      • et al.
      An fMRI study of inhibitory control and the effects of exposure to violence in Latin-American early adolescents: Alterations in frontoparietal activation and performance.
      ,
      • Gonzalez M.Z.
      • Allen J.P.
      • Coan J.A.
      Lower neighborhood quality in adolescence predicts higher mesolimbic sensitivity to reward anticipation in adulthood.
      ,
      • Tomlinson R.C.
      • Burt S.A.
      • Waller R.
      • Jonides J.
      • Miller A.L.
      • Gearhardt A.N.
      • et al.
      Neighborhood poverty predicts altered neural and behavioral response inhibition.
      ) was associated with patterns of neural reactivity indicative of accelerated brain maturation and either dampened or sensitized neural reactivity in multiple brain regions that control behavior and emotion. For example, reduced inferior frontal gyrus activation during a Go/No-Go task accounted for the association of greater neighborhood poverty and poorer response inhibition in children and adolescents (
      • Tomlinson R.C.
      • Burt S.A.
      • Waller R.
      • Jonides J.
      • Miller A.L.
      • Gearhardt A.N.
      • et al.
      Neighborhood poverty predicts altered neural and behavioral response inhibition.
      ). Considering peripheral effects, as with lower family SES, lower neighborhood SES was associated with diurnal hypocortisolism in adolescents (
      • Chen E.
      • Paterson L.Q.
      Neighborhood, family, and subjective socioeconomic status: How do they relate to adolescent health?.
      ). Neighborhood SES also is conflated with variation in exposure to pollutants that can have neurotoxic effects (
      • Morello-Frosch R.
      • Zuk M.
      • Jerrett M.
      • Shamasunder B.
      • Kyle A.D.
      Understanding the cumulative impacts of inequalities in environmental health: Implications for policy.
      ). Independent of family and neighborhood SES, greater neighborhood-level exposure to air (e.g., particulate matter 2.5) and water (e.g., lead, arsenic) pollutants from age 10 to 16 years predicted stronger sympathetic and weaker parasympathetic influence over ANS activity at age 17 years in U.S. Mexican–origin adolescents, which could increase risk for myriad illnesses in adulthood (
      • Ugarte E.
      • Johnson L.E.
      • Robins R.W.
      • Guyer A.E.
      • Hastings P.D.
      The impact of social disadvantage on autonomic physiology of Latinx adolescents: The role of environmental risks [published online ahead of print May 30].
      ). Hence, neighborhood economic disadvantage exposes developing neurobiological systems to multiple kinds of threats.

      Social and Structural Determinants, Neurobiology, and Mental Health

      Decades of research have shown that the central and peripheral systems affected by structural and social determinants are intricately linked to mental health (
      • Shim R.
      • Koplan C.
      • Langheim F.J.P.
      • Manseau M.W.
      • Powers R.A.
      • Compton M.T.
      The social determinants of mental health: An overview and call to action.
      ,
      • Harnett N.G.
      Neurobiological consequences of racial disparities and environmental risks: A critical gap in understanding psychiatric disorders.
      ,
      • Parra L.A.
      • Hastings P.D.
      Integrating the neurobiology of minority stress with an intersectionality framework for LGBTQ-Latinx populations.
      ,
      • Paradies Y.
      • Ben J.
      • Denson N.
      • Elias A.
      • Priest N.
      • Pieterse A.
      • et al.
      Racism as a determinant of health: A systematic review and meta-analysis.
      ). Multiple neurobiological processes are theorized to function as mechanistic biomarkers, conveying structural and social determinants’ effects on mental health (
      • McEwen B.S.
      Stress, adaptation, and disease. Allostasis and allostatic load.
      ,
      • Levine S.
      Developmental determinants of sensitivity and resistance to stress.
      ,
      • Hostinar C.E.
      • Swartz J.R.
      • Alen N.V.
      • Guyer A.E.
      • Hastings P.D.
      The role of stress phenotypes in understanding childhood adversity as a transdiagnostic risk factor for psychopathology. J Psychopathology and Clinical Science.
      ,
      • Myers H.F.
      Ethnicity- and socio-economic status-related stresses in context: An integrative review and conceptual model.
      ,
      • Hatzenbuehler M.L.
      How does sexual minority stigma “get under the skin”? A psychological mediation framework.
      ). Evidence indicates that links between childhood adversities (e.g., family poverty) and later psychopathology are mediated through accelerated maturation of emotion processing via frontolimbic functional connectivity, and deficits in reward processing via functional connectivity of the salience network and the amygdala (
      • Herzberg M.P.
      • Gunnar M.R.
      Early life stress and brain function: Activity and connectivity associated with processing emotion and reward.
      ). SES has consequences for family processes (
      • Conger R.D.
      • Conger K.J.
      Understanding the processes through which economic hardship influences families and children.
      ), and links between family SES and brain functioning and development are themselves mediated by effects of economic adversity on family functioning (
      • Brieant A.
      • Herd T.
      • Deater-Deckard K.
      • Lee J.
      • King-Casas B.
      • Kim-Spoon J.
      Processes linking socioeconomic disadvantage and neural correlates of cognitive control in adolescence.
      ). The clinical implications of these effects on connectivity may be realized in transdiagnostic, symptom-relevant manifestations such as emotion dysregulation, attention inflexibility, and inefficiencies and biases in processing information. Considering other neurobiological mechanisms, diurnal hypercortisolism accounted for the association between heterosexist discrimination and elevated depressive symptoms in LGB young adults (
      • Parra L.A.
      • Benibgui M.
      • Helm J.L.
      • Hastings P.D.
      Minority stress predicts depression in lesbian, gay, and bisexual emerging adults via elevated diurnal cortisol.
      ). Neurobiological mediation is not always evident, however. In U.S. Mexican–origin adolescents, greater exposure to social threats including discrimination and crime predicted both internalizing problems and multisystem coupling of the PFC and ANS reactivity to emotional faces, but multisystem coupling did not mediate links between these social determinants and mental health (
      • Weissman D.G.
      • Guyer A.E.
      • Ferrer E.
      • Robins R.W.
      • Hastings P.D.
      Tuning of brain-autonomic coupling by prior threat exposure: Implications for internalizing problems in Mexican-origin adolescents.
      ). Stronger downregulatory coupling of increased PFC activity with less ANS reactivity may have been an adaptation to chronically threatening contexts that could carry longer-term risks to mental health in the future (
      • Ellis B.J.
      • Del Giudice M.
      Developmental adaptation to stress: An evolutionary perspective.
      ).
      Building on biopsychosocial models of mental health (
      • Cicchetti D.
      A multiple-levels-of-analysis perspective on research in development and psychopathology.
      ,
      • Ellis B.J.
      • Boyce W.T.
      • Belsky J.
      • Bakermans-Kranenburg M.J.
      • van Ijzendoorn M.H.
      Differential susceptibility to the environment: An evolutionary–neurodevelopmental theory.
      ), researchers have begun to examine the combined or moderating roles of social and structural determinants and brain structure and function in adolescent mental health (
      • Guyer A.E.
      Adolescent psychopathology: The role of brain-based diatheses, sensitivities, and susceptibilities.
      ). U.S. Mexican–origin adolescents with larger hippocampal volumes showed more depressive symptoms when they experienced more neighborhood crime, but fewer symptoms when less exposed to crime (
      • Schriber R.A.
      • Anbari Z.
      • Robins R.W.
      • Conger R.D.
      • Hastings P.D.
      • Guyer A.E.
      Hippocampal volume as an amplifier of the effect of social context on adolescent depression.
      ). Neighborhood crime was unrelated to symptoms in adolescents with smaller hippocampal volumes, suggesting that larger hippocampi may potentiate the effects of these social determinants. In this same sample, greater neighborhood and school crime exposure also predicted elevated externalizing problems, but only for adolescents with reduced activity in the posterior cingulate cortex, temporoparietal junction, and amygdala when thinking about how another person’s emotional cues made them feel, referred to as emotion introspection (
      • Weissman D.G.
      • Gelardi K.L.
      • Conger R.D.
      • Robins R.W.
      • Hastings P.D.
      • Guyer A.E.
      Adolescent externalizing problems: Contributions of community crime exposure and neural function during emotion introspection in Mexican-origin youth.
      ). Adolescents with weaker neural evidence of emotional awareness, potentially indicative of dampened engagement with others’ emotional needs, appeared to be more affected by crime exposure.
      A moderated-mediation pattern involving the subgenual ACC, hostile environments, deviant behavior, and family connection also has been found with these Mexican-origin youths (
      • Schriber R.A.
      • Rogers C.R.
      • Ferrer E.
      • Conger R.D.
      • Robins R.W.
      • Hastings P.D.
      • Guyer A.E.
      Do hostile school environments promote social deviance by shaping neural responses to social exclusion?.
      ). Experiencing high levels of hostility at school predicted stronger subgenual ACC activation to social exclusion, which in turn predicted more deviant behavior. As found for attribution of racial discrimination (
      • Masten C.L.
      • Telzer E.H.
      • Eisenberger N.I.
      An fMRI Investigation of attributing negative social treatment to racial discrimination.
      ,
      • Akdeniz C.
      • Tost H.
      • Streit F.
      • Haddad L.
      • Wüst S.
      • Schäfer A.
      • et al.
      Neuroimaging evidence for a role of neural social stress processing in ethnic minority-associated environmental risk [published correction appears in JAMA Psychiatry 2014;71:888].
      ), the brain’s processing of social exclusion may be a mechanism linking hostile experiences with deviant behavior, perhaps as the subgenual ACC becomes sensitized to social threat. This mediation effect was moderated, though. Adolescents who felt less family connection showed the most deviant behavior if they had high subgenual ACC reactivity to social exclusion, yet the least deviant behavior if subgenual ACC reactivity was low. Adolescents who felt more family connection were buffered from deviant behavior, regardless of their neural response to exclusion. Family connection functioned as a protective contextual factor and could be a potential target for biologically informed interventions.

      Advancing the Work on Structural and Social Determinants: Challenges in the Field

      Given the accumulating evidence for the pervasive and enduring effects of structural and social determinants on neurobiology and mental health, an immediate reaction could be to do more, do better. Certainly more research is needed, and, we would argue, particularly more research on 1) how the effects of structural and social inequities on multiple neurobiological systems shape the course of mental health disparities across development, 2) what can be done to mitigate said effects of these inequities, and 3) how to reduce or remove the inequities themselves. Yet, this reaction may be too superficial, because there are challenges to reaching an effective understanding of social and structural determinants within biological psychiatry. These include representation of diversity within researchers and the populations they study, biological reductionism, and access to care and training.
      There is a woeful lack of representation of diverse communities, and particularly of racially and ethnically minoritized and economically marginalized peoples, within biological psychiatry (
      • George S.
      • Duran N.
      • Norris K.
      A systematic review of barriers and facilitators to minority research participation among African Americans, Latinos, Asian Americans, and Pacific Islanders.
      ,
      • Oh S.S.
      • Galanter J.
      • Thakur N.
      • Pino-Yanes M.
      • Barcelo N.E.
      • White M.J.
      • et al.
      Diversity in clinical and biomedical research: A promise yet to be fulfilled.
      ), owing at least in part to histories of structural oppression and exclusion (
      • Bassett M.T.
      • Graves J.D.
      Uprooting institutionalized racism as public health practice.
      ,
      • Kline W.
      Building a Better Race: Gender, Sexuality, and Eugenics From the Turn of the Century to the Baby Boom.
      ). Yet, there is a corollary of working in a homogeneous profession: most who have been privileged enough to do this work are, themselves, the products of the same systemic, structural, and social determinants that have excluded and harmed those who are underrepresented (

      Ledgerwood A, da Silva Frost A, Kadirvel S, Maitner A, Wang YA, Maddox KB (in press): Methods for advancing an open, replicable, and inclusive science of Social cognition. In: Hugenberg K, Johnson K, Carlston DE, editors. Oxford Handbook of Social Cognition. Oxford, UK: Oxford University Press.

      ,
      • Remedios J.D.
      Psychology must grapple with Whiteness.
      ). The effects of being the beneficiaries of these determinants are, to be sure, quite different than the effects discussed previously, but they are likely to include unrecognized biases in the questions we ask, the approaches used to address those questions, the populations studied, what is prioritized in the data generated, the interpretations of those data, and the evaluation of others’ research (
      • Campbell L.G.
      • Mehtani S.
      • Dozier M.E.
      • Rinehart J.
      Gender-heterogeneous working groups produce higher quality science.
      ,
      • Coiro P.
      • Pollak D.D.
      Sex and gender bias in the experimental neurosciences: The case of the maternal immune activation model.
      ,
      • Hofstra B.
      • Kulkarni V.V.
      • Munoz-Najar Galvez S.
      • He B.
      • Jurafsky D.
      • McFarland D.A.
      The diversity–innovation paradox in science.
      ).
      One such bias is that, in studying neurobiology, many assume they are studying things that are objective, measurable, and interpretable as having consistent and specific meaning. We must escape assumptions of universality and biological reductionism. The same size of a brain region, the same magnitude of an event-related potential component, the same level of a circulating hormone will not necessarily have the same implication for mental health when observed between individuals with very distinct life histories. While plausible that some neurobiological processes may be expected to unfold in a similar manner regardless of life history, it requires additional research with diverse populations to ascertain where such commonalities exist.
      Access to psychiatric providers and services is affected by limited regional access and insurance constraints, particularly in communities ridden with structural and social challenges. Marginalized communities have learned to mistrust researchers because of an extensive history of scientific abuses (
      • George S.
      • Duran N.
      • Norris K.
      A systematic review of barriers and facilitators to minority research participation among African Americans, Latinos, Asian Americans, and Pacific Islanders.
      ,
      • Hussain-Gambles M.
      • Atkin K.
      • Leese B.
      Why ethnic minority groups are under-represented in clinical trials: A review of the literature.
      ) and failures to keep personally identifiable biological data protected (
      • Rothstein M.A.
      Is deidentification sufficient to protect health privacy in research?.
      ). This limits the pool from which to recruit research participants in clinical settings. Both psychiatric clinicians and researchers need training in understanding issues pertaining to cultural and diversity competency.

      Actionable Steps

      Diversify Biological Psychiatry

      The relatively scant empirical attention to structural and social determinants of neurobiology and mental health likely stems from limited diversity within the field of biological psychiatry (
      • Jones-London M.
      NINDS strategies for enhancing the diversity of neuroscience researchers.
      ). Most scientists have not come from marginalized, minoritized, or disadvantaged communities; consequently, they have not attended to the forces affecting those communities. Acknowledging that fact behooves the field to recruit, mentor, retain, and scaffold the success of researchers and scientist-practitioners who reflect the diverse populations with which the field should be engaging. This will require financial investments of fellowships and stipends to defray the high costs of education that individuals from economically marginalized backgrounds cannot be expected to shoulder, and also investments of time and effort for scientists from advantaged and majority positions to learn how to effectively mentor and scaffold people with different life experiences. Given their life experiences, this next generation of scientists may apply alternative theoretical frameworks, pose unasked questions, implement innovative approaches, achieve novel insights, and train future scientists differently. Compared with past and current scientific norms, such changes should be recognized as (at least) equally likely to be valid models of practicing biological psychiatry.
      A more diverse biological psychiatry would more effectively engage and work with diverse communities. Engaging in community partnerships through participatory action research and citizen science approaches could help biological psychiatry better identify the mental health issues of greatest relevance to a given community, and the research procedures that community is more likely to accept and support (
      • Ballonoff Suleiman A.
      • Ballard P.J.
      • Hoyt L.T.
      • Ozer E.J.
      Applying a developmental lens to youth-led participatory action research: A critical examination and integration of existing evidence.
      ,
      • Roskams J.
      • Popović Z.
      Power to the people: Addressing big data challenges in neuroscience by creating a new cadre of citizen neuroscientists.
      ,
      • Friesen P.
      Participatory neuroscience: Something to strive for?.
      ). Community partnerships could shift the field from deficits-based to strengths-based models of adaptation and resilience by recognizing and incorporating community-specific assets into our understanding of the multiple paths toward mental health and well-being across diverse populations. This also could help to strengthen the pipeline for engaging the interests of young people from diverse communities in the pursuit of biological psychiatry as a profession.

      Integrate Structural and Social Determinants Into the Biologically Informed Practice of Psychiatry

      Psychiatrists could be better supported to consider the roles of structural and social determinants of mental health when working with those living in disadvantaged contexts. The DSM-5 (
      American Psychiatric Association
      Diagnostic and Statistical Manual of Mental Disorders.
      ), used to define, classify, and diagnose mental disorders in the United States, has pending the DSM-5-Text Revision [DSM-5-TR (
      American Psychiatric Association
      Diagnostic and Statistical Manual of Mental Disorders.
      )] that will incorporate the impacts of racism and discrimination into the diagnosis and manifestations of mental disorders. This is a step in the right direction given the evidence reviewed above. Diagnostic tools could incorporate the impacts of structural and social determinants on mental health, for example, by including a life stress interview approach in assessments. Psychiatric service providers’ ability to better account for the life experiences of diverse clients, and what these may mean for their neurobiological adaptations to context, should contribute to more effectively person-centered care. For example, psychotherapy is less effective for Black youth living in more racist communities (
      • Price M.A.
      • Weisz J.R.
      • McKetta S.
      • Hollinsaid N.L.
      • Lattanner M.R.
      • Reid A.E.
      • Hatzenbuehler M.L.
      Meta-analysis: Are psychotherapies less effective for Black youth in communities with higher levels of anti-Black racism?.
      ); more research, informed by models of structural and social determinants of mental health, is needed to develop adequate health practices for this underserved population.
      Psychiatric assessment and diagnosis may be further aided by including biological assays of peripheral markers indicative of exposures to structural and social determinants of mental health. For example, testing blood for exposure to toxins such as lead or mercury that can result in psychiatric symptom–like behaviors (
      • Brown Jr., J.S.
      Environmental and Chemical Toxins and Psychiatric Illness.
      ) would be straightforward. More big data research with large samples of participants from diverse communities will be needed to confirm those for whom specific neural and peripheral biomarkers of exposures to adversity actually do confer susceptibility to mental health problems. From such efforts, physiological tests of hormones, cytokines, and other biomarkers that can be assessed from minimally invasive biospecimens may also become informative components of community-appropriate assessments.
      Preventive approaches to reduce suffering from mental disorders and promote good mental health must acknowledge that early-life periods constitute particularly key windows in which to apply prevention strategies (
      • Fusar-Poli P.
      • Correll C.U.
      • Arango C.
      • Berk M.
      • Patel V.
      • Ioannidis J.P.A.
      Preventive psychiatry: A blueprint for improving the mental health of young people.
      ). Implementing appropriate and valid screening measures, including assessments of contextual influences, in community settings frequented by all youth, such as schools, would reach those constituencies with less access to primary care. Prevention and intervention strategies must be designed with structural and social determinants in mind and then evaluated for evidence of efficacy and effectiveness.

      Translate Research Into Structural and Social Action

      Standard interventions for individuals’ mental health problems typically treat the symptoms rather than the root causes of problems. Identifying and understanding neurobiological mechanisms by which adversity, classism, sexism, heterosexism, transphobia, and racism contribute to mental health disparities (
      • Parra L.A.
      • Hastings P.D.
      Integrating the neurobiology of minority stress with an intersectionality framework for LGBTQ-Latinx populations.
      ) is necessary for developing systems-level interventions to disrupt these fundamental structural and social causes of disease at both individual and community levels (
      • Hatzenbuehler M.L.
      • Phelan J.C.
      • Link B.G.
      Stigma as a fundamental cause of population health inequalities.
      ,
      • Link B.G.
      • Phelan J.
      Social conditions as fundamental causes of disease.
      ). Bolstering antidiscrimination policies may help dismantle barriers to access to housing, employment, education, and fair treatment among economic, ethnic, racial, sexual, and gender minorities. More inclusive laws, policies, and practices support healthier brain and peripheral physiological development (
      • Hatzenbuehler M.L.
      • Weissman D.G.
      • McKetta S.
      • Lattanner M.R.
      • Ford J.V.
      • Barch D.M.
      • McLaughlin K.A.
      Smaller hippocampal volume among Black and Latinx youth living in high-stigma contexts.
      ,
      • Hatzenbuehler M.L.
      • McLaughlin K.A.
      Structural stigma and hypothalamic–pituitary–adrenocortical axis reactivity in lesbian, gay, and bisexual young adults.
      ), which in turn promote better mental and physical health.
      Some such laws and policies exist but often are not upheld, and governments need to be held accountable in exercising these protective measures (
      • Sauer A.T.
      • Podhora A.
      Sexual orientation and gender identity in human rights impact assessment.
      ). This extends to violence prevention and gun control legislation, social safety net programs, natural disaster emergency response programs, and pollution control efforts, all of which disproportionately adversely affect marginalized and minoritized communities (
      • Parra L.A.
      • Helm J.L.
      • Hastings P.D.
      Adrenocortical responses of emerging adults in California in the two months following the Pulse Night Club massacre: Evidence for distal stress responses.
      ,
      • Brandt E.B.
      • Beck A.F.
      • Mersha T.B.
      Air pollution, racial disparities, and COVID-19 mortality.
      ,
      • Bui C.N.
      • Peng C.
      • Mutchler J.E.
      • Burr J.A.
      Race and ethnic group disparities in emotional distress among older adults during the COVID-19 pandemic.
      ,
      • Casselman B.
      • Conlen M.
      • Fischer-Baum R.
      Gun deaths in America.
      ,
      • Morello-Frosch R.
      • Shenassa E.D.
      The environmental “riskscape” and social inequality: Implications for explaining maternal and child health disparities.
      ). Simultaneously, new legislation being enacted in many jurisdictions that further marginalize already vulnerable populations, such as denying gender-affirming health care to transgender minors (
      • Luneau D.
      Breaking: Arizona house passes anti-transgender sports and medical care bans.
      ) or restricting school curricula from addressing the topic of structural and social determinants (
      • Greene P.
      Teacher anti-CRT bills coast to coast: A state by state guide.
      ), is itself imposing new structural inequities. Knowing the profound effects of structural and social determinants of mental health behooves psychiatric scientists and practitioners to become social and political advocates for positive change to improve the life contexts of those we study and treat.

      Globalize Biological Psychiatry

      Internationalizing basic research, translational efforts, and social policy changes should be a priority. Mental health research involving neurobiology is being conducted in low- and middle-income countries (LMICs) (
      • Memiah P.
      • Nkinda L.
      • Majigo M.
      • Humwa F.
      • Haile Z.T.
      • Muthoka K.
      • et al.
      Mental health symptoms and inflammatory markers among HIV infected patients in Tanzania [published correction appears in BMC Public Health 2021;21:1535.
      ,
      • Musana J.W.
      • Cohen C.R.
      • Kuppermann M.
      • Gerona R.
      • Wanyoro A.
      • Aguilar D.
      • et al.
      Association of differential symptoms of stress to hair cortisol and cortisone concentrations among pregnant women in Kenya.
      ), yet it remains the case that biological psychiatrists overwhelmingly pursue their science in high-income countries. The majority of the world lives in LMICs, and they too are subject to structural and social determinants of neurobiology and mental health. There are mutual, bidirectional benefits to rectifying this disparity in empirical work across the global population. For example, increasing investment in the necessary physical and personnel infrastructure (equipment and training) for scientists and practitioners in LMICs to pursue biological psychiatry would advance theory, research, and practice with diverse cultures and communities, and would bring more diverse perspectives and approaches into scientific endeavors. The Fogarty International Center at the National Institutes of Health provides one example of how infrastructure and research grants can be targeted toward scientific capacity-building within LMICs.
      More work remains to validate biological and psychiatric constructs across cultures and countries. ICD-11 (
      International Classification of Diseases, Eleventh Revision (ICD-11), World Health Organization (WHO) 2019/2021.
      ) is widely used in Europe and across the globe. Working to bridge future revisions of the DSM-5-TR and ICD-11 with globally informed understandings of structural and social determinants of mental health could advance the training of clinicians and researchers by, for example, recognizing variations in the relevant criteria for diagnoses within different cultures and communities, and across the lifespan.
      Globally, countries with steeper income gradients (more wealthy and more impoverished members, relative to fewer middle-income members) have overall worse health across the economic spectrum than countries with less economic disparity (
      • David R.J.
      • Collins J.W.
      Layers of inequality: Power, policy, and health.
      ,
      ). Even while acknowledging that marginalized and disempowered members suffer the most, living in a country with greater structural and social inequity is unhealthy for everyone in that country, paralleling research on the biological tolls of structural and social inequities (
      • Bellatorre A.
      • Finch B.K.
      • Phuong Do D.
      • Bird C.E.
      • Beck A.N.
      Contextual predictors of cumulative biological risk: Segregation and allostatic load.
      ,
      • Parra L.A.
      • Helm J.L.
      • Hastings P.D.
      Adrenocortical responses of emerging adults in California in the two months following the Pulse Night Club massacre: Evidence for distal stress responses.
      ). Translating biological psychiatry into advocacy for reducing collective stress stemming from economic and other disparities could promote better global mental health and well-being.

      Conclusions

      The increasing empirical attention from biological psychiatry to structural and social determinants is revealing that they have pervasive and lifelong impacts on the brain and other neurobiological systems, with profound consequences for mental health. More research on these processes clearly is needed, and particularly for structural determinants, to advance both the science and the practice of biological psychiatry. Doing this work well will require creative thinking and novel approaches from scientists who have experience with and understanding of these structural and social determinants, and competence at building effective research partnerships with communities that have been disadvantaged by structural and social inequities. Building diversity within biological psychiatry and allied disciplines by involving more people who identify as members of marginalized racial, ethnic, gender, sexual, and economic groups will require intentional efforts for culture change within the field. Although diversifying the ranks of scientists serves to increase scientific innovation, the work of scientists from underrepresented backgrounds is systematically devalued (
      • Hofstra B.
      • Kulkarni V.V.
      • Munoz-Najar Galvez S.
      • He B.
      • Jurafsky D.
      • McFarland D.A.
      The diversity–innovation paradox in science.
      ), contributing to their greater likelihood of leaving academia (
      • Jones-London M.
      NINDS strategies for enhancing the diversity of neuroscience researchers.
      ,
      • Roskams J.
      • Popović Z.
      Power to the people: Addressing big data challenges in neuroscience by creating a new cadre of citizen neuroscientists.
      ). These inequities within our professions must be addressed, because to better promote national and global well-being, we need more research on the structural and social determinants of neurobiology and mental health, by the people who are best positioned to engage effectively with this challenging work.

      Acknowledgments and Disclosures

      We thank Ms. Enya Daang for assistance in preparing the manuscript.
      The authors report no biomedical financial interests or potential conflicts of interest.

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