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. Author manuscript; available in PMC: 2019 Mar 25.
Published in final edited form as: Lancet Psychiatry. 2018 Oct 10;5(11):940–944. doi: 10.1016/S2215-0366(18)30342-0

Curtailing the communicability of psychiatric disorders

Milton L Wainberg 1, Liat Helpman 2, Cristiane S Duarte 3, Sten H Vermund 4, Jennifer J Mootz 5, Lidia Gouveia 6, Maria A Oquendo 7, Karen McKinnon 8, Francine Cournos 9
PMCID: PMC6433373  NIHMSID: NIHMS1017707  PMID: 30316807

Abstract

Although psychiatric disorders are classified as non-communicable diseases, we believe this classification is too rigid and limiting. We present evidence of the communicability of psychiatric disorders through three major pathways: infectious and ecological, familial, and sociocultural communicability. Successful strategies developed to control the spread of communicable infectious diseases are relevant to curtailing the communicability of psychiatric disorders, thereby reducing their burden. Current interventions and policies that conceptualise psychiatric illnesses as non-communicable mostly focus on the individual. By applying strategies from infectious disease and chronic illness prevention models within a socioecological framework, we posit a broad communicable chronic disease psychiatric illness control plan for effectively treating the patient with the psychiatric disorder (host) as early as possible, providing benefits to their family and the community, and preventing transmission to others.

Introduction

WHO defines communicable diseases as those caused by infectious agents or their toxic products directly or indirectly transmitted from person to person, from animal to person, and from the environment to person (eg, through food, air, water, body fluids).1 We believe that well established strategies developed to contain the spread of infectious diseases could be successfully applied to other illnesses that are transmitted from one person to another (either directly or through the indirect pathways noted above).

This Personal View examines how substance use and other mental health illnesses can be communicated through three major pathways.

Evidence for the communicable nature of psychiatric disorders

Infectious and ecological communicability

Pathogens and microorganisms that invade the brain can directly affect organ function, causing delirium, psychosis, mania, and depression.25

The brain–gut axis and the microbiome can interfere with fermentation processes in the intestinal flora that produce fatty acids such as butyrate, which is a neuropsychiatric regulator.6 Shifts in the gut microbiome, due to changes in diet or as a response to stress,7 can manifest as depression8 and post-traumatic stress disorder.9

Exposure to environmental factors such as toxins (eg, lead, tobacco) or contaminated water sources put children at an increased risk of later developmental and psychiatric disorders.10 Urbanicity is associated with an increased risk of psychosis, possibly related to individual-level environmental exposure to cannabis use, social adversity, exclusion, and discrimination.11 Similar to man-made disasters,11,12 natural disasters are associated with psychiatric illness, including depressive, anxiety, and post-traumatic stress disorders.12

Familial communicability

Risks associated with having family members with psychiatric illness are multifaceted, including genetic, behavioural, prenatal and perinatal, and developmental pathways.

Whereas low-prevalence disorders such as schizophrenia (1–3% prevalence worldwide) and autism (1–2% prevalence) are highly heritable (0·70 heritability for schizophrenia13 and 0·64–0·91 for autism14), more common disorders such as depression (4·67% prevalence) and anxiety (7·30% prevalence) have lower heritability (0·37–0·67 for depression and 0·32–0·49 for anxiety15). Substance use disorders have a worldwide prevalence of 6·8% and an estimated heritability as high as 0·50.16 The established genetic basis of most psychiatric disorders17 cannot explain the increased prevalence of psychiatric disorders among family members with no genetic relationship, such as spouses, and it cannot explain the adverse effects of psychiatric disorders on family members who do not have psychiatric illness.18

Assortative mating is the non-random mating pattern of people with specific attributes. This mating pattern might augment existing shared traits, behaviours, and life circumstances, which can explain why psychiatric disorders are highly heritable when they are associated with reduced fecundity, why some disorders are more highly heritable than others, and the genetic comorbidity across psychiatric disorders.19 Assortative mating between people with psychiatric illness could lead to increased communicability within families through both genetic and nurturing influences.20

Perinatal and parenting-related patterns also have a role in familial communicability. A psychiatric disorder within a family is associated with poorer mental health in offspring than in families who do not have a psychiatric disorder. Aside from genetics, this association could be attributed to exposure to stress at multiple levels21 (ie, biological, behavioural, socioeconomic) during developmentally formative years. In addition, maternal depression is associated with adverse outcomes in the fetus, infant, and child.22,23 Brain development begins in utero, and is influenced by maternal stress, anxiety and depression, and the toxic effects of alcohol and other substances, which all have negative effects on neurodevelopment.22,2426 Postnatal maternal anxiety and depression affect early development and mental health, possibly through changes in maternal behaviours such as caressing the infant27 and provision of support28—crucial factors in the development of stress and emotion regulation systems during infancy. Maternal depression, anxiety, and stress are shown to be bidirectionally associated with offspring depression and experiences of stress.29 Symptoms of post-traumatic distress have been shown to affect the psychiatric disorders of those close to the patient with post-traumatic distress.30 Both maternal stress specifically, and parental psychopathology generally, have been shown to be associated with the psychiatric health of children.31,32 Living with a relative with a psychiatric disorder as a young child can be an adverse childhood event.33 Substance use disorders are a powerful risk factor for household dysfunction, abuse and neglect, and placement into alternative living arrangements such as foster care.33

Epigenetic patterns are caused by molecular alterations (eg, DNA methylation, microRNA expression, and histone modifications) that can turn genes on or off selectively. They change in association with stress and the family nurturing environment3436 Altered epigenetic regulation can explain some of the intergenerational and intrafamilial correlation, including endocrine and brain development. Alterations of gene expression due to stress exposure can also contribute to clustering of psychiatric illness, termed transgenerational epigenetic inheritance,34 and can begin during intrauterine development, emphasising once more the crucial role of mothers in the communicability of psychiatric diseases. A 9-year follow-up study of a birth cohort in 20 large American cities (n=2420) showed that children with father loss have significant epigenetic changes—shorter telomeres. Paternal death had the largest association with shorter telomeres; interestingly, when fathers were lost due to separation or divorce, loss of telomere length was greatly mediated by loss of income. However, loss of income had a less substantial contribution to loss of telomere length when fathers were lost due to death or incarceration, emphasising the role of fathers beyond provision of tangible goods and the strong negative effects of parental incarceration.37

Sociocultural communicability

In addition to the well described social determinants, including social inequities, ongoing racism, discrimination, and physical health disparities,38,39 psychiatric illnesses show a pattern of transmission within cultures40 and social networks,41 particularly in young people.42

Poverty, famine, social disadvantage, and structural discrimination are common risk factors for psychiatric illness.10,38 Natural12 and man-made disasters increase the prevalence of psychiatric illness and can have long-term and intergenerational effects. Many so-called epidemics of psychiatric illness have been recorded in areas afflicted by ongoing armed conflict and forced migration,43 terrorist attacks,44 and financial crises.45 Rape, female genital mutilation, societal restrictions, and violence directed at girls and women are associated with adverse psychiatric consequences.46,47 Among the lesbian, gay, bisexual, and transgender (LGBT) population, prejudice and stigma—from self, family, and community institutions, in addition to discrimination, childhood abuse, sexual victimisation, and harsh criminal prosecution—might account for some of the enhanced risk for poor mental health.4852 Indeed, any minority identity—eg, historically colonised Indigenous populations—can have a heightened risk of collective generational and lifespan traumas, increased vulnerability to multiple lifetime disorders (through pathways of childhood adversity and negative family environments), and collective generational adversity.39

Substance use disorders are the most prevalent and burdensome example53 of a psychiatric disorder arising from institutional culture, with both a familial54 and a social pattern of communicability, particularly when use occurs as part of the institutional culture observed in correctional facilities, schools, and colleges.55 The diversity of pathways in the initiation of so-called gateway substances (ie, tobacco, alcohol, cannabis) and how this initial substance use can progress to use of other illicit drugs provides evidence for communicability.56

Suicide clusters57 have been described in various institutional and community contexts, suggesting a substantial social contagion effect, particularly in young people.42 Proposed underlying mechanisms have included direct transmission, imitation, common context, and affiliation.57 Mass psychogenic illness has been reported globally from North America58 to Africa59 and southeast Asia.60 Symptoms are often attributed to witchcraft61 or environmental toxicity,58 but can be evoked in psychology laboratory settings.62 Culture-bound syndromes, such as koro (an anxiety disorder associated with the fear that one’s genitals are shrinking), also appear in clusters, suggesting transmission.40

Addressing the communicability of psychiatric illness

We believe that successful strategies developed to control the spread of communicable infectious diseases are relevant to curtailing the communicability of psychiatric disorders, thereby reducing their burden. Interventions and policies that conceptualise psychiatric illnesses as non-communicable mostly focus on the individual. By applying strategies from infectious disease63 and chronic illness prevention models64 within a socioecological framework,65 we suggest a broad communicable chronic disease psychiatric illness control plan (figure) to effectively treat the psychiatric patient (host) as early as possible and prevent transmission to others.

Figure:

Figure:

Communicable chronic disease psychiatric illness control plan

At the individual level

Undiagnosed patients with psychiatric disorders, and patients at risk of these disorders, should be identified by integrating routine (self-administered or easy to administer), state-of-the-art, multilevel validated screenings (including household assessments and, eventually, biological testing) into primary care and the community, through public health strategies across urban, suburban, and rural settings.

Linking to care, and treating and retaining in care, patients who have a positive screen for psychiatric illness should be prioritised, as is facilitating adherence to maximise treatment outcomes, reduce disability, and prevent further transmission by using evidence-informed treatment as prevention.

At the family level

Intervention and prevention strategies should be developed, targeting people at a high-risk of developing psychiatric disorders, including first-degree relatives and household members of patients with psychiatric illness.

Intervention and prevention strategies targeting those whose psychiatric disorders will impact others, including parents and other caregivers of children, should be implemented. Keeping such people free of, or in remission from, psychiatric disorders can be expected to reduce the risk of communicability.

At the community and systems level

Awareness and prevention strategies should be promoted, within and beyond the health system, including overall communities and their specific constituents: families, schools, hospitals, churches, jails, and the armed forces. Structural interventions to maximise salutary psychiatric outcomes should be applied, including psychosocial support, prevention of interpersonal violence, discrimination, bullying, and traumatic brain injuries, organisation of community youth activities, and implementation of effective alcohol and substance misuse policies. Such interventions would increase knowledge, reduce incidence and burden, decrease stigma and social isolation, reduce barriers to care, and, for individuals with the most severe psychiatric disorders, provide opportunities for employment and housing.

Surveillance, identification, and early intervention should be prioritised for specific communities at a high risk of developing psychiatric disorders. Communities that would benefit from this strategy include conflict zones, high crime and low-resourced neighbourhoods, areas affected by natural disasters and those affected by epidemics of substance use, psychogenic illness, and suicide cluster incidence.

This novel framework applies successful strategies developed to control the spread of communicable infectious diseases to curtail the communicability of psychiatric disorders and reduce their burden. Implementing multiple interventions—some of them already in use—within public systems of care, would offer an efficient way of utilising resources, particularly important in low-resource settings, to reduce the communicability and chronic occurrence of psychiatric disorders. Although a few countries have recognised the need to scale up mental health services using some of these strategies for various disorders,6668 and some funding agencies have allocated monies to address the global mental health treatment gap,69 the comprehensive approach described here is yet to be implemented. An ongoing hybrid cost-effectiveness and implementation scale-up study in Mozambique will provide evidence regarding this framework (NCT03610750).

Even though psychiatric disorders are the leading cause of years lost to disability globally70 and are estimated to account for more than half of the projected total economic burden from non-communicable diseases by 2030,71 on average, only 0·5% (in low-income and middle-income countries) to 5·1% (in high-income countries) of national health-care budgets have been devoted to mental health disorders.72 In contrast, low-income and middle-income countries affected by the HIV epidemic have instituted multiple approaches to eradicate this epidemic, combining local and global funding. Global funding for infectious diseases and non-psychiatric non-communicable diseases are, respectively, 17 times and four times higher than funds targeted to mental health disorders.73,74 Classifying diseases as either communicable or non-communicable might create conceptual barriers to effective public health strategies and skew funding priorities. The little funding available for psychiatric illness typically facilitates intervention at the individual level. Funding for interventions at the family level, to address the communicability embedded in the mother–child dyad, should target integration of psychiatric services into care for women and children63 as a feasible, cost-effective way of delivering services and curtailing communicability. Substance misuse and domestic violence would be other important targets of intervention at the family level. Community gateways, such as schools and primary care with community health workers, family-oriented centres and associations, and hospitals, should have staff trained in the delivery of family-level and community-level strategies, enlisting medical, psychiatric, and social welfare professionals, along with community and social leaders. Policy reform and collaboration with governments and legal systems are needed to implement this framework. A shift from a purely non-communicable disease approach, to incorporating communicable disease strategies for psychiatric illnesses would enable families, networks, and communities to mobilise resources and integrate treatment into care systems aimed at psychiatric illness awareness and prevention.

One of the arguments against developing a stronger focus on expanding efforts to treat mental illnesses in resource-limited environments is that health-care systems are already overburdened and imposing additional tasks is unrealistic, especially without an expansion of the health-care workforce. However, we believe that our approach will lessen the burden on the health-care system. The communicable chronic disease psychiatric illness control plan must first be reviewed to determine where it will be implemented, who will be responsible for each phase, and the best methods to train those who will carry it out and monitor and sustain its implementation.

The brain and the body function as an integrated system, but the care system for conditions affecting the brain and body usually operates in silos. Stigma about mental illness, which pervades the education of all health-care providers, creates the belief that treating mental illnesses can be avoided through triage to specialists. In practice, people with common mental health disorders routinely present to medical providers with somatic complaints such as those seen in anxiety disorders (eg, palpitations, shortness of breath, gastrointestinal problems) and depressive disorders (eg, fatigue and pain). Failure to diagnose and treat psychiatric disorders results in multiple futile medical visits. Recognising that the brain and the body are one system, and that diseases can be both chronic and communicable, creates the unity we need to better improve the health of all populations.

Acknowledgments

This research was supported by a National Institute of Mental Health Grant U19 MH113203, PRIDE sSA—Partnerships in Research to Implement and Disseminate Sustainable and Scalable Evidence Based Practices in sub-Saharan Africa (FC, LG, MLW, and MAO), the Fogarty International Center and National Institute of Mental Health Grant D43 TW009675—PALOP MH Implementation Research Training (LG,MLW, and MAO), a National Institute of Mental Health Grant P30MH062294, Center for Interdisciplinary Research on AIDS (SHV), and a National Research Service Award grant T32 MH096724, Global Mental Health Research Fellowship: interventions that make a difference (LH, CSD, JJM, and MLW).

Footnotes

Declaration of interests

MAO receives royalties for the commercial use of the Columbia-Suicide Severity Rating Scale. MAO’s family owns stock in Bristol-Myers Squibb. All other authors declare no competing interests.

Contributor Information

Prof Milton L Wainberg, New York State Psychiatric Institute and Columbia University College of Physicians and Surgeons, New York, NY, USA.

Liat Helpman, Psychiatric Research Unit, Tel Aviv Sourasky Medical Center, Tel Aviv-Yafo, Israel.

Cristiane S Duarte, New York State Psychiatric Institute and Columbia University College of Physicians and Surgeons, New York, NY, USA.

Sten H Vermund, Yale School of Public Health, New Haven, CT, USA.

Jennifer J Mootz, New York State Psychiatric Institute and Columbia University College of Physicians and Surgeons, New York, NY, USA.

Lidia Gouveia, Department of Mental Health, Mozambique Ministry of Health, Avenida Eduardo Mondlane, Maputo, Mozambique.

Maria A Oquendo, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

Karen McKinnon, New York State Psychiatric Institute and Columbia University College of Physicians and Surgeons, New York, NY, USA.

Francine Cournos, Mailman School of Public Health, Columbia University, New York, NY, USA.

References

  • 1.WHO. Health topics: infectious diseases http://www.who.int/topics/infectious_diseases/en/ (accessed Aug 7, 2018).
  • 2.van Gool WA, van de Beek D, Eikelenboom P. Systemic infection and delirium: when cytokines and acetylcholine collide. Lancet 2010; 375: 773–75. [DOI] [PubMed] [Google Scholar]
  • 3.Wainberg ML, McKinnon K, Cournos F. Epidemiology of psychopathology in HIV. In: Joska JA, Stein DJ, Grant I, eds. HIV/AIDS and psychiatry West Essex: Wiley Blackwell, 2014: 1–60. [Google Scholar]
  • 4.Buka SL, Tsuang MT, Torrey EF, Klebanoff MA, Bernstein D, Yolken RH. Maternal infections and subsequent psychosis among offspring. Arch Gen Psychiatry 2001; 58: 1032–37. [DOI] [PubMed] [Google Scholar]
  • 5.Klein HC, Doorduin J, de Witte L, de Vries EF. Microglia activation, herpes infection, and NMDA receptor inhibition: common pathways to psychosis? In: Müller N, Myint AM, Schwarz MJ, eds. Immunology and psychiatry, from basic research to therapeutic interventions Cham: Springer, 2015: 243–54. [Google Scholar]
  • 6.Stilling RM, van de Wouw M, Clarke G, Stanton C, Dinan TG, Cryan JF. The neuropharmacology of butyrate: the bread and butter of the microbiota-gut-brain axis? Neurochem Int 2016; 99: 110–32. [DOI] [PubMed] [Google Scholar]
  • 7.Cryan JF. Stress and the microbiota-gut-brain axis: an evolving concept in psychiatry. Can J Psychiatry 2016; 61: 201–03. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Dash S, Clarke G, Berk M, Jacka FN. The gut microbiome and diet in psychiatry: focus on depression. Curr Opin Psychiatry 2015; 28: 1–6. [DOI] [PubMed] [Google Scholar]
  • 9.Leclercq S, Forsythe P, Bienenstock J. Posttraumatic stress disorder: does the gut microbiome hold the key? Can J Psychiatry 2016; 61: 204–13. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Johnson SB, Riis JL, Noble KG. State of the art review: poverty and the developing brain. Pediatrics 2016; 137: e20153075 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.Heinz A, Deserno L, Reininghaus U. Urbanicity, social adversity and psychosis. World Psychiatry 2013; 12: 187–97. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Goldmann E, Galea S. Mental health consequences of disasters. Annu Rev Public Health 2014; 35: 169–83. [DOI] [PubMed] [Google Scholar]
  • 13.van Dongen J, Boomsma DI. The evolutionary paradox and the missing heritability of schizophrenia. Am J Med Genet B Neuropsychiatr Genet 2013; 162B: 122–36. [DOI] [PubMed] [Google Scholar]
  • 14.Tick B, Bolton P, Happé F, Rutter M, Rijsdijk F. Heritability of autism spectrum disorders: a meta-analysis of twin studies. J Child Psychol Psychiatry 2016; 57: 585–95. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Guffanti G, Gameroff MJ, Warner V, et al. Heritability of major depressive and comorbid anxiety disorders in multi-generational families at high risk for depression. Am J Med Genet B Neuropsychiatr Genet 2016; 171: 1072–79. [DOI] [PubMed] [Google Scholar]
  • 16.Hart AB, Kranzler HR. Alcohol dependence genetics: lessons learned from Genome-Wide Association Studies (GWAS) and post-GWAS analyses. Alcohol Clin Exp Res 2015; 39: 1312–27. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17.Gratten J, Wray NR, Keller MC, Visscher PM. Large-scale genomics unveils the genetic architecture of psychiatric disorders. Nat Neurosci 2014; 17: 782–90. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Trump LJ, Lamson AL, Lewis ME, Muse AR. His and hers: the interface of military couples’ biological, psychological, and relational health. Contemp Fam Ther 2015; 37: 316–28. [Google Scholar]
  • 19.Zietsch BP, Verweij KJH, Heath AC, Martin NG. Variation in human mate choice: simultaneously investigating heritability, parental influence, sexual imprinting, and assortative mating. Am Nat 2011; 177: 605–16. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Nordsletten AE, Larsson H, Crowley JJ, Almqvist C, Lichtenstein P, Mataix-Cols D. Patterns of nonrandom mating within and across 11 major psychiatric disorders. JAMA Psychiatry 2016; 73: 354–61. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Newman L, Judd F, Olsson CA, et al. Early origins of mental disorder—risk factors in the perinatal and infant period. BMC Psychiatry 2016; 16: 270. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 22.Stein A, Pearson RM, Goodman SH, et al. Effects of perinatal mental disorders on the fetus and child. Lancet 2015; 384: 1800–19. [DOI] [PubMed] [Google Scholar]
  • 23.Weissman MM, Berry OO, Warner V, et al. A 30-year study of 3 generations at high risk and low risk for depression. JAMA Psychiatry 2016; 73: 970–77. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.Bock J, Wainstock T, Braun K, Segal M. Stress in utero: prenatal programming of brain plasticity and cognition. Biol Psychiatry 2015; 78: 315–26. [DOI] [PubMed] [Google Scholar]
  • 25.Entringer S, Kumsta R, Hellhammer DH, Wadhwa PD, Wüst S. Prenatal exposure to maternal psychosocial stress and HPA axis regulation in young adults. Horm Behav 2009; 55: 292–98. [DOI] [PubMed] [Google Scholar]
  • 26.Glover V Maternal depression, anxiety and stress during pregnancy and child outcome; what needs to be done. Best Pract Res Clin Obstet Gynaecol 2014; 28: 25–35. [DOI] [PubMed] [Google Scholar]
  • 27.Sharp H, Hill J, Hellier J, Pickles A. Maternal antenatal anxiety, postnatal stroking and emotional problems in children: outcomes predicted from pre- and postnatal programming hypotheses. Psychol Med 2015; 45: 269–83. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Albers EM, Riksen-Walraven JM, Sweep FCGJ, de Weerth C Maternal behavior predicts infant cortisol recovery from a mild everyday stressor. J Child Psychol Psychiatry 2008; 49: 97–103. [DOI] [PubMed] [Google Scholar]
  • 29.Hammen C, Hazel NA, Brennan PA, Najman J. Intergenerational transmission and continuity of stress and depression: depressed women and their offspring in 20 years of follow-up. Psychol Med 2012; 42: 931–42. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Landolt MA, Ystrom E, Sennhauser FH, Gnehm HE, Vollrath ME. The mutual prospective influence of child and parental post-traumatic stress symptoms in pediatric patients. J Child Psychol Psychiatry 2012; 53: 767–74. [DOI] [PubMed] [Google Scholar]
  • 31.Borelli JL, Smiley P, Bond DK, et al. Parental anxiety prospectively predicts fearful children’s physiological recovery from stress. Child Psychiatry Hum Dev 2015; 46: 774–85. [DOI] [PubMed] [Google Scholar]
  • 32.Gureje O, Oladeji B, Hwang I, et al. Parental psychopathology and the risk of suicidal behavior in their offspring: results from the World Mental Health surveys. Mol Psychiatry 2011; 16: 1221–33. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Dong M, Anda RF, Felitti VJ, et al. The interrelatedness of multiple forms of childhood abuse, neglect, and household dysfunction. Child Abus Negl 2004; 28: 771–84. [DOI] [PubMed] [Google Scholar]
  • 34.Nestler EJ. Transgenerational epigenetic contributions to stress responses: fact or fiction? PLoS Biol 2016; 14: e1002426. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.McEwen BS. In pursuit of resilience: stress, epigenetics, and brain plasticity. Ann NY Acad Sci 2016; 1373: 56–64. [DOI] [PubMed] [Google Scholar]
  • 36.Monk C, Feng T, Lee S, Krupska I, Champagne FA, Tycko B. Distress during pregnancy: epigenetic regulation of placenta glucocorticoid-related genes and fetal neurobehavior. Am J Psychiatry 2016; 173: 705–13. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37.Mitchell C, Mclanahan S, Schneper L, Garfinkel I, Brooks-Gunn J, Notterman D. Father loss and child telomere length. Pediatrics 2017; 140: e20163245. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 38.Allen J, Balfour R, Bell R, Marmot M. Social determinants of mental health. Int Rev Psychiatry 2014; 26: 392–407. [DOI] [PubMed] [Google Scholar]
  • 39.Brave Heart MYH, Lewis-Fernandez R, Beals J, et al. Psychiatric disorders and mental health treatment in American Indians and Alaska Natives: results of the National Epidemiologic Survey on alcohol and related conditions. Soc Psychiatry Psychiatr Epidemiol 2016; 51: 1033–46 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Bernstein RL, Gaw AC. Koro: proposed classification for DSM-IV. Am J Psychiatry 1990; 147: 1670–74. [DOI] [PubMed] [Google Scholar]
  • 41.Rosenquist JN, Fowler JH, Christakis NA. Social network determinants of depression. Mol Psychiatry 2011; 16: 273–81. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42.Niedzwiedz C, Haw C, Hawton K, Platt S. The definition and epidemiology of clusters of suicidal behavior: a systematic review. Suicide Life Threat Behav 2014; 44: 569–81. [DOI] [PubMed] [Google Scholar]
  • 43.Shultz JM, Garfin DR, Espinel Z, et al. Internally displaced “victims of armed conflict” in Colombia: the trajectory and trauma signature of forced migration. Curr Psychiatry Rep 2014; 16: 475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Neria Y, DiGrande L, Adams BG. Posttraumatic stress disorder following the September 11, 2001, terrorist attacks: a review of the literature among highly exposed populations. Am Psychol 2011; 66: 429–46. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 45.Chang S-S, Stuckler D, Yip P, Gunnell D. Impact of 2008 global economic crisis on suicide: time trend study in 54 countries. BMJ 2013; 347: f5239. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46.Mulongo P, Hollins Martin C, McAndrew S. The psychological impact of female genital mutilation/cutting (FGM/C) on girls/women’s mental health: a narrative literature review. J Reprod Infant Psychol 2014; 32: 469–85. [Google Scholar]
  • 47.Dillon G, Hussain R, Loxton D, Rahman S. Mental and physical health and intimate partner violence against women: a review of the literature. Int J Family Med 2013; 2013: 313909. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 48.Austin A, Herrick H, Proescholdbell S. Adverse childhood experiences related to poor adult health among lesbian, gay, and bisexual individuals. Am J Public Health 2016; 106: 314–20. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 49.Katz-Wise SL, Hyde JS. Victimization experiences of lesbian, gay, and bisexual individuals: a meta-analysis. J Sex Res 2012; 49: 142–67. [DOI] [PubMed] [Google Scholar]
  • 50.Hatzenbuehler ML, McLaughlin KA, Keyes KM, Hasin DS. The impact of institutional discrimination on psychiatric disorders in lesbian, gay, and bisexual populations: a prospective study. Am J Public Health 2010; 100: 452–59. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 51.Choi M, Ahn S, Yang E-J, et al. Hippocampus-based contextual memory alters the morphological characteristics of astrocytes in the dentate gyrus. Mol Brain 2016; 9: 72. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 52.White Hughto JM, Reisner SL, Pachankis JE. Transgender stigma and health: a critical review of stigma determinants, mechanisms, and interventions. Soc Sci Med 2015; 147: 222–31. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 53.Ferrari AJ, Norman RE, Freedman G, et al. The burden attributable to mental and substance use disorders as risk factors for suicide: findings from the Global Burden of Disease Study 2010. PLoS One 2014; 9: e91936. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 54.Pears KC, Capaldi DM, Owen LD. Substance use risk across three generations: the roles of parent discipline practices and inhibitory control. Psychol Addict Behav 2007; 21: 373–86. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 55.Galea S, Nandi A, Vlahov D. The social epidemiology of substance use. Epidemiol Rev 2004; 26: 36–52. [DOI] [PubMed] [Google Scholar]
  • 56.Degenhardt L, Dierker L, Chiu WT, et al. Evaluating the drug use “gateway” theory using cross-national data: consistency and associations of the order of initiation of drug use among participants in the WHO World Mental Health Surveys. Drug Alcohol Depend 2010; 108: 84–97. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57.Cheng Q, Li H, Silenzio V, Caine ED. Suicide contagion: a systematic review of definitions and research utility. PLoS One 2014; 9: e108724. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 58.Jones TF, Craig AS, Hoy D, et al. Mass psychogenic illness attributed to toxic exposure at a high school. N Engl J Med 2000; 342: 96–100. [DOI] [PubMed] [Google Scholar]
  • 59.Beyene BB, Teka A, Luce R. Outbreak of mass psychogenic illness at a high school, Amhara region, Ethiopia, April, 2010. Int Invent J Med Med Sci 2014; 1: 157–61. [Google Scholar]
  • 60.Roy D, Hazarika S, Bhattachary A, Das S, Nath K, Saddichha S. Koro: culture bound or mass hysteria? Aust N Z J Psychiatry 2011; 45: 683. [DOI] [PubMed] [Google Scholar]
  • 61.Colligan MJ, Pennebaker JW, Murphy LR. Mass psychogenic illness: a social psychological analysis Abingdon: Routledge Taylor & Francis Group, 2013. [Google Scholar]
  • 62.Broderick JE, Kaplan-Liss E, Bass E. Experimental induction of psychogenic illness in the context of a medical event and media exposure. Am J Disaster Med 2011; 6: 163–72. [PMC free article] [PubMed] [Google Scholar]
  • 63.Centers for Disease Control and Prevention. A CDC framework for preventing infectious diseases October, 2011. https://www.cdc.gov/oid/docs/id-framework.pdf (accessed Dec 14, 2017).
  • 64.Epping-Jordan JE, Galea G, Tukuitonga C, Beaglehole R. Preventing chronic diseases: taking stepwise action. Lancet 2005; 366: 1667–71. [DOI] [PubMed] [Google Scholar]
  • 65.Dahlberg LL, Krug EG. Violence—a global public health problem. In: Krug E, Dahlberg LL, Mercy JA, Zwi AB, Lozano R, eds. World Report on Violence and Health Geneva: World Health Organazation, 2002: 1–56. [Google Scholar]
  • 66.Santos PF, Wainberg ML, Caldas-de-Almeida JM, Saraceno B, Mari JD. Overview of the mental health system in Mozambique. Int J of Ment Health Syst 2016; 10: 1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 67.Van’t Hof E, Cuijpers P, Waheed W, Stein D. Psychological treatments for depression and anxiety disorders in low- and middle-income countries: a meta-analysis. Afr J Psychiatry (Johannesbg) 2011; 14: 200–07. [DOI] [PubMed] [Google Scholar]
  • 68.Chibanda D, Cowan FM, Healy JL, Abas M, Lund C. Psychological interventions for common mental disorders for people living With HIV in low- and middle-income countries: systematic review. Trop Med Int Health 2015; 20: 830–39. [DOI] [PubMed] [Google Scholar]
  • 69.National Institute of Mental Health. Research partnerships for scaling up mental health interventions in low- and middle-income countries https://www.nimh.nih.gov/about/organization/gmh/scaleuphubs/index.shtml (accessed Aug 7, 2018).
  • 70.Whiteford HA, Ferrari AJ, Degenhardt L, Feigin V, Vos T. The global burden of mental, neurological and substance use disorders: an analysis from the Global Burden of Disease Study 2010. PLoS One 2015; 10: e0116820. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 71.Bloom DE, Cafiero ET, Jané-Llopis E, et al. The global economic burden of non-communicable diseases September, 2011. http://www3.weforum.org/docs/WEF_Harvard_HE_GlobalEconomicBurdenNonCommunicableDiseases_2011.pdf (accessed Sept 26, 2018).
  • 72.WHO. WHO mental health atlas 2011 Geneva: World Health Organization, 2011. [Google Scholar]
  • 73.Sridhar D Who sets the global health research agenda? The challenge of multi-bi financing. PLoS Med 2012; 9: e1001312. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 74.WHO. Programme budget 2016–2017 2015. http://www.who.int/about/finances-accountability/budget/PB201617_en.pdf?ua=1 (accessed Jan 12, 2017).

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