Many times in movies, we encounter characters who are institutionalized after enduring a severe trauma. Something devastating happens, and the person who once seemed psychologically stable undergoes a striking transformation, almost as if a switch has been flipped in the mind.
The camera moves through the window of a psychiatric ward and into the character’s room. Some appear detached from the world around them. Some withdraw completely, becoming unresponsive to external reality. Some speak only to themselves. Some see or hear things that no one else can perceive.
Scenes like these can leave us with a question: can this really happen to someone who had shown no prior signs of mental illness? Can overwhelming life events lead someone to what we call “madness”?
Let us approach this question through a book that attempts to explain the causes of such experiences.
First things first: defining and even using the term madness is controversial and sensitive. It is not an observable entity in itself, but rather a label attributed by others. For that reason, it carries more subjectivity than objectivity.
Therefore, a full discussion of the concept would require a separate and much more extensive analysis across different disciplines. For the purposes of this text, however, we need a working definition.
In everyday language, and in the cinematic scenes I described earlier, “madness” is often used as a shorthand for psychosis. When people ask whether someone can “go crazy,” they are usually referring to symptoms such as hallucinations, delusions, disorganized behavior, or a marked withdrawal from reality. In other words, the curiosity behind the question often concerns the possibility of developing psychotic symptoms.
Briefly put, psychosis refers to a significant disruption in one’s ability to distinguish between internal experiences and external reality. During an acute psychotic episode, a person may appear detached from the shared world around them. However, the experience is not simply an absence of reality; rather, it involves the presence of an alternative reality that feels subjectively real to the individual.
This self-generated reality may include perceptions that others cannot access. A person may see figures or hear voices that are not externally present (hallucinations). At the same time, their attention may be absorbed by these internal experiences, making interaction with the external world difficult.
Cognitive organization can also be affected. Thoughts may become fragmented, which is often reflected in disorganized speech. This may include rapid shifts between unrelated topics, tangential or irrelevant responses, incoherent phrasing, or the creation of new words (neologisms) that carry meaning only within the person’s internal framework.
Psychosis is not a separate disorder in itself. Rather, it is recognized as a symptom that can appear across a range of psychiatric conditions. In addition to primary psychotic disorders, psychotic features may also occur within other diagnostic categories, for example, major depressive disorder with psychotic features.
Despite this, psychosis is often immediately associated with schizophrenia, largely because schizophrenia is the most widely known psychotic disorder and psychotic symptoms constitute its core clinical feature. The etiology of schizophrenia has traditionally been discussed within predominantly biological frameworks, with a strong emphasis on genetic vulnerability and heritability.
This perspective can lead to the assumption that individuals without a family history of psychotic disorders are unlikely to develop psychosis solely in response to adverse life events. However, clinical observations and empirical findings suggest that the picture may be more complex.
If psychotic experiences can emerge in individuals without clear genetic risk, how should this be understood? And more broadly, is psychosis primarily a biological phenomenon, or can it also be meaningfully linked to what a person has experienced in their life?
In Models of Madness, Read, Mosher, and Bentall (2004) critically examine the dominant medical conception of schizophrenia by drawing on a wide range of empirical findings. The authors argue that many symptoms commonly associated with schizophrenia can be understood as psychological responses to adverse and traumatic life experiences.
According to this perspective, the traditional medical model, which conceptualizes schizophrenia primarily as a biologically determined disorder rooted in genetic vulnerability, does not fully account for the complexity of existing evidence. Although genetic and neurobiological factors have been widely emphasized, the authors highlight research suggesting that environmental stressors, trauma, and social context play a substantial role in the development of psychotic experiences.
They further argue that a strictly reductionist interpretation, one that locates causality almost exclusively in inherited “faulty genes,” risks overlooking the psychological and social realities individuals have faced. Such a framework may unintentionally shape expectations about recovery by implying that symptoms are fixed, biologically predetermined, and primarily manageable through pharmacological intervention.
The authors also raise broader concerns about how dominant explanatory models influence public policy and resource allocation. When schizophrenia is framed almost entirely as a genetic illness, preventive efforts aimed at improving social conditions, addressing trauma, or reducing environmental stress may receive less attention. In this sense, theoretical models do not remain purely scientific; they shape institutional practices and societal responses.
Finally, Read and colleagues suggest that the persistence of the medical model cannot be understood solely in scientific terms. They point to the powerful institutional and economic forces, including the influence of the pharmaceutical industry, that contribute to maintaining its dominance within mental health systems (pp. 3–5).
If you have ever read a textbook chapter or article on schizophrenia, you may have noticed a recurring pattern. The discussion often begins with an emphasis on heredity. Genetic vulnerability is typically introduced as one of the most fundamental and established facts about the disorder. Frequently, this claim is supported by reference to twin studies, presented as strong scientific evidence.
Over time, repeated exposure to this narrative can make the genetic explanation feel almost self-evident. It becomes framed as the starting point of understanding schizophrenia, rather than one explanatory model among others.
For that reason, the perspective proposed in Models of Madness may initially feel unfamiliar, perhaps even counterintuitive. If the genetic basis of schizophrenia has been repeatedly emphasized as foundational, how can a different framework be justified?
Let us now look more closely at how the authors develop their argument.
The authors present findings from a range of studies as counter-evidence to the strictly medical model and highlight methodological limitations within research that support a predominantly hereditary explanation of schizophrenia. Here, I will briefly focus on their critique of twin studies, largely because twin research is often regarded as one of the most robust methods for estimating genetic influence. For that reason, their challenge to this methodology initially appears surprising.
The central target of their critique is the so-called equal environment assumption. Twin studies typically assume that monozygotic (identical) and dizygotic (fraternal) twins share their environments to the same extent. Therefore, any greater similarity observed in identical twins is interpreted as evidence of stronger genetic influence.
However, the authors question whether this assumption is empirically justified. Identical twins not only share more genes; they also tend to be treated more similarly by parents, teachers, and peers. Greater genetic similarity may increase environmental similarity, rather than being independent of it. If this is the case, then monozygotic and dizygotic twins may not, in fact, experience statistically comparable environments.
To illustrate this point, the authors refer to studies suggesting that identical twins show higher rates of identity confusion, potentially reflecting more intertwined developmental experiences (p. 69)[i]. If environmental experiences differ systematically between twin types, then attributing higher concordance rates solely to genetic factors becomes more problematic.
In this sense, the critique does not reject genetic influence outright. Rather, it challenges the methodological certainty with which genetic conclusions are sometimes presented.
And naturally, this raises the next question: what about adoption studies?
Adoption studies have traditionally been considered particularly strong evidence for genetic explanations. The logic appears straightforward: if a child who is biologically related to a parent with schizophrenia is adopted early in life and raised in a different family environment, yet later develops schizophrenia at higher rates than adopted children without such biological risk, this pattern is interpreted as support for genetic transmission. Because the biological and rearing environments are presumed to be separated, adoption designs have often been presented as a way to disentangle genetic influence from environmental factors.
In the book, the authors also reconsider six major adoption studies that have historically been interpreted as strong evidence for the genetic basis of schizophrenia. However, Read and colleagues provide a detailed critique of their methodological limitations (pp. 73–74). I will briefly summarize some of the key points.
First, the diagnostic definitions used across these studies lack consistency. The term “schizophrenia” is not uniformly defined, and several studies include not only chronic schizophrenia but also broader, non-psychotic schizophrenia spectrum conditions. In some cases, diagnoses such as manic depression, bipolar psychosis, or depressive psychosis are grouped within the same analytical framework.
Importantly, when analyses are restricted strictly to chronic schizophrenia, the results in some studies become far less compelling. For example, in one study, 65 biological relatives were reported to have a spectrum disorder, yet none met criteria for chronic schizophrenia[ii]. In another, only one child among 76 adopted children whose biological parents had a spectrum disorder was diagnosed with schizophrenia[iii].
Despite these nuances, findings from broadly defined spectrum categories are often aggregated and interpreted as evidence for a strong genetic basis of schizophrenia. The authors argue that such aggregation risks overstating the specificity of genetic influence.
Second, despite the central importance of environmental variables in studies attempting to disentangle gene–environment effects, many of these adoption studies provide limited information about the adoption process itself. Details regarding the age at which children were adopted, the duration of pre-adoption institutionalization, the psychological state of the child at placement, and the characteristics of the adoptive family environment are often insufficiently reported.
Given that environmental exposure before and after adoption may significantly influence developmental outcomes, the absence of such information makes it difficult to isolate genetic contributions with confidence.
The relevance becomes clear when we return to the initial question: can severe life events lead ordinary individuals to develop psychotic symptoms?
The central argument of Models of Madness is precisely that many experiences labeled as “schizophrenia” may be better understood as responses to adverse and traumatic life events. Rather than viewing psychosis exclusively as the manifestation of an inherited biological defect, the authors propose that it can emerge in the context of overwhelming psychological and social experiences.
In this sense, the book suggests that the answer to the question is not merely hypothetical. Psychotic experiences following trauma have been documented across different populations. The more complex issue is how these experiences are interpreted.
To support their position, the authors review extensive research on childhood abuse among psychiatric inpatients (pp. 226–239). Across studies, both male and female mental health inpatients are reported to be at least twice as likely as the general population to have experienced childhood abuse. When focusing specifically on schizophrenia, one study cited in the book reports that 35% of outpatients diagnosed with schizophrenia had experienced emotional abuse, 42% physical neglect, and 73% emotional neglect[iv].
Moreover, higher rates of childhood sexual abuse have been reported among women diagnosed with schizophrenia (78%) compared to women with other diagnoses such as panic disorder (26%), anxiety disorders (30%), and major depressive disorder (42%)[v].
Beyond prevalence rates, the authors emphasize patterns linking trauma history with symptom expression. Studies indicate that adults with histories of abuse are more likely to report hallucinations than non-abused individuals. In some cases, the type of hallucination (e.g., visual, auditory, tactile) appears to vary in relation to the type of abuse experienced. Similarly, the thematic content of delusions and hallucinations often reflects traumatic experiences, suggesting that life events may shape not only the emergence but also the form of psychotic symptoms.
The authors extend their analysis beyond childhood adversity and examine the role of traumatic experiences in adulthood. For example, they cite a study conducted with 409 female psychiatric inpatients reporting a significant association between sexual assault in adulthood and a diagnosis of schizophrenia[vi].
Importantly, they do not treat childhood and adulthood trauma as independent phenomena. Instead, they emphasize the cumulative and interactive nature of traumatic exposure. Individuals who experience abuse in childhood are statistically more likely to encounter further trauma later in life. In such cases, adult trauma may function not as an isolated event but as a trigger that reactivates earlier unresolved experiences, potentially contributing to the emergence or intensification of psychotic symptoms.
The book also explores broader structural factors, including poverty, urbanization, and gender differences in the prevalence of schizophrenia (pp. 161–177). Numerous studies are cited showing significantly higher rates of diagnosis among individuals from lower socioeconomic backgrounds and among those living in densely populated urban areas.
These findings raise a critical question. If schizophrenia were purely a genetically determined disorder, why would its prevalence vary so markedly across social and environmental conditions? The authors use these disparities to argue that social context cannot be treated as secondary. Instead, living conditions, chronic stress, and social adversity may play a substantial role in shaping vulnerability to psychosis.
The authors also address gender differences in the onset and course of schizophrenia. They propose that socially constructed gender roles may help explain why men are, on average, diagnosed at an earlier age than women.
According to the literature they cite, symptom onset in men often occurs in late adolescence or early adulthood, a developmental period characterized by efforts to establish independence, assert autonomy, and negotiate social identity. This phase may involve heightened interpersonal conflict and stress, which, in vulnerable individuals, could contribute to the emergence of psychotic symptoms.
In contrast, the onset in women is reported to be more frequently associated with periods involving major life transitions, such as childbirth or significant family-related stress. Rather than attributing these differences solely to biology, the authors suggest that gender-specific stress exposures and social expectations may shape both timing and expression of symptoms.
Gender differences are also discussed in relation to prognosis. Men are often reported to experience a more severe course. One proposed explanation concerns differences in social and familial support. Parents and families may, on average, adopt a more protective stance toward daughters, whereas sons are more often expected to demonstrate independence and emotional stability. When symptoms emerge, lower tolerance and reduced support may contribute to poorer outcomes among men.
This interpretation again reflects the authors’ broader argument: that social context, expectations, and relational dynamics interact with vulnerability in shaping the trajectory of psychosis.
Taken together, the authors interpret these findings as evidence that adverse life events and difficult social and economic conditions play a substantial role in the development of psychotic symptoms. This perspective is not presented as something to fear, as if anyone might suddenly develop these symptoms at any moment. Rather, it reframes psychosis as a human response that can be understood within the context of lived experience.
There is a meaningful difference between being told that symptoms reflect a fixed disease written into one’s genes and being told that they may be connected to what one has endured. The latter interpretation can open space for agency, recovery, and social change in ways that strictly biological models sometimes do not.
From a therapeutic standpoint, this distinction has practical consequences. If psychosis is viewed only and exclusively as a neurochemical imbalance, medication might be overemphasized at the expense of other important interventions. If it is understood, at least in part, as a response to trauma, then working through traumatic experiences, building safe therapeutic relationships, and strengthening social support become central components of treatment. In reality, many patients likely need a combination of both approaches.
At the societal level, the implications are even broader. If poverty, urban stress, and gendered social expectations contribute to the risk of psychosis, then the response cannot be exclusively medical. It becomes a social responsibility.
Ultimately, Models of Madness leaves us with a simple question: is psychosis primarily genetic, or is it shaped by lived experience? The answer may lie somewhere in between.
Whether their arguments fully persuade you is another matter. Here, I have only been able to outline the core ideas. The book spans nearly 400 pages, dedicating substantial space to critiquing the medical model, presenting psychosocial formulations, and reviewing evidence-based psychosocial interventions. Its arguments are supported by an extensive body of empirical research.
For that reason, any quick judgment, whether in favor of or against the authors’ position, would not do justice to the depth of the material. If the question interests you, reading the book itself may provide a deeper understanding than this overview can offer.
REFERENCES
[i] Jackson, D. D. (Ed.). (1960). The etiology of schizophrenia. Oxford, England: Basic Books, 37-87.
[ii] Kety, S. S., Rosenthal, D., Wender, P. H., & Schulsinger, F. (1968). The types and prevalence of mental illness in the biological and adoptive families of adopted schizophrenics. Journal of Psychiatric Research, 6, 345-362. https://doi.org/10.1016/0022-3956(68)90026-5
[iii] Rosenthal, D., Wender, P. H., Kety, S. S., Welner, J., & Schulsinger, F. (1971). The Adopted-Away Offspring of Schizophrenics. American Journal of Psychiatry, 128(3), 307-311. https://doi.org/10.1176/ajp.128.3.307
[iv] Holowka, D. W., King, S., Saheb, D., Pukall, M., & Brunet, A. (2003). Childhood abuse and dissociative symptoms in adult schizophrenia. Schizophrenia Research, 60(1), 87-90. https://doi.org/10.1016/S0920-9964(02)00296-7
[v] Friedman, S., Smith, L., Fogel, D., Paradis, C., Viswanathan, R., Ackerman, R., & Trappler, B. (2002). The incidence and influence of early traumatic life events in patients with panic disorder: A comparison with other psychiatric outpatients. Journal of Anxiety Disorders, 16(3), 259-272. https://doi.org/10.1016/S0887-6185(02)00097-X
[vi] Cloitre, M., Tardiff, K., Marzuk, P. M., Leon, A. C., & Portera, L. (1996). Childhood abuse and subsequent sexual assault among female inpatients. Journal of Traumatic Stress, 9(3), 473-482. https://doi.org/10.1002/jts.2490090306
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