Front Matter

This book has both intellectual and personal roots. One of my motivations in writing this second edition is to summarize what I have learned in 50 years as a psychiatrist. At the same time, I want to share with readers what I have had to unlearn. When I began my training in the 1960s, there was not much contact between strains of thought that favored nature or nurture. They ran in parallel without ever meeting. Like many North American residents at that time, I had psychoanalysts as teachers who believed that the causes of common mental disorders lie in an unhappy childhood. Their models were seductive because they offered an understanding of almost every form of psychopathology, but these ideas were inaccurate and simplistic.

At the same time, psychiatry was in the midst of a psychopharmacological revolution. In the most severe disorders, drugs were usually superior to psychotherapy. Moreover, drugs were starting to be applied to patients who were symptomatic but less impaired. I could not anticipate that millions of patients would be taking psychiatric drugs, sometimes for a lifetime. A new paradigm has replaced a biopsychosocial mode (Engel 1980) with what, among others, Bentall (2009) has called a “bio-bio-bio” model.

I have never disagreed with the principle that mental disorders are brain disorders. Of course they are! However, that does not mean that thoughts, behaviors, and emotions are best understood by reduction to a neuronal level. Moreover, a biopsychosocial model leads to different clinical implications. For a good number of patients, ranging from those with mild depression to those with a personality disorder, medication is of doubtful value and psychotherapy is the treatment of choice. For others, a combination of drugs and talking therapy is the best option.

When I began to practice psychiatry, I wanted to justify my years of training in medicine and treat patients who were sick enough to require the services of a physician. I was particularly interested and challenged by patients who were chronically suicidal. These patients were often avoided by nonmedical clinicians, and if, by the end of treatment, they decided to go on living, I would know that they had benefited. This is why I became interested in the treatment of borderline personality disorder. At the time, a psychodynamic model seemed to have the most to offer, and that is what I offered my patients in the early years of my career. Like most clinicians, I started with high hopes but achieved mixed results. Some patients did brilliantly—these are the cases clinicians like to write up and talk about. Other patients deteriorated in spite of my best efforts. Most showed middling levels of improvement.

I also took a psychodynamic perspective as a teacher of psychiatric residents. Whatever the presenting problems, I could come up with a plausible explanation based on the patient’s personal history. I later came to the conclusion that this way of thinking was specious, and I began to adopt a hardheaded approach based on empirical evidence. I came to consider myself a “born-again” proponent of evidence-based practice. I have wondered if I should undertake a “product recall” and inform residents from the 1970s to ignore my earlier views, but my students have almost certainly forgotten most of what I taught them.

In the course of a long career, my ideas about psychiatry have changed dramatically. For nearly 50 years, I have been in charge of an outpatient consultation clinic evaluating a large number of new patients referred from the community. I have now seen about 50,000 cases—approximately the population of a small town. Exposure to a very broad range of psychopathology helped me to appreciate the complexity of the pathways to mental illness. I benefit, at least in principle, from this experience. However, as this book argues, clinical experience is not a reliable guide to understanding causes. Like any scientific hypothesis, intuitive impressions need to be confirmed by systematic research.

I have been fortunate to have colleagues who helped me to develop a second career as a researcher. In spite of my late arrival on the scientific scene, beginning as a clinician-teacher had some advantages. My experiences led me to address the question as to why some patients develop one type of illness under adverse circumstances while other patients, faced with the same life events, develop a completely different type of illness, and still others develop no illness at all. My own research has focused on patients who do not benefit from standard treatments. This lack of response requires an explanation. Traditionally, clinicians believed that the intractability of personality disorders derived from their roots in early childhood. However, research does not confirm this view and shows that most people who experience early adversities never develop a mental disorder (Paris 2020). Life events alone do not account for the development of personality disorders or, for that matter, of most mental disorders.

Several lines of evidence, described in detail in this book, support this conclusion (Cicchetti 2016). Many patients with mental disorders have no history of childhood adversity. Patients with similar life experiences can develop completely different illnesses. Children experiencing severe adversities show high levels of resilience, and only a minority will develop diagnosable psychopathology in adulthood. Moreover, children raised in the same family and exposed to the same environment do not necessarily have the same outcome as adults. Finally, research in behavior genetics shows that about half of the variance affecting most mental disorders is genetic (Plomin 2018).

Psychopathology in any individual is not predictable, either from inborn temperament alone or from life experience by itself. The problem with current models in psychiatry is that they heavily tilt the scales, one way or the other, toward genes or environment. The biomedical model attempts to view psychopathology as entirely a function of abnormal neuroconnectivity or neurochemistry. In doing so, it radically oversimplifies the complexity of the human brain and mind. This model works best for psychoses, as well as neurodevelopmental disorders and neurocognitive disorders, but even there has limitations.

A purely psychological or psychosocial model of psychopathology is equally simplistic and misleading. When events in an individual’s life have been adverse, it may seem plausible to account for present difficulties by personal history. However, what clinicians do not always realize is that their patients are a highly selected subsample of those exposed to any given risk factor. When researchers go out into the community and interview nonclinical samples, they find that most people exposed to negative life events develop mild difficulties or none at all.

These facts are striking. To explain them, we need a different and more interactive theoretical model, one that integrates nature and nurture (Tabery 2014). This book describes how predisposing genetic factors particular to the individual, interacting with environmental stressors, can be the basis of a general model that can be applied to most categories of mental disorder. I apply these principles to most of the more common conditions that psychiatrists see.

I do not, however, focus on disorders in which the gene-environment model is not quite appropriate, particularly in conditions whose etiology is mainly biological. Thus, I do not discuss autism spectrum disorders, or neurocognitive disorders in which research shows that the environment plays only a minor role. Although schizophrenia is also highly genetic, I discuss research supporting a role for environmental risk factors. I also, much more briefly, describe the weaker evidence for environmental risk in bipolar disorders. I omit many other conditions listed in DSM manuals that are insufficiently researched to determine whether they fit the model.

In recent years, my critique of modern psychiatry has focused on the idea of biological reductionism. The pendulum has swung so far that the effects of psychosocial environment are dismissed, or at best paid lip service. Reductionism in science has had great success but has great limitations. We cannot understand water by reducing it to the properties of hydrogen and oxygen. Complex phenomena have emergent properties that cannot be explained by their components (Gillett 2016).

Moreover, the pathways leading to mental disorders are not linear but involve an enormously complex set of interactions. The principle that disorders have multiple causes may seem a truism. Yet contemporary psychiatry honors it “more in the breach than in the observance.” Like other disciplines that face complexity, psychiatry has been susceptible to reductionistic theories. We are tempted to reduce cognitive dissonance and to look for simple ways to explain what we observe.

Psychiatry has suffered from what Snow (1958/1993) called the problem of “two cultures.” A biomedical mental health culture takes the world view that mental disorders are primarily the result of factors inside the person. A psychosocial culture takes the world view that mental disorders are primarily the result of factors outside the person. Both models tend to be reductionistic, applying unidimensional theories in which one risk factor causes one disorder. The historical background of these models is illuminating. Biological theories dominated psychiatry during the nineteenth century but went into decline in the first half of the twentieth century, largely because few brain abnormalities could be observed and because no effective biological treatments for mental disorders were available. The postwar years were the heyday of psychoanalysis and other psychological therapies. In the latter decades of the twentieth century, however, and even more in the twenty-first century, successful pharmacological treatment came of age, and brain science again came to dominate psychiatric theory. Even so, modern psychiatry still lacks a comprehensive biological theory (Harrington 2019).

These world views suffer from reductionism, even at the biological level. The effects of genes are extremely complicated, and hundreds of them can be involved in a single disorder. Similarly, the role of life events in psychopathology is complex, and one should not assume that single traumatic events cause mental disorders, a complexity that has sometimes led to the use of the term “environome” (Plomin 2018).

The theoretical models that psychiatrists use are not just a matter of intellectual interest. They profoundly affect what these psychiatrists do clinically. If a psychiatrist believes that mental disorders arise from single causes, he or she will tend to treat patients with single methods. In a biomedical model, clinicians search for aberrant neurotransmitter pathways that can be specifically targeted by carefully designed pharmacological agents. In an environmental model, clinicians may search for life events and psychological conflicts or assumptions that can be addressed through psychotherapy. To do justice to the complex causes of psychopathology, we need much more sophisticated explanations of the relationship between risks and disorders (Kendler 2019). Any comprehensive and clinically relevant approach must be multivariate. (Modern statistics reflect this approach, replacing t-tests and chi-squares with regression equations.)

The psychosocial risk factors for psychiatric illness are important, but we must be cautious in attributing pathology of patients to negative events that are common in human life. Because clinicians only see people who became disordered, they tend to develop a distorted view of the relationship between adversity and illness. In biologically vulnerable people, however, negative events have a stronger effect. For example, in PTSD, adverse experiences, unless they activate predispositions, usually cause only short-term, not long-term effects (Yehuda 2002). Many of the associations in the literature between psychosocial risks and mental disorders can be accounted for by predisposed subpopulations.

Thinking interactively helps us avoid assuming simple relationships between causes and effects. Instead, the model encourages us to address complex relationships between many causes and many effects. It also offers a nonreductionistic way of conceptualizing the origins of psychopathology. Unfortunately, reductionism is alive and well. Clinicians of the future need to become more comfortable with complexity. In the long run, the weight of scientific evidence can change the way we think.

My aim is to provide the reader with an intelligible summary of the gene-environment model and to illustrate its application to the understanding of mental disorders. I do not claim to present a new or an original theory. I am hardly the first author to advocate an interactive approach. For those who want to delve further into the details of this subject, I recommend Michael Rutter’s (2006) seminal volume Genes and Behavior.

In principle, gene-environment interaction theory is in the mainstream of contemporary psychiatry. The idea that diseases arise from interactions between constitution and experience can be traced as far back as the writings of Galen (Monroe and Simons 1991). However, as subdisciplines of psychiatry have become separate and have taken on a narrower vision, interactions have been downplayed. This is particularly true in clinical practice, where ideology too often trumps evidence.

A few words are also needed to explain what this book is not about. A great deal of research has been done concerning the precise mechanisms that mediate biological predispositions to mental illness. Yet in spite of all the progress made in recent years, we are still very far from defining how genes act on brain chemistry and connectivity. Therefore, although neuroscience is one of the “hottest” areas of research in psychiatry, this volume only deals with this subject peripherally. One can study genetic influences without knowing exactly how they affect neurotransmitters. Moreover, this is a fast-changing field, in which today’s breakthrough often becomes tomorrow’s blind alley. In the future, when these issues are better understood, we should be in a position to develop a model fully grounded in neurobiology.

In showing how the model can be usefully applied to a very wide range of psychopathology, I have had to review a very wide literature. Synthesizing this information requires making compromises between the needs of different readers. Specialists may find some sections lacking in detail. However, this book is primarily directed at practicing clinicians. Its aim is to show how the model should guide evidence-based practice. Most of the references in this book consist of research reports published in scientific journals, but it is impossible to review a complex literature without picking and choosing. Wherever my conclusions seem controversial, readers should pursue their own inquiries, making use of the extensive reference list provided at the end of this book.

In science, difficult problems are rarely settled by single studies. Only the overall weight of evidence allows firm conclusions. This is why I have referenced many of my conclusions with review articles or books, which are themselves summaries of the research literature. Wherever individual papers shed particular light on questions, I have highlighted them. But as I tell my students, no matter how impressive a research finding is, one needs to wait for a meta-analysis.

Lise Laporte read the entire manuscript and offered many useful suggestions for improvement. Laura Roberts, Erika Parker, and the American Psychiatric Association Publishing staff offered crucial help and support.