Locating Environmental Factors in Mental Disorders Within a Biopsychosocial Model

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What are the connections between environmental factors and the development of mental disorders?

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COMMENTARY

There have always been 2 kinds of psychiatry: 1 rooted in neuroscience and the other focusing on the impact of environmental adversities. In the past few decades, psychiatry has adopted a strong biological orientation in both research and practice. Although biological reductionism has come under criticism,1 it still dominates our discipline.

On the other hand, quite a few psychotherapists, both within psychiatry and in other disciplines, carry out a practice based on environmental theories. One is the idea that childhood trauma lies behind many mental disorders.2

A biopsychosocial (BPS) model describes a much broader picture than biological reductionism—one of nature and nurture interacting with each other to produce psychopathology.3 Most mental disorders can best be understood as the result of gene-environment reactions.4 That model of psychopathology can guide clinical work toward a comprehensive, evidence-based practice.

Behavior genetic research shows that virtually all common mental disorders have a moderate heritable component.5 Heritability has a larger effect in more severe disorders, such as psychoses, but still accounts for nearly half the variance in most mood and anxiety disorders. The other half of the variance may be shaped by life experiences; however, these findings leave plenty of room for environmental effects.

At the same time, environmental risk factors do not consistently determine a particular outcome. For example, posttraumatic stress disorder (PTSD), defined as a reaction to psychosocial stressors, occurs in only 5% to 10% of those who are exposed to traumatic events.2 Moreover, longitudinal follow-up studies of individuals who grew up with serious adversities in childhood show that only a minority go on to develop mental disorders.6,7

A useful variant of the BPS model is based on gene-environment interactions in what has been called “differential sensitivity to the environment.”8 Thus, some individuals are highly sensitive to stressors, usually based on trait neuroticism, while others are less sensitive and usually more resilient to adversity. There are many other sources of resilience, such as a supportive family environment and a well-functioning social network.4

Finally, social factors can also raise the risk for developing mental disorders.6,7 The most important example is low socioeconomic status, particularly when associated with poverty and bad neighborhoods. Although psychiatrists are clinicians who lack the expertise or the influence to ameliorate social risks, they need to keep these risk factors in mind when treating patients who have been disadvantaged.

Clinical Implications of the Biopsychosocial Model

Theories that focus exclusively on either biological or psychosocial factors in mental disorders can lead to misleading conclusions. Thus, the assumption that mood and anxiety disorders reflect some form of “chemical imbalance” leads to an overreliance in practice on psychopharmacological interventions. Similarly, the idea that trauma is the sole cause of PTSD (and of other common mental disorders) has supported psychotherapy methods that are not necessarily effective.2

In principle, psychiatrists have the advantage of having been trained both in drug prescription and in psychotherapy—yet they do not always take advantage of this broader education.

For example, major depression is diagnosed in a large number of patients we see on the basis of a very low bar (5 out of 9 criteria for only 2 weeks). Yet patients who are depressed are very heterogeneous, and some may not even have a diagnosable disorder.9 Patients with less severe depressions—who make up the majority of cases—carry a weaker genetic load and are more influenced by environmental precipitants. It is therefore logical to provide different treatment options for different forms of illness with different levels of biological or psychosocial risk factors.

Moreover, all these risk and protective factors interact with each other. For example, depression changes the brain and it interferes with the social connections that support resilience. Yet there is also evidence that cognitive behavior therapy for depression has more long-lasting benefits than antidepressant treatment.10

In summary, the assumption that a diagnosis of a mental disorder, by itself, provides sufficient information to make decisions about treatment is not supported by empirical research. In fact, our diagnostic manuals do not define any of their categories on the basis of treatment response. To consider an example of complex comorbidity, most patients with personality disorders are also depressed, while up to half of patients with depression also have a diagnosable personality disorder.11

There is also extensive and convincing literature showing that psychotherapy is effective for complex mental disorders shaped by a large environmental component.12 The effects of environmental risks are not simple, but rather a process that is complex and cumulative.4

Avoiding Environmental Reductionism in Psychotherapy

Environmental reductionism occurs when clinicians focus on life events without considering biology, which determines how patients vary in sensitivity to their environment. Those who consistently favor environmental causes may think that doing so provides a more hopeful prognosis, and that heredity implies irreversibility. But these conclusions are mistaken.

First, the mechanisms by which genes affect the mind are complex and indirect. Second, genetic influences on behavior are not usually fully independent of the environment. Third, individuals with problematic heritable traits can change in therapy.

It follows that clinicians always need to take individual differences into account. When the tailor has only 1 size, the customer should not have to pay for the adjustments. One of the strengths of the BPS-based gene-environment model is that it addresses individuality while leaving sufficient space for personal responsibility and choice.

In the future, psychological treatments will probably be based on this interactive approach, taking into account how the same experiences have different effects on individuals with different personality traits. It need not follow current fads, such as the attribution of all symptoms to trauma, whether such events are simple or complex.

Although it can be difficult to access, talking therapy is crucial for the management of many mental disorders. In a BPS model, psychotherapy would be based on a broader and truly complex view of treatment in which patients spend less time searching for past traumas and more time learning skills that will help them manage emotions and relationships.

Acknowledging the role of heritable traits need not be seen as “blaming the victim.” By taking both nature and nurture into account, we can avoid such attributions. Those with high trait neuroticism generally need more emotional support than others, and if that is not available in a family or other support system, we are more likely to see symptoms develop.

For most patients, effective therapy usually needs to focus less on past life events and more on current difficulties. That is why clinicians need to help teach patients how to move on from their past traumas, as described by the concept of “radical” acceptance.13

Those who seek treatment from clinicians for symptoms that emerge from environmental neglect or trauma need not focus totally on past sorrows. They need to maximize their free will and learn how to moderate their responses to adversity. Although some events always lie outside control, patients need to seek agency—the sense of being in charge of the trajectory of their lives.

Dr Paris is emeritus professor of psychiatry at McGill University in Montreal, Quebec.

References

1. Moncrieff J, Cooper RE, Stockmann T, et al. The serotonin theory of depression: a systematic umbrella review of the evidence. Mol Psychiatry; 2023;28(8):3243-3256.

2. Paris J. Myths of Trauma. Oxford University Press; 2023.

3. Engel G. The clinical application of the biopsychosocial model. Am J Psychiatry. 1980;137(5):535-544.

4. Rutter M, Moffitt TE, Caspi A. Gene-environment interplay and psychopathology: multiple varieties but real effects. J Child Psychol Psychiatry Allied Discip. 2006;47(3-4):226-261.

5. Jang KL. The Behavioral Genetics of Psychopathology: A Clinical Guide. Routledge; 2005.

6. Paris J. Nature and Nurture in Psychiatry: A Gene-Environment Model. 2nd ed. American Psychiatric Publishing; 2020.

7. Paris J. Nature and Nurture in Personality and Psychopathology: A Guide for Clinicians. Routledge; 2022.

8. Belsky J, Pluess M. The nature (and nurture?) of plasticity in early human development. Perspect Psychol Sci. 2009;4:345-351.

9. Horwitz AV, Wakefield JC. The Loss of Sadness: How Psychiatry Transformed Normal Sorrow Into Depressive Disorder. Oxford University Press; 2007.

10. Cuijpers P, Miguel C, Harrer M, et al. Cognitive behavior therapy vs. control conditions, other psychotherapies, pharmacotherapies and combined treatment for depression: a comprehensive meta‐analysis including 409 trials with 52,702 patients. World Psychiatry. 2023;22(1):105-115.

11. Friborg O, Martinsen EW, Martinussen M, et al. Comorbidity of personality disorders in mood disorders: a meta-analytic review of 122 studies from 1988 to 2010. J Affect Disord. 2014;152:1-11.

12. Markham M, Lutz W, Castonguay L, eds. Bergin and Garfield’s Handbook of Psychotherapy and Behavior Change. 7th ed. Wiley; 2021.

13. Linehan MM. Cognitive Behavioral Therapy for Borderline Personality Disorder. Guilford; 1993.

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