Multidimensional Approaches to Understanding Mental Illness

Learning Objectives

  • Explain why unidimensional explanations of mental disorders are insufficient
  • Explain the interaction between biological, psychological, and social factors in the development of psychopathology
  • Describe how the diathesis-stress model and gene-environment correlation models explain the etiology of mental disorders

Problems with Unidimensional Models in Understanding Mental Illness

The interior dashboard and steering wheel of a car.

Figure 1. Just as a car is a system of parts working together, our brains and bodies are complex systems with a multitude of parts and pieces. Mental disorders do not have any single, simple biological or psychological explanations but are systemic outcomes, influenced by multiple factors, including biological, psychological, social, and cultural forces that regularly interact.

A system is a set of elements that interact or are interdependent on one another, but forms a coherent whole and interacts with its environment and/or other systems. For example, the car or bus you use for transportation is a mechanical system. It has multiple parts that interact such as the fuel system, the electrical system, the engine, the drive train, the wheels, etc. All these parts work together in a unified way to create movement and speed. If any part of the system fails, such as the engine, the electrical system, or the wheels, the system experiences dysfunction and may no longer work well. In this example, the car is a system and its purpose is transportation or movement. Cars or buses interact with street systems, highway systems, traffic patterns and so, forth as well as gas stations and more, which represent other, larger systems of which it is a part. Similarly, our own bodies are biological systems made up of interdependent parts.

Our brains, heart, circulatory system, respiration, digestion, etc., are all interdependent parts that work together. If one part of the system becomes damaged or disabled such as by high blood pressure, diabetes, or a broken leg, it affects the entire system. Our body/biological systems together make life, and of course, we interact with our environment and many other social systems around us such as the medical system, families, schools, churches, and more.

Multidimensional Approaches to Mental Disorders

X-ray type image of a person showing their brain in front of a magnified image of neural activity.

Figure 2. Multidimensional approaches to explaining behavior contend that mental illness is not simply caused by “chemicals in the brain.”

Understanding how systems work, and how interdependent the parts are, helps us to realize why simplistic, unidimensional explanations of mental disorders such as that they are caused by a “chemical imbalance”—a reductionistic or overly simplified biological explanation—or alternatively, that they are caused by a negative relationship with one’s mother—an overly simplified psychological and social explanation—are inadequate to fully understand the disorder and its causes. Unidimensional explanations limit both our ability to understand how a mental disorder develops and may limit our ability to find effective treatments. If we are to make progress in reducing stigma against the mentally ill and improving the effectiveness of treatments, we need to begin by seeking to understand more multidimensional models and consider how multiple systems interact in contributing to mental disorders.

To be fair, there are a few specific conditions that mimic mental disorders that can be attributed to a single, unitary cause. An example of this is untreated syphilis, which can spread throughout the body, creating damage in multiple organ systems, including the brain, and lead to psychosis and dementia, possibly even death. However, these types of conditions today are rare, and would not be classified as mental disorders because they are thought of more as medical conditions with biological treatments. In contrast, mental disorders such as attention deficit hyperactivity disorder, major depression, anorexia nervosa, or schizophrenia do not have any single, simple biological or psychological explanation; they are systemic outcomes, influenced by multiple factors, including biological (genetics, hormones, neurotransmitters, and other systems), psychological (learned behaviors, attitudes, emotional responses, cognitive, or social developmental stage), and social and cultural forces (social support or lack of it, rejection, stress) that frequently interact.

For instance, there are some studies that implicate prenatal exposure to a virus, which has cultural implications as well as biological, in the development of some forms of schizophrenia. Epigenetics is a newer field of study shedding light on how social, psychological, and environmental influences can actually change which genes in a person’s DNA may activate or may be turned off, having significant implications for the development of disorders. Epigenetic effects are a normal part of human development. Every cell in your body has the same DNA, the same genetic code for an entire human being. But as cells develop in the body, they become specialized, meaning that some genes may be activated in some cells and not in the other cells. A good example are the genes that allow cells to detect light; these are turned on or activated in your eye cells, but are turned off or deactivated in all other cells.[1] Thus, it is not surprising that some environmental events or experiences may activate or deactivate specific genes that may increase or decrease (in the case of protective factors like positive social support) the chance someone may develop a mental disorder. Environmental epigenetic effects do not change the DNA itself but influence the expression of our genes. Thus, it is clear that both nature and nurture are relevant to all forms of mental disorders, not just one or the other.

This modern, multidimensional approach to understanding mental disorders can help us to avoid labeling persons with mental disorders (or even medical illnesses) as being due to just one cause, thereby reducing stigma. We need to approach each person individually and seek to understand their own biological, psychological, and social history to better understand them and their symptoms. You will learn later in this module that most approaches to the treatment of mental disorders arose from unidimensional perspectives on mental disorders; clinicians today (and researchers), even when they may focus on a particular approach or way of treating a mental disorder, will better serve their clients by recognizing that they are approaching only one element of a system and be open to new information and thorough in their assessments.

The next several sections of this module will focus on describing different “models” that explain how mental disorders occur. We begin by exploring multidimensional models and then will explore unidimensional parts or elements of the biopsychosocial system. These elemental models are important because they reflect the history of scientific attempts to understand the etiology of mental illnesses in a coherent way. Newer models built on older ones or were reactions against previous thinking. Although most of them are unidimensional and therefore limited, they each explore different aspects of the whole multidimensional picture and can be useful when we think about what each of them teaches us. These models also lead to the development of different treatment approaches or “orientations.”

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The Biopsychosocial Model

Pie chart showing three equal sections—biological, psychological, and social/cultural

Figure 3. The biopsychosocial model emphasizes the interaction between biological, psychological, and social/cultural forces.

The major multidimensional model that is useful in understanding the causes of mental disorders is usually called the biopsychosocial model (BPS). The biopsychosocial model (BPS) was first proposed by George L. Engel and Jon Romano of the University of Rochester in 1977. As opposed to the medical model, which emphasizes mental illness as disease, this model aimed for a more holistic approach by recognizing that each patient has their own thoughts, feelings, and history. In developing the model, Engel framed this model for both medical illnesses and mental problems.

Specifically, Engel revolutionized medical thinking by removing the supposed separation of body and mind. The idea of mind-body dualism goes back at least to the French philosopher René Descartes in the 17th century, but was forgotten during the emergence of the biomedical approach, which largely ignored individual psychological and social development. Engel emphasized that the biomedical approach is flawed because the body alone does not contribute to illness. Instead, the individual’s mind (psychological and social factors) plays a significant role in how an illness is caused and how it is treated. Figure 3 presents a simplified graphical representation of the biopsychosocial model, emphasizing the interaction of all three elements. This model could be used, for example, by clinicians as a way to make sure they are evaluating the medical or genetic conditions a person may have while also exploring the person’s psychological experiences and upbringing, and their social and cultural environmental stresses to better understand them. Researchers could use this model as a general way to think about specific research findings, or to explore the interactions between these three major elements of the model.

In the biopsychosocial model (BPS), the biological element can include such things as genetic inheritance related to risk of developing a disorder, malfunctions or disruptions of the system of neural transmission between neurons in the brain, potential damage to parts of the brain, infections or diseases that might affect brain or nervous system functioning, and hormonal influences or brain-hormone interactions, among others. As noted above, epigenetic research has found that environmental stressors or events, especially those occurring early in life, may interact with a person’s genome (set of all our genes in our DNA), creating expanding biological effects.

The psychological element of the BPS includes a wide range of thoughts, feelings, and behaviors including things like: learned behaviors (conditioning or observed behaviors), thought patterns that increase or intensify emotions like sadness or anxiety, events occurring during key developmental stages in life, strengths and weaknesses in ability to cope with different life stressors, sense of confidence or self-efficacy, personality or cognitive development, and more.

The social/cultural element of the BPS involves a wide range of external situations that can shape how people respond to events and other people, often by influencing the degree of stress a person experiences in their life. These can include experiences of abuse, being a victim of a crime, experiencing racism and discrimination, poverty, war, the impact of cultural expectations and demands, state of physical health and nutrition, levels and type of stress in the environment (rural living versus city living, for example), extent of social support network (friends, family, and others one can turn to for help and comfort), and more.

Predisposed for anxiety?

Consider Erin. Erin is born into a family that has strong genetic connections to anxiety. Several of her family members have diagnosable mood and anxiety disorders. Does this mean that Erin will develop a phobia or panic disorder?

Erin likely inherited at least some genes that may make her more likely to react strongly to life events and may shape how her body’s stress response works. A lot may also depend on how her parents raise her, as well as the behaviors she sees her family and friends exhibit as she grows up; do they demonstrate effective coping reactions to stress and frightening experiences or do they strongly react to situations and increase symptoms by trying to avoid frightening situations? Do her parents teach her that life is dangerous and unpredictable and that she needs to be on her guard all the time, or do they encourage her to explore, demonstrate how to cope with events that happen, and provide emotional support?

It may also depend a lot on where she lives, whether she experiences severe negative events in life, is discriminated against, or teased and bullied by kids at school. This is only a small set of possible alternatives that could happen in Erin’s life, and it is fairly easy to see that whether or not she would develop an anxiety or mood disorder could be influenced by the interaction of these biological, psychological, and social forces. Don’t forget that epigenetics would also suggest that it is possible that depending on her life experiences, the way her brain and hormonal systems function might also change as a result, either increasing or decreasing her likelihood of developing a disorder.

In addition, it is important to realize that the particular patterns of how the biopsychosocial model functions also vary by the disorder. Some disorders have a heavier influence due to genetic and other biological factors while other disorders are more heavily influenced by social or psychological elements. If you examine Figure 4(a) for depression, you’ll see that biological elements have slightly greater influence on how a person’s life will turn out than the other elements, although both the psychological and social/cultural elements still play major roles. In contrast, in Figure 4(b), biological elements have a significantly smaller role in the development of eating disorders while social/cultural and psychological elements have a stronger influence. Even with a condition such as schizophrenia (see Figure 4(c)) which is often incorrectly thought of by many as a “mental disease,” the biological elements still contribute less than 50% of the influence on whether a person will develop the disorder or not. This statistic is based on multiple studies demonstrating that the concordance rate between identical twins is less than half, a measure of the likelihood of an identical twin developing schizophrenia if the co-twin already has it. Said another way, this means that more than half of the time, even with a strongly biologically influenced disorder, an identical twin, a person with identical genes, will not develop schizophrenia. Clearly, social/cultural and psychological elements also play important roles even in this case, and it is possible that epigenetics also has some influence. You will learn more about these issues in later modules.

Three pie charts showing showing the balance between biological, psychological, and social/cultural components for depression, eating disorders, and schizophrenia. For Depression, biological is 40%, and psychological and social/cultural make up 30% each. For eating disorders, there is a large portion of social/cultural influences (45%), and 35% psychological, and 20% biological. For schizophrenia, the breakdown is roughly 48% biological, 30% social/cultural (stigma, stress), 22% psychological.

Figure 4. (a) Depression has strong biological elements to it, but psychological and social/cultural forces also make significant contributions. (b) Eating disorders are more widely influenced by social and cultural factors. (c) Schizophrenia is the most biologically/genetically influenced set of disorders in this example; however, even with schizophrenia, there is evidence that psychological and social/cultural forces can impact on symptoms and prognosis (future course of the disorder).

Clearly, the biopsychosocial multidimensional model is very useful at helping us understand the elements that contribute to mental disorders in a more complete and useful way, but it does not specifically explain how a person like Erin might actually develop a disorder. Fortunately, two BPS-related models have emerged that give us insight into this situation:  the diathesis-stress and gene-environment correlation models.

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This video further explains what some of the biological, psychological, and social factors are that all interact in contributing to our mental wellness.

You can view the transcript for “biopsychosocial model” here (opens in new window).

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The Diathesis-Stress Model

The biopsychosocial model gives a broad, general idea of how the three major elements all interact with each other to produce mental disorders. The diathesis-stress model, first applied to schizophrenia by Paul Meehl in the 1960s, is more specific and helps us understand why one person might develop a disorder, or why two people from similar backgrounds might develop different disorders. The term diathesis comes from the Greek word meaning “predisposition.” Professionals sometimes talk about “vulnerability” to a disorder, but these terms are all interchangeable. The key assumption of the diathesis-stress model is that both factors, diathesis (usually genetic or biological) and environmental stress, are necessary in the development of a disorder. It is important to note that a large range of differences exists among individuals’ vulnerabilities to the development of a disorder and that the brain and how it functions, contrary to popular belief, continue to change over the lifespan, even at the genetic level, in response to environmental events (Durand & Barlow, 2013).[2]

A given person’s diathesis or vulnerability to developing a mental disorder represents the person’s pre-existing risk or probability of developing a mental disorder if they are exposed to sufficient stress. For example, a person who grew up in a family with a long history of alcoholism and drug use is much more likely to develop a substance disorder than a person raised in a family with no such history. Diathesis is often thought to refer to genetic, biological, and physiological conditions such as variations in genes or combinations of multiple genes that increase the chance for someone to develop a disorder, but they can also include cognitive, personality-related, and even environmental factors (such as loss of parent early in life). However, remember that there is no simple genetic inheritance that leads to a mental disorder; having a vulnerability or a diathesis for a disorder does not mean the person will actually develop the disorder.

For example, let’s assume that the diathesis for a person with a strong family history of alcoholism may include biological effects perhaps like an attraction, stronger than most, for the taste of alcohol, and/or that alcohol has a stronger and more immediate impact on the brain than is true for someone else. However, a lot depends on the interaction with environmental stress. If the person who inherits this diathesis learns alternative ways to cope with stress in their life (rather than drinking) and never, or rarely, drinks alcohol, they may never become an alcoholic. However, if the person follows the example of family members, takes up drinking at a young age, and uses drinking to cope with job loss, relationship problems, and so forth, that person is much more likely to develop alcohol dependence.

Similarly, someone could be exposed to significant life stressors, meaning life events that disrupt a person’s stability or functioning in life, and not develop a disorder, if they do not have a diathesis or vulnerability to a disorder or if that diathesis is weak. For example, someone who comes from a family with no history of alcoholism or addiction, may drink and party in college, drink occasionally through life, and may experience divorce, chronic illness, and/or a motor vehicle accident and not develop alcohol dependence. This is because the diathesis-stress model also presumes that for each person there is a threshold, a point at which the person’s coping abilities and social, psychological, and biological defenses cannot manage their level of life stress; when the combination of a diathesis/vulnerability and life stress exceeds the person’s threshold, they will develop a disorder that aligns with their vulnerability.

Stick broken in half

Figure 5. The diathesis-stress model can be compared to a stick that breaks under strain.

Think of picking up a stick on a walk. If you hold the stick in your hands and bend it, it does not immediately break. It may bend and experience strain until it reaches a threshold point at which it will break. Now consider all the factors that may cause that threshold to vary from stick to stick:  is the stick green (not dried out), the thickness of the stick, the type of wood the stick comes from, and so on. Each stick will have its own distinctive threshold for how much stress it can take before it breaks.

Water bucket overflowing with water.

Figure 6. Another metaphor to understand the diathesis-stress model is that of a bucket. Buckets may be of varying sizes and come with different amounts of material already inside, and stressors that cause the water to overflow may trigger a mental disorder in someone who is vulnerable.

Another common metaphor for understanding the diathesis-stress model is the visual image of a bucket filling with water. Genetics influence the size of the bucket we have or the amount of the material that is already inside of the bucket. Life stressors and other events can add water to the bucket, while coping mechanisms and positive experiences can open taps on the bucket to remove some of that stress. We can think of genetic/biological diathesis as the sand that is already inside of the bucket. The larger that vulnerability, the less life stress (the water on top) is necessary to exceed the threshold and trigger the disorder. The reverse is also true; if a person has a very low vulnerability to a particular disorder, the same amount of stress will not exceed the threshold and no disorder will be triggered. Alternatively, the person would have to experience a significant and large amount of stress to exceed the threshold which is possible, but not as likely. This model reinforces the importance of understanding how nature and nurture interact in the etiology of mental disorders.

There are a few other aspects of the diathesis-stress model that are worth considering. Protective factors, such as positive parent-child relationships, positive social networks, effective coping strategies or high self-esteem, can counteract the effects of stressors and prevent or curb the effects of disorder. Many psychological disorders have a window of vulnerability, during which time an individual is more likely to develop the disorder than others. For these reasons, diathesis-stress models are often conceptualized as multi-causal developmental models, which propose that multiple risk factors over the course of development interact with stressors and protective factors contributing to normal development or psychopathology.

The development of the diathesis-stress model was a significant advance from the biopsychosocial model in helping to understand how people would vary in their symptoms and diagnoses even if they had similar genetics or came from similar environments. However, the model was still based mostly in a simple additive idea: the biological diathesis (vulnerability) plus the amount of environmental stress experienced would cause a disorder if it was enough to cross the threshold. A newer model called the gene-environment correlations model or rGE[3], emphasizes, even more, the interactions that can occur between a person’s biological elements (genetics, neurotransmitter systems, brain development) and the psychosocial and cultural environment.

Gene-Environment Correlation Models

The rGE (the little r is the statistical symbol for correlation) model and related studies have greatly expanded since the decoding of the human genome was finished in 2003, creating the possibilities of new research into genes and genetic variants (alternative copies of the same gene such as genes that code for brown eyes versus blue eyes) and how they interact with the environment. However, because this field is rapidly evolving, there are still areas of controversy and new information is emerging regularly.

A review of 315 studies conducted through 2015 found that a large number of them (67–83%) showed significant interactions between genes and the environment. The gene-environment correlation model (rGE) is defined as the tendency of individuals to select and/or generate their environment based on genetic features that influence behavior, thoughts, and feelings[4].

In other words, instead of the simple diathesis-stress additive model of a diathesis plus sufficient stress to cross the threshold producing a disorder, the rGE model has demonstrated evidence that a person’s genetically influenced personality traits and behaviors may either select for or create the stressful life events or experiences that exceed the threshold and trigger the diathesis. The rGE model differs from epigenetics which emphasizes the influence of environmental forces on genetic expression, although that field has also greatly benefited from the mapping of the human genome. Some evidence suggests that cultural forces may also be involved, although this is not yet fully understood. Leighton and colleagues (2017) noted that some gene-environment interactions are robust in western nations like the United States, but have not been replicated in eastern nations. They further concluded that there is an increasing consensus among experts that “most common psychiatric disorders, such as depression and anxiety, are best explained as complex disorders involving dysfunctions in several biological systems in interaction with environmental factors” (p.2).[5].[/footnote]

As an example of how the rGE model works, Jaffee and Price (2007)[6] described a study conducted in 2006 that found that persons with a variant gene that conveyed high risk (diathesis) for alcoholism also showed personality traits, such as less desire to please other people, that increased their risk for a diagnosis of antisocial personality disorder. These personality traits are more likely to lead to disrupted relationships and increased social isolation as well as life events that could generate stress including divorce, never marrying, and potential criminal behavior that could increase a desire to drink, exceeding the threshold and triggering the underlying vulnerability to alcohol dependence.

In the diathesis-stress and gene-environment correlation models, we see the evolution and increased complexity of the biopsychosocial model over time; at the same time, this more complete understanding of the mechanisms involved in how biological forces interact with and are shaped by environmental influences (including psychological and social/cultural elements) holds out promise of greater understanding and new treatments to come. These models also reinforce the inadequacy of simplistic unidimensional explanations of mental disorders, like the “chemical imbalance” explanation. That said, we will now explore different elements of the biopsychosocial model and the treatment approaches they have generated over time.

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concordance rate: the percentage rate of twins sharing a particular attribute

diathesis-stress model: suggests that people with a predisposition or vulnerability for a disorder (a diathesis) are more likely to develop the disorder when faced with stress; it is one model of psychopathology

epigenetics: the study of how social, psychological, and environmental influences can actually change which genes in a person’s DNA may activate or may be turned off—a change in phenotype without a change in genotype

gene-environment correlation model (rGE): is defined as the tendency of individuals to select and generate their environment based on genetic features that influence behavior, thoughts, and feelings

multidimensional models: explanations involving multiple approaches or interacting elements

system: a unified whole made up of parts that interact and are interdependent with each other

  1. Shrindhar, N. & Walker, L. (August, 2016). Gene-environment interactions and epigenetics. Retrieved from:
  2. Durand, V. and Barlow, D., 2013. Essentials of Abnormal Psychology. 6th ed. Wadsworth: Cengage Learning.
  3. Jaffee, S.R. & Price, T.S. (2007, May). Gene-environment correlations: A review of the evidence and implications for prevention of mental illness. Molecular Psychiatry, 12(5), 432-442. doi:10.1038/ PMC 3703541.
  4. Leighton, C., Botto, A., Silva, J.R., Jiménez, P.J., & Luyten, P. (2017). Vulnerability or sensitivity to environment? Methodological issues, trends, and recommendations in Gene-Environment interactions research in human behavior. Frontiers in Psychiatry, 8(106), 1–14
  5. [footnote]Leighton, C., Botto, A., Silva, J.R., Jiménez, P.J., & Luyten, P. (2017). Vulnerability or sensitivity to environment? Methodological issues, trends, and recommendations in Gene-Environment interactions research in human behavior. Frontiers in Psychiatry, 8(106), 1–14.
  6. Jaffee, S.R. & Price, T.S. (2007, May). Gene-environment correlations: A review of the evidence and implications for prevention of mental illness. Molecular Psychiatry, 12(5), 432–442. doi:10.1038/ PMC 3703541.