biopsychosocial model of health essay

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Understanding the Biopsychosocial Model of Health and Wellness

A holistic approach to well-being

Maskot/Getty Images

The Three Aspects of the Biopsychosocial Model

How the Biopsychosocial Model Impacts Mental Health

Criticism of the Model

How Healthcare Professionals Use the Biopsychosocial Model

How clients and patients can use the biopsychosocial model.

The biopsychosocial model is an approach to understanding mental and physical health through a multi-systems lens, understanding the influence of biology, psychology, and social environment. Dr. George Engel and Dr. John Romano developed this model in the 1970s, but the concept of this has existed in medicine for centuries.

A biopsychosocial approach to healthcare understands that these systems overlap and interact to impact each individual’s well-being and risk for illness, and understanding these systems can lead to more effective treatment. It also recognizes the importance of patient self-awareness , relationships with providers in the healthcare system, and individual life context.

Dr. Akeem Marsh, MD , physician and author of Not Just Bad Kids , described the biopsychosocial model as “at its core, centering around social determinants of mental health in connection with the ‘standard’ biomedical and psychological models. One of the more common ways in which it is represented when using the model is through the four ‘Ps’ of case formulation: predisposing, precipitating, perpetuating, and protective factors.”

Learn more about how providers can use the biopsychosocial model to offer holistic care and how clients and patients can benefit from this approach.

What Are the Three Aspects of the Biopsychosocial Model?

When understanding an individual’s physical and mental health through the biopsychosocial model, we consider physiological factors such as genetics and illness pathology (biological); thoughts, emotions, and behavior (psychological); and socioeconomic components, social support, and culture (social). How do each of these components inform the model as a whole?

“Biology” refers to our genetics , physical health, and the functioning of our organ systems. Our physical well-being impacts our mental health for multiple reasons. First, our brain is an organ and can become unwell just like any other organ. Second, physical health conditions can wear on mental health. For example, chronic pain can lead to symptoms of depression.

Additionally, just like we can have genetic predisposition to a physical disability, mental health has genetic roots as well. According to Dr. Marsh, “Genetics are the most basic level by which mental health is influenced, and on some level has an impact for everyone.” In other words, “Whatever the phenotypical expression, genetics does play a role to some degree.” The expression is in turn influenced by the environment.

Psychological

Mental health is health, and one’s psychological well-being impacts both mental and physical health. Unhealthy and maladaptive moods, thoughts, and behaviors can all be symptoms of mental health conditions, and in turn can contribute to our overall health. Mental health and behavior can be cyclical; for example, an individual who self-isolates as a symptom of depression may experience increased depressive symptoms as a result of isolation.

Routine physical activity is known to promote positive mental wellness, while inadequate or excessive physical activity can contribute to different types of mental health struggles.

Addressing these symptoms is key in improving mental health.

Dr. Marsh shares the impact of external factors on health: “The expression [of genetics] is in turn influenced by environment.” Changes in one’s environment can impact mental health, both positively and negatively. In the previous example of depression and isolation , individuals who have appropriate social support experience fewer mental health issues compared to those without this support.

An individual who is struggling with their mental health might need social support and environmental changes just as much as they need therapy or medication intervention for their symptoms.

Traditionally, healthcare has focused primarily on the medical and biological side of the patient’s needs, and mental health care has focused on the psychological side. While it makes logical sense to address manifesting symptoms, a holistic approach to care that aims to address the social as well as the psychological and biological contributions to illness can be more health-promoting.

Sometimes, for instance, addressing an underlying social need or environmental stressor can improve mental health more effectively than other psychological or biological treatments. This may allow for less-invasive treatments and interventions, and it can improve the individual’s well-being in a way that non-holistic models overlook.

Criticism of the Biopsychosocial Model

Although many providers support a holistic approach to care and implement the biopsychosocial model in practice, like any model it has limitations. Dr. Marsh notes that there are concerns about its evidence backing: “Some people believe that [the biopsychosocial model] is not scientific, as in it has not quite met the ‘gold standard’ of being validated through multiple randomized trials, as it is a uniquely challenging study prospect.” How can researchers study controlled variables in a model that requires holistic care that takes individual needs into account?

At the same time, the model has many strengths and can benefit patients in the healthcare and mental health systems: “It has been researched extensively and shown positive results when applied in different ways,” Dr. Marsh said.

Mental health professionals who utilize the biopsychosocial model in practice include extensive medical history, family history, genetics, and social factors in assessments in addition to psychological information.

Additionally, they use this information to ensure that all of the client’s needs are met , as many medical issues can manifest with mental health symptoms. Therapy services to treat, for example, depression caused by an under-functioning thyroid is unlikely to be effective.

When adopted appropriately, health professionals conceptualize patients that they work with in a broad context that attempts to understand and see patients as a whole person—complex human being with nuance, so much more than just a cluster of symptoms or diagnosis.

This model lets providers see the whole person beyond their presenting symptoms.

While the biopsychosocial model has its place in the healthcare and mental healthcare systems, individuals might also implement tenants of this model in their own lives. This means being aware of how environmental factors impact their mental and physical health, as well as how their genetics and medical history in turn influence behaviors, thoughts, and emotions.

It can help individuals better understand themselves as complex, whole beings as well. “I believe that [the biopsychosocial model] could enhance their self-awareness and understanding of themselves, along with broadening their personal sense of what issues or challenges may be going on with them," says Dr. Marsh.

Engel GL. The need for a new medical model: a challenge for biomedicine . Science . 1977;196(4286):129-136. doi:10.1126/science.847460

Soltani S, Kopala-Sibley DC, Noel M. The co-occurrence of pediatric chronic pain and depression: a narrative review and conceptualization of mutual maintenance . The Clinical Journal of Pain . 2019;35(7):633-643. doi:10.1097/AJP.0000000000000723

Alsubaie MM, Stain HJ, Webster LAD, Wadman R. The role of sources of social support on depression and quality of life for university students . International Journal of Adolescence and Youth . 2019;24(4):484-496. doi:10.1080/02673843.2019.1568887

By Amy Marschall, PsyD Dr. Amy Marschall is an autistic clinical psychologist with ADHD, working with children and adolescents who also identify with these neurotypes among others. She is certified in TF-CBT and telemental health.

Biopsychosocial Model: Examples, Overview, Criticisms

Viktoriya Sus (MA)

Viktoriya Sus is an academic writer specializing mainly in economics and business from Ukraine. She holds a Master’s degree in International Business from Lviv National University and has more than 6 years of experience writing for different clients. Viktoriya is passionate about researching the latest trends in economics and business. However, she also loves to explore different topics such as psychology, philosophy, and more.

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Chris Drew (PhD)

This article was peer-reviewed and edited by Chris Drew (PhD). The review process on Helpful Professor involves having a PhD level expert fact check, edit, and contribute to articles. Reviewers ensure all content reflects expert academic consensus and is backed up with reference to academic studies. Dr. Drew has published over 20 academic articles in scholarly journals. He is the former editor of the Journal of Learning Development in Higher Education and holds a PhD in Education from ACU.

George Engel first articulated the b iopsychosocial model in 1977, proposing that understanding a person’s medical condition requires assessing not only their biology but also psychological and social influences.

The biopsychosocial model encompasses three primary elements: physiological, psychological, and sociocultural aspects.

For example, biological factors can include a person’s age, genetic makeup, health history, and gender. Psychological influences can include the individual’s emotions, thoughts, and behavior.

Finally, social aspects like economic status, family relationships, and access to healthcare services can drastically alter one’s choices.

This method emphasizes that people possess unique well-being needs, recognizing the interrelationship of these three components for optimal care.

By taking a comprehensive approach to patient healthcare, medical practitioners can understand the root causes of illness, thus enabling them to craft individualized care plans.

Overview of the Biopsychosocial Model

A biopsychosocial model is a holistic approach to understanding health and illness considering multiple influences. It recognizes the interplay between biological, psychological, and social factors on health throughout a person’s lifespan (Bolton & Gillett, 2019).

Through this model, practitioners can gain insight into how physical, psychological, and social stressors can interact to affect an individual’s overall health.

According to Erb and Schmidt (2021), a biopsychosocial model:

“…is a general model of care, positing that biological, psychological (i.e., thoughts, emotions, and behaviors), and social factors all play a significant role in human functioning in the context of disease or illness (p. 29).

While traditional medical models focus purely upon problems’ pathological origins, this alternative considers multiple aspects beyond mere biological cause.

This method focuses on comprehending how combined biological, psychological, and social aspects can affect our well-being.

Kusnanto and colleagues (2018) state that:

“…the biopsychosocial model is an ideal representation of science and humanism in medical practice, although many argue that the model is hard to implement” (p. 497).

Integrating mental, physical, and social factors into patient care can be arduous. Its primary goal is to give a complete view of patient care by concentrating on nurturing the individual as an entirety rather than solely focusing on their medical symptoms.

For example, a person suffering from persistent pain could find relief through integrated physical and psychological therapies, along with the assistance of their psychologist. The treatment plan must always be carefully tailored to an individual’s needs accordingly.

Simply, the biopsychosocial model allows practitioners to understand the root causes of ailments or discomfort, enabling them to create more tailored treatment strategies.

Three Components of the Biopsychosocial Model

The biopsychosocial healthcare model comprises three interrelated components: biological, psychological, and social (Landow, 2006).

Let’s look at each of these components:

1. Biological Component

This component refers to the physiological and genetic characteristics of the individual that affect his health. It includes predisposition to certain diseases, immune system, age, gender, and other biological factors.

For instance, hereditary factors may make a patient with a family history of type 2 diabetes more prone to developing the disorder.

2. Psychological Component

The psychological aspect covers the patient’s emotional and psychological state, including stress, anxiety, mood, and consciousness.

Psychological factors can influence health through behavioral and cognitive processes.

As in the first case, in a patient with a chronic condition such as arthritis, increased stress levels can increase pain and cause depression.

3. Social Component

This component affects the social environment and cultural factors that affect human health.

For example, it may include health care availability and quality, family support, economic status, and educational attainment.

A patient with low socioeconomic status may have limited access to quality health care or a healthy diet, leading to chronic diseases.

Biopsychosocial Model Examples

Eating Disorders : The biopsychosocial model offers invaluable insights into the development of eating disorders, such as anorexia nervosa, bulimia nervosa, and binge eating, by exploring their biological, psychological, and social nuances. Evidence affirms that these conditions cannot be attributed to any cause but rather a combination of factors from several domains. So, treatment plans must look at all aspects of an individual’s condition rather than solely focusing on physical symptoms.
Anxiety Disorders : Anxiety can be attributed to biological, psychological, and social factors. Thus, by blending biological elements such as neurotransmitter imbalances with psychological approaches like cognitive behavioral therapy (CBT) and social paradigms , including supportive networks – it is achievable to mitigate the symptoms of anxiety conditions, for example, panic disorder or OCD.
Depression : This psychological condition can be caused by various components, such as genetics, hormone imbalances, detrimental thought patterns and environmental pressures. An effective treatment should take into consideration each of these contributing aspects to successfully tackle depression symptoms.
Addiction : Addictive behaviors may have a biological base due to chemical imbalances in the brain or genetic predispositions. Still, they can also be triggered by personal struggles or difficult situations in a person’s life. So, before developing a treatment strategy, it’s important to consider all the contributing factors to an individual’s addiction.
Chronic Pain : If you experience persistent pain, there is likely to be a physiological cause. Additionally, psychological and environmental elements can contribute to distress. To successfully handle chronic soreness requires physical treatments that address the root of your condition and cognitive-behavioral strategies designed to lessen its emotional impact while receiving support from family members or friends.
Heart Disease : Biological risk factors like smoking or high cholesterol levels and psychological elements like stress and lack of physical activity can contribute to this chronic condition. Understanding these different components helps healthcare professionals create comprehensive prevention plans for individuals at risk of developing heart disease.
Autism Spectrum Disorders : Like many other conditions, ASD can be the result of biological factors such as neural development or genetic makeup. Psychological issues, including anxiety, or social problems, such as communication or social interaction difficulties, can also influence it. Integrating all of these components into treatment plans can help to improve the lives of those struggling.
ADHD/ADD : Biological causes, like an increase in certain neurotransmitters levels alongside environment elements e.g. absence/or not enough parental monitoring and inadequate nutrition are known causes culminating to Attention Deficit /Hyperactive disorder (ADHA/ADD). So, treatment plans should take all of these factors into consideration to help those affected by this condition.
Schizophrenia : This mental disorder is associated with multiple biological changes in the brain and possible genetic influences. However, social factors, including trauma or relationship issues, may trigger its onset or exacerbate existing symptoms. Thus, creating an effective treatment plan should include assessing these contributing components.
Insomnia : Studies suggest that there are both physical and emotional drivers behind insomnia. Thus, if you have insomnia, a comprehensive treatment plan should include not just lifestyle interventions such as reducing caffeine and alcohol intake. In addition, consider taking some form of mental health guidance such as CBT (cognitive behavioral therapy) aimed at detecting and addressing underlying emotions capable of disrupting adequate slumber.

Origins of the Biopsychosocial Model

In the 1970s, George L. Engel – an American psychiatrist – proposed a biopsychosocial model as an alternative to the biomedical model that was then prevailing (Smith, 2002).

The biomedical model focused exclusively on the physical and biological aspects of the disease. It marked the beginning of a revolutionary new era in psychiatry and medicine.

Still, this model took a reductionist approach and only looked at the disease from an anatomical, physiologic, and chemical perspective of the body. Thus, psychological and social influences were disregarded.

According to Smith (2002), based on various studies and clinical experience, Engel proposed the biopsychosocial model to combine diseases’ biological, psychological, and social aspects.

This model emphasizes the significance of taking into account all three elements in combination in order to gain a comprehensive insight into diseases and their causes.

Over time, the biopsychosocial model has earned immense global recognition from researchers.

It found considerable traction in many current approaches to diagnosing, curing, and averting ailments ranging from psychological conditions to chronic illnesses.

Criticisms of the Biopsychosocial Model

While the biopsychosocial model may look a promising unified approach to patient treatment, its ambiguity in terms of outcomes, lack of unity amongst practitioners, and its complexity have been heavily criticized.

Here are some key criticisms of this model:

Lack of c larity and s tructure : One major criticism of the biopsychosocial model is its relative uncertainty and absence of structure. The lack of clear boundaries and criteria for each component (biological, psychological, and social) can make developing and evaluating standard treatment techniques challenging (Carey et al., 2014).
Lack of unity : The biopsychosocial model is often seen as an alternative to the biomedical model but is not always integrated with it. This separation can lead to interaction problems between specialists in different fields and a lack of a unified treatment strategy.
Complex ity : Measuring and evaluating psychological and social factors can be complex and subjective. Determining the relationship between these components and diseases can take time, creating difficulties in developing and evaluating treatment effectiveness (Carey et al., 2014).
Resource limitations : The biopsychosocial model requires a broader and deeper approach to treatment, which can require significant resources and time. Implementing such an approach can be challenging, especially with limited budgets and overburdened healthcare facilities.

To gain insight into every aspect of one’s well-being requires a comprehensive perspective such as what’s provided by the biopsychosocial model.

This evidence-based approach helps us gain greater insight into how physical and mental issues come about – giving us an invaluable tool for improving our overall health.

Developed by George Engel in the late 1970s, healthcare practitioners have widely adopted this model due to its comprehensive and integrative approach.

Despite its advantages, the biopsychosocial model has been criticized for its lack of certainty, structure, unity, complex process, and resource limitations.

Still, it serves as a significant means of comprehending and dissecting physical and mental healthcare challenges, whilst devising potent treatments for multiple conditions.

Bolton, D., & Gillett, P. G. (2019). The biopsychosocial model 40 years on. In www.ncbi.nlm.nih.gov . Palgrave Pivot. https://www.ncbi.nlm.nih.gov/books/NBK552030/

Carey, T. A., Mansell, W., & Tai, S. J. (2014). A biopsychosocial model based on negative feedback and control. Frontiers in Human Neuroscience , 8 . https://doi.org/10.3389/fnhum.2014.00094

Erb, M., & Schmid, A. A. (2021). Integrative rehabilitation practice: The foundations of whole-person care for health professionals . Jessica Kingsley Publishers.

Kusnanto, H., Agustian, D., & Hilmanto, D. (2018). Biopsychosocial model of illnesses in primary care: A hermeneutic literature review. Journal of Family Medicine and Primary Care , 7 (3), 497–500. https://doi.org/10.4103/jfmpc.jfmpc_145_17

Landow, M. V. (2006). Stress and mental health of college students . New York: Nova Science Publishers.

Smith, R. C. (2002). The biopsychosocial revolution. Journal of General Internal Medicine , 17 (4), 309–310. https://doi.org/10.1046/j.1525-1497.2002.20210.x

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The biopsychosocial model of illness: a model whose time has come

Affiliations.

1 1 Faculty of Health and Life Sciences, Oxford Institute of Nursing, Midwifery and Allied Health Research, Oxford Brookes University, Oxford, UK.
2 2 School of Psychology, Cardiff University, Cardiff, UK.
PMID: 28730890
DOI: 10.1177/0269215517709890

The biopsychosocial model outlined in Engel's classic Science paper four decades ago emerged from dissatisfaction with the biomedical model of illness, which remains the dominant healthcare model. Engel's call to arms for a biopsychosocial model has been taken up in several healthcare fields, but it has not been accepted in the more economically dominant and politically powerful acute medical and surgical domains. It is widely used in research into complex healthcare interventions, it is the basis of the World Health Organisation's International Classification of Functioning (WHO ICF), it is used clinically, and it is used to structure clinical guidelines. Critically, it is now generally accepted that illness and health are the result of an interaction between biological, psychological, and social factors. Despite the evidence supporting its validity and utility, the biopsychosocial model has had little influence on the larger scale organization and funding of healthcare provision. With chronic diseases now accounting for most morbidity and many deaths in Western countries, healthcare systems designed around acute biomedical care models are struggling to improve patient-reported outcomes and reduce healthcare costs. Consequently, there is now a greater need to apply the biopsychological model to healthcare management. The increasing proportion of healthcare resource devoted to chronic disorders and the accompanying need to improve patient outcomes requires action; better understanding and employment of the biopsychosocial model by those charged with healthcare funding could help improve healthcare outcome while also controlling costs.

Keywords: Biopsychosocial model; biomedical model; healthcare organization.

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Library Mental Disorders Mental Health Treatments The Bio-Psycho-Social Model

The Bio-Psycho-Social Model

The idea of being broad in your assessment of the nature of your problems remains a good one, even when your problems ultimately turn out to be simple ones and the full bio-psycho-social model doesn’t really apply. It is always a good idea to keep in mind that your problems will sometimes be more complicated than you initially thought and require you to try a variety of solutions before you are able to make any headway with them. It is also a good idea to keep in mind that you might benefit from using more than one self-help method at a time, and that such methods might address seemingly very different aspects of your experience and still be effective.

Mental health professionals’ use of the bio-psycho-social model reflects their understanding that human beings are biological, psychological and social creatures all at the same time. People seeking to benefit from scientific wisdom for purposes of helping themselves better manage life problem are wise to copy this comprehensive professional approach and do what they can to learn about these three important aspects of human experience. A basic understanding of medicine and human biology theory helps people to understand how their bodies and brains are constructed and then affected by disease. A little background in psychological theory helps people to understand how minds develop and operate, how thoughts and feelings work, and how behaviors and attitudes can be changed. Finally, knowledge about how relationships and other social processes (gained from learning a little about sociology and social work theories ) helps people to develop an appreciation for the social systems in which people live and the impact these systems have on their group and individual health.

It can feel overwhelming to think about needing to learn about medicine, psychology and social sciences all at once! And yet, all of these fields are important in their own right with regard to informing self-help. None of them can be sacrificed or set aside in favor of another if you are to understand a balanced picture of how human problems occur and can best be fixed. Fortunately, it is not necessary to become an expert in any one of these fields to benefit from them. Learning certain basic ideas and observations which are fundamental to these fields is all that is needed. Learning these basic ideas will help you to determine when problems are serious and require professional help, and when they aren’t serious and can probably be handled well on your own. They can help you to know what general directions to go in; what basic steps to take to successfully handle different types of problems.

Before discussing the various ideas and theories, we want to point out a non-obvious truth. Just because a theory or method we describe here is “scientifically based”, doesn’t mean that it will be able to offer you a good and accurate fit for your issues. Scientifically supported ideas and theories are developed based on systematic group observations. The solutions and concepts they offer accurately describing group behavior (at least for whatever groups were studied), but they are not always a good fit to any given individual. You need to use your judgment, and the judgment of others whose opinions you value (because they are wise) to help you determine what fits you and what does not. If a theory or method doesn’t make sense then don’t choose it.

MentalHealth.com is a health technology company guiding people towards self-understanding and connection. The platform offers reliable resources, accessible services, and nurturing communities. Its mission involves educating, supporting, and empowering people in their pursuit of well-being.

The content on this page was originally from MentalHelp.net, a website we acquired and moved to MentalHealth.com in September 2024. This content has not yet been fully updated to meet our content standards and may be incomplete. We are committed to editing, enhancing, and medically reviewing all content by March 31, 2025. Please check back soon, and thank you for visiting MentalHealth.com. Learn more about our content standards here .

We take mental health content seriously and follow industry-leading guidelines to ensure our users access the highest quality information. All editorial decisions for published content are made by the MentalHealth.com Editorial Team, with guidance from our Medical Affairs Team.

The Biopsychosocial Model 40 Years On

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First Online: 29 March 2019

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Derek Bolton 3 &
Grant Gillett 4

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The first chapter outlines George Engel’s proposal of a new biopsychosocial model for medicine and healthcare in papers 40 years ago and reviews its current status. The model is popular and much invoked in clinical and health education settings and has claim to be the overarching framework for contemporary healthcare. On the other hand, the model has been increasingly criticised for being vague, useless, and even incoherent—clinically, scientifically and philosophically. The combination of these two points signifies something of a crisis in the conceptual foundations of medicine and healthcare. We outline some of the emerging evidence implicating psychosocial as well as biological factors in health and disease, and propose the following solution to the vagueness problem: that the scientific and clinical content of the model relates to specific conditions and stages of conditions, so that there is, for example, a biopsychosocial model of cardiovascular disease, diabetes or depression. Much the same point applies to the narrower biomedical model. However this raises the question: what is the point of having a general model? Our response is that it is needed to theorise biopsychosocial interactions in health and disease. In the light of historical prejudices against psychosocial causation deriving from physicalist reductionism and dualism, recognised by Engel and current commentators on the biopsychosocial model, this is a non-trivial task that occupies subsequent chapters.

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Biomedical model
Biopsychosocial model
Philosophy of medicine
Medical models

1.1 Doing Well—But with Underlying Problems

1.1.1 engel’s proposed improvement on the biomedical model.

In his classic paper published in 1977 George Engel proposed a new model for medicine, the biopsychosocial model, contrasted with the existing biomedical model [ 1 ]. While recognising the great advances in biomedicine, Engel argued that nevertheless the biomedical model was limited, and insufficient for many aspects of medical science and healthcare. These limitations were extensive, comprising failure to take account of the following: the person who has the illness, the person’s experience of, account of and attitude towards the illness ; whether the person or others in fact regard the condition as an illness; care of the patient as a person; for some conditions such as schizophrenia and diabetes, the effect of conditions of living on onset, presentation and course; and finally, the healthcare system itself also cannot be conceptualised solely in biomedical terms but rather involves social factors such as professionalisation ([ 1 ], pp. 131–135). Engel argued that a broadening of the biomedical approach, a new biopsychosocial model, was needed to take account of all these factors ‘contributing to both illness and patienthood’ ([ 1 ], p. 133).

1.1.2 The Presumed ‘Overarching Framework’

In his review of a recent book on the biopsychosocial model by Nassir Ghaemi [ 2 ], in The American Journal of Psychiatry , Kenneth Kendler starts with the sentence: “This book is about a very important topic—the overarching conceptual framework of our field of psychiatry” ([ 3 ], p. 999).

Whether the biopsychosocial model has this status for the rest of medicine is less clear, given the prominence of biomedicine and its biomedical model. Nevertheless, ‘the rest of medicine’ is not one thing, and the various medical specialities differ in their relative involvement with the biological, the psychological and the social. Primary care, also known as general practice or family medicine, is well-known to be much involved in psychological and social factors, and another clear example is public health. The relevant contrast here is with biomedicine, but biomedicine is not itself a medical speciality, but a particular kind of biological science-based medicine that can be applied across medical specialities, in some more than in others. Although Engel starts his paper referring to the ‘medical model’, he soon switches to ‘biomedical model’ and this is the term he uses for the contrast with his new proposed ‘biopsychosocial model’. In short it is not only psychiatry but also all the other non-biomedical aspects of medicine and its specialities that apparently require the broader biopsychosocial model.

We will review some of the health science suggesting the need for a biopsychosocial model in the next section, but first let us consider some current major trends in health, disease and healthcare that point to the same conclusion.

Engel was primarily concerned with psychosocial aspects of managing illness within hospitals, complementing the biomedical approach in hospital care. The example he discussed in detail in his 1980 ‘clinical applications’ paper was of myocardial infarction [ 4 ]. However, it has become clear in the intervening decades that managing illnesses in hospital is a particular and expensive way of providing healthcare. Illness severe enough to require hospital admission has high burden of suffering and disability, and high costs of hospital care, including biomedical investigations and treatments. It would be better all round to prevent illness altogether, or to detect and manage it earlier to prevent worsening, and also better to provide community and social care where possible to avoid or shorten hospital admissions. Implementing this last strategy involves practical psychological and social factors, such as availability of social supports or social care. The first two strategies, primary and secondary prevention, interact with psychosocial factors such as lifestyle, social capital and health literacy.

At the same time the importance of many of the areas of neglect that Engel conveniently listed under one heading—as shortcomings of the biomedical model—have been ratcheted up by diverse trends including socio-cultural changes, economics and globalisation. The voice of the service user has gained strength from civil rights and general emancipatory social changes; rising costs of healthcare in economically developed countries have focussed minds on containing costs by service reorganisations of diverse kinds; health has become globalised in many ways, such as improving health services in economically developing countries, or in the need for international policy to manage epidemics that can now spread more rapidly worldwide.

Other trends since Engel wrote that have also broadened the focus to include more than the biomedical model have to do with changing patterns of population health. Among the greatest achievements of biomedicine have been the identification, treatment and control of infectious diseases. However, and connected, the current burden of ill health in the population now includes many conditions that are not infectious diseases and which have no available complete cure—the so-called non-infectious diseases (NCDs), sometimes also called long-term conditions (LTCs)—such as cardiovascular disease, diabetes, recurrent depression and schizophrenia. In addition, as people live longer, for many reasons including biomedical advances, the proportion of the elderly increases, especially in the absence of immigration, and care of the elderly in hospital accounts for a high proportion of healthcare costs. In short, what biomedicine is good at no longer solves a large part of the population health burden and costs, and can contribute to rising costs by keeping us alive longer (thank you at a personal level) but at great expense—to someone, especially the younger generations. What is needed to theorise all these developments is much more complicated than biomedicine or the biomedical model were ever designed for. As well as biomedicine, what is needed is a complex mix of social science , politics, economics, environmental and social epidemiology and psychology —and no doubt more scientific specialities under development.

A further development in the decades since Engel ’s papers that has added overwhelming weight to the case for a model that can encompass biological, psychological and social factors has been accelerating research on the causes of illness , the basis for primary prevention. The recent research, to be reviewed briefly in the next section, makes two things clear: first, that for many diseases, causes or risks are present from very early on, and second, that for many these causes or risks are combinations of biological, psychological and social. Prospective epidemiological studies suggest that risks for many major illnesses, physical and mental, start early in development, many in childhood, and that risks include social factors such as poverty and other forms of social exclusion , some specific family level factors such as neglect and abuse, and life - style factors such as exercise and diet. Findings on what have come to be called ‘social determinants of health ’ were summarised and publicised for example by Michael Marmot in his 2010 Strategic Review of Health Inequalities in England [ 5 ]. At the same time, but proceeding largely separately, there have been rapid advances in genetics . Over the past few decades many physical and mental health conditions have been found to have a genetic risk—and genetic risk starts from conception, and interacts with non-genetic factors including but not limited to psychosocial factors of the sort identified in the social epidemiological literature. In short, these sciences combined have produced a whole new dimension of the claim of the biopsychosocial model that conditions of living—as well as biological factors—may affect the onset, presentation and course of an illness .

For all these various kinds of reasons, since Engel wrote his papers some 40 years ago, the biopsychosocial model has become the orthodox overarching model for health, disease and healthcare. It is much cited and taught in healthcare trainings of all sorts and in workshops and ward rounds the world over. In simple terms it recommends to healthcare to take into account all three aspects, the biological, the psychological and the social. It is particularly useful in psychology and social work healthcare professions, and in medical practice that has to deal with the psychological and the social as much as the biomedical, primary care (family medicine) being the clearest example [ 6 ], and in-hospital medical training that emphasises the importance of a comprehensive management plan. In all these contexts the biopsychosocial model easily wins, facilitating identification and integration of different aspects of care aimed at different aspects of the patient’s life, disease and management. To illustrate further good fit with much current practice, the biopsychosocial model obviously aligns with the rationale of multidisciplinary teams, and with the increasing recognition of the value of the service user’s views in providing good and effective healthcare.

Given the prominent status and use of the biopsychosocial model, it is clearly of great importance that the model is clear and robust. At this point, however, there is a very large problem, because there have been increasing charges in the medical literature that in fact the biopsychosocial model—popular and accommodating as it may be—is far from being clear and robust, but is in fact deeply flawed.

1.1.3 But Lacks Content, Validity and Coherence

Engel’s biopsychosocial model has long been criticised for having various kinds of limitation, along with suggestions for improvements (e.g. [ 7 , 8 , 9 ]). Increasingly, however, there have been more radical criticisms. Such radical criticisms are of two main types: first, that the model lacks specific content , is too general and vague ; and second, that it lacks scientific validity and philosophical coherence. Given the popularity of the biopsychosocial model and its presumed status as overarching framework for medicine and healthcare, such radical criticisms signal significant underlying theory problems.

The first broad heading of criticism is well argued by Nassir Ghaemi , a psychiatrist at Tufts, in his 2010 book with the telling title: ‘ The Rise and Fall of the Biopsychosocial Model ’ [ 2 ]. Ghaemi argues that the model is vague, too general, tells us nothing specific of value, hence is inefficient and sometimes distracting; it ‘gives mental health professionals permission to do everything but no specific guidance to do anything’ ([ 2 ], p. 82). The way Ghaemi tells the story, the biopsychosocial model arose in the context of competing general views about illness , favouring one or other of the social, the psychological/psychoanalytic and the biological. These general views—one might call them ideologies without criticism—were views of the whole domain of illness , offering general accounts, discriminating not much between kinds of case to which they applied and kinds of case to which they did not. Ghaemi interprets the biopsychosocial model as an elegant—if problematic and ultimately unviable—solution to these ideological conflicts: the unseemly turf wars could be ended, a truce could be declared, if all the participants won, if they were not really in opposition at all, but were in fact all true general accounts of illness and healthcare in all their aspects. The problem whether the cause of illness, and hence in theory its prevention and treatment, is biological, psychological or social is solved, because the answer is ‘all three’ ([ 10 ], p. 3; [ 2 ], ch. 6).

It has to be said that this line of thought is not apparent in Engel’s main papers [ 1 , 4 ]. Ghaemi does however quote a characterisation of the biopsychosocial model from another of Engel’s papers consistent with presumed generality: ‘all three levels, biological, psychological, and social, must be taken into account in every health care task’ ([ 11 ], p. 164; [ 10 ], p. 3). This claim Ghaemi understands as meaning that the three levels ‘are all, more or less equally, relevant, in all cases, at all times’ ([ 10 ], p. 3). In these quotes one can see the point of the allegations that the biopsychosocial model is a slogan, too vague to be of any use. And moreover, when pinned down, more than likely just wrong, counter-evidenced exactly by the successes of biomedicine, in which biological factors alone adequately explain diseases and treatments, such as bacterial infections and anti-biotics cures. Effective biomedicine is an anomaly for any general claim to the effect that ‘everything is biopsychosocial’, an obvious point that warrants repetition (e.g. [ 2 , 12 ]).

So, the charge is that the biopsychosocial model is vague without specific content. If, on the other hand, the model is firmed up to a very general proposition about the general relevance of all three kinds of factors, it is likely to be just false, exactly because of biomedicine. Faced with this obvious enough fact, a possible move is retreat to vagueness, but at the cost of content, as highlighted increasingly by critical commentary.

As mentioned above when illustrating the current important status or aspirations of the biopsychosocial model, Kenneth Kendler opens his review of Nassir Ghaemi ’s book with the statement that its topic is very important, the overarching conceptual framework of psychiatry ([ 3 ], p. 999). In his review Kendler goes on to quote Ghaemi’s negative conclusion, ‘The BPS model has never been a scientific model or even a philosophically coherent model. It was a slogan…’ ([ 2 ], p. 213), and comments: ‘While the reader may think this a little harsh…, I think he is substantially correct in this assessment’ ([ 3 ], p. 999). On the other hand, Kendler ends his review with a reminder of the importance of the biopsychosocial model as a teaching tool in family medicine, concluding: ‘While I agree with Ghaemi that the Biopsychosocial model has been a failure as a scientific paradigm, it probably continues to serve a useful clinical and teaching function in psychiatry and medicine’ ([ 3 ], p. 999). Kendler correctly identifies the major tension here: the biopsychosocial model is a useful tool for clinical and teaching functions, but apparently lacks scientific validity and philosophical coherence.

But then probably all cannot be problem free on the teaching front either. Here is Chris McManus , Professor of Psychology and Medical Education at University College London, reviewing an earlier edited book on biopsychosocial medicine in The Lancet ([ 13 ], p. 2169):

Biopsychosocial medicine’s challenge is to transcend the vague, aspirational inclusivity of its name, and to create a model that truly merits being called a model, and is properly explanatory and predictive … Arm-waving and the inclusion of everything ultimately says and does little of practical consequence.

Ghaemi , Kendler and McManus all basically agree in their negative assessments of the biopsychosocial model.

Given the popularity of the biopsychosocial model, its use in teaching and the clinic, its presumed status as the overarching framework for psychiatry and perhaps for medicine generally, such authoritative negative assessment signals significant problems at the conceptual foundations.

We believe that these two kinds of charge put to the biopsychosocial model, querying its content, validity and coherence, are cogent, but can be met. What they signal is not the end of the model—witness the fact that it persists, for good reasons already indicated—but the need to rethink and reinvigorate it. The answer to the content problem, we suggest, is that the content lies in scientific and clinical specifics , not generalities. This is proposed in the next section, beginning with a brief review of the emerging basic and clinical science supporting the biopsychosocial model. This response to the content problem, however, immediately raises the question: if the content of the biopsychosocial model lies in specifics, what is the point of the general model? We suggest that this question relates to core scientific theory, at the place where it merges into philosophy, and is therefore here that the problem of scientific validity and philosophical coherence is to be addressed. We define this problem in Sect. 1.3 , and address it in detail through subsequent chapters.

1.2 Locating the Content of the Biopsychosocial Model

1.2.1 emerging evidence of psychosocial causation.

Just as the biomedical model is of interest because of the substantial and well-established evidence base of biomedicine, so the biopsychosocial model warrants attention insofar as there is evidence of psychological and social as well as biological factors in health and disease. There has been an accumulation of such evidence in recent decades, and before moving the main theoretical argument forwards, we pause to review some of it.

This review carries a health warning! It is uncritical and unsystematic; we have usually not distinguished strength of evidence of the studies cited below (uncontrolled to randomised controlled and replicated), nor commented on other aspects of methodological strengths (such as sampling strategies and sample size), nor on conflicting and uncertain results, nor have we employed a systematic literature search strategy. Many of the papers cited are reviews, more or less systematic. The purpose here is only to orientate the unfamiliar reader to wide range of research that has supported on-going interest in the interplay of biological, psychological and social factors in health and disease and hence the biopsychosocial model.

Over the past few decades the picture that has emerged for causes of disease onset, especially for the non-communicable diseases, also known as the LTCs, is one of complex, multifactorial causation, involving many risk factors of relatively small effect, affecting multiple outcomes. The recent research on social factors as causes or risks for poor health—the so-called ‘social determinants of health ’—is probably the most well-known, new face validation of the need for a broad biopsychosocial model. Among the most influential social epidemiological research programmes are the Whitehall Studies of British civil servants, led by Michael Marmot [ 14 , 15 , 16 ]. These longitudinal cohort studies found robust correlations between variance in incidence for a wide range of health conditions—coronary heart disease, premature mortality, some cancers, lung disease, gastrointestinal disease, depression, suicide, sickness absence, back pain and general feelings of ill-health—and civil service grade. The social gradient in health —the correlation between indices of social status and health outcomes—is now well-established; much is now known about the social determinants of health [ 17 , 18 ], and something like the biopsychosocial model has to be invoked in order to comprehend it. As typically for epidemiology, most findings on the social gradient in health come from association studies only, retrospective or prospective. Establishing causation is more complex, using such as controlled cohort studies, natural experiments or animal models.

Other large research programmes have investigated associations between adverse psychosocial exposure in childhood and later health outcomes. A landmark programme is the Adverse Childhood Experiences Study (ACE Study) in the United States, carried out by Kaiser Permanente and the Centers for Disease Control and Prevention. The ACE study has demonstrated associations between adverse childhood experiences, such as physical and emotional neglect and abuse, and a large range of physical as well as mental health outcomes (e.g. [ 19 ]).

Lifestyle factors, comprising behaviours and associated beliefs, attitudes and values, have been increasingly implicated as risks, or conversely as protective factors, for a wide range of physical health conditions [ 14 , 18 ]. For example risk factors for some cancers and cardiovascular disease include such as smoking, alcohol use, diet, exercise and chronic stress . Lifestyle factors can be covered under the same heading as social factors, or separately. Either way, lifestyle factors interact strongly with social context, reflecting Engel’s insight that the person is essentially within a social context: diet for example, depends to some extent on choice, but also on what is available and affordable; stress —to be considered in Chapter 4 —depends on individual characteristics but also on task demands and available resources.

Lifestyle and psychological factors can be distinguished: the former are behavioural, while the latter, such as beliefs, attitudes and values, are mental. At the same time they are closely linked. One reason is that psychological factors motivate lifestyle, but there is also a general linkage between our psychology and our behaviour, namely, that we respond to reality at it appears to us, at any given time, to be. We pick this up as a theoretical point in more detail later, in Chapter 3 (Sect. 3.1 , heading “ Mind Is Embodied ”). In the present context it appears in evidence suggesting that it is not objectively measured social status but social status as perceived , so-called ‘subjective social status’ that accounts for more of the variance in health outcomes (see e.g. [ 20 , 21 ]). This interesting finding becomes part of the complex jigsaw puzzle of biopsychosocial aetiology.

Over the same past few decades that evidence for psychosocial factors in health and disease has been accumulating, so also has evidence of genetic effects. For some health conditions such as Huntington’s chorea, and some cancers, there are massive genetic effects, but for the majority of health conditions, the proportion of population variance attributable to genetic influence is much less than 100%, the picture being rather of relatively small effects of multiple genes , with the remaining variance attributable to non-genetic, environmental factors. Combining these broad kinds of research programmes presents a biological-psychological-social and-environmental picture, and new epigenetics is likely to help explain how the various kinds of factor interact. These issues are taken up in Chapter 3 , Sect. 3.4 .

Post-onset course of disease raises different causal questions: what are the processes determining course, for example, progression, stability, fluctuation or recovery? Treatment effects are a special case, assessed using a range of designs including randomised controlled trials. There has been accumulating evidence from randomised controlled treatment trials since the late 1970s of treatment effects of psychosocial interventions on some mental health conditions. Among the first was a randomised controlled trial of cognitive behaviour therapy for depression published by Beck et al. [ 22 ] showing effectiveness, but further, the same effectiveness as for anti-depressant medication. In effect this trial showed that a psychological intervention could achieve the same result as a biomedical intervention, and it paved the way for accelerating developments of tested psychological treatments for a wide range of mental health conditions and the translation of these into national health service provisions. There are complications, as always, for example, as to the extent to which psychological therapy outperforms pill placebo control, but the principle that some psychotherapies help some mental health conditions has been established (e.g. [ 23 ]).

The position is different with physical illnesses . Put strongly, there is a glaring gap in the evidence for the biopsychosocial picture as a whole, namely, absence of persuasive evidence of psychosocial treatment effects on the course of major physical illnesses. There is no clinical trial that finds effects of psychological therapy on physical illnesses such as, say, diabetes, cancers, cholera or advanced cardiovascular disease. We just wish to make the point that no psychotherapy or any other kind of psychosocial intervention turns around such disease processes once established, and this is a major apparent fact that needs to be taken into account in discussing the relative merits of the biomedical model and the broader biopsychosocial model. This is linked to the fact that for the many conditions that are managed biomedically in acute hospitals, successfully in some cases, there need be no special interest in the broader biopsychosocial model, and any advocate of the broader model has to accommodate the fact that whatever other significant roles they may have, psychosocial factors apparently make no difference to the course or treatment of major physical illnesses .

That said—and we intend it to be a big that —there is emerging evidence that psychosocial factors may be implicated in the prognosis of some among the very large range of medical conditions. For example: breast cancer (e.g. [ 24 ]), atopic disease, generally [ 25 ], including for asthma [ 26 ]; HIV [ 27 , 28 , 29 ] and musculoskeletal disorders (e.g. [ 30 ]). In addition, psychosocial factors have been implicated in outcomes of surgical procedures, for example, chronic pain [ 31 ]; lumbar and spinal surgery [ 32 , 33 , 34 , 35 , 36 , 37 , 38 ]; liver transplant (e.g. [ 39 ]) and coronary artery bypass (e.g. [ 40 , 41 , 42 ]). In addition, there is evidence for psychosocial factors in wound healing [ 43 , 44 ], and extent of fatigue after traumatic brain injury [ 45 ]. Psychosocial factors have also been implicated in responses to other interventions for medical conditions, such as inpatient rehabilitation for stroke patients (e.g. [ 46 ]), and effects of hospitalisation on older patients (e.g. [ 47 ]).

Reference to psychosocial factors affecting course of medical and post-surgical conditions is not intended to be read as either conclusive or general. Many studies on this general topic are of associations only, and there are many mixed results. Hence the subtitle of this section, ‘emerging evidence’, and the explicit qualification of specificity to particular conditions and stages. Further, absence of reports of psychosocial effects on medical conditions, while it may suggest simply that the research has not yet been done, may also indicate that results have been negative and unpublished, and further back in the clinical research sequence, that clinicians have not seen evidence warranting case study research reports, progressing to cohort studies, and so on. This takes us back to the point made first, that some major medical conditions, such as the primary dysfunction in diabetes, or advanced cancers, or advanced cardiovascular disease, appear to be influenced exclusively by biological factors, impenetrable to psychosocial processes and interventions, and in some cases also unresponsive to biological interventions.

An old-fashioned way of making this point is to say that the mind cannot control biological processes such as abnormal cell growth. In the old dualist framework, however, the mind couldn’t really control anything material, not cell growth, but not arms and legs either, so the discriminating point got lost in the metaphysics. In the new post-dualist scientific framework, to be outlined in Chapter 3 , the ‘mind’ is not immaterial, not causally impotent, but more a matter of the central nervous system regulating some internal systems as well as the behaviour of the whole in the environment, and in these terms there are researchable differences between what the central nervous system can control and what it cannot. Extent of control may be modifiable, subject to individual differences, training and practice, but we know now that even at its best the central nervous system is not an omnipotent controller: there are places and processes that CNS signalling pathways do not reach, for example, cell growth, linked to the fact that the cells are very basic, similar in humans as in yeast; nor does the brain control the journey and final resting place of an embolus, and a long list of other biological processes and outcomes, benign or catastrophic. And this list can be contrasted with a list of biological processes and pathways that can or might have CNS involvement, as suggested by studies cited above. These issues and options only open up, however, in a new post-dualist metaphysics and biopsychological scientific paradigm, which are large themes to be addressed through the book. For now, we return to review the findings on biopsychosocial factors.

The next point to note is that, even for those physical health conditions that are unaffected by psychosocial factors, generally or at specific stages, still such factors may be relevant to clinically significant aspects of disease progression and management. These are factors such as access to treatment, participation in the recommended treatment regime, associated pain, psychological/mental health complications and health-related quality of life . Some details and literature as follows:

Access to healthcare is an obvious heading, covering diverse factors such as public health screening to ensure timely detection, health literacy, availability, accessibility and affordability of care, and quality of care—all factors heavily dependent on personal, class and state economics, associated therefore with the social gradient in health [ 5 , 48 , 49 and e.g. 50 ].

Acceptability of/participation in the recommended treatment regime. Psychosocial factors are associated with medication non-adherence, for example, following acute coronary syndrome [ 51 ], in haemodialysis patients [ 52 ], in youth with newly diagnosed epilepsy [ 53 ]. One systematic review of study of psychosocial factors predicting non-adherence to preventative maintenance medication therapy produced a negative result and call for more research [ 54 ].

Psychosocial factors in pain. Pain as an important phenomenon and concept spanning the biopsychosocial and will be considered further in Chapter 4 . Clinical studies implicating psychosocial factors include: in chronic pain [ 55 , 56 ] and in pain associated with specific conditions/sites, such as multiple sclerosis [ 57 ]; musculoskeletal pain [ 58 , 59 ]; low back pain [ 60 , 61 ]; spinal pain [ 62 ]; chronic prostatitis/chronic pelvic pain syndrome in men [ 63 ]; osteoarthritis [ 64 ]; cancer-related pain [ 65 ] and pain after breast cancer surgery [ 66 ].

Psychological/mental health complications of medical conditions . This is an increasingly recognised issue, with implications for quality of life (on which more below), social impairments and costs, in primary care [ 67 ], in LTCs [ 68 ] and in oncology [ 69 , 70 ]. Accumulating clinical experience and research has led to a new UK NHS policy directive requiring psychological therapy services to be integrated into physical healthcare pathways [ 71 ].

Quality of life . There is a substantial literature on psychosocial factors and health-related quality of life in medical conditions, for example, in patients with haematological cancer [ 72 ]; children with myelomeningocele [ 73 ]; colorectal cancer survivors [ 74 , 75 ]; myocardial infarction [ 76 ]; after hip fracture in the elderly [ 77 ]; newly diagnosed coronary artery disease patients [ 78 ]; adults with epilepsy [ 79 ], and after surgery [ 80 ]; and youth-onset diabetes myelitis [ 81 ].

Accumulating health data of the sort indicated above implicating psychosocial as well as biomedical factors, taken together, cover a large proportion of population health and health service provision in clinics and hospital beds. In other words, they are massively important, looked at in terms of population health, individual suffering, or economic costs; they are not a side-issue compared with conditions or stages of conditions that involve biological factors alone.

The psychosocial data have accumulated over the past few decades and have vindicated Engel’s proposal of a new model for medicine and healthcare. Engel was ahead of the game, and the popularity of his model is explained at least partly by the fact that it appeared as a ready-made framework for accommodating the emerging evidence of psychological and social causal factors in determining health and disease.

In these terms its clear that we need a biopsychosocial model of the sort that Engel anticipated, but one that can meet the criticisms reviewed previously that the model, at least as we currently invoke it, has serious problems including lack of content and incoherence. We propose in the next section a solution to the content problem, based, as would be expected, on emerging findings implicating psychosocial as well as biological factors of the sort outlined above. As to the coherence problem, this will involve theorising the categories of ‘biological’, ‘psychological’ and ‘social’ in such a way that they can interact in health and disease. This theorising will occupy the rest of the book. One strand was already mentioned earlier in this section: the old dualism between mind and body is replaced by a partial and to some extent negotiable interaction between the central nervous system and other biological systems. This theory-shift will be taken up in Chapter 3 , along with the proposal that the primary concept of the psychological is embodied agency , with implications for health, drawn out further in Chapter 4 : a person’s psychological health depends on the development of a viable enough sense of agency , while conversely, if agency is seriously compromised, such as in conditions of chronic stress , their mental health is liable to suffer, and so also, via complex biopsychosocial pathways, is their physical health.

1.2.2 The Scientific and Clinical Content Is in the Specifics

Let us pick up the line of argument in this chapter. The biopsychosocial model is much invoked, with claim to be the overarching framework for psychiatry and other branches of medicine such as primary care, perhaps for medicine generally. It has however been severely criticised, for being vague, without scientific or clinical content. Here is our suggested remedy: the scientific content and clinical utility of the biopsychosocial model is not to be found in general statements, but rather is specific to particular health conditions, and, further, specific to particular stages of particular health conditions . We provided above a brief, non-systematic, non-critical review of some of the emerging evidence of involvement of psychological and social as well as biological factors. All the evidence refers to particular health conditions or classes of conditions, and particular stages: risks for onset, post-onset course, including under treatment, adjustment and quality of life .

At the time Engel wrote there was not much evidence of causes of diseases and treatment effects, with important exceptions in the case of some major infectious diseases. But especially, compared with now, relatively little was known, though much was speculated, about the role of psychosocial factors in health and disease. Since then, in the intervening decades, there have been massive new research programmes, not only in biomedicine, but in clinical psychology , neuroscience , social epidemiology and genetics , and in treatment trials, pharmacological and psychological. Much more is now known about the causes of diseases and about possible disease mechanisms, with associated technologies for prevention, early detection and treatment. This broad evidence base has led in turn to treatment guidelines for specific conditions, to the whole apparatus of evidence-based clinical care, to be used alongside a thorough assessment of the individual case. Much of the science and clinical management is now psychological and social as well as biological. Given this situation as it is now, the scientific and clinical content of the biopsychosocial model is in the specifics, not in a ‘general model’. Much the same, by the way, can be said of biomedicine and its associated biomedical model: medicine, whether biomedical or biopsychosocial, deals with complex, specific systems.

The proposal that the content problem is resolved by focussing on specifics not generality also helps explain how the problem arises. In brief, it is because the specifics are too many and too complex, that some shorthand, vague gesturing, is sometimes useful. The basic and clinical sciences of the past few decades invoke very many kinds of factors in their models: biological factors—biological systems, including neural systems and genetic mechanisms—but also psychological factors—such as temperament, personality, lifestyle, adjustment, quality of life —and also social determinants of health and disease—variants on social inclusion or exclusion—together with the implication that all these things interact over time, in the course of life and the illness , in complicated and barely understood ways. So, on occasions when the question arises, for example in clinical consultation or healthcare education systems: ‘and what are the factors involved in this or that disease, or individual presentation?’—the quick answer would be: ‘it’s all biopsychosocial’, or ‘it’s as the biopsychosocial model says’. The full answer is much longer, in the systemic reviews of the epidemiological and clinical sciences, treatment trials and clinical guidelines—but this full story does not fit in a ward round or clinical consultation; it more makes up years long healthcare educational training programmes. As workable compromise, the brief throwaway—‘it’s all biopsychosocial’ could be expanded into something more informative along these lines: ‘In this condition there are possibly (or probably) biological, psychological and social factors involved, in some stages, some of which have been identified, with more or less confidence, combining together in such-and-such ways, though interactive causal pathways are bound to be complex and (typically) not yet well understood—the details of what is known and hypothesised about the condition to date is in the literature/is among the topics in one of your teaching modules’.

Such an answer, and the science it refers to, is about a particular health condition, such as diabetes, or depression. In this sense there are multiple specific biopsychosocial models: a model for diabetes, depression, cardiovascular disease, schizophrenia; and so forth. Further, much depends on what stage or what aspect of a particular condition we have in mind, whether pre-onset aetiological risks for onset, or post-onset course, involving many issues including maintaining factors, treatment responses, complications, psychological adjustment and factors affecting quality of life . The factors involved in these various stages and aspects typically differ within any particular condition, and especially they differ in the relative involvement of biological, psychological and social. For example, social epidemiological studies suggest that social factors as well as biological are implicated in the aetiology of a wide range of health conditions, such as cardiovascular disease and depression, while treatment might not be so, as in surgical intervention for advanced cardiovascular disease, or pharmacological therapy for depression. This latter is typically best combined with psychological therapy, which might also be indicated to aid adjustment and recovery of quality of life following cardiovascular surgery. In short, there is need for much discrimination between what conditions we are talking about, what stages of conditions and questions of interest in each. This is the specificity and complexity of diseases and therefore of the science and its models.

We stress here that we mean no implication that particular diagnostic categories are valid once and for all, or optimal in terms of explanation or prediction. Rather, they simply represent the current consensus state of clinical practice and clinical science and are liable to revision, to subtyping or supra-typing, or to replacement altogether. The proposal is that biopsychosocial medicine, like biomedicine, is applied to specific health conditions, in terms of which the science at any one time is conducted; but identification and classification of these conditions are subject to change.

In brief, our proposal is that, while the biopsychosocial model can sometimes appear as vague hand-waving, absent any scientific or clinical content, this is because we are looking for content in the wrong place, in the general model, rather than in the epidemiological and clinical science literatures about particular conditions. This proposal, if accepted, solves the content problem.

On the other hand, that said, such a solution immediately raises a still more radical problem for the biopsychosocial model: if it’s all about specifics, what is the point of having a ‘general model’?!

1.2.3 So What’s the Point of a ‘General Model’?

Engel wrote about the biopsychosocial model in a way that suggested it had scientific content and clinical utility. His 1980 paper [ 4 ] was on clinical applications of the biopsychosocial model, the main example being myocardial infarction, consistent with the reasonable expectation that the model specified biopsychosocial causal pathways in particular conditions and hence could guide clinical practice. However, the position regarding what is known in the science has radically changed in the intervening decades, and now, as argued in the preceding section, the ‘general model’ is probably now not the place to look for causal pathways, clinical applications and treatment guidance, which are rather to be found in the health science literatures.

One possibility in the circumstances, as the evidence accumulates, is that the general model might summarise the evidence for all the health conditions, along something like the following lines: “Psychological and social factors as well as biological factors (each of these being of many different kinds) are relevant to all health conditions and all healthcare, though they vary in their relative contributions, depending on the condition and the stage of the condition, between 0-100%, or mostly between, say, 20-80% – summing to something like 100%”.

However, while such a general proposition might be true, give or take some percentage points, it clearly has no or not much content, or use, in for example shaping guidance about prevention or clinical management. It is certainly less informative and useful than the full picture for a specific health condition. It is true that a general statement of the model such as the above can serve to remind us and our students to keep one’s mind open to the range of biopsychosocial factors, but the treatment guidelines and the science behind them already now say this, if applicable, and there is limited gain from repeating the fact—vaguely. Used in this way, the model runs the risk of being, minimally, a bucket to throw research findings into, convenient for hand-waving purposes. As for basic scientists and clinical trialists, they investigate the causes, mechanisms and treatment of cardiovascular disease, depression, and so forth; with definitely or probably not much need or time for a ‘general model’.

So what is the point of a general model? Perhaps as a theory of health and disease. But the line of thought we are pursuing is exactly that health and disease are not one thing, or two things, but each many things, depending which system within us is functioning well or poorly. Even so, the general picture still matters when the whole of health is in question, for example in estimating and projecting population health, planning and prioritising health services and research funding, on treatment, primary or secondary prevention, planning syllabuses for health education, or modelling linkages between health outcomes and outcomes in other sectors such as education, productivity or national happiness. Clinicians, patients and researchers may well be concerned with specific conditions, but for many other purposes views of the whole are required. The concept of biomedicine arose in the recognition that many effective health technologies had in common that they relied on biological factors only, notwithstanding complex biopsychosocial presentations. Such a concept then drives further lines of enquiry, investigating biological factors in other conditions. An analogous point applies to the biopsychosocial model. A related point is a need for a framework to organise accumulating research findings, to recognise emerging patterns, to identify what is known, with more or less certainty, and what is not known. This applies to specific conditions such as cardiovascular disease, or addictions, but it also applies across health conditions as a whole.

There are many purposes for a general model and accordingly many ways of constructing such a thing. We focus here on the general biopsychosocial model as a core philosophical and scientific theory of health, disease and healthcare, which defines the foundational theoretical constructs—the ontology of the biological, the psychological and the social—and especially the causal relations within and between these domains .

While the details of the relative roles of biological, psychological and social factors in specific health conditions, at particular stages, are matters for the health sciences, the general, or core, biopsychosocial model is more of an exercise in the philosophy of science—in this case, philosophy of biology , philosophy of mind and social theory, but especially as applied to health and disease. These philosophies are especially relevant in the present case, because there is massive historical baggage, carried in the long history of physicalism , dualism and reductionism , that makes biopsychosocial ontology and causation deeply problematic. This whole problem area needs rethinking and reconceptualising in the light of current scientific paradigms and philosophical theory.

1.3 The General Model: Biopsychosocial Ontology and Interactions

1.3.1 defining the problem.

Engel was well aware of the philosophical problems involved in the shift from the biomedical model to the biopsychosocial. This is how he characterises the biomedical model ([ 1 ], p. 130):

The biomedical model embraces both reductionism , the philosophic view that complex phenomena are ultimately derived from a single primary principle, and mind-body dualism , the doctrine that separates the mental from the somatic. Hence the reductionist primary principle is physicalistic; that is, it assumes that the language of chemistry and physics will ultimately suffice to explain biological phenomena.

The biomedical model so understood, as based on these philosophical views, is antithetical to any extension to a biopsychosocial model, and conversely, if the biopsychosocial model is to be viable, it has to overcome the challenges they pose. This is well recognised by thoughtful commentators on the biopsychosocial model, including those, quoted previously, who criticise the model for its hand-waving tendencies. Here is Chris McManus in his review for The Lancet cited previously ([ 13 ], p. 2169):

The challenges for the Biopsychosocial Model involve reductionism , dualism , mechanism, methodology, and causality. The psychological and the sociological are ineluctably phenomena of the mind, and the reductionist challenge is how to integrate the mental with the cellular, molecular, and genetic levels at which biomedicine now works.

Ken Kendler in his review quoted earlier, goes on to identify the philosophical issues relevant to the biopsychosocial model and the work that needs to be done ([ 3 ], p. 999):

[These are] the issues that the Biopsychosocial model at least seemed to be addressing—how to integrate the diverse etiologic factors that contribute to psychiatric illness and how to conceptualize rigorously multidimensional approaches to treatment. [There is] a range of exciting recent developments in the philosophy of science on approaches to complex biological systems, which are quite relevant to these issues… [which] examine scientific approaches to complex, nonlinear living systems and explore various models of explanatory pluralism, from DNA to mind and culture….

The importance of understanding causal interactions between kinds of factors is also highlighted by Dan Blazer in his review of Nassir Ghaemi’s book [ 82 ] (p. 362):

[There are] emerging efforts across all of medicine to integrate biological, psychological, and social factors in the exploration of the causes and outcomes of both physical and psychiatric illnesses …. These efforts are not eclectic but transdisciplinary, efforts which are leading to a much better understanding of how biological, psychological, and social factors interact through time.

Both Kendler and Blazer identify the current challenge of constructing a coherent view of causation in health and disease that can encompass biological, psychological and social factors. Kendler refers to recent philosophical developments and Blazer to emerging efforts in health sciences, both implying a historical dimension and that something new needs to happen and is happening, at a conceptual level as well as a scientific level.

Engel’s characterisation of the biomedical model, a reasonable one in the 1970s, had it supposing that only the biological exists, or is alone causal in health and disease, and it exists as physics and chemistry, with the same principles or laws of causation. The ontology was flat and reductionist: nothing new grew out of the basic physics and chemistry, and any other domain with aspirations to be causal had to be ultimately reduced back to the basics. To construct an alternative to this set of assumptions it is necessary to envisage ontology and causal relations other than, and in some metaphorical sense ‘above’, those in physics and chemistry. Engel proposed systems theory for this purpose, and as we shall consider in later chapters, we think this is fundamentally the right way to go.

A systems theory approach in fact already underlies the solution to the content problem we proposed in the previous section. We proposed in Sect. 1.2 , heading “ The Scientific and Clinical Content Is in the Specifics ”, that the content is to be found in the science and clinical guidelines on specific health conditions. This is the indicated move because specific systems are distinctive, with their own distinctive functions, operating principles and vulnerabilities to dysfunction, which therefore have to be modelled separately. Healthcare science along with other systems sciences, essentially deals in specifics. This has always applied to biomedicine, which deals with particular biological systems. It also applies in psychology , which deals with particular psychological systems, such as motivation and fear, and in clinical psychological theory—for example, cognitive behaviour therapy has specific models for such as depression, obsessive-compulsive disorder and panic disorder.

The question arises then: what is the core theory linking together the various applications to specific systems? For biomedicine, in the way that Engel characterised it in the 1970s, the core theory was that biology is physics and chemistry, and biological causation is physico-chemical causation. This has changed; it is no longer true of current biomedicine; this is the topic of the next chapter. The core theory underpinning cognitive behavioural therapy, as stated by its founders Aaron Beck and colleagues [ 22 ] (p. 3) is startlingly brief, that cognitions cause affect and behaviour. However, even this brief statement of the core model does crucial work: it highlights the working assumption that intervening with cognition is the way to modify troubling emotions and behaviour, and it links together the various types of cognitive behaviour models for diverse conditions. Even in the absence of explicit theory of causation, there can be evidence of causal connection from well-designed treatment trials, but also, in this particular case there is a long and respectable history of the cognitive theory of the emotions and the philosophy of practical reason that provides conceptual familiarity for working purposes.

The contrast here is with the biopsychosocial core model: there is no long and respectable history of philosophy and science theorising causal interactions between the biological, the psychological and the social. To the contrary, the history since the beginnings of modern science in the seventeenth century consists of assumptions and arguments that psychological and social causation are impossible or even incomprehensible, that there is no distinctive biological causation either, over and above physics and chemistry. The historical background is entirely hostile to the whole idea of biopsychosocial causal pathways, and there is therefore a need for an explicit theory as to what the new idea is. It is this, we propose, that is the purpose of the general biopsychosocial model; in short, to theorise biopsychosocial causal interactions.

We review some main relevant historical background below, under the heading “ Prejudicial Theory: Physicalism, Reductionism, Dualism ”. First, in the next section, we consider how the search for biopsychosocial theory is not only of interest to reworking a model proposed some 40 years ago, but has arisen in the health sciences themselves.

1.3.2 Biopsychosocial Data in Search of Theory

The emerging evidence of psychosocial causation in health and disease of the sort briefly outlined in Sect. 1.2 , comes from studies using empirical methodologies that have been developed and applied substantially since Engel wrote his papers on the biopsychosocial model. Prior to these new research methods, there was little or no demonstrated evidence of psychological and social causes of physical health conditions. Their effects were not as plain—as massive—as those identified by biomedicine, as for example effects on incidence of cholera of drinking contaminated water from a particular pump, or recovery following treatment by antibiotics. In the absence of a significant body of evidence of a causative or curative role of psychological and social factors in particular diseases, claims as to their importance were bound to have an uncertain status: were such claims meant to be general, to apply to all conditions, meant to be obvious, or based on prejudice or expert consensus—or specific to particular conditions? In the absence of much evidence, the appearance of ideology was inevitable—and this is one of the key points behind Ghaemi’s critique of Engel’s biopsychosocial model [ 2 ], considered previously (Sect. 1.1 ). However, the amount of evidence and most importantly the type of evidence bearing on these issues has changed radically in the 40 years since Engel proposed the model. We refer to use of novel statistical methodologies and associated study designs that are sensitive to multiple factors, relatively small, partial causal influences, usually called risk factors, contributing in some way to a complex nexus of causation associated with a particular outcome of interest. The development of these new methodologies was based on nineteenth-century conceptual work on the scientific demonstration of causation, and early twentieth-century work in the theory of statistical inference.

Much of the intellectual work clarifying the scientific methodology required for the determination of causes was done by J. S. Mill in his A System of Logic [ 83 ]. Hume [ 84 ] had seen that causality is linked to generality, that the statement ‘A causes B’ implies that events of type A are always followed by events of type B. This implies also that knowledge of causes enables prediction, that the next A will be B. Mill saw, however, that in practice what is observed on any one occasion is not simply an event of type A being followed by an event of type B, but this conjunction in a complex of circumstances, C. To establish a causal link between A and B the possible confounding effects of C have to be determined. This involves observing the effects of C without A, on the one hand, and A without C on the other. These principles, elucidated by Mill as the ‘methods of agreement and difference’, underlie our modern idea of controlled experimentation.

Robert Koch’s pioneering work in microbiology in the closing decades of the nineteenth century made four postulates as methodology to determine the causal relationship between a microbe and a disease, applied to the aetiology of cholera and tuberculosis [ 85 , 86 ]. Koch’s postulates tapped similar principles to Mill’s , including assumptions of generality and isolation of the suspected active causal ingredient—‘isolation’ here requiring cutting edge technology of the time. Interestingly Koch himself recognised that there was a problem with the generality requirement, which takes us on to the next main point.

Hume , Mill and Koch supposed that causality is general—applies to ‘all’. However, in practice in the lifesciences, medicine, psychology and the social sciences we rarely find universal generalisations, but rather partial ones, of the form: A is followed by B in a certain proportion of observed cases. One function of a universal generalisation is to license the simple inductive inference: the next observed A will be followed by B. In the absence of a universal generalisation, the problem is to determine the probability of the next A being followed by B, given that the proportion in the sample so far observed. This is the problem for the theory of statistical inference, developed in the first decades of the twentieth century.

The theory of statistical inference is a necessary condition of being able to detect reliable small correlations between two factors, between say amount of daily exercise and cardiovascular function at a later time. The implications of correlations being small—much less than 1 and not much above 0—is that other factors are at work, signalling the need for investigation of multiple factors associated with the particular outcome of interest. Investigation requires a group study in which each factor is each measured and their association or correlation with the outcome computed. Analysis of variance, ANOVA, is one class of statistics that can be used for such purposes: there is an outcome of interest, the so-called dependent variable, and several independent variables, hypothesised to effect it. For example, the dependent variable may be onset of cardiovascular disease by 40 years, the independent variables are individual characteristics such as weight, diet, smoking, exercise, multiple deprivation index, family history as assumed proxy for genetic vulnerability, and the results of the ANOVA will quantify the amounts of variance in outcome and hence risk attributable to these several factors, alone or in combination. Other classes of statistical analyses can be used, more or less closely related, depending for example on the nature of the variables (e.g. categorical or continuous) and on study design (e.g. cross-sectional or longitudinal). Use of such methods has become pervasive in the human sciences in the past few decades, reflecting the fact that the phenomena are complex with multiple causes; instances when a single variable completely explains a phenomenon (accounts for all or most of the variance) are rare.

Naturalistic studies of populations in the first instance establish correlations only, and further investigation is needed to establish causation, using or approximating to experimental methods of the sort elaborated by Mill and Koch. Experimental designs for establishing causation typically involve at least two groups, assumed to be identical in relevant respects—either known or suspected to affect the outcome of interest—except for one factor, the factor of interest. Differences of outcome between the two groups are then attributable to the factor of interest in accordance with Mill’s method of difference. The factor of interest is often a treatment—an ‘intervention’. Confidence in the assumption that the two groups are otherwise identical in relevant respects is critical in these methodologies, and there are many methods of ‘matching’ groups to achieve this. The philosophical justification for regarding controlled designs as the appropriate methodology for establishing causation such as treatment effects has been argued elsewhere [ 87 ]. The gold standard for maximising this confidence—the true experimental design—is taken to be randomisation, with sufficiently large numbers, such that possible confounding causal factors can be reasonably assumed to be distributed equally between the groups. Quasi-experimental designs, such as matching cohorts, can also be used, though the confidence that unknown confounders are equally matched is less. There are also ‘natural experiments’ (see e.g. [ 88 ]), and sometimes the background base rates absent the putative cause are safely assumed.

If we establish that a universal correlation is causal, the finding can be expressed as A causes B. Typically in the life and human sciences, correlation between factors is partial—variation in A accounts for only part of the variance in outcome B—in which case the correlation can be expressed as: A raises probability of B, in some specified degree depending on the size of the correlation. If B is a harmful outcome, such as a poor health outcome, this is often expressed: A raises risk of B, in some specified degree.

Population studies of risk factors for the onset of disease cannot use randomisation designs, plainly for ethical reasons, and are generally limited to more or less refined quasi-experimental methodology. Experimentation is left to animal studies. Treatment studies of the effect of an intervention on the course of a disease once onset can use randomisation designs—again subject to ethical constraints.

The new study designs and analytical methodologies showed effects—typically small—of psychological and social factors. The same methodology of course can show the importance of biological factors of small effect, such as genetic and epigenetic effects.

Relevant to our main theme, however, we can note that while these new study designs and statistical methodologies are well theorised, as is the determination of causes by experimental and related methods, they provide in themselves no theory of the factors indexed by the variables and no theory of causal mechanisms linking them. They can provide evidence of biopsychosocial causal connections, but no theory about them. This absence of theory is important because of the historical background of dualism and physicalist reductionism , noted at the beginning of this section (under the heading “ Defining the Problem ”), that would exclude any distinctive forms of biological (as opposed to physico-chemical), psychological and social causation . We review some main points of this historical background next.

1.3.3 Prejudicial Theory: Physicalism , Reductionism , Dualism

Engel’s characterisation of the biomedical model—quoted at the beginning of this section, uses a few key technical terms: reductionism , physicalism and physicalist reductionism (Engel uses ‘physicalistic’). These terms refer to complex and controversial concepts with long histories, and we will use working characterisations as follows:

Physicalism is the view that everything that exists is physical. This is an ontological statement—about what there is. It has often been combined with the corresponding statement about causation: that all causation is physical, covered by physical laws. On the assumption that chemistry is basically physics, physicalism can be expressed in terms of physics + chemistry. The contemporary philosophical literature on physicalism is substantial (for recent review see e.g. [ 89 ]). Working around physicalism is necessary to establish a biopsychosocial model and is addressed in more detail in the next chapter.

Reductionism has various meanings. In one of the senses used by Engel in his characterisation of the biomedical model, quoted at the beginning of this section, it is a scientific claim that complex phenomena have a main cause of a particular type. In the medical context, reductionism in this sense would claim that there is a main cause of one or other kind: biological (e.g. an infection or lesion), or psychological (e.g. unconscious conflicts, or maladaptive cognitive style), or social (e.g. social exclusion ; labelling). There is also a philosophical or metaphysical doctrine of reductionism , deriving from physicalism , as follows:

Physicalist reductionism follows from the strong version of physicalism which has ontology and causation as all a matter of physics. It is a strict consequence for other sciences, such as chemistry, biology , psychology and social science : either they are true causal sciences, in which case they must ultimately reducible to the concepts and laws of physics; or, otherwise, they are pseudo-sciences, or at least, ‘sciences’ that do not deal with causation. Physicalist reductionism so understood is a philosophical or metaphysical doctrine in the sense that it is known or alleged a priori; it is not based on scientific research, but rather prejudges what there is to be discovered. Physicalist reductionism along with its roots in physicalism is taken up in the next chapter.

Physicalism has a long history, its roots lying in what historians of science refer to as the ‘mechanisation of the world picture’ in the seventeenth century [ 90 , 91 , 92 ]. This involved defining the primary qualities of nature in mathematical terms, as mass, extension and motion, covered by the few universal laws of Newtonian mechanics. The mechanisation of nature created mind–body dualism , because the thing that never did seem to be physical was immediate experience: sense-perceptions, thinking, pain and the like. Physical objects including the human body have the primary qualities, while the mind was something else, immaterial and unlocated. Physicalism and dualism are twins, one born straight after the other, combative from the start, each refuting the other, the one supported by the great edifice of modern mechanics, the other known immediately by experience, battling ever since.

It is impossible to overstate the massive influence of modern physics and its accompanying philosophy of nature on the subsequent development of western science through the eighteenth and nineteenth centuries. As sciences developed, studying apparently distinctive domains and processes, the dominant physicalism applied its stringent reductionist test: either the new aspiring science was valid as causal science, in which case it should be reducible to physics, or, it was not reducible to physics, in which case it was pseudo-science, or at best, a ‘science’ studying non-causes. The chemistry that emerged in the nineteenth century passed the test and joined physics. As to biology , psychology and social science , on the other hand, physicalist reductionism aided by dualism caused disunity and more or less havoc—some key points in brief as follows, to be picked up in later chapters:

Biology as we now understand it developed in the nineteenth century, drawing from previous roots in medicine, natural history and botany (see e.g. Ernst Mayr’s seminal work on the history and philosophy of biology, [ 93 ]). This large, complex field, comprising many subfields, with distinctive domains, questions and methods, had an ambiguous relation with physicalism and reductionism . In some areas of biology , especially in medicine, physiology and new subspecialities such as microbiology—there was the possibility of reduction of biological phenomena as chemistry. A key development was Lavoisier’s work on the relation between combustion and respiration, initiating the scientific research programme that became biochemistry. However, for other parts of the broad and diverse field of biology, reducing the phenomena of life to chemistry was not such a clear option. This applied especially to developmental embryology and evolutionary biology , which aimed to understand the formation of individual organisms and whole species, and which used explanatory concepts more akin to older, Aristotelian concepts such as form and function. Such alternative concepts, contrasted with physics and chemistry, will appear in later chapters as we develop biopsychosocial theory. Biology could embrace physicalist reductionism , or ignore it, or argue against it head on. This third option was the doctrine of ‘vitalism ’, which posited a biological life force in addition to mechanical, or more broadly physico-chemical, forces. Vitalism is in this sense a direct response to the mechanisation of the world picture in modern science, a point made by Bechtel and Richardson [ 94 ] (p. 1051):

Vitalism is best understood… in the context of the emergence of modern science during the sixteenth and seventeenth centuries. Mechanistic explanations of natural phenomena were extended to biological systems by Descartes and his successors. Descartes maintained that animals, and the human body, are ‘automata’, mechanical devices differing from artificial devices only in their degree of complexity. Vitalism developed as a contrast to this mechanistic view.

As to psychology , this new science inherited the Cartesian dualist assumptions: immaterial mind evident immediately in consciousness, and the mechanical body. Psychology struggled with the oddness of mind as its subject matter for several decades, then shifted to the other option, compatible with physicalism and reductionism , aligning psychology with physics and chemistry. This was behaviourism, and here is Watson [ 95 ] (p. 158) summarising the new approach:

Psychology , as the behaviorist views it, is a purely objective, experimental branch of natural science which needs introspection as little as do the sciences of chemistry and physics. It is granted that the behaviour of animals can be investigated without appeal to consciousness… This suggested elimination of states of consciousness as proper objects of investigation in themselves will remove the barrier from psychology which exists between it and the other sciences. The findings of psychology become the functional correlates of structure and lend themselves to explanation in physico-chemical terms.

The social sciences , on the other hand, as they emerged through the nineteenth century never were going to lend themselves to comprehension in physico-chemical terms. This would be desperate business. Their subject-matter was, briefly stated, forms and processes of social organisation, which looked a very long way from physics and chemistry, further away than even psychology . As to principles of social causation , perhaps there were universal laws governing change, but equally, social systems and events appeared as specific, even unique. In short, the ontology of the natural sciences was no use to the emerging social sciences , and their methodology was of limited or questionable use. Accordingly alternative approaches developed, drawing from philosophical traditions other than physicalism , emphasising understanding and meaning, ‘hermeneutics’, rather than causal explanation of nature. Here is Anthony Giddens on this point [ 96 ] (pp. viii–ix):

The tradition of the Geisteswissenschaften, or the ‘hermeneutic’ tradition, stretches back well before Dilthey, and from the middle of the eighteenth century onwards was intertwined with, but also partly set off from, the broader stream of Idealistic philosophy. Those associated with the hermeneutic viewpoint insisted upon the differentiation of the sciences of nature from the study of man. While we can ‘explain’ natural occurrences in terms of the application of causal laws, human conduct is intrinsically meaningful, and has to be ‘interpreted’ or ‘understood’ in a way which has no counterpart in nature. Such an emphasis linked closely with a stress upon the centrality of history in the study of human conduct, in economic action as in other areas, because the cultural values that lend meanings to human life, it was held, are created by specific processes of social development.

To sum up, physicalist reductionism had a massive influence on the development of the biological, psychological and social sciences . It prioritised physics, subsequently physics and chemistry, as the benchmark of empirical science and causal explanation. Parts of biology measured up, as biochemistry, evolutionary biology didn’t; psychology struggled; and the social sciences were so far off the mark that new views of science including alternatives to causal explanation were needed.

Against this background, deeply entrenched theory, antithetical to any distinctive forms of biological (as opposed to physico-chemical), psychological and social causation , Engel’s proposal of the biopsychosocial model was audacious. It was, however, prescient, because in the intervening decades the empirical evidence has built up, as outlined in Sect. 1.2 , under the heading “ Emerging Evidence of Psychosocial Causation ”. A main virtue of the empirical, empiricist methodology of Hume and Mill , outlined in Sect. 1.3 , under the heading “ Biopsychosocial Data in Search of Theory ”, is that it can accumulate evidence of causal connections, driving the science forwards, unhindered by theoretical prejudice. The scientific methodology for determining associations and causal connections between one or more factors and a health outcome in indifferent to the nature of the factor variables involved, in particular it has no interest in whether they are called ‘biological’, ‘psychological’ or ‘social’; the methodology has no interest in ontological matters at all—it cares only that the variables are measurable. Equally the empirical and statistical methodology has not much or nothing to say about causal mechanisms . Free of the historical theoretical baggage, it has been able to study relations between biological, psychological and social factors and health outcomes of interest, the upshot of which has been accumulation of evidence that psychological and social factors are at least associated with some health outcomes, physical and mental, and with some evidence of causal impact. Such free creativity is typical of empirical science. On the other hand, the downside is that we have apparently established biopsychosocial ontology and causal interactions, but so far untheorised, and—still feeling the effects of physicalist reductionism in the last few centuries of science—with perplexity and incredulity that such a thing is possible.

1.3.4 Theorising Biopsychosocial Interactions—Not Parallel Worlds

The proposal of biopsychosocial ontology and causal relations—under the weight of philosophical and scientific prejudice according to which psychological and social causation are impossible, even incomprehensible, and there is no distinctive biological causation either, over and above physics and chemistry—is audacious and the task of making theoretical sense of it is non-trivial.

Engel’s biopsychosocial model is a very suitable heading for examining these issues. His papers certainly identified many of them, probably all that were apparent at the time he wrote them. However, Engel’s model is only a heading for the major task of elucidating theory that can comprehend the paradigms and findings of the health sciences of the past few decades that invoke the full range of and interactions between biological, psychological and social factors in health and disease.

We propose to start with biology and especially its relation to physics and chemistry. It is the assumption that biology is no more than physics and chemistry that locks in the physicalist philosophy that the laws of physics and chemistry are the only causal laws. While that philosophical position remains in play, without viable alternative, it is difficult to make out any distinctive psychological or social causation and especially difficult to theorise biopsychosocial interactions. There is simply too much historical conceptual baggage in the way, variations of dualism and the disunity of the sciences.

We will be considering theory changes that have accelerated in the decades since Engel wrote. Up to the 1970s, just about everybody supposed that biology (as least as physiology) was reducible to physics and chemistry, but psychology and social sciences hardly, and so much the worse for them. In the 1970s, however, the reducibility of biology to physics became questionable, with recognition that all the ‘special sciences’, apart from physics/chemistry, had distinctive concepts and apparently causal explanations. However, exactly what the other sciences are sciences of, and what becomes of physicalism , dualism and reductionism , and especially how the various sciences are meant to relate to one another— all remained unclear and contested. Jerry Fodor’s 1974 paper [ 97 ] had the full title ‘Special Sciences (Or: The Disunity of Science as a Working Hypothesis)’. Fodor’s 1997 [ 98 ] update was equally informatively titled, as ‘Special Sciences: Still Autonomous After All These Years’, concluding ‘The world, it seems, runs in parallel, at many levels of description. You may find that perplexing…’

This parallel world view—or perhaps it should be parallel worlds plural—in which it is supposed that as well as the physico-chemical world, there is also a biological world (unless that is the same as the physico-chemical world), and a psychological world, and the social world—is certainly perplexing. It does not get much less perplexing if ‘parallel world(s)’ is replaced by ‘many (parallel) levels of description’. Such a view however is exactly what is intellectually arrived at when forced to acknowledge, when no longer able to deny, that the biological, psychological and social sciences are now established as valid sciences including causal determinations, in some reasonable sense of ‘causal’, such as: can predict; when no longer able to deny this, while at the same time continuing to assume that the physico-chemical world is closed to anything other than physico-chemical causation.

This parallel worlds/levels of description approach can be applied in the health sciences, leading to the idea that psychological and social models of health and disease, as well as the biomedical, can somehow all be valid, but at different levels of description. As indicated previously in Sect. 1.1 , Nassir Ghaemi argued that the biopsychosocial model has been used exactly to resolve turf wars between these various disciplines, by allowing them all to claim validity at the same time, the upshot being irredeemable vagueness and incoherence. We noted however that this thought is not prominent in Engel’s papers, which philosophically relies rather on systems theory in which there is interaction between domains.

Philosophically, the parallel world(s) move, historically inevitable as it probably was, is not really coherent; what is needed rather is a more liberal view of worldly ontology and causation that can encompass not only physics and chemistry but also biological, psychological and social processes and principles of change. In any case, so far as the current sciences are concerned, and especially the health sciences, the idea of parallel causal explanations is unhelpful; rather, what is needed is theory of multifactorial interactive causation. Specifically, data of the sort reviewed in Sect. 1.2 under the heading “ Emerging Evidence of Psychosocial Causation ”, suggesting biopsychosocial involvement in health and disease, need to be theorised in terms of biopsychosocial interactions. The quotes from Chris McManus , Ken Kendler and Dan Blazer considered at the beginning of this section, when setting up the task of the general biopsychosocial model, all refer to the need to integrate biological, psychological and social factors. Another aspect of the same point is that the various kinds of factors are found in the science to account for different proportions of the variance in health outcomes, with relative proportions of the three varying between health conditions and stages of condition. From the point of view of the science, a sentence along such lines as: ‘biological, psychological and social factors (always) each severally account for 100% of the variance – at different levels of description’—is completely incomprehensible.

1.3.5 Finding the Right Metaphor: Evolution and Development

It is not straightforward to find the right metaphor for the relation between the biological, the psychological and the social. The most common is in terms of hierarchical levels, but it suffers from reductionist connotations that lower levels are more basic, more causal, than higher ones. Alternatively, as a transitionary move away from reductionism , appraised in the previous section, it can be interpreted as different levels of ontology and/or description running in parallel, but this makes interactions mysterious. Systemic approaches that envisage interactions are the key, major improvement, but still the metaphors struggle. One, used by Engel in his 1980 paper [ 4 ], is ‘nested squares’ of systemic inter-activity, from the within-body biological, outwards to self-organised activity in the external environment, including interactions with immediate conspecifics, through to complex patterns of social organisation and regulation. This ‘nested’ domains metaphor is not up to much either, however, insofar as it lends itself to the implicit though odd presumption that the inner domain is sorted out first, then the next grows around it, then the next around that; in effect to the idea, absurd once spelt out, that our internal biology comes first, then activity in the outside world, then activity with conspecifics. This sequencing beginning with ‘first’ makes no sense temporally or systemically. Internal biology, functioning in the environment, including with other biological beings, cannot be separated from one another, conceptually or temporally.

What is missing from and obscured by these two-dimensional picture metaphors of levels and nested domains is the temporal, evolutionary and developmental, parameter . Everything is present in the original, primitive, prototypic forms . A cell is an individual unit, separate from but essentially interacting with the environment, extracting and expending energy, including interaction with other biological entities such as viruses. Parent sea birds catch fish and put it in the mouths of developmentally immature offspring, promoting the biologically necessary energetic reactions by bringing the chemicals into close enough proximity, acting like a catalyst—unless the fish is taken away first by a bigger bird of the same or different species. All these biological-environmental-individual-within-and-between-species-interactive processes are involved from the start in the simple forms , which become ever more complex. In short, no static metaphor, whether in terms of levels or nested systems, capable of being drawn on a page, does justice to the new systems sciences, which essentially invoke dynamical interaction in present time, on the basis of co-evolution through deep time.

1.3.6 Developing the General Model

Evolution and development involve increasing complexity of forms , and our argument will be that these forms bring with them new causal properties. Another way of expressing this is to say that what comes into being are increasingly complex systems, and that these systems have new and distinctive causal properties. There is in particular a quantum leap at the boundary between inanimate and biological material in which new forms or systems appear that manage the physics and chemistry of the matter, specifically energy exchanges governed by physico-chemical equations. This is the argument of Chapter 2 , Sect. 2.1 . The biological/biomedical sciences in the last half-century have done all the work to undo the restrictive assumption that biology is only physics and chemistry and to construct instead new deep theory involving another kind of ontology , turning on dynamical forms , and causation as regulation and control. The way out of physicalist reductionism starts here—exactly at the place where physics and chemistry become biology. This is the argument of Chapter 2 , Sect. 2.2 .

The evolution of life forms ends up with human psychological and social phenomena. This ‘ends up with’, as currently understood in the science, is not a matter of logic or scientific law, but is entirely contingent—accidental. In this sense, biopsychosocial systems theory is unlike some traditional philosophical systems, which start with axioms and deduce the rest, or which elucidate natural law that covers everything. So when we move from defining key features of biology , in Chapter 2 , to defining key features of psychological and hence social phenomena in Chapter 3 , there is a gap, evident at the start in Sect. 3.1 , one which cannot be filled in by logic or natural law, but only by contingent facts of evolution , development and change.

Human psychological and social phenomena have lives of their own—multiple distinctive modes of operation, turning on systemic concepts and principles already evident in biology, such as form , organisation , ends , communication , rules and regulations . In the evolution and development of new forms or systems, it can be said that they all share—from the start, and remaining in—the same ‘ontological space/time’. This is a good way of capturing the fact that they can bump into one another and affect one another, that they causally interact, as opposed to being in parallel universes. This is to say, the ontological point is at the same time essentially a point about causal interaction. We propose defining key features of psychosocial phenomena and causation in the first sections of Chapter 3 , Sects. 3.1 – 3.4 , consistent with the key features of biology proposed in Chapter 2 . With the whole biopsychosocial system in view, we return in Sect. 3.4 , to the general theory of biopsychological systems, interwoven ontology and causal theory. We address the vexed issues of top-down causes, vexed from the point of view of physicalist reductionism : psychological effects on biological processes, and social effects on our biology and psychology . However, by this stage in the argument—and in the current science we intend to be tracking—the prejudicial concepts and assumptions of physicalist reductionism are nowhere to be seen. Rather, in the new approach, there are coherent core concepts and principles of causation by regulatory control , which are found already in biology , and which can elucidate in a relatively straightforward way the logic of what is traditionally regarded as top-down processing in biological, psychological and social domains. In brief, control mechanisms employ agents at the lower level, compliant with any laws that may apply at that level, but also acting as messengers from higher levels, defined by networks of relations at those higher levels.

The detailed arguments elucidating the general theory of biopsychosocial interactions are developed through the next two chapters. The fourth chapter expands on relevance to health and disease. In fact, however, the whole theory is at its core, from the start, a theory of health and disease. This is because the theory is fundamentally normative, in terms of concepts such as functioning well or badly, being well or unwell. The contrast here with physicalist reductionism is striking: the old theory makes a point of excluding any hint of normativity, with no interest in any difference between life and death or anything else related.

Engel, G. L. (1977). The need for a new medical model: A challenge for biomedicine. Science, 196 (4286), 129–136.

Article PubMed Google Scholar

Ghaemi, S. N. (2010). The rise and fall of the biopsychosocial model: Reconciling art and science in psychiatry . Baltimore, MD: Johns Hopkins University Press.

Google Scholar

Kendler, K. S. (2010). [Book Review] The rise and fall of the biopsychosocial model: Reconciling art and science in psychiatry. American Journal of Psychiatry, 167 (8), 999–1000. https://doi.org/10.1176/appi.ajp.2010.10020268 .

Article Google Scholar

Engel, G. L. (1980). The clinical application of the biopsychosocial model. American Journal of Psychiatry, 137 (5), 535–544.

Marmot, M. (2010). Fair society, healthy lives: Strategic review of health inequalities in England post-2010 . London, UK: Department of Health.

Frankel, R. M., Quill, T. E., & McDaniel, S. H. (Eds.). (2003). The biopsychosocial approach: Past, present, and future . Rochester, NY: University of Rochester Press.

Sadler, J. Z., & Hulgus, Y. F. (1990). Knowing, valuing, acting: Clues to revising the biopsychosocial model. Comprehensive Psychiatry, 31 (3), 185–195.

Lindau, S. T., Laumann, E. O., Levinson, W., & Waite, L. J. (2003). Synthesis of scientific disciplines in pursuit of health: The interactive biopsychosocial model. Perspectives in Biology and Medicine, 46 (Suppl. 3), S74–S86.

Article PubMed PubMed Central Google Scholar

Smith, R. C., Fortin, A. H., Dwamena, F., & Frankel, R. M. (2013). An evidence-based patient-centered method makes the biopsychosocial model scientific. Patient Education and Counseling, 91 (3), 265–270. https://doi.org/10.1016/j.pec.2012.12.010 .

Ghaemi, S. N. (2009). The rise and fall of the biopsychosocial model. The British Journal of Psychiatry, 195 (1), 3–4.

Engel, G. L. (1978). The biopsychosocial model and the education of health professionals. General Hospital Psychiatry, 1 (2), 156–165.

Davey Smith, G. (2005). The biopsychosocial approach: A note of caution. In P. D. White (Ed.), Biopsychosocial medicine: An integrated approach to understanding illness (pp. 77–102). New York, NY: Oxford University Press.

McManus, C. (2005). Engel, Engels, and the side of the angels. The Lancet, 365 (9478), 2169–2170. https://doi.org/10.1016/S0140-6736(05)66761-X .

Marmot, M. (2005). Remediable or preventable social factors in the aetiology and prognosis of medical disorders. In P. D. White (Ed.), Biopsychosocial medicine: An integrated approach to understanding illness (pp. 39–58). New York, NY: Oxford University Press.

Marmot, M. (2006). Status syndrome: A challenge to medicine. Journal of the American Medical Association, 295 (11), 1304–1307.

Marmot, M. G., Rose, G., Shipley, M., & Hamilton, P. J. (1978). Employment grade and coronary heart disease in British civil servants. Journal of Epidemiology and Community Health, 32 (4), 244–249.

Link, B. G., & Phelan, J. (1995). Social conditions as fundamental causes of disease. Journal of Health and Social behavior , Special Issue, 80–94.

Cockerham, W. C. (2007). Social causes of health and disease . Cambridge: Polity Press.

Felitti, V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz, A. M., Edwards, V., et al. (1998). Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults. The Adverse Childhood Experiences (ACE) Study. American Journal of Preventative Medicine, 14 (4), 245–258.

Adler, N. E., Epel, E. S., Castellazzo, G., & Ickovics, J. R. (2000). Relationship of subjective and objective social status with psychological and physiological functioning: Preliminary data in healthy, white women. Health Psychology, 19 (6), 586–592.

Singh-Manoux, A., Adler, N. E., & Marmot, M. G. (2003). Subjective social status: Its determinants and its association with measures of ill-health in the WhiteHall II study. Social Science and Medicine, 56 (6), 1321–1333.

Beck, A. T., Rush, A. J., Shaw, B. F., & Emery, G. (1979). Cognitive therapy of depression . New York, NY: Guilford Press.

Hunsley, J., Elliott, K., & Therrien, Z. (2013). The efficacy and effectiveness of psychological treatments. Report to the Canadian Psychologial Association. https://cpa.ca/docs/File/Practice/TheEfficacyAndEffectivenessOfPsychologicalTreatments_web.pdf . Accessed 21 December 2018.

Falagas, M. E., Zarkadoulia, E. A., Ioannidou, E. N., Peppas, G., Christodoulou, C., & Rafailidis, P. I. (2007). The effect of psychosocial factors on breast cancer outcome: A systematic review. Breast Cancer Research, 9 (4), R44. https://doi.org/10.1186/bcr1744 .

Chida, Y., Hamer, M., & Steptoe, A. (2008). A bidirectional relationship between psychosocial factors and atopic disorders: A systematic review and meta-analysis. Psychosomatic Medicine, 70 (1), 102–116.

Ritz, T., Meuret, A. E., Trueba, A. F., Fritzsche, A., & von Leupoldt, A. (2013). Psychosocial factors and behavioral medicine interventions in asthma. Journal of Consulting and Clinical Psychology, 81 (2), 231–250.

Chida, Y., & Vedhara, K. (2009). Adverse psychosocial factors predict poorer prognosis in HIV disease: A meta-analytic review of prospective investigations. Brain, Behavior, and Immunity, 23 (4), 434–445.

Ironson, G. H., & Hayward, H. (2008). Do positive psychosocial factors predict disease progression in HIV-1? A review of the evidence. Psychosomatic Medicine, 70 (5), 546–554.

Langford, S. E., Ananworanich, J., & Cooper, D. A. (2007). Predictors of disease progression in HIV infection: A review. AIDS Research and Therapy, 4 (1), 1–11.

Laisné, F., Lecomte, C., & Corbière, M. (2012). Biopsychosocial predictors of prognosis in musculoskeletal disorders: A systematic review of the literature (corrected and republished). Disability and Rehabilitation, 34 (22), 1912–1941.

Berk, H. O. S. (2010). The biopsychosocial factors that serve as predictors of the outcome of surgical modalities for chronic pain. Agri, 22 (3), 93–97.

Block, A. R., Ben-Porath, Y. S., & Marek, R. J. (2013). Psychological risk factors for poor outcome of spine surgery and spinal cord stimulator implant: A review of the literature and their assessment with the MMPI-2-RF. The Clinical Neuropsychologist, 27 (1), 81–107.

Celestin, J., Edwards, R. R., & Jamison, R. N. (2009). Pretreatment psychosocial variables as predictors of outcomes following lumbar surgery and spinal cord stimulation: A systematic review and literature synthesis. Pain Medicine, 10 (4), 639–653.

den Boer, J. J., Oostendorp, R. A. B., Beems, T., Munneke, M., Oerlemans, M., & Evers, A. W. M. (2006). A systematic review of bio-psychosocial risk factors for an unfavourable outcome after lumbar disc surgery. European Spine Journal, 15 (5), 527–536.

Epker, J., & Block, A. R. (2001). Presurgical psychological screening in back pain patients: A review. The Clinical Journal of Pain, 17 (3), 200–205.

Gaudin, D., Krafcik, B. M., Mansour, T. R., & Alnemari, A. (2017). Considerations in spinal fusion surgery for chronic lumbar pain: Psychosocial factors, rating scales, and perioperative patient education. World Neurosurgery, 98, 21–27.

Lall, M. P., & Restrepo, E. (2017). The biopsychosocial model of low back pain and patient-centered outcomes following lumbarfusion. Orthopaedic Nursing, 36 (3), 213–221.

Wilhelm, M., Reiman, M., Goode, A., Richardson, W., Brown, C., Vaughn, D., et al. (2015). Psychological predictors of outcomes with lumbar spinal fusion: A systematic literature review. Physiotherapy Research International, 22 (2), e1648.

Fineberg, S. K., West, A., Na, P. J., Oldham, M., Schilsky, M., Hawkins, K. A., et al. (2016). Utility of pretransplant psychological measures to predict posttransplant outcomes in liver transplant patients: A systematic review. General Hospital Psychiatry, 40, 4–11.

Pignay-Demaria, V., Lespérance, F., Demaria, R. G., Frasure-Smith, N., & Perrault, L. P. (2003). Depression and anxiety and outcomes of coronary artery bypass surgery. The Annals of Thoracic Surgery, 75 (1), 314–321.

Rosenberger, P. H., Jokl, P., & Ickovics, J. (2006). Psychosocial factors and surgical outcomes: An evidence-based literature review. Journal of the American Academy of Orthopaedic Surgeons, 14 (7), 397–405.

Tully, P. J., & Baker, R. A. (2012). Depression, anxiety, and cardiac morbidity outcomes after coronary artery bypass surgery: A contemporary and practical review. Journal of Geriatric Cardiology, 9 (2), 197–208.

Alexander, S. J. (2013). Time to get serious about assessing—and managing—psychosocial issues associated with chronic wounds. Current Opinion in Supportive and Palliative Care, 7 (1), 95–100.

Soon, K., & Acton, C. (2006). Pain-induced stress: A barrier to wound healing. Wounds UK, 2 (4), 92–101.

Mollayeva, T., Kendzerska, T., Mollayeva, S., Shapiro, C. M., Colantonio, A., & Cassidy, J. D. (2014). A systematic review of fatigue in patients with traumatic brain injury: The course, predictors and consequences. Neuroscience and Biobehavioral Reviews, 47, 684–716.

Chang, E. Y., Chang, E., Cragg, S., & Cramer, S. C. (2013). Predictors of gains during inpatient rehabilitation in patients with stroke: A review. Critical Reviews in Physical and Rehabilitation Medicine, 25 (3–4), 203–221.

Admi, H., Shadmi, E., Baruch, H., & Zisberg, A. (2015). From research to reality: Minimizing the effects of hospitalization on older adults. Rambam Maimonides Medical Journal, 6 (2), e0017. https://doi.org/10.5041/RMMJ.10201 .

Felix-Aaron, K., Moy, E., Kang, M., Patel, M., Chesley, F. D., & Clancy, C. (2005). Variation in quality of men’s health care by race/ethnicity and social class. Medical Care, 43 (3), I-72–I-81.

Grintsova, O., Maier, W., & Mielck, A. (2014). Inequalities in health care among patients with type 2 diabetes by individual socio-economic status (SES) and regional deprivation: A systematic literature review. International Journal for Equity in Health, 13 (1), 43. http://www.equityhealthj.com/content/13/1/43 .

Davidson, E., Liu, J. J., & Sheikh, A. (2010). The impact of ethnicity on asthma care. Primary Care Respiratory Journal, 19 (3), 202–208.

Crawshaw, J., Auyeung, V., Norton, S., & Weinman, J. (2016). Identifying psychosocial predictors of medication non-adherence following acute coronary syndrome: A systematic review and meta-analysis. Journal of Psychosomatic Research, 90, 10–32.

Ghimire, S., Castelino, R. L., Lioufas, N. M., Peterson, G. M., & Zaidi, S. T. R. (2015). Nonadherence to medication therapy in haemodialysis patients: A systematic review. PLoS One, 10 (12), e0144119.

Loiselle, K., Rausch, J. R., & Modi, A. C. (2015). Behavioral predictors of medication adherence trajectories among youth with newly diagnosed epilepsy. Epilepsy & Behavior, 50, 103–107.

Zwikker, H. E., van den Bemt, B. J. F., Vriezekolk, J. E., van den Ende, C. H. M., & Dulmen, S. (2014). Psychosocial predictors of non-adherence to chronic medication: Systematic review of longitudinal studies. Patient Preference and Adherence, 8, 519–563.

Edwards, R. R., Dworkin, R. H., Sullivan, M. D., Turk, D. C., & Wasan, A. D. (2016). The role of psychosocial processes in the development and maintenance of chronic pain. The Journal of Pain, 17 (9), T70–T92.

Ong, K. S., & Keng, S. B. (2003). The biological, social, and psychological relationship between depression and chronic pain. The Journal of Craniomandibular & Sleep Practice, 21 (4), 286–294.

Harrison, A. M., McCracken, L. M., Bogosian, A., & Moss-Morris, R. (2015). Towards a better understanding of MS pain: A systematic review of potentially modifiable psychosocial factors. Journal of Psychosomatic Research, 78 (1), 12–24.

Mallen, C. D., Peat, G., Thomas, E., Dunn, K. M., & Croft, P. R. (2007). Prognostic factors for musculoskeletal pain in primary care: A systematic review. British Journal of General Practice, 57 (541), 655–661.

PubMed Google Scholar

Whibley, D., Martin, K. R., Lovell, K., & Jones, G. T. (2015). A systematic review of prognostic factors for distal upper limb pain. British Journal of Pain, 9 (4), 241–255.

Pincus, T., Burton, A. K., Vogel, S., & Field, A. P. (2002). A systematic review of psychological factors as predictors of chronicity/disability in prospective cohorts of low back pain. Spine, 27 (5), E109–E120.

Ramond-Roquin, A., Bouton, C., Bègue, C., Petit, A., Roquelaure, Y., & Huez, J. F. (2015). Psychosocial risk factors, interventions, and comorbidity in patients with non-specific low back pain in primary care: Need for comprehensive and patient-centered care. Frontiers in Medicine, 2 (73), 1–6.

Campbell, P., Wynne‐Jones, G., & Dunn, K. M. (2011). The influence of informal social support on risk and prognosis in spinal pain: A systematic review. European Journal of Pain, 15 (5), 444. e1–14. https://doi.org/10.1016/j.ejpain.2010.09.011 .

Riegel, B., Bruenahl, C. A., Ahyai, S., Bingel, U., Fisch, M., & Löwe, B. (2014). Assessing psychological factors, social aspects and psychiatric co-morbidity associated with Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) in men: A systematic review. Journal of Psychosomatic Research, 77 (5), 333–350.

Somers, T. J., Keefe, F. J., Godiwala, N., & Hoyler, G. H. (2009). Psychosocial factors and the pain experience of osteoarthritis patients: New findings and new directions. Current Opinion in Rheumatology, 21 (5), 501–506.

Novy, D. M., & Aigner, C. J. (2014). The biopsychosocial model in cancer pain. Current Opinion in Supportive and Palliative Care, 8 (2), 117–123.

Schreiber, K. L., Kehlet, H., Belfer, I., & Edwards, R. R. (2014). Predicting, preventing and managing persistent pain after breast cancer surgery: The importance of psychosocial factors. Pain, 4 (6), 445–459.

Von Korff, M. (2005). Fear and depression as remediable causes of disability in common medical conditions in primary care. In P. D. White (Ed.), Biopsychosocial medicine: An integrated approach to understanding illness (pp. 117–131). New York, NY: Oxford University Press.

Naylor, C., Parsonage, M., McDaid, D., Knapp, M., Fossey, M., & Galea, A. (2012). Long-term conditions and and mental health: The cost of co-morbidities. The King’s Fund and Centre for Mental Health. Available at https://www.kingsfund.org.uk/sites/default/files/field/field_publication_file/long-term-conditions-mental-health-cost-comorbidities-naylor-feb12.pdf . Accessed 21 December 2018.

Parle, M., Jones, B., & Maguire, P. (1996). Maladaptive coping and affective disorders among cancer patients. Psychological Medicine, 26 (4), 735–744.

Cordella, M., & Poiani, A. (2004). Behavioural Oncology: Psychological, communicative, and social dimensions . New York, NY: Springer-Verlag.

NHS England & NHS Improvement. (2018). The Improving Access to Psychological Therapies (IAPT) pathway for people with long-term physical health conditions and medically unexplained symptoms . London, UK: NHS.

Allart, P., Soubeyran, P., & Cousson-Gélie, F. (2013). Are psychosocial factors associated with quality of life in patients with haematological cancer? A critical review of the literature. Psycho-Oncology, 22 (2), 241–249.

Bakaniene, I., Prasauskiene, A., & Vaiciene‐Magistris, N. (2016). Health‐related quality of life in children with myelomeningocele: A systematic review of the literature. Child: Care, Health and Development, 42 (5), 625–643.

Sales, P. M. G., Carvalho, A. F., McIntyre, R. S., Pavlidis, N., & Hyphantis, T. N. (2014). Psychosocial predictors of health outcomes in colorectal cancer: A comprehensive review. Cancer Treatment Reviews, 40 (6), 800–809.

Bours, M. J. L., van der Linden, B. W. A., Winkels, R. M., van Duijnhoven, F. J., Mols, F., van Roekel, E. H., et al. (2016). Candidate predictors of health-related quality of life of colorectal cancer survivors: A systematic review. Oncologist, 21 (4), 433–452.

Kang, K., Gholizadeh, L., Inglis, S. C., & Han, H. R. (2017). Correlates of health-related quality of life in patients with myocardial infarction: A literature review. International Journal of Nursing Studies, 73, 1–16.

Peeters, C. M. M., Visser, E., Van de Ree, C. L. P., Gosens, T., Den Oudsten, B. L., & De Vries, J. (2016). Quality of life after hip fracture in the elderly: A systematic literature review. Injury, 47 (7), 1369–1382.

Pragodpol, P., & Ryan, C. (2013). Critical review of factors predicting health-related quality of life in newly diagnosed coronary artery disease patients. Journal of Cardiovascular Nursing, 28 (3), 277–284.

Taylor, R. S., Sander, J. W., Taylor, R. J., & Baker, G. A. (2011). Predictors of health-related quality of life and costs in adults with epilepsy: A systematic review. Epilepsia, 52 (12), 2168–2180.

Seiam, A. H. R., Dhaliwal, H., & Wiebe, S. (2011). Determinants of quality of life after epilepsy surgery: Systematic review and evidence summary. Epilepsy & Behavior, 21 (4), 441–445.

Walders-Abramson, N. (2014). Depression and quality of life in youth-onset type 2 diabetes mellitus. Current Diabetes Reports, 14 (1), 449. https://doi.org/10.1007/s11892-013-0449-x .

Blazer, D. (2010). [Book Review] The rise and fall of the biopsychosocial model: Reconciling art and science in psychiatry. The International Journal of Psychiatry in Medicine, 40 (3), 361–362. https://doi.org/10.2190/PM.40.3.j .

Mill, J. S. (1843). A system of logic . London: John W. Parker.

Hume, D. (1902). An enquiry concerning human understanding (L. A. Selby-Bigge, Ed.). Oxford: Oxford University Press (Original work published 1777).

Koch, R. (1890). Uber bacteriologische forschung. Deutsche Medizinische Wochenschrift, 16, 756–757.

Evans, A. (1976). Causation and disease: The Henle-Koch postulates revisited. The Yale Journal of Biology and Medicine, 49, 175–195.

PubMed PubMed Central Google Scholar

Bolton, D. (2008). The epistemology of randomized, controlled trials and application in psychiatry. Philosophy, Psychiatry & Psychology, 15 (2), 159–165.

Rutter, M. (2000). Psychosocial influences: Critiques, findings, and research needs. Development and Psychopathology, 12 (3), 375–405. https://doi.org/10.1017/S0954579400003072 .

Stoljar, D. (2015)., “Physicalism”, The Stanford Encyclopedia of Philosophy (Winter 2017 Edition), Edward N. Zalta (ed.), URL = < https://plato.stanford.edu/archives/win2017/entries/physicalism/ >. Accessed 12/21/2018.

Burtt, E. A. (1932). The metaphysical foundations of modern physical sciences . London: Routledge and Kegan Paul.

Dijksterhuis, E. J. (1961). The mechanization of the world picture (C. Dikshoorn, Trans.). Oxford: Oxford University Press.

Koyré, A. (1968). Metaphysics and measurement: Essays in the scientific revolution . London: Chapman and Hall.

Mayr, E. (1982). The growth of biological thought: Diversity, evolution, and inheritance . Cambridge, MA: Harvard University Press.

Bechtel, W., & Richardson, R. C. (2005). Vitalism. In E. Craig (Ed.), The shorter Routledge encyclopedia of philosophy (p. 1051). Oxford: Routledge.

Watson, J. B. (1913). Psychology as the behaviorist views it. Psychological Review, 20 (2), 158–177.

Giddens, A. (2005). Introduction to the protestant ethic and the spirit of capitalism, by Max Weber (T. Parsons, Trans.). London: Routledge.

Fodor, J. (1974). Special sciences (Or: The disunity of science as a working hypothesis). Synthese, 28 (2), 97–115.

Fodor, J. (1997). Special sciences: Still autonomous after all these years. Philosophical Perspectives, 11, 149–163.

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Bolton, D., Gillett, G. (2019). The Biopsychosocial Model 40 Years On. In: The Biopsychosocial Model of Health and Disease. Palgrave Pivot, Cham. https://doi.org/10.1007/978-3-030-11899-0_1

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Bolton D, Gillett G. The Biopsychosocial Model of Health and Disease: New Philosophical and Scientific Developments [Internet]. Cham (CH): Palgrave Pivot; 2019. doi: 10.1007/978-3-030-11899-0_4

Cover of The Biopsychosocial Model of Health and Disease

The Biopsychosocial Model of Health and Disease: New Philosophical and Scientific Developments [Internet].

Chapter 4 biopsychosocial conditions of health and disease.

Published online: March 29, 2019.

This chapter continues from the previous chapter on themes in biopsychosocial conditions of health and disease, picking up some core questions familiar in the theory and philosophy of medicine. We argue that the concepts and boundaries of health and disease are themselves biopsychosocial. Controversies about whether such-and-such a condition is or is not a medical matter, as opposed to difference or lifestyle choice, the consequences of being which involve benefits such as access to healthcare and/or harms such as stigma, and the terms in which such debates are conducted—are all thoroughly biopsychosocial-political. Core defining features of illness—activity limitations, pain and distress—likewise involve our psychology and social life as well as our biology. On the theme of causation, we endorse scientific method as the route to identifying causal mechanisms, note the major role of chronic stress in models of causal mechanisms linking psychosocial factors with biological damage, and spell out that chronic stress is a quintessential biopsychosocial concept. We consider the Research Domain Criteria (RDoC) proposed recently by the N.I.M.H. as a framework for research in mental health as an illustration of a biopsychosocial research framework, potentially extendable to cover physical health and biomedicine. Physical and mental health conditions are brought together in the new biopsychosocial model rather than being axiomatically separate—as they were in the old context of reductionism and dualism.

4.1. Conditions of Biopsychosocial Life

So far, we have reviewed the rationale as well as the challenges for the biopsychosocial model, in Chapter 1 , and, drawing on contemporary life and human sciences, presented conceptualisations of the biological, in Chapter 2 , and the psychological and social, in Chapter 3 . In the later parts of Chapter 3 , we drew out features of the biopsychosocial whole, especially that causal interactions run within and between these three, or rather four, since the natural environment is thoroughly involved with all, a point made explicit in Sect. 2.3 . Critical for the biopsychosocial model as a model of health and disease, foundational biopsychosocial concepts already have the relevant normative distinction built into them. Chapter 2 characterised biological processes as local areas running contrary to the general direction of the second law of thermodynamics, temporarily; this feat achieved by metabolic regulatory mechanisms, which, as and when they fail, jeopardise the viability of the organism, which in any case eventually inevitably ends up back as dust, more or less prematurely. Some familiar conditions of biological life were listed in Sect. 3.3 , such as food, water, oxygen, suitable ambient temperature, accommodation, on the way to the less obvious conditions of psychological life as agency, which include opportunity, access to resources such as education and training, which involves, picking up themes in Sect. 3.2 , recognition by a supportive, encouraging and resourced social group, which is also necessary, along with peace and an uncompromised natural environment, for basic biological security.

In short, the conditions of biological, psychological and social life—risks and protective factors for developing and recovering from health conditions—are pervasive. As this has become clear in science and our thinking, health policy has recognised that it should be cross-sectoral, involving much more than the healthcare sector. As a general rule, the healthcare sector is trained and funded to treat people who have fallen below the or their normal level of functioning, in important domains, with the aim of restoration of function, or optimising lowered function, or reducing avoidable further loss. The healthcare sector also has a limited role in primary prevention, but this has turned out to be a multifaceted, cross-sectoral task, in which the illness-related language of healthcare gives way to more general concepts such as promoting resilience, or well-being, thriving, or further away still, happy enough family life, access to and use of educational opportunity, satisfying and well enough paid work, friendships and meaningful civic engagement.

The biopsychosocial model is a model of health and disease, but this roughly divides up, for reasons understandable in terms of the model, into, on the one hand, the business of the healthcare sector—illness, with the negative conception of health as avoidance of or recovery from illness—and, on the other hand, prevention of illness, which merges into resilience and thriving, which are protections against ill health from the point of view of healthcare, but which from all other, non-illness preoccupied sectors, are another thing altogether: education, work, economics, politics, environmental policy and security. In this fourth chapter, we pursue further implications of biopsychosocial theory as a model of disease and health as absence of disease, leaving aside the broader questions of health and well-being.

4.2. Biopsychosocial Conceptualisation of Health Conditions

Concepts and boundary disputes.

What health and illness mean in general are matters which concern the physician least of all. He deals scientifically with life processes and with particular illnesses. What is ‘ill’ in general depends less on the judgement of the doctor than on the judgment of the patient and on the dominant views in any given cultural circle.

In conditions of certainty, there is no need to spell out what illness means; all concerned, at home and in the hospital, know only too well, and they have other serious tasks to be getting on with. And if and when the need for a definition of illness or disease arises, in a textbook or classroom or the clinic, it is easy enough to give one simply by using some other term with similar meaning, such as abnormal structure or function, or disruption , disturbance , dysregulation , etc. The medical textbook descriptions of signs, syndromes and diseases are full of such terms, and they can all be used to define each other well enough for most purposes. This family of disease/illness related terms are all typically systemic, referring to abnormalities or disturbances of structural forms, regulation and functional ends.

The meaning of illness—and all the cognates to do with abnormality—becomes an issue in conditions of uncertainty and dispute as to whether such and such a condition is an illness or not, in circumstances when it seems that no further observation or laboratory test would settle the matter clearly one way or the other. This uncertainty arises when criteria that normally go together, in the paradigm or prototypical kind of case, fall apart. Three key features of illness typically go together: the person complains of distress or pain; second, they are unable to do things they need to do, there is incapacity or activity limitation, loss of agency; and third, there is the assumption that these things are because something is not well with the person’s body or mind. This last assumption implies that medical/psychological expertise is required, hopefully, to reduce the harm (the distress/pain and incapacity) and not create more. When these features and assumptions are all present and correct, there are conditions for certainty—but insofar as they cleave apart, some present, some absent, or dubious, the position becomes ambiguous; attribution of illness and the closely linked perceived need for healthcare professional attention, become uncertain. With uncertainty comes controversy. Examples of general kinds of case where attribution of illness and/or need for medical attention is commonly contested include: some mental health diagnoses, especially those associated with non-voluntary admissions; ‘medically unexplained’ conditions; alleged over-medicalising and overtreating of conditions that are regarded rather as ‘normal’, self-limiting, or less harmful compared with harms from treating; pathologising/stigmatising difference and diversity, and lifestyle choices—even if they carry raised risk of illness.

The reference to ‘pathologizing/stigmatising’refers to a downside of the illness attribution—a harmful side effect, linked to the main effect. The main effect of illness is to decrease our agency, up to and including the ultimate ending of it all. The adverse effects of illness on agency, and the experience of illness as pain and distress, cue interpersonal and institutionalised responses to help, to provide resources including care and treatment. At the same time, social expectations are reduced: the ill person is excused from normal social role obligations, from moral responsibility, and hence from blame; the attribution of causation of behaviour, or of inactivity, is to the illness, not to the person as agent. In short, illness attribution implies excuse for and not being blamed for the downturn in functioning, and the right to access available healthcare. However, at the same time, and for the same reasons, pathologising carries the risk of disqualification of the person from their full recognition as a self-determining agent in the social world—with knock-on risks of being stigmatised and subjected to the many varieties of social exclusion. The relative benefits and losses of being seen as ill depend on many general and individual factors. For sudden onset, treatable conditions, the benefits are typically high and the costs (of the above psychosocial sort) relatively low. For long-term conditions, with no treatment, or with treatments that—from the person’s point of view—may do as much harm as good, the balance shifts, costs may outweigh benefits, leading to a rejection of the ‘illness’ label, in favour of ‘difference’ and ‘diversity’.

Conditions of so-called ‘disability’ are a special case, distinguished from ‘illness’, for complex reasons including absence of treatment, and, commonly, the absence of complaints of distress. However, the ‘disability’ label functions like the ‘illness’ label in that it imputes deficit in ability, hence excuse from ‘normal’ social role obligations, and hence at the same time carries risk of demotion from full recognition as an equal agent. Furthermore, for lifelong conditions, ‘disability’ is not relative to the person’s own previous functioning, and for acquired chronic conditions, the downturn in personal functioning does not come with implied upturn, and becomes ‘difference’. The implication is that the critical notion of ‘deficit in relation to normal’ is benchmarked not against the person’s own normality but against normality of the majority. Further, since ability to act is a function not only of personal abilities but that always in the context of task demands and available resources and opportunities, the cause of ‘disability’ can be legitimately attributed to these external factors; for example, people who have to use wheelchairs are handicapped in mobility by the way the majority build transport systems, not by their condition in itself. These kinds of points are well theorised in the ‘social model of disability’ (e.g. [ 2 , 3 ]).

In short, conceptual issues around illness—and disability-related concepts and practices involve a complex range of and interaction between biological, psychological, social, moral and policy factors. They cannot be so much as articulated without a full biopsychosocial framework.

The Logic of Disease Attribution Is Top-Down

The fundamental feature of disease in a system is that it causes—or significantly raises risk of—disruption of the function of the system, thus leading to adverse outcomes for a dependent system. ‘Adverse outcomes for a dependent system’ implies disruption of functionality of that dependent system, and that dysfunctionality in turn means that it causes or raises of adverse outcomes on a further dependent system… and so on. This cascade continues until we reach dysfunctionality/adverse outcomes for the organism as a whole in its activity in the environment. It is poor outcomes at the level of the whole that ultimately drives attribution of dysfunctionality downwards to the parts that serve the whole. In short, the difference between function and dysfunction (or between good enough function and not good enough function) of parts, ultimately turns on the difference between function and dysfunction (or between good enough function and not good enough function) of the organism as a whole.

In short, the logic of disease attribution is top-down, not bottom-up. The causal pathways, by contrast, can be bottom-up, as for example atherosclerosis causing an embolus causing cardiac arrest causing the person’s death. Causal pathways can also be top-down as previously considered; for example, chronic unhealthy diet and lack of exercise raising risk for atherosclerosis. But the point made here is a different one, namely, that the logic of dysfunction, as opposed to function, is top-down, in the sense that it flows from whole to part.

The Centrality of the Person

The implication of the line of argument in the preceding section is that, in biopsychosocial systems theory, health conditions have to be understood in terms of the person as a whole, specifically how it affects their agency, values and achievement of personal goals. The centrality of the person was identified by Engel as a feature of the biopsychosocial model in his original papers [ 4 , 5 ]. In this respect, there are some connections between the biopsychosocial model and the Patient- or Client-centred Care Model, and many papers have examined the relation between the two approaches (e.g. [ 6 – 9 ]).

There are also connections with the Recovery model, a relatively recent, important and radical influence on mental health services [ 10 – 12 ]. The model focuses on chronic health conditions, on the centrality of the person’s life and values, on achieving a good quality-of-life, on the need for good medical and nursing care, especially in acute phases, and on issues of access to social resources and opportunities. Many if not all aspects of the Recovery model can be applied as much to chronic physical health conditions as to mental health conditions, though so far this extension is in its infancy (see e.g. [ 13 ]).

The focus on chronic conditions has implications for a distinction often drawn in the literature between illness and disease , illness being the condition of the person, and hence involved in the personal and social world, and disease being a dysfunctional condition of a bodily organ or system, and not so involved (e.g. [ 14 , 15 ]). Although this is an important distinction, it applies most clearly in cases where there is an identifiable somatic disease process, in an otherwise unaffected person, which subsequently remits, spontaneously or with treatment. The distinction becomes blurred, however, in chronic conditions that have to be accommodated in the person’s life and hence involved with the development of the whole personality. William Osler’s famous remark: It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has [ 16 ]—applies especially well to chronic conditions. This blurring of the difference between disease and illness is another aspect of the shift from the (infectious) disease paradigm to focus on non-communicable conditions, which require a biopsychosocial approach.

The number of people living with chronic diseases for decades is increasing worldwide… In this context, the WHO definition becomes counterproductive as it declares people with chronic diseases and disabilities definitively ill. It minimises the role of the human capacity to cope autonomously with life’s ever changing physical, emotional, and social challenges and to function with fulfilment and a feeling of wellbeing with a chronic disease or disability.

Consistent with this last sentence, the authors go on to propose a conceptualisation of health as the ability to adapt and to self-manage , discussing this in relation to physical health, mental health and social health.

A concept of health along these lines makes personal agency fundamental, though in its broad biopsychosocial context, interacting with resources and opportunities. A person’s sense of agency, whether they can do enough to have a viable life, and with it whether they wish for life, as it is, or better, with treatment or with none, are all matters that depend on the person. The condition of the biological body matters, but insofar as it affects the person. It is of fundamental importance in healthcare that it is the person who feels ill and wants treatment, any or more, or feels well enough without it. We attend to the person, not the body part—and not to psychological signs and symptoms in isolation either. The centrality of the person also shows up in the next section. We will quote from Wittgenstein: the pain may be in the hand, but we comfort the person, not the hand.

Pain and Distress Have Personal Biopsychosocial Meaning

Activity limitation is the core behavioural feature of illness or injury, pain and distress are their subjectively experienced aspects. But even these subjective experiences turn out to be thoroughly biopsychosocial, whichever way one approaches them: by philosophical analysis of ‘subjective experience’, or in terms of neuropsychological models of causal pathways, or behavioural models of interpersonal pain signalling functions.

‘But doesn’t what you say come to this: that there is no pain, for example, without pain-behaviour? ’ It comes to this: only of a living human being and what resembles (behaves like) a living human being can one say: it has sensations; it sees; is blind; hears; is deaf; is conscious or unconscious.

But isn’t it absurd to say of a body that it has pain?——And why does one feel an absurdity in that? In what sense is it true that my hand does not feel pain, but I in my hand? What sort of issue is: Is it the body that feels pain?—How is it to be decided? What makes it plausible to say that it is not the body?— Well, something like this: if someone has a pain in his hand, then the hand does not say so (unless it writes it) and one does not comfort the hand, but the sufferer: one looks into his face.

Reconstructions of pain that involve moving away from preconceptions of mind/body dualism, appear increasingly in the humanities literatures (e.g. [ 19 , 20 ]).

Turning to the subjective experience: there are three distinct components […] First, there is the purely discriminative part that includes recognizing the quality of the sensation as a burn and localizing it to your hand. Second, there is the motivational aspect associated with the desire to pull your hand away or to terminate the sensation. Third, there is an evaluative component the thought of the damage that has been done to your hand and how that will affect your life in the hours and days ahead. (italics added)

It is this third component—italicised in the quotation above—that is of special interest here, because we take it to involve: the thought of the impact of the damage to oneself, one’s agency and way of life, including its always important social aspects. In short, this evaluative component that is central to the experience of pain is thoroughly biopsychosocial. The ‘biopsychosocial’ appears here in the intentionality of pain, i.e. in what it is ‘about’, its meaning or representational content, which is, briefly: threat of loss of significant biopsychosocial function.

In addition to its role in pain perception, the limbic system mediates emotional responses to a variety of factors including personal loss, anticipation of harm, and so on. The dysphoric states such as depression and anxiety share limbic system circuits with somatic pain. It is thus no accident that the word “pain” is often used to denote emotional pain that has no somatic component.

The evaluative component in pain perception figures prominently in psychological models of pain and distress, with clinical applications. Highly negative (fearful) appraisals about the effect of damage, or other negative events, and indeed of the pain or distress itself, on one’s future life are sometimes referred to as catastrophizing , and they typically risk having the effect of amplifying the experience. These models have the implication that psychological management of pain and distress should target among other things reduction of catastrophising [ 23 ].

A further psychosocial aspect of pain and distress is their function in interpersonal signalling and regulation of behaviour. This aspect is already implied in Wittgenstein’s account of pain expression: expressions of pain, behavioural, facial and verbal, induce caring responses from others. It has been theorised in various ways, for example in the Social Communication Model of Pain [ 24 ] and in evolutionary theoretic terms [ 25 ].

4.3. Locating Causes in Biopsychosocial Systems

Identifying dysfunctions and modifiable causes.

While disease is contextualised in the person as a whole, the immediate question is where the dysfunctional process is located: which system within the whole is dysfunctional, causing problems for the whole? The methodological assumption of healthcare is that the person as a whole is in trouble because of some dysfunctional part, a dysfunctional subsystem within the body/mind. It underlies the traditional individual focussed medical model of identification of clinical syndromes and diagnoses, and models of psychological processes in the individual that give rise to distress and activity limitations. The scientific details are in the medical and clinical psychological textbooks and will not be taken further here. We focus more on the broader implications of systems theory and the biopsychosocial approach. The main issue is that systems theory envisages (causal) interactions everywhere, including within and between the organism and the environment, in which context the question arises: what is the logic of attributing causes of dysfunction to the organism rather than the environment?

In systems theory, one cannot begin to talk about the function of systems without reference to their operating environments. All biological systems function in interaction with others and ultimately in relation to fitness of the whole organism in a range of environmental conditions. One broad kind of pathway to dysfunction of the whole is poorness of fit between the expected environment, to which behaviour is adapted, and the actual environment, to which it isn’t. This general point applies in the evolutionary context, for example in the so-called ‘thrifty phenotype’ hypothesis applied to obesity. Hales and Barker [ 26 ] hypothesise that in poor dietary conditions in utero metabolic mechanisms are set to maximise fat storage in expectation of subsequent, poor post-natal dietary intake; this mechanism would be highly adaptive in environments where poor dietary conditions in utero were reliably followed by poor dietary conditions postnatal, as may be reasonably assumed to be the case in our original evolutionary environments; but if this association breaks down, as in postnatal dietary environments that are actually high in accessible sugar/fats, the consequence would be a hard to modify tendency to excessive fat storage. The general idea of poorness of fit of previously adaptive mechanisms to later environments has an ontogenetic version in the learning theories in psychological science: behaviour shaped up by one set of environmental contingencies may be maladaptive in a subsequent environment. For example, if toddlers are reared in parenting styles involving multiple and conflicting commands, the child is likely to learn to ignore them and to seek to satisfy their own goals regardless, but this behaviour pattern will likely lead to poor outcomes in the classroom [ 27 , 28 ].

Notwithstanding these considerations, we still locate the problem—the dysfunction—in the person. An obvious reason for doing so is the centrality of the person: it is the person to whom harm accrues—who suffers pain, distress, significant impairment of agency and loss. However, this consideration alone is superficial in a systemic context, because the cause may still lie outside the person, being done to, and this is the force behind the social model of disability which we have already had occasion to cite in this section. A more promising key to this issue is the one increasingly found in the health literature: the concept of identifying modifiable causes. The idea is that, among all the criss-crossing causal pathways, what needs to be identified are promising targets for intervention. This approach is consistent with the interventionist approach to causality referred to in Chapter 3 , Sect. 3.1 , and is well suited to healthcare as applied science, seeking to change things, for the better. From this point of view, dysfunction attribution is in part—and somewhat paradoxically—shorthand for belief about promising possibilities for change. While ‘dysfunction’ and its cognates connote deficit, promising possibilities for change are opportunities.

In complex systems where there is a poor fit between the person’s behaviours and the environment, the question arises: where is potential for change? In conditions of the person that are lifelong, not amenable to change, the potential for change lies elsewhere, not in the person, but in social attitudes and resources—and this is a compelling argument of the social model of disability. For acquired long-term health conditions, it is likely that optimal outcomes from the person’s point of view come from a combination of—in no order—available high-quality healthcare, self-management, social support, plus non-discrimination by broader society.

Effective treatment or prevention technologies rely on targeting a cause of large enough effect, i.e. a causal factor identified in group studies that accounts for a large proportion of the outcome variance. The main point for the present purpose is that there are few causes of currently common health conditions with so large an effect that targeting them leads to complete prevention or complete cure, and for the majority, a multimodal approach to multiple factors is required.

These issues relate to the problem of reduction of disease to a single primary cause . If a normal function of a biological system is carried out by only that one system, then the failure of that function will be reducible to processes within that one system. For example, insofar as it is only the cardiovascular system that delivers oxygen to cells, failure to achieve that functional end, depleted oxygen delivery to cells, is attributable only to—and in this sense is reducible to—cardiovascular dysfunction, to a cardiovascular disease process such as atherosclerosis. In many cases however, and this may be the general rule, biological functions are affected by multiple subsystems, with the effect that achievement of a particular function is not a matter of processes in any one system, but may be affected by many interacting systems. However, such factors may not be relevant to the disease process once onset: for example, advanced arteriosclerosis is not likely to be reversed by social policy affecting dietary changes, and quite different interventions may be needed, such as bypass surgery. On the other hand, for acquired, chronic health conditions, there is typically ongoing interaction with environmental, psychological and social factors. There is, in brief, no reduction to a primary cause, biological, psychological or social, but rather multiple systems of all kinds are involved at varying stages, some contributing risk for poor outcomes, others contributing to protection, including restorative and compensatory mechanisms.

Identifying Causal Mechanisms

In setting the scene for developing biopsychosocial theory in the first chapter, we noted that evidence of biological, psychological and social causal factors in many health conditions comes from group statistical data in controlled study designs. The inference to causation relies on the empiricist approach to causation, after Hume and Mill, as association or correlation determined in experimental or quasi-experimental study designs. We noted however that such data in themselves provide no theoretical account of what kind of thing the variables stand for, or what kind of causal properties they have, separately or in combination. This absence of ontological-causal theory is particularly noticeable given the long-standing assumptions that physical(-chemical) processes alone are causal, covered by inviolable physical laws, that therefore biological factors can be causal only because biology is physics and chemistry, while mental events are scientifically odd epiphenomena, and social processes can hardly be conceptualised at all within this particular world view. The task of Chapter 3 and this chapter is to elucidate a general biopsychosocial theory capable of comprehending biopsychosocial data.

The health sciences infer causal relations from mixed evidence: on the one hand, mechanisms and theoretical knowledge, and, on the other, statistics and probabilities. Statistics are used to show that the cause makes a difference to the effect, and mechanisms allow causal relationships to explain the occurrence of an effect.

A mechanism for a behaviour is a complex system that produces that behaviour by the interaction of a number of parts, where the interactions between parts can be characterised by direct, invariant, change relating generalisations.

This is more informative, but is so exactly because it reintroduces the importance of invariant generalisations consistent with the empiricist approach to causation.

So what is a causal mechanism over and over what is established by controlled experimentation? The life sciences deal with complex systems changing over time, with probabilistic associations between inputs and outputs that are separated spatially by the inner workings of the system and by time. Confidence in having identified a causal mechanism is raised when the events are proximate, with fewer or no intervening processes and closer in time. So one idea behind ‘causal mechanism’ is just that we fill in the intervening steps , spatial and temporal, finding causal connections of ever closer proximity between inputs and effects, between, for example, environmental exposures at one time and poor health at a later time. This approach to ‘causal mechanism’—filling in the intermediate steps—is suggested by Illari and Williamson [ 30 ], and supported by considerations in, for example, Kincaid [ 33 ]. It is, however, readily accommodated in the empiricist approach to causation, a point well-argued by Kendler and Campbell [ 34 ]. A corollary of filling in the intervening steps, with ever closer proximity of links in the causal chain, taking into account other proximate factors at each step, in effect increases probabilities from lower to higher. Further, as probabilities of association and correlations approach 1, the sample size required for confidence in generalisability reduces: a few well-designed, replicated experiments with relatively small samples will do. All this can be understood in terms of the empiricist approach.

There is however the famous limitation of empiricist epistemology, whether in the knowledge of causes or knowledge generally, namely, that it omits theory , envisaging knowledge by observation only. In the statement of their thesis quoted above Russo and Williamson bring together ‘(causal) mechanisms and theoretical knowledge’ contrasted with statistics and probabilities, but it is worth distinguishing them. It is true that experimental method or approximations to it only ever establish correlations and associations, albeit generalisable and counter-factual that can support intervention to make a difference. The theory goes further, however, explaining why the correlations exist and why the intervention works, ‘explaining’ in the sense of fitting into a more or less well-established body of knowledge. On the other hand, it should be said that the additional need for theory is not a totally different requirement compared with establishing causal connections; rather, theory is typically a broader class of causal connections, themselves established or confirmed using experimental methodologies or approximations. So, if we elucidate the concept of ‘causal mechanism’ in terms of ‘theory’, just as if we elucidate it in terms of intervening steps, the process of identifying a causal mechanism and identifying a cause are similar—and specifically, identifying causal mechanisms is not a separate epistemological route to establishing causes. This conclusion is consistent with Alex Broadbent’s discussion of these issues in epidemiology [ 35 ], and with Bert Leuridan’s and Erik Weber’s discussion of mechanistic evidence and the International Agency for Research on Cancer (IARC) [ 36 ].

As to what theorised biopsychosocial causal mechanisms are, the general concepts and principles have been the main topic in preceding chapters, including systems , structures or forms , functioning towards ends , information and communication , coding , regulation and control . And for causal mechanisms responsible for breakdown, their relevant negations, such as such as error , abnormal , dysfunction and dysregulation . These are the general concepts and principles; the specifics are diverse, depending on which system, vulnerable structures, ends and control mechanisms are being modelled.

Stress as a Biopsychosocial Causal Mechanism

Chronic stress carries an attributable risk for cardiovascular disease that is on par with other recognised risk factors, such as smoking, increased lipid concentrations, hypertension, and diabetes. Despite the prevalence and potency of this risk factor, little is known about the mechanisms that translate stress into cardiovascular disease events… Our study provides several observations that together define a mechanism linking stress to cardiovascular events…, specifically that the amygdala could be a key structure in the mechanism… and that upregulation of haemopoietic tissue activity and increased atherosclerotic inflammation are additionally implicated in a neural–haemopoietic–arterial axis.

A good way of thinking about stressful person-environment relationships is to examine the relative balance of forces between environmental demands and the person’s psychological resources for dealing with them. If the environmental load substantially exceeds the person’s resources, a stressful relationship exists… In psychological stress, the comparison is between the power of the environmental demands to harm, threaten, or challenge, and the psychological resources of the person to manage these demands… From the standpoint of this way of thinking, stress is particularly powerful when the individual must struggle with demands that cannot easily be met… If the ratio of demands to resources becomes too great, we are no longer talking about high stress but trauma… The person feels helpless to deal with the demands to which he or she is exposed, and this can result in feelings of panic, hopelessness, and depression.

Psychologically, stress arises from exposure to salient negative, uncontrollable events, jeopardising the sense of agency. Salience covers what is essential to our biological and psychological life. Further, psychological stress essentially involves social factors such as task demands and access to resources. At the same time psychological stress is also biological, physiological: it is the activation of the arousal system, preparing for action to achieve important goals—but if the goals cannot be achieved, ever, or never enough, or never reliably, the arousal system is chronically active, and it is this chronic (hyper-) activity of the arousal system that is hypothesised to be the source of long-term biological damage. In short, chronic stress as the key hypothesised mechanism linking psychosocial factors with poor physical and mental health outcomes is—as to be expected—a mechanism that explicitly addresses criss-crossing biological, psychological and social processes. Key features of the hypothesised chronic stress mechanism are aspects of the core features we have proposed for biopsychosocial theory: the psychological sense of agency and action itself are compromised, raising risk for mental health problems, because social task demands are excessive and social resources inadequate, and the consequences of this chronic psychosocial misfortune is top-down dysregulation of critical biological processes raising risk of physical health problems.

Biopsychosocial Research Framework

Extension to physical health : A research framework of this sort could be to apply to biological systems below as well as above the neck, to include such as the cardiovascular system as well as the central nervous system, in effect incorporating biomedicine, and potentially then able to have relevance to physical as well as to mental health conditions. Importantly, it would be able to accommodate the many kinds of pathways and conditions that do not fit neatly into either of these two categories, such as risks involving chronic stress, or the so-called psychosomatic conditions or medically unexplained symptoms. The expanded framework would in effect have the advantage of recognising interactions between the brain and other biological systems, and hence be able to accommodate the emerging evidence outlined in Chapter 1 , Sect. 1 .2 , implicating psychosocial factors in the aetiology and course of medical conditions. Assuming the grid has explicit relevance to both systemic function and dysfunction in the rows, on which more below, some aspects of research findings relevant on mental health on the one hand and physical health on the other would diverge significantly, for example, confirmation of primary biological progressive disease mechanisms and treatments in some physical diseases. But in other areas of the grid, particularly relating to aetiological risk factors accumulating through the lifespan, or in areas of the grid—to be proposed for addition below—on management of chronic conditions and factors affecting quality-of-life, similarities among mental and physical health conditions would be more apparent.

More discrimination among kinds of psychological and social factors relevant to health and disease . For example, to accommodate aspects of agency: agency as perceived, and agency related to social factors including task demands (e.g. work; dependents) and access to resources and opportunities (these of many kinds, including access to treatment). This would require more columns. The RDoC framework is work in progress, adaptable as the science develops; current versions have around 5 columns for biological factors, around 1 for psychological, and around 0–1 for social factors (e.g. [ 45 , 46 ]).

Acknowledgment of non-social environmental health risks , especially important if physical health is included, again requiring more columns, to include factors such as ambient air quality and available diet.

Explicit specification of health conditions or ‘diseases’ , not only the biological systems. The RDoC framework at present has no explicit conceptualisation or characterisation of mental health conditions, connected with the aim of replacing current psychosocial diagnostic criteria with biological criteria [ 47 – 49 ]. To accommodate specification of health conditions, probably a third dimension of the grid would be needed. This is easier to see if we imagine the grid incorporating biomedicine in which the issues are better worked out: the rows would be specific systems such as the immune system, with implicit reference to its components and functions, and the columns would specify factors affecting functioning, but probably a third dimension of the grid, distinct though theoretically closely connected to the rows and the columns, would be needed to specify the dysfunctions and disorders of the immune system. The cells in this now 3-dimensional grid could then accommodate findings of the specific subsystems responsible for harmful health conditions warranting healthcare attention.

Need to discriminate among stages of health conditions would arise once a dimension specifically for health conditions was explicitly in place. It would also be necessary, as we have emphasised previously, to distinguish between research questions referring to, first, aetiology of disease incidence, in population samples; second, disease progression or maintenance, in patient samples; and third, factors affecting quality-of-life in chronic conditions. These discriminations are necessary because they are distinct research questions, requiring distinctive methodologies and sampling, and also—especially relevant to our main theme—because the balance of biological, psychological and social involvement can vary substantially depending on the stage of a condition. For example, for cardiovascular disease biological processes dominate as maintaining factors and targets for intervention such as surgery in the advanced stages of the disease; whereas, if the question is the aetiology of cardiovascular disease, accumulation of risk factors in the population, to be applied as basis for prevention technologies, or application to advising an at-risk individual patient, then lifestyle social and factors, such as exercise and time of access to treatment, figure large. And for chronic diseases, in fact for all diseases where the person is alive and managing, not in coma, there are always issues of agency and the quality of life. A framework for organising or planning research into management of chronic diseases would, therefore, need to accommodate the full range of biological, psychological, environmental and social factors.

Population level as opposed to individual level questions , for example, incidence vs. susceptibility, might require different grids, the one to do with differences between individuals (types), the other differences between populations. The UK NICE conceptual framework for public health [ 50 ], for example, distinguishes between individual and population patterns of disease and their causal mechanisms; both include biological, social and related factors, but the latter has additional interactions with a range of other factors including political and economic.

Finally, a further dimension of variation is developmental . All biological and psychological systems in health and disease have developmental trajectories, within which there is variation in the relative influence of biopsychosocial and environmental factors, including in factors affecting vulnerability and resilience to adversities and illness. Hence all the research questions would have to allow for age variation.

The points above indicate what, based on considerations so far in this essay, would constitute an adequate framework for organising health research and identifying areas of relatively certainty and important unknowns. Possibly further dimensions could be added, for example on ‘impact’, estimating the relative importance of knowing more about a specific health condition at a specific stage, for treatment or prevention, depending on, for example, prevalence, projected prevalence, among what age-group, healthcare costs, associated cross-sectoral costs, etc. But, in any case, the elaborated framework as sketched above is already multidimensional, needs far more than a two-dimensional grid, can hardly be represented diagrammatically, though could be split up into different diagrams, but it is bound to be complicated if able to accommodate and organise the entire basic and clinical science health research—this can hardly be expected to be simple. In practice of course such a multidimensional monster grid to organise biopsychosocial research across the whole of healthcare will never be constructed because too big, too complicated and of no practical use. Small segments of the hypothetical framework are written up in reviews for circumscribed specifics: for some conditions, some treatments, some stages, some health economic analyses, some policies, other angles. Otherwise, it exists in the scientific literature as a whole, broadly construed, across the range of biopsychosocial and environmental sciences applied to health.

In the next section, we consider the tension—intrinsic to healthcare as it has developed over the past few decades—between research data of the kinds considered above, on groups, and clinical care of the individual.

Clinical Epistemology

It is something of an irony that while health research has made such strides over the past few decades, while knowledge has increased, certainty in the clinic is just as likely to have gone down as up! This is connected with the fact that much of what has been discovered is about complex, multifactorial causation. We know more about the body and mind, their functions and dysfunctions, and their interaction with the environment, and more about the treatment of biological and psychological health problems, but this has come along with increasing appreciation of the complexity of the problems, beyond physically damaged tissue or biological infection, involving multiple interacting biological systems, along with increased understanding of regulating systems with wide interactive reach, including the central nervous system and psychological functioning. Linked with multifactorial complexity, this new complicated knowledge is statistical, based on group studies, delivering associations such as relative risk and odds ratios, and quantifications of treatment effects such as effect size and number-needed-to-treat—and how all these statistics relate to a particular patient is unsettled. Notwithstanding the benefits of evidence-based practice, the challenges of inference from population-based aetiological risk studies and clinical treatment trials to preventative management and treatment of the individual patient are significant [ 51 , 52 ]. The challenges here do not disqualify the application of the experimental method, following Mill’s methods of agreement and difference, or approximations to them, to determine causes and effects (as outlined in Chapter 1 , Sect. 1.3 , under the heading “ Biopsychosocial Data in Search of Theory ”). There are in fact no other serious players on this particular pitch. Application includes reliance on randomised controlled treatment trials (or better, meta-analyses of multiple such trials) as being the most logically valid way of identifying treatment effects (see e.g. [ 53 ]). Experimental method can result in reliable positive findings, but also, and of high importance, reliable negative findings, likelihoods of no or no clinically significant effect of a treatment, compared with no treatment, or with a harmless placebo. The epistemological problem is not how to establish that a treatment technology has some effect or no effect in group samples, but rather that, because of many kinds of complexity (in the condition, in the sampling, in individual differences), treatments are rarely effective for all individuals, and application of the data to care of the individual patient is not straightforward. For this, as is often said, thorough assessment and clinical judgement are needed to combine with knowledge of the basic and clinical science.

Complexity and uncertainty are most marked where there is evidence of causation by multiple factors of small effect. Conversely, simplicity and certainty are most marked where single, primary causative factors are presumed. The single, primary factor approach works well in some specialist areas of biomedicine and psychological therapy, and less well in clinical settings with caseload is not restricted to a narrow range of conditions, in settings such as primary care, palliative care, care of the elderly, and community mental health. Other limitations of the single factor approach are apparent in medical wards and outpatient clinics in which some patients present with pain, distress and activity limitations in the absence of biomedically determined conditions. All these contexts require a broader causal theory, more complex, about which much is unknown at present, to do with biological/psychological/social interactions of the sort being explored for example in the chronic pain, health psychology and public health literatures.

This new complexity creates much uncertainty, in clinicians, patients and students. It can be resolved by a dogmatic certainty that the real cause must be one or another sort—something biological, psychological or social—though at the cost of selective inattention to other factors, the risk of over-reliance on one treatment approach, and detachment from anomalies. More adaptively, the uncertainty has to be tolerated. The more responsibility a clinician has, the more obligation they have to know the science as well as the patient and to keep a mind open to complexity and alternatives, at the same time as needing to make definite decisions and recommendations one way or the other.

There are occasions, in response to questions from patients or from students as to causes, in complex cases, where single aetiology of large effect has been excluded, and the picture looks more like multiple aetiology of small effect, it is as correct as anything else to say:‘it is a complex biopsychosocial picture’. This move is by all means somewhat vague and hand-waving, connected to the criticism of the biopsychosocial model reviewed in the first chapter, that it is vague and too often used for unhelpful hand-waving. Engel’s model has stood ready to accommodate emerging findings of biopsychosocial complexity, and being so accommodating has made it hard to capture in a few words except vaguely. However, complexity and uncertainty have come from the science; they are not peculiar features of a model—no point blaming the messenger. And, in fairness to the biopsychosocial model, the generalised single primary cause models are the same—vague hand-waving to everything being biological/biomedical, or else all psychological, or social. The science of the past few decades has all but ruled out these single primary cause general models, and endorsed the broader biopsychosocial approach. The broader approach is also able to be more discriminating, more empirically based than the previous generalised single factor models. Biological, psychological and social factors may be involved in specific health conditions, at specific stages, but whether they are or not, and in what degree, is not known in advance, but only by doing the science.

4.4. Compare and Contrast Physical and Mental Health Conditions

Psychiatry and ‘the rest of medicine’.

Psychiatry is obviously psychological, at first glance, but also obviously social, at second glance, while biological to a degree, while the rest of medicine—according to the biomedical model—manages well enough with the biological only. In this sense, the question of psychiatry’s relation to ‘the rest of medicine’ stands proxy for the rationale and validity of the biopsychosocial model—and vice versa. In fact, Engel chose just this issue as the starting place for his 1977 paper; he turned on its head the aspiration for psychiatry to emulate the rest of medicine, recommending the opposite: make the rest of medicine more like psychiatry—more psychosocial, not biological only [ 4 ] (p. 129).

On the other hand, as we noted at the beginning of the first chapter (under the heading “ The Presumed ‘Overarching Framework’ ”), the ‘rest of medicine’ is not one thing, and the various medical specialities differ in their relative involvement with biological, psychological and social factors. Primary care (also known as general medical practice, or family medicine) is much involved with the psychosocial, as is public health, and palliative care, as well as many aspects of care on acute medical wards. In this sense, the contrast is not so much between psychiatry with the rest of medicine, but between psychiatry along with many other areas of medicine, contrasted with biomedicine. Taking these considerations things into account much qualifies the idea that psychiatry is so different because of its involvement with the psychosocial. Nevertheless, psychiatry can still be regarded as the odd one out compared with ‘the rest of medicine’, for reasons that go much deeper than detailed and discriminating considerations of the above sort about varying degrees of involvement with the psychosocial.

The Difference Is Deeply Theorised and Institutionalised

The perceived difference between mental and physical health conditions and healthcare is underpinned by the great historical dichotomies outlined in the first chapter, Sect. 1.3 (under the heading “ Prejudicial Theory: Physicalism, Reductionism, Dualism ”): mind/body dualism, and the separation of the social and moral sciences from the natural sciences. Thomas Szasz’s highly influential 1960s critique of psychiatry [ 54 ] relied on these dichotomies. But worse, the two sides of the dichotomies were not equally balanced in respect of scientific validity, especially in connection with determining causes and interventions—matters fundamental to medicine. Rather, against the background of physicalist reductionism, which underpinned the dichotomies, as reviewed in Sect. 2.2 , while physical health conditions involved recognised causes and effects, researchable and manageable by proper biological/biomedical science, mental disorders were something else altogether, barely recognisable let alone theorised, and psychiatry along with them.

Built on top of the historical dichotomies in deep theory are the reinforcing, maintaining effects of having organised the whole of healthcare training and delivery around physical health problems on one side of the road and mental health problems on the other. On one side, biomedicine performs best with biological mechanisms in physical diseases, and psychosocial involvement, if any, is out of scope. On the other side, theoretical or practical preoccupation with ‘mental abnormalities’ such as delusions and other hard to understand mental states and behaviour tends to neglect somatic signs and symptoms, and does not bring into focus people as a whole and their social circumstances. The dichotomy between mental and physical health conditions is historically theorised and currently institutionalised and practised.

The Biopsychosocial Model Highlights Similarities

There are several reasons why the picture is changing however. Mental health conditions are more evident, linked to increasing public awareness and efforts to decrease stigma, and the extent of associated activity impairments such as days lost to work is better understood and increasingly recognised as comparable with those in physical health conditions. It is increasingly recognised that physical and mental health problems often co-occur, complicating each other, and therefore also complicating our healthcare system, given that it is currently organised on the basis of separating them out, along with the clinical expertise for managing them. And as regards aetiology, public health and prevention, recent epidemiology suggests that the two kinds of health problem can share aetiological risk factors, possibly implicating shared mechanisms. These social and scientific developments change policy, as for example in the UK NHS policy paper ‘No health without mental health’ [ 55 ]. In this section, we review these issues in more detail, with reference to the biopsychosocial theory and science set out in previous chapters.

Considering aetiology, we noted in the first chapter, Sect. 1.2 , the emerging epidemiological evidence that implicates psychosocial as well as biological risk factors including genetic for many physical health conditions. It also suggests that some risks of all sorts are shared between some physical health conditions and some mental health conditions; it is not the case that risk factors divide neatly into those to physical health on the one hand and those to mental health on the other. Drilling into hypothesised mechanisms, we saw in section Stress as a Biopsychosocial Causal Mechanism that chronic stress and its biological effects are commonly implicated in the aetiology of many physical and mental health conditions. Again, it is not the case that pathogenic mechanisms neatly divide between those for physical health conditions and those for mental health conditions. As corollary, preventative strategies and technologies, for many physical and mental health conditions, overlap. Public health does not have two unconnected tasks, one for physical health promotion and another for mental health promotion.

Post onset, especially for the long-term conditions, also considered in Sect. 1.2 under the heading “ Emerging Evidence of Psychosocial Causation ”, psychosocial factors affect biomedical management, in matters such as access and collaboration over management plan, for example ongoing medication; as well as affecting psychological adjustment and quality of social life. These diverse psychosocial issues coincide or at least overlap for both physical health and mental health long term conditions. We went on to note the connected finding that physical health problems raise risk for mental health problems and vice versa. The causal pathways are diverse, but include such as chronic physical ill-health imposes activity restrictions and loss of amenity, and pain, all of which raise risk of high anxiety and low mood; mental health chronic conditions can be associated with risk factors for physical health problems, such as social exclusion, poor diet, smoking, and higher thresholds for medical attention to physical health problems. The picture that emerges, therefore, is not that of patients with physical health problems, and an entirely different set of patients with mental health problems. All these considerations—regarding aetiology, adjustment, quality of life, and bidirectional complications—serve to break down the dichotomy between mental health conditions and physical health conditions. They highlight the importance of psychological and social as well as biological factors in health and disease, and they need broad biopsychosocial theory to accommodate them.

The general drift of the biopsychosocial systemic approach—as can be expected from its name—is to view physical and mental health conditions under a unified ‘health problem’ heading. The core common feature is a substantial negative effect on the person’s agency, associated with distress: with worry and fear about their safety and their future and their dependents.

In the broader biopsychosocial picture, the key secondary difference between physical health problems and health problems is that some but not all physical health problems have a biomedically identifiable maintaining cause—a disease process or lesion—while this is probably not the case for mental health problems. This is a critical difference and it stands out most clearly for physical health problems that are biomedically well understood and treatable, in a relatively short timeframe, without therefore impacting on what is presupposed as an otherwise normal life. Cure of infectious disease by antibiotics, surgical interventions that are now routine such as hip replacements and even cardiac surgery, especially where all the psychological and social conditions for access, detection and intervention are in place, and which therefore can be ignored, stand out as triumphs of biomedicine. If we start with the underlying presumption that physical health problems are purely physical—and entirely different from mental health problems—these are the cases we will attend to, and we would tend to neglect the kinds and aspects of physical health problems that don’t fit the picture: regarding aetiology, chronic conditions and comorbidities as reviewed briefly above. And, coming from the other direction, the assumption that mental health problems are quite different from physical health problems because exclusively to do with the mind, or the person, is also problematic. For example, some mental health conditions have some response to pharmacotherapy. It is true that psychological therapy is often indicated along with medication for mental health conditions, but equally, as is now being recognised, it is often indicated alongside medical management of physical health conditions [ 56 ]. As to mental health conditions, as opposed to physical health conditions, being integral to the personality, the contrast is less marked for long-term conditions of either type, as previously remarked in Sect. 4.2 . Also, some mental health conditions such as obsessive-compulsive disorder are typically seen by the person as externally imposed, rather than as integral to themselves. This is probably the rule for mental health conditions rather than the exception. This is a complicated clinical area but the point, in short, is that only for a particular sub-class of mental health conditions is there a strong presumed link with personality, that is, the so-called ‘personality disorders’.

Another way of viewing the similarities and differences between mental health conditions and physical health conditions is through the lens of the hypothetical virtual biopsychosocial research framework sketched above (Sect. 4.3 ). In addition to the specification of biological and neurological systemic functioning, this framework was imagined to include specification of health problems, physical and mental, and to have complete coverage of stages, from risks of onset through to post-onset maintaining causal mechanisms, interventions, and factors affecting adjustment and quality-of-life in long-term conditions. The columns of the grid would include biological, psychological and social factors, and the cells research findings. The upshot of this is that the relative importance of biological compared with psychosocial factors would be most marked between mental and some physical health problems at just one—albeit very important—point, namely post-onset maintaining causal mechanisms and interventions. For some physical health problems, these would be mainly biological with little psychosocial. But for all other stages: aetiological pathways to onset, and post-onset adjustment and quality-of-life, the pattern of relative weights of biological, psychological and social would be evened out and would certainly not be all biological for all physical health problems, and all psychological and social for mental health problems.

4.5. Locating the Biopsychosocial Model

We noted in the first chapter that the biopsychosocial model has been charged with vagueness in the clinic, as well as vagueness as a scientific theory and as a ‘model’. It is true that Engel wrote his 1980 paper [ 5 ] on clinical application of the model, giving rise to the reasonable inference that the biopsychosocial model was a guide to clinical practice. However, as we went on to note in Sect. 1.2 , there have been many developments in the intervening decades with more direct relevance to scientific content and guiding clinical practice. There have been new research programmes to investigate the causes of diseases and disease mechanisms, and technologies for prevention, early detection and treatment. These, in turn, have led to treatment guidelines for specific conditions at specific stages, to the whole apparatus of evidence-based clinical care, to be used alongside a thorough assessment of the individual case. The point is simply that, given all this basic and clinical science of the last few decades, the biopsychosocial model cannot usefully be regarded as some additional statement of the science or as a tool to guide clinical decision-making. It is true the model advises us to keep one’s mind open to the range of biopsychosocial factors, but the treatment guidelines and the science behind them already now say this, if applicable, and we don’t need a general model to repeat the fact—especially not to repeat it vaguely instead of paying close attention to the science of specific conditions and stages.

While this may be a solution for the biopsychosocial model of the vagueness problem, it works only, as we noted in section “ So What’s the Point of a ‘General Model’? ”, by raising the more fundamental question: what is the point of having a general model at all? We then located the task of the general model as defining biopsychosocial ontology and causation, in Sect. 1.3 , noting the special need for this because of the deeply entrenched assumptions of physicalism, dualism and reductionism that have been so influential in the development of the life and human sciences. With these assumptions, only physical properties and causation appear real, while the mind is a non-causal epiphenomena, and social organisation and processes can hardly be comprehended at all. In short, the scientific and philosophical back story is more or less entirely antithetical to theorising biopsychosocial ontology and interactions. Hence the need for a new general theory for this purpose. We pursued this, tracking the science, in Chapters 2 and 3 .

In Chapter 2 on biology we used the approach especially suited for the present purpose that relates biological processes to physics. Life forms do extraordinary things with energy, holding up the general direction of the second law of thermodynamics, for a while, the key being control by genetic code, essentially prone to error, to doing it differently, making space for evolutionary diversification. The key ontological shift compared with physicalism is away from few primary physical qualities and laws, variations on the theme of energy and energy conservation, towards multiplicity and diversity of dynamical forms with their own distinctive principles of change and causal interaction, all however retaining consistency with the physics of the matter. The corresponding key epistemological shifts are from generality to specificity, simplicity to complexity, and from knowledge of inviolable facts to active knowing, something more like ‘trial and error’. Moving on from biology, the psychological and the social were considered in Chapter 3 . The primary concept of the psychological is identified as agency. This connotes altogether: causation, in the sense of regulatory control, authorship, individual differences, and self-determination. Agency is thoroughly biological: it is embodied, and accordingly has to secure the conditions necessary for biological life, specifically those related to maintaining appropriate energy differentials. At the same time, agency for us social beings needs recognition in the social group, and generally assumes a socio-political dimension, connoted by the related concept of autonomy. The primary function of the social is identified in the model as the regulatory control of the distribution of resources necessary for biological life, but also of resources and opportunities for psychological development and cultivation of agency.

In this biopsychosocial theory, concepts of health and disease appear in prototypical form at the beginning, in the differences between survival and non-survival of biological organisms, between a biological system’s working or breaking down. The basic facts of biological health and disease carry through into the biopsychosocial whole, being joined by concepts of psychological health and ill-health, related to agency, and concepts of psychosocial health and disadvantage, marked by exclusion from social relationships, resources and opportunities. Causal pathways run within and between all these systems and the many subsystems that serve them, in health and ill-health. The exact pathways and the size of effects vary with the health condition, its stage, and the challenges it presents to the person as agent.

As well as major developments in the basic and clinical sciences since Engel’s original papers, there have been other major developments in dedicated models of health and disease and clinical practice. Three such have been mentioned so far in this chapter, Sect. 4.2 : the social model of disability, which contests attribution of cause of activity limitations to the person rather than to the ill-resourced, socially excluding environment; the model of patient-centred care, which locates the person as patient, their aims and values, at the centre of healthcare, and the Recovery model, which theorises the need of the person with a chronic health condition to recover their life notwithstanding. These dedicated models emphasise specific important aspects of healthcare that broadly relate to individual differences, the person, the broader social and political context, and managing with chronic conditions—typically with explicit contrast with a perceived simple and over-simple ‘medical model’, with its focus on biological disease processes in the individual. In this sense, these models have taken up challenges and tasks of the sort that Engel identified, but with more elaboration, depth and detail than the biopsychosocial model itself.

As proposed here, biopsychosocial theory and the biopsychosocial model define the conceptual foundations of a new approach to health, disease and healthcare, one that responds to the accumulating evidence implicating many and diverse processes of kinds indicated by the name, and more besides, particularly the physics and chemistry of our bodies and the environment, at one end, and social and economic policy at the other. It is more general than the science of specifics, or single disciplines, or dedicated models of clinical care. It is more like a view of human nature, based in the current science, one that includes propensity to health and disease. As a view of human nature and its vulnerabilities, the biopsychosocial model is comparable to the biomedical model. The biomedical model has two versions however: the old version, running to approximately mid-twentieth century, assuming, as Engel saw, physicalist reductionism and dualism, the other brand new and going from strength to strength since, at the cutting edge of reconstructing the relationship between biology, physics and chemistry, and articulating new models involving not only the inviolable physics and chemistry of energy, but also vulnerable forms regulated to ends. The new research programmes have advanced biomedicine, but at a conceptual level they open up worlds beyond the biological to include the psychological and the social. This conceptual opening up is of huge importance given that the conceptual foundations of health science and healthcare need to be able to comprehend and respond to all the new findings on psychosocial factors that have been accumulating over the past few decades, on the social determinants of health, the effectiveness of psychological and social treatments, and the increasing prevalence of long-term health conditions.

Biopsychosocial theory, incorporating the psychosocial and the political, also involves morality. The biopsychosocial model of health and disease has conceptual connections with bioethics. This is a contrast with the biomedical model, in either its old or new forms. To the extent that the biomedical model embraced physicalist reductionism, it was not entitled to any normative concepts, not even the difference between health and disease, and definitely not morals. Normativity has no place in physics and chemistry. The new biomedical model that invokes regulatory control mechanisms has normativity, but so far restricted to internal somatic systems and does not yet comprehend the whole human being as an agent in the interpersonal, socio-political world. To have this reach, the biopsychosocial model is required, and the term ‘bioethics’ could be expanded to ‘biopsychosocial ethics’. At the foundational level, all normativity is interconnected. The 4 principles of bioethics laid out by Beauchamp and Childress [ 57 ] employ terms and relations that are foundational in biopsychosocial theory: autonomy of the person, harm and benefits to the person, social distribution of resources. The biopsychosocial theory does not resolve ethical disputes but indicates their terms and the friction points where they arise. Biological health, psychological health, autonomous exercise of agency and values, social provision of resources necessary for these things—are all goods from our point of view as biopsychosocial beings, but they can be hard to achieve together since they can come into conflict one with one another. The individual may come into conflict with family, clinicians or the law, over what is good for them; what is in the interests of the individual may conflict with what is in the interests of the community; attribution of ‘illness’ or ‘disability’ may have benefits in terms of access to healthcare and support, but it downgrades recognition of autonomy, with potential for harm; provision of resources can conflict with promoting agency; equal distribution of resources competes with individual and group interests. And there are boundary issues, for example as to when biological life becomes psychological life with moral value protected by law, or as to when psychological life has come to an end in severe brain damage while the biology continues. Biopsychosocial theory cannot resolve these many kinds of moral dilemmas, but their terms and the potential for conflicts over priorities and boundaries appear at its foundations.

Monographs, or book chapters, which are outputs of Wellcome Trust funding have been made freely available as part of the Wellcome Trust's open access policy

Cite this Page Bolton D, Gillett G. The Biopsychosocial Model of Health and Disease: New Philosophical and Scientific Developments [Internet]. Cham (CH): Palgrave Pivot; 2019. Chapter 4, Biopsychosocial Conditions of Health and Disease. 2019 Mar 29. doi: 10.1007/978-3-030-11899-0_4
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Conditions of Biopsychosocial Life
Biopsychosocial Conceptualisation of Health Conditions
Locating Causes in Biopsychosocial Systems
Compare and Contrast Physical and Mental Health Conditions
Locating the Biopsychosocial Model

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Introducing the Biopsychosocial Model for good medicine and good doctors

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Introducing the Biopsychosocial approach as the model for good medicine and good doctors.

Development of a new model

Until recent decades the traditional approach towards health and disease has been the medical or biological model where a person’s ill- health was exclusively treated by medical means. At the time this seemed satisfactory but recent research in psychology and the social sciences has challenged this approach and sought to develop a new more extensive model of health that can be applied in clinical practice.

In spite of the traditional dominance of the biomedical model, the time seems right for expanding the model to the Biopsychosocial Model as the social and psychological influences of today’s health problems do not fit the narrow framework of the biomedical model. There has been much discontentment with the medical model to the extent that Engel (1977) suggested that it had acquired the authority and tradition of dogma. It was this same author who devised the Biopsychosocial Model and stated in his landmark paper that,

“We are now faced with the necessity and the challenge to broaden the approach to disease to include the psychosocial without sacrificing the enormous advantages of the biomedical approach”.

The Biopsychosocial Model of health and illness as proposed by Engel (1977) implies that behaviours, thoughts and feelings may influence a physical state. He disputed the long-held assumption that only the biological factors of health and disease are worthy of study and practice. He argued that psychological and social factors influence biological functioning and play a role in health and illness also. This is a more realistic model in light of the role lifestyles play in a society having entered the new millennium. This new theoretical model therefore has been developed in an attempt to improve on the disease approach and narrow view with respect to health and illness held by the medical model so that psychological and social factors of the individual can also be considered.

The Biopsychosocial Model is a very important step in medical care as it broadens the scope with which health and illness can be examined in clinical practice. Considering this model leads to the patient being interviewed as a person with an individual lifestyle and not simply as a patient with a disease which has deviated them from normal functioning. Thus the clinician will have many avenues to explore before they make their diagnosis and hopefully they will be able to provide preventative information to the patient about how they may adjust their lifestyle in order to have a better quality of life. This model can be used in medical schools to train doctors in the art of good communication, understanding and compassion.

The Biopsychosocial Model in Clinical Practice

One of the primary criticisms of new theoretical models is that they may lack scientifically proved evidence that they can work. This would be an unjust criticism of the Biopsychosocial Model however as there has been substantial and extensive research into how this model can interface with modern health problems and exert a considerable improvement. Many of the modern illnesses such as heart disease and cancer have been found to have psychological and social components to their aetiology. For example it has been estimated that 30% of cancers are associated with tobacco use and that diet accounts for some incidence of digestive tract cancers (Doll and Peto, 1981). Psychological factors such as self-esteem and perceived control have been identified as potential markers to help increase health- promoting behaviours like exercise and reduction of over-consumption. Also since it is known that individual’s susceptibility to coronary heart disease is increased by factors such as hypertension, smoking, high cholesterol and type A personality traits, then interventions can be designed to seek change in a person’s lifestyle.

Possibly the most general biopsychosocial illness is that caused by excess stress, that term used to describe situations in which individuals are faced with environmental or other demands which exceed their immediate ability to cope (Lazarus and Folkman, 1984). Very often these situations produce adverse psychological and physiological changes and sometimes they are associated with a disease outcome. With the Biopsychosocial model, stress can be examined from each of these perspectives. Firstly, biological factors like high blood pressure levels, muscle tension and an individual’s decreased resistance to disease as a result of immuno- suppression could be sources of investigation. Psychological factors like increasing risk behaviours (smoking, large alcohol intake), coping mechanisms and predisposition to anxiety could be examined. In fact a study conducted on stress and burnout in psychiatric nurses showed that the biggest factor in causation of burnout as measured on the Maslach Burnout Inventory (MBI) was not job-demands but high trait anxiety levels (Mc Inerney,1999).

Different interventions for modifying risk behaviours and so incidence of disease can be carried out on an individual or small group basis using stress- management or relaxation techniques. However, it has been found that it is very difficult for individuals to give up risky behaviours and adopt more healthy lifestyles. It is therefore necessary to alter the cognitions (beliefs, perceptions and attributes) that patients have about their health and illness which play a role in determining their behaviour. Cognitive-behavioural therapy, once exclusively used in the domain of clinical psychology has proved successful in dealing with illnesses that would previously have been viewed as requiring medical intervention e.g. cardiovascular disease.

Social factors like loneliness, lack of participation in social activities like exercising, the effects of unemployment and the effects of working in an environment where long and unsociable working hours are the norm are examples of where interventions may be implemented. Good research will need to be continued to identify the health risks associated with different behaviours and social conditions. This data should then be brought to the attention of the Government to bring about changes at a political, economic and social level so we may seek to eliminate conditions like poverty, unemployment and loneliness. Since many high-risk behaviours are often associated with these adverse social conditions, it may only be after changes occur at a political level that the vicious cycle of social circumstances affecting psychological and medical circumstances will be broken. At an individual level, families can exert a range of either positive or negative influences on the health status and psychosocial adjustment of patients. Family support can reduce the stressful impact of illness, assist in the development of coping mechanisms by the patient and encourage compliance with medical regimens (Flor& Turk,1985) Biopsychosocial interventions may be achieved in clinical practice by introducing these psychological or social interventions at the primary care level. For example, GPs and hospital doctors should be able to apply some psychological techniques themselves to intervene in the patients lifestyle to avoid them needing medical treatment given that there is an increased amount of training in these areas being offered in medical schools. It is no longer sufficient that doctors feel that they only deal with broken bones; they must also seek to mend the mind.

There are far-reaching implications of this model to the training of good doctors and for good medical practice. An interesting area where this model is being used is in the psychiatric hospital where a multi- disciplinary team consisting of a consultant psychiatrist, junior doctor, psychologist, social worker and psychiatric nurse consider the patients problem firstly as a whole and then divide their resources. This has a very effective result as all the needs of the patient are met and the team is aware of the needs of the patient to improve their quality of life.

Sadly, it appears that there is a scarcity of psychological or social intervention in Irish general hospitals. Hospital doctors should have clear guidelines about what health professional they should contact if they believe that a patient may benefit from psychological or social intervention. Also junior doctors, having benefited from exposure to behavioural science should be able to apply some psychological techniques themselves to intervene in the patients lifestyle to reduce the likelihood of them needing medical treatment for conditions like coronary heart disease.

World Health Organisation (WHO) Challenge

“Health is a positive concept emphasising social and personal resources, as well as physical capabilities.” WHO,1986.

As a basis of meeting the WHO challenge proposed by this statement, medical professionals will need to be familiar with the research identifying the health risks associated with different behavioural and social conditions and not just the biological illness itself. Therefore it is no longer sufficient for clinicians to state that treatment is successful in terms of its effect on a specific biological illness but it is now also necessary to know whether the treatment gives significant improvement in the way in which a person lives.

The model inherently places a lot of emphasis on the individuals control over their body and health and this may be difficult and confusing for the chronically ill or those who battle in vain with weight, smoking or drinking habits. However this is where the doctor uses his or her expertise and experience in knowing how to approach the sensitive issues of a patient’s daily life.

Doll,R., Peto,R. (1981) The causes of cancer. New York: Oxford University Press.

Engel,G. (1977) The need for a new medical model: a challenge for biomedical science. Science, 196:126-9.

Flor, H., Turk, D.C. (1985) Chronic Illness in an adult family member: Pain as a prototype.

Lazarus,R.S., Folkman,S. (1984) Stress, appraisal and coping. New York: Springer-Verlag.

Competing interests: No competing interests

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Biopsychosocial model in Health Psychology
Supremacy of the Biopsychosocial Model of Health Over the Biomedical
Biomedical and Biopsychosocial Models of Health and Illness
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Biomedical and Biopsychosocial Model
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5.1b. Several perspectives on trauma disorders

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Understanding the Biopsychosocial Model of Health
A holistic approach to well-being. The biopsychosocial model is an approach to understanding mental and physical health through a multi-systems lens, understanding the influence of biology, psychology, and social environment. Dr. George Engel and Dr. John Romano developed this model in the 1970s, but the concept of this has existed in medicine ...
Biopsychosocial Model: Examples, Overview, Criticisms
Overview of the Biopsychosocial Model. A biopsychosocial model is a holistic approach to understanding health and illness considering multiple influences. It recognizes the interplay between biological, psychological, and social factors on health throughout a person's lifespan (Bolton & Gillett, 2019). Through this model, practitioners can ...
The Biopsychosocial Model 40 Years On
The first chapter outlines George Engel's proposal of a new biopsychosocial model for medicine and healthcare in papers 40 years ago and reviews its current status. The model is popular and much invoked in clinical and health education settings and has claim to be the overarching framework for contemporary healthcare. On the other hand, the model has been increasingly criticised for being ...
Biopsychosocial Model of Health Case Study
Case Based Essay. The biopsychosocial model of health (Engel, 1977) claims that health and illness are: the product of a combination of factors including biological characteristics (e.g. genetic predisposition), behavioural factors (e.g. lifestyle, stress, health beliefs), and social conditions (e.g. cultural influences, family relationships, social support).
A revitalized biopsychosocial model: core theory, research paradigms
Introduction: the problem area and a proposal. The biopsychosocial model (BPSM) was proposed by George Engel in 1977 as an improvement to the biomedical model (BMM), necessary to account for psychological and social factors in health and disease as well as biological (Engel, 1977).This proposal remains critical in science and in service planning (Wade & Halligan, 2017).
The biopsychosocial model of illness: a model whose time has come
While evaluations of the model over the past 40 years are mainly positive, with the biopsychosocial approach securing considerable success and traction in several areas of healthcare, an American observer recently wrote, 'the unfortunate reality is that … since Engel's seminal paper the integration of the biopsychosocial approach into everyday medical care hasn't happened yet'. 2 The ...
The past, present, and future of the biopsychosocial model: A review of
In The Biopsychosocial Model of Health and Disease: New philosophical and scientific developments, Derek Bolton and Grant Gillett (2019) present a summary of four decades of scholarship. They conclude that the model has fallen short clinically, scientifically, and philosophically. ... In a systematic review of the 48 empirical research papers ...
Rethinking the biopsychosocial model of health: Understanding health as
The biopsychosocial model has dominated research and theory in health psychology. This article expands the biopsychosocial model by applying systems theories proposed by developmental scholars, including Bronfenbrenner's ecological models and Sameroff's transactional model, as well as contemporary philosophical work on dynamic systems.
Preface
The problem area of this essay is set within a broad trend of increasing recognition that crossdisciplinary approaches are needed for addressing the aetiology, prevention and management of diseases. The recognition of this need goes by the name of the 'biopsychosocial model', originally proposed by the physician and psychoanalyst George Engel in a paper published in 1977. By now, some 40 ...
The biopsychosocial model of illness: a model whose time has come
Psychophysiology*. United Kingdom. The biopsychosocial model outlined in Engel's classic Science paper four decades ago emerged from dissatisfaction with the biomedical model of illness, which remains the dominant healthcare model. Engel's call to arms for a biopsychosocial model has been taken up in several healthcare fields, but it ….
(PDF) Biopsychosocial Model of Health
In Wikipedia, biopsychosocial model (2020) is defined as an interdisciplinary model that looks at the interconnection between biology, psychology and socio-environmental factors. Its founder ...
The Bio-Psycho-Social Model
When professional mental health clinicians are asked to figure out what is wrong with a patient, they assess that patient broadly, using something they call the "bio-psycho-social" model as a guide. The bio-psycho-social model assumes that mental health problems are hardly ever limited to just one domain of human experience (say, just a "mental" problem).
The Biopsychosocial Model
The biopsychosocial model generally accounts of biological, psychological and sociological which are interrelated spectrums (Lakhan, 2006). Today, this model was widely used as a solving problem in clinician practice. The biological referred to the aetiology of diseased from functioning of individual's body. The psychological and sociological ...
Rethinking the biopsychosocial model of health: Understanding health as
The biopsychosocial model has dominated research and theory in health psychology. This article expands the biopsychosocial model by applying systems theories proposed by developmental scholars, including Bronfenbrenner's ecological models and Sameroff's transactional model, as well as contemporary philosophical work on dynamic systems. The proposed dynamic biopsychosocial model construes human ...
In defence of the biopsychosocial model
It is now 40 years since George Engel, a psychiatrist from the University of Rochester, New York, NY, USA, put forward his idea of the biopsychosocial model. Engel argued that if psychiatry aimed to generate a fully scientific and inclusive account of mental disorder, then bioreductionist accounts should be superseded by a new model that adhered to the insights of the General Systems Theory ...
The Biopsychosocial Model 40 Years On
Abstract. The first chapter outlines George Engel's proposal of a new biopsychosocial model for medicine and healthcare in papers 40 years ago and reviews its current status. The model is popular and much invoked in clinical and health education settings and has claim to be the overarching framework for contemporary healthcare.
Biopsychosocial Model in Contemporary Psychiatry: Current Validity and
The biopsychosocial model (BPS) was proposed by George L. Engel in 1977 as a needed medical model to explain psychiatric disorders. [1] Since then, this model had gained wide acceptability across the globe. It systematically explained the complex interplay of three major dimensions (biological, psychological, and social) in the development of ...
The Biopsychosocial Model
Science, 196 (4286), 129-136; Engel, G. L. (1980). The clinical application of the biopsychosocial model. The American Journal of Psychiatry, 137 (5), 535-544) because he felt that the traditionally embraced biomedical reductionist model in medicine was outdated in light of the newer advances in medicine. He emphasized that modern medicine ...
Biopsychosocial Model Essay
Biopsychosocial Model Essay Cindy Lopez College of Psychology, Grand Canyon University PSY 352-O501: Health Psychology Tanya Harrell January 21, 2024 A Holistic Approach to Health The biopsychosocial model offers a comprehensive structure for understanding health and illness by incorporating biological, psychological, and social factors ...
Biopsychosocial Conditions of Health and Disease
The centrality of the person was identified by Engel as a feature of the biopsychosocial model in his original papers [4, 5]. In this respect, there are some connections between the biopsychosocial model and the Patient- or Client-centred Care Model, and many papers have examined the relation between the two approaches (e.g. [6-9]).
Introducing the Biopsychosocial Model for good medicine and good
The Biopsychosocial Model of health and illness as proposed by Engel. (1977) implies that behaviours, thoughts and feelings may influence a. physical state. He disputed the long-held assumption that only the. biological factors of health and disease are worthy of study and practice.