What are the basic forces in the biopsychosocial framework and how does the timing of these forces affect their impact?

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 [14–16]. 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 [27–29] 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 [32–38]; liver transplant (e.g. [39]) and coronary artery bypass (e.g. [40–42]). 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.

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’?!

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.