What is Vantage Sensitivity?


Vantage sensitivity is a psychological concept related to environmental sensitivity, initially developed by Michael Pluess and Jay Belsky. It describes individual differences in response to positive experiences and supportive environmental influences. According to vantage sensitivity, people differ considerably in their sensitivity to positive aspects of the environment, with some people benefitting particularly strongly from positive experiences such as parental care, supportive relationships, and psychological interventions, whereas others tend to respond less or not at all.

Refer to Diathesis-Stress Model.


The concept of vantage sensitivity is related to other theories of environmental sensitivity such as differential susceptibility according to which some people are more sensitive than others to both negative and positive experiences. Vantage sensitivity provides a specific theoretical perspective and terminology to describe individual differences in response to exclusively positive experiences.

According to vantage sensitivity theory, people who benefit from positive experiences display vantage sensitivity as a function of vantage sensitivity factors (i.e. genetic, physiological, or psychological traits) whereas those who benefit less show vantage resistance due to the presence of vantage resistance factors (or the absence of vantage sensitivity factors). Differences in vantage sensitivity are considered to reflect neurobiological differences in the central nervous system, which are influenced by genetic as well as environmental factors.

Figure 1: Graphical illustration of vantage sensitivity; in response to a positive exposure, the level of functioning increases in Individual A, reflecting vantage sensitivity, whereas it remains unchanged in Individual B, reflecting vantage resistance.


A growing number of studies provide empirical evidence for individual differences in vantage sensitivity across a wide range of established sensitivity markers, including genetic, physiological, and psychological ones.

Genetic Markers

Several studies report that differences in response to positive experiences are associated with genetic sensitivity. For example, Keers et al. created a polygenic score for environmental sensitivity based on thousands of gene variants and found that children with higher genetic sensitivity responded more strongly to higher quality of psychological treatment.

Physiological Markers

Studies suggest that a higher physiological reactivity to stress (indicated by cortisol) is associated with a stronger positive response to positive influences. For instance, a study testing the efficacy of exposure-based psychotherapy, a type of psychological treatment that is used with people suffering from panic disorders and agoraphobia, found that people whose cortisol response was higher during exposure were also more likely to recover faster and benefit more from the treatment.

Psychological Markers

A number of studies have shown that children who score high on the Highly Sensitive Child (HSC) scale, a psychometric tool designed to measure sensitivity, respond more positively to psychological interventions. For example, Nocentini et al. conducted a randomised controlled trial to investigate whether sensitivity was associated with greater response to a school-based anti-bullying intervention. Results indicated that sensitive children benefitted significantly more from the positive effects of the intervention. Vantage sensitivity has also been found to influence the socio-emotional well-being of young people in school. The wellbeing of sensitive adolescents increased in response to positive changes in the school environment. In adults, high sensitivity has been found to predict a greater response to positive pictures and increased leader-rated employee task performance.

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What is Differential Susceptibility?


The differential susceptibility theory proposed by Jay Belsky is another interpretation of psychological findings that are usually discussed according to the diathesis-stress model.

Both models suggest that people’s development and emotional affect are differentially affected by experiences or qualities of the environment. Where the Diathesis-stress model suggests a group that is sensitive to negative environments only, the differential susceptibility hypothesis suggests a group that is sensitive to both negative and positive environments.

A third model, the vantage-sensitivity model, suggests a group that is sensitive to positive environments only. All three models may be considered complementary, and have been combined into a general environmental sensitivity framework.

Differential Susceptibility versus Diathesis-Stress

The idea that individuals vary in their sensitivity to their environment was historically framed in diathesis-stress or dual-risk terms. These theories suggested that some “vulnerable” individuals, due to their biological, temperamental and/or physiological characteristics (i.e. “diathesis” or “risk 1”), are more vulnerable to the adverse effects of negative experiences (i.e. “stress” or “risk 2”), while other “resilient” individuals are not affected by these negative experiences (see Figure 1). The differential susceptibility hypothesis and the related notion of biological sensitivity to context suggested that individuals thought to be “vulnerable” are not only sensitive to negative environments, but also to positive environments (see Figure 2). Thus, according to the differential susceptibility hypothesis, some individuals are “susceptible” or “plastic”, in that they are more influenced than others by environmental influences in a “for better and for worse” manner.

Figure 1. The diathesis-stress/dual-risk model. Developmental outcome as it relates to environmental quality. A “vulnerable” group experiences negative outcome when exposed to a negative environment, although this group is identical to the other, “resilient” group in a positive environment.
Figure 2. The differential susceptibility model. The lines depict two categorical groups that differ in their responsiveness to the environment: the “plastic” group is disproportionately more affected by both negative and positive environments compared to the “fixed” group.

Theoretical Background

Belsky suggests that evolution might select for some children who are more plastic, and others who are more fixed in the face of, for example, parenting styles.

Belsky offers that ancestral parents, just like parents today, could not have known (consciously or unconsciously) which childrearing practices would prove most successful in promoting the reproductive fitness of offspring – and thus their own inclusive fitness. As a result, and as a fitness optimising strategy involving bet hedging, natural selection might have shaped parents to bear children varying in plasticity. This way, if an effect of parenting had proven counterproductive in fitness terms, those children not affected by parenting would not have incurred the cost of developing in ways that ultimately proved “misguided”.

Importantly, natural selection might favour genetic lines with both plastic and fixed developmental and affective patterns. In other words, there is value to having both kinds at once. In light of inclusive-fitness considerations, children who were less malleable (and more fixed) would have “resistance” to parental influence. This could be adaptable some times, and maladaptive other times. Their fixedness would not only have benefited themselves directly, but even their more malleable siblings indirectly. This is because siblings, like parents and children, have 50% of their genes in common. By the same token, had parenting influenced children in ways that enhanced fitness, then not only would more plastic offspring have benefited directly by following parental leads, but so, too, would their parents and even their less malleable siblings who did not benefit from the parenting they received, again for inclusive-fitness reasons. The overall effect may be to temper some of the variability in parenting. That is, to make more conservative bets.

This line of evolutionary argument leads to the prediction that children should vary in their susceptibility to parental rearing and perhaps to environmental influences more generally. As it turns out, a long line of developmental inquiry, informed by a “transactional” perspective, has more or less been based on this unstated assumption.

Criteria for the Testing of Differential Susceptibility

Belsky, Bakermans-Kranenburg, & Van IJzendoorn, (2007) delineated a series of empirical requirements – or steps – for evidencing the differential susceptibility hypothesis. Particularly they identify tests that distinguish differential susceptibility from other interaction effects including diathesis-stress/dual-risk.

While diathesis-stress/dual-risk arises when the most vulnerable are disproportionately affected in an adverse manner by a negative environment but do not also benefit disproportionately from positive environmental conditions, differential susceptibility is characterised by a cross-over interaction: the susceptible individuals are disproportionately affected by both negative and positive experiences. A further criterion that needs to be fulfilled to distinguish differential susceptibility from diathesis-stress/dual-risk is the independence of the outcome measure from the susceptibility factor: if the susceptibility factor and the outcome are related, diathesis-stress/dual-risk is suggested rather than differential susceptibility. Further, environment and susceptibility factor must also be unrelated to exclude the alternative explanation that susceptibility merely represents a function of the environment. The specificity of the differential-susceptibility effect is demonstrated if the model is not replicated when other susceptibility factors (i.e. moderators) and outcomes are used. Finally, the slope for the susceptible subgroup should be significantly different from zero and at the same time significantly steeper than the slope for the non- (or less-) susceptible subgroup.

Susceptibility Markers and Empirical Evidence

Characteristics of individuals that have been shown to moderate environmental effects in a manner consistent with the differential susceptibility hypothesis can be subdivided into three categories: Genetic factors, endophenotypic factors, phenotypic factors.

Bakermans-Kranenburg and Van IJzendoorn (2006) were the first to test the differential susceptibility hypothesis as a function of Genetic Factors regarding the moderating effect of the dopamine receptor D4 7-repeat polymorphism (DRD4-7R) on the association between maternal sensitivity and externalizing behaviour problems in 47 families. Children with the DRD4-7R allele and insensitive mothers displayed significantly more externalizing behaviours than children with the same allele but with sensitive mothers. Children with the DRD4-7R allele and sensitive mothers had the least externalising behaviours of all whereas maternal sensitivity had no effect on children without the DRD4-7R allele.

Endophenotypic Factors have been examined by Obradovic, Bush, Stamperdahl, Adler and Boyce’s (2010). They investigated associations between childhood adversity and child adjustment in 338 5-year-olds. Children with high cortisol reactivity were rated by teachers as least prosocial when living under adverse conditions, but most prosocial when living under more benign conditions (and in comparison to children scoring low on cortisol reactivity).

Regarding characteristics of the category of Phenotypic Factors, Pluess and Belsky (2009) reported that the effect of child care quality on teacher-rated socioemotional adjustment varied as a function of infant temperament in the case of 761 4.5-year-olds participating in the NICHD Study of Early Child Care and Youth Development (NICHD Early Child Care Research Network, 2005). Children with difficult temperaments as infants manifest the most and least behaviour problems depending on whether they experienced, respectively, poor or good quality care (and in comparison to children with easier temperaments).

Table 1: List of Proposed Susceptibility Factors that emerge across studies, according to Belsky and colleagues.

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What is the Trauma Model of Mental Disorders?


The trauma model of mental disorders, or trauma model of psychopathology, emphasises the effects of physical, sexual and psychological trauma as key causal factors in the development of psychiatric disorders, including depression and anxiety as well as psychosis, whether the trauma is experienced in childhood or adulthood. It conceptualises people as having understandable reactions to traumatic events rather than suffering from mental illness.

Trauma models emphasise that traumatic experiences are more common and more significant in terms of aetiology than has often been thought in people diagnosed with mental disorders. Such models have their roots in some psychoanalytic approaches, notably Sigmund Freud’s early ideas on childhood sexual abuse and hysteria, Pierre Janet’s work on dissociation, and John Bowlby’s attachment theory. There is significant research supporting the linkage between early experiences of chronic maltreatment and severe neglect and later psychological problems.

In the 1960s trauma models became associated with humanist and anti-psychiatry approaches, particularly in regard to understanding schizophrenia and the role of the family. Personality disorders have also been a focus, particularly borderline personality disorder, with the role of dissociation and ‘freezing responses’ (more extreme reactions than fight-flight when someone is terrified and traumatised) thought to have a significant role in the aetiology of psychological disturbance. Extreme versions of trauma models have implicated the foetal environment and the trauma of being born, but these are not well-supported in the academic literature and have been associated with recovered memory controversies.

People are traumatised by a wide range of people, not just family members. For example, male victims of sexual abuse report being abused in institutional settings (boarding schools, care homes, sports clubs).

Trauma models thus highlight stressful and traumatic factors in early attachment relations and in the development of mature interpersonal relationships. They are often presented as a counterpoint to psychiatric orthodoxy and inform criticisms of mental health research and practice in that it has become too focused on genetics, neurochemistry and medication.

Refer to Models of Mental Health and The Mental Health Continuum.

Brief History

From the 1940s to the 1970s prominent mental health professionals proposed trauma models as a means of understanding schizophrenia, including Harry Stack Sullivan, Frieda Fromm-Reichmann, Theodore Lidz, Gregory Bateson, Silvano Arieti and R.D. Laing. Based on their clinical work they theorised that schizophrenia appears to be induced by children’s experiences in profoundly disturbed families and reflect victims attempts to cope with such families and live in societies that are inherently damaging to people’s psychological well-being. In the 1950s Sullivan’s theory that schizophrenia is related to interpersonal relationships was widely accepted in the United States. Silvano Arieti’s book Interpretation of Schizophrenia won the American National Book Award in the field of science in 1975. The book advances a psychological model for understanding all the regressive types of the disorder.

Some of the psychogenic models proposed by these early researchers, such as the “schizophrenogenic mother”, came under sustained criticism, from feminists who saw them as ‘mother-blaming’ and from a psychiatric profession that increasingly moved towards biological determinism. From the 1960s pharmacological treatments became the increasing focus of psychiatry, and by the 1980s the theory that the family dynamics could be implicated in the aetiology of schizophrenia became viewed as unacceptable by many mental health professionals in America and Europe. Before his death in 2001, at 90, Theodore Lidz, one of the main proponents of the “schizophrenogenic” parents theory, expressed regret that current research in biological psychiatry was “barking up the wrong tree”. Like Lidz, Laing maintained until his death that the cause of both schizoid personality disorder and schizophrenia was influenced by family relationships. Some more recent research has provided support for this; for instance, child abuse has been shown to have a causal role in depression, PTSD, eating disorders, substance abuse and dissociative disorders, and research reveals that the more severe the abuse the higher the probability that psychiatric symptoms will develop in adult life.

Judith Herman’s book Trauma and Recovery has heavily influenced therapeutic approaches. Recovery entails three phases which are best worked through sequentially: First ‘establishing safety’; secondly ‘a process of remembrance and mourning for what was lost’; thirdly ‘reconnecting with community and more broadly, society’.


Critics of the model, such as August Piper, argue that the logic that childhood trauma causes insanity has a serious flaw: If the claim was true, the abuse of millions of children over the years should have caused higher prevalence rates of mental disorders than the literature reveals. Other critics, particularly proponents of behaviour family therapy, have seen trauma models as parent blaming, and have emphasised the fact that families are usually the main, and often only, source of support for people diagnosed with severe mental illness. Lucy Johnstone has pointed out that some critics advocate family interventions for adult psychiatric patients whilst at the same time maintaining that childhood experiences are not causal as regards mental illness – as if family members can only have a helpful or damaging impact on their adult children.

In response to Piper’s assertion, it has been noted that Arieti stated in Interpretation of Schizophrenia that a trauma is more significant when committed by people to whom young human beings are emotionally bonded, and abuse is often interwoven with other forms of neglect and confusing behaviours from care-givers:

First of all we have to repeat here what we already mentioned…, that conditions of obvious external danger, as in the case of wars, disasters, or other adversities that affect the collectivity, do not produce the type of anxiety that hurts the inner self and do not themselves favor schizophrenia. Even extreme poverty, physical illness, or personal tragedies do not necessarily lead to schizophrenia unless they have psychological ramifications that hurt the sense of self. Even homes broken by death, divorce or desertion may be less destructive than homes where both parents are alive, live together, and always undermine the child’s conception of himself.

Recent Approaches

A 2005 meta-analysis of schizophrenia revealed that the prevalence of physical and sexual abuse in the histories of people diagnosed with psychotic disorders is very high and has been understudied. This literature review revealed prevalence rates of childhood sexual abuse in studies of people diagnosed with schizophrenia ranging from 45% to 65%. An analysis of the American National Comorbidity Study revealed that people who have endured three kinds of abuse (e.g. sexual, physical, bullying) are at an 18-fold higher risk of psychosis, whereas those experiencing five types are 193 times more likely to become psychotic. A 2012 review article supported the hypothesis that current or recent trauma may affect an individual’s assessment of the more distant past, changing the experience of the past and resulting in dissociative states. Several reviews of risk factors for common mental disorders have emphasised trauma. Such research has rejuvenated interest in this field, both from clinicians, researchers and service user organisations such as the Hearing Voices movement.

Psychiatrist Colin Ross calls his model the “trauma model of mental disorders” and emphasises that, unlike biological models, this addresses the literature on comorbidity of trauma with mental disorders. Ross describes the theoretical basis of his trauma model as common sense:

“The problem faced by many patients is that they did not grow up in a reasonably healthy, normal family. They grew up in an inconsistent, abusive and traumatic family. The very people to whom the child had to attach for survival were also abuse perpetrators and hurt him or her badly…. The basic conflict, the deepest pain, and the deepest source of symptoms, is the fact that mom and dad’s behavior hurts, did not fit together, and did not make sense.”

In terms of psychoses, most researchers and clinicians believe that genetics remains a causative risk factor but “genes alone do not cause the illness”. Modern views of genetics see genes more like dimmer switches, with environmental factors switching the genes on; the more severe the environmental stress, the more effect genes have.

In the field of criminology, Lonnie Athens developed a theory of how a process of brutalization by parents or peers that usually occurs in childhood results in violent crimes in adulthood. Richard Rhodes’s Why They Kill describes Athens’s observations about domestic and societal violence in the criminals’ backgrounds. Both Athens and Rhodes reject the genetic inheritance theories.

Criminologists Jonathan Pincus and Dorothy Otnow Lewis believe that although it is the interaction of childhood abuse and neurological disturbances that explains murder, virtually all of the 150 murderers they studied over a 25-year period had suffered severe abuse as children. Pincus believes that the only feasible remedy for crime would be the prevention of child abuse.

The logical conclusion of the trauma model is that the task for clinicians is not to treat biological disorders but to help people manage and modify their learned, and often embedded, responses to traumas they have experienced. As such, services need to be reconstituted to focus on this aim.

This page is based on the copyrighted Wikipedia article < https://en.wikipedia.org/wiki/Trauma_model_of_mental_disorders >; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

Book: A Manifesto for Mental Health

Book Title:

A Manifesto for Mental Health: Why We Need a Revolution in Mental Health Care.

Author(s): Peter Kinderman.

Year: 2019.

Edition: First (1st).

Publisher: Palgrave Macmillan.

Type(s): Paperback and Kindle.


A Manifesto for Mental Health presents a radically new and distinctive outlook that critically examines the dominant ‘disease-model’ of mental health care. Incorporating the latest findings from both biological neuroscience and research into the social determinants of psychological problems, Peter Kinderman offers a contemporary, biopsychosocial, alternative. He warns that the way we care for people with mental health problems is creating a hidden human rights emergency and he proposes a new vision for the future of health organisations across the globe.

The book highlights persuasive evidence that our mental health and wellbeing depend largely on the society in which we live, on the things happen to us, and on how we learn to make sense of and respond to those events. Kinderman proposes a rejection of invalid diagnostic labels, practical help rather than medication, and a recognition that distress is usually an understandable human response to life’s challenges. Offering a serious critique of establishment thinking, A Manifesto for Mental Health provides a well-crafted demonstration of how, with scientific rigour and empathy, a revolution in mental health care is not only highly desirable, it is also entirely achievable.

Book: Models for Mental Disorder: Conceptual Models in Psychiatry

Book Title:

Models for Mental Disorder: Conceptual Models in Psychiatry.

Author(s): Peter Tyrer.

Year: 2013.

Edition: Fifth (5th).

Publisher: Wiley-Blackwell.

Type(s): Paperback and Kindle.


Models for Mental Disorder, first published in 1987, anticipated the
move towards integration of psychiatric services into multidisciplinary teams (doctor, psychologist, nurse, social worker, etc) and the need to bring together the different philosophies of mental illness.

Peter Tyrer has identified four different models of mental disorder that are relevant to clinical practice: the disease, psychodynamic, cognitive-behavioural and social models.

Each model is described and reviewed, with reference to case studies and
illustrations, to show how it relates to mental health disorders and can be
used to interpret and manage these disorders.

The book has been widely read and is often used for training purposes so that
each professional can understand and appreciate that differences in viewpoint
are often a consequence of one or more models being used in a different way
rather than a fundamental schism in approach.

Since the fourth edition was published in 2005, the disciplines of mental health
have moved even closer together with the growth of assertive outreach and
more integrated community teams. This, combined with the greater awareness
of mental health among users of services, which leads to more penetrating and
informed questions at interviews with professionals, has emphasized the need
for a wider understanding of these models.

  • The only book to describe the models framing mental health diagnosis and management.
  • A great review for those wanting a better grasp of psychiatric disorders and for integration of concepts for treatment planning.
  • New information on formal classifications of mental disorder.
  • New information on mindfulness and mentalisation regarding the dynamic model.
  • Clearly written in a style which includes some humour and a conversational presentation – a joy to read for the beginner and more experienced practitioner alike.
  • Features a teaching exercise for use when training students in the various models.

Mental Health: Model Navigator!

Research Paper Title

Mental Health Navigation – A Model.


The need for mental health care services is a growing concern around the world.

This article proposes a conceptual model for the role a mental health care navigator to meet the growing needs of consumers who are seeking greater access to fragmented and confusing mental health care services.

This conceptual model proposes integrating mental health into primary care with a more patient-centered approach to the care of the whole person.

This approach is congruent with The Ottawa Charter for Health Promotion Charter calling for the reorienting of health services focusing on the total needs of the individual as a whole person.

Although USA focused, the model has potential for sharing across countries to build capacity for mental health care in other countries around the world.

The conceptual model focuses on matching consumer mental health care needs with the correct mental health care services.

This would ensure that patients get the appropriate mental health care services while allowing the primary care physician to maintain the role of coordinator of care for all of the patient’s health care needs.

The main intent of the model is to stimulate discussion and exploration around the role of a proposed mental health care navigator that can lead to creating models reflecting local need and adaptation.

Successful models can lead to collaborative discussion encouraging capacity building in other countries.

The authors maintain that coordination of health care, including mental, medical and surgical care, is the best approach to controlling costs and ensuring the health of the whole person.


Knesek, G. & Hemphill, T. (2020) Mental Health Navigation – A Model. Health Promotion International. 35(1), pp.151-159. doi: 10.1093/heapro/day109.

Models of Mental Health

There are many different ways of explaining mental health issues, and of explaining the factors that influence our health. Different models emphasise different aspects of mental health, such as the impact society and culture have on a person’s mental health.

It is important to note that there is more to mental health than whether or not a person has a diagnosis of an illness.

For the purposes of this website, I have selected the mental health continuum as a useful model to show that mental health changes over time and that mental health issues are about everyone (I learnt about the mental health continuum as part of the Scotland’s Mental Health First Aid course).

Other models of health and mental health are briefly described below.

Dahlgren and Whitehead Model

After the mental health continuum, another popular model to give an overview of one alternative way of considering health is the model by Dahlgren and Whitehead (1991).

This model pays closer attention to the impact of lifestyle, social, economic circumstances, culture, and the environment. It attempts to show how these things influence an individual’s health and how they interact with one another.

The model shows that health is affected by a range of different factors, from those specific to the individual, to wider cultural and social issues.

An individual’s health will be influenced by their gender, age, by their individual personality, and relative strength or resilience. However, health is much more than individual factors. A person’s health is affected by their local community and the extent to which they have sense of belonging. Education, work, the ability to access and prepare healthy food, housing and sanitation are also significant factors, as are economic, cultural, and environmental conditions.

This model is useful for considering the extent to which a person has control over their own health, and how much health improvement needs to be driven by policy that recognises the impact of all these factors.

The model also acts as an important reminder that health is not purely about the individual. It is therefore unhelpful and misguided to blame those who are experiencing poor health.

Kinderman’s Psychological Model of Mental Disorder

A coherent conceptualisation of the role of psychological factors is of great importance in understanding mental disorder (Kinderman, 2005). Academic articles and professional reports alluding to psychological models of the aetiology of mental disorder are becoming increasingly common, and there is evidence of a marked policy shift toward the provision of psychological therapies and interventions.

This article discusses the relationship between biological, social, and psychological factors in the causation and treatment of mental disorder. It argues that simple biological reductionism is not scientifically justified, and also that the specific role of psychological processes within the biopsychosocial model requires further elaboration. The biopsychosocial model is usually interpreted as implying that biological, psychological, and social factors are co-equal partners in the aetiology of mental disorder.

The psychological model of mental disorder presented here suggests that disruption or dysfunction in psychological processes is a final common pathway in the development of mental disorder. These processes include, but are not limited to, cognitive processes.

The model proposes that biological and social factors, together with a person’s individual experiences, lead to mental disorder through their conjoint effects on those psychological processes. Implications for research, interventions, and policy are discussed.

The Biopsychosocial Model

The biopsychosocial approach was developed at Rochester decades ago by Dr’s. George Engel and John Romano, and published in 1977 (Engel, 1977; Frankel et al., 2003). While traditional biomedical models of clinical medicine focus on pathophysiology and other biological approaches to disease, the biopsychosocial approach emphasises the importance of understanding human health and illness in their fullest contexts. The biopsychosocial approach systematically considers biological, psychological, and social factors and their complex interactions in understanding health, illness, and health care delivery.

  • Biological, psychological, and social factors exist along a continuum of natural systems, as depicted in the diagram above.
  • Systematic consideration of psychological and social factors requires application of relevant social sciences, just as consideration of biological factors requires application of relevant natural sciences. Therefore, both the natural and social sciences are ‘basic’ to medical practice. In other words, psychological and social factors are not merely epiphenomena: they can be understood in scientific ways at their own levels as well as in regard to their biological correlates.
  • Humanistic qualities are highly valued complements to the biopsychosocial approach, which involves the application of the scientific method to diverse biological, psychological, and social phenomena as related to human health.
  • While the biomedical approach takes the reductionistic view that all phenomena are best understood at the lowest level of natural systems (e.g., cellular or molecular), the biopsychosocial approach recognises that different clinical scenarios may be most usefully understood scientifically at several levels of the natural systems continuum.

To apply the biopsychosocial approach to clinical practice, the clinician should (Engel, 1980):

  • Recognise that relationships are central to providing health care.
  • Use self-awareness as a diagnostic and therapeutic tool.
  • Elicit the patient’s history in the context of life circumstances.
  • Decide which aspects of biological, psychological, and social domains are most important to understanding and promoting the patient’s health.
  • Provide multidimensional treatment.

Rethinking the Biopsychosocial Model of Health

In 2017, Lehman colleagues suggested that the biopsychosocial model had dominated research and theory in health psychology. Their 2017 article expanded 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 construed human health as a product of the reciprocal influences of biological, psychological, interpersonal, and macrosystem contextual dynamics that unfold over personal and historical time. The importance, or centrality, of these influences varies within a person over time. The model is explicated using two hypothetical case studies derived from existing interdisciplinary health research. Implications for health, theory, research, and policy are discussed.

The Biomedical Model of Mental Disorder

Deacon (2013) states that the biomedical model posits that mental disorders are brain diseases and emphasises pharmacological treatment to target presumed biological abnormalities.

A biologically-focused approach to science, policy, and practice has dominated the American healthcare system for more than three decades. During this time, the use of psychiatric medications has sharply increased and mental disorders have become commonly regarded as brain diseases caused by chemical imbalances that are corrected with disease-specific drugs.

However, despite widespread faith in the potential of neuroscience to revolutionise mental health practice, the biomedical model era has been characterised by a broad lack of clinical innovation and poor mental health outcomes.

In addition, the biomedical paradigm has profoundly affected clinical psychology via the adoption of drug trial methodology in psychotherapy research. Although this approach has spurred the development of empirically supported psychological treatments for numerous mental disorders, it has neglected treatment process, inhibited treatment innovation and dissemination, and divided the field along scientist and practitioner lines.

The neglected biopsychosocial model represents an appealing alternative to the biomedical approach, and an honest and public dialog about the validity and utility of the biomedical paradigm is urgently needed.


Dahlgren, G. & Whitehead, M. (1991) Policies and Strategies to Promote Social Equality in Health. Stockholm: Institute for Future Studies.

Deacon, B.J. (2013) The Biomedical Model of Mental Disorder: A Critical Analysis of its Validity, Utility, and Effects on Psychotherapy Research. Clinical Psychology Review. 33, pp.846-861.

Engel, G.L. (1977) The Need for a New Medical Model: A Challenge for Biomedicine. Science. 196, pp.129-136.

Engel, G.L. (1980) The Clinical Application of the Biopsychosocial Model. American Journal of Psychiatry. 137, pp.535-544.

Frankel, R.M., Quill, T.E. & McDaniel, S.H. (Eds). (2003) The Biopsychosocial Approach: Past, Present, Future. Rochester, New York: University of Rochester Press.

Kinderman, P. (2005) A Psychological Model of Mental Disorder. Harvard Review of Psychiatry. 13(4), pp.206-217.

Lehman, B.J., David, D.M. & Gruber, J.A. (2017) Rethinking the Biopsycholosocial Model of Health: Understanding Health as a Dynamic System. Social and Personality Psychology Compass. 11(8).