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 Case Formulation
After Engel—The 4P
Model:
A Philosophical Case
Conference
Abstract: The best known model for case formulation
in the last 50 years was George Engel’s Biopsychosocial
model. It expanded the compass of medical investiga-
tion and it promised a scheme by which to organize
clinical information for more adequate understanding
and more effective interventions. Despite its claimed
advantages, it has not been adopted by clinicians.
This article examines reasons for this failure. It argues
for the therapeutic value of case formulation (as a
complement to diagnosis), and presents an alternative
schema by which clinicians can organize information
into the four moments of a clinical problem: its origins
(preconditions), precipitating factors, perpetuating
factors, and protective factors. Unlike Engel’s hierarchi-
cally organized, synchronic schema, the 4P schema is
developmental, diachronic, and clinically intuitive. The
4P schema encourages ‘thick’ case formulations as the
basis of wise treatment interventions. The last section
describes two seminar series in which the structure and
elements of the 4P schema were presented to third-year
psychiatry residents.
Keywords: Biopsychosocial model, diagnosis, medical
education, illness behavior, sick role, interpretation,
practice.
© 2015 by The Johns Hopkins University Press
Jonathan W. Bolton
“Case formulation is considered passé.” (In-patient
attending psychiatrist 2012)
W
ould this view, if true (and it seems
to be), confirm George Engel’s late-life
despair about medicine after he had
spent so much energy trying to get physicians to
broaden their understanding of illness? Ironically,
it might have been, at least in part, because of
Engel’s efforts that clinicians are now disinclined
to try to understand their patients from biologi-
cal, psychological, and sociological perspectives.
In this article, I review Engel’s Biopsychosocial
model as a schema for case formulation. I then
defend the utility of case formulation in practice
and present an alternative model that avoids some
of the conceptual and practical problems of the
Biopsychosocial model. Finally, I describe the
organization of a seminar that was designed to
train psychiatric residents how to formulate their
cases within this alternative model, which I call
the 4P model. Although the seminar was designed
for psychiatric residents, the organization and
much of the content are applicable to trainees in
180 ■ PPP / Vol. 21, No. 3 / September 2014
other medical disciplines and medical students
more generally.
Engel’s Biopsychosocial
Model
Engel proposed his Biopsychosocial model of
disease as a corrective to what he called the Bio-
medical model. As he described it, the Biomedical
model was (or is, as it has not gone away) a frac-
tional–analytic model, typical of ‘classical science’
that seeks to understand disease by breaking it
down into its constituent parts and elucidating
simple, linear causal sequences. Diseases, including
behavioral abnormalities if they are to be consid-
ered diseases, should ultimately be reduceable to
basic biochemical or physical derangements. If a
phenomenon cannot be reduced in this way, then
it is not a disease, and therefore it is not within
the domain of medicine (Engel 1977).
Engel challenged psychiatry to not adopt the
Biomedical model, and advised that medicine as
a whole should reconsider its attachment to it. By
excluding psychological and social influences on
behavior and illness, clinicians have a narrow vi-
sion of disease. With this argument, Engel was in
harmony with some of the moderate voices of the
then influential Psychosocial movement. However,
Engel went further. He looked for ways to link the
biological, the psychological, and the social into a
conceptual whole. This was a time of Grand Theo-
ries: Structuralism in linguistics and anthropology,
Functionalism in sociology, Psychoanalysis, and
Marxism. Engel hitched his arguments to the
writings of the biologist von Bertalanffy, whose
ambitious General Systems Theory called for a
‘reorientation of science’ toward thinking about
phenomena as manifestations of transcendental
organizational principles (von Bertalanffy 1968).
The General Systems Theory is a ‘meta-model’ in
that it seeks to identify the ‘universal principles
applying to systems in general’ rather than to
understand any particular system. von Berta-
lanffy contrasted closed systems or unorganized
complexities, for which classical science might be
adequate, and open systems, which include life
forms, for which it is not. Understanding open
systems or organization involves identifying the
structural uniformities, organizational principles,
or isomorphisms common to apparently different
systems or levels of organization. A foundational
organizing principle is hierarchy: “nature is or-
dered as a hierarchically arranged continuum. . . .
Each level in the hierarchy represents an organized
dynamic whole…” (Engel 1980, 536). In his 1980
article, Engel sought to illustrate how hierarchi-
cally connected levels of organization—from cel-
lular to social—were implicated in the case of a
man with chest pain.
Post Mortem
For reasons best elucidated by historical re-
search Engel’s model, or at least the term Biopsy-
chosocial, was adopted by medical educators, be-
coming institutionalized over the last few decades,
for example, in the phrasing of competencies,
learning objectives, and conferences.
Now, 35 years later, what are we to make of
the Biopsychosocial model? It is quite difficult to
answer this question, in part because it has be-
come part of the ideology of medicine. Preclinical
medical students are still being asked to consider
problems from biological, psychological, and
sociological perspectives, although without being
taught an integrating metaphysics of the sort that
Engel and especially von Bertalanffy proposed.
If it was such an advance over the Biomedical
model, why has it not caught on? Why do we not
hear teams of rounding physicians trying to make
links between changes at the cellular level with
psychological states or social dynamics? There are
epistemological and pragmatic reasons that are
intrinsic to the model itself, and external reasons
for it’s failure to be adopted by clinicians.
Reasons intrinsic to the model include the
following. First, the central motif of the Biopsy-
chosocial model is a hierarchy of levels of orga-
nization. It is a stratigraphic model, and as the
anthropologist Clifford Geertz (1973, 41) wrote
of stratigraphic models, “Once culture, psyche,
society, and organism have been converted into
separate ‘levels,’ complete and autonomous in
themselves, it is very hard to bring them back
together again.” This is Biopsychosocial model’s
Humpty-Dumpty problem. It is difficult or impos-

sible for researchers, let alone clinicians, to be able
to trace connections beyond two or three levels
(e.g., DNA, protein, structure); it is too much to
expect that clinicians be able to make these sorts
of cognitive connections for each of the myriad
clinical problems that they are asked to respond to.
Second, the inclusion of supra-individual levels
of organization within the Biopsychosocial model
is necessary for its claim to comprehensiveness;
however, it assumes a too happy state of affairs
among the disciplines that claim these levels of
organization as their own (e.g., sociology, an-
thropology, political science, economics). These
fields are in Kuhn’s term ‘pre-paradigmatic’ (Kuhn
1970). There is little reason to believe that two
social scientists will agree on even fundamental
concepts within their field. For example, there is no
agreed-upon model, e.g., of ‘culture,’ ‘personality’,
or ‘motivation.’ This lack of agreement makes it
unlikely that a conceptual model that attempts to
link events within their level and with other levels
could be described or would be accepted as true.
Third, there is an incommensurability between
kinds of knowledge pertinent to different organi-
zational levels. The possession of self-awareness
by individuals, and its absence in organs and mol-
ecules, makes it difficult to extrapolate from the
dynamics of organs to the dynamics of individuals,
or groups of individuals.
Fourth, the emphasis in General Systems Theo-
ry, on which the Biopsychosocial model is based, is
less concerned with how a particular system (e.g.,
a patient) works and more concerned with how
systems of that sort work, that is, what they share
with other types of similar systems. This interest in
systems as systems is more the concern of research-
ers who occupy a different social role to clinicians,
who must respond to individual patients.
Influences external to the Biopsychosocial
model that contributed its failure to be adopted
by clinicians include the social organization and a
division of labor within medicine that has resulted
in greater specialization and, with it, a greater
standardization in the definition of problems. This
in turn has resulted in a narrowing of the range of
phenomena to be made sense of, a containment of
uncertainty requiring explanation, and a tendency
to reduce the domain of statements made by clini-
cians to the identification of an entity or a state-
Bolton / The 4P Model ■ 181
ment that it is not one of the clinician’s claimed
entities. All of this has resulted in a reduction in
the felt need for such integrative models as the
Biopsychosocial model.
Another, more generic reason for its failure
might derive from an exaggerated sense of the
importance of theory in clinical work. The Bio-
psychosocial model, even more than the Biomedi-
cal model, is a theoretical or rational model. It is
arguable that medical practice is actually more
empirical than its theoreticians realize (Foster
1994). Much of clinical work proceeds by pattern
recognition, lore, and simple axioms. In Peirce’s
typology, medical practice is more deductive than
inductive, but it is mostly abductive in the sense of
generating logically risky hypotheses (Peirce 1992).
In psychiatry, the third edition of the Diagnostic
and Statistical Manual of Mental Disorders and
its descendants encourage a simple empiricism and
deductive reasoning. Modern psychiatric diagnosis
is explicitly acausal, and as such it is antithetical
to Engel’s model. In short, elaborated theories, like
the Biopsychosocial model, are not particularly
relevant to day-to-day practice, although they do
have significant ideological relevance in the medi-
cal and political marketplace.
Implications
For all of these reasons, the Biopsychosocial
model, as an interpretive or explanatory schema,
has not been adopted by the majority of physicians
in general or psychiatrists in particular. Instead,
we seem to be doing essentially what Engel tried
to move us away from doing: we are making
diagnoses.
The relationship between diagnosis and case
formulation is the relationship between type and
case. Diagnosis encourages the clinician to see
the person or the person’s problem as a type of
problem; formulation encourages the clinician to
see the person or problem as something unique,
complex, and situated. Diagnosis is a label; formu-
lation is a map. It is a map of the extensions and
connections of a problem and a map for action.
Case formulation respects Andre Gide’s famous
request, “Please don’t understand me too quickly.”
Clearly, Engel’s emphasis was on case formulation
rather than diagnosis.
182 ■ PPP / Vol. 21, No. 3 / September 2014
The 4P Model of Case
Formulation
How do we approach the problem or the pa-
tient in its uniqueness? What would a model of
case formulation, shorn of high theory but em-
bodying the spirit of the Biopsychosocial model,
look like? What would clinicians want it to do?
First, and minimally, it should encourage us to
tell better stories, thicker stories.
Second, the model should be true to the process
of investigation. The act of giving a diagnosis con-
veys a sense of finality (not to mention how sticky
diagnoses can be once given; Biehl 2005; Rosenhan
1973), but it is actually one moment in an ongo-
ing process, and frequently the diagnosis is either
revised or forgotten. As Elvin Semrad observed,
“so often, when you get to know a patient, they
lose their diagnosis, you know” (Rako and Mazer
1980, 176). A case formulation should be seen
as a provisional statement: not right or wrong,
but more or less adequate, and in William James’
pragmatic sense more or less true (James 1948).
The process of understanding a patient’s problem
or situation is more akin to reflection-in-action, as
Schön described the process of listening to how a
problem ‘talks back’ to a prod, prodding again,
listening again, and so on (Sch n 1983). It is the
iterative process of the hermeneutic circle by which
the part is understood with reference to the whole,
and the whole is understood by reference to the
individual parts.
Formulating a case ought not to be done free
form. Clinicians are assisted by at least a minimal
framework to guide their examination. As we have
seen, Engel’s synchronic, hierarchically organized
model has not proven to be useful clinically. What
is called for, instead, is a diachronic approach that
examines how a problem arose, what sustains
it, and what limits it within the lived life of an
individual.
One model that encourages this perspective is
what I call the 4P model. Elements of the model
have long been part of a common lore approach
(apparently more common to English medicine
than American medicine) to case formulation, but
the elements are rarely integrated into a frame-
work. The four Ps are preconditions, precipitating
factors, perpetuating factors and protective fac-
tors. Each of the four Ps poses a question:
UÊ *ÀiVœ˜`ˆÌˆœ˜Ã\ʼ7…ÞʈÃÊ̅ˆÃÊ«iÀܘÊÛՏ˜iÀ>LiÊ̜Ê̅ˆÃÊ
problem?’
UÊ *ÀiVˆ«ˆÌ>̈˜}Ê v>V̜ÀÃ\Ê 7…ÞÊ ˜œÜ¶Ê /…ˆÃÊ V>˜Ê ÀiviÀÊ ÌœÊ
‘why is this person having symptoms now?’ and/
or ‘why is this person presenting to this healer for
treatment now?’
UÊ *iÀ«iÌÕ>̈˜}Êv>V̜ÀÃ\ʼ7…ÞʈÃÊ̅ˆÃÊ«iÀܘÊÃ̈Êˆ¶½
UÊ *ÀœÌiV̈ÛiÊv>V̜ÀÃ\ʼ7…ÞʈÃÊ̅ˆÃÊ«iÀܘʘœÌʓœÀiʈ¶½
These four questions encourage the clinician
to see the patient as a case rather than a type by
revealing the dramatically different situations
of individual patients, and how similar clinical
problems affect individuals differently. Together
the four questions elicit and organize information
into a ‘plot’ for the problem in question.
The four questions elicit ‘actionable’ informa-
tion: by focusing the clinician’s attention on the
relevant biological, social, and psychological
perpetuating and protective factors, in particular,
the clinician can design comprehensive and effec-
tive treatment plans, namely by decreasing the
perpetuating and increasing the protective fac-
tors. Indeed, supportive psychotherapy attempts
to do just that. In this way, the model emphasizes
prognosis over diagnosis: the model draws atten-
tion to the fixed and modifiable factors that are
currently in place that might influence the course
of the illness episode?
How Do You Teach the 4P
Model?
This last section is based on my experience
organizing two, 9-month, weekly seminar series
for third-year psychiatry residents—one at the
Cambridge Hospital and the other, more recently,
at the University of New Mexico.
The course was coordinated by myself; guest
lecturers were informed of the structure and peda-
gogical goals of the seminar series and were asked
to try to link their discussion with as many of the
other topics as possible. The seminar was intended
to complement other disease-, diagnosis-, and
treatment-focused seminar series. It was conceived
as a foundation course to encourage sophisticated
case formulations by introducing residents to bod-

ies of knowledge not fully covered in other courses
but which are relevant to the understanding of
individual patients’ illnesses.
The organizing principal to the seminar is that
the course and prognosis of a disease in any given
person is not determined solely by an intrinsic
(biological) disease process; the course of illness is
importantly affected by sociological and psycho-
logical influences that need to be understood and
made explicit if interventions are to be appropri-
ate and effective for that person. This approach
is at odds with a view of medical practice as only
(or even ideally) the application of standardized
treatments based on standardized knowledge to
standardized problems, but it is consonant with
Engel’s view. It is a view of medicine as a practical
activity involving (often) unstandardized prob-
lems; it calls for practical wisdom, what Aristotle
called phronesis. According to this view, physi-
cians are not scientists but problem solvers. Jonsen
and Toulmin described the difference between
scientist and clinician:
Where scientists study specific cases for any light they
can throw on general theoretical ideas, members of
the service professions [which include physicians],
conversely study general ideas for any help they can
give in dealing with specific practical cases. (Jonsen and
Toulmin 1990, 31)
This is the justification for exposing physicians-
in-training to the general ideas of psychology and
sociology: it brings into awareness the diverse
influences on illness, and this should lead to more
imaginative, intentional and effective therapeutic
interventions in particular cases.
The organization of any seminar reveals a num-
ber of assumptions about the subject matter (and
the audience). The organization of this seminar
is intended to acquire knowledge required for
the ‘situation analysis’ of the problems presented
by any particular person: why the person might
be vulnerable to the problem, how and why it
arose, and what sustains it and what might help
to resolve or ameliorate it. It encourages clinicians
to draw on relevant biological, sociological, and
psychological knowledge to make fuller sense of
these questions.
This seminar is organized into a sequence of
four modules mirroring the chronological develop-
Bolton / The 4P Model ■ 183
ment of and influences on any clinical problem.
The four modules are i) preconditions to illness,
ii) precipitating factors in illness episodes (or in
health-seeking behavior), iii) perpetuating, and
iv) protective factors in illness. The organiza-
tion of this sequence is important. Research in
clinical reasoning shows that how knowledge is
presented, and organized in memory and which
cognitive associations are established influences
how it is recalled (Bordage 1994). The medium
of the seminar series is the message. Appendix 1
provides a syllabus of the course.
The seminar has a number of pedagogical
objectives. First, the organization of the seminar
itself provides a structure by which to organize
clinically relevant information. The organization
of the seminar itself contains a built-in redundancy
to the pedagogical objective that understanding a
patient’s problem(s) means putting it/them into a
developmental, biographical, and social context,
as well as understanding physiological or anatomi-
cal derangements. A related benefit of clustering
lectures into the four stages of a problem is that it
encourages a broad and cross-disciplinary under-
standing of phases of the problem. For example,
understanding why a person remains ill involves
not just understanding the organic progression
of a pathological process, but might also involve
recognizing the iatrogenic consequences of past
medical interventions, the enclosure that occurs
with stigmatization of some medical and psychi-
atric conditions, how the person has become an
identified patient within the family system, the
‘functions’ of resisting medical advice, and so on.
Second, the juxtaposition of approaches deriv-
ing from different theoretical perspectives encour-
ages a critical understanding of their arguments,
especially as they are applied to medical practice
(Bolton 1995). This increases the likelihood that
our trainees will become discriminating consum-
ers of knowledge. This style of learning is found
more commonly in graduate schools than in
medical schools or residencies, which continue to
emphasize rote memorization over integrative and
critical understanding.
Third, the schema introduces topics (e.g., race,
poverty, transgenerational influences, immigra-
tion, communication patterns, stigma) that are
184 ■ PPP / Vol. 21, No. 3 / September 2014
not commonly included in medical/psychiatric
assessment. By integrating these knowledges into
an overall schema of sickness, the course demon-
strates how they can be influential in vulnerability
to and the course of illness. Appendix 2 lists top-
ics according to their contribution to phases of a
medical problem.
Fourth, gathering and organizing information
according to this model naturally leads to an ap-
preciation of pragmatic and ethical issues pertinent
to any particular patient and their problem(s).
Sadler and Hulgus (1992) distinguished three
aspects of clinical problems: the epistemic aspect,
which tries to understand the clinical nature of
the problem; the ethical aspect, which considers
the preferable course of action, depending on the
values of patient and doctor; and the pragmatic
aspect, which considers the most practical course
of action as influenced by the epistemic and ethical
aspects. They pointed out the danger of crossed-
aspect decision making in which, for example, a
practical aspect is mistaken for an ethical aspect
or an epistemic solution is offered for an ethical
problem. In exploring the perpetuating and protec-
tive factors relevant to a problem, in particular,
the clinician inevitably discovers practical and
ethical aspects that have to be reckoned with in
treatment planning.
Finally, the approach presents a clinician’s-eye
view on medical practice. Freidson (1986) dis-
tinguished three types of medical work: clinical
practice, administrative practice, and research
practice. Researchers limit their focus to narrow
or abstract problems; administrators consider
general problems of organizing services, but cli-
nicians must deal with the often messy problems
of individuals. Of the three types of practice,
clinical practice is the least theorized, and as a
result it is at risk of being ‘trumped’ by the logics
of entrepreneurial practice or bureaucratic/ratio-
nal practice (Freidson 2001). Expanding upon
William James’s metaphor of the ‘rich thicket of
reality’ (James 1948, 152), Donald Schön (1987,
3) contrasted researchers who stay on the high,
hard ground with clinicians who descend into the
swampy lowland of confusing problems that defy
technical solutions. Schön is among those who
recognize the tension between demands for pure,
abstract knowledge and the need for practical,
reflexive, and contextually sensitive knowledge.
Abraham Flexner emphasized the pragmatic
nature of medical education and the need for a
consciously organized curriculum in the service
of case formulation:
Medical education is a technical or professional dis-
cipline; it calls for the possession of certain portions
among many sciences arranged with a distinct practical
purpose in view. That is what makes it a ‘profession’.
Its point of view is not that of any one of the sciences
as such. It is difficult to see how separate acquisitions
in several fields can be organically combined, can be
brought to play upon each other, in the realization of a
controlling purpose, unless this purpose is consciously
present in the selection and manipulation of the mate-
rial. (Flexner 1910, 58)
As clinicians, we must do our work in the
absence of coherent integrated knowledge. Our
model for case formulation should be true to the
fact that we are more bricoleurs than systems
builders (Levi-Strauss 1966). We should not be too
worried that the 4P model lacks a reductive model
of causation from vulnerability to perpetuation of
a problem; for clinicians it is enough to be able to
help us tell better, thicker, truer stories to ourselves
and to our patients.
References
Biehl, J. 2005. Vita: Life in a zone of social abandon-
ment. Berkeley: University of California Press.
Bolton, J. W. 1995. Medical practice and anthropo-
logical bias. Social Science and Medicine 40, no.
12:1655–61.
Bordage, G. 1994. Elaborated knowledge: A key to
successful diagnostic thinking. Academic Medicine
69:883–5.
Engel, G. 1977. The need for a new medical model:
A challenge for biomedicine. Science 196, no.
4286:129–36.
———. 1980. The clinical application of the biopsy-
chosocial model. American Journal of Psychiatry
137:535–44.
Flexner, A. 1910. Medical education in the United States
and Canada. New York: Carnegie Foundation for
the Advancement of Teaching.
Foster, G. 1994. Hippocrate’s Latin American legacy.
Humoral medicine in the new world. Langhorne,
Penn: Gordon and Breach.
Freidson, E. 1986. Professional powers. A study of the
institutionalization of formal knowledge. Chicago:
The University of Chicago Press.

———. 2001. Professionalism: The third logic. Chicago:
University of Chicago Press.
Geertz, C. 1973. The impact of the concept of culture on
the concept of man. The interpretation of cultures.
New York: Basic Books.
James, W. 1948. What pragamatism means. Essays in
pragmatism. New York: Hafner Publishing.
Jonsen, A., and S. Toulmin. 1990. The abuse of casu-
istry. Berkeley: University of California Press.
Kuhn, T. S. 1970. The structure of scientific revolutions.
Chicago: University of Chicago Press.
Levi-Strauss, C. 1966. The savage mind. Chicago: Uni-
versity of Chicago Press.
Peirce, C. S. 1992. Deduction, induction, and hypoth-
esis. In The essential Peirce: Selected philosophical
writings (1867–1893), ed. N. Houser and C. Kloesel,
186–99. Bloomington: Indiana University.
Rako, S., and H. Mazer, eds. 1980. Semrad. The heart
of a therapist. Northvale, NJ: Jason Aronson.
Rosenhan, D. L. 1973. On being sane in insane places.
Science 179:250–8.
Sadler, J. Z., and Y. F. Hulgus. 1992. Clinical problem
solving and the biopsychosocial model. American
Journal of Psychiatry 149, no. 10:1315–23.
Schön, D. A. 1983. The reflective practitioner. New
York: Basic Books.
———. 1987. Educating the reflective practitioner. San
Francisco: John Wiley and Sons.
von Bertalanffy, L. 1968. General systems theory. New
York: George Braziller Inc.
Appendix 1
Case Formulation
A Seminar Series for Third-Year Psychiatry
Residents
1. Introduction to Case Formulation Seminar
series
2. Are you (just) a disease hunter? The PPPP
model of case formulation
a. Discussion of the difference between diag-
nosis and case formulation; type and case/
token. Examination of alternative models
of case formulation.
3. Preconditions: Overview
a. Genetics
Primer on genetic contributions to disease,
including patterns of inheritance, models
of gene-environment interaction, epigenetic
influences, role of mutations, methods of
Bolton / The 4P Model ■ 185
investigation (McClellan and King 2010;
Rutter and Silberg 2002).
b. Does where you work and how you live
hurt you?
Discussion of influence of position in social
hierarchy and stress on health and disease
(Marmot et al. 1991, 1997, 2006).
c. What are the effects of trauma?
Discussion of the epidemiology, vulner-
abilities, and sequelae of trauma (Herman
1992; MacFarlane 1989).
d. Does social integration help and/or hurt
people?
Discussion of the research into social net-
work analysis; historical shifts in patterns of
relatedness; relationship based obligations
and expectations; types of relationship-
based resources and strain (Berkmand and
Glass 1989; Seeman 14996).
e. What gets transmitted across generations?
Does trauma, divorce, parenting styles,
guilt, suicide risk get transmitted from
generation to generation (Serbina and Karp
2004; Amato 1996; Kellerman 2001)?
f. Development
Primer on personality/identity development,
including models of adult development
(Erikson); sexual identity; research in neu-
rological development (Erikson 1950).
4. Precipitating Factors: Overview
a. Why do/don’t people seek help?
Discussion of ‘hierarchies of resort’; types
of ambivalence about Biomedicine; impedi-
ments to receiving care (Merton et al. 1983;
Vogel et al. 2007).
b. What do people want from you?
Discussion of the research into ‘requests’
that patients make of doctors and how they
make them (Lazare et al. 1975; Barry et al.
2000).
c. Contagion
Examination of the biological and social
spread of risk (Bollen and Phillips 1982;
Phillips 1974).
d. Can you predict suicide? Can you under-
stand suicide?
Why do people consider/attempt suicide
when they do? Examination of the ‘motiva-
186 ■ PPP / Vol. 21, No. 3 / September 2014
tion’ behind suicide (Menninger 1938; Buie
and Maltsberger 1983).
e. Prodrome and First Break: What does it feel/
look like? What can/should you do (Dazzan
and Murray 2002)?
f. The ‘motivated accident’:
Discussion of the research into whether
some people are some people ‘accident
prone’ (Visser et al. 2007; Shapiro 1965).
g. What happens to people when they emi-
grate/ immigrate?
Review of the motivations and forces behind
migration; differences between refugees and
immigrants; stages of acculturation; influ-
ences on identity formation/development;
stresses associated with being a migrant
(Akhtar 1995; Fadiman 1997).
5. Perpetuating Factors: Overview
a. Hazard accumulation, cumulative injury
How does one condition predispose one
to other conditions/stresses (Holland et al.
2000)?
b. Demoralization
What is demoralization, and how is it dif-
ferent from depression (Clarke and Kissane
2002; Frank and Frank 1991)?
c. Why are some people undertreated?
Examination of sources of under-treat-
ment—related to patient, provider and
social factors.
d. How do we hurt our patients?
Discussion of varieties of iatrogenic effects,
including labeling, stigma, ‘side-effects’,
medical mistakes, psychological regression,
financial costs, etc. (Nath and Marcus 2006;
Rosenhan 1973).
e. What is the interaction between pain, per-
sonality and suffering?
Does personality style lead to vulnerability
or repetitive injury? Are some people ‘prone’
to suffering (Stone 1993; Tyrer 1992)?
f. What’s to gain from suffering?
Examination of notions of primary and sec-
ondary gain (van Egmond 2003; Fishbain
1994).
g. Why/how do some people avoid change?
Discussion of role of avoidance in perpetu-
ating illness.
h. Deficits: How does disease affect adapta-
tion?
Examination of how some diseases can
interrupt the processes of secondary and
tertiary socialization (Carter and Flesher
1995).
i. Interpersonal and family dynamics
Introduction to the research into the influ-
ence of family dynamics on illness behavior
and experience, including Expressed Emo-
tion, scapegoating, neglect, etc. (Butzlaff
and Hooley 1998).
j. Maladaptive coping
Discussion of the variety of coping styles/
mechanisms of defense, their adaptive/mal-
adaptive consequences, including substance
abuse, acting out, avoidance, distortion
(Vaillant 1992; Warner et al. 1994; Khant-
zian 1985).
k. Shame, stigma, guilt
Discussion of the differences between shame
and guilt; how they compound illness ex-
periences; interpersonal dynamics involved
in stigma and responses available to the
stigmatized (Miller 1988).
l. How do people’s thoughts keep them ill?
Introduction to principles of cognitive
therapy and positive psychology (Deale
1998).
6. Protective Factors: Overview
a. Why are some people protected from illness?
Introduction to the research into genetic/
social advantage and resilience (Rutter
1985; Vanderpol 2000; Frankl 1959).
b. Self-care and intelligence: How do some
people stay healthy?
Examination of ‘self-care’ as a form of intel-
ligence and influences on it (Khantizan and
Mack 1983).
c. Recovery
Discussion of the patient advocacy, peer
support; disability studies; modes of coping
Davidson et al. 2005).
d. Social support
Examination of the role of social capital
in health and recovery; patterns of social
relationships found in people with different
types of illness (Khantzian and Mack 1994;
Fowler and Christakis 2008).

e. Does religion protect people from getting
ill or dying?
Review of research on religious beliefs
and practices, and spirituality and health/
protection from illness (Powell et al. 2003;
Vaillant 2008).
f. Role and relevance
Discussion of the health benefits of ‘genera-
tivity’ and continued social relevance, e.g.,
volunteering (Yum and Lightfoot 2005).
7. Review and wrap-up
References
Akhtar, S. 1995. A third individuation: Immigration,
identity, and the psychoanalytic process. Jour-
nal of the American Psychoanalytic Association
43:1051–84.
Amato, P. R. 1996. Explaining the intergenerational
transmission of divorce. Journal of Marriage and
Family 58:628–40.
Barry, C., C. P. Bradley, N. Britten, F. A. Stevenson, et al.
2000. Patients’ unvoiced agendas in general practice
consultations: qualitative study. BMJ 320:1246–50.
Berkman, L., and T. Glass. 2000. Social integration,
social networks, social support, and health. In So-
cial Epidemiology, ed. L. Berkman and I. Kawachi,
137–73. Oxford: Oxford University Press.
Bollen, K., and D. Phillips. 1982. Imitative suicides:
A National study of the effects of television news
stories. American Sociological Review 47:802–9.
Brent, D., and N. Melhem. 2008. Familial transmission
of suicidal behavior. Psychiatric Clinics of North
America 31:157–77.
Buie, D., and J. Maltsberger. 1983. The practical for-
mulation of suicide risk. Cambridge Mass: Firefly.
Butzlaff, D., and J. Hooley. 1998. Expressed emotion
and psychiatric relapse. Archives of General Psy-
chiatry 55:547–52.
Carter, M., and S. Flesher. 1995. The neurosociology
of schizophrenia: vulnerability and functional dis-
ability. Psychiatry 58:209–24.
Clarke, D. M., and D. W. Kissane. 2002. Demoraliza-
tion: its phenomenology and importance. Australian
and New Zealand Journal of Psychiatry 36:733–42.
Davidson, L., et al. 2005. Recovery in serious mental
illness: A new wine or just a new bottle? Professional
Psychology: Research and Practice 36:480–7.<AQ1>
Dazzan, P., and R. M. Murray. 2002. Neurological soft
signs in first-episode psychosis: A systematic review.
British Journal of Psychiatry 181(Suppl. 43):50–7.
Deale, A. 1998. Illness beliefs and treatment outcome in
chronic fatigue syndrome. Journal of Psychosomatic
Research 45:77–83.
Bolton / The 4P Model ■ 187
Erikson, E. H. 1950. Eight stages of man. In Childhood
and Society, E.H. Erikson, ed, 247–74. New York:
W.W. Norton.
Fadiman, A. 1997. The spirit catches you and you fall
down: A Hmong child, her American doctors, and
the collision of two cultures. New York: Farrar,
Straus, and Giroux.
Fishbain, D. A. 1994. The secondary gain concept: Defi-
nition problems and its abuse in medical practice.
American Pain Society Journal 3:264–73.
Fowler, J. H., and N. A. Christakis. 2008. Dynamic
spread of happiness in a large social network: lon-
gitudinal analysis over 20 years in the Framingham
Heart Study. BMJ 337:1–9.
Frank, J. D., and J. B. Frank. 1991. Persuasion and
Healing. 3rd ed. Baltimore, Md: The Johns Hopkins
University Press.
Frankl, V. 1959. Man’s Search for Meaning. Boston,
Mass: Beacon Press.
Herman, J. 1992. Trauma and Recovery. New York:
Basic Books.
Holland, P., L. Berney, D. Blane, G. D. Smith, et al.
2000. Life course accumulation of disadvantage:
childhood health and hazard exposure during adult-
hood. Social Science and Medicine 50:1285–95.
Khantzian, E. 1985. The self-medication hypothesis
of addictive disorders: focus on heroin and co-
caine dependence. American Journal of Psychiatry
142:1259–64.
Khantzian, E., and J. Mack. 1983. Self-preservation
and the care of the self—Ego instincts reconsidered.
Psychoanalytic Study of the Child 38:209–32.
Khantzian, E. J., and J. E. Mack. 1994. How AA works
and why it’s important for clinicians to understand.
Journal of Substance Abuse Treatment 11:77–92.
Kellerman, N. P. 2001. Transmission of Holocaust
trauma—An integrative view. Psychiatry 64:256–67.
Lazare, A., S. Eisenthal, and L. Wasserman. 1975.
The customer approach to patienthood. Attending
to patient requests in a walk-in clinic. Archives of
General Psychiatry 32:553–8.
MacFarlane, A. 1989. The aetiology of post-traumatic
morbidity: Predisposing, precipitating and perpetuat-
ing factors. British Journal of Psychiatry 154:221–8.
Marmot, M., H. Bosma, H. Hemingway, E. Brunner, et
al. 1997. Contributions of job control and other risk
factors to social variations in coronary heart disease
incidence. Lancet 350:235–9.
Marmot, M. G. 2006. Status syndrome. JAMA
295:1304–6.
Marmot, M. G., G. D. Smith, S. Stansfeld, C. Patel, et
al. 1991. Health inequalities among British civil ser-
vants: The Whitehall II study. Lancet 337:1387–93.
McClellan, J., and M.-C. King. 2010. Genomic analysis.
JAMA 303:2523–4.
188 ■ PPP / Vol. 21, No. 3 / September 2014
Menninger, K. 1938. Man against himself. New York:
Harcourt, Brace and World.
Merton, R., V. Merton, and E. Barber. 1983. Client am-
bivalences in professional relationships: The problem
of seeking help from strangers. In New Directions
in Helping, ed. B. M. DePaulo, 2:13–44. New York:
Academic Press.
Miller, S. B. 1988. Humiliation and shame. Bulletin of
the Menninger Clinic 152.
Nath, S., and S. Marcus. 2006. Medical errors in psy-
chiatry. Harvard Review of Psychiatry 14:204–11.
Phillips, D. 1974. The influence of suggestion on sui-
cide: Substantive and theoretical implications of
the Werther effect. American Sociological Review
39:340–54.
Powell, L. H., L. Shahabi, and C. E. Thoresen. 2003.
Religion and spirituality: Linkages to physical health.
American Psychologist 58:36–52.
Rosenhan, D. L. 1973. On being sane in insane places.
Science 179:250–8.
Rutter, M. 1985. Resilience in the face of adversity. Pro-
tective factors and resistance to psychiatric disorder.
British Journal of Psychiatry 147:598–611.
Rutter, M., and J. Silberg, 2002. Gene-environment
interplay in relation to emotional and behavioral dis-
turbance. Annual Review of Psychology 53:463–90.
Seeman, T. 1996. Social ties and health: The ben-
efits of social integration. Annals of Epidemiology
6:442–51.
Serbin, L. A., and J. Karp. 2004. The intergenerational
transfer of psychosocial risk: mediators of vulner-
ability and resilience. Annual Review of Psychology
55:333–63.
Shapiro, D. 1965. Neurotic Styles. New York: Basic
Books.
Stone, M. 1993. Pain-dependent personality types. In
Abnormalities of Personality, 373–91. New York:
W.W. Norton.
Tyrer, S. 1992. Psychiatric assessment of chronic pain.
British Journal of Psychiatry 160:733–41.
Vaillant, G. E. 1992. The beginning of wisdom is
never calling a patient a borderline: Or the clinical
management of immature defenses in the treatment
of individuals with personality disorders. Journal
of Psychotherapy Practice and Research 1:117–34.
Vaillant, G. E. 2008. Positive emotions, spirituality and
the practice of psychiatry. Mental Health, Spiritual-
ity, Mind 6:48–62.
Vanderpol, M. 2002. Resilience: A missing link in our
understanding of survival. Harvard Review of Psy-
chiatry 10:302–6.
van Egmond, J. J. 2003. The multiple meanings of
secondary gain. American Journal of Psychoanalysis
63:137–47.
Visser, E., Y. J. Pijl, R. P. Stolk, J. Neeleman, et al.
2007. Accident proneness, does it exist? A review
and meta-analysis. Accident Analysis and Preven-
tion 39:556–64.
Vogel, D., S. Wester, and L. Larson. 2007. Avoidance of
counseling: Psychological factors that inhibit seek-
ing help. Journal of Counseling and Development
85:410–22.
Warner, R., D. Taylor, J. Wright, A. Sloat, et al. 1994.
Substance abuse among the mentally ill: Prevalence,
reasons for use, and effects on illness. American
Journal of Orthopsychiatry 64:30–9.
Yum, T., and E. Lightfoot. 2005. The effects of volun-
teering on the physical and mental health of older
people. Research on Aging 27:31–55.
Appendix 2

Predisposing Factors: Precipitating Factors: Perpetuating Factors: Protective Factors:

“Why Is This Person “Why Now?” “Why Is This Person Still Ill?” “Why Is This Person Not More Ill?”
Vulnerable?”

Biological
Genetics Accumulation of vulnerabilities Relapse and remission Resilience
Sex differences in development Medical illness Chronic illness Full treatment
Neurobiological development Iatrogenic events Addiction Genetic protection
Prenatal and postnatal exposures First-break episodes Pain
Childhood exposures Pregnancy Undertreatment
Iatrogenic influence
Psychological
Development Life events Avoidance Self-care
Temperament (including Loss Confidence and despair Spirituality/religious belief
“neuroticism”)
Intelligence Role change Behaviorist models Coping styles
Sexuality and gender identity Trauma Cognitive distortions Acceptance
Trauma Helplessness Resistance
Exposures ‘Stress’ Primary and secondary gain
Attachment ‘Accidents’ Disability acceptance
Lack of emotional support ‘Noncompliance’
Adaptive pathology and
pathological adaptation
Interrupted socialization
Hopelessness/demoralization

Bolton / The 4P Model ■ 189

Social
Abuse and neglect Family crises Stigma Health-related values
Transgenerational family dynamics Immigration Family dynamics, including Social support
expressed emotion
Parents with illness Homelessness and poverty Interrupted socialization Financial security
Political economy of sickness Violence Disability payments Supportive networks
Discrimination Influences on presentation to Social/work skills deficits Social ethos regarding suffering
healers
Cultural definitions of normal and Barriers to care Access to care
abnormal
Cohort variations in incidence of mental Poverty
illness
Social networks and illness