## 1. Introduction




Scholars and textbooks alike agree (though they might not like it)
that psychiatry now adheres to the "medical model", which
advocates "the consistent application, in psychiatry, of modern
medical thinking and methods" (Black 2005, 3) because
psychopathology "represents the manifestations of disturbed
function within a part of the body" (Guze 1992, 44) to wit, the
brain. But what does it mean to adopt this view of psychiatry, and what
difference does it make?




One might think that the medical model merely commits us to a
brain-based view of mental illness with few implications for science,
and it is true that clinical or scientific differences across
practitioners seldom seem to have much to do with divergent
interpretations of the medical model. However, many theorists have
argued that our current diagnostic categories, as compiled into DSM-5
(American Psychiatric Association 2013: I refer to different editions
of this work by its abbreviated title), are faulty because they are
derived from observable phenomena rather than underlying physical
pathologies. These theorists are sceptical about many existing
psychiatric diagnoses, and not just on empirical grounds; they see DSM
diagnoses as collections of symptoms rather seeing them as medicine
understands diseases--in terms of destructive processes realized
in bodily tissues. Genuine mental illnesses, on this view, are not
just sets of co-occurring symptoms but destructive processes taking
place in biological systems. Following Murphy (2009), this may be
termed the strong interpretation of the medical model. In contrast, a
minimal interpretation of the medical model thinks of mental disorders
as collections of symptoms that occur together and unfold in
characteristic ways, but it makes no commitments about the underlying
causes of mental illness.




These two interpretations are set out in section 2. Explanation is
discussed in section 3. The strong interpretation naturally suggests
that psychiatry should embrace the practices of medical
explanation. If disease is a pathological process in bodily systems,
then there must be a way of understanding how such processes occur in
the brain, and how they explain the clinically observable facts about
mental illness. But it seems that the logic of the medical model does
not force us to privilege any one level of explanation--notably,
it does not commit us to explanations restricted to the resources of
molecular biology. Psychiatry, then, is a multi-level science. But we
often know very little about the mental illnesses that psychiatrists
study, and much explanation in psychiatry involves case studies or
narrative accounts that cite the characteristics of a disorder, rather
than underlying systems. Theorists disagree over whether these should
be seen as different kinds of explanation, or as rudimentary forms of
a full causal explanation. Section 3 also discusses the difficulties
raised by cross-cultural issues. Section 4 discusses some recent approaches to mental illness that are broadly within the medical model but dissent from the mainstream.


## 2. The Medical Model and its Implications




 It may be helpful to distinguish
*minimal* and *strong* interpretations. A
minimal interpretation makes no commitments about the underlying
physical structure that causes mental illness. The *strong*
interpretation of the medical model, in contrast, dissents on just this
issue. It says that the proper medical understanding of disease is in
terms of morbid anatomy. It is committed to specific causal hypotheses
in terms of abnormalities in underlying neurobiological systems.
Minimalists treat diagnostic labels as useful heuristics rather than
natural kind terms, whereas a strong interpretation commits psychiatry
to a view of mental illness as a medical disease in the strongest
sense, that of a pathogenic process unfolding in bodily systems.


### 2.1 The Minimal Interpretation




Minimalists employ a concept of disease as the observable, regular
unfolding of a suite of symptoms. Kraepelin applied it to psychiatry as
the basis for differential diagnosis, for example between dementia
praecox (schizophrenia) and other forms of insanity (1899, 173-175). It
is a familiar idea that the DSM's syndrome based conception of
mental illnesses stands in the tradition of Kraepelin, who argued that
"*only the overall picture of a medical case from the
beginning to the end of its development* can provide justification
for its being linked with other observations of the same kind"
(1899, 3). This familiar neo-Krapelinian picture is that mental
illnesses are regularly co-occurring clusters of signs and symptoms
that doubtless depend on physical processes but are not defined or
classified in terms of those physical processes.




Guze (1992), for example, is a minimalist. In saying that
psychiatry as a part of medicine he means that we can classify
disorders in terms of their characteristic symptoms and courses. McHugh
and Slavney (1998) seem to agree. They say that a disease "is a
construct that conceptualizes a constellation of signs and symptoms as
due to an underlying biological pathology, mechanism and cause
(302)." To diagnose a patient as suffering from a mental
disorder, for McHugh and Slavney (48), is to label them in a way that
we judge helpful as a starting point for investigating physical
processes.




McHugh and Slavney deny that a disease is a physical
process--"its essence is conceptual and inferential"
(48). This way of thinking about diseases prescinds from
theorizing about underlying causes of a disease entity in favor of a
concentration on observable phenomena, not hidden causes. However, it
is diseases understood as destructive processes that make up the taxa
of medicine. Similarly, the successive editions of the DSM have sought
to classify mental illnesses based on course and symptoms but not
specific causes.




 Many scholars have argued (e.g. Bynum 1994, Carter 2003,
Whitbeck 1977) that in the nineteenth century medicine changed in many
ways, including a shift in thinking about disease. Instead of seeing
disease as the identification of symptoms, it was the linkage of
symptoms to distinct pathologies, understood as departures from normal
function, that came to define disease. Heinrichs (2001, 271), for
example, insists that psychiatry needs to employ this basic medical
outlook, and therefore needs a developed theory of how the mind/brain
works that can be used to identify psychological abnormalities and
explain how they arise. Andreasen (2001, 172-76) embraces the strong
interpretation. She argues that psychiatry, now emerging as a form of
cognitive neuroscience, is for the first time able to identify the
specific pathophysiologies that underpin the symptoms of mental
illness. This development fits the pattern suggested by Hempel (1965),
who expected psychiatry, as it matured, to develop a theory-driven
classification scheme based on an understanding of the objective nature
of mental illness rather than just pragmatic factors (Hempel 1965; See
Fulford et. al 2006: 324-341: Thornton 2008: 169-74).


### 2.2 The DSM Conception of Mental Illness And Its Critics.




The DSM treats mental disorders as syndromes along the lines of the
minimal medical model. Individuals who share a DSM diagnosis have a
subset of symptoms in common, often drawn from a larger list so that
although some people may have all their symptoms in common, there may
be no overlap at all in other cases. These collections of symptoms are
also supposed to unfold over time in more or less the same way, once
we make due allowances for some individual variation. They are also
expected to respond to treatment in the same way. The previous version
of the DSM assumed that each
diagnosis represented malfunction in some mental, physical or
behavioural trait or capacity (DSM-IV-TR, xxi). However, the diagnoses
were listed without worrying about what that underlying malfunction
might be, and in most cases there was (and remains) no agreement about
what causes what. DSM-5 defines mental disorders (p. 20) as syndromes
comprising clinically significant disturbances of cognition, emotion
or behaviour that reflect underlying dysfunctions. These are normally
associated with distress or social disability, but cannot be diagnosed
if the behaviour is culturally normal or merely socially deviant,
unless it reflects a dysfunction. 




DSM diagnoses are usually taken to reflect a conventional concept of
disease, despite the talk of underlying malfunction, because of the
emphasis on syndromes and the lack of causal hypotheses. In the
manner of the minimal medical model, they let us make use of
descriptive and statistical reasoning and offer the hope of accurate
prediction and effective control. In the opinion of some philosophers,
that is all science ever aspires to. I began by citing a textbook
declaration that psychiatry uses normal medical methods, and there is
certainly nothing within McHugh and Slavney's discussion of mental
illness that makes scientific methods inapplicable.




Other philosophers, though, will tell you that the job of science is
to discover the causal structure of the world. Furthermore, there are
plenty of students of psychopathology who argue that the neglect of
causal structure in psychopathology is getting in the way of science
(Poland, Von Eckardt and Spaulding 1994, Murphy 2006, Gerrans
2014). They worry that we are lumping together different groups of
people based on behavioral evidence alone, when in fact their
observable similarities mask important underlying differences,
including differences between normal people who are troubled but
basically healthy, and their pathological counterparts. From this
philosophical-cum-clinical perspective it looks like dereliction of
duty when any scientific discipline isolates itself from inquiry into causes. Suppose we ask why
the conventional view of diseases is successful in organizing
prediction and control (what psychiatrists sometimes call
"predictively valid"). The obvious answer is that
successful predictive categories are actually tracking the causal
structure in the world that accounts for the shared nature of the
different instances, so we should aim for a stronger validation of the
diagnosis than mere predictive validity. Whilst the reliability of a
diagnosis is a gauge of agreement across measurements and observers,
validity is supposed to be about what is really there. It looks
obvious that even the most expert observers could all agree but
nonetheless be wrong, whereas proper validation reassures us that we
are measuring something that is really there. (Psychiatrists employ
the concept of validity in several ways; for help in sorting them out,
see Fulford et al. (2006: 318-19), Schaffner (2012) and the
essays in Zachar et al. 2014.)




Someone committed to a strong version of the medical model sees
validating a diagnosis as understanding its underlying causal
structure: a valid diagnosis rests on a biological process
that can be identified by experiment and observation using the methods
of the biological and cognitive sciences. Any approach to psychiatry
that looks to science to validate its categories in this way must meet
at least two conceptual challenges. First, there is a metaphysical
challenge, which is that a concept of validity tied to the uncovering
of neurobiological processes seemingly adopts a realist philosophical
position, thinking that science can tell us how the world is really
put together. Many philosophers think that realism is a wholly
unnecessary and unwarranted metaphysical commitment, and that all
science can really tell us about is a set of relationships among the
data. These relationships let us make predictions and exert some
control over nature, but do not tell us what is really out
there. Philosophical disputes over realism have often centred on the
notion of the unobservable. In psychiatry
the situation is different; theories and constructs refer to latent
variables rather than unobservables. Schizophrenia, as a
construct, is not a further type of stuff that lies behind the
appearances and explains them: it is constituted by visible
phenomena. We are not looking for an unobservable, but asking which
observable phenomena (neurological, genetic, developmental, social)
explain the symptoms. If the strong conception of the medical model is
philosophically realist, it is so in light of its commitment to
causes, not to unobservables. We may look for a hidden variable that
explains the observable phenomena, or for some other hypothetical
underlying cause. Gold and Gold (2014, p.163-66) for example, suggest
that many delusions and other psychotic symptoms may reflect a
malfunctioning "Suspicion System" that has evolved to
detect and monitor social threats. If such a system exists it is not
directly observable, but its components should be open to observation
and manipulation via the standard methods of the cognitive
sciences. Psychiatry, like many sciences, deals in hidden variables or
hypothetical causal structures, but it is not helpful to think of
these as unobservable in the traditional sense. 




The second conceptual challenge to the realist interpretation of
validity is normative. The challenge is that there is an important
sense in which diagnoses cannot be validated at all, if by
"validation" we mean "shown to be a real
disorder". All validation can do is show that a pattern of
behaviour deemed to be clinically significant depends on a physical
process. Whether that pattern of behaviour is really pathological -
rather than immoral or harmlessly odd- is another matter. The second
challenge probably is very hard to meet. It requires that judgements
of pathology be scientifically
grounded, rather than human judgements. If
so, there has to be some natural fact of the matter about whether some
physical system is dysfunctional. If this cannot be done, then
predictions about physical states can be validated, but disorders
cannot be. 


 
The DSM classification has been designed to improve communication
between psychiatrists and across disciplines and provide a basis for
education. But it is not advertised as the jumping-off point for a
mature system of causally organised classification and practice. This
reflects a minimal interpretation of the medical model; it can guide
empirical research but not uncover causal structure. This leaves it
open to the charge that a classification which groups together
observable phenomena can sort entities into heterogeneous classes,
with underlying diversity masked by surface similarities so that like
cases are not grouped with like cases (Tabb 2015). We already know
from other areas of medicine that what looks like the same
phenomenon--a cough, say, or a sore throat, or chest
pain--can reflect different biological processes and hence may
really signify different conditions. A taxonomy that is content with
surface features risks lumping different conditions together and
keeping related ones apart.




Here are some examples of this charge in the recent literature (for
others, see Murphy 2006 (chapters 1-3) and McNally, 2012). Ross
et al. (2008, 33-34, 200-01) suggested some revisions to the current
diagnostic category of Pathological Gambling (PG) (see DSM-IV-TR, 671-74).
The category of pathological gambling is designed to operationalize a
concept whose content is, roughly, gambling that causes problems for
the gambler. But Ross et al. reasoned as follows: the existing category
"maps relatively smoothly onto the class of people who exhibit
classic patterns of addictive behaviour as a result of a specific kind
of dysfunction in their dopaminergic reward system and consequent
neuroadaptation impairing frontal control circuits. We therefore
believe that clarity would be served ... by replacing the
behaviourally derived concept of PG with the neuroscientifically
anchored concept of addictive gambling (200)".




A judgment that DSM categories have insufficient validity led the
National Institute of Mental Health to introduce the Research Domain
Criteria (RDoC) in grant proposals (Insel et al. 2010). The
originators of the RDoC acknowledged that the system entrenched by
previous versions of the DSM has increased diagnostic reliability. But
they worried that it was too detached from the nature of mental
illness, which they conceived of as disorders of brain circuits. For
example, rather than existing categories such as depression, the RDoC
envisaged a domain of negative valence including symptoms of anxiety
or depression that might come to be seen as expressions of an
underlying disorder of specific brain circuits (Sanislow et al 2010)
. These disorders could be studied at many levels and need not be
identified with simple lesions. But future models of mental illness
are expected, on this vision, to draw on psychological, neurological,
and genetic mechanisms, as well as information about the wider
cultural context. In this case, validating a diagnosis is thought of
as understanding its underlying causal structure: a diagnosis is valid
if it rests on a biological process that can be identified by
experiment and observation using the methods of the biological and
cognitive sciences. (For philosophical discussion of the RDoC in the
context of precision medicine, see Tabb 2020).




Ross and his colleagues argued along similar lines in their discussion
of gambling. They thought there were two benefits to the conceptual
change that they wanted. First, it would provide a clearer and
principled demarcation of the addicted gambler from the "problem
gambler" which is currently somewhat arbitrary (201). They also
showed the way to a better understanding of the nature of the addictive
disorders more generally via the use of their preferred approach,
which combined neuroscience and behavioural economics. They drew on
prior research (ch. 6.2) to suggest that addictive gambling resembles
dependence on stimulants (like cocaine) more than it does alcoholism,
and hence enlarges our understanding of addiction more fully than
purely behavioural criteria would do. The worry is that a behavioural
approach misses the similarities and differences between forms of
addiction by treating all as more or less the same, based on shared
behavioural and phenomenological effects.




To make these arguments we have to distinguish the truly
pathological gambler, whose life is dominated (and typically wrecked)
by gambling, from merely habitual gamblers. Habitual gamblers might
engage in gambling more than they feel they should, or periodically
lose more than they can afford, but there is a qualitative difference
between this population and the population of genuinely addicted
gamblers. This qualitative difference is detected by observing
behaviour and rating the results of questionnaires. However, if we
classify gamblers according to quantitative measures alone, we miss the
reason why different groups behave differently. The reason is a causal
process. The brains of the real addicts don't work like the
brains of the merely troubled; thinking of addiction merely in terms of
habitual behaviours will not let us make the discriminations among
gamblers that neuroscientific evidence detects.




A stronger but similar argument was made by Horwitz and
Wakefield (2007). They claim that only a hypothesis about causes
distinguishes a normal population from a disordered one. They
begin with the DSM criteria for diagnosing major depression. A subject must suffer from
five of the following nine symptoms in a two week period (including
either or both of depressed mood or diminished interest or pleasure in
almost all activities): depressed mood; diminished interest; weight
gain or loss (without dieting) or change in appetite; insomnia or
excessive sleep; observable psychomotor agitation or retardation;
fatigue or loss of energy; feeling worthless or excessively guilty;
diminished ability to think or concentrate, or indecisiveness;
recurrent thoughts of death or suicide or a planned or attempted
suicide.




Obviously many ordinary episodes in a person's life can cause
behaviors or feelings from this list, such as losing one's job.
The traditional concept of melancholy or depression, which in the West has a
continuous history going back to classical antiquity (Radden 2000),
sees pathology only where
one's circumstances do not justify a normal melancholy response.




The DSM, however, ignores this tradition. Anyone who fits the syndrome
receives the diagnosis regardless of how their life is going. The
sole exception stipulates that grief following bereavement does not
count towards diagnosis of Major Depressive Disorder until two months
have elapsed, after which one may diagnose major depression. But not
even that qualification is made if you show depressive symptoms after
your intended jilts you at the altar or you fail all your exams or get
your legs blown off. In subsequent work Horwitz and Wakefield (2012)
 extended their analysis to the anxiety disorders. They argued
that normal human anxieties are being pathologized and that the
diagnostic criteria for anxiety and depression have been much too
sharply distinguished from those for depression, leading to an
inability to explain why depression and anxiety so often co-occur.




During the run-up to DSM-5 the Mood Disorders Work Group proposed
eliminating the bereavement exclusion. This met considerable
professional and public opposition (see
Zachar 2014, ch. 10 for a summary of the debate and a discussion of
the issues). From the standpoint of Horwitz and Wakefield, the
proposal appeared to be pathologizing a normal human
reaction. However, it was never suggested that grieving itself was
pathological. Rather, the proposal was based on the idea that
stressful life events often precipitate episodes that meet the
criteria for a major depressive episode, and there is no reason to
exempt bereavement. Many people, after the death of a loved one,
exhibit symptoms very like those of major depression, and are at risk
for subsequent episodes. From this perspective, the elimination of the
bereavement exclusion is justified by science, regardless of common
sense (Kendler et al 2007; Lamb et al 2010). Why should bereavement
alone be exempted from the general claim that depression is caused by
stressful life events?




Horwitz and Wakefield suggest that genuine depression is caused by a
dysfunction on the part of a loss-response system that evolved to
respond to losses that threaten to deprive us of reproductive
resources. In depression the system misfires. It causes a
loss-response in situations where it should not. Whether or not that
is convincing, the argument that Horwitz and Wakefield make about the
conflation of depression and sadness stands on its own merits. They
make the case that the DSM conception of depression respects neither
folk psychological common sense nor previous psychiatric consensus
about depression. They conclude that the concept of depression defined
by this diagnostic syndrome represents a major conceptual break. Our
use of the new concept, they suggest, means that many people who are
just normally miserable for understandable and ordinary reasons are
being diagnosed as depressed. This leads to unnecessary alarm about an
epidemic of depression as well as carrying unfortunate consequences
for many people who are wrongly diagnosed. However, it is certainly
open to those theorists opposed to the bereavement exclusion to insist
that if depression is the result of an underlying system that
misfires, it could misfire in response to bereavement. The proposal is
not that everyone who grieves should be called depressed, but that
there are reactions to bereavement that are severe enough to meet the
criteria for major depression and should be classed as such. 




The DSM concept of depression, on the face of it, lumps together
different psychological and behavioral types in the same category. It
does this because it neglects the diverse etiologies that may produce
similar signs and symptoms. There is no way to answer this charge, or
to arrive at a satisfactory taxonomy that mirrors that of general
medicine, unless we adopt a causal foundation for nosology as suggested
by psychiatrists who urge the adoption of what I have called the strong
medical model. Indeed, without an account of underlying causal
structure, it becomes difficult to give a principled answer to the
question why some conditions should be seen as pathological to begin
with. Merely saying that members of a class have certain properties
does not tell us whether, let alone why, they are mentally ill. To
answer that question we need some basis for making the judgment. The
DSM, as we have seen, states that we have such a basis; mental disorder
is an outward sign of dysfunction. But to make that argument, we need a
commitment to finding dysfunction somewhere on the basis of the
outward, observable phenomena. The minimal model can only
answer questions about the relationship between membership in a taxon
and some other variable: it will not explain why the taxon has the
nature that it has, or why it should be seen as a kind of disorder.




Doing that involves not just the empirical study of mental disorder,
but a strong interpretation of the medical model, with its commitment
to a view of disease as not just a syndrome but a destructive process.
It is certainly possible to collect data using the DSM concept of
depression, especially information about epidemiology and natural
history. In that sense normal medical reasoning can indeed be employed,
but much medical reasoning is directed at trying to
understand causes. It is here that we come to the strong
interpretation, with its commitment to the idea that a mental disorder,
like any other disease, is not just a construct to guide inquiry, but a
genuine part of the causal structure of the biological world--a
destructive entity with a distinctive pathophysiology which explains
the observable phenomena that the minimal model is content with.


### 2.3 The Strong Interpretation of the Medical Model




Proponents of the strong interpretation, then, can agree with Guze
that there are distinct mental illnesses with characteristic symptoms
and natural histories. But they go further. If psychiatry is really a
branch of medicine, they suspect, we should see the specific causal
hypotheses emerge about mechanisms that cause the symptoms of mental
illness. Both Andreasen and Guze assume that to find the specific
causes of disease we need a background theory of normal function.
Psychopathology is to be identified as the departure of a psychological
system from its proper state. (We should note what counts as a
malfunction is often contested in psychology and neuroscience.
Furthermore, the presence of a malfunction does not suffice for mental
illness. Most scholars agree that our thoughts about the nature of
disease are sensitive to biological abnormalities but are also guided
by judgments that such abnormalities impede human flourishing (See
Cooper 2007, Murphy 2006, Sadler 2004, Wakefield 1992). The medical
model also sees abnormalities or dysfunctions as necessary but not
sufficient for mental illness. The broader issues involved will be put
aside here. Our question is: how far can psychiatry adopt medical
reasoning about pathogenic neurobiological processes? )




The strong interpretation seeks explanations that cite pathogenic
processes in brain systems, just as bodily diseases are explained by
processes in other organs. The process at issue need not be
destructive, in the sense that it makes the system collapse. Bolton and
Hill (2004, 252) note that many mental illnesses seem to be the
outcome of systems in a poorly regulated state that is stable, albeit
suboptimal. But, as they say, the same is true of hypertension and
Cushing's disease; the idea of a specific pathogenic process in
medicine includes dysregulation.




Heinrich and Andreasen assume that since the brain is an information
processing organ the obvious background theory is cognitive
neuroscience. Other thinkers have argued that the correct background
theory for psychiatry is molecular biology (Kandel 2005, ch.2).




Bolton and Hill worry that whatever background theory the medical
model employs, it will require explanations in terms of biological
rather than intentional phenomena. They conclude that biological
psychiatry can only accommodate disorders in which
"intentionality has run out" (2004, 256). If true, this
rules out using the medical model to explain the many psychopathologies
that appear to involve irreducibly intentional or meaningful processes
(cf. Thornton 2007, ch 4). The worry is founded on the assumption that
there is an unbridgeable distinction between understanding a phenomenon
in intentional terms and providing a causal explanation of it.
But the brain is a cognitive organ--and, indeed, a social one.
Many disciplines study the effects of healthy cognition on behaviour,
and there is no reason to expect that cognition will suddenly become
irrelevant to the explanation of behaviour when we study mental
illness. For instance, Kendler and Prescott (2006, 148ff) found that
"stressful life events" are among the chief causes of
depression, that they are especially depressogenic if they involve
experiences of humiliation (160), and that humiliation cannot be
given a molecular reduction (350). Kendler and Prescott call Major
Depression one of the oldest diagnoses in medicine (52) and they are
committed to finding specific etiologies. Yet they are happy to employ
"classically mental constructs" (350) as parts of their
causal models of mental illness.




As presented so far, the strong interpretation of the medical model
includes a demand for understanding biological systems in terms of
their normal function if we are to understand why they become abnormal.
Kincaid (2008, 375) has argued that a demand like that is
unreasonable, because we can conduct research on depression (his
example), as we do medical research more generally, based on
"partial and unsystematic" causal understanding. Kincaid
identifies the demand for a background theory with the search for a
"complete wiring diagram of the organism from fertilization to
maturity" (377) and he identifies that search with a
conception of science as a search for laws of nature and natural kinds.
But these seem to be separable: a background theory could comprise a
number of partial wiring diagrams arrived at by piecemeal
investigation, nor does it have to be driven by a desire for
explanation in terms of kinds participating in laws. The questions are,
what sort of general orientation toward mental phenomena does the
medical model permit, and what sorts of explanations can it encompass?
We do not need a complete theory of how biological systems work in
order to conduct fruitful research. The issue is whether, at a minimum,
there need to be some rough theoretical frameworks and shared empirical
claims within which otherwise abnormalities can be identified and
outcomes assessed.




First, nothing in the strong interpretation of the medical model
rules out explanations that cite cognitive processes in brains:
Andreasen (1997) argues that schizophrenia and depression are cognitive
pathologies and sees psychiatry as both a form of medicine and
"the discipline within cognitive neuroscience that integrates
information from all these related disciplines in order to develop
models that explain the cognitive dysfunctions of psychiatric patients
based on knowledge of normal mind/brain function" (1586).
This conception of psychiatry is fully biological but not committed to
a particular metaphysical interpretation of what biological explanation
must look like. It sees mental illness as the result of pathogenic
processes taking place in brain systems but does not force us to choose
reductive explanations as a matter of logic. So Bolton and Hill's
worry about the compatibility of the medical with their "neural
encoding" theory (2005, ch.2) seems overstated. They are right to
stress that the brain can be seen as a socially situated, cognitive
organ, but there are advocates of a strong medical model who are
equally attuned to this conception of neuroscience. Existing medical
and biological practice already cites processes that cross levels of
explanation (Schaffner 1993, 1994) and incorporate environmental
information about stress or other risk factors. There is in principle
no objection to adding an intentional level to the mix. Any conception
of normal neurological functioning must take information-processing
into account, because processing information is what brains are for.





Most mental illnesses are caused by diverse environmental and
genetic factors. We have little reason to think that all the relevant
causes can be given a reductive analysis, for as Schaffner dryly points
out, to specify and measure environmental variables in purely molecular
terms "would be a very long-term project" (1994, 287).
But one might still think that molecular processes are the root
causes of mental illness even if many other contributory factors exist
and define the context within which genes work. Kandel (2005) offers a
very stringent version of this view, which assigns all explanatory
significance to proximal genetic causes on the grounds that "all
of 'nurture' is ultimately expressed as
'nature' (39)" He means that behavioral and
cultural factors influence gene expression, but he also seems to think
that this implies that psychiatric explanations need only mention gene
expression, which will screen off everything else.




Kandel's genetic reductionism is a metaphysical position aimed
at identifying a privileged level in nature and a general explanatory
strategy that unifies the phenomena and offers lawlike explanations.
However, in medicine the goal of causal explanation is instrumental. We
seek the factors that make a difference in a given case, not a
metaphysically privileged level or a general unifying account. There is
little reason so far to believe that the reductionistic approach Kandel
urges has been more fruitful.




In studying eating disorders, for example, we find that social
factors may explain particular epidemiological patterns, like different
levels of eating disorder across populations. But social factors
don't tell us why only one girl in a family gets bulimia. To
explain that we can look at a particular brain chemistry that puts her
at risk (Steiger et al 2001). But that does not establish that
neurobiology really is fundamental. Rather, nothing is fundamental.
Culture or trauma may require biological mediation to have its
pathological effect, and vice-versa. Neither one should be considered
fundamental, but seen rather as the best way to answer a specific
question about what makes a difference in a context.




The identification of a cause of a disease often depends on what we
want to control. The reason for this, as Whitbeck (1977) and Kincaid
(2008) have convincingly argued, is that physicians care about causes
for instrumental reasons. The goal is to understand why a biological
system has departed from a functional state and identify components and
processes within the system that can be manipulated so as to understand
the abnormal character of the system, and, ideally, mitigate it.
In looking for the relevant factors we do not seek a final
description of the system or look for the ultimate sources of an
abnormal or disvalued outcome. Rather, we hope to identify the
variables that made a difference to the outcome.




That is why alternative etiologies can complement, rather than
compete with, each other, as in Meehl's (1977) example of an
elderly man, genetically somewhat at risk for depression, who develops
it after his spouse dies. It seems wrong to call this a genetically
caused episode of depression: the genes needed an unusual environment,
so that in most other circumstances the man would not be depressed. But
he would not have developed clinical depression had his genes been
different. Both factors are causally relevant.




Because of this stress on figuring out what makes a difference in a
context, medicine is a natural home to manipulationist accounts of
causation, as Whitbeck also saw (1977, 627-28). The basic idea behind
the manipulationist approach is that it puts us in a position to begin
explaining a phenomenon "when we have identified factors or
conditions such that manipulations or changes in those factors or
conditions will produce changes in the outcome being explained"
(Woodward 2003, 10). We may have a correlation--say that
between smoking and heart disease. We get from there to a causal
explanation if we can intervene so as to manipulate the value of the
causal variable by itself--by stopping one group from smoking
and letting an otherwise identical group smoke, for example. If smoking
causes heart disease, we will see an effect on the cancer variable that
reflects our meddling with the smokers. If smoking doesn't cause
heart disease then there will not be a correlation between the two
variables. (This view is compatible with many proposals about the
underlying metaphysics. There will be more on this account of causation
in section 3.1. For the technical details see Spirtes et al 2000, Pearl
2009).




Kandel's avowed molecular reductionism dissents from the
goal-driven, manipulationist view. Kandel bets that molecular
explanation picks out nature's own preferred level. He assumes
that as we learn more we will be able to supply fundamental
explanations at such a level. Kandel invites us to give up a fruitful
approach in favor of a promissory note, on which we have scant reason
to expect payment. Molecular explanations do not appear to be
flourishing alone among all possible approaches to mental illness.
(Schaffner (1998) points out how hard it is to supply reductive
explanations even for simple model organisms.)




Things may turn out as Kandel expects, but it is not clear that they
will, based on the current fortunes of different kinds of psychiatric
explanation. In any event, it seems that the medical model does not
require any particular level of explanation. Rather, it seems to be
marked, in its strong interpretation, by a search for explanations of a
particular form that can involve many different levels. These are
explanations that show how symptoms of mental illness systematically
depend on disruptions to the normal functioning of biological and
cognitive processes. The strong interpretation of the medical model
bets on such explanations being available and--which is a
further claim--being clinically useful when they are finally
uncovered. Whether the ensuing explanations privilege one form of
explanation over others is an empirical question to be answered case by
case. However, psychiatry currently recognizes many different causal
factors and we should expect that to continue. One way of cashing out
this idea is to say that psychiatry must pay attention to different
levels of explanation. The next section, on explanation, will begin
with a discussion of this point.


## 3. Explanation


### 3.1 Levels of Explanation




I begin with a picture that is familiar to philosophers of psychology,
Marr's (1982, 24-5) distinction between three levels of
explanation in cognitive science. The highest specifies the
computational task accomplished by the system of interest. It tells us
what the goal of the system is, specified in terms of what it
computes. The middle level describes the actual representations and
algorithms that carry out the goal. The lowest level tells us how
brain tissue or other material substrate, such as the parts of a
machine, can implement the algorithm. Note that the
levels of description are different perspectives on the same
mental process - Marr thinks of vision as the construction of a 3D representation from a 2D input, and the three levels are three different ways to understand that construction. Other cognitive phenomena can also be understood in these three ways. 




Marr sought to understand psychological capacities in the abstract
without worrying about biology: although he certainly assumed that
capacities could be realised in a physical set up, he thought that the
details of the particular set up would not make a difference to the way
the psychology was understood. But as the sciences of the mind have
become more interested in the brain we are learning that this idea may
need to be amended. Cognitive neuroscience is learning to look for
physical structures in the brain that carry out information-processing
jobs, or what Glymour (1992) calls "cognitive parts". Our
understanding of biological realization feeds back into and constrains
our understanding of the abstract processes of cognition (Bechtel and
Richardson 1993). Rather than relating abstract psychological
capacities to each other, higher level descriptions of the mind/brain
in cognitive neuroscience relate capacities understood as functional
descriptions of fairly coarse-grained brain areas, not purely abstract
computational task specifications. Theories of the normal system
specify the nature and interrelation of cognitive parts. Armed with
these assumptions about cognitive parts, psychiatrists can see a
disorder as a breakdown in normal functioning within and between
cognitive parts. Marr's first level might seems to be useful as a
source of background theory for doing psychiatry, because it asks
"what is it for?" and much of psychiatry is about finding
out psychological systems fail to do what they are for.




However, we still face the question of how psychological deficits
are related to other levels of explanation, and here Marr's
picture comes under real stress. Marr's three levels are
different representations of the same process. But in psychiatry
different levels typically represent distinct causal processes. For
example, the causes of many mental illnesses include a mix of genes and
environmental factors, as in Meehl's example, cited above, of
genetics and bereavement conspiring to cause depression. The genes and
environmental effects are different kinds of processes, not different
levels of one process. If we were dealing with one process,
describable in different ways, then we could anticipate a reductive
account, in which higher-level variables are mapped on to lower-level
ones. But even though it is hard enough to imagine a molecular or
neurological reduction of a psychological construct like humiliation
(which, we saw above, is depressogenic), it is even harder to imagine a
reductive analysis of socio-cultural factors like unemployment or
childhood sexual abuse. They have brain effects, but the brain effects
vary across classes of individuals in ways that depend on other
environmental and genetic contexts (see Kendler and Prescott 2006 for a
comprehensive review.)




Schaffner (1993, 1994) suggests this structure is the norm
throughout biology, and sees it as relating causes and effects at
different levels of explanation. Appealing to levels of explanation is
unobjectionable if it just involves a reminder that we need to relate
variables of many sorts. But it is not clear that we have any
principled grounds for sorting phenomena into levels. Marr did, because
he imagined levels as descriptions of the same process (the
construction of a 3D image from 2D retinal impacts) couched in the
vocabularies of different sciences. But when we move outside the skull
and begin introducing environmental factors and other kinds of cause,
the Marrian picture looks less plausible.




Another way in which levels talk has featured in recent philosophy
of psychiatry is as a constraint on permissible kinds of explanation.
Chris Frith (1992, 26) for example, imagines what we would say if we
found a strong correlation between a spike in dopamine levels and
delusions of thought insertion (in which, for example, one has the
experience of another person's thoughts in one's own mind).
He argues that such a correlation is "simply not
admissible" as an explanation because we would remain in the dark
about why a sudden upsurge in dopamine causes thought insertion rather
than something else. To show why thought insertion comes about, Frith
thinks, we need a cognitive story which shows us how it is caused by
failures of normal subpersonal processing.




Frith's idea is that a causal explanation of a psychotic
phenomenon, or some other mental symptom, must cite properly cognitive
variables to be explanatory. That is, explanations should relate
variables from the same level. The relationship between dopamine
and thought is just opaque to reason, and we want variables that are
related in ways that are transparent to reason. There is a constraint
here; the idea that explanations of psychological phenomena should
relate cause and effect in ways that we find intelligible. Campbell
(2008) in attacking this picture, notes that talk of levels of
explanation is often wheeled in at this point, as it is by Frith, to
supply relations that are transparent to reason in the right way. The
idea is that only processes at a level let us grasp explananda at that
level. Explanantia at a different level are not intelligible in the
right way, so although lower-level processes may realise the higher
ones they cannot explain them. This amounts to a constraint on
acceptable explanation. Should we accept it?



The debate here quickly gets into technical arguments about the
concept of causation. Campbell argues against Frith in favour of the
Humean idea that we simply cannot tell in advance of inquiry what
causal relations obtain in nature. Anything can cause anything and it
is just as unwarranted to suppose that the relevant explanatory
variables for psychotic or affective phenomena must be cognitive as it
is to adopt a simple reductionism and insist on their being
biological. Decades of research have revealed that mental illness is
caused by, and causes in turn, many different physical, psychological
and social factors. We simply have to take our causal relations where
we find them, including interlevel ones. Craver and Bechtel (2007,
554) on the other hand, argue that it stretches the concept of
causation to breaking point to admit interlevel causes: they say that
"to accept interlevel relationships as causal violates many of
the central ideas associated with the concept of
causation". Craver and Bechtel argue from the perspective of
mechanistic explanation. Mechanisms explain effects in terms of
interlocking parts, and the relation across levels, they affirm, is
one of constitution, not causation; causation can only be
intra-level. Interlevel causation, on this view, amounts to something
causing itself, because different levels are different ways of talking
about the same thing. However, talk of levels in psychiatry often
involves relating different parts of the world, as in Meehl's example:
genetics and bereavement may be seen as requiring different levels,
but they are not different ways of describing the same process. Causal
models must interrelate phenomena of very different types.



In part because of these issues, that levels in psychiatry are not
Marrian, Campbell (2006) argues for an interventionist approach to
causation. This is the view that when we say *X* is a cause
of *Y* we are saying that intervening on *X* is a way of
intervening on *Y* (Woodward and Hitchcock 2003, Woodward 2003,
Pearl 2000): manipulating one variable makes a difference to
another. This is not a reductive analysis of causation, since it makes
use of causal ideas--it just states that questions about
whether *X* causes *Y* are questions about what would
happen to *Y* if there were an intervention
on *X*. Kendler and Campbell (2009) have argued that an
interventionist model provides a rigorous way of articulating the idea
that any combination of variables might characterize the causes of a
disorder, whilst at the same time providing a clear test of what
variables are actually involved, thus avoiding a simple-minded holism
that just says that lots of things are relevant. They further note
(2009, 997) that interventionism "permits the clear separation
of causal effects from the mechanistic instantiations of those
effects", thus directly confuting the approach favored by
Bechtel and Craver.




Appealing to levels of explanation in psychiatry, then, might just
be a reminder that we need to relate variables of many sorts in
explaining the causes of disorder. But it may also be connected with
particular perspectives on reduction, explanation and causation. We
won't go into these debates here; rather, we will move on to
discuss a further problem. As well as great diversity in causal
factors, psychiatry also confronts the problem of diverse symptoms;
many mental illnesses take a different form in different people.
Although two people might both be diagnosed with major depression, they
need share few symptoms. Both are very likely to feel miserable and
lose interest in activities they normally enjoy. However, one might
lose weight, sleep less and becomes physically agitated while the other
sleeps more and becomes lethargic and tormented by feelings of guilt
and thought of suicide. The philosophical problem arises from the
confrontation between the great variation in clinical reality and the
need to simplify in order to render that reality scientifically
tractable. In summary form, the problem is; what are we trying to
explain when we explain a mental illness? Is it a diverse set of
real-world phenomena, or some simplified representation of those
phenomena?


### 3.2 Disorders as Statistical Networks




One way to start thinking about what we have to explain in
psychiatry is to borrow from Thagard's (1999, 114-5) account of
diseases as networks of "statistically based causal
relations" which are discovered using epidemiological and
experimental methods. This fits the picture that Kendler and Prescott
present for depression quite neatly (although their models are designed
to incorporate both causal relations between variables and
correlations). Thagard's causal-statistical networks, like
Kendler and Prescott's path models, provide "a kind of
narrative explanation of why a person becomes sick" (p15). They
incorporate information about the typical course of a disease as it
unfolds over time, including information about typical risk factors for
the disease--such as the finding that heavy use of aspirin increases
acid secretion which makes a duodenal ulcer more likely. The causal
network does not specify how each causal factor produces its effects,
though. It is really a descriptive model that lets us ask the question;
what facts make it true that people get sick in these ways?




In effect we have a set of exception-prone generalizations about the
pathways a disorder takes: people in this situation are likely to
become depressed unless such and such intervenes. And when they are
depressed they will probably have the following experiences, unless
they have these other ones. Thagard's idea of a narrative is
helpful here; path models represent typical stories about
characteristic ways of getting sick. But a narrative by itself might
not explain anything; if it is explanatory, it is because earlier
events mentioned in the narrative pick out the causes of later
events.


 Rachel Cooper (2007) presents a way of thinking about psychiatric
explanation that fits well with the idea that a diagnosis lets us tell
a story. We often find ourselves with narratives that tell us how
someone gets sick, and it might be that a useful narrative is one
which isolates the temporally prior variables and lets us see how
later phenomena depend on them. One way to think about this is that a
good narrative is one that talks about a natural kind. If we have a
natural kind, with some causal structure underpinning it, the
systematic dependence of later states on earlier ones is easy to
grasp. Several theorists have defended a view of psychiatric disorders
as natural kinds. Influential recent philosophical treatments have
rejected the idea that mental disorders have essences, but have
defended the idea that mental disorder are natural kinds in
Boyd's sense of homeostatic property clusters (Beebee and
Sabbarton-Leary 2010; Kendler et al. 2010; Parnas et al. 2010; Samuels
2009, Zachar 2014, Pereira 2020), in which properties occur together
often enough, and reliably enough, to support ampliative inferences,
even if the mechanisms responsible for the kind do not make every
member of it the same as every other member. When inductive reasoning
works, thinks Boyd, it works because we have have latched onto these
underlying causal mechanisms that bring about the
clustering. Successful inductions track the observable manifestations
of the causal mechanisms responsible for the characteristics of the
kind. The mechanisms, we might say, leave an identifiable causal
signature in the world. The HPC account seems to suit mental
disorders. They often vary across cases, with characteristic symptoms
sometimes absent even when the patient presents a typical cluster of
signs and symptoms. So it is understandable that theorists who are
sympathetic to the medical model in psychiatry should be drawn to the
homeostatic property cluster idea. 


### 3.3 From Histories to Causes




Cooper distinguishes natural-history based explanations from case
studies. She presents them as distinct kinds of psychiatric
explanation, but she doesn't go into detail about what the other
types might be, so her overall position is hard to grasp. But one idea
is very clear; at least some mental illnesses are natural kinds, and
natural history explanations work by "invoking natural
kinds" (2007, 47). Once we know which kind an object belongs
to, we can explain and predict its behaviour based on its kind
membership: we can say why a substance has expanded upon being heated
by invoking the fact that it's a bit of metal, and metals expand
when heated. Or we can predict that if Rex is in the kitchen then
leaving the roast beef there unattended is a bad idea, since Rex is a
dog and dog-meat interactions take a predictable form. And, it is
hoped, we can explain why Laura hears voices by appealing to the fact
that she has schizophrenia. And our confidence that she is
schizophrenic warrants (pessimistic) predictions about her future.




Cooper also talks about case histories and argues that they explain
another person's unique situation by drawing on our capacities
for simulation of other people's states of mind. This claim
involves commitments in the explanation of theory of mind that would
take this essay too far astray. The relation of folk psychology to case
histories is unexplored, as is the nature of reasoning from cases more
generally: we lack a good general account of what a case history
explains or is otherwise good for, in psychiatry or in any other field.
(Forrester (1996) points out that reasoning with cases seems to be a
distinctive and ubiquitous style of thought in science and elsewhere,
and we have no good account of it.) So for now, we must put case
histories aside.




Cooper argues that a natural history explanation needs to cite
natural kinds if it is to be helpful. But in order to work the
explanations do not need to cite the actual causal mechanisms
responsible for the behaviour of the members of the kind in question.
We know that Rex will devour the roast if we leave him in the kitchen
with it, and we can safely make this prediction despite total ignorance
of canine physiology. The history of psychiatry offers a number of
instances in which pharmacology has led to the recognition of new kinds
even in the absence of detailed causal knowledge. For example
Cade's (1949) discovery that lithium greatly inhibited the
startle reflex and other forms of anxiety in guinea pigs was useful
even without good information about their underlying cognitive
neurobiology, since it led him to predict that whatever was going on
might also apply in humans.




Invoking kinds give us power over the world, by making it easier to
predict, control or mitigate the outcomes we care about. One
philosophical question we can ask, of course, is whether science wants
anything more. If you think science just aims for empirical adequacy,
then it may seem that sorting patients into kinds is enough, provided
that we can understand the course of the disease.




In particular, natural history explanations fit a conception of
diseases as syndromes unfolding over time that is enshrined in both
DSM-IV-TR and the minimal construal of the medical model. It does not
deny that there are causal processes, but sees mental illnesses as
collections of signs and symptoms with characteristic histories. They
doubtless depend on physical processes but are not defined or
classified in physical terms. This picture of disease naturally goes
along with the employment of natural history explanations, since they
too invoke natural kinds without worrying about the mechanisms that
explain the behaviour of members of the kind. It's enough to be
able to identify kind membership, thereby giving us a degree of
explanatory and predictive control.



Natural history explanations fit Thagard's disease network
nicely; if a disease network provides a narrative account of why people
get ill, and predicts some outcomes, we can see it as a graphical
representation of the historical pathway typical of a kind. Much
epidemiological work in psychiatry fits the pattern here; we try to
isolate the causal factors that define a disease history that is met
with regularly. These histories display relations between variables
that show how later phenomena, like the symptoms of depression or
substance abuse, depend on earlier phenomena, like the genes you were
born with, or the parental abuse you endured.




Unlike some of the more homespun examples, the natural histories
uncovered by systematic longitudinal research can be quite surprising
and genuinely explanatory. But (as Cooper and Thagard both suggest)
they leave us with a lot to do; whatever the philosophers of science
may say about how empirical adequacy is good enough, physicians have
spent a century and a half looking for causal explanations of
pathological phenomena (Carter 2003).


### 3.4 Causal Explanatory Strategies




Cooper suggests (174n2) that natural history explanations
provide us with what Murphy (2006) calls causal discrimination, as
opposed to causal understanding. We can know two kinds are causally
different even if we don't why they are different, because the
details of the underlying causal structure evade us. Different types of
plant may need to be put in the ground at different times, or in
different seasons, in order to maximize crop yield, for instance, and
we may be able to predict accurately that different patients will
respond to different drugs even if the basis for these differences
remain unknown. But we assume that these differences rest on an
underlying causal structure. In psychiatry, differential
diagnosis follows a similar logic, but sceptics wonder if the degree of
variation makes the predictions too unreliable for this approach to
really work.




An explanation of this type places entities in kinds, thereby
tracking the as yet unknown causal factors that regularly make the same
kind of difference in patients of the same type. Rather than
identifying the causal factors, then, the natural history approach
tracks the operation of hitherto unknown causes, by sorting patients
into kinds with a presumed common nature, based on the natural history
of their conditions, or on other grounds that I have not talked about,
like differential responses to drugs.




Our complete explanatory job is to explain the observed
causal-statistical network by identifying the mechanisms and other
forces that give rise to it, viz. the causal structure of disorders.
The problem, of course, is the sheer variety of the phenomena, which
does not give us the degree of epistemic security we get when we sort
phenomena into kinds in other sciences. One way to make this variety
tractable, suggested by the natural history approach, is to look for
some stable phenomena that do not vary. These are not likely to be
found at the level of diagnoses, because in many cases two people with
the same diagnosis will exhibit different behaviours and other symptoms
depending on their personal lives, cultural background, other mental
illnesses, and so on. There is too much variety at the level of
diagnosis. So we must search for smaller units of explanation.




We can think of this first approach as zooming-in on one small
portion of the overall network, looking for a unit that has enough
stability across histories to allow for an explanation in which there
are cause-effect regularities; if the underlying causal structure is
too diverse, look for causal units that stably replicate across
patients, explain them, and then put these well-understood parts
together to explain individuals. Another advantage of this approach is
that it promises to treat patients as individuals rather than clumping
together into kinds that they only approximately fit.




This zoom-in approach is exemplified by Bentall (2005) and
Spaulding et al (2003). They both look for the smallest unit of
reliable explanation or manipulation. Spaulding et al. argue from a
clinical perspective for seeing patients as collections of
"problems", with the problems in each case drawn from a
repertoire of clinically significant phenomena that different patients
exemplify in different ways. Bentall argues that diagnoses like
depression or schizophrenia have proved helpless in the face of all the
variation that patients exhibit. He sees individual cases as
mosaics made up of recurring symptoms like hallucinations, which can be
separated out and studied in isolation. According to this view, there
is no such thing as schizophrenia. That's not because there is
nothing wrong with schizophrenics, but because schizophrenia is not a
natural kind. The natural kinds of psychiatry are specific pathologies
that schizophrenics display in shifting conjunctions. These are
distinct psychotic phenomena that should be approached separately and
treated as distinct symptoms or complaints.




Bentall thinks "we should abandon psychiatric diagnoses
altogether and instead try to understand and explain the actual
experiences and behaviours of psychotic people" (2005, 141). But
in fact he tries to relocate diagnosis at a more reliable level. For
example, Bentall (ch. 15) objects to the old model of inferring
thought disorder on the basis of disordered speech. His sees
disordered speech as a failure of communication, which is especially
likely when subjects are emotionally aroused. In Bentall's tentative
model, initial deficits in working memory caused by emotional arousal
interact with other deficits in semantic memory, theory of mind and
introspective monitoring. The result is a failure to communicate and a
lack of self-awareness of one's failure to communicate (which
distinguishes psychotic patients from normal subjects in the grip of
powerful emotions who are struggling to get their ideas across). This
is a stable phenomenon, in the sense that we can give the same causal
story in all cases of thought disorder, thus giving us a robust
account that transfers across patients. A general theory of
schizophrenia would have too many qualifications and varieties to
transfer in this way.




Zooming-in faces two problems. First, where do we stop when looking
for smaller units? There is always the chance that some finer causal
discrimination will uncover an even more stable structure.




A proponent of zooming-in can always argue that the idea, as in any
science,
is to develop the descriptive apparatus empirically in a way that
ultimately fits one's theory of the domain. Bentall and Spaulding
et al. are betting that any clustering
of problems or symptoms will not line up neatly with the DSM
categories, and this is probably a good bet for any approach.
Bentall's chosen approach stresses the cognitive science of
psychotic phenomena, whereas Spaulding et al. tend to look for
correlations between clinically significant problems and a wider
variety of underlying phenomena; for Spaulding et al, the relevant
sciences for identifying problems span many levels of analysis from the
intra-cellular to the socio-cultural. Their examples include low levels
of cortisol and learning deficits (127-130).




Nonetheless, there will always be differences across patients in the
phenomena when we zoom in. This is likely to be
especially problematic when these independently characterised
lower-level phenomena start to combine in actual patients. Zooming in
should not, therefore, be thought as an alternative to idealization,
since any search for commonalities across patients will involve some
degree of idealization. The rival approach is another form of
idealization, but zooms out to think in terms if idealized patients,
rather than idealized problems.




Zooming out begins by accepting that mental illness almost always
depends on complex interactions between diverse lower-level phenomena
and tries to deal with this variety by treating disease networks as
idealizations that are more or less similar to actual histories. It is
a recurring theme in the history of psychiatry that the textbook
expression of a disorder can be realized in individuals in different
ways. Charcot (1887-88) distinguished *archetypes,* which are
ideal types of disorder, from *formes frustes*, which are the
imperfect forms the ideal type manifests in individual subjects.
Birnbaum's (1923) distinction between the *pathogenic*
features of a psychosis and its *pathoplastic* features is
similar. The former define its essential structure, and the latter
express the personal circumstances of the patient.



Murphy (2006) argues that the variety in mental illness requires us to
explain psychiatric phenomena not by looking for stable regularities
but by constructing exemplars. Murphy sees the exemplar as an imaginary
patient who has the ideal textbook form--something like
Thagard's network, and the narrative it provides--of a disorder,
and only that disorder, although the textbook needs to thought of as a
statement of the final theory, and not any current work in
psychiatry. As with zooming-in, the approach assumes that
commonalities across patients will be revealed by inquiry. The
idea is to model all the causes that contribute to a natural history so
as to explore how they work together in different contexts to produce
the various outcomes of interest, and then understand patients as
idiosyncratic instances of the exemplar. When we explain a disease, we
construct an exemplar and model it. But the causal structure that
explains the exemplar resembles real world patients to varying degrees.
So when we talk about individuals we explain their symptoms by
identifying processes in the patient and showing how they resemble some
part of the model. Godfrey-Smith (2006), following Giere, suggests that
there may not be a helpful general treatment of these resemblance
relations. They are not formal relations but the sort of comparisons
between imaginary and real states of affairs that we all perform
effortlessly. If there is a general theory, then, it is likely to be
found not by philosophers but by cognitive scientists studying
analogical thought (e.g. Hummel and Holyoak 2005). And because it is
instrumental concerns that drive our search for explanations in
psychiatry, as in medicine more generally, the clinically significant
relations between disease, model and patient are likely to be highly
context-specific; they will be determined in part by whether they offer
opportunities for successful therapeutic interventions, which depend
not just on how the world is arranged, but also on what our resources
and opportunities are.




The exemplar lets us identify *robust processes* (Sterelny
2003, 131-2, 207-8) that are repeatable or systematic in various
ways, rather than the actual processes that occur as a disorder unfolds
in one person. But we do not stop there: the ultimate goal is causal
understanding of a disease. We build a model to serve this end. It aims
to represent the pathogenic process that accounts for the observed
phenomena in the exemplar. To explain an actual history in a patient is
to show how the processes unfolding in the patient resemble those that
are assumed to occur in the exemplar. Exemplars provide an idealized
form of the disorder that aims to identify the factors that remain
constant despite all the individual variation. Not every part of a
model will apply to a given patient. Once we understand the resemblance
relations that exist between parts of the model and the exemplar, we
can try to manipulate the model so as to change or forestall selected
outcomes in the real world.




In commenting on this approach, Mitchell (2009) points out that her
own work (2003) contains an alternative approach to model-based
explanation in complex sciences. Her "integrative
pluralism" aims to isolate individual causes and model them
individually, seeing how each makes a causal contribution on its own.
Theorists then put together a collection of models of individual
phenomena and try to integrate them by applying multiple models as
seems necessary to explain a particular case. Mitchell's approach
resembles the zoom-in in its search for decomposing, but it tries to
isolate causes that can recombine--such as genes or
interpersonal difficulties--rather than searching for explanations of
particular clinical phenomena like thought disorder (see also Tabery
2009). This is similar to the way Spaulding et al. seek the development
and integration of causal models in the service of developing a
comprehensive clinical understanding of people and their problems.




Mitchell (2009, 131) suggests that we might need both her models and
Murphy's as circumstances dictate. And there might be room for
zoom-in models as well. There seems no reason why psychiatric research
could not aim to be pluralist about explanation and combine elements
drawn from all these explanatory styles as we learn more about what
works when we try to figure out mental illness.



Ghaemi (2003. ch 12) offers a different defense of zooming-out. He
argues that current DSM diagnoses function as ideal types in
Weber's sense. One way to understand Weber's idea is just
as a forerunner of modelling, in which essential variables are isolated
and inessential ones put aside. Ghaemi, though, locates it in a
tradition of hermeneutic understanding that is most closely associated
in psychiatry with Karl Jaspers (1997). This approach looks for
meaningful psychological connections between phenomena and is
contrasted with causal, scientific explanation. In Ghaemi's view
the DSM categories are designed to foster understanding of this type by
directing clinical attention to aspects of the patient's life
that are relevant to the disorder at hand. He sees this as an
application of the methods of the humanities, rather than those of the
sciences.



One argument that might be made against zooming-out is that it assumes
that mental disorders are categorical, rather than dimensional. The
neo-Kraepelinian approach is often faulted for assuming that disorder
is an all or nothing affair, whereas it might mark an extreme point on
a dimension that is present to a greater or lesser degree throughout
the population (Kendell 1975, McHugh and Slavney 1998, Poland et. al
1994, Widiger and Sankis 2000). So schizophrenia might be seen either
as condition that is present or not--just as one either is of
voting age or not. But we might also see it as like having high blood
pressure--marking a point on one or more dimensions where normal
psychological traits become aggravated enough to constitute a
population of clinical concern. Some psychiatrists have supported one
approach or the other. Others, like Ghaemi (203), have argued that
some conditions, like the major psychoses and mood disorders, are
probably categorical, whereas other conditions, especially the
personality disorders, are dimensional.



This is clearly an empirical issue in the end, so if the zooming-out
approach is committed to a categorical approach it is a cause for
concern. However, a zooming out approach could treat its models as end
points on a spectrum that usefully capture differences between
populations (Ghaemi, 199); this is compatible with looking for causal
stories that explain the model. Furthermore, in so far as the
zooming-in approach relies on idealizations too, it faces the same
problem. Bentall's approach, for instance, faces the issue of
what degree of language difficulties counts as pathological, and
Spaulding et al. need to find a way of distinguishing a clinical
problem from a phenomenon that is normal but unwelcome.


### 3.5 Cross-Cultural Issues




Successive editions of the DSM have been published in North America,
and questions have always arisen about the applicability of its
categories outside the West. DSM-5 follows its predecessor in coping
with cross-cultural variety in two ways. First, some conditions, such
as depression and anxiety, are treated as universal - found in
every culture, despite local differences in character. We may term
this the unificationist project. The DSM-IV-TR averred that major DSM
categories occur all around the world but with symptoms and courses
that are influenced by local cultural factors. Second, DSM-IV-TR employed the concept of culture-bound syndromes, which were
defined as "recurrent, locality-specific patterns of aberrant
behavior and troubling experience that may or may not be linked to a
particular DSM-IV diagnostic category" (p. 898). Culture-bound
syndromes occur in a limited number of specific societies or cultural
areas. They are local, often traditional, diagnostic categories that
make sense of patterns of thought and behaviour that are treated as
deviant or troubling in that context. 




In theory, culture-bound syndromes are those folk illnesses in which
alterations of behaviour and experience figure prominently, relative
to local norms. Standard DSM diagnoses are not thought of in this way,
even if they are culturally limited. Multiple Personality Disorder/
Dissociative Identity Disorder, for example, was widely diagnosed in
the USA in the 1980s, but seldom found elsewhere. That did not lead
psychiatrists to treat it as a culture-bound syndrome, even though it
seems to fit the definition. The assumption in mainstream psychiatry
is that Western conditions are not culture-bound; they represent
abnormalities in a universal human endowment. This is the case even
for conditions (such as some kinds of body dysmorphia) for which
prevalence data only exists in a few western nations. 




DSM-5 has moved away from concept of a culture-bound syndrome and
adopted that of "cultural concepts of distress" (p.758).
These are ways in which "cultural groups experience, understand
and communicate suffering, behavioural problems or troublesome
thoughts and emotions". DSM-5 distinguishes three main types of
cultural concepts: syndromes, idioms (ways of expressing distress),
and local explanations. The last is particularly interesting: a
standard picture of mental illness in both non-Western and premodern
societies represents it as explained by supernatural forces like ghost
possession. But Edgerton (1966) reported that the East African tribes
he studied were divided over the explanation of psychosis. Some tribes
did understand it in terms of ghost possession, but others thought of
it as having an organic cause ("brain worms"). DSM-5 makes
room for such findings as part of the integration of local
explanations into a theory of mental illness.




DSM-5 supplements this conceptual reform with a thorough overhaul of
the "Outline for Cultural Formulation". This is an
interview outline introduced in DSM-IV-TR, in part in response to
pleas from cross-cultural psychiatrists dissatisfied with the old ways
(e.g. Canino and Alegria 2008). It reflects an unprecedented
investment in applying anthropology to psychiatry by the DSM-5
Cultural Issues Subgroup, who ran field trials of the new Cultural
Formulation Interview (CFI) in 6 sites around the world (Aggarwal
2013). The CFI is designed to assess both the cultural or ethnic
groups that the subject belongs to and the ways in which those groups
understand the problem and affect the subject's experience of
it. It comprises a series of questions designed to gather information
from the point of view of the patient and his or her cultural peers,
including specific questions that tell the patient not to repeat what
the doctor has told them but to express their problems as they see
them and describe which aspects of their identity are most important
to them. It could be used with any subject anywhere, and the manual
acknowledges that all mental illness, including the DSM diagnoses, is
shaped by the surrounding culture. On the other hand, the CFI and its
associated conceptual material are poorly integrated into the DSM-5
- many diagnoses pay no attention to cultural formulation at all
- and the culture-bound syndromes do in fact survive. They have
been renamed "Cultural Concepts of Distress" but the
appendix listing them survives, so one may wonder how thorough the
overhaul has been.




The other approach to cultural variation, as mentioned, is to treat
different diagnoses as manifestations of the same underlying DSM
condition. The issue is how different a diagnosis needs to be before
it stops being a form of a DSM condition and becomes a culture-bound
syndrome. It has been suggested that anxiety disorders, for example,
should have their "worry domains" expanded because people from other
cultures may worry about things that Euro-Americans don't fret
over (Lewis-Fernandez et al 2010). The assumption here is that anxiety
disorders are common enough in all human cultures to merit treating as
a universal, but that this can be missed if clinicians do not
appreciate the different triggers, reactions and conceptions that
distinguish the anxiety disorders in different populations. We need to
recognise the greater variety of symptoms among sufferers from anxiety
who live in Western cultures but don't show the typical symptoms
of a Westerner. Lewis-Fernandez and his team (2010) argue that a
majority of Latino sufferers from ataque de nervios would meet panic
disorder criteria, for example, if the DSM amended the requirement
that a panic attack lasts only a few minutes. Ataque de nervios was
listed as a culture-bound syndrome in DSM-IV-TR. Its symptoms commonly
include a mix of classic panic attack symptoms like palpitations and
sensations of bodily heat and loss of control. But it may also involve
uncontrollable shouting and threats of violence, together with other
symptoms less often found in panic attacks, and it may last much
loner. Lewis-Fernandez is interested in the idea that ataque de
nervios can be assimilated to existing anxiety diagnoses provided we
take the variation in symptomatology more seriously.




This unificationist approach may be used to argue that the diagnostic
entity itself is the same in all cases - some shared underlying
process that adapts or responds to different cultural settings to
produce different behaviors. Some scholars argue that the underlying
abnormality, even if it exists, is beside the point. Our response to
the condition should be determined by its expression, even if there is
an underlying psychological kind. Kleinman argued that depression in
the West and in East Asia are different enough in their expression and
course that they should be seen as different conditions (1987, 450):
"Depression experienced entirely as low back pain and depression
experienced entirely as guilt-ridden existential despair are such
substantially different forms of illness behavior with different
symptoms, patterns of help-seeking, course and treatment responses
that though the disease in each instance may be the same, the illness
rather than the disease is the determinant factor." 




Horwitz and Wakefield (2007, p. 199) opt for universality in response:
"we agree with Kleinman's distinction between disease as a
universal underlying dysfunction and illness as the culturally shaped
expression of a given dysfunction ... [but] if there are indeed
underlying common dysfunctions, then treatment presumably depends in
large part on the science of identifying and intervening in such
dysfunctions irrespective of their cultural presentation." 




The unificationist project is an empirical bet that is based on the
assumption that human psychology is enough alike to treat at least
some culturally distinctive forms of mental disorder as expressions of
a shared human nature that is differently shaped by local culture. The
appeal to culture bound syndromes is also a perfectly good bet,
reflecting the idea that some forms of behaviour are entirely local
and not assimilable to a universal model. Both unificationism and
recognition of culture-bound syndromes could be pursued at the same
time. Given the boring but probably correct observation that people
around the world are both alike and different, that may be the obvious
course. However, pursuit of these strategies should be freed from the
apparent assumption in DSM-5 that western minds are the blueprint for
the world. The western form of a condition may be unusual: the more we
look, the more it seems as though the cognitive aspects of depression
- the complex psychology of self-blame and immiserating
introspection - may be distinctively Western. There may be
conditions that DSM treats as universal but which in fact are
culture-bound syndromes that only exist in NATO countries.


### 3.6 Clinical Application




Psychiatric models explain idealization of some sort. The point of it
all, though, comes when that understanding lets us help patients.
Guze (1992) calls this the move from the biological perspective to the
clinical one. In making the move we shift from a general description
of a disease process to a specific description of the biology of an
individual. The clinician takes the imaginary ideal patient and
specifies more real-world detail, so as to produce a description of a
smaller set of patients, perhaps even a single case. The scientific
project idealises, whereas the clinical one uses the resources of the
science to help individuals. In displaying causal relations that give
rise to features of the model we present opportunities for therapeutic
action, whether we have zoomed in or out. The model defines a set of
relations that differ from those present in a real patient along
various dimensions. One is precision: the causal relations the model
represents may need to be made more precise when we look at real
patients. The degree to which a symptom is present, for example, might
need to be specified precisely in a clinical setting, whereas in the
exemplar the symptom can be defined as inhabiting some range of
values, any one of which might apply in nature. Or we can supply a
determinate story that embraces the details of the beliefs and other
intentional states of the patient, instead of just citing the fact
that a particular information-processing pathway is implicated in
patients of that type. An important strand in recent philosophy,
however, regards the key to successful understanding as humanistic or
non-reductive, and is skeptical about the chances of understanding
mentally ill persons through the medium of research categories
inspired by the medical model (Glover 2014: Tekin 2019) 



> 
> Supplement on Philosophical Psychopathology
> 


## 4. Alternatives to the Medical Model


### 4.1 Introduction




A number of scholars in recent years have argued that existing
psychiatry is flawed in terms of its philosophy of psychology, even if
one accepts the basic commitments of the medical model rather than a
more normative view. On this view, psychiatry has bought into several
philosophical mistakes, being unduly reductive or internalist. There
are longstanding objections to psychiatry along these lines,
including the idea that psychiatric disorders should not be assimilated
to general medical conditions (Arpaly 2005, Graham 2009). But there are
specific criticisms within a broadly naturalistic approach to
philosophical psychopathology that we will review here.


### 4.2 4E Philosophy of Psychiatry



An important development that is avowedly sceptical of the existing
biomedical paradigm in psychiatry is the rise of approaches inspired by
the 4E movement in philosophy of mind - the "embedded,
embodied, extended and enactive" tradition. Many philosophers of
psychology and cognitive scienctists dispute the viability of
what they see as an unduly reductive and anti-environmental tradition
of philosophical psychology. To this internalist tradition is
attributed the view that the mind is confined to the 'skin and
skull' of individual agents and that psychological processes and
their pathologies are entirely explained by the brain and central
nervous system. On this view, whatever is responsible for cognition is
wholly within the agent, and thus can be studied while
'bracketing off' an agent's social and material
environment. Externalists have argued that this tradition has both
driven and been reinforced by approaches to psychiatry that are too
brain-centred (Sneddon 2002, Roberts et al 2019) and lobby for greater
attention to environmental or other extra-cranial factors.
(Internalists, or proponents of traditional views of  cognition,
one should add, often disagree with this view of what they are
committed to or find the commitments of 4E too vague to be helpful
(Aizawa 2018, Rupert 2016)).  As well as externalists, the 4E
movement includes 'embedded' theorists who stress the
dependency of minds on environmental scaffolding (Hutchins 1995) and
"embodied" theorists who believe that bodies or aspects of
the wider environment are constitutive of mental states, and often that
sensorimotor phenomena are constitutive parts of cognition, rather than
just the input and output of cognition (or what Hurley (1998) calls the
'sandwich model'). Enactivism tends to be the more radical
view that mental life can be explained via the dynamic interaction of
nervous system, body and environment without reference to mental
representation (Hutto and Myin 2013).



Clark and Chalmers (1997) motivated the extended mind thesis using a
thought experiment centring upon memory. Its protagonists, Otto and
Inga, each need to remember how to get to MOMA for an exhibition. Inga
has been to MOMA many times and gets there via introspective recall. But
Otto has an impaired
capacity to produce, store and retrieve memories. To cope with this, he
carries a notebook containing important information. Otto routinely
consults and updates his notebook, he always carries it with him, and
he endorses its contents. A variant of this view holds that agents are
typically embedded in wider set of environmental and social phenomena,
and that these exogenous factors are explanatorily vital and often
neglected when it comes to cognition, but that cognition is
intra-cranial.



The consensus among 4E proponents is that psychiatry is wedded to a
number of outdated philosophical positions, although there is not
always agreement about what these positions are. Zoe Drayson
(2009), for example, thinks that psychiatry is committed to old
fashioned models of artificial intelligence that ignore embodiment,
whereas other theorists (Davies 2016) think that psychiatry is too
neglectful of the environment, or has the wrong picture of explanation
and causation (de Haan 2019). Indeed, it is unclear whether any
particular scientific research program derives from core 4E
commitments. One might see the movement as what Godfrey-Smith (2001)
calls a philosophy of nature or (in this case) a piece of philosophical
anthropology (cf Gallagher 2017). As Godfrey-Smith puts it (2001,
p.284-5) a philosophy of nature comes after science, and aims to
describe and interpret the world as disclosed by science. One can see
4E as giving us a view of human nature that stresses the
interdependence of person and environment and emphasizes the dynamic
aspects of cognition, which is seen as a special kind of animacy.
Because of this variety within the movement it is not easy to construct
a core program for philosophical psychiatry that every scholar with
some 4E attachments would accept, but there are recurrent themes that
can be assessed here.



To begin with, many externalist approaches to psychiatry contest
what they see as the basic ontological commitments of psychiatry when
it comes to mental illness, by objecting to what is seen as a reductive
or internalist thesis that psychiatric conditions are neurological
disorders. Competing conceptions of mental illness may accept that
psychiatric conditions involve neural dysfunction in some sense, but
they argue that no psychic process, including pathological ones,
"can be reduced to the brain or to localized neural activities:
they are embodied, inherently intentional, and context related"
(Fuchs 2018, p. 253)



This claim can be made in ways that are more or less committed to 4E
machinery. It is possible, for example, to argue, as Levy (2007) does
for addiction, that a condition cannot be seen as a brain disorder
because its symptoms only arise in specific social environments. Davies
(2016) asserts that many psychiatric categories are committed to
'constitutive externalism', by which he means that one
cannot be diagnosed with those conditions unless one stands in certain
relations to features of the environment, including the social
environment. This position could be adopted even if one has only very
weak commitments in the 4E vein; it is based on claims about the
relations between subjects and environments rather than theories about
the nature of the mind. Furthermore, although Davies asserts that these
features distinguish psychiatry from somatic medicine, they plainly do
not. As Glackin notes (2017) each of Davies' examples has
parallels in somatic medicine. In a similar vein, Fuchs (2018) argues
that the tendency of contemporary psychiatry is to isolate the patient
from their surroundings and study disorder independently of the
environment.



It is not easy to evaluate claims like these, given that psychiatry
does pay attention to social and biographical contingencies in a
patient's life. It may be that the force of the objection is that
these extra-cranial factors are acknowledged but not taken seriously in
treatment, which tends to be too much directed at aspects of the
condition inside the patient that can be addressed by drugs. In defence
of psychiatry, one might point out that changing a patient's
brain is often a lot easier than changing society or even the
patient's local environment or life circumstances. However, it
does seem clear that prescinding from the details of the situation and
assessing a patient in a context insensitive way does happen, and it
can be a source of problems.



The purpose of the Otto/Inga example is to challenge the assumption
that only processes that take place "in the head" are
psychological. When Otto consults his diary, he has the occurrent
belief that MOMA is located on Fifty-third street. What the authors
claim, in addition to this, is that, like Inga, who remembers it
unaided, Otto also has the dispositional belief that MOMA is located on
Fifty-third street before he consults his notebook. Otto's
capacity for storage and retrieval of memories extends beyond the
brain, and encompasses the notebook as a resource, in the same way that
Inga's storage and retrieval depends on neural resources. Drayson
and Clark (2019) discuss cases in which sufferers of Alzheimer's
disease perform poorly in standard tests but live alone successfully.
Their homes are carefully scaffolded by personalised mnemonic props,
including post-it notes, labelled pictures, strategically placed items,
and messaging centres. If we are interested in an accurate assessment
of an agent's mental health we will be led astray if we do not
find room in standard capacity tests for the role that an agent's
environment might play in their cognitive functioning. Further, the
role of the environment must also be considered in therapeutic
contexts: decisions to relocate subjects from their homes to
residential care facilities, for example, are typically accompanied by
decline in cognitive health.



According to an internalist or scaffolded/situated approach,
external artefacts (such as notebooks) or other agents (such as life
partners) can only be props that compensate for an incapacity. On this
view, Otto suffers from a deficit Inga does not have, and is thus less
healthy than she is. However, if we think, as externalists do, that
Otto's notebook is a part of his cognitive architecture, we
should attribute him the same capacity to remember as Inga, for the
only difference between Otto and Inga, in this respect, is that
Otto's psychological capacity is realised by an agent-environment
system of which he is part.




Hoffman (2016) argues that the extended mind thesis thus has
implications for how we judge the mental health status of an agent,
including whether or not they meet diagnostic criteria for particular
disorders. Based on this discussion, we can draw a distinction between
narrow, situated and wide theories of mental disorder (Murphy, Donovan
and Smart forthcoming). The narrow construal is strongly internalist:
the only genuine psychological capacities are those realized by
cognitive architecture internal to the agent. The situated view
construes psychological capacities as intimately dependent upon
environmental states of affairs, and so prohibits methodological
solipsism. A full understanding of the capacities exercised require an
understanding of agent-world dynamics.



A wide account tells a different story. Otto's mental health is not
compromised, whatever the state of  his brain, because using his
notebook he can store and retrieve memories in a functionally
equivalent manner to Inga. Poor mental health can be the outcome of
neural dysfunction, but it can also owe to problems with the
environments in which agents are situated, as well as with their
capacity to fruitfully exploit environmental resources (Sneddon 2002;
Roberts, Krueger, and Glackin 2019). The externalist claims that she
can discern types of explanations, interventions and strategies that an
internalist picture misses.


### 4.3 Network models



The medical model is widely believed to borrow the "common
cause" structure of general medicine, in which observed variables
(symptoms) indicate the existence of a latent variable that is their
cause. The network model (Nuijten et al 2016), however, makes a very
different bet. Rather than an underlying cause or latent variable, it
attributes the joint occurrence and course of the clustered symptoms to
the fact that they are part of the same network: "instead of
being effects of a common cause, psychiatric symptoms have been argued
to cause each other" (Borsboom 2017, p.5). This can be
represented as a network  in which symptoms are nodes, and the
connections between nodes indicate causal relations, which we can
understand using interventionist models of causation.



Each symptom is a node, and a change in a node changes the
probability distribution of the other symptoms which are connected to
the original node. For example, difficulties in sleeping is likely to
be strongly connected to fatigue, and both nodes may be connected to
depressed mood, indicating that tired, sleep-deprived people are more
likely to feel down and feel bad about themselves. (The connections
could run in the other direction too, from low mood to difficulty
sleeping.) Eventually we see a set of connections stabilizing the
network as the symptoms of depression switch each other on and even
symptom nodes that are not directly connected influence each other via
shared neighbours (Borsboom 2017, p.6).



The intuitive appeal of the network model relies on the idea that
standard conceptions of medical disease, with their separation of
underlying condition and visible symptom, make no sense in psychiatry
and are implausibly reductive (Borsboom et al 2019, Borsboom 2017).
However, it has been argued in response that the (Bringmann and Eronen
2018) network and latent variable models are not so easy to
distinguish, and that the choice between them is orthogonal to
questions of reductionism. Further, although a disease such as
depression cannot function as a part of the network, we can include in
the network neurological or genetic processes that are taken to be part
of the underlying state, so that the line between networks and
traditional models is blurry. Bringmann and Eronen's review of
the literature suggests that model choice should not be made on the
basis of background pictures of disease, but on the basis of other
factors, especially the dynamic relations among variables stressed by
network theorist. The philosophical appeal of a conception of mental
illness by itself does not legitimate any choice of model.