Behavioural Brain Research 389 (2020) 112665

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Behavioural Brain Research

journal homepage: www.elsevier.com/locate/bbr

Addiction from the harmful dysfunction perspective: How there can be a T

mental disorder in a normal brain
Jerome C. Wakefield
Silver School of Social Work, Department of Psychiatry, and Center for Bioethics, New York University, 1 Washington Square North, New York, NY 10025, United States

ARTICLE INFO ABSTRACT

Keywords: Is addiction a medical disorder, and if so, what kind of disorder is it? Addiction is considered a brain disease by
Addiction NIDA, based on observed brain changes in addicts that are interpreted as brain damage. Critics argue that the
Substance use disorder brain changes result instead from normal neuroplasticity and learning in response to the intense rewards pro-
Brain disorder vided by addictive substances, thus addiction is not a disorder but rather a series of normal-range if problematic
Intentionality
choices. Relying on the harmful dysfunction analysis of medical disorder to evaluate disorder versus nondisorder
Diagnosis
Harmful dysfunction
status, I argue that even if one accepts the critics’ reinterpretation of NIDA’s brain evidence and rejects the brain
Philosophy of psychiatry disease account, the critics’ conclusion that addiction is not a medical disorder but is rather a matter of pro-
blematic nondisordered choice does not follow. This is because there is a further possible account of addiction,
the evolutionary “hijack” view, that holds that addiction is due to the availability of substances and stimuli that
were unavailable during human species evolution and that coopt certain brain areas concerned with human
motivation, creating biologically undesigned peremptory desires. I argue that if the hijack theory is correct, then
it opens up the possibility that addiction could be a true motivational medical disorder for which there is no
underlying neurological-level dysfunction. Finally, I explore the implications of this account for how we see the
social responsibility for addiction and how we attempt to control it.

1. Introduction: Is addiction a disorder?
To formulate a useful vision of how the disparate interdisciplinary
efforts that now exist to address addiction might be integrated into a
coherent overall approach, it would be helpful to have a conceptual
understanding of the target of those efforts. Addiction is classified as a
mental/psychiatric medical disorder in official diagnostic manuals such
as DSM-5 [1] and ICD-10 [2], which rely on the intuitive notion of
compulsive use as the justification for classifying addiction as a dis-
order. Yet, despite the standard classifications and the enormous recent
advances in research on addiction, addiction theorists and philosophers
remain sharply divided over the fundamental conceptual question: is
addiction a disorder? Unlike most other conditions classified as mental
disorders, there is active controversy as to whether even clear-cut
prototypical cases of addiction that are devastating to the addicted
individual and perhaps to others such as family members as well are in
fact medical disorders, and a great number of prominent theorists reject
the disorder designation.
It is this question of the diagnostic status of addiction—whether or
not it is a disorder, and if it is, what kind of disorder it might be—that I
am going to address. In the course of doing so, I will propose a way of
thinking about addiction according to which it is indeed a mental
disorder, but of a kind that has some unorthodox implications for how
we should conceptualize our overall efforts to address this challenge.
First, a few caveats are in order. I aim to analyze the intuitive notion
of substance addiction and not the official substance use disorder di-
agnostic criteria in DSM-5 [1], which I have argued are quite flawed
[3–7]. Moreover, I aim my analysis primarily at substance addictions,
but I believe it may be applicable as well to behavioral addictions to
such activities as gambling, video gaming, or internet pornography,
although I will not develop that topic here. Further, my account is not
claimed to cover all possible substance addictions but to identify what I
believe illuminates most major substance addictions of current concern.
Addictions are of such a great variety that the generalizations below
must be taken as first approximations to addressing some significant
subset of addictions, and not a universal account. Finally, some pas-
sages in this presentation are revised versions of ideas put forward in
various previous publications [8–12], and I thank the respective pub-
lishers and blogs for permission to reproduce and revise those passages.
2. The phenomenological/descriptive nature of addiction:
Peremptory desire that transforms the intentional field
Before attempting to address the question of the diagnostic status of

E-mail address: jw111@nyu.edu.

https://doi.org/10.1016/j.bbr.2020.112665
Received 24 November 2019; Received in revised form 29 January 2020; Accepted 21 April 2020
Available online 26 April 2020
0166-4328/ © 2020 Elsevier B.V. All rights reserved.
J.C. Wakefield
addiction, I first consider addiction from a phenomenological and de-
scriptive perspective. I will be elaborating here in somewhat different
language an idea that is common and even fundamental to the field of
addiction studies, that addiction is a motivational dysfunction that has
affinities to compulsive behavior (e.g., [13–17]). For a useful listing of a
great variety of definitions of addiction in which this common theme
frequently emerges, see West and Brown [18]. Restating this common
perspective is a step towards exploring new ways to construe it so as to
situate it in a somewhat novel way within the field’s broader debates.
Addiction is often characterized descriptively simply as compulsive
use. However, compulsion is a very general and vague notion, and a
somewhat more elaborated characterization of this particular type of
compulsion would be useful. Indeed, the notion of compulsion fre-
quently has been misinterpreted by critics of NIDA to imply total
compulsion and thus lack of any choice, a strawman argument, as we
shall see. Of course, DSM symptom criteria are also intended to identify
addiction from a phenomenological and descriptive perspective, but
DSM symptom criteria are mostly rather weak indirect indicators of
compulsive use or addiction. It will be useful to try to say more directly
what it is the DSM criteria are attempting to measure.
No doubt the intuition that addictions are medical disorders is based
on an implicit hypothesis that biological design has failed due to
compulsivity. The intuition appears to be that the individual’s delib-
erative consideration of various motives and lines of evidence that leads
to quasi-rational choice and action has gone wrong. That is, the in-
dividual’s exercise of quasi-rational regulatory control over a delib-
erative process that takes place in a space of desire/deliberation/choice
that leads to an appropriate decision and the actions that follow has
become dysfunctional, in the sense that it is failing to perform as it was
biologically designed to perform. The agency that such a deliberative
space allows is central to social interaction over time and appears to be
part of our biological design as social animals.
This desire/deliberation/choice process can certainly become dis-
ordered. To take some extreme examples, children with Lesch-Nyhan
genetic syndrome have a peremptory urge to chew off their fingers, and
various brain parasites are able to manipulate their hosts’ brains to
create desires that further the parasite’s life cycle, for example by
creating a desire in an animal to wallow in pooled water which is re-
quired for the parasite’s propagation. These harmful peremptory desires
are pathological given the causal pathway, the content, and the context
that have no evolutionary roots. A similar judgment of pathology is
applied to self-harming addictive behavior.
Intense and even overpowering desire is of course not in itself pa-
thological, and when such desire occurs, there may be concomitant
effects on an individual’s entire mental system. For example, when in
the throes of passionate erotic love, suffering from starvation, or ex-
periencing an intense highly aroused emotion such as rage or terror, it
is normal for one’s perceptions and reactions to reorganize so as to be
highly influenced by the now-central motive, with other motives and
strands of psychological processing fading somewhat into the back-
ground. I will call such motivation that is not only episodically intense
but also episodically distorting or rearranging of other priorities and
interactions among mental states a “peremptory desire.” Here, “per-
emptory” suggests its usual meanings of “insisting on immediate at-
tention or obedience” and, in law, “not open to appeal or challenge.”
Even so, a peremptory desire is not absolute and with effort generally
can be held in check or overcome, or else we would have a lot more
crimes of passion than we do.
A common feature of normal peremptory desire is that it is time
limited and a response to specific circumstances. For example, intense
emotions create peremptory desires—to run, to attack— that would be
maladaptive if they persisted after the transient circumstances that
trigger them. The peremptory desire for food in a starving person
subsides over time when the individual becomes well-fed. The default
“resting state” of the intentional system is optimal for usual processing
of information and is overridden only under specific urgent
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Behavioural Brain Research 389 (2020) 112665
circumstances.
When a desire becomes peremptory, not only are other desires to
some extent weakened or put aside, but overall mental processing is
transformed in a way that leaves challenging desires and thoughts less
salient. When you are very thirsty, it is the water-related aspects of the
world that you see most saliently. I will use the term “intentional field”
to refer to the momentary status of the dynamically changing system of
active beliefs, desires, memories, emotions, and other representational
psychological states that comprise an individual’s psychological system
at a given time. The intentional states that are the parts of this system
possess what philosophers refer to as “mental content.”
As the philosopher Franz Brentano [19] explained when he for-
malized the concept of intentionality as the fundamental theoretical
concept of psychology, when you believe, you believe something; when
you desire, you desire something; when you remember, you remember
something; when you perform an action, it is with a purpose to do
something, and when you fear or love, you fear or love something. An
intentional state—a belief, desire, and so on—is directed at the “thing”
or state of affairs that is its object via its representational content that
can take various forms (e.g., images, thoughts). These representations
dynamically interact in accord with their contents and their modes (i.e.,
belief, desire, fear), as when the desire “I want a beer” and the belief
“there is a beer in the refrigerator” yield an action with the purpose of
walking to the refrigerator to get a beer. The contents of the intentional
field can change in organized ways that produce sequences of thoughts
or other states that may be anything from a rational argument to an
emotional reaction to a random fantasy, and these sequences will be
greatly affected if there is a peremptory desire.
Obviously, the intentional field is altering at every second due to
new perceptual inputs and the processes of memory, emotion, desire,
and thought. A peremptory desire is one that transforms the intentional
field to support its own dominance. I don’t think these are difficult
concepts to understand for anyone who has been head over heels in
love, or been enraged during an argument with a partner who is in fact
loved for many wonderful and legitimate reasons but who at the mo-
ment of rage seems unlovable and unworthy, and so on. A conclusion
that seems obvious at the moment in the midst of such an episode may
become evidentially absurd a few minutes later when arousal wanes.
Everything I have described above is quite normal. We are biolo-
gically designed to experience such peremptory desires transiently at
certain times and to have our intentional systems react in these dis-
torted ways that focus us because they enable us to adaptively deal with
certain kinds of immediate challenges. Perhaps this is why in some
cultures there is an allowance for leniency for “crimes of passion”
committed under circumstances in which it is known that intense
emotions are likely to create a distortion of the intentional field. Such
transient psychological changes are no more abnormal than, say, the
heart beating rapidly when we exercise, at a rate that under conditions
other than exercise or emotional arousal might represent a pathological
condition. Similarly, non-transient intentional field transformations
that occur for reasons not linked to our biologically shaped functioning
can constitute a medical—in this case, mental—disorder.
3. The harmful dysfunction analysis of medical disorder
To determine whether addiction is a disorder and if so what kind of
disorder it may be, one needs some account of “medical disorder.” I
approach the discussion of the diagnostic status of addiction within the
framework of my “harmful dysfunction analysis” of the concept of
medical, including mental, disorder [20–29]. According to this analysis,
a medical disorder exists when two conditions are both met. First, the
condition must be caused by a dysfunction, that is, by a failure of some
physiological or psychological mechanism to perform a natural function
that it was biologically designed to perform. “Biological design” and
“natural function” are understood here not in terms of any theistic
beliefs or social or human intentionality or purpose but simply in terms
J.C. Wakefield
of the natural selection of mechanisms in the process of evolution. The
effects of a mechanism that cause it to be naturally selected and become
part of human biological design constitute the mechanism’s natural or
biological functions. Thus “biological function” and “biological dys-
function” construed as a failure of biological design are factual concepts
in the sense that they are scientifically descriptive and not evaluative
[30–32].
However, the failure of a biological mechanism to be capable of
performing a natural function does not by itself constitute our concept
of medical disorder. Such failures are ubiquitous and often harmless, as
in the myriad harmless genetic mutations that occur when one goes out
into the sun. So, a medical disorder also requires that the dysfunction
must cause significant harm to the individual [33]. Thus, the harmful
dysfunction analysis is known as a “hybrid” fact/value view due to the
insistence that both factual and value components are involved in dis-
order attributions.
4. Addiction versus addictive disorder
Getting somewhat ahead of my analysis, note that the harmful
dysfunction view allows a distinction to be drawn between harmless
dysfunctions that are not medical disorders versus harmful dysfunctions
that are medical disorders. Among addictions, assuming that an ad-
diction is a dysfunction and that some addictions are indeed medical
disorders, the harmful dysfunction analysis allows a distinction to be
drawn between “addiction” per se as a phenomenon that is a dysfunc-
tion versus “addictive disorder” in which such a dysfunction causes
harm. Various cultures may have practices that render certain addic-
tions harmless and not disorders, and the harmful dysfunction analysis
allows such cross-cultural variations to be respected without denying
that an addiction is an abnormality even when socially accepted and
harmless.
For example, in our society, a moderate addiction to caffeine can be
harmless and not qualify as a medical disorder because caffeine use is
accepted for performance enhancement to meet the demands for
alertness that our workday imposes, and caffeine is freely available and
relatively affordable. However, if caffeine intake becomes harmful due
to medical issues, caffeine addiction in which cessation of high caffeine
intake is difficult or impossible for the individual may then qualify as an
addictive disorder.
However, the addictions listed in the DSM and that are most dis-
cussed in the addiction research literature are clearly frequently
harmful to the addicted individual. So, like most writers on addiction, I
will frame my discussion within this harmful subset of addictions and
consider only such harmful addictions here. This allows me to simplify
the terminological complexities and use the term “addiction” here
specifically for addictive disorder.
5. Addiction as a brain disorder
I now briefly describe three views of addiction that bear on its di-
agnostic status. First, addiction is considered—and assertively re-
presented—as being not merely a mental disorder but specifically a
brain disorder by the National Institute of Drug Abuse (NIDA). This
claim rests on extensive research that observed well-documented neu-
ronal changes in addicts. NIDA interprets these changes as substance-
induced damage to the brain’s reward, inhibitory, and other systems
[34,35]. (Note that I refer here to NIDA’s position as that addiction is a
“brain disorder” even though in fact NIDA specifically terms addiction a
“brain disease” because brain damage of the type they describe, even if
truly a brain disorder, would not clearly qualify for the label ‘disease’ as
it is commonly used.) NIDA’s position that addiction is a brain disorder
is repeated frequently in public statements and shapes research grant
awards. So, the “brain disorder” account of addiction can justifiably be
considered the standard current view among psychiatrists and re-
searchers.
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Behavioural Brain Research 389 (2020) 112665
6. Addiction as constrained normal choice
The claim that addiction is caused by brain damage and thus is a
brain disorder has been widely questioned (e.g., [36–50]) and been
challenged by a second view that addiction is a matter of choice. Al-
though tissue damage may occur from excessive substance use, it is
puzzling that many addictive substances should happen to cause da-
mage at multiple brain loci in precisely the way that brings about in-
tense motivation to continue using that substance, yielding intensified
desire, heightened sensitivity to cues of availability, reduced interest in
other rewards, willingness to undergo painful tradeoffs to obtain the
substance, reduction of inhibitory functioning of the cortex that usually
restrains impulsive action, increased delay discounting favoring im-
mediate gratification, and so on. These forms of “damage” look like
what happens when one develops an overriding “peremptory” desire
that grips one such that mental functioning reorganizes in primary
pursuit of the object of the desire.
We observed earlier that when in the throes of passionate erotic love
or suffering from starvation, it is normal for one’s perceptions and re-
actions to reorganize around that central motive, and surely there are
accompanying brain alterations. Consequently, simply identifying brain
processes corresponding to the addicted individual’s increased desire/
wanting, reduced inhibitory control, and lessened interest in alternative
rewards does not resolve the puzzle of whether addiction is normal or
disordered. For example, drug-preferring rats have larger neuronal as-
semblies firing in response to the drug [51], but rather than being in-
terprted as a brain disorder this could be understood as the normal
brain instantiation of strong preference. Critics of NIDA’s “brain dis-
order” claim argue that the observed changes, rather than being brain
damage, are the expectable results of a normal brain’s neuroplasticity,
habituation, and restructuring in reaction to the intense learning pro-
cess that occurs in response to substance use [45].
The obvious fact is that taking a substance to which one is addicted
is a voluntary action and thus in some sense a choice. Many critics of
the standard brain-disease view react to the implausible claims of total
lack of choice or control that they believe is implied by the brain-da-
mage account, emphasizing instead, from various perspectives, that the
addicted individual is in fact making choices. These choices may look
less like choices than our typical choices because they are constrained
by decisional calculations that are themselves constrained by circum-
stances ranging from poverty and self-medication for other psycholo-
gical problems to sheer pursuit of pleasure. These critics therefore deny
that the series of such choices that constitute an addiction is a medical
disorder.
7. The evolutionary view of addiction as a “hijacking” of desire/
deliberation/choice motivational mechanisms
The third view is the evolutionary view of addiction, which is
neutral on whether there is tissue damage from substance use. One can
hold that the evolutionarily novel nature, purity, ease of access, routes
of administration, or amounts of substances of abuse that exist in their
present form due to our technological capabilities can lead to genuine
functional pathology without any tissue damage being necessary,
simply as the “normal” response of biologically designed mechanisms to
a novel input. As Nesse and Berridge [52] explain: “Pure psychoactive
drugs and direct routes of administration are evolutionarily novel fea-
tures of our environment. They are inherently pathogenic because they
bypass adaptive information processing systems and act directly on
ancient brain mechanisms that control emotion and behaviour. . . and
can result in continued use of drugs that no longer bring pleasure” (pp.
63–64).
It is not a disorder to ingest novel substances that go outside of
biologically designed domains in the quest for pleasure, even if such
activities entail risks of harm. Moreover, of those who engage in sub-
stance use, only a small percentage become addicted. Taking such
J.C. Wakefield
substances can cause motivational dysfunctions in some individuals but
not others, likely as a result of normal brain variation between in-
dividuals. Such variations likely were not a problem in the environ-
ments in which we evolved precisely because of the limited availability
and purity of these substances. However, at present the result can be
overwhelming peremptory motivations to take the substance despite
good reasons not to do so, constituting a motivational disorder.
It should be noted that the pure hijack view of addiction as resulting
from the evolutionarily novel nature or purity or routes of adminis-
tration of psychoactive drugs interacting with brain mechanisms not
designed for them is not the only evolutionary model of psychoactive
substance response. The hijack view is the dominant evolutionary view
of substance response and vulnerability to addiction, but there are al-
ternative evolution-based research programs that are exploring whether
human response to psychoactive drugs is not entirely accidental but
instead might be a biologically designed response to certain chemical
features of such drugs that may provide overall fitness benefits, for
instance anti-pathogen effects that offer disease protection, despite
their toxicity (e.g., [53–58]). Even if this theory should turn out to be
correct and explain some receptivity to substance ingestion or even
some specific cases where a degree of hunger for a substance is within
biologically designed range, it would not make a major difference to the
larger point here because it is clear that in many cases substance ad-
diction goes well beyond any plausible fitness benefits that make sense
as part of biological design. On either approach, given how we are
biologically designed, novel changes in the availability and purity of
various substances relative to the environment in which we evolved is
likely the reason that certain substances are able to coopt our motiva-
tional machinery to the degree that they cause a motivational dys-
function in the form of addiction without there necessarily being any
brain damage underlying addiction.
8. Must all mental disorders be brain disorders?
One might ask: If addiction is a disorder at all, then isn’t NIDA’s
claim trivially true? Mustn’t all mental disorders be brain disorders,
given that all psychological states occur in brain tissue?
To see why the claim is not trivial, one must first understand,
conceptually speaking, how one distinguishes a brain disorder from
other mental disorders. This distinction depends on the kinds of con-
cepts essential to describing the function that is failing and the reason
for the failure. Cartesian ontological worries aside, brain descriptions
and mental content/representational descriptions of the intentional
field form two theoretical domains with their own functions and lawful
relations. I thus interpret the notion of a brain disorder as follows: a
brain disorder is a harmful dysfunction of brain mechanisms in which
the function that is failing to be performed can be fully specified in
brain-anatomical and brain-physiological terms without any essential
reference to the psychological/mental level of description involving the
intentional field or conscious experiences.
The doctrine that all mental disorders must be brain disorders is
commonly embraced today. It is a tenet of an influential movement
known as “neo-Kraepelinianism” [59,60], named after the 19th-century
psychiatrist Emil Kraepelin [61,62]. Influenced by the discovery that
syphilitic infection of the brain was responsible for the scourge of
general paresis at the time and by the identification of brain pathology
in Alzheimer’s disease, Kraepelin hypothesized that distinct brain
pathologies would eventually be found to correspond to each mental
disorder. Modern neo-Kraepelinians have been highly influential in
psychiatry over the past half century. As Samuel Guze, one of the neo-
Kraepelinian movement’s founding theoreticians, put it: “The conclu-
sion appears inescapable to me that what is called psychopathology is
the manifestation of disordered processes in various brain systems that
mediate psychological functions. Psychopathology thus involves
biology” ([63], p. 317). Nobel prize-winning neuroscientist Eric Kandel
states: “All mental processes are brain processes, and therefore all
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Behavioural Brain Research 389 (2020) 112665
disorders of mental functioning are biological diseases….The brain is
the organ of the mind. Where else could [mental illness] be if not in the
brain?” [64]. Similarly, Nancy Andreasen [65] former Editor-in-Chief of
The American Journal of Psychiatry, asserts that “people who suffer from
mental illness suffer from a sick or broken brain” (p. 8, emphasis in
original).
Given that every occurrence of a mental state is an occurrence of a
physical brain state and so takes place in the brain, it is fair to say that
in a locational sense every mental disorder is indeed a brain disorder.
However, that does not imply that every mental disorder is a brain
disorder in the stricter sense that there is a neurobiologically specifiable
dysfunction. Functions and dysfunctions describable at the psycholo-
gical level of organization might not correspond to functions and dys-
functions describable in purely non-psychological neurobiological
terms. It seems prima facie possible that biologically designed psy-
chological-level processes might go awry for purely psychological-level
reasons without any underlying physiological disorder.
Malfunctions at the level of the interaction of psychological con-
tents—where contents are designed to interact with each other in cer-
tain ways that make cognitive, conative, and emotional sense—may not
entail malfunctions describable at the brain circuit level. Of course,
even if a dysfunction at the psychological level does not correspond to a
dysfunction at the physiological level, it does correspond to some
physiological process and it is still the case that processes at the phy-
siological level have causal influences on processes at the psychological
level. However, granting Kandel’s locational premise, it remains at least
conceptually possible that there are mental dysfunctions that are not
brain dysfunctions in the narrower sense. The invalidity of “all mental
disorders are located in the brain, therefore all mental disorders are
brain disorders” is suggested by the invalidity of the analogous argu-
ment: All computer software runs in computer hardware, therefore all
software malfunctions must be hardware malfunctions. Every step in
the running of a computer program is an occurrence in the computer’s
hardware, but the functions of software involve the symbolic meanings,
not the silicon-level descriptions, of the hardware configurations. Thus,
there are software problems in which symbolic processing is mal-
functioning that don’t involve any hardware problems.
To take a familiar example, the “Y2K” panic about the potential
breakdown of our information processing infrastructure involved no
feared hardware malfunctions. Rather, the problem was that, once the
year 2000 arrived, the two-digit “year” register in most commercial
software, designed only for inputs of twentieth-century years using just
the last two digits of a year, would have provided inappropriate inputs
(e.g., “01” would be interpreted as “1901” rather than “2001”), yielding
software malfunction. For example, software calculating interest on a
bank account might yield nonsense as output, yet nothing would be
wrong with the computer hardware. Considering again the Kandel
passage quoted above, intentional contents do occur “in the brain,” but
the software analogy suggests that the fact that all mental occurrences
take place in brain tissue does not imply that every mental dysfunction
is a dysfunction specifiable in purely anatomical/physiological terms.
The Kandel-type argument equivocates in moving from the correct
premise that all mental disorders are brain disorders in the locational
sense to the conclusion that all mental disorders are brain disorders in
the narrower sense that there is an underlying dysfunction describable
sheerly in anatomical/physiological terms.
All this only suggests that it is conceptually possible that some
mental disorders might not be brain disorders. But it does not yet prove
that there are such conditions, and it does not suggest anything speci-
fically about addiction one way or the other. In fact, the neo-
Kraepelinian axiom that all mental disorders are brain disorders seems
to be accepted by many opponents of NIDA’s view. Opponents of the
brain disorder model of addiction tend to assume that since addiction is
not a brain disorder, it therefore must not be a mental disorder at all. I
am going to take a different position. I will argue that the idea that
there can be a medical/mental disorder in a biologically normal brain is
J.C. Wakefield
more than a conceptual notion and actually can occur. Thus, I will
argue that even if the “brain damage” account of addiction is rejected,
addiction can still be a medical disorder.
9. The fallacy that pathology precludes choice
Some philosophers have rejected the brain-disorder account and any
other pathological account of addiction because they believe that the
pathology view entails that addicted individuals are acting in-
voluntarily and cannot make choices. This would have the unwanted
and implausible implication of paralyzing common therapeutic efforts
that often depend on supporting the addicted individual in making
painful choices. Thus, the field suffers from a false “pathology versus
choice” paradigm that assumes that either addictive behavior is caused
by an underlying pathology and thus is not a matter of choice and is
involuntary, or addicts retain some degree of choice and control over
drug use most and can be responsive to incentives, thus retain agency
and are thus nondisordered.
The problem with this argument is that it is a fallacy to infer from
the fact that addicts retain some degree of choice and agency that
therefore there is no underlying pathology or dysfunction. Most dys-
functions in medical conditions involve partial, not total, loss of func-
tion. In addiction, the dysfunction is in the distortion of the preference
function and the functioning of the intentional system on the basis of
which agency and choice are exercised. Choice is pathologically biased
or restricted in certain ways but not eliminated, so “choice versus pa-
thology” is a false dichotomy. The primary symptom of addiction lies
not in the taking of a drug—there is nothing pathological about such an
action in itself—but in the set of background perceptions and desires
that shape the likelihood of that choice, which despite the distortions in
the default state of the intentional system is still a choice.
Understanding that the addicted individual has the capacity for
choice is critical for a sensible approach to treatment that exploits the
addicted individual’s ability to make choices. Importantly in terms of
correcting the critics’ confusions, there is no conflict between addiction
being a pathology of choice and the possibility of exploiting remaining
capacities for choice in treatment of addiction. Here is a vivid (to me)
analogy. I recently suffered from an excruciatingly painful malady
called frozen shoulder, in which the range of motion of my shoulder
was severely impaired due to inflammation-caused pain. The orthope-
dist’s prescription for physical therapy specified the treatment in one
elegant but terrifying phrase: “aggressive stretching.” Now, a medical
sophist might argue that there is a tension here: how can I treat my
condition by undergoing “aggressive stretching” when the stretching
movement involved in the treatment is precisely the function that is
impaired and exquisitely painful? Common sense answers that, with
courage, one can push the shoulder at the threshold where the pain and
movement inhibition occurs to gradually increase the range of motion;
one can treat motion impairment by systematically using motion to
push back the impairment’s boundaries. Analogously, one can think of
addiction treatment as painful “aggressive stretching” of an impaired
choice function, where, with courage, a choice disorder is treated by
systematic and gradual “stretching” of the individual’s choices in ways
that have hitherto seemed impossible. Although choice is mal-
functioning, its healthy aspects can be exploited for treatment progress.
Nor does the degree of retained choice mean that addiction itself is a
voluntary action. Having your choice function altered is not a voluntary
action. Becoming addicted has an ontological status analogous to falling
asleep; you can voluntarily engage in the actions that place you in the
circumstances where it is likely to happen and you can even intend to
bring it about as a result of placing yourself in those circumstances, but
it is not itself an action but rather something that happens to you once
you are in those circumstances. You cannot will yourself to be addicted
any more than you can will yourself not to be addicted, although of
course you can will yourself to engage in actions that bring about your
being addicted or non-addicted.
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Behavioural Brain Research 389 (2020) 112665
Nor is the fact that circumstances, such as poverty, can influence an
addicted individual’s choice in tension with a disorder attribution.
Many disorders are context-sensitive with symptoms that emerge only
under certain circumstances. (E.g., both my brothers had terrible
asthma in New York and moved to Arizona where their pathology was
no longer triggered to yield symptoms.) Circumstances such as poverty
may explain drug use, but they do not explain the development of ad-
diction per se. One must also keep in mind that the degree of context
dependence depends on the addictive agent. For example, the opioid
epidemic in the U.S. appears to be an example of an iatrogenic scourge
generated by the decision to widely prescribe opioids for noncancer
pain, and it has had deleterious effects on middle class intact families
and communities that have traditionally not had social problems of the
sort appealed to by those who attribute addiction to deprivation.
It is important to emphasize that even severe addiction involves
some degree of choice and is not the zombie-like total suspension of
self-control sometimes portrayed by brain-disease proponents or at-
tributed to their view by their critics. A pathologically narrowed space
of desire/deliberation/choice processes is not the same as no space at
all. The addict may be able to exploit his or her own remaining degree
of will to expand and exercise greater control over the space of choice
and deliberation. However, the fact that a degree of choice and will is
possible for addicts and that exploiting these capacities should be en-
couraged as a route to change does not conflict with the claim that
addiction is a medical disorder because, as noted, most medical dis-
orders do not involve total cessation of compromised functions. Rather,
they involve pathological degrees of hyperactive or hypoactive func-
tioning that is outside biologically designed bounds, or alternatively
they involve normal-level activity that is misdirected, as in paraphilias
or autoimmune disorders. The brain-disease and medical-disorder
models entail at most a pathological degree of diminution of control,
not complete loss of control. Consequently, showing that addicts pos-
sess some control or can make choices does not demonstrate that ad-
diction is not a disease or disorder. Disruption of the desire/delibera-
tion/choice system by peremptory desire that the system was not
designed to experience is a dysfunction that is a matter of degree and
not generally total.
10. The gosling and the fox: An example of a mental disorder in a
normal brain
Computer hardware-software metaphors aside, is it possible for
there to be a mental disorder without a brain disorder? Prevailing neo-
Kraepelinian psychiatric ideology holds that every mental disorder
implies brain damage, setting up the dichotomy: either addiction is a
disorder because it involves brain damage, or addiction is not a disorder
at all. I am arguing for a third approach that holds that addiction can be
a genuine medical disorder even if there is no brain damage. Before I
can argue for the plausibility of such a third view, I have to vanquish
the dominant neo-Kraepelinian doctrine and establish that in principle
it is possible for there to be a mental disorder that involves no brain
damage. In this section, I develop such a counterexample to the neo-
Kraepelinian claim—an example in which something is wrong with the
mind and in which it is clear that there is a mental disorder despite
there being nothing wrong with the brain.
To prepare the way, let me first back up for a moment and clarify a
point about the definition of “dysfunction.” It is sometimes said that a
dysfunction occurs when a mechanism cannot perform its function.
However, obviously that is not sufficient because, for example, a
blindfolded person’s eyes cannot perform the function of seeing and an
isolated person’s sexual organs cannot perform their function of re-
production, yet neither have a dysfunction or disorder. So, dysfunction
requires that the mechanism cannot perform its function because of
internal reasons. However, this is not quite sufficient either. As
Christopher Boorse [66] points out, it is not a dysfunction of your blood
clotting mechanisms if they never actually perform the function of
J.C. Wakefield
causing your blood to clot, if the reason is that you never are injured.
Indeed, it is the internal structure of the clotting mechanisms that
prevents them from performing their function of causing clotting when
there is no injury; that is part of their design. There is no dysfunction as
long as the clotting mechanisms are capable of performing their func-
tion should the appropriate conditions occur for which the clotting
capacity was selected, namely, an injury. Or, for example, erectile
dysfunction is not the lack of an erection, and it is not the incapability
of having an erection under current conditions, but the incapability of
having an erection when confronted with the standard appropriate
environment in which erection is the biologically designed re-
sponse—say, a sexually desired and responsive partner. So, we might
say: a dysfunction is the inability of a mechanism to perform its function for
internal reasons even under the appropriate circumstances for which it was
selected to perform that function.
Now, to my counterexample to the neo-Kraepelinian thesis: goslings
(baby geese) famously have neural assemblies dedicated to an “im-
printing” function. The imprinting system is biologically designed to
store an image of the first creature the gosling sees upon hatching. Once
imprinted, the gosling then has an irresistible and irreversible desire to
stay close to and follow the represented creature. The mechanical
nature of the imprinting system was famously demonstrated when
Konrad Lorenz [67,68] caused goslings to imprint on him and follow
him around as if he was their mother.
The evolutionary explanation for the imprinting mechanism is that,
first, almost invariably the first creature the gosling sees upon hatching
is its mother, given her involvement in bringing about the hatching. The
mechanism’s selection depended on this correlation, so imprinting on
the mother is a higher-level function of the imprinting mechanism.
Second, linking the gosling specifically to its mother is the function of
imprinting because the development and survival of the gosling depend
on staying close to its mother after hatching, and on multiple correla-
tions with being imprinted specifically on the mother. This is due to the
existence of a variety of naturally selected coordinated mechanisms in
mother and gosling such as the mother’s inclination to protect, feed,
and teach the gosling, all of which is triggered by the hatching and the
subsequent interaction between gosling and mother goose.
The gosling’s imprinting mechanism is associated with such a
hierarchy of functions, some of which depend for their success on ex-
pectable environmental correlations. The storage of the image of the
first seen creature after hatching has the function of storing the image
of the mother, and the success of the latter function depends on the
expectable environmental correlation of the mother being the first
creature seen after hatching. Storing the image of the mother in turn
has the function of activating the follow-and-stay-close program when
seeing the mother that matches the image, and the evolution of the
function of the staying-close program depended on a strong correlation
between being the mother goose and having a variety of caretaking,
protective, and teaching programs triggered around the time of the
gosling’s hatching.
Now, consider a gosling that accidentally imprints on a passing fox
that happened to be in its visual field when hatching and thus follows
the fox around until it is eaten. I claim that this gosling has a disorder in
virtue of having a psychological dysfunction that clearly causes harm.
In this example, the claimed dysfunction is not in the failure of the
imprinting function itself at the most basic level– that of imprinting on
whatever creature the gosling first observes upon hatching. That
function is successfully performed in this example because by un-
fortunate chance the fox is the first creature the gosling sees upon
hatching. However, there is nonetheless a failure of a function higher in
the hierarchy of functions, namely, a failure of the function of the im-
printing mechanism to imprint the gosling on its mother.
One might object that this is not a dysfunction because the gosling’s
difficulties are due entirely to an unexpectable environmental circum-
stance of the fox being in the gosling’s visual field at the time of the
gosling’s hatching. If the failure to perform a function is due sheerly to
6
Behavioural Brain Research 389 (2020) 112665
unexpectable environmental circumstances but the mechanism is still
capable of performing its function if placed in the expectable, evolu-
tionarily relevant circumstances, then this is a mismatch but not a
dysfunction. This explains why, even though one of the functions of the
sexual motivational system is to bring about sexual activity with a
partner, lack of potential sexual partners in the local environment is not
a sexual dysfunction despite the fact that a function of the sexual mo-
tivational system cannot be performed; the sexual system is still capable
of performing its function if the organism is placed in a more expectable
environment in which there are potential sexual partners.
However, it is an entirely different situation and not merely a de-
viant environment if a developmental mechanism with a critical
window for a developmental stage transition is operating in an un-
expectable environment. That can disrupt development in such a way as
to trigger an irreversible developmental pathway that becomes a fixed
feature of the organism, potentially making downstream functions im-
possible to perform. In a critical-window situation, the “wrong” input
can render the mechanism incapable thereafter of performing its
function even in the standard expectable environmental circumstances.
Regarding the gosling’s dysfunctional and disordered status once it is
imprinted on a fox and thus leaves its mother and follows the fox
around to its death, something has certainly gone wrong with the
gosling’s naturally selected psychological functioning. Note that the
closest human equivalent to such a condition, in which a child’s at-
tachment occurs to arbitrary strangers rather than a caregiver, is la-
beled “disinhibited social engagement disorder” and listed as a category
of mental disorder in DSM-5.
The crucial fact in the gosling case is that the imprinting process
permanently and irreversibly locates an image of the target of the im-
printing in the brain. Once that occurs, subsequent failures of function
are due not to events in the environment but to the internal state of the
gosling. Once the imprinting on the fox takes place, there is a true
developmental disruption in which the gosling is incapable even under
ideal circumstances—for example, if placed in the presence of its mo-
ther—of performing basic functions that are developmentally essential
and for which the mother alone is primed to provide a complementary
interactor. In the biologically designed developmental sequence, the
gosling following its mother triggers many other developmental pro-
grams and expectable inputs as the gosling learns from watching its
mother hunt for and share food, is warmed and sheltered by her
feathers, is protected by her from predators, is helped to learn and re-
cognize species-specific behaviors and vocalizations, and thus is en-
abled to recognize conspecifics so that the gosling can eventually select
an appropriate mate. Of course, all this could fail to occur due to a
deviant environment where the mother is not available to the gosling
(e.g., the mother is eaten by the fox). However, in the mis-imprinting
example, it is not the environment that makes all these later develop-
mental performances impossible contrary to the naturally selected
trajectory of biologically designed functioning. Rather, it is an internal
change in the gosling that makes the gosling incapable of later re-
sponding to these various stimuli. That internal change is the perma-
nent and irreversible developmental disruption that occurs when, in the
critical window for imprinting, the gosling imprinted on a passing fox
rather than its mother. This would seem to be a clear case of dysfunc-
tion according to standard criteria that there is an incapacity to perform
various functions for internal reasons even under appropriate en-
vironmental conditions [69].
Turning to the neo-Kraepelinian challenge, if one concedes that
nothing is wrong with the gosling’s brain at the level of neurological
description, how can anything be wrong with the gosling’s functioning
at the psychological level? The answer is that the dysfunction at the
psychological level concerns intentional representational content, not
neurophysiology; and it concerns not whether the psychological process
of imprinting took place successfully (it did), but what it is that the
gosling imprinted on, a question outside of neurophysiology. The image
in the brain refers to a passing fox, not to the mother, and thus involves
J.C. Wakefield
the failure of a higher level of function of the imprinting mechanism,
namely, that the gosling imprint on the mother. One can identify what
has gone wrong only by going beyond brain descriptions and referring
to meanings (i.e., what the gosling’s brain-stored image in fact re-
presents).
Even if one examined the brain of the gosling in a way that allowed
one to identify the nature of the image within the imprinting register,
one would still not know for sure whether the image was of a fox or of
an unusual-looking mother goose facially similar to a fox. Even if the
image looks like a goose, the accidental target of imprinting could be a
passing gosling-hating goose that resembles the mother goose.
Examining the stored image alone cannot establish the object whose
image was stored, thus cannot establish whether the imprinting me-
chanism performed its higher-order function of imprinting on the mo-
ther goose. For that, one must go beyond the facts about the gosling’s
brain and understand the relationship of the image to the gosling’s
environment and to the biologically designed functions of the involved
mechanisms.
The point is that there is nothing wrong with the gosling at the
brain-descriptive level. The gosling’s problem is a matter not of brain
functioning per se but of the reference or meaning of the image stored
in its brain, a psychological-level mental-content construct. So, we have
here an example of a psychological dysfunction that is not a brain
dysfunction because it cannot be described in sheerly brain-physiolo-
gical terms.
Of course, there are many known animal and human developmental
processes that are analogous to gosling imprinting in that they involve
critical periods and the possibility of developmental disruption if cer-
tain environmental triggers do not occur during that period. These
range, for example, from critical periods in human language learning
and in visual focus to bird misimprinting on non-conspecific birdsongs
or sexual signals, and many others. Almost any of these other examples
would serve as well to make the conceptual point, via examples of
critical-period developmental disruption due to unexpectable environ-
mental signals, that psychological dysfunction does not require brain
dysfunction. The gosling imprinting process is simply one of the simpler
and best-known cases to make this conceptual point.
11. Dysfunction without tissue damage: Mimicry
The gosling example, in which the fox “hijacks” the gosling’s im-
printing mechanism, establishes the principle that there can be mental-
level disorders without any brain-level dysfunction. However, that ex-
ample involves no ingested substance. Still, there are plenty of ex-
amples analogous to addiction of evolutionarily unexpectable sub-
stances that coopt systems in other areas of functioning. One much-
discussed example is hormone-mimicking chemicals, such as estrogen
mimics, that leach from plastics and trigger hormone receptors, po-
tentially disrupting developmental programming. The hormone re-
ceptors are perfectly normal, but their activation by plastic-based hor-
mone mimics is a dysfunction.
Another example is carbon monoxide poisoning. Carbon monoxide
gas in significant environmental amounts is an evolutionarily novel
product of incomplete human-caused combustion. Carbon monoxide
happens to have chemical properties that allow it to perfuse from en-
tirely normal lungs to blood cells and bind successfully with entirely
normal hemoglobin in Lewis acid-base reactions of the kind that are
biologically designed to occur with oxygen. The problem is that carbon
monoxide binds more strongly than oxygen to hemoglobin, so does not
disengage when it reaches the cells and does not allow a subsequent
adequate rate of exchange for fresh oxygen. One can die of such hi-
jacked hemoglobin transport even though the hemoglobin is normal
and in many respects is doing exactly what it was designed to do. The
dysfunction derives from the fact that the hemoglobin is performing its
function with a novel substance with which it was not designed to in-
teract.
7
Behavioural Brain Research 389 (2020) 112665
Addiction is analogously a kind of overly strong “binding” of desire/
choice systems to a kind of motivating reward they were not designed
to handle. Because addictive substances act directly on reward-de-
tecting systems each time they are used, they do not allow for natural
processes of habituation. During such processes, the brain usually be-
comes increasingly sensitive to unexpected levels of potential reward,
and motivational salience typically migrates from the reward itself at
expectable levels to various indirect cues of unexpected reward levels
[70,71]. Because this biologically designed reduction of motivational
salience does not occur in response to addictive substances, the an-
ticipated reward is thus repeatedly strengthened in a way that it was
not designed to be, yet there is no tissue damage underlying this dys-
function. Many people have died from the hijacking of hemoglobin in
carbon monoxide poisoning, but many more have died from a hijacked
desire system in which choice is reshaped by a substance for which the
choice system was not designed. An individual with carbon monoxide
poisoning has perfectly normal lungs and hemoglobin, and an in-
dividual responding to leached hormone mimics from plastic can have
perfectly normal hormone receptors. Similarly, an addicted individual
can have a perfectly normal brain. Yet each of them has a dysfunction
due to binding to the wrong thing.
However, there is a crucial difference: carbon monoxide’s binding to
hemoglobin is universally powerful enough to cause harm at high levels
despite some variations in sensitivity, whereas most addictive sub-
stances cause a harmful level of addiction in only a minority of in-
dividuals even when taken in substantial amounts over time. This im-
plies that there are additional psychological or biological risk factors
involved in addiction. The most likely such additional factor is normal
genetic variations that were not problematic in evolutionarily ex-
pectable environments but create vulnerability to substance-caused
motivational dysfunction in evolutionarily unexpectable environments
like ours. For example, one such normal variation that influences al-
cohol addiction susceptibility is whether one has the so-called “Asian
alcohol gene” found in East Asian populations that lowers the like-
lihood of alcohol addiction by inactivating the aldehyde dehydrogenase
gene and thereby making drinking less enjoyable [72].
There are many metabolism-influencing genetic variations that are
perfectly normal when in a heterozygous combination but that can
cause vulnerabilities when one is homozygous for that variant. Many
normal genetic variants are equally adequate for health under the en-
vironment of evolutionary adaptedness (EEA) conditions in which hu-
mans evolved, but under novel environments can become deleterious.
For example, under the depleted intake of certain B vitamins in our
modern environment, some normal-range genetic variants that were
perfectly adequate for processing B vitamin pre-metabolism in the EEA
are no longer adequate and thus, although they are normal variants
evolutionarily, become risk factors for disorder in our present en-
vironment due to altered vitamin intake. It is also conceivable, of
course, that in addition to such normal variations that interact patho-
genically with novel substance intake, there are some mutations that
are themselves harmless dysfunctions under other conditions but that
create vulnerability to harm in a substance-novel environment.
12. Implications for an integrative view of addiction studies
I have argued that there is a coherent conceptually defensible
middle ground between NIDA and its critics in which NIDA is right that
addiction is a medical disorder but wrong about it being a brain dis-
order, and the critics are right that addiction is not a brain disorder but
wrong about addiction therefore being simply a matter of normal
problematic but nondisordered choice functions exercised under unu-
sual circumstances. The middle ground is that addiction comes about
due to evolutionarily novel inputs to the brain that cause a true harmful
psychological dysfunction of choice mechanisms that were not designed
for these inputs—thus there is a medical disorder—despite there being
no underlying brain disorder. I have explored the possibility and
J.C. Wakefield
implications of this conceptual option, but it is an empirical matter
whether this is in fact the best account of addiction. If it is correct, then
I believe that it has vast ramifications for how we see the social re-
sponsibility for addiction and how we attempt to control it.
In particular, the view of addiction suggested in this paper has
dramatic implications for the relationship among and integration of the
addictive sciences, and places considerable responsibility on society at
large for the problem of addiction. This is not only for the usual reason
that negative social circumstances such as poverty and lack of life op-
tions increase drug use and thus addiction. From the harmful dys-
function perspective, the primary direct social factor in creating the
phenomenon of addiction is the social creation and availability of
evolutionarily novel addictive substances and activities that are capable
of producing addiction in interaction with normal genetic and psy-
chological variations that create addiction vulnerability. An analogy is
to the misguided “blaming” of many individuals who are obese due to
normal variations in genes regulating fat storage that were adaptive
during our evolutionary past interacting with the unprecedented
amount of high-calorie food marketed in temptation-maximizing ways
to people in contemporary societies. Similarly, most addicted in-
dividuals would be fine in evolutionarily expectable environments.
Thus, society bears a heavy responsibility for the problem of addiction.
On this view, offering treatment is not just a matter of compassion but
also a matter of justice [73].
Society exists in virtue of the fact that the desire/deliberation/
choice systems of large number of human beings can be coordinated to
some extent via socialization processes. The occurrence of severe
widespread deviations from expectable desire functions due to a variety
of addictions thus can pose a serious challenge not only to the in-
dividual’s ability to benefit from social institutions but to social func-
tioning. Obviously, there are novel incentives routinely offered by
changing social institutions to reorient individuals to new motivational
goals. However, the creation of deviant and problematic choice func-
tions due to addiction seems to be a consequence of technical social
progress that inevitably creates new ways that external substances and
forms of stimulation interact with endogenous motivational systems.
Just as there is now routine evaluation of new chemical substances
for teratogenic and carcinogenic effects on our biochemistry and ge-
netic systems, so there should be routine evaluation of both substances
and novel behavioral stimulations for addictive potential. To some ex-
tent, such testing is done now, but it is often done by those who wish to
addict us to their products for monetary gain. Whether it is gambling
machines, “click bait” online, or foods with their salt-sugar-fat irresis-
tible taste for some genetic variants, our weaknesses for motivational
dysfunction are being massively exploited. Given that just as in the
design of medications, the design of addictive motivational techniques
and substances is only going to get more sophisticated, addictive po-
tential should become a routine part of product testing and disclosure
on labels. Just as in current European “freedom to disappear” laws that
prevent the internet from overriding one’s reasonable choices to let
things go from the past, new social institutions need to be created that
allow people to live together and yet have pathways that eliminate
certain temptations that they don’t want to confront or to which they
have a demonstrated weakness. It is unjust to approach this issue as we
have in the gambling industry, by letting loose on the community an
activity with known addictive casualty rates and then siphoning off a
portion of the profits for treatment. This is like allowing a company for
profit to let loose a virus that renders devastatingly ill only a small
percentage of the population if the company agrees to contribute to
medical care for the infected. Addictive threats to health should be
considered in the same way other kinds of threats to health are con-
sidered, not only with regard to treatment and cure but within a
comprehensive approach to everything from pre-testing of products to
mitigation of risk factors to provision of the ability to enter niche social
trajectories and environments that preclude confrontation for certain
addictive pathogens.
8
Behavioural Brain Research 389 (2020) 112665
Declaration of Competing Interest
None.
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