ORIGINAL RESEARCH
published: 18 December 2018
doi: 10.3389/fsoc.2018.00039
Re-socializing the Vulnerable Brain:
Building an Ethically Sustainable
Brain Disease Model of Addiction
Jaakko Kuorikoski 1* and Susanne Uusitalo 2
1
New Social Research, University of Tampere, Tampere, Finland, 2 Department of Philosophy, Contemporary History and
Political Science, University of Turku, Turku, Finland
Edited by:
Veljko Dubljevic,
North Carolina State University,
United States
Reviewed by:
Adrian Carter,
Monash University, Australia
Larissa J. Maier,
Department of Psychiatry, University
of California San Francisco,
United States
*Correspondence:
Jaakko Kuorikoski
jaakko.kuorikoski@uta.fi
Specialty section:
This article was submitted to
ELSI in Science and Genetics,
a section of the journal
Frontiers in Sociology
Received: 29 June 2018
Accepted: 30 November 2018
Published: 18 December 2018
Citation:
Kuorikoski J and Uusitalo S (2018)
Re-socializing the Vulnerable Brain:
Building an Ethically Sustainable Brain
Disease Model of Addiction.
Front. Sociol. 3:39.
doi: 10.3389/fsoc.2018.00039
Frontiers in Sociology | www.frontiersin.org
According to the brain disease model of addiction (BDMA), substance addiction is a
chronic, relapsing brain disease. The BDMA is currently influential in informing addiction
policy and the development of new treatments, but remains highly controversial across
the addiction research community. We draw on resources from philosophy of science and
applied ethics to re-examine the methodological and ethical implications of the BDMA
and offer a new forward-looking and constructive conceptualization of the BDMA as a
heuristic reductionist research hypothesis. We argue that this not only allows a sharper
delineation of the empirical shortcomings of the BDMA, but also helps skeptical social
scientists appreciate and incorporate the empirical successes of the BDMA to a broader,
social understanding of addictions. We apply this view to the ethical implications of the
BDMA, especially to the key concept of vulnerability. The BDMA states that it is the brain
that has been hijacked by the drug and the brain thus compels the individual to act in
ways that are often disastrous for the individual. The proponents of the BDMA ascribe
“vulnerability” to multiple levels of organization, such as genes, specific neural systems,
the brain, and the person, thus resulting in confusion and highly problematic ethical,
social and even legal implications. The BDMA locates the vulnerability firmly within the
individual and treats it as a matter of susceptibility to changes in brain chemistry. This may
well be a part of the phenomenon, but the kind of vulnerability relevant for understanding
and treating addiction is, however, embedded in normativity, as it concerns the agency
of individuals with addiction. Agency is not simplistically reducible to the competencies
of the individual, but rather it is also constituted in the interactions with their environment.
Keywords: brain disease model of addiction, reductionist heuristics, vulnerability, localization, agency
INTRODUCTION
The human brain is susceptible to psychoactive substances. This fact has been widely acknowledged
and utilized in medicine, recreational activities, spiritual experiences, as well as in the enhancement
of physiological and psychological performance (see e.g., Goodman et al., 2007). As the human
brain’s susceptibility to such substances is shared by all human kind, societies have felt the need to
control the substances in various ways (e.g., establishing agencies, such as European Monitoring
Centre for Drugs and Drug Addictions). With psychoactive substances, there is a risk of abuse
and misuse. The pharmacological effects of psychoactive substances often lead to using more than
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reality and the lived experience of people using psychoactive
substances.
This tug-of-war between the neurobiological and sociological
perspectives on addiction is but one front in the broader
re-negotiation of boundaries of expertise and authority on
normatively contested behavior brought about by advances in
neuroscience (e.g., Pickersgill, 2013; Rose and Abi-Rachid, 2013).
However, in few other areas of application has the neuroscientific
picture gained such prominence in the public as well as in the
governing sphere (in the United States) as in addiction research.
In what follows, we consider these fundamental challenges from
the perspectives of philosophy of science and applied ethics, in
that order.
initially intended or using a prescribed substance to purposes
not covered by the original purpose of the prescription. As
such misuse can result in substantial harm, control, and
governance is often warranted. In fact, one of the motivations
for control stems from the fact that individuals are in
danger of losing control in drug use, i.e., becoming addicted
(e.g., Manchikanti et al., 2010). While we acknowledge that
the concept of addiction is contested, historically contingent
and that addictive behaviors display significant cross-cultural
variation, in the following we adopt a suitably loose and broad
understanding of addiction as a persistent problem in selfcontrol related to substance use possibly resulting in harm to the
agent.
Addiction has been viewed as one of the undesirable
consequences of psychoactive substances, no matter what the
original purpose of the consumption has been. However, the
nature of addiction is contested; there are various competing
and complementary views on the condition, ranging from a
non-pathological condition grounded on subjective preferences
to an agency-deleting disease. Whilst each view has its own
challenges and strengths, one account has received a great deal
of attention (and funding). The brain disease model of addiction
(BDMA) states that addiction is a chronic relapsing brain disease.
This immediately suggests that the right response to addiction
is the development of pharmaceutical and other medical
interventions for the destructive condition that is portrayed in
the model. Although substance use is initially voluntary, the
pharmacological effects in the brain reduce the individual’s ability
to control her own behavior (e.g., Leshner, 1997). Whether or
not this is factually so, the view has nonetheless ethical, legal
and social implications that need scrutiny. In what follows we
will focus on the brain disease model of addiction, as it has
been argued to be the view that is shared by scientists (Animal
Farm, 2014). Although neuroscientific (especially dopaminergic)
perspectives have also gained prominence in the scientific and
public understanding of behavioral addictions, most notably of
pathological gambling, we focus here on substance addictions, as
these are the phenomena to which the full BDMA has been most
explicitly formulated (for a neuroscientific model of pathological
gambling, see, e.g., Potenza, 2008).
Nevertheless, the full scientific picture is not that simple.
BDMA is a deeply contested model (Hall et al., 2015;
Heather et al., 2018)—despite its proponents’ insistence on
its prominence in the US or even worldwide (Animal
Farm, 2014)—and it faces many empirical and normative
challenges. Despite its original rationale of reducing the
moralistic stigma associated with addiction (e.g., Leshner, 1997),
the BDMA is seen as empirically and ethically problematic
in downplaying the role of social and cultural context in
creating and sustaining addiction. Existing surveys suggest
that among scientists and clinicians, the model is usually
endorsed only with a string of caveats about ignored contextual
factors attached (Bell et al., 2014; Barnett et al., 2018). The
empirical and normative problems of the model arise out of
the fundamental difficulties in integrating the ever-increasing
empirical findings about altered brain functionality to the
broader social scientific bodies of knowledge about the social
Frontiers in Sociology | www.frontiersin.org
DIAGNOSING THE BDMA
The brain disease model of addiction was “launched” as a
specifically scientific way of understanding addiction by the then
director of the National Institute of Drug Abuse (NIDA) Alan
Leshner (1997). BDMA was positioned explicitly as an alternative
to the stigmatizing view of addiction as a personal moral failure
and as a political tool for securing better access and insurance
cover for treatment, as well as for influencing public opinion and
legislation (Dackis and O’Brien, 2005). Underneath the two main
components of “disease” and “the brain,” the model is in fact more
like an umbrella term that covers various alternative and often
competing neuroscientific models that focus on habits, learning,
pleasure, and incentive salience. As a poignant symbol of the
prominence of the BDMA within the institutions responsible
for control and treatment, the directors of the NIDA and
the National Institute on Alcohol Abuse and Alcoholism have
provided an integrative neurobiological account that attempts to
combine all of these mechanisms into a coherent whole (Koob
and Volkow, 2016).
The model is based on diverse experimental and physiological
evidence. The results of animal models on self-administration
of drugs and of neuroimaging studies on individuals with
drug addiction support the idea that dopamine activation
plays a key role in the “addicted brain,” especially in the
mesocortical, mesolimbic and mesostriatal pathways (Volkow
et al., 2011). The model is also supported by genetic research
on addiction in twin-studies, not only demonstrating the
(population-level) heredity of the increased risk of addiction,
but also suggesting corresponding biological pathways from the
genome to behavioral patterns (Kendler et al., 2012).
The opponents of the BDMA nevertheless deride the model
as being a dogma upheld more by appeals to authority rather
than by solid empirical evidence (Satel and Lillenfield, 2014).
They, for instance, refer to epidemiological evidence that most
people “mature out” of problematic patterns of substance use on
their own (Heyman, 2009; e.g., Granfield and Cloud, 2001), and
suggest that addiction as such does not amount to a (medical)
problem, but that its problems are mostly due to comorbidities
(e.g., Pickard and Pearce, 2013). The agency-deleting disease
model is also hard to reconcile with the fact that most people with
problems related to substance use do nevertheless respond to
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insists that such false hypotheses are useful, even necessary.
The reason is that it is epistemically useless to approach
complexity holistically, by simply acknowledging it or by
amassing observations without any roadmap for putting these
observations into a coherent whole. Reductionist hypotheses,
although literally false, are useful in that by looking at the way
in which they fail to empirically account for the full richness
of the phenomenon studied provides further hypotheses about
the way in which the whole is more than simply a sum of
its parts. The necessity of such simplifying working hypotheses
is deeply ingrained, although often implicit, in the training of
natural scientists, but may be a more alien mindset to many
social scientists. We hypothesize that the failure to recognize this
insight is a major factor in the skepticism toward neuro-centered
perspectives on addiction, especially among researchers with a
more social scientific or anthropological orientation.
Adapting this key lesson to our context, we hold that pointing
out that a social-behavioral phenomenon, such as addiction is
complex, context sensitive, historically contingent and socially
embedded (e.g., Reinarman and Granfield, 2015), is not, as such,
yet a deep insight about the phenomenon. It is more of an
admission that the phenomenon is not yet well-understood. As
Derek Heim(2014, 40), along with 94 signatories, puts it in his
response to the prominent BDMA editorial in Nature (2014),
“Addiction is too complex to be fought on a medical-research
front alone. A variety of approaches based on diverse levels
of analysis is required.” Again, few would disagree with this
statement. The real challenge is in figuring out the form of
complexity, the dynamics of the different aspects, ways in which
context matters, and when and how the extrinsic social and
environmental factors influence the phenomenon. The challenge
is all the more daunting in a case, such as addiction, in which
the biological, and the social are so obviously intertwined in
the treatment and regulation of the phenomenon. Answering
these challenges, and moving beyond the mere acknowledgment
of the interconnectedness of the brain, the body and the social,
requires epistemically strategic simplifications1 —a point often
misunderstood and overlooked by the critics of the BDMA.
Our modest contribution to answering these challenges is the
suggestion that we should treat the empirical failures of the
BDMA as opportunities to learn more about the form of the
interaction between the neurobiological and the social. We
will next delineate the empirical failings of the BDMA as
consequences of reductionist heuristics, and point to ways in
which these failings could serve as empirical entry points for
understanding the interaction between the biological and the
social.
The BDMA is a reductionist hypothesis on two levels. First,
it conceptualizes the problematic behavior of the individual as
even small changes in incentives or personal situations (Heyman,
2009; Satel and Lillenfield, 2014), and that only a subset develop
these problems in the first place. More generally, and what is most
important for our present purposes, BDMA is accused of leading
to an impoverished and reductionist understanding of addiction,
devoid of important social and cultural contextual variables
(Fraser et al., 2014; Reinarman and Granfield, 2015). Although
we agree with most of the opponents’ criticism, the problem with
this confrontational attitude is that it also renews and maintains
the barriers between the vast bodies of empirical understanding
about the social and societal factors relevant for understanding
addiction and recovery, and the neuroscientific insights about the
sub-personal mechanisms relevant for understanding the selfregulation of our behavior. We take our intervention to be timely
as the newly launched European Addiction Theory–network
positions itself explicitly in opposition to the BDMA (Heather
et al., 2018).
Fenton and Wiers (2017) correctly identify the BDMA as
actually consisting of a cluster of empirical hypotheses and that,
given the evidence at hand, the jury should still be out on all
of them. Their take is that, at the moment, evidence seems
to point that the full BDMA does apply to a small segment
of people with substance use problems, but that most within
this population fall short on what the BDMA seems to entail.
Although in broad agreement with the assessment of Fenton and
Wiers, we now present an alternative way of conceptualizing the
BDMA. We take the most constructive way of understanding
the BDMA not simply as (a set of) empirical hypotheses, but
as a strategic simplification—a heuristic reductionist hypothesis.
We will next show how the BDMA can be seen as a natural
consequence of applying a particular set of research heuristics
aimed at understanding complexity: first try to understand the
phenomena by treating it as a sum of the properties of its
parts and then learn about the role of context, organization and
interaction by looking at the specific ways in which this initial
simplifying hypothesis fails. The question of whether the BDMA
is “true” or “false” is therefore transformed into whether and
when it is false in an informative way.
We do not claim that this is what the proponents of the
BDMA have in mind (on the contrary, we take the proponents
to fully intend that the BDMA is the final scientific verdict on
the matter). Instead, we propose this as a forward-looking way
of repositioning the debate—one that also helps the opponents
of the model to appreciate more what has been learnt about
the constitution of agency in addiction by looking inside the
heads of individuals with addiction. Whereas, much of the
earlier criticism of the BDMA has concentrated on the agencydeleting aspect (the disease component), our conceptualization
additionally explicates the empirical and normative limitations
of the reductionist localization aspect of the model (the brain
component).
The concept of reductionist research heuristic is taken
from the work of philosopher of science William Wimsatt,
who has studied the epistemic strategies used for untangling
and understanding (especially biological) complexity (2007).
Although much of his work has been about explicating the
fallacies arising from reductionist hypotheses, he nevertheless
Frontiers in Sociology | www.frontiersin.org
1 Behavioral analytical perspectives on addiction utilizing economic reasoning (e.g.,
Rachlin, 2007; Ainslie, 2013) are a good example of a successful integration of
the neuroscientific, behavioral, and to a modest extent also social dimensions in
a tractable manner. Nevertheless, even these models and associated experimental
designs are subject to the reductionist fallacies delineated below. Furthermore, in
practice the picoeconomic models emphasizing the dopaminergic system end up
having much of the same problematic ethical implications as “standard” BDMA,
outlined in the latter sections.
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should first be looked for inside the individual agent and
any such inner difference-makers found should be regarded
as “the essence” of the behavior (Wimsatt, 2007, 348). Within
the individual, this suggests that addiction “boils down” into
a dysfunction of a specific subsystem, such as the hysteresis
of the dopamine system with its associated biomarkers. This
one true cause of the behavior is also taken to be particularly
“real” in being robustly physical. The immediate, and mistaken,
implication is that the most effective strategy for influencing
the phenomenon is to intervene on this inner essence. As Nora
Volkow has stated in an interview, “we will be treating addiction
as a disease, and that means with medicine.”2
The idea of an inner essence of addiction leads to default biases
in the explanation of related social problems and comorbidities:
if and when individuals with addictions exhibit a clustering of
different social and health problems, the default explanation is
that the inner essence is the common cause of these problems.
For example, the concurrence of heroin and amphetamine
use in many US cities is by default taken to result from the
common neurological vulnerability, rather than from the fact that
draconian anti-vagrancy laws force homeless individuals with
heroin-dependence to use amphetamines to stay awake and avoid
confrontation with the law—a structural cause (Langegger and
Koester, 2017).
A more subtle bias resulting from these localization steps is
the default assumption that all the relevant interactions respect
the agent-environment boundary (“interface determinism”)
(Wimsatt, 2007, 348). For example, the current integrated
neuroscientific model seems on the outset to take into
account many context sensitive aspects of addictive behavior
by emphasizing, e.g., the neurological basis of skewed incentive
salience and cue reactivity (Jasinska et al., 2014) and the
importance of environmental stressors in compromising topdown executive control in terms of physiologically measurable
changes in cortical connectivity and the amygdala (Kwako and
Koob, 2017). What falls beyond this localization is that agency
itself is distributed into the wider social context and that agencyundermining vulnerabilities can arise directly from changes in
these social relations (see e.g., Anderson, 2017). For example
the draconian anti-vagrancy laws that ban loitering in public
and thus deprive the individual basic human rights of homeless
people to be able to rest (Langegger and Koester, 2017). This
turns into a vicious circle for such vulnerable individuals, as
their attempts to reduce the need to rest with meth they further
dispose themselves to other agency-undermining vulnerabilities,
e.g., sleep deprivation.
Localizing the problem to be within the agent leads one to
ignore or downplay observations of historical and interactional
patterns. If addiction is a chronic brain disease, then all
information about the etiology of the condition is screened-off
by the resultant changes in brain functioning, i.e., knowledge
of the history of the addictive behavior is relevant only to the
extent that it helps in diagnosing what is wrong with the agent
(or her brain) here and now. This rules out the possibility that the
being exclusively caused by “abnormalities” or ”dysfunctions”
in specific brain systems, caused in turn by continuous
substance use (Vrecko, 2010). The main locus of addictionwithin-the-brain has long been thought to be the mid-brain
dopaminergic system realizing a reward-based reinforcement
learning mechanism (for criticism, see Nutt et al., 2015), but the
current picture now includes other systems and functionalities as
key components of addictive behavior (for a review see Volkow
and Morales, 2015, Koob and Volkow, 2016). Functional and
physiological correlates for compromised top-down executive
control, skewed cue salience, and reduced ability to handle
stress and anxiety, now figure prominently in the neuroscientific
understanding of addiction (Koob and Volkow, 2016). These
empirical advances show that the reductionist strategies have
proven powerful in disentangling the complex organization
within the inner mechanisms regulating our behavior; the
empirically exposed limitations of the original “reward-system”
model of addiction, localizing addiction to the mid-brain
dopaminergic system, have provided opportunities to learn
piecemeal lessons about the role of other systems, such as the
consequences of the deterioration in the handling of internal and
external stressors. Nevertheless, even the current model is clearly
“incomplete” in not yet including neural mechanisms responsible
for, for example, false beliefs induced by motivated reasoning or
representations of long-term goals. Note that this is not intended
as a criticism of the current model, since simply pointing out that
such things are important is not very constructive until we have
learned in what way they should be incorporated into the full
picture of the neurology of addiction.
Second, and much more problematically, BDMA
conceptualizes addiction as a stable property of the individual.
The locus of the problems in the alignment of short-term desires
and long-term goals, commitments to others, and the normative
and legal expectations of the society, is taken to be a specific
deficit in individual agency, caused by the use of a foreign
psychoactive substance or excessive engagement in an addictive
behavioral pattern, such as gambling. This second reductionist
localization hypothesis probably seems so obviously correct to
the proponents of the brain disease model that its nature as a
drastic simplification is anything but transparent.
Nevertheless, we hold that also this second localization step is
also literally speaking false. Addiction is a phenomenon of selfcontrol and agency, and agency, as such, is also constituted by
the social relations we have with each other (e.g., Mackenzie and
Stoljar, 2000; see also Jennings, 2016; Enfield and Kockelman,
2017). Coherent and meaningful agency or autonomy, i.e., acting
according to our long term goals, reflectively endorsed beliefs and
self-identity, is possible and meaningful only with the help of
social scaffolding and socially distributed strategies of self-control
(Enfield, 2017, Stoljar, 2018), as well as of the socially provided
symbolic resources for envisioning possible alternative courses of
action and for constructing a narrative self, capable of holding
time-consistent plans and projects (McConnell, 2016).
The much criticized empirical shortcomings of the BDMA
are direct consequences of the predictable and, in a sense,
unavoidable biases of these reductionist simplifications. First,
BDMA suggests that explanations for puzzling social behavior
Frontiers in Sociology | www.frontiersin.org
2 Nora Volkow, interview by Jeneen Interlandi, “What Addicts Need” Newsweek
February 23, 2008.
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value or enjoy. Folk-psychological concepts are also ill-fitted to
handle “loss of control” that comes in degrees: we are either
in or not in control—our behavior is caused by our beliefs
and desires—or it is caused by something else entirely. Hence
the empirically suspect dichotomy between the “rational” or
volitional view of addiction as choice behavior and the agencydeleting view of the BDMA.
The tension between addiction and our folk-psychological
understanding of action is one of the key hurdles in constructing
an integrated and socially enriched empirical picture of
addiction. Our understanding of social interaction is, almost
by necessity, based on folk-psychological concepts, whereas the
neuroscientific picture of the drivers of addictive behavior does
not map neatly unto these concepts. We suggest that both
the empirical failures of the reductionist BDMA hypotheses as
well as the mismatches of folk-psychological accounts of action
and addictive behavior flag contact points between the biological
and the social in need of a new conceptualization. This should
be taken as the heuristic for building a sociologically and
neuroscientifically informed model of addiction. The empirical
failings also point to potentially informative foci for future
empirical research on the interaction between the biological
and the social: the possibly self-enforcing feedback between
changes in, say, cue salience or affective self-regulation, and
changes in the social relations or self-identity; comparison of
comorbidities across social contexts; comparison of life-histories
and current behavioral patterns within groups of subjects with
similar biomarkers associated with heavy use, to name a few. We
return to these tentative suggestions in the concluding remarks.
problematic behavior is, at least partly, due to the development
of behavioral patterns detrimental to agency (within a particular
social context), but which do not necessarily correspond to any
“pathological” changes in the brain. Heavy substance use is
often accompanied with ways of organizing one’s life and friends
facilitating the use, and it is often as hard to quit these as it
is to quit the consumption of the substance itself. In contrast,
many frameworks for understanding addiction not based on the
BDMA emphasize the systematic differences in the histories of
different kinds of problems of self-control, differences which are
very much relevant to whether treatment should be considered,
and what form this treatment should take. A prominent example
in the context of behavioral addictions is the “pathways model”—
typology of problem gamblers, which takes the history of the
problematic gaming behavior into account—with implications to
effective treatment (Blaszczynski and Nower, 2002).
The two localization steps also have pronounced effects
on the experimental designs used to study addictions. The
reductionist hypotheses imply a preference for experimental
designs with constant environmental variables and manipulation
of the intrinsic states of the subject, over designs in which
environmental variables are manipulated (Wimsatt, 2007, 349–
350). This makes the BDMA partly self-vindicating. The classic
paradigm of drug self-administration in rats is a good example of
this bias: controlling for the experimental environment produced
strongly biased results concerning the behavioral consequences
of self-administration, whereas as soon as the animals had
access to meaningful social interaction with their fellows, they
stopped “choosing” self-administration of even highly “addictive”
substances, such as cocaine or heroin (For instance Solinas
et al., 2008, see also Alexander et al., 1978, Alexander et al.,
1981). When talking about neuroscientific experiments on
human subjects, it is, of course, prohibitively difficult to devise
meaningful designs which would not impose drastic controls on
the environment. It is simply not feasible to, for instance, scan the
subject’s brain across different social contexts of substance use.
Nor are we aware of studies correlating physiological changes in
the brain to substance use across different social contexts.3
Agency is also a folk-psychological concept: we are agents in
virtue of our behavior being conceptualized in terms of beliefs
and desires. By folk-psychology (or common-sense psychology)
we refer to the set of more-or-less automatic capacities and
practices used to interpret and predict the behavior of others
and ourselves in terms of internal “mental states” like beliefs and
desires (Stich and Ravenscroft, 1994). One of the main reasons for
the endless controversies in theorizing addiction is that addictive
behavior does not fit neatly into this folk-psychological template
for understanding human behavior. One of the key insights
into addiction, based partly on the neuroscientific picture of
the reward system, has been that addictions really do decouple
wanting from liking: individuals with addictions can be, at least
momentarily, motivated to pursue goals that they do not really
VULNERABILITY AND AGENCY
We will now move from the purely empirical to more
normatively laden implications of the two reductionist
hypotheses by looking at how they mold the way in which
individuals’ vulnerability in addiction is conceived as one of the
important reasons for prevention and treatment. Vulnerabilities
in addiction are typically connected to various aspects of drug
use and its induced pathologies of the brain (see e.g., NIDA.,
2014), but what exactly does this vulnerability amount to? In the
psychological literature on psychopathology, there seems to be
no general agreement (see e.g., Ingram and Price, 2010) on how
to define vulnerability. Yet, a significant corpus of knowledge
exists, as researchers are taken to “already know vulnerability
when they see it,” and to also be able to identify groups of
vulnerable people using mainly pre-theoretic criteria (Ingram
and Price, 2010, 5, for discussion on the concept of vulnerability
in bioethics, see Rogers et al., 2012; ten Have, 2016). We now
question the view that vulnerabilities in addiction can always
be traced down to brain pathology, as the BDMA seems to
suggest. We argue that the reductionist fallacies localizing agency
inside individuals and unto particular neuronal populations
have pernicious effects on the identification and treatment of
substance-related vulnerabilities.
To give some idea of how the BDMA shapes the conception
of vulnerability, let us review the ways in which two leading
3 For example, Siegel (2001) reviews experiments studying contextual effects (the
presence of cues previously paired with the substance) on the physiological effects
of a substance on rats. We acknowledge the difficulties in translating such designs
to humans.
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2014; ten Have, 2016; Straehle, 2017): all living organisms are
vulnerable in the sense that they are finite and fragile to many
forces. Psychoactive substances, by definition, are substances
that bring about reactions in the brain and the human brain
is therefore inherently susceptible to these kinds of substances.
Of course, the intoxication that, say, a suitable dose of opiates
brings about in humans may vary from individual to individual,
but all human beings become intoxicated after consuming
enough opiates. In the same vein, long-term use results in
changes in the brain and again there is individual variation.
These susceptibilities and changes nevertheless, as such, do not
necessarily result in individual harm with the same inevitability
as neuronal degeneration in Parkinson’s disease, for instance.
Human brain’s susceptibility to psychoactive substances is
therefore a fact that need not be normatively loaded, as it does
not in and of itself entail positive or negative outcomes of
the use of these substances. In this light, susceptibility of the
brain to psychoactive substances does not, as such, constitute
a threat to human agency: Our brains react to psychoactives
in different ways, depending, partly, on our genetic make-up,
the constitution of the substance, dose, and the circumstances
in which the anticipated reaction takes place. By consuming
psychoactive substances, we are able to intervene and modify the
(dys)functioning brain. Opioids take away pain, sedatives relieve
anxiety, and stimulants help us to stay focused and alert, and the
context partly determines whether those pharmacological effects
on human agency result in such desired outcomes. Of course,
medical use of psychoactive substances is not and has not been
the only purpose of these substances. Be it for a shaman or a
raver, psychoactive drugs have also been used as enhancing some
desired traits, sources of feeling pleasure and for reaching altered
states of consciousness (Goodman et al., 2007) These purposes
typically involve different people in different social and cultural
circumstances.
If all consumption of psychoactive substances leaves a mark
on the brain, research on mere use, and the marks that this
use leaves on the brain, does not suffice for something to be
identified as an addiction, as not all people lose control over their
drug use, even when the use is frequent and heavy. For instance,
many chronic pain patients could qualify for this group. They
consume opioids for their pain, and this, as such, does not make
them individuals who suffer from addiction—even if they are
physically (and even psychologically) dependent on the substance
that they are using. Their prescription is typically such that it does
not (further) undermine the agent’s ability to act in ways in which
they see best in the light of their identity and long-term goals.
Yet Rehm et al. (2013) have argued that the very fact that current
neuroscientific studies cannot reliably differentiate between truly
addicted individuals and heavy users (because all the subjects
used in the studies have had a long history of substance affecting
the brain) as reason to doubt the scientific or even clinical
meaningfulness of the distinction. Nevertheless, there seem to be
populations of heavy user that do not have the kinds of problems
true addiction is likely to bring about (see e.g., Van der Pol
et al., 2013). Epidemiological studies show that vulnerabilities
are dependent on many demographic, social and historical
variables (e.g., Van der Pol et al., 2015). Insofar as addiction is
figures in the BDMA camp—Koob and Volkow (2016)—use the
concept in several points in their review of the neurobiology
of addiction. We take this authoritative review to exemplify
ways in which vulnerability can be unreflectively localized to
different levels of organization—unless due care is taken to keep
in mind that such localizations are not really valid outside their
heuristic use. Koob and Volkow discuss “initial vulnerability”
of transduction and transcription factors in addiction-relevant
neurocircuitry (Koob and Volkow, 2016, 760) and “molecular
basis of vulnerability to relapse” (Koob and Volkow, 2016,
767) not only on neurobiological level, but also on that of the
individual, where these vulnerabilities are directly translated into
individuals subjected to “greater vulnerability” to addiction and
“vulnerability to relapse” (Koob and Volkow, 2016, 761). In
using the concept of vulnerability, the article bundles up many
levels of explanation: it discusses “genetic and environmental
vulnerability to addiction” (Koob and Volkow, 2016, 766), and
“[genetic] vulnerability in the human population” (Koob and
Volkow, 2016, 768), but also “vulnerability for drug and alcohol
use disorder” (768), and more generally “vulnerability to drug
use and relapse” (Koob and Volkow, 2016, 768). The authors
do not limit their interest to strictly endogenous features and
are also interested in environmental factors, but only insofar as
they contribute to “resilience against vulnerability” (Koob and
Volkow, 2016, 761) and to ways to “influence vulnerability to the
development and perpetuation of addiction” (Koob and Volkow,
2016, 764). They claim to do so by identifying features that
contribute “to an individual’s vulnerability to addiction” (Koob
and Volkow, 2016, 766). Vulnerability is therefore attributed
to everything from genes and brain-chemistry to persons and
populations. Is it really the same notion or does the meaning
vary from use on one level to use in another? Purely descriptive
notions relying on statistics and biochemical mechanisms differ
in an important sense from notions that refer to socially
meaningful action. From a normative perspective, it arguably
matters whether we are discussing vulnerability on the level of
the population, the individual or that of genes and molecules.
Vulnerability as susceptibility on a genetic and molecular
levels is constituted and modified by a range of different
predispositions and modifiers, which are often multifactorial.
Although detailed analyses of the molecular and genetic
susceptibilities are beyond the scope of our paper, what needs
to be emphasized is that the relation of these descriptive
sub-personal attributes to the normative sphere of individual
action regarding substance use is anything but straightforward.
According to Ingram and Price, 2010, the core features of
psychopathological vulnerability include that it is a stable trait,
endogenous and latent in nature, and that stress has a role in
“actualizing vulnerability” (Ingram and Price, 2010, 6). What
is noteworthy about this is that it, first, firmly locates the
vulnerability within the individual. It is a property of the
agent in question. Second, the “actualization” of vulnerability
implies a deviation from the agent’s normal functioning. Third,
vulnerability is a matter of degree: one can be more or less
vulnerable due to changes in brain chemistry. This third point
can be traced back to a point much discussed in the bioethical
literature on vulnerability (see discussion e.g., Mackenzie et al.,
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the prevailing prescription practices and the heavy promotion
of drugs and the active suppression of concerns about overprescription by the pharmaceutical industry certainly played a
key role (Manchikanti et al., 2010; Fischer et al., 2014; Global
Commission on Drug Policy, 2017a), 3) has released a position
paper in which they state that most addictions in the US opioid
crisis start with “diverted supplies rather than among pain
patients.” Most prescription opioid users fail to develop addiction
(furthermore, heroin, not prescription opioids, has now become
the most common first opioid). These facts suggest that an
exclusive focus on the direct pharmacological effects of the drugs
falls short of explaining the crisis (Dasgupta et al., 2018 and
Rigg et al., 2018 review institutional and socioeconomic factors
explaining geographical heterogeneity in the opioid epidemic).
Nevertheless, when weighing in on the crisis in a recent comment
in The Lancet, Volkow emphasized the importance of the access
to treatment and that “medications are the gold standard of
treatment for opioid use disorder” (Volkow, 2018, 285). For
her, the answer to the epidemic seems to lie not in figuring
out why so many people suddenly engage in patterns of opioid
use deleterious to their health and autonomy, but in therapy
making use of medication “allowing the patient’s brain to heal”
(cf. Volkow, 2018, 285).4
In sum, the BDMA seems to flirt with an unfair description
of vulnerabilities in its conflation of the levels of explanation
and in lumping together the different kinds of vulnerabilities
that are in play in addiction. The kind of vulnerability we
should be interested in here is embedded in normativity, as it
concerns the agency of individuals with addiction. The reason
we are concerned with certain behavioral patterns partially
resulting from the use of psychoactive substances is the associated
loss of control, impaired agency. But agency is not situated
within the brain, or even within the individual. Agency is more
than merely the competencies and psychological states of the
individual: it is also constituted by the individuals’ interactions
with their social and material environment (e.g., Enfield and
Kockelman, 2017). Agency, especially pathological agency, is
a normative concept and, as such, is socially constituted. We
are in control of our own behavior not in virtue of having
the right sort of psychological processes causing the behavior,
but in virtue of our behavior being appropriately responsive
to reasons and incentives in our social environment. We form
intentions about future actions and hold on to them unless
a right kind of reason requires us to adjust the intentions
(see Holton, 2009). When we are considering vulnerabilities
in addiction, we should be considering the susceptibility
of this socially upheld responsiveness to reasons to all the
consequences of the practices of using psychoactive substances,
not merely the susceptibility of the brain to the substances
themselves.
not automatically developed simply after a certain amount of
drug use, it could be the case that long-term effects differ in
non-addicted heavy drug users and addicted drug users. Some
animal models seem to suggest interesting differences between
individuals subjected to heavy use in terms of “compulsive
drug consumption that occurs in spite of adverse consequences”
(Volkow and Morales, 2015, 715). However, care should be taken
in extrapolating these model findings to human agency in that the
“adverse consequences” in the form of immediately administered
electric shocks are something altogether different than long term
problems in the (lack of) control of one’s life (Ahmed, 2018).
Willingness to undergo pain for an expected reward hardly tells
us inevitably about loss of control.
Nonetheless, most of the neuroscientific science evidence rests
on changes in the brain processes of chronic drug users. But
one can be physically and psychologically dependent on things
that are beneficial for one’s identity and long term goals, like
chronic pain patients. The concept of vulnerability should also
be seen in this broader normative context, not just in terms of
physical susceptibility: it implies that in certain circumstances,
the population or the individual are in an increased, or even
likely, danger of being harmed and wronged (see Hurst, 2008;
Martin et al., 2014). Insofar as the susceptibility and dependency
to psychoactive substances actualizes the descriptive vulnerability
of individuals and their constitution, it as such does not
suffice for automatically amounting to problematic behavior and
suffering.
There are no neuroscientific studies (that we know of)
comparing the physiological or functional differences between
people with heavy substance use patterns and people with
addictions. However, we do not take this to be an argument
against the distinction. In contrast, we surmise that the very
absence of such studies is itself a consequence of a reductionist
bias, localization of a systemic function (self-control required for
full-blown autonomous agency) to a single neuronal subsystem
directly affected by the substance. Yet it is arguably the
individual’s self-endorsed agency and the vulnerabilities related
to it that matter normatively, rather than the ever-present subagentive biochemical susceptibility to substances per se. We
would therefore, contrary to Rehm et al. (2013), like to see
future neuroscience of addiction take the distinction between
heavy use and addiction more seriously. This may present quite
a challenge to research. Insofar as the research is conducted with
animal models, the distinction between heavy use and addiction
on the basis of self-control may understandably be difficult to
operationalize (these are the same challenges that are discussed in
research on decision-making and problem gambling with animal
studies, see Ahmed, 2018).
We definitely do not intend to downplay the causal role of
the psychoactive substance, however. One could, for example,
bring up the increasing problematic opioid use in the US, the
opioid epidemic (Global Commission on Drug Policy, 2017b; US
Department of Health Humanities Services (HHS), 2018). The
mere fact that the number of people who develop problematic
opioid use in the US is increasing does not, of course, by itself
imply that the only cause of this increase is the drug and its
effects in the brain and that no other factor plays a role. Although
Frontiers in Sociology | www.frontiersin.org
4 Very
much in line with this statement, NIDA is also part of the NIH HEAL
Initiative seeking answers to the opioid crisis on two fronts: improving medicationassisted treatment and researching alternative resources for pain management
(https://www.nih.gov/research-training/medical-research-initiatives/healinitiative). Again, this reflects a very individualistic understanding of the epidemic;
a brain disease caused by opioids originally taken as pain killers.
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REFLECTIONS ON THE ETHICAL
IMPLICATIONS FOR PRACTICE
the risk of more and more individuals failing to identify with
the symptoms. Consequently, the chances of early prevention
and treatment may decrease due to this non-identification with
the BDMA. It may even raise the threshold for seeking help, as
individuals do not consider their state severe enough to seek help.
In the worst scenario they may choose not to seek help at all,
as they reject the idea that they are suffering from an agencydeleting disease of the brain, the treatment of which takes place
in psychiatric wards. These issues matter on individual as well
as on public health scale. People’s willingness to seek help may
also depend on the kind of place in which the service is offered
(see Lagisetty et al., 2017). The same kind of advice and help
may be easier to accept for instance in a safe injection site than
in medical facility, even if the personnel have the same training.
Vulnerability that one may experience in losing control over one’s
drug consumption involves feelings of shame (see e.g., Wiechelt,
2007). These kinds of states are likely to make the individual
with addiction even more vulnerable and further complicate
addressing the problem and seeking help.
A question can be raised whether BDMA, in its current
formulation, creates unfair circumstances to individuals
with addiction: Not only does it highlight the automatic
aspects of human behavior and thus runs the risk of eating
away the agency of individuals with addictions, but also
seems complicate access to help by raising the threshold
of what constitutes addiction and by labeling it in a way
that may results in individuals not identifying with the
condition.
Assumptions within the BDMA have ethical implications on
the society and stakeholders, especially for individuals with
addictions. When the reductionist hypotheses are bundled
together, the individual is deprived of full agency. As Pickard
(2013) points out, it is challenging to form effective intentions
if one does not believe one is capable of executing those
intentions to begin with. Like the rest of us, people with problems
in controlling their substance use have a folk-psychological
understanding of their own agency and they may well experience
frustration and confusion about their own actions. It may be
difficult to understand why they fail to act in ways they regard as
better and explain why they continue to act in ways in which they
know to have grave consequences. In this light, it is reasonable
that they may come to question their agential competence, their
efficacy for desired action. On the first blush, BDMA may sound
like a plausible solution, as it offers a compelling explanation for
this behavior: the drug has “hijacked” the brain. This solution,
however, seems to come with a high price as motivation has been
identified as a key factor in recovery in addiction (see e.g., Sayegh
et al., 2017) and the BDMA implies that the agent’s efficacy is
lacking. Moreover, the BDMA implies that agency is impaired in
a stable manner, grounded in uncontestable physiological reality.
Consequently, an individual with addiction seeking help may
find it impossible to be motivated and form intentions of acting
contra-addiction due to BDMA-informed beliefs about his or her
condition. Their self-efficacy is likely be low to begin with and this
kind of further “evidence” may run the risk that their beliefs are
further confirmed. Depriving agency will also reduce “positive
stigma,” i.e., the normative expectations of others, crucial for the
social constitution of long-term agency. Some studies suggest
that a biological disease-conceptualization of addiction actually
increases the social distance kept by other people to those with
addiction (Satel and Lillenfield, 2014). If we are not treated as
responsive to reasons and incentives by our fellows, we lose a
key resource for actually doing so. We can therefore argue that
the picture portrayed by the BDMA’s reductionist view questions
the agency of individuals with addiction on a very fundamental
level and thus amounts to a violation of one of the main ethical
principles in biomedicine, namely the principle of respect for
autonomy (e.g., Beauchamp and Childress, 2001).
It seems clear that if we took the vocal proponents of the
BDMA seriously and applied the model to all cases of problematic
substance use, we would end up misdescribing a great number
of substance abusers and misusers. To be clear, this is not
what happens in the practice of prevention and treatment.
Nevertheless, it could still be argued that BDMA in its severe
form applies to a sub-population and that these individuals are,
in fact, beyond non-medical help. These individuals may find
it comforting to understand why they persistently fail to act in
ways they would like to and keep on acting in ways in which
they accept to have detrimental consequences for them and
others. Narrowing down the population regarded as “addicted”
may generate yet another problem for prevention and treatment,
however. As the severity of the condition is highlighted, it runs
Frontiers in Sociology | www.frontiersin.org
CONCLUDING REMARKS: TOWARD A
MORE SUSTAINABLE
NEUROSCIENTIFICALLY INFORMED
PICTURE OF ADDICTION
Nobody denies that addiction involves changes in the brain—any
significant behavioral change probably involves alterations in the
brain—and that, in the case of substance addictions, substance
use is one important cause of these changes. The challenge is
to articulate how these changes in the brain affect, and are also
partially caused by, changes in the socially constituted guidance
of our behavior in the light of our long-term projects and goals,
i.e., agency. According to our proposal, we should look for the
empirical shortcomings of the reductionist hypotheses implied
by the BDMA for lessons about the persistent problems in selfcontrol related to the use of psychoactive substances—something
over and above the truism that these problems are complex,
contextual and socially embedded.
A socially embedded neuroscientific picture of addiction
should recognize that the contrast between choice and disease
is a false dichotomy. Individuals with addictions do respond
to incentives and, in fact, the current integrated neuroscientific
model (e.g., Koob and Volkow, 2016) already points to the ways
in which environmental and inner factors skew decisions toward
substance use even when other considerations speak against it.
The ways in which addictive substances link environmental cues
to motivational states (skewed incentive salience), reduce the
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Kuorikoski and Uusitalo
Re-socializing the Vulnerable Brain
efficacy of representations of long-term goals (executive control),
compromise affective self-regulation and increase the role of
stress function all point ways in which the folk-psychological
template of action should be enriched and modified in the context
of use of psychoactive substances.
But most importantly, a neuroscientifically informed model of
addiction should not localize agency itself to be a property of the
brain. Agency is not a homunculus inside our skulls, waiting to
be hijacked by devious substances. We control our own conduct
not only by “sheer willpower,” but, perhaps more importantly,
by also making commitments to others, by modifying our lived
environment so as to make certain courses of actions more
“costly” than others, and by re-writing the narratives that define
who we are.
Consequently, whereas the BDMA conceptualizes the inner
essence of addiction as the primary target of pharmacological and
other medical interventions, such as Deep Brain Stimulation (for
a review on neuromodulation in treating addictions see Bari et al.,
2018), a socially integrated brain perspective would conceptualize
medication as a possible additional resource in reorienting and
reconstituting socially distributed agency. There is a fundamental
difference in conceptualizing medication as restoring “a healthy
brain,” and using psychoactive substances to manage oneself and
one’s life, so as to facilitate the creation and pursuit of meaningful
long-term goals. This broader understanding of “medication”
could therefore also remove some of the moralistic skepticism
regarding the therapeutic use of the addicting substance itself
in helping to regain control of one’s life (such as heroin-assisted
treatment, see Ferri et al., 2012).
In the end, even when one regards the advances in
the neuroscience of addiction as greatly contributing to
our understanding of not only addiction, but also to our
understanding of the motivational architecture and self-control
in general, the empirical shortcomings and the practical and
ethical costs of the brain disease model of addiction should
force us to reconsider the usefulness of the notion. Addiction
is certainly not a disease of the brain in the same sense
as neurodegenerative diseases are. As addiction as a social
phenomenon is affected by the self-understanding of the
people involved (i.e., via the “looping effect”), the concept of
a brain disease, no matter how well-informed and nuanced,
may be too liable for harmful public misunderstandings as to
warrant scientific or administrative usage. An empirically and
ethically viable neuroscientific picture of addiction should not
conceptualize addiction neither as a biological disease nor as
localized in the brain. An ethically sustainable neuroscientific
picture should focus on tractable (piecemeal) models of the
interaction (feedback) between the cognitive, affective, and
motivational changes brought about by substance use and
the lived social environment, and treat cognitive and affective
processes within the individual only as one resource among many
in the constitution of personal autonomy.
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All authors listed have made a substantial, direct and intellectual
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ACKNOWLEDGMENTS
This research has been supported by the Academy of Finland
(project 301689), part of the INSOSCI consortium, ERA-NET
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Conflict of Interest Statement: The authors declare that the research was
conducted in the absence of any commercial or financial relationships that could
be construed as a potential conflict of interest.
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