If Addiction is not Best Conceptualized a Brain Disease, then What

ORIGINAL PAPER

If Addiction is not Best Conceptualized a Brain Disease,

then What Kind of Disease is it?

Sally L. Satel & Scott O. Lilienfeld

Received: 10 August 2016 /Accepted: 22 August 2016

Springer Science+Business Media Dordrecht 2016

Abstract A modest opposition t o the brain dis ease

concept of addiction has been mounting for at least the

last decade. Despite the good intentions behind the brain

disease rhetoric – to secure more biomedical funding for

addiction, to combat Bstigma,^ and to soften criminal

approaches – the very concept of addiction as a brain

disease is deeply conceptually confused. We question

whether Lewis goes far enough in his challenge, robust

as it is, of the brain disease concept. For one thing, the

notion that addiction is a disease (especially within the

behavioral realm) is challenging to refute or confirm

because the disease concept itself is poorly defined in

medical and psychological nosology. More important,

quibbling over what kind of disease addiction is unlikely

to be productive. The rational response to adjudicating

whether addiction is a brain disease is not to engage in

potentially fruitless debates over the question of disease

classification but rather to view addiction as an enor-

mously complex set of behaviors that operate on several

dimensions, ranging from molecular function and

structure and brain physiology to psychology, the psy-

chosocial environment, and social and cultural relations.

Keywords Addiction

Brain disease

Reductionism

Levels of analysis

National Institute on Drug Abuse

Neurocentrism

Philosophy of medicine

Over-

medicalization

What is a Disease?

In his thought-provoking essay, Lewis makes the case

that addiction is not a brain disease because it can be

overcome as a result of willpower, changing perspec-

tives, changing environments, mindfulness, or emotion-

al growth. Although we are sympathetic to many of

Lewis’s arguments, we part ways with him in several

respects.

Lewis, like most participants on both sides of this

ongoing debate, appears to assume that the question of

whether a given condition, in this case the condition of

addiction, is or is not a Bdisease^ is scientifically an-

swerable. This assumption causes Lewis (and his cham-

pions and critics alike) to neglect a basic point: the very

question of what constitutes a disease entity in psychi-

atry, and in other domains of medicine, is largely or

entirely unresolved. Philosophers of medicine have long

debated, and continue to debate, the criteria used to

adjudicate whether a given condition is a disease. They

have advanced various criteria, including statistical rar-

ity, degree of social impairment, patient’sordoctor’s

perceived need for treatment, biological dysfunction,

Neuroethics

DOI 10.1007/s12152-016-9287-2

S. L. Satel

American Enterprise Institute, Washington DC, USA

S. L. Satel (*)

Yale University School of Medicine, New Haven, CT, USA

e-mail: slsatel@gmail.com

S. O. Lilienfeld

Samuel Candler Dobbs Professor of Psychology, Emory

University, Atlanta, GA, USA

e-mail: slilien@emory.edu

and decrea sed evolutionary fitness. Yet all of these

criteria have their serious shortcomings, and none ap-

pears to be sufficient to account for all conventional

diseases [1, 2]. Others in the field, such as Donald Klein

and Jerome Wakefield, have argued that disease is in-

stead a hybrid concept involving a conjunction of evo-

lutionary dysfunction (a breakdown in a naturally se-

lect ed system) and harm (distress or impairment in

everyday life), but this view, too, has its critics [3–5].

Still other authors have maintained that Bdisease,^ much

like many other concepts in nature (e.g., mountain,

continent, planet), is inherently a fuzzy, family-

resemblance concept that does not lend itself to a strict

definition [6, 7]. From this lattermost perspective, the

question of whether a given condition (e.g., addic-

tion) is t ruly a Bdisease^ is as scientifically unre-

solvable as the question of whether a given large

object orbiting the solar system (e.g., Pluto, Ceres)

is truly a Bplanet^ [8]. Although we do not intend to

resolve this knotty conceptual controversy here, suf-

fice it to say that before one can decide whether a

given set of behaviors constitutes a brain disease,

one must first decide whether it constitutes a dis-

ease. At present, it is not at all clear that this issue

can be resolved strictly by means of scientific data.

If not a Disease, then What?

The rational response to adjudicating whether addiction

is a brain disease, we believe, is not to engage in poten-

tially fruitless debates over the question of disease clas-

sification but rather to view addiction as a complex set

of behaviors that operates on several dimensions, rang-

ing from molecular function and structure and brain

physiology to psychology, the psychosocial environ-

ment, and social relations [6]. Given the myriad concep-

tual ambiguities associated with the disease concept, we

are concerned here with the more pressing and arguably

more important question of whether addiction is best

construed as a brain disease.

Addiction is typically associated with brain changes,

to be sure, but in contrast to conventional brain pathol-

ogies, such as Alzheimer’s disease, those alterations

rarely if ever preclude individuals’ capacity to alter their

behavior based on foreseeable consequences. The term

Bbrain disease,^ which in most cases implies a lack of

control over behavior, obscures that crucial distinction.

Moreover, although severe addictions are partly rooted

in genetic predispositions that are themselves manifest-

ed in brain functioning, these conditions can be profit-

ably understood at multiple levels of analysis (e.g.,

psychological, social, cultural) in addition to the neural

level.

These dimensions are best organized not as a sim-

plistic reductionist scheme arrayed hierarchically from

least complex to most, but rather as a side-by-side

arrangement in which each level is complex in its own

way. We imply no sense of a pinnacle, or ultimate frame

of analysis; the point is that each dimension plays a

distinctive explanatory role in addiction, with some

being more clinically or scientifically relevant than

others depending upon the question posed and the con-

text in play. We start with the neurobiological level,

which comprises the central nervous system, and most

prominently the brain and its constituent cells. Genes

help to direct neuronal development; neurons assemble

themselves into brain circuits. Information processing,

or computation, and neural network dynamics are next.

The subsequent dimension consists of conscious mental

states, such as thoughts, feelings, motives, perceptions,

knowledge, and intentions. Social and cultural spheres,

which play powerful roles in shaping our thoughts,

feelings, and behavior, occupy the next phases.

Problems arise when we ascribe too much importance

to only one dimension, as in the case of the brain disease

model and brain-based explanations, and not enough to

psychological or social ones. Psychiatrist Kenneth Kendler

warned of the hazards of Bfervent monism,^ that is, the

tendency to value one approach to human nature while

undere

mphasizing or neglecting others [9]. The heart of

what we term B neurocentrism^ is a particular brand of

fervent monism, one that prioritizes brain-based explana-

tions for human behavior above all others [10–12]. Just as

one obtains differing perspectives on the layout of a

sprawling city while ascending in a skyscraper’sglass

elevator , we can acquire different insights into human

behavior at different dimensions of analysis [13].

Consider a da Vinci painting It is an assemblage

of subatomic particles, but it is not merely an

assemblage of such particles. Conceptualizing it exclu-

sively at only the subatomic level misses critical aspects

of analysis, especially the level of the meaning afforded

by the nua nced higher-orde r i nteractions am ong

the features of the painting [14]. Philosopher Daniel

Dennett referred to this brand of eliminative

reductionism as “greedy reductionism,” because it ad-

vocates replacing one level of analysis with others rather

Satel S.L., Lilienfeld S.O.

than attempting to integrate them by constructing bridg-

ing laws across them [15, 16]. Psychologist Steven

Pink er has aptly argued for an alternative brand of

reductionism: “Good reductionism (also called hierar-

chical reductionism) consists not of replacing one field

of knowledge with another but of connecting or unify-

ing them” [17]. Such an ecumenical approach to addic-

tion would, in our view, would be far more fruitful than

the effort to conceptualize this enormously complex

behavioral condition by means of a single and inevitably

myopic lens.

The key to this approach is recognizing that some

explanations are more informative for certain purposes

than others. This principle is profoundly important in

therapeutic intervention. A scientist trying to develop a

medication for Parkinson’s disease will work within the

biological realm of the explanatory spectrum, perhaps

developing compounds aimed at boosting the activity of

dopamine in affected brain regions. In contrast, a psy-

chotherapist helping a distraught spouse who has recent-

ly undergone a divorce must focus on the psychological

realm of analysis. Efforts by this therapist to understand

the patient’s psychological pain by subjecting his or her

brain to an fMRI could be worse than useless because

doing so would draw attention away from his or her

thoughts, feelings, and assumptions about the world —

the domains in which intervention would be most

helpful.

Overemphasizing the neural dimension of analysis

when conceptualizing addiction impedes our progress in

treating and preventing it. This is because it distracts us

from considering users’ motives, their unappreciated, if

constrained, decision-making capacities, and their well-

documented abilities to respond to incentives, central

psychological factors in the theatre of addiction. Ironi-

cally, Lewis’ emphasis on the neurobiological dimen-

sions of addiction in his essay and in his 2011 book,

Memoirs of an Addicted Brain inadvertently reinforces

the notion that addiction is a brain disease. Although he

focuses on the Blearning^ aspects of addictive behavior,

an undeniably useful perspective on mechanism, the

story he tells is rendered almost exclusively in the lan-

guage of biology – the lingua franca of physical disease

[18]. As a consequence, we are doubtful that Lewis’

otherwise careful analysis will sway champions of the

brain disease model of addiction because it does not

explicitly address the value of levels of explanation

beyond the biological. To be fair, Lewis does present

textured patient vignettes in depth in his 2015 book, The

Biology of Desire, and he mines his own experience in

his 2013 book, Memoirs of an Addicted Brain.Indeed,

he attributes his own recovery to psychological

transformation.

To be sure, addiction can be explained in part accord-

ing to how it operates neurobiologically. Indeed, scien-

tists studying the role of dopamine transmission in rein-

forcement will, naturally, address themselves to to neu-

rophysiology. In this respect, arguably, addiction is in

part a pathological condition of the brain. At the same

time, however, it is every bit as much a personality

disease, a motivational disease, a social disease, a cul-

tural disease, and so on. Why privilege one aspect of

analysis above all of the others? On every one of those

dimensions we can find elemen ts that contribute to

excessive and repeated drug use. Understanding those

elements can lead to strategies that help individuals

bring their behavior under control.

The NIDA Misconception

Some background about the nature of the debate sur-

rounding the Bbrain disease^ formulation is in order. By

the mid-1990s, the longstanding truism Bonce an addict,

always an addict^

was reinvigorated and repackaged

th a neurocentric twist: BAddiction is a chronic and

relapsing brain disease^ [19]. This view was promoted

tirelessly by psych ologist Alan I. Leshner, then the

director of the National Institute on Drug Abuse

(NIDA), the nation’s premier addiction research body

and part of the National Institutes of Health. It is now the

dominant view of addiction in the scientific field [20].

The brain disease model is a staple of medical school

education and drug counselor training and even appears

in antidrug lectures given to high-school students [21,

22]. Rehab patients similarly learn that they have a

chronic brain disease. The American Society of Addic-

tion Medicine, the largest professional group of physi-

cians specializing in drug problems, calls addiction Ba

primary, chronic disease of brain reward, motivation,

memory and related circuitry^ [23]. Drug czars under

Presidents Bill Clinton, George W. Bush, and Barack

Obama have all endorsed the brain disease framework at

one time or another [24–26]. From being featured in a

major documentary on HBO, on talk shows and Law

and Order, and on the covers of Time and Newsweek,

the brain disease model has become dogma in most

What is Addiction?

quarters. Like all articles of faith, it is typically accepted

without question, as Lewis observes [24, 27–29].

A recent article in the New England Journal of

Medicine confirms that the brain disease formulation

is the government-approved narrative for addiction.

Three esteemed researchers, including NIDA head

Dr. Nora Volkow and National Institute on Alcohol

Abuse and Alcoholism chief Dr. George Koob, both

of whom work under the auspices of the National

Institutes of Health, wrote the article, entitled

BNeurobiologic advances from the brain disease

model of addiction.^ They laid out the neural path-

ways involved in various stages of drug abuse, such

as anticipation and craving, intoxication, and with-

drawal. It is a fine summary of the latest brain-based

findings.

They begin: In the past two decades, r esearch has

incr easingly supported the view that addiction is a dis-

ease of the brain.… the underlying concept of substance

abuse as a brain disease continues to be questioned,

perhaps because the aberrant, impulsive, and co mpul-

sive behaviors that are characteristic of addiction have

not been clearly tied to neurobiology [30].

As two vocal critics of the brain disease model, we

can attest to the fact that their interpretation is incorrect.

The brain disease model indeed Bcontinues to be

questioned^ by us and others, but not because the link-

ages between addiction and biological processes have

not always been clearly tied to neurobiology. Those

linkages, regardless of how detailed they are, demon-

strate only that the brain is somehow involved with drug

addiction. This assertion is merely a scientific truism

given that virtually all contemporary neuroscientists

agree that the mind is ultimately what the brain and rest

of the central nervous system do. The linkages between

brain and behavior do not, per se, make the case that

addiction is best conceptualized as a brain-based phe-

nomenon. Nor does the trivial fact tha t a da Vinci

painting is composed of subatomic particles implies that

it is best conceptualized as a subatomic phenomenon

that is most profitably analyzed by chemists and phys-

icists. Indeed, we fully expect more details about the

biology of addiction to be uncovered in the near future;

as important as they may be, such discoveries will not

make addiction any more a brain disease than it is – or is

not – at present.

Similarly, to contend that knowing about the brain in

addiction makes addiction a brain disease makes no

more sense than concluding that because we now know

more about the role of personality traits, such as neurot-

icism, in increasing risk for anxiety disorders, we can, at

last, recognize that anxiety disorders are purely disor-

ders of personality. The brain disease model captures

only one important part of a remarkably multilayered

causal story.

To be sure, addiction is associated with and contrib-

utes to brain changes. Individuals with such brain alter-

ations are sometimes less likely to make certain deci-

sions and find it more difficult to act on certain choices,

but those changes do not come close to eradicating the

capacity to choose. Volumes of research show that most

people who are addicted respond to incentives and

consequences, such as small cash payments, the oppor-

tunity to participate in work programs, or threats of an

overnight jail stay [31]. The implications for contingen-

cies, choice, and motivation in recovery are well

established [32, 33]. The data on the power of rewards

and sanctions in reducing drug use are potent evidence

that addiction is a set of behaviors that many, if not most,

users can control when consequences are foreseeable. In

contrast to many neurological illnesses, addiction thus

has an important voluntary dimension. In his writing,

Lewis makes the point that users indeed make choices,

and that some of these are self-destructive whereas

others are life-saving. He emphasizes that these positive

changes, like addiction itself, also represent a form of

learning. Imagine, by way of contrast, promising a re-

ward to people with amytrophic lateral sclerosis (Lou

Gehrig’s disease) if they could prevent their neurological

symptoms from worsening. That would be both pointless

and cruel because the kinds of brain changes intrinsic to

this illness leave sufferers resistant to rewards or penalties.

The same would hold for dementias, such as Alzheimer’s.

Hence, the oft-cited analogy between addiction and most

other neurological diseases does not hold.

e of the major shortcomings of the neurocentric

view of addiction is that it ignores the fact that people

use drugs and sustain their addiction because substances

temporarily quell their pain: persistent self-loathing,

anxiety, alienation, deep-seated intolerance of stress or

boredom, and pervasive loneliness. The brain disease

model is of little use here because it does not accommo-

date the emotional logic that triggers and sustai ns

addiction.

The brain disease model can also lead us to over-

value medication. As commonly conceptualized, this

model implies that addicts cannot stop using drugs until

their brain chemistry returns to normal, and it

Satel S.L., Lilienfeld S.O.

overemphasizes the value of brain-level solutions, such

as pharmace utical interventions. In 1997 , Leshn er

ranked the search for a medication to treat methamphet-

amine addiction as a Btop priority^ [33]. A decade later,

Volkow forecasted that BWe will be treating addiction as

a disease [by 2018], and that means with medicine^ [21,

29]. The search for a magic bullet is folly— and even

NIDA concedes that it has finally given up hope of

finding a wonder drug— but the brain-disease narrative

continues to inspire unrealistic goals and guide funding

priorities.

Methadone and buprenorphine, both opiate substi-

tutes, suppress withdrawal and craving and are thus

stabilizing for many patients. But rarely are medications

sufficient to change longstanding habits of behavior –

responding to psychic distress with other self-defeating

behavior, yielding to cue-induced craving – without

professional counseling or a self-imposed schedule of

self-binding. Self-binding refers to devising ways to

shield oneself from predictable provocation, to cope

with stress, and to maintain the motivation to do so.

Closing and Policy Implications

Lewis rightly views addiction as a learned behavior that

can also be unlearned. This visi on clashes with the

standard NIDA-approved brain disease model that fo-

cuses on Btissue damage,^ as Lewis puts it, and that

denies the capacity for choice making. We find Lewis’

insights to be valuable. At the same time, we believe that

a more explicit consideration of the alternative dimen-

sions of analysis would enrich his conceptualization of

addiction.

In his policy writings, Lewis recommends laissez-

faire policies for addicts (e.g., sanctioned drug distribu-

tion; decriminalization of minor drug-related crime). His

prescriptions reflect one way of seeing the addict: name-

ly, as a person who can make better choices in a different

environment and who does not require external control

or benign paternalism. We draw somewhat different

policy conclusions, however. We urge accountability

and applaud strategies that divert non-violent substance

abusers into contingency management programs with

the goal of achieving abstinence or responsible use of

opiate replacement medications. This course of recovery

will involve shifts in personal identity, social networks,

and values – dimensions that Lewis, too, rightly regards

as important.

The recent opiate epidemic in America has afforded

an opportunity to replay longstanding debates surround-

ing conceptualizations of drug addiction and the addict.

The major emphasis among public health officials and

addiction experts has been on opiate replacement be-

cause, as the standard narrative goes, addiction is a

Bbrain disease.^ We agree that medications can be useful

and in some cases even necessary – one of us works in a

methadone clinic – but they must not be emphasized at

the expense of the other dimensions of recovery that

take place on the psychological, social, and environ-

mental levels. A neurocentric view of addiction, which

Lewis’ analysis paradoxically reinforces despite his

overt rejection of the simplistic brain disease model,

can lead us into such a trap. Once the nature of choice

in addicti on i s better app reciated, the value of

employing contingency management and of modifying

expectations of user behavior becomes apparent.

Acknowledgments The a uthors would like to thank Mr.

Clayton Hale, research assistant at the American Enterprise Insti-

tute, for his astute technical and editorial help.

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