POINT
Addiction Is
a Choice
by Jeffrey A. Schaler, Ph.D.
Many activities that are not
themselves diseases can cause diseases, and a
foolish, self-destructive
activity is not necessarily a disease. When we
find a parallel between
physiological processes and mental or personality
processes, we can
mistakenly assume the physiological process is what is
really going on, and
the mental process is just a passive result of the
physical
process.
COUNTERPOINT
Addiction Is a Disease
by
John H. Halpern, M.D.
Addiction-as-disease or addiction-as-choice may
be better defined by
delineating initial experimentation with addictive drugs
from ongoing drug
use. Repeated exposure to addictive substances changes the
molecules and
neurochemistry of the addict. Addiction-as-disease accepts
the
responsibility of the health care professional to treat the patient
and
precludes the stigmatization that addiction is a
choice.
POINT
Addiction Is a Choice
by Jeffrey A.
Schaler, Ph.D.
Psychiatric Times October 2002 Vol. XIX
Issue 10
(Please see Counterpoint article by John H. Halpern,
M.D. below)
Is addiction a disease, or is it a choice? To think clearly
about this
question, we need to make a sharp distinction between an activity
and its
results. Many activities that are not themselves diseases can
cause
diseases. And a foolish, self-destructive activity is not necessarily
a
disease.
With those two vital points in mind, we observe a person
ingesting some
substance: alcohol, nicotine, cocaine or heroin. We have to
decide, not
whether this pattern of consumption causes disease nor whether it
is foolish
and self-destructive, but rather whether it is something
altogether distinct
and separate: Is this pattern of drug consumption itself
a disease?
Scientifically, the contention that addiction is a disease is
empirically
unsupported. Addiction is a behavior and thus clearly intended by
the
individual person. What is obvious to common sense has been corroborated
by
pertinent research for years (Table 1).
The person we call an
addict always monitors their rate of consumption in
relation to relevant
circumstances. For example, even in the most desperate,
chronic cases,
alcoholics never drink all the alcohol they can. They plan
ahead, carefully
nursing themselves back from the last drinking binge while
deliberately
preparing for the next one. This is not to say that their
conduct is wise,
simply that they are in control of what they are doing. Not
only is there no
evidence that they cannot moderate their drinking, there is
clear evidence
that they do so, rationally responding to incentives devised
by hospital
researchers. Again, the evidence supporting this assertion has
been known in
the scientific community for years (Table 2).
My book Addiction Is a
Choice was criticized in a recent review in a British
scholarly journal of
addiction studies because it states the obvious
(Davidson, 2001). According
to the reviewer, everyone in the addiction field
now knows that addiction is
a choice and not a disease, and I am, therefore,
"violently pushing against a
door which was opened decades ago." I'm
delighted to hear that addiction
specialists in Britain are so enlightened
and that there is no need for me to
argue my case over there.
In the United States, we have not made so much
progress. Why do some
persist, in the face of all reason and all evidence, in
pushing the disease
model as the best explanation for addiction?
I
conjecture that the answer lies in a fashionable conception of the
relation
between mind and body. There are several competing philosophical
theories
about that relation. Let us accept, for the sake of argument, the
most
extreme "materialist" theory: the psychophysical identity
theory.
Accordingly, every mental event corresponds to a physical event,
because it
is a physical event. The relation between mind and the relevant
parts of the
body is, therefore, like the relation between heat and molecular
motion:
They are precisely the same thing, observed in two different ways. As
it
happens, I find this view of the relation between mind and body
very
congenial.
However, I think it is often accompanied by a serious
misunderstanding: the
notion that when we find a parallel between
physiological processes and
mental or personality processes, the
physiological process is what is really
going on and the mental process is
just a passive result of the physical
process. What this overlooks is the
reality of downward causation, the
phenomenon in which an emergent property
of a system can govern the position
of elements within the system (Campbell,
1974; Sperry, 1969). Thus, the
complex, symmetrical, six-pointed design of a
snow crystal largely governs
the position of each molecule of ice in that
crystal.
Hence, there is no theoretical obstacle to acknowledging the
fact that
thoughts, desires, values and other mental phenomena can dominate
bodily
functions. Suppose that a man's mother dies, and he undergoes the
agonizing
trauma we call unbearable grief. There is no doubt that if we
examine this
man's bodily processes we will find many physical changes, among
them
changes in his blood and stomach chemistry. It would be clearly wrong to
say
that these bodily changes cause him to be grief-stricken. It would be
less
misleading to say that his being grief-stricken causes the bodily
changes,
but this is also not entirely accurate. His knowledge of his
mother's death
(interacting with his prior beliefs and values) causes his
grief, and his
grief has blood-sugar and gastric concomitants, among many
others.
There is no dispute that various substances cause physiological
changes in
the bodies of people who ingest them. There is also no dispute,
in
principle, that these physiological changes may themselves change
with
repeated doses, nor that these changes may be correlated with
subjective
mental states like reward or enjoyment.
I say "in
principle" because I suspect that people sometimes tend to run
away with
these supposed correlations. For example, changes in dopamine
levels have
often been hypothesized as an integral part of the
reward/reinforcement
process. Yet research shows that dopamine in the
nucleus accumbens does not
mediate primary or unconditioned food reward in
animals (Aberman and
Salamone, 1999; Nowend et al., 2001; Salamone et al.,
2001; Salamone et al.,
1997). According to Salamone, the theory that drugs
of abuse turn on a
natural reward system is simplistic and inaccurate:
"Dopamine in the nucleus
accumbens plays a role in the self-administration
of some drugs (i.e.,
stimulants), but certainly not all" (personal
communication, Nov. 26,
2001).
Garris et al. (1999) reached similar conclusions: "Dopamine may
therefore be
a neural substrate for novelty or reward expectation rather than
reward
itself." They concluded:
[T]here is no correlation between
continual bar pressing during
[intracranial self-stimulation] and increased
dopaminergic neurotransmission
in the nucleus accumbens.our results are
consistent with evidence that the
dopaminergic component is not associated
with the hedonistic or 'pleasure'
aspects of reward.Likewise, the rewarding
effects of cocaine do not require
dopamine; mice lacking the gene for the
dopamine transporter, a major target
of cocaine, will self-administer
cocaine. However, increased dopamine
neurotransmission in the nucleus
accumbens shell is seen when rats are
transiently exposed to a new
environment. The increase in extracellular
dopamine quickly returns to normal
levels and remains there during continued
exploration of the new
environment.dopamine release in the nucleus accumbens
is related to novelty,
predictability or some other aspects of the reward
process, rather than to
hedonism itself.
Perhaps, then, some people have been too ready to jump
to conclusions about
specific mechanisms. Be that as it may, chemical rewards
have no power to
compel--although this notion of compulsion may be a
cherished part of
clinicians' folklore. I am rewarded every time I eat
chocolate cake, but I
often eschew this reward because I feel I ought to
watch my weight.
Experience with addiction treatment must surely make us
even more dubious
about the theory that addiction is a disease. The most
popular way of
helping people manage their addictive behavior is Alcoholics
Anonymous (AA)
and its various 12-step offshoots. Many observers have
recognized the
essentially religious nature of AA. The U.S. courts are
increasingly
regarding AA as a religious activity. In United States v Seeger
(1965), the
U.S. Supreme Court stated that the test to be applied as to
whether a belief
is religious is to enquire whether that belief "occupies a
place in the life
of its possessor parallel to that filled by the orthodox
belief in God" in
religions more widely accepted in the United States. This
requirement is met
by members of AA and other secular programs that help
people with addictive
behaviors and encourage their members to turn their
will and lives over to
the care of a supreme being. What kind of disease is
this for which the best
available treatment is religion (Antze, 1987)?
Clinical applications are
based on explanations for why the behavior occurs.
An activity based on a
religious belief masquerading as a clinical form of
treatment tells us
something about what the activity really is--an ethical,
not medical,
problem in living.
What passes as clinical treatment for
addiction is psychotherapy, which
essentially consists of various forms of
conversation or rhetoric (Szasz,
1988). One person, the therapist, tries to
influence another person, the
patient, to change their values and behavior.
While the conversation called
therapy can be helpful, most of the
conversation that occurs in therapy
based on the disease model is potentially
harmful. This is because the
therapist misleads the patient into believing
something that is simply
untrue--that addiction is a disease, and, therefore,
addicts cannot control
their behavior. Preaching this falsehood to patients
may encourage them to
abandon any attempt to take responsibility for their
actions.
The treatment of drug effects, at the patient's request, is well
within the
domain of medicine, what passes as evidence for the theory that
addiction is
a disease is merely clinical folklore.
Dr. Schaler
teaches at American University's School of Public Affairs in
Washington,
D.C., and at Johns Hopkins University in Baltimore. Addiction is
a Choice
(Open Court Publishers, 2000) is among his published works
on
addiction.
References
Aberman JE, Salamone JD (1999), Nucleus accumbens dopamine depletions
make
rats more sensitive to high ratio requirements but do not impair
primary
food reinforcement. Neuroscience 92(2):545-552.
Antze P
(1987), Symbolic action in Alcoholics Anonymous. In: Constructive
Drinking:
Perspectives on Drink From Anthropology, Douglas M, ed. New York:
Cambridge
University Press, pp149-181.
Campbell DT (1974), 'Downward causation' in
hierarchically organized
biological systems. In: Studies in the Philosophy of
Biology: Reduction and
Related Problems, Ayala FJ, Dobzhansky T, eds. London:
Macmillan.
Davidson R (2001), Conspiracy, cults and choices. Addiction
Research &
Theory 9(1):92-92 [book review].
Garris PA, Kilpatrick
M, Bunin MA et al. (1999), Dissociation of dopamine
release in the nucleus
accumbens from intracranial self-stimulation.
Nature
398(6722):67-69.
Nowend KL, Arizzi M, Carlson BB, Salamone JD
(2001), D1 or D2 antagonism in
nucleus accumbens core or dorsomedial shell
suppresses lever pressing for
food but leads to compensatory increases in
chow consumption. Pharmacol
Biochem Behav 69(3-4):373-382.
Salamone
JD, Cousins MS, Snyder BJ (1997), Behavioral functions of nucleus
accumbens
dopamine: empirical and conceptual problems with the anhedonia
hypothesis.
Neurosci Biobehav Rev 21(3):341-359.
Salamone JD, Wisniecki A, Carlson
BB, Correa M (2001), Nucleus accumbens
dopamine depletions make animals
highly sensitive to high fixed ratio
requirements but do not impair primary
food reinforcement. Neuroscience
105(4):863-870.
Sperry W (1969), A
modified concept of consciousness. Psychol Rev
76(6):532-536.
Szasz TS
(1988), The Myth of Psychotherapy: Mental Healing as Religion,
Rhetoric, and
Repression. Syracuse, N.Y.: Syracuse University Press.
United States v
Seeger, 980 US 163
(1965).
COUNTERPOINT
Addiction Is a
Disease
by John H. Halpern, M.D.
Psychiatric Times October
2002 Vol. XIX Issue
10
----------------------------------------------------------------------------
----
(Please
see Point article by Jeffrey A. Schaler, Ph.D.)
The practice of medicine
obligates physicians to accept the responsibility
of promoting the overall
health of their patients. When dealing with
patients who abuse substances, we
can find direct and indirect adverse
consequences from such use. Lung cancer,
although rare in the general
population, is linked to chronic tobacco
smoking, for example. Cigarette
smokers who begin this addiction in their
teen years appear to have a higher
incidence of adult depression (Goodman and
Capitman, 2000); so, either early
tobacco use is a marker for later mental
illness or, more ominously, this
legal drug of abuse may promote the
development of mental illness. Multiple
warning labels describing tobacco's
toxicity and other risks to health have
been printed for decades on each pack
of cigarettes sold, yet more than 20%
of Americans continue to "choose" to
smoke (Centers for Disease Control and
Prevention [CDC], 2001). Despite the
hundreds of millions of dollars spent
in anti-tobacco messages and education,
the ever-increasing state and
federal "sin" taxes collected on every pack of
tobacco product sold, the
harsh restrictions on tobacco advertisements by
legislative mandate, and the
high-profile lawsuits and settlements, the
median prevalence figures of
current tobacco use in the United States have
held steady for the last five
years.
Perhaps, then, "choice" has
little to do with the decision to continue
tobacco use. Cigarette smokers are
so concerned about their drug use that
each year some 1 million of them
attempt to quit; but, sadly, less than 15%
succeed in abstinence for a full
year (Rose, 1996). Despite understanding
that risks outweigh perceived
benefits, addicted individuals compulsively
continue their drug use in a
chronic, relapsing fashion. It is not that
these individuals are devoid of
any choice when engaging in behaviors that
support and reinforce continued
drug use; rather, we must accept that not
all choices are equally easy to
make, especially when there exists a host of
genetic, environmental and
non-environmental factors supporting continued
drug use.
Clinical
research reveals that some individuals may be more vulnerable to
drug
dependence than others due to genetic and developmental risk factors.
The
best-validated risks are family history and male gender (Hyman,
2001).
Studies of separated, adopted twins, for example, have found the risk
for
alcoholism and other addictive drugs is greater for those twins
whose
biological parents also had drug dependence, regardless of drug use
status
in the adoptive parents (Cadoret et al., 1995; Kendler et al., 2000;
Tsuang
et al., 1996). Drug craving and relapse are triggered by exposure
to
drug-related cues (e.g., photos of drugs and paraphernalia), as well
as
stress. Neuroimaging studies of former cocaine-dependent individuals
have,
for example, identified neural correlates of cue-induced craving for
cocaine
(Childress et al., 1999; Wexler et al., 2001).
Preclinical
studies also indicate that repeated exposure to highly addictive
substances
alters, perhaps permanently, a number of molecular and
neurochemical indices,
thereby changing physiologic homeostasis. In other
words, even after
detoxification, an individual may be sensitized to relapse
because of changes
in the brain from prior repeated use. We know the
molecular targets in the
central nervous system for most of the addictive
drugs. As examples, opioids
are agonists at µ opioid receptors; alcohol is
an agonist at g-alphabutyric
acid-A (GABA-A) receptors and an antagonist
at -methyl-D-aspartate (NMDA)
glutamate receptors; and tobacco's nicotine is
an agonist at nicotinic
acetylcholine receptors (Hyman, 2001). We also know
that the principal CNS
pathway for processing reward, punishment and
reinforcement extends from the
ventral tegmental area (VTA) to the nucleus
accumbens (NAc), mediated, in
particular, by the release of the
neurotransmitter dopamine (Spanagel and
Weiss, 1999). Preclinical evidence
supports the "final common pathway" theory
that addictive drugs, despite
discordant molecular targets, all result in an
increased release and
dysregulation of synaptic dopamine in this region of
the brain (Nestler,
2001). For example, the same dose of cocaine administered
weekly to monkeys
results in increased extracellular release of dopamine in
the CNS, a
phenomenon called neurochemical sensitization. When a second dose
of cocaine
is administered after the first dose is wearing off, a decreased
release of
extracellular dopamine is found in the CNS, a phenomenon called
acute
tolerance (Bradberry, 2000). As tolerance builds, increased amounts of
the
drug are ingested in an attempt to achieve the same rewards, which, in
turn,
will also further drive molecular changes in the brain. Drug
dependence,
then, is reinforced at the cellular level as the CNS adjusts to
continued
drug exposure. Such conditioning may be unmasked by abrupt
cessation of drug
use, resulting in a period of observable and reproducible
symptoms of
withdrawal.
Chronic exposure to addictive substances also
shifts signal transduction
pathways within neurons, thereby altering gene
expression (Matsumoto et al.,
2001; Walton et al., 2001). New or different
concentrations of regulatory
proteins, in turn, are synthesized, directing
neurons to form new synaptic
branches and altered concentrations of cellular
receptor density. Cocaine,
for example, has been found to increase spine
density and dendritic
branching of neurons in the NAc and prefrontal cortex
of rats (Robinson and
Kolb, 1999). The remodeling of neurons involved with
the maintenance of the
brain's reward center also may continue long after
drug use has ceased
(Hyman and Malenka, 2001; Ungless et al., 2001). There
are probably hundreds
of transcription factors involved in gene regulation;
already the cyclic-AMP
response-element-binding protein (CREB) and FosB are
implicated in addiction
(Nestler, 2001). Interestingly, biochemically
modified isoforms of FosB
appear only slightly after acute drug exposure, but
they accumulate over
time with repeated drug administration. Other regulatory
proteins of the Fos
family rapidly break down after synthesis, but FosB is
highly stable,
persisting for months after drug withdrawal. Here, then, is
one example of a
molecular mechanism for drug-induced changes in gene
expression persisting
long after last use. Preclinical models reveal that
chronic, but not acute,
administration of cocaine, amphetamine,
phencyclidine, alcohol, nicotine and
opiates induces FosB release in the NAc
and dorsal striatum (Kelz and
Nestler, 2000).
In short, both human and
preclinical data converge to suggest that addiction
is associated with frank
biological abnormalities that cannot be easily
explained by a simple
hypothesis of "choice." It is a strange set of
societal circumstances that
people may still consider the ingestion of some
drugs as outside the purview
of physicians, when clearly the practice of
medicine deals with the impact of
exogenous substances upon the human body
and mind. Those individuals who
abuse drugs do so absent the legal
mechanisms for which society provides,
i.e., a prescription or
recommendation from a physician. Whether legal or
not, all addictive
substances should be carefully reviewed with our patients
precisely because
physicians must obtain all information that may assist in
the diagnosis and
treatment of disease and in the improved preventive health
of patients.
Drug dependence changes the lives of users and those around
them. Tobacco,
for example, is the single greatest cause of preventable death
in the United
States (CDC, 2001). Certainly, then, tobacco is a menace to
public health
and its continued popularity supports nicotine dependence as a
chronic,
relapsing disease in which volitional choice becomes but one
negotiable
variable in the struggle to achieve good health throughout the
life cycle.
Moral rejectionists mislabel drug dependence as a failure of
volition only
and, thereby, claim a right to assign judgment and blame. The
absurdity of
looking through such a narrow lens is that if addiction really
were merely a
choice, people would stop after experiencing more harm than
perceived
benefits!
Accepting drug dependence as another mental
illness does not typically
abrogate responsibility for an addict's actions:
Thousands each year are
arrested, prosecuted and sentenced to serve jail time
for simple drug
possession, and, as for mental illness in general, consider
that the two
psychiatric inpatient facilities in the United States in which
the largest
numbers of patients reside are the Los Angeles County Jail and
New York City
Rikers Island Prison (Geller, 2000; Torrey, 1999; Watson et
al., 2001).
Obviously, such individuals' moment-to-moment decision-making can
have
long-term consequences that were never wished for or accurately
anticipated.
Not all choices can be equally entertained at every given
moment either, and
sometimes other options are not even known. For example, a
young woman,
supporting herself and her drug habit through prostitution, may
not know of
the different "ethical" choices available to her, especially when
as a child
she had been introduced to both drugs and her career by her
mother's
example. The reasons for experimenting with addictive drugs, then,
may be
quite different from the motivations fueling continued use. Relapse is
not
due to an absolute loss of volitional control but rather to loss of
a
perspective that cherishes good health and mental well-being above
other,
less healthy choices. In high-risk situations, this long-term desire
for
maintaining better health through abstinence is overwhelmed by the cued
wish
to re-experience a known, anticipated "high" available at that
moment.
Stigmatization of illness continues against many patients
afflicted with
brain pathology. Substance dependence is particularly
stigmatized by those
who wish to make this illness a debate over volition
while denying the
biological underpinnings of behavior. Moreover, demands for
precise
linguistic definitions of addiction and disease, as if they must
forever be
hermetically sealed within specific denotations of legalese and
ethics, is
of little value to physicians charged with the observation and
treatment of
pathology. History reveals many examples of debates over illness
versus
individual responsibility: Hansen's disease ("leprosy" from
Mycobacterium
leprae), seizure disorders ("epilepsy"), cancer and major
depression are
some examples of medical disorders now vindicated with the
discovery of
effective medications and procedures. Physicians, and
psychiatrists in
particular, are needed now more than ever to stand up and
explain to the lay
public how substance abuse and dependence can
significantly alter brain
function and physical health and that a variety of
treatment modalities are
available.
Effective management of drug
dependence requires a medical model so as to
tailor therapy according to the
condition of the individual. Faith-based
support groups, Alcoholics Anonymous
and its affiliates, and long-term
residential programs have a long history of
assisting people in achieving
and maintaining abstinence via a combination of
direct therapy, education,
cognitive skill-building exercises, expanded
non-drug social supports and
providing a drug-free environment. Contingency
management skills can be
taught to provide individuals with extra time to
anticipate the high-risk
situations and emotions for relapse and then,
hopefully, re-script behavior
to minimize such exposures (Carroll et al.,
2001). This helps individuals
learn to avoid night clubs or other users
because such settings and people
may make the choice for continued abstinence
appear less valuable than the
immediate reward anticipated with
use.
Current pharmacotherapy for drug dependence includes screening for
an
underlying psychiatric condition after the patient has
successfully
completed detoxification. People may choose to self-medicate
with an
addictive drug, all the while unaware that they have a treatable
psychiatric
illness. For example, rates for alcoholism and other drug abuse
are much
higher in people with untreated bipolar disorder and depression.
For
motivated individuals, disulfiram (Antabuse) may particularly aid
in
maintaining sobriety from alcohol. Smoking tobacco while on
the
antidepressant buproprion (Zyban, Wellbutrin) is another aversive
treatment,
as the drug induces an undesirable taste when some smokers
relapse. Agonist
replacement medications assist with detoxification and/or
offer a stable,
safer maintenance therapy for those who repeatedly fail pure
abstinence
(e.g., methadone for opiate dependence, nicotine gum or patch for
tobacco
dependence). Many new medications are also in development including
more
opiate antagonists for the treatment of alcoholism and opiate dependence
and
NMDA antagonists such as acamprosate [Campral] for alcoholism (Tempesta
et
al., 2000). One day, perhaps there will even be a vaccine to confer
natural
immunity against cocaine (Schabacker et al., 2000). As Krystal et al.
(2001)
reported regarding the efficacy of naltrexone (ReVia), an opioid
antagonist,
in the treatment of alcoholism, sometimes medications do not
prove to be as
effective as promised. Evidence still suggests, however, that
naltrexone may
be quite effective if taken intermittently on the days that
the individual
feels at greater risk for relapse, rather than ingesting it
every day
(Boening et al., 2001).
Whether addiction is a disease or
merely a choice, the utility of the
medical model is needed to address
resultant risks to public and individual
health. A careful review of this
growing body of scientific literature
should offer hope that real solutions
are possible. All other models for
addressing drug dependence have, to date,
proven to be costly failures, and
doctors are not going to ignore viable
treatment options for healing those
suffering with drug dependence. Defining
addiction as a choice only
abdicates our responsibility for seeking health
and true healing for our
patients and, instead, leaves crushed lives
dehumanized by a chronic
relapsing condition with no hope for cure. As every
doctor knows, "Remember
to do some good" should quickly follow the first rule
to "do no harm."
Dr. Halpern is an instructor in psychiatry at
Harvard Medical School and on
staff at McLean Hospital and Brigham &
Women's Hospital. He is the recipient
of a Career Development Award (K23)
from the National Institute on Drug
Abuse for ongoing research at McLean
Hospital's Alcohol and Drug Abuse
Research
Center.
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