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Johnny Wilkinson's Addiction

Malcolm Horne
Philosophy, Psychiatry, & Psychology, Volume 17, Number 1,
March 2010, pp. 31-34 (Article)
Published by The Johns Hopkins University Press
DOI: 10.1353/ppp.0.0280

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Johnny Wilkinsons
Malcolm Horne

Keywords: addiction, choice, frontal lobes.

brief poll of my scientific colleagues

confirmed that, to a person, they regard
addiction as a disease, whereas most nonscience acquaintances consider it to be a failure of
willpower. Reconciliation of these polarized views
seems difficult and rather than finding a middle
path, such as suggested by Foddy and Savulescu.
I am an entrenched supporter of the view that
addiction can be a disease. I first should declare
my position as a card-carrying biologist, holding
the view that behavior emanates from the brain
and, accordingly, that behavior and emotions result from brain function. This brain function also
produces addiction and related behaviors, whereas
Foddy and Savulescu seem to credit humans with a
greater capacity to choose than biological evidence
suggests. The second problem relates to definitions
of disease: I argue that there are at least three ways
addiction might be considered a disease.

1. Addiction is a disease because it results in pathology. For example, hypertension is a disease. Hypertension per se does not cause dysfunction, but leads to
pathologically definable conditions such as stroke and
myocardial infarction. Smoking, like hypertension, can
result in pathologies such as emphysema and cancer.
The problem is not smoking per se, or even addiction
to nicotine, rather it is the consequent diseases caused
by tobacco. Nevertheless, if hypertension is a disease,
so is smoking. The question of choosing to persist
with smoking has no bearing on whether it is disease.
2010 by The Johns Hopkins University Press

Whether a person chooses to care for their hypertension

or ignore it does not alter the fact that they have hypertension; it is still a disease and it will still harm them.
Whether addiction affects the capacity to choose is not
relevant because it does not alter the fact that smoking
causes pathology and hence is a disease.
2. Foddy and Savulescu argue that addiction leaves
no tell-tale pathology to set it aside from normal
physiology. Although this claim is debatable, disease
can nevertheless be present without measurable pathology, especially if it causes dysfunction. There is no
diagnostic test or hallmark pathology of schizophrenia,
which nevertheless is a devastating disease. Undoubtedly, future research will reveal the pathology, but the
same arguments hold for addiction, which can also have
devastating effects on quality of life, social integration,
and employment, and eventually destroy health and life
without pathognomonic pathology or tests. There are
two points to be made: Disease can be present without
us knowing the nature of the pathology, and dysfunction
in itself is sufficient to call a process a disease.
3. Disease and normality lie at opposite ends of a continuum: The extremes are readily recognized, but the
boundaries can be difficult to define. Cancer is unambiguously a disease, but the border between malignancy
and benign hyperplasia can be difficult to define. Blood
pressure and cholesterols levels are other examples of
spectrums, risk of pathology being directly proportional
to blood pressure or serum cholesterol. Low is clearly
normal whereas trouble is inevitable with extremely
high levels of either cholesterol or blood pressure: But
where does the border lie? Addiction is also a continuum
and it has been recognized for over 500 years that at one
end of this continuum, addiction takes a form in which
people lose control, or autonomy, to the addicting agent.

32 PPP / Vol. 17, No. 1 / March 2010

The first meaning of addiction was to give over or

cede control in legal sense, and long before addiction
carried its modern opprobrium, it was recognized that
some addicted people cede control to the addicting
agent. This is demonstrated by the alcoholic, who has
lost job and family, who suffers from delirium tremens,
and has brain injury and liver failure from alcohol, yet
continues to drink. It becomes difficult to argue that this
person acts autonomously. Although some addiction
may not be pathological, it does not follow that none
are. To mix the caffeine addiction of the functioning
middle class with the broken life of the street addict
seems to be mixing categories. Although both may be
addicted, according to the definitions, one has a disease
but the other does not.

Thus, there are at least three ways that some

addictions could be considered a disease. I have
also argued that whether a person chooses to care
for their hypertension or diabetes or ignore it does
not alter the fact that they have a disease called hypertension or diabetes and it will still harm them.
Similarly, choosing between ceasing or persisting
with addiction has no bearing on whether it is
disease. Of course, hypertension comes unbidden, whereas there is a view that people choose,
for example, to smoke. However, I wish now to
argue that addiction does, at the core, decrease
the capacity to choose and this is a consequence
of frontal lobe function.
The behaviors governed by the frontal lobe are
anchored deep in our evolutionary past. They are
the innate or highly learned impulses necessary for
survival of the species: The impulses to eat, procreate, and other behaviors necessary for survival.
Cole Porter observed that Birds do it, bees do it,
and even humans do. However, humans spend far
more time than either birds or bees reflecting on
issues of unrequited and undying love, infidelity,
lust, and many other emotions and passions. This
capacity to reflect and perhaps reason requires
the biological processes of awareness and attention. However, the brain has limited capacity to
attend, so some behaviors are subjugated to an
automatic mode, thus allowing attention to
be directed toward achieving goals that depend
on these automatic behaviors. For example, attending to the goal of driving home is achieved
because peak hour traffic and handling the car are
carried out automatically and without conscious

attention. It is a central role of the frontal lobes to

make behaviors so well learned that they become
automatic, so that other goals, which depend on
these automatically executed behaviors, can be
The circuits of the frontal lobes function in a
relatively uniform manner. Somewhat arbitrarily,
there are at least six recognized circuits, subserving a range of behaviors including movement,
emotions, and cognition. Their apparent diversity
of functions reflect diverse inputs and outputs,
rather than differences in their inner workings.
As a result, much can be gained by using movement as an exemplar to apply to other aspects of
frontal lobe function and dysfunction. Without
dwelling on the complexities, practice produces
skilled movements such as driving a car, piano
playing, or a tennis serve by processes that reinforce or strengthen the circuits connecting relevant
movement related regions of the frontal lobe: The
frontal lobe circuits are the neural substrates of
this aspect of learning. This learning produces
automatically executed movements so that piano
playing and the tennis serve become learned and
stereotyped in much the same way as tics or mannerisms. The result is that the pianist attends to
making music rather than playing notes and the
tennis player concentrates on the strategy of winning rather than the mechanics of serving the ball.
Those familiar with Johnny Wilkinson, Englands
Rugby goal kicker, will recognize his stereotyped,
tic-like ritual for goal kicking: Attention is only
on kicking the goal by allowing the automatic
and overlearned behavior of the ritual of kicking
to take charge.
However, the frontal lobe movement circuits
can dysfunction. When they fail, such as with
Parkinsons disease, automatic movements also
fail, whereas abnormal function produces tic disorders, such as Tourettes syndrome, or the guild
dystonias, which distort the skilled movements of
high-performance musicians. These examples of
stereotyped movements reflect abnormal learning
in these loops. Tics are purposeless movements
that can be a disease when they impair social
function; guild dystonias are diseases because
they distort movement, preventing a person from
pursuing their career. People with tics or dystonia

Horne / Johnny Wilkinson 33

do not choose to make these movements, they

are impulsive and under almost no voluntary
The movements circuits were discussed to provide insights into the frontal lobe circuitry that
are affected by addiction. These circuits produce
automated behaviors, such as compulsive and
obsessive traits. Without them children would not
be cared for and most of us would not go to work.
They lead to attention to detail and the following
of routine that makes us get up and go to work
every day. These normal and important behaviors are the product of learning in the frontal
lobes of normal people. On the other hand, when
these circuits are destroyed or damaged, people
are unreliable, no longer persisting in reliable or
learned patterns of behavior. A famous example
is Phineas Gage, whose frontal lobe injury in the
late nineteenth century provided early insights into
frontal lobe function. Before his injury he was a
reliable, thoughtful, and considered person, but
afterwards became capricious and vacillating,
devising many plans of future operations, which
are no sooner arranged than they are abandoned in
turn for others appearing more feasible (Harlow
1848/1999, 280). Injuries like Gages are analogous to Parkinsons disease, causing these circuits
to fail. On the other hand (and in a similar manner
to the production of tics and guild dystonia in motor circuits), overactivity in these circuits causes
disabling compulsions and obsessions instead of
the normal constructive and useful compulsions.
Addiction is, in effect, a compulsion produced by
these circuits.
To summarize, a normally functioning frontal
lobes make behaviors automatic so that other
goals, which depend on these automatically executed behaviors, can be attended to. Just as the
piano player makes music by playing the notes
automatically, the mother acts automatically
indeed impulsivelyto care for her child. When
the frontal lobes misfunction, they produce unwanted impulsive movements (tics, stereotypes)
and behaviors (compulsions). Acting through
these loops, addictive agents cause unwanted
compulsive behavior.
Clearly, the brain of humans (and probably
non-human primates) do produce rational and

reasoned thought about past and current events

and make future predictions. One of the functions
of the frontal lobe is to juggle the competing directions of reason and the impulsive demands of
the highly learned circuits. If the impulse is strong
enough, rational conclusions will be overridden.
When the balance is swung too far toward impulsive drive over reflective control, it is referred to
as an impulse control disorder. People who develop Parkinsons disease are, as a generalization,
abstemious and careful. When treated with drugs,
known as D2 receptor agonists, some develop an
impulse control disorder causing gambling and
heightened interest in sex. They do not enjoy
feeding these impulses or wish to continue the
treatment and indeed these impulses can adversely
affect their lives and bank balances. Addiction
should be considered as an aspect of frontal lobe
function and not as a separate and discrete entity
with its own name. Addictive agents shift the balance from rational to impulsive: It is the extent
of the shift rather than the agent or its use that is
Foddy and Savulescus claim is that addictive
desires are just strong, regular appetitive desires
(2010, 14). However, it misstates the role of the
frontal lobe circuits to call them reward or pleasure pathways. Although these circuits are the
substrates of learning, reward is not a constant accompaniment. For example, activation or learning
in motor circuits produce little emotional affect.
Although it is well known that addictive drugs
can alter mood, it is not universally euphoria and
hedonism that they produce. Some drugs remove
anxiety (e.g., benzodiazepine or cannabis) rather
than causing euphoria or pleasure. Literature and
music are laced with example of people who drink
alcohol to avoid pain rather than gain reward.
Brick Pollitt in Tennessee Williams Cat on a
Hot Tin Roof drank to escape self-disgust and
not for any reward. Thus, hedonistic reward is
not the main reason for use of drugs or indeed the
function and purpose of these loops.
Impulsive behavior and the emotional consequences, whether fearful or pleasurable, are normal and the consequence of normal frontal lobe
function. When these same circuits produce tics
that do not cause dysfunction or disability, we do

34 PPP / Vol. 17, No. 1 / March 2010

not call this disease, even if statistically abnormal.

In the case of obsessive behavior, it may even lead
to academic success! Similarly, addiction may be
minor, causing no social, physical, or emotional
disruption and thus hardly rates as disease. In
these circumstances Foddy and Savulescus three
claims about addiction may hold. However, guild
dystonias, complex tics, and compulsions all result from dysfunction of the frontal lobes. Why
call it dysfunctional? Because their consequences
fulfill the definitions of disease, causing disability
and unhappiness (as with obsessive-compulsive
disorder) and changes in brain wiring (as in guild
dystonia). Similarly, the alcoholic, who wishes to
cease but cannot shake the demon from his back,
surely fits this definition of disease. Were we to
substitute addiction with the more accurate failed

impulse control, would it be so easy to accept

Foddy and Savulescus closing paragraph? A full
and correct account of failed impulse control
would take seriously the claim that pleasure as
a sensation can be a part of an autonomous and
even rational life plan. A full account of failed
impulse control will make it a term we can use
in a liberal way (2010, 20).

Foddy, B., and J. Savulescu. 2010. A liberal account
of addiction. Philosophy, Psychiatry & Psychology
17, no. 1:122.
Harlow, J. M. 1848/1999. Passage of an iron rod
through the head. The Journal of Neuropsychiatry
and Clinical Neurosciences 11:2813.