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Addictive Behaviour
bio explanations
evaluating dopamine
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SUPPORTING SCIENTIFIC RE
Volkow
et al (
03
)
fMRI
- during
drug
intoxication
>
areas
associated
with
dopamine
-
activated
including
b
circuits
involved
with
reward
,
motivation
and
cognitive
control
shows
link
between
dop
and
substance
A
>
credible
explanation
CONTRADICTORY EVIDENCE > doesn't explain all types
Stokes
et al (
09
) -
no
significant
increase
in
dop
for
volunteers
who took
cannabis
(
depressant
)
Yoder
-
no
consistent
increase
in
dop
across
people
who took
alc
(
depressant
)
engage
in
AB
>
doesn't
produce
an
increase
in
dopamine
}
insufficient
explanation
- explains
some
not
all
> is
gene
explanation
better
Counter =
Professor
Nutt
(
15)
-
criticised
method
sample
-
often
small
and
ppts
given
substances
in
different
form
and
in
a
lab
USEFUL APPLICATIONS FOR TREATMENT -
therapy
-
target
strategies
to
reduce
rewarding
dopamine
properties
E.G.
Naltrexone
-
antagonist
for
AB
binds
to
opioid
receptors
and
blocks
AB
effects
> if used =
no
pleasure
/
increase
in
dopamine
> Ab -
less
rewarding
and
less
likely
to
engage
prevents
dop
release
by
binding
and
blocking
gives
validity
to
theory
that
dop
release
is
involved
in
A
antagonists
-
most
effective
when
used
with
other
methods
- suggests
dopamine
isn't
the
sole
cause
REDUCTIONIST
A -
complex
B >
reduced
to
role
of
dopamine
and
reward
pathways
AB -
very
complex
>
explanation
=
too
simplistic
and
ignores
other
important
influences
with
supporting
research
evidence
(
Bosari
and
Carey
)
CONCLUSIONS
explanation
is
valid
:
scientific
,
supporting evidence
,
successful
applications
and
dop
can be
scientifically tracked
and
measured
lacks
reliable
and
conclusive evidence
,
unlikely
to be
sole
cause
,
reductionist
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