As the pattern of use is
established, John’s attempted cessation on tobacco is further perturbed by
conditioned tolerance. John describes that in certain situations such as when
he was drinking alcohol, he would consume many more cigarettes. When he has
quit smoking, he experiences greater unease and stronger cravings, and finds it
particularly hard to avoid smoking when he is out having a beer with his
friends. Both conditioned tolerance and negative reinforcement can be
identified as the learning phenomenon that leads to the pattern of relapse in
this case. Conditioned tolerance as explained by Macrae et al (1987) involves
homeostatic process by which animals maintain their internal environment within
acceptable limits. As drugs produce pharmacological effects on the body,
animals react to the effects with compensatory mechanism that reduce the drug’s
effects. In addition to reacting to disruptions of homeostatic systems resulted
from acute drug taking, animals also learned association between significant
cues with drug taking behaviour, and through Pavlovian conditioning their
bodies learn to anticipate the effects when conditioned stimuli are present. Over
time, tolerance on particular drug will occur as the strength of the
compensatory response increases with repeated drug administration. In light of
John’s case, drinking alcohol and social situation are the neutral stimuli.
With homeostasis, smoking behaviour (US) induces compensatory process that
reduce the nicotine effect in John’s body (UR). When neutral stimuli are paired
repeatedly with the US, Pavlovian conditioning occurs and neutral stimuli
becomes CS which animals learn to anticipate and activate compensatory
mechanism (CR). This explains the greater unease for John when he is out having
beers with friends as his body undergoes compensatory process in anticipation
of the drug taking yet without the effect of nicotine, the opposite effect of
pleasant feeling is not counterbalanced. Without the modulating effect of
analgesia and other neuropharmacological effects brought by nicotine, opposite feelings
amplified, hence the greater unease and stronger cravings. Conditioned
tolerance as a phenomenon in substance use has been demonstrated in extensive
experiments. For example, Azorlosa et al (2006) studies on the acquired
conditioned tolerance on lab rats. Rats were either in the paired group given
contextual environmental cue with nicotine, unpaired group with nicotine alone,
or control group with saline alone. The tail flick test was conducted and
results show that both the unpaired and paired group had shorter latencies than
the control group. This highlights the developed tolerance to analgesic effect
of nicotine on both experimental groups. Furthermore, with the present of
contextual cues, the paired group showed shorter latency in the tail flick test
than the unpaired group, demonstrating that conditioned tolerance is developed,
which further diminishes the analgesic effect of nicotine through stronger
homeostatic reaction. Additionally, if drug tolerance is in part attributable
to conditioning, tolerance should be subject to extinction. Azorlosa et al
(2006) exhibits the extinction of such conditioned withdrawal. By presenting
the contextual cue without nicotine, rats in paired group showed similar
latency length as unpaired group. This suggests that drug tolerance was
completely attenuated when animal was given nicotine in new environment and the
compensatory mechanism is not elicited when cues were absent from new
environment. The theory of using Pavlovian conditioning to explain the
phenomenon of conditioned tolerance is thus justified. 


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