Smoking-related deficits in brain dopamine, a chemical released by neurons to send signals to other nerve cells, return to normal levels three months after quitting, according to a new study.
The normalisation of dopamine systems suggested smoking-related deficits are a consequence of chronic smoking, rather than a risk factor, said the study published recently in the journal Biological Psychiatry.
It also suggested that the first three months after one stops smoking may be a particularly vulnerable time for relapse.
These findings by a team of researchers from Germany raise the possibility that treatments might be developed that normalise the dopamine system in smokers.
A major challenge in understanding substance-related disorders lies in uncovering why only some individuals become addicted, according to study lead author Lena Rademacher from the University of Lubeck.
To answer this question, Rademacher's team examined dopamine function in chronic smokers before and after long-term cessation.
The researchers used a brain imaging technique called positron emission tomography to measure an index of the capacity for dopamine production in 30 men who were nicotine-dependent smokers and 15 non-smokers.
The initial scan revealed a 15-20 per cent reduction in the capacity for dopamine production in smokers compared with non-smokers.
The researchers expected this impairment to persist even after quitting, which would suggest it could be a marker of vulnerability for nicotine addiction.
"Surprisingly, the alterations in dopamine synthesis capacity normalised through abstinence," Rademacher said.
The study suggests that the first three months after one stops smoking may be a particularly vulnerable time for relapse, in part, because of persisting dopamine deficits. This observation raises the possibility that one might target these deficits with new treatments.