Three months after quitting smoking, levels of dopamine in the brain return to normal, according to a new study published in the journal Biological Psychiatry. The findings suggest that dopamine deficits found in smokers are due to the smoking itself and are not necessarily a pre-existing risk factor.
A major challenge in understanding substance-related disorders lies in discovering the reasons why only some individuals become addicted, according to first author Dr. Lena Rademacher, postdoctoral fellow at the University of Lübeck in Germany.
Researchers believe that some individuals possess certain traits making them more vulnerable to addiction. They also suspect that brain circuits involving dopamine may be involved. Drugs of abuse release dopamine, and addiction to nicotine is connected to abnormalities in the dopamine system.
But it is still unknown whether smoking induces those abnormalities or if they already exist and contribute to risk of nicotine addiction.
For the study, senior author Dr. Ingo Vernaleken, Professor at RWTH Aachen University in Germany, led a team of researchers to examine dopamine function in chronic smokers before and after long-term cessation.
Using a brain imaging technique called positron emission tomography, the researchers measured the capacity for dopamine production in 30 men who were nicotine-dependent smokers as well as in 15 nonsmokers. After performing an initial scan on all participants, 15 smokers who successfully quit were scanned again after three months of abstinence from smoking and nicotine replacement.
The first scan showed a 15-20 percent reduction in the capacity for dopamine production in smokers compared with nonsmokers. The researchers expected this deficit to remain even after quitting, which would suggest it could be a marker of vulnerability for nicotine addiction. But they discovered that dopamine functioning returned to normal as time went on.
“Surprisingly, the alterations in dopamine synthesis capacity normalized through abstinence,” said Rademacher.
While the role of dopamine in vulnerability toward nicotine addiction cannot be excluded, the findings suggest that altered dopamine function of smokers is a consequence of nicotine consumption rather than the cause.
The findings raise the possibility that treatments might be developed that could help normalize the dopamine system in smokers.
“This 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,” said Dr. John Krystal, editor of Biological Psychiatry.