Philadelphia, PA, July 28, 2016 - A new study in Biological Psychiatry reports that smoking-related deficits in brain dopamine, a chemical implicated in reward and addiction, return to normal three months after quitting. The normalization of dopamine systems suggests smoking-related deficits are a consequence of chronic smoking, rather than a risk factor. These findings raise the possibility that treatments might be developed that normalize the dopamine system in smokers.
According to first author Dr. Lena Rademacher, postdoctoral fellow at the University of Lübeck in Germany, a major challenge in understanding substance-related disorders lies in uncovering why only some individuals become addicted.
Researchers think some people could possess a trait that predisposes them to addiction, and suspect that brain circuits involving dopamine may be involved. Drugs of abuse release dopamine, and addiction to nicotine is associated with abnormalities in the dopamine system. But researchers are uncertain if smoking induces those abnormalities or if they already exist and contribute to risk of nicotine addiction.
Senior author Dr. Ingo Vernaleken, Professor at RWTH Aachen University in Germany, led a team of researchers examining 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 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 initial scan revealed a 15-20% reduction in the capacity for dopamine production in smokers compared with nonsmokers. 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 normalized through abstinence," said Rademacher.
The role of dopamine in vulnerability toward nicotine addiction cannot be excluded, but the findings suggest that altered dopamine function of smokers is a consequence of nicotine consumption rather than the cause.
Dr. John Krystal, Editor of Biological Psychiatry, noted the implications of these findings for developing better ways to help smokers trying to quit. "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."
Notes for editors
The article is "Effects of Smoking Cessation on Presynaptic Dopamine Function of Addicted Male Smokers," by Lena Rademacher, Susanne Prinz, Oliver Winz, Karsten Henkel, Claudia A. Dietrich, Jörn Schmaljohann, Siamak Mohammadkhani Shali, Ina Schabram, Christian Stoppe, Paul Cumming, Ralf-Dieter Hilgers, Yoshitaka Kumakura, Mark Coburn, Felix M. Mottaghy, Gerhard Gründer, and Ingo Vernaleken (doi: 10.1016/j.biopsych.2015.11.009). It appears in Biological Psychiatry, volume 80, issue 3 (2016), published by Elsevier.
Copies of this paper are available to credentialed journalists upon request; please contact Rhiannon Bugno at +1 214 648 0880 or firstname.lastname@example.org. Journalists wishing to interview the authors may contact Lena Rademacher at Rademacher@snl.uni-luebeck.de or Ingo Vernaleken at email@example.com.
The authors' affiliations, and disclosures of financial and conflicts of interests are available in the article.
John H. Krystal, M.D., is Chairman of the Department of Psychiatry at the Yale University School of Medicine, Chief of Psychiatry at Yale-New Haven Hospital, and a research psychiatrist at the VA Connecticut Healthcare System. His disclosures of financial and conflicts of interests are available here.
About Biological Psychiatry
Biological Psychiatry is the official journal of the Society of Biological Psychiatry, whose purpose is to promote excellence in scientific research and education in fields that investigate the nature, causes, mechanisms and treatments of disorders of thought, emotion, or behavior. In accord with this mission, this peer-reviewed, rapid-publication, international journal publishes both basic and clinical contributions from all disciplines and research areas relevant to the pathophysiology and treatment of major psychiatric disorders.
The journal publishes novel results of original research which represent an important new lead or significant impact on the field, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Reviews and commentaries that focus on topics of current research and interest are also encouraged.
Biological Psychiatry is one of the most selective and highly cited journals in the field of psychiatric neuroscience. It is ranked 5th out of 140 Psychiatry titles and 11th out of 256 Neurosciences titles in the Journal Citations Reports® published by Thomson Reuters. The 2015 Impact Factor score for Biological Psychiatry is 11.212.
Elsevier is a world-leading provider of information solutions that enhance the performance of science, health, and technology professionals, empowering them to make better decisions, deliver better care, and sometimes make groundbreaking discoveries that advance the boundaries of knowledge and human progress. Elsevier provides web-based, digital solutions -- among them ScienceDirect, Scopus, Elsevier Research Intelligence and ClinicalKey -- and publishes over 2,500 journals, including The Lancet and Cell, and more than 35,000 book titles, including a number of iconic reference works. Elsevier is part of RELX Group, a world-leading provider of information and analytics for professional and business customers across industries. http://www.elsevier.com
Editorial Office, Biological Psychiatry
+1 214 648 0880