Chai Rin Kim

A smoker’s chances of developing a nicotine dependence may be determined by genetics, suggests a recent study published in the journal “Translational Psychology.”

The study, co-authored by Yale School of Medicine psychiatry professor Joel Gelernter determined that nicotine dependence can be associated with variants in a particular gene: CHRNA4. The study — the largest to date investigating the genetics of nicotine dependence — provided statistical evidence for the link between CHRNA4 and nicotine addiction. Study authors and experts on nicotine dependence said that by identifying the genetic cause of nicotine dependence, the research has potential to assist in the development of smoking-cessation treatment.

“This study, for the first time, was able to … provide very strong statistical evidence that indeed the variants of [CHRNA4] are associated with nicotine dependence,” said Dana Hancock, study author and genetic epidemiologist at Research Triangle Institute International.

Hancock and her fellow researchers began by assembling a cohort of 17,074 smokers of European descent. Next, they collected data about study participants’ nicotine dependence by asking not only how often they smoked, but also under what conditions. Hancock added that including questions such as “How early in the morning do you smoke?” or “Do you still smoke while you’re ill?” allowed researchers to assess subjects’ smoking dependence, as opposed to just smoking patterns.

When the researchers compared the results of these surveys to the smokers’ genomes, they found that smokers with a particular variant of the CHRNA4 gene had an increased risk of developing nicotine dependence by about 10 percent. Though the findings of previous studies have strongly suggested that CHRNA4 is responsible for nicotine dependence, none had been able to provide definite statistical evidence, Hancock said. The larger sample size made the study results confirming that CHRNA4 plays a role in nicotine dependence more significant and definitive than the results of previous studies.

“This study raises the possibility of developing treatments for nicotine dependence that selectively act at nicotine receptors that contain the [CHRNA4 gene variant],” said John Krystal, Yale School of Medicine psychiatry department chair.

According to Krystal, the study’s findings allow for the development of more precise methods to aid smokers in the process of quitting. By targeting a specific gene, the research also guides future treatment development for nicotine dependence, he added.

However, Caryn Lerman, co-director of the Penn Medicine Neuroscience Center, said further research needs to be conducted before the study’s findings can be applied for the development of further nicotine-dependence treatments.

“It’s conceivable that the genetic regulatory mechanism could be targeted [for treatment], but the next steps would be to validate the findings,” Lerman said.

Lerman, whose primary area of research is the genetics of smoking cessation, added that eventually this research may contribute to the development of medications that target the CHNRA4 gene.

Still, Hancock said that she hoped the study would spur further research in the field of nicotine addiction, with the intention of ultimately of reducing the public health effects of smoking.

“Our ultimate goal, [is] to reduce the risk of the public health burden on cigarette smoking,” she said.

According to the Centers for Disease Control and Prevention, nearly 18 of every 100 U.S. adults 18 years or older currently smoke cigarettes.

  • type_b

    Just 10%? Doesn’t sound like a strong effect to me.

  • petergkinnon

    While the rather weak association of this gene with nicotine “addiction” might well have influence upon nicotine receptor activity it is improper to speak of “a gene for nicotine addiction,”/
    Unfortunately ,such descriptions are not uncommon among those still embedded in the now obsolete paradigm propagated in the seventies in the epidemic of “gene fever” that occurred in the wake of the elucidation of the structure of DNA.  A gross over-simplification which sadly is uncritically of those accepted by even some working in the field today, as well, it would seem bythe author of the article.  

    The crucial  aspect which is regularly overlooked is that the “turning on” or “turning off” of a gene is a function of the cell and not directly attributable to the genome itself.

    The very common notion that “DNA creates the organism” is very wrong. Implications of this kind can all too easily help propagate the myth that morphogenesis and structural and behavioral changes are driven by the gene (or group of genes) rather than by selection pressure, a function of the overall evolutionary network.

    It is important to bear in mind that the genome is merely a rather small library of protein recipes. It is entirely passive. It is actively manipulated, maintained and accessed by RNA and other cellular machinery.

    Machinery that is directly inherited, complete with RNA, organelles, the transcriptome, and all other structures required for function. All as a result of cell division. DNA being merely a rather small reference library that is accessed for instructions for the manufacture of “spare parts”.

    In my writings, I employ the analogy of a piano to represent DNA. The piano itself is entirely passive, as is DNA. But a pianist can produce innumerable musical variations by using this passive array of strings.

    In biology, the pianist corresponds to the machinery of the cell together with the inputs from its environment. Some of which control differentiation.

    Biological evolution is, after all, a network function.

    The network model of inheritance and morphogenesis is explored more fully in my latest book “The Intricacy Generator: Pushing Chemistry and Geometry Uphill”, a 336 page illustrated paperback now available from Amazon, etc

    Also of great relevance to this topic is Franklin M Howard’s excellent “The Way of The Cell”. A “must read”.for anybody interested in such matters

  • Jack Listerio

    More questionnaire JUNK SCIENCE………then find something they might or could have in common in the genome tree and call it the nicotine gene………..well done BS and junk science YALE now go have another ALE. Im sure Harvard school of public health can out junk science these dweebs

  • CyZane

    If it is the nicotine effects they were researching why do the study with smokers only? Nicotine is only a contributing factor to the dependence of smoking. Why not do the same study with let’s say e–cigs, patches, gum, pharma inhalers? Only then the effects of nicotine in isolation from the other components of tobacco can be properly assessed. As far as I am concerned this study is totally worthless.

  • Randall

    Millions of e-cigarette users demonstrate that nicotine alone is a very weak dependance factor. This study is only about tobacco consumers, not ‘pure’ nicotine: this difference makes invalidates the conclusion…

  • cigarbabe

    This is just another piece to back the very poor science used by many of the ANTZ researchers.