A new study confirms that genetics plays a role in addiction to nicotine found in tobacco. This discovery could open the way to a possible more effective treatment against addiction.
We are not all equal when it comes to cigarettes. Nicotine addiction does not happen by chance; on the contrary, it is written in our genes, demonstrates a American-Mexican study published Tuesday in the scientific journal Nature Communications. This confirms an already documented genetic reality.
To reach this conclusion, scientists scanned the genomes of more than 250,000 smokers on three different continents. They discovered that some of the people carrying one or two variants of the CHRNB3 gene smoked less, or even significantly less, than the others.
More resistance
In detail, those with a CHRNB3 gene variant smoked 21% fewer cigarettes per day, while people with two mutations smoked 78% fewer cigarettes daily.
Their brain is less receptive to nicotine. “These minority people have a receptor – which could be represented by a lock where the key would be nicotine – which is less effective and more resistant”, illustrates Thierry Favrod-Coune, doctor responsible for the addictions unit at the University Hospitals of Geneva (HUG), in the 7:30 p.m. of the RTS.
Thanks to this receptor, people carrying the CHRNB3 gene will tend to smoke less.
Towards a more effective treatment?
Medications that block the nicotine receptor in the body already exist today, but their effectiveness is only partial.
This new scientific discovery raises hopes of developing a drug capable of imitating the inhibitory effect of the genetic variant studied.
“Given that the reduction in smoking is 80% among people who have the two abnormal genes, we could imagine that this new treatment would be 3 to 4 times more powerful than current medications,” underlines Thierry Favrod-Coune.
In Switzerland, tobacco is responsible for 14% of deaths. According to the Federal Office of Public Health (FOPH), it is the substance that kills the most, ahead of alcohol and drugs.
Cécile Durring/iar
