Struggling to ditch the durries? Blame it on your genes.
Even though we smoked our last lungbuster more than 30 years ago, your Back Page scribbler still worries about the lingering damage his younger self may have inflicted on his organs.
While it would be easy to cite our tobacco-adjacent social environment for this particularly brainless adolescent life choice, the fact is we can really only blame our personality at the time, which in hindsight we would charitably characterise as “impressionable idiot”.
Or maybe not.
Perhaps our early addiction to the coffin nails was the result of something more sinister, such as something buried deep in our genetic code.
According to new research published this week in the journal Nature Communications, scientists reveal that a propensity to become a heavy smoker, or not, may be linked to a particular form of gene that interacts with the body’s nicotine receptors.
This connection was uncovered when boffins from the US-based Regeneron Genetics Center looked at the entire genetic codes of nearly 38,000 smokers in Mexico.
What they found was variants in the genes which encode “nicotinic acetylcholine receptors”. These receptors are responsible for mediating the “rewarding”’ effects of nicotine on the brain which therefore could be linked to changes in smoking behaviour in individuals.
“We have discovered that people carrying rare, naturally occurring mutations in a gene called CHRNB3 tend to smoke significantly fewer cigarettes per day,” the study’s lead authors, geneticists Veera Rajagopa and Giovanni Coppola, told media.
According to the researchers, the CHRNB3 gene controls a particular subunit of the nicotine receptors, called β3.
People with one or two copies of the variant gene smoked approximately 21% or 78% fewer cigarettes, respectively, than people with the more common version of the gene.
To establish that this wasn’t just a Mexican thing, the study team then tested to see if the link produced the same result in other populations.
Using local genetic data for 130,000 British and 180,000 Japanese folks, the team found the connection produced the same result.
These findings could prove significant down the track, the authors say, because having identified the subunit β3, it could become a potential target for treatments aimed helping smokers quit the habit.
Having said that, the team were quick to point out that a lot more work needed to be done before anybody got their hopes too high.
For instance, a therapy that potentially inhibited the CHRNB3 gene might help reduce or stop someone smoking, but nobody has any idea what other effects that might have.
That’s because while the gene and its subunit may well have been identified, the mechanism for exactly how they influence smoking, and for that matter, any other functions in the brains, are still unknown.
So in the meantime, let’s all lament the fact that New Zealand’s coalition government last year repealed that nation’s world-first “generational” smoking ban, reversing laws that would have prohibited tobacco sales to anyone born after 1 January 2009.
Because, in our humble opinion, if you really want to wean folks off the gaspers, that’s how you go about it.
Talking about brainless.
Send story-idea-shaped smoke signals to Holly@medicalrepublic.com.au
