The mystery behind why some smokers still have healthy lungs despite a lifetime of smoking has been explained by UK scientists.
According to BBC News, the analysis of more than 50,000 people showed favorable mutations in people’s DNA enhanced lung function and masked the deadly impact of smoking.
The Medical Research Council scientists say that the findings could lead to new drugs to improve lung function. However, cessation from smoking is still and will always be the best option, they say.
Scientists were looking to see if there was a genetic basis behind why some people getchronic obstructive pulmonary disease (COPD), and some don’t. COPD is the name given for a collection of diseases which cause people to have breathlessness, chest infections and persistent coughs, and is due to a narrowing of the airways, causing airflow obstruction. It is the third leading cause of death globally and causes an estimated 135,000 deaths annually in the United States alone.
By studying over 50,000 people, who ranged from heavy smokers to those who had never smoked in their life, the researchers were able to show that lung function and health in both smokers and non-smokers were associated with a handful of independent genetic variations. According to the researchers, these seem to be affecting how the lungs grow and repair themselves, and are the first example of how variations in our genes may affect lung health. Exactly how these genes do this is not yet known.
These findings, taken together with previous findings, will help define pathways underlying predisposition to development of COPD and smoking behaviours. A full understanding of the biological mechanisms underlying these genetic associations will improve our understanding of the pathophysiology of COPD and smoking behaviour, and potentially give rise to novel therapeutic strategies for the management of airway disease and prevention of nicotine addiction.”
Using this data alongside a new genetic analysis technique which allowed the team to look at a vast number of differences in the participants DNA very quickly, they were able to measure over 800,000 genetic variations. They then compared lung health and self-reported smoking behavior to both common and rare genetic variations. Of these, they found six genetic variations were associated with lung health.
Hence, smokers with “good genes” had a lower risk of COPD than those with “bad genes”.
In a nutshell, upon understanding how our genes might be impacting lung health could help in developing new treatments for sufferers, although the best way to protect against COPD is to simply either not to smoke in the first place, or stop if you already do.