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A new study has found that some life long smokers seem to have healthy lungs due to a DNA mutation that enhances lung function.
British researchers looked at data collected from a little over 50,000 people in the UK’s Biobank project and noticed that they had favorable mutations in their DNA. These rare mutations serve to enhance lung function and mask the nefarious effects of smoking.
The team from the Medical Research Council believes that its research may lead to the development of new, more efficient drugs that can improve lung function in smokers and treat lung disease.
For their study, Professor Ian Hall, field expert from University of Nottingham’s Queen’s Medical Centre, and his colleagues set out to investigate the genetic basis behind smoking behavior and airflow obstruction. They believe that this is essential in figuring out what the cause of chronic obstructive pulmonary disease (COPD) is.
Researchers have long said that both indoor air pollution and smoking are the main risk factors for chronic obstructive pulmonary disease. However the health community also says that there’s also a strong genetic component in developing chronic obstructive pulmonary disease, as well as in one’s smoking behavior.
An interesting finding is that people who’ve never smoked and people classified as heavy smokers share some of the genetic causes linked to lung disease. This discovery suggests that smoking acts independently of the genetic component to cause the development of chronic obstructive pulmonary disease.
The study involved a total of 152,030 subjects, all of European ancestry. Some of them (46,758) were heavy smokers, while others (105,272) were non-smokers who’ve never lit up a cigarette. All of the subjects fell into one of the extremes of lung function – some of them had high forced expiratory volume (FEV), others had low forced expiratory volume.
When Professor Hall and his colleagues checked to see if there were any shared genetic causes between the forced expiratory volume extremes and the phenotypes associated with each of them, they noticed that there are six (6) different genetic variants that affect chronic obstructive pulmonary disease and general lung health.
But one of the genetic variants that affect chronic obstructive pulmonary was also found in subjects who had never smoked in their life – chromosome 17 had the same “numbers of copies of duplicated sequence of the genome” in both groups.
The research team concluded that the findings offer new insight into the very mechanisms that are underlying airflow obstruction, tobacco addiction, and chronic obstructive pulmonary disease.
What’s more, the scientific community now has proof that there’s a shared genetic architecture between airflow obstruction in heavy smokers and airflow obstruction in non-smokers.
The study was published earlier this month, in The Lancet Respiratory Medicine.
Image Source: pixabay.com
