According to a paper published in Nature, the same defect could also act as a protection against smoking-related cancers.

A team from the University of Toronto studied variations in the gene for an enzyme called CYP2A6. The body uses this particular enzyme in the liver to break down nicotine, the addictive component of cigarettes.

They found that people with a common defect in the gene could only metabolise nicotine very slowly. This meant they were less likely to develop an addiction, and if they did smoke, they smoked fewer cigarettes than people without the fault.

Kicking the habit

The researchers said the discovery opened the way for completely new treatments for nicotine addiction. It was possible a pill or patch that blocked the enzyme could be developed to help people kick the smoking habit.

Dr Rachel Tyndale: New drug therapy could be just a few years away

"This is the first gene that has clearly been identified that affects the development of the regular smoking pattern," Dr Rachel Tyndale, an assistant professor in the University's department of pharmacology, said.

"We're interested therapeutically because we believe we can imitate the genetic defect and use this as a (drug) therapy."

She said it was also possible that smokers who carry the defective gene could be protected against lung cancer, since they would be less efficient at producing the carcinogens that come from tobacco smoke.

Genetic protection

The Toronto team first discovered the role of CYP2A6 in the metabolism of nicotine last year. There are three types of CYP2A6 genes: one normal and two defective. Everyone has two of the genes, one inherited from each parent.

The team first discovered the role of CYP2A6 last year

One percent of the population carry two deficient CYP2A6 genes, which gives them the most protection from tobacco. People who have one functioning and one faulty gene also have the defect.

Rachel Tyndale and her colleagues, Edward Sellers and Michael Pianezza, studied 184 people who had never smoked and 244 people who were addicted. Among the smokers, the researchers found those with the faulty gene smoked an average of 129 cigarettes a week, compared to 159 a week for people without the defect.

Dr Tyndale said a drug therapy could be just a few years away. "Even just having one half of the impairment can make a big difference in terms of whether people are likely to become smokers. If we can imitate that, or imitate the people who have no nicotine metabolism, we feel that this would be a really strong therapeutic approach."