London - Being able to eat as much cake as you want and never put on any weight may not just be down to luck.
Scientists believe they have discovered a gene which is linked to thinness.
Some people have a biological quirk meaning this gene does not work properly and so are believed to burn fat at a greater rate, keeping them slim.
To find the gene, researchers trawled through a database of more than 47 000 people, comparing the DNA of those who were a normal weight with those who were naturally thin.
They wanted to know what skinny people – who were not athletes and did not suffer from an eating disorder which made them thin – had in common.
The answer is a quirk in part of the DNA called the ALK gene.
When the scientists removed this gene from mice, they could feed them a high-fat diet and the animals did not get fat.
The result is hoped to lead to a pill to help those who are not naturally skinny to stay thin – and it could be available in four years.
Professor Josef Penninger, senior author of the study from the University of British Columbia in Canada, said: "Most of us know someone who appears to eat whatever they want and never puts on weight.
"That can seem unfair to those of us who eat the same amount and become a little bit chubby.
"These findings suggest there is a genetic underpinning for this, and that a gene expressed in the brain is encouraging their body to burn fat.
"We know this gene is druggable, so there could well be a pill in future which people could take to get the same effect." Experts believe less than one percent of the population has the version of the ALK gene linked to thinness.
It means they have a biological difference which stops the gene working properly and may keep them slim.
After finding the gene in a database of people aged 20 to 44 in Estonia, researchers tested how it worked on mice.
They took gene-edited mice without the ALK gene and compared them to normal mice.
When both mice ate the same diet, those missing the gene were thinner. When the animals were fed high-fat meals, normal mice became obese, while those missing the gene stayed lean.
The study, published in the journal Cell, found mice missing the gene had smaller fat cells.
They also had higher levels of an enzyme which causes fat to be burned off quicker – as did 30 of the naturally thin people.
Knocking out the gene kick-starts a circuit in the brain which tells fat in the body to burn more calories, the authors believe.
Drugs already exist which do this, because the ALK gene is also linked to cancer.
Therefore it might be possible to develop a new drug to block the gene to help people keep weight off. Professor Penninger said: "It’s targetable. We could possibly inhibit ALK, and we actually will try to do this in the future."