As the rest of the world has been packing on the pudding during COVID lockdown, about 1 per cent of the population has remained rail thin, no matter how many comfort cakes they eat – or how little exercise they do.
We tend to say to such people: You must have good genes.
And it seems to be true.
Researchers have identified “a gene linked to thinness that may play a role in resisting weight gain in these metabolically healthy, thin people”.
The scientists found that thin people have a variant of what’s known as the ALK gene.
It’s this variant of the gene that facilitates a resistance to weight gain, no matter what diet you’re on, a finding suggested by follow-up experiments with mice and flies.
The science of thinness is a new frontier
“We all know these people: It’s around 1 per cent of the population,” said senior author Dr Josef Penninger, the director of the Life Sciences Institute and professor of the department of medical genetics at the University of British Columbia.
“They can eat whatever they want and be metabolically healthy. They eat a lot, they don’t do squats all the time, but they just don’t gain weight,” he said, in a prepared statement
“Everybody studies obesity and the genetics of obesity. We thought, ‘Let’s just turn it around and start a new research field’. Let’s study thinness.”
According to a statement from Cell Press, publisher of the study, Dr Penninger’s team analysed data from the Estonian Biobank, which includes 47,102 people aged 20 to 44 years old.
The team compared the DNA samples and clinical data of healthy thin individuals with normal-weight individuals and discovered genetic variants unique to thin individuals in what’s in the ALK gene.
According to Cell Press: “Scientists have known that the ALK gene frequently mutates in various types of cancer, and it gained a reputation as an oncogene, a gene that drives the development of tumours.
“The role of ALK outside of cancer has remained unclear. But this new finding suggested that the gene may play a role as a novel thinness gene involved in weight-gain resistance.”
It’s not a matter of simply having the ALK gene.
Rather, the variation found in thin people has an inhibiting effect on the gene, which in turn produces resistance “to diet-induced obesity”.
The researchers found that flies and mice without ALK remained thin, “despite having the same diet and activity levels as normal mice.”
The team’s mouse studies also suggested that ALK, which is highly expressed in the brain, plays a part there by instructing the fat tissues to burn more fat from food.
Is there something in it for everybody?
The researchers say therapeutics targeting the gene might help scientists fight obesity in the future.
“If you think about it, it’s realistic that we could shut down ALK and reduce ALK function to see if we did stay skinny,” Dr Penninger said.
“ALK inhibitors are used in cancer treatments already. It’s targetable. We could possibly inhibit ALK, and we actually will try to do this in the future.”
The researchers plan to further study “how neurons that express ALK regulate the brain at a molecular level to balance metabolism and promote thinness.”
Meanwhile, the researchers need to confirm their findings with other data banks through meta-analysis.