There really is a ‘thinness gene’ but unfortunately only 1% of us have it: Why some people ARE able to eat whatever they want and not put on weight
- Authors examined the health profile of 47,102 people aged 20-44 from Estonia
- They found 1 per cent of the studied population were ‘naturally slim and healthy’
- This meant they could eat what they like without having to exercise to stay slim
- The team say they also didn’t have an ALK gene that can also be linked to cancer
- They say it might be possible to turn the ALK gene off in others to fight obesity
Just one per cent of the population are able to eat whatever they want and not put on weight, according to researchers, who have discovered a ‘thinness gene’.
In a clinical trial by the University of British Columbia, Canada, researchers looked at the genetic profile of 47,102 people aged 20 to 44 years old living in Estonia.
The team found that when the ALK gene – linked to thinness – was shut down in flies and mice they didn’t gain weight when overfed a fatty and sugary diet.
Lead author, Josef Penninger, said it might one day be possible to create a treatment that shuts down the gene in humans struggling with obesity.
Just one per cent of the population are able to eat whatever they want and not put on weight, according to researchers, who have discovered a ‘thinness gene’
The ALK protein has been of interest to scientists for a number of years – and there are are already medications that target it.
This is because it frequently mutates in a number of forms of cancer, earning its reputation as an ‘oncogene’ that fuels tumour development.
Professor Penninger, of the University of British Columbia, Canada, wants to use a similar technique used in the treatment of cancer to help people lose weight.
‘If you think about it, it is realistic we could shut down ALK and reduce ALK function to see if we did stay skinny,’ he said.
‘ALK inhibitors are used in cancer treatments already. It is targetable. We could possibly inhibit ALK, and we actually will try to do this in the future.’
The study published in Cell sheds fresh light on why some people stay slim – whatever their lifestyle most have to diet and hit the gym hard to remain in shape,
‘We all know these people – it is around one percent of the population,’ he said.
‘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.
‘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.’
His team used data from the Estonian Biobank that has been tracking the population’s health since 2000.
This enabled them to compare DNA samples and clinical data of healthy thin individuals with those of normal weight. The latter had mutated forms of ALK.
The gene’s role outside cancer has remained unclear until now – the new finding suggests it plays a vital role in thinness.
More research will be required to see if drug inhibitors are effective for this purpose before they are tried on humans, say the researchers.
The team found that when the ALK gene – linked to thinness – was shut down in flies and mice they didn’t gain weight when overfed a fatty and sugary diet
The next step is to carry out what scientists call a ‘meta-analysis’ which will involve pooling data from other other data banks, including the UK Biobank that holds genetic information on half a million Brits, to see if they get the same results.
‘You learn a lot from biobanks,’ said Penninger. ‘But, like everything, it is not the ultimate answer to life.’
They are the starting points and very good points for confirmation, very important links and associations to human health.’
The team says that its work is unique as it combines exploration of the genetic basis of thinness on a population with genome-wide scale and analyses of living organisms – mice and flies.
Penninger added: ‘It is great to bring together different groups, from nutrition to biobanking, to hardcore mouse and fly genetics.
‘Together, this is one story including evolutionary trees in metabolism, the evolutionary role of ALK, human evidence, and hardcore biochemistry and genetics to provide causal evidence.’
The findings have been discovered in the journal Cell.
WHAT IS OBESITY? AND WHAT ARE ITS HEALTH RISKS?
Obesity is defined as an adult having a BMI of 30 or over.
A healthy person’s BMI – calculated by dividing weight in kg by height in metres, and the answer by the height again – is between 18.5 and 24.9.
Among children, obesity is defined as being in the 95th percentile.
Percentiles compare youngsters to others their same age.
For example, if a three-month-old is in the 40th percentile for weight, that means that 40 per cent of three-month-olds weigh the same or less than that baby.
Around 58 per cent of women and 68 per cent of men in the UK are overweight or obese.
The condition costs the NHS around £6.1billion, out of its approximate £124.7 billion budget, every year.
This is due to obesity increasing a person’s risk of a number of life-threatening conditions.
Such conditions include type 2 diabetes, which can cause kidney disease, blindness and even limb amputations.
Research suggests that at least one in six hospital beds in the UK are taken up by a diabetes patient.
Obesity also raises the risk of heart disease, which kills 315,000 people every year in the UK – making it the number one cause of death.
Carrying dangerous amounts of weight has also been linked to 12 different cancers.
This includes breast, which affects one in eight women at some point in their lives.
Among children, research suggests that 70 per cent of obese youngsters have high blood pressure or raised cholesterol, which puts them at risk of heart disease.
Obese children are also significantly more likely to become obese adults.
And if children are overweight, their obesity in adulthood is often more severe.
As many as one in five children start school in the UK being overweight or obese, which rises to one in three by the time they turn 10.
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