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The subjects of the study had been meager all their lives, not because they had an unusual metabolism. They did not care much about the food.
They have never eaten huge amounts, never obsessed with the next meal. A group of British researchers may have found the reason.
People carry a genetic alteration that cuts appetite. This also greatly reduces their chances of getting diabetes or heart disease.
The scientific study, published Thursday in the journal Cell, is based on data from the British biobank, which includes half a million people aged 40 to 69 years. Participants provided DNA samples and medical records, and allowed researchers to track their years.
A second study in the same journal also used data from this population for develop a genetic risk score for obesity. This can help predict, right from childhood, who is at high risk of suffering from obesity all his life and who is not.
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Together, the studies confirm a truth that researchers want to make more people understand. There are biological reasons why some struggle violently with their weight and others do not, and biological impacts are often perceived on appetite and not on metabolism. People who are gaining too much weight or struggling to stay slim are more hungry than naturally thin people.
The appetite mutation study was led by Dr. Sadaf Farooqi, professor of metabolism and medicine at the University of Cambridge, and Nick Wareham, an epidemiologist at the university.
The study is based on Dr. Farooqi's research on a gene, MC4R. She has been probing it for 20 years, but for the opposite reason: understand why some people are overweight, not why some are thin.
People with MC4R mutations tend to be obese. Researchers have recorded up to 300 mutations in this gene, which are the most common. single gene cause of obesity. Mutations in the gene represent 6% of children with severe obesity.
Mutations destroy satiety, the feeling of fullness after a meal, Dr. Farooqi and her colleagues found.
Normally, when people eat a meal, the gene is activated and sends a signal to people that they are full. Then the gene goes out on its own. But some people carry a rare mutation in MC4R that prevents the gene from working.
As a result, their bodies never receive the signal that they have eaten enough. They always to be hungry and are often overweight. Their risk of diabetes and heart disease is 50% higher, compared to those without the mutation.
In the new study, Dr. Farooqi and her colleagues found that in some thin individuals, the MC4R gene was always activated, not always deactivated, because of different mutations involving previously unknown metabolic pathway.
These people feel continually satiated. About 6% of the population carries such protective mutations.
"This proves that MC4R is an important weight controller, if not the most important," said Dr. Farooqi. And the new pathway is an obvious target for drugs against obesity.
Researchers are finding more and more that appetite and satiety determine who gains weight and who does notCecilia Lindgren, Professor of Genomic Endocrinology and Metabolism at Oxford University.
"We believe that regulating hunger and satiety is the key," she said. "There is food everywhere. If you are a little hungry and someone distributes a large plate of donuts during your meeting, who will pick up the donuts? "
In the other data study of the British Biobank, Dr. Amit V. Khera, Massachusetts General Hospital cardiologist, and his colleagues looked for a way to predict, from a vast collection of tiny variations in DNA which is destined to be big fight with the weight, and which would be spared by a problem of weight.
Scientists have established an obesity risk score based on changes in DNA at two million locations in the genome. People with the highest scores averaged 30 pounds more than those with the lowest scores. Among the very obese, 60% had a high score.
"We were shocked by the difference," said Dr. Sekar Kathiresan, co-author of the paper and geneticist at Massachusetts General Hospital.
But the population of the British biobank was composed solely of adults. "We wondered when does this start?" Said Dr. Kathiresan.
The researchers turned to additional data, confirming their findings in 300,000 participants in other genetic studies. At birth, scientists found that babies with high scores had the same weight as those with low scores.
At the age of 3.5, they were significantly heavier on average than others of their age. At age 8, children were often obese and by the end of adolescence, they weighed an average of 30 pounds more than those with a low risk score.
Having a high score "is not deterministic," said Dr. Kathiresan. "That does not mean that the fact that you are in the first percentile is a condemnation." But a high score indicates that weight control can be difficult.
Dr. Joel Hirschhorn, a geneticist at Boston Children's Hospital, noted that most of the genome spots that make up the risk score have nothing to do with weight. We do not yet know which are the most important.
He was struck by the fact that obesity does not really seem resolved until children are 8 years old. "These eight years could be magical and give you a unique opportunity to make a difference," he said.
This might not be easy, said Ruth Loos, director of the Obesity Genetics Program at Mount Sinai's Icahn School of Medicine. Children who are always hungry find a way to get more food.
"In an environment like ours, there is a lot of seduction," she said.
Cheap, tasty and high-calorie foods are available almost everywhere, and snacks and pastures are commonplace. People at high risk of obesity "may be more easily seduced," said Dr. Loos.
But risk scores could also reveal strategies that could work, said Dr. Lee M. Kaplan, director of the Institute for Obesity, Metabolism and Nutrition at Massachusetts General Hospital.
Of the 10% of the population with the highest risk scores, many are not large. Why is that?
Are there still unknown genes against those who cause people to overeat? Or do these people have good strategies to fight hunger and control food?
"At the end of the day, this opens up new lists of questions that can be asked and answered," said Dr. Kaplan.
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