Found it! Gene mutation causes morbid obesity in children

Found it! Gene mutation causes morbid obesity in children

Modern people live a wealthy life with abundant food. Not only are adults beginning to face the problem of obesity, but even on campus one can see a bunch of "little fat boys and girls", which makes us worry about the health of our next generation. Recent studies have found that childhood obesity is not only closely related to eating and lifestyle habits, but is also related to mutations in certain groups of genes in the body. In other words, some children are really born to be "chubby."

American scientists have successfully found two sets of key obesity genes that can easily cause children to lose weight!

The latest report from Time Magazine pointed out that the Center for Applied Genomics at Children's Hospital of Philadelphia analyzed 14 related research reports and examined the genetic sequences of more than 10,000 children from the United States, Canada, Australia and Europe, of which 5,500 were classified as obese or overweight. The researchers found that these children had clear mutations in the OLFM4 gene on chromosome 13 and the HOXB5 gene on chromosome 17, which may affect the biological performance of intestinal bacteria and thus affect the overall digestive function.

According to a statistic from the US health department, the number of obese children has tripled in the past 30 years alone, which is related to family, school and social education. Many people attribute obesity to lazy lifestyle or overeating, but the results of this study overturned previous assumptions and argued that slight genetic mutations are the key to changes in physique and digestive system, that is, the same food eaten by different people will have completely different effects on body shape. The researchers are optimistic that once several key genes in the body are locked down, the corresponding targeted drugs can be successfully developed and the problem of obesity in some children can be fundamentally solved.

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