IF we are always hungry, the reason may be written in our DNA. A mutation that unites one in 340 people, more than 23 million in the world, causes a greater probability of being fat from early childhood, reaching an average of 17.7 kilos more than the ideal weight as adults.
The culprit is there melanocortina 4, also called Mc4r: a protein receptor that communicates to the appetite centers how much fat we have in store. When the Mc4r gene isn’t working properly, our brains believe that our fat stores are lower than real ones, so it starts telling us that we absolutely need to eat, guiding us to the cookie jar.
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The study conducted by scientists from the Mrc Metabolic Diseases Unit of the University of Cambridge and the Mrc Integrated Epidemiology Unit of the University of Bristol, just published in Nature Medicine, is based on a random sample of about 6 thousand participants recruited by Children of the 90s, one of the most representative and complete multi-generational study of its kind, which includes data on mothers and children of 80% of births in the district Bristol between 1990 and 1992. The authors analyzed the Mc4r gene in the participants’ DNA and each time they found a mutation, they continued to study its functional effects in the laboratory. A meticulous approach that provided reliable estimates on the frequency and impact of the mutation on weight and body fat percentage.
According to their calculations, making a comparison, in Italy over 177 thousand people have a greater amount of fat accumulated precisely because of this genetic mutation. It is not new that obesity has a familiarity and that specific genes can affect our weight starting in early childhood. “Mutations in the leptin-melanocortin system often occur in severe early-onset human obesity, but the extent of the phenotypic impact of these mutations is unclear,” the British researchers write. “The G protein associated melanocortin 4 receptor is widely expressed in the central nervous system and its binding to natural agonists results in a sense of satiety. On the contrary, when leptin acts on hypothalamic neurons to promote the release of melanocortins, it suppresses the secretion of the antagonist and makes you hungry ”. But fortunately this mutation does not always lead to obesity, if anything it predisposes us to hyperphagia, or an increase in the feeling of hunger that directs us towards more fatty and energetic foods at the expense of fruit and vegetables.
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In general, obesity is a multifactorial pathology, in which the environment and psychology are also important. On the other hand, obesity due to melanocortin 4 receptor deficiency is a rare disease whose prevalence does not exceed two thousand people. Other studies had already detected the presence of Mc4r mutations in obese people and their families and correlated this gene to adiposity, but this is not always the case: to give an example, a cohort study carried out in Germany went in search of the peculiarities genetics common in the obese and have identified this specific mutation in only 1.7% of cases. Also according to data collected by the UK Biobank, those with this mutation are not obese, just overweight.
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For this study, age-specific analyzes were conducted showing a clear association between the Mc4r mutation and a high Bmi in childhood, adolescence and adulthood, with gradual weight gain starting at age 5 it becomes evident after the age of 18, where the average difference between carriers and not is 17.76 kilos. The researchers also found a significant association of fat mass at the expense of lean, with an average weight difference of 14.78 pounds.
“Our results show that it is not uncommon for weight gain in childhood to be genetic. This should encourage a more compassionate and rational approach to overweight children and their families, including the genetic analysis of all severely obese, “says Professor Stephen O’Rahilly of the University of Cambridge, among the authors of the study. “This work helps to recalibrate our understanding of the frequency and functional impact of rare Mc4r mutations and will help shape future management of this important health factor,” adds Professor Nic Timpson, head of the Children of the 90s study. “A job like this was only made possible thanks to the extraordinary properties presented by a studio like Children of the 90s. Having biological samples for sequencing, rich data on the course of life, within a representative sample of the population, is fundamental to allow a new understanding and a deep characterization of important biological genetic effects such as these “, emphasizes the doctor. Kaitlin Wade of the University of Bristol.
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Although the Mc4r gene is a prime example, “this is just one of many that affect our weight and it is likely that there are more examples that will emerge as genetic sequencing becomes more common,” the researchers conclude. And given that there is currently no specific treatment for Mc4r deficiency, “knowledge of the brain pathways controlled by melanocortin 4 could aid in the design of drugs that bypass the blocking of signaling and help restore people to a healthy weight,” really managing to modulate the sense of hunger.
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