If you’re taller than your great-grandparents – and you probably are – you have a sensor in your brain to thank. That’s according to a new paper published in the journal Nature this week which has finally puzzled out the precise mechanism behind humanity’s general increase in height over the past century. If you were to step into a time machine and go back a hundred years or so, you’d probably stand out a bit. Not because of the mask or the social distancing – that was all the rage back in the era of the Spanish flu – but because you’d most likely just be so darn tall compared to the people around you. If you’re in the USA, you’d probably be about 10 centimeters (four inches) taller than your counterparts in the 1900s; in Europe, today’s time travelers would find themselves towering up to 15 centimeters (6 inches) above their forebears. That alone may not be completely surprising to you. People in the past grew up with bad nutrition and shaky child labor laws, after all – and that’s before we even get to the smoking rates and levels of general malaise – so it’s no wonder they weren’t reaching their full potential, height-wise. It might not even surprise you to learn that people a century ago reached certain puberty milestones later than today’s teens, and for much the same reasons: poor nutrition, lack of reliable access to food, and all the other stressors you’d expect from living in a time when almost everybody was walking around with a blood alcohol level that could knock out a rhino. While that’s all true, it doesn’t quite explain the problem fully. Sure, having reliable access to good and plentiful food makes a population taller, but why, exactly? The key is a receptor called MC3R. It is expressed in the hypothalamus – the part of the brain which regulates hormones and bodily processes in order to keep everything ticking along nicely. “It tells the body we're great here, we've got lots of food, so grow quickly, have puberty soon and make lots of babies,” study senior author Prof Sir Stephen O'Rahilly, told the BBC. “It's not just magic - we have the complete wiring diagram for how it happens.” How did the researchers figure this out? As with quite a few discoveries in recent years, it was thanks to the massive database which is the UK Biobank: they collected genetic and health information from over half a million volunteers. The team scoured the data looking for people with mutations that would interfere with the proper functioning of MC3R to see what effects they would experience. The few thousand that turned up all had something in common: they were shorter on average, and entered puberty later, than the general population. “This is such an exciting time for human genetics,” said senior study author Professor John Perry in a statement about the research. “By analyzing the genetic sequences of large numbers of research participants, we can now understand fundamental biological processes that have remained elusive until now.” One particularly unlucky person who turned up in the data had not one but two copies of a damaging mutation in their MC3R genes. The result: they ended up not going into puberty until they were over 20 years old. At their maximum height, the researchers reported, they were still “markedly short”. “[T]he brain can sense nutrients and interpret this to make subconscious decisions that influence our growth and sexual development,” O'Rahilly explained. “Identifying the pathway in the brain whereby nutrition turns into growth and puberty explains a global phenomenon of increasing height and decreasing age at puberty that has puzzled scientists for a century.” The discovery has immediate benefits for public health, the authors explained, and particularly for children with delayed growth, O'Rahilly said. But the implications aren’t just limited to child development – the findings also offer a potential therapy for people suffering from chronic illnesses. “Many chronic diseases are associated with the loss of lean mass, including muscle, with resultant frailty,” said O'Rahilly. “The finding that the activity of the MC3R pathway influences the amount of lean mass carried by a person suggests that future research should investigate if drugs that selectively activate the MC3R might help redirect calories into muscle and other lean tissues with the prospect of improving the physical functional of such patients.” Source
