This week’s Sunday Science is focused on bodies…fossil bodies, dead bodies and the causes and consequences of obesity…The exciting discoveries about human evolution just keep coming at the moment. The latest is the most complete fossil remains yet found of a Denisovan, half of a jaw plus two teeth, found at very high altitude on the Tibetan plateau, and dated to over 160,000 years old (see featured image). The researchers were unable to access any DNA, but unusually managed to get a protein analysis from the teeth. It also helps explain a mystery: it’s known that some modern Tibetans carry a genetic variant that allows them to cope with low oxygen available at high altitude, but it is clear that it evolved thousands of years before modern humans lived that high. It’s known that Asian and Oceanic populations carry some genes inherited from Denisovans, but until now, Denisovan remains have only been found at relatively low altitude. This study indicates that Denisovans evolved the adaptation on the Tibetan Plateau and later passed it to Homo sapiens, around 30,000-40,000 years ago, when they arrived in the area. There is a nice editorial speculating on this and other recent hominid fossil findings here, (open access) and the original study here (paywalled).

Moving on from fossils to the far more recently dead, the UK is set to open up its’ first “body farm”, otherwise known as a forensic cemetry or taphonomy (a new word for me). This long-overdue change (they have existed for many years in the US, for example) will allow forensic scientists to study the decay of bodies under controlled, monitored conditions, providing valuable insights for criminal and forensic investigations. In related news, the state of UK forensic science was roundly condemned in a recent parliamentary report, with a fragmentation of resources, lack of research and facilities not being up to standard, leading to unsolved crimes and even possible miscarriages of justice. Scientists warned this would happen with the closure of the Forensic Science Service in 2011 (but hey, who listens to experts?)

Obesity has been regarded as more of a problem in urban environments, where factors such as poverty, easy access to high-calorie, nutrient-poor food, good transport and sedentary work all conspire to produce expanding waistlines. Poverty in rural areas, the received wisdom goes, is more likely to be associated with malnutrition and underweight. Except that, actually, it turns out that obesity is more of a problem in rural areas. An important study reveals that levels of overweight and obesity are greater in rural than in urban areas in all high-income countries, and will soon match urban levels even in low to middle income countries. It’s probably due at least in part to the increasingly easy availability of those cheap high-calorie foods even in rural areas.  This has very important policy implications. Original study here (open access).

What is one of the risks of all this obesity? Fatty liver disease (also associated with excessive alcohol intake, but, increasingly, now, with obesity). A frankly alarming finding of an ongoing study monitoring the health of a cohort of young people in the UK has found an “epidemic” of fatty liver disease. At just 24, 1 in 5 of these young people had evidence of fatty deposits on their liver, half of them “severe”, and 1 in 40 actually had fibrosis, or scarring. This is very worrying as it is something previously seen only in much older people (rather like the related condition of type 2 diabetes) and can lead ultimately to cirrhosis and liver cancer. Yet at these stages it would otherwise be undetectable without a scan. Obesity and overweight in young people is setting them up for a shortened lifetime of significant ill-health; this must be countered. Original study here.

And finally, obesity isn’t all down to diet and exercise – there is a highly heritable component as to whether you are likely to become obese or not. Around 4 million people in the UK carry genetic variants that make them less likely to become overweight and, significantly, develop type 2 diabetes, a serious disease. A new study has found around 60 genetic variants in one gene alone, MCR4, that either protect or encourage obesity. This gene acts as a “switch” to regulate appetite. Original study published in Cell here (open access).

Featured image

A virtual reconstruction of the Denisovan jawbone found on the Tibetan Plateau. Credit: Jean-Jacques Hublin/MPI-EVA via Nature publications.

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