Last week, you probably heard about a study purporting to show that consuming any amount of red meat significantly upped your risk of premature death. If that news has you freaked out, I highly recommend reading Deborah Blum's roundup of high-quality news coverage of this study. Her piece explains what the study does say, what it doesn't say, and why some evidence is better than other evidence. The takeaway: You should probably be reducing the amount of processed meat that you eat (but we already knew that). Read the rest
There was some interesting research out of the Mayo Clinic announced this week. The study focused on a new method to combat aging, though not, significantly, one that could extend life. Instead of living forever, Darren Baker and colleagues would just like to help people enjoy the time they do have—by reducing the physical downsides of aging, such as lost muscle and stiff joints.
Their method centers around something called senescent cells, normal cells that have basically shut down all growth, but continue to release chemicals into the body. Some scientists have suspected this process of cellular senescence contributes to the negative physical effects of aging and Baker's team was able to provide some big support for that theory. They killed senescent cells in the bodies of fast-aging mice. Those mice went on to age more gracefully, delaying the physical breakdown of their bodies. Ed Yong explains:
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Baker exploited the fact that many senescent cells rely on a protein called p16-Ink4a. He created a genetic circuit that reacts to the presence of p16-Ink4a by manufacturing an executioner: a protein called caspase-8 that kills its host cell. Caspase-8 is like a pair of scissors – it comes in two halves that only work when they unite. Baker could link the two halves together using a specific drug. By sneaking the drug into a mouse’s food, he activated the executioners, which only killed off the cells that have lots of p16-Ink4a. Only the senescent ones get the chop.
Baker tested out this system in a special strain of genetically engineered mice that age very quickly.
Oldupai Gorge in Tanzania is kind of the human race's institute of higher learning. It was one of the places where our ancient ancestors congregated and changed. And it's become famous for the quantity and variety of fossil remains it still holds, giving us way more information about human evolution than we otherwise would have had. We're all alumni of OGU.
But we aren't alone. Other creatures lived in Oldupai besides proto-humans. Some were our food. And some, it seems, might have fed on us.
Crocodylus anthropophagus—that's "man-eating crocodile" for those keeping score at home—lived 1.84 million years ago. Technically, scientists can't say for sure that C. anthropophagus was actually killing people, but there is good, solid evidence that it at least gnawed on them a bit. In a newly published paper researchers analyzed a fossil left foot and a left leg that had once belonged to early hominids and which bear the marks of crocodile teeth. These fossils were found relatively close to fossils of C. anthropophagus. It's not exactly a smoking gun, but it does provide some evidence that the crocodile species and the hominids who'd been bitten by crocodiles lived around the same place and time. Correlation is not causation, but it does wink suggestively, and perhaps flash its sharp teeth.
This paper is a bit weird in that it was accepted for publication back in 2008, but only published this month. In the meantime, a paper that used this research as a source was actually published first. Read the rest
My friend Jim captured this excellent moment in science reporting this morning. Thankfully, as I check Google News now, the headlines are drifting more towards the real story, which is fairly interesting. Turns out, deadly car accidents aren't so much a function of driver age as they are a function of driver experience.
Basically, over the past few decades, several states have placed stringent limits on teenage drivers—usually when they can drive, and who they can drive with. The idea was to separate first-time drivers from risky driving situations, and a lot of people assumed these measures were saving lives. Instead, we now know, the rules merely shifted when the deadly accidents happened. Some lives were saved. But, in general, the results were pretty much a wash.
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The researchers found that states with the most restrictive graduated licensing programs — such as those that required supervised driving time as well as having night-driving restrictions and passenger limitations — saw a 26% reduction in the rate of fatal crashes involving 16-year-old drivers compared with states without any restrictions.
But the rate of fatal crashes among 18-year-old drivers in those states jumped 12% compared with the states without restrictions.
A similar trend was seen when comparing drivers in states with strong graduated licensing programs with those in states with weak programs: The rate of fatal crashes among 16-year-old drivers was 16% lower but was 10% higher among 18-year-old drivers.
Overall, since the first program was enacted in 1996, graduated programs were linked to 1,348 fewer fatal crashes involving 16-year-old drivers and 1,086 more fatal crashes involving 18-year-old drivers.