A popular type of heartburn medicine could hasten wear and tear of blood vessels.

Proton pump inhibitors, or PPIs, gunk up cells that typically line the veins and arteries like a slick coat of Teflon, researchers report May 10 in Circulation Research. Excess cellular junk ages the cells, which could make blood vessels work less smoothly.

The results, though controversial, are the first inkling of evidence that might explain why PPIs have recently been linked to so many different health problems, from heart attacks to dementia.
“The authors present a compelling story,” says Ziyad Al-Aly, a nephrologist at the Veterans Affairs Saint Louis Health Care System in Missouri. It begins to outline how using PPIs could spell trouble later on, he says. But Al-Aly notes that the study has one big limitation: It was done in cells, not people.

Gastroenterologist Ian Forgacs from King’s College Hospital in London agrees. Drawing conclusions about humans from cells grown in the lab requires “a huge leap of faith,” he says. So far, scientists have found only correlations between PPIs and their alleged side effects. “We need to know whether these drugs really do cause dementia and coronary disease and renal disease,” he says.

In the last few decades, proton pump inhibitors have emerged as a kind of wonder drug for heartburn. The drugs switch off molecular machines that pump acid into the stomach. So less acid surges up to burn the esophagus.

In 2012, nearly 8 percent of U.S. adults were taking prescription PPIs, according to a survey published last year in JAMA. (Some PPIs are also available over-the-counter.) Many people use PPIs for longer than they’re supposed to, says study coauthor John Cooke, a cardiologist at Houston Methodist Research Institute in Texas. “These are very powerful drugs­ — they’re not Tums,” he says. “They have side effects.”

Several of these side effects are still under debate. And if PPIs do increase the risk of dementia, say, or kidney disease, no one knows how. So Cooke and colleagues explored what chronic exposure to the drugs, which travel through the bloodstream, does to cells lining the blood vessels.
Human cells treated with a PPI called esomeprazole (sold as Nexium) seemed to age faster than untreated cells, the researchers found. The cells lost their youthful shape and instead “looked kind of like a fried egg,” Cooke says. They also lost the ability to split into new cells, among other signs of aging.

Cooke traced the rapid aging to mishaps in acid-filled cellular chambers called lysosomes. These chambers act as tiny garbage disposals; they get rid of junk like broken-down proteins. But PPIs, which work so well at shutting down acid production in the stomach, also seemed to shut down the acidic garbage disposals, too, the researchers found. That caused proteins to pile up, forming “little heaps of rubbish,” Cooke says.

Mucking with blood vessels’ lining could trigger all sorts of problems. For instance, instead of gliding easily through, platelets and white blood cells could get hung up, sticking to vessel walls like Velcro. “That’s how hardening of the arteries starts,” Cooke says.

The next step is to see if similar damage occurs in people. Doctors and regulatory agencies should take a second look at the widespread use of PPIs, too, Cooke says. “There’s enough data now that we have to be very cautious in our use of these agents.”

But some researchers think PPIs are getting a bum rap. “Everybody and their mother now want to hammer PPIs,” says gastroenterologist David Metz of the University of Pennsylvania. “It’s unfortunate because they’re spectacular drugs and they save people’s lives.”

The real question, Al-Aly says, is whether the benefits outweigh the risks.

In the scorching heat of the Kalahari Desert, some birds still manage to keep their cool.

Thermal imaging reveals that the southern yellow-billed hornbill (Tockus leucomelas) vents heat from its beak, a phenomenon previously observed in toco toucans (Ramphastos toco). A team of South African researchers snapped infrared photos of 18 hornbills on a farm in the southern edge of the desert at temperatures from 15° to 45° Celsius.

When air temperatures hit 30.7° Celsius, the difference between beak surface temperature and air temperature spikes — indicating the birds were actively radiating heat through their beaks. At most, the birds lost about 25.1 watts per square meter through their beaks. Hornbills probably manage this cool trick by dilating the blood vessels to increase flow in their uninsulated beaks, the team writes May 18 in PLOS ONE.

Toucans lose about 60 percent of their total heat loss through their beaks, but hornbills only shed up to 20 percent of their heat loss through this method. The researchers chalk that difference up to larger beak-to-body-size in toucans.

A last-ditch weapon against drug-resistant bacteria has met its match in Pennsylvania.

A 49-year-old woman has tested positive for a strain of Escherichia coli resistant to the antibiotic colistin, researchers report May 26 in Antimicrobial Agents and Chemotherapy.

It’s the first time in the United States that scientists have found bacteria carrying a gene for colistin resistance known as mrc-1, write study coauthor Patrick McGann of Walter Reed Army Institute of Research in Silver Spring, Md., and colleagues.
But perhaps even more alarming is that the gene rides on a transferable loop of DNA called a plasmid.

“That means we now see a possibility of spread,” says physician and clinical microbiologist Robert Skov. And not just from mother cell to daughter cell, he says, but to neighboring strains of bacteria, too.

Bacteria carry most of their genetic information in a tangle of DNA contained in chromosomes inside the cell. But tiny loops of DNA called plasmids hang around outside of the tangle. These loops carry extra information that bacteria can use, like how to protect themselves from antibiotics. Bacteria can swap plasmids like trading cards, effectively spreading instructions for antibiotic resistance.

In December, Skov and colleagues discovered a Danish patient carrying bacteria with mcr-1 plasmid DNA, like the woman in Pennsylvania. And in November of 2015, researchers reported something similar in China.

Until then, all known colistin resistance was due to tweaks in chromosomal DNA (which, unlike plasmid DNA, isn’t easily spread among bacteria), says Skov, of the Statens Serum Institut in Copenhagen, who was not involved with the new work.

Colistin, a 50-year-old drug that doctors largely stopped prescribing in the 1970s because of its side effects, has made a comeback in the last five to 10 years. It’s used when other antibiotics fail; it’s a treatment option for people infected with multidrug-resistant bacteria. Now, with colistin-resistant bacteria, Skov says, antibiotic treatment options are becoming more and more limited.

The problem, scientists have been pointing out for years, is that people are taking antibiotics too frequently. More use means more opportunity for bacteria to develop resistance.

Still, even with colistin-resistant bacteria emerging all over the world, Skov says he doesn’t expect thousands of people to become infected.

“The scenario now is that once in a while, we’ll see a patient carrying bacteria that we don’t have any good antibiotics left for.” But that, he adds “is dreadful enough.”