Why did people think cannibalism was good for their health? The answer offers a glimpse into the zaniest crannies of European history, at a time when Europeans were obsessed with Egyptian mummies.

Driven first by the belief that ground-up and tinctured human remains could cure anything from bubonic plague to a headache, and then by the macabre ideas Victorian people had about after-dinner entertainment, the bandaged corpses of ancient Egyptians were the subject of fascination from the Middle Ages to the 19th century.

Mummy mania

Faith that mummies could cure illness drove people for centuries to ingest something that tasted awful.

Mumia, the product created from mummified bodies, was a medicinal substance consumed for centuries by rich and poor, available in apothecaries’ shops, and created from the remains of mummies brought from Egyptian tombs back to Europe.

By the 12th century apothecaries were using ground up mummies for their otherworldly medicinal properties. Mummies were a prescribed medicine for the next 500 years.

In a world without antibiotics, physicians prescribed ground up skulls, bones and flesh to treat illnesses from headaches to reducing swelling or curing the plague.

Not everyone was convinced. Guy de la Fontaine, a royal doctor, doubted mumia was a useful medicine and saw forged mummies made from dead peasants in Alexandria in 1564. He realised people could be conned. They were not always consuming genuine ancient mummies.

But the forgeries illustrate an important point: there was constant demand for dead flesh to be used in medicine and the supply of real Egyptian mummies could not meet this.

Apothecaries and herbalists were still dispensing mummy medicines into the 18th century.

Mummy’s medicine

Not all doctors thought dry, old mummies made the best medicine. Some doctors believed that fresh meat and blood had a vitality the long-dead lacked.

The claim that fresh was best convinced even the noblest of nobles. England’s King Charles II took medication made from human skulls after suffering a seizure, and, until 1909, physicians commonly used human skulls to treat neurological conditions.

For the royal and social elite, eating mummies seemed a royally appropriate medicine, as doctors claimed mumia was made from pharaohs. Royalty ate royalty.

Dinner, drinks, and a show

By the 19th century, people were no longer consuming mummies to cure illness but Victorians were hosting “unwrapping parties” where Egyptian corpses would be unwrapped for entertainment at private parties.

Napoleon’s first expedition into Egypt in 1798 piqued European curiosity and allowed 19th century travellers to Egypt to bring whole mummies back to Europe bought off the street in Egypt.

Victorians held private parties dedicated to unwrapping the remains of ancient Egyptian mummies.

Early unwrapping events had at least a veneer of medical respectability. In 1834 the surgeon Thomas Pettigrew unwrapped a mummy at the Royal College of Surgeons. In his time, autopsies and operations took place in public and this unwrapping was just another public medical event.

Soon, even the pretence of medical research was lost. By now mummies were no longer medicinal but thrilling. A dinner host who could entertain an audience while unwrapping was rich enough to own an actual mummy.

The thrill of seeing dried flesh and bones appearing as bandages came off meant people flocked to these unwrappings, whether in a private home or the theatre of a learned society. Strong drink meant audiences were loud and appreciative.

The mummy’s curse

Mummy unwrapping parties ended as the 20th century began. The macabre thrills seemed in bad taste and the inevitable destruction of archaeological remains seemed regrettable.

Then the discovery of Tutankhamen's tomb fuelled a craze that shaped art deco design in everything from the motifs of doors in the Chrysler Building to the shape of clocks designed by Cartier. The sudden death in 1923 of Lord Carnarvon, sponsor of the Tutankhamen expedition, was from natural causes but soon attributed to a new superstition — "the mummy's curse."

Modern mummies

In 2016 Egyptologist John J. Johnston hosted the first public unwrapping of a mummy since 1908. Part art, part science, and part show, Johnston created a an immersive recreation of what it was like to be present at a Victorian unwrapping.

It was as tasteless as possible, with everything from the Bangles’ Walk Like an Egyptian playing on loud speaker to the plying of attendees with straight gin.

The mummy was only an actor wrapped in bandages but the event was a heady sensory mix. The fact it took place at St Bart’s Hospital in London was a modern reminder that mummies cross many realms of experience from the medical to the macabre.

Today, the black market of antiquity smuggling – including mummies – is worth about US$3 billion.

No serious archaeologist would unwrap a mummy and no physician suggest eating one. But the lure of the mummy remains strong. They are still for sale, still exploited, and still a commodity.

This article was originally published on The Conversation. You can see the original version here.

Ben Franklin may have had it partly right with his belief that "early to rise" makes one "healthy, wealthy and wise." Natural early risers may experience greater overall well-being and better mental health compared with night owls, a new study suggests.

But what Franklin likely didn't know is that your chronotype, or tendency to sleep and rise at a particular time, is heavily dependent on your genes — and there might not be much you can do to change it.

In the new study, published today (Jan. 29) in the journal Nature Communications, researchers identified 351 regions in the human genome associated with being an early bird, only 24 of which were known previously. Those people in the study with the most gene variants associated with early rising tended to go to sleep upward of a half hour sooner than others with fewer of these variants. [5 Surprising Sleep Discoveries]

What's more, the study found that these genomic regions were linked to the body's circadian clock and to the retina, supporting the theory that the brain's ability to detect light through the retina sets the body's clock to a 24-hour cycle of sleep and wakefulness.

"Part of the reason why some people are up with the lark while others are night owls is because of differences in both the way our brains react to external light signals and the normal functioning of our internal clocks," lead study author Samuel Jones, a research fellow studying the genetics of sleeping patterns at the University of Exeter Medical School in the U.K, said in a press statement.

The study tapped into genomic data from nearly 700,000 participants in a U.K.-based nonprofit health project called the U.K. Biobank and the U.S.-based private genome analysis company 23andMe. The 23andMe participants were asked via a health survey whether they were a "morning person" or a "night owl," or somewhere in between.

As such an answer could be subjective, the researchers validated their findings with information from wristband activity trackers worn by more than 85,000 individuals in the UK Biobank project, which revealed with no bias when they went to sleep and woke up.

The researchers found differences in sleep timing but not sleep quality. They also found no increased risk of obesity and diabetes among night owls, contrary to some earlier studies. But they uncovered an apparent causal link between being a night owl and being more prone to depression, anxiety and schizophrenia.

That is, through their statistical analysis, the researchers showed that the more of a night owl someone is, as defined by their genetics, the greater their risk of schizophrenia and the lower their wellbeing. This was not dependent on factors such as poor sleep quality or lack of sleep, they found.

The reason for this link between sleep timing and poor mental health remains unknown but perhaps is due to a combination of factors, said co-lead study author Jacqueline Lane, an instructor and researcher at the Massachusetts General Hospital Center for Genomic Medicine. These factors could include unknown protections offered by the genes in early risers, or the physical stimulation of morning light that early risers receive, or societal advantages of feeling awake in the morning and midday in a culture dominated by a 9-to-5 work cycle, Lane said. [The Science of Jet Lag: 5 Surprising Findings]

"Our current study really highlights the need for further study of how chronotype is causally linked to mental health and, until these studies are done, we can only speculate on the mechanism," Lane told Live Science.

If you are a bona fide night owl who needs to function in an early-riser world, you aren't entirely out of luck, said Nancy Rothstein, a sleep consultant known as The Sleep Ambassador with a focus on business productivity.

Rothstein said you can better prepare for sleep by not consuming caffeine in the afternoon and by tuning out of technology at least an hour before going to bed, so that sweet sleep can arrive soon after you hit the pillow.

"Asking yourself to get to bed a few hours earlier is not always realistic," Rothstein told Live Science. "Your body clock needs to adapt to the change in timing. Fill the hour [before bed] with a shower, reading with a dim light, having a conversation, or doing some gentle stretching," Rothstein said. "Practice a simple mindfulness technique that gets you out of your head and into your breathing and body awareness."

• Top 11 Spooky Sleep Disorders
• 5 Things You Must Know About Sleep
• 10 Things You Didn't Know About the Brain

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science

Recreational marijuana use is becoming increasingly legal across the U.S., but that doesn't mean that it's safe. As with alcohol and tobacco, the drug comes with risks. And a new study finds regular marijuana may — similar to alcohol and tobacco — affect a man's sperm count and vitality.

While the study was small — just 24 participants — researchers found, for the first time, that higher concentrations of tetrahydrocannabinol (THC) in urine corresponded to a lower sperm count. (THC is the compound in marijuana responsible for the drug's high.) The study also found that pot smokers had changes in their sperm genetic profile that, in other studies, have been associated with abnormal growth and cancer.

The study, which was published today (Dec. 19) in the journal Epigenetics, could not determine whether these changes in sperm quantity and quality could affect the fertilization process and the health of the offspring, but the researchers advise caution nonetheless. [25 Odd Facts About Marijuana]

"In the absence of a larger, definitive study, the best advice would be to assume these changes are going to be there [in sperm]," said lead author Susan Murphy, the chief of the Division of Reproductive Sciences in the Department of Obstetrics and Gynecology at Duke University Medical Center in North Carolina. "I would say, as a precaution, stop using cannabis for at least six months before trying to conceive."

Previous studies have hinted that smoking marijuana can lower sperm count, that is, the number of sperm in semen when ejaculated. The new study, however, is the first to show a strong correlation between THC concentrations in urine and the number of viable sperm. On average, the sperm concentration in the semen of the 12 non-smokers in the study was about twice as high as it was in the 12 smokers, the study revealed.

More worrisome for the researchers was the degree of epigenetic changes among pot smokers. Epigenetics refers to the suite of small chemical "tags" that are added to the DNA structure and regulate gene expression. While this is a normal process, it can be altered by environmental exposures.

The researchers found that the men who smoked marijuana had epigenetic changes in their sperm DNA involving hundreds of genes and two important regulatory pathways: one for helping bodily organs reach their full size; the other for basic growth during development. Several kinds of cancer are associated with the interference of these pathways, though this study did not find a specific link between marijuana use and cancer.

As with sperm count, the higher the concentration of THC in the men's urine, the more pronounced the epigenetic changes to their sperm were. The research group's corresponding study on rats revealed a similar pattern in the same group of genes.

"We don't yet know what that means, but the fact that more and more young males of child-bearing age have legal access to cannabis is something we should be thinking about," senior study author Scott Kollins, a professor in psychiatry and behavioral sciences, also at Duke, said in a statement.

Changes in sperm quantity and quality induced by marijuana smoking might not be permanent, Murphy told Live Science. Men generate new sperm daily. Sperm take about 70 days to mature and then, if not ejaculated, will die shortly after that and be reabsorbed into the body.

"The sperm DNA… is not mutated in the traditional sense" by marijuana, Murphy said. "By definition, epigenetic alterations can affect gene regulation without changing the DNA sequence.

This means that, in the absence of marijuana use, new sperm may be able to develop normally. Nevertheless, damaged sperm from marijuana use could theoretically adversely affect the offspring, "assuming that said sperm is viable, capable of fertilization and results in a viable embryo," Murphy added.

Tim Jenkins, an epigenetics and male fertility expert at the University of Utah School of Medicine, who was not involved in the study, told Live Science that "despite the limited sample size in this study, a real strength are the animal data which comport remarkably well with the human data," which "makes the results significantly more convincing."

However, Jenkins stressed the importance of addition research. "It is imperative that additional work is performed in this realm to identify the real risk of cannabis use on sperm function but most importantly, on offspring health," he said. "This study represents a great first step in that effort, but there is still a great deal of work that is required.”

For their next study, Murphy said they'd like to at least double the sample size to improve the statistical significance of the results.

• Trying to Conceive: 12 Tips for Men
• 7 Ways Marijuana May Affect the Brain 
• Marijuana Could Treat These 5 Conditions

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

If you're already feeling stressed out, sorry, but there's one more thing you might need to worry about: A new study finds that stress may impair your memory now and quicken cognitive decline later in life.

And if that's not stressful enough, stress might also be tied to a slight shrinking of the brain, according to the study, published today (Oct. 24) in the journal Neurology.

In a study with more than 2,000 healthy, middle-age volunteers, doctors found that those with higher blood levels of the hormone cortisol — an indicator of stress — performed more poorly on memory tests and had a slightly shrunken brain volume compared to those with a normal level of the hormone. The effect was more evident among women in the study. [10 Things You Didn't Know About the Brain]

But before you panic, know that the researchers emphasized (stressed, really) that the findings do not mean that stress causes brain damage. Rather, the study reveals an association between stress and brain function that's consistent with laboratory-based studies on mice.

Don't stress — it's natural

The stress response is a natural part of life, as the bodymust react when confronted by danger or other threats. And cortisol is central to that stress response, said lead study author Dr. Justin Echouffo-Tcheugui, an assistant professor of medicine at the Johns Hopkins School of Medicine in Baltimore.

During stressful moments, cortisol levels rise and, together with another hormone called adrenaline, signal the body into making a fight-or-flight response. Specifically, cortisol increases glucose, or sugar, in the bloodstream; enhances your brain's use of that glucose for energy; and suppresses bodily functions that aren't immediately needed during an emergency, such as digestion, reproduction and growth. [11 Tips to Lower Stress]

Once the stressful event passes, cortisol levels should fall. This, however, isn't always the case, Echouffo-Tcheugui told Live Science. The body may still perceive stress or, for reasons not well understood, retain high levels of cortisol. Or, in this modern life, one's home or work life may cause daily stress.

Persistently higher cortisol levels can cause damage to the heart and skin. So, the idea that stress and higher cortisol levels could also affect memory and brain function is not surprising, Echouffo-Tcheugui said. Indeed, people with Cushing syndrome, a condition that's defined in part by a high and persistent level of cortisol, often experience poor memory, attention deficit, moodiness and depression.

Stress and the brain

In the new study, Echouffo-Tcheugui, who was based at Harvard Medical School while conducting the analysis, tapped into the Framingham Heart Study database, a massive, government-sponsored study that has followed the health of thousands of residents in the Framingham, Massachusetts, area for more than 70 years. Echouffo-Tcheugui and his colleagues identified 2,231 people with an average age of 49 who were free of dementia.

At the beginning of the study, each participant had a psychological exam and assessments for memory and thinking skills. Their memory and thinking skills were tested again an average of eight years later. At the end of the study,the participants also provided a blood sample, and about 2,000 of them had a a series of MRI brain scans to measure brain volume.

The researchers found that people with high levels of cortisol had lower scores on tests of memory and thinking skills than those with normal levels of cortisol. High cortisol was also linked to lower total brain volume.

Echouffo-Tcheugui said the study is only a snapshot of the effects of cortisol at one period in time for one group of people, largely of European descent. Yet, given the known deleterious effects of elevated cortisol levels on various body tissues, he said doctors and the public should pay heed to the potential for brain damage.

"Our research detected memory loss and brain shrinkage in middle-aged people before symptoms started to show" in ordinary, daily activities, said Echouffo-Tcheugui. "So, it's important for people to find ways to reduce stress."

Dr. Paul George, an assistant professor of neurology and neurological sciences at Stanford Medicine, who was not involved with the research, said the community-based study "raises many questions which need further exploration about how cortisol affects the brain and our cognition."

"One of the strengths is the assessment of these brain volumes using multiple imaging assessments to evaluate brain changes," George told Live Science. "The size of the study also adds to its impact, [and] they provided sound analysis to eliminate confounding factors such as depression."

The limitations, George added, are inherent in the nature of such epidemiological studies: The researchers cannot be certain of the cause, existence or persistence of stress, because they are relying on a one-time morning blood sample of cortisol levels.

Echouffo-Tcheugui said that he agrees with that assessment. Still, reducing stress can have a range of benefits, he said, whether it's accomplished through better sleep, exercise, relaxation techniques, or asking one's doctor about cortisol-reducing medication, if needed.

"There's nothing wrong in reducing stress," he said.

Follow Christopher Wanjek @wanjekfor daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

You'd be hard-pressed to find someone to say something good about Salmonella, a pervasive family of bacteria that sickens more than a million people each year in the United States.

But as bad as Salmonella's reputation is, the bug is certainly good at something: infecting us and causing misery. And now, scientists have discovered part of the reason why the bacteria are so talented at this: They've learned how to, quite literally, hide their tails and avoid detection by the immune system. And the discovery of that method is a good thing for us, because it may give scientists a new way to target and fight the bacteria. [Tiny & Nasty: Images of Things That Make Us Sick]

In a new study, published today (Oct. 23) in the journal Cell Reports, researchers found a tricky property of Salmonella Typhimurium (STM), the subspecies of this bacteria family that makes humans and other mammals sick. These bacteria can temporarily turn off their flagella, the tail-like appendages that whip to and fro, propelling the bacteria through the body.

"If you are bacteria [with] lots of flagella, it's like wearing a neon sign around your neck, basically alerting the immune system to your presence," said lead study author Brian Coombes, a professor in the Department of Biochemistry and Biomedical Sciences at McMaster University in Hamilton, Ontario. "Without that alert, it is a lot harder for the host to contain the bacteria's spread [and prevent them from going] to more cells."

In other words, by turning off that neon sign — or, in this case, those many neon propellers — the bacteria make it harder for your body's immune system to track down the invader and stop it.

Evading detection

Once STM bacteria invade a host cell — in this case, both mice and human cells in a laboratory setting — they use a genetic switch to stop their flagella activity, only to reactivate it when they leave to infect another cell, the researchers found. Coombes said he doesn't know of any other bacteria that behave this way, not even Salmonella bongori, the species that infects reptiles and other cold-blooded animals and has the same flagella genes.

"The loss of flagella has been reported in certain strains of bacteria that cause chronic infections of the gut and other mucosal surfaces … [but that] loss of flagella is permanent," Coombes told Live Science. "The process we identified [in Salmonella] is all controlled by regulation of the genes, so the bacteria doesn't have to delete them or mutate them. They just figured out how to turn them off at the right time. This allows them to turn [the genes] on … again later when the time is right."

Salmonella, which is spread through contaminated food, causes about 1.2 million illnesses; 23,000 hospitalizations; and 450 deaths in the United States every year, according to the Centers for Disease Control and Prevention (CDC). And while the illness can, in most cases, be treated with antibiotics, doctors are concerned because some strains of the bacteria have become resistant to the drugs. Currently, a multidrug-resistant strain of Salmonella has contaminated raw chicken products in 29 states, leading to 21 hospitalizations, according to the CDC. [6 Superbugs to Watch Out For]

Disarming a threat

Dana Philpott, a professor of immunology at the University of Toronto, who was not involved with the study, said that the "findings highlight yet another way these pathogens hide from the host’s immune system."

But the newfound understanding of STM's invasion strategy may open up new ways to thwart the spread of the pathogen and perhaps other Salmonella types as well, Philpott told Live Science.

Indeed, the authors of the new study said they hope their findings will one day lead to non-antibiotic drugs that can fight even the resistant strains. Antibiotics directly kill bacteria, but bacteria can mutate in ways that make these drugs useless. A more effective approach may be to develop drugs that help the immune system kill the bacteria, Coombes said.

In the case of Salmonella, Coombes said he envisions a drug that prevents the bacteria from entering into their stealth mode, thus enabling the immune system to do its thing.

"Finding drugs that 'disarm' rather than outright kill bacteria, like antibiotics do, is an emerging area to help beat the antibiotic-resistance crisis," Coombes said. "Our immune systems are as close to the perfect natural antibiotic [as] you can find, and so by disarming bacteria of their virulence factors, the immune system regains the upper hand."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, "Bad Medicine," appears regularly on Live Science.

Many cancer cells can divide indefinitely by flicking on an "immortality switch," a trick most other cell types can't perform. Now, researchers have discovered a way to short-circuit that switch, which may slow or halt the spread of more than 50 types of cancer, including the kind of brain cancer that Sen. John McCain died from last month.

In the new study, researchers examined glioblastoma brain cancer cells that had been removed from cancer patients, finding that a tiny segment of a common protein called GABP was the key in enabling cancer cells to activate the so-called immortality switch. When the researchers removed that protein segment, the cancer cells — both in lab dishes and when transplanted into mice — stopped their voracious multiplying and behaved like mere-mortal cells. [10 Do's and Don'ts to Reduce Your Risk of Cancer]

The researchers, led by Joseph Costello, a professor of neurosurgery and a neuro-oncology expert at the University of California, San Francisco, said they hope to develop a drug that could inhibit just that tiny segment of GABP, depriving cancer cells of their key to the switch while avoiding harming other cells. (Costello disclosed in the study that he and a co-author are founders of Telo Therapeutics, which is partnering with the pharmaceutical company GlaxoSmithKline to search for small molecules that have potential as drugs.)

The findings were published today (Sept. 10) in the journal Cancer Cell.

Unchecked division

A signature of cancer cells is their ability to divide unchecked. Almost all other cells can divide only a set number of times before they die. The main exceptions are stem cells, which can divide throughout an organism's lifetime to replenish all those other cells that are dying, such as blood and skin cells.

Cellular life spans are set by structures called telomeres, which cap the ends of chromosomes, serving like aglets on a shoelace. With each cell division, the telomeres get a little shorter, until, eventually, they are too short to protect the integrity of the chromosomes. That's when cell division stops.

Stem cells escape this mortality by using telomerase, an enzyme that rebuilds the telomere. In an indirect way, many cancer cells do much the same thing, by exploiting mutations in a gene called TERT, short for telomerase reverse transcriptase. Cancer cells that can switch on this gene can, like stem cells, divide indefinitely.

Scientists have understood cancer's use of the immortality switch for years. Previous research has found that more than 90 percent of tumors have mutations that enable the growths to turn on TERT expression and produce telomerase. But cancer drugs that simply block telomerase have proven to be too toxic for patients, because the medicines choke stem cells, too, limiting a patient's ability to produce new blood cells and other vital cells.

Focusing on glioblastoma, the most aggressive form of brain cancer, Costello's group discovered a way to limit access to the immortality switch only for cancer cells, sparing stem cells. Specifically, the researchers found that cancer cells were using a part of the GABP protein, called GABPbeta1L, to activate the switch.

The GABP protein is used by many types of cells for a multitude of tasks, so inhibiting this protein entirely would have adverse effects throughout the body. The researchers instead experimented with removing only the GABPbeta1L element, using the gene-editing tool CRISPR to do so.

And it worked. The GABP protein lacking beta1L had a detrimental effect on cancer cells but no effect on other cells, according to experiments the researchers did in lab dishes and in mice.

"These findings suggest that the beta1L subunit is a promising new drug target for aggressive glioblastoma and potentially the many other cancers with TERT promoter mutations," Costello said in a press statement.

Glioblastoma target?

McCain and former Vice President Joe Biden's son Beau Biden both died from glioblastomas. Although it is not publicly known whether their form of glioblastoma had TERT promoter mutations, Costello told Live Science it was probable, given that an estimated 83 percent of glioblastomas have such mutations. [5 Facts About Brain Cancer]

Dr. John Laterra, co-leader of the Brain Cancer Program at the Johns Hopkins Sidney Kimmel Comprehensive Cancer Center in Baltimore, who was not part of this research, said the findings "are of high potential significance given the known role of TERT in driving cancer cell immortality and glioma malignancy.

"The findings provide a compelling argument for future work directed at identifying [molecules] that inhibit GABPbeta1L or other regulators of" GAPB's ability to activate the immortality switch, Laterra told Live Science.

He added that it will be important to replicate this experiment in other tumor models, preferably those derived directly from patient samples. Also, although the cancer cells already deficient in GABPbeta1L grew less aggressively after transplantation into mice, more work in mice is necessary, Laterra said. Researchers need to design an experiment to determine if cancer that has already developed in mice can be stopped by blocking or removing GABPbeta1L, he said.

Costello said his group and other collaborators will pursue two approaches in parallel: the creation of a small-molecule drug that targets GABPbeta1L and the development of a CRISPR-based therapy that can alter human genes so they will not produce GABPbeta1L. The CRISPR approach was done for the human brain cancer cells transplanted into mice in this experiment. The researchers are working with GSK on the former project. Both approaches are highly experimental, though, and will take several years to develop, Costello told Live Science.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Followers of science and health news, particularly those with a terminal illness, may get the impression that the dawn of a new, disease-free era is upon us — and nowhere is this idea more evident than in the latest buzzword in the health sciences, CRISPR.

With this tool, a form of genetic engineering, scientists can edit a genome — that is, alter a set of genes among the tens of thousands contained in an organism's DNA. With CRISPR, scientists may have the ability to remove or correct disease-causing genes or insert new ones that could theoretically cure disease, including cancer.

But the technology comes with both potential benefits and risks. [10 Amazing Things Scientists Just Did with CRISPR]

Two important CRISPR studies published this month underscore the promise and concerns. The first, from a multi-institute team led by researchers at the University of California, San Francisco (UCSF) and published in the journal Nature, revealed a new, more efficient way of making changes in the genome using CRISPR. This method, which uses electrical fields, drew widespread praise from the biomedical research establishment, as relayed in numerous news reports.

The second study, from the laboratory of Allan Bradley at Wellcome Sanger Institute in England, published a few days later in the journal Nature Biotechnology, suggested that CRISPR gene editing may be doing more damage than scientists thought.

So, what's going on? And how close are scientists to actually using CRISPR to effectively treat cancer?

CRISPR getting crisper

CRISPR is one tool among many in the 40-year-old field of genetic engineering, storming onto the scene in 2012. The technology offers unprecedented precision in editing the genome — that is, opening up a strand of DNA and correcting an error typed into the genetic code. CRISPR is not the first method for editing genes, but it seems to be the most precise so far.

Here's how it works: CRISPRs, short for clustered regularly interspaced short palindromic repeats (don't worry — most scientists can't remember this), are stretches of DNA found in bacteria and other microbes. These microorganisms use CRISPRs to find and remove viral DNA that has invaded their genomes. It's a host defense system. The CRISPRs and associated proteins, such as Cas9, essentially snip out the viral DNA and patch things up.

The technology is just now entering the realm of clinical application, with still only a handful of patients receiving the treatment, all starting in 2017. However, CRISPR is used now — broadly and remarkably successfully — in creating laboratory animals and cell lines with key genetic characteristics that help scientists better study human diseases.

In this regard, part of the CRISPR promise has already been realized in terms of "really advancing the landscape of research in biomedicine in a way nobody thought possible," said Fyodor Urnov, deputy director of the Altius Institute for Biomedical Sciences in Seattle, who uses CRISPR and other methods to edit human genes in the lab. [7 Diseases You Can Learn About from a Genetic Test]

And as for the other promise, clinical application, "There's really good news on the horizon," Urnov told Live Science.

CRISPR advances — and pitfalls

For CRISPR to work, the short strands first need to get into the nucleus of a cell, where DNA is found. To transport CRISPRs there, scientists use modified viruses, a decades-old delivery method. These harmless viruses invade the cell, as they are wont to do, and deposit the package. But manufacturing these viruses in significant numbers for clinical use can take months or a year, and critically ill patients usually don't have that long to wait.

That's why the new Nature article elicited such excitement and praise. In that work, scientists used electrical stimulation, not viruses, to ferry genetic material into the cell nucleus. This is called "electroporation," and it shortens the process to a few weeks. The method could greatly speed research efforts.

But the other new study, though it didn't reference the research on electrical stimulation, warned that CRISPR remains rife with danger. The technique can alter more parts of the DNA than scientists realized, including those parts located farther away from the region targeted by CRISPR, the researchers said.

In short, CRISPR can snip too much, and depending on what's snipped, this inaccuracy could spell trouble, the researchers wrote. Scientists using CRISPR might inadvertently cut out a cancer-suppression gene, for example.

And these errors could occur regardless of the ferry mechanism used, whether electroporation or viral vector, lead study author Michael Kosicki, a graduate student at the Wellcome Sanger Institute in England, told Live Science.

But Urnov, who wasn't involved in either study, said that he cautioned against drawing broad conclusions from the second paper. That study used mouse cells, not clinic-grade human cells, and did not use a CRISPR-Cas9 strain engineered for clinical use, he said. You can't compare the off-target cleavage seen in the mouse DNA to what might happen in the human studies, he added.

In the U.S. and Europe, no clinical trial would begin without passing through "rigorous safety review," Urnov said.

There are two primary safety concerns: 1) making sure the genetic change was made correctly, without snipping other regions, a danger that the second study highlighted and 2) ensuring the genetic change of interest, even if done correctly, is safe and that its alteration or removal has no unforeseen ramifications.

What cancer patients need to know

CRISPR has the potential to revolutionize cancer therapy, chiefly in the realm of immunotherapy. In cancer immunotherapy, the treatment genetically engineers immune cells called T cells to find and kill cancer cells, as if they were a cold virus. In 2017, the U.S. Food and Drug Administration approved two drugs for a type of immunotherapy called chimeric antigen receptor (CAR-T) immunotherapy. Neither treatment involved CRISPR, though.

But doctors worldwide are using both traditional immunotherapy and new CRISPR techniques to increase the number of cancer types that they can treat reliably, albeit all at the preliminary experimental level.

If you are cancer patient, the first thing you need to realize is that you don't necessarily want to be in need of these experimental therapies. If you do need one, that means the conventional treatments — chemotherapy, radiation and surgery — have failed. [7 Side Effects of Cancer Treatment, and How to Cope with Them]

The second thing that cancer patients must understand is that experimental CRISPR treatments are, well, experimental and not available to many. These treatments are offered primarily at research hospitals, and they don't work for the majority of patients. Doctors in those settings are trying to figure out if and how these therapies work, or how they need to be tweaked, so these physicians need to recruit patient-volunteers who have well-defined cancer types.

So, this is the key question: How close are we, really, to curing cancer with CRISPR? Of course, no expert can say for sure. Urnov said that he is confident that CRISPR technology will bring about more and more cures to a broad range of diseases, including certain cancer types, in the next few years.

Dr. Alexander Marson of UCSF, senior author on the electroporation study, suggested that we may get an answer about CRISPR's cancer applications rather soon. His team hopes to treat siblings who have an autoimmune disease so rare that it lacks a name. These patients' T cells have already been corrected using the non-viral gene-targeting method in the lab. The goal is to transfer corrected cells back into the children to treat their disease. Important  work remains ahead to develop clinical-grade corrected cells, test their safety and seek regulatory approval, Marson told Live Science.

Marson and other members of this team also are partnering with the Parker Institute for Cancer Immunotherapy in San Francisco to engineer cells to treat a variety of cancers, now that CRISPR-mediated immune cell reprogramming can be done so effectively without relying on viruses.

This, hypothetically, would quicken the pace of CRISPR's entry into clinical studies and arrival as a mainstream treatment.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Could an aspirin a day keep the Alzheimer's away? If only it were that simple. And yet, new research suggests that there does seem to be some hope that aspirin, one of the most widely used medications in the world, may help to treat some aspects of this devastating brain disease.

Scientists have discovered that aspirin works with certain subcellular machinery in the brain to prevent the buildup of amyloid plaque, sticky blobs of protein around brain cells that are thought to be the primary cause of Alzheimer's disease, according to the new study, which was done in mice.

In the study, mouse experiments revealed that aspirin enhanced the ability of lysosomes, which are sort of like the cells' waste processors and recyclers, to clear amyloid plaque or stop it from forming in the first place. Aspirin should have the same effect on the human form of Alzheimer's, too, said the researchers, who published their findings today (June 2) in The Journal of Neuroscience.

Alzheimer's disease, the most common type of dementia, is a progressive brain disease that affects nearly 6 million Americans and is the sixth-leading cause of death among all U.S. adults, according to the Centers for Disease Control and Prevention. There's no cure, and medications have had very limited success in slowing the progression of the disease. [9 Surprising Risk Factors for Dementia]

Aspirin, also known as acetylsalicylic acid, is an inexpensive drug with a century-long history of being safe in low doses, aside from possible stomach irritation and a small risk of internal bleeding. Many adults take a low-dose aspirin daily as a mild blood thinner to help prevent heart attacks.

In fact, several population-wide studies on aspirin and heart health have found that aspirin may also lower the risk of Alzheimer's disease, albeit modestly. A meta-analysis that Chinese researchers published in March 2018 in the journal Frontiers in Aging Neuroscience reviewed 18 population-wide studies and found that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, was associated with a 20-percent lower risk, on average, of developing Alzheimer's disease.

Aspirin and Alzheimer's

Building on the possible connection between aspirin and Alzheimer's prevention, first observed more than a decade ago, researchers at Rush University Medical Center in Chicago crafted experiments that entailed giving aspirin to mice with a mouse version of Alzheimer's disease and also applying aspirin directly to mouse brain cells growing in the lab.

Both approaches — in vivo and in vitro — appeared to prevent or reverse the biological signs of Alzheimer's disease, said lead study author Kalipada Pahan, a professor of neurological sciences at Rush University.

Aspirin activates a cellular receptor called PPARα, which, in turn, regulates a protein called TFEB, a so-called master regulator of lysosomal activity, Pahan explained. In short, aspirin helps cells clear cellular debris, including proteins that form amyloid plaque. [5 Interesting Facts About Aspirin]

"We expect to see similar results in human brain cells," Pahan told Live Science.

Indeed, other drugs, such as the triglyceride-lowering drug gemfibrozil (sold as Lopid), also target TFEB, Pahan said, but aspirin is safe enough to be available without a prescription and has fewer side effects.

Rajini Rao, a professor of physiology at Johns Hopkins University School of Medicine in Baltimore who was not involved with this research, said the new study "offers an elegant mechanistic explanation for protective effects of aspirin seen at the cellular and model animal level."

However, she noted that it was unclear from the study whether the degree of improvement in amyloid removal would translate into better brain function.

"Results from epidemiological studies on aspirin use and dementia are mixed," Rao told Live Science. "While there have been some indications of protection, other studies have failed to replicate this. Unfortunately, this is the case for virtually every drug used in Alzheimer's trials — over 99 percent have failed in the clinic — which is why Alzheimer's research is especially challenging."

Pahan said that, although aspirin is relatively safe, it does carry some risks when used daily and shouldn't be used casually as an unproven way to treat or prevent Alzheimer's disease. He added that for aspirin to stimulate lysosomal activity, the cellular receptor PPARα needs to be present, and thus any person with Alzheimer's who lacks a sufficient number of PPARα receptors wouldn't benefit from aspirin. That may explain the mixed results of population-wide studies, Pahan said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Physical activity is good for both the body and mind. Indeed, doctors have long known that exercise improves thinking and slows the rate of cognitive decline, particularly among older adults. But what kind — and how much — exercise is needed to achieve a healthier brain?

The answer seems to be just about any kind of exercise that gets you moving, as long as you stay with it, according to an international study published yesterday (May 30) in the journal Neurology Clinical Practice.

Walking, running, weight training, yoga or tai chi … it's all good, provided you do it a few times a week for at least 52 hours over the course of six months or so. A key finding in the study was that the exercise doesn't need to take place within a set number of hours per day or week. [7 Ways the Mind and Body Change With Age]

"The real-world impact is that you can break that [52 hours] up" into an hour here or there, said lead study author Joyce Gomes-Osman, a clinical neuroscientist at the University of Miami Miller School of Medicine. "This is encouraging, because it tells you that you may not necessarily need an hour a day. If you exercise a few days a week and start racking up those 'points,' and you do this over several months and you get to that 52-hour mark, this is when you can expect that your mind is going to become sharper."

Gomes-Osman noted that low-intensity "mind-body" exercises (such as yoga and tai chi) work just as well as high-intensity, strength-training and aerobic exercises.

The new research examined nearly 100 previously published studies on exercise and cognition, with a total of more than 11,000 participants whose average age was 73. The common denominator across all these studies was that various forms of exercise all led to sharper thinking if the participants achieved this minimum 52-hour target over roughly six months, Gomes-Osman said. Studies with fewer hours of exercise or shorter time scales did not yield positive results.

Gomes-Osman told Live Science that, as a neuroscientist practicing physical therapy, she has long desired to prescribe a "dose" of exercise to her patients, employing the same precision and individualized approach that a physician would use to prescribe a heart medication. Now, she's closer to that goal, she said.

"We often hear advice to be more active" given with the aim of improving thinking, Gomes-Osman said. But, "What does that mean? Does that mean the person needs to do 30 minutes a day every weekday? Or an hour a day? And what kind of exercise?"

Referring back to heart disease, Gomes-Osman said there are recommendations for the precise amount of rigorous or moderate exercise needed to improve heart health. But a corresponding dose of exercise for cognitive health was not known … until now. This is an important new understanding, she said, because there are no drugs to improve or slow cognitive decline. Exercise, for now, is the only approach.

Dr. Douglas Scharre, director of the Center for Cognitive and Memory Disorders at The Ohio State University Wexner Medical Center, who was not involved with new research, agreed with the study's conclusions.

"I believe that the take-home message is that physical exercise should be done consistently for the long term to gain maximum cognitive benefits," Scharre told Live Science. "It does not seem to matter how much or how long or what type of exercise, just that you do it regularly over the long term."

The researchers found that real cognitive gains were in specific areas of thinking — namely, planning and initiation of tasks, processing speed and executive function, which is the ability to focus and manage tasks, Gomes-Osman said. Her team found that participants’ memory improvement was only seen in about half of the studies analyzed, so averaged together, they could not conclude that exercise improved memory.

That makes sense, according to Scharre, because those nonmemory elements of cognition make common use of frontal brain regions that get more of a workout during exercise than brain regions related to memory. [10 Things You Didn't Know About the Brain]

"Exercise is a fabulous brain activity," Scharre said. "The brain is being activated very much during exercise. We have to learn how to control our muscles to do the exercise; we need to focus attention on doing the tasks; we have to determine if we are feeling tired or … plan to go slower the next time to avoid a certain activity that causes pain. Basically, 'use it or lose it,' I believe, is just as true for the brain as it is for muscles."

Scharre added that watching TV and not socializing does not use your brain as much as exercise.

The researchers, who include scientists from Brazil and Spain, wrote that those brain functions that consistently improved with exercise across all studies examined — processing speed, planning and focus — are the very same functions that start to falter with the onset of age-related cognitive decline.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Why are infections from the viruses that cause West Nile fever, dengue and even Zika deadly for some people but mild in others? 

The answer thus far has been chalked up to being mostly a matter of human genetics. But a major factor in whether these viruses wreck your health may come down to the profile of bacteria that inhabit your intestines, called the gut microbiome, a new study in mice suggests.

The study, published today (March 27) in the journal Cell Reports, found that these particular viral infections were more likely to be deadly if the infected mice had been treated in advance with antibiotics. (More research is needed to confirm the findings in humans, whose microbiomes differ from those of mice.) [9 Deadliest Viruses on Earth]

The reason is that antibiotics wipe out the gut microbiome, and this weakened microbiome somehow"impairs your immune system," senior study author Dr. Michael Diamond, a professor of medicine, molecular microbiology, pathology and infectious disease at Washington University School of Medicine in St. Louis.

"The immune system is activated differently if the gut does not have a healthy microbiome," Diamond said in a statement. "If someone is sick with a bacterial infection, they absolutely should take antibiotics. But it is important to remember that there may be collateral effects. You might be affecting your immune response to certain viral infections."

Antibiotics kill bacteria, not viruses. Nevertheless, some doctors prescribe antibiotics for viral infections such as colds and the flu as an extra precaution, perhaps to ease the concerns of patients who think they need medicine, or to prevent a subsequent bacterial infection from arising while the body is weak. But that practice — giving antibiotics as a preventive measure— may backfire. 

"Taking antibiotics [by chance] could affect [the] responses" of the immune system to a variety of viruses, Diamond told Live Science. "That would be an implication of our study, but, of course, [this] requires further validation — especially in humans."

Gut bugs and viruses

Scientists have uncovered many beneficial roles of the gut microbiome. Microbes in the small intestine help digest food, synthesize vitamins and regulate metabolism. What's more, the dominance of "good" bacteria helps to prevent the establishment of harmful bacteria, such as Clostridium difficile (C. diff.), which can cause a difficult-to-treat infection that can be life-threatening.

Only in recent years, however, have scientists homed in on the direct connection between the gut microbiome and the immune system. The presence of healthy bacteria seems to improve the body's ability to produce T cells, a type of white blood cell that attacks and destroys viruses and other disease-causing microbes, Diamond said.

In the new study, the researchers infected mice with the Zika, West Nile and dengue viruses, all of which are part of a group of viruses called flaviviruses. All three viruses were more harmful to the mice who had received antibiotics prior to infection than to the mice that didn't receive antibiotics, the researchers found.

The researchers then examined West Nile virus in greater detail. This virus is typically spread by mosquitoes and can cause swelling in the brain. The researchers gave mice either a placebo or a cocktail of four antibiotics — vancomycin, neomycin, ampicillin and metronidazole — for two weeks before infecting them with the virus. About 80 percent of the mice that received no antibiotics survived the infection, while only 20 percent of the antibiotic-treated mice did. [5 Things You Need to Know About West Nile Virus]

Different antibiotic treatments administered separately or in combinations led to different changes in the bacterial community in the mouse gut, and these changes correlated with vulnerability to the viral infection in the study. For example, treatment with ampicillin or vancomycin alone made the mice more likely to die from West Nile infection. Metronidazole had no effect alone, but it amplified the effect of ampicillin or vancomycin.

"Once you put a dent in a microbial community, unexpected things happen," lead study author Larissa Thackray, an assistant professor of medicine also at Washington University School of Medicine in St. Louis, said in a statement. "Some groups of bacteria are depleted, and different species grow out. It's likely that antibiotic use could increase susceptibility to any virus that is controlled by T-cell immunity, and that's many of them."

Independent research on rodents has found that a healthy microbiome may also help control influenza virus and lymphocytic choriomeningitis virus, a type of virus that infects rodents and is similar to the virus that causes Lassa hemorrhagic fever and similar diseases in humans.

The big question, the researchers said, is to what degree the microbiome outweighs other factors in disease progression, such as age, genetics, prior viral exposures and other diseases a person might have. In other words, does a person's microbiome play a larger role than these other factors in how bad a viral infection will be? More research is needed, particularly in humans.

Still, the findings suggest that for humans, taking antibiotics unnecessarily may be unwise because of the potential effects on immune responses, Diamond said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Could your pee reveal your youth? Or perhaps your advanced age? Scientists in China think so. In a study published today (Feb. 27) in the journal Frontiers in Aging Neuroscience, researchers say they have identified a natural chemical in urine that appears in higher concentrations as we age.

The researchers said the chemical may serve as a marker of your "biological age," or how fast you're aging, as opposed to your chronological age, which is based on your birth date. It's easy to detect in urine, too, they added.

The name of the chemical is a mouthful — 8-oxo-7,8-dihydroguanosine, or 8-oxoGsn for short. It's a byproduct of slow, lifelong damage to RNA, an important molecule that interacts with DNA to enable gene expression and to create proteins in the core of most cells. [7 Ways the Mind and Body Change with Age]

If aging is defined as a prolonged buildup of damage to cells and tissues, then something that measures the deterioration of RNA, a molecule essential for maintaining healthy cell function, would be a proxy for measuring aging, said lead study author Dr. Jian-Ping Cai, of the MOH Key Laboratory of Geriatrics at Beijing Hospital and the National Center of Gerontology in Beijing.

Humans age at vastly different rates, based on a combination of genetics and environmental factors. So, finding an accurate biomarker to measure the rate of aging has been akin to a search for the Holy Grail for many in the field of geriatric medicine.

Such a biomarker could be used to determine a person's age at the cellular level and thus identify their risk for developing age-associated diseases, such as arthritis, heart disease and Alzheimer's disease.

Physical features such as wrinkles and gray hair can belie the internal youthfulness that many older people might still have. Someone in their 50s with no gray hair, for example, may be aging faster and at a greater risk for age-related diseases than a gray-haired grandmother in her 70s.

Searching for a marker

Cai and his colleagues, from West China Hospital at Sichuan University in Chengdu, China, searched for a biomarker that would be based on a leading aging theory, called the free radical theory of aging. A free radical is a highly reactive atom or molecule that is produced in the presence of oxygen, in a process called oxidation. If not neutralized by an antioxidant, the free radical can interact with and damage other molecules at a subcellular level.

Free radicals "produced during normal metabolism can cause oxidative damage to biomolecules in cells, such as DNA and RNA," Cai told Live Science. "As we age, we suffer increasing oxidative damage, and so the levels of oxidative markers increase in our body."

The molecule 8-oxoGsn is one such marker; it is a well-known byproduct of the oxidation of guanine, one of the four base pairs found in DNA and RNA.

In previous studies on mice, rats and monkeys, Cai and his colleagues found that levels of 8-oxoGsn increased in the urine of these animals as they aged. In their latest work, the researchers turned to humans — more than 1,200 Chinese males and females between 2 and 90 years old. Similarly, they found an age-dependent increase in urinary 8-oxoGsn in participants 20 years and older. In other words, levels of the biomarker were higher in people ages 20 and older.

Levels of 8-oxoGsn were about the same between men and women, except in postmenopausal women, who showed higher levels. This may be a result of the decrease in estrogen levels that happens during menopause, as estrogen is known to have antioxidant effects, the researchers said.

Cai said his group hopes to validate their findings in a much larger study, which is feasible because the measurement technique they developed can analyze 10 urine samples per hour.

Should 8-oxoGsn prove to be an accurate biomarker for the rate of aging, it could be used in rodents, monkeys and humans to test interventions to slow aging, such as calorie restriction, because changes in the levels of 8-oxoGsn could be tracked over a short span of time instead of the entire life span of the test subject, as is the case for such studies now.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

These "biohybrid" robots could be endowed with muscle cells to help them perform subtle movements. And on a microscopic scale, tiny robots could be merged with bacteria to ferry them through the body for precision medical procedures.

And the future, it seems, is happening now. [Super-Intelligent Machines: 7 Robotic Futures]

In a new review of studies, an international group of scientists and engineers described the state of biohybrid robotics — a field that is entering a "deep revolution in both [the] design principles and constitutive elements" of robots. The review was published today (Nov. 29) in the journal Science Robotics.

"You can consider this the counterpart of cyborg-related concepts," said lead author Leonardo Ricotti, of the BioRobotics Institute at the Sant'Anna School of Advanced Studies, in Pisa, Italy. "In this view, we exploit the functions of living cells in artificial robots to optimize their performances."

Scientists have created robots of all shapes and sizes with increasing complexity in recent decades. Some robots function well on assembly lines, tightening bolts or welding together sheets of metal. Miniaturized robots smaller than a millimeter are being developed to be placed in the body to kill cancer cells or heal wounds.

But what's lacking among all these fascinating robots is the range of fine movement and the energy efficiency found in living organisms, which evolved toward perfection over the course of millions of years, Ricotti told Live Science. That's why it's necessary to incorporate elements of living organisms into robots, he said.

If robot movement and efficiency are fine-tuned, scientists could be use them to explore the human body, monitor environments too small or intricate for current robots, or manufacture products with greater precision, the authors wrote in the review.

Actuation, or the coordination of movement, is a persistent hurdle in robotics, Ricotti said. For example, robots can be designed to easily lift heavy weights or make precision cuts, but they have difficulty coordinating actions as subtle as cracking an egg cleanly into a bowl or caressing a distressed individual. Their initial movements are jerky.

Animal movements, in contrast, start gently on a micro scale as a cascade of molecular machinery becomes activated inside nerve cells, and culminate in large-scale muscular motion, according to the review.

This raises the possibility that animal tissue, such as cardiac muscle or insect muscle, could provide precise actuation and steady movement in robots. For example, a group led by Barry Trimmer of Tufts University, a co-author of the Science Robotics paper, has developed worm-like biohybrid robots that move via the contraction of insect muscle cells.

Another problem in robotics is the power supply, particularly for micro-robots, in which the powering device can be bigger than the robot itself. Biohybrid robots can overcome this obstacle as well, Ricotti said. His colleague Sylvain Martel, of Polytechnique Montréal, also a co-author of the Science Robotics paper, is using magnetotactic bacteria, which naturally move along magnetic field lines, to transport medicine to hard-to-reach cancer cells. Martel's group can direct the bacteria with external magnets.

There are limits to what these biohybrid robots can achieve, though, Ricotti said. Living cells need to be nourished, which means that, for now, these robots tend to be short-lived. Also, biohybrid robots can operate only in the temperature range suitable for life, meaning that they can't be used in extreme heat or cold.

Despite these challenges, Ricotti and his colleagues said, the field of biohybrid robots is rapidly evolving from the "art of possible" to the science of "reliable manufacturing."

It may be that, in the near future, our cyborg descendants will be cured by biohybrid robotic medicine — administered, no doubt, by an android doctor.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

WASHINGTON — Humans and many other animals express a range of social behaviors, from cooperation to aggression. But as innate as these behaviors may be, little is known about which brain regions control them.

But now, new tools can probe the brains of living animals while they are engaged in social interactions, providing insights into how the brain controls certain behaviors.

These tools — which involve electrodes implanted into the brains of animals — have also revealed that brains likely don't operate in isolation. [10 Things You Didn't Know About the Brain]

Four independent studies, presented here yesterday (Nov. 13) at the annual meeting of the Society for Neuroscience, highlighted some particularly interesting findings about the "social brain."

Among some surprises were findings that social aggression is closely associated with the brain's memory region, that cooperation is more a self-serving strategy than an empathetic one, and that there is biological evidence that two minds really can be on the same wavelength.

"We're beginning to see a striking aspect of the brain … that brains are wired for social interactions," said Dr. Robert Green, a professor of neuroscience and psychiatry at the University of Texas Southwestern Medical Center, during a news conference about the studies.

Although scientists have seen hints there must be an underlying brain architecture guiding social behavior, only now are they observing this architecture directly in living brains, Green told Live Science. This understanding could lead to treatments for antisocial behaviors, he said.

Green also noted these new insights are a result of studying brains interacting with each other simultaneously, as opposed to traditional studies of probing only one brain at a time in isolation.

Social aggression

One research group, from Columbia University in New York, investigated the phenomenon of social aggression, which is aggression toward a fellow species member as opposed to prey. The researchers found that the hippocampus, which is the brain's memory center, appears to drive this type of aggression in mice — in this case, the attack of one mouse by another who didn't recognize it as a friend.

"The second that aggression started is when [nerve signals from the hippocampus] turned on really strongly," said Félix Leroy, a neuroscience associate research scientist at Columbia University who led the study. "We're now trying to look at the exact relay of signals in these brain regions to confirm that this burst of activity precedes aggression."

Leroy's team also found that they could block aggression by stimulating a region of the hippocampus called CA2. The findings imply that CA2 could be a therapeutic drug target to treat abnormal aggression associated with neuropsychiatric diseases, Leroy said, though much more research is needed to confirm such effects in humans. [Fight, Fight, Fight: The History of Human Aggression]

Strategic thinking

In another study, scientists at the University of Pennsylvania found that strategic thinking, not empathy, may underlie cooperative behavior so common in primates. These researchers constructed an experiment in which rhesus macaques were taught play a computerized version of the classic game of "chicken," which itself sounds like an amazing feat. But there's more.

When playing against each other, two monkeys could strategize on ways to avoid crashing into one another and reap the highest rewards together. When just one monkey played against a machine, though, and the other one simply watched, the game-playing monkey suddenly had no interest in maximizing rewards for his one-time game companion. Instead, the game-playing monkey employed a different strategy to get the highest rewards only for himself.

"We found that neurons in a part of the brain [previously] linked to strategic thinking, but not in a part of the brain linked to empathy and shared experience, respond selectively when rhesus macaques cooperate," said Wei Song Ong, a postdoctoral neuroscience researcher at the University of Pennsylvania, who led the study.

Ong said she wasn't ready to concede that empathy isn't an important human trait, but she added that social cooperation may be much more of a selfish act than people would like to think.

Syncing up

What could be more social than brains acting in sync? Similar brain activity may be fundamental for how animals, including humans, interact to form social bonds, according to Dr. Miguel Nicolelis, a professor of neuroscience at Duke University School of Medicine in North Carolina.

Nicolelis' group built an experiment in which one monkey drives a vehicle to get a fruit reward while another monkey watches. Each time the driver monkey gets a fruit reward, the spectator monkey gets one, too. So they are linked, Nicolelis said during the news conference.

"To our shock, what we found is that as these animals are interacting … both brains are highly synchronized," Nicolelis said. "We have, in fact, in some instances, 60 percent of [the firing of neurons] in the motor cortexes of both monkeys [happening] precisely the same time."

The synchronicity became more precise as the monkey got closer to the fruit reward or, as shown during a second experiment in the study, as the spectator monkey helped control the vehicle remotely, Nicolelis said. The finding suggests that the optimal performance of social tasks, such as gathering food, requires synchronization of brain activity across the brains of all subjects involved — in other words, with everyone being on the same wavelength.

Conversely, Nicolelis said that some antisocial neurological disorders, such as autism, may result in an inability to establish such interbrain synchronization. He said he hopes to test this in his lab with human subjects.

The "social brain"

Taken together, the collection of studies presented at the news conference "opens a new chapter in neuroscience, [as we] have the ability to assess multiple brains simultaneously," Nicolelis said.

"We can no longer think of brains in isolation," Nicolelis said. "The 'social brain' idea that we are talking about supersedes the notions that [scientists] have developed for brains in isolation, because the brain is not just a passive device alone in the world. … The action on one animal involves the actions of other animals."

Whereas neuroscience has, up until recently, focused on the study of neurons or networks of neurons, the new reality is that behavior arises from a network of different brains interacting, Nicolelis said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Viruses are tricky beasts. Some of these "submicroscopic" pathogens can "go to sleep" inside a person's body, essentially hiding from the immune system indefinitely, only to reactivate and cause illness later.

Now, scientists have learned how to prevent one type of virus, the herpes virus, from slipping into its sleep-like dormant phase and out of sight. This is a major step in understanding the virus's unique ability to essentially hide from the immune system, the scientists say.  

More than 80 percent of the world's population is infected with herpes simplex virus (HSV), according to the World Health Organization, which includes HSV-1, which causes cold sores, and HSV-2, which causes genital warts.

But most people who are infected with the virus have no symptoms until something external — stress, illness or even sunlight, for example — triggers the virus to wake up and start replicating and spreading. This, in turn, prompts the immune system to attack the virus, resulting in inflammation and the characteristic blisters around the mouth, lips, nose or genitals. It's during this "reactivation" that the virus can spread from person to person. [The 9 Deadliest Viruses on Earth]

Unlike viruses such as those that cause the common cold or the flu, the herpes virus usually quickly enters a latent, or dormant, mode, in the human body. Scientists have tried to study this process. But in a laboratory setting, they have had difficulty placing the live virus to "sleep" without extreme and harmful measures, akin to clubbing your subject into an unconscious state and hoping it wakes up normally.

Now, in the first of two advances, scientists at Princeton University have developed a laboratory technique that more naturally induces the herpes virus into a latent mode, as gently as a lullaby, allowing them to better simulate the natural life cycle of the herpes virus. The same group of researchers then used this technique to find a key set of proteins involved in the virus's tendency to sleep and wake.

The findings were published yesterday (Oct. 27) in the journal PLOS Pathogens.

Sleeping viruses

Viruses that don't quickly go into hiding are easier for the immune system to find and kill. But this is not the case for the herpes viruses, which stay with you for life.

These viruses are part of a subfamily of the virus called alphaherpesvirinae, which is known to infect and then hide in nerve cells. The immune system has learned to treat these viruses with kid gloves, because immune cells can't outright kill these herpes viruses without killing the nerve cells that serve as a host.

"Usually, killing a virus infection by the immune system involves killing the infected cells," said senior study author Lynn Enquist, a professor in molecular biology at Princeton University. But "in this case, these cells would be the [nerve cells] that are irreplaceable. So, 'putting the virus to sleep' is a better and more protective way for the nervous system."

A major question about herpes, however, is although the virus can sometimes cause symptoms immediately, why, most of the time, does it go into hiding right away?. The answer would reveal better ways to control infections.

"Escape from silencing"

To get to the heart of the issue — what causes the natural virus to stay awake and "escape from silencing," as the researchers described it — the scientists used a type of herpesvirus called pseudorabies virus, which is closely related to HSV-1.

The researchers' first step was to develop a method that would essentially put the virus to sleep in infected nerve cells. The technique involved using a novel three-chamber environment in which the nerve cell's nucleus and its tentacle-like axon structures are isolated.

Then, the researchers focused on how to wake the virus up. They discovered two ways to do so: with chemical stress signals present at the time the virus enters the cells, as expected; or in the presence of a cluster of proteins called viral tegument proteins, a new concept.

Further analysis ruled out a hypothesis that perhaps it's the size of the viral load, or the amount of virus in a person's system, that somehow overrides the typical immune response to let the viruses sleep. Rather, the researchers found that the viral tegument proteins alone were the key trigger, acting like a splash of ice water on the face of the viruses, waking them up or otherwise keeping them awake and active.

"The question we and others are working on now is to determine if" this approach for waking viruses up in the lab is the same as what goes on naturally in the immune system when a virus wakes up, Enquist told Live Science. "We think there is a lot in common." [Tiny & Nasty: Images of Things That Make Us Sick]

The Princeton researchers' technique "represents an important advancement," in studying the virus latency cycle and controlling infections, said Felicia Goodrum Sterling, an immunologist at the University of Arizona Cancer Center, who was not involved in the research.

"In understanding herpesvirus latency, model systems are everything," Goodrum Sterling said. "This is the first model system that does not require drug treatment" to put viruses to sleep.

A better understanding of this mechanism, the researchers said, may lead to a class of drugs that could target viral tegument proteins to prevent them from waking up viruses or keeping them awake, thus preventing symptoms and the spreading of the virus to other people.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Want to follow conversations better in a noisy restaurant or bar? There soon may be an app for that.

Researchers in Boston have developed a computer game that trains the brain to better understand words in noisy situations. After playing the game a few hours per week for two months, elderly people who had hearing loss were able to correctly identify 25 percent more words spoken in noisy conditions, compared with before the study began.

Their hearing didn't get better, strictly speaking. Rather, it was their ability to make sense of what they'd heard that improved. In other words, the computer game helped their brains better discern signal from noise. [7 Ways the Mind and Body Change with Age]

"The test we used was designed to try to assess 'real-world' hearing abilities," said lead study author Jonathon Whitton, an audiologist at the Massachusetts Eye and Ear Infirmary in Boston. "Some participants reported being able to hear better in noisy situations or that their spouses noticed that they weren't asking for repetition as much."

The findings were published today (Oct. 19) in the journal Current Biology.

To test how well the game worked, the researchers conducted a double-blind, placebo-controlled study in which neither the participants nor the researchers knew who was playing the game that was intended to improve the individual's ability to understand what he or she heard and who was playing an ordinary, placebo game.

The study enrolled 24 adults, with an average age of 70, who had mild to severe hearing loss and who had worn hearing aids for an average of seven years. The participants were randomly assigned to one of two training groups and asked to spend 3.5 hours per week for eight weeks playing a game. The members of the placebo group played a game that challenged their auditory memory but that wasn't intended to improve hearing. The other group played the "real" game that was a bit like the children's game "hot-cold," Whitton said.

"As you get closer to or farther from some hidden target, sound changes in an informative way," Whitton told Live Science. "Participants had to track subtle changes in an ongoing sound to guide their finger along a tablet screen while trying to ignore [auditory] distractions."

When tested a few days after their brain training, the participants who played the placebo game didn't have any improvement in their ability to hear in a noisy situation. Those who played the real game, however, could discern 25 percent more words in the presence of high levels of background noise compared to the baseline test that was conducted at the start of the study. The boost amounted to three times more words than those provided by their hearing aids alone.

"Even catching a few extra words can make the difference between being able to stay in a conversation or fall out," Whitton said. And although the test was done on older adults with hearing aids, "there is reason to believe that this approach would also provide benefit for middle-aged individuals who have trouble hearing but do not use hearing aids," he added.

The researchers noted that the study is small, and more research is needed before the game could be recommended to help with hearing.

Indeed, they hope to enroll more people and enlarge their study as they fine-tune the game, which was developed from more than a decade of research on laboratory rodents.

The researchers said that they envision a time when hearing challenges might be managed through a combination of auditory training software coupled with the latest in-ear listening devices.

"We look forward to a future where auditory perceptual training software that has been inspired by principles of brain plasticity, not audiological testing, is packaged with new advances in these listening devices," said senior study author Daniel Polley, an associate professor of otolaryngology at Harvard Medical School and director of the Lauer Tinnitus Research Center at Massachusetts Eye and Ear.

"There is reason to believe that the sum of these benefits would be greater than could be expected from any one approach applied in isolation," Polley told Live Science.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Have you ever struggled to open a stubborn package? If so, that may be a good thing…if your baby is watching.

A new study finds that babies as young as 13 months old can learn perseverance by watching you muddle through failure and repeatedly attempt to reach a goal.

In the study, researchers presented babies with a challenge to activate a musical toy box. Babies who had just witnessed an adult struggle with a different kind of task a few seconds earlier, such as removing a key chain from a carabiner, tried harder to overcome their own little challenge, compared with babies who didn't witness such a struggle. [11 Facts Every Parent Should Know About Their Baby's Brain]

The findings, published today (Sept. 21) in the journal Science, suggest there is "potential value in letting children 'see you sweat,'" the researchers wrote in their paper. "Showing children that hard work works might encourage them to work hard too."

Previous studies have shown that school-age children who persevere through modestly complicated tasks tend to be more successful academically later in life. However, scientists have not been able to determine how and when children develop such true grit.

Most studies in this area have focused on children in grade school and middle school. Researchers at Stanford University, for example, found that seventh-graders who thought that intelligence was malleable and that effort determines achievement outperformed their peers who thought intelligence was fixed. The study was conducted over a two-year period through middle school.

In the new study, researchers at the Massachusetts Institute of Technology (MIT) wanted to see if babies might be inspired to persevere by witnessing a struggle that resulted in success. To do so, they recruited more than 260 babies (and their guardians).

The babies, ages 13 to 18 months, were placed in three testing categories: A third of them watched an adult struggle and succeed with a task; a third watched adults succeed in a task easily; and a third were in a control group, not witnessing adults perform any kind of task.

The task was either opening a container or removing a key chain from a carabiner. In the first group, the adult would pretend to struggle for 30 seconds with the task and then succeed, all the while making eye contact with the baby and saying things such as, "Hmm, I wonder how I can get my toy out of here?"

In the second group, the adult completed the task without struggling in 10 seconds, and then repeated this task twice more over the next 20 seconds.

In all the groups, an adult would give the baby a trick music box with a big button that was inert and a hidden button that played music. The adult would activate the musical sound, hand the toy to the baby and leave the room. [Top 5 Benefits of Play]

Although no babies found the hidden button, those who had witnessed an adult struggle pushed the inert button significantly more often and probed the toy longer before giving up, compared with the babies in the other groups. In fact, there were no significant differences in the amount of time both other groups examined the toy.

The researchers hope that "the study reassures parents that they don't have to make everything look like it comes easily," said lead study author Julia Leonard, a graduate student at MIT.

Leonard added that more research is needed to gauge the effects of watching adults struggle through tasks on babies' perseverance. "We have a lot of respect for parents and wouldn't presume to use a single laboratory study as a basis for parenting advice," Leonard told Live Science.

"However, we hope the study might interest parents, and we'd be interested in knowing from parents whether simply showing children a couple of examples of struggling before succeeding seems to help their children persist more on tasks where the parent is confident that the child might succeed with effort," she said.

And what about watching parents struggle through a task unsuccessfully? The researchers said they hope to investigate this in future studies. If an adult fails to achieve a goal, the baby might conclude that the task is beyond its ability, the researchers said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Living in your gut are trillions of microscopic squatters, mostly bacteria. There are likely thousands of different kinds of them, and they started moving in soon after you were born.

The bacteria may not be a part of your body like your brain or heart, but they nevertheless play a major role in shaping who you are. These microbes, known as the gut microbiome, help digest your food, set your metabolism rate, regulate your weight and moderate your immune system.

But in recent years, scientists have wondered whether the wrong balance of microbial populations — brought about by an unhealthy, Western-style diet — might be responsible, at least in part, for the rise in some modern chronic diseases, such as obesity and irritable bowel syndrome. [Body Bugs: 5 Surprising Facts About Your Microbiome]

So, a group of scientists led by microbiologist Justin Sonnenburg of Stanford University decided to study the gut microbiome in its most natural, preindustrial setting: by examining the Hadza people of Tanzania.

The Hadza comprise one of the last groups of humans living a traditional, nomadic, hunter-gatherer lifestyle, as all humans once did just a few tens of thousands of years ago. Despite having no access to modern health care, the Hadza are largely free from the chronic diseases that plague Americans.

What the scientists found is that the Hadza have a far more diverse gut microbiome compared to Americans. What's more, the types of gut bacteria vary greatly in number as the Hadza alter their diet from season to season.

The new study, published Aug. 25 in the journal Science, suggests that a person's diet strongly dictates the diversity of the gut microbiome, and that those people living in the industrialized world have a far less vibrant gut microbiome that may adversely affect their health.

An unchanged, ancestral lifestyle

The Hadza are an indigenous population living in the central Rift Valley of north-central Tanzania. There are fewer than 1,000 Hadza people left. Among them, only about 200 live a completely traditional lifestyle unchanged from that of their ancestors, gathering food daily and moving from region to region seasonally.

The Hadza's homeland has two main seasons: wet and dry. During the wet season, the Hadza forage for berries and honey; during the dry season, they hunt game such as antelope. Their diets differ dramatically during these two seasons, and the only common elements are fiber-rich tubers and the fruit of the baobab tree, both available year-round. But the Hadza eat no processed food, nor do they eat farmed food. [11 Ways Processed Food is Different from Real Food]

To study the gut microbiome of the Hadza people, the researchers took stool samples from nearly 190 Hadza men and women over a period of four seasonal changes, or about 18 months — seven collection dates in all.

Sonnenburg's group then analyzed the samples and found that the gut microbiome varied along with the change in diet from season to season, the first such evidence of a cyclical change in humans. Bacteria species present in stool samples collected in the dry season all but disappeared in the wet season, only to return in the next dry season.

Aside from having a greater diversity of gut bacteria compared with Americans, the Hadza have many bacteria species that other traditional groups in South America and Papua New Guinea also have — and that Americans lack, the researchers found. It's as if something about modern society is causing the disappearance of microbial gut species, the researchers said.

"The challenge is to understand the importance of the ecological role and functional contributions of [microbial] species with which humans coevolved but that are now apparently underrepresented or missing in industrialized populations," the researchers concluded.

One factor influencing gut microbiome diversity may be dietary fiber, the researchers said. The Hadza consume upwards of 150 grams (5.3 ounces) of fiber daily, 10 times more than what Americans consume, on average, according to the researchers. 

Sonnenburg said that his group cannot determine whether the Hadza microbiome is protective against chronic diseases, but there are "many arrows pointing in this direction right now."

He added that the relatively low life expectancy for the Hadza, 46 years, is due primarily to a high infant mortality rate and dying from accidents, such as falling out of a tree while collecting honey. But chronic diseases are rare, even among the older Hadza, he said.

Care for some raw honey comb and bee larvae? They're in season.

Follow Christopher Wanjek @wanjekfor daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Consider it another strike against not getting enough sleep: A new study finds that getting too little REM sleep may be linked to a higher risk of dementia later in life.

REM, or "rapid eye movement," sleep is one of four sleep stages, which also include two stages of light sleep and a stage of deeper sleep called slow-wave sleep. REM sleep is characterized by vivid dreams and high levels of brain activity, similar to the brain's state when its awake. Humans typically cycle through several periods of REM sleep between the other stages of sleep each night.

In the new study, published today (Aug. 23) in the journal Neurology, researchers found that the people who developed dementia had gotten significantly less REM sleep when examined overnight years earlier compared with the people who didn't develop cognitive problems. [Get Better Sleep in 2017]

The study does not prove that low levels of REM sleep cause dementia; rather, it shows an association between the two, said lead study author Matthew Pase, a senior research fellow at Swinburne University of Technology in Australia.

Pase offered several ideas for how REM sleep and dementia might be linked.

"On one hand, REM may help protect connections within the brain that are vulnerable to damage with aging and Alzheimer's disease," Pase told Live Science. "On the other hand, perhaps lower REM is caused by other potential dementia risk factors, such as heightened anxiety and stress. This requires further study."

Doctors have long known that poor sleep can result in mental and emotional health problems. But details about which types of sleep are associated with dementia and long-term cognitive decline have been lacking. More than 10 percent of Americans over age 65 have some form of dementia, according to the Centers for Disease Control and Prevention.

In the new study, the researchers looked at more than 320 people in the U.S. whose average age was 67. These people were already part of an ongoing, larger study on heart health. The researchers collected sleep data approximately half way through the as they followed the participants for an average of 12 years. During that time, 32 people (about 10 percent) were diagnosed with some form of dementia; among those 32 people, 24 were diagnosed with Alzheimer's disease.

The people who developed dementia spent an average of 17 percent of their sleep time in REM sleep, compared with 20 percent for those who did not develop dementia. The researchers found that for every 1-percent reduction in REM sleep, there was a 9-percent increase in the risk of dementia. The results held up even after the researchers adjusted for other factors that could affect dementia risk or poor sleep, such as heart disease, depression and medication use.

Also, the time that the people spent in stages of non-REM sleep was not associated with dementia risk, the study found. [5 Surprising Sleep Discoveries]

"The study is valuable, since it has identified inadequate REM sleep as correlating with dementia risk," said Dr. Pinky Agarwal, a neurologist at EvergreenHealth in Washington and a professor of neurology at the University of Washington. Agarwal was not part of the study.

"The current [scientific] literature is mixed and mostly identifies inadequate 'slow wave sleep' [a type of deep, non-REM sleep] as a risk, but these have been much shorter-duration studies," Agarwal told Live Science. Because REM sleep is thought to be related to how the brain processes and retains memories, the new findings make sense, she said; dementia is, in part, marked by memory problems. The research points to the need for closer follow-up to recognize signs of dementia in patients with decreased REM sleep, she added.

Indeed, Pase noted that his research group would like to understand why a lower amount of REM sleep is tied to an increased risk of dementia. He hopes to tap into a larger sample of data to examine the relationship between sleep and signs of accelerated brain aging, such as poor thinking, memory problems and loss of brain volume.

This further research might provide more information about how getting less REM sleep, or even poor sleep in general, could lead to the development of dementia, Pase said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

If you have ever taken an antibiotic, you likely know the drill: Finish the entire course of treatment, even if you are feeling better, or else you risk a relapse.

Worse, by not finishing, you might contribute to the dangerous rise of antibiotic-resistant bacteria.

The advice to always finish your antibiotics has long been considered medical dogma, and can be seen today on the websites of the World Health Organization, the U.S. Food and Drug Administration and other leading health authorities. [7 Medical Myths Even Doctors Believe]

But the advice is wrong, according to an opinion article published today (July 26) in the journal The BMJ.

"'Complete the course' is taught very widely, but it's been known to be wrong for quite a while," said Dr. Martin Llewelyn, a professor of infectious diseases at Brighton and Sussex Medical School in the U.K. and the lead author on the opinion piece.

Llewelyn said the advice is, at best, overly simplistic. The idea that stopping an antibiotic treatment early encourages antibiotic resistance is not supported by scientific evidence, he said.

Moreover, having everyone finish their antibiotics all the time may actually be increasing antibiotic resistance worldwide, because it's the taking of antibiotics for longer than absolutely necessary that increases the risk of resistance, Llewelyn said.

The original theory was this: Treating bacterial infections with an antibiotic kills those bacteria, but this may take a week or more to accomplish. If you stop treatment early, you have only killed the weaker of the bacteria, those bugs most readily wiped out by the antibiotic. The ones leftover are the tougher bacteria, which would have been killed if the treatment continued but now, in the absence of antibiotics, have room to multiply and pass their genetic-based resilience to their progeny. Next time around, the infection is that much tougher.

On one level, the theory made sense. Bacteria that do survive an onslaught of antibiotics do indeed reproduce quickly and pass along those traits that made them resistant to the antibiotics.

Yet infectious disease experts have known for at least two decades that this theory is flawed. The British microbial specialist Harold Lambert wrote in a 1999 Lancet journal article that antibacterial resistance rarely arises in one patient from one treatment. Rather, it is a populationwide phenomenon in which bacteria spread from host to host, acquire all kinds of genetic traits, and may be resistant to a particular antibiotic before the bacteria even enter your body.

Most experts agree that the widespread use of antibiotics — both in humans and in animals raised for food — has placed increased evolutionary pressure on bacteria to adapt and become resistant to the antibiotic. [6 Superbugs to Watch Out For]

"It's a hot topic; everyone is interested in using less," said Dr. Helen Boucher, an infectious disease physician and director of the Infectious Diseases Fellowship Program at Tufts Medical Center in Boston, who was not part of the BMJ opinion article.

Boucher said she agrees with the BMJ authors' stance that "completing the course" merely for the sake of lowering the risk of antibacterial resistance is not based on solid scientific evidence. She added, however, that doctors don't often know when a shorter course of antibiotics is as effective as a longer one.

As an example, she said that recent studies have shown that a six-day regimen of antibiotics is as effective as 10 days for people with skin infections, as originally prescribed; and a five-day regimen is as effective as 10 days for people with pneumonia. But shorter durations did not prove as effective for ear infections in very young children, she said.

The length of the antibiotic regimen for any given case is not arbitrary. Regimens are based on clinical studies done when the drugs were first tested, Boucher said. Newer, more refined studies often reveal more effective lengths that strike the balance between killing the bacteria causing an infection and not flooding the environment with more antibiotics.

Boucher is also involved in the leadership of the Infectious Diseases Society of America, and she noted that this professional society of more than 10,000 health specialists has a strong interest in conducting studies to understand the best minimal dose of antibiotic regimens.

Both Boucher and Llewelyn said patients should not "self-medicate" with antibiotics, or simply stop when they are feeling better. Rather, they should follow their doctor's instructions about when to stop.

The opinion piece stated that some health authorities have recently replaced the phrase "complete the course" with messages advocating taking antibiotics "exactly as prescribed."

"'Exactly as prescribed' is OK and at least it gives flexibility in the discussion between doctor and patient about when to stop — perhaps when [the patients] have been reviewed, or have a certain test result, or have been better for a certain period of time," Llewelyn told Live Science.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Could the idea that there are "good" and "bad" bacteria be a false dichotomy? A study appearing today (July 21) in the journal Science Immunology suggests so.

In a study on mice, scientists found that a group of bacteria called Helicobacter, long associated with ulcers, stomach cancer and intestinal distress, turned "bad" only when placed in a bad gut environment.

These bacteria triggered two very different kinds of immune-system responses, depending on the health of the mice. In healthy mice raised in a nearly germ-free, controlled environment, the Helicobacter induced an immune response associated with tolerance, as if the body were saying it accepted the new bacteria along with its existing gut bacteria, collectively known as the gut microbiome. [Body Bugs: 5 Surprising Facts About Your Microbiome]

However, in mice bred to have colitis, a condition that involves inflammation of the bowel, the Helicobacter made the inflammation worse. The immune systems treated the bacteria as foreign invaders.

The study suggests that Helicobacter and similar bacteria labeled as "bad" may, in fact, be neutral or even beneficial, depending on the health of the individual. A person's level of stress, poor diet or genetics all may influence the good or bad nature of gut bacteria, the scientists said.

"An interesting issue about Helicobacter species is that they're thought of as pathobionts, which means they don't necessarily have a well-described function in terms of promoting host health," said Dr. Chyi-Song Hsieh, an assistant professor of medicine and of pathology and immunology at the Washington University School of Medicine in St. Louis, who led the study. "But in the wrong context, in the wrong person, with the wrong genetics, it can cause inflammation in various parts of the gastrointestinal tract."

Hsieh said the discovery could lead to a better understanding of the causes of inflammatory bowel disease, as well as treatments for the condition, which affects upward of 3 million Americans, according to the Centers for Disease Control and Prevention. [5 Ways Gut Bacteria Affect Your Health]

The human gut contains trillions of bacteria and other microorganisms that mostly contribute to good health by aiding in digestion and regulating the immune system. Many of these bacteria elicit responses from the immune system cells, called T cells. These responses improve the body's tolerance to beneficial molecules and keep the immune system in check, so it doesn't run rampant and attack the body's own tissues.

"Gut bacteria [are] constantly interacting with immune cells of the host and can promote barrier function [or protection] in the intestinal tract," said Jiani Chai, a graduate student in Hsieh's lab who was the first author on the paper.

Some bacteria, however, such as the Helicobacter species, cause the T cells to increase inflammation and attack cells within the body that they recognize as foreign.

The study on mice doesn't imply that all gut bacteria are inherently neutral, waiting for the gut to determine their fate as good or bad, Hsieh told Live Science. After all, one type of Helicobacter, called H. pylori, clearly can cause dangerous ulcers and stomach cancer. But it is interesting to observe that Helicobacter, thought to be solely bad, can trigger an immune response that is good for the body, he added.

It remains unclear exactly why Helicobacter elicits certain responses from T cells, but this could be key to maintaining tolerance to bacteria. And figuring this out could potentially lead to the development of new drug targets for treating IBD, he said.

Hsieh said his group's future studies may investigate the possibility of using bacteria as sort of a medical delivery system, like a vaccine, to directly access the immune system to help regulate autoimmune diseases.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

If you were to wrestle a chimpanzee in some kind of bizarre battle of the species, you'd be at a serious disadvantage.

Pound for pound, our closest cousins in the animal kingdom are about 1.35 times more powerful than humans, according to the first study to compare the underlying biology and mechanics of chimpanzee muscle to human muscle, along with reviewing previous research on the topic.

In terms of jumping, pushing, pulling and lifting, humans are indeed weaker than most primates, the group of mammals that includes apes and monkeys, the study authors noted. [Meet Your Muscles: 6 Remarkable Human Muscles]

But don't let that get you down. Human muscles have enabled us to walk and run great distances, providing us with the foraging and hunting abilities that ultimately made us human.

These differences in muscles likely emerged within the past 7 million years, when early human ancestors developed more slow-twitch muscle fibers (which are good for endurance) than fast-twitch muscles (which are good for speed and punch), according to Matthew O'Neill, an assistant professor at the University of Arizona College of Medicine in Phoenix. O'Neill led the research group that reported the findings, which were published today (June 26) in the journal Proceedings of the National Academy of Sciences.

"Previous studies have shown that slow fibers are more fatigue resistant and less costly to contract than fast fibers," O'Neill said. "We can … do things like run marathons, unlike chimpanzees."

This greater number of slow-twitch fibers may have evolved because it gave early humans the advantage of being able to travel long distances and forage, and allowed them to rely less on powerful movements for survival and fitness, O'Neill said.

For years, scientists have suspected that chimpanzees are more powerful than humans, but that suspicion was based largely on anecdotal evidence. Adult chimps are generally smaller than adult humans; on average, the apes weigh about 100 lbs. (45 kilograms). Therefore, it has been difficult to accurately compare strength between the two primates. [10 Things That Make Humans Special]

The notion that chimpanzees and other apes have superhuman strength dates back first to tall tales from European explorers in sub-Saharan Africa in the early 19th century and then to research in the 1920s by biologist John Bauman, who studied chimps in zoos. In a series of studies later revealed to have poor methodology, Bauman found that chimps could pull weights five times heavier than the beefiest college football players could.

One particular chimpanzee, named Suzette, supposedly pulled 1,260 lbs.(572 kg) in a fit of rage, which was nearly 10 times her body weight, although no other study has recorded anything close to that show of strength.

The "five times stronger" figure stuck for decades until more modern studies in the 1960s refined the estimation to about two times stronger. O'Neill's group reviewed even more recent, laboratory-controlled studies on chimpanzee mass-specific muscle performance and found that, on average, the animals outperformed humans by a factor of approximately 1.5 in tasks involving pulling and jumping.

Then, the group compared the skeletal muscles under a microscope.

"One of the advantages of our approach is that we avoid all the complexities involved in trying to elicit maximal performance from a chimpanzee of unknown motivation or interest, and instead gets right to the measurement of the muscle tissue," O'Neill told Live Science.

The researchers found that the so-called contractile properties of human and chimpanzee skeletal muscle fibers — that is, how muscle fibers pull two joints together to enable the body to lift or move — are similar. [6 Strange Things the Government Knows About Your Body]

However, human skeletal muscles differ in fiber length and protein composition, the study found. Chimp muscles contain a balanced mixed of three variants of a protein called MHC: I, IIa and IId. But human muscles are dominated by the MHC I variant. This variant enables slower twitching, or contracting, which is important for endurance and energy conservation.

The researchers' computer simulations revealed that these differences in muscle characteristics increase the maximum dynamic force and power-producing capacity of chimpanzees by a factor of 1.35 compared to humans. The price of that power, though, is that chimps and other apes tire more easily and cannot walk great distances to find food — or, for that matter, to find new lands and make new discoveries.

The finding is independent of body size and instead concerns the physical property of individual muscle fibers, O'Neill said. Both humans and chimps can gain strength through exercise and the creation of more muscle fibers.

Rather, pound for pound, chimps have the advantage in a fight. So you'd better stick to long-distance running.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

A major doctors' group hopes to put an end to a great irony served up daily at most U.S. hospitals: The food offered there tends to contribute to obesity, diabetes, heart disease, stroke and cancer — the very same conditions for which many of the hospital patients are seeking treatment.

Refried, frozen chicken patties on doughy white bread; greasy pizza slices that turn the paper plate translucent; waxy, flavorless beans poured straight from a can constituting the only vegetable option; orange drink purporting to have 10 percent real orange … So much for a hospital being a beacon of health.

At its annual meeting on June 14, the American Medical Association (AMA) House of Delegates, which represents more than 200,000 physician members, issued a policy statement that called for the reduction of sugar-sweetened beverages and processed meats, and an increase in the availability of healthful, plant-based foods in hospitals. [7 Foods You Can Overdose On]

Under the resolution, physicians and hospital staff are encouraged not only to counsel their patients about the health consequences of a poor diet but also to lead by example by offering healthier foods at the hospital.

Specifically, the resolution states that the "American Medical Association hereby call on U.S. hospitals to improve the health of patients, staff, and visitors by (1) providing a variety of healthful food, including plant-based meals and meals that are low in fat, sodium, and added sugars, (2) eliminating processed meats from menus, and (3) providing and promoting healthful beverages."

Removing sugary drinks from vending machines and replacing them with water, unflavored milk, and unsweetened teas and coffees may be the easiest place to start making hospital food choices healthier, according to the AMA.

"Excessive sugar consumption has been linked to some of the nation's most debilitating diseases, and limiting the consumption of sugar-sweetened beverages will go a long way toward helping people prevent the onset of these diseases, improve health outcomes and rein in health costs associated with chronic diseases," Dr. William E. Kobler, an AMA board member who was part of the policy decision, said in a statement from the organization.

Yet health experts have lamented for years that hospitals' food options, not just the drinks, are unhealthy — a concept that contradicts hospitals' health-oriented mission. A study published in 2002 in the Journal of the American Medical Association found that more than a third of the top 16 U.S. hospitals had contracts with fast-food restaurants to offer their food in the hospital.

Similarly, a 2014 study conducted by the Physicians Committee for Responsible Medicine (PCRM), a nonprofit health group of 12,000 doctors who advocate plant-based diets, found that more than 20 percent of the 208 hospitals they surveyed housed fast-food restaurants. The same study found that the cafeteria food in these hospitals, where the staff eats every day, was dominated by foods that were high in sugar, salt and cholesterol, such as processed meats. [9 Snack Foods: Healthy or Not?]

Speaking at the AMA meeting, PCRM President Dr. Neal Barnard compared unhealthy food served in hospitals to tobacco. "A generation ago, the AMA supported doctors who were working to get tobacco out of their hospitals. And that helped everyone, especially those patients who needed to break a bad habit," Barnard said in testimony.

Barnard noted that, as with cigarettes, hot dogs and similar processed meats are now known to contain cancer-causing agents. "[M]any doctors and administrators would like to replace them with healthier foods," he said.

The Washington, D.C.-based PCRM started a national campaign in 2016 to encourage hospitals to ban processed meats such as hot dogs, which are a choking hazard for children. Several hospitals have since pledged to remove these foods as a result of the campaign.

The tide may be turning elsewhere, as well. A 2015 study published in the journal Preventive Medicine Reports found that creating hospital gardens for staff, patients and the community can lower rates of obesity in communities they serve and reduce public health disparities by providing more people with easy access to fresh, healthy, plant-based foods. More than 100 hospitals have such gardens, the study found.

So the day might come when you can go to the hospital to fix a broken leg and not have to return for a hospital-food-induced angioplasty.

Other policy resolutions announced at the AMA meeting included reducing the consumption of sugary drinks nationwide, destigmatizing obesity, strengthening vaccine policy and using the phrase "gun violence mitigation" in lieu of "gun control," among 11 other resolutions.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

You may want to run and hide from chronic pain. But pain, it seems, does its best to hide from medication taken to provide relief.

An international team of researchers has found that chronic pain can be hard to treat because pain receptors normally found on nerve cell surfaces can move, migrating into the cell, which places them out of the reach of pain medications while they continue to pump out pain signals to the brain.

Yet the same group of researchers has found a way to ferry medication into the nerve cell to numb these pain receptors, providing long-lasting pain relief.

The researchers said the discovery, in rodents, may lead to the creation of new medications for people with chronic pain that are more potent but less prone to side effects, such as the risk of addiction that comes with pain-relieving opioids. Their work appears today (May 31) in the journal Science Translational Medicine.

Pain is the body's way of telling you something is wrong, and can be beneficial, raising your awareness of danger. Acute pain, such as the burn from a hot surface, tells your brain to move your hand away quickly. [5 Surprising Facts About Pain]

Chronic pain, as the term implies, is long-lasting; there's no universally agreed-upon definition, but most doctors consider pain lasting several months to be chronic. Arthritis, nerve damage and diseases such as multiple sclerosis are common causes of chronic pain. Nearly 50 million American adults experience chronic pain, according to statistics compiled by the Centers for Disease Control and Prevention.

Drugs that control pain include opioids, such as morphine and oxycodone, and nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Yet opioids can be highly addictive, and NSAIDs can cause stomach, kidney and liver problems when taken in excess.

"Opioids and NSAIDs do not work for everyone and have unacceptable side effects, particularly when used over a long period of time," said Nigel Bunnett, a professor of surgery and pharmacology at Columbia University Medical Center in New York, who led the study.

In studying the pathways of pain signals, Bunnett's team may have found a better way to block pain that could require lower doses and thus fewer side effects, he said.

Many current pain medications work by targeting molecules, called G protein-coupled receptors (GPCRs), on the surface of nerve cells. These receptors help transmit signals to the brain. Activation of opioid receptors, one type of GPCR, blocks pain. Activation of another type of GPCR, called neurokinin 1 receptor (NK1R), causes the sensation of pain along with inflammation.

Disabling the NK1R is one approach to blocking pain, but most clinical trials of potential drugs targeting NK1R have been unsuccessful, Bunnett said. Now he knows why.

Bunnett and his colleagues discovered that NK1R, when stimulated by pain, quickly moves from the nerve cell's surface into intracellular compartments, called endosomes. In this protective bubble, NK1R continues to function for a prolonged period, pumping out signals for pain and inflammation. [America's Opioid-Use Epidemic: 5 Startling Facts]

Drugs created to deactivate cell-surface NK1R may not penetrate the cell membrane and reach the receptors hiding out in the endosomes, which is why these types of drugs often are less effective than hoped for, Bunnett said.

But the solution may be simple enough. Bunnett's group, based mostly at Monash University in Melbourne, Australia, where Bunnett maintains a dual appointment, attached a fat molecule to an NK1R-targetting drug to ferry the drug through the cell membrane and into the endosomes hiding the receptors. Fat molecules can easily pass through cell membranes. Piggybacking on the fat molecule enabled the drug to deactivate NK1R, providing lasting pain relief in rodents.

"[T]he really fascinating aspect of this work is the realization that by blocking the NK1 receptor in endosomes, rather than on the cell surface, as is traditional, we see quite different, and in this case beneficial, outcomes," said Christopher Porter, a professor of pharmaceutical sciences at Monash, who worked on the project.

G protein-coupled receptors are involved not only in the perception of pain but also in taste and smell and the regulation of mood and the immune system. More than a third of all available drugs act on certain G protein-coupled receptors in some way, Bunnett said. [7 Bizarre Drug Side Effects]

Moreover, many kinds of G protein-coupled receptors can migrate toward the endosomes once activated, previous studies have found. So, transporting drugs into the cell to moderate the activity of these receptors may have the potential to enhance the effectiveness of many different classes of medications, the researchers said.

"Could endosomal-targeting strategies be applied to 'tune' the activity of many currently marketed drugs — or, indeed, future drugs — that target GPCRs? We think so, at least for those that internalize, and this is an ongoing focus," Porter told Live Science.

If further experiments on rodents prove successful, the group hopes to test its technique on humans.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

BALTIMORE — Scientists and engineers are 3D printing all types of objects these days, including eyes: A group of eye specialists and eye-care providers from the Netherlands has used 3D-printing technology to create artificial eye structures, called conformers, in a small study of five children.

The technique could help children with conditions called microphthalmia and anophthalmia, in which they are born with underdeveloped or missing eyes, respectively, the research team says. These conditions, which can occur in one or both eyes, affect more than 10 percent of blind children worldwide and as many as 30 in 100,000 children, according to previous studies.

Although the sculpted eyes don't enable the child to see, they do provide critical support of the eye socket so that the child's face can have a natural, proportional look, the researchers said today (May 11) here at the annual meeting of the Association for Research in Vision and Ophthalmology (ARVO), the world's largest gathering of eye and vision researchers.

"If there's no eye present, there's not enough adequate stimulus for the bone [around the eye socket] to grow," Maayke Kuijten, a postdoctoral fellow at the VU University Medical Center in Amsterdam who conducted a study on five children fitted with the conformers, said at ARVO. [The 10 Weirdest Things Created by 3D Printing]

Because children with these conditions may have malformed eye sockets, the face and the areas around the eyes cannot expand to their natural contour, Kuijten said. The advantage of 3D-printed eye conformers is that they can be replaced often with slightly larger sizes by the parent at home as the child grows, or as frequently as weekly when the child is a few months old, she said.

"Symmetry of the face is our end goal," Kuijten told Live Science.

Traditionally, a child or adult who is missing an eye would be fitted with a device called an ocular prosthesis. (This was commonly called a "glass eye" because it was originally made with glass, but it is now mostly made of a medical-grade plastic acrylic.) These ocular prostheses are made by ocularists, professionals who are trained in both the fabrication and fitting of the prostheses.

The ocular prosthesis can be nearly spherical, like the eyeball, or cup-like, to fit over an existing, malformed and nonfunctioning eye. A conformer is often used for temporary support, such as after the accidental loss of an eye, to maintain the eye socket for several months until a more permanent prosthesis can be fitted.

But making and fitting an ocular prosthesis, or even a conformer, is a laborious process, Kuijten said. The ocularist typically must visually gauge the size of the socket, create an orb based on educated guesswork and polish it until it fits perfectly. It is as much artwork as it is medical care.

For infants with microphthalmia or anophthalmia, time is critical because their rapidly growing heads need the stimulation of a full-size eyeball for the frame of the eye socket to expand accordingly. Without such stimulation, that section of the skull can cave inward.

3D-printed conformers help address this challenge because they can be printed quickly, cheaply and in a range of sizes varying by less than a millimeter in diameter, Kuijten said.

To test the utility of 3D-printed conformers, Kuijten's team looked at patients being treated by Dr. Dyonne Hartong, an oculoplastic surgeon at the VU University Medical Center who is currently treating about 50 patients with microphthalmia or anophthalmia. Hartong was the senior investigator on the study.

As part of the standard care of children with these eye conditions in the Netherlands, they have several ultrasounds of their head taken during their first 3 months of age, followed by an MRI scan when they're about 3 months old. (MRIs require anesthesia because babies cannot be instructed not to move during the scans. But administering anesthesia to newborns under 3 months is considered too dangerous.)

Using data from these scans, the researchers determined the extent of the eye malformation and the size of the eye socket. The doctors also injected a soft gel into the affected eye socket to create a crude mold of its shape.

Based on these measurements and data on natural growth development, Kuijten devised an eye-growth chart for these children for their next 10 years of development. Then, her group used a 3D printer to create customized conformers in a vast array of sizes matching the prediction of the growth charts. [7 Cool Uses of 3D Printing in Medicine]

The conformers don't look like eyes. In fact, the original batch of eyes were green, with no pupils colored in. But they are convenient enough for parents to fit into their baby's eye socket after they're trained by ocularists on how to do so. Kuijten said the treatment is noninvasive and not painful for the child.

Early evaluation has shown that socket volumes of the treated eyes doubled, on average, over the treatment time of about a year, thus indicating that significant socket expansion occurred, the researchers said. The study on these children is ongoing.

"This is certainly a novel approach with several advantages," said Dr. Irene Gottlob, a professor of ophthalmology at the University of Leicester Ulverscroft Eye Unit at the Leicester Royal Infirmary who was not involved in the study. "This is a good example of individualized treatment, or 'precision medicine.' It is also a good example of how 3D printing can be used in medicine."

"However, so far, only five patients have been treated, and we need to see the results of a larger group," Gottlob added.

Gottlob said she was encouraged by the researchers' plan to improve mathematical models to better predict eye-socket growth and development. She also noted that better refinement of ultrasound scans could help bring the method to younger infants, before they reach the age when they can safely undergo an MRI scan.

"I think this is a very promising … method, but experience with more patients and further development will improve this even further," Gottlob told Live Science.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

In a medical first, surgeons have used a robot to operate inside the human eye, greatly improving the accuracy of a delicate surgery to remove fine membrane growth on the retina. Such growth distorts vision and, if left unchecked, can lead to blindness in the affected eye.

Currently, doctors perform this common eye surgery without robots. But given the delicate nature of the retina and the narrowness of the opening in which to operate, even highly skilled surgeons can cut too deeply and cause small amounts of hemorrhaging and scarring, potentially leading to other forms of visual impairment, according to the researchers who tested out the new robotic surgery in a small trial. The pulsing of blood through the surgeon's hands is enough to affect the accuracy of the cut, the researchers said.

In the trial, at a hospital in the United Kingdom, surgeons performed the membrane-removal surgery on 12 patients; six of those patients underwent the traditional procedure, and six underwent the new robotic technique. Those patients in the robot group experienced significantly fewer hemorrhages and less damage to the retina, the findings showed. [5 Experts Answer: What's the Best Way to Preserve My Eyesight?]

The technique is "a vision of eye surgery in the future," Dr. Robert E. MacLaren, a professor of ophthalmology at the University of Oxford in the United Kingdom, who led the study team and performed some of the surgeries, said in a statement. MacLaren presented the results today (May 8) at the annual meeting of the Association for Research in Vision and Ophthalmology (ARVO), happening this week in Baltimore.

"These are the early stages of a new, powerful technology," said MacLaren's colleague Dr. Marc de Smet, an ophthalmologist in the Netherlands who helped design the robot. "We have demonstrated safety in a delicate operation. The system can provide high precision [at] 10 microns in all three primary [directions], which is about 10 times" more precise than what a surgeon can do, de Smet said. (The three primary directions are up/down, left/right, and towards the head/towards the feet.)

Membrane growth on the retina results in a condition called epiretinal membrane, a common cause of visual impairment. The retina is the thin layer at the back of the eye that converts light waves into nerve impulses that the brain then interprets as images.

An epiretinal membrane can form because of eye trauma or conditions such as diabetes, but more commonly it is associated with natural changes in the vitreous, the gel-like substance that fills the eye and helps it maintain a round shape. As people age, the vitreous slowly shrinks and pulls away from the retinal surface, sometimes tearing it.

The membrane is essentially a scar on the retina. It can act like a film, obscuring clear vision, or it can distort the shape of the retina. The membrane can form over the macula, a region near the center of the retina that sharply focuses images, a crucial process for reading or seeing fine detail. When membranes form here, a person's central vision becomes blurred and distorted, in a condition called a macular pucker. [10 Medical Conditions That Sound Fake but Are Actually Real]

Removing the membrane can improve vision, MacLaren said, but the surgery is very intricate. The membrane is only about 10 microns thick, or about a tenth the width of a human hair, and it needs to be dissected from the retina without damaging the retina … all while the eye of the anesthetized patient is jiggling with each heartbeat, MacLaren said.

Faced with the need for such precision, de Smet and his Dutch-based group developed a robotic system over the course of about 10 years. Robot-assisted surgery is now commonplace, particularly for the removal of cancerous tumors and diseased tissues, as in the case of hysterectomies and prostatectomies. But it has never been tried on the human eye, given the finer precision needed, the researchers said.

De Smet's group had a working model of the robotic system in 2011, devised by de Smet and Maarten Steinbuch, an engineering professor at the University of Eindhoven in the Netherlands. They demonstrated the system's utility in 2015 on pigs, which have similar size eyes as humans.

MacLaren's team first used the system on a human, a 70-year-old priest from Oxford, England, in September 2016. Upon the success of that surgery, MacLaren's team conducted a study on 11 more patients in a randomized clinical trial, hoping to measure the robotic system's accuracy compared to the human hand.

The robot acts like a mechanical hand with seven independent motors that can make movements as precise as 1 micron. The robot operates inside the eye through a single hole less than 1 millimeter in diameter and goes in and out of the eye through this same hole during various steps of the procedure. But the surgeon is in control, using a joystick and touch screen to maneuver the robot hand while monitoring movements through the operating microscope, MacLaren explained.

During the trial, two patients who underwent the robotic surgery developed micro-hemorrhages, which means a little bit of bleeding, and one experienced a "retinal touch," which means there was an increased risk of retinal tear and detachment. In the traditional surgery group, five patients experienced micro-hemorrhages, and two had retinal touches.

MacLaren said the precision offered by the robotic system may enable new surgical procedures that surgeons have dreamed about but figured were too difficult to accomplish. For example, MacLaren said he hopes to next use the robotic system to place a fine needle under the retina and inject fluid through it, which could aid in retinal gene therapy, a promising new treatment for blindness.

"The robotic technology is very exciting, and the ability to operate under the retina safely will represent a huge advance in developing genetic and stem cell treatments for retinal disease," MacLaren told Live Science.

The surgical system was developed by Preceyes BV, a Dutch medical robotics firm established at the University of Eindhoven by de Smet and others.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Could shining bright lights on comatose patients to encourage their natural circadian rhythms help them awaken? A small study from Austria says yes.

The body's ability to awaken from a coma after severe brain injury is tied to its maintenance of its natural circadian rhythms, according to the study, which included 18 patients in various unconscious states.

The scientists found that the chances of regaining consciousness may improve once the body falls back into its natural, healthy cycle of rising and falling body temperatures throughout the day. [The 7 Biggest Mysteries of the Human Body]

The scientists also found that, in a subset of eight patients, two showed increased levels of consciousness after a treatment with carefully timed bright lights that were intended to trigger circadian rhythm activity and natural daily body-temperature fluctuations.

"[T]he closer the body-temperature patterns of a severely brain-injured person are to those of a healthy person's circadian rhythm, the better they scored on tests of recovery from coma," said study leader Christine Blume, a postdoctoral researcher at the Laboratory for Sleep & Consciousness Research at the University of Salzburg in Austria.

The new findings are very preliminary, but they suggest that monitoring circadian rhythms may one day serve as a diagnostic tool to monitor a comatose patient's chance for recovery, the researchers said. In addition, therapies aimed at tweaking those rhythms may ease patients into a more aware state, the research team wrote, in their study, published today (April 19) in the journal Neurology.

Circadian rhythms are daily cycles that tell the body when to eat, sleep or wake. They are set by environmental cues, such as daylight and nightfall. In healthy people, these rhythms include small changes in body temperature. Generally, body temperature increases during the day, with a peak at about 4 p.m., and decreases during the night, with the low point occurring at about 4 a.m., Blume said.

For the new study, the researchers monitored 18 people with severe brain injuries. Some were diagnosed with unresponsive wakefulness syndrome, also called a vegetative state. People in this state have awakened from a coma (which is a state of complete unconsciousness), and may open their eyes and have periods of sleep but otherwise remain unresponsive. Other patients in the study were in a minimally conscious state, meaning that they showed some signs of awareness.

For one week, the researchers continually monitored the body temperatures of these study participants with external skin sensors. They also evaluated the level of consciousness for each person with the Coma Recovery Scale, measuring things such as their responses to sound and their ability to open their eyes with or without stimulation. They found that the patients who scored better on that scale also had body temperature patterns that more closely aligned with a healthy 24-hour rhythm.

Then, the researchers tried to nudge eight of the patients back into a more natural temperature cycle. The researchers exposed these patients to cyclical periods of bright light stimulation over the course of a week. Two participants responded positively to this therapy, expressing increased signs of consciousness.

Blume cautioned, however, that her team's study sample, comprising only eight patients, was too small to show whether the light stimulation is a beneficial therapeutic tool to help patients with brain injuries regain alertness and awareness. [10 Things You Didn't Know About the Brain]

"This is promising, but preliminary, and should be investigated in a larger cohort," Blume told Live Science.

"We indeed hope we can encourage the cycle to return," Blume added. "We therefore encourage doctors to create an environment in the hospital that mimics the natural cycle of light during the day and darkness during the night — especially, daylight lamps may be helpful."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Deep breaths can settle your nerves, and now scientists have discovered the neural pathway in the brain that controls this process.

In an experiment on mice, scientists identified a circuit of neurons — a tiny cluster of a mere 350 nerve cells, among millions in the mouse brain — that regulate the connection between breathing and the higher-order brain activity that affects how calmly or worked up the mice behaved.

When the scientists removed these cells, they found that the mice still breathed normally, but they were uncharacteristically calm. This discovery, the researchers said, may someday lead to therapies to help people who have anxiety, stress and panic attacks. [11 Tips to Lower Stress]

A paper describing the work was published today (March 30) in the journal Science.

Breathing is largely an unconscious, involuntary action that's among the most basic rhythms of life. It is the process in which most animals inhale oxygen to create energy at a cellular level and then exhale carbon dioxide, the byproduct of this cellular respiration.

Yet humans have known for millennia that taking long, slow, deep breaths can have a calming effect and reduce stress. Conversely, panic attacks can cause a person to take short, fast breaths, further exacerbating the sense of unease.

Researchers have known that neural circuits throughout the brain regulate breathing, but until now, they had not pinpointed the neural pathway that connects breathing to the emotional states of anxiety and calmness.

In the new work, a team led by Dr. Mark Krasnow, a biochemistry professor at Stanford University School of Medicine in Stanford, California, searched the main region of the brain that controls breathing rhythms — called the pre-Bötzinger complex — which is nestled in a rudimentary section of the brain stem called the pons. In an experiment that was the culmination of years of work involving techniques such as neural mapping and genetically engineered mice, Krasnow's team zeroed in on the responsible circuitry.

The team found a subset of neurons in the pre-Bötzinger complex that transmits signals to a region in the pons that moderates feelings of alertness, attention and stress. [10 Interesting Facts About Caffeine]

They also found that these neurons express two proteins, cadherin-9 (CDH9) and developing brain homeobox protein 1 (DBX1), which are controlled by the Cdh9 and Dbx1 genes, respectively.

The researchers then turned to genetically engineered mice, in which they could mute the Cdh9 and Dbx1 genes. This enabled the researchers to select and kill the approximately 350 neurons that are thought to connect breathing to arousal, yet leave all the other neurons untouched, according to the study's lead author, Dr. Kevin Yackle, an assistant researcher at the UCSF School of Medicine. Afterward, the researchers found that the mice spent more time in a calm state.

Although deep breathing is an easy and safe way to control anxiety and stress, Yackle sees potential for developing medicines that target these genes.

"In panic disorders, it may be nearly impossible for one to control breathing," Yackle told Live Science. "Therefore, a pharmacological approach may be critical for preventing these panic attacks triggered by hyperventilation."

Yackle also said that sudden infant death syndrome (SIDS) may result when the brain doesn't sense a lack of oxygen while the infant is sleeping, and thus doesn't arouse the body. Some babies may be at higher risk for SIDS for reasons of genetics or because they were born prematurely. In these cases, babies at the highest risk for SIDS might benefit from a therapy that improves the neural signaling between oxygen intake and arousal, Yackle said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Your brain may start aging at a dramatically faster rate when you hit age 65 — or it may not, depending on which version of a particular gene you have, a new study suggests.

In the study, scientists identified a gene that appears to control the speed at which the brain ages, and they say that a particular version of it may offer protection against a host of age-related neurological diseases, including dementia. [7 Ways the Mind and Body Change With Age]

The gene, called TMEM106B, kicks into action at about age 65. Soon after that, people with bad copies of this gene will have a brain that looks 10 to 12 years older than people of the same age who have working copies, the scientists said.

The discovery may allow doctors to identify which people are at an increased risk for neurological diseases by virtue of having a faulty TMEM106B gene. It also may help develop drugs that target this gene to promote healthier brain aging, the researchers said. The study describing this work appears today (March 15) in the journal Cell Systems.

In recent years, scientists have identified numerous genes associated with Alzheimer's disease, Parkinson's disease and other neurological conditions.

"But those genes explain only a small part of these diseases," said study co-leader Herve Rhinn, an assistant professor of pathology and cell biology in the Taub Institute for Alzheimer's Disease and the Aging Brain at Columbia University Medical Center in New York. "By far, the major risk factor for neurodegenerative disease is aging. Something changes in the brain as you age that makes you more susceptible to brain disease."

The genetic-based instructions expressed by TMEM106B may be that "something," Rhinn said. The instructions may either protect against or accelerate the ravages of aging. [6 Big Mysteries of Alzheimer's Disease]

"If you look at a group of seniors, some will look older than their peers, and some will look younger," said Dr. Asa Abeliovich, a professor of pathology and neurology at the Taub Institute and a co-author of the study. "The same differences in aging can be seen in the frontal cortex, the brain region responsible for higher mental processes."

Previous studies have associated TMEM106B with a rare form of dementia called frontotemporal lobar degeneration. However, the new study shows that the TMEM106B gene is more broadly associated with brain age, and underlies how well seniors maintain their cognitive abilities, according to Rhinn and Abeliovich.

To determine what might control brain aging, the two researchers analyzed genetic data from more than 1,200 autopsied human brains from people who had not been diagnosed with a neurodegenerative disease while alive. They focused on a few hundred genes whose levels of expression had previously been found to either increase or decrease with aging. From this information, they compiled a chart of what they called "differential aging" denoting the difference between someone's true or chronological brain age compared with an apparent brain age.

One gene, TMEM106B, popped out of the data as a genetic driver of differential aging. TMEM106B appears to control inflammation and neuronal loss in the brain. There are two forms of the gene, or alleles: One form is associated with an increased rate, or risk, of brain aging, and the other allele is protective and is thought to prevent such an acceleration of aging.

Everyone has two copies of the gene, and in the general population, about 30 percent of people have two risk alleles; about 50 have one risk allele and one protective allele; and 20 percent have two protective alleles, Rhinn said. [6 Foods That Are Good For Your Brain]

"From what we could see, the effect of the [TMEM106B] risk allele is additive, in the sense that the brain of elderly people with two copies of the risk allele 'looks' five years older than the [brain] of people with only one copy of risk allele, and [they] themselves 'look' five years older than people with no risk allele," Rhinn told Live Science. "It is indeed one of our hypotheses that TMEM106B regulates systematic response to age-associated stressors in [the] human brain."

In the same study, Rhinn and Abeliovich also looked at the brains of people who had been affected by Alzheimer's disease and/or Huntington's disease during their lives, and they observed the same effect of TMEM106B on brain aging in those people.

"TMEM106B begins to exert its effect once people reach age 65," Abeliovich said. "Until then, everybody's in the same boat, and then there's some yet-to-be-defined stress that kicks in. If you have two good copies of the gene, you respond well to that stress. If you have two bad copies, your brain ages quickly."

TMEM106B may be an attractive target for researchers hoping to create treatments that could slow down brain aging, although such therapies would take many years to develop, the researchers said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

The falsehood that vaccines cause autism has regained traction since the election of President Donald Trump, and this misinformation may leave Americans blind to a real risk: a loss of health and learning services for people with autism that will result from the coming changes in health care and cuts to research funding, researchers say.

Vaccines do not cause autism. But Trump's "apparent openness to a long-debunked link between vaccines and autism risks" may cause advocates for services for people with autism and policymakers to focus on defending well-established scientific facts instead of fighting the potential rollback of protections for people with autism, the researchers wrote today (March 8) in an editorial in The New England Journal of Medicine.

These threatened protections include the Affordable Care Act's (aka Obamacare or ACA) key provision that health insurance companies cannot deny coverage because of a pre-existing condition, the researchers said. Also, the Individuals with Disabilities Education Act (IDEA), which predates the ACA, guarantees appropriate education for all children with disabilities. [Beyond Vaccines: 5 Things that Might Really Cause Autism]

Both acts may be on the chopping block, said Colleen Barry, a professor and chair of health policy and management at the Johns Hopkins Bloomberg School of Public Health. Barry co-authored the editorial with David Mandell, a professor and director of the Center for Mental Health Policy and Services Research at the University of Pennsylvania.

"We have no idea what will come out of Congress," Barry told Live Science. But there is a "real risk" that the changes could reverse gains made in autism care over the past two decades, she said.

The Republican-led Congress and the president have pledged to repeal and replace the ACA. Among the ideas favored by many Republicans in Congress is a plan to open up health insurance markets across state lines, the researchers said.

"If interstate insurance purchasing became possible, out-of-state insurance companies would not have to comply with the autism-mandate requirements in consumers' state of residence," Barry and Mandell wrote. "[S]uch freedom from requirements might easily precipitate a 'race to the bottom,' in which state legislators would repeal autism mandates (and other types of insurance mandates and consumer protections) to make in-state health insurance products price-competitive. As a result, gains achieved to date in access to autism-specific services could be reversed."

The ACA also requires marketplace health plans to cover 10 essential health benefit categories, including services important to people with autism and other disabilities. These services include therapies aimed at helping people with autism improve their skills of daily living, speech and language therapy, and mental health treatment.

Concerning the IDEA, Barry said that Secretary of Education Betsy DeVos and Attorney General Jeff Sessions have publicly questioned the value of the act's protections. DeVos has suggested that states should be able to decide whether to enforce the IDEA, Barry added. [6 Politicians Who Got the Science Wrong]

As for government-sponsored research funding, Trump has proposed cutting  $54 billion from some federal agencies, such as those that fund scientific research.

Autism is a developmental disability that can cause significant social, communication and behavioral challenges. The number of children diagnosed with autism has risen dramatically in recently decades, from 1 in 2,000 people in 1970 to 1 in 150 people today, according to the Centers for Disease Control and Prevention.

Yet scientists are not sure whether the rise is due to better diagnosis and the broadening of the clinical definition of autism, or an actual increase in the true prevalence. Nor do scientists understand what causes autism.

This week, researchers at the University of North Carolina School of Medicine reported that they found that infants as young as 6 months old, who were later diagnosed with autism at age 2, had a substantially greater amount of cerebrospinal fluid — the clear liquid that cushions the brain within the skull — compared with the 6-month-olds who did not go on to develop autism. This is the latest in a series of studies demonstrating how some infants are born with symptoms linked to autism long before they receive vaccines.

Barry and Mandell are worried because Trump has rehashed the discredited link between vaccines and autism, as recently as January 2017.

"The risk of getting drawn into an outdated debate about vaccines and autism is that advocates and policymakers will spend their time and resources fighting on that flank and could miss the window to respond on proposed cuts to critical services for those with autism coming from the other direction," Barry said.

Those who care about preserving and expanding services for people with autism need to pay attention to the conversations in Washington around the ACA repeal and threats to IDEA to make sure important protections and guarantees are not lost, Barry said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Europeans who came to the Americas inadvertently introduced germs — including smallpox and measles — that killed upward of 90 percent of the native people. But now a new study finds that these now-infamous germs weren't the only ones the Europeans were carrying.

The Europeans (and their African slaves) also brought new strains of bacteria called Helicobacter pylori, known to cause gastric ulcers and stomach cancer, according to an international team of researchers.

The twist is that these "foreign" H. pylori strains didn't kill the local people quickly, like the smallpox virus did. Instead, the strains supplanted the local strain of H. pylori already present in the Americas, and eventually, led to a near extinction of the local strains. [27 Devastating Infectious Diseases]

The effects of this may be seen today. These Old World strains of H. pylori now infecting the multiethnic populations of the Americas may be one reason why South America, in particular, currently has some of the world's highest rates of ulcers and stomach cancer, the researchers said.

The provocative new study — a mix of anthropology, genetics and public health — appears today (Feb. 23) in the journal PLOS Genetics.

H. pylori is a bacterium found in the stomach, transmitted from person to person most commonly through exchange of saliva (oral-oral route) or poor hygiene in food preparation (oral-fecal route). More than half of the world's population is infected with the bacteria, although, globally, fewer than 20 percent of people will develop ulcers and fewer than 2 percent will develop stomach cancer as a result of the infection, according to the World Health Organization.

The rates of disease resulting fromH. pylori infection tend to be lower in the wealthier countries of North America, Europe and East Asia, but the rates remain high in South America and Central Asia. People can be treated with a regimen of antibiotics if they are diagnosed with a gastric ulcer caused by H. pylori.

In the new study, led by research fellows Kaisa Thorell of the Karolinska Institute in Sweden and Koji Yahara of the National Institute of Infectious Diseases in Japan, scientists analyzed more than 400 H. pylori genome sequences from strains collected in North, Central and South America. They found that European and African strains were mixed together across the Americas, with little sign of the original American strains, suggesting that after the arrival of the newcomers, the foreign bacterial populations spread rapidly to people of different ethnicities, wiping out the local H. pylori strains.

"The pre-Columbian Americans had strains of East Asian ancestry [from their migration from Asia millennia ago], of which we nowadays only see traces of in remote communities," said Daniel Falush of the University of Bath in the U.K., the senior author on the study. "However, the reasons for the replacement will require more detailed investigation," he told Live Science. [Body Bugs: 5 Surprising Facts About Your Microbiome]

But one reason why some populations living in the Americas today have high rates of ulcers and stomach cancer once infected may have to do with a "mismatch" between the ethnicity of the patient and the origin of the H. pylori strain they carry, Falush said. Studies have found a link between having such a mismatch and an increased risk of disease.

For example, in 2014, researchers at Vanderbilt University Medical Center in Nashville reported that the African H. pylori strain was relatively benign in people of African ancestry yet far more disease-causing in people of mixed Amerindian ancestry. A similar study of this same group found that the European H. pylori strain was more likely to cause precancerous lesions in populations with native American ancestry than in European populations.  

Falush said the new findings may be useful for future research on the connection between individual bacterial strains and their associated risk of causing gastric ulcers and stomach cancer in different human populations.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Scientists have coaxed sound-sensing cells in the ear, called "hair cells," to grow from stem cells. This technique, if perfected with human cells, could help halt or reverse the most common form of hearing loss, according to a new study.

These delicate hair cells can be damaged by excessive noise, ear infections, certain medicines or the natural process of aging. Human hair cells do not naturally regenerate; so as they die, hearing declines.

More than 20 million Americans have significant hearing loss resulting from the death or injury of these sensory hair cells, accounting for about 90 percent of hearing loss in the United States, according to the Centers for Disease Control and Prevention.

In the new study, scientists at Harvard University and the Massachusetts Institute of Technology reported that they isolated stem cells from a mouse ear, discovered how to get them to multiply in a laboratory setting, and then converted them into hair cells. Their previous efforts, in 2013, produced only 200 hair cells. With a new technique, however, the research team has increased this number to 11,500 hair cells that were grown from one mouse ear. [Inside Life Science: Once Upon a Stem Cell]

Their paper describing the stem cell advance appears today (Feb. 21) in the journal Cell Reports.

Jeffrey Corwin, an expert on hair-cell regeneration and a professor of neuroscience at the University of Virginia School of Medicine, who was not part of this new research, called it "a very impressive study…by a dream team of scientists" and "a big advance" in the pursuit of regenerating these sensory hearing cells in humans.

Hair cells grow in bundles in the inner ear, and are so named because they look like hairs. Many hair cells within the ear are involved in balance, not hearing. But in the cochlea, the hearing organ deep in the ear canal, there are two kinds of specialized hair cells: outer hair cells, which amplify pitch and enable humans to discern subtle differences in sound; and inner hair cells, which convert sound into electrical signals sent to the brain. Humans have two cochleae (one in each ear), and each has only about 16,000 hair cells.

In fish, birds, lizards and amphibians, cochlear hair cells that die can be regenerated in as fast as a few days. However, in mammals, for the most part, the cells cannot regenerate — except for mice and other small mammals when they are newly born. But since so many species can naturally regenerate hair cells from a stem cell precursor, including some newborn mammals, many researchers have been motivated to find a way to rekindle hair-cell regeneration in adult mammals and, of course, in humans, Corwin said.

The new research was done by a team led by Albert Edge, director of the Tillotson Cell Biology Unit at the Massachusetts Eye and Ear Infirmary and professor of otolaryngology at Harvard Medical School in Boston.

In 2012, Edge's group discovered stem cells in the ear called Lgr5+ cells. These cells are also found in the gut, where they actively regenerate the entire lining of human intestines every eight days. The research team soon found a way to coax the Lgr5+ cells to differentiate into hair cells, instead of intestinal cells. But the process was slow, and the yield was low.

Now, the researchers have increased the yield dramatically by inserting a new step. After removing Lgr5+ cells from mice, the researchers first get them to divide in a special growth medium. This step produced a two-thousandfold increase in Lgr5+ cells, Edge told Live Science. Then, the researchers moved these stem cells into a different kind of growth culture and added certain chemicals to turn the Lgr5+ cells into hair cells. [7 Ways the Mind and Body Change With Age]

These laboratory-grown hair cells appear to have many of the characteristics of actual inner and outer hair cells, although they might not be fully functional, Edge said. The most immediate use for this new technique will be to create a large set of the cells to test drugs and to identify compounds that can heal damaged hair cells or regrow them and restore hearing, Edge said.

Scientists have had difficulty testing drugs on large batches of actual hair cells because there are so few in mammalian ears and they are deep in the cochlea, hard to extract, Edge said.

The researchers have reason to believe the technique to regenerate fully functional hair cells in humans could someday work. As reported in their paper, the team tested the technique on a sample of healthy ear tissue from a 40-year-old patient who underwent a labyrinthectomy (removal of parts of the inner ear) to access a brain tumor. The adult human stem cells isolated from this tissue also multiplied and differentiated into hair cells, although not as robustly as the mouse cells did.

But as Corwin noted about Edge's research, "You can see in their paper that they are perfecting their technique as they go along."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Men who are expecting a child or whose partner has recently had a baby may experience depression just as women sometimes do, according to a new study.

In recent years, much attention has been focused on recognizing and treating maternal depression, and this treatment has had positive effects on the health of moms and babies, the research team said. Yet identifying fathers who are at risk for paternal depression also can be beneficial to these men and their families, the researchers noted.

The new study of fathers — one of the largest studies on both prenatal and postnatal paternal depression — included more than 3,500 men and was part of the ongoing "Growing Up in New Zealand" project. The results are published today (Feb. 15) in the journal JAMA Psychiatry. [7 Ways Depression Differs in Men and Women]

Previous studies have shown that as many as 20 percent of women experience prenatal or postnatal depression, the researchers wrote in their article. The condition may result from hormonal changes during and after pregnancy or external factors such as an unplanned pregnancy, domestic violence, or a lack of social or relationship support.

In the new study, the researchers found that 2.3 percent of the men in New Zealand had prenatal depression and 4.3 percent had postnatal depression. Although that rate is much lower than that of women, it can still have serious public health consequences, said Lisa Underwood, a research fellow at The University of Auckland in New Zealand, who led the study.

Paternal depression could strain the family's relationships in a way that could cause financial hardships for the family or lead to poor cognitive development for the child, "including emotional and behavioral problems," Underwood said.

"Given that around 4 million babies are born in the United States each year, these apparently small percentages translate to a large number of men, and consequently children, who are affected," Underwood told Live Science. "The antenatal [prenatal] and postnatal periods are critical times of fathers' influence on long-term child well-being [and] outcomes." [5 Ways Fatherhood Changes a Man's Brain]

The new study also found that depression in the dads was seen across the population, and was not significantly associated with men's age, general socioeconomic status, marital status or whether the pregnancy was unplanned.

However, prenatal depression in the dads was associated with experiencing stress or poor health during the pregnancy. Postnatal paternal depression was associated with stress, poor health, no longer being in a relationship with the mother, being unemployed, or having a history of depression.

Underwood said she hopes that doctors can learn to identify the factors that may lead to depression, recognize the symptoms of depression itself, and recommend treatment options for fathers as they are increasingly doing for mothers.

"Fathers, as well as mothers, have a significant impact on children's development," Underwood said. "Both parents' mental well-being affects their relationship, their parenting and their involvement with their children. Therefore, it is vital that we recognize and treat symptoms of mental ill health among fathers — and mothers — early."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Ah, to sleep, perchance … to shrink your neural connections? That's the conclusion of new research that examined subtle changes in the brain during sleep.

The researchers found that sleep provides a time when the brain's synapses — the connections among neurons — shrink back by nearly 20 percent. During this time, the synapses rest and prepare for the next day, when they will grow stronger while receiving new input — that is, learning new things, the researchers said.

Without this reset, known as "synaptic homeostasis," synapses could become overloaded and burned out, like an electrical outlet with too many appliances plugged in to it, the scientists said.

"Sleep is the perfect time to allow the synaptic renormalization to occur … because when we are awake, we are 'slaves' of the here and now, always attending some stimuli and learning something," said study co-author Dr. Chiara Cirelli of the University of Wisconsin-Madison Center for Sleep and Consciousness. [10 Things You Didn't Know About the Brain]

"During sleep, we are much less preoccupied by the external world … and the brain can sample [or assess] all our synapses, and renormalize them in a smart way," Cirelli told Live Science.

Cirelli and her colleague, Dr. Giulio Tononi, also of the University of Wisconsin-Madison, introduced this synaptic homeostasis hypothesis (SHY) in 2003.

Now, Cirelli and Tononi have direct visual evidence of SHY after observing the shrinking of synapses in mice while the animals slept, an intricate experiment spanning four years. The researchers described their findings today (Feb. 2) in the journal Science.

Sleep is the price people pay for brains that are able to keep learning new things, the researchers said.

Russell Foster, who directs the Sleep and Circadian Neuroscience Institute at the University of Oxford in the United Kingdom, who was not associated with the study, called it a "very nice, clear piece of work." The findings support the notion that sleep is necessary for the consolidation of memories and thus learning, Foster said.

For millennia, humans have probed the nature and purpose of sleep. Aristotle suggested that sleep was restorative, a time to replace or rebuild all that was burned up throughout the body during the day. Modern science supports this idea, with researchers identifying sets of genes associated with restoration and metabolic pathways that turn on only during sleep.

Cirelli and Tononi focused on sleep's effect on the brain. In a paper published in 2003, they hypothesized about sleep's role in the growth of synapses, which serve as avenues to ferry information among neurons. Synapses are constantly strengthening, or widening, during the day to accommodate the flow of traffic as the brain soaks up new experiences. But that strengthening cannot go on indefinitely, or else the synapses will become saturated — think "information overload."

The researchers suggested in their earlier paper that synapses get pruned back during sleep. This pruning doesn't necessarily cause the body to need sleep; rather, the body is taking advantage of the decreased brain traffic that occurs while an individual sleeps. [7 Mind-Bending Facts About Dreams]

To find evidence for this, the researchers used a new form of electron microscopy that can discern the miniscule changes in the shrinking and subsequent expansion of these microscopic synapses at the nanometer level in mice brains. They found that a few hours of sleep led to an 18 percent decrease in the size of the synapses on average.

Cirelli said that one interesting finding was that this pruning occurred in about 80 percent of the synapses but spared the largest ones. These larger synapses may be associated with the most stable and important memories, connections the brain does not want to lose, the researchers speculated. Yet, the way in which the brain decides what synaptic connections to prune is another mystery to explore, Cirelli said.

"It is critical to have pruning back at night, so that the huge amount of information encoded by temporary synapses during the day won't overwhelm the brain," said Foster. "Pruning ensures that only the most important information is retained."

Foster said he can envision follow-on experiments based upon the Cirelli-Tononi work that would use mouse models to explore the connections among circadian rhythms (the body's "internal clock"), sleep, synapse pruning and psychiatric disorders. Some of the key features of these disorders seem to be a disruption in neural circuitry, sleep disruption, and impaired cognition and memory, said Foster, who is also a co-author of the upcoming book "Circadian Rhythms: A Very Short Introduction," (Oxford University Press, 2017).

Foster added that resetting synapses may be a core feature of sleep, particularly for humans, with their advanced cognitive abilities compared to other animals. However, pruning is likely to be just one of many essential functions that takes place during the sleep phase, a period during which the body takes advantage of physical inactivity to perform a range of essential housekeeping activities, he said.

So Aristotle wasn't too far off.

Original article on Live Science.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

To eat soy or not: That's the question many U.S. women have been asking. Tofu, miso paste and other soybean-based foods are high-quality sources of protein that are low in calories and saturated fat. And studies have shown that they can help prevent cancer.

Yet many doctors recommend that women who have, or are at risk of developing, a common form of breast cancer called estrogen-receptor-positive breast cancer  avoid eating soybean-based foods because they contain compounds called isoflavones. Some studies suggest that isoflavones can mimic the hormone estrogen and encourage tumor growth.

Now, in an animal study, researchers at the Georgetown Lombardi Comprehensive Cancer Center in Washington, D.C., have uncovered a possible reason for the apparent Jekyll-and-Hyde nature of soy — how it can both prevent cancer and fuel its spread. [Top 10 Cancer-Fighting Foods]

The researchers found that rats that were given soybean isoflavones to eat throughout their lives — in particular, one type of soybean isoflavone called genistein — had improved immunity against cancer. But rats that weren't given the isoflavone until after developing breast cancer didn't have that same immune response to kill cancer cells. Instead, these rats had higher rates of cancer growth and higher rates of recurrence after their tumors were removed.

The study may explain why women in Asian countries, who tend to consume high amounts of soybean-based foods throughout their lifetime, have rates of breast cancer that are five times lower than those of women in the United States, the researchers said. The findings were published today (Feb. 1) in the journal Clinical Cancer Research.

More than 200,000 U.S. women are diagnosed each year with breast cancer, and the majority have estrogen-receptor-positive breast cancer, according to the Centers for Disease Control and Prevention. One of the most common drugs to combat this type of cancer is tamoxifen, which acts to reduce estrogen's ability to promote cancer growth.

In their animal study, the researchers induced cancer growth in rats that had a steady diet of genistein and in rats that never had any genistein until after the cancer developed. All of the rats were then treated with tamoxifen to kill the cancer. The researchers found that the rats raised on genistein had only a 7 percent chance of breast cancer recurrence after tamoxifen treatment, but the rats that were recently given genistein had a 33 percent recurrence rate.

It's not clear why genistein would have this effect but it may be related to the body's immune system being activated by the isoflavone, recognizing it as a nutrient from its longtime consumption, said study senior author Leena Hilakivi-Clarke, a professor of oncology at the Georgetown Lombardi Comprehensive Care Center.

"The immune system was not activated in animals that started consuming genistein for the first time with tamoxifen," Hilakivi-Clarke told Live Science. This may have resulted in the genistein appearing more like the cancer-fueling estrogen and less like a tumor-fighting agent, she said.

In other words, the paradox is in the timing. It may be that soy consumption is protective only if started before cancer develops.

Despite the lingering ambiguity of whether the same is true in humans, Hilakivi-Clarke thinks the animal study can inform doctors and their patients.

"We have solved the puzzle of genistein and breast cancer in our rat model, which perfectly explains the paradox seen in earlier animal studies and patients," Hilakivi-Clarke said. "While many oncologists advise their patients not to take isoflavone supplements or consume soy foods, our findings suggest a more nuanced message — if these results hold true for women. Our results suggest that breast cancer patients [who ate soy before their diagnosis] should continue consuming soy foods after diagnosis, but not to start them if they have not consumed genistein previously." [6 Foods That May Affect Breast Cancer Risk]

Maggie Neola, a staff dietitian for the Barnard Medical Center and Physicians Committee in Washington, who wasn't part of the study, said that findings from animal experiments often don't translate to humans and that she'd like to see research from population studies with women.

"What we know about soy consumption in humans is that whole and minimally processed soy foods, such as edamame, tofu, and tempeh, have been shown in several studies to protect women from breast cancer recurrence," Neola said.  "Of course, women who want to make any dietary changes following a cancer diagnosis should consult their physicians."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Does your housemate have a strange, unexplainable effect on your behavior? Well, there's a gene for that…and that gene belongs to your housemate.

In a new study, researchers found that the genetics of a mouse's cage mate can affect its own health in a multitude of ways. Moreover, cage mates do this by influencing traits once thought to be controlled solely by an animal's own genes, such as growth rate and the functioning of its immune system.

"The take-away message here is that we need to pay attention to the genetic makeup of social partners, since in some cases it affects health more than the individual's own genes," said Amelie Baud, a postdoctoral fellow at the European Bioinformatics Institute in Hinxton, England, and first author on the study.

"This is something we did not know before," Baud told Live Science. "It means we need to stop looking at individuals in isolation and include social partners when we look at an individual's health." [7 Diseases You Can Learn About from a Genetic Test]

Scientists have long known that social interactions contribute to health and disease. For example, peer pressure can increase the chances that a teenager will take up smoking. However, the extent to which the genetic makeup of one animal can impact the traits of another that it lives with — an emerging concept called social or indirect genetic effects — is poorly understood.

In the new study, the researchers identified more than 40 traits in mice that a neighboring mouse's genetic profile may influence. They found that a cage mate's genetics contribute, on average, to about 10 percent of its partner's anxiety level, immune function, body weight, wound-healing speed and other traits.

The findings, published today (Jan. 25) in the journal PLOS Genetics, may apply to studies of complex traits in human populations, and further studies should look at this possibility, the researchers said.

Baud gave the example of a morning person living with a night owl. The morning person might develop an illness that's exasperated by a lack of sound sleep resulting from her staying up late with her partner. So, her partner's genetics — a natural inclination to stay up late — alters her own behavior and contributes to poorer health.

In the study on mice, however, the outcomes were not as obvious or explainable. For example, black mice housed with gray mice healed better than black mice housed with other black mice, but the researchers weren't sure why. Gray mice were less anxious when they were housed with black mice than when they are housed with gray mice. No type of mouse had universally positive or negative effects on its cage mates across all traits, the researchers said. [Unraveling the Human Genome: 6 Molecular Milestones]

For some traits related to the immune system, social genetic effects accounted for nearly 30 percent of how genes were expressed, the study revealed.

The research was led by Oliver Stegle of the European Bioinformatics Institute, part of the European Molecular Biology Laboratory, which has labs in five European countries supported by 22 member states. Stegle's group aims to unravel how genetic background and environment jointly shape phenotypic traits — that is, how one's genes are expressed.

Baud said that her team's ongoing research "could inform patients and doctors on social contributions to disease and provide clues as to how to mitigate social influence, or indeed enhance it when it has beneficial effects."

The findings highlight the fact that some important traits underlying health and disease appear to be beyond the individual and, instead, in the hands of one's partner, the researchers said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Tuberculosis in mice can be cured much faster than normal by simply tweaking the standard regimen of antibiotics, new research shows.

Scientists reduced treatment time in mice by up to 75 percent; they did so by optimizing the combinations and doses of the standard drugs. The finding may lead to a markedly shorter course of treatment for tuberculosis in humans and may reduce the risk of the infection becoming resistant to the antibiotics.

Treating tuberculosis in humans can be long and onerous; the infected person must take a regimen of antibiotics for eight months or more. As a result of this lengthy treatment, patients often fail to complete the full course of medication; this is particularly true in poor countries, where people may not have easy access to medical care. Failing to complete the course of antibiotics can lead to disease relapse, further spread of the illness and drug resistance. [27 Devastating Infectious Diseases]

The newly optimized combinations of antibiotics could reduce the spread of even the most virulent strains of tuberculosis, the researchers said. Their findings were published today (Jan. 24) in the journal Nature Communications.

Tuberculosis, or TB, is a leading cause of death worldwide, with more than 10.4 million cases and 1.8 million deaths in 2015, according to the World Health Organization (WHO). The disease is caused by the Mycobacterium tuberculosis bacterium. TB is an airborne disease spread by coughing, sneezing or any exchange of saliva.

Most worrisome to infectious-disease experts is the rise of multi-drug-resistant and extensively drug-resistant TB, against which few if any drugs are effective. There were more than 500,000 such cases in 2015, according WHO, mostly in China, India and Russia.

In the United States, 10 drugs are approved to treat TB. And the first line of defense is a set of four antibiotics: isoniazid, rifampin, ethambutol and pyrazinamide. These are usually given together for eight weeks, often followed by just isoniazid and rifampin for the next 16 to 24 weeks. [6 Superbugs to Watch Out For]

This standard regimen evolved from the 1950s to the present by a process of adding or replacing drugs one by one, rather than by a systematic search to identify the most highly synergistic drug combinations, explained the research team in the new study.

Given the literally billions of possible combinations of drugs and doses, the team set out to find which combination could be most effective at killing M. tuberculosis. The researchers were led by Dr. Marcus Horwitz, a professor of medicine at the University of California, Los Angeles (UCLA) David Geffen School of Medicine. The team used a special drug-screening technique developed at UCLA to rapidly identify the most promising drug combinations, and then tested them in a cell culture. That work was reported in March 2016.

This approach allowed the scientists to rank more than 1,000 three- and four-drug combinations in order of their potency in killing M. tuberculosis, Horwitz said.

In the new study, the team tested the most promising combinations on mice that were infected with TB. Two regimens stood out: One had four common and inexpensive drugs (clofazimine, ethambutol, prothionamide and pyrazinamide) and cured the mice in 12 weeks. The other had a similar set of four drugs but with a less-common, more-expensive drug (bedaquiline) replacing prothionamide. It cured the mice in only four weeks, a 75 percent reduction in time compared to the standard treatment. [7 Bizarre Drug Side Effects]

Dr. Daniel Clemens, an adjunct professor of medicine at the Geffen School of Medicine and a co-first author on the study, said he is guardedly optimistic that the regimens could work in humans.

"Showing markedly greater efficacy than the standard regimen in the mouse model makes our regimens very promising for further study in humans, but does not guarantee that they will be more effective in clinical trials," Clemens told Live Science.

"There are differences between TB in mouse and human that could cause our mouse model to overestimate the clinical efficacy of our regimens," he said. "On the other hand, the mouse model might underestimate the efficacy… [because] whereas a few residual bacteria in a mouse can cause relapse, the stronger human immune response may control a small number of bacteria and prevent relapse."

Clemens said his team found other drug combinations in the cell-culture studies that hold potential as "universal regimens for treatment of multi-drug-resistant TB" and that the researchers hope to test in mice and ultimately in humans.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Never mind unraveling the mysteries of the human brain. A new study suggests that neuroscientists might not even have the analytical tools to understand the far simpler logic that drives the "brain" in "Donkey Kong."

In a thought experiment, two researchers asked the question: Could a neuroscientist understand a microprocessor? That is, if one considers the human brain to be an extremely complicated computer, could neuroscientists apply their widely used neuroscience approaches to analyze a simple computer?

How simple? They decided to try the Atari 2600, which in 1981 was a state-of-the-art game console — with what was then a blisteringly fast 6502 microprocessor — that introduced the world to the menacing, chest-beating, damsel-snatching gorilla named Donkey Kong. [Top 10 Mysteries of the Mind]

The researchers — Eric Jonas, a postdoctoral fellow at the University of California, Berkeley, and Konrad Kording, a professor of physical medicine and rehabilitation/physiology at Northwestern University in Chicago — chose the Atari 2600 as their "model organism" because it was complicated enough to present an analytical challenge, yet the engineers who created it had mapped it out thoroughly and understood it completely.

To mimic a typical brain study, they examined three types of "behaviors" for the Atari 2600 in the form of three different games: "Donkey Kong," "Space Invaders" and "Pitfall!" They then applied some of the data analysis methods that are commonly used in neuroscience to see whether those methods would reveal how the Atari "brain" — its microprocessor — processes information. [10 Things You Didn't Know About the Brain]

The methods did "reveal interesting structure" within the microprocessor, the researchers wrote in the paper describing the experiment. "However, in the case of the processor, we know its function and structure, and our results stayed well short of what we would call a satisfying understanding" of the Atari brain.

The results of their experiment were published today (Jan. 12) in the journal PLOS Computational Biology.

The field of neuroscience is expecting a windfall of data from new, large and well-funded research programs that have been developed to understand the human mind, like the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, Jonas told Live Science. Yet Jonas said that he questions the value of such data if the results cannot be properly understood.

"As people doing computational neuroscience, we really struggle to make sense of even the comparatively small data we acquire today, partly because we lack any sort of 'ground truth,'" Jonas said. "But if various synthetic systems like classic microprocessors can serve as a test bed, maybe we can make faster progress."

So, it is "game over" for neuroscience's current methods?

"I am actually very positive about progress in neuroscience," said Kording, who is also a research scientist at the Rehabilitation Institute of Chicago. "The fact that the field is able to take our contribution seriously shows that they at least have plans to overcome the problems we highlight."

Kording said that more than 80,000 people viewed an earlier version of the paper on a preprint server. Many loved it, he said, although many hated it, too. But he was happy that he and Jonas have started a dialogue.

Terrence Sejnowski, who directs the Computational Neurobiology Laboratory at the Salk Institute for Biological Studies in San Diego, told Live Science that he appreciates the need for researchers to develop a better conceptual framework for understanding neural processing. Indeed, Sejnowski was the first author on a 2014 paper in the journal Nature Neuroscience, which many in the field consider to be a road map for how to analyze the massive and diverse sets of neuroscience data that are expected to come from research projects in the coming years.

But he's not convinced that the Atari 2600 is a suitable model organism for testing out neuroscience's analytical tools.

"The microprocessor and the brain are two completely different types of computers, and one should not be surprised that different methods are needed to analyze them," Sejnowski said. "Let's do the converse experiment and analyze the brain using methods that work for micros [or, microchips], using a logic analyzer. This works great in reverse-engineering micros but would fail completely with the brain because the brain isn't a digital chip."

To be sure, the brain is a daunting kind of computer. And as neuroscientists go about unraveling its mysteries, they must feel a bit like little Mario, forever battling obstacles in their seemingly endless journey into unknown realms.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Babies as young as 4 months old process the faces and scenes that they see much like adults do, according to a new study. The findings suggest that the structure of the brain's visual cortex is already highly organized at birth or soon after.

The visual cortex is the part of the brain that processes all visual information. In adults, this area is highly compartmentalized into regions specialized to process certain kinds of objects, such as faces, houses or trees. Scientists have long wondered how the visual cortex got this way: Are these regions specified at birth, before the brain even knows what a face or tree looks like, or do they develop later as people grow and learn?

A definitive answer has eluded scientists, however, because of the inherent challenges of studying the brains of infants. The primary tool for studying these brain areas is the functional magnetic resonance imaging (fMRI) brain scan, which is challenging to use on infants. While the scan poses no radiation danger, subjects need to stay still and awake in the machine for several minutes at a time to produce a clear image. [10 Things You Didn't Know About the Brain]

Babies aren't exactly known for staying still, particularly when they are awake …  and particularly when they are placed in the long tube of an MRI machine.

In what may be a feat more monumental than herding cats, researchers at the Massachusetts Institute of Technology (MIT) and Harvard Medical School have managed to capture crisp fMRI scans of nine squirming, gurgling, burping or otherwise unruly infants. The scientists employed various tactics to keep the kids relatively still, such as placing them in a specially designed infant seat and climbing into the MRI scanner with the babies to help them feel safe. [7 Baby Myths Debunked]

The scans revealed that the visual cortex of 4- to 6-month-old human infants is clearly spatially organized, with distinct regions responding preferentially to human faces versus natural scenes. Additionally, the results showed that the babies' responses to these images resembled those observed in adults. That is, brain activity extended throughout the cerebral cortex, from the front to back of the brain, the researchers wrote in their study, published today (Jan. 10) in the journal Nature Communications.

Neuroscientists hotly debate how much of the structure of the brain is specified at birth and how much of that structure arises from experience, said Rebecca Saxe, a professor of cognitive neuroscience at MIT who was the senior author on the study.

"Some people think only the simplest, most basic functions are specified at birth … and everything else is learned from the pattern of experience," Saxe told Live Science. "Other people think lots of high-level 'cognitive' functions are supported by pre-existing machinery that is 'ready to go' at birth in one way or another." [11 Facts Every Parent Should Know About Their Baby's Brain]

The answer may lie somewhere in between, according to Saxe's project with infants, which was led by Ben Deen, then a graduate student in Saxe's lab and now a postdoctoral fellow at the Rockefeller University in New York. The team found that the visual cortices of infants and adults are not identical, though they are similar, suggesting that the structure becomes refined through development, the researchers said.

Still, the new findings support the hypothesis that specification in the brain at birth provides a sort of scaffolding that ultimately leads to precise category-selective brain regions in adults, the researchers said. As another example, Saxe cited the part of the brain called the "visual word form area" where humans process alphabets and ideograms. Reading is a relatively new phenomenon in the human experience; for all humans to possess such a specified brain area for visualizing words, it must be built upon innate scaffolding.

In a TEDx talk in June 2016, Saxe explained that she turned to studying infant brains to better understand the origin of the human mind. She wanted to answer questions like, "What is innate, what is learned, and how much of what people think about the world is universal?" Her own newborn boy was one of her first test subjects in her group's fMRI project.

Follow Christopher Wanjek @wanjekfor daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Diagnosing cancer is about to get more accurate, with the help of artificial intelligence.

Pathologists have diagnosed diseases in more or less the same way for the past 100 years, by laboring over a microscope reviewing biopsy samples on little glass slides. Working almost robotically, they sift through millions of normal cells to identify just a few diseased ones. The task is tedious and prone to human error.

But now, scientists and engineers have created a technique that uses artificial intelligence (AI) and can differentiate cancer cells from normal cells almost as well as a top-notch pathologist. A Harvard-based team demonstrated the AI method as part of a competition at the 2016 International Symposium of Biomedical Imaging in Prague, showing how it could pinpoint, with 92 percent accuracy,cancer cells among samples of breast tissue cells. That accuracy was far better than the other AI methods in the competition, landing the team first place.

Humans + AI

Humans still have the edge: Pathologists beat the robots in this competition with their ability to identify 96 percent of the biopsy samples with cancer cells. [Super-Intelligent Machines: 7 Robotic Futures]

But the real surprise came when pathologists were teamed up with the Harvard team's AI. Together, the artificial intelligence and good, ole human intelligence identified 99.5 percent of the cancerous biopsies.

While the thought of trusting Dr. Robot with your medical analysis may seem a bit scary, some scientists see great promise in AI-assisted doctor services.

"Our guiding hypothesis is that 'AI plus pathologist' will be superior to pathologist alone," said Dr. Andrew Beck, of Beth Israel Deaconess Medical Center and Harvard Medical School in Boston, who led the creation of the winning AI design. "If we and the larger research community are able to demonstrate that the use of AI tools significantly reduces diagnostic errors, I believe patients, physicians, health care payers and health systems will be supportive of the addition of AI tools in the clinical workflow," he told Live Science.

Why breast cancer cells?

The contest, held in April, invited AI designs from around the world created by private companies and academic research organizations. The goal was to spur interest in creating more accurate AI methods of disease diagnosis.

"The fact that computers [in the April competition] had almost comparable performance to humans is way beyond what I had anticipated," said Jeroen van der Laak of Radboud University Medical Center in the Netherlands, who organized the contest. "It is a clear indication that artificial intelligence is going to shape the way we deal with histopathological images in years to come." [Infographic: The History of Artificial Intelligence (AI)]

The contest organizers chose the topic of breast cancer detection — more specifically, metastatic cancer cells in sentinel lymph node biopsies — as a real-world test of an important public health issue. Among U.S. women, breast cancer is the second most common type of cancer (after skin cancer) and the second deadliest type of cancer (after lung cancer), according to the Centers for Disease Control and Prevention.

A sentinel lymph node biopsy is a surgical procedure in which a sample of tissue is removed from a sentinel node, the first in a group of lymph nodes, or glands, where cancer cells might spread after leaving the original site. A multicenter study published in 2003 in the Journal of the American College of Surgeons found that these biopsies, using traditional human analysis, were 96-percent accurate, with a false-negative rate of 8 percent.

Because cancer surgeons rely on the biopsies to decide what tissue to remove or leave in place, often at the very moment a cancer is beginning to spread, accuracy in the biopsy analysis is crucial.

Machines that learn

Beck's group used a process called "deep learning" to essentially teach a computer to better recognize what cancer cells look like. This process is a machine-learning algorithm used in applications such as speech recognition; it makes the system more and more accurate with each use. In preparation for the contest, Beck's group fed the computer thousands of images of cancer cells.

The team identified examples for which the computer was prone to make a mistake in cancer identification and retrained the computer using greater numbers of more difficult examples.

The development of such automated diagnostics has been a goal for the AI field for the past 30 years, as computers became more commonplace in labs, Beck said. But only recently has the field seen the improvements in scanning, storage, computational power and algorithms necessary to make this possible.

Don't worry, pathologists won't be fading away. Beck said the field will evolve to adopt new skill sets. For example, pitfalls to avoid with AI include a system that routinely misses a particular rare form of cancer the AI hasn't seen before or that is routinely thrown off by an artifact in the biopsy image, he said. Humans will be needed to continuously teach the robots.

Beck's team includes postdocs in his Harvard lab, Dayong Wang and Humayun Irshad, along with Harvard graduate student Rishab Gargya and MIT researcher Aditya Khosla. A technical report describing this work was posted yesterday (June 20) on the open-access e-print archive arXiv.org.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Placebos offer real therapeutic value: Although they cannot cure an illness, they can make patients feel better. So why not incorporate them into medical practice?

In a provocative essay published today (July 1) in The New England Journal of Medicine, Harvard Medical School professor Ted Kaptchuk proposes that placebos should be considered valuable components of medical care and important tools in relieving patients' symptoms — and not simply an inconvenient baseline that "real medicines" are compared to within medical studies.

A placebo — the word comes from the Latin phrase meaning "I shall please" — is a fake pill or procedure that can provide a psychological benefit because the patient thinks he or she is getting real treatment. The placebo effect is an improvement in symptoms that can be attributed to fake medicines, or even standard symbols of healing, such as a medical doctor's white coat and diploma, or a witch doctor's menacing mask.

"A significant body of research has resulted in a shift from thinking of placebos as just 'dummy' treatments to recognizing that placebo effects encompass numerous aspects of the health care experience and are central to medicine and patient care," Kaptchuk said.

And Kaptchuk would know. As director of a research program at Harvard that studies placebos, he has led much of this research. In recent years, Kaptchuk and his colleagues have demonstrated that patients' symptoms may be relieved even if they know they are taking a placebo pill; that sometimes a placebo can cause negative side effects, such as nausea; and that some placebos work better than others.

In 2012, Kaptchuk even took placebos to the genetic level and found that patients with a certain variation of a gene associated with the brain chemical dopamine were more likely to respond positively to fake acupuncture for the treatment of irritable bowel syndrome. Such insights may help scientists design better drugs for certain people by ruling out certain side effects or elements of symptom relief that are psychological, rather than biochemical, in origin.

But exactly how to capitalize on the placebo effect in the doctor's office, ethically, is an open-ended question that Kaptchuk is posing to the clinicians who read The New England Journal of Medicine. [11 Surprising Facts About Placebos]

"Medicine comprises two things: the moral care of a patient … and effective therapy," Kaptchuk told Live Science. "You can't lie to patients."

Doctors need to think of clinical interventions designed to elicit placebo effects without deceptions, Kaptchuk said. This could include research into how a doctor's touch, gaze or capacity for listening can have positive effects on a patient, or how stern warnings about drug side effects could actually induce those side effects in the patient.

Or, a placebo could be ethical in situations when no cure or relief is otherwise available, Kaptchuk added.

For centuries, physicians have debated the proper role of placebos in patient care. Some have considered placebos completely harmless, while others have claimed they're damaging tools of charlatans and quacks. A steady flow of medical advances in the early 20th century relegated the placebo effect to the backwoods of clinical care.

A 1955 paper by Henry Beecher of Harvard Medical School titled "The Powerful Placebo" changed that by introducing the concept that placebos have therapeutic value that can be exploited. But then, the tide turned, again, with a study published in The New England Journal of Medicine in 2001 by Dutch researchers, who found that most placebo studies were methodologically flawed. With a rub to Beecher, their paper was playfully titled "Is the Placebo Powerless?"

Kaptchuk has claimed in previous interviews to have learned much from the Dutch study and has since collaborated with one of the Dutch authors.

Nevertheless, there are many critics of using placebos in medical care. In a 2011 article in The Atlantic, in reaction to a study that Kaptchuk conducted on asthma, retired family physician Harriet Hall said, "Asthma can be fatal. If the patient's lung function is getting worse, but a placebo makes them feel better, they might delay treatment until it is too late."

But critics argue that placebo effects tend to be small, temporary and inconsistent, and that they have little proven positive effect on disease outcome, which should be the ultimate goal.

Kaptchuk conceded that placebo effects are modest in comparison to lifesaving surgery and powerful medications. But he noted that a placebo can enhance the effectiveness of these methods — a central point he hopes his fellow clinicians will consider.

"The New England Journal of Medicine rarely entertains studies on placebos," Kaptchuk said. "I am happy they are considering this."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Children and teens from families with lower incomes have differences in their brain structure compared with wealthier children, a new analysis of MRI scans reveals.

Scientists report today (March 30) in the journal Nature Neuroscience a correlation between growing up in a lower-income family and having a smaller surface area in brain regions associated with skills that are important for academic success.

The association is independent of the children's race or ethnicity, the researchers found. Encouragingly, however, they also found that even small increases in income among the poorest seem to be associated with relatively large increases in brain surface area, and thus learning potential.

"We do not know exactly what [it is] about having more money [that] leads to these brain size differences, but we suspect it involves all the resources that more affluent people can afford, such as good nutrition, health care, better schools, etc.," said Elizabeth Sowell, senior author on the report and a professor of pediatrics at Children's Hospital Los Angeles and the University of Southern California Keck School of Medicine.

The researchers examined nearly 1,100 individuals between ages 3 and 20, the largest study of its kind. The children's family income levels were assessed through questionnaires, and measurements of the surface area of the brain were assessed with high-resolution brain MRIs. [10 Things You Didn't Know About the Brain]

The researchers found that as family income increases so, too, does the brain surface area of the child, on average, in regions supporting language, reading, spatial skills and executive functions, which are the mental processes that enable focusing, remembering and multitasking.

The study also showed that parental education was linked with a child's total brain surface area, implying that the more education the parent had, the greater the brain surface area for the child throughout his or her development.

However, the link between higher income levels and greater brain surface area showed a "logarithmic" increase among poor families. This means that small increases in income among the poor — for example, from $20,000 a year to $30,000 a year — translated to proportionally larger gains in surface area, far greater than the same $10,000 increase for those in the middle- or high-income brackets.

When the researchers compared children whose families make $25,000 or less per year to families with $150,000 or more, they found about a 6 percent difference in brain surface area; whereas when they compared children of parents with a high school education or lower to a college degree or higher, they found a 3 percent difference, Sowell calculated.

The findings do not imply that income is causing the brain differences (for example, there could be some other underlying factor that affects both brain size and family income level). Nor do they imply that a child's socioeconomic circumstances would necessarily dictate a child's cognitive or brain development in all cases, the researchers stressed.

"The important thing to realize is that, even though we are able to measure differences in brain structure in childhood and adolescence as a function of SES [socioeconomic status], it does not mean that disadvantaged children were or are 'doomed,'" said lead author Dr. Kimberly Noble, assistant professor of pediatrics at Columbia University Medical Center and an associate professor of neuroscience and education at Teachers College, Columbia University, in New York.

"We strongly believe that these differences reflect differences in experience --- learning experiences inside and out of the home, family stress, nutrition, environmental toxicants, quality child care --- that themselves shape brain development," Noble said. "By intervening at the level of those experiences, especially early in childhood, we could prevent or redirect children's detrimental outcomes."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

If you want to protect your mind, be mindful of what you eat. Doctors say that a diet rich in fruits, vegetables and lean meats that includes a little wine can lower the risk of developing Alzheimer's disease. 

The researchers have aptly named their diet the "MIND diet" — it is a hybrid of the Mediterranean diet and the DASH (Dietary Approaches to Stop Hypertension) diet. MIND stands for Mediterranean-DASH Intervention for Neurodegenerative Delay.

In a decade-long study of about 1,000 people, those who followed this diet reduced their risk of Alzheimer's disease by 53 percent, compared with people who did not follow it, according to the researchers. Even the people who only casually followed the diet had a lower risk of Alzheimer's, the researchers added.

The results appear online this month in the journal Alzheimer's & Dementia.

Alzheimer's disease, the most common form of dementia, affects more than 40 million people globally, according to Alzheimer's Disease International. Among developed nations, the prevalence rates tend to be highest in North America and northern Europe and lowest in Asia and the Mediterranean region. [6 Foods That Are Good for Your Brain]

Doctors believe that Alzheimer's disease is caused by a mix of genetic, environmental and lifestyle factors. Previous studies have found that Alzheimer's disease is associated with obesity, high blood pressure, high cholesterol, cardiovascular disease and diabetes.

A study published in the journal Neurology in 2011 found that people with diabetes were at least twice as likely to develop Alzheimer's disease, compared with people who don't have diabetes. In fact, researchers at Brown University have called Alzheimer's disease "Type 3 diabetes," given its connection to high blood-sugar levels and insulin resistance, hallmarks of Type 2 diabetes.

Alzheimer's disease rates are relatively low in Japan and in Italy, leading researchers to further ponder the connection between diet and loss of cognitive function among the elderly. In 2013, researchers in China found that the Japanese and Mediterranean diets may offer protection against Alzheimer's disease. These diets share an emphasis on fruits, vegetables, beans and fish, and include little red meat.

The latest study, conducted by researchers at Rush University Medical Center in Chicago, looked at the effects of a hybrid Mediterranean and DASH diet, the latter developed specifically to improve heart health. The study enlisted 923 participants, ages 58 to 98 years, and followed them for upward of 10 years.

The MIND diet emphasizes 15 dietary components, including 10 foods to eat daily — green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, fish, poultry, olive oil and wine — and five foods to avoid: red meats, butter and stick margarine, cheese, pastries and sweets, and fried or fast food.

Lead author Martha Clare Morris, a nutritional epidemiologist at Rush, said her group focused on this mix of two well-known healthy diets because it would be easy for Americans to follow. The Mediterranean diet, for example, calls for much more fish consumption.

"We devised a diet and it worked in this Chicago study," Morris said. "The results need to be confirmed by other investigators in different populations and also through randomized trials."

Even those participants who didn't follow the diet perfectly had a 35 percent reduction in the risk of developing Alzheimer's disease. The longer and more consistently a person follows the MIND diet, the less risk that person will have of developing Alzheimer's disease, Morris added.

"[P]eople who eat this diet consistently over the years get the best protection," she said. "You'll be healthier if you've been doing the right thing for a long time."

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Energy drinks might give you some pep — but they might also be priming you for heart problems, a new study finds.

Researchers found that energy drinks can raise blood pressure to potentially unhealthy levels. The effect was far more prominent in young adults who did not consume caffeine regularly, according to the study, presented March 14 at an American College of Cardiology meeting in San Diego.

In this study, the research team — led by Dr. Anna Svatikova, a cardiovascular-diseases fellow at the Mayo Clinic in Rochester, Minnesota — gave a can of a commercially available energy drink to 25 healthy volunteers, whose ages ranged from 19 to 40. On a different day, the participants drank the same amount of a placebo drink. The researchers measured the participants' heart rate and blood pressure before and after the drinks.

The participants experienced a more marked rise in blood pressure after consuming the energy drink than after drinking the placebo, according to the findings. The participants' average systolic blood pressure (the top number in a blood pressure reading) increased by 3 percent more after they drank an energy drink, compared with after they drank the placebo drink. [5 Health Problems Linked to Energy Drinks]

The effect was most dramatic in people who did not typically consume more than a small cup of coffee or other caffeinated drink daily. In this so-called "caffeine-naive" group, the blood pressure increase was twice as high as the increase seen in the people who drank at least the equivalent of a cup of coffee on a daily basis, the researchers said in a statement.

Even a small increase in blood pressure can have deadly consequences, depending on your age and resting blood pressure, said Sachin Shah, an associate professor of pharmacy at the University of the Pacific in Stockton, California, who was not involved in the study.

"An acute, moderate increase in blood pressure is typically not a cause of worry in healthy subjects," said Shah, who has done research on the effects of energy drinks. However, in older people or those with hypertension, a moderate increase may be a cause for concern, he said.

At a population level, an increase of three or four points on a systolic blood pressure reading could mean a significant increase in deaths from stroke, he told Live Science.

Scientists do not know whether it is the caffeine, taurine or other ingredients found in energy drinks — or a combination of ingredients — that can adversely affect the heart.

In a separate study, presented last year at an American Heart Association meeting by Maj. Emily Fletcher of the David Grant Air Force Medical Center, healthy volunteers experienced a greater increase in blood pressure after they consumed an energy drink compared to after they drank a coffee drink that had an equal amount of caffeine. This result, Fletcher said, suggests that ingredients in the energy drink other than caffeine were conspiring to raise blood pressure.

According to the Mayo Clinic, consuming up to 400 milligrams of caffeine a day appears to be safe for most healthy adults. That's roughly the amount of caffeine in four cups of brewed coffee, 10 cans of cola or two "energy shot" drinks.

Previous studies have associated the consumption of energy drinks with poor memory and learning, anxiety, hallucinations, abnormal heart rhythm, substance abuse, and risk-taking behaviors. A study published in the journal Pediatrics in 2011 found that children, in particular, are at high risk of cardiac abnormalities from consuming energy drinks because of their smaller body size.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

With obesity rates continuing to rise around the globe and the majority of Americans now obese or overweight, it's easy to see that we are losing the battle of the bulge.

Aside from isolated areas of improvement where people are, in fact, losing weight — in a city here, a neighborhood there — no country has succeeded in reversing its obesity epidemic. That failure has begun to have dire consequences: shortened lives, compromised life quality and skyrocketing health care costs, scientists reported Wednesday (Feb. 18) in a special issue of the journal The Lancet.

In a series of six critical articles covering the health, policy, economics and politics of obesity, scientists lay out what society has been doing wrong and call for a new global action plan to meet what they call the "modest" goal of the World Health Organization: no increase in the prevalence of obesity from now through 2025.

"There are clear agreements on what strategies should be implemented and tested to address obesity," said Christina Roberto, an assistant professor of social and behavioral sciences and nutrition at the Harvard School of Public Health, and lead author of the first report of the series. "The challenge now is [figuring out] how to implement the specific actions within those strategies."

"Even outside public health, there is no question that obesity is a complex problem and that reversing the epidemic will require substantial and urgent actions not only from governments, but from a range of actors, including industries [and] civil society," Roberto told Live Science.

Of the 7 billion people on Earth, more than 2 billion are overweight or obese, according to a study published last year in The Lancet. The condition affects people in countries large and small, rich and poor. The Pacific islands of American Samoa, Nauru and the Cook Islands are the most obese countries in the world, according to the WHO, and at least a dozen countries, including Mexico, now have obesity rates higher than that of the United States. [8 Reasons Our Waistlines Are Expanding]

The diverse group of obesity experts reporting in The Lancet said society has gone wrong by following false dichotomies about obesity, thus laying the foundation for poor policy or inaction. For example, people argue over whether obesity is something people bring on themselves or is caused by the environment (when, in fact, both factors play a role); whether the responsibility to take action against obesity lies with individuals or society (again, the best courses of action will include both); whether the high rate of consumption of unhealthy food is due to a too-big supply of it or a too-big demand for it; and whether the government should regulate the food industry or the industry should self-regulate.

Roberto said researchers now better understand the complexity of obesity, that it's not black-and-white and that the goal is to "merge these competing perspectives to provide an understanding of obesity's causes and solutions that integrates what seem like opposing beliefs."

Corinna Hawkes, head of policy at World Cancer Research Fund International, wrote in the second article of the Lancet series about a vicious cycle in people's preferences and demand for unhealthy food that starts in childhood. Research has revealed how children, even as infants, learn to like foods from influences in the world around them. The food industry targets these tastes, Hawkes said, and the resulting food preferences can be stubborn and set the tone for longer-term food habits.

So, while individuals bear some personal responsibility for their health, environmental and marketing factors exploit humans' biological and economic vulnerabilities that promote the consumption of unhealthy foods, Hawkes and other scientists explained.

"The future benefits to society of raising a generation for whom healthier food choices are the preferred choices are huge," Hawkes said. "Kids who enjoy healthy eating when they are young have a better chance of keeping hold of those habits in later life. In turn, they are likely to be a positive influence on others, including their own children."

The Lancet authors wrote that they support policy actions proposed in the NOURISHING framework, which was created by the World Cancer Research Fund International. Each letter in NOURISHING represents a concept, such as "Nutrition label standards" and "Offer healthy foods."

The framework covers three broad areas: the food environment (nutrition labeling, advertising restriction and food taxes); the food system (supply-chain incentives for production); and behavior-change communication (nutrition-counseling interventions and public awareness campaigns).

The researchers cite successes such as New York City's ban on trans fat in restaurant foods, which has had a positive, rippling effect around the country; and Mexico's tax on sugary drinks, which has significantly reduced soda consumption since being instituted last year.

"There is reason to be optimistic," Roberto said, but she added that "there are a number of barriers to progress" that governments and health organizations must seriously address. [7 Diet Tricks That Really Work]

Dr. William Dietz of the Milken Institute School of Public Health at the George Washington University wrote a Lancet piece on medical bias against obesity and the dearth of health professionals trained to help obese patients, stating that the medical community has yet to rise to the call. Other authors cited obstacles such as food industry lobbying, a shortfall of empirical evidence demonstrating effective policy, governments too weak or unwilling to implement changes and the menace of childhood obesity, which sets people up for a lifetime fight against their weight.

The Lancet editors concluded that the obesity epidemic will not be reversed without government involvement, and they outlined a systems approach that includes food producers, retailers, schools and, at the heart of the system, the individual.

The article abstracts, commentary and infographics are available on The Lancet website.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Smoking a pack of cigarettes a day will cost a person upwards of $2 million in tobacco costs and other expenses over his or her lifetime — at least according to a study conducted last month by WalletHub, a financial advice website. But is that claim true?

The study says the main driver of this exorbitant price tag was the "tobacco cost per smoker," which WalletHub estimated to be between $800,000 and $1.5 million, depending on which U.S. state a person lives in; cigarettes are the cheapest in South Carolina and most expensive in Alaska.

The study's numbers were shocking. And although WalletHub's calculations were posted on its website and not in a peer-reviewed journal, the study was widely reported by news outlets, even financial websites.

Yes, the results are shocking. But are they true? Not at all. From a public health perspective, this cost is inflated by at least a factor of 10.

The primary reason the WalletHub number is inflated is that the company's calculation is based on the idea that if smokers weren't spending their money on cigarettes, they would be investing every penny of it and that their investment would give them a 7 percent rate of return for 51 years. (The 51 years, by the way, does indeed reflect a sad truth that someone who starts smoking a pack daily at age 19 likely won't live past age 70. The 7 percent rate of return is the historical average annual return of the S&P 500, which is generally considered a good measure of the stock market returns.)

If that were the case, then presto! A person could be a millionaire by age 70. [Kick the Habit: 10 Scientific Quit-Smoking Tips]

But as any 70-year-old lifetime nonsmoker on a fixed income will tell you, it just doesn't work that way.

In fact, public health experts don't speculate about costs this way when they calculate the societal impact of smoking, for two reasons: No one diverts all the money that would have been spent on a bad habit into an investment, and investing money offers no guarantee for such a high financial return.

Still, smoking clearly is unhealthy and costly, for society and the individual. So, let's do the straight math.

The price of cigarettes varies greatly from state to state, and country to country. Assuming a $6-per-pack average (the American Lung Association estimates $5.51) and for simplicity, like the WalletHub study, disregarding inflation, the cost would be $6 per day, times 365 days, times 51 years — a total of $111,690.

That's a hefty hunk of change, and this alone should alarm smokers. But to grow that sum to more than $1 million, you would need to be diligent about investing that $6 per day, or $2,160 per year, and pray for an average rate of return of 7 percent over 51 years.

WalletHub's calculation is based on something called the "latte factor" — the notion, largely discredited by financial planners, that if you cut back on a store-bought latte each day, you would be a millionaire in the future.

Cost calculations in the public health realm don't employ the latte factor. For example, the average cost of raising a child is about $25,000 a year, according to the USDA. This does not mean that not having a child will make you a millionaire in 20 years. If this were true, you could choose not to have twins and have nearly $2 million in 20 years!

WalletHub conceded as much.

"We did not conduct this study based on a smoker versus nonsmoker approach," WalletHub told Live Science via email. "We assumed that a smoker saved the amount spent daily on cigarettes and avoided some of the extra costs associated with smoking and, in the end, added up how much money that person could save."

Another questionable element of WalletHub's cost calculation is "the costs for victims of secondhand-smoke exposure," as stated in its report. "This approach assumes that, in a perfect society, smokers would also pay the costs related to the harmful smoke that tobacco releases into the air," the study authors wrote.

But alas, we don't live in a perfect society, so one cannot add these costs to an individual's financial burden from smoking, because they are not tangible costs, and the smoker isn't being burdened by them.

Even the health cost associated with smoking is widely speculated. WalletHub calculated costs between $100,000 and $200,000 depending on the state where one lives, based on a recalculation of data from the Centers for Disease Control and Prevention at a population-wide level.

However, previous estimates haven't been close to this level. Last year, the Campaign for Tobacco-Free Kids updated a well-established calculation made in the 1990s by Thomas Hodgson, a CDC scientist. This group found the lifetime health costs to be $21,000.

To its credit, the WalletHub calculation included some expenses that some smokers might not realize: the extra cost of health insurance, life insurance, homeowners insurance and possible loss of income as a result of absenteeism or workplace prejudice against smokers.

(Actually, there are more costs not included in the WalletHub calculation, such as cleaning costs, lower trade-in value for cars and shorter life for electronic equipment sullied by smoking residue.)

So, what is the lifetime cost of a pack-a-day smoking habit? You can assume you'll burn through about $100,000 for the cigarettes. Beyond that, costs are very speculative.

Smoking is an expensive habit. It's a dirty habit. It's an unhealthy habit. It's an annoying habit for the 80 percent of Americans who don't smoke. But it is not a $2 million habit.

Smokers need true facts to help them quit smoking, not hyperbole.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Editor's note: This column was updated on Feb. 6 to indicate the fact that the 7 percent rate of return is the historical average of the S&P 500. 

The brains of psychopathic violent criminals have abnormalities in regions related to punishment that are not seen in the brains of violent criminals who are not psychopathic, according to new research using brain scans.

These MRI scans suggest that psychopaths don't grasp punishment the same way as other people, the researchers said. This is likely why psychopaths do not benefit from rehabilitation programs, as other violent criminals often do, the scientists report today (Jan. 28) in the journal Lancet Psychiatry.

However, understanding these neurological underpinnings of psychopathy may improve interventions during childhood, when psychopathic behavior emerges as something distinct from ordinary delinquency, the scientists said.

"Psychopathic offenders are different from regular criminals in many ways," said Dr. Nigel Blackwood of King's College London, a senior author on the paper. "Regular criminals are hyper-responsive to threat, quick-tempered and aggressive, while psychopaths have a very low response to threats, are cold, and their aggressive behavior is premeditated."

In previous research, Blackwood has described psychopaths as "cold-hearted" and other violent offenders as "hot-headed." [Top 10 Controversial Psychiatric Disorders]

To understand this difference, Blackwood and his colleagues conducted MRI scans of the brains of 12 violent criminals with psychopathy, 20 violent criminals with antisocial personality disorder but not psychopathy, and 18 healthy people who were not criminals. The criminals had been convicted of murder, rape, attempted murder or grievous bodily harm in the United Kingdom.

While their brains were being scanned, the participants were asked to play a matching game to assess their ability to change their behavior when confronted with rewards and punishment.

In the group of criminals who were psychopathic, the scientists observed lower volumes of gray matter in brain regions involved in empathy, moral reasoning, and the processing of social emotions such as guilt and embarrassment. They also found abnormalities in white matter fibers leading to the prefrontal cortex, in regions involved in learning from reward and punishment.

The other violent criminals performed similarly to the people who were not criminals in this test, the researchers found.

For any person, deciding on how to behave involves generating a list of possible actions, weighing the negative and positive consequences of each, and, hopefully, choosing the behavior most likely to lead to a positive outcome, explained Sheilagh Hodgins, a professor of psychiatry at the University of Montreal, who co-led the study with Blackwood.

"Offenders with psychopathy may only consider the possible positive consequences and fail to take account of the likely negative consequences," Hodgins said. "Consequently, their behavior often leads to punishment rather than reward as they had expected."

So, approaches to rehabilitation that are based on treating the behavior problems of psychopaths similarly to those of criminals who are not psychopathic are bound to fail, the researchers said.

"Offender rehabilitation focuses on changing behavior, but to succeed it must take account of the personality characteristics of the offenders," Hodgins told Live Science. "Those with psychopathy are less empathetic, more callous, more manipulative, and they commit more violent crimes, some of which are premeditated."

What can be done to help psychopaths control their behavior? The researchers suggest focusing on learning-based interventions during childhood, when there still is the potential to alter brain structure and function.

Hodgins said that researchers are "only beginning to learn about the childhood antecedents of the syndrome of psychopathy," but that her group's study provides a hypothesis on the emergence of psychopathy and how to test for it in children.

There is ongoing research trying to understand how to help children with psychopathic characteristics — that is, being callous, unemotional and prone to disruptive conduct — to become more emotionally responsive, Hodgins said. This may include focusing on reward and using negative reinforcement sparingly when interacting with these children.

"Since most violent crimes are committed by men who display conduct problems from a young age, learning-based interventions that target the specific brain mechanisms underlying this behavior pattern and thereby change the behavior would significantly reduce violent crime," Hodgins said.

But the abnormalities of brain structure and function associated with persistent violent behavior are subtle and complex, Blackwood added. And little is still known about how genes and the environment conspire to create a cold, ruthless killer.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Consider it a wake-up call for generations X and Y: You may think you are healthy, but having cholesterol levels that are even slightly high during your 30s may double your risk for heart disease later in life, new research shows.

People can lower their risk of developing heart disease by refraining from smoking and maintaining a healthy weight and blood pressure. But regardless of whether you do those things, if your cholesterol is above the healthy range starting in your mid-30s, you might be setting yourself up for a heart attack or chest pains by the time you're in your 60s, the results of the new study suggest.

Moreover, if you wait until you're 50 to lower your cholesterol, it may be too late to reverse the damage already done, the researchers said. Their message is for young adults to get their cholesterol level checked and, if it's high, do something about it now.

"Several of my co-authors and I are members of generations X and Y, so for us, this research wasn't just scientific; it's personal," said lead author Dr. Ann Marie Navar-Boggan of the Duke Clinical Research Institute, part of the Duke University Medical Center in Durham, N.C. "After I saw the results of our study, I called all of my family members between the ages of 20 and 50, and told them they needed to have their cholesterol levels checked."

Heart disease is the leading cause of death in the United States for both men and women, and is responsible for one in four deaths in the U.S., according to the Centers for Disease Control and Prevention. But fewer than half of adults ages 20 to 35 have had a cholesterol test, according to a 2010 CDC report. Cholesterol screening is not usually performed on young adults unless they have a risk factor for heart disease, such as obesity.

In this latest study, the researchers looked at data from the Framingham Heart Study, which has tracked the heart health of thousands of adults throughout their lifetimes, since 1948. The researchers focused on approximately 1,500 adults who are now in their 70s and who had been free of heart disease at age 55.

They found that the people in this group who'd had high cholesterol for at least 10 years by the time they reached age 55 had a 16.5 percent chance of developing heart disease after age 55. In comparison, people in the study who had normal cholesterol levels during those early years had a 4.4 percent risk of developing heart disease after age 55. [5 Surprising Ways to Be Heart Healthy]

Each decade of high cholesterol raised people's risk of heart disease by about 40 percent, suggesting that the cumulative effects of even mild or moderate elevations in cholesterol pose a significant risk to heart health, the study found.

The "wealth of data collected over time made it possible to analyze the long-term effects of cholesterol in young people — a topic on which not enough is known because it requires decades of tracking," said Michael Pencina, a professor of biostatistics and bioinformatics at Duke and a senior author on the paper.

The researchers considered people to have elevated cholesterol if their levels were 160 mg/dL or higher for non-HDL cholesterol. Non-HDL is the total cholesterol minus the "good" HDL, leaving the "bad" LDL plus other types of harmful cholesterol. The researchers noted, however, that they found similar results for patients with LDL cholesterol of 130 mg/dL or higher.

Most experts agree that diet and exercise are the best methods of lowering your bad cholesterol and raising your "good" cholesterol. Numerous studies have shown that moderate physical exercise for 30 minutes a day can lead to at least modest improvements in a person's cholesterol profile; that is, some exercise is better than none, but more is much better than some.

Foods that can improve cholesterol levels include oats and other high-fiber grains; beans; oily fish, such as salmon; most nonsalted nuts; olive oil; and a plant-based diet in general.

And then there's the possibility of medication.

"Our research does not imply that all young adults in their 30s and 40s with high cholesterol should be on statins," which are cholesterol-lowering drugs, Navar-Boggan told Live Science. "We do not have great long-term data about the long-term safety and effectiveness of statin therapy when started in early adulthood for mild to moderately elevated cholesterol."

"That said, there are adults who will be unable to control their cholesterol with diet and exercise alone," Navar-Boggan said. "For these people, the decision to start statin therapy will ultimately be a personal one … hopefully grounded in an informed conversation with their health care provider."

Other members of the research team are based at Boston University and McGill University in Montreal.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Diabetes appears to be a disease written deeply in human genes, a feature millions of years old, which can emerge yet also retreat through the influence of environmental forces such as diet, a new study suggests.

Researchers looked at how obesity, in particular, can trigger the onset of Type 2 diabetes in both mice and humans by manipulating how genes are expressed.

They found that obesity, in effect, can change the chemical tags associated with DNA, called the epigenome. These epigenetic changes modify how genes behave and can alter the production of proteins necessary for proper metabolism and secretion of insulin, the hormone that controls blood sugar levels.

The good news is that diseases brought on by such epigenetic changes can be reversed, the scientists at Johns Hopkins University in Baltimore said in their study, published Jan. 6 in the journal Cell Metabolism.

The study may help explain why Type 2 diabetes, a disease that was hardly seen a few generations ago, now affects more than 300 million adults worldwide, with some populations far more affected than others — a conspiracy of both genetic and epigenetic factors. [8 Reasons Our Waistlines Are Expanding]

In people with Type 2 diabetes, the body has lost either the ability to produce enough insulin, or the ability to respond to the insulin that is produced. Insulin is the hormone that triggers the body's cells to take up sugar from the bloodstream, so in people with Type 2 diabetes, the level of sugar in the blood rises too high.

It is well established that people who are obese are at increased risk of developing Type 2 diabetes, so the Hopkins scientists first studied obese mice to understand how obesity is related to the disease. The mice in the study were clones — all had identical genetics. The researchers found that the mice placed on a high-fat diet grew obese and diabetic; mice on a regular diet stayed lean and healthy. This much was expected.

Yet although the mice started life with identical genes, it was clear that the lean and obese mice had radically different gene expression as adults. An analysis of DNA isolated from their fat cells revealed changes in the epigenome: at certain sites along their DNA, chemical tags called methyl groups were present in the lean mice but missing in the obese mice; at other sites, vice versa. These methyl groups prevent genes from making proteins.

The scientists then looked at a dataset of obese people who underwent gastric bypass surgery, and, to their surprise, found nearly the exact same pattern of epigenetic changes at key sites in DNA isolated from their fat cells.

"Mice and humans are separated by 50 million years of evolution, so it's interesting that obesity causes similar epigenetic changes to similar genes in both species," said Dr. Andrew Feinberg, director of the university's Center for Epigenetics, who led the study.

The findings mesh nicely with other recent discoveries about the role of diet in the development of diabetes.

A study published in April 2012 in The New England Journal of Medicine found that 75 percent of people with diabetes who underwent gastric-bypass surgery saw a reversal of their disease. The Hopkins study supports this by revealing how the epigenome in obese patients becomes more like the epigenome in lean people after this weight-loss surgery.

A study published in August 2014 in Cell Metabolism found that grizzly bears essentially become diabetic during hibernation, and then "recover" when they awaken. The bears' diabetes is induced by the accumulation of fat in the months preceding their winter sleep. Once in a diabetic state, insulin stops working, and, in the absence of more food while hibernating, the insulin resistance allows the bears to effectively break down their fat stores for energy.

This finding points to the idea that diabetes is a feature encoded in our DNA that can have evolutionary advantages in a feast-or-famine world, the researchers said.

"It's likely that when food supplies are highly variable, these epigenetic changes help our bodies adapt to temporary surges in calories," Feinberg said. "But if the high-calorie diet continues over the long term, the same epigenetic pattern raises the risk for disease."

Feinberg stressed, however, that the new findings highlight the "complementary nature of genetics and epigenetics in disease." Diet is still the main contributor to type 2 diabetes, he said.

Some of the epigenetic changes that the scientists discovered were associated with genes already known to raise diabetes risk. Many more were tied to genes not linked conclusively to the disease but rather metabolism in general.

Together, they offer "new potential targets for treating Type 2 diabetes," said G. William Wong, an associate professor of physiology at Johns Hopkins and a co-author on the paper.  The study also suggests that researchers could develop an epigenetic test to identify people on the path to diabetes much earlier than can now be done.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

Twelve athletes will embark tomorrow (Jan. 16) on an extraordinary feat — to run across the United States from California to Maryland, more than 3,000 miles, completing a marathon a day, nearly every day for the next four and a half months.

And scientists plan to tag along, capitalizing on this unique opportunity to study the impact of ultra-endurance running on the human body.

The extreme endurance event could provide insight into how the rest of us mere mortals can better cope with the trials and tribulations of more moderate exercise, the scientists said.

The event is called Race Across USA, and its primary goal is to raise money and awareness for childhood obesity. In the past 30 years, obesity rates have more than doubled in children and quadrupled in adolescents, according to the Centers for Disease Control and Prevention. [8 Reasons Our Waistlines Are Expanding]

Ten of the runners have agreed to participate in scientific studies. Scientists want to look at how these runners burn calories; how ultra-endurance running changes the percentages of body fat and muscle mass in the body; and how such an extreme athletic endeavor impacts cardiovascular health, gut bacteria, sleep patterns, bodily injuries and mental health. Multiple research teams from across the country are participating.

"The core team runners will experience a variety of obstacles throughout the Race Across USA, and our research program is positioned to examine how they respond and how the body and mind adapts," said research director Bryce Carlson, an assistant professor of anthropology at Purdue University in West Lafayette, Indiana.

And Carlson should know. On top of running the study project, he's also running the actual race, all 3,080 miles of it.

Carlson's own part of the larger scientific study will be on what he calls biocultural adaptation to stress, which means attempting to determine the role nutrition plays in buffering stress or promoting recovery, and how runners modify their behavior or use technology to shield themselves from stress.

Lara Dugas, an assistant professor at Loyola University Chicago Stritch School of Medicine, is part of a team studying energy metabolism. Among the key questions she hopes to answer are how does a person's body composition change during sustained endurance activity, and how do total energy expenditure and resting metabolic rate vary across the climates, altitudes and types of terrain the runners will encounter throughout the race.

Dugas said it will be important to do such tests noninvasively, as the runners already have enough obstacles to worry about. So, to gather the necessary measurements, her research team will rely on lightweight heart-rate monitors that the runners will wear, and urine samples taken daily.

"It is not unusual for athletes to already be training with heart-rate monitors or other wearable sensors," she said.

Dr. Aaron Baggish, associate director of the Cardiovascular Performance Program at the Massachusetts General Hospital Heart Center in Boston, said he plans to conduct what he describes as the first longitudinal study on the heart health of extreme-long-distance runners. He will ask runners to undergo CT angiography, echocardiography and blood sampling before and after the race.

Baggish, an expert on marathoners' health, is a co-medical director for the Boston Marathon and was at the finish line treating victims of the bombing at the 2013 marathon. He said that scientists "really don't have any idea" whether running ultramarathons is beneficial or harmful to the heart.

He said an important message about Race Across USA is to motivate people everywhere to move their bodies a little more, because when it comes to exercise, even "a little goes a long way."

"It doesn't take a whole lot of exercise to maximize cardiovascular health," Baggish told Live Science. He added that significant benefits in heart health can be realized with 10 or 15 minutes of exercise a few times a week, at an intensity that leaves you speaking in broken sentences.

The Race Across USA runners themselves are an eclectic bunch, including nine men and three women ranging in age from 29 to 74. Two are barefoot runners, two will run in minimalist sandals, two usually run in kilts, and one runner (Rob Young, a kilt-wearer from the U.K.) had already completed more than 260 marathons in the past 240 days.

Suffice it to say that none of the runners are overweight.

You can follow the race and make a donation in a runner's name at http://raceacrossusa.org.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.

A woman's garbled text message to her son had an underlying message: She was having a stroke.

Her case, published last month in the journal BMJ Case Reports, is now the fourth reported incident in which garbled texting, similar to slurred speech, was a symptom of a stroke. Doctors are calling this a new phenomenon.

Clumsy thumbs and devious auto-correction aside, the inability to write a coherent text message is called dystextia, and it was first described as medical symptom in 2006, seen in people with migraine headaches. Texting requires the coordination of several brain regions. Thus, dystextia may be a sign of abnormal brain function that otherwise wouldn't be seen in a person speaking or  writing longhand, stroke experts say.

Its is not clear exactly what causes dystextia, but it includes disruption of multiple brain functions, including fine motor skills, said Dr. Samer Al-Hadidi, a medical resident at the Hurley Medical Center in Flint, Michigan, who treated the woman and is the lead author on the case report. [16 Oddest Medical Cases]

Dystexia is similar to aphasia, a language disorder often caused by stroke in which a person may be able to speak coherently but not read or write, or vise versa, Al-Hadidi said. "Aphasia is well described, and it [manifests itself in] different ways according to the area of the brain affected," Al-Hadidi said. In contrast, as a newly identified condition, dystextia remains poorly understood.

The first reported case in which dystextia was seen as a stroke symptom was published in the journal JAMA Neurology in December 2012. A 25-year-old pregnant woman was rushed to the emergency room upon sending her husband strange messages about their baby's due date, such as "everywhere thinging days nighing" followed by "some is where."  Her speech was mostly coherent.

It turned out that the woman was suffering from a mild stroke. She was treated successfully with blood thinners and ultimately delivered a healthy baby.

At the American Academy of Neuroscience annual meeting in 2013, doctors presented another case, dating back to 2011, of a 40-year-old man who similarly sent his wife a series of disjointed messages while on a short business trip. Doctors subsequently found that he could read, write and speak just fine. Yet when they asked him to precisely text the phrase "the doctor needs a new BlackBerry," the man typed "Tjhe Doctor nddds a new bb."

The man did not recognize his typing errors. A thorough examination with brain scans revealed that he had recently had a stroke, although it was unclear exactly when it happened.

In this latest case, a 61-year-old woman sent her son strange text, prompting him to call for an ambulance. The woman's text was nearly coherent, though, a series of three quick messages: "Oh honey your" followed by "I am weak" and then "I am out, don't know how sleep, can't sense, I can't type, lov you."

The wording is curiously similar to that of man on the business trip, who texted his wife: "Oh baby your" followed by "I am happy" and "I am out of it, just woke up, can't make sense."

The woman was treated at Hurley Medical Center and quickly recovered her ability to text. Her case underscores the importance of recognizing stroke symptoms and seeking medical help immediately, Al-Hadidi said. The sooner a stroke is detected and treated, the better the outcome, he said.

Garbled text messages could be valuable in treating patients. Because texts are time-stamped they can help doctors to narrow in on when a stroke occurred and to determine the best course of treatment, he said.

Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science.