TIME medicine

DIY Drugs: Antibiotics Could Soon Be Made Out of Your Own Bacteria

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Our own gut bacteria may be the next source of antibiotics dra_schwartz—Getty Images

There’s a universe of friendly bacteria living within us, and they may be the next source of powerful drugs, including antibiotics

Scientists have known for a long time that there’s no better drug-maker than nature. A third of our medicines come from plants and microbes so it’s not such a surprise that the millions of bacteria that inhabit our gut, mouths, nose, skin and reproductive tracts—called our microbiome—might be an untapped resource for new drugs. That’s what Michael Fischbach, an assistant professor in the department of bioengineering at the University of California, San Francisco, was counting on, and, he reports in the journal Cell, he was right.

He and his team analyzed the genomes of microbes living in various parts of the human body, and using an algorithm they developed called ClusterFinder, they found 3,118 groups of genes that churned out drug-like molecules. This suggests that these groups of genes could be a rich trove of potentially new drugs or other important compounds that keep our bodies healthy. “When the results of the search came back, it was a eureka moment,” he says. “It was a big surprise to us, because in retrospect the human microbiome was one place we hadn’t thought to look,” he says of the results.

MORE: The Good Bugs: How the Germs in Your Body Keep You Health

Not satisfied with simply identifying the bacteria that make these small molecules, Fischbach also wanted to see if any of them were making drugs that could prove useful in treating human disease. And indeed, he found that some made antibiotics that mimiced those developed by pharmaceutical companies and are already on the market. To see how effective a human microbiome-based antibiotic might be, he isolated one of these gene products from the vaginal microbiome of a Texas woman.

Dubbed lactocillin, it turned out to be a strong antibiotic against some familiar infections, including Staphylococcus aureus and Enterococcus faecalis, but not against E. coli. In fact, a compound similar to lactocillin is being developed by Novartis as a new member of the antibiotic class.

The results were so robust, says Fischbach, that “we completely changed what we are working on. We stopped working on soil bacteria and started working on gut, skin and oral bacteria.” While he doesn’t expect that most of the genes will yield antibiotics, he is confident that they will produce other critically important compounds that are important in regulating our immune systems, for example, and in keeping our metabolism—the way we burn calories and store fat—in check. Those compounds may explain some of the other intriguing things scientists are learning about the microbiome: that the community of bacteria in the guts of normal weight people differ from those of obese individuals, for example, and that different bacterial communities might be responsible for everything from cancer to allergies and asthma.

That’s why he’s eager to move on to the next steps, triaging the thousands of genes he’s identified to tease out those that make drug-like molecules, and then systematically figuring out what those molecule do. That will lead to a better understanding of how we might be able to exploit them—either by making the same molecules in a lab or transplanting the right communities of bacteria to the gut or other places and putting the microbes to work for us.

MORE: Colon Cancer’s Newest Culprit: Gut Bacteria

TIME medicine

Woman Receives First Stem Cell Therapy Using Her Own Skin Cells

A Japanese woman is the first to receive retinal cells made from her own skin cells

Researchers at the RIKEN Center for Developmental Biology in Japan surgically transplanted a sheet of retinal pigment cells into the eye of a 70-year old woman on Friday.

The cells are the first induced pluripotent stem cells, or iPS cells, given to a human patient. They were made by Masayo Takahashi, who grew them from the patient’s own skin cells, which were treated with four genetic factors to revert back to an embryonic-like state. Takahashi then soaked the cells with the appropriate growth factors and other compounds so they developed into retinal pigment cells.

The patient was losing her sight due to macular degeneration, because her retinal pigment endothelial cells were damaged by an overgrowth of blood vessels. Replacing them with a new population of cells can restore her sight.

MORE: Stem-Cell Research: The Quest Resumes

Stem cell scientists are starting to test their treatments in eye-related diseases, because parts of the eye are protected from the body’s immune system, which could recognize the introduced cells as foreign and destroy them. That’s not a problem with the iPS cells, since they are made from the patient’s own skin cells, but it’s an added safety net to ensure that the therapy is safe and hopefully effective.

Because iPS cells are genetically treated to erase their skin cell development and revert them back to an embryonic-like state when they can become any type of cell, there are still concerns about their safety when transplanted into patients. The U.S. Food and Drug Administration has not yet approved a trial involving iPS cells – so far, only stem cells made from excess IVF embryos have been approved for treating macular degeneration. A 19-member committee of the Japanese ministry of health approved the experimental procedure four days ago, according to Nature, after Takahashi made her case, with the help of Dr. Shinya Yamanaka of Kyoto University, who shared the 2012 Nobel Prize for discovering iPS cells.

MORE: Stem Cell Miracle? New Therapies May Cure Chronic Conditions like Alzheimer’s

Japan’s stem cell scientists are hoping the surgery is a success; the field has been struggling since a well-publicized paper about a new way to make iPS cells was retracted amid allegations of fraud.

It’s not known whether the cells will continue to grow and form abnormal tumors, or whether they will migrate to other parts of the body. But now that the first patient has received them, those questions – and more, about the effectiveness of stem cell therapy – might be answered soon.

TIME sleep

The Power of Sleep

sleep illustration
Photo-Illustration by Timothy Goodman for TIME

New research shows a good night's rest isn't a luxury--it's critical for your brain and for your health

When our heads hit the pillow every night, we tend to think we’re surrendering. Not just to exhaustion, though there is that. We’re also surrendering our mind, taking leave of our focus on sensory cues, like noise and smell and blinking lights. It’s as if we’re powering ourselves down like we do the electronics at our bedside–going idle for a while, only to spring back into action when the alarm blasts hours later.

That’s what we think is happening. But as scientists are now revealing, that couldn’t be further from the truth.

In fact, when the lights go out, our brains start working–but in an altogether different way than when we’re awake. At night, a legion of neurons springs into action, and like any well-trained platoon, the cells work in perfect synchrony, pulsing with electrical signals that wash over the brain with a soothing, hypnotic flow. Meanwhile, data processors sort through the reams of information that flooded the brain all day at a pace too overwhelming to handle in real time. The brain also runs checks on itself to ensure that the exquisite balance of hormones, enzymes and proteins isn’t too far off-kilter. And all the while, cleaners follow in close pursuit to sweep out the toxic detritus that the brain doesn’t need and which can cause all kinds of problems if it builds up.

This, scientists are just now learning, is the brain on sleep. It’s nature’s panacea, more powerful than any drug in its ability to restore and rejuvenate the human brain and body. Getting the recommended seven to eight hours each night can improve concentration, sharpen planning and memory skills and maintain the fat-burning systems that regulate our weight. If every one of us slept as much as we’re supposed to, we’d all be lighter, less prone to developing Type 2 diabetes and most likely better equipped to battle depression and anxiety. We might even lower our risk of Alzheimer’s disease, osteoporosis and cancer.

The trouble is, sleep works only if we get enough of it. While plenty of pills can knock us out, none so far can replicate all of sleep’s benefits, despite decades’ worth of attempts in high-tech pharmaceutical labs.

Which is why, after long treating rest as a good-if-you-can-get-it obligation, scientists are making the case that it matters much more than we think. They’re not alone in sounding the alarm. With up to 70 million of us not getting a good night’s sleep on a regular basis, the Centers for Disease Control and Prevention considers insufficient sleep a public-health epidemic. In fact, experts argue, sleep is emerging as so potent a factor in better health that we need a societal shift–and policies to support it–to make sleep a nonnegotiable priority.

THE CONSEQUENCES OF SKIMPING

Despite how great we feel after a night’s rest–and putting aside what we now know about sleep’s importance–we stubbornly refuse to swallow our medicine, pushing off bedtime and thinking that feeling a little drowsy during the day is an annoying but harmless consequence. It’s not. Nearly 40% of adults have nodded off unintentionally during the day in the past month, and 5% have done so while driving. Insomnia or interrupted sleep nearly doubles the chances that workers will call in sick. And half of Americans say their uneven sleep makes it harder to concentrate on tasks.

Those poor sleep habits are trickling down to the next generation: 45% of teens don’t sleep the recommended nine hours on school nights, leading 25% of them to report falling asleep in class at least once a week, according to a National Sleep Foundation survey. It’s a serious enough problem that the American Academy of Pediatrics recently endorsed the idea of starting middle and high schools later to allow for more adolescent shut-eye.

Health experts have been concerned about our sleep-deprived ways for some time, but the new insights about the role sleep plays in our overall health have brought an urgency to the message. Sleep, the experts are recognizing, is the only time the brain has to catch its breath. If it doesn’t, it may drown in its own biological debris–everything from toxic free radicals produced by hard-working fuel cells to spent molecules that have outlived their usefulness.

“We all want to push the system, to get the most out of our lives, and sleep gets in the way,” says Dr. Sigrid Veasey, a leading sleep researcher and a professor of medicine at Perelman School of Medicine at the University of Pennsylvania. “But we need to know how far we can really push that system and get away with it.”

Veasey is learning that brain cells that don’t get their needed break every night are like overworked employees on consecutive double shifts–eventually, they collapse. Working with mice, she found that neurons that fire constantly to keep the brain alert spew out toxic free radicals as a by-product of making energy. During sleep, they produce antioxidants that mop up these potential poisons. But even after short periods of sleep loss, “the cells are working hard but cannot make enough antioxidants, so they progressively build up free radicals and some of the neurons die off.” Once those brain cells are gone, they’re gone for good.

After several weeks of restricted sleep, says Veasey, the mice she studied–whose brains are considered a good proxy for human brains in lab research–“are more likely to be sleepy when they are supposed to be active and have more difficulty consolidating [the benefits of] sleep during their sleep period.”

It’s the same thing that happens in aging brains, she says, as nerve cells get less efficient at clearing away their garbage. “The real question is: What are we doing to our brains if we don’t get enough sleep? If we chronically sleep-deprive ourselves, are we really aging our brains?” she asks. Ultimately, the research suggests, it’s possible that a sleep-deprived brain belonging to a teen or a 20-year-old will start to look like that of a much older person.

“Chronic sleep restriction is a stress on the body,” says Dr. Peter Liu, professor of medicine at Harbor-UCLA Medical Center and L.A. Biomedical Research Institute. And the cause of that sleep deprivation doesn’t always originate in family strife, financial concerns or job-related problems. The way we live now–checking our phones every minute, hyperscheduling our days or our kids’ days, not taking time to relax without a screen in front of our faces–contributes to a regular flow of stress hormones like cortisol, and all that artificial light and screen time is disrupting our internal clocks. Simply put, our bodies don’t know when to go to sleep naturally anymore.

This is why researchers hope their new discoveries will change once and for all the way we think about–and prioritize–those 40 winks.

GARBAGEMEN FOR YOUR BRAIN

“I was nervous when I went to my first sleep conference,” says Dr. Maiken Nedergaard, the chatty and inquisitive co-director of the Center for Translational Neuromedicine at the University of Rochester. “I was not trained in sleep, and I came to it from the outside.” In fact, as a busy mother and career woman, she saw sleep the way most of us probably do: as a bother. “Every single night, I wanted to accomplish more and enjoy time with my family, and I was annoyed to have to go to bed.”

Because she’s a neuroscientist, however, Nedergaard was inclined to ask a seemingly basic question: Why do our brains need sleep at all? There are two competing evolutionary theories. One is that sleeping organisms are immobile and therefore less likely to be easy targets, so perhaps sleep provided some protection from prey. The time slumbering, however, took away from time spent finding food and reproducing. Another points out that sleeping organisms are oblivious to creeping predators, making them ripe for attack. Since both theories seem to put us at a disadvantage, Nedergaard thought there had to be some other reason the brain needs those hours offline.

All organs in the body use energy, and in the process, they spew out waste. Most take care of their garbage with an efficient local system, recruiting immune cells like macrophages to gobble up the garbage and break it down or linking up to the network of vessels that make up the lymph system, the body’s drainage pipes.

The brain is a tremendous consumer of energy, but it’s not blanketed in lymph vessels. So how does it get rid of its trash? “If the brain is not functioning optimally, you’re dead evolutionarily, so there must be an advantage to exporting the garbage to a less critical organ like the liver to take care of it,” says Nedergaard.

Indeed, that’s what her research shows. She found that an army of previously ignored cells in the brain, called glial cells, turn into a massive pump when the body sleeps. During the day, glial cells are the unsung personal assistants of the brain. They cannot conduct electrical impulses like other neurons, but they support them as they send signals zipping along nerve networks to register a smell here and an emotion there. For decades, they were dismissed by neuroscientists because they weren’t the actual drivers of neural connections.

But Nedergaard found in clinical trials on mice that glial cells change as soon as organisms fall asleep. The difference between the waking and sleeping brain is dramatic. When the brain is awake, it resembles a busy airport, swelling with the cumulative activity of individual messages traveling from one neuron to another. The activity inflates the size of brain cells until they take up 86% of the brain’s volume.

When daylight wanes and we eventually fall asleep, however, those glial cells kick into action, slowing the brain’s electrical activity to about a third of its peak frequency. During those first stages of sleep, called non-REM (rapid eye movement), the firing becomes more synchronized rather than haphazard. The repetitive cycle lulls the nerves into a state of quiet, so in the next stage, known as REM, the firing becomes almost nonexistent. The brain continues to toggle back and forth between non-REM and REM sleep throughout the night, once every hour and a half.

At the same time, the sleeping brain’s cells shrink, making more room for the brain and spinal cord’s fluid to slosh back and forth between them. “It’s like a dishwasher that keeps flushing through to wash the dirt away,” says Nedergaard. This cleansing also occurs in the brain when we are awake, but it’s reduced by about 15%, since the glial cells have less fluid space to work with when the neurons expand.

This means that when we don’t get enough sleep, the glial cells aren’t as efficient at clearing the brain’s garbage. That may push certain degenerative brain disorders that are typical of later life to appear much earlier.

Both Nedergaard’s and Veasey’s work also hint at why older brains are more prone to developing Alzheimer’s, which is caused by a buildup of amyloid protein that isn’t cleared quickly enough.

“There is much less flow to clear away things in the aging brain,” says Nedergaard. “The garbage system picks up every three weeks instead of every week.” And like any growing pile of trash, the molecular garbage starts to affect nearby healthy cells, interfering with their ability to form and recall memories or plan even the simplest tasks.

The consequences of deprived sleep, says Dr. Mary Carskadon, professor of psychiatry and human behavior at Brown University, are “scary, really scary.”

RIGHTSIZING YOUR SLEEP

All this isn’t actually so alarming, since there’s a simple fix that can stop this nerve die-off and slow the brain’s accelerated ride toward aging. What’s needed, says Carskadon, is a rebranding of sleep that strips away any hint of its being on the sidelines of our health.

As it is, sleep is so undervalued that getting by on fewer hours has become a badge of honor. Plus, we live in a culture that caters to the late-nighter, from 24-hour grocery stores to online shopping sites that never close. It’s no surprise, then, that more than half of American adults don’t get the recommended seven to nine hours of shut-eye every night.

Whether or not we can catch up on sleep–on the weekend, say–is a hotly debated topic among sleep researchers; the latest evidence suggests that while it isn’t ideal, it might help. When Liu, the UCLA sleep researcher and professor of medicine, brought chronically sleep-restricted people into the lab for a weekend of sleep during which they logged about 10 hours per night, they showed improvements in the ability of insulin to process blood sugar. That suggests that catch-up sleep may undo some but not all of the damage that sleep deprivation causes, which is encouraging given how many adults don’t get the hours they need each night. Still, Liu isn’t ready to endorse the habit of sleeping less and making up for it later. “It’s like telling people you only need to eat healthy during the weekends, but during the week you can eat whatever you like,” he says. “It’s not the right health message.”

Sleeping pills, while helpful for some, are not necessarily a silver bullet either. “A sleeping pill will target one area of the brain, but there’s never going to be a perfect sleeping pill, because you couldn’t really replicate the different chemicals moving in and out of different parts of the brain to go through the different stages of sleep,” says Dr. Nancy Collop, director of the Emory University Sleep Center. Still, for the 4% of Americans who rely on prescription sleep aids, the slumber they get with the help of a pill is better than not sleeping at all or getting interrupted sleep. At this point, it’s not clear whether the brain completes the same crucial housekeeping duties during medicated sleep as it does during natural sleep, and the long-term effects on the brain of relying on sleeping pills aren’t known either.

Making things trickier is the fact that we are unaware of the toll sleep deprivation takes on us. Studies consistently show that people who sleep less than eight hours a night don’t perform as well on concentration and memory tests but report feeling no deficits in their thinking skills. That just perpetuates the tendency to dismiss sleep and its critical role in everything from our mental faculties to our metabolic health.

The ideal is to reset the body’s natural sleep-wake cycle, a matter of training our bodies to sleep similar amounts every night and wake up at roughly the same time each day. An even better way to rediscover our natural cycle is to get as much exposure to natural light as possible during the day, while limiting how much indoor lighting, including from computer and television screens, we see at night. And of course, the best way to accomplish that is by making those seven to nine hours of sleep a must–not a luxury.

“I am now looking at and thinking of sleep as an ‘environmental exposure,'” says Brown University’s Carskadon–which means we should look at sleep similarly to how we view air-pollution exposure, secondhand smoke or toxins in our drinking water. If she and other researchers have their way, checking up on sleep would be a routine part of any physical exam, and doctors would ask about our sleep habits in the same way they query us about diet, stress, exercise, our sex life, our eyesight–you name it. And if we aren’t sleeping enough, they might prescribe a change, just as they would for any other bad health habit.

Some physicians are already taking the initiative, but no prescription works unless we actually take it. If our work schedule cuts into our sleep time, we need to make the sleep we get count by avoiding naps and exercising when we can during the day; feeling tired will get us to fall asleep sooner. If we need help dozing off, gentle exercises or yoga-type stretching can also help. Creating a sleep ritual can make sleep something we look forward to rather than something we feel obligated to do, so we’re more likely to get our allotted time instead of skipping it. A favorite book, a warm bath or other ways to get drowsy might prompt us to actually look forward to unwinding at the end of the day.

Given what scientists are learning about how much the body–and especially the brain–needs a solid and consistent amount of sleep, in-the-know doctors aren’t waiting for more studies to prove what we as a species know intuitively: that cheating ourselves of sleep is depriving us from taking advantage of one of nature’s most powerful drugs.

“We now know that there is a lasting price to pay for sleep loss,” says Veasey. “We used to think that if you don’t sleep enough, you can sleep more and you’ll be fine tomorrow. We now know if you push the system enough, that’s simply not true.”

–WITH REPORTING BY MANDY OAKLANDER AND ALEXANDRA SIFFERLIN/NEW YORK CITY

TIME neuroscience

Alzheimer’s Linked to Sleeping Pills and Anti-Anxiety Drugs

New research suggests that people who take benzodiazepines may have a higher risk of developing Alzheimer’s

About 9 million Americans rely on sleeping pills or some sort of sedative to doze off at night, and 11% of middle-aged women take anti-anxiety medications. The most common of these include benzodiazapines, and now scientists say the drugs are associated with a higher risk of Alzheimer’s.

In a report published Wednesday in The BMJ, researchers say that among 1,796 people with Alzheimer’s disease and 7,184 controls, those who have used benzodiazepines showed a 51% higher risk of the neurodegenerative disorder. Among people who took the drugs more than 180 days, the risk escalated to about two-fold higher.

Previous studies have linked the drugs to memory and cognitive problems, but primarily in those taking them short term. But in the current study, in which the scientists, led by Sophie Billioti de Gage, a PhD student at INSERM, University of Bordeaux, followed the participants for six years, the connection to dementia appeared strong. The interaction remained even after the scientists adjusted for potential confounding effect on Alzheimer’s rates such as blood pressure, heart disease, depression and insomnia.

In order to rule out the possibility that it was happening the other way around—that Alzheimer’s was causing a rise in insomnia and anxiety—the authors focused on people who had been prescribed sleeping and anxiety meds more than five years before they were diagnosed with Alzheimer’s. “We believe that the likelihood that the results are mainly driven by reverse causation is low,” de Gage said in an email discussion about the results.

It’s not clear why the drugs might increase the risk of Alzheimer’s, although de Gage speculates that the short-term effects on memory and cognitive functions may deplete reserve capacities that might help to offset reduce nerve functions as the disease’s hallmark protein plaques start to build up.

She also said that the study did not find an effect among those who used benzodiazepines for less than three months. That’s how most of the medications are prescribed, so people shouldn’t stop using them to treat anxiety disorders, social phobias and insomnia. But, she added, “It seems crucial to encourage physicians to carefully balance the benefits and risks when initiating or renewing a treatment [with benzodiazepines].”

TIME Developmental Disorders

Autism Symptoms Disappeared With Behavioral Therapy In Babies

Baby on fur rug
Getty Images

Parents using ground-breaking new techniques with infants essentially cured their babies of developmental delays

For the first time, researchers report that treating early signs of autism in infants as young as 6 months can essentially help them to avoid developmental delays typical of the disorder. And the intervention doesn’t involve pills or invasive surgery but an intensive behavioral therapy provided by the babies’ parents, according to the Journal of Autism and Developmental Disorders.

Kristin Hinson was one of those parents. She knew what autism looked like. With two of her three children showing developmental delays, she was on the lookout for similar signals when her son Noah was born. And at 6 months, they came. Noah began avoiding eye contact with her and other family members, his muscle tone was low, and he started lagging in the early infant milestones like rolling over and responding to sounds and people. “He was doing everything, but everything was a little sloppy,” says Hinson.

Because she had two children affected by autism, Noah was enrolled in a study of infant siblings of autistic children at the University of California Davis. Noah’s symptoms appeared relatively early — at that age, doctors can’t diagnose the developmental disorder, but they know the hallmarks that are strongly associated with it. Noah’s sibling history also meant there was a good chance he would eventually show delays in language and social skills as well.

MORE: Brain Imaging Could Detect Autism Risk in Infants as Young as 6 Months

He was fortunate enough, however, to be one of seven children to begin an intensive, parent-based program for treating autism in infants as young as 6 months. The goal of the program is to slow or avoid the symptoms of autism that often mean affected children need special education or other formal care as they get older.

Hinson attended 12 sessions for an hour once a week at the Institute, and continued to apply what she had learned there during each of her interactions with Noah at home for six weeks while following up with their counselor. The techniques she and the other parents learned were based on the Early Start Denver Model, which was developed by Sally Rogers, a professor of psychiatry at UC Davis, and Dr. Geraldine Dawson at Duke University.

The program involved intensive and intentional play by trained therapists at children’s homes. Once a week, the therapists went to the families’ homes and purposefully engaged with the toddlers, who were between three years and five years old. Even when they were rebuffed, the therapists would persist, finding objects that appealed to the children and inserting themselves into the child’s play with that object so they were forced to have more social engagement. Eventually, the children responded, and even showed brain changes that suggested their brain patterns were normalizing to look more like those of children unaffected by autism.

With the latest group, Rogers moved the program earlier, to babies between 6 months and 15 months old, well before autism is usually diagnosed. Because the babies were so young, Rogers wanted to test whether parents could be taught the same techniques that therapists used, so the strategy could be applied more consistently and frequently than a few times a week, and during daily interactions with the infants—while they were fed, diapered, bathed and more.

MORE: Study: Siblings of Autistic Kids Show Similar Brain Activity

The results were astounding. Six of the seven infants in the study essentially caught up in their learning and language skills by age two or three. They no longer showed developmental delays in social communication or language, and behaved just as a control group of children unaffected by the disorder.

“At 18 months, Noah just blossomed,” says Hinson. “He started talking, and really socializing. Before, he wasn’t really engaging with others, and all of a sudden it felt like a light flipped on.”

Noah is attending a mainstream preschool, and Hinson doesn’t anticipate he will need any special education or tutoring to keep up with his classmates once he enters kindergarten,

Doctors, especially psychiatrists, don’t like to use the word “cure.” But, says Rogers of the small, promising group of infants like Noah who were part of the study, “We are curing their developmental delays.”

MORE: Behavior Therapy Normalizes Brains of Autistic Children

She’s careful not to suggest that the behavioral therapy can cure children of autism, since the only a handful of babies were involved, and they haven’t been studied long-term yet. But the findings do support the idea that intervening early, and with intensive therapy, can make a difference in the trajectory of the disorder.

The results also suggest that the progression of autism isn’t inevitable, and that its symptoms aren’t entirely biologically or genetically preordained. “If a baby doesn’t smile at you, doesn’t make eye contact, doesn’t respond pleasurably to your many interactions or doesn’t ever call for your attention, you don’t know if you’re on the right track,” she says of the typical early signs of autism. “If the message you get from them is that they aren’t interested, then you’re not going to continue.” Over, time, she says, that limits the number of social learning opportunities that the babies have, and they may spiral deeper and deeper into their own world. “Over time, the parents and children accommodate the child’s interest in objects and lack of interest in people.”

The behavioral training that she provides parents counters this cycle, and forces parents to find ways to engage their child, even if it means using the inanimate objects that appeal to them. If an infant is captivated by a stuffed animal, for example, then parents are trained to enter their baby’s field of vision, and play with the animal by using it to tickle the child, or tickle himself. The parent might even hide the stuffed toy under her shirt, and encourage the baby to find it. “The parent takes over so the child is now interested in the parent because there is a game going on with the toy and the parent,” says Rogers. “The key is to create a social game so the object is now serving the people instead of taking over the child’s attention.”

That shift takes effort, however, and it isn’t easy. “The first month I felt really frustrated,” admits Hinson. “There was a lot of pressure on me.” She says that it took most of the 12 week program before she felt completely comfortable with the new way of interacting with Noah, with inserting herself into his “circle” of attention at every opportunity, and with waiting for him to respond to her forays at communication.

But, she says, it was well worth the effort, and it comes easily. “Every new skill, like teaching him nursery rhymes and songs, or trying to get him to share something, and show me something, didn’t come natural to me at first. But when he started giving me some reciprocation, like smiling and babbling, it was like I was getting rewarded for the hard work.”

The skills are “completely doable,” says Hinson, and far less intrusive than having therapists visit the home once a week, which she did for her two older children who were developmentally delayed. “It’s brilliant if you can get the hands-on training. Because as parents, we are in their circle all the time, every day of their lives, and what better way to help them than to do it every day at every opportunity.”

While she’ll never know if the program was actually responsible for helping Noah to avoid developmental delays, Hinson is sure of one thing. “If they could have had something like this for my other children, I think they would be completely different children today.”

 

TIME Cancer

Lung Cancer May Be Detected With a Thermometer

Detecting lung cancer may be as simple of taking the temperature of your exhaled breath, say researchers

In the continuing effort to find less invasive ways of detecting lung cancer, scientists from Italy announced that your breath’s temperature could be a giveaway of tumors within.

In a report presented at the European Respiratory Society International Congress, Giovanna Carpagnano, from the University of Foggia, said that among 82 people who showed potential signs of lung cancer on X-rays, those who had confirmed lung cancer had higher breath temperatures than those whose readings weren’t as high.

While many factors could contribute to breath temperature, the team also found that the readings were higher the more the participants had smoked, and among those with later-stage cancer.

The findings need to repeated and confirmed, but efforts to find easier ways of diagnosing lung cancer that don’t require biopsies of lung tissue, are gaining ground. Scientists are also working on ways to identify specific chemicals that made by tumors and the odors they emit in the breath. “If we are able to refine a test to diagnose lung cancer by measuring breath temperature, we will improve the diagnostic process by providing patients with a stress-free and simple test that is also cheaper and less intensive for clinicians,” Carpagnano wrote in a statement describing the research.

TIME medicine

Kate Middleton Has Morning Sickness—Again

It’s déjà vu for Duchess of Cambridge. Another pregnancy, another battle with morning sickness.

Along with the good news that Kate Middleton is pregnant and expecting her second child, who would be fourth in line to the throne, Middleton also revealed that she is suffering from hyperemesis gravidarum, a severe form of morning sickness that landed her in the hospital during her first pregnancy.

Having the condition during a previous pregnancy increases the chances that it will recur, which may explain Middleton’s circumstances. Consistent nausea and vomiting can lead to dehydration and deficiencies in some important nutrients, say experts, so expectant moms who can’t keep food down are treated with IV fluids. It’s generally not dangerous to the developing fetus, unless the mom-to-be doesn’t gain enough weight during pregnancy, which can lead to lower-birth weight babies. (George, her first child, was born at a healthy 8 pounds, 6 ounces.)

This time, the Duke and Duchess’ office says, she is being treated at home, which for her is Kensington Palace.

For those who might have forgotten, hyperemesis gravidarum can be caused by hormonal changes occurring during the first three months of pregnancy—specifically the steep rise in human chorionic gonadotropin (HCG), which is released by the placenta as it readies to nourish the fetus.

Presence of hydatidform moles, or a growth inside the uterus, can also trigger the severe nausea and vomiting.

There’s something else that often triggers the morning sickness: twins. No word just yet from the royals on whether George will be joined by more than one sibling.

TIME Healthcare

Joan Rivers’ Death Raises Questions About Outpatient Care Centers

Joan Rivers Signs And Discusses Her New Book "Diary Of A Mad Diva"
Comedian Joan Rivers poses before signing copies of her new book "Diary Of A Mad Diva" at Barnes & Noble bookstore at The Grove on July 10, 2014 in Los Angeles, California. Amanda Edwards—WireImage

The comedien apparently went into cardiac arrest while undergoing a procedure at an outpatient center, and had to be transported to a hospital for emergency care

The New York Department of Health is still investigating the death of Joan Rivers, who died Thursday when she did not recover from cardiac arrest. Rivers, 81, was at Yorkville Endoscopy, an outpatient surgical center, for an elective procedure when she ceased breathing and her heart suddenly stopped. An autopsy proved inconclusive, the New York chief medical examiner’s office said Friday.

Rivers’ death is raising questions about how outpatient or ambulatory centers are accredited, and what regulations are in place to ensure patient safety. Each state health department oversees such facilities; some are part of hospitals and therefore regulated by the same organizations that oversee hospitals, while others are independently owned and operated by physicians.

Just under half of states, including New York, require that the latter centers receive accreditation from any of four organizations that set criteria for patient care and safety. The New York Department of Health lists threeAccreditation Association for Ambulatory Health Care, American Association for Accreditation of Ambulatory Surgery Facilities (AAAASF), and the Joint Commission.

As one of the organizations that accredits centers for which Medicare reimburses procedures, the AAAASF has a 162 page checklist of items, from requiring that a circulating nurse is in both the operating room and the recovery rooms, to board certification of surgeons performing the procedures and the presence of crash carts for resuscitating patients should complications occur. Centers also need to have an agreement with a nearby hospital to respond to any emergencies. Because of these criteria, says Dr. Geoffrey Keyes, president of AAAASF, death rates at ambulatory surgery centers that are accredited are similar to those at hospitals.

But if states do not require accreditation or licensure, then centers have to voluntarily apply for the status, which can cost $10,000 over three years and require regular inspections for compliance.

While the majority of ambulatory surgery centers are accredited by one of the four agencies perform the service in the U.S., the bulk of the smaller practices run by one or two physicians who perform surgical procedures at their offices are not. “One of the first questions a consumer should ask a surgeon is what environment do they intend to do the procedure, and whether that environment is accredited, whether it’s a hospital or outpatient center,” says Michael Kulczycki, executive director of the Ambulatory Care Accreditation Program of the Joint Commission.

If the facility is accredited, while it’s no guarantee that complications won’t occur, it’s a reassurance that a high level of patient safety and surgical standards are being met. “My personal belief is that with proactive risk and safety measures in place, and appropriate plans to mitigate emergencies, care in the ambulatory care environment would be as safe as care in an inpatient environment,” says Dr. Daniel Ross, field director for ambulatory programs at the Joint Commission.

TIME medicine

What May Have Caused an American Pilot to Crash

Socata Plane
A Socata TBM-900 (700N) at Glasgow airport in Scotland on March 14, 2014. Iain Marshall

An unresponsive pilot whose plane crashed off Jamaica may have suffered from hypoxia

A New York real estate executive was piloting his his small plane from Rochester to Florida on Friday when he stopped communicating with air traffic controllers before eventually crashing near Jamaica.

Larry Glazer, who frequently flew that route, was traveling with his wife. FAA officials said the private plane had reached an altitude of 25,000 feet, prompting some officials to speculate he may have suffered from something known as hypoxia, in which parts of the brain are deprived of adequate oxygen.

It’s far too early to know for sure. But at that altitude, oxygen is so thin that brain cells can only survive for several minutes before they start dying off. Without enough oxygen, people become inattentive, show poor judgment and eventually stop breathing. With extended exposure at high altitudes, the brain shuts off and slips into a coma. Military pilots dispatched to track the aircraft after it failed to respond to air traffic control signals reported seeing the pilot slumped over.

The FAA has warned non-commercial pilots of the dangers of high altitude changes and hypoxia—in its first phases, the pilot won’t necessarily be aware that he’s experiencing oxygen deprivation. On the FAA site’s training section, a member of the agency’s education team urges more physiology training of pilots so they are aware and prepared for the dangers of hypoxia.

According to an official 1991 FAA report, Civilian Training in High-Altitude Flight Physiology, “Some National Transportation Safety Board staff members have expressed a concern that high-altitude flight physiology training for civilian flight personnel should receive greater emphasis than it currently does.” The report goes on to say, “When pilots combine their private flying skills with their business transportation needs and use their aircraft to meet those needs, it is inevitable that in order to meet a schedule, arrive at a destination, or get home after a meeting, the urge to complete a mission will lead the pilot into a physiologically-unsafe altitude or into conditions for which there has been insufficient training or experience.”

TIME Research

Journal Retracts Paper that Questioned CDC Autism Study

A paper that claimed government scientists covered up data showing a connection between vaccines and autism has been pulled by its publisher

Earlier in August, the journal Translational Neurodegeneration, an open access, peer-reviewed journal, published a re-analysis of a 2004 paper published in Pediatrics that looked at MMR vaccines and autism. The re-analysis of the data, by biochemical engineer Brian Hooker of Simpson University, claimed to find a higher rate of vaccination against MMR among a subset — African-American boys — of the original study population who developed autism than among those who did not, a finding that Hooker claims was suppressed by the authors of the original paper from the Centers of Disease Control. One of the co-authors of the 2004 paper, William Thompson, released a statement admitting to omitting the data after a secretly recorded conversation he had with Hooker was released on YouTube. (Thompson was not available for comment.)

MORE: Whistleblower Claims CDC Covered Up Data Showing Vaccine-Autism Link

Now, however, the editors of Translational Neurodegeneration have retracted Hooker’s paper, noting on its site that “This article has been removed from the public domain because of serious concerns about the validity of its conclusions. The journal and publisher believe that its continued availability may not be in the public interest. Definitive editorial action will be pending further investigation.”

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