TIME ebola

FDA Cracks Down on Unproven Ebola Cures

Ebola virus
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The agency says a product marketed as a treatment for Ebola violates laws that require drugs to be approved by the FDA for safety and effectiveness

On Sept. 23, the Food and Drug Administration (FDA) issued a warning letter to Rima Laibow and Ralph Fucetola of Natural Solutions Foundation informing them that the company’s products, including Silver Sol Nano Silver and High Potency CBD Hemp Oil, which are marketed as Ebola treatments, violate the Federal Food, Drug and Cosmetic Act.

Based on the claims made on the company’s website as well as in a YouTube video, the FDA says the products are marketed as drugs, and therefore fall under the agency’s jurisdiction.

In the letter, the FDA notes

Your “Personal Protection Pack,” “Family Protection Pack,” “Dr. Rima Recommends™ The Silver Solution,” and “CBD Organic Dark Chocolate Bars” products are not generally recognized as safe and effective for the above referenced uses and therefore, these products are “new drugs” under section 201(p) of the Act [21 U.S.C. § 321(p)]. New drugs may not be legally introduced or delivered for introduction into interstate commerce without prior approval from the FDA, as described in section 505(a) of the Act [21 U.S.C. § 355(a)]; see also section 301(d) of the Act [21 U.S.C. § 331(d)]. FDA approves a new drug on the basis of scientific data submitted by a drug sponsor to demonstrate that the drug is safe and effective.

The company’s claims about its Ebola treatments also violate Federal Trade Commission laws, which prohibit advertising that a product can prevent, treat or cure human disease without reliable and valid scientific evidence.

In the past month, the World Health Organization as well as the FDA have warned consumers about such unproven therapies. Both remind the public that there are no known cures or treatments for Ebola; the therapy received by a handful of care workers in the U.S. are still considered experimental and only used as an exception to the agency’s usual drug approval process.

The company has 15 days to correct the violations, or face legal action and seizure of the products.

TIME Developmental Disorders

How Brain Waves May Be the Clue to Diagnosing Autism

Unique EEG fingerprints reveal how autistic brains process sights and sounds

Diagnosing autism as early as possible, even before the first noticeable symptoms of social and developmental delays emerge, is becoming a critical strategy for reducing the condition’s most severe symptoms. Experts have long known that children with autism process sensory information – sights and sounds in particular – in different ways than unaffected children.

In a new study published in the Journal of Autism and Developmental Disorders, Sophie Molholm, from the departments of pediatric and neuroscience at Albert Einstein College of Medicine, proposes that those differences may lay the foundation for social and communication deficits in some children later on.

Molholm and her team took electroencephalogram (EEG) readings from more than 40 children aged six years to 17 years diagnosed with autism and compared their patterns to those of unaffected children of similar age and other characteristics. All children were given either a flash cue, a beep cue or a combination of both, and asked to press a button when these stimuli occurred. A cap with 70 sensors picked up the children’s brain responses every two milliseconds during these tasks, including those that recorded how the brain first processed the sensory information.

MORE: Behavior Therapy Normalizes Brains of Autistic Children

The children with autism showed a distinctly different brain wave signature from those without the condition. Specifically, the signals in those with autism showed differences in the speed in which the sights or sounds were processed, and in how the sensory neurons recruited neighbors in more far-flung areas of the brain to register and make sense of the information. And the more abnormal this multi-processing was, the more severe the child’s autistic symptoms. “By developing this tool in the older cohort of children we can then figure out which ones are the most promising and then go test them in younger children,” says Molholm.

It’s also possible that because the children she studied were older, the differences in their EEG patterns were the result of autism, rather than a sign of changes that precede the disorder. But, she says, “If you ask me to make an educated guess, I would say these are part of autism, and they represent neuropathology related to having the disorder. It seems unlikely to me that you get autism and then develop atypical auditory processing.”

MORE: Autism Symptoms Disappeared With Behavioral Therapy In Babies

Molholm says the sample was too small to use the profile for diagnosing autism, but it could lead to such a test if the results are confirmed and repeated. To confirm the findings, scientists will have to intervene with behavioral strategies for helping the different regions of the brain work in a more coordinated way when confronted with visual and auditory cues. If that reduces autism symptoms, then EEG profiling could become one of a number of new ways that doctors can start identifying those at highest risk – however young — of developing autism.

TIME health

Obama Plan to Fight Antibiotic Resistance ‘Disappointing,’ Critics Say

Publix First To Offer Free Antibiotics To Customers
Roxana Selagea, a Publix Supermarket pharmacy manager, counts out the correct number of antibiotic pills to fill a prescription August 7, 2007 in Miami, Florida. Joe Raedle—Getty Images

The President’s plan to address the growing health threat of bacteria that are resistant to antibiotics doesn’t go far enough, say some, in containing the heaviest users of the drugs – agriculture.

President Barack Obama is taking the health problems posed by antibiotic resistant bacteria seriously. He signed an Executive Order Thursday to create a task force – led by the secretaries of Defense, Agriculture and Health and Human Services – to develop an action plan on the issue. He also created a non-governmental advisory council to inform and develop recommendations concerning antibiotic resistant bacteria, and directed the Food and Drug Administration (FDA) to “continue taking steps to eliminate agricultural use of medically important antibiotics for growth-promotion purposes.”

That last action will likely become the most important, given that 80% of antibiotics in the country aren’t used by people but by animals. So while over-prescribing of the drugs to treat everything from colds to viral infections (for which they aren’t effective) are part of the problem, their use in animals, which can then pass the resistant strains on to people, is the much bigger challenge. And most of the animals receiving antibiotics aren’t sick, but are fed low doses of the drugs in order to grow faster and larger.

MORE: Farm Drugs: The FDA Moves to Restrict (Somewhat) the Use of Antibiotics in Livestock

In 2012, the FDA did restrict the use of one class of antibiotics commonly used in people, cephalosporin drugs, in animals that weren’t actively fighting infections. It also called for makers of antibiotics to voluntarily phase out claims that the medications would enhance growth, and pushed for greater veterinary oversight of antibiotic prescriptions.

But earlier this year, the Natural Resources Defense Council (NRDC) revealed evidence that the FDA allowed 18 antibiotics that it rated as high risk to human health to remain on the market, where farmers used them to boost the feed and water of their animals.

MORE: New Report Says FDA Allowed ‘High Risk’ Antibiotics to Be Used on Farm Animals

And, as Mae Wu, an NRDC attorney who wrote a blog post about the need to address farm practices, says, while animal drug makers may be removing growth claims about their products, they may still be touting their “disease prevention” features. So “they can easily switch from one to the other without changing practices,” says Wu. “It’s a change in name only.”

That’s why Wu argues that the President’s actions, while important, aren’t enough to change such long-standing agricultural practices.

“It’s great that the President has elevated [the problem of antibiotic resistance] to this level, and the White House is really talking about the problem and developing a plan over the next five years about how to do it,” she says. “But it’s disappointing that they are being so passive on one of the largest issues – the largest use of antibiotics in this country [in agriculture].”

The President’s Council of Advisors on Science and Technology (PCAST) also released a report on the matter, and among its eight recommendations for combating antibiotic resistant is a call for limiting the use of antibiotics in agriculture.

What that means will be up to the task force to determine, since the report didn’t specify a strategy. Even if the latest presidential actions don’t change the way antibiotics are currently prescribed, however, the heightened awareness that the White House is bringing to the problem may start to push things in the right direction. Already, Perdue, one of the country’s largest producers of poultry, announced that it will no longer use human antibiotics with 95% of its chickens.

TIME Diet/Nutrition

Artificial Sweeteners Aren’t the Answer to Obesity: Here’s Why

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Artificial sweeteners may be contributing to the very health problems they were supposed to prevent, say researchers Tetra Images—Getty Images/Tetra images RF

They’re supposed to be the sweet alternative to high-calorie, diabetes-causing sugar. But the latest science shows that artificial sweeteners may actually set us up for obesity and diabetes

Aspartame, saccharin, sucralose—sugar alternatives go by many names, but share an almost irresistible promise: all the sweetness of sugar without the calories, weight gain and increased risk of diabetes that comes with uncontrolled amounts of sugar in the blood.

But studies on artificial sweeteners and weight loss—as well as research about whether sugar substitutes helped people avoid metabolic disorders like diabetes—have been mixed. And in a paper published Wednesday in Nature, Dr. Eran Elinav from the Weitzmann Institute of Science in Israel found that the sugar stand-ins actually contribute to changes in the way the body breaks down glucose. How? Fake sugars aren’t digested and therefore pass directly to the intestines, impacting the millions of invisible bacteria that live in our gut. And when he and his colleagues gave seven people who didn’t normally use artificial sweeteners the sugar substitutes for seven days, about half of the people showed higher blood glucose levels after just four days.

MORE: 5 Steps to Quitting Artificial Sweeteners

“What our comprehensive genetic profiling of the microbiome pointed to is that exposure to artificial sweeteners directly impacts the microbes,” Elinav says. “We found that the artificial sweeteners we think of as beneficial and that we use as treatment or preventive measures against obesity and its complications are contributing to the same epidemics they are aimed to prevent.”

In the intestines, gut microbes are hard at work, pulling out some nutrients from food that are helpful in stopping tumor growth, for example, and squirreling away others to store as energy for later use. But while artificial sweeteners aren’t absorbed by our own cells, they may be absorbed by our bacteria—and when that happens, things appear to go haywire.

Higher amounts of the sweetener substitutes, Elinav and his team found, can change the makeup of these bacterial communities. And that in turn can change how those bugs behave, leading to weight gain and poorer glucose breakdown. These alterations in intestinal bacteria were the same as those in a group of 400 people who reported using artificial sweeteners—and those changes were the same in mice as well.

MORE: Why Your Brain Isn’t Fooled By Sugar Stand-Ins

In the mouse studies, Elinav’s team found that the artificial sweeteners pushed one particular group of bacteria, Bacteroides, to thrive, while inhibiting growth of another, Clostridiales. Bacteroides are the microbial equivalent of hoarders, hungrily pulling energy out of food and squirreling it away as fat. The end result of a Bacteroides-heavy gut is a physically heavy gut as well. In studies by other research groups, its dominance, and the resulting drop in diversity of other microbes, is typical of obese people compared to normal weight individuals.

MORE: 7 Not-So-Sweet Lessons About Sugar

The metabolic consequences were also dramatic in both the mice and people studied. In the mouse experiments, animals who were fed the same dose of saccharin that the U.S. Food and Drug Administration considers safe for daily use showed a drop in their ability to break down glucose. When he gave those mice antibiotics, their ability to break down glucose returned to normal, suggesting that wiping out the abnormal balance of bacteria could return the animals back to a healthier state.

And to confirm that the changing microbial communities were indeed responsible for the glucose changes, he also transplanted fecal samples from the people using artificial sweeteners into mice whose own guts had been wiped clean. These mice then developed the same abnormalities in glucose breakdown that the human donors and the mice who were fed saccharin did—even though they never actually ate artificial sweeteners. Simply harboring the microbes that had been exposed to the sweeteners was enough to disturb their glucose metabolism.

MORE: Can Sugar Substitutes Make You Fat?

The good news is that as easily as the gut microbiome can shift toward an unhealthy state, it can just as easily be brought back into line with the proper balance of bacterial communities. The best way to do that isn’t clear yet, but, says Eran Segal, a co-author of the study and a professor of computer science and applied mathematics at the Weitzmann Insttitute, “We believe that the situation today at the very least needs to be re-examined. We were able to induce glucose intolerance in a few days in some individuals, so this massive, unsupervised and unregulated use [of artificial sweeteners] should at the very least be reassessed and perhaps re-examined in additional studies.”

Elinav, for one, isn’t waiting. Based on his findings, he’s stopped adding artificial sweeteners to his coffee.

 

TIME Cancer

Our Global Cancer Report Card Is Here

In its annual cancer status report, the American Association for Cancer Research highlights new tumor-fighting drugs, and the inevitable spike in cancer cases expected in coming years

The Food and Drug Administration (FDA) approved six new cancer treatments between July 2013 and July 2014, five of them representing innovative ways to target tumors more precisely with fewer side effects. Thanks to those therapies, and advances in understanding how the body’s own immune system can be co-opted into fighting cancer, patients diagnosed with any of the 200 or so forms of the disease have never been in a better position to survive it. In fact, the number of cancer survivors has increased nearly five-fold from when Congress declared a war on cancer in 1971 and 2014. But despite advances in diagnosing and treating cancer, incidence and death rates may start to rise again, say experts in a new report.

That’s in part because most cancers emerge in older age—and the population of people over-65 is expected to double by 2060. “We face a future in which the number of cancer-related deaths will increase dramatically unless new and better ways to prevent, detect, and treat cancer can be developed,” according to the 2014 American Association for Cancer Research (AACR)’s Cancer Progress Report 2014. “These trends are being mirrored globally, and the number of people dying of cancer worldwide is expected to increase from 8.2 million in 2012 to 14.6 million in 2035.”

The (AACR), which has been compiling the report every year since 2011 as an educational tool to update Congress and the public on the progress and needs in the fight against cancer, also provided a “prescription” for addressing this coming wave, and for maintaining the momentum of recent victories against the disease. Noting that research grants from the National Institutes of Health (NIH), the largest funder of basic biomedical research that has contributed to many of the new anti-cancer therapies now on the market, are $3.5 billion lower than where they should be even if the funding only kept up with the rate of inflation for biomedical equipment and personnel, the AACR urges more federal investment in cancer research.

That money, they point out, can also be directed toward training the next generation of cancer researchers, since fewer grants are turning promising young scientists away from the field. They write:

We are now at a crossroads in our country’s long struggle to prevent and cure cancer; we must choose between two paths, but there is only one viable path forward to continue transforming lives.

On the viable path we seize the momentum at this exciting time in biomedical research by committing to budget increases for the NIH and NCI so that the remarkable progress of the past can continue at a rapid pace.

To take the alternative path is simply unacceptable. This particularly dangerous path leads us to a place where federal funding for biomedical research remains stagnant, or even worse, declines, seriously jeopardizing the rate at which we are able to make progress. On this path, breakthroughs and discoveries will be slowed, meaning that delivery of the cures that patients and their loved ones desperately need is delayed.

…Our federal government can do no better than invest robustly in the NIH and NCI so that the path forward will lead us to a brighter future for the millions of people whose lives have been touched by cancer.

TIME Mental Health/Psychology

A Blood Test for Depression? Science Says It’s Possible

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It may even tell doctors whether patients will respond to some kinds of therapy

As with any disease, detecting depression early is critical for reducing suffering and for finding an effective course of treatment. Now, in a study released Tuesday, scientists led by Eva Redei at Northwestern Medicine say it may be possible to test for depression in the blood—and figure out which patients will benefit most from behavior-based therapy as a treatment.

While a blood test alone can only tell us so much, some 26 markers in the blood had previously been associated with depression—something Redei, a professor of psychiatry and behavioral sciences, and her team had discovered in lab animals. They also applied those findings to human subjects, and found that some of those compounds were present in teens with major depressive disorder. This prompted Redei to put their suite to the test with a sample of patients aged 23 year to 80 years recruited from a Northwestern University general medicine clinic.

In her report, published in the journal Translational Psychiatry, Redei focused on nine markers whose levels in the blood differed between people with depression those who were not depressed. Depressed people went on to receive cognitive behavioral therapy, and Redei and her colleagues followed them to see if they could find any additional markers for whether these patients responded well to the therapy or not.

“What we didn’t bargain for, but what we got, was that by looking at [patients' blood] before they received cognitive behavioral therapy (CBT), we could identify patterns that tell us who will respond to therapy and who will not,” she says. About 60% of the patients did not experience another depressive episode during the study period’s 18 weeks. But 40% of them did, and they showed differences in three gene products that were measured in the blood.

MORE: A New Key to Understanding Depression

In addition, the team also found three markers among the original nine that remained different even among the depressed patients who benefited from CBT, and the controls. That suggests these markers could be harbingers of a person’s vulnerability to the mood disorder. In other words, they could be predisposing factors that make depression more likely in the face of stress or anxiety or trauma. Of the remaining six markers in the panel, Redei says they could be useful measures of the changing state of a patient’s depression, similar to fluctuating levels of cholesterol or blood pressure, and they could be a helpful gauge for doctors in figure out how much treatment or medication a patient might need.

MORE: Doctors Treat Depression With Brain Magnets

And these genes, she says, “are a complete and utter surprise because they are relatively unknown. Some of them are genes that are known in other areas of science or medicine but have never been associated with depression before.”

That means they could lead to a better understanding of the disease and, possibly, better treatments. “It’s very dangerous to delay treatment,” says Redei. “We don’t want anybody to suffer, so the goal is to develop a Food and Drug Administration-approved test that is very easy to administer anywhere.”

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

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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].”

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