TIME Exercise/Fitness

The Drug-Free Way to Fight Depression

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Exercising throughout adulthood can help to keep depression at bay Jupiterimages—Getty Images

A 50-year study shows that physical activity may help fight the disease

Exercise can do a lot of physical good, from making hearts healthy to keeping weight down—and now there’s strong new evidence that it can give a mental boost as well.

In a study appearing in JAMA Psychiatry, researchers from the UK and Canada found that people who were more physically active throughout most of their adult years experienced fewer depressive symptoms than those who were less active. That finding is familiar, but these results are extremely affirming because they involved both a large number of same-aged people—11,000, who were born the same week in March 1958—and a long period of time—50 years.

The volunteers answered questions about how many times they exercised a week on average at four points during the study: when they were 23, 33, 42 and 50 years old. They also took standardized tests that measured depressive symptoms such as depressed mood, fatigue, irritability and anxiety.

At every stage, those who reported more physical activity also had fewer depressive symptoms. What’s more, those who became more active between the recordings also showed fewer signs of depression. That means someone who exercised more each week at 42 than they did at 33 also benefited from having fewer depressive symptoms at 42. In fact, getting more physically active at any age—going from never working out to working out three times a week—lowered the chances of depression by 19% five years later.

The results add to previous studies that found similar associations between exercise and lower depression rates among younger and older people, but this study shows that the connection exists throughout adulthood.

Understanding the link could help doctors better treat both obesity and depression; with some people, depression could be a barrier to becoming physically active, while with others, being overweight could feed into cycle of depression. “Our study suggests that practitioners helping patients to recover from depression might address activity within their treatment plan for lifestyle factors,” the authors write.

TIME medicine

Stem Cells Allow Nearly Blind Patients to See

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Stem cells could lead to new treatments for eye disorders Photography by Peter A. Kemmer—Getty Images/Flickr RF

Embryonic stem cells can be turned into a therapy to help the sight of the nearly blind

In a report published in the journal Lancet, scientists led by Dr. Robert Lanza, chief scientific officer at Advanced Cell Technology, provide the first evidence that stem cells from human embryos can be a safe and effective source of therapies for two types of eye diseases—age-related macular degeneration, the most common cause of vision loss in people over age 60, and Stargardt’s macular dystrophy, a rarer, inherited condition that can leave patients legally blind and only able to sense hand motions.

In the study, 18 patients with either disorder received transplants of retinal epithelial cells (RPE) made from stem cells that came from human embryos. The embryos were from IVF procedures and donated for research. Lanza and his team devised a process of treating the stem cells so they could turn into the RPE cells. In patients with macular degeneration, these are the cells responsible for their vision loss; normally they help to keep the nerve cells that sense light in the retina healthy and functioning properly, but in those with macular degeneration or Stargardt’s, they start to deteriorate. Without RPE cells, the nerves then start to die, leading to gradual vision loss.

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

The transplants of RPE cells were injected directly into the space in front of the retina of each patient’s most damaged eye. The new RPE cells can’t force the formation of new nerve cells, but they can help the ones that are still there to keep functioning and doing their job to process light and help the patient to see. “Only one RPE can maintain the health of a thousand photoreceptors,” says Lanza.

The trial is the only one approved by the Food and Drug Administration involving human embryonic stem cells as a treatment. (Another, the first to gain the agency’s approval, involved using human embryonic stem cells to treat spinal cord injury, but was stopped by the company.) Because the stem cells come from unrelated donors, and because they can grow into any of the body’s many cells types, experts have been concerned about their risks, including the possibility of tumors and immune rejection.

MORE: Early Success in a Human Embryonic Stem Cell Trial to Treat Blindness

But Lanza says the retinal space in the eye is the ideal place to test such cells, since the body’s immune cells don’t enter this space. Even so, just to be safe, the patients were all given drugs to suppress their immune system for one week before the transplant and for 12 weeks following the surgery.

While the trial was only supposed to evaluate the safety of the therapy, it also provided valuable information about the technology’s potential effectiveness. The patients have been followed for more than three years, and half of the 18 were able to read three more lines on the eye chart. That translated to critical improvements in their daily lives as well—some were able to read their watch and use computers again.

“Our goal was to prevent further progression of the disease, not reverse it and see visual improvement,” says Lanza. “But seeing the improvement in vision was frosting on the cake.”

TIME ebola

CDC Deploys Ebola SWAT Team to Dallas

The agency says it will send a team of Ebola experts to any hospital with an Ebola case in the future

A team of experts with experience treating Ebola patients in Africa and containing outbreaks there is now in Dallas working to contain the deadly disease after the first two diagnoses on U.S. soil, a top health official said Tuesday.

Tom Frieden, the director of the Centers for Disease Control and Prevention (CDC), said the team is helping officials at Texas Health Presbyterian, and was joined by two nurses from Emory University Hospital, where U.S. aid workers were successfully treated for Ebola. The team’s job is to enhance safety and infection control measures at the hospital.

“A single infection in a health care workers is unacceptable,” Frieden said. “What we are doing at this point is looking at everything we can do to minimize the risk so those caring for her can do so safely and effectively.”

Frieden said that it’s still not clear how a nurse, Nina Pham, got infected while caring for Thomas Eric Duncan, the first patient diagnosed on U.S. soil who later died. But every step in how Ebola patients are handled will be scrutinized and improved, Frieden said.

Asked why the CDC didn’t send a team as soon as Duncan was diagnosed, Frieden said: “We did send some expertise in infection control but think in retrospect, with 20-20 hindsight, we could have sent a more robust hospital infection control team, and been more hands on at the hospital on day one about exactly how this [case] should be managed. We will do that from now on any time we have a confirmed case.”

In an encouraging sign, health officials said Pham has only had direct contact with one person— and that person isn’t sick, but is being monitored. Dozens of people who had direct or indirect contact with Duncan are still being monitored. “It is decreasingly likely that any of them will develop Ebola,” Frieden said.

TIME ebola

Nurses ‘Infuriated’ By Suggestion of Dallas Ebola Protocol Breach

The National Nurses Union is pushing for the CDC to mandate better gowns, masks and training to prepare them for treating Ebola

When Thomas Duncan, the first person to be diagnosed with Ebola in the U.S. was admitted to Texas Health Presbyterian Hospital, the nurses and doctors who took over his care became the frontline in the battle with the virus. According to the Centers for Disease Control (CDC), proper infection control procedures should have protected those health care workers from getting infected, and should have stopped the virus from spreading any further than Duncan and anyone he may have had direct contact with before falling ill.

But they didn’t. Nina Pham, one of the nurses assigned to care for Duncan before he died, tested positive for Ebola on Oct 13. Initially, CDC director Dr. Tom Frieden attributed the infection to a “breach in protocol.”

“That infuriated me,” says Karen Higgins, co-president of National Nurses United (NNU) and a nurse at Boston Medical Center. “What it should have been attributed to was a breakdown in the system. It never should have been stated. Instead, we should figure out what the problem was and fix it, not say that it was her fault that she didn’t follow protocol and that’s why it happened.”

MORE: 5 Ways U.S. Hospitals Need to Get Ready For Ebola

CDC has since acknowledged that they and the Texas health department are still investigating how the infection occurred, but according to the nurses’ group, there are serious gaps in the country’s preparedness for treating Ebola patients. For one, there is no standard protocol for what a hospital needs to have in place and how a hospital should handle an Ebola case. The CDC has published guidelines on its website, but it’s up to each hospital to decide how to implement those recommendations. And according to a recent survey of more than 2,200 nurses in 46 states, those policies vary widely and are haphazard. Eighty five percent of the nurses questioned felt their hospitals had not provided education about Ebola in a format in which they could ask questions and learn more about best practices for protecting themselves, the patient and their communities. Most were directed to a video or website or handed a piece of paper informing them of Ebola’s symptoms and urging them to ask patients with fevers about their recent travel history. Some were provided a Hazmat suit in the breakroom and told to try it on if they had time. Most said their hospitals did not have Hazmat suits for the nurses. Forty percent of them said their hospitals did not have enough protective equipment, including face shields or the fluid-barrier gowns that are required when treating infectious patients. “Are we prepared for infectious diseases? Yes we are. Are we prepared for Ebola? No we are not,” says Higgins.

The fact that two hospitals in the U.S.—Emory University Hospital and Nebraska Medical Center—successfully treated Ebola patients without any spread of the virus supports Frieden’s conviction that it’s possible to contain Ebola and protect health care workers.

MORE: Ebola Health Care Workers Face Hard Choices

But in order to do that, the NNU says a strong mandate is needed from the CDC and public health departments that specifies exactly what type of equipment health care providers should be wearing, how they should put the equipment on and take it off, and how they should dispose of them once they have been contaminated. That’s especially important if the CDC expects every hospital to be able to properly care for Ebola patients, something that Frieden says is possible. “We are challenging the CDC and saying we are past the time of guidelines and recommendations,” says Higgins. “What we need are standards, high standards of care. Say that this is now what is expected of your equipment, the right gloves, the right outfits, masks and covers.”

Specifically, the nurses want Hazmat suits for anyone who will be treating an Ebola patient. Health departments and the CDC have been reluctant to mandate these, since putting them on or taking them off improperly may put health care workers at greater risk of contamination. But with training, the nurses say, the suits could prevent further spread of the virus, like what happened in Dallas. “The equipment is one thing, but training has to be the second part,” says Higgins. “And not just a web site or a video, but people working with people one on one to make sure everyone understands what they are doing, how to get in and out of the equipment, and how to do it right.”

At Boston Medical Center, hospital staff have recognized that current procedures aren’t enough, and in the past week have increased hands-on training and drills to make sure health care workers are prepared to properly handle an Ebola patient, should one walk through the door. Those procedures include making sure that anyone gowning to go into an infectious patient’s room has a buddy to observe or gown with them, and point out any missed steps or improperly worn protective gear.

MORE: Ebola Lessons We Need To Learn From Dallas

Waste from a potential Ebola patient is also getting the same stepped-up vigilance. Previously, the waste wasn’t given any additional care beyond the usual treatment for hazardous materials—a separate bin and a separate removal process that generally ended in incineration. But now, the hospital is requiring any Ebola material to be double or triple bagged and put in a separate box to be removed by a properly trained hazardous waste management team who will dispose of it in the right way to prevent further contamination.

For now, the nurses aren’t confident that they are able to properly protect themselves and their community from Ebola, but they’re convinced that with the proper equipment and training, they can be. “This is our test and we need to do it right,” says Higgins. “We feel extremely upset that any [healthcare worker] got infected. Hopefully she will be fine, but we don’t want to have to face another person or family that ends up getting infected because we are not as good as we should be in treating patients.”

Read next: CDC Chief Urges U.S. Hospitals to ‘Think Ebola’

TIME neuroscience

This Alzheimer’s Breakthrough Could Be a Game Changer

Scientists recreated what goes on in the brains of Alzheimer’s patients in a 3D culture dish that could speed development of new drugs for the disease

Researchers have overcome a major barrier in the study of Alzheimer’s that could pave the way for breakthroughs in our understanding of the disease, a new report shows—and that new understanding could, in turn, pave the way for drugs that treat or interrupt the progression of the neurodegenerative condition.

For decades, animals have been the stand-ins for studying human disease, and for good reason. Their shorter lifespans mean they can model human conditions in weeks or months, and their cells can be useful for testing promising new drug treatments.

But they haven’t been so helpful in studying Alzheimer’s disease. Two factors contribute to the neurodegenerative condition — the buildup of sticky plaques of the protein amyloid, and the toxic web of another protein, tau, which strangles healthy nerve cells and leaves behind a tangled mess of dead and dying neurons. Despite attempts by scientists to engineer mice who exhibit both factors, they haven’t been able to generate the tau tangles that contribute to the disease.

Now, Dr. Rudolph Tanzi and Dr. Doo Kim at the Mass General Institute for Neurodegenerative Diseases at Massachusetts General Hospital, have devised a work-around that doesn’t involve animals. They have developed a way to watch the disease progress in a lab dish.

“In this new system that we call ‘Alzheimer’s-in-a-dish,’ we’ve been able to show for the first time that amyloid deposition is sufficient to lead to tangles and subsequent cell death,” said Tanzi in a statement.

MORE: Blood Test for Alzheimer’s

While autopsies showed evidence of both amyloid and tau in the brain, Alzheimer’s experts have been debating for years which came first — do amyloid plaques trigger the formation of tau tangles, or does the presence of tau cause amyloid to get stickier and bunch together in the brain? Tanzi and his colleagues showed definitively for the first time that amyloid is the first step in the Alzheimer’s process, followed by tau tangles. When he blocked the formation of amyloid in the culture with a known amyloid inhibitor, tau tangles never formed.

The disease-in-a-dish model is an emerging way of understanding conditions that either can’t be recapitulated accurately in animals, or diseases that make it difficult to study and test in human patients. In recent years, for example, scientists have successfully recreated the process behind amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, using stem cells from patients and allowing them to develop into the motor neurons that are affected by the disease. The technique led to a breakthrough in understanding that a certain population of nerve cells known as glial cells poison the motor neurons and impede their normal function. Now experts are focusing on finding ways to control the glial cell activity as possible treatment for ALS.

MORE: How Moodiness and Jealousy May Lead to Alzheimer’s

Tanzi and his team are hoping that something similar will come from their model of Alzheimer’s.

While the genes responsible for the inherited form of Alzheimer’s differ slightly from those involved in the more common form that affects people as they age, the end result — the build up of amyloid plaques and tau tangles — are the same. So now that they can see both the clumps of amyloid and the tau tangles, form, they can start to tease apart the processes that link the two processes together.

That will open the way toward finding drugs or other ways of interrupting the process more quickly than they could working with animals. It took six to eight weeks for the cells in the dish to form plaques and then tangles, compared to a year or so in mice. “We can now screen hundreds of thousands of drugs in this system that recapitulates both plaques and tangles…in a matter of months,” Tanzi said. “This was not possible in mouse models.” The system also makes it possible to test these drug compounds at one-tenth the cost of evaluating them in mice, he said. And that means that finding a way to prevent Alzheimer’s may come both faster and cheaper than scientists had expected.

TIME Obesity

How Family Dynamics at the Dinner Table Affect Kids’ Weight

A stock photograph of a family dinner
Getty Images

It's not just what kids eat, but who they eat with that matters when it comes to their weight

“Eat together” is a mantra that doctors and nutritionists use regularly when they talk with families about eating healthy and maintaining normal weight. Children who eat regular family meals tend to have lower rates of obesity and eat more nutritiously. A new study published Monday morning in the journal Pediatrics takes a novel look at why.

A team led by Jerica Berge, in the department of family medicine and community health at University of Minnesota, asked the families of 120 children aged 6 to 12 to record eight days of meals. The families didn’t have to eat every meal together, and didn’t even have to eat dinner together every one of those nights, but did have to share at least three meals during that time. Half of the children were overweight or obese, and half were normal weight.

To tease out what features of the family meal might be influence weight, Berge’s team laboriously coded the interactions occurring at the table into two broad groups — those relating to the emotional atmosphere at the meal, such as how much the family members seemed to be enjoying the time together, how much hostility the diners showed one another, and how many uncomfortable silences or awkward pauses occurred — and those involving food specifically, including how much hostility emerged from discussions about food, including weight issues, and how much the parents controlled or limited what and how much children ate.

Children who were overweight or obese had family meals that included more negative emotional interactions — hostility, poor quality interactions, little communication and more controlling behavior from their parents — compared to children who weren’t obese. Their meals tended to have a warmer, more communicative atmosphere. For example, these children were given positive reinforcements to eat, and were encouraged to eat foods to get stronger or run faster, while heavier children experienced more negative pressures including threats and made to feel guilty about those in the world who can’t afford to eat three meals a day. If parents or caregivers talked constantly throughout the meal about food, and lectured about homework or attempted to control what the children ate, the youngsters were also more likely to be heavy.

“I was surprised by how consistent the patterns were,” says Berge. “Almost every single one of the emotional factors we coded were in the right direction, and there were really clear patterns in how much positive or negative interactions were associated with overweight and non overweight.”

The analysis also revealed other things that distinguished the family meals of overweight children and normal weight youngsters. Heavier children tended to have shorter meals — spending 13.5 minutes on average eating with their family compared to 18.2 minutes for non obese kids. Children who weren’t obese were also more likely to have a father or step-father at the table. The reason, says Berge, may be practical. “It might be a matter of having one more person at the table for crowd control, another person to help make the meal and be a model for children to emulate,” she says.

The team only coded the types of interactions between the family members during the meal, and did not include an in-depth look at what the families were eating. But that’s the focus of their next study.

In the meantime, the current data suggests that simply sitting down at the same table at the same time isn’t enough to influence obesity. And it’s up to pediatricians and family doctors to help families understand how to take full advantage of breaking bread together. “There is clear evidence that family meals are important in protecting kids against overweight,” says Berge, “so it’s important to start the conversation with families. It’s important to focus on making the meal environment more positive.” And, as her study showed, it doesn’t take lengthy repasts either — just 20 minutes as many times a week as possible.

Read next: Why I Don’t Eat With My Kids

TIME Obesity

Why Brown Fat May Be the Key to Weight Loss

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Can you think your way thinner?

Not all fats we eat are created equal. We all know that, trying to dodge the less healthy ones that come from animals and dairy products and load up on those less likely to clog our arteries and add to our waistlines.

But it turns out that even after we consume fat, we store it in different forms as well, and scientists reporting in the journal Cell have identified a pathway in the brain that can direct our bodies to convert stubborn waistline-growing fat into a different fat that’s easier to burn off.

MORE: Having The Right Kind of Fat Can Protect Against Diabetes, Study Says

Brown fat, so-called because it is rich in the darker hued energy factories of cells known as mitochondria, is a calorie-hungry machine. It consumes a lot of energy and generates just as much, mostly in the form of heat. That’s why brown fat is more common in newborns, who need to be protected from getting chilled after nine months in the toasty womb. As we age and are better able to regulate our body temperature, we lose brown fat, and until recently scientists thought most adults had little brown fat, if any.

Now researchers at Yale School of Medicine have identified the process that turns white fat, the more common kind in the average adult body and the primary culprit in weight gain, into the energy-consuming brown fat.

MORE: How Now, Brown Fat? Scientists Are Onto a New Way to Lose Weight

Working with mice, the scientists honed in on a set of neurons in the brain that regulate the body’s energy balance, including the breakdown of glucose, which is the primary source of fuel for most cells. When mice fast, for example, their bodies shift into a type of emergency mode, conserving energy and shutting off systems and cells that require high amounts of energy, such as the heat-generating brown fat cells. Fasting resembles times of starvation, so evolutionarily, this makes sense; when food is scarce, the body shunts its energy toward essential processes, such as keeping the heart pumping and getting oxygen to the brain.

Xiaoyong Yang, an associate professor of comparative medicine and physiology at Yale, showed that this switch to conserve energy is intimately tied to hunger signals in the brain. “We showed that hunger itself is a signal that controls the browning of white fat, so the brain can actually control the browning of white fat.”

That means it’s the brain that regulates what type of fat, and how much of it, is burned. In obese animals, Yang found, these hunger signals are dysfunction; overweight and obese mice eat regardless of whether they are hungry, so the normal physical signals from the stomach don’t function properly. Heavier animals continuously feel hungry, even if they’ve eaten enough for their energy needs. That perpetuates the cycle of obesity, since it shuts off the transformation of white fat into energy-consuming brown fat, and therefore keeps more fat in an inert, pound-packing form.

“Obese animals, and people, lose the response to hunger,” he says. “Although there is plenty of food and plenty of energy, the hunger neurons send a false message that the body needs to conserve energy, not burn it.”

Eventually, he says, it might be possible to intervene with the hunger signal anywhere along its journey from the brain to the fat cells, and that may shift the balance in favor of burning fat rather than storing it, which might open the door to weight loss. But calibrating the switch will be critical, since favoring the burning of fat can also lead to other physiological problems such as wasting and malnutrition. “You don’t want to set the body’s energy balance to zero,” says Yang. “You want to reset it to normal levels.”

TIME Cancer

Why Cancer Drugs May Work Better While You Sleep

The body doesn't process drugs in the same way throughout the day, so it's possible to time your doses to make anti-cancer meds more effective

It’s news to no one that your body works differently when you’re awake and when you’re sleeping. But could the different states also affect how your body processes certain life-saving drugs? Researchers, reporting Friday in the journal Nature Communications, found that when it comes to cancer drugs, the answer may be yes.

Researchers at the Weizmann Institute of Science discovered—by happy accident—that some of the body’s molecular functions during the day may interfere with the effectiveness of certain cancer medication. Specifically, they found that the normal day-time production of some steroid hormones in the body actually inhibited the work of epidermal growth factor (EGF) receptors—which are the proteins targeted by a class of anti-cancer drugs. Tumor cells plant these receptors on their surfaces to attract nutrients that help them survive and grow. Drugs, including the breast cancer agent lapatinib, can block these receptors on tumors, and such medications are a popular way to treat breast cancers expressing epidermal growth factor.

But Yosef Yarden, a professor in the department of biological regulation, and his team found that when the tumor cells simultaneously bind to something else—such as steroid hormones—the EGF receptors are less active, making drugs like lapatinib less potent.

The findings are still preliminary, but there is other evidence that the day-night cycle may be a potentially important factor in determining cancer treatment dosing in coming years. Some studies showed, for example, that when the 24-hour rest and activity cycle is broken metabolically, and the EGF receptors aren’t given enough time to be active, certain tumors in animals grow two to three times faster.

“The study developed out of a mistake. We accidentally omitted a synthetic steroid…from the medium in which we routinely grow mammary gland cells,” Yarden wrote in an email response to TIME. “And we noticed that the cells acquired a faster rate of migration when we followed them under a microscope.”

Intrigued, they turned to mice to answer some more questions. Knowing that steroid levels peak during the day and drop off during sleep, Yarden and his colleagues wondered whether the timing of anti-tumor drugs would affect tumor growth. So they gave a group of mice with breast cancer tumors lapatinib at different times over a 24-hour period and tracked any differences in the size and growth of the tumors.

Indeed, the mice given the drug while they slept showed significantly smaller tumors after seven days than those who received the drug during the day. Yarden suspects that the lower levels of steroid hormones circulating at night allows more of the EGF-targeting drug to hone in on its receptors on the tumor cells and inhibit their growth. Not only that, but the tumors in the mice taking the drug at night looked different; they showed less blood vessel infiltration which meant they were less robust.

Does that mean it’s better to get cancer therapy at night? So far, the results only apply to animal models, and to cancers driven by EGF. More work needs to be done, but if it’s validated, shifting therapies to just before bed “seems logical,” says Yarden. Especially since drugs like lapatinib come in pill form, so it would be relatively easy to take medications before turning in rather than in the morning.

TIME diabetes

Type 1 Diabetes Treatment Gets Boost from Stem Cells

Human stem cell derived beta cells
Insulin-making cells grown from stem cells glow green two weeks after they are transplanted into mice (c) Douglas Melton 2014

Scientists started with stem cells and created the first insulin-making cells that respond to changes in glucose

Scientists are closer to a potential stem cell treatment for type 1 diabetes.

In a new article in the journal Cell, Douglas Melton, co-director of the Harvard Stem Cell Institute (and one of the 2009 TIME 100) and his colleagues describe how they made the first set of pancreatic cells that can sense and respond to changing levels of sugar in the blood and churn out the proper amounts of insulin.

It’s a critical first step toward a more permanent therapy for type 1 diabetics, who currently have to rely on insulin pumps that infuse insulin when needed or repeated injections of the hormone in order to keep their blood sugar levels under control. Because these patients have pancreatic beta cells that don’t make enough insulin, they need outside sources of the hormone to break down the sugars they eat.

MORE: Stem-Cell Research: The Quest Resumes

Melton started with two types of stem cells: those that come from excess embryos from IVF procedures, and those that can be made from skin or other cells of adults. The latter cells, known as iPS cells, have to be manipulated to erase their developmental history and returned back to an embryonic state. They then can turn into any cell in the body, including the pancreatic beta cells that produce insulin. While the embryonic stem cells from IVF don’t require this step, they aren’t genetically matched to patients, so any beta cells made from them may cause immune reactions when they are transplanted into diabetic patients.

Both techniques, however, produced similar amounts of insulin-making beta cells—something that would have surprised Melton a few years ago. But advances in stem cell technology have made even the iPS cells pretty amenable to reprogramming into beta cells. Melton’s group tested more than 150 different combinations of more than 70 different compounds, including growth factors, hormones and other signaling proteins that direct cells to develop into specific cell types, and narrowed the field down to 11 factors that efficiently turned the stem cells into functioning beta cells.

MORE: Woman Receives First Stem Cell Therapy Using Her Own Skin Cells

The two populations of stem cells churned out hundreds of millions of insulin-making cells, which is the volume of cells that a patient with type 1 diabetes would need to cure them and free them from their dependence on insulin. An average patient, says Melton, would need one or two “large coffee cups” worth of cells’, each containing about 300 million cells. Melton and his team then conducted a series of tests in a lab dish to confirm that the cells were functioning just like normal beta cells by producing more insulin when they were doused with glucose, and less when glucose levels dropped. That was a huge advance over previous efforts to make beta cells from stem cells—those cells could produce insulin, but they didn’t respond to changing levels of glucose and continuously pumped out insulin at will.

Next, the scientists transplanted about five million of the stem cell derived beta cells into healthy mice, and two weeks later, gave them an injection of glucose. About 73% of the mice produced enough insulin to successfully break down the sugar. What’s more, that was similar to the proportion of mice responding to glucose after getting a transplant of beta cells from human cadavers. That was especially encouraging since some type 1 diabetics currently receive such transplants to keep their diabetes under control. “We’ve now shown that we can produce an inexhaustible source of beta cells without having to do to cadavers,” he says.

MORE: First Stem Cells Cloned From Diabetes Patient, Thanks to Egg Donors

Taking the tests even further, the group showed that even mice that were already diabetic showed improved blood sugar levels after receiving a transplant of the stem cell beta cells—in other words, the transplanted cells effectively cured their diabetes. “We showed you can give three sequential challenges of glucose—similar to breakfast, lunch and dinner—and the cells responded properly,” says Melton.

But he acknowledges that as exciting as the advance is, it only solves half the problem for those with type 1 diabetes. The reason their beta cells aren’t able to make enough insulin may be due to the fact that they are attacked by the body’s own immune system for reasons that scientists still don’t understand. So the next step in turning these findings into a potential therapy is to find ways to protect the beta cells from destruction, either by encapsulating them in a mesh-like device similar to a molecular tea bag, or finding ways to genetically modify them to carry ‘don’t attack me’ proteins, the same way that fetal cells do so that an expectant mother’s immune cells don’t attack the growing baby.

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

“It’s taken me 10 to 15 years to get to this point, and I consider this a major step forward,” says Melton, who began researching ways to treat type 1 diabetes when first his son, then his daughter were diagnosed with the condition more than two decades ago. “But the longer term plan includes finding ways to protect these cells, and we haven’t solved that problem yet.”

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