TIME Health Care

The Price of Staying Alive For the Next 3 Hours

Stayin' alive—and cheap at the price
Stayin' alive—and cheap at the price ZU_09; Getty Images

A new study suggests a little spending now can buy you a lot of time later

How much do you reckon you’d pay not to be dead three hours from now? That probably depends. If you’re 25 and healthy, a whole lot. If you’re 95 and sickly, maybe not so much. But for people in one part of the world—the former East Germany—the cost has been figured out, and it’s surprisingly cheap: three hours of life will set you back (or your government, really) just one euro, or a little below a buck-thirty at current exchange rates.

That’s the conclusion of a new study out of Germany’s Max Planck Institute, and it says a lot about the power of a little bit of money now to save a lot of suffering later—with implications for all manner of public health challenges, including the current Ebola crisis.

The new findings are a result of one of the greatest, real-time longitudinal studies ever conducted, one that began the moment the Berlin Wall fell, on Nov. 9 1989. Before that year, there were two Germanys not just politically, but epidemiologically. Life expectancy in the western half of the country was 76 years; in the poorer, sicker east, it was 73.5. But after unification began, social spending in the East began rising, from the equivalent of €2,100 per person per year to €5,100 by the year 2000. In that same period, the difference in lifespan across the old divide went in the opposite direction, shrinking from 2.5 years to just one year as the east Germans gained more time. Crunch those numbers and you get the three extra hours of extra life per person per euro per year.

“Without the pension payments of citizens in east and west converging to equivalent levels,” said Max Planck demographer Tobias Vogt in a statement, “the gap in life expectancy could not have been closed.” Increased public spending, Vogt adds, is often framed as an unfortunate knock-on effect of longer life. “But in contrast,” he says, “our analysis shows that public spending can also be seen as an investment in longer life.”

The idea that generous, tactical spending now can be both a money-saver and lifesaver is one that health policy experts tirelessly make—and that people in charge of approving the budgets too often ignore. Bill Gates often makes the point that $1 billion spent to eradicate polio over the next few years will save $50 billion over the next 20 years, not just because there will no longer be any cases of the disease to treat, but because the global vaccination programs which are necessary just to contain the virus can be stopped altogether when that virus is no more.

As TIME reported in September, British inventor Marc Koska made a splash at the TEDMed conference in Washington DC when he unveiled his K1 syringe—an auto-destruct needle that locks after it’s used just once and breaks if too much force is used to pull the plunger back out. That prevents needle re-use—and that in turn not only reduces blood-borne pathogens from being spread, it does so at a saving. According to the World Health Organization (WHO), $1 spent on K1 syringes saves $14.57 in health care costs down the line—or $280 for a $20 order of the shots.

All across the health care spectrum, such leveraging is possible. Critics of the Affordable Care Act have slammed the law for the cost of the preventative services it provides, and while it’s way too early to determine exactly how successful the law will be, the encouraging stabilization in the growth of health costs suggests that something, at least, is working.

Global health officials are making a similar, though more urgent, preventative argument concerning the Ebola epidemic in West Africa. Americans are rightly jumpy over the few cases that have landed on our shores, but the 1,000 new infections per week that are occurring in the hot-spot nations of Liberia, Guinea and Sierra Leone make our concerns look small. Frighteningly, according to the WHO’s newest projections, that figure will explode to 10,000 cases per week by December if the resources are not deployed to contain the epidemic fast.

“We either stop Ebola now,” WHO’s Anthony Banbury said in a stark presentation to the U.N. Security Council on Sept. 14, “or we face an entirely unprecedented situation for which we do not have a plan.”

Suiting up and wading into the Ebola infection zone is a decidedly bigger and scarier deal than spending an extra euro on public health or an extra dollar for a new syringe. But the larger idea of intervention today preventing far larger suffering tomorrow remains one of medicine’s enduring truths. We lose sight of it at our peril.

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 medicine

FDA Approves Combined Hepatitis Drug

Harvoni
Harvoni, the first single medication to treat hepatitis C, was recently approved by the FDA. Gilead Sciences

Harvoni is the third hepatitis C drug approved in the past year

The Food and Drug Administration approved the first single medication to treat hepatitis C on Friday, green-lighting one pill in the place of multiple treatments. The new drug, Harvoni, is the third hepatitis C drug approved in the past year.

“With the development and approval of new treatments for hepatitis C virus, we are changing the treatment paradigm for Americans living with the disease,” said FDA official Edward Cox.

Harvoni, developed by Gilead Sciences, will be the first hepatitis drug to require a pill only once daily. A full 12-week treatment will cost $94,500, less than existing treatments, Reuters reports.

TIME Obesity

Why Brown Fat May Be the Key to Weight Loss

brown fat
Getty Images

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 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.”

TIME medicine

New Genes Found that Determine Your Height

The latest analysis doubles the number of genes connected to height

How tall you are is strongly related to the genes you inherit, and previous studies suggested that as much as 80% of the variance in height among people is due to their DNA.

And in the largest genetic study of height-related genes to date, scientists involved in the appropriately titled GIANT consortium (Genetic Investigation of Anthropometric Traits) identified 423 genetic regions connected to height — which could explain as much as 60% of that genetic component.

Dr. Joel Hirschhorn, leader of the GIANT consortium at Boston Children’s Hospital, Harvard Medical School and the Broad Institute of MIT says that for a trait like height, which isn’t determined by a single gene but likely the combined effects of multiple genes involved in multiple different processes from bone growth to cell growth, the new findings are like finding biggest nuggets of gold in a riverbed. The latest analysis, published in the journal Nature Genetics, describes the gene variants most commonly shared among people (not the rare mutations) that likely contribute to height.

They emerged from a sweep of the genomes of more than 250,000 people of various heights, and from correlating their stature with their genetics. Many of the known and familiar factors related to height, including those dealing with skeletal growth and collagen that are mutated in people with medically short stature, for example, appeared in the study, confirming their role in determining how tall people get.

But there were also some surprises — genetic regions that previous had never been thought to be related to height, including a gene known to be involved in cell growth but not in skeletal functions. “It’s a mix ranging from completely known things, to those that make sense to things that are completely surprising and things we don’t even know what to think about them,” says Hirschhorn.

What the group has identified are gene regions of interest, and a new round of studies will have to delve deeper into those areas to isolate specific genes — and the proteins they make, such as growth factors, enzymes, or other agents — that are actually responsible for determining height. But it’s a critical first step, and could lead to potential new ways of treating medical conditions of short stature or gigantism that can have health negative health effects on the heart and joints.

TIME Innovation

Five Best Ideas of the Day: October 3

The Aspen Institute is an educational and policy studies organization based in Washington, D.C.

1. With 3D printing, prosthetic technology is poised to change millions of lives.

By Tom McKay in Mic

2. Dysfunctional oversight of the Department of Homeland Security undermines its mission.

By Daniel Kaniewski in The Hill

3. The web isn’t killing newspapers. Print readership has been in decline for 20 years.

By Whet Moser in Chicago Magazine

4. Skyrocketing drug traffic has deeply affected life on Indian reservations at the US-Mexico border.

By Shannon Mizzi in Wilson Quarterly

5. With Chinese elites joining the movement, the protests in Hong Kong could yield a partial win.

By Zack Beauchamp in Vox

The Aspen Institute is an educational and policy studies organization based in Washington, D.C.

TIME Ideas hosts the world's leading voices, providing commentary and expertise on the most compelling events in news, society, and culture. We welcome outside contributions. To submit a piece, email ideas@time.com.

TIME ebola

Ebola Patient in Texas Is Not Allowed Any Visitors

Thomas Eric Duncan remains in serious condition at a Dallas hospital

Thomas Eric Duncan remains in serious condition at Texas Health Presbyterian Hospital, kept under close watch by law enforcement officials. He’s not allowed any visitors, but is communicating with family and friends via phone.

In a news conference on Thursday, Dr. Tom Frieden, director of the Centers for Disease Control and Prevention, said CDC-trained health officials in Monrovia, Liberia, took Duncan’s temperature before he boarded a plane on Sept. 19 to begin his journey to the United States. As part of the screening process to prevent the spread of Ebola into this country, passengers’ temperatures are taken and those with fevers are pulled off the flight. Duncan’s temperature, according to Frieden, was 97.3 (or 36.3C) — normal.

Frieden said more than a dozen people from the countries most affected by Ebola were prevented from boarding flights to the U.S. in September. Duncan did not develop fever and symptoms until four days after he arrived in Dallas.

The four people in the apartment where he stayed are now under quarantine, prevented from leaving their home by a law enforcement officer stationed outside the complex. If any of the individuals violate the order, a formal court order will be issued. None of the people are symptomatic, but, said Dr. David Lakey, commissioner of the Texas Department of State Health Services, he “had concern about our ability to be confident that monitoring was going to take place the way we needed it to take place.” People who might have had contact with Duncan are being monitored with twice daily temperature checks and, he said, without elaborating on the reasons, “we felt this [quarantine order] was needed.”

Food is being delivered to the four people in the apartment and Lakey said a cleaning service had been found to thoroughly clean the residence as well. Health officials visited the apartment when Duncan was admitted to the hospital, and helped the residents bag Duncan’s belongings, along with trash and towels that he used. In an interview with Anderson Cooper 360° due to air Thursday evening, however, Duncan’s partner, Louise, with whom he stayed and is one of those quarantined, said the sheets he used were still on the bed. She and the other four people in the apartment were also instructed about how to decontaminate areas that Duncan might have touched, until more thorough cleaning could be done.

For now, Lakey said, “I have no intention to put other individuals under a control [quarantine] order.” Together with the CDC, the Texas health department is monitoring 100 people with daily temperature checks; most are unlikely to be at high risk of developing Ebola, and only about a dozen had direct contact with Duncan. The state is also investigating how Duncan could have been sent home after his first visit to hospital, when he had a fever and told the nurse that he had recently arrived from Liberia.

TIME ebola

Pentagon Dispatches 101st Airborne to Africa to Tackle Ebola

Ebola
Getty Images

Headquarters unit from the storied division to coordinate U.S. efforts to tackle the disease

While the U.S. military has dispatched some 1,600 troops to Iraq in recent weeks to deal with the threats posed by Islamic militants there, it apparently was saving its big guns for a more insidious threat: the Ebola virus.

On Tuesday, the Pentagon announced it will soon have about 1,600 troops in western Africa dealing with the spreading scourge—and that nearly half of them will come from the Army’s storied 101st Airborne Division.

“It’s not an armed threat,” Rear Admiral John Kirby, the Pentagon spokesman, said of the Ebola virus Tuesday. But “just like any other threat, we take it very, very seriously.” While U.S. troops will not be tending to those infected with the disease, he said, they will be “trained on personal protective equipment and on the disease itself…we’ll make sure that they’ve got the protection that they need.”

Like the war against the Islamic State in Iraq and Greater Syria (ISIS), the battle against Ebola is open-ended, Kirby said. He announced that a 700-strong headquarters unit from the 101st would head to Liberia by the month’s end to help coordinate the response to the epidemic. The virus has so far killed over 1,800 in Liberia, the country worst affected by the outbreak.

A second group of 700 engineering troops are headed there to build treatment units to treat the infected, he said. Nearly 200 U.S. troops are already in West Africa dealing with the threat.

“These deployments are part of a whole-of-government response to the Ebola outbreak,” Kirby said. “The U.S. military is not in the lead, but we are fully prepared to contribute our unique capabilities.”

Last week, 15 Navy Seabees—the service’s construction arm—arrived in the Liberian capital of Monrovia to begin help building treatment and training centers. “We’re establishing command and control nodes, logistics hubs, training for health care workers, and providing engineering support,” Army General Martin Dempsey, chairman of the Joint Chiefs of Staff, said. “The protection of our men and women is my priority as we seek to help those in Africa and work together to stem the tide of this crisis.”

The World Health Organization said Tuesday that the number of Ebola patients in Guinea, Liberia and Sierra Leone had topped 6,500, with nearly half of them dying from the disease.

It was only two weeks ago that President Obama declared the U.S. would dispatch 3,000 troops to battle Ebola. “If the outbreak is not stopped now,” he warned, “we could be looking at hundreds of thousands of people infected, with profound political and economic and security implications for all of us.”

On Tuesday, in another echo of the fight against ISIS, Kirby said that might not prove sufficient. “They’ll come in waves,” he said of U.S. troops deployments. “It could go higher than 3,000 troops eventually.”

TIME medicine

Soon You Can Send Your Expired Painkillers Through the Mail

painkiller pills
Getty Images

The DEA has a new way to get rid of extra meds

How to get rid of leftover medication is a tricky question—keep it around and it can get into the wrong hands, but dispose of it improperly and you risk contaminating the environment.

That’s why in the past, the U.S. Drug Enforcement Administration (DEA) has held National Prescription Drug Take-Back Day. Last April, the DEA reported that it collected 780,000 pounds of prescription drugs, and during the event on Sept. 27, a single county in Virginia dropped off 1,200 pounds of drugs. But even though half a ton of drugs for one county is certainly a coup, it was the last event of its kind—because soon, through an innovative new program, Americans will be able to safely abandon their unused pills at any time.

The DEA first recognized the leftover pill problem because the Controlled Substances Act had no outlined provisions for how people could get rid of their unused or expired prescription drugs. According to the DEA, people would keep them in their medicine cabinets (which made it possible for them them to be abused), toss them in the trash or flush them down the toilet. The latter method was discovered to contaminate water supplies.

In 2010, the Drug Disposal Act gave the DEA the authority to create a framework for how the general public and facilities could dispose of prescription pills properly and safely. On Sept. 9 the regulations were approved, and the DEA says it will start implementing the plan in early October. The new regulations allow Americans to get rid of their excess drugs at pharmacies or police departments with drop-off receptacles. Patients will also be able to grab envelopes from places like hospitals that they can use to mail their pills to authorized collectors, who will make sure the pills are properly incinerated. “It will be more convenient because once these rules are implemented, then people can do it all the time,” a DEA spokesperson told TIME.

The number of Americans abusing prescription drugs has dropped in the last couple years, but the DEA says the 6.5 million people who reportedly abused prescription drugs in 2013 is double the number of people who use hard drugs like cocaine, heroin, LSD and Ecstasy combined.

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