TIME Diet/Nutrition

This Diet Is Better for Your Brain Than Low-Fat

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Simply adding more olive oil and nuts to your diet may help prevent memory problems and loss of cognitive skills that come with old age

You’ve heard a million times that the modern Mediterranean diet is good for you. Now there’s stronger evidence the diet may be good for your brain, too.

In a study published in JAMA Internal Medicine, Dr. Emilio Ros from the Hospital Clinic in Barcelona, Spain and his colleagues conducted a study of 447 men and women aged 55 to 80 years to see whether changing their diet could affect their performance on cognitive tests. The volunteers were healthy but at higher risk of developing heart-related problems; some smoked or had hypertension, for instance, others had a family history of heart issues. Everyone in the study was randomly assigned to eat, for about four years, a Mediterranean diet supplemented with 1 liter of extra virgin olive oil a week, a Mediterranean diet enhanced with 30 grams of nuts a day, or a low-fat diet. The researchers performed a series of brain functioning tests on the participants at the start of the study and then at the end of the study.

MORE: Here’s Another Reason to Try the Mediterranean Diet

Both Mediterranean diet groups showed improvements compared to the low-fat diet group; those consuming more olive oil showed better memory scores at the end of the study while those eating more nuts showed improvements in executive function skills. The low-fat diet group, on the other hand, showed declines in many of the cognitive measures.

“It’s never too late to change your dietary patterns to improve your health,” says Ros. “This surprised even myself.” The results, he says, are especially encouraging since the people in the study were at higher risk of developing cognitive problems because of their heart-related risk factors, which can also impair cognitive function by increasing risk of stroke and compromising blood flow to the brain. “If you intervene with a healthy dietary pattern in people who are at risk of cognitive failure, even in people who still haven’t had any memory complaints or loss of cognitive function, you can prevent cognitive deterioration,” he says.

MORE: This Diet Has Been Linked to a Longer Life—Again

The findings support a growing body of evidence that connects the Mediterranean diet, which is high in antioxidant-rich foods like rich vegetables and fats, and improved brain function. Because researchers now believe that the brain is damaged by free radicals produced by stress, a diet that is rich in antioxidants may help to counter that harm. A previous study involving the same group of participants found similar brain benefits of olive oil and nuts, but that trial did not follow volunteers over time to measure the change associated with the dietary change.

MORE: Mediterranean Diet Better Than Low-Fat Diet in Keeping Aging Brains Sharp

While these results are promising, Ros says that more work is needed to confirm them; the current study is relatively small and did not find, for example, a strong correlation between the Mediterranean diet and the rate of mild cognitive impairment, a measure of cognitive decline that often precedes conditions like Alzheimer’s. “I think these results contribute to our understanding of healthy aging,” he says. “With a change in lifestyle as simple making some healthy choices in your food, it can make a difference.”

TIME medicine

How Concussions Can Lead to Poor Grades

Head injuries can have long lasting effects, not just on the field but in the classroom too

When it comes to concussions, the biggest question, especially on the minds of parents of student-athletes, is whether and when their child should get back in the game. But researchers at the Children’s National Health System say that there’s potentially bigger question that parents and educators aren’t asking: how concussions affect children’s performance in the classroom.

In a study published in the journal Pediatrics, Danielle Ransom, a postdoctoral fellow in neuropsychology, and her colleagues found that children who had concussions may experience more problems concentrating, keeping up and paying attention in school. The symptoms are worse for students who have recently been injured, but remained significant even for those who had recovered.

MORE: Longer Rest After Concussions Might Not Be Good, Study Says

“My colleagues and I have been hearing for years that kids with concussions have problems in school, but there was no evidence to show what the problems are, and how frequently they are occurring,” she says.

So she focused on 349 students ages 5 to 18 years old who had all been diagnosed with concussion. Some were still recovering, and experiencing symptoms, while others were no longer feeling any effects from their injury. Of the students who were still recovering, 88% reported more than one symptom including headaches, fatigue, difficulty understanding lessons or problems concentrating. And 77% said they had more trouble taking notes and spent more time completing homework assignments.

MORE: A New Blood Test to Diagnose Concussions on The Field

Students who experienced more-severe head injuries were also more likely to have the most trouble in school. But Ransom admits that diagnosing the severity of concussions is still a challenge. “At this point we really don’t have tools to clinically say, this is what you can expect in your kid’s recovery,” she says.

Still the results highlight the need to pay attention to the extra support that children with concussions need in order to recover. That may include, at least in the first days back from a head injury, a shorter school day, since students may feel more tired and overwhelmed by a full day, and even breaks throughout the day so they can rest when they feel headaches or symptoms occurring.

“Instead of trying to get the kid back to school doing things 100% as they usually would, we need to allow the symptoms to ebb and flow in a more natural way,” says Ransom. “Kids should be paying attention to their bodies, and teachers need to be attuned to their symptoms.”

MORE: Football Players Have More Concussions Than Are Diagnosed, Study Suggests

Such strategies could not only help to ease the transition back to school, and but also potentially lessen the effects of the concussion, says Ransom. There is evidence that children who push themselves to return too quickly to their normal workload can slow recovery and even make symptoms worse.

Unfortunately, she says, there is no magic threshold for when students can handle working at their full capacity; it varies with each child and with the injury. But recognizing that concussions can affect how children do in school could lead to better ways of helping them to return to their normal workload sooner. “We really think the findings in our study highlight the importance of targeting specific problems, and can ease the transition back for kids,” says Ransom.

TIME medicine

Exclusive: Meet the World’s First Baby Born With an Assist from Stem Cells

This newborn is the first baby in the world born using a breakthrough IVF treatment

Doctors in Canada have begun a new chapter in medical history, delivering the first in a wave of babies expected to be born this summer through a technique that some experts think can dramatically improve the success rate of in vitro fertilization (IVF).

Now 22 days old, Zain Rajani was born through a new method that relies on the discovery that women have, in their own ovaries, a possible solution to infertility caused by poor egg quality. Pristine stem cells of healthy, yet-to-be developed eggs that can help make a woman’s older eggs act young again. Unlike other kinds of stem cells, which have the ability to develop into any kind of cell in the body, including cancerous ones, these precursor cells can only form eggs.

In May 2014, Zain’s mother, Natasha Rajani, now 34, had a small sliver of her ovarian tissue removed in a quick laproscopic procedure at First Steps Fertility in Toronto, Canada, where she lives. Scientists from OvaScience, the fertility company that is providing Augment, then identified and removed the egg stem cells and purified them to extract their mitochondria.

Mitochondria are the powerhouses of the cell, a molecular battery that energizes everything a cell does. Adding the mitochondria from these egg precursor cells to Natasha’s poor-quality eggs and her husband Omar’s sperm dramatically improved their IVF results. In the Rajanis’ first traditional-IVF attempt, Natasha produced 15 eggs, but only four were fertilized—just one of those matured to the point were Natasha’s doctor felt comfortable transferring it. “I knew it wasn’t the best-quality embryo, but it was what she had,” says. Dr. Marjorie Dixon, of First Steps Fertility.

With Augment, the Rajanis produced four embryos, two of which have been frozen should the couple decide to have more children. Another one became baby Zain.

It’s not currently available in the U.S., since the Food and Drug Administration (FDA) considers the process of introducing mitochondria a form of gene therapy, which it regulates. So far, some three dozen women in four countries have tried the technique, and eight are currently pregnant. All of the women have had at least one unsuccessful cycle of IVF; some have had as many as seven.

“We could be on the cusp of something incredibly important,” says Dr. Owen Davis, president of the American Society of Reproductive Medicine (ASRM). “Something that is really going to pan out to be revolutionary.”

The Next Big Thing in IVF

The technique is indeed poised to usher in the next big advance in IVF; since the first baby, Louise Brown, was born using the process in 1978, the procedure has changed little. Scientists have made incremental advances in fine-tuning the procedure, but taken together, these improvements have nudged pregnancy rates upward by only a percent or two over the course of 35 years. As it stands, the IVF success rate is about 38% for women in their late 30s and 18% for those in their early 40s. Natasha’s first IVF cycle differed little from the one that produced Brown more than 35 years ago.

Augment emerged from a breakthrough made in 2004 by biologist Jonathan Tilly, then at Harvard Medical School and now chair of biology at Northeastern University. He found that cells scraped from the outer surface of the ovary contain the precursor cells that can provide a more reliable source of energy to older eggs. “The technique addresses a void now in IVF,” says Tilly. “No cell culture can circumvent poor egg quality or an egg that is simply too tired to execute what it is capable of doing. We are taking patients with a zero percent pregnancy rate, patients who have failed IVF because of poor egg quality, and getting them pregnant.”

The Rajanis had tried for four years to get pregnant, turning to fertility drugs, intrauterine insemination, and a naturopath before trying their first attempt at IVF. Natasha became pregnant once, but miscarried a few weeks later. “I tried to remain positive, thinking there is a light at the end of the tunnel, and that a baby will be there at the end,” she says of all the misses.

What finally made the difference wasthe population of her own egg stem cells. What makes these cells so enticing to scientists is that they come from the mother herself. Mitochondria contain their own DNA, and in a controversial decision the U.K. government recently approved so-called “three-person babies,” where mitochondrial DNA from a donor is introduced into the egg of a woman with mitochondrial disease. When the egg is then fertilized and results in a live birth, it can raise ethical questions, biological concerns and conflicts about parenthood.

With Augment, the cells used—and their mitochondrial genes—are from the mother’s own ovaries. Still, the FDA requested more studies on the effect of adding mitochondria, even from the mother who provides the egg, to the IVF process. OvaScience plans to conduct 1000 cycles using Augment this year, and generate more data that will help bring the procedure to the U.S.

Because the procedure is so new, some reproductive science experts are skeptical. What’s lacking, they say, is convincing evidence comparing pregnancy rates of women undergoing Augment to those with similar infertility problems who didn’t use the technique. So far, no formal clinical trials have been conducted; the only data on the procedure comes from recent presentations by Dr. Robert Casper of University of Toronto and Dr. Kutluk Oktay from Gen-ART IVF in Ankara, Turkey, both of whom are advisors to OvaScience.

“We’re not yet sure the scientific model has proven what the outcomes would be if you use the mitochondria of a younger egg, or from an egg stem cell,” says Davis of ASRM. “It’s a fascinating concept but we just haven’t seen the studies yet.”

In the world of infertility, however, such data are historically hard to come by. A lack of regulation of most reproductive technologies—the ones that don’t fall under the jurisdiction of the FDA as either drugs, devices or gene therapy—and the dominance of business-minded scientists has rushed new methods to clinics, often before their effectiveness has been fully proven.

Tilly counters doubters with evidence from other species that these cells can do what OvaScience has said they can. Egg precursor cells extracted from ovarian tissue from rats, mice, monkeys, pigs and women, for instance, have developed into immature eggs and, in the case of rats and mice, those eggs have mature and produced viable offspring. “Mitochondria from egg precursors rejuvenate the egg to bring it back to a high quality state,” says Tilly.

That appears to be the case with the Rajanis, and time will tell whether that ends up holding true for the other women trying Augment, too. “We see Zain as a symbol of hope for all couples struggling with infertility,” says Natasha. “While the process is long, emotional and physically draining, there is light at the end of the tunnel—and that light for us is Zain.”

For more on Zain and this new approach for infertility, see the May 18, 2015, issue of TIME.

TIME Sex/Relationships

Why Menopause Isn’t the Sex Killer You Thought It Was

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Oppenheim Bernhard—Getty Images

A woman's sex drive isn’t as affected by menopause as we once thought

Hormones are generally at the center of any discussion about sex. At puberty, the surge in estrogen and testosterone is responsible for the emergence of a sex drive, launching the most fertile period in our lives, while at the other end, a decline in hormones means a waning libido.

But we shouldn’t be so quick to blame that change in hormones, at least in women, say researchers led by Dr. Tim Spector, professor of genetic epidemiology at King’s College, London.

In a report published in the Journal of Sexual Medicine, Spector and his colleagues studied four years’ worth of answers that women provided about their sexual health both before and after menopause. It’s the first study to analyze how various domains in sexuality, including desire, arousal, orgasm, satisfaction and pain, interact with each other and change over time.

They expected that sexual drive and problems with sexual function would increase with time and be higher among women after menopause. But the rate of sexual dysfunction over the four-year study period was about the same—22% to 23%—for both pre- and post-menopausal women. That suggests that menopause, which marks the end of a woman’s reproductive years and is biologically triggered by a decline in estrogen levels, isn’t as important a contributor to sexual issues as once thought.

“We were surprised by the results a little bit,” says Spector. “They suggest that menopause has been exaggerated as an excuse for everything.”

What’s more, the proportion of women reporting improvements in sexual function during the study also remained about the same in pre- and post-menopausal women, hinting that declines in things like desire or arousal can be reversed to a certain extent. “Women do see improvements in sexual functioning after menopause,” Spector says. “What that says is that you are not necessarily stuck” if you experience sexual dysfunction.

The best predictor of how your sex life will change, in fact, is where you start. Women reporting issues with desire, arousal or orgasm at the start of the study, for instance, were more likely to continue to have those issues at the end of the study. But, as the results show, where you start doesn’t have to dictate where you end up when it comes to sexual function. “By modifying your life and attitudes about sexual desire,” Spector says, “you can change things sometimes surprisingly for the better, although you are getting older.”

TIME medicine

The Best Way to Quit Smoking Isn’t E-Cigs

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In the latest in-depth review of studies investigating which smoking cessation methods work best, experts say there isn’t enough evidence to support using e-cigarettes to kick the habit

The U.S. Preventive Services Task Force, a government-convened group of experts, says that if you want to quit smoking, you’re better off with drug-based methods, behavior modification programs or a combination of both—not puffing on e-cigarettes. There isn’t enough evidence to support claims that e-cigs, which have been touted as the latest way to wean people off tobacco, can actually help people quit.

The task force focused on studies that investigated how effective various smoking cessation methods are, for both adults and pregnant women. Drugs that address nicotine’s effects on the body, as well as nicotine replacement options, are better ways to quit, and the data suggest that they are even more effective if used together. In addition, behavioral interventions, including support groups and counseling sessions, can boost quit rates from 7-13% compared to rates of 5-11% among those who don’t use them.

MORE: E-Cigs Are Smokers’ Favorite Quitting Tool

“We have an embarrassment of riches in terms of a menu of things to offer patients who want to quit smoking,” says Dr. Francisco Garcia, director and chief medical officer of the Pima County Health Department in Arizona and member of the task force. “But every individual is different; some might respond better to behavioral therapy, some might respond better to varenicline, some might feel nicotine replacement is important to bridge them away from tobacco use.” For most people, it’s a matter of discussing with the smoker which method has the most appeal, and which one they are more likely to stick with long enough to go smoke-free.

But for certain populations, there isn’t enough data to support one strategy over another. Among pregnant women, for example, there haven’t been many studies to show how drug-based methods might affect the developing fetus, so it’s hard to determine if the benefits of quitting outweigh he risks represented by the medications. So for now, the task force advises that pregnant women rely on behavioral, non-drug strategies to help them stop smoking.

MORE: This Is The New Best Way to Quit Smoking, Study Finds

And for e-cigarettes, the data is sparse. The panel concluded that there was “insufficient” evidence to determine whether e-cigarettes improve or hinder quit rates.

TIME Longevity

Scientists Discover the Secret to Keeping Cells Young

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Researchers say it may be possible to slow and even reverse aging by keeping DNA more stably packed together in our cells

In a breakthrough discovery, scientists report that they have found the key to keeping cells young. In a study published Thursday in Science, an international team, led by Juan Carlos Izpisua Belmonte at the Salk Institute, studied the gene responsible for an accelerated aging disease known as Werner syndrome, or adult progeria, in which patients show signs of osteoporosis, grey hair and heart disease in very early adulthood.

These patients are deficient in a gene responsible for copying DNA, repairing any mistakes in that replication process, and for keeping track of telomeres, the fragments of DNA at the ends of chromosomes that are like a genetic clock dictating the cell’s life span. Belmonte—together with scientists at the University Catolica San Antonio Murcia and the Institute of Biophysics at the Chinese Academy of Sciences—wanted to understand how the mutated gene triggered aging in cells. So they took embryonic stem cells, which can develop into all of the cells of the human body, and removed this gene. They then watched as the cells aged prematurely, and found that the reason they became older so quickly had to do with how their DNA was packaged.

MORE: The Cure for Aging

In order to function properly, DNA is tightly twisted and wound into chromosomes that resemble a rope in the nucleus of cells. Only when the cell is ready to divide does the DNA unwrap itself, and even then, only in small segments at a time. In patients with Werner syndrome, the chromosomes are slightly messier, more loosely stuffed into the nuclei, and that leads to instability that pushes the cell to age more quickly. Belmonte discovered that the Werner gene regulates this chromosome stability. When he allowed the embryonic stem cells that were missing this gene to grow into cells that go on to become bone, muscle and more, he saw that these cells aged more quickly.

“It’s clear that when you have alterations in [chromosome stability], the process of aging goes so quickly and so fast that it’s tempting to say, yes, this is the key process for driving aging,” says Belmonte.

Even more exciting, when he analyzed a population of stem cells taken from the dental pulp of both younger and older people, he found that the older individuals, aged 58 to 72 years, had fewer genetic markers for the chromosome instability while the younger people aged seven to 26 years showed higher levels of these indicators.

MORE: What Diet Helps People Live the Longest?

“What this study means is that this protein does not only work in a particular genetic disease, it works in all humans,” says Belmonte. “This mechanism is general for aging process.”

Before it can be considered as the Fountain of Youth, however, Belmonte says new and better techniques need to be developed that can more specifically and safely alter the Werner gene in people, not just a culture dish of human cells. He also stresses that there may be other processes contributing to aging, and it’s not clear yet how important chromosome stability is compared to those factors. But, he says. “having technologies like this will allow us to determine how important each of these parameters are for aging.” And if the findings hold up, they could be first step toward finding a way to help cells, and eventually people, live longer.

TIME Diet/Nutrition

How to Block the Hunger Pangs When You Diet

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The hardest part of a diet are the cravings. That’s because dieting goes against the body’s developed-over-millions-of-years instinct to feed when energy levels drop. There’s a network of neurons that is exquisitely designed to sense when the body’s cells need more calories to fuel the metabolic, enzymatic, muscular, neurologic and sensory things they do. So when the body wants calories, we eat.

But what if it were possible to fool the body into thinking that it was full — without eating a bite?

Now scientists say you may be able to have your cake and not eat it — at least a little more easily. They worked with mice, but their findings could lead to new obesity treatments for people as well. In two papers published in Nature and Nature Neuroscience, researchers from different groups culminate a 15-year search for the specific nerve circuits in the brain responsible for hunger and satiety.

Scott Sternson, a researcher and group leader at the Howard Hughes Medical Institute’s Janelia Research Campus, investigated the signals that prompt us to eat. Do we eat to silence the negative sensations we get when we’re hungry? Or do we eat simply because we like the taste of food? Previous studies in animals suggests the latter, and the fact that we eat even when we’re not hungry also supports the idea.

But Sternson reports in Nature that his team found evidence it’s the desire to get rid of the unpleasant feelings associated with hunger that drives eating. Something called agouti-related peptide neurons (AgRP) are critical for regulating when animals eat. When calories dwindle and energy drops, AgRP are active, fueling appetite. “When we start to lose 5%, or 10% of body weight, that’s when these neurons are kicking in. And they are a big part of why most diets fail even though people do succeed in initially losing weight,” he says.

That may explain why diets go awry too. Sternson says AgRP nerves may not be active at the start of the diet, but as we lose weight, and the body senses that fewer calories are coming in, the neurons become more active, compelling us to fill up the missing calories and making us feel unpleasantly hungry all the time.

Sternson gave recently-fed mice mice different flavored capsules. Those flavors were associated each with either turning on or turning off the AgRP; when the mice were offered the flavored capsules again, they tended to favor the flavor they associated with when AgRP was turned on, and they felt hungry.

But when they did the same test on mice who hadn’t eaten in a while, the animals tended to favor the flavor linked to when AgRP was turned off — that’s when they didn’t feel the hunger pangs and the physical pain associated with hunger. Indeed, when they did more experiments that allowed them to peer inside the animals’ brains and see which nerves were active, the AgRP neurons started to quiet down as soon as the animals saw food, even before they began eating. But if the mice did not eat after seeing the food, the neurons would rev up again and remind the animals — painfully — that they hadn’t eaten.

But simply interrupting AgRP neurons wouldn’t be the safest way to support weight loss, says Dr. Bradford Lowell, professor of medicine at Harvard Medical School and Beth Israel Deaconess Medical Center and senior author of the other paper, published in Nature Neuroscience. Not only do AgRP neurons regulate appetite by driving animals to eat, but it also tries to conserve what energy remains by helping the body burn fewer calories. It signals the sympathetic nervous system, which controls things such as heart rate and blood pressure, to work less efficiently. And that could have negative effects on the heart.

The ideal situation would be to find something downstream of AgRP’s signaling that can be manipulated more safely. And that’s what Lowell spent the past 15 years doing. In his latest paper, he reports on a cluster of cells in the hypothalamus that might be just such a target. Unlike the neurons that trigger the heart-related symptoms when AgRP is activated, these nerves act as the hunger hub. Called melanocortin 4 receptor cells (MC4) hey are responsible, Lowell found, for feelings of satiety. Activating AgRP normally turns these cells off, so animals will feel the uncomfortable symptoms of hunger and start eating.

But one question that Lowell was keen on answering was whether animals eat to quiet down the hunger pangs of whether they simply eat because it activates reward and pleasure centers in the brain. By using the latest laser-technology that can activate specific neurons, they studied hungry mice and turned the MC4 cells on in one room and off when the mice wandered into another room, essentially tricking them into thinking they had just eaten, even if they hadn’t. Not surprisingly, the mice tended to spend more time in the room where the cells were turned on, and they felt “full.” “They were not eating any food but the mice chose to hang out in the room where their satiety signals were turned on. And they really liked it,” says Lowell.

But when they repeated the study with mice that had dined on chow, the results were different. This time, the mice didn’t show any preference and the satiety signals didn’t seem to affect them. That means that the animals ate mainly to get rid of the hunger pangs, and that given a choice, they would rather feel full.

That’s the same with people, and explains why diets are so hard to keep up. It’s a challenge to constantly fight the instinctive desire to quiet those hunger calls. But, says Lowell, it may be possible to manipulate the MC4 cells and fool the body into feeling the same satisfaction that comes with a full belly. “If we artificially turn on the downstream neurons of MC4, we are countering the adverse effect caused by AgRP being active. We are artificially removing the effect of the AgRP neurons on them,” he says.

And doing that, says Sternson, could help people who start a diet to stick with it. “We think it’s critical to understand all we can about these neurons, and how they control hunger when we start to loose weight. The more we understand the proteins that these neurons express, the more intelligently we can conceive potential treatment strategies,” he says. And those therapies might even make it possible to be hungry without feeling hungry, making them them the ultimate diet enabler.

TIME medicine

Hormone Treatments Raise Cancer Risk Even After They’re Stopped

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Estrogen and progestin therapy to treat menopause has led to controversial and confusing recommendations. But in the latest and longest term look at the data, experts say the risks of the hormones may last long after women stop taking them

Researchers admit that when it comes to hormone therapy — estrogen and progestin — to treat the symptoms of menopause for women, they don’t have a lot of consistent or convincing answers. They thought the medications could not only help menopause symptoms but also protect against heart disease, although some studies showed the added hormones could also raise risk of breast cancer. The resulting advice to women seeking answers about whether hormone therapy is for them has been anything but satisfying.

Now the scientists involved in the first large trial of hormone therapy, the Women’s Health Initiative (WHI), have continued to study those women who participated in the 1990s and found some surprising results. Reporting in the journal JAMA Oncology, they say that the risk of breast cancer for women taking the combination of estrogen and progestin remains the same seven to eight years after they stop the drugs than while they were taking them.

MORE: Hormone Replacement Therapy After Menopause: What Women Need to Know

The estrogen helps to maintain levels of that hormone as natural amounts start to drop during menopause, and the progestin protects the uterus from potential tumors arising from excess amounts of estrogen. They also found that for the quarter or so post-menopausal women who have had a hysterectomy, and can take estrogen alone, the hormone can lower their risk of breast cancer.

The WHI was created to study the health effects of hormone therapy on the millions of women taking them. Some small studies had suggested that the hormones could protect women from heart disease; women tend to have heart attacks about a decade or so later than men on average, and researchers believed some of that protection came from estrogen. But doctors were concerned about the known connection between estrogen and breast cancer, since during puberty estrogen contributes to breast tissue growth, and wanted to understand how the benefits for the heart matched up against the risks to the breast, so they enrolled more than 26,600 women aged 50 to 79 years in the WHI.

MORE: Estrogen After Menopause Lowers Breast Cancer Risk for Some Women

They intended to study them until 2005, but in 2002, they stopped the trial when it became clear that there was a group of women experiencing higher heart disease rates. It turned out that these were the women taking hormones, either the combination or estrogen alone.

MORE: The Truth About Hormones

The results completely changed menopause treatment, and led to a precipitous drop in the use of the medications; in the U.S., where about 40% of women turned to the hormones, only 15% did after most experts agreed that they should only be used in the short term, for about a year or so during and just after menopause. The assumption was that the benefits in lowering breast cancer risk would be similar — if women stopped taking the hormones, then their risk would decline.

That seemed to be true, at least for the first year or so after discontinuing the therapy. But in 2013, Dr. Rowan Chlebowski, an oncologist at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, and one of the initial investigators on WHI, reported that the benefit didn’t hold for long. He found that if women who had previously been on estrogen and progestin therapy were studied for more than eight years, their risk of breast cancer started climbing back up, to levels that were on par with when they were taking the medications.

That finding, however, contradicted other results from studies. And to make matters more confusing, the women who had had a hysterectomy, and no longer had a uterus so could take estrogen alone, did not seem to experience the same increased risk of breast cancer. All of this data prompted Chlebowski to do a more detailed analysis of the WHI data on women who agreed to continue to participate years after they stopped taking the hormone therapy.

MORE: Making Sense of Hormone Therapy After Menopause

In the current study, it’s clear that the combination of estrogen and progestin increases breast cancer risk, he says. The drop in risk that occurs immediately after the therapy is stopped is likely due to the changing hormone environment. Any small or emerging tumors that were already present before hormone treatment started may eventually start growing again years later.

For women who have had a hysterectomy, taking estrogen alone does not increase breast cancer risk and may, according to the latest results, even provide some protection against the disease.

“It looks like hormones have longer term lingering effects,” says Chlebowski. “For estrogen and progestin together, we see an increase in risk even years after you stop. But for estrogen alone, it looks like the hormone may be more favorable in reducing breast cancer risk than we thought before. The estrogen alone findings are now quite compelling that we may had to call lit risk reduction.”

The results should stress the importance of defining what menopausal symptoms are, and how much they interfere with women’s daily lives. Most health groups now recommend short term hormone therapy, but it’s clear that the risks of breast cancer remain even after exposure. So doctors and patients need to weigh the relief of symptoms against the unhealthy legacy of taking these medications. “There is a little more risk than we thought with estrogen and progestin,” says Chlebowski. “But it’s always difficult to figure out how to categorize that risk. It’s different for each woman.”

TIME Infectious Disease

An Experimental Ebola Drug Shows More Promise

TKM Ebola, which at least a few US and European health care workers may have received to treat their Ebola infection, is upgraded and proves effective in animal studies

When the Ebola outbreak hit last spring, there were a handful of potential treatments at the experimental stage in labs around the world. Some of them—like the drug TKM Ebola—that had shown promise in primates were given to U.S. and European health care workers who had been infected. Assessing how effective these drugs were in humans, however, posed some unique challenges.

That’s because many of the patients who got experimental treatments were also given a number of other therapies—making it impossible to know what was responsible for their recovery. But in a new paper published Wednesday, several of the scientists responsible for developing TKM Ebola, led by Thomas Geisbert of the University of Texas Medical Branch, report that the drug worked on all the monkeys it used it on, even after the monkeys were given a lethal dose of Ebola.

The animals exposed to Ebola that didn’t get the drugs all died at day eight or nine.

The study used an updated version of the drug that is made up of snippets of the Ebola virus’ genome encapsulated in fatty particles. The fragments bind to their matching counterparts on the circulating virus and become a genetic monkey wrench that prevents Ebola from copying itself and infecting more cells.

MORE: WHO Outlines Timeline for Experimental Ebola Drugs

It turns out that the virus responsible for the current outbreak in west Africa differs from the 1976 strain at three points in the Ebola genome, so Geisbert and his team adjusted the drug accordingly. That’s one of advantages of the TKM Ebola approach, he says, compared to therapies such as vaccines or other drugs that rely on antibodies to the virus. These regimens are designed to attack the broadest range of virus strains possible, but in doing so, they may give up some of their virus-fighting potency. With gene sequencing technology becoming more refined and accessible, however, having drugs that are specifically targeted against a particular strain of a virus is actually a realistic goal. “It’s especially important when you look at how big this outbreak is, and it’s continuing for over a year,” says Geisbert of such matched therapies. “With this technology, we could theoretically turn around a new treatment in something like weeks. This outbreak taught us a lot about how to prepare for the future.”

MORE: The Ebola Fighters

These results will still have to be repeated in human patients, to ensure TKM Ebola is both safe and effective, but they strongly hint that the drug could be a critical part of future anti-Ebola strategies. The company that is developing TKM, Tekmira Pharmaceuticals, is now testing this latest form of the drug in Ebola patients in Sierra Leone, west Africa.

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