TIME Diet/Nutrition

How to Block the Hunger Pangs When You Diet

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.

TIME medicine

Vaccines Don’t Cause Autism, Even in Kids at Higher Risk

"We are able to look at the vaccines and show there is no association with autism"

In the latest study on the vaccines, researchers find even more evidence that childhood immunizations aren’t linked to autism.

In a study published in the Journal of the American Medical Association, a group led by Dr. Anjali Jain of the Lewin Group, a health care consulting organization, found that brothers and sisters of children with autism were not at any higher risk of developing the disorder if they were vaccinated compared with brothers and sisters of those without autism.

Numerous studies have found an increased risk of autism among those with older siblings with the condition, and some parents who believe that their older child’s autism is connected to vaccinations, specifically the MMR vaccine, have been reluctant to immunize their younger children. Indeed, Jain found that vaccination rates among siblings of autistic children were lower, at about 86% at 5 years, compared with 92% among those without autistic brothers or sisters.

But among the 95,000 children with older siblings included in the study, children who received the MMR and had autistic older siblings were no more likely to develop autism than children who were vaccinated and didn’t have any autistic older siblings. In fact, the relative risk of autism among those with older autistic brothers or sisters was lower if they were vaccinated compared with those who were not vaccinated.

“Our study confirmed that in kids with older siblings who we know are at increased risk of developing autism themselves, those kids are being vaccinated less,” says Jain. “But in the kids who did develop autism who were vaccinated, there was no increased risk from the vaccine compared to kids who did not get the vaccine.”

The results, she says, should put to rest any concerns that parents of autistic children might have that vaccinating their younger kids will somehow increase their risk of developing autism. The large size of the study, and the fact that vaccination and autism information wasn’t collected for purposes of a vaccines-and-autism study but as part of a larger health insurance database, also reinforce the strength of the findings. (The Lewin Group is an editorially independent part of Optum company, which collected the data.)

“We may not understand what is causing autism in these kids or families,” says Jain. “There could be a host of both genetic and environmental factors. But we are able to look at the vaccines themselves and show there is no association with autism.”

Read next: HPV Vaccine May Work for People Who Already Had the Virus

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TIME medicine

This Is a Baby’s Brain on Pain

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For the first time, scientists map newborn babies’ brains on pain, and the results are surprising

In a first, researchers at Oxford University have watched infants as young as a day old as their brains process a light prodding of their feet. The results confirm that yes, babies do indeed feel pain, and that they process it similarly to adults. Until as recently as the 1980s, researchers assumed newborns did not have fully developed pain receptors, and believed that any responses babies had to pokes or pricks were merely muscular reactions. But new research published Tuesday morning changes that.

Taking advantage of the fact that newborns less than a week old tend to sleep through anything, Rebeccah Slater, an associate professor of pediatric neuroimaging at Oxford, and her colleagues placed 10 infants who were 1-6 days old in an fMRI machine. The researchers, who reported their findings in eLife, observed which areas of the infants’ brains became more active, or consumed more oxygen, as the scientists lightly poked their feet. They did the same for adults and compared the brain images.

In adult brains, 20 regions were activated by the painful stimulus, and the newborns shared 18 of these. “The infant’s brain is much more developed than I was expecting,” says Slater. “I might have thought that some information might have gone to the sensory areas of the brain — telling the baby something was happening on the foot, for example — but I didn’t necessarily think it would go to areas more commonly involved in emotional processing such as the anterior cingular cortex, which is thought be involved in the unpleasantness associated with an experience.”

Even at birth, then, a baby’s brain possesses the foundation for quickly evaluating anything he or she experiences, including painful stimuli. “I hope this provides incentive to more researchers to find better ways of measuring pain in babies, and prioritize the importance of providing the best pain relief possible in children,” says Slater.

Slater found that newborn brains are still immature in some ways, however. Any stimulus, whether it’s a painful one or a sensory one such as a smell, tends to activate widespread regions of the brain. That signals that the baby’s brain is still trying to learn what’s what and distinguish different stimuli. The poking triggered even the newborns’ olfactory system, for example, even though the sensation had nothing to do with smell.

Second, babies tend to register all stimuli as having the same intensity. Even light pokes “feel” the same as harder ones, reflecting their still inexperienced system in distinguishing levels of activation.

But the fact that they are experiencing pain in almost the same ways as adults do is very revealing. Now that there’s evidence that the brains of babies do indeed process pain, that may change the way doctors treat newborns, especially those who are premature or need extra medical attention in the neonatal intensive care unit. In a recent study, scientists tallied an average of a dozen procedures including needle sticks that babies experienced every day; more than 60% of those infants did not receive any pain medication, either in the form of a topical numbing cream or other pain relief. Having these experiences may make these babies more sensitive to pain later in life, says Slater. A study of circumcised baby boys, for example, found that those who received pain relief felt less pain when getting vaccinations three months later than those who didn’t receive any pain medication.

“Now that we have seen for the first time what is happening in babies’ brains while they experience something mildly painful,” says Slater, “there should be a big drive to try to treat pain in these children, especially those having a high number of procedures performed in their early days.”

TIME medicine

Smokers Don’t Think a Few Cigarettes Will Harm Their Health

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Nearly everyone knows that smoking is harmful for your health. But some refuse to admit that their habits may be killing them

Heart disease, lung cancer, throat cancer, diabetes—the list of bad things that smoking does to your health is long and growing longer. Thanks to public health warnings and education campaigns, most of us have heard that cigarettes can be dangerous to your wellbeing and can shorten your life.

But one group who should be getting that message loud and clear may be in a bit of denial. In a study of more than 1,600 French smokers and non-smokers, 34% said that lighting up 10 cigarettes a day would not put them at higher risk of lung cancer. And fewer than 40% knew that their risk of lung cancer wouldn’t disappear if even if they quit smoking. The results were presented at the European Lung Cancer Conference in Geneva, Switzerland.

“The fact that one third of subjects wrongly considered that a daily consumption of up to 10 cigarettes was not associated with any risk of lung cancer is particularly impressive and threatening,” writes study author Dr. Laurent Greillier from Aix Marseille University in response to questions about the findings.

The results were especially worrisome since the participants in the study were 40 years old to 75 years old and therefore spent most of their adult lives hearing strong public health warnings about the dangers of smoking. That means that while anti-smoking campaigns have been effective, they may not have educated people deeply enough about the dangers of tobacco. That’s especially true for people who engage in what they consider to be “safe” or “light” smoking, the study finds. “Our results suggest that public health policies must continue to focus on the tobacco pandemic, and notably initiate campaigns concerning the risk of any cigarette,” says Greillier.

TIME medicine

The Strange Way a Diabetes Drug May Help Skin Scars

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We all form scars, but most of us don’t want them. There may soon be a way to make them disappear

We all have them — scars that won’t let us forget the spill we took off a bike, the burn we got from a hot stove, or even the legacy of radiation therapy. Scarring is a good thing in some ways — it’s the body’s quick response to a deep injury, its way of protecting and sealing up the wound to keep infections and other noxious agents away.

Now scientists led by Dr. Michael Longaker, co-director of the Institute for Stem Cell Biology and Regenerative Medicine at Stanford University, report in the journal Science that they have teased apart the molecular steps behind scarring, and also discovered a way to inhibit them from forming.

While training to become a plastic surgeon, Longaker operated on fetuses still in the womb and became intrigued by the fact that they did not scar; any incisions surgeons made disappeared practically without a trace. Why, if babies did not change their genes from the womb to the time they are born, do infants form scars?

Working with mice, the team focused on two kinds of fibroblasts, which are cells responsible for maintaining the structural integrity of organs, tissues and more. One is primarily responsible for wound healing, and the formation of tumors like melanoma. “This type of fibroblast starts out as less than 1% of the developing skin, but by the time an animal is a month old, it’s 80% of the fibroblasts in skin on the back of the animals,” he says.

When he treated the cells with diphtheria toxin, which destroys the fibroblasts, the animals scarred less. It turns out that these fibroblasts carry a marker on their surface that helps scientists to pick them out. And even more fortuitous, there is a drug approved for treating type 2 diabetes that inhibits the work of this marker.

In the mice, the drug reduced scarring but did not compromise the integrity of the wounded skin at all, making it a promising potential treatment for scar in people. Each year in the US people get 80 million operations, the bulk of which require incisions that leave a mark, not to mention the millions more who get cuts or scrapes during accidents or who develop fibrous tissue after radiation to treat cancer. If the scar-inhibiting drug is used on those wounds before they begin to heal, says Longaker, it’s possible they won’t leave a scar.

Whether the same could be true of existing scars isn’t clear yet. But he says that doctors may be more eager to do revision surgery to minimize scars if such a compound exists. And, if the results are repeated and confirmed, doctors may be able to reduce scars not just for cosmetic purposes but for medical ones as well, such as in the heart after a heart attack, following spinal cord injury and in deep tissues treated with cancer-fighting radiation.

TIME medicine

The Scary Connection Between Snoring and Dementia

Sleep disorders, including sleep apnea and snoring, can have harmful effects on the brain over the long term

If you don’t snore, you likely know someone who does. Between 19% and 40% of adults snore when they sleep, and that percentage climbs even higher, particularly for men, as we age. It’s a nuisance for bed partners, but researchers say we shouldn’t be so quick to write off snoring or other forms of disrupted breathing while asleep as mere annoyances; instead, they could be affecting the brain, according to new research.

Snoring is a form of sleep apnea, in which people stop breathing for a few seconds or several minutes dozens of times in an hour. Any disruption of breathing during sleep can affect the brain, say researchers of a new study published in the journal Neurology. They found that people with sleep apnea tended to develop memory problems and other signs of mild cognitive impairment (MCI) earlier than people without such sleep disorders.

MORE The Power of Sleep

Ricardo Osorio, MD, research assistant professor of psychiatry at NYU Center for Brain Health, and his colleagues studied 2,000 people enrolled in the Alzheimer’s Disease Neuroimaging Initiative (ADNI)—a population of 55 to 75 year olds, some of whom are cognitively normal, some who have mild cognitive impairment and others who have Alzheimer’s dementia. Everyone was asked about their snoring or sleep apnea, and researchers followed up every six months for two to three years to record any changes in their cognitive status.

Those who reported having sleep apnea or snoring tended to develop signs of mild cognitive impairment, including memory lapses and slower speed on cognitive skills, about 12 years earlier on average than those who didn’t report any sleep-disordered breathing. Mild cognitive impairment often precedes Alzheimer’s dementia, but not all people who develop MCI go on to get Alzheimer’s. The connection between disrupted sleep breathing and MCI remained strong even after Osorio accounted for the effects of Alzheimer’s-related genes, gender, education, depression and heart disease risk factors, all of which have been associated with increased risk of cognitive decline.

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

Osorio also saw a connection between sleep apnea or snoring and Alzheimer’s dementia, but it wasn’t as robust as the link to MCI. That might be because other studies have found that not only are sleep disorders a risk factor for Alzheimer’s, but they are also a symptom of the degenerative brain disease—so those who already developed Alzheimer’s dementia may not have been accurately reporting their sleep habits.

Osorio is careful not to implicate all snoring as a precursor to memory problems or Alzheimer’s. But particularly in the elderly, he says doctors should consider the potential effect that disrupted breathing during sleep can have on the brain. While it’s not clear how sleep disorders might be increasing the risk of MCI or Alzheimer’s, it’s possible that the cumulate effects of even the short periods when the person isn’t breathing could deprive brain neurons of critical oxygen, and Alzheimer’s has been linked to slower or abnormal blood flow caused by hypertension and high cholesterol levels. Other studies have also shown that the protein responsible for Alzheimer’s, amyloid, tends to build up during the day when the nerves are active and decline at night during deep sleep. If people are being roused from deep sleep by their apnea or snoring, then they aren’t enjoying prolonged periods of low amyloid production, so the substance can build up and potentially form plaques.

MORE Here’s How Much Experts Think You Should Sleep Every Night

Osorio also found that it’s possible to counteract some of the effects of sleep apnea or snoring. He also studied people who used a device to prevent apnea, known as a continuous positive airway pressure (CPAP) machine, which keeps airways open during sleep. Even though they snored or had sleep apnea, people who used the device developed MCI or Alzheimer’s at the same rate as those who didn’t have these sleep problems. CPAP machines are cumbersome and uncomfortable to use, and many people drop them after a few weeks. But, says Osorio, they may have more reason to stick with them now. “A lot of people don’t use them because they see no benefits,” he says, “but if they know it can improve their memory, they may definitely try to do better.”

Read next: 7 Signs You’re Not Getting Enough Sleep

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TIME Heart Disease

What Divorce Does to Women’s Heart Health

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When it comes to the fallout from a divorce, one spouse is harmed more by it’s biological and psychological effects on the heart

Dissolving a marriage is hard on everyone, but researchers say the psychological stress of a divorce can have serious physical effects on the heart, especially for women.

Women who divorced at least once were 24% more likely to experience a heart attack compared to women who remained married, and those divorcing two or more times saw their risk jump to 77%. In the study published in the journal Circulation: Cardiovascular Quality and Outcomes, Matthew Dupre of Duke University and his colleagues found that men weren’t at similar risk. Men only saw their heart attack chances go up if they divorced two or more times compared to men who didn’t split with their spouses. If men remarried, their heart risk did not go up, while for women who remarried, their chances of having a heart attack remained slightly higher, at 35%, than that of divorced women.

MORE: Divorce More Likely When Wife Falls Ill

These findings remained strong even after Dupre’s team adjusted for other potential contributors to heart attack, including age, social factors such as changes in occupation and job status and health insurance coverage, and physiological factors including body mass index, hypertension and diabetes. Previous studies have found links between divorce or widowhood and heart disease that were explained, at least in part, by changes in people’s access to health care and their ability to keep up healthy eating and exercise habits.

But these are the first results from tracking people over a longer period of time—18 years—to capture the cumulative effects of changes in marital status, says Dupre. “We looked at lifetime exposure to not only current marital status, but how many times someone has been divorced in the past. What we found was that repeated exposure to divorce put men and women, but particularly women, at higher risk of having a heart attack compared to those who were married.”

MORE: Study: Marriage is Good For The Heart

And it wasn’t simply changes in health insurance coverage or financial status resulting from the divorce that explained the higher heart risk. Even after Dupre’s group accounted for these, the relationship held. While he admits that the trial did not investigate exactly how divorce is seeding more heart attacks, other studies hint at a possible explanation. Dramatic life changes such as divorce, which signal an end to not only a significant relationship but potentially to stable financial and social circumstances as well, can lead to spikes in the stress hormone cortisol, which in turn can push blood pressure, cholesterol and blood sugar to unhealthy heights.

The long term scope of the study revealed the impact that social and life events can have on the physical functioning of the body. “The health consequences of social stresses are real,” says Dupre. For women, the 77% higher risk of heart attack connected to multiple divorces was on par with well-established factors such as hypertension (which boosts risk by 73%) and diabetes (which elevates heart problems by 81%).

MORE: Do Married People Really Live Longer?

That’s doesn’t mean, of course, that women should avoid getting divorced to save their hearts. “Another way to put it is to say that women who are stably married are at an increased advantage of preventing heart attacks than women who may have had to go through transitions where they weren’t,” says Dupre.

It also makes a good case for doctors including discussion about potential stressors, including lifestyle and social circumstances, in their health assessment of patients. Recognizing that divorce may be a life event that can contribute to higher heart attack risk, for example, they can monitor patients experiencing divorce more carefully, and be alert to the first signs of potential problems with cholesterol, blood pressure or blood sugar. “Understanding all of the factors that lead to a physiological response are equally important,” says Dupre. And potentially life saving.

TIME medicine

How Traumatic Life Events During Childhood Affect Diabetes

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Researchers say that traumatic life events can play a role in raising risk of type 1 diabetes

Type 2 diabetes tends to get more attention than type 1, mainly because the risk factors for type 2—obesity, for instance—are thought to be more in our control. Type 1 is believed to be primarily a genetic disease, triggered by an unfortunate DNA configuration that signals the body’s immune system to destroy insulin-producing beta cells.

Now, in a report published in the journal Diabetologia, Dr. Johnny Ludvigsson, a pediatrician from Linkoping University in Sweden, and his colleagues say that life events, including traumatic experiences such as the death of a family member or a serious accident, can triple the risk that young children have of developing the disease.

The researchers studied 10,495 families with children born between 1997 and 1999 and asked them to participate in at least one of four follow-up sessions when the children were between two and 14 years old. The parents filled out questionnaires about whether the children had experienced anything that might be considered a serious life event, including things like the death of a family member, a new sibling, divorce or a move. Parents were also asked about their own stress and whether they felt they had social support.

Once the scientists adjusted for factors that also contribute to type 1 diabetes, such as BMI, mother’s age and a history of diabetes in the family, children who experienced deaths and accidents in their early years showed a three-fold higher risk of developing diabetes than those who didn’t live through these events.

“People may be worried and have feelings of guilt that not only did their child get diabetes, but that in a way they contribute to it,” says Ludvigsson of the results. But parents should take some solace in the fact that after he adjusted for other factors that can contribute to type 1 diabetes, including BMI, mother’s age at child’s birth, and family history of diabetes, events such as divorce, new siblings and other changes in the family structure weren’t as strongly associated with an increased risk for the disease.

What may be happening is that some children may have a genetic predisposition to developing type 1 diabetes, but these genetic triggers aren’t “activated” unless they experience some extreme stress or trauma, such as the death of a loved one. Biologically, scientists believe that high stress situations may lead to a boost in the hormone cortisol, and that pushes the beta cells that produce insulin to work harder and release other potentially toxic factors as well. The added influx of insulin may be viewed by the immune system as abnormal and undesirable, which may prompt them to start attacking the beta cells and destroying them.

“This study does not say that you should never divorce,” says Ludvigsson. “But stress from life events can be one factor that influences the immune balance, just like many other factors do, like sleep, physical activity and so on.” Which highlights the need to address traumatic experiences and children’s reactions to them. Supporting families that go through difficult times, whether caused by marital conflicts or financial worries, could also be an important way to keep young children even healthier and to avoid certain chronic diseases. “If society could be a bit supportive, we could perhaps save some families and relationships, and that would be good for the children,” says Ludvigsson.

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