TIME medicine

5 Ways to Make Binge Watching Less Terrible for You

Your brain will undoubtedly thank you for the one benefit of binge watching — not having to wait in suspense to see what happens next. But your body might not be so forgiving.

It’s time for season three of Orange Is the New Black on Netflix, so we know where most of you will be this weekend. If you must get your OITNB dose in one mammoth session on your couch, here’s some advice on how to break it up so at least some of health harms from all that sitting—the perils of which cannot be overstated—don’t come back to haunt you.

Get up halfway through each episode.

The latest data shows that getting up every 30 minutes (whether you’re binge watching or at your desk at work) can keep your metabolism from flagging and your heart muscle from getting too relaxed. You don’t have to run a mile but getting up and walking upstairs or downstairs can get your circulation going.

Go easy on the snacks.

Just keep enough around you to keep you sated through the next half hour—because, per above, you’ll be getting up anyway. But don’t eat nonstop, either. Have episode-on, episode-off rules for eating.

Don’t eat just chips and pizza and beer.

If it’s impossible to avoid the binge-watching staples, at least mix in a few fruits and nuts—which just got another thumbs up from a health perspective, or these veggies that are even healthier than kale. That will keep your taste buds occupied too and you won’t get bored eating the same thing for hours. And in case you are so inclined to snack on fries, read this: Should I Eat French Fries?

Drink water.

Side benefit — it will make you want to go to the bathroom more often, and that will force you to get up (see above). Skip soda, juice and even seemingly healthy beverages like coconut water and just grab yours from the tap. You, like most American kids, probably aren’t drinking enough of the stuff anyway.

Do something physical for 1 minute whenever your favorite character comes on.

Think of it like a drinking game, but with exercise. Use each appearance of your favorite prisoner to do a minute of jumping jacks. Or squats. Or lunges. Anything, in other words, that gets you off your butt and moving. Recent research shows that micro-workouts as short as 1 minute make a big difference when you add it all up.

TIME Diet/Nutrition

Mom’s Diet During Pregnancy Can Affect Child’s Lifetime Cancer Risk

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Expectant mother’s nutrition during pregnancy can have lasting effects on their children’s health, especially when it comes to cancer risk

In a new report published in the journal Genome Biology, researchers combed the genome to find regions that are particularly vulnerable to outside influences, such as diet, nutrition and environmental exposures, to determine how these factors might affect a developing fetus.

While the genes encoded in every person’s genome determines his characteristics, a second layer of genetic activity, called epigenetics, controls which genes are turned on and which are shut off, at different times in different cells. It’s epigenetics that is responsible for ensuring that a hair cell becomes a hair cell and not a liver cell, and so on. For the most part, these instructions are set during early development in the embryo.

But, as Robert Waterland, associate professor of pediatrics and molecular and human genetics at Baylor College of Medicine and his team found, there are discrete places in the genome where epigenetic changes are more vulnerable to external influences like diet. They conducted a genome-wide survey to find these regions, and then tried to match them up with easily measurable factors such as nutrition or mothers’ diets.

They did this in a population of women in Gambia, where changing seasonal availability of food allowed them to compare women who conceived during times when food was scarce, to those who conceived when crops were more abundant. Indeed, they honed in on a specific variant in a gene that is involved in suppressing tumors. When this gene is epigenetically activated, it leads to protection against cancer, but may lead to lower immune system function and this activation is influenced by a mother’s nutrition. Lower levels of vitamin B2 may contribute to inceeased cancer suppressing activity, and that may establish an lower risk for cancer among children while they are still in the womb.

“Very different maternal nutritional status nudges the distribution of the epigenetic state in one direction or the other,” says Waterland. “In the next phase of research we want to directly test whether individual epigenetic variations in fact leads to changes in the risk of diseases included cancer and immune-related conditions.”

What’s encouraging about the findings is the fact that in addition to the gene they studied in detail, the scientists also found 108 other genes that might be influenced by factors such as diet. Other such external contributors that Waterland is hoping to investigate are things such as mother’s obesity and the effect of IVF, in addition to environmental contaminants such as pollution or cigarette smoke.

TIME Brain

Mental and Social Activity Delays the Symptoms of Alzheimer’s

Rich Seymour—Getty Images

There’s evidence that such activities do little to change the underlying drivers of Alzheimer’s, but doctors say they delay symptoms

Among the many frustrations surrounding an Alzheimer’s diagnosis is the fact that there is little that patients can do to halt or treat the disease. While promising drugs are under development, the only advice physicians give patients is to stay as mentally active as they can — by learning new languages, reading, piquing the brain with puzzles, and maintaining their social life. Such constant stimulation is supposed to keep the healthy parts of the brain as unaffected by the disease for as long as possible. There’s also evidence that a lifetime of such activity can build up so-called reserves, which can compensate for brain functions when Alzheimer’s sets in.

In a report published in the journal Neurology, Dr. Keith Johnson from Massachusetts General Hospital and Harvard Medical School and his colleagues reveal that people who report higher levels of intellectual stimulation throughout their lifetimes don’t actually exhibit lower levels of protein plaques and other signs of Alzheimer’s compared to those who don’t. But they also found that staying mentally and socially active can push back the appearance of memory problems and other symptoms of Alzheimer’s.

So while the results don’t show that mental activity can affect the biology of Alzheimer’s in any way, it can have a meaningful impact on symptoms. And that is “huge,” says Dr. David Knopman, professor of neurology at Mayo Clinic College of Medicine, who reviewed the paper and recommended it for publication. “If that resulted in a year or two delay in symptoms across the population, that would be a huge effect.”

MORE: Many Doctors Don’t Tell Patients They Have Alzheimer’s

The study involved 186 healthy volunteers with an average age of 74 years who agreed to report their current and past cognitive activities, as well as undergo a brain scan to measure levels of the Alzheimer’s-associated protein called amyloid and the volumes of specific regions of the brain responsible for memory. The group reporting more intellectual activity over their lifetimes did not show lower levels of Alzheimer’s progression as those who reported less cognitive stimulation. But the former group were able to delay the appearance of symptoms, presumably because their stronger intellectual base compensated for the effects of the disease for a longer period of time.

“If two people had the same amount of Alzheimer’s pathology, and one had higher education and engaged in more cognitively stimulating activities, and one had lower educational attainment and didn’t participate in as many mentally stimulating activities, then the symptoms [of Alzheimer’s] would appear earlier in the person with less cognitively stimulating activity,” says Knopman.

MORE: This Alzheimer’s Breakthrough Could Be a Game Changer

While earlier studies relied on studies on autopsy brains to draw connections between cognitive activity and Alzheimer’s disease, this is among the first to investigate the connection in healthy living people, by using state-of-the-art imaging techniques to pick up protein deposits in the brain and following the volunteers to see if any develop the disease. Next up will be studies looking at whether picking up more cognitive activities after an Alzheimer’s diagnosis can have the same effect of slowing memory problems as having a lifetime of such skills.

TIME medicine

Woman Gives Birth After a Transplant of Her Own Frozen Ovarian Tissue

Case hailed as a scientific breakthrough

Over a decade ago, a bone marrow transplant left a Belgian girl infertile. Now, a transplant of her own frozen ovarian tissue has helped her get pregnant and give birth to a healthy baby boy, Sky News reports.

The scientific breakthrough is likely to benefit other sick children who lose their fertility through cancer treatments.

“Freezing ovarian tissue is the only available option for preserving their fertility,” Dr Isabelle Demeestere, a fertility specialist at the Universite Libre de Bruxelles, Brussels, told media. The details of the transplant were published in Human Reproduction, a medical journal.

The patient, who suffered from sickle cell anemia, was 13 when her ovary was frozen and she had yet to start her period.

A decade later, four pieces of the frozen tissue were transplanted onto the patient’s remaining ovary at her request. Two years after the transplant, she was pregnant, Sky News reports

Doctors reportedly expect the woman’s ovary function to remain normal, allowing her to have more children in the future.

[Sky News]

TIME medicine

The Next Big Drug to Treat Heart Disease

The Food and Drug Administration may soon approve blockbuster drugs that can lower cholesterol better than anything on the market today. Here’s what you need to know about the heart disease game changers.

There’s a well accepted dogma in heart disease: too much cholesterol flowing through the blood vessels can jam up heart byways and lead to heart attacks, stroke and other problems. So lowering cholesterol, by eating fewer high-fat foods or taking advantage of drugs that can keep levels under control, can protect you against heart trouble.

A drug that promises to drop cholesterol levels to unprecedented levels—some say to as low as those found in infants—has to be a good thing. That’s what a Food and Drug Administration (FDA) advisory committee decided after reviewing data on the first candidate in a new class of heart drugs since the cholesterol-lowering statins emerged in the 1980s. The committee looked at studies involving alirocumab, developed by Sanofi and Regeneron Pharmaceuticals, and will do the same for a similar compound, evolocumab from Amgen, on Wednesday. Another drug, developed by Pfizer, is further behind the approval process. All three belong to a new class called PCSK9 inhibitors, which work by pumping out more LDL cholesterol receptors on liver cells; these can pull cholesterol out of the blood like sponges and keep vessels clear of the artery-clogging fats.

The committee voted 13-3 to recommend approval of alirocumab, determining that it was safe enough and provided significant enough benefits over existing therapies that it should be approved. The FDA usually follows its advisory committee recommendations, but isn’t bound by the advice.

The recommendation isn’t a surprise given the encouraging data so far on the drugs, but it is a bit unusual because there aren’t any long-term data yet on how patients taking these drugs fare. Normally, the FDA likes to see studies that follow people taking heart drugs, for example, for several years, and that demonstrate that they have fewer heart-related events and are less likely to die from heart problems than people not taking the medications. But the PCSK9 inhibitors have a unique advantage on this issue that may have helped them shortcut that process.

Some people are born with mutations that make them deficient in the PCSK9 enzyme, which tends to eat up and degrade LDL receptors. These individuals are blessed with low LDL levels throughout their lifetime and don’t seem to show any other adverse health effects. “These people are effectively experiencing the functional equivalent of taking one of these drugs for their entire life,” says Dr. Elliott Antman, professor of medicine at Brigham and Women’s Hospital and Harvard Medical School and president of the American Heart Association. “They almost never get vascular disease and tolerate their low levels of LDL very well. So they were the inspiration for developing drugs that inhibit PCSK9.”

Further studies of the drugs that mimicked the effect of the genetic mutation showed that almost everyone taking them enjoyed a drop in LDL cholesterol levels of up to 65%. Some people in the trials have seen their LDL levels go down to 25 mg/dL or below; in previous guidelines, heart experts advised people without a history of heart events to aim for LDL levels of 100 mg/dL or below and for heart attack patients to shoot even lower, for 70 mg/dL or less.

“These drugs are a big deal,” says Dr. Steven Nissen, chariman of cardiovascular medicine at Cleveland Clinic who is leading a study on the Amgen drug to see if it can not only lower cholesterol, but actually reverse existing plaques in the arteries. The dramatic effect that PCSK9 inhibitors have on cholesterol is making doctors also rethink how they treat heart disease. The latest guidelines from the American Heart Association and the American College of Cardiology did away with target cholesterol levels, and the new class of drugs may support that trend, pushing doctors to advise patients to go as low—meaning as close to zero cholesterol in their blood—as they can.

“I think right now that will scare most people,” says Dr. Seth Martin, assistant professor of medicine and cardiology at Johns Hopkins School of Medicine. “But the science supports that it’s safe.”

The FDA would still have to determine for which patients the drugs should be prescribed. Some panel members recommended that the first indication include only those with genetic conditions that make them more vulnerable to abnormally high cholesterol levels, or those who can’t tolerate statins. Because statins are generally effective, the new drugs may also be recommended as second line therapy, to be used only after patients have failed to respond to statins, Unlike statins, which remain the best-selling prescription drugs in the U.S., the PCSK9 inhibitors need to be self-injected, either every two weeks or once a month.

If approved, even for a limited group initially, the drugs are likely to make their way into the broader-based heart-disease patient population—and quickly. “I have patients keeping an eye on this, who said to me, ‘This sounds pretty good, how can I get some now?’” says Antman. “They asked me to give them a call if it gets approved.” Not all of them have a genetic predisposition to high cholesterol levels, but, Antman notes, “they are sophisticated patients and say ‘I’ve had a good response to statins, so if I took this on top of the statin, I could cut my current LDL in half. Doesn’t that mean good things for reduction of my risk?’ And the answer is yes, it does.”

If the FDA does decide to approve alirocumab and other PCSK9 inhibitors, the agency will likely require the manufacturers to keep registries of patients using the drugs and monitor any side effects or other adverse events that may arise.

TIME medicine

See What Diseases You’re at Risk For Based on Your Birth Month

Researchers say there are sound and possibly scientific reasons to pay more attention to the month you were born in

“Whenever I present our work, I have to allow for laugh time,” says Nicholas Tatonetti, a scientist at Columbia University Medical Center.

Not a common practice for a serious academic researcher, but then again, Tatonetti studies something quite unfamiliar to those more accustomed to the intricacies of biological and molecular explanations for the human condition. “I study the month people were born in, to see if that changes their risk of developing disease in their entire lifetime,” he says. And in his latest report, published in the Journal of the American Medical Informatics Association, those results are pretty eye-opening.

By delving into the extensive database of patients seen at Columbia Medical Center over 14 years, beginning in 2000, Tatonetti and his team did a first-of-its kind look at whether birth month has anything to do with disease risk. Some previous studies have looked at the potential connection, but these investigations focused on individual conditions such as asthma and brain conditions, and therefore might have suffered from disease- or population-biases.

Tatonetti found that among 1,688 conditions for which patients were seen, 55 showed a strong relationship with birth month that could not be explained by chance alone. These included 20 conditions that were already described from previous, smaller studies, and 16 completely new associations. These included a surprisingly large number of heart-related diseases.

“Not only was it surprising that nobody had studied the relationship between heart disease and birth month yet, but we found not just one association but several with the same trend of increased lifetime risk of heart disease for those born in late winter and early spring,” says Tatonetti. “That’s suggestive of a mechanistic relationship, although we don’t yet know what that is.”

Earlier studies, for example, had connected birth in late summer or fall with asthma or respiratory problems, since mothers pregnant during the winter may be more likely to catch the flu or other respiratory infections. Tatonetti’s group is collaborating with 40 other institutions around the world to standardize patient electronic health records so the anonymized data can be studied for possible explanations of the birth month trends. The database will include environmental data as well, since it’s well known that environmental exposures — to things such as pollution, second hand smoke and more — can influence expectant moms and their developing fetuses.

He prefers to call what he does a study of seasonality rather than birth month. “Astrology puts a lot of stock on what month you were born in, and that really hurts this type of research, since there isn’t much scientific evidence to support that,” says Tatonetti. “But seasonality is a proxy for variable environmental factors present at the time of your birth, and we are learning more about the very large role that environment, and gene-environment interactions, plays in our development. This could be one way to start mapping out those gene-environment effects.”

To see which conditions you might be more vulnerable to developing, find your birth month in the wheel below.

Dr. Nick Tatonetti, Columbia University Medical Center

Read next: How Your Cat Could Make You Mentally Ill

TIME medicine

Memory Loss Not Caused By Cholesterol Drugs After All

Chris Gallagher—Getty Images/Photo Researchers RM

Some cholesterol-lowering drugs, called statins, could contribute to short-term memory lapses, but new data suggest that risk may not be real

About 25 million Americans currently take a drug to lower their cholesterol, so it’s no surprise that the most popular among them, statins, consistently top the list of best-selling prescription medications. But recent studies hinting that they were associated with memory problems have led some patients to shy away from them.

According to the latest data, though, there’s probably no need to avoid taking statins for this reason if a doctor prescribes them to protect against heart disease. In a report published in JAMA Internal Medicine, Dr. Brian Strom, chancellor of biomedical and health sciences at Rutgers University, and his colleagues say that while statins may contribute to short term memory issues, these tend to resolve over the long term and that such memory problems are not unique to the statins.

MORE: Who Really Needs To Take a Statin?

Previous studies had reported a possible connection between statins and memory loss, but those studies compared statin users to non-statin users. In his study, Strom included another group for comparison: people prescribed cholesterol-lowering drugs that were not statins. Among a large group of 482,543 statin users, 26,484 users of non-statin cholesterol-lowering drugs and 482,543 controls who weren’t on any drugs, Strom and his team found that both cholesterol-lowering drug groups showed short-term memory problems in the first 30 days after they started taking their medications compared to the controls. For statin users, the increased odds of memory lapses was four-fold, and for the other drug group, nearly the same, at 3.6-fold.

Because both groups taking drugs showed similar memory effects, Strom says that it’s unlikely that statins are uniquely to blame for the short-term cognitive issues. And because statins and the other cholesterol-lowering drugs work in vastly different ways, it’s also unlikely that the effect can be blamed on the drugs themselves. Strom proposes that the groups’ short-term memory issues, which were recorded by doctors in the patients’ medical records, is more likely the result of these patients simply being more aware of and sensitive to any changes in their functions after starting a new medication. In other words, people may have been having memory issues before they started their medications, and the problems might have occurred if they had not started taking them, but the symptoms became more noticeable because the users were more attuned to changes after filling their new prescription. The control group might have been experiencing similar memory issues but didn’t report them to their doctors; therefore, the issues might not have been recorded. “People on new medicines are more likely to notice a problem, more likely to blame problems on the drug and more likely to go back to the doctor and report these problems,” Strom says.

MORE: Statins May Seriously Increase Diabetes Risk

While it’s possible that the drug-taking group is also at higher risk to begin with for memory-related problems, since they have more potentially vessel-blocking cholesterol in their blood that can also impede blood flow to the brain, the results remained strong even after the group adjusted for risk factors such as diabetes and other blood-related conditions.

What’s more, Strom and his team also looked at users who might have been prescribed statins, stopped taking them because they were uncomfortable with the short-term memory issues, and then were prescribed them again at a later time. These patients did not report memory problems at the same rate, suggesting that the effect has less to do with the drugs themselves than with a hyper-vigilance for any changes associated with new drugs—the second time around, the drugs weren’t novel any more. “If the memory problems were real, we would expect that those who took statins for the second time would develop memory problems again,” he says. “The fact that we saw this as a problem so infrequently in this group suggests that it was more because the statins were a new drug the first time around.”

Based on the results, Strom says he informs his own patients that for some, statins may be linked to a short-term memory issue but that these tend to disappear over the long term. He also warns that even the short-term problems may not be a true effect of the drugs but rather a misinterpretation of the studies. “People should not steer away from statins because of a fear of short-term memory problems,” he says, “because they probably are not real.”

TIME medicine

Explaining ‘Epigenetics’: The Health Buzzword You Need to Know

Atomic Imagery—Getty Images

Getting a bad genetic draw from mom and dad is the most common way to inherit risks for diseases like cancer and heart problems. But there’s another way to pick up genetic changes that researchers are starting to pay attention to

Most of us get an introduction—whether we remember it or not—to genetics in our first biology class. We learn that genes, made up of DNA, are the molecular blueprint that make us who we are, and that this DNA code is a unique combination of instructions from both our mothers and fathers. Which genes we pick up from mom and which from dad is somewhat random, and that genetic roulette in turn determines, at least in part, which disease we’re most at risk for developing during our lifetimes.

But in recent decades scientists have learned that DNA alone is not destiny, and they’ve been focusing on another layer of genetic inheritance called epigenetics, which also play a role in determining what our DNA blueprints look like (more on that below). And in a new study published in the journal Cell, researchers show how it’s possible to pass on these epigenetic changes — which are not permanent alterations to the genome — created by exposure to things like tobacco, environmental pollutants and diet, as well as lifestyle behaviors.

What are epigenetic changes?

Every cell in the body contains the entire complement of genes it needs to develop properly — and that includes instructing liver cells to become liver cells and bone cells to function as bone cells and so on. How each cell knows to turn on the right genes in the genome to assume its correct identity involves epigenetics. Every gene is regulated by a region called the promoter, and epigenetics involves the process of turning specific genes on or off in particular cells. The most common way of controlling this gene expression is by plunking a molecule known as a methyl group on the promoter region. Where these methyl groups end up and how many of them crowd a gene on the genome determines whether that gene is turned on or off, and if it’s turned on, how much it is expressed.

What controls epigenetic changes?

This is a question that researchers are still trying to answer, but some of the leading candidates include exposure to things like tobacco and environmental pollutants. Diet may play a role as well as things like stress.

Can these epigenetic changes be passed from parent to child?

Studies show that some epigenetic changes might be transmitted from one generation to the next, but, says Azim Surani of the Wellcome Trust/Cancer Research Gurdon Institute at the University of Cambridge, and senior author of the Cell paper. “It’s still an open question to what extent that happens.”

In his latest study, Surani and his colleagues studied how egg and sperm, known as germ line cells, are formed in an embryo. They found that these cells undergo a type of epigenetic erasure, in which any methyl groups added from the mother’s egg and the father’s sperm are removed, so the growing fetus can create its own, tabula rasa egg or sperm, depending on its sex.

“I would say this is an extremely robust erasure mechanism that’s unique to the germ line cells,” says Surani. “It’s really designed to clear out the epigenetic information before transmission of the genome to the next generation, almost like it’s trying to clean out the genome and prevention transmission of so-called aberrant epigenetic information being passed on.”

But about 5% of the methyl changes aren’t wiped out, and these escapees, as Surani calls them, may explain how some epigenetic changes re-appear in the offspring of parents, even if they aren’t permanent alterations to the genome but more like external modifications to how genes are regulated — similar to a renovation of a house whose original structure and layout remain the same.

Are there benefits or risks of having epigenetic changes passed from parent to child?

Surani’s results raise interesting questions about why epigenetic changes might be “inherited” in the first place.

Of the changes that they documented in the small sample of human embryos they studied, as well as among mice, they found that a certain core of genes may preferentially escape from the epigenetic cleansing. These genes are predominantly involved in nerve and brain cell function, as well as metabolic conditions, so they could preferentially impact conditions such as obesity and schizophrenia.

More work needs to be done before the exact role of epigenetics, and de-methylation, might play in these conditions, but the findings do point to an other potential contributor to these conditions, and possibly some helpful therapies.

But any epigenetic-based treatments are still a ways off, Surani says, since there is still a lot about methylation and de-methylation that remains a mystery. In addition to orchestrating which genes turn on and off and when, for example, methyl groups also have a very critical role in sitting on so-called jumping genes, or the dark matter of the genome. These are portions of DNA that are more mobile when the twisted strands of DNA open and close when cells divide. As they move around, these elements can cause mutations if they land in important genes and disrupt their function. Of the 5% of methylation that doesn’t get erased, most of it, says Surani, involves this dark matter of the genome.

So is that good or bad?

It may be that having some epigenetic changes escape from one generation to the next is a good thing, a defense mechanism of sorts, although what the right balance is for how much of the methyl groups should remain isn’t clear yet. “Future studies will start to illuminate some of the questions that these results raise now,” says Surani.

TIME medicine

The Vaccine for Type-1 Diabetes Is Moving Forward

A promising vaccine to reverse type 1 diabetes heads to a next level trial

A promising vaccine that has the potential to reverse the symptoms of type I diabetes—an autoimmune disease often diagnosed in childhood—is heading on to a phase II trial, which will test the vaccine on humans with the chronic disease.

The vaccine, called bacillus Calmette-Guérin (BCG) has succeed in reversing type 1 diabetes in a trial among mice and in a phase I trial in 103 humans. The new trial, which the researchers announced on Sunday at the Scientific Sessions of the American Diabetes Association, will last for five years and will test the effect of the vaccine on people with type 1 diabetes among adults between ages 18 to 60. The vaccine may be able to improve the disease in people who have small but detectable levels of insulin coming from their pancreas. Lead researcher Dr. Denise Faustman, director of immunobiology at Massachusetts General Hospital (MGH), estimates that about one million people with type 1 diabetes still produce some insulin.

BCG is already FDA-approved as a vaccine for tuberculosis and as a bladder cancer treatment. Researchers have shown that the vaccine can eliminates problematic white blood cells that lead to type 1 diabetes by destroying the beta cells that make and release insulin into the blood.

Previously, the study authors showed they were able to temporarily eliminate the abnormal white blood cells and provide a small return of insulin. The new trial will provide more frequent doses of the vaccine over a five year periods in 150 adults with the disease. The researchers hope that the vaccine will produce better blood sugar control and could be used to treat advanced disease.

“Type 1 diabetics are a pretty skeptical audience,” says Faustman. “There’s been a lot of disappointment [from other research].”

Faustman says the trial is ambitious because it is focusing on people who have had type 1 diabetes for many years. Other research has looked at treating people with diabetes close to diagnosis. Faustman says that the trial will also help determine what type of dosing may be needed for the vaccine to be successful.

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