TIME Cancer

Genetic Test Impacts Chemo Choices In Surprising Ways

Maciej Frolow—Getty Images

A study investigates for the first time how a gene-based test is affecting women’s decisions to get chemotherapy

Correction appended, Aug. 31, 2015

In the new era of personalized medicine, having more information on hand is considered the ideal situation for making more customized, and ideally, effective decisions about medical care.

And in a new study of breast cancer patients, researchers show that a relatively new genetic test for evaluating tumors is doing just that. It’s just that the test isn’t necessarily leading to the decisions that experts expected.

The Oncotype DX Breast Cancer Assay is a test launched in 2004 to help women decide how likely their breast cancer is to recur. The score, from zero to 100, is for women with breast tumors that have not spread to the lymph nodes. It places women on a scale of probability, based on an analysis of 21 genes in her tumor. Most doctors and patients use the score to decide, in part, whether the woman should receive chemotherapy following surgery.

MORE: A Major Shift in Breast Cancer Understanding

In previous studies, about 20% to 30% of doctors say they changed their recommendation about chemotherapy based on the Oncotype DX score. But none of the studies looked at how Oncotype DX affected the likelihood a woman would undergo chemotherapy rates in a real-world setting— outside of a trial. In clinics, says Michaela Dinan, assistant professor in medical oncology at the Duke Cancer Institute, many other factors contribute to treatment decisions, including fear, family history and physician advice. So she and her colleagues conducted a review of data on more than 44,044 breast cancer patients to see how the Oncotype test affected chemotherapy decisions.

MORE: Here’s the Amount of Exercise That Lowers Breast Cancer Risk

The results, published in JAMA Oncology, showed that overall, the test had no effect on their decision. Women who were tested were no more or no less likely to opt for chemotherapy than those not getting Oncotype DX. Younger age and a higher risk disease were more likely to predict chemotherapy use than the assay.

While many assumed that the test would lead to fewer treatments, Dinan’s data shows that how the testing affects chemotherapy decisions is less predictable. When Dinan delved further into the numbers, she found an interesting pattern. Those rated as having high-risk breast cancer according to the National Comprehensive Cancer Network guidelines were less likely to get chemo than women who were not tested. And among people with low-risk disease, those getting the genetic test were more likely to get chemotherapy than low-risk patients who did not.

Because the study did not take into consideration what the Oncotype DX scores were, it’s possible, for example, that women considered high risk who received intermediate or low Oncotype DX scores decided not to undergo chemotherapy since the testing showed their response might not be as positive as they might have expected. On the other hand, women who have low risk disease and receive an intermediate test score might decide to undergo chemotherapy since the intermediate risk might represent a slightly higher risk of recurrence than they were anticipating.

“It’s a more nuanced finding,” says Dinan. “The Oncotype DX test is impacting the receipt of chemotherapy, but the impact isn’t in one direction or another in terms of whether people are more or less likely to get chemotherapy.”

As more options for personalized treatments make their way into the clinic, Dinan says it’s worth remembering that they shouldn’t dictate decisions but inform them. “The nuanced finding of the difference between high risk and low risk patients says to me that whether or not a woman with early stage breast cancer undergoes chemotherapy is going to be affected by a number of different factors, not just this assay. It’s a personalized discussion about the individual patient’s case.”

Correction: The original version of this story misstated that the Oncotype DX test is FDA approved. It is a commercial test regulated by different laboratory guidelines.

TIME Cancer

How Doctors Cured This Woman’s Brain Cancer

MaryAnn Anselmo Memorial Sloan Kettering
Christopher Morris—VII for TIME MaryAnn Anselmo in New York City on March 13, 2015

Earlier this year, TIME explored the promise of precision medicine in treating cancer patients. We featured one woman who was taking a drug typically used for melanoma to treat her brain tumor. Here’s an update on how she’s doing

In November 2013, MaryAnn Anselmo—who was on the cover of TIME in March—heard the words that most of us dread the most: she had cancer. Worse, it was stage 4 glioblastoma, a particularly aggressive brain tumor that often takes a patient’s life in a matter of months. Having just recovered from a devastating car accident, Anselmo thought, “Somebody wants me dead here.”

Nearly two years later, the New Jersey resident is receiving some completely different, and more welcome news. “The latest scan doesn’t show any tumor any more,” her physician, Dr. David Hyman, acting director of Developmental Therapeutics ad Memorial Sloan Kettering Cancer Center (MSKCC), tells TIME. The results from Hyman’s most recent study, which Anselmo participated in, is published in the latest issue of the New England Journal of Medicine (NEJM).

“I’m tired all the time,” she says, “but I’m dealing with it, living with it. I feel awesome compared to what this tumor could have done to me.”

MORE: The Cancer Gap

Hyman is reluctant to call it a “cure” for certain cancers—the burden of proof is higher than this one study or this one patient—but Anselmo’s cancer is gone. And for that, Anselmo can thank something called a basket trial, a new way for doctors to test promising cancer treatments that more precisely target the right therapies to the right patients at the right time. This is the first such trial of its kind.

The trial puts the idea of precision medicine to the test. At 23 cancer centers around the world, 122 patients with advanced cancer signed up for a last-resort treatment covered in the new study. All had their tumor genomes sequenced, so doctors could get a better sense of which mutations were driving the cancers, and whether there were any targeted therapies for those mutations.

Anselmo had three mutations fueling the growth in her brain, but she and her doctors at MSKCC decided to focus on one, called BRAF. A recently approved drug to treat BRAF mutations in melanoma helped shrink or halt tumor growth in half of treated patients, so doctors wanted to know whether the drug could help patients with the same mutation but with different kinds of cancer, like Anselmo. But while BRAF mutations occur in about 50% of melanoma cases, they are much rarer in other types of cancers. So creating a trial for patients like Anselmo would take both time and money that researchers couldn’t justify.

A basket trial, however, capitalizes on the growing understanding that cancers should be characterized by not just where they start (in the breast, colon or lung, for example) but also by how they grow — which mutations are driving them. A basket trial collects patients, all of whom have BRAF mutations, for instance, but who might have different types of cancer.

In the NEJM study, patients with non small cell lung cancer, colon cancer, thyroid cancer, multiple myeloma and, glioblastomas, among others, were included. By studying them as a group, Hyman says it’s possible to get a better idea of how feasible it is to target mutations like BRAF among those who don’t have melanoma.

So far, the results are encouraging. Patients with non small cell lung cancer seemed to have the best response rate to vemurafenib, 42%, after a year. More than 70% of the patients with this cancer saw their tumors shrink by at least 30% in length. There were promising signs that patients with the other, untreatable cancers also responded and took longer before their tumors progressed than they would have without the experimental therapy.

Anselmo was among the extraordinary responders. “It is unusual,” says Hyman of the apparent shrinkage of her tumor. “She really is an outlier in any way you measure it.”

NEJM 373; 8; 2015. Courtesy Dr. David Hyman: Anselmo’s brain tumor at the start of the study in 2014 (left) and on Aug. 11, 2015 (right)

But it’s precisely for patients like Anselmo that basket trials are being considered — the possibility that there may be one, two or however many patients who, rather than facing a poor prognosis with existing or non-existent options for treating their disease, may have a chance, however small, of living longer and even controlling their cancer.

“One of the things that gets lost when we talk averages and medians is how many patients benefit and for how long,” says Hyman. “There is a tremendous range and a concern that promoting the best successes sets the bar very high. But it also lets people know that things are not entirely hopeless, that there are people who have tremendous benefit from therapies and not get completely caught up in medians and averages.”

That being said, Hyman cautions that more work needs to be done to better apply the principles of precision medicine to improve patients’ outcomes. Since most tumors have many mutations, how can doctors determine which one, or ones, to target with drugs? Why do some patients respond very well, while others do not?

Another looming question has to do with how cancer doctors can start to incorporate what they are learning about mutations and cancer-causing pathways with their more traditional knowledge based on where tumors start. In the study, for example, patients with BRAF colon cancers did not respond to vemurafenib; but some started to show responses when vemurafenib was combined with another drug, cetuximab. That suggests that knowing where the cancer originates may still be an important part of the puzzle in figuring out which treatments might work best for which types of cancers.

In an editorial accompanying the study, researchers at the T.H. Chan Harvard School of Public Health and Boston University note that basket trials may be just the first step in a precision medicine approach to cancer. Once doctors figure out which types of cancers might respond best to, for example, a BRAF-focused drug, they might conduct additional trials on each of these cancers to determine which patients, like Anselmo, would benefit most.

For her, the trail has provided the chance to sing again. A jazz vocalist, she performed at a friend’s birthday party and attended a song-writing retreat in upstate New York. She makes weekly visits to her doctors — to the dermatologist to monitor any side effects from the drug, to Hyman every two months for a brain scan, and to get lab tests done to check on her immune system. And she’s tired all the time. “But that’s par for the course,” she says. “I’m just lucky to be alive at a time when cancer care is so different than it was years ago. Who would have known that treatments could be so customized? It’s so amazing, and I’m very thankful to be a part of it.”


TIME Research

There’s a New Theory About Native Americans’ Origins

Chlaus Lotscher / Getty Images An Eskimo harpoons a whale in the Bering Sea off Alaskan shores.

The question at hand: Did Native Americans come to the Americas in one migratory wave or two?

New research is turning a centuries-old hypothesis about Native Americans’ origins on its head. A team of geneticists and anthropologists published an article in Science on Tuesday that traces Native Americans to a single group that settled in what’s now America far later than what scientists previously thought.

The researchers looked at sequenced DNA from bones as well as the sequenced genomes of Native American volunteers with heritage from not only the Americas but also Siberia and Oceania, says according to Rasmus Nielsen, a computational geneticist at the University of California, Berkeley, and one of the authors of the study. The researchers contacted people whose heritage indicated they were of Amerindian or Athanbascan—the two ethnic derivations of Native Americans—descent. Specifically, they looked at their mitochondrial DNA (mDNA), which is passed from mother to child.

What they found fundamentally changes what scientists previously thought. The team found that Native Americans most likely had a common Siberian origin, contradicting theories that an earlier migration from Europe occurred.

The timeline Rasmus and his colleagues propose goes something like this: About 23,000 years ago, a single group splintered off from an East Asian population. The group, hailing from northeast Asia, crossed the Bering Land Bridge between northeast Asia and Alaska, eventually making their way to the rest of the Americas. About 13,000 years ago—much more recent than previous theories—Native Americans started to split into different groups, creating the genetic and cultural diversity that exists today.

“We can refute that people moved into Alaska 35,000 years ago,” Rasmus says. “They came much more recently, and it all happened relatively fast.”

Rasmus’ team’s theory contradicts another line of thought, which points to two different populations coming from Siberia, settling in the Americas more than 15,000 years ago.

David Reich, a senior author of a different Nature paper detailing the competing theory and a professor at Harvard, told the New York Times that their results were “surprising”: “We have overwhelming evidence of two founding populations in the Americas,” he said. Reich’s group divides the migration groups into two: one is the First Americans, and another they identify as Population Y, which “carried ancestry more closely related to indigenous Australians, New Guineans and Andaman Islanders than to any present-day Eurasians or Native Americans.”

Despite their differences, both groups agree on the notion that Native Americans can trace their ancestry to Eurasian migrants with Australasian ancestry.

Rasmus emphasizes that their team’s new findings don’t close the case. But as simple as the finding seems to be, Rasmus says it is truly astonishing. “The original hypothesis isn’t true,” he says. “All Native Americans are descendants of one migration wave.”

TIME Science

The Molecule Behind the Golden Rule

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

We have this deep evolutionary system that motivates us to care about complete strangers

I want to start out by telling you about a woman that I interviewed in the San Diego County jail a couple of years ago. Let me call her Lisa. Lisa had been arrested for the 13th or 14th time for possession of methamphetamine for sale. She had served time many times. And I was part of a team that was interviewing her to understand how she had gotten to where she was and if we might help her change the course of her life.

You have to imagine this tiny little room in the county jail. We’re sitting almost knee to knee, about to have a long clinical interview. She’s in an orange jumpsuit, her hands are shackled, and there’s a guard outside the door. Slowly I start talking to her, asking her questions. “When did you first start smoking marijuana?” She said age thirteen. And then I asked, “When did you first start smoking methamphetamine?” She said age thirteen.

So what’s the natural question? “Gee, what happened to you when you were 13?”

She said, “Oh, my mom was a meth user, and she wanted to have someone to party with, so she introduced me to meth.” And then she started to cry, and she said, “And now when my mother calls me in prison to say she loves me, I can’t say it back to her.”

Breaking all appropriate clinical protocol, I said, “I don’t think you have to. Your mother did a terrible thing to you.” And indeed, Lisa had been raped because of meth, she had prostituted herself to get meth, she had married a man who was a meth user who beat her regularly, once fracturing her skull. She had two teenage children who lived in a state far from her because she couldn’t care for them. And she supported herself — though she was homeless — by selling meth.

The deeper question, then, I think, is how is it possible for a mother to do something so horrendous to her child? The trivial answer is, well, her brain was addled by drugs. But when she invited her daughter to start using meth, she was not high, right? She was sober. And she made a decision, a very bad decision.

So then the larger question, which I spent about twelve years in my life trying to understand, is why do any of us treat each other well at all, particularly when no one is looking?

I’m staying at a hotel right now and all the windows in my room are open because it’s hot. My computer is in there, all my stuff is in there. It would not be hard to just walk in there and take all my stuff, right?

Why do I have the windows open? Because I have a sense somehow that it’s safe based on the environment, the people. Earlier, I sat next to this stranger, Marissa, and we were chatting. And she didn’t look stressed out or anything, even though I’m some giant stranger.

How do we do that? How do we navigate through the sea of strangers that we all live in without having something in our brains that tells us who to be around and who not to be around, who is safe and who’s not safe? That’s what we began studying around 2001.

Oxytocin, this molecule that’s classically associated with child birth and breastfeeding, is released in all kinds of settings in which humans have positive social interactions, and it plays the role of a safety-signaling molecule. So when I see Marissa, her brain releases oxytocin, she feels safe to be around me, and now we can interact with each other.

Now, if I did something scary and crazy and weird, her stress hormones would turn on and she would immediately get away from me. Part of this story is that we have this built-in ability to come together as human beings to form relationships with people we have no direct genetic relationship to, and we can extract value from those relationships.

I want to tell you a little about how we’ve actually done this science. These field studies are fun. They show that this really works in the world that we live in.

`Maybe there’s a reason why people behave nicely even when they don’t have to. There is a rich literature in social animals showing that oxytocin allows members of the same species to identify burrow-mates. This is generally done by smell. So when I see my friend Bavindra — but I don’t really see him, I smell him, and he’s in my burrow — I think, Bavindra, he is my friend, I like him. And my brain makes oxytocin and then we can affiliate; we can huddle up for warmth or for safety.

Human beings, I thought, might do the same kind of thing. We don’t initially smell each other, but we recognize through all kinds of signals like body language that someone is safe or not safe. And we can do the same thing. We can affiliate and get all the value of relationships, except as human beings we do it very broadly.

We do it all of the time. We can’t help it. On airplanes, in meetings, all the time we see people we like, they’re friendly, and we can do projects with them or we can form friendships or romantic relationships. It’s all the same molecule. But in 2001, this was really a heterodox.

One of my colleagues actually said, “Paul, this is the world’s stupidest idea. It’s a career-ending decision.” I said, okay, maybe, but there is a big animal literature, and there must be a way to measure oxytocin in humans.

He said, “It’s irrelevant, just a female hormone,” indicating that if this is for women, it can’t be that important.

This was a guy, by the way. And I said, “Yeah, but men’s brains make oxytocin too. There must be a reason why.”

He said, “It’s just residual. You know, it’s not important.”

I said, “Well, I think I can test this, and if I can test it, then I can actually determine for men and for women or for both if oxytocin really matters.”

We decided to tempt people with virtue and vice by using money. Here’s the experiment. Let’s do it, we’ll do it right now. We’ll split the room in half. So half of you guys have $10. You guys have $10, too. You get matched up by computer. We don’t do face-to-face interactions because, since it’s a reproductive hormone, imagine if you’re sitting across from a cute guy or girl, of course you will be totally nice to them. We know that. We don’t want that confound. You’re matched by computer to somebody. You’ll have ten dollars and you’re randomly assigned in this pairing. And it says you’re first decision-maker or you’re second decision-maker. And here’s the task: If you are first decision-maker, you can give up some of your $10, ship it by computer to the other person you are matched to.

You can’t see them, you can’t talk to them, you make just one decision. Whatever you send comes out of your account and gets tripled in the other person’s account. Then the second person gets a message by computer saying, “Person 1 sent you say $15. With the $10 you got for joining the study, you now have $25. Do you want to keep it all, or send some amount back?” No one will know, you get paid in a different building. You’re totally in private.

So the standard view in economics was that if you’re Person 2, money is good. I think it’s a sort of caveman economics: “Oh, money good, me keep money.” It almost never happens in these experiments. What we see happening is that the more money someone sends you, the more money you tend to return to that person.

Person 1 has to sacrifice to make Person 2 better off. What do they expect you to do? Share the money with me, all right, and almost everybody does that. We didn’t care how people feel, we just followed the money. A kind of a Jerry Maguire approach to research: Show me the money, I’ll show you what I care about.

We did blood draws before and after, and we found that the more money you received as the second person in this transaction, the more your brain made oxytocin, and the more oxytocin your brain made, the more money you reciprocated.

This is actually really amazing. This basically blows up all standard economics, and it tells us something important about human nature: Oxytocin is the biological basis for the golden rule.

You play nice with me, I’ll play nice with you — usually. And the “usually” is where the story gets interesting, so I’ll get to that in a minute.

So we’ve done this now for hundreds of people, and in 95 percent of them, their brains make oxytocin and they reciprocate the money.

The next question we asked was, is this just a trust molecule or does it apply to a larger set of moral behaviors? I’m using the word “moral” here in an agnostic sense. I have no religious or philosophical tradition that I’m trying to support. I just mean those social behaviors that we recognize as positive: social behaviors like generosity, trustworthiness, honesty, compassion.

I’m going to study all the behaviors I can. I have a great tool now, and actually oxytocin is hard to measure and has a very short half-life — it is a quick on/off switch. Meaning, if I cause your brain to release oxytocin and you trust me, you don’t leave that switch on because you might run into some bad guy, and this guy might steal all your money.

So we had to do very rapid blood draws. Oxytocin degrades at room temperatures. You have to get the blood fast to keep them cold. So we have to work out these kinds of protocols that now everybody uses, which is great. But it wasn’t an obvious thing when we started.

And I should say lastly that the oxytocin in your blood actually reflects what’s going on in your brain because oxytocin is an evolutionarily old molecule. It actually pre-dates mammals. And we can see in humans we have many more receptors — particularly in the front of the brain — for oxytocin. We’re kind of hyper-social. We are social with people we don’t even know, and it’s because we’re much more sensitive to oxytocin.

We studied that by just changing these tasks over and over and over until we could figure out when this effect kicked in and when it didn’t. In addition, because nothing in the brain or the body happens in isolation, we wanted to make sure that we could actually show a direct causal relationship between oxytocin and these moral behaviors.

We did that by manipulating the oxytocin system. We took these really big drills and we drilled into people… No, we didn’t do that. Instead, we developed this nasal inhaler with which you can spray oxytocin in your brain, it will actually go in your sinuses and kind of leak into brain after about an hour. And it turns out that when you give people intranasal oxytocin, we can turn on moral behaviors like opening up a garden hose. They just spurt out.

People know what they’re doing with others, they just don’t care as much about their own welfare and care more about others. So I think oxytocin is this little molecule that evolved in mammals to motivate care for offspring, and when your brain releases oxytocin, it’s signaling that I’m a member of your family. So it causes us to treat strangers like family, and that’s really beautiful.

We have this deep evolutionary system that motivates us to care about complete strangers.

One of the questions that we asked was, what is the feeling that people have when their brains make oxytocin? Could you tell your brain was making it? The short answer is no, but let me tell you how we discovered it. I had a graduate student in my lab, now a faculty member at Claremont, who’s a social psychologist. He said that in social psychology, we use all kind of things like videos to try to change people’s social states. I wonder if it changes people’s physiologic states, too?

Well, I’m not so keen on that because I don’t want to rely on people telling me how they feel. I’m more interested in behavior. Anyway, he presented this little video that he got from St. Jude Children’s Hospital about a little boy with cancer, and the video runs 100 seconds. I’m not going to play it for you today because the last time I played was at a law conference at UCLA, and several lawyers actually cried when they saw it, and you guys are aware lawyers don’t have souls, right?

So, you nice people would definitely cry, too. It’s quite sad and it’s actually a real case. The little boy’s name is Ben and he died of terminal brain cancer. So it’s emotional, and we took blood before and after and people watched this video and then did these same share-the-money tasks. What we found was that the more oxytocin your brain made, the more empathic you felt towards Ben and his father; you felt emotionally connected to them. So that’s really interesting. And, people who watched the video were generous towards others and to a childhood cancer charity.

So now we have this underlying psychological mechanism that the physiology induces. For example, it’s not that I don’t want to steal Bavindra’s phone — I really do — it’s just that I’m going to feel bad if I do that. And then he’ll feel bad. If I’m a social creature, and if I have any sense of empathy, I’m going to feel bad because he feels bad and then that feeling makes me not want to steal from him.

I think that’s the same reason why in our studies people donate money to childhood cancer charity. When people’s brains release oxytocin, they’re giving up their money — even though we’re torturing them with needles and all kinds of things, they’re giving their money to the childhood cancer charity, not because they can fix Ben, but because they feel terrible that a child was suffering. Again this is a really beautiful thing about human beings — that we care about people at a distance. It’s not just the face-to-face interactions; it’s really the connection to the entire human family.

So why are people moral? What’s the punch line? We can think of three ideas. One is that we’re moral because God made us that way. So as a scientist, I don’t know if God exists or not, it’s not my place to say that; if that works, fine. I’m just not going to go there. Well, we’re going to go halfway there — I’ll tell you about that later.

The second is the government is watching us. Big Brother is here. There must be cameras in this room somewhere, we’re all being recorded, the NSA knows everything we’re doing. I can’t cheat because I’ll get caught, right? Well, these experiments give people a lot of privacy, you can do whatever you want to do, and honestly there are all kinds of situations we’re in which no one knows what we’re doing.

And the last idea is that, as social creatures, we actually care about what the other humans think about us. You know, we say we don’t, but of course we do. And this idea actually is quite old and traces back to Adam Smith, who you guys may remember from Econ 101. He wrote The Wealth of Nations in 1776. It turns out The Wealth of Nations was his second-best book. His best book was written 17 years earlier. It was called a The Theory of Moral Sentiments. It turns out Smith was a moral philosopher, and he was a kind of a nobody in Scotland — no one heard about him. He writes this book in 1759, and Smith becomes an absolute rock star in Europe.

He’s having dinner with the king of France, he’s hanging out with Thomas Jefferson, Benjamin Franklin. He developed the first fully terrestrial theory of why people are moral, and he said, “Why are we moral?” Because we have what he called “fellow feeling.” If I do something to hurt somebody, I share that emotion. Since I don’t like pain, I avoid doing those things.

If I do something that brings you joy, I get to share that joy. I like doing that. So most of the time, I’m going to behave in a way that keeps me embedded in the social fabric in which I am. So why is this Smith’s best book? Because he revised The Wealth of Nations three times, he revised The Theory of Moral Sentiments six times, including on his deathbed. He thought it was his more important work.

We have this sense of emotional connection to others which works as sort of a moral compass. It doesn’t always work, and that’s the second half of this lecture.

It doesn’t always work, and when it doesn’t work, the neuroscience is really interesting on what shuts down morality. Smith was doing this by intuition and casual observation of people. But now we can run experiments to ask what inhibits this response, what promotes this response.

But I think he was mostly right. So we can’t help but feel empathy when we see the dog, the homeless person, the child with cancer, and that motivates us to do things that improve our social standing, that make us better human beings, that motivate us to serve others which is just amazing to me. And now we know why.

I want to give you a cautionary note on how not to improve society from a moral perspective. When we first published the research for the oxytocin inhaler, the media frenzy was enormous and overwhelming and mostly wrong. We used synthetic oxytocin, a drug, to show the direct causal relationship between oxytocin and positive social behaviors. We spent most of our time in the intervening six or seven years working on the large variety of situations that causes your brain to make its own oxytocin, and how that affects your behavior. Synthetic oxytocin administration is not the way to improve society.

That’s what I really want to talk about. That’s where the rubber hits the road. Everyone isn’t nice all the time. Why is that? That’s what we started investigating. It turns out that there’s a larger brain circuit that oxytocin activates which I call the HOME circuit, Human Oxytocin-Mediated Empathy circuit, and this circuit utilizes oxytocin and two other neuro-chemicals.

I’ll spend thirty seconds on this because it’s important. One is called dopamine, which is this reinforcement-learning chemical. So when we do something that’s nice, say, I hold the door for Ken and he says “thank you,” our brain makes a little oxytocin and it releases this little reinforcement chemical that says, “Oh, that’s nice. Apparently he must like it when you do that, you should keep doing that.”

We learn from an early age that these are the important behaviors that help sustain us in the community of humans. Second, oxytocin facilitates the release of serotonin, a neuro-chemical you all have heard about. When you have more serotonin, you have an improvement in mood and reduction in anxiety.

So social interactions change body states. So it actually feels good to do good for others.

Given that, the question is what inhibits activity in the circuit, and what promotes activity?

The first is something that you all have experienced, which is high levels of stress. When you’re super-stressed out, you are not your best self, right? You’re grumpy, you’re cranky, you’re not nice to people.

Then what do you have to do the next day? You’ve got to go to your spouse, to your work colleagues or whatever, you say, “I was such a jerk yesterday, I’m sorry.” “I was having a bad day, I got in a car accident and my dog died.” Whatever it is, we understand that. We can have a bad day, it doesn’t mean you’re a bad person, you’re just having a bad day.

So high levels of stress inhibit the release of oxytocin, and we become less focused on others and more on ourselves. We’re in survival mode. It turns out that moderate levels of stress increase oxytocin release. So for all the single folks out there, for your first date, I recommend riding a roller coaster, tandem skydiving, or bungee jumping. You have this big arousal response and you really want to now be with this person. Or just flying out of the Aspen Airport, I think that will do it, too.

So high stress is one inhibitor. The second inhibitor for oxytocin is the most important chemical for half the people in this audience, which is testosterone. When we administer testosterone to men and compared their behavior to themselves on placebo, men on testosterone are more selfish and more entitled.

For those of you with teenage boys at home, this is not news to you. Why is that testosterone focuses our brain on ourselves? It’s like your brain whispering to you, you have the best genes on the planet, you’re a little god, everyone should bow down in front of you. Now, this is not only valuable for people with teenage boys at home — it turns out that if you win a chess match, your testosterone goes up.

If you do anything challenging, your testosterone goes up. Testosterone goes up both in men and women. It turns out that in men it’s about ten times higher than in women, so the effect is more egregious. But for both sexes, testosterone increases make interactions all about you.

You are the center of attention. By the way, what happens when you speak in public? Your testosterone goes up. So I’m sorry, I’ll try to be more empathic later. So we know a lot about how this system works. We also know that for every study we’ve done in twelve years, on average women release more oxytocin than men. Again, not surprising. Women are nicer than men, we know that. Except when they’re not. Now you know why.

So it turns out that estrogen primes the brain to be more sensitive to oxytocin. And it turns out that progesterone inhibits this response. So it puts on a little brake.

Women are nicer than men but also more complicated.

We also looked at developmental factors that affect oxytocin. Animals that are abused or neglected, not cared for by the mother, have fewer oxytocin receptors, particularly in the front of the brain, which is part of the feel-good circuit.

We studied women who have terrible life histories, who as children were repeatedly sexually abused. So really long-term sexual abuse. We find about half of them don’t have a functional oxytocin system. And they’re socially withdrawn, they are clinically depressed, they have a lot of difficult issues.

On the other hand, the other half was resilient against that abuse, and it didn’t depend on the length of abuse, the extent of the abuse. So the oxytocin system seems fairly robust to moderate amounts of abuse, although all abuse is bad for sure. This system is mostly protected, but enough abuse shuts this system down. By the way, we talked about methamphetamine earlier. Stimulants, like methamphetamine and cocaine, also damage oxytocin receptors. This may be one reason stimulant addicts become socially withdrawn.

I said earlier that 95 percent of people we have tested in a variety of situations release oxytocin in the appropriate way and reciprocate, but 5 percent don’t. Who are the 5 percent? About half of those are people who are just having a really bad day. They are stressed out, but otherwise they are okay people.

The other half have all the attributes of psychopaths.

Last summer my lab and I spent two weeks in the cornfields of Wisconsin at a treatment center for criminal psychopaths. And we took blood from a 161 of these wonderful human beings, all men, and we found that on average when they watched that cancer kid video that makes lawyers cry, nothing. They don’t produce oxytocin. One hallmark of psychopathology is a lack of empathy. It’s not that these individuals are necessarily planning to hurt others. They just don’t care. They see individuals as a tools to an end. They’re going to use you for sex or for drugs or for money. You’re just a hurdle they have to jump over. They just don’t have the same feeling that we do. So they’re dangerous. I recommend you avoid them. Not good people to be around. It’s 2 percent of the free roaming population; it’s around 40 percent of prison population.

But 2 percent isn’t bad, right? Three percent of people are having bad days, and 95 percent are releasing oxytocin and behaving quite nicely. Most of the time, for most people, the system works pretty well. But how do we really know it works well? I’m going to show you some experiments we’ve done around the world in different populations, not just in North America or Europe, and also what I think one of the interesting legal implications, a defense against criminal responsibility.

Let me tell you about a case of a gentleman named Hans Reiser. Reiser was a rising star in the Internet world in Silicon Valley. He started a couple of companies. One of those hit big. He’s married. They have a little child together, a little girl. And at some point, his wife decided she is going to divorce Reiser. And then what happens?

She goes missing. You wonder how that happened, right? It’s always the spouse. You guys know that, you’ve seen all the crime shows, you’ve seen the data, particularly when a woman dies. About 90 percent of the time it’s the spouse. So Reiser is arrested, but they have not found the body. He goes to trial and by the last day of the trial, it’s clear that he’s going to get convicted, and he’s up for the death penalty. So he agrees to plead guilty to avoid the death penalty. He’ll get life in prison if he shows them where the body is.

They go to the Berkeley hills, and he shows them where he dumped her body. He’s in jail for life in San Quentin. After a year at San Quentin, he writes a four-page handwritten appeal in pencil to the governor of California requesting a new trial, citing my research, claiming that his lawyer had what I’ve called oxytocin deficit disorder, ODD. He’s saying his lawyer was a psychopath. Think of the irony of this. Reiser is clearly a psychopath and he’s claiming his lawyer couldn’t represent him fully because his lawyer wasn’t empathic enough.

So that appeal was turned down. I didn’t get to be on the stand as an expert witness (yet). But this is coming, and I think that’s a conversation we need to have as a society.

If my genes made me do it, if my lack of oxytocin made me do it, am I fully responsible for that act? I don’t know.

I’m going to conclude with what you can do with this information. As I started writing my book The Moral Molecule, I spent a bunch of time thinking about why I spent ten years of my life trying to understand morality.

It started out with work I had done on cross-country levels of trust which are predictive of countries’ levels of prosperity. High-trust countries have more social interactions. More social interactions lead to more economic transactions that create wealth that sustains prosperity. The highest trust countries in the world, Norway, Sweden, Denmark, are very homogenous and have good governments. There is almost no social strife. Everything works well in these societies. So trust is a very good measure of a well-functioning society. That’s the dishonest answer about why I studied oxytocin.

Once I understood trust at the country level, then I wanted to understand it at the individual level. But I started writing the book, and I realized that I had another motivation for this, and it was driven by this woman, Sister Mary Maris Stella, also known as…my mother.

My mother was a former Catholic nun. And when I was a child, mom was the ultimate moral authority in our house because she was trained and we were not. You know, the white glove test: dust in your room, you could be going to hell. So mom was a little experimenter with her family, and God bless her, she just passed away about a year ago. But as I got older, I thought, why does mom know best, or why is promoting a top-down morality? Why do some words in a book apply to me?

Why isn’t there a ground-up morality? Why don’t we know what morality is? So I rejected her views, and because of that, in our experiments, we asked the most simple questions about people’s religious beliefs, but basically I didn’t want to touch this issues, it’s the third rail of science. We just asked things like “Do you believe in God?,” “Do you pray?,” “Do you go to church?” None of that really mattered for the experiments, it didn’t affect oxytocin, and it didn’t affect people’s behavior. We just ignored it.

And as I was writing the book, I thought to myself, you should actually address this issue. So we got permission to actually go into churches and take blood before and after religious services, everything from Buddhist to Quakers to Protestants. And we went to different rituals that have the aspects of religious services, but aren’t religious at all.

We had soldiers march around our lab for fifteen minutes and took their blood. We went to folk dances and took blood before and after people danced. And we found in all these situations that a majority of people would release oxytocin, and when they did that, they felt closer to the communities they were in. We did not find that the release of oxytocin changed their sense of connection to God or some ultimate reality.

We used lots of different words to get at this issue. So whatever that feeling comes from, it doesn’t seem to be an oxytocin effect; it’s driven by something else. But I still think that these rituals, just like weddings, are important because they connect us to communities.

So this story I’ve told to you sounds like a kind of human universal, and this work has been replicated now by lots and lots of labs. And we can talk about all the details of the studies if you want, but one question that also nagged me was, is it really universal? Because honestly we did these studies first on college students in the U.S. and in Europe. Then we did free roaming humans. We found in all the same response.

But what about as far away from the developed world as we can get? So to address that question, I flew for thirty hours to the highlands of Papua New Guinea, which is a rainforest. There are 700 distinct languages in Papua New Guinea. It’s the Stone Age there. No running water, no electricity, no bathrooms. I was embedded in a village for a week and took blood before and after an ancient war dance was done by indigenous tribe members. It was really an amazing and life-changing experience. This tribe, it’s about 1,000 people. They live in huts. They live way in the highlands, too far from any markets to grow cash crops. They trade pigs for brides.

It’s really an amazing place in many ways. None of these men had ever been to a doctor or dentist in their life, so they had never seen their blood drawn. So it was an interesting experience for them.

So we had them do the dance. We did a baseline blood draw, had them do their dance for twenty minutes, and then took their blood again. These people are pretty healthy. They’re vegetarian. They do do drugs because they’ve got a lot of spare time. So they smoke pot which, you know, not surprising for you guys in Colorado, and they also use an indigenous drug called betel nut which stains their gums red. It’s a euphoric, and so some of them are kind of spaced out.

Anyway, what we found is that just like in all the other rituals we studied, a majority of men who danced in this ritual released oxytocin, and when they released oxytocin, they felt more connected to the community, they said they were more willing to volunteer to help their community. For example, they are subsistence farmers. They just grow roots, tubers, broccoli, and collect nuts. The people who are addicted to betel nut don’t tend their plots.

What happens to the drug users? Do they starve? I mean, what happens to their plots? They said, “Ah, no, we just take care of it for them. There’s this real sense of community in which if you’re not able to feed yourself, we’ll just take care of you, no big deal.”

So it looks like oxytocin is a universal factor in promoting morality. A moral molecule. The Papua New Guinea experiment was so compelling for me because if you remember this old saying from World War II, FUBAR, this is the FUBAR experiment. Everything went wrong. The liquid nitrogen evaporated on the flight. It was gone. The generators, the voltage was wrong, that didn’t work. We had all these things set up. We had an anthropologist who had to work with this tribe, who had arranged all this. We had gotten permission from the government. Their government, our government, lots of permissions. It took two years to do this. And you’re exhausted, and you get there, and you can do nothing.

So I’m in the village. People are sitting around the hillsides kind of watching the show, the weird white people with cameras coming in. And there’s nothing I could do. The crew was trying to work on getting more liquid nitrogen. In fact, I was so freaked out the camera crew told me, “We do this for a living, you need a break, just take a break.” So I sit down on the grass. People start coming over, looking at me, and in Papua New Guinea, they’re very touchy, they like to touch your hands. And I’m thinking, oh my God, I have to eat with these hands, like, we’ve brought all our own food. Where’s the Purell? Oh my gosh, the body odor is powerful.

And then the little children came up to me, and they started looking at me and I started making faces at them. I don’t speak in this language at all of course. I started making faces, I started playing with them. All of a sudden, we were laughing, we were having fun, and I just relaxed and enjoyed this wonderful opportunity to be in people’s homes.

Amazing people. And I felt so close to my village. So when I got ready to leave with our blood samples, with more liquid nitrogen coming in from Tokyo, we have to get down the mountain and get these things back to LA. And the chief who’s got a fifth grade education says, “Stop, you need to sit down, we have gifts for you.” So I sat down. And the film crew sat down.

These people have nothing. They have no money at all and they made me this beautiful hand-spade, and the chief had someone translate into English a little note that said “In our village, all leaders have hand-spades to till their fields to feed their people, and we thought you needed a hand-spade.” Isn’t this amazing? That’s amazing.

So how stupid are we if we can’t connect to the people around us where we speak the same language, we’re in the same culture, and yet we go around the world and we’re connecting to people who are in some sense totally different than us and another sense, completely the same as us. They have the same things, they love their kids, they want to have a good life. They want to be healthy, they want to enjoy themselves.

We have this sense of morality or appropriate social behaviors, and one of those is trust. As I said earlier, we showed that trust is a big engine for prosperity at the level of countries, and when prosperity is higher, if that wealth is shared equally enough, it means we’re reducing poverty, which reduces the stress people have, which gives them the luxury of releasing more oxytocin, increasing morality.

If prediction by the neuroscience were true, we should see evidence for it.

When we look at cross-country data, we find measures tolerance for people who are different than ourselves increases with income. We find that happiness levels increase with income.

And we recently looked at this in individuals — those who release more oxytocin are more satisfied with their lives. Why? Because they have high quality relationships of all types — romantic, with friends, with family, and even with strangers.

I want to tell you what happened to Lisa, the prisoner. Lisa was either going to serve a three-year jail term for her sentence or do a — a three-year jail term usually is a year-and-a-half for good behavior. So it’s a year-and-a-half in jail or a year-and-a-half in lockdown rehab. And through a series of interviews she was eligible to do a year of lockdown rehab. She learned about drug use. She learned how to stay away from the cues that motivate drug use.

Her goal was to get out of San Diego, where she had been sucked into this drug lifestyle, and move to the state where her children lived. And she indeed did that. The last I heard from her, she had rented an apartment in the same city in which her children lived with her aunt and uncle. And she was beginning to rebuild her relationship with her children. She wasn’t able to care for them yet, but at least she started to rebuild that relationship. And the last note she sent me, she said she had not contacted her mother.

So what’s the take-home? Oxytocin is sometimes called the love molecule. It makes us care about our offspring, our romantic partners. My lab showed that it also makes us care about complete strangers. And we looked at lots of ways we could cause oxytocin release, and one of those was touch. In rodents, if you stroke the belly, you can cause the release of oxytocin. I thought, oh, that’s a good experiment. You’ll come in, I’ll rub your belly and then… That’s kind of weird, right? So I thought, maybe I can do an experiment where you come in and have all the participants hug each other for like ten minutes.

So what’s wrong with that experiment? First of all, I get sued because someone gets their butt grabbed, and that’s not good, and also it’s just creepy, right? So instead we thought, who gets to touch you who you don’t know? Your doctor. Your hairstylist. Your massage therapist.

So we did this study at UCLA, and this was the easiest recruiting of a study we’d ever done. You came in, you get a blood draw, you get ten minutes professional massage therapy, another blood draw, then do a “share the money” task. We found, indeed, that touch released oxytocin and made people much more generous towards strangers. So I thought, how do I apply this to my own life?

I decided some years ago to refuse to shake hands with people and begin to hug everybody. So the students in my lab like to tease me, and they starting saying you’re Dr. Love now, you’re hugging people. Whatever. Anyway I had a reporter come down a couple of years ago from Fast Companymagazine. He wanted to interview me, be in some experiments. It’s always kind of weird when reporters come out because I don’t really know what they want from me and why they’re there and — anyway, he’s getting ready to go, so I said, “Before you go I’m going to give you a hug because I’m the oxytocin guy and I’m all about connection.”

So he titles his article “Introducing Dr. Love.” So I’m outed now as Dr. Love. At first I was kind of unhappy, I’m a serious scientist, I do this work every day. It’s hard, you know, we spend a lot of money on experiments. We work hard to do this work right.

But then when I thought about it, I thought, what a great thing he gave me. I get to go places and talk about love.

Love is a biological reality. Your brain is designed for love. We need love. It’s super important to us. We’ve shown that touch not only increases oxytocin, it reduces stress hormones and improves the immune system. So we need those social relationships. So I encourage you to embrace the “L” word, tell the people around you that you love them.

Even at work, I encourage people to say “love.” It just means I’m interested in you as a human being. I care about what happens to you. And generally people will reciprocate and care about what happens to you as well.

That’s how oxytocin works. I can’t force you to love me, I can only give you love. In the same way, I can’t make my brain make its own oxytocin, but I can give you the gift of oxytocin by, for example, giving you a hug, and you will generally reciprocate. You might even try to use the “L” word.

This article was originally published by The Aspen Institute on Medium

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

TIME medicine

Scientists Find a Gene That Regulates Sleep

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It's a study in flies but it could have implications for us, too

Flies, it turns out, sleep about as much as young children do. Males need about 12 hours a day, while females can do with about 10 hours. To find out which genes might be responsible for guiding how much slumber flies get a night, Kyunghee Koh did a massive experiment that you can only do with fruit flies.

She and her team at Thomas Jefferson University reported in the journal Current Biology that they took 3,000 flies, introduced random mutations in them and then monitored how well they slept. That allowed them to zero in on the genes that most directly affected slumber, and they found one, taranis, that may become an important target for sleep-related research even in people.

Flies with abnormal forms of taranis only get about 25% of their daily sleep; removing the gene keeps the flies buzzing almost non stop.

Koh’s team found that taranis works with a couple of other proteins to balance sleeping and waking. Normally, taranis and cyclin A pair up to keep the activity of another enzyme down. That enzyme generally keeps the flies awake. So when all three are working in concert, taranis and cyclin A shut down the enzyme so flies can get 10 to 12 hours of sleep. But when taranis is mutated, it doesn’t do its job as well, and the enzyme keeps the flies alert and unable to sleep.

It turns out that taranis has a related gene in mammals that may work in similar ways. The gene typically controls the way cells divide, “We don’t know yet whether these genes have a role in sleep in mammals or humans, but our hope is that somehow these genes we find in flies may have similar roles in people, and might ultimately give us some novel drug targets to help us sleep better,” says Koh.

TIME medicine

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

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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 Longevity

Scientists Discover the Secret to Keeping Cells Young

Nude mature woman with grey hair, back view.
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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 Research

Relatives of Sex Offenders Are 5 Times More Likely to Commit Similar Offenses Finds Study

Genetic factors were found to increase the risk of a sex crime conviction

A new study of thousands of male sex offenders found that close relatives of people convicted of sexual offenses were up to five times more likely than average to commit similar offenses themselves.

Researchers found that about 2.5 percent of brothers and sons of convicted sex offenders are themselves convicted of sexual offenses, compared to about 0.5 percent of the wider public. The correlation, according to the study, is largely due to genetic factors rather than shared family environments.

“Importantly, this does not imply that sons or brothers of sex offenders inevitably become offenders too”, Niklas Langstrom, professor of Psychiatric Epidemiology at Sweden’s Karolinska Institutet and the study’s lead author, said in a statement. “But although sex crime convictions are relatively few overall, our study shows that the family risk increase is substantial. Preventive treatment for families at risk could possibly reduce the number of future victims.”

The study, which analyzed data on 21,566 men convicted of sex offenses in Sweden between 1973 and 2009, was published in the International Journal of Epidemiology.

TIME animals

Young Male Monkeys Prefer Spending Time With Daddy, Study Says

A rhesus macaque monkey grooms another on Cayo Santiago, known as Monkey Island off the eastern coast of Puerto Rico, Tuesday, July 29, 2008.
Brennan Linsley—AP A rhesus macaque monkey grooms another on Cayo Santiago, known as Monkey Island off the eastern coast of Puerto Rico, on July 29, 2008

Turns out quality father-son time is not just a human phenomenon

Male rhesus macaque monkeys prefer the company of their fathers, according to a new study, marking one of the first times gender partiality has been exhibited in primates before they leave the colony.

Rhesus macaques are generally found in Asia, but by studying a colony on the small Puerto Rican island of Cayo Santiago the team was able to identify individual moneys and document socialization patterns, according to the BBC, citing a report in the American Journal of Primatology.

Researchers discovered that infants and juveniles spent more time with their mothers, but as they developed into adulthood the role of the father (and his relatives) becomes increasingly important.

Scientists think this is because male monkeys eventually leave the colony, so young adults spend more time with their fathers to help them prepare for the challenges of a nomadic lifestyle.

While gender preference had been observed in primates before, the new study shows that parental bias begins before the males go off on their own — a departure from the previous idea that favoritism is the result of females forming strong bonds with their relatives by remaining in the group when the males leave.


TIME medicine

What We Learn When We Sequence the Genes of an Entire Nation

In a genetic milestone, researchers have amassed DNA data from an entire population of people. Here’s what we can learn from that information

Experts say that genetic sequencing may be the future of medicine, shaping how we understand and ultimately treat disease. If that’s the case, then the people of Iceland have a leg up on the rest of us.

In four groundbreaking papers published in Nature Genetics, scientists from Iceland describe the results of a massive gene-sequencing effort involving 2,636 people. Because the island country is relatively isolated, it’s a genetic goldmine. It enjoys a founder effect, which means that most residents can trace their lineage back to a few founding fathers, and that genetic variants have been passed down from generation to generation. That makes it possible to infer the distribution of the genetic variants found in the study’s 2,636 people to the remaining 325,000 Icelanders.

When they did that, the researchers, led by Kari Stefansson, CEO of deCODE Genetics/Amgen, were able find mutations linked to Alzheimer’s disease, liver disease, thyroid disorders and atrial fibrillation. They also identified almost 8% of the population who have lost function of at least one of their genes and calculated the rate of mutations in the Y-chromosome among men.

In recent years, the practice of mining large numbers of human genomes by comparing people with and without specific diseases has led to a growing list of genetic culprits behind conditions such as Alzheimer’s, cancer and more. But by studying such a genetically unique population, Stefansson says, he was able to pick up even rare genetic changes that have emerged more recently and occur less frequently but might still be important contributors to disease. Those, he says, will be important clues to better understanding the biological roots of health problems, as well as finding new drugs and treatments for them. “What we anticipate is that all human diversity is going to be explained by the diversity in the sequence of the genome, either solely by the diversity in the sequence or by the interface of that diversity and the environment,” he says. “That includes the diversity and risk of disease and the ability to resist them.”

MORE: The Iceland Experiment

The mutation associated with Alzheimer’s, for example, in the ABCA7 gene, hasn’t popped up in previous searches, but the gene is involved in transporting lipids across membranes, a process that may contribute to the build up of sticky protein plaques in the brains of Alzheimer’s patients.

The people who have lost function of at least one gene—called knockout genes in the genetic world—could also provide valuable hints about the pathways to disease. Even with a gene knocked out, most of these people are functioning, and Stefansson says researchers still study them in more detail to figure out how they are affected by their non-functioning genes. In animal research, knockouts are useful to see how prominent and important a gene is for health functioning. Stefansson anticipates that there may be redundancies built into the human genome to compensate for some knockouts, so finding these backup systems might be key to understanding why certain people get sicker with a disease while others remain relatively unaffected.

MORE: Scientists Identify Rare Gene Mutation that Protects Against Alzheimer’s

The sequences are also giving scientists a sharper picture of our past. The Y chromosome analysis shows that the last common ancestor sharing the Y chromosome among homo sapien men dates back 239,000 years, putting it closer to the common ancestor for the mitochondrial DNA passed down by women via their eggs. It also revealed how quickly mutations on the Y chromosome are occurring, which “gives us information about the age of our species, which is related to how diverse we are,” says co-author Agnar Helgason of deCODE and University of Iceland. “It tells us how quickly we are evolving.”

deCODE, which was acquired by the biotechnology company Amgen in 2012, is also investigating the new trove of genetic information for possible drug targets. “What this kind of work and insight into the human genome does is make approaches to influence the genome [and find treatments for disease] more rational,” says Stefansson.

How quickly that will happen isn’t clear yet, but having more information could make the process more efficient. “I’m willing to go so far as to say that there is nothing in human nature that may not have a reflection in the genome, or have something in the genome that associates with it,” he says. “We are made from the basis of the information coded in the genome.”

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