The Key to Weight Loss Is Diet Quality, Not Quantity, a New Study Finds

The Key to Weight Loss Is Diet Quality, Not Quantity, a New Study Finds

Anyone who has ever been on a diet knows that the standard prescription for weight loss is to reduce the amount of calories you consume.

But a new study, published Tuesday in JAMA, may turn that advice on its head. It found that people who cut back on added sugar, refined grains and highly processed foods while concentrating on eating plenty of vegetables and whole foods — without worrying about counting calories or limiting portion sizes — lost significant amounts of weight over the course of a year.

The strategy worked for people whether they followed diets that were mostly low in fat or mostly low in carbohydrates. And their success did not appear to be influenced by their genetics or their insulin-response to carbohydrates, a finding that casts doubt on the increasingly popular idea that different diets should be recommended to people based on their DNA makeup or on their tolerance for carbs or fat.

The research lends strong support to the notion that diet quality, not quantity, is what helps people lose and manage their weight most easily in the long run. It also suggests that health authorities should shift away from telling the public to obsess over calories and instead encourage Americans to avoid processed foods that are made with refined starches and added sugar, like bagels, white bread, refined flour and sugary snacks and beverages, said Dr. Dariush Mozaffarian, a cardiologist and dean of the Friedman School of Nutrition Science and Policy at Tufts University.

“This is the road map to reducing the obesity epidemic in the United States,” said Dr. Mozaffarian, who was not involved in the new study. “It’s time for U.S. and other national policies to stop focusing on calories and calorie counting.”


In a new study, people who ate lots of vegetables and whole foods rather than processed ones lost weight without worrying about calories or portion size. CreditAndrew Scrivani for The New York Times

The new research was published in JAMA and led by Christopher D. Gardner, the director of nutrition studies at the Stanford Prevention Research Center. It was a large and expensive trial, carried out on more than 600 people with $8 million in funding from the National Institutes of Health, the Nutrition Science Initiative and other groups.

Dr. Gardner and his colleagues designed the study to compare how overweight and obese people would fare on low-carbohydrate and low-fat diets. But they also wanted to test the hypothesis — suggested by previous studies — that some people are predisposed to do better on one diet over the other depending on their genetics and their ability to metabolize carbs and fat. A growing number of services have capitalized on this idea by offering people personalized nutrition advice tailored to their genotypes.

The researchers recruited adults from the Bay Area and split them into two diet groups, which were called “healthy” low carb and “healthy” low fat. Members of both groups attended classes with dietitians where they were trained to eat nutrient-dense, minimally processed whole foods, cooked at home whenever possible.

Soft drinks, fruit juice, muffins, white rice and white bread are technically low in fat, for example, but the low-fat group was told to avoid those things and eat foods like brown rice, barley, steel-cut oats, lentils, lean meats, low-fat dairy products, quinoa, fresh fruit and legumes. The low-carb group was trained to choose nutritious foods like olive oil, salmon, avocados, hard cheeses, vegetables, nut butters, nuts and seeds, and grass-fed and pasture-raised animal foods.

The participants were encouraged to meet the federal guidelines for physical activity but did not generally increase their exercise levels, Dr. Gardner said. In classes with the dietitians, most of the time was spent discussing food and behavioral strategies to support their dietary changes.

The new study stands apart from many previous weight-loss trials because it did not set extremely restrictive carbohydrate, fat or caloric limits on people and emphasized that they focus on eating whole or “real” foods — as much as they needed to avoid feeling hungry.

“The unique thing is that we didn’t ever set a number for them to follow,” Dr. Gardner said.

Of course, many dieters regain what they lose, and this study cannot establish whether participants will be able to sustain their new habits. While people on average lost a significant amount of weight in the study, there was also wide variability in both groups. Some people gained weight, and some lost as much as 50 to 60 pounds. Dr. Gardner said that the people who lost the most weight reported that the study had “changed their relationship with food.” They no longer ate in their cars or in front of their television screens, and they were cooking more at home and sitting down to eat dinner with their families, for example.

“We really stressed to both groups again and again that we wanted them to eat high-quality foods,” Dr. Gardner said. “We told them all that we wanted them to minimize added sugar and refined grains and eat more vegetables and whole foods. We said, ‘Don’t go out and buy a low-fat brownie just because it says low fat. And those low-carb chips — don’t buy them, because they’re still chips and that’s gaming the system.’”

Dr. Gardner said many of the people in the study were surprised — and relieved — that they did not have to restrict or even think about calories.

“A couple weeks into the study people were asking when we were going to tell them how many calories to cut back on,” he said. “And months into the study they said, ‘Thank you! We’ve had to do that so many times in the past.’”

Calorie counting has long been ingrained in the prevailing nutrition and weight loss advice. The Centers for Disease Control and Prevention, for example, tells people who are trying to lose weight to “write down the foods you eat and the beverages you drink, plus the calories they have, each day,” while making an effort to restrict the amount of calories they eat and increasing the amount of calories they burn through physical activity.

“Weight management is all about balancing the number of calories you take in with the number your body uses or burns off,” the agency says.

Yet the new study found that after one year of focusing on food quality, not calories, the two groups lost substantial amounts of weight. On average, the members of the low-carb group lost just over 13 pounds, while those in the low-fat group lost about 11.7 pounds. Both groups also saw improvements in other health markers, like reductions in their waist sizes, body fat, and blood sugar and blood pressure levels.

The researchers took DNA samples from each subject and analyzed a group of genetic variants that influence fat and carbohydrate metabolism. Ultimately the subjects’ genotypes did not appear to influence their responses to the diets.

The researchers also looked at whether people who secreted higher levels of insulin in response to carbohydrate intake — a barometer of insulin resistance — did better on the low-carb diet. Surprisingly, they did not, Dr. Gardner said, which was somewhat disappointing.

“It would have been sweet to say we have a simple clinical test that will point out whether you’re insulin resistant or not and whether you should eat more or less carbs,” he added.

Dr. Walter Willett, chairman of the nutrition department at the Harvard T. H. Chan School of Public Health, said the study did not support a “precision medicine” approach to nutrition, but that future studies would be likely to look at many other genetic factors that could be significant. He said the most important message of the study was that a “high quality diet” produced substantial weight loss and that the percentage of calories from fat or carbs did not matter, which is consistent with other studies, including many that show that eating healthy fats and carbs can help prevent heart disease, diabetes and other diseases.

“The bottom line: Diet quality is important for both weight control and long-term well-being,” he said.

Dr. Gardner said it is not that calories don’t matter. After all, both groups ultimately ended up consuming fewer calories on average by the end of the study, even though they were not conscious of it. The point is that they did this by focusing on nutritious whole foods that satisfied their hunger.

“I think one place we go wrong is telling people to figure out how many calories they eat and then telling them to cut back on 500 calories, which makes them miserable,” he said. “We really need to focus on that foundational diet, which is more vegetables, more whole foods, less added sugar and less refined grains.”


This article was originally published in The New York Times.  Read the original article.

What Makes Us Vibe?

What Makes Us Vibe?

Think about your friends—the people you spend a lot of time with, see movies with, those people you’d text to grab a drink or dinner after a long week. Now think back to why you first became friends and ask yourself: was it because you like them? Or because you are like them? A recent study, led by Carolyn Parkinson, a psychologist at the University of California, Los Angeles, suggests that the answer may involve a complex network of brain regions that gets to the root of how friendship exists in our brains.

When I spoke with her, Parkinson told me that a key focus of her research is learning how social networks might shape or be shaped by how our brains process information. Her previous work explored how the brain encodes one’s social standing, or where one sits in relation to another within a social hierarchy. She now wanted to understand how friendship itself was fleshed out in the brain.

Parkinson and her co-authors, Adam Kleinbaum and Thalia Wheatley of Dartmouth College, used a measure called social distance to define the friendship networks of 279 graduate students. Four months into their academic semester, Parkinson asked the students to consider an online list of their classmates and click on their friends. This Facebookian measure can be used to count how closely tied two individuals are based on their degree of social connection. Social distance, similar to sixdegrees of separation (or, alternatively, of Kevin Bacon), expresses how closely tied two individuals are within a larger social group.

Consider three people: Bill, Grace and Thomas. Bill and Grace are friends. Grace and Thomas are also friends. But Bill and Thomas have never met. In this scenario, Bill & Grace and Grace & Thomas are friends with one degree of separation while Bill & Thomas are two degrees of separation from each other (linked by their mutual friend Grace).

Parkinson used the questionnaire data to create a network that showed how far in social ties each of the students were from one another. These distances ranged from one degree of separation, meaning the students were friends with one another, to five degrees of separation, meaning that to draw a connection between two students in the friendship network, one would have to traverse a chain five friendships long.

Parkinson then showed 42 of the students a series of short video clips that resemble the way your TV would look if you were flipping through channels: three minutes of the earth from space, a few minutes of journalists debating, some slapstick comedy, a brief interlude watching a soccer match. Each student watched the same series of videos while their brain activity was recorded with functional MRI.

After the scan, Parkinson took the resulting MRI data and separated them based on where they originated in the brain. She then created what is known as a time series plot that represents how, on average, a brain region’s activity changed as each student viewed the video sequence. With each time series plot in hand, Parkinson could then determine whether an individual’s social relations were correlated with how their brain responded to viewing those videos.

Parkinson discovered that, indeed, the closer the social tie, the more similarly the student’s brains responded to the videos. And interestingly enough, the brain regions that were most similar across friends were those involved in attention and social cognition. The take-home: friends think alike.

These results fascinate me. If our engagement with social media is any indication, we spend an enormous amount of time thinking about our friends—about friends we have now, those we’ve had in the past, those we wish to have; the joys, the pains, the suspense of friendships. But I wager we don’t often think about how that all happens, how beneath our veneer of consciousness, neural assemblies are churning through sensory information, trying to make sense of the world and struggling to understand how to act within it. Yes, we are a social species, so friendships and social ties are extremely important—but what does that mean? And how does that happen at the level of those neural assemblies? It turns out that our brains appear, in a very real way, to synchronize with people we befriend, an incarnation of social unity. Perhaps it’s not simply that you feel close to your friends, but rather that you are experiencing the world more closely.

And of course I wondered which happens first. To (conversationally) binarize the question, I wondered about two chicken/egg scenarios: One, do we become friends with someone because their brain processes information like our own? Or two, does the act of befriending cause our brains to process information more similarly to our friends?

Parkinson was careful to remind me that because her study was cross-sectional—meaning she took a snapshot of the students and how their brains function—she can’t draw conclusions regarding cause and effect. In other words, she can’t say whether it was scenario one or two.

Either way, I see her results as an argument for some level of neural determinism. Consider the first scenario, wherein people with similar brains are drawn toward one another. This is an obvious case wherein your neurobiology has sculpted your social relationships. You may think you are choosing your friends, but your brain is really just responding to some neurophysiologic reflection; you see the world similarly, and so become friends.

The other scenario is a bit spooky. Say you somehow become friends with someone, perhaps by sitting next to them in class. As you get to know one another, you exchange some cognitive contagion that alters the way both of your brains perceive reality. By befriending, you become somehow not you.

It’s probably a little bit of both; nature births chickens and eggs simultaneously. And given the fact that collectively, humans have been befriending one another for thousands of years, no neurological danger was revealed here. But still I wonder whether “falling into the wrong crowd” or “marrying up” have some neurological correlate. And what of inter-species friendships—do cat people and dog people’s brains process information more like their pets? And vice-versa? (I’m imagining the urge to stick my head out my car window.)

Fortunately Parkinson told me she is hard at work conducting a longitudinal study, one that follows people (which is to say human brains) from before they meet until they form friendships. So hopefully she’ll give us an answer soon. In the meantime, choose your friends wisely. If you can.



This article was originally published in Scientific American. Read the original article.

The First Step Toward a Personal Memory Maker?

The First Step Toward a Personal Memory Maker?

Decent memory is a matter of livelihood, of independence, most of all of identity.

Human memory is the ghost in the neural machine, a widely distributed, continually changing, multidimensional conversation among cells that can reproduce both the capital of Kentucky and the emotional catacombs of that first romance.

The news last week that scientists had developed a brain implant that boosts memory — an implantable “cognitive prosthetic,” in the jargon — should be astounding even to the cynical.

App developers probably are already plotting yet another brain-exercise product based on the latest science. Screenwriters working on their next amnesia-assassin scripts got some real-life backup for the pitch meeting.

The scientists are in discussions to commercialize the technology, and so people in the throes of serious memory loss, and their families, likely feel a sense of hope, thin though it may be. These things take time, and there are still many unknowns.

But for those in the worried-well demographic — the 40-is-the-new-30 crowd, and older — reports of a memory breakthrough fall into a different category.

What exactly does it mean that scientists are truly beginning to understand the biology of memory well enough to manipulate it? Which reaction is appropriate: the futurist’s, or the curmudgeon’s?

The only honest answer at this stage is both.

The developers of the new implant, led by scientists at the University of Pennsylvania and Thomas Jefferson University, built on decades of work decoding brain signals, using the most advanced techniques of machine learning.

Their implant, in fact, constitutes an array of electrodes embedded deep in the brain that monitor electrical activity and, like a pacemaker, deliver a stimulating pulse only when needed — when the brain is lagging as it tries to store new information.

When the brain is functioning well, the apparatus remains quiet.

“We all have good days and bad days, times when we’re foggy or when we’re sharp,” said Michael Kahana, a psychology professor at the University of Pennsylvania and senior author of last week’s report.

“We found that jostling the system when it’s in a low-functioning state can jump it to a high-functioning one.”

If this system, once refined, one day provides support for people with extreme deficits, it will sharply improve lives (insurers willing). The older person with creeping dementia will have more years living independently. The veteran with traumatic brain injury may regain just enough sharpness to find a decent job, or a career.

For most everyone else, the central discovery behind the device — that goosing a wandering brain can make it somewhat sharper — is already deeply familiar. Human beings have been doing this deliberately, and forever: with caffeine, nicotine, prescription drugs like Ritalin, or more virtuously, with a brisk run around the park.

“We have good evidence that things like nicotine and aerobic exercise improve some aspects of attention,” said Zach Hambrick, a professor of psychology at Michigan State University. “The stimulation may be activating some of the same systems, only more directly and precisely.”

One such ability that people with extraordinarily precise memory have in common is known as selective attention, or “attentional control.” In a common measure of this, the Stroop test, people see words flash on a computer screen and name the color in which a word is presented.

Answering is nearly instantaneous when the color and the word are the same — “blue” displayed in blue — but slower when there’s no match, like “blue” displayed in red. The men and women who compete in memory competitions score very highly on such tests and often do so well into their thirties, when the ability is typically on the wane.

This skill is partly inherited, but psychologists have shown that just about anyone can stretch his or her native ability using the same technique that the memory champs do: mentally arranging new names, facts or words in a deeply familiar place — along subway stops, for example, or in a childhood room.

In one continuing study, researchers at Washington University in St. Louis trained a group of 50 older adult volunteers to memorize word lists using location imagery — a so-called memory palace.

“One woman in her sixties got to where she could recall more than 100 words in correct order,” said David Balota, who collaborated on the study. “Others were well up to fifty and sixty words.”

And all without surgery, or Ritalin.

But there was a catch. “That ability didn’t transfer to any improvement in general cognition, like the ability to concentrate, to store new information without using the technique, or speed of processing,” Dr. Balota said.

In short, ramping up the ability to recall lists of facts, whether with use of an electric brain implant or imagery-based training, may mean nothing for overall quality of life in people whose memories are functioning normally.

It is in those with serious deficits that the equation changes.

A device that even partly corrects those injuries might keep crucial details — whom to call for help, how to use the phone, even navigating back and forth to the bathroom — firmly lodged in mind. For now, that is where a brain implant is most relevant.

In the years to come, scientists are likely to turn this new technology to the task of memory retrieval, rather than just storage.

“We find there’s even more variability during retrieval than encoding,” Dr. Kahana said — meaning more potential to ramp up performance. When that happens, the game changes.

Giving people with serious deficits a way to master the crucial facets of daily existence would certainly be a medical advance.

But giving them, and others, a more vivid and deeper reach into the vast pool of what they already know — well, there are angels and demons buried there, in addition to facts and names.

That will be a real-life screenplay we should all watch carefully.


This article was originally published in The New York Times.  Read the original article.

Can Coffee Rev Up Your Workout? It May Depend on Your Genes

Can Coffee Rev Up Your Workout? It May Depend on Your Genes

Whether athletes can enhance their performance with caffeine may depend on their genes.

According to a new study of the genetics of caffeine metabolism, athletes with a particular variant of one gene show notable improvements in their endurance performance after swallowing caffeine.

But those with a different variant of that gene may perform worse if they first have caffeine, raising questions about who should be using the drug to bump up performance and about the broader interplay of nutrition, genetics and exercise.

For many of us, caffeine, usually in the form of coffee, is as necessary to the morning as sunrise.

But different people respond differently to the effects of caffeine. Some become jittery and later have difficulty sleeping. Others can drink the same amount of coffee and report increased alertness but no jitters or sleep disruptions.

The same range of reactions occurs in athletes. In multiple past studies, most people will work out longer, faster or more strenuously after they swallow a moderate dose of caffeine, but a few perform no better or even worse.

A few years ago, these disparities drew the attention of Ahmed El-Sohemy, a professor of nutritional science at the University of Toronto in Canada, who studies how people’s genes influence their bodies’ reactions to foods and diets. He is the founder of Nutrigenomix, a company that provides genetic testing related to nutrition.

By then, other geneticists had established that a specific form of one gene affects how people metabolize caffeine. That gene, prosaically called CYP1A2, controls the expression of an enzyme that affects the breakdown and clearance of caffeine from the body.

One variation of the CYP1A2 gene prompts the body to rapidly metabolize caffeine. People who have two copies of this variant, one from each parent, are known as fast caffeine metabolizers; the drug gives them a quick jolt and is gone.

By most estimates, about half of us are fast metabolizers.

Another variant of the gene slows caffeine metabolism. People with one copy of this version and one of the faster-metabolizing type are considered to be moderate metabolizers, whereas people with two copies of the slow-metabolizing variant are, of course, slow caffeine metabolizers.

About 40 percent of us are thought to be moderate metabolizers, with the remaining 10 percent being genetically slow metabolizers.

In 2006, Dr. El-Sohemy and his colleagues published a study in JAMA showing that slow metabolizers had a heightened risk of heart attacks if they frequently drank coffee, compared to people who were genetically classified as fast caffeine metabolizers. The scientists theorized that the drug, which can constrict blood vessels, hung around and produced longer-lasting — and in this case undesirable — cardiac effects among the slow metabolizers.

But few large experiments had focused on how people’s CYP1A2 genetic profile might influence their athletic performance after swallowing caffeine.

So for the new study, which was published this month in Medicine & Science in Sports & Exercise, Dr. El-Sohemy, together with his graduate student Nanci Guest and other colleagues, decided to ply about 100 willing, young, male athletes with various doses of the drug. (The study was funded in part by Nutrigenomix, as well as Coca-Cola and the Canadian Institutes of Health Research; the funders did not influence the results, Dr. El-Sohemy says.)

The scientists swabbed the men’s cheeks, analyzed their CYP1A2 genes and, based on which variants each man carried, categorized them as fast, moderate or slow caffeine metabolizers.

Then they had the athletes complete three separate sessions of pedaling a stationary bicycle for 10 kilometers as quickly as possible. Before one ride, the men received a low dose of caffeine (2 milligrams for every kilogram of their body weight, or about the amount found in one large cup of coffee). Before another, they swallowed twice as much caffeine; and before a third, a placebo.

Their subsequent time trial results showed that, on aggregate, the men performed better with caffeine, especially after the higher amount.

But there were substantial differences by gene type.

The fast metabolizers rode nearly 7 percent faster after they had downed the larger dose of caffeine compared to the placebo. The moderate metabolizers, by contrast, performed almost exactly the same whether they had received caffeine or a placebo.

It was the slow metabolizers, however, who showed the greatest impact, although in a negative direction. They completed the 10 kilometer ride about 14 percent more slowly after the higher dose of caffeine than after the placebo.

Just how caffeine differentially boosted or blunted the men’s athletic performance remains unclear.

But Dr. El-Sohemy suspects that, as in the heart-attack study, caffeine lingered in the slow metabolizers, narrowing their blood vessels and reducing the flow of blood and oxygen to tiring muscles.

In fast metabolizers, the drug likely provided a quick gush of energy and then was cleared from their bodies “before it could do the bad stuff,” he says.

This study involved only healthy young men and bicycling. It cannot tell us whether caffeine likewise gooses or inhibits performance for other people in other sports.

And it cannot answer the broader question of whether we need a genetic test before deciding if we should mainline coffee in advance of our next workout.

Physical performance involves, after all, so many factors, including motivation, sleep, stress, overall nutrition, and the working of a vast number of genes, many still unidentified.

So if you find that coffee seems to impede your performance, you could use a genetic test to characterize your CYP1A2 gene and confirm that you are a slow metabolizer. Or you could not drink coffee before you exercise.


This article was originally published in The New York Times.  Read the original article.

The coffee cannabis connection

The coffee cannabis connection

It’s well known that a morning cup of joe jolts you awake. But scientists have discovered coffee affects your metabolism in dozens of other ways, including your metabolism of steroids and the neurotransmitters typically linked to cannabis, reports a new study from Northwestern Medicine.

In a study of coffee consumption, Northwestern scientists were surprised to discover coffee changed many more metabolites in the blood than previously known. Metabolites are chemicals in the blood that change after we eat and drink or for a variety of other reasons.

The neurotransmitters related to the endocannabinoid system — the same ones affected by cannabis — decreased after drinking four to eight cups of coffee in a day. That’s the opposite of what occurs after someone uses cannabis. Neurotransmitters are the chemicals that deliver messages between nerve cells.

Cannabinoids are the chemicals that give the cannabis plant its medical and recreational properties. The body also naturally produces endocannabinoids, which mimic cannabinoid activity.

In addition, certain metabolites related to the androsteroid system increased after drinking four to eight cups of coffee in a day, which suggests coffee might facilitate the excretion or elimination of steroids. Because the steroid pathway is a focus for certain diseases including cancers, coffee may have an effect on these diseases as well.

“These are entirely new pathways by which coffee might affect health,” said lead author Marilyn Cornelis, assistant professor of preventive medicine at Northwestern University Feinberg School of Medicine. “Now we want to delve deeper and study how these changes affect the body.”

Little is known about how coffee directly impacts health. In the new study, Northwestern scientists applied advanced technology that enabled them to measure hundreds of metabolites in human blood samples from a coffee trial for the first time. The study generates new hypotheses about coffee’s link to health and new directions for coffee research.

The paper was published March 15 in the Journal of Internal Medicine.

Drinking lots of coffee for science

In the three-month trial based in Finland, 47 people abstained from coffee for one month, consumed four cups a day for the second month and eight cups a day for the third month. Cornelis and colleagues used advanced profiling techniques to examine more than 800 metabolites in the blood collected after each stage of the study.

Blood metabolites of the endocannabinoid system decreased with coffee consumption, particularly with eight cups per day, the study found.

The endocannabinoid metabolic pathway is an important regulator of our stress response, Cornelis said, and some endocannabinoids decrease in the presence of chronic stress.

“The increased coffee consumption over the two-month span of the trial may have created enough stress to trigger a decrease in metabolites in this system,” she said. “It could be our bodies’ adaptation to try to get stress levels back to equilibrium.”

The endocannabinoid system also regulates a wide range of functions: cognition, blood pressure, immunity, addiction, sleep, appetite, energy and glucose metabolism.

“The endocannabinoid pathways might impact eating behaviors,” suggested Cornelis, “the classic case being the link between cannabis use and the munchies.”

Coffee also has been linked to aiding weight management and reducing risk of type 2 diabetes.

“This is often thought to be due to caffeine’s ability to boost fat metabolism or the glucose-regulating effects of polyphenols (plant-derived chemicals),” Cornelis said. “Our new findings linking coffee to endocannabinoids offer alternative explanations worthy of further study.”

It’s not known if caffeine or other substances in coffee trigger the change in metabolites.

Although Cornelis studies the effects of coffee, she didn’t drink it growing up in Toronto or later living in Boston.

“I didn’t like the taste of it,” Cornelis said.  But when she moved to join Northwestern in 2014, she began to enjoy several cups a day. “Maybe it’s the Chicago water,” she mused, “but I do have to add cream and sweetener.”



This article was originally published in NIH. Read the original article.

Genes have a role in empathy, study says

Genes have a role in empathy, study says

It helps us to make close connections with people, and influences how we behave in a range of situations, from the workplace to a party.

Now scientists say empathy is not just something we develop through our upbringing and life experiences – it is also partly inherited.

A study of 46,000 people found evidence for the first time that genes have a role in how empathetic we are.

And it also found that women are generally more empathetic than men.

‘Important step’

Empathy has an important role in our relationships.

It helps us recognise other people’s emotions and it guides us to respond appropriately, such as by knowing when someone is upset and wants to be comforted.

It is largely considered to be something we develop through childhood and our life experiences.

But in this new paper, published in the journal Translational Psychiatry, scientists looked to see if how empathetic we are can be traced to our genes.

Participants in the study had their “empathy quotient” (EQ) measured with a questionnaire, and gave saliva samples for DNA testing.

Scientists then looked for differences in their genes that could explain why some of us are more empathetic than others.

They found that at least 10% of the differences in how empathetic people are is down to genetics.

Varun Warrier, from the University of Cambridge who led the study, said: “This is an important step towards understanding the role that genetics plays in empathy.

“But since only a tenth of the variation in the degree of empathy between individuals is down to genetics, it is equally important to understand the non-genetic factors.”

blue double helix modelsImage copyrightGETTY IMAGES
Image captionIt is the first time a study has looked to see if empathy can be traced to our genes

The research also found differences in empathy between the sexes.

Out of a maximum of 80 from the EQ questionnaire, women on average scored 50, as opposed to 41 for men.

But researchers said they were unable to find any genetic differences behind this.

The scientists also found genetic differences that are associated with lower empathy were also linked to a higher risk of autism.

However, they acknowledged there were limitations to the research.

The empathy quotient is a self-reported survey, which can skew results.

And although they found genetic differences between people who were more and less empathetic, they were not able to find specific “empathy genes” that were responsible for this.

They added that future research to find the genes that affect empathy would benefit from more people taking part in the study.

Gil McVean, professor of statistical genetics at the University of Oxford, told the BBC the study established that genes had a role in empathy, but this was “minor” compared to environmental factors.

“We know that basically anything you can measure in humans has a genetic component, and this establishes that empathy does have some heritable component.”

Dr Edward Barker, a reader at the department of psychology at King’s College London, said the paper had some “very interesting” findings and was a “first step” in exploring the link between our genes and empathy.

“But as the authors say, it’s the first analysis of its kind and could benefit from a larger study,” he added.


This article was originally published in NPR. Read the original article.