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.

[BBC]

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.”

TIME medicine

5 Things to Know on World Down Syndrome Day

World Down Syndrome Day 2014 Celebrated in Indonesia
Robertus Pudyanto—Getty Images A girl with Down syndrome takes part in planting a tree during World Down Syndrome Day on March 21, 2014 in Surabaya, Indonesia.

From how it happens to what it does

Saturday is World Down Syndrome Day, a day recognized each year by the United Nations to raise awareness about the genetic disease. Here are five things you need to know about Down syndrome.

1. Down syndrome is caused by an extra set of chromosome 21. Every cell in the body has 23 pairs of chromosomes, one from each parent, but Down occurs when one parent contributes extra genetic material. Older mothers have a higher chance of having a Down baby.

2. More than 400,000 people live with Down in the U.S.

3. The most common symptoms of Down include cognitive delays, low muscle tone and a small stature.

4. People with Down can lead full, independent lives. They are, however, at higher risk of developing heart, respiratory problems and certain cancers.

5. People with Down are living much longer than in the past, thanks to treatments for their health issues. While the average life expectancy in 1983 was 25 years, today it is 60 years.

MONEY Entrepreneurs

Here’s a New Theory About Why People Become Entrepreneurs

mother and daughter shopkeepers
Ariel Skelley—Getty Images

Nurture beats nature when it comes to small business ambitions, according to a new study.

It’s long been known that children with entrepreneurial parents are more likely to become entrepreneurs themselves. But new research quantifies that effect—and goes a step further by suggesting why exactly that might be.

The study, published in the latest Journal of Labor Economics, found that upbringing, rather than genetics, seems to have the biggest effect on the offspring of self-started business owners. The researchers did something prior studies (which mainly focused on twins) hadn’t: They examined the career choices of thousands of Swedish children raised by either adoptive or biological parents to compare the relative effects of nature and nurture on the entrepreneurial impulse.

Adopted children, they found, were 20% more likely to become entrepreneurs if their biological parents were also entrepreneurs. But if it was their adoptive parents who were entrepreneurs, it was 45% more likely children would follow suit.

“The importance of adoptive parents is twice as large as the influence of biological parents,” wrote authors Joeri Sol and Mirjam Van Praag of the University of Amsterdam, and Matthew Lindquist of Stockholm University.

The authors controlled for the possibility that kids might just be inheriting the family business (or money to start a new business) and continued to find the same effect—which suggests that kids were simply seeing their parents as role models. That would also explain why gender had a big impact on children: Daughters in the study were most likely to become entrepreneurs if their mothers were—and sons if their fathers were.

These findings may also have implications for educators and policymakers who care about growing small businesses. The greater the effect of nurture on career choices, the authors wrote, “the larger the potential benefit of programs aimed at fostering entrepreneurship.”

The biggest takeaway for parents? If you want your kids to become start-up success stories, you should first try to become one yourself.

TIME medicine

Here’s How 23andMe Hopes to Make Drugs From Your Spit Samples

The company is making a bold move to enter the drug-making business by using the genetic information donated by its clients

On March 12, 23andMe, the genetic testing company best known for analyzing your DNA from a sample of spit, announced the creation of a new therapeutics group. The group’s mission: to find and develop drugs from the world’s largest database of human genetic material.

That’s a huge shift for the company, which must now build a research and development arm from scratch. Richard Scheller, formerly of the biotechnology corporation Genentech, will lead the group and will also be 23andMe’s chief science officer.

Scheller admits that for now, he’s the therapeutics group’s only member. But soon after he starts on April 1, he anticipates that things will move quickly, as they do in the genetics world. That’s what attracted him to 23andMe after overseeing early drug development at Genentech for 14 years. “I’ve seen over the last couple of years how human genetics has impacted the way Genentech does drug discovery, and I thought it might be fun and interesting to work in an unrestricted way with the world’s largest human genetic database,” he says. “The questions we will ask are research based, but we could identify a drug target extremely quickly. I believe there is the real possibility to do really, really great things for people with unmet medical needs.”

MORE: Genetic Testing Company 23andMe Finds New Revenue With Big Pharma

More than 850,000 people have paid 23andMe to sequence their DNA since the company launched in 2006 until 2013, when the Food and Drug Administration requested that the company stop selling its medical genetic information services over concerns that their marketing claims weren’t supported by strong enough evidence about how the genetic information influenced human health. The company still retains that genetic information and continues to sell kits, but provides only non-medical information now while it continues to work with the FDA on further regulatory issues.

That experience “transformed” the company, as CEO Anne Wojcicki said to TIME earlier this year. Since then, the company has expanded its collaborations with pharmaceutical companies to access its database. The latest addition of drug development is a further evolution in the company’s identity.

Of those who have sent in samples, 80% have agreed to allow their genetic information to be used for research purposes. That’s the database that Scheller is eager to investigate. While at Genentech, he helped broker a collaboration between the biotech firm and 23andMe in which Genentech would have access just to the genetic testing company’s Parkinson’s disease patients, to search for any genetic clues to new therapies. Now, he says, “I plan on asking hundreds or maybe thousands of times more questions of the database than any pharmaceutical partner.”

MORE: 23andMe Finds Genes for Motion Sickness

He will be looking, for example, at whether patients who develop a certain disease tend to have specific hallmark genetic changes in their DNA, which could serve as potential launching points for new drugs. Or he might focus on the extreme outliers: people who have advanced cancer, for example, but somehow survive, or those who seem to succumb early. Mining their genomes might yield valuable information about what makes diseases more or less aggressive, and might become targets for drugs as well.

To do this, Scheller will have to create a drug development team from the ground up. The company is not divulging how much it intends to invest in this effort, but is soliciting another round of financing in the coming months. Initially, Scheller anticipates that even before the company has labs set up, he and his team will take advantage of labs-for-hire, or contract research organizations, to start doing experiments within weeks. Because his drug candidates will be more targeted and designed to address specific mutations or processes in the body, he anticipates that the cost of developing drugs that patients might eventually benefit from may be “substantially reduced” from the average $1 to $2 billion most pharmaceutical companies now spend.

MORE: Time Out: Behind the FDA’s Decision to Halt Direct to Consumer Genetic Testing

As for which disorders or medical issues he will tackle first, Scheller is being democratic. “We are going to be opportunistic,” he says. “That’s the nice thing about being part of 23andMe. We don’t really have a say. We can look generally at the database, and try and let it teach us what we should be working on.” In other words, anything is game.

MONEY Credit

Your Genes Might Affect Your Credit Score

150311_FF_DNAMoney
Jon Boyes—Getty Images

Your credit score isn't controlled by any one cause, but your genes may be a key factor.

There is the standard list of factors that influence your credit score: payment history, outstanding balances, the types of credit that you use and so on. But what you probably don’t realize is that your genes may also play an important role. Yes, your biological wiring might make you more likely to be more risk-seeking and take on more debt, which could lead to a lower FICO score.

I came across this intriguing discovery while researching my book Coined: The Rich Life of Money And How Its History Has Shaped Us. I wrote the book because I was working at a Wall Street investment bank during the credit crisis, and I wanted to know what leads people to make bad decisions with money. I learned that there are many things that guide our financial decisions, including our genes.

To understand how genes could sway our decisions, I asked a neuroeconomist. Neuroeconomics is an emerging and interdisciplinary field in which brain scans and other technologies are used to understand how we make financial decisions. Brian Knutson, a neuroeconomist at Stanford University, explained a study that he conducted with two colleagues, Camelia Kuhnen and Gregory Samanez-Larkin, on the link between our genes, financial decisions and even life outcomes.

They started with the multi-part question, “Do genes influence cognitive abilities, do they shape the way people learn in financial markets, or do they determine risk attitudes?” They concentrated on a gene known as 5-HTTLPR because it had been identified in previous studies as playing a role in how we make financial decisions. Specifically, they wanted to know whether there was causation between people who have a variant of this gene, possessing a short or long allele, and their financial outcome.

In the trial, they selected 60 individuals from San Francisco to participate. The participants shared demographic information such as their age, marital status and ethnicity. They also provided personal financial information such as their occupation, income level and debts. Some participants also disclosed their FICO scores. All participants had their DNA collected via cheek swabs for an analysis of whether they possessed the short or long alleles. Participants were then presented a series of financial decisions like how to allocate $10,000 across stocks, bonds and cash.

It turned out that those with short alleles made more conservative financial decisions than those with long alleles. Participants with short alleles allocated less money in equities and more in low-performing assets like cash. Moreover, in real life these participants had fewer lines of credit than the others. Those with two short alleles had higher FICO scores, some 93 points, than those with a long allele. FICO scores typically range between 300 and 850, so a swing of 93 points, or 17%, is statistically noteworthy.

Before concluding that genes were the reason for the variance in behavior, the researchers considered other possible factors: income, wealth and financial literacy. But they didn’t find that any of these things were meaningful in explaining the outcome of their study. Ultimately, they settled, “Overall, these results indicate that individual variation in the 5-HTTLPR genotype influences financial choice.”

Their conclusion is in line with other academic studies that find there are genetic determinants for financial decisions. For example, researchers compared the investment portfolios of fraternal and identical twins. They found that almost one third of the divergence in asset allocation might be attributable to genetic factors. Indeed, twins that were frequently in touch invested in a similar manner. But identical twins who grew up separately also demonstrated similar financial decisions. The researchers explain, “We attribute the genetic component of asset allocation—the relative amount invested in equities and the portfolio volatility—to genetic variation in risk preferences.”

However, Knutson and his colleagues sound a cautionary note: not all participants acted in accordance with how their genes might predict. Just because several studies reveal that genes appear to play a role in determining the financial decisions, doesn’t mean that they are the only things that matter. Even if someone is biologically wired to be risk-averse, they might demonstrate risk-seeking behavior depending on the situation. For example, say someone in her late 20s who is predisposed to risk aversion is setting up a retirement account. She has also taken two online courses that recommend more aggressive investing early in one’s career, so she decides to be more risk-seeking, and invests more money in stocks than bonds. In this case, knowledge triumphed over genetics.

That genes can influence our credit scores is an intriguing finding of neuroeconomics. Maybe one day, credit reports won’t just outline our borrowing and repayment history but how it deviates from expected behavior based on our genes.

More from Credit.com

This article originally appeared on Credit.com.

TIME sexuality

No Ben Carson, Homosexuality Is Not a Choice

Pointing the wrong way: Carson is just plain wrong on the science
Richard Ellis; Getty Images Pointing the wrong way: Carson is just plain wrong on the science

Jeffrey Kluger is Editor at Large for TIME.

A presidential hopeful (and a doctor) gets the science all wrong—and makes things worse when he tries to explain himself

If you’re a candidate dreaming of the White House with virtually no chance of actually winding up there, it sometimes helps to say something ridiculous—if only to get your name-recognition numbers up. That is the very best and most charitable explanation for comments by Dr. Ben Carson, a neurosurgeon, on CNN, arguing that homosexuality is “absolutely” a choice. His evidence? Prison.

“A lot of people who go into prison go into prison straight and when they come out, they’re gay,” he said. “So did something happen while they were in there?”

Prison, of course, is the worst of all possible examples Carson could have chosen—conflating sexuality with circumstance. Men confined together for years without women remain sexual beings and may take whatever outlet is available to them. Something similar was true in a less enlightened era of gay men and women who were forced to marry people of the opposite sex, and who dutifully produced children and tried to satisfy their partners despite the fact that they were getting little satisfaction themselves.

Carson, who was blowtorched in both social and mainstream media for his remarks, quickly walked them back, issuing a statement that, in some ways, only made things worse. “I’m a doctor trained in multiple fields of medicine, who was blessed to work at perhaps the finest institution of medical knowledge in the world,” he wrote. “Some of our brightest minds have looked at this debate, and up until this point there have been no definitive studies that people are born into a specific sexuality.”

That statement could indeed have the virtue of being true—provided it was issued in 1990. But since then, there’s been a steady accumulation of evidence that sexuality—like eye color, nose size, blood type and more—is baked in long before birth. The first great breakthrough was the 1991 study by neuroscientist Simon LeVay finding that a region in the hypothalamus related to sexuality known as INAH3 is smaller in gay men and women than it is in straight men. The following year, investigators at UCLA found that another brain region associated with sexuality, the midsagittal plane of the anterior commissure, is 18% larger in gay men than in straight women and 34% larger than in straight men.

One cause of the differences could be genetic. In 1993, one small study suggested a connection between sexual orientation and a section on the X chromosome called Xq28, which could predispose men toward homosexuality. The small size of the study—only 38 pairs of gay brothers—made it less than entirely reliable. But a study released just last year expanded the sample group to 409 pairs of brothers and reached similar conclusions.

Genes are not the only biological roots for homosexuality. Womb environment is thought to play a significant role too, since part of what determines development of a fetus is the level and mix of hormones to which it is exposed during gestation. In 2006, psychologist Anthony Bogaert of Brock University in Canada looked into the never-explained phenomenon of birth order appearing to shape sexuality, with gay males tending to have more older brothers than straight males. Working with a sample group of 944 homosexual and heterosexual males, Bogaert found that indeed, a first born male has about a 3% chance of being gay, a number that goes up 1% at a time for each subsequent boy until it doubles to 6% for a fourth son.

The explanation likely involves the mother’s immune system. Any baby, male or female, is initially treated as an invader by the mother’s body, but multiple mechanisms engage to prevent her system from rejecting the fetus. Male babies, with their male proteins, are perceived as slightly more alien than females, so the mother’s body produces more gender-specific antibodies against them. Over multiple pregnancies with male babies, the womb becomes more “feminized,” and that can shape sexuality.

A range of other physical differences among gay men and lesbians also argue against Carson’s thinking—finger length for instance. In heterosexual men, the index finger is significantly shorter than the ring finger. In straight women, the index and ring fingers are close to the same length. Lesbian finger length is often more similar to that of straight males. This, too, had been informally observed for a long time, but in 2000 a study at the University of California, Berkeley, seemed to validate it.

Lesbians also seem to have differences in the inner ear—of all unlikely places. In all people, sound not only enters the ear but leaves it, in the form of what are known as otoacoustic emissions—vibrations that are produced by the interaction of the cochlea and eardrum and can be detected by instruments. Heterosexual women tend to have higher frequency otoacoustic emissions than men, but gay women don’t. Still other studies have explored a link between homosexuality and handedness (with gays having a greater likelihood of being left-handed or ambidextrous) as well as hair whorl (with the hair at the crown of gay men’s heads tending to grow counterclockwise), though there are differing views on these last two.

Clearly, none of us choose our genetics or finger length or birth order or ear structure, and none of us choose our sexuality either. As with so many cases of politicians saying scientifically block-headed things, Carson either doesn’t know any of this (and as a doctor, he certainly should) or he does know it and is pretending he doesn’t. Neither answer reflects well on his fitness for political office.

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 Innovation

Five Best Ideas of the Day: March 4

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

1. We’re measuring family poverty wrong. We should measure access to opportunity to find out what’s really working.

By the Annie E. Casey Foundation

2. Anxiety, depression and more: “Four to five times more” high school athletes struggle with mental health issues than concussions.

By Gary Mihoces in USA Today

3. They provide social order and an economic structure. What if prison gangs actually make life better behind bars?

By Shannon Mizzi in Wilson Quarterly

4. Scientists have released the genetic sequence of the 2014 Ebola virus to crowdsource solutions to future outbreaks.

By Fathom Information Design

5. If new technology really cut jobs, we’d all be out of work by now.

By Walter Isaacson in the Aspen Journal of Ideas

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

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 Research

Humans Are Genetically More Similar to Their Fathers, Study Finds

Sorry mom

Every parent wants their child to be just like them, but new research shows that dads may have an advantage at least from a genetic standpoint.

According to a study by the University of North Carolina’s School of Medicine and published in the journal Nature Genetics, mammals use more DNA from the father than the mother when undergoing mutations — the genetic process that makes us who we are.

The researchers, led by genetics professor and senior author Fernando Pardo-Manuel de Villena, tested the genetic mutations of specially crossbred mice to see which mutations altered gene expression. Of the 80% that did, several hundred genes showed a “genome-wide expression imbalance in favor of the dad,” first author James Crowley told Science Daily. “This imbalance resulted in offspring whose brain-gene expression was significantly more like their father’s.”

The authors believe a similar bias would exist for human subjects. Pardo-Manuel de Villena called the results “an exceptional new research finding that opens the door to an entirely new area of exploration in human genetics.”

[Science Daily]

TIME Obesity

New Genes Mean the Future of Obesity Treatment Could Get Personal

Broken scale
Getty Images

Scientists have uncovered a trove of new genetic targets that could lead to better treatments for obesity

It took the genomes of nearly 340,000 people and more than 400 researchers in two dozen countries, but we now have the most comprehensive picture so far of the genetic contributors to obesity.

Two new papers in the journal Nature describe the results of two studies that connected the obesity-related factors of body mass index (the ratio between height and weight) and fat distribution to their potential genetic drivers. The studies did not isolate specific genes—at least not yet—but identified areas in the human genome where people with different BMIs and different patterns of fat distribution varied in their genetic code. Those variants will lead scientists to the genes they code for, and eventually to how those genes work in contributing to obesity.

MORE: Healthy-Obesity Gene Found—But Genes Aren’t Everything

“I think we have so many more opportunities now to learn about the biology of obesity through genetic contributions to these traits,” says Karen Mohlke, professor of genetics at University of North Carolina and the senior author of the report focusing on body fat distribution.

Those genetic clues may yield new weight-management treatments that are both more powerful and more personalized. “What the data supports is the fact that there are a lot of different causes of obesity,” says Dr. Elizabeth Speliotes, assistant professor of internal medicine and computational medicine and bioinformatics at the University of Michigan and senior author of the paper on body mass index. “If you’re hoping for one cause of obesity, that’s not reality. What causes you to be obese is probably slightly different from what causes me to be obese.”

Currently, however, all obesity is treated pretty much the same way. With the new knowledge gleaned from the genetics of what’s driving different types of obesity, that may change.

MORE: Gym vs. Genes: How Exercise Trumps Obesity Genes

In the study involving factors contributing to BMI, Speliotes and her team discovered 97 genetic regions, or loci that account for nearly 3% of the variation among people on BMI. Of those, 56 are entirely new. Many of the regions are in areas that code for nervous system functions, or brain systems. Some aren’t so surprising—they confirm previous studies that have implicated genetic regulators of areas that control appetite, for example—but others were more unexpected. They involved regions responsible for learning, memory and even emotional regulation, hinting that some of weight and obesity may be tied to the addiction and reward pathways that help to reinforce behaviors like eating with feelings of pleasure and satisfaction. “There were definitely a lot more loci involving the brain than I would have guessed,” says Dr. Joel Hirschhorn, director of the center for basic and translational obesity research at Boston Children’s Hospital and Harvard Medical School and one of the co-authors. “That makes obesity much more of a neurobehavioral disorder than just the fact that your fat cells are more efficient or less efficient.”

MORE: Study Identifies Four New Genetic Markers For Severe Childhood Obesity

They also uncovered some truly head-scratching connections between some genetic variants that contributed to higher BMI and lower risk of diabetes, heart disease and triglyceride levels. That suggests that there may be some protective genetic factors that counteract the effects of higher BMI, and exploiting these may be an entirely new way of treating obesity.

The group that zeroed in on the genetic factors directing how body fat is distributed had similar findings. Mohlke and her colleagues looked at the waist-hip ratio and found 49 areas in the genome that varied among the participants, 33 of which were entirely new. Most of the variants involved logical processes such as the formation of HDL and LDL cholesterol, triglycerides and processing of insulin.

MORE: New Genes Identified in Obesity: How Much of Weight is Genetic?

What was interesting, however, was the fact that many of these exerted much more power on women than on men, suggesting the need to recognize gender-based differences as a critical factor in future obesity therapies.

The findings, all of the authors stress, are just the beginning of a deeper understanding of what is driving obesity in its many forms, and how best to intervene with more personalized and potentially more effective treatments. Genes, they say, only play a part in obesity, but these studies are the first step toward a better appreciation of how genes are involved in behaviors that influence what and how much we eat. “We don’t know how much impact each of these genetic loci are going to have on whether people will need different treatments,” says Hirschhorn. “But these papers provide the tools to start answering that question. It’s possible that if we know a lot more about how somebody came to be obese, then we will know more about what to do about it.”

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