TIME medicine

Scientists Find a Gene That Regulates Sleep

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Vincent Besnault—Getty Images

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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Atomic Imagery—Getty Images

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

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

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

What are epigenetic changes?

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

What controls epigenetic changes?

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

Can these epigenetic changes be passed from parent to child?

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

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

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

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

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

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

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

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

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

So is that good or bad?

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

TIME Longevity

Scientists Discover the Secret to Keeping Cells Young

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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.

[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

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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

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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.

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This article originally appeared on Credit.com.

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