TIME Sex/Relationships

How Previous Sexual Partners Affect Offspring

At least, if you’re a fly. But the research suggests that it may be time to take into account more than just DNA when it comes to our offspring

It’s a long-held belief among animal breeders that pure-bred progeny are best produced by females who have never mated before. Call it puritanical or ridiculous, but in breeding, it’s been a long-standing practice—even though there has never been much science to back it up. Now, however, researchers at University of New South Wales in Australia believe they may finally have some evidence to give that notion some scientific support.

Working with flies, Angela Crean, a research fellow at the evolution and ecology research center, picked up on her mentor’s work of looking at how male factors can influence offspring outside of the DNA in his semen.

“The genetic tests showed that even though the second male fertilized the eggs, the offsprings’ size was determine by the condition of the first male,” she says of her findings, published in the journal Ecology Letters. “The cool thing is that the non-genetic effects we are seeing are not necessarily tied to the fertilization itself.”

Cool, or really disturbing. The implications of the study are that any mates a female has had may leave some legacy—in the form of physical or other traits that are carried in the semen (but not the DNA-containing sperm)—that could show up in her future offspring with another mate.

While there’s a growing body of work showing that a mother’s diet, her smoking status, and other lifestyle habits can have an influence on her offspring, the data on similar factors on the father’s side is just emerging. With flies it’s known, for example, that males who eat a maggot-rich diet while they’re mere larvae, develop into larger than average adults, and on top of that, sire larger than average offspring as well. Males fed a meager maggot diet tend to be smaller have have smaller progeny.

Eager to learn how this was happening, Crean conducted a series of mating experiments with female flies when their eggs were immature. At that stage, the eggs are more receptive to absorbing factors in semen, but because they aren’t fully developed, they can’t be fertilized and won’t result in baby flies. When she and her colleagues “mated” these females with males who were larger, then allowed the females to actually mate with smaller males once they were mature, the offspring turned out to be large, just like the first males the females had sexual contact with. Genetically, they were the offspring of the second, smaller male, but physically, they resembled the larger males.

The same was true when they reversed the experiment and first exposed the females to smaller flies and then mated them with the larger ones.

To be sure that the was indeed due to something in the semen, Crean repeated the studies with an unfortunate group of male flies who had their genitalia glued down so they could not pass on any semen during their encounters. (“It’s horrifying but seemed nicer than cutting them off,” she says.) When these males, both large and small, were the first “mates” for females, their size did not have an effect on the offspring when the female mated with her second mate and had offspring. In other words, those offspring were large if the second male was large, and small if the second male was small.

Crean says the idea of a female’s previous mates having an effect on their offspring isn’t unheard of. In fact, this very idea, called telegony, was proposed by ancient scholars such as Aristotle but dismissed with the advent of genetics. But new findings about epigenetics — how our behaviors, such as diet, smoking and drinking — can affect our genes and how those changes can be passed on, make the idea of such non-genetic inheritance possible. “This could be seen as a maternal effect [such as diet or smoking] where the mother’s environment are her previous mating partners,” she says. “We have to realize that it’s not just DNA that gets passed on. It opens up the opportunity for all these other pathways that we had excluded.”

And while flies aren’t people, what are the chances that the same phenomenon is occurring in human reproduction? “It’s something we definitely don’t want to speculate about yet with humans,” she says. “There is no direct scientific evidence for that at all.” At least, for now.

TIME Parenting

The Pain of Passing My Disability on to My Child

Parenting
Cecilia Cartner—Getty Images

When my daughter was six weeks old, we received official word that she had inherited my bone disorder, a condition that would likely cause her many fractures and possibly painful corrective surgeries

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This article originally appeared on Patheos.

When my oldest daughter Leah was born, many people made the same observation: “Look at those fingers! So long and skinny…just like yours, Ellen.” Right after she was born, my husband went with her for a bath as I was stitched up after my c-section. When he returned, he mentioned that her eyes were a “funny color.” All of those observations, straightforward and innocent on the surface, let me know that some of my darkest fears were probably being realized.

My daughter’s long, skinny fingers and toes, the bluish color in the whites of her eyes—these were signs that Leah had inherited a scrambled gene that would wreak havoc on her skeleton. When she was six weeks old, we received official word that Leah had indeed inherited my bone disorder, osteogenesis imperfecta (OI)—a condition that would likely cause her many fractures (I had about three dozen before the age of 11) and possibly painful corrective surgeries. I clutched her fiercely against my chest and told God that he had damn well better take care of this child. That day 14 years ago was the hardest day of my life.

I have spent much of the past 10 years or so writing about genetics and disability and the choices made possible by increasingly sophisticated technologies that allow parents to choose, to some extent, what sort of child they might have. I have talked to dozens of potential parents who, like me, have some serious genetic baggage and fear putting its weight on their children’s shoulders. And I have talked to some people who wonder whether, if their child does inherit some genetic menace that wreaks havoc on that child’s health and well-being, will they regret that they took such chances with a genetic lottery stacked against them?

I tell such people that I think it’s impossible, barring extreme psychological dysfunction, to regret your own child’s existence. And I tell them about my daughter Leah, who is bearing the weight of my own genetic baggage on her fragile skeleton, who has, yes, broken a dozen bones and deeply mourned the losses that come when yet another broken bone messes with our plans. I have watched Leah sink into a place that is really dark and really sad. But I have other stories to tell about Leah, not just the dark and sad ones.

There’s this story: One Sunday morning several months ago, I slipped on some black ice when going to get our newspaper. Landing hard on my back, I broke two ribs and a shoulder bone, and partially collapsed a lung—the kind of injuries that stronger-boned people incur when they fall from trees and roofs. I managed to crawl from the frozen front walk into our entrance hall, but couldn’t go any farther. While I lay there waiting for the ambulance to arrive, as my husband reassured my two younger children and called my mom to come stay with the kids, as I struggled to breathe, Leah sat next to me on the floor. She just sat there, silent. At one point, I said to her, “You know, Leah, don’t you? You know how I’m feeling.” I wasn’t talking just about the pain, but also the crushing disappointment of a regular day ruined, the weightier knowledge of the ruined days to come. I was talking about feeling powerless in the face of something as stupidly mundane as ice, and being betrayed by the fragile body gaining the upper hand on the strong spirit. Leah nodded. Yes, she knew.

A few months later, I was heading to pick Leah up from church choir practice. I was dreading it, because I knew that Leah would be getting some bad news at the rehearsal. For Leah, singing is a passion, and when she joined our church choir about three years ago, she found another family, a community. The choirmaster was a young man called Dr. Roberts. Dr. Roberts is a talented musician but also a gifted teacher. Leah will, I’m sure, remember him for the rest of her life as the kind of teacher and mentor who changed her life. I knew that during this particular rehearsal, Dr. Roberts was planning to let the kids know that he had taken a job in New York City and would be leaving. I knew Leah would be devastated.

She came out from the church to the parking lot and with tears streaming down her face, she said, “You know Mom? This is his dream, this job he’s taking in New York. It’s good. It’s just all good.”

So it seems that, at not quite 15 years old, Leah knows what love looks like. She knows how to help carry another’s burden. She knows that sometimes an empathic presence is more helpful than words. She knows about wanting the best for someone you care about, even when their best is your worst. That she is capable of such wisdom at such a young age is proof to me that I can never regret anything about the person Leah is and is becoming, brittle bones and all.

I want to be perfectly clear, though, about what I don’t mean. I hate those clichés about how we should be grateful for the shitty stuff in our life because it teaches us so much, about how “Everything happens for a reason.” I don’t believe that one bit.

But I’m beginning to understand that Leah’s inheritance from me is not merely a faulty gene and a fragile skeleton, but also the truest kind of compassion—the kind that arises when you know what pain looks like and feels like, and you recognize another’s need, and know just what to do.

Do I regret that Leah inherited my fragile bones? I don’t love it. I even sometimes hate it.

But while I sometimes wish I could have spared her that particular genetic fate, I’m also profoundly grateful that it was not in my power to decide what kind of kid I would get.

Because I never could have predicted, much less devised, the wounded and gracious person my daughter is becoming.

Ellen Painter Dollar is the author of No Easy Choice: A Story of Disability, Parenthood, and Faith in an Age of Advanced Reproduction (Westminster John Knox, 2012). She blogs about faith, family, disability, and ethics at Patheos. Dollar also serves on a working group sponsored by the Yale University Interdisciplinary Center on Bioethics, exploring bioethical issues related to health care and people with disabilities.

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TIME Mental Illness

Schizophrenia Linked to 108 Genes

In a groundbreaking study, researchers reveal a host of new genes involved in schizophrenia, making it possible to develop desperately needed treatments

It took 80,000 genetic samples, seven years and the work of 300 scientists from around the world, but scientists now have the most complete dossier on schizophrenia ever.

In an historic paper published in the journal Nature, the Schizophrenia Working Group of the Psychiatric Genomics Consortium identified 108 new regions on the genome linked to the psychiatric disorder, which is associated with hallucinations and psychotic episodes and affects about 1% of people worldwide.

The genetic clues are the most dramatic hints that experts have gotten so far about what causes that mental illness. Schizophrenia has had a rocky history in the psychiatric community, with some doctors early on not even recognizing it as a disorder, and others debating whether its origins were biological or caused by traumatic events or other experiences. Now, by comparing the genomes of people with and without the disorder, it’s clear that at least some of the psychotic symptoms can be traced to changes in the genes.

“For the first time, we are starting to see the underlying biological basis of the disease, and that can lay the foundation for understanding the disorder, and eventually developing treatments,” said Eric Lander, founding director of the Broad Institute of MIT and Harvard, where about one third of the DNA samples were sequenced.

MORE: Older Fathers Linked to Kids’ Autism and Schizophrenia Risk

The study used genome wide association, a technique that sequences the genomes of affected and unaffected individuals, and then compares where they differ. Those DNA differences may be hints about why people develop schizophrenia in the first place, and therefore lead to new drugs or treatments.

The 108 genetic regions aren’t all located in specific genes, nor is it known yet if this is what actually causes schizophrenia. But, like evidence at a crime scene, they may point to certain molecular pathways that are responsible for the mental illness. It’s already known that some of the identified regions, for example, are involved in how adaptable or plastic the brain is, and in regulating the immune system, a connection that experts have previously not investigated before. Other genes may also reveal new ways to potentially treat the disease, a significant improvement over the existing therapies, which only address one brain system, involving dopamine. “Thorazine was approved in 1954 as the first anti-psychotic medication, and every antipsychotic since then has relied on the same fundamental mechanism of action,” Steve Hyman, director of the Broad Institute’s Stanley Center for Psychiatric Research and professor of stem cell and regenerative biology at Harvard University said. “And their efficacy has plateaued since the 1960s.”

MORE: Most Common Psychiatric Disorders Share Genetic Roots

Having a greater suite of potential areas of inquiry, the researchers hope, will attract pharmaceutical companies back to the field of mental illness. “We now have more than 100 genes pointing to distinct pathways – calcium channels, glutamate, the immune system – this is concrete stuff, and it means that the pharmaceutical companies who left [this area of drug development] because they didn’t have anything concrete to work on, are beginning to get their toes in the water, and are thinking of jumping back in the water,” says Lander.

The genetic windfall can also help scientists piece together how genetic changes may work in tandem to cause symptoms of psychoses. They warn that these advances, and new treatments, may not come in the next year, but they may be able to provide better answers to questions about which drugs may work better in which patients, and in finding ways to detect and hold off symptoms of schizophrenia earlier, before they become debilitating. All of the genetic information released in the paper will be deposited in a public database for researchers to access and advance the understanding of the disorder.

TIME Genetics

How Our Social Networks Impact Our Health

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A new study says we may be genetically similar to our friends Digital Vision.—Getty Images

We share more than similar interests with our friends, we share genetics too

We might think we pick our pals based on who will best complement us—the old “opposite attracts” adage—but there may be something else at play. A new study published in the journal in the journal Proceedings of the National Academy of Sciences of the United States (PNAS) shows we are more genetically similar to our friends than to strangers. In fact, we’re about as genetically equivalent to our friends as we are our fourth cousins.

Though the latest findings were primarily reserved to a group of white people of European origin, the researchers say their findings suggest there is a genetic factor at play beyond physical appearance. Though the researchers say we only share about 1% of our genes with our friends, these underlying markers may make noteworthy patterns when it comes to who we decide to spend our time with, and could even influence our health.

The study is the second to recently show that the people we are closest to are also genetically similar to us. In May, another study published in PNAS found that people also tend to be genetically similar to their spouses. But why?

These questions are central to the work of researchers, James Fowler, a professor of medical genetics and political science at the University of California, San Diego, and Dr. Nicholas Christakis, a social scientist at Yale University. The pair have been building a growing body of research about why we choose our friends, and what evolutionary benefits these choices might have.

“Sharing genes with friends appears to enhance your utility to them,” says Dr. Christakis. “Consider the hypothetical example of speech. If you evolve the capacity to speak, its use to you is greatly enhanced if you form ties with others who have evolved the same capacity.” On the other hand, the researchers found that we tend to hang out with people whose immune system make up is different from ours, which also makes genetic sense, since evolutionarily we don’t want to be susceptible to the same illnesses as our best friend or partner. We could pass it to each other, and then who takes care of who?

In the past, the researchers have looked at how social contagion can spread generosity and have reported thar people are more likely to light up a cigarette if their friends do. And in a 2007 study, the pair showed that friends can influence our weight more than genetics or family members, showing that when a study participant’s friend become obese, there was a 57% greater chance that the participant would also become obese too. They believe it’s not just that we share lifestyle behaviors with our friends, but that friends change our opinions on what we believe to be appropriate social behavior. Conversely, friends could also help us stay on a weight loss plan for the same reasons. The researchers also show that social networks could also have the potential to predict epidemics given that most are set up in a similar way, where certain people are more connected and popular than others, and subsequently more likely to come in contact with disease.

In earlier studies on friendship and genetics, Christakis and Fowler suggested that genetics can influence social behavior in networks of friends, even impacting whatever predispositions those friends already have. For example, if someone is genetically predisposed to alcoholism, and they end up associating with people of similar genotypes who are more likely to have alcohol available, that could be a problem for them. But on the other hand, if that same person chooses a group of friends with a different make-up, alcohol may not be frequently present, and their predisposition remains un-triggered.

That means friendships might modify the way our own genes are expressed, the authors propose. Meaning human evolution is not just limited to the influence of physical and biological environments, but social ones as well.

TIME Friendship

Study: BFFs May Have Similar DNA

RyanJLane—Getty Images

Really close friends might be as genetically similar as fourth cousins

Next time someone says “You would really like my friend, she’s just like you,” try to refrain from giving her the side eye. It turns out she might have some science to back her up. According to a new study from Yale University and the University of California at San Diego, good friends are often genetically similar, and can share as much as 1% of the same gene variants. In genetic terms, that’s a lot. As close as, say, fourth cousins.

“This gives us a deeper accounting of the origins of friendship,” says Nicholas Christakis, professor of sociology, evolutionary biology, and medicine at Yale, who co-authored the study with James Fowler, professor of medical genetics and political science at UC San Diego. “Not only do we form ties with people superficially like ourselves, we form ties with people who are like us on a deep genetic level. They’re like our kin, though they’re not.”

To do their study, which was published in July in the Proceedings of the National Academy of Sciences, Christakis and Fowler looked at 1.5 million gene variants from the Framingham Heart Study, a dataset which has details on the friendships and genetics of its participants. Most of the participants were of European descent. Researchers genetically compared pairs of friends with pairs of strangers from among the same 1,932 subjects they studied. None of the pairs were related to each other.

The study found that, oddly, close friends are often genetically similar in their sense of smell. But it also concluded that friendship may play a role in evolution. The genes that were shared by friends saw the most “evolutionary activity”, or have evolved the fastest over the past 30,000 years. Whether the friendship or the genetic similarity came first is up for debate. Do we seek out genetically similar friends or do our friendships and mating affect what genes get passed on

“Human beings are one of the few species who form long-term, non-reproductive relationships with other members of our species,” says Fowler. “This role of affiliation is important. It ties into the success of our species.”

TIME Obesity

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

DNA is not always destiny

Austrian researchers have discovered a possible genetic explanation for why about a quarter of obese people are “metabolically healthy”—meaning they don’t have the risk factors for type 2 diabetes.

In their mice study, published in the journal Cell, the researchers were able to determine that high levels of a molecule called HO-1 was linked to poor metabolic health and a higher risk for diabetes in people who are obese. If that molecule is blocked, as they suggest it might be in people who don’t have those risks, it could reverse those consequences. Though the researchers’ study is very specified to one molecule, it brings into question once again the larger debate about whether there really is such a thing as healthy obesity.

For the last couple of years, there’s been back and forth within the medical community on the topic. The scientific concept of healthy obesity stems from recent studies that show some overweight or obese people are just as healthy as normal-weight individuals since they have normal blood pressure, they are not diabetic and they good cholesterol levels. There has even been one study that found overweight individuals lived longer than healthy-weight people. On the other hand, researchers at Mount Sinai Hospital in Toronto reviewed studies dating back to the 1950s and came to the conclusion that people cannot be both overweight and healthy. Another recent study published in the Journal of the American College of Cardiology looked at 14,828 metabolically healthy Korean adults came to the same conclusion.

“Obese individuals who are considered healthy because they don’t currently have heart-disease risk factors should not be assumed healthy by their doctors,” study author Dr. Yoosoo Chang in a statement.

But what is often overlooked in the debate is that while genes influence the body’s responses to various environments, they do not guarantee a person will be thin or overweight. “Most obesity…probably results from complex interactions among multiple genes and environmental factors that remain poorly understood,” states the Centers for Disease Control and Prevention’s explainer on obesity and genetics. And indeed, many things can play a part in whether a persons’ genes express themselves or not.

“In genetics, there are exceptions to almost every rule,” says Joy Larsen Haidle, the president-elect of the National Society of Genetic Counselors. “Studies have been done looking at identical twins with a predisposition to obesity. Not surprisingly, the twins who were physically active had less issues with body mass than the twins who were more sedentary.”

So yes, perhaps the HO-1 molecule has some implications but in the grand scheme of influence, it’s just a drop in the pond. What matters more is that efforts to lower the obesity rate in the U.S. take a comprehensive approach.

TIME Genetics

Basketball Star’s NBA Dreams Crushed by Marfan Syndrome Diagnosis

Baylor center Isaiah Austin shoots during the second half of an NCAA men's college basketball tournament regional semifinal, in Anaheim, Calif. on March 27, 2014.
Baylor center Isaiah Austin shoots during the second half of an NCAA men's college basketball tournament regional semifinal, in Anaheim, Calif. on March 27, 2014. Jae C. Hong—AP

Isaiah Austin was diagnosed with Marfan syndrome. But what's that?

Former Baylor center Isaiah Austin’s hopes of playing in the NBA were dashed this weekend when he was diagnosed with a disorder called Marfan syndrome. A standard EKG during a routine exam for the NBA draft revealed an abnormality, and further genetic testing showed he has Marfan syndrome.

But what is that exactly?

Marfan syndrome is a genetic disorder that affects the connective tissues in the body, and can interfere with the functionality of the heart, eyes, blood vessels and skeleton. According to the Mayo Clinic, it’s common for people with Marfan syndrome to be tall with disproportionately long arms, legs, fingers and toes. Austin is 7 ft. 1 in. tall.

The severity of the disease can differ from person to person, but if the heart and blood vessels are affected it can become a fatal disease. For example, aortic enlargement is a possible life threatening side effect and some players have died in the middle of a game due to the disease.

“They said I wouldn’t be able to play basketball anymore at a competitive level,” Austin told ESPN. “They found the gene in my blood sample. They told me that my arteries in my heart are enlarged and that if I overwork myself and push too hard that my heart could rupture. The draft is four days away, and I had a dream that my name was going to be called.”

According to the Marfan Foundation, around 1 in 5,000 people have Marfan syndrome across all races and ethnicities, though only about half of those with the disorder know they have it. The majority of people with the disease inherited it from a parent, since children of an individual with the disease have a 50% chance of getting the mutated gene that causes the disorder. About 25% of people will be the first to have the gene, meaning the disease can also be spurred by what’s called a spontaneous mutation.

It’s been rumored but not confirmed that Michael Phelps has Marfan syndrome, and in 1962, Cincinnati doctor Abraham Gordon was the first to propose that former president Abraham Lincoln suffered from the disease — just one of several theories to explain Abe’s lanky stature.

Treatment for Marfan syndrome usually includes taking medication to make sure blood pressure stays in check so that heart strain stays low. In some cases, heart, spine or eye surgery may be necessary.

“This is devastating news, but Isaiah has the best support system anyone could ask for, and he knows that all of Baylor Nation is behind him,” head coach Scott Drew said in a statement. “His health is the most important thing, and while it’s extremely sad that he won’t be able to play in the NBA, our hope is that he’ll return to Baylor to complete his degree and serve as a coach in our program.”

TIME Genetics

Genetics In Court Is a Very Messy Business

Courts may soon face the challenge of determining whether genetics can be linked to criminal behavior

The “my genes made me do it” defense is not solely reserved for Law and Order SVU. At least, not for long.

As science continues to tell us more and more about genetics, geneticists and medical ethicists believe it’s only a matter of time before people start using genetic predispositions to get them out of guilty verdicts. A precedent has been set with a number of recent cases, but scientists and lawyers alike flag that a poor understanding of genetics and behavior could result in a dangerous misuse of science in the legal system. That’s what Dr. Paul Appelbaum, the director of Columbia University’s Center for Research on Ethical, Legal and Social Implications of Psychiatric, Neurologic and Behavioral Genetics argues in an essay published today in the journal Neuron.

The problem is that a genetic predisposition for, say, violence, is not the same as a diagnosed mental disorder. “The ‘my genes made me do it’ argument is problematic because there is no evidence that genes make a person behave in a certain way that is beyond their capacity to control or recognize is wrong,” says Appelbaum. So far, studies on some of the leading genetic markers are only associational, and do not draw definite conclusions about a person’s behavior. Even if a person has a genetic mutation that puts them at a higher risk for cancer, there’s no guarantee they will develop the disease.

A genetics argument in criminal court may make scientists squeamish, and Appelbaum says that should apply to civil court—which handles things like divorce and some property damage cases—as well. An interesting case in Canada raised this red flag. In Adacsi v Amin, a woman named Tammy Adacsi sued her landlords after the house she was staying in caught on fire. She was hospitalized for months and claimed that her injuries prevented her from ever working again. The landlords demanded in court that Adacsi be ordered to submit a blood sample to test for whether she is a carrier of a gene mutation for Huntington’s Disease, which runs in her family. The landlords argued some of her symptoms could be a result of that disorder. The court ruled in their favor. Appelbaum says it’s not out of the question that a similar thing could happen in the U.S.

In the future, it might be even easier for courts to get access to defendants’ genetic data. “If it’s true that more and more of us will have our genomes sequenced, then this information will be sitting somewhere. It will be much easier for litigants in civil cases and prosecutors or defense attorneys in criminal cases to subpoena something that already exists,” says Applebaum. “The increased availability of this information in the future might spur its introduction into court.”

His recommendation is that courts allow genetics to enter arguments very, very slowly.

TIME The Weekend Read

What Science Says About Race and Genetics

DNA
Illustration by Umberto Mischi for TIME

The New York Times' former science editor on research showing that evolution didn't stop when human history began.

A longstanding orthodoxy among social scientists holds that human races are a social construct and have no biological basis. A related assumption is that human evolution halted in the distant past, so long ago that evolutionary explanations need never be considered by historians or economists.

New analyses of the human genome have established that human evolution has been recent, copious, and regional.In the decade since the decoding of the human genome, a growing wealth of data has made clear that these two positions, never at all likely to begin with, are simply incorrect. There is indeed a biological basis for race. And it is now beyond doubt that human evolution is a continuous process that has proceeded vigorously within the last 30,000 years and almost certainly — though very recent evolution is hard to measure — throughout the historical period and up until the present day.

New analyses of the human genome have established that human evolution has been recent, copious, and regional. Biologists scanning the genome for evidence of natural selection have detected signals of many genes that have been favored by natural selection in the recent evolutionary past. No less than 14% of the human genome, according to one estimate, has changed under this recent evolutionary pressure.

Analysis of genomes from around the world establishes that there is a biological basis for race, despite the official statements to the contrary of leading social science organizations. An illustration of the point is the fact that with mixed race populations, such as African Americans, geneticists can now track along an individual’s genome, and assign each segment to an African or European ancestor, an exercise that would be impossible if race did not have some basis in biological reality.

Racism and discrimination are wrong as a matter of principle, not of science. That said, it is hard to see anything in the new understanding of race that gives ammunition to racists. The reverse is the case. Exploration of the genome has shown that all humans, whatever their race, share the same set of genes. Each gene exists in a variety of alternative forms known as alleles, so one might suppose that races have distinguishing alleles, but even this is not the case. A few alleles have highly skewed distributions but these do not suffice to explain the difference between races. The difference between races seems to rest on the subtle matter of relative allele frequencies. The overwhelming verdict of the genome is to declare the basic unity of humankind.

Genetics and Social Behavior

Human evolution has not only been recent and extensive, it has also been regional. The period of 30,000 to 5,000 years ago, from which signals of recent natural selection can be detected, occurred after the splitting of the three major races, so represents selection that has occurred largely independently within each race. The three principal races are Africans (those who live south of the Sahara), East Asians (Chinese, Japanese, and Koreans), and Caucasians (Europeans and the peoples of the Near East and the Indian subcontinent). In each of these races, a different set of genes has been changed by natural selection. This is just what would be expected for populations that had to adapt to different challenges on each continent. The genes specially affected by natural selection control not only expected traits like skin color and nutritional metabolism, but also some aspects of brain function. Though the role of these selected brain genes is not yet understood, the obvious truth is that genes affecting the brain are just as much subject to natural selection as any other category of gene.

Human social structures change so slowly and with such difficulty as to suggest an evolutionary influence at work.What might be the role of these brain genes favored by natural selection? Edward O. Wilson was pilloried for saying in his 1975 book Sociobiology that humans have many social instincts. But subsequent research has confirmed the idea that we are inherently sociable. From our earliest years we want to belong to a group, conform to its rules and punish those who violate them. Later, our instincts prompt us to make moral judgments and to defend our group, even at the sacrifice of one’s own life.

Anything that has a genetic basis, such as these social instincts, can be varied by natural selection. The power of modifying social instincts is most visible in the case of ants, the organisms that, along with humans, occupy the two pinnacles of social behavior. Sociality is rare in nature because to make a society work individuals must moderate their powerful selfish instincts and become at least partly altruistic. But once a social species has come into being, it can rapidly exploit and occupy new niches just by making minor adjustments in social behavior. Thus both ants and humans have conquered the world, though fortunately at different scales.

Conventionally, these social differences are attributed solely to culture. But if that’s so, why is it apparently so hard for tribal societies like Iraq or Afghanistan to change their culture and operate like modern states? The explanation could be that tribal behavior has a genetic basis. It’s already known that a genetic system, based on the hormone oxytocin, seems to modulate the degree of in-group trust, and this is one way that natural selection could ratchet the degree of tribal behavior up or down.

Human social structures change so slowly and with such difficulty as to suggest an evolutionary influence at work. Modern humans lived for 185,000 years as hunters and gatherers before settling down in fixed communities. Putting a roof over one’s head and being able to own more than one could carry might seem an obvious move. The fact that it took so long suggests that a genetic change in human social behavior was required and took many generations to evolve.

Tribalism seems to be the default mode of human political organization. It can be highly effective: The world’s largest land empire, that of the Mongols, was a tribal organization. But tribalism is hard to abandon, again suggesting that an evolutionary change may be required.

The various races have evolved along substantially parallel paths, but because they have done so independently, it’s not surprising that they have made these two pivotal transitions in social structure at somewhat different times. Caucasians were the first to establish settled communities, some 15,000 years ago, followed by East Asians and Africans. China, which developed the first modern state, shed tribalism two millennia ago, Europe did so only a thousand years ago, and populations in the Middle East and Africa are in the throes of the process.

Two case studies, one from the Industrial Revolution and the other from the cognitive achievements of Jews, provide further evidence of evolution’s hand in shaping human social behavior within the recent past.

The Behavioral Makeover Behind the Industrial Revolution

The essence of the Industrial Revolution was a quantum leap in society’s productivity. Until then, almost everyone but the nobility lived a notch or two above starvation. This subsistence-level existence was a characteristic of agrarian economies, probably from the time that agriculture was first invented.

Perhaps productivity increased because the nature of the people had changed.The reason for the economic stagnation was not lack of inventiveness: England of 1700 possessed sailing ships, firearms, printing presses, and whole suites of technologies undreamed of by hunter gatherers. But these technologies did not translate into better living standards for the average person. The reason was a Catch-22 of agrarian economies, called the Malthusian trap, after the Rev. Thomas Malthus. In his 1798 Essay on the Principle of Population, Malthus observed that each time productivity improved and food became more plentiful, more infants survived to maturity, and the extra mouths ate up the surplus. Within a generation, everyone was back to living just above starvation level.

Malthus, strangely enough, wrote his essay at the very moment when England, shortly followed by other European countries, was about to escape from the Malthusian trap. The escape consisted of such a substantial increase in production efficiency that extra workers enhanced incomes instead of constraining them.

This development, known as the Industrial Revolution, is the salient event in economic history, yet economic historians say they have reached no agreement on how to account for it. “Much of modern social science originated in efforts by late nineteenth and twentieth century Europeans to understand what made the economic development path of western Europe unique; yet these efforts have yielded no consensus,” writes the historian Kenneth Pomeranz. Some experts argue that demography was the real driver: Europeans escaped the Malthusian trap by restraining fertility through methods such as late marriage. Others cite institutional changes, such as the beginnings of modern English democracy, secure property rights, the development of competitive markets, or patents that stimulated invention. Yet others point to the growth of knowledge starting from the Enlightenment of the 17th and 18th century or the easy availability of capital.

This plethora of explanations and the fact that none of them is satisfying to all experts point strongly to the need for an entirely new category of explanation. The economic historian Gregory Clark has provided one by daring to look at a plausible yet unexamined possibility: that productivity increased because the nature of the people had changed.

Clark’s proposal is a challenge to conventional thinking because economists tend to treat people everywhere as identical, interchangeable units. A few economists have recognized the implausibility of this position and have begun to ask if the nature of the humble human units that produce and consume all of an economy’s goods and services might possibly have some bearing on its performance. They have discussed human quality, but by this they usually mean just education and training. Others have suggested that culture might explain why some economies perform very differently from others, but without specifying what aspects of culture they have in mind. None has dared say that culture might include an evolutionary change in behavior — but neither do they explicitly exclude this possibility.

To appreciate the background of Clark’s idea, one has to return to Malthus. Malthus’s essay had a profound effect on Charles Darwin. It was from Malthus that Darwin derived the principle of natural selection, the central mechanism in his theory of evolution. If people were struggling on the edge of starvation, competing to survive, then the slightest advantage would be decisive, Darwin realized, and the owner would bequeath that advantage to his children. These children and their offspring would thrive while others perished.

“In October 1838, that is, fifteen months after I had begun my systematic inquiry,” Darwin wrote in his autobiography, “I happened to read for amusement Malthus on Population, and being well prepared to appreciate the struggle for existence which everywhere goes on from long-continued observation of the habits of animals and plants, it at once struck me that under these circumstances favorable variations would tend to be preserved, and unfavorable ones to be destroyed. The results of this would be the formation of a new species. Here then I had at last got a theory by which to work.”

Given the correctness of Darwin’s theory, there is no reason to doubt that natural selection was working on the very English population that provided the evidence for it. The question is that of just what traits were being selected for.

The Four Key Traits

Clark has documented four behaviors that steadily changed in the English population between 1200 and 1800, as well as a highly plausible mechanism of change. The four behaviors are those of interpersonal violence, literacy, the propensity to save, and the propensity to work.

Profound events are likely to have profound causes.Homicide rates for males, for instance, declined from 0.3 per thousand in 1200 to 0.1 in 1600 and to about a tenth of this in 1800. Even from the beginning of this period, the level of personal violence was well below that of modern hunter-gatherer societies. Rates of 15 murders per thousand men have been recorded for the Aché people of Paraguay.

Work hours steadily increased throughout the period, and interest rates fell. When inflation and risk are subtracted, an interest rate reflects the compensation that a person will demand to postpone immediate gratification by postponing consumption of a good from now until a future date. Economists call this attitude time preference, and psychologists call it delayed gratification. Children, who are generally not so good at delaying gratification, are said to have a high time preference. In his celebrated marshmallow test, the psychologist Walter Mischel tested young children as to their preference for receiving one marshmallow now or two in fifteen minutes. This simple decision turned out to have far-reaching consequences: Those able to hold out for the larger reward had higher SAT scores and social competence in later life. Children have a very high time preference, which falls as they grow older and develop more self-control. American six-year-olds, for instance, have a time preference of about 3% per day, or 150% per month; this is the extra reward they must be offered to delay instant gratification. Time preferences are also high among hunter-gatherers.

Interest rates, which reflect a society’s time preferences, have been very high — about 10% — from the earliest historical times and for all societies before 1400 AD for which there is data. Interest rates then entered a period of steady decline, reaching about 3% by 1850. Because inflation and other pressures on interest rates were largely absent, Clark argues, the falling interest rates indicate that people were becoming less impulsive, more patient, and more willing to save.

These behavioral changes in the English population between 1200 and 1800 were of pivotal economic importance. They gradually transformed a violent and undisciplined peasant population into an efficient and productive workforce. Turning up punctually for work every day and enduring eight eight hours or more of repetitive labor is far from being a natural human behavior. Hunter-gatherers do not willingly embrace such occupations, but agrarian societies from their beginning demanded the discipline to labor in the fields and to plant and harvest at the correct times. Disciplined behaviors were probably evolving gradually within the agrarian English population for many centuries before 1200, the point at which they can be documented.

Clark has uncovered a genetic mechanism through which the Malthusian economy may have wrought these changes on the English population: The rich had more surviving children than did the poor. From a study of wills made between 1585 and 1638, he finds that will makers with £9 or less to leave their heirs had, on average, just under two children. The number of heirs rose steadily with assets, such that men with more than £1,000 in their gift, who formed the wealthiest asset class, left just over four children.

The English population was fairly stable in size from 1200 to 1760, meaning that if the rich were having more children than the poor, most children of the rich had to sink in the social scale, given that there were too many of them to remain in the upper class.

Their social descent had the far-reaching genetic consequence that they carried with them inheritance for the same behaviors that had made their parents rich. The values of the upper middle class — nonviolence, literacy, thrift, and patience — were thus infused into lower economic classes and throughout society. Generation after generation, they gradually became the values of the society as a whole. This explains the steady decrease in violence and increase in literacy that Clark has documented for the English population. Moreover, the behaviors emerged gradually over several centuries, a time course more typical of an evolutionary change than a cultural change.

In a broader sense, these changes in behavior were just some of many that occurred as the English population adapted to a market economy. Markets required prices and symbols and rewarded literacy, numeracy, and those who could think in symbolic ways. “The characteristics of the population were changing through Darwinian selection,” Clark writes. “England found itself in the vanguard because of its long, peaceful history stretching back to at least 1200 and probably long before. Middle-class culture spread throughout the society through biological mechanisms.”

Economic historians tend to see the Industrial Revolution as a relatively sudden event and their task as being to uncover the historical conditions that precipitated this immense transformation of economic life. But profound events are likely to have profound causes. The Industrial Revolution was caused not by events of the previous century but by changes in human economic behavior that had been slowly evolving in agrarian societies for the previous 10,000 years.

This of course explains why the practices of the Industrial Revolution were adopted so easily by other European countries, the United States, and East Asia, all of whose populations had been living in agrarian economies and evolving for thousands of years under the same harsh constraints of the Malthusian regime. No single resource or institutional change — the usual suspects in most theories of the Industrial Revolution — is likely to have become effective in all these countries around 1760, and indeed none did.

That leaves the questions of why the Industrial Revolution was perceived as sudden and why it emerged first in England instead of in any of the many other countries where conditions were ripe. Clark’s answer to both these questions lies in the sudden growth spurt in the English population, which tripled between 1770 and 1860. It was this alarming expansion that led Malthus to write his foreboding essay on population.

But contrary to Malthus’s gloomy prediction of a population crash induced by vice and famine, which would have been true at any earlier stage of history, incomes on this occasion rose, heralding the first escape of an economy from the Malthusian trap. English workmen contributed to this spurt, Clark dryly notes, as much by their labors in the bedroom as on the factory floor.

Clark’s data provide substantial evidence that the English population responded genetically to the harsh stresses of a Malthusian regime and that the shifts in its social behavior from 1200 to 1800 were shaped by natural selection. The burden of proof is surely shifted to those who might wish to assert that the English population was miraculously exempt from the very forces of natural selection whose existence it had suggested to Darwin.

Explaining Ashkenazi IQ

A second instance of very recent human evolution may well be in evidence in European Jews, particularly the Ashkenazim of northern and central Europe. In proportion to their population, Jews have made outsize contributions to Western civilization. A simple metric is that of Nobel prizes: Though Jews constitute only 0.2% of the world’s population, they won 14% of Nobel prizes in the first half of the 20th century, 29% in the second and so far 32% in the present century. There is something here that requires explanation. If Jewish success were purely cultural, such as hectoring mothers or a zeal for education, others should have been able to do as well by copying such cultural practices. It’s therefore reasonable to ask if genetic pressures in Jews’ special history may have enhanced their cognitive skills.

It’s reasonable to ask if genetic pressures in Jews’ special history may have enhanced their cognitive skills.Just such a pressure is described by two economic historians, Maristella Botticini and Zvi Eckstein, in their book “The Chosen Few.” In 63 or 65 AD, the high priest Joshua ben Gamla decreed that every Jewish father should send his sons to school so that they could read and understand Jewish law. Jews at that time earned their living mostly by farming, as did everyone else, and education was both expensive and of little practical use. Many Jews abandoned Judaism for the new and less rigorous Jewish sect now known as Christianity.

Botticini and Eckstein say nothing about genetics but evidently, if generation after generation the Jews less able to acquire literacy became Christians, literacy and related abilities would on average be enhanced among those who remained Jews.

As commerce started to pick up in medieval Europe, Jews as a community turned out to be ideally suited for the role of becoming Europe’s traders and money-lenders. In a world where most people were illiterate, Jews could read contracts, keep accounts, appraise collateral, and do business arithmetic. They formed a natural trading network through their co-religionists in other cities, and they had rabbinical courts to settle disputes. Jews moved into money-lending not because they were forced to do so, as some accounts suggest, but because they chose the profession, Botticini and Eckstein say. It was risky but highly profitable. The more able Jews thrived and, just as in the rest of the pre-19th century world, the richer were able to support more surviving children.

As Jews adapted to a cognitively demanding niche, their abilities increased to the point that the average IQ of Ashkenazi Jews is, at 110 to 115, the highest of any known ethnic group. The population geneticists Henry Harpending and Gregory Cochran have calculated that, assuming a high heritability of intelligence, Ashkenazi IQ could have risen by 15 points in just 500 years. Ashkenazi Jews first appear in Europe around 900 AD, and Jewish cognitive skills may have been increasing well before then.

The emergence of high cognitive ability among the Ashkenazim, if genetically based, is of interest both in itself and as an instance of natural selection shaping a population within the very recent past.

The Adaptive Response to Different Societies

The hand of evolution seems visible in the major transitions in human social structure and in the two case studies described above. This is of course a hypothesis; proof awaits detection of the genes in question. If significant evolutionary changes can occur so recently in history, other major historical events may have evolutionary components. One candidate is the rise of the West, which was prompted by a remarkable expansion of European societies, both in knowledge and geographical sway, while the two other major powers of the medieval world, China and the house of Islam, ascendant until around 1500 AD, were rapidly overtaken.

Civilizations may rise and fall but evolution never ceases.In his book The Wealth and Poverty of Nations, the economic historian David Landes examines every possible factor for explaining the rise of the West and the stagnation of China and concludes, in essence, that the answer lies in the nature of the people. Landes attributes the decisive factor to culture, but describes culture in such a way as to imply race.

“If we learn anything from the history of economic development, it is that culture makes all the difference,” he writes. “Witness the enterprise of expatriate minorities — the Chinese in East and Southeast Asia, Indians in East Africa, Lebanese in West Africa, Jews and Calvinists throughout much of Europe, and on and on. Yet culture, in the sense of the inner values and attitudes that guide a population, frightens scholars. It has a sulfuric odor of race and inheritance, an air of immutability.”

Sulfuric odor or not, the culture of each race is what Landes suggests has made the difference in economic development. The data gathered by Clark on declining rates of violence and increasing rates of literacy from 1200 to 1800 provide some evidence for a genetic component to culture and social institutions.

Though equivalent data does not exist for the Chinese population, China’s society has been distinctive for at least 2,000 years and intense pressures on survival would have adapted the Chinese to their society just as Europeans became adapted to theirs.

Do Chinese carry genes for conformism and authoritarian rule? May Europeans have alleles that favor open societies and the rule of law? Obviously this is unlikely to be the case. But there is almost certainly a genetic component to the propensity for following society’s rules and punishing those who violate them. If Europeans were slightly less inclined to punish violators and Chinese slightly more so, that could explain why European societies are more tolerant of dissenters and innovators, and Chinese societies less so. Because the genes that govern rule following and punishment of violators have not yet been identified, it is not yet known if these do in fact vary in European and Chinese populations in the way suggested. Nature has many dials to twist in setting the intensities of the various human social behaviors and many different ways of arriving at the same solution.

For most of recorded history, Chinese civilization has been pre-eminent and it’s reasonable to assume that the excellence of Chinese institutions rests on a mix of culture and inherited social behavior.

The rise of the West, too, is unlikely to have been just some cultural accident. As European populations became adapted to the geographic and military conditions of their particular ecological habitat, they produced societies that have turned out to be more innovative and productive than others, at least under present circumstances.

That does not of course mean that Europeans are superior to others — a meaningless term in any case from the evolutionary perspective – any more than Chinese were superior to others during their heyday. China’s more authoritarian society may once again prove more successful, particularly in the wake of some severe environmental stress.

Civilizations may rise and fall but evolution never ceases, which is why genetics may play some role alongside the mighty force of culture in shaping the nature of human societies. History and evolution are not separate processes, with human evolution grinding to a halt some decent interval before history begins. The more that we are able to peer into the human genome, the more it seems that the two processes are delicately intertwined.

Nicholas Wade is a former science editor at The New York Times. This piece is adapted from the new book, A Troublesome Inheritance, published by the Penguin Press.

TIME Aging

Long-Life Secrets From The 115-Year-Old Woman

Hendrikje van Andel-Schipper, 113 years
HOOGEVEEN, NETHERLANDS: Hendrikje van Andel-Schipper at 113 years old, CONTINENTAL—AFP/Getty Images

We've thoroughly exhausted the search for the "Fountain of Youth," yet scientists are still trying to decode the secret to longevity.

The secret to a longer life may be discovered in the body of one of the world’s oldest humans.

When Hendrikje Van Andel-Schipper donated her body to science, she gave longevity researchers a truly special gift. She was the oldest person in the world when she died at age 115, and her body, in the hands of a team of Dutch researchers, launched a slew of breakthrough investigations into why some people live longer than others. In 2010, scientists led by Dr. Henne Holstege at the VU University Medical Center in Amsterdam sequenced Andel-Schipper’s genome with the hope they would uncover something about the secrerts of longevity from her genes.

In Holstege’s latest study, published in the journal Genome Research, the researchers looked for gene mutations in Andel-Schipper’s blood. When stem cells divide, they generate different types of blood cells, like white blood cells. But these divisions can also cause mutations. They wanted to determine whether mutations can occur in healthy white blood cells over time, and if they have any impact on health. They discovered that although she was a mostly healthy person, there were hundreds of genetic mutations in her cells, which they thought was curious. So the researchers explored where these white blood cells were coming from, and took a look at her stem cells.

Scientists estimate that everyone starts their life with about 20,000 stem cells, 1,300 of which are considered “active.” To the researchers’ surprise, Andel-Schipper only had two active stem cells at the time of her death. “At first I could not believe that it was true. I thought it must be a technical error. It cannot be true that this person can still be alive with two stem cells,” says Holstege.

The researchers then looked at the length of the telomeres on Andel-Schipper’s blood cells and discovered they were extremely short compared to all her other organs. As cells age, their telomeres get shorter. Therefore, the researchers realized that there may be a limit to the number of divisions our stem cells can make, and that at a certain point, they must start to die from division exhaustion. It’s possible that stem cell exhaustion was the cause of death of Andel-Schipper, and that it could also be the cause of death among many people who live to great ages, although the researchers acknowledge that more research needs to be done to determine whether this holds true.

If proven, the implications for aging are significant. If there’s a limit to the life of stem cells, that’s a limit to human life. But what if you could replenish them?

Aging is a puzzling phenomenon for researchers, and even businesses like Google are setting their sights on life expectancy. In September, TIME broke the news that Google co-founder Larry Page plans to launch a firm called Calico, which will focus on solving health problems, specifically expanding the human lifespan. The details of the endeavor remain undisclosed, but it’s more evidence that the desire to understand aging reaches far beyond the lab. Meanwhile, Dr. Holstege’s team is still searching Andel-Schipper’s genome for answers. Dr. Holstege is in the process of searching her genome for elements that protect against Alzheimer’s, since Andel-Schipper grew old with no signs of dementia.

“We need to analyse the genomes of more individuals just as special as Mrs. van Andel-Schipper: cognitively healthy and extremely old,” says Dr. Holstege.

So while there are likely several overlapping factors at play, the new research suggests that perhaps we should consider stem cells one of the secrets to a longer life.

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