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.

TIME Genetics

3D Mugshots Created From DNA Samples? It’s a Tantalizing Possibility

An officer at the forensic laboratory of the Turkish National Police. In the future, crime busters might be able to create mugshots from a single strand of hair Halil Sagirkaya—Anadolu Agency/Getty Images

Scientists have found genes that are associated with defining facial features

If the technology keeps making headway, CSI teams can expect an enormously powerful tool in the future: three-dimensional mug shots gleaned from a single strand of hair.

Researchers led by anthropologist Mark Shriver of Pennsylvania State University published a study in PLOS Genetics Thursday, outlining their attempts to understand how the genetic code shapes our facial appearance.

By creating 3D-models of 592 people of mixed European and West African ancestry, and comparing the subjects’ genomes, the scientists pinpointed 24 ‘single nucleotide polymorphisms’ (SNP) that were significantly associated with facial shape.

However, seemingly rudimentary characteristics like sizes are so far proving extremely challenging to predict.

“One thing we’re certain of: there’s no single gene that suddenly makes your nose big or small,” says Kun Tang, a biologist at the Shanghai Institutes for Biological Sciences in China.

Tang’s research team has however managed to find a gene that strongly predicts lip shape in Han Chinese women. As for crime scene investigations, though, it seems like the police will have to stick to good old, well-tested forensics methods for a little while yet.

[Nature]

TIME Obesity

Fried Foods Are Bad for Fat Genes

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Melodie DeWitt—Getty Images/fStop

Study shows frequent consumption can have twice the weight gain effect than those at risk for obesity

We know that some people are dealt a genetically more difficult hand when it comes to obesity, as studies have shown that genes play a role in how we process high-fat and high-sugar diets. Now it’s time to cross fried foods off that list, if you haven’t already.

Of course, fried food isn’t good for anyone’s health. But a new study published in the journal BMJ found that eating fried food interacts with genes associated with obesity and can double one’s risk for becoming obese.

The researchers studied 37,000 men and women, and had them fill out questionnaires that asked how often they consumed fried food. They also assessed the participants’ genetic risk based on 32 different gene variants known to be related to body mass index (BMI) and obesity. Participants who had the highest genetic score for obesity and ate fried foods four or more times a week had a BMI around two pounds greater than those who ate fried foods once a week. But for people with the lowest genetic scores, the differences were closer to one pound. Eating fried food more than four times a week had twice the effect on the body for people at the greatest genetic risk for obesity.

But not being genetically predisposed to obesity hardly makes one immune. Another recent study published in BMJ reports that people who are exposed to a lot of takeaway restaurants around their homes or work are more likely to consume those foods, and subsequently more likely to be obese. Other research has shown that food deserts–places where fresh food is hard to come by–contribute to the obesity epidemic as well.

“This work provides formal proof of interaction between a combined genetic risk score and environment in obesity,” Alexandra Blakemore and Dr. Jessica Buxton, professors at Imperial College London wrote in a corresponding editorial. But they’re not exactly hopeful that this knowledge will made a difference. The results “are unlikely to influence public health advice,” they write, “since most of us should be eating fried food more sparingly anyway.”

TIME mental health

More Bad News for Older Dads: Higher Risk of Kids With Mental Illness

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The effect of paternal age on autism, schizophrenia, and ADHD may be greater than previously thought

For so long, mothers – particularly older moms — bore the brunt of responsibility for genetic disorders in their children. And for good reason. Eggs are stockpiled from birth, not made anew with each monthly reproductive cycle, so eggs stored for decades until childbearing can develop genetic mutations. The older the mother, the greater the chance of abnormalities that can contribute to conditions such as Down syndrome, especially after age 35. Fathers, on the other hand, constantly make sperm, so their reproductive contribution was supposed to be fresher and free of accumulated DNA damage.

That may not actually be the case, however, according to the latest study in JAMA Psychiatry investigating how advanced paternal age can affect rates of mental illness and school performance in children. After a groundbreaking genetic analysis in 2012 highlighted the surprising number of spontaneous mutations that can occur in the sperm of older men, scientists have been delving into the relationship to better quantify and describe the risk. While some studies confirmed the connection, others failed to find a link.

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

In the latest research, Brian D’Onofrio, associate professor of psychological and brain sciences at Indiana University, and his colleagues attempted to address one of the biggest problems with studying the trend. Most of the previous investigations compared younger fathers and their children to different older fathers and their offspring. “That’s comparing apples and oranges,” says D’Onofrio. “We know young fathers and old fathers vary on many things.”

So his team turned to birth registry data from Sweden and compared children born to the same fathers, evaluating the siblings on various mental health and academic measures. The study included 2.6 million children born to 1.4 million fathers.

What they found surprised them – so much so that they spent about two months re-evaluating the data to make sure their numbers were correct. While the previous genetic study found that an older father’s DNA may account for about 15% of autism cases, D’Onofrio’s group found that the increased risk for children of fathers older than 45 years soared to 3.5 times compared to that of younger fathers. Children of older fathers also showed a 13 fold higher risk of developing attention deficit-hyperactivity disorder (ADHD), a 25 times greater chance of getting bipolar disorder, and twice the risk of developing a psychosis. These kids also had doubled risk of having a substance abuse problem and a 60% higher likelihood of getting failing grades in school compared with those with younger fathers.

MORE: Too Old to Be a Dad?

“What this study suggests is that the specific effect of older paternal age may actually be worse than we originally thought,” says D’Onofrio.

The scientists controlled for some of the well-known factors that can account for poor grades and psychoses and mental illnesses, such as the child’s birth order, the mother’s age, the mother’s and father’s education level, their history of psychiatric problems, and their history of criminality. Even after adjusting for these possible effects, they still found a strong correlation between higher rates of mental illness among younger siblings compared with their older ones.

The 2012 genetic study pointed to a possible reason for the higher rates of mental illnesses – because genetic mutations tend to accumulate each time a cell divides, older men may build up more spontaneous, or de novo, changes each time the sperm’s DNA is copied. While a 25-year-old father may pass on an average of 25 mutations to his child, a 40-year-old dad may bequeath each offspring as many as 65; the researchers calculated that the de novo mutation rate doubled with every 16.5 years of the father’s age. In contrast, regardless of her age, a mother tends to pass on about 15 mutations via her eggs.

The findings still need to be repeated by other groups, but the large sample size and the careful way that the researchers designed the study – to analyze the same fathers over time – suggest that the association is significant and worth considering for those who put off having a family. “This study suggests that paternal age does need to be considered as one of many risk factors associated with children’s mental health,” says D’Onofrio.

MORE: Fewer Drugs Being Prescribed to Treat Mental Illness Among Kids

Whether it gains the same amount of weight that maternal age does in family planning decisions isn’t clear yet, but even if it is confirmed, he notes that the correlation doesn’t predict that every child born to an older father will develop a mental illness. Older parents also have protective factors against these disorders, including more maturity and financial and social stability, that can offset some of the effect.

TIME Evolution

Did Miserably Wintry Weather Give Humans a Thirst for Milk?

Spilt Milk
Christopher T Stein / Getty Images

Geneticists find new clues in mankind's sudden and mysterious love of milk

Somewhere in the course of human evolution, our European ancestors learned to stop loathing lactose and love the udder, and a new study sheds light on our sudden and mysterious love of milk.

NPR reports that geneticists in Sweden have traced the love story back to recent history. Even though one-third of Spaniards are more than a little tolerant of lactose (Manchego is exhibit A), geneticists found lactose intolerant genes in the bones of their ancestors just 5,000 years ago.

In other words, Spaniards seem to have experienced a sudden burst of lactose love, and this finding pokes a hole in a competing theory of our evolution. It was hypothesized that lactose tolerance spread among sun — starved Europeans in the north, hungry for vitamin D. They got their fix of D from cow’s milk, and the more milk they could digest, the more they thrived. So why would the gene proliferate in sun-drenched regions of the South?

Good question, and for scientists hard on the case, the plot has just thickened.

[NPR]

MONEY health

DNA Testing: Crack Open Your Genetic Code

Genetic testing is getting cheaper and easier. What you should know before you use it.

For as little as $100, here are some secrets you can unlock from your DNA: Whether you could have inherited a risk factor for certain kinds of cancer. Or how much of your genetic makeup comes from Neanderthals.

You might also learn whether your genes raise your chances of getting diabetes — but your doctor will still probably be more interested in other, more obvious risk factors, such as your family history and diet.

In short, although technology is quickly making it cheaper and easier to get data about yourself, it’s not always clear which information is worth getting and which isn’t.

Here’s a guide to using, and paying for, genetic tests.

What you can find out — and what you’ll pay

Roughly, two kinds of tests are available.

The first is ordered by a doctor and will often involve finding all the variations in specific genes. Research has found some variations that point to a higher risk of diseases, including breast cancer and a kind of colon cancer.

A doctor might recommend a screen based on risk factors like family history or ethnic background. Other tests, says David Fleming, an internist and health ethicist at the University of Missouri, can provide clues to how you’ll respond to certain drugs or treatments.

The tests can cost $300 to $3,500. If your doctor recommends it, insurance will generally cover it like any other test. But call your insurer first: Some might require an advance letter from your doctor or a visit to a genetic counselor, a professional trained to help people use genetic information to manage their health.

The second kind of test is a home kit that lets you mail in a saliva sample and log on to a website to get results. It’s generally not covered by insurance. (The Food and Drug Administration has said it’s concerned about unregulated consumer tests but allowed companies to keep them on the market if they began the process of getting approval; none are yet FDA approved.)

One big player, 23andMe, has made a publicity splash by cutting its price to $99 for a report on up to 250 indicators, from that Neanderthal DNA to markers of health risk. This test may differ from one your doctor would order; it won’t read all the variations in a gene but looks for common markers.

For concerns about a specific disease, use a doctor, not a kit.

Why you shouldn’t face the serious stuff alone

Experts caution that the results of tests can be difficult to interpret on your own. That’s fine if you are looking for fun info on your ancestry. But discuss with a counselor or doctor in advance whether you should do a screen for a disease, and what a positive or negative result would mean.

You also need to think about what you’ll do if you get a worrying result.

A test can find markers of an elevated risk for late-onset Alzheimer’s, for example, but you can have them and never get the disease. And since there’s little to do now to prevent Alzheimer’s, you may feel better off not knowing.

Other screens, such as those for cancer, could leave you with difficult choices about how aggressively to respond. “The issue is when we make decisions based on fear rather than what we know,” says Fleming.

You’ll want professional help to sort through the facts. Visits to genetic counselors are often covered by insurers and billed like doctor’s visits. You can find a counselor at nsgc.org.

What tests don’t tell you

With some diseases, such as diabetes, it may be more accurate to simply look at your own family history, says Michael Dougherty, director of education at the American Society of Human Genetics. What’s more, he adds, “the genetic test doesn’t take into consideration all of the environmental factors.”

So it’s a good idea to eat right and exercise no matter what the result.

How safe are your records?

A law passed in 2008 prevents health insurers from using genetic information against you. Employers can’t use it either. But federal law doesn’t offer the same protection on long-term-care, life, and disability coverage. (Some states have stricter rules.)

“The concern is the insurance company could require you to show certain medical records,” says Harvard Medical School geneticist Robert Green. Or even just ask if you’ve been tested. It doesn’t appear to be happening yet, but it’s one more thing to keep in mind as you weigh whether you want to see what’s written in your DNA.

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