The histories of Indigenous peoples of the Americas are fascinating. Looking at the spectacular buildings of Machu Picchu, the walrus ivory carvings of the Canadian Arctic, and the effigy stone pipes of the Eastern Woodlands, and considering the extraordinary diversity of past and present Indigenous cultures, many people wonder at their origins.

How did the First Peoples survive the ice age and arrive on the continents? How did they adapt to the new environments in these lands?  Did they arrive 15,000 years ago, or 30,000 years ago? Where did their ancestors come from? How did they travel beyond the massive ice sheets that covered the northern portions of the continents during the Last Glacial Maximum? Indigenous peoples themselves have diverse and ancient histories of their own ancestors, some of which align with archaeological and genetic models of the past, and some of which do not.  A thousand questions drive legitimate and respectful conversations about the past.

In recent years, “alternative historians” have exploited this thirst to learn. Self-appointed “experts” or journalists such as Graham Hancock variously claim that the first people to enter the Americas were: from Europe, from sub-Saharan Africa, from Egypt  (some claim there’s an Egyptian city in the Grand Canyon and Egyptian artifacts in Burrow’s Cave in Illinois), giants (descended from an extinct human relative known as the Denisovans), travelers from the Black Sea region, Atlantean refugees, aliens, and alien mentees. The proponents of these claims have landed shows on Netflix and the History Channel, and book contracts. Sensationalism sells, as the viewership of the latest series in the genre, Netflix’s Ancient Apocolypse, demonstrates. Profiting off their visibility from media appearances, some grifters organize conventions, and offer “informal research expeditions” to “investigate megalithic sites without bias.”

While these purveyors make millions, their theories perpetuate a harmful and incorrect view of the origins of Native Americans. They cook up pseudo-histories by cherry picking “evidence” (often faked, misunderstood, or paranormal) to support a pre-determined outcome, and by eschewing hypothesis testing, peer review, and other tools of rigorous scientific inquiry. Scientists, skeptics, and scholars have debunked these claims, pointing out factual inaccuracies, identifying faked evidence, noting anti-Indigenous rhetoric, and delving into history and context that explain why the bogus claims emerged in the first place. But a lie can go halfway around the world before experts can debunk it.

Scientists, Indigenous knowledge holders, and scholars from multiple disciplines have spent decades compiling evidence about the First Peoples of the Americas—using genetics, professional archaeology, and knowledge passed down many generations among Indigenous communities to understand the histories of Indigenous peoples. One of the most recent tools available is the study of complete genomes from ancient peoples, which has allowed scholars to produce powerful models of biological histories and test relationships between past and present populations.

DNA recovered from ancient remains shows us that the First Peoples of the Americas have ancestral roots in Asia, and that they descend from two populations who mixed during the Upper Paleolithic era: One group related to the ancestors of present-day East (with affinities to some Southeast) Asians, and another group descended from a population called Ancient North Eurasians. The East Asian and Ancient North Eurasian groups came together approximately 25,000 years ago; soon after, the DNA evidence suggests, the intermingled population became isolated for a few thousand years, coinciding with the peak of the global climactic event called the Last Glacial Maximum, also known as the ice age.

During this period, human populations across the globe retreated to locations where resources were more abundant. Based on paleoclimactic reconstructions, some archaeologists, geneticists, and paleoclimatologists hypothesize that the population ancestral to the First Peoples may have moved to the southern coast of central Beringia (the land bridge which connected East Asia and West Alaska until the Earth warmed and sea levels rose, creating the Bering Strait).

The DNA evidence suggests that the Beringian population split into several branches. One moved into the Americas as soon as routes past the glacial ice sheets became accessible, after about 17,000 years ago, and gave rise to all peoples south of Alaska. Genetics and some traditional Indigenous histories indicate that people were present in the Pacific Northwest extremely early; the first movements into the Americas were likely by boat along the coast.   There is no genetic evidence that the earliest Native Americans were Europeans, ancient Israelites, or African mariners, as pseudo-historians sometimes assert.

At human occupation sites throughout North America and South America, a vast preponderance of archaeological evidence—securely dated physical traces of human activities in undisturbed geological contexts—demonstrates that these First Peoples were making homes in North and South America by around 15,000 to 16,000 years ago, and that they had no contact with any outside group (with very limited exceptions) before 1492.

There were some exceptions to their isolation. Genetic evidence hints that there may have been brief contact between Polynesian and South American populations approximately 800 years ago. The L’Anse aux Meadows site in northern Newfoundland contains wood-framed buildings and artifacts that confirm Norse people lived there between 900 and 1,300 years ago (congruent with narratives from both Vinland Sagas and Indigenous traditional histories). Human and animal footprints at the White Sands Locality 2 site may date back between 21,000 and 23,000 years, one group of scientists has (somewhat controversially) suggested. If their data—which align with the traditional histories of Indigenous peoples in the region—hold up to additional scrutiny, it would indicate that an earlier population predated the post-ice age expansion out of Beringia. This is one of the most exciting developments in the field in recent years, and is an area of active research by multiple archaeologists and geneticists.

But such exceptions do not support “alternative history” claims, particularly that the First Peoples of the Americas were anything other than the ancestors of present-day Native Americans, or that other Europeans besides the group at L’Anse aux Meadows entered the Americas prior to 1492. No burial mounds, stone pyramids, or ancient settlements were built by Egyptians, aliens, or a “lost race.”

Scientists don’t agree on a single, unified model for the peopling of the Americas. We debate which sites contain valid evidence of a human presence, how old they may be, and their significance. That’s a good thing. Disagreeing about how to interpret the archaeological record is the strength of the scientific method, not a weakness. It creates space for rigorous scrutiny of evidence and testing of hypotheses, which leads to a gradual accumulation of knowledge and the development of more accurate models of the past. It requires a profound humility to articulate how your ideas may be tested and proven wrong.

Archaeologists, biological anthropologists, and geneticists studying the earliest histories of the First Peoples are not immune to criticism. We are grappling with legacies of racisim against Native Americans, some which continue to persist within our disciplines. All too often, non-Native scientists ignore or treat disrespectfully traditional histories and Indigenous perspectives on their own past. We can and must do better.

But “alternative historians” and pseudo-archaeologists do not even acknowledge—let alone seek to root out—the racism and anti-Indigenous perspectives that are so integral to the stories they tell. Instead of trying to test hypotheses, they build cases for their pet theories—whether by co-opting Indigenous traditional histories to support racist theories, speculating wildly over single artifacts, or even looting Indigenous sacred sites to manufacture evidence.  When scholars or institutions attempt to debunk this charlatanism, the alternative historians deride them as part of a conspiracy to suppress “the great secrets of Earth history.”

But scientists care about what is actually true; the YouTube algorithm does not. There is a special kind of joy at the intersection of our love of the past and our love of solving puzzles. It’s familiar to those of us who feel goosebumps walking amid the ruins of ancient buildings, who read every historical marker on road trips, or who delight in the fingerprints of the potter marking ancient ceramics. We want to understand these large and tiny histories, and to see what the past was really like.

Embracing the joy in learning about the past and present cultures of the Indigenous peoples of the Americas—including learning about the peoples whose lands you are on and rejecting harmful and inaccurate narratives that drive a wedge between these peoples and their own histories—is the heart of science and the soul of humanity. Respectful curiosity is the starting point for understanding the past, including just how long Indigenous peoples have been on these continents. And it can start close to home: Close your laptop, and pay a visit to an ancient site.

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Nurse, currently the founding director and CEO of the Francis Crick Institute, visited Zócalo yesterday with Caltech developmental biologist Magdalena Zernicka-Goetz, author of The Dance of Life, for a conversation that reflected on his scientific and philosophical insights into human life throughout his career as a geneticist. The Zócalo/Caltech event touched on the similarities between artists and scientists, the prospects for curing cancer, and Nurse’s startling discovery of his own genetic history. The scientists also reflected on striking similarities between their professional and personal lives.

Nurse recalled his initial interest in natural history in his youth, when observing butterflies spurred him to question the differences between living and nonliving things. He later recognized that cellular reproduction lay at the core of that question, and that its simplest instances promised to shed light on the mechanisms behind human life. Leland Hartwell, who was studying genetic methods for cell cycle studies to understand cancer, inspired Nurse to learn about yeast development and genetics.

“I wasn’t a geneticist at that time, and I wasn’t working on yeast at that time, but I decided I would learn both of those things,” Nurse said, recalling that the line of research wasn’t highly regarded by other scientists back then. Still, he decided it would be more fulfilling to investigate an important but under-studied area than to focus on a topic already receiving heavy attention.

That choice eventually resulted in a Nobel Prize in 2001, which Nurse shared with Hartwell and biochemist and molecular physiologist Tim Hunt. Their discovery of protein molecules that control cell division in yeast cells shed light on cell reproduction in general, and also had important implications for understanding the growth of cancer cells.

From Nurse’s work, the conversation turned to his personal genetic history as Nurse recalled growing up in a working-class household in Great Britain and being the first in his family to attend college. As an adult, when Nurse requested a complete copy of his birth certificate for a visa to the United States, the document revealed to him that his sister was, in fact, his mother, and his father was unknown. It was a deeply ironic revelation for the geneticist, who described having to reorganize his personal understanding of his entire family tree.

Zernicka-Goetz also asked Nurse about his view that “the best research is both intensely individual and utterly communal.” Researchers are often driven by personal motivations for success and their own interests, but support from one’s broader community is equally essential, Nurse explained. He stressed the importance of finding a balance between respect for individuals’ work, and for the communal support that enables their contributions to scientific research. It was this philosophy that led Nurse to step into a role outside of the lab as director general of the Imperial Cancer Research Fund (now Cancer Research UK), in 1996.

Over the course of the conversation, the scientists constantly returned to the links and similarities between artists and scientists, and the importance of creative thinking to academic research. Creativity, they agreed, drives ideas. By putting certain ideas or concepts that don’t normally go together, “they produce something else that’s different and new,” said Nurse, adding that it’s “the juxtaposition that’s interesting.” Often, Nurse said, scientists can get stuck on the same track. But by embracing creativity, he said, it fosters the ability “to change your mind and think of things in a different way.”

During an audience question-and-answer session, one person over the live YouTube chat circled back to the question driving the event: What is the meaning of life?

“I don’t know what the meaning of life is,” Nurse prefaced, but remarked on the meaning individuals can find in supporting their family, friends, and colleagues. He also offered a broader perspective:

“On a bigger scale, the meaning of life, whilst you’re on the planet, is to try and improve the lot of humankind. That may be through some intellectual discovery, it may be entirely local, it may be by producing some wonderful piece of art, it may be by political leadership in some sense, but it has to be aimed at improving the lot of humanity—whether small or big—in whatever arena you can be most effective.”

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The first successful de-extinction occurred long before the advent of CRISPR. The Pyrenean ibex (Capra pyrenaica pyrenaica), a type of wild mountain goat commonly known as a bucardo, once was a common sight in the French Pyrenees and northern Spain. By the late 19th century, hunting had reduced the species to fewer than 100 individuals. When the last one, a female known as Celia, died in January 2000, the Pyrenean ibex joined the estimated 5 billion species that have become extinct since life arose on this planet. But in this case, three years later, on July 30, 2003, a team of French and Spanish scientists gathered around a pregnant domestic goat and delivered by cesarean section a live kid genetically identical to the extinct bucardo. For the next seven minutes (after which the animal died from respiratory failure), the Pyrenean ibex was extinct no more.

The extinct bucardo was returned to life through the well-established technology of cloning through nuclear transfer. This technique, in which a cell containing the complete genome of the extinct species is inserted into the egg of a living animal, was used to clone Dolly the sheep in 1996. But now, with CRISPR, de-extinction does not require a live or frozen cell from the extinct species. Instead, all scientists need are organic remnants—such as pieces of bone—that contain fragments of DNA. Those fragments allow geneticists to discover the complete genome of the extinct animal (a process scientists refer to as “sequencing”). Once they have this “recipe” for the extinct species, CRISPR enables scientists to edit the DNA of its closest living relative to create a genome that, as edited, approximates the genetic code of the extinct species. Think of the living animal’s DNA as version 2.0 of a piece of software: the goal is to get back to version 1.0. You compare all of the millions of lines of code to spot differences, and then painstakingly edit the lines with differences to restore the code to its original state.

Once the DNA has been edited to reintroduce the key traits of the extinct plant or animal, the edited DNA is inserted into the nucleus of a reproducing cell. The resulting individual may not be genetically identical to the extinct species, but the key traits that made the extinct species unique are reintroduced, and the resulting animal or plant has the potential to be the functional equivalent of its extinct relative. So, for example, the scientists working on the de-extinction of the woolly mammoth (which last roamed the Earth about 4,000 years ago) are starting with the DNA of an Asian elephant, and then using CRISPR to reintroduce the traits that made the woolly mammoth unique, such as the metabolism, subcutaneous fat, and shaggy coat that allowed it to survive in the sub-Arctic tundra.

But why do this? Most proponents of de-extinction make an argument based on ecological restoration. For example, large herbivores such as the woolly mammoth played a critical role—through trampling, grazing, and fertilization—in the maintenance of the grassy cap that insulated the permafrost of the great northern tundra. When these large grazing beasts disappeared, the grassy cap declined, allowing the thawing of the permafrost below and consequential release of massive volumes of previously trapped greenhouse gases, significantly accelerating global warming. To reverse this effect, Russian scientists in a remote part of Eastern Siberia are working on an effort called “Pleistocene Park.” Their vision is a restored Mammoth Steppe—a place where the Siberian permafrost is again insulated by treeless grasslands extending to the horizon in all directions, on which vast herds of wild horses, bison, and de-extincted mammoths graze in symbiotic partnership with the restored cold-weather savanna.

Another de-extinction currently being attempted for purposes of ecological restoration is that of the passenger pigeon, once North America’s most abundant bird species, with billions of individuals as late as the 1870s. The entire population was shot, netted, hunted, or otherwise slaughtered by humans. In 1914, the last individual, Martha, died in a Cincinnati zoo. The consequences of the rapid extinction of a keystone species at this scale are not precisely understood, but we know enough to expect them to be widespread and profound. For example, the loss of the passenger pigeon caused disruption of the forest regeneration cycle and significant declines in forest health. It also may have precipitated the proliferation of Lyme disease. “Re-wilding” proponents such as Stewart Brand’s Long Now Foundation also point out that any de-extinction enhances the biodiversity that is the foundation for healthy ecosystems.

One of the other justifications for pursuing de-extinction is a moral one: possession of the power to bring back lost species implies a moral duty to use that power, at least in the case of species whose extinctions were caused by human beings. In other words, we have a duty to right our prior wrong. It is notoriously difficult to estimate the number of species whose disappearance can be blamed primarily on human interference. But all scientists agree that humanity’s greed, recklessness, and negligence have greatly accelerated the natural pace of extinction, harming both the planet and ourselves.

The enthusiasm of de-extinction’s supporters is nearly matched by the skepticism of its detractors. Many of the issues are practical, such as doubts that man can create populations with sufficient numbers and genetic diversity to be sustainable in the wild; concerns that the de-extincted animals are neither genetically identical to the extinct species nor benefit from the non-genetic drivers (such as parental nurturing) that determined their behaviors; and arguments that plants and animals created based on ancient genomes will not flourish in contemporary conditions. For example, the passenger pigeon, if revived, would face a world in which the American chestnut, which provided a major part of its habitat and food, has disappeared.

Conservation biologists are split on the matter. Some argue that belief in the possibility of de-extinction creates a moral hazard, opening the door for those benefiting economically from the destruction of habitat to argue that even if a species is lost, it can always be “brought back.” Others simply say that in the current era of human-caused mass extinction, society should prioritize those endangered species that can be saved rather than dreaming of returning lost ones to life. They argue that CRISPR, instead of being deployed for de-extinction, should be used to increase the genetic diversity of a surviving endangered population, increasing its odds of survival.

One thing is certain. Like the gift of fire to humanity by Prometheus, the cat is out of the bag. Efforts by governments and NGOs to limit or control use of genetic technologies—such as the 2020 guidelines issued by an international commission convened by the U.S. National Academy of Medicine, the U.S. National Academy of Sciences, and the U.K.’s Royal Society—are unlikely to deter further experiments involving the editing of the heritable human genome. What scientists can do, at least some, somewhere, will do.

And why do I argue that the result may be the most important thing to happen on the planet for 4.5 billion years? Since the dawn of life on Earth, species have developed through the process of random genetic mutation followed by natural selection—by evolution. But from this moment forward, that has changed. CRISPR-Cas9 gives us the ability to hack evolution. Rather than waiting for mutations to occur randomly, we can amend our genetic inheritance (or that of the other life forms). This means the substitution of human desire and choice for the process of natural selection. Is this inevitably the disaster that many predict?

Humanity has a long tradition of making interventions designed to improve, restore, and steward the natural world. Virtually no agricultural or horticultural species has been unaffected by hybridization, and most of those altered plants are now valued citizens of the natural world. Wheat, grapefruit, and peppermint all resulted from interspecies breeding (as did, on other branches of the tree of life, cattle, bison, African bees, and honeybees). Genetic editing is, without a doubt, a new and different tool, but the result, species created by man (rather than by the operation of natural selection), is not.

Those instinctively suspicious of these types of interventions in nature tend to view the natural world as static. But we now understand that nature is not some stable, passive stage on which the dance of life plays out. Instead, the relationship between an environment and the life it hosts is highly interactive. Species adapt to their habitat and then change it. From the moment Homo sapiens emerged during the Middle Paleolithic, we inserted ourselves into this dance by transforming habitats and the organisms they supported. Population growth and technology mean that the scale of our impact is now global. By the act of conceiving the current geological era as the Anthropocene, where human activity is the dominant influence on the planet, we have started to come to grips with the fact that we are now the creator, and no longer merely the created. It’s a responsibility that cannot be dodged. Human moral and ethical frameworks must catch up to our technology. Will we use our power in selfish, shortsighted, and reckless ways—or instead dedicate ourselves to deploying the new technologies to mitigate our past wrongs and reestablish a healthy Earth?

Of course, caution is always important. But too often, timidity and hostility to progress disguise themselves under the guise of prudence. If tools like CRISPR allow us to replace keystone species like the woolly mammoth and passenger pigeon in order to keep greenhouse gases in the tundra or to restore healthy ecosystems, then we should use them. We cannot escape choice through inaction. Now that we have the technology for de-extinction, the failure to use it to heal the planet is also a choice for which we will be held accountable by future generations.

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My doubts, as it happened, had some validity. The name Central Metric Office proved to be a red herring, since the office’s purposes were narrow. Scotland Yard had something very specific in mind: a system of criminal identification, imported from France, relying on card files of prisoners that were sorted according to an array of bodily measurements. The office in question, though, offered evidence that police devotion to data was quite real, and the office was linked to an impressive network of measurement activities. Probing the episode of the Central Metric Office opened up a new perspective on the history of genetic knowledge, and even on its human meaning.

Most textbook accounts have genetics emerging quite suddenly in 1900. Historians have long treated this moment as pivotal. The year 1900 is when Gregor Mendel’s decades-old hybridization experiments on peas suddenly became famous. Almost immediately, his work was celebrated as the foundation for a science of biological inheritance.

At almost the same time, in 1899, measurements such as those collected by the Central Metric Office drew the attention of anthropologists. A year later they appeared in the first issue of a pioneering statistical journal, Biometrika, with a triumvirate of editors that included eugenic pioneers Francis Galton and Karl Pearson. Their movement to investigate how heredity shaped abilities and “defects” was just then getting off the ground, and they worked to support it with vast repositories of data from schools, universities, prisons, hospitals, and insane asylums. The Mendelian and biometric strains of eugenics thus began to flourish almost simultaneously. However, modern scholarship, taking a more cultural approach, is uncovering a much richer and longer history for the investigation of human heredity.

In fact, as further probing revealed, the biological inheritance of criminality had been widely suspected, often simply assumed, for decades before the London police first spoke of a Central Metric Office. But prison officials had very little access to family data. It was only around 1900 that hereditary information on criminals began to appear in connection with a crisis, as it seemed, of “feeblemindedness.”

What brought about this supposed crisis, paradoxically, was the expansion of schooling. Beginning about 1870, as governments made elementary education universal and even mandatory in much of Europe and North America, they created a category of child known as “feebleminded.” Those who fell behind in school were given this label. They were sometimes sent to special schools, where they were subject to medical and psychological examination. Followers of the Italian criminologist Cesare Lombroso claimed that such children were biologically and morally backward: in short, born criminals. Others denied this, arguing that the defective children were not specifically criminal, but simple and gullible, hence vulnerable to bad influences.

It was, however, the supposed link of criminality to feeblemindedness that sparked systematic data collection on criminal heredity. Felons, arriving in jails or prisons as adults and attended by police officers with no medical training, were unlikely to provide information on the mental health of their families. The opposite was true for schoolchildren under the watch of teachers, doctors, and school officials. The role of heredity in feeblemindedness became a hot topic in the late 19th century, and schools for such children turned into sites for hereditary investigation. It was a huge stimulus to the nascent eugenics movement, which in many respects took off long before 1900, though it was not known as such.

Breeding results on peas and poultry provided a basis for genetic explanations, but did not create these hereditary concerns. Rather, medical-social anxieties contributed to the excitement about breeding and heredity that made biometric as well as Mendelian methods seem thrilling and even fateful. From about 1880, special schools were the most important sources of data on human heredity and of proto-eugenic anxieties.

To get the full picture, however, we need to look even further back to earlier sources for hereditary and eugenic study. Record keeping on inheritance of feeblemindedness was shaped by an enterprise whose first beginnings can be traced back at least to 1789. In January of that year, King George III’s symptoms of madness became alarming enough to precipitate a constitutional crisis in England. Was the king likely to recover, or would it be necessary to appoint his son as regent?

Dr. William Black, a veteran of studies of smallpox inoculation, knew how to proceed with such questions. He found his way to private records on the insane (there were no good public ones) from the royal asylum of Bethlem. Within months, Black published tables of cure rates in relation to several variables, including one on causes of insanity. “Family and hereditary” appeared here as perhaps the most important cause of all.

Black’s statistics were exceptional, but a vast expansion of insane asylums in the early 19th century stimulated new routines of recordkeeping. Causes of insanity were of particular interest. Lay as well as medical witnesses endorsed the key role of hereditary causation right from the start. Although the new public asylums at first reported abundant cures, patient numbers increased with hyper-Malthusian fury. Disappointed by their failure or inability to cure their patients, the doctors (known as “alienists”) focused more and more on the presumed causal role of heredity. If this alarming epidemic could not be checked by medicine, the key might be to persuade young men and women tainted by bad heredity to refrain from marriage.

When King George III’s madness became clear, Dr. William Black searched the records of the royal asylum, Bethlem Hospital, to understand which patients had recovered. Courtesy of the Wellcome Trust/Wikimedia Commons.

This project, eugenic in all but name, was anchored in data collection on patients and their families. A Norwegian alienist, for example, compiled the first family pedigrees of insanity in 1859, and then labored to track the migration of these hereditary factors from generation to generation. Two German doctors compiled data to calculate the increased probability of madness when one or both parents had been diagnosed insane.

When statisticians and geneticists turned their attention to questions of human heredity around 1900, they learned immediately that psychiatrists and school psychologists already possessed not just unmatchable data on the transmission of mental illness and mental weakness, but sophisticated tools to compile and analyze the numbers. All this data work led to modest scientific successes punctuated by embarrassments, as claims for the discovery of a single hereditary factor for mental illness soon appeared scandalous. Data files also facilitated the injustice, as it is now recognized, of forced sterilization—which was legal for a time in much of the United States and abroad—as well as mass killings of asylum patients in Nazi Germany.

Partly in reaction to these horrors, postwar human and medical geneticists tried to model their science on fruit fly genetics. But doctors, psychologists, and geneticists could not put aside this old faith in genetic causes of schizophrenia, mental disability, even criminality. Geneticists in the 1970s gathered data from prisons in the expectation that much violent crime might be explained by the presence of an extra Y chromosome, and the campaign or the Human Genome Project was included promises to identify the genes for schizophrenia.

The science of human genetics has deep roots in eugenic doctrines and projects that go back more than two centuries. The use of numbers to support ideas arising from fear or bigotry is not limited to benighted days gone by.

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Even science has carried this idea to extremes. Genes, for example, are said to account for the difference between people who are perpetual cheaters and those in a lifelong committed relationship. Genes are said to be the reason why some people vote conservative while others vote liberal and why some don’t vote at all. Genes supposedly determine our ability to get through those last years of college, to keep ourselves out of credit card debt, or to invest in the stock market in order to plan for our retirement. And on and on.

If you take this narrative literally, you might think that humans have little free will or sense of right and wrong, and that our environments, educations, and societies play a minor role in how we act or the choices we make. We are, in this version, fleshy computers running hardware provided by our genes.

Why are genes so popular now? Why do they seem to explain everything so perfectly? And how did we come to want to know ourselves through our DNA?

These questions first came to me as I was wrapping up a book on the Human Genome Project and ideas about race. Looking at the state of genetic science, I noticed a push toward investigating the genetics of social phenomena arising in my own field of sociology. I decided to talk to scientists, experts, and everyday people to get a sense of why so many things previously understood in terms of social relations and environmental conditions were coming to be explained in terms of our genomes.

What I discovered is that science and pop culture each spin a narrow version of what genes are and how they impact us, together professing that genes are the deepest essence of ourselves. These two strands combine and reinforce each other.

Recently, researchers, even social scientists, have been focused on finding genetic causes for things in ways that leave out the environment, culture, and social upbringing. Pop culture has seized on these scientific reports, relaying findings as the ultimate truth. And as public interest in genetics and genetic testing has grown, the organizations that fund scientific research have begun putting a premium on studies that seek answers in the genes, closing a feedback loop.

Looking at phenomena beyond disease has become the newest trend, and there is a great deal of energy being spent on opening up opportunities for it. Scientists who are willing to risk their reputations on the new arena of social behavior are being rewarded by the biggest funders and health organizations out there. The National Institutes of Health and National Science Foundation, for example, are eager supporters of studies as well as efforts to build out a new field of science wholly focused on the genetics of social phenomena.

The space opened up is now being populated by social scientists who are new to genetics, but who believe that they will be able to revolutionize the hunt for genetic associations. This is most striking in the spate of new gene-focused fields, fields like “genopolitics” and “genoeconomics,” that creatively mash up natural and social science methods to apply genetics to new arenas of life, such as political participation and financial decision-making.

A prominent example of the kind of research that these fields are doing is the ongoing search for genes associated with educational attainment. A consortium of political scientists, economists, and sociologists have been mining the human genome for genetic culprits that have an impact on how far people make it through school. Another example is the hunt for rage genes. Scientists have linked the MAOA gene to violent behavior, rape, and even gang participation.

Despite arising from complex interdisciplinary approaches, these hybrid sciences all too often promote genetic determinism. Though they aim to characterize the special way that genes and environments interact to make us who we are, most often they use methods common to genetic science that analyze only the DNA portion of the gene-environment equation. It is expensive and challenging enough to tackle genes alone, and funders do not require that genetic studies pay detailed attention to the environment, so scientists leave the environment out of the picture. Instead of showing us how nature and nurture work together, they reinforce a nature versus nurture way of thinking. This isn’t the fault of individual scientists, but rather is built into the way things are done when hunting for genes. Even the most seasoned social scientists end up checking deep environmental analysis at the door.

For the general public, an even more reductive sense of how genes work and what they mean reigns supreme. TV shows like CSI convince viewers that genes are entities that trump all else. Cultural analysts who have studied the rise of genes in pop culture say that DNA has a certain mystique, seeming indivisible and irreducible, like atoms. And in a world where everyday people are increasingly being asked to manage their own health, to optimize it in any way possible, genetic susceptibilities seem to be one bit of outside reassurance for an uncertain future.

This potent combination of data and cultural resonance gives relatively flimsy scientific conclusions tremendous potency. When I spoke with experts across society—teachers, attorneys, prison wardens, and more—about genetic tests, I learned that they believed that genes had a uniquely predictive power. Many were concerned that tests could be misused by non-experts, but they nevertheless believed that knowing about someone’s DNA would help in working with them. IQ tests could be used to track kids into different types of schools. Criminality tests could determine how to handle repeat offenders. Moreover, tests could be given in infancy, or even administered prenatally.

The belief that nature is really what’s driving us is not new. It’s an idea that can be traced to the earliest thinking about genes and evolution, back to Darwin—and also to his infamous cousin, the founder of eugenics, Francis Galton. Darwin allowed for nurture to kick in as soon as individuals were born, but Galton popularized the idea that the transfer of traits via DNA was all that mattered. In his version, nature and nurture were at odds, with nature winning every time. Francis Galton’s vision went beyond the notion that nature determined the essence of humanity; he believed that the only way to rid humanity of undesired traits was to rid it of the people with those traits.

Though most people today would not want to live in a eugenic society, where DNA decides everyone’s fate, it could be a real possibility if we don’t change the way we think about genes. Our increasing belief in genetic determinism, in an era in which tests are proliferating like mad, threatens to bring us to a world in which people will be slated for totally different experiences, relationships, and life outcomes based on their genes. This will be nothing less than a high-tech eugenic social order, even though people will feel they’ve bought into it voluntarily—through dating apps and hobby tests.

In fact, if you take our current cultural attitudes to their likely conclusion, eventually, there could be two genetic classes. The haves will be able to test their embryos and use IVF to select for things like high intelligence and bullish fiscal attitudes. The have-nots will be tested in infancy or as they enter school, where they will be tracked for certain classrooms and educational and fitness programs, or given no school at all. Educational institutions will become closed-off places where like meets like, as will the labor programs and trade schools offered to those who have “less fit” DNA. If we don’t develop a more critical approach to the information offered by DNA testing, a social order built from the most insidious inequality truly could be our future.

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Fruit fly research has long provided fundamental insights that turn out to apply to humans. Fly research has helped us learn how fertilized eggs grow into mature adults, how cells in our bodies communicate with one another, and what controls the “biological clocks” within us. Several times—and as recently as 2017—findings that began with research on the fly have been honored with a Nobel Prize for Physiology or Medicine.

Now fruit fly studies are getting personal: They are becoming integrated into research with direct impact on patients.

In the new and promising field of genomic medicine, teams of experts use data from the DNA sequences of patients suffering from genetic diseases to figure which of our 20,000 genes is responsible for the disease. Superficially, the path from genome sequencing to treatment is clear. Step one, use the sequence data to figure out which genes have changes when compared with genes in healthy family members. Step two, use what we know about the genes to make a specific diagnosis. Step three, customize a treatment plan based on these findings.

Yet cases are rarely so straightforward. The genome of a patient with a genetic disease is likely to contain differences in hundreds of genes when compared with healthy family members, and in some cases, we cannot identify which one or more is the cause. Even when a genetic cause is identified, a treatment might not be available. Moreover, when a genetic disease is rare, few patients exist who can participate in a clinical trial, so the development of new therapies can be especially challenging.

Enter the fruit fly.

With more than a century of knowledge in the bank, we know more about fruit flies than we do about most other multicellular organisms on the planet. Researchers have developed countless tools to manipulate fly genes, as well as tests that let us study everything from cell shape to organ size, from physiology to complex behavior.

One of the biggest surprises of the last 25 years has been the discovery that the genes controlling fundamental cell functions—the parts, the assembly lines, the machines—are largely the same in flies, humans, and other animals. With flies, we do not have to ponder these commonalities in the abstract; we can test and experiment.

Fruit fly researchers have begun to partner with physicians and others to use this knowledge to bridge the gap between what is learned from genome sequence data and what is required for clinicians to make a specific diagnosis and treatment plan.

A few years ago, the U.S. National Institutes of Health expanded an existing program called the Undiagnosed Disease Network (UDN) to include a group dedicated to using fruit flies (as well as fish) to figure out which of several genes identified using a genomic medicine approach is the cause of a given rare or new disease. The group, led by Hugo Bellen, a fruit fly biologist at Baylor College of Medicine, introduces changes into the fly genome that mimic changes found in genes from human patients. Sometimes they even insert a human gene into a fly. Then they watch the flies to see if they get symptoms that resemble the symptoms of the human disease.

By applying “synchronized bench and bedside investigations,” the group has succeeded in diagnosing what had been mystery cases. One of the newly identified genetic diseases was named Harel-Yoon syndrome, after clinician Tamar Harel and fruit fly biologist Wan Hee Yoon, whose work was instrumental in the case.

In at least one UDN case, identification of the gene affected in a young patient led physicians to prescribe a treatment that they predicted would counteract the effects of a change discovered in a gene called CACNA1A. Following the first diagnosis, other cases in which the CACNA1A gene is similarly affected were identified, suggesting that the results will impact additional families.

But knowing the cause of a genetic disease does not always help identify or design a treatment. For many genes, we do not know enough about their functions to understand what cellular process should be targeted or whether the activity of a gene should be ramped up or down to improve the patient’s life. In other cases, we might understand a gene’s function in detail but lack a safe drug that can modulate its activity in a way that helps the patient.

Here again, biomedical research is turning to the fly. By engineering fly genes so that flies bear characteristics of a genetic disease, the insects can serve as simpler but similar stand-ins for human patients. These “disease model flies” can then be used to find genes that might be good therapeutic targets or to identify small molecules that improve disease-related symptoms in the flies, suggesting a path for development of new drugs. They can also be used to discover whether existing drugs can be “repurposed” to treat other diseases.

For rare diseases in particular, the fact that flies are such prolific reproducers is a significant advantage. Within a relatively short time, large numbers of flies can be tested with thousands of possible drugs. Another advantage is that flies can be studied throughout their lifecycle—as they grow and develop from embryo to adult—and across their lifespan, which for a normal adult fly is about two or three months. In addition, flies process drugs in organs similar to our own liver and kidneys, giving a fuller picture of what might happen when a patient takes a drug than might be learned from testing cells in a petri dish.

Some of the challenges researchers face in conducting these studies are practical ones. How do you get a fly to take its medicine? How much of a drug do you give it? How do you monitor outcomes and analyze results? Scientists such as Daniela Zarnescu of the University of Arizona and Tin Tin Su, of the University of Colorado and SuviCa, Inc., have organized workshops at which Drosophila researchers discuss their experiences of working with fruit flies and drugs.

Private industry is jumping into the game as well. The biotech company Perlara, PBC, is using fruit flies, as well as yeast, worms, and fish, to develop drug treatments for rare genetic diseases such as NGLY1 deficiency, which can affect the development of speech, cause uncontrolled movement, and result in other problems for children with the disorder. The expectation is that the advantages offered by using the fly will help in the development of new drugs to treat NGLY1 deficiency. According to the Grace Science Foundation, research related to NGLY1 deficiency is likely to have impact on other, less rare conditions, such as cancer and Parkinson’s disease.

Fruit fly research has had a profound positive impact on our understanding of general biological principles and the functions of individual genes. We can now look to a future in which this foundation expands our ability to diagnose and treat human diseases. In the words of Clement Chow of the University of Utah and Lawrence Reiter of the University of Tennessee, the fruit fly is “far from a quaint genetic model of the past, but rather, continues to evolve as a powerful system for the study of human genetic disease.”

The post Why Fruit Flies Are the New Lab Rats appeared first on Zócalo Public Square.

Reading the article, you might be left with the impression that even thinking about designer babies would be alarmist, unscientific, or just silly.

As public interest advocates who are focused on the social implications of human biotechnologies, my colleagues and I see how often the term “designer babies” serves as a distraction in these discussions—and we usually avoid using it ourselves. But recently I’ve been thinking that maybe it’s not the idea itself, but the way we’ve been talking about it, that’s the problem.

What if we could use discussion of designer babies productively, to unpack some of the complex issues surrounding gene editing? Actually talking about such imaginary babies—however far-fetched their existence seems—could help us start that discussion. Only by acknowledging that a future defined by designer DNA is possible can we decide whether we are comfortable with the risks, or even aspire to that future.

First of all, just thinking about designer babies could help people understand important aspects of new gene editing technologies, including the difference between two distinct applications that often get conflated. Both involve CRISPR, a relatively easy-to-use gene editing tool that has revolutionized genetic research. Using CRISPR, scientists can make pinpoint changes in the genes of many kinds of cells, from bacteria to plants to animals to humans. There is both great hope and great hype surrounding CRISPR, because it might prove useful for medical purposes. For example, editing the DNA of human blood cells could treat or even cure diseases like sickle cell or beta-thalessemia—providing tremendous relief to people who are sick.

Editing specialized cells in existing people is called somatic editing, and these kinds of genetic changes would not be passed on to the next generation. A very different application of CRISPR is required to make a designer baby: a scientist has to alter the genes in eggs, sperm, or early embryos, making changes that shape the human germline—the DNA passed down from one generation to the next.

Widespread media coverage has made this kind of gene editing experiment using human embryos seem ubiquitous. In fact, only a handful of researchers around the world have done this research and none have attempted to start a pregnancy using a genetically altered human embryo. Still, some of these researchers do hope to use germline gene editing for reproduction, and this is a disturbing prospect because it risks unintended permanent consequences, not only in terms of its safety, but also in its impact on society.

That’s why, before we decide whether to go forward with germline editing, we need to have a much broader society-wide conversation about what its risks are, technologically, socially, and morally. The way we talk about CRISPR makes that hard to do. For example, calling CRISPR a “gene editor” and comparing it to a word processor for DNA makes the technology seem relatively minor and familiar, when in fact it is neither. And vague terms like “genome surgery” conflate somatic gene therapies with embryo or germline editing. A more serious dialogue about designer babies could begin to change the conversation.

It also could help us unpack why “designer babies” come up in the media at all. Frequently, we find, proponents start talking about designer babies when they want to stop real discussion about the risks of gene editing. Hoover Fellow Henry I. Miller, for instance, dismisses concerns over genetically enhanced embryos as downright sinister—“excessive introspection” that will “cause patients to suffer and even die needlessly,” or, as prominent bioethicists Peter Sykora and Arthur Caplan recently charged, hold patients “hostage” to “fears of a distant dystopian future.”

In fact, there are no desperate patients who will suffer without germline gene editing, because by definition it will be done on people who don’t exist yet. Though some proponents claim that editing the genes of embryos is the best or only way to prevent the birth of children with inherited genetic diseases, another technology already exists that accomplishes the same thing. For decades, people who want children but carry genes known to cause disease have used pre-implantation genetic diagnosis (PGD) to test embryos created via in vitro fertilization. With PGD, a few cells of a days-old embryo are tested for specific genetic conditions, allowing parents to identify and implant only those that are unaffected.

PGD carries its own ethical concerns: It prompts difficult decisions about what kind of children will be welcomed into the world and how those choices might stigmatize individuals already living with inherited conditions. But gene-editing human embryos raises such concerns to an even greater degree, by allowing parents to alter genes or even introduce new traits, and carries additional societal risks of increased inequality.

This brings up a third issue worth discussing: What makes a baby a designer baby in the first place? Some try to make a tricky distinction between “bad” reasons for germline gene editing, like enhancing appearance or talent, and “good” reasons for germline gene editing, like preventing serious diseases. Children who resulted from embryos edited for looks or smarts would be the “designer babies;” those created from embryos edited for disease prevention would be … something else.

But in fact such distinctions are difficult to parse in real life. Configuring the genetic makeup and traits of future children is a way of designing them—even if the choices seem unambiguously good, as when choosing to remove a genetic variant that causes serious disease. Any child born from an engineered embryo is, in a sense, a designer baby. Only considering the products of the most frivolous choices to be “designer babies” makes it seem as if there is a clear and easily enforceable line between acceptable and unacceptable uses of germline editing.

But we really don’t have a consensus about which inherited traits are desirable or undesirable. What counts as disease? What conditions are “serious” enough to correct? Who gets to decide? Beliefs can change over time in ways that underscore how problematic it would be to alter future generations. Up until 1973, to cite one example, homosexuality could be diagnosed as a psychological illness; we think about it much differently now.

Decisions to edit out diseases impose present-day values on future generations. Autism has been proposed as one of the serious diseases that might be prevented through embryo editing—but the definition of autism has changed radically over the past few decades. Would editing autism out of people’s genes really be a social good? Many people—advocates, authors, and even employers—argue that we should value the neurodiversity that the autism spectrum represents.

Already, a few scientists are drawing up lists of genes to target for enhancement, and transhumanist proponents of gene editing advocate that we should go beyond preventing disease. Some, including Oxford philosopher Julian Savulescu, argue that it would be unethical for parents not to try to enhance their children if the technology were safe and available. But that oversteps another important issue: If it were possible, who would provide consent? We don’t know the long-term health risks of germline gene editing for a future child or adult, nor for future generations as edited genomes are passed down. Would designer babies feel a loss of autonomy or individuality if they found out their DNA had been changed before they were born? Arguing that there is an ethical obligation to enhance children treats them like commodities—rather than people.

Finally, talking about designer babies can help us understand how germline gene editing would affect social inequality. Another meaning of “designer” is expensive or exclusive. It’s easy to imagine that if designer babies became possible, only the very wealthy would be able to access whatever real or perceived biological “improvements” the edits offered. The advantages that children of the wealthy already have would be reproduced in biology—or would at least be perceived as biological. But the problem is not just who has access: The idea that some genes are better than others has been the basis of dangerous social divisions and injustice, from racism to eugenics. Editing the genes of future generations could exacerbate the inequalities that already exist, and even introduce new forms.

Before we decide whether to go ahead with embryo or germline editing we need a broad societal consensus, and to gain that, the discussion must go beyond the experts and their issues, to a debate by the public at large.

When you dig deeply instead of dismissing concerns about designer babies, you can see what a complicated thicket of issues it presents. Human gene editing is complex—technically, socially, morally—and our discussion of this powerful emerging technology ought to involve everyone. Designer babies provide a figure around which people’s fears, hopes, and questions coalesce. We’re missing a chance to engage when we won’t talk about them.

The post Designer DNA Isn’t Just for ‘Designer Babies’ appeared first on Zócalo Public Square.

Then scurvy would break out—as it has recently in a mental hospital in Bulawayo, Zimbabwe, and at a clinic for diabetics in Sydney—with typical lesions on the skin and mucous tissue, aching joints, and various kinds of vascular damage. Once this happens, vitamin C (ascorbate) has to be ingested immediately to prevent sustained damage to the bones, the blood vessels, the network of nerves, and the brain. Teeth fall out, cartilage disappears, and internal bleeding begins. The heart is under pressure, and the brain can start to hemorrhage. At the same time, scurvy sufferers experience either stupor or powerful dreams and hallucinations. Untreated, scurvy will kill you.

The story of our mutated gene bears strong similarities to the Biblical account of the fall of man, with one important difference. Fruit then was the cause of original sin and our mortality, and fruit (lemons and oranges) now is what infallibly will cure scurvy. But in both scenarios choice of food is a life and death issue.

“Govern well thy appetite, lest sin/ Surprise thee, and her black attendant Death,” Raphael warms Adam in Milton’s Paradise Lost, first published in 1667.

Around the same time, Robert Hooke, an eminent member of the Royal Society of London for Improving Natural Knowledge, remembered the warning when anticipating the great improvements to life and health that experimental science was about to deliver: “And as at first, mankind fell by tasting of the forbidden Tree of Knowledge, so we, their Posterity, may be in part restor’d by the same way … by tasting too those fruits of Natural Knowledge, that were never yet forbidden.”

Hooke’s optimism about human ingenuity didn’t blind him to the fact that we all carry in our bodies the seed of mortality, of which that mutated gene is the physical specimen and scurvy, the specific proof. From Hooke’s era to ours, the biological defect we share with guinea pigs and fruit bats has been a constant in our lives, and for much of that time we have been ignorant of what we need to make us whole. We are none of us perfect, being unable to extract from otherwise nourishing food the vital principle without which we shall die: fat, protein, carbohydrate, and sugar don’t contain it, neither do preserved fruits or boiled vegetables.

Like goiter and rickets, scurvy is a nutritional disease. You don’t catch it, like Ebola or bubonic plague. It waits for an interruption in the ingestion of fresh food, and then—if the interruption is long enough—makes its fatal appearance. On hearing that she had scurvy last year, a patient in the Sydney clinic for diabetics, with a scorbutic ulcer on her leg cried out, “I didn’t realize you could be obese and malnourished at the same time.” A lot of people don’t realize this, which explains why scurvy will always be with us.

A survey of college students in North America found 14 percent with ascorbate below the level for good health. In the Sydney clinic where the outbreak of scurvy occurred, 60 percent of the target group was in a more dire state of depletion. Amnesia about our peculiar gene isn’t limited to people who choose to eat badly. According to The Guardian, since the onset of austerity economics in Britain five years ago, “the number of bed days accounted for by someone with a primary or secondary diagnosis of malnutrition,” including many elderly people, has risen 44 percent.

There is however another reason why alertness or indifference to the dangers of scurvy is part of our history. The difference between neo-Platonic and empirical beliefs about the perfection of the human entity was exhibited when Hooke started inventing machines designed to supplement the deficiencies of the senses. He designed microscopes for the eye, hygrometers (to measure moisture) for the nose, a sort of telegraph for the ear.

John Locke, the Enlightenment philosopher, was incredulous: Why be dazzled, suffocated, and deafened by impressions our nature was never intended to feel?

Hooke thought we needed the supplement of machines if we were ever to feel things as they truly are, and shed our sin and mortality. Locke, on the other hand, was an empiricist to the extent he believed that all we know comes to us via the senses, but like Descartes and Plato he believed we needed no additional help in order for our perceptions to be perfect—or as perfect as was consistent with God’s will. His empiricism was flexible enough to accommodate Plato’s and Descartes’ belief that truly good and wise humans are never in a state of becoming, but already complete in their faculties unless seduced and enslaved by false representations. Margaret Cavendish, the 17th century English aristocrat and scientist, was of the same opinion and, later, so was Locke’s pupil, the elegant philosopher-earl Anthony Ashley Cooper, Lord Shaftesbury.

Hooke thought we needed all the prostheses we could lay our hands on if we were to regain what we lost in Paradise; so he ably abetted his friend, Robert Boyle, in the management of an air-pump, a sort of artificial lung, in his efforts to discover the vital principle of air.

And Hooke’s colleagues Thomas Willis and Walter Charleton, two great 17th century specialists on scurvy, came as close as any scientists, before the isolation of vitamin C in 1933, to the secret of the vital principle of food. They called it a nitrous salt, a latex, a nutritive sap which, they showed, directly affected the efficiency of the nerves as well as the scaffolding of the body. They knew it added nothing to body mass, but that without it even the most robust constitution would fail.

Almost a hundred years after their hypotheses were confirmed by bio-chemical proofs, a significant fraction of the population remains at risk of diseases that supervene when ascorbate levels are low—a risk that can in many cases be minimized with a healthy dose of vitamin C. It has recently been discovered that large intravenous injections of vitamin C will reduce deaths from sepsis by three-quarters. Current research at Vanderbilt University indicates that seizures are much more likely when the body is carrying insufficient ascorbate. A colleague assured me that five years of his life were lost to chronic fatigue syndrome until he started intensive doses of vitamin C.

It is not for nothing that the first outbreak of scurvy in Australia in almost 200 years occurred at a clinic for diabetics. Type 2 diabetes is largely caused by a poor diet cooperating with oxidative stress, a major factor in depleting reserves of ascorbate.

Is it because we thought we were perfect that scorbutic imperfection dogs us? Or is it that artificial perfection is too tedious to attain, and we would rather dally with our sin?

The post Why Scurvy Is Still a Snake in Our Nutritional Lost Paradise appeared first on Zócalo Public Square.

But what if there was a sense in which you really could tell the future? And what if we could also make a particular outcome more likely, even certain? The emerging technology known as gene drives offers just such a prospect for favoring particular traits in future plants and animals—to increase agricultural output, to reduce the risk of infectious disease transmission, or something we haven’t yet imagined. Indeed, some have already suggested using gene drives to eliminate certain mosquitoes that can spread Zika, malaria, and other ailments. But is that a good idea? How should we think about employing such a technology in ways that anticipate, and weigh, its benefits and harms for current and future generations?

Over the past year, at the request of the National Institutes of Health and the Foundation for the NIH, a committee of the National Academies of Sciences, Engineering, and Medicine considered these questions. Last month, the committee, which I co-chaired with Elizabeth Heitman from the Center for Biomedical Ethics and Society at Vanderbilt University Medical Center, released its report—“Gene Drives on the Horizon: Advancing Science, Navigating Uncertainty, and Aligning Research with Public Values.” So what did we conclude? I will get to that in a minute, but first, a lesson on the science.

Gene drive technology allows scientists to alter the normal rules—odds, if you will—of genetic inheritance in sexual reproduction. Through gene drives, we can significantly enhance the chances (from nature’s 50-50 odds in most sexually reproducing species) of a particular gene being passed to an offspring. The gene drive technology combines an altered genetic trait, such as producing a male, with an increased likelihood the trait passes throughout a population.

This is a new tool in a well-established pursuit. Inheritance is an area in which humans put a lot of effort into managing future outcomes. Breeders may work for years or decades to ensure that characters such as a plant’s seed size, or a horse’s strength or speed, pass predictably from generation to generation. How predictably? Well, throughout history the essence of “good breeding” is making passage of a desirable trait between generations as reliable as possible.

It was only in the late 1800s, however, that experiments with pea plants by an Austrian monk, Gregor Mendel, raised the prospect that managing the passage of traits between generations could move beyond best practices or even best guesses. Mendel demonstrated that for at least some parental traits he could predict the average frequency with which they would occur in offspring. For example, if parent plants in a sexually reproducing species had red flowers or yellow seeds, a prediction might be that half of all offspring would have red flowers or yellow seeds. It was a remarkable advance. By early in the 20th century, Mendel’s results were among the fundamental insights leading to the science of genetics.

Geneticists work to reveal the rules of inheritance by understanding the processes that link an individual’s DNA, or genotype, to the expression of a particular trait, the phenotype of a developing organism or an adult. This requires understanding the molecular and environmental variables controlling an outcome, such as having a male or female offspring. We know that in most species with two sexes, we can expect on average the offspring generation will have about half males and half females. This is a basic rule of inheritance. Absent forces such as gene mutation or natural selection, the frequency of many traits in the offspring generation will equal that of the parental generation. But what if you had the technology to alter that basic rule and cause the ratio in the offspring generation to be 60:40 males to females, or 70:30, or even 99:1?

Gene drive technology opens up such possibilities. A gene drive could be designed to increase the likelihood a female produces males as opposed to females. In addition, with the passing of each generation the fraction of males in a population increases as the trait “drives” through a population—the future becomes more certain. In an extreme, much or all of a population could become males, and of course for a species with sexual reproduction the result would be reduction or elimination of a population, or even extinction of a species.

But should gene drives be used to alter population sizes, perhaps to the point of extinction? On the upside, gene drive modified organisms hold the promise of improving human health and agricultural productivity, conserving other species, and advancing basic research. Imagine eliminating a mosquito species that carries malaria.

There are, however, possible downsides to releasing gene drive modified organisms in natural ecosystems. How should we consider using such gene drive power? What should we consider before deciding whether to use it?

The NIH committee report issued in June devotes a lot of attention to responsible science and the need for continuous evaluation and assessment of the social, environmental, regulatory, and ethical considerations of releasing gene drive modified organisms into the environment. Each step in research and deployment, we emphasized, rests on values held by individuals and communities. Public engagement in pursuit of uncovering and understanding these values cannot be an afterthought. The governance of research on gene drive modified organisms should begin with the personal responsibility of the investigator and extend from there to research institutions and regulators. But what regulators: state, federal, global? After all, upon release, a gene drive modified organism is designed to spread. The borders of private property, states, or countries are not barriers to dispersal. A key message of the report is:

There is insufficient evidence available at this time to support the release of gene drive modified organisms into the environment. However, the potential benefits of gene drives for basic and applied research are significant and justify proceeding with laboratory research and highly-controlled field trials.

Some of the gaps in understanding the full impacts of gene drive technology include ecological and evolutionary processes in natural ecosystems. If we diminish or even eliminate a species like a mosquito that transmits a pathogen that infects humans, what will that mean for the ecosystem’s stability? This action, for example, may then open an opportunity for one or more additional insect species that transmit even less desirable infectious diseases to become established or increase in numbers.

The committee’s blueprint for moving forward includes a gradual framework for testing that stretches from laboratory development to field release and monitoring of gene drive modified organisms. We recommended ecological risk assessment as a method for quantifying how a specific change or changes in the environment will affect something of value to society—such as water quality or the chance that an unwanted pest species that transmits an infectious pathogen might become established.

Controlling the future of inheritance across entire populations and species is a powerful scientific advance, one that is hard to overstate. And, as often happens, there is a risk of scientific research outpacing the development of a broader ethical framework to determine whether, and how best, to deploy this newly acquired scientific power. Let’s hope scientists, and governments everywhere, heed the report’s call to proceed with caution. The promise of gene drive technology is immense, but when we’re talking about the power to make certain species extinct, it’s a technology we can’t afford to misuse.

The post How to Control the Incredible Promise and Profound Power of Gene Drive Technology appeared first on Zócalo Public Square.

As we gain greater power over these units of heredity, we have to ask deep questions about how far we are willing to go. Earlier this month The New York Times reported that scientists are privately discussing manufacturing the entire DNA contained in human chromosomes out of chemicals. The activity raises the specter of being able to create a human being without parents through cloning, but according to the Times report, an organizer of the proposed project was quick to circumscribe its ambitions, saying it was aimed at creating cells, not people. Their goal, he said, was to improve scientists’ ability to synthesize DNA, techniques that could apply to animals, plants, and microbes.

With so much promise and peril in the air, how should we navigate this new scientific frontier? In advance of an upcoming Zócalo Public Square event with Pulitzer Prize-winning author and physician Siddhartha Mukherjee asking “Will genetic engineering endanger humanity?”, we posed to experts a related question: “What is the greatest possible benefit—and the biggest danger—of gene manipulation?”

The post Will Modern Genetics Turn Us Into Gene “Genies”? appeared first on Zócalo Public Square.