At first, Everly Green’s parents didn’t understand why her doctors wanted genetic testing. Their daughter was behind on her milestones at 18 months, but was gradually making progress, and they expected that to continue.
Then, when she turned 2, the seizures started. She suddenly began to lose skills. Three months later, Everly needed a feeding tube. Now, at 8, she can only move her eyes, allowing her to communicate via a screen.
Everly, whose family lives in Fort Collins, has a rare mutation in a gene called FRRS1L, pronounced “frizzle,” which affects how cells in her brain communicate. Her parents, and other members of the tiny community of children with the condition, have worked with researchers and small-scale manufacturers to develop a treatment that could restore some of her ability to move — but only if they can raise $4 million to develop and test it.
Everly clearly understands what happens around her and loves school, where she learns in a mainstream classroom with support and has several best friends, said Chrissy Green, Everly’s mother. Still, she wants to do things she can’t, such as holding toys on her own or going on the occasional family trip with her brothers, Green said.
“These kids are in there, they want to play like other kids, they just can’t move,” she said.
Green is co-president of the foundation Finding Hope for FRRS1L, which is collecting funds for the next stage of drug development. Children with FRRS1L gene disorder, the foundation’s website says, “are trapped in a body they can’t move, however still retain high cognitive function, understanding, communication and awareness.”
Worldwide, only a few dozen children currently have a diagnosis of the same mutation in FRRS1L, meaning there’s little interest from drug companies. Families are on their own to fund research and, if all goes well, convince the U.S. Food and Drug Administration that the treatment is safe and effective enough to go on the market.
And, even if they succeed with the FDA, they’ll still face a battle with insurance companies that may not want to pay the steep price for a drug to correct a faulty gene. (Even though the families aren’t looking to make a profit, these types of treatments are expensive, and the company under contract to do the manufacturing isn’t doing it for free.)
Chrissy Green sits with her daughter Everly, 8, as her two boys Colton, 9, left, and Ryle, 4, play at their home in Fort Collins on Dec. 18, 2025. (Photo by RJ Sangosti/The Denver Post)
Normally, drug companies take on the financial risk of turning basic research that’s often publicly funded into treatments, with the hope of eventually making a profit. For gene therapies, that model can break down because of the small number of patients. Green’s FRRS1L foundation knows of about three dozen patients worldwide, though other children with unexplained seizures could have the mutation.
A drug that treats so few patients will never be profitable, so parents are largely on their own in trying to fund research and development, said Neil Hackett, a researcher who has worked with families on gene therapies and advised the FRRS1L foundation. Usually, they can’t do it unless they happen to have one or more business-savvy parents with the time and resources to run a foundation while caring for a child with complex needs, he said.
“They need specific expertise, which is not easy to find, and they need massive amounts of money,” he said.
Steve Green supports his daughter Everly’s head as the family plays with toys together at their home in Fort Collins on Dec. 18, 2025. (Photo by RJ Sangosti/The Denver Post)
When they first received Everly’s diagnosis, her doctor told the family to make the most of the time they had left, because medicine couldn’t offer anything to extend her life or reduce her symptoms, Green said. She didn’t initially question that, but focused on loving her daughter and trading tips for daily life with other families via Facebook.
Green connected with a mother in London who had a child the same age as Everly. Viviana Rodriguez was exploring whether researchers had found any evidence to suggest they could repurpose existing drugs to reduce FRRS1L symptoms.
Everly Green, 8, lies next to her mother, Chrissy Green, as she reads to her at their home in Fort Collins on Dec. 18, 2025. (Photo by RJ Sangosti/The Denver Post)
Through a “providential” series of events, one of Rodriguez’s contacts knew a doctor at the University of Texas Southwestern Medical Center who worked on gene therapies. That doctor had read a paper from a German researcher who bred mice with the FRSS1L mutation so he could study it. The German scientist had given the mice a gene therapy as part of his experiments, but his work wasn’t focused on the clinical applications, Green said.
Green and Rodriguez, along with a small group of other parents, formed the foundation to raise $400,000 for the UT Southwestern researchers to breed their own group of FRSS1L mice and give them a gene therapy in a study that was set up to show results. The mice that received the gene therapy had near-normal movement after it took effect, she said.
“We saw major recovery in the animals, so we’re really hopeful for our kids,” she said.
The next step was testing for toxic side effects, then finding a manufacturer who could do the complicated work of inserting the corrected gene into a harmless virus, Green said. If they can raise the necessary money and all goes as expected, children could receive their doses through a clinical trial starting in September, she said.
Colton Green, 9, pushes his sister Everly, 8, into the family’s living room at their home in Fort Collins on Dec. 18, 2025. (Photo by RJ Sangosti/The Denver Post)
Many treatments that look promising in mice don’t pan out in humans. Even if they do, foundations must navigate the complex process of getting permission from the FDA to sell the treatment, Hackett said. Then they face the separate battle of convincing insurance companies, or national health systems serving patients in other countries, that they should pay for it, he said.
Theoretically, a foundation could keep a treatment in reserve for patients diagnosed with the FRSS1L mutation in the future, but that likely isn’t feasible, Hackett said.
“At the end, I think you have to turn it over to a commercial entity, and I don’t think anyone knows what that looks like,” he said.
Green is hopeful, however, that the treatment she’s trying to fund will not only help children like Everly, but also ease the path for future gene therapies.
“All the diseases can kind of help each other move forward,” she said.
Chrissy Green lifts her daughter Everly, 8, out of bed at their home in Fort Collins on Dec. 18, 2025. (Photo by RJ Sangosti/The Denver Post)
In 2005, scientists announced that moss could grow inside of spaceships. The little plants the scientists sent up on NASA Space Shuttle missions grew in a breathtakingly weird shape, a sort of fuzzy spiral, an apparent reaction to the low-gravity environment.
It was not as whimsical an experiment as you might think. As researchers contemplate how humans might someday feed ourselves beyond Earth, it’s anyone’s guess how plants that evolved on Earth, with Earth’s gravity and atmosphere and protection from the radiation of outer space, will handle such strange habitats.
Since that space moss took its journey, many research teams have sent seeds and spores to the International Space Station (ISS) and arranged for plants to be grown there. Now, following in the steps of those researchers, a team publishing Nov. 20 in the journal iScience demonstrates that more than 80% of moss spores left on the outside of the ISS for nine months and brought back to Earth germinated normally. The findings confirm that moss spores, already known to be hardy, handily survive the stresses of near-Earth orbit.
This particular moss species, called spreading earthmoss, is often used by scientists in the lab, says Tomomichi Fujita, a professor at Hokkaido University and an author of the new paper. Its spores, each containing everything needed to build a new moss plant, went to space because Fujita and his colleagues were curious how they might handle long-term exposure to those harsh conditions, with an eye to someday growing such mosses on other planets. On Earth, “moss is a pioneering land plant,” he says. When plant life on this planet first moved from the seas to the land, it’s thought that mosses were some of the first to take to the new living situation.
Before the spores took flight, the researchers first checked to see how they handled stresses on Earth. They recorded how many spores germinated after being exposed to extreme heat and cold, to ultraviolet radiation, and to very low pressure, confirming that when compared to other life stages of the moss, spores were more resilient. Then, the spores were kept on the outside of the ISS for nine months, where they were exposed to numerous challenges at once.
Fujita and his colleagues weren’t sure if any spores would make it; each of the challenges on Earth seemed to knock down their viability substantially. But in the end, “[more than] 80% of the spores survived. That was very surprising,” he says. He hopes the results can help advance research about how plants from Earth could someday grow on Mars or the moon.
One factor that spores might face once they leave low-Earth orbit, which this study could not address, is how they handle cosmic ionizing radiation, says Agata Zupanska, a research scientist at the SETI Institute, a nonprofit dedicated to studying the origins of life in the universe. Earth’s magnetic field largely deflects these rays before they can tear into genetic material and cause mutations, and the ISS is low enough that it is fairly protected. But that kind of protection isn’t available in deeper space, and it is a serious concern that crop seeds on their way to another planet might take so much damage that they are no longer viable on arrival, Zupanska says.
To address this issue in her own work, Zupanska bombards hardy Antarctic mosses with radiation in a particle accelerator. “The most resistant-to-radiation plant is moss. This is why I got into moss,” she says. (Also, she adds, with a laugh, “moss is cute.” It has surprising charisma for a small green entity.) Her group has sent these bombarded plants up to the ISS to see how low-gravity conditions affect their ability to recover from radiation; results from that experiment have not yet been published.
If mosses—either their spores or whole plants—can weather the trials of space travel, perhaps their strategies could be adapted to aid other plants. And mosses themselves, both Fujita and Zupanska believe, might have a role to play in making other planets hospitable for earthly life. After all, mosses are thought to have helped pump large amounts of oxygen into Earth’s atmosphere more than 400 million years ago.
“It’s a pioneering plant. Here on Earth, even when you have a forest devastated by wildfires, the first plants to creep in and restore the ecosystem are going to be moss,” Zupanska says. Maybe someday there will be cushions of green on red Martian dust, adapting to a new environment and modifying it in turn.
Sip a glass of wine, and you will notice liquid continuously weeping down the wetted side of the glass. In 1855, James Thomson, brother of Lord Kelvin, explained in the Philosophical Magazine that these wine “tears” or “legs” result from the difference in surface tension between alcohol and water. “This fact affords an explanation of several very curious motions,” Thomson wrote. Little did he realize that the same effect, later named the Marangoni effect, might also shape how embryos develop.
In March, a group of biophysicists in France reported that the Marangoni effect is responsible for the pivotal moment when a homogeneous blob of cells elongates and develops a head-and-tail axis — the first defining features of the organism it will become.
The finding is part of a trend that defies the norm in biology. Typically, biologists try to characterize growth, development, and other biological processes as the result of chemical cues triggered by genetic instructions. But that picture has often seemed incomplete. Researchers now increasingly appreciate the role of mechanical forces in biology: forces that push and pull tissues in response to their material properties, steering growth and development in ways that genes cannot.
Modern imaging and measurement techniques have opened scientists’ eyes to these forces by flooding the field with data that invites mechanical interpretations. “What has changed over the past decades is really the possibility to watch what happens live, and to see the mechanics in terms of cell movement, cell rearrangement, tissue growth,” said Pierre-François Lenne of Aix Marseille University, one of the researchers behind the recent study.
The shift toward mechanical explanations has revived interest in pre-genetic models of biology. For example, in 1917 the Scottish biologist, mathematician, and classics scholar D’Arcy Thompson published On Growth and Form, which highlighted similarities between the shapes found among living organisms and those that emerge in nonliving matter. Thompson wrote the book as an antidote to what he thought was an excessive tendency to explain everything in terms of Darwinian natural selection. His thesis—that physics, too, shapes us—is coming back into vogue.
Time-lapse movie of a gastruloid developing a head-to-tail axis.
Video: Sham Tlili/CNRS
“The hypothesis is that physics and mechanics can help us understand the biology at the tissue scale,” said Alexandre Kabla, a physicist and engineer at the University of Cambridge.
The task now is to understand the interplay of causes, where genes and physics somehow act hand in hand to sculpt organisms.
Grow With the Flow
Mechanical models of embryo and tissue growth are not new, but biologists long lacked ways of testing these ideas. Just seeing embryos is difficult; they are small and diffusive, bouncing light in all directions like frosted glass. But new microscopy and image analysis techniques have opened a clearer window on development.
Lenne and his coworkers applied some of the new techniques to observe the motion of cells inside mouse gastruloids: bundles of stem cells that, as they grow, mimic the early stages of embryo growth.
More than 3,000 years ago, in what is now Kazakhstan, six dogs were laid carefully in the ground. Were they beloved pets? Sacrifices, since they seem to have ritually arranged? No one can say for sure. But for scientists studying how dogs threaded themselves into human history, archaeological finds like these are precious. They provide a chance to peek into the DNA of dogs, to see just how they leapt from one group of humans to another, making their own migrations across continents.
Advances in sequencing ancient DNA have revealed that over millenia, people have moved into new regions in successive waves, sometimes intermingling with local folk, sometimes replacing them entirely. Researchers curious if the same was true for other creatures living alongside them turned to DNA from 17 dogs that lived in the last 10,000 years in Eurasia, including one from the burial in Kazakhstan. In a study published Nov. 13 in the journal Science, they reveal that dogs traveled with their humans into new lands, and sometimes, even if the human newcomers didn’t stick around, the dogs did.
Dogs have lived among humans for far longer than you might realize—before there were cities, before there were even farms, they were with us, says Laurent Frantz, a professor at the Ludwig Maximilian University of Munich and an author of the paper. Chickens, horses, pigs, sheep, goats, and cows are all more recent additions to humans’ menagerie than dogs. And these pooches seem to have been well-traveled, even millennia ago; previous work by Frantz and collaborators suggests dogs living in North America before the arrival of European colonists originally came from Eurasia, as humans did.
But it can be surprisingly tricky to find their remains among the vast numbers of other animal bones humans leave behind. “I travel a lot with a colleague of mine that works on horses,” Frantz says. “We go together through boxes trying to find material coming from these sites, and we find sheep, sheep, sheep, sheep.” But dogs are more likely than other animals to have been buried specially, he says, in their own graves, with some care.
For their paper in Science, Frantz and his collaborators were curious about a pivotal moment in Asian history: the arrival of bronze in China. The technology to make the metal traveled from the western part of the continent to the east about 5,000 to 4,000 years ago, he says, and “it completely transformed society.” The people who brought bronze seem to have come with horses, cattle, and sheep. Did they also bring new types of dogs?
Using never-before-analyzed DNA from dogs living in Eurasia over the last 10,000 years, the team pieced together an intriguing picture. At first, before the Bronze Age, dogs in western and eastern Eurasia were distinct populations. Between the two, in a place called Botai in Kazakhstan, there were even dogs whose ancestors came from the Arctic, perhaps reflecting the cold local climate or the specific needs of the Botai people.
But as the human migration linked to the spread of bronze crept eastward, genetics suggests the people of Botai mostly disappeared, subsumed by the newcomers. “It’s like the end of the world, in a way,” Frantz says. “Their way of life is gone, and a lot of their genetics also disappear.” The same was true of Botai’s dogs.
When bronze reached East Asia, something different happened: The locals picked up the newcomers’ bronze technology and their dogs, but they didn’t pick up their genes. “What’s really interesting with the dogs,” says Frantz, “is they seem to flow more like the technology than the people.”
That’s an apt comparison, says Audrey Lin, a paleogeneticist at the American Museum of Natural History who was not involved in the current study. “They are a technology,” she says.
While it’s impossible to know from DNA what dogs were up to with humans all those years ago, they were likely used for hunting, herding, or perhaps as a kind of alarm system once humans had turned in for the night. So it makes sense that they might have been traded.
Frantz is eager to explore how dogs spread through Southeast Asia, down into Australia. And he is curious, too, not just about the anthropological questions dogs can answer, but how they shaped themselves to live so long in tandem with humans. They traveled with hunter-gatherers, they were bred by the Romans, they lived on remote islands in Siberia—all long before there was easy exchange between these parts of the world.
“There are lots of questions that we have,” he says, “about dogs themselves.”
In a step toward the wider use of gene editing, a treatment that uses Crispr successfully slashed high cholesterol levels in a small number of people.
In a trial conducted by Swiss biotech company Crispr Therapeutics, 15 participants received a one-time infusion meant to switch off a gene in the liver called ANGPTL3. Though rare, some people are born with a mutation in this gene that protects against heart disease with no apparent adverse consequences.
The highest dose tested in the trial reduced both “bad” LDL cholesterol and triglycerides by an average of 50 percent within two weeks after treatment. The effects lasted at least 60 days, the length of the trial. The results were presented today at the American Heart Association’s annual meeting and published in The New England Journal of Medicine.
The Nobel Prize–winning Crispr technology has mostly been used to address rare diseases, but these latest findings, while early, add to the evidence that the DNA-editing tool could be used to treat common conditions as well.
“This will probably be one of the biggest moments in the arc of Crispr’s development in medicine,” Samarth Kulkarni, CEO of Crispr Therapeutics, tells WIRED. The company is behind the only approved gene-editing treatment on the market, Casgevy, which treats sickle cell disease and beta thalassemia.
The American Heart Association estimates that about a quarter of adults in the US have elevated LDL levels. A similar number have high triglycerides. LDL cholesterol is the waxy substance in the blood that can clog and harden arteries over time. Triglycerides, meanwhile, are the most common type of fat found in the body. High levels of both raise the risk of heart attack and stroke.
The Phase I trial was conducted in the UK, Australia, and New Zealand between June 2024 and August 2025. Participants were between the ages of 31 and 68 and had uncontrolled levels of LDL cholesterol and triglycerides. The trial tested five different doses of the Crispr infusion, which took about two and a half hours on average to administer.
“These are very sick people,” says Steven Nissen, senior author and chief academic officer of the Heart, Vascular and Thoracic Institute at Cleveland Clinic, which independently confirmed the trial’s results. “The tragedy of this disease is not just that people die young, but some of them will have a heart attack, and their lives are never the same again. They don’t get back to work, they develop heart failure.”
One trial participant, a 51-year-old man, died six months after receiving the lowest dose of the treatment, which was not associated with a lowering of cholesterol and triglycerides. The death was related to his existing heart disease, not the experimental Crispr treatment. The man had a rare, inherited genetic form of high cholesterol and previously had several procedures to improve blood flow to his heart.
In 2018, Chinese scientist He Jiankui shocked the world when he revealed that he had created the first gene-edited babies. Using Crispr, he tweaked the genes of three human embryos in an attempt to make them immune to HIV and used the embryos to start pregnancies.
The backlash against He was immediate. Scientists said the technology was too new to be used for human reproduction and that the DNA change amounted to genetic enhancement. The Chinese government charged him with “illegal medical practices,” and he served a three-year prison sentence.
Now, a New York–based startup called Manhattan Genomics is reviving the debate around gene-edited babies. Its stated goal is to end genetic disease and alleviate human suffering by fixing harmful mutations at the embryo stage. The company has announced a group of “scientific contributors” that includes a prominent in vitro fertilization doctor, a data scientist who worked for de-extinction company Colossal Biosciences, and two reproductive biologists from a major primate research center. A scientist who pioneered a technique to make embryos using DNA from three people is also involved.
“I like to take on challenges when I see them,” says cofounder Cathy Tie, a former Thiel fellow who left college at 18 to start her first company, Ranomics, a genomics screening service. As Tie sees it, that challenge is to make the idea of human embryo editing more acceptable in society.
The idea of editing human embryos is tantalizing, because any changes made to the reproductive cells are heritable. Snip out a disease-causing mutation in an embryo and it would be deleted from future generations as well. But gene-editing technology also has the potential to cause unintended “off-target” effects. Edit the wrong gene by mistake and it could give rise to cancer, for instance. Those mistakes would also be passed down to any future children.
While newer forms of gene editing are more precise, there are still ethical issues to contend with. The prospect of being able to manipulate the DNA of a human embryo has raised fears of a new kind of eugenics, where parents with the means to do so could make “designer babies” with traits that they select.
Tie says the goal of Manhattan Genomics—originally called the Manhattan Project when the company first launched in August—is disease correction, not enhancement. Unlike the original Manhattan Project, a secretive US government program during World War II that produced the first nuclear weapons, Tie says her venture will operate openly and transparently. “We’re revolutionizing medicine, and this technology is definitely very powerful. That’s what I think is the commonality here with manipulating the nucleus of the atom and manipulating the nucleus of the cell,” she says.
For decades, the discussion around autism has been a hotbed of misinformation, misinterpretation, and bad science, ranging from the long-discredited link between the neurodevelopmental condition and vaccines, to newer claims that going gluten-free and avoiding ultra-processed foods can reverse autistic traits.
On Monday night, this specter arose again in the Oval Office, as President Donald Trump announced his administration’s new push to study the causes of autism with claims that the common painkiller Tylenol, otherwise known as acetaminophen, can cause the condition. The FDA subsequently announced that the drug would be slapped with a warning label citing a “possible association.”
David Amaral, professor and director of research at the UC Davis MIND Institute, was among those watching in dismay as the president launched into a diatribe about Tylenol, repeatedly warning pregnant women not to take it, even to treat fevers.
“We heard the president say that women should tough it out,” says Amaral. “I was really taken aback by that, because we do know that prolonged fever, in particular, is a risk factor for autism. So I worry that this admonition to not take Tylenol is going to do the reverse of what they’re hoping.”
The speculation surrounding Tylenol stems from correlations drawn by some studies that have touted an association between use of the painkiller and neurodevelopmental disorders. One such analysis was published last month. The problem, says Renee Gardner, an epidemiologist at the Karolinska Institute in Sweden, is that these studies often reach this conclusion because they don’t sufficiently account for what statisticians describe as “confounding factors”—additional variables related to those being studied that might influence the relationship between them.
In particular, Gardner points out that pregnant women needing to take Tylenol are more likely to have pain, fevers, and prenatal infections, which are themselves risk factors for autism. More importantly, given the heritability of autism, many of the genetic variants that make women more likely to have impaired immunity and greater pain perception, and hence use painkillers like acetaminophen, are also linked to autism. The painkiller use, she says, is a red herring.
Last year, Gardner and other scientists published what is widely regarded within the scientific field as the most conclusive investigation so far on the subject, one that did account for confounding factors. Using health records from nearly 2.5 million children in Sweden, they reached the opposite conclusion to the president: Tylenol has no link to autism. Another major study of more than 200,000 children in Japan, published earlier this month, also found no link.
Doctors are worried that Trump’s claims will have adverse consequences. Michael Absoud, a pediatric neurodisability consultant and a researcher in pediatric neurosciences at King’s College London, says he fears that pregnant women will start using other painkillers with a less well-proven safety profile.
Gardner is concerned that it will also lead to self-blaming among parents, a flashback to the 1950s and ’60s, a time when autism was wrongly attributed to emotionally cold “refrigerator mothers.” “It’s making parents of children with neurodevelopmental conditions feel responsible,” she says. “It harks back to the early dark days of psychiatry.”
The world of pregnancy is going to radically change, predicts Noor Siddiqui. “I think that the default way people are going to choose to have kids is via IVF and embryo screening,” she said at the WIRED Health summit last week. “There’s just a massive amount of risk that you can take off of the table.”
Siddiqui is the founder and CEO of Orchid, a biotech company that offers whole-genome screening of embryos for IVF. By analyzing the DNA of different embryos before selecting which one to implant, Orchid says, parents can lower the risk their children grow up affected by conditions with a genetic basis. Siddiqui was speaking with George Church—a pioneer in genomics and a professor of genetics at Harvard Medical School—at the summit in Boston, exploring the promise and potential of whole-genome sequencing.
An estimated 4 percent of people worldwide have a disease that’s caused by a single genetic mutation. With embryo screening, “these monogenic diseases can be just completely avoided,” Siddiqui said. On top of this, roughly half the world’s population suffers from a chronic disease with at least some genetic basis. Analyze five embryos ahead of implanting one, Siddiqui said, “you can now mitigate the genetic component of that risk by these double-digit numbers. You’re talking about in the worst case 30 percent and in the best case up to 80 percent.”
Orchid’s website, which references statistical analysis on how much risk reduction can be achieved through embryo screening, explains that the exact reduction in relative risk will depend on a number of factors. These include, among others, how prevalent the disease is, the number of embryos analyzed, and how much influence the genetic variants screened for have on the likelihood of developing the disease.
Church is an investor in Orchid, and believes the type of embryo screening it offers is among the most cost-effective medical technologies ever created. The Human Genome Project, the first effort to map all human genes, cost $3 billion, but since then, the cost of sequencing a genome has fallen dramatically. Orchid’s whole-genome sequencing costs several thousand dollars per embryo. That’s “maybe a 10-fold return on investment,” Church believes. “A huge fraction of our health care costs, psychological problems, and family issues could be solved by this method.”
Siddiqui has used the technology to screen her own embryos. She shared the story of her mother, who experienced adult-onset blindness as a result of a genetic variation in her genome. “Fortunately, all embryos are negative for that,” she said. “But the other thing that’s quite common in most South Asian families is an incredibly high risk for heart disease and diabetes. So that’s really the other thing that we’re prioritizing based on.”
The blindness that Siddiqui described is monogenic, meaning it was caused by just a single genetic variation. Of the single-gene diseases that are known, “95 percent have no treatment, much less of a cure,” Siddiqui said. But many other conditions—such as schizophrenia, or bipolar disorder, or heart disease—are polygenic, driven by the cumulative impact of many genetic variants. For these, genetic risk scores can quantify the risk of potentially developing a disease, and they can be calculated both for adults and embryos. Orchid’s embryo tests look for both disease types.
Few living thinkers have been as influential—or controversial—as Richard Dawkins. An evolutionary biologist by training, Dawkins rose to prominence with his 1976 book The Selfish Gene, which revolutionized the public understanding of evolution by shifting the focus from organisms to the genes that shape them (as well as surfacing the now-ubiquitous concept of the meme, which Dawkins defined as units of cultural transmission or imitation). In the decades since, he has become almost as well known for his critiques of religion as for his scientific work, with 2006’s The God Delusion establishing him as one of the world’s most outspoken atheists. Dawkins’ work shows why free inquiry and the scientific method are essential for human progress, especially when they are under threat from religious dogma or new forms of ideological orthodoxy.
In this wide-ranging conversation with Reason‘s Nick Gillespie, recorded live in September 2024 in Milwaukee as part of Dawkins’ Final Bow tour, the two discuss the central metaphor of Dawkins’ latest book, The Genetic Book of the Dead, which presents every organism as a kind of living archive of evolutionary history. He explains how cooperation among genes—not just competition—drives natural selection. The two also explore the role of atheism in a changing moral landscape, whether science requires a specific cultural or political environment to thrive, and what humans might gravitate toward next as belief in traditional religion continues to decline.
Reason: I first encountered your work as an undergrad. I was a double major in psychology and English. When reading your work, I couldn’t believe that I was reading science because I understood what you were saying. But in The Genetic Book of the Dead, you use a term—palimpsest—as a controlling metaphor. What is a palimpsest, and why is it so important to what you’re doing in this book?
Dawkins: A palimpsest is a manuscript which is erased and then the parchment is used again. In the days when paper was not available, people wrote on parchment. It was quite scarce; they would reuse it. The point of it in the book is that every animal bears in itself—in its genes and in its body—a description of the worlds in which its ancestors survived. This, it seems to me, follows from natural selection. The animal has been put together by a whole lot of selection pressures over many millions of years.
In the book, you talk about how that palimpsest is sometimes literally on the organism’s skin or shell. What’s a good example of that?
Any camouflaged animal that sits on the background that it resembles. I use the example of a lizard in the Mojave Desert, which has, more or less, painted on its back a picture of desert. The whole of its back is a painting of the desert. Any camouflaged animal is an obvious example. My thesis is that that principle must apply to every cell, every biochemical process, every detail, every part of the animal.
In The Selfish Gene, you debunked the idea that we’re in control as humans—you said we’re being used by genes. In this book, you’ve outdone yourself by saying that we are actually a cooperative of viruses. I guess my question is: What do you have against human beings?
Well, The Selfish Gene had what you would call a sting in the tail—the last chapter switched to a different topic, which was memes. I thought this book should have a sting in the tail as well, and so this is this idea that we are a gigantic colony of cooperating viruses.
One of my books is called The Extended Phenotype. This is the idea that the genes in an animal work to survive not just by influencing the body of the animal in which they sit—they reach outside the animal, and part of the so-called phenotype of the genes is outside the body. An obvious example is a bird’s nest or a bowerbird’s bower, which is not a part of the animal but which nevertheless is a Darwinian adaptation. It’s shaped by natural selection. And this must mean that there are genes for nest shape, genes for bower shape. This principle of the extended phenotype applies not just to inanimate objects like nests and bowers. It applies to other individuals. A parasite can influence the behavior of the host in which it sits in order to further its designs as a parasite. That means that the genes in the parasite are having phenotypic effects on the body and behavior of the host.
Now, if you think about a parasite in an animal—like a worm or a virus or a bacterium—its task is to get into the next host. There are two ways in which it can do this.
It can be expelled from the host in some way, like sneezed out or coughed out of the host, and then breathed in by the next host. When a parasite exits the body by some such route, it has no great interest in the survival of the host in which it sits. For all it cares, the host can die.
But what about a parasite which passes to the next host via the gametes, via the eggs or sperms of the present host? Well, a parasite whose hope for the future is to go into the progeny, into the offspring of the present host, if you think about it, its extended phenotype, its aims, its desires, its hopes for the future will be identical to the genes of the host. It will want the host to be a successful survivor. It will want the host to be a successful reproducer. It will want the host to be sexually attractive, to be a good parent, because everything about what the host regards as success, namely having offspring, will be the same as what the parasite regards as a success, namely, the host having offspring.
All our own genes: The only reason they cooperate in building us—in building the body, in building any animal—is that they all have the same interests at heart. They all get into the next generation via the gametes of the host. In other words, they have the same interest at heart in exactly the same way as a virus that gets passed on in the gametes, or a bacterium that gets passed on in gametes. So that’s why I say that all our own genes can be regarded as equivalent to a gigantic colony of cooperating viruses.
Are you becoming a softy? When you published The Selfish Gene in 1976, evolution seemed to me more about competition and the survival of the fittest. Now you’re speaking more about cooperation. What moved you away from competition and toward cooperation?
I think that’s a misunderstanding. I’m not becoming a softy, or rather, I always was a softy, because The Selfish Gene is not really about selfishness. It’s about selfishness at the level of the gene, but that translates out into altruism at the levels of the individual, or it can. And that’s largely what the book is about. Genes are selfish in the sense that they are striving to get into the next generation. That’s what they do. They are, in a sense, immortal. But they do it by cooperating. I’ve always said that.
In The Selfish Gene, there’s a chapter in which I have the analogy of a rowing race where you have eight men sitting in a row in a boat, and they’re cooperating. That’s what the genes are doing. The genes are cooperating in building a body that will carry all of them to the next generation via reproduction. So they have to cooperate.
We’re always looking for the gene that controls this or controls that. You say that’s a misnomer. Where does that misunderstanding come from?
When you talk about a gene for anything, it’s tempting to think that there’s a gene for this bit and a gene for this bit. It’s not like that. Genes are more like the words of a recipe or a computer program, where they work together to produce a whole embryo, and then a whole body. Genes cooperate in the process of embryology.
The reason why you can, to some extent, talk about a gene for that is that you focus on the differences between individuals. Gregor Mendel, for example, studied wrinkled peas and smooth peas. Well, what he’s really talking about there is individual differences. A genetic difference controls an individual difference. Say, the Habsburg chin—the hereditary malformation of the chin which affected the royal families of Europe. There are lots and lots of genes that enter into the making of a chin, but what this particular gene does is to make the difference between somebody who has the Habsburg chin and somebody who doesn’t. So “gene for X” always means “gene for the difference between somebody who has X and somebody who doesn’t have X.”
You also talk about how a cultural change can have evolutionary consequences, such as the taming of fire and the shrinking of jaws and teeth.
There’s a book by Richard Wrangham, who’s an anthropologist at Harvard, about the importance of cooking on human evolution. One of the things you see as you look at the human fossil record is that our jaws have shrunk. Our ancestors had much bigger, more powerful jaws than we have. Wrangham thinks that this is because of the discovery of fire, the invention of cooking, which enabled us to make food less tough. We didn’t need such powerful jaws. And so that’s an interaction between culture, namely the taming of fire and the development of cooking, and genetic evolution.
Over what time period does that emerge?
Well, it looks as though Homo erectus, which is our immediate ancestor species, which lived about a million years ago, had fire. It’s not absolutely definite, but there do appear to be archeological remains of hearths suggesting that they had fire, and they probably had cooking. At least Wrangham thinks so. So maybe a million years.
Last year, you wrote an article in The Spectator called “Why I’m sticking up for science” about the adoption of certain Māori origin myths being presented as science in New Zealand schools. What was going on there?
This is a very strange business. I arrived in New Zealand and was immediately aware that I was in the midst of a great controversy. The New Zealand government—which was then a socialist government; it’s changed now, but the present government is doing the same thing—is importing compulsorily into science classes in New Zealand schools, Māori myths. And they are being given equal status to what they call “Western science.” Which is just science. It’s not “Western”; it’s just science.
So the children in New Zealand are, I would have thought, being bewildered by, on the one hand, learning about the big bang and the origin of life and DNA and things like that; on the other hand, they’re being told it’s all due to this sky father and the earth mother probably having it off together. It’s pandering to, I think, a kind of guilt that white New Zealanders feel toward the Māori indigenous population, and bending over backward to show respect to the indigenous population. And I think that’s fine—it would be great for New Zealand children to learn about Māori culture and myths in classes on anthropology and history. But to bring them into science classes—that’s just not science.
I became involved because a number of distinguished scientists in New Zealand—fellows of the New Zealand Royal Society, which is the New Zealand equivalent of the National Academy of Sciences here—had written a letter protesting about this to a New Zealand journal called the Listener. As a consequence, they had their lectures canceled, they were threatened with expulsion, really quite unpleasant victimization of these distinguished scientists. And I had lunch with about half a dozen of them and heard all about it from them.
Broadly speaking, how important is it that you were born at a time when you were able to take advantage of a liberal political era so that you could do a lot of the work that you did? If you had been born 200 years earlier or 20 years later, maybe not, right?
Totally. Very, very important.
What do you think accounts for that kind of social and moral progress that makes us more open as a society?
I am fascinated by this. In one of my books, The God Delusion, I talk about the shifting moral zeitgeist. Something changes as the centuries go by. You’ve only got to go back to, say, the mid–19th century, where people like Abraham Lincoln and Thomas Henry Huxley—who were in the vanguard of enlightened liberal thought—by today’s standard were the most terrible racists. So the shifting moral zeitgeist is something that changes not just over the centuries but over decades.
I am genuinely curious about what it is in the air that changes. It seems to me to be a bit like Moore’s law in computing, which is a definite mathematical straight line on a long scale in computer power. It’s not due to any one thing; it’s a composite of things that I think the shifting moral zeitgeist is the same, it is a composite of conversations at dinner parties, journalism, parliamentary/congress decisions, technological innovation, books. Everything moves on.
What do you think the role of atheism—or a challenge to the supremacy of religion—has been, if not as a kind of scientific theory of order, then a social or cultural theory of order?
Well, I think atheism is just sensible. If you look at polls in America and in Western Europe, the number of people who profess religion is steadily going down. There are more religious people in America than there are in the rest of Western Europe. But it is coming down. So that’s part of the shifting zeitgeist.
Part of that has to do with books that you—or the colony of bacteria that are you—wrote. What do you see as the most convincing arguments that you advanced?
If you want to believe something, you’ve got to have reason to do so. It’s rather better to say, “What are the most convincing arguments for theism?” And I’m not sure there are any. But, obviously, there are a lot that appear convincing to many people. The argument from design is probably the most powerful one.
In a way, you kind of advance a godless design with evolution, don’t you? Everything is designed?
Yes, yes. Absolutely. It’s an astonishingly powerful illusion of design. And it breaks down in certain places where there’s bad design, like the vertebrate retina being backward, that kind of thing. But one of the things that I try to do in most of my books, actually, is to show how beautifully perfect the animals are. They really, really do look designed. I think this is probably why it took so long for a [Charles] Darwin to come on the scene. People just couldn’t fathom the idea that it could come about through unconscious laws of physics.
Do you feel good that atheism, or maybe a better term is godlessness, is ascendant?
Yes, I do.
Despite not believing in God, you have called yourself a cultural Christian for at least a decade. What do you mean by that?
Nothing more than the fact that I was educated in Christian schools and a Christian society. It doesn’t mean I’m sympathetic toward it, doesn’t mean I believe it.
You have said that if you had to live in a Christian country or an Islamic country, you would pick the Christian country every time.
Yes, I would not wish to live in a country where the penalty for apostasy is death, and gay people are thrown off high buildings, and women are stoned to death for the crime of being raped.
There is an argument that liberal political philosophy, which allows for limited government, free speech, and open inquiry, has its roots in Christianity and the English Civil War. Part of the argument there was that the king did not have dominion over other men because we are all equal in front of God. I read a critique of you saying that you have been in the tree of Christianity and you’ve been sawing the branch off your whole time, and now by calling yourself a cultural Christian, you’re in a way free riding on something. How do you respond?
Well, I’m rather sorry I said that thing about being a cultural Christian, because people have taken it to mean I’m sort of sympathetic toward the belief.
Now that thing about the society which lets science be free to do what it does being a Christian society, that’s a matter for historians. And they might be right. It is possible that Christendom was the right breeding ground for science to arise in the 17th, 18th, 19th centuries. And your point about the English Civil War could be valid as well.
Research suggests, with obvious exceptions, that religiosity is declining. Religion has been a part of human history and civilization. Is there an issue that replaces it?
G.K. Chesterton is possibly wrongly thought to have said, “When men stop believing in religion, they believe in anything.” It’s rather a pessimistic view. I would like to think you believe in evidence. And I think it’s rather demeaning to human nature to suggest that giving up one sort of nonsense, you’ve immediately got to go and seize on some other sort of nonsense.
What do you hope you will be remembered for? You are a palimpsest—you are writing over the work of previous scientists and thinkers. What is the message that sticks around long enough to influence people after you?
I suppose the message of The Selfish Gene: that natural selection chooses among immortal replicators, which happen to be genes on this planet. It will be the same principle, the Darwinian principle of the nonrandom survival of randomly varying, potentially immortal replicators.
This interview has been condensed and edited for style and clarity.
For a molecule of RNA, the world is a dangerous place. Unlike DNA, which can persist for millions of years in its remarkably stable, double-stranded form, RNA isn’t built to last—not even within the cell that made it. Unless it’s protectively tethered to a larger molecule, RNA can degrade in minutes or less. And outside a cell? Forget about it. Voracious, RNA-destroying enzymes are everywhere, secreted by all forms of life as a defense against viruses that spell out their genetic identity in RNA code.
There is one way RNA can survive outside a cell unscathed: in a tiny, protective bubble. For decades, researchers have noticed cells releasing these bubbles of cell membrane, called extracellular vesicles (EVs), packed with degraded RNA, proteins, and other molecules. But these sacs were considered little more than trash bags that whisk broken-down molecular junk out of a cell during routine decluttering.
Then, in the early 2000s, experiments led by Hadi Valadi, a molecular biologist at the University of Gothenburg, revealed that the RNA inside some EVs didn’t look like trash. The cocktail of RNA sequences was considerably different from those found inside the cell, and these sequences were intact and functional. When Valadi’s team exposed human cells to EVs from mouse cells, they were shocked to observe the human cells take in the RNA messages and “read” them to create functional proteins they otherwise wouldn’t have been able to make.
Valadi concluded that cells were packaging strands of RNA into the vesicles specifically to communicate with one another. “If I have been outside and see that it’s raining,” he said, “I can tell you: If you go out, take an umbrella with you.” In a similar way, he suggested, a cell could warn its neighbors about exposure to a pathogen or noxious chemical before they encountered the danger themselves.
Since then, a wealth of evidence has emerged supporting this theory, enabled by improvements in sequencing technology that allow scientists to detect and decode increasingly small RNA segments. Since Valadi published his experiments, other researchers have also seen EVs filled with complex RNA combinations. These RNA sequences can contain detailed information about the cell that authored them and trigger specific effects in recipient cells. The findings have led some researchers to suggest that RNA may be a molecular lingua franca that transcends traditional taxonomic boundaries and can therefore encode messages that remain intelligible across the tree of life.
In 2024, new studies have exposed additional layers of this story, showing, for example, that along with bacteria and eukaryotic cells, archaea also exchange vesicle-bound RNA, which confirms that the phenomenon is universal to all three domains of life. Another study has expanded our understanding of cross-kingdom cellular communication by showing that plants and infecting fungi can use packets of havoc-wreaking RNA as a form of coevolutionary information warfare: An enemy cell reads the RNA and builds self-harming proteins with its own molecular machinery.
“I’ve been in awe of what RNA can do,” said Amy Buck, an RNA biologist at the University of Edinburgh who was not involved with the new research. For her, understanding RNA as a means of communication “goes beyond appreciating the sophistication and the dynamic nature of RNA within the cell.” Transmitting information beyond the cell may be one of its innate roles.
Time-Sensitive Delivery
The microbiologist Susanne Erdmann studies viral infections in Haloferax volcanii, a single-celled organism that thrives in unbelievably salty environments such as the Dead Sea or the Great Salt Lake. Single-celled bacteria are known to exchange EVs widely, but H. volcanii is not a bacterium—it’s an archaean, a member of the third evolutionary branch of life, which features cells built differently from bacteria or eukaryotes like us.
Because EVs are the same size and density as the virus particles Erdmann’s team studies at the Max Planck Institute for Marine Microbiology in Germany, they “always pop up when you isolate and purify viruses,” she said. Eventually, her group got curious and decided to peek at what’s inside.
Some people get a lot of things from their parents. Their eye color, or the shape of their nose, or a crushing, inexplicable loyalty to a terrible sports team, which must be genetic, because why would anyone choose this agony? (Even with the heartache, Go, Habs, Go!) We also inherit some far less obvious attributes, including genetic coding that makes everything else we do possible.
Within each of our cells—indeed, the cells of most organisms that have DNA—is a structure called mitochondria, which produces a substance called adenosine triphosphate (ATP), a vital component of the energy we need to stay alive. These tiny cell batteries have their own form of DNA, which is different from that found in cells’ nuclei. In nearly all animals, including humans, that mtDNA is inherited only from mothers. Why that’s the case has puzzled biologists, but new data could provide an answer, and lead to new treatments for some rare disorders.
While there are cases of humans having mtDNA from both parents, it’s extremely rare. In 2016, Ding Xue, a professor of molecular and developmental microbiology at the University of Colorado Boulder set out to find out why that is. He discovered a complicated process that causes paternal mitochondrial DNA to essentially destroy itself.
“It could be humiliating for a guy to hear, but it’s true,” Xue said in a statement. “Our stuff is so undesirable that evolution has designed multiple mechanisms to make sure it is cleared during reproduction.”
In the intervening years, Xue set out to learn what happens in the rare cases where that self-destruct sequence isn’t initiated, and paternal mitochondria is passed down to offspring. He chose to experiment on C. elegans, a tiny roundworm consisting of only around 1,000 cells, but still has some tissues in common with humans, such as a nervous system, gut, and muscles.
Describing the experiment in the journal Science Advances, Xue said the worms didn’t display any defects when it came to their sensory responses, but were affected in other ways, such as showing a reduced ability to remember or learn from negative stimuli. The altered worms were also less active in their movements.
None of this is particularly surprising. Around one in 5,000 humans are affected by a mitochondrial disease, and the symptoms can often include developmental delays, impaired cognition, muscle weakness, and poor growth. Previous experiments revealed that when mice were altered to have two different mtDNA sequences, there were a number of negative effects on their metabolism, activity level, and cognition.
What was surprising was that Xue and his colleagues were able to significantly reverse the effects, including returning ATP levels to normal. When they treated the worms with a form of vitamin K2, they found the worms’ learning and memory performance “significantly improved.”
Xue’s paper not only explained the benefits of inheriting mitochondria from a single parent—since adding a second parent’s mitochondrial DNA can lead to adverse effects—but also may have laid the groundwork for future treatments of mitochondrial disorders. He said it’s possible that delays in eliminating paternal mtDNA could be what leads to the disorders occurring in humans. “If you have a problem with ATP it can impact every stage of the human life cycle,” he said.
Roundworms are simple creatures, and it’s unlikely that simply giving humans with mitochondrial disorders vitamin K2 will fully cure their conditions. But the disorders can be hereditary, and Xue said that, while much more research needs to be done, it’s possible that giving vitamin K2 to mothers with a family history of the disease could lessen the chances of passing them on to their kids.
There’s still no hope for a cure for the annual disappointment of missing the playoffs. Thanks, dad.
Kteily says by the time the company rolled out these services, it was too late. Customers had already left the platform. “I think they hit on something viral, which was the concept of where you’ve come from. People found that so fascinating. But once you know that information, you’re not going to come back five years later and pay for a subscription,” he says.
Sumit Nagpal, a serial entrepreneur in the health tech space and a self-described early adopter of 23andMe, says he was among the company’s subscribers but eventually stopped logging into the online platform. He says the reports didn’t provide much “actionable” health advice. “It never had any life-changing value,” he says.
Nagpal’s latest company, Cherish, which he founded in 2020, is developing radar-based sensor platforms equipped with AI for health and safety monitoring. He thinks 23andMe could have had more offerings earlier on—for instance, personalized coaching on diet, exercise, and other lifestyle factors on an ongoing basis to keep customers engaged.
In many ways, 23andMe’s conundrum is similar to the Instant Pot problem. Its initial product was so successful that people never needed to come back to buy another one.
23andMe has tried to diversify its revenue streams, making deals to allow pharmaceutical companies to mine its vast genetic database for drug leads. It partnered with Genentech back in 2015, and when that ended, it struck an exclusive deal with GlaxoSmithKline in 2018. The pharma company invested $300 million in 23andMe, but that agreement expired in 2023, with no big partners stepping in to fill Glaxo’s shoes. And while 23andMe recently shut down its drug discovery unit, it is continuing to advance the drug candidates it already has in clinical trials.
Now, the company has turned to growing its telehealth business. In 2021, it acquired telehealth service Lemonaid. Capitalizing on the Ozempic craze, Lemonaid started offering Ozempic, Wegovy, and compounded semaglutide in August through a weight-loss program. After an initial consultation with a clinician, the membership is $49 per month with weight-loss medication starting at $299 a month for compounded semaglutide. “The addition of weight-loss management for our customers fits directly within our strategy of delivering services to approved individuals’ health through preventive actions,” Wojcicki said in an earnings call in August.
But it may not be enough. Estelle Giraud, CEO and founder of Trellis Health, which is building a health app for pregnancy, says the anti-obesity space is already crowded. 23andMe will have to prove that it offers something unique compared to other telehealth providers. “If I’m a customer looking for a telehealth solution, it comes down to brand and trust,” she says.
And establishing trust may be 23andMe’s biggest challenge after last year’s data breach exposed personal information from nearly 7 million customers’ profiles. It doesn’t help that there’s always been confusion among users over the company’s data practices. Customers must give their express consent to share their deidentified genetic data for research purposes, but one survey conducted in 2017 and 2018 by university researchers found that more than 40 percent of customers polled were not aware that using and sharing customer data was part of 23andMe’s business model. When users opted into sharing their data for research, likely many of them didn’t realize that “research” included helping Big Pharma develop new drugs.
There were many challenges in the process of confirming the role of the MAL gene, including a study by rival researchers that suggested a completely different gene could be responsible. “We suddenly thought, ‘Oh no, maybe all this work we’ve been doing has been wasted,’” recalls Tilley. “That was a real low point.” Thornton chimes in: “But we were convinced we were right.”
In the end, the other study turned out to be wrong, and one of its authors later joined forces with Tilley, Thornton, and their colleagues. Together, the group was subsequently able to prove the significance of the MAL gene in some key experiments. First, following painstaking efforts to find antibodies that would react with it, they established that the crucial AnWj antigen (encoded by the MAL gene) was indeed present on the surface of most people’s red blood cells. Then, they took AnWj-negative blood cells, lacking said antigen, and inserted a complete MAL gene into those cells. This had the hoped-for effect of generating the antigen on the cell surface, turning the cells AnWj-positive. That was definitive proof that the researchers had found the gene responsible for this rare red blood cell variation.
Now that they know the gene in question, it should make it much easier to find AnWj-negative people who could become blood donors so that, if people affected by this blood group ever need a transfusion, they can have one safely.
“What they did was really clever,” says Sara Trompeter, a consultant hematologist and pediatric hematologist at University College Hospitals London. Trompeter also works for NHS Blood and Transplant but was not involved in the AnWj study. “They presented it at a conference, some of their early work. It was like watching one of those detective shows where they’re just picking up on tiny clues and testing hypotheses—things that other people might have ignored.”
Mark Vickers, a hematologist at the University of Aberdeen, who also was not involved in the study, agrees that the results are robust. “They’ve really gone to town and done some very nice work,” he says. “As far as this blood group is concerned, this is going to be the unequivocal landmark paper.”
There are few indications as to what factors might influence someone to have genes that make their blood AnWj-negative. One family of AnWj-negative individuals in the paper was Arab-Israeli, but the authors stress that there is no clear link to ethnicity at this stage. The vast majority of people who are AnWj-negative are not genetically predisposed to it. Rather, they have such blood because of a hematological disorder or because they have one of the cancers that can affect their MAL gene. “It’s not truly negative. It’s just suppressed,” says Thornton, referring to those cases.
There are questions remaining though. Babies don’t actually develop the AnWj antigen on their red blood cells until they’re seven days old. The mechanisms as to why that is remain murky. Vickers suggests it could be something to do with the variety of changes that happen in a fetus’s blood around the time of birth—for example, when its dependence on nutrition and oxygen from its mother’s blood ends.
Tilley, Thornton, and colleagues were also responsible for discovering the genetic basis for the 44th blood group system, called Er, in 2022, as well as the MAM blood group system in 2020, among others. During the past decade or so, blood researchers around the world have described roughly one new blood group system every year, on average. “We’ve got some more in the pipeline,” teases Thornton.
There are still a handful of enigmatic blood samples—blood that reacts to other people’s blood in unexpected ways—out there, tucked away in lab storages. Scientists—mindful of the patients whose lives are affected by this, who will struggle to find matching blood donors, or who, in some cases, may suffer devastating complications during pregnancy—regularly pore over those samples, hoping to explain them one day.
At least one more mystery has been solved. Describing how she feels upon seeing her and her colleagues’ paper published at last, and reflecting on nearly 20 years of work, Tilley just says: “It’s a huge relief.”
Cystic echinococcosis (CE) is a significant zoonotic disease caused by the tapeworm Echinococcus granulosus, affecting various intermediate hosts, including livestock and humans. The disease manifests through the formation of cysts in the viscera, particularly the liver and lungs. Understanding the molecular mechanisms governing parasite-host interactions and immune evasion is crucial for developing effective control and treatment strategies. This is the focus of research in Dr. Rodolfo Paredes’s laboratory at the Veterinary School of the Life Science Faculty at Universidad Andres Bello in Santiago, Chile.
Dr. Paredes and colleagues employ Weighted Gene Co-expression Network Analysis (WGCNA) on RNAseq data from Echinococcus granulosus protoscoleces, a parasite structure found inside liver and lung cysts. They identified 34 gene modules in protoscoleces of liver origin, with 12 showing differential co-expression compared to those of lung origin. Key hub genes related to immune evasion, such as tegument antigen, ubiquitin hydrolase isozyme L3, and COP9 signalosome complex subunit 3, were discovered. This is the first evidence of distinct gene expression networks in protoscoleces from different organs, highlighting the influence of the microenvironment on parasite development and immune evasion.
Dr. Paredes said, “Our research uncovers the intricate gene networks that Echinococcus granulosus sensu stricto utilizes to evade the host’s immune system, offering potential new targets for medical intervention.” Dr. Christian Hidalgo, a co-investigator, added, “The differential gene expression in protoscoleces from liver and lung cysts underscores the importance of considering organ-specific environments in developing effective treatments for cystic echinococcosis.” Dr. Ismael Pereira, a co-investigator, stated, “This study marks a significant advancement in our understanding of the molecular mechanisms of Echinococcus granulosus, paving the way for novel therapeutic strategies.”
Dr. Goodman, Editor-in-Chief for Experimental Biology and Medicine, said: “This pioneering application of WGCNA to Echinococcus granulosus protoscoleces reveals crucial insights into the parasite’s immune evasion strategies. The identified co-expression networks and hub genes provide new potential molecular targets for medical interventions. These findings have significant implications for improving control strategies and therapeutic approaches for cystic echinococcosis, a neglected disease, and emphasizes the need for organ-specific treatments.”
Experimental Biology and Medicine is a global journal dedicated to the publication of multidisciplinary and interdisciplinary research in the biomedical sciences. The journal was first established in 1903. Experimental Biology and Medicine is the journal of the Society of Experimental Biology and Medicine. To learn about the benefits of society membership visit www.sebm.org. If you are interested in publishing in the journal, please visit https://www.ebm-journal.org/journals/experimental-biology-and-medicine.
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On a recent trip to Giant Eagle, my local grocery store in Pittsburgh, I noticed something new in the fruit section: a single pineapple packaged in a pink and forest-green box. A picture on the front showed the pineapple cut open, revealing rose-colored flesh. Touted as the “jewel of the jungle,” the fruit was the Pinkglow pineapple, a creation of American food giant Fresh Del Monte. It cost $9.99, a little more than double the price of a regular yellow pineapple.
I put the box in my cart, snapped a picture with my phone, and shared the find with my foodie friends. I mentioned that its color is the result of genetic modification—the box included a “made possible through bioengineering” label—but that didn’t seem to faze anyone. When I brought my Pinkglow to a Super Bowl party, people oohed and aahed over the color and then gobbled it down. It was juicier and less tart than a regular pineapple, and there was another difference: It came with the characteristic crown chopped off. Soon enough, my friends were buying pink pineapples too. One used a Pinkglow to brew homemade tepache, a fermented drink made from pineapple peels that was invented in pre-Columbian Mexico.
At a time when orange cauliflower and white strawberries are now common sights in American grocery stores, a non-yellow pineapple doesn’t seem all that out of place. Still, I wondered: Why now with the flashy presentation? And why pink? And why had my friends and I snapped it right up?
When I brought my questions to Hans Sauter, Fresh Del Monte’s chief sustainability officer and senior vice president of R&D and agricultural services, he began by offering me a brief history of the fruit. You may assume, like I did, that pineapples have always been sweet and sunny-colored—but that wasn’t the case prior to the 1990s. Store-bought pineapples of yesteryear had a green shell with light yellow flesh that was often more tart than sweet. Buying a fresh one was a bit of a gamble. “Nobody could tell, really, whether the fruit was ripe or not, and consumption of pineapples was mostly canned product, because people could trust what they would eat there,” Sauter says. The added sugar in some canned pineapple made it a sweeter, more consistent product.
In 1996 the company introduced the Del Monte Gold Extra Sweet, yellower and less acidic than anything on the market at the time. Pineapple sales soared, and consumers’ expectations of the fruit were forever changed. The popularity of the Gold led to an international pineapple feud when fruit rival Dole introduced its own varietal. Del Monte sued, alleging that Dole had essentially stolen its Gold formula. The two companies ended up settling out of court.
With the success of its Gold pineapple, Del Monte was looking for new attributes that could make the pineapple even more enticing to consumers, Sauter says. But breeding pineapples is a slow process; it can take two years or longer for a single plant to produce mature fruit. Del Monte had spent 30 years crossbreeding pineapples with certain desired characteristics before it was ready to launch the Gold. Sauter says the possibility of waiting 30 more years for a new variety was “out of the question.” So in 2005 the company turned to genetic engineering.
Del Monte didn’t set out to make a pink pineapple per se, but at the time, Sauter says, there was interest from consumers in antioxidant-rich fruits. (Acai bowls and pomegranate juice, anyone?) Pineapples happen to naturally convert a reddish-pink pigment called lycopene, which is high in antioxidants, into the yellow pigment beta-carotene. (Lycopene is what gives tomatoes and watermelon their color.) Preventing this process, then, could yield pink flesh and higher antioxidants. The company set its dedicated pineapple research team to the task of figuring out how to do it.
The team landed on a set of three modifications to the pineapple genome. They inserted DNA from a tangerine to get it to express more lycopene. They added “silencing” RNA molecules to mute the pineapple’s own lycopene-converting enzymes, which also helped reduce its acidity. (RNA silencing is the same technique used to make non-browning GMO Arctic apples.) Finally, Del Monte added a gene from tobacco that confers resistance to certain herbicides, though representatives for the company say this was simply so its scientists could confirm that the other genetic changes had taken effect—not because Del Monte plans to use those herbicides in production.
Walk me through your own decision to do this—to use Orchid’s technology on yourself.
I mean, I started the company because I wanted to test my own embryos.
Because of your mom, or because of who you are as a person?
Both. Reproduction is one of the most fundamental things in life. It’s like you die, taxes, and, you know, people have kids.
You always knew you wanted to have kids.
Oh, yeah. Yeah.
How old were you when you were like, “I should be able to sequence my embryos”?
I don’t think it was sequence my embryos specifically. I’ve always had an interest in genetics. I’ve always had an interest in fertility and reproductive tech.
Even as, like, a teenager?
I remember one of my applications for the Thiel Fellowship definitely had a version of Orchid on there.
That was, what, over a decade ago, and a lot of prospective parents still rely on the same genetic testing we used back then.
I would consider it negligent to use the old technology. Because you’re by definition missing hundreds of things that could have been detected. Parents who are not told that this new technology exists are being done a huge disservice and will probably be suing if their child ends up with a condition.
You think that’s a legitimate lawsuit?
Of course. If your doctor doesn’t tell you that there’s a way for you to screen for your child to not have a condition that would be either life-threatening or life-altering for them—I mean, it’s already happened. [Parents have been suing physicians for failing to perform genetic tests since the late 1980s.]
How much does an Orchid screening cost?
It’s $2,500 per embryo.
And presumably you’d be screening several embryos. What about for families that can’t afford that?
We have a philanthropic program, so people can apply to that, and we’re excited to accept as many cases as we can.
Your clientele, at the moment, must tend toward well-off optimizers—people who really fuss about numbers.
I guess you’re right. I mean, I don’t know.
Do you ever worry about that? Giving people, like, more things to worry about?
No, no, no. I think it’s the opposite. For the vast majority of our patients, it reduces worry.
There must be exceptions.
There are some people who, I agree, are kind of anxious. And I just don’t think they should do any genetic testing.
Oh yeah?
I mean, everyone’s different. It’s just that I want to expand the menu of choice. You get to choose your partner. You get to choose when and if you have kids. This is, like, this is your kid. Why would you censor information about that?
But this still makes a lot of people extremely uncomfortable. There’s a fear, so often, around anything that touches reproduction. Are we, I don’t know, afraid of playing God or something?
Every other time we examine something, we develop—we develop insulin, right? We’re like, “That’s great!” It’s not like you’re playing God there. But you actually are, right? You’re creating something that didn’t exist before.
Researchers believe they have discovered a new biological mechanism for obesity, pointing to rare variants on two genes that dramatically increase the risk of carrying excess weight.
Research published in the journal Nature Genetics on Thursday points to variants that raise the chance of being obese by as much as six times. Unlike other known variants that affect weight gain in children, these only appear to play a role in adults.
Unraveling obesity’s mechanisms could help scientists develop new drugs, or tailor existing ones, for a condition that now affects one in eight people. For the first time, patients can now take highly effective medicines to shed unwanted weight. The revolution, led by drugmakers Novo Nordisk A/S and Eli Lilly & Co., carved open a market that could surpass $100 billion globally by 2030.
Using data from over 500,000 people, scientists from the Medical Research Council at the University of Cambridge found variants in two genes called BSN and APBA1 that increased the risk of obesity in adults.
The variants in BSN, also known as Bassoon, were associated with an increased risk of diabetes and fatty liver disease. The Bassoon variants affect about 1 in 6,500 adults, the researchers said.
The hypothesis is that as people who have these gene variants get older, neurons in their brain start to degenerate, removing “some of the key circuits within the brain controlling food intake and therefore you end up with obesity,” said Giles Yeo, one of the authors of the study and a professor at the MRC Metabolic Diseases Unit.
The Bassoon variant may one day help drugmakers develop preventive medicines, according to Yeo. The question would be, “can we actually slow down the process, prevent the process from happening to begin with, so that then we prevent more people from ending up with obesity, particularly in adulthood.”
The researchers used the UK Biobank database and worked with AstraZeneca Plc to check that their findings applied beyond people of European ancestry, using data from Pakistan and Mexico.
Astra is one of the latest drugmakers to join the obesity race, having clinched a deal last year to buy an experimental pill that’s still in early-stage tests.
Sometime you go out and a few drinks hit you must different they they usually do…there is a wide variety of reasons why, and genetics is one of them. The body is a complex systems scientists and physicians are still trying to figure out. And when you add things to your body, they don’t always know it is going to react.
Like alcohol, marijuana has been around since early man and has been used for worship, medicine and for pure recreations…but it remains unpredictable. Even seasoned users have a variation of there usually journey. But they can usually manage the effect marijuana has on them, while also staying calm during an unpredictable high. For newcomers, however, it’s different; novice users usually can’t predict how the drug will affect them, whether it’ll lead to a paranoid high or giggle fest.
Cannabis functions by binding itself to the cannabinoid receptors in our bodies, which are located in our cells, containing our individual DNA. Mutations in CB1 or CB2 receptors can make you more vulnerable to different illnesses, such as Chron’s disease or anorexia. These changes could also impact how your cells bind to different molecules including the ones in cannabis. It is one explanation on why different people have different reaction to the same strain.
In a study, published in the journal Nature Neuroscience, researchers found a variable in the gene CHRNA2 could increase the risk of becoming addicted to cannabis. Cannabis addiction is something that’s not all that understood, with many people doubting its existence. Symptoms of marijuana withdrawal include depression, irritability, a higher heart rate and more.
While this gene doesn’t indicate whether or not someone is a marijuana addict, it does increase the odds of these kinds of responses to heavy use of the drug.
Photo by VICTOR HABBICK VISIONS/SCIENCE PHOTO LIBRARY/Getty Images
All of this means that when sharing a bong or a joint with friends, a few of them can have slightly different reactions depending on several factors including their genome, personal experience with the drug and the strain they’re ingesting.
Genes are extremely complex. Although we’re born with some genetic mutations, other mutations can occur due to the things we’re exposed to throughout our lives, such as the foods we eat, the germs we interact with, our levels of stress, and more.
There’s a lot we don’t understand about genetics yet, but organizations like the Allen Institute are doing research to under more. This will lead to a better understand of cannabis and its impact on our genes. There’s a lot of possibilities once you start playing around with these variables, hopefully resulting in more medicinal and recreational benefits.
Hearing loss is one of the most common conditions affecting older adults. According to the National Institute on Deafness and Other Communication Disorders, one in three people between the ages of 65 and 74 has hearing loss, and nearly half of those older than 75 have difficulty hearing.
The effect of hearing loss on an older person can be devastating. Having trouble hearing can make it hard to understand and follow a doctorâs advice. Hearing doorbells and alarms becomes difficult. Having conversations becomes hard. This can be frustrating, embarrassing and at worse, dangerous.
But, these are not the only problems that can follow hearing loss.
In a study that tracked 639 adults for nearly 12 years, a Johns Hopkins research team found that mild hearing loss doubled dementia risk. Moderate loss tripled risk, and people with a severe hearing impairment were five times more likely to develop dementia.
There are options to help with hearing loss, but first you need to detect its occurrence. Here are some questions based on a tool for hearing loss. If you answer yes to three or more of these questions you could have a hearing problem and you should check with your doctor. Do you:
Sometimes feel embarrassed when you meet new people because you struggle to hear?
Feel frustrated when talking to members of your family because you have difficulty hearing them?
Have difficulty hearing when someone speaks in a whisper?
Feel restricted or limited by a hearing problem?
Attend religious services less often than you would like because of hearing problem?
Argue with family members because of hearing problem?
Have trouble hearing the TV or radio at levels that are loud enough for others?
Believe that any difficulty with your hearing limits your personal or social life?
Have trouble hearing family or friends when you are together in a restaurant? Or when visiting friends, relatives, or neighbors?
Hearing loss can happen for a number of different reasons. Hearing loss might be a genetic trait or may be caused by illness or injury. Another reason for hearing loss is having been exposed to extended periods of loud noise. Many construction workers, farmers, musicians, airport workers, and people in the armed forces are subject to hearing loss.
There are ways to address hearing loss. You must determine what works best for you and your circumstances. Here are a few ways to counteract hearing loss:
Hearing aids. They make sounds louder. Often things will sound different than you are used to, which can make getting use to a hearing aid difficult. You may need to try a number of hearing aids before you find the one that works for you.
Cochlear implants. These are small electronic devices surgically implanted in the inner ear. These implants are for people whose hearing loss is severe.
Assistive listening device. These include amplifying devices for the telephone, or cell phone. They can also be helpful in places of worship, theaters, and auditoriums.
Lip reading. People who use this method pay close attention to others when they talk, by watching how the speakerâs mouth moves.
Hearing aids and other devices are rarely covered by insurance, and they are not inexpensive. But, the cost to the individual with hearing loss is much more in loss of quality of life.
SeniorCare keeps a list of organizations that assist with hearing aids and other hearing assistance devices. To learn more, call SeniorCare at 978-281-1750 or TTY: 978-282-1836 and ask to speak with an information and referral specialist.
Tracy Arabian is the communications officer at SeniorCare Inc., a local agency on aging that serves Gloucester, Beverly, Essex, Hamilton, Ipswich, Manchester-by-the-Sea, Rockport, Topsfield and Wenham.
Tracy Arabian is the communications officer at SeniorCare Inc., a local agency on aging that serves Gloucester, Beverly, Essex, Hamilton, Ipswich, Manchester-by-the-Sea, Rockport, Topsfield and Wenham.
