This week marked a rather unpleasant anniversary: It’s a year since Texas reported a case of measles—the start of a significant outbreak that ended up spreading across multiple states. Since the start of January 2025, there have been over 2,500 confirmed cases of measles in the US. Three people have died.

As vaccination rates drop and outbreaks continue, scientists have been experimenting with new ways to quickly identify new cases and prevent the disease from spreading. And they are starting to see some success with wastewater surveillance.

After all, wastewater contains saliva, urine, feces, shed skin, and more. You could consider it a rich biological sample. Wastewater analysis helped scientists understand how covid was spreading during the pandemic. It’s early days, but it is starting to help us get a handle on measles.

Globally, there has been some progress toward eliminating measles, largely thanks to vaccination efforts. Such efforts led to an 88% drop in measles deaths between 2000 and 2024, according to the World Health Organization. It estimates that “nearly 59 million lives have been saved by the measles vaccine” since 2000.

Still, an estimated 95,000 people died from measles in 2024 alone—most of them young children. And cases are surging in Europe, Southeast Asia, and the Eastern Mediterranean region.

Last year, the US saw the highest levels of measles in decades. The country is on track to lose its measles elimination status—a sorry fate that met Canada in November after the country recorded over 5,000 cases in a little over a year.

Public health efforts to contain the spread of measles—which is incredibly contagious—typically involve clinical monitoring in health-care settings, along with vaccination campaigns. But scientists have started looking to wastewater, too.

Along with various bodily fluids, we all shed viruses and bacteria into wastewater, whether that’s through brushing our teeth, showering, or using the toilet. The idea of looking for these pathogens in wastewater to track diseases has been around for a while, but things really kicked into gear during the covid-19 pandemic, when scientists found that the coronavirus responsible for the disease was shed in feces.

This led Marlene Wolfe of Emory University and Alexandria Boehm of Stanford University to establish WastewaterSCAN, an academic-led program developed to analyze wastewater samples across the US. Covid was just the beginning, says Wolfe. “Over the years we have worked to expand what can be monitored,” she says.

Two years ago, for a previous edition of the Checkup, Wolfe told Cassandra Willyard that wastewater surveillance of measles was “absolutely possible,” as the virus is shed in urine. The hope was that this approach could shed light on measles outbreaks in a community, even if members of that community weren’t able to access health care and receive an official diagnosis. And that it could highlight when and where public health officials needed to act to prevent measles from spreading. Evidence that it worked as an effective public health measure was, at the time, scant.

Since then, she and her colleagues have developed a test to identify measles RNA. They trialed it at two wastewater treatment plants in Texas between December 2024 and May 2025. At each site, the team collected samples two or three times a week and tested them for measles RNA.

Over that period, the team found measles RNA in 10.5% of the samples they collected, as reported in a preprint paper published at medRxiv in July and currently under review at a peer-reviewed journal. The first detection came a week before the first case of measles was officially confirmed in the area. That’s promising—it suggests that wastewater surveillance might pick up measles cases early, giving public health officials a head start in efforts to limit any outbreaks.

There are more promising results from a team in Canada. Mike McKay and Ryland Corchis-Scott at the University of Windsor in Ontario and their colleagues have also been testing wastewater samples for measles RNA. Between February and November 2025, the team collected samples from a wastewater treatment facility serving over 30,000 people in Leamington, Ontario. 

These wastewater tests are somewhat limited—even if they do pick up measles, they won’t tell you who has measles, where exactly infections are occurring, or even how many people are infected. McKay and his colleagues have begun to make some progress here. In addition to monitoring the large wastewater plant, the team used tampons to soak up wastewater from a hospital lateral sewer.

They then compared their measles test results with the number of clinical cases in that hospital. This gave them some idea of the virus’s “shedding rate.” When they applied this to the data collected from the Leamington wastewater treatment facility, the team got estimates of measles cases that were much higher than the figures officially reported. 

Their findings track with the opinions of local health officials (who estimate that the true number of cases during the outbreak was around five to 10 times higher than the confirmed case count), the team members wrote in a paper published on medRxiv a couple of weeks ago.

There will always be limits to wastewater surveillance. “We’re looking at the pool of waste of an entire community, so it’s very hard to pull in information about individual infections,” says Corchis-Scott.

Wolfe also acknowledges that “we have a lot to learn about how we can best use the tools so they are useful.” But her team at WastewaterSCAN has been testing wastewater across the US for measles since May last year. And their findings are published online and shared with public health officials.

In some cases, the findings are already helping inform the response to measles. “We’ve seen public health departments act on this data,” says Wolfe. Some have issued alerts, or increased vaccination efforts in those areas, for example. “[We’re at] a point now where we really see public health departments, clinicians, [and] families using that information to help keep themselves and their communities safe,” she says.

McKay says his team has stopped testing for measles because the Ontario outbreak “has been declared over.” He says testing would restart if and when a single new case of measles is confirmed in the region, but he also thinks that his research makes a strong case for maintaining a wastewater surveillance system for measles.

McKay wonders if this approach might help Canada regain its measles elimination status. “It’s sort of like [we’re] a pariah now,” he says. If his approach can help limit measles outbreaks, it could be “a nice tool for public health in Canada to [show] we’ve got our act together.”

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

Earlier this week, MIT Technology Review published its annual list of Ten Breakthrough Technologies. As always, it features technologies that made the news last year, and which—for better or worse—stand to make waves in the coming years. They’re the technologies you should really be paying attention to.

This year’s list includes tech that’s set to transform the energy industry, artificial intelligence, space travel—and of course biotech and health. Our breakthrough biotechnologies for 2026 involve editing a baby’s genes and, separately, resurrecting genes from ancient species. We also included a controversial technology that offers parents the chance to screen their embryos for characteristics like height and intelligence. Here’s the story behind our biotech choices.

A base-edited baby!

In August 2024, KJ Muldoon was born with a rare genetic disorder that allowed toxic ammonia to build up in his blood. The disease can be fatal, and KJ was at risk of developing neurological disorders. At the time, his best bet for survival involved waiting for a liver transplant.

Then he was offered an experimental gene therapy—a personalized “base editing” treatment designed to correct the specific genetic “misspellings” responsible for his disease. It seems to have worked! Three doses later, KJ is doing well. He took his first steps in December, shortly before spending his first Christmas at home.

KJ’s story is hugely encouraging. The team behind his treatment is planning a clinical trial for infants with similar disorders caused by different genetic mutations. The team members hope to win regulatory approval on the back of a small trial—a move that could make the expensive treatment (KJ’s cost around $1 million) more accessible, potentially within a few years.

Others are getting in on the action, too. Fyodor Urnov, a gene-editing scientist at the University of California, Berkeley, assisted the team that developed KJ’s treatment. He recently cofounded Aurora Therapeutics, a startup that hopes to develop gene-editing drugs for another disorder called phenylketonuria (PKU). The goal is to obtain regulatory approval for a single drug that can then be adjusted or personalized for individuals without having to go through more clinical trials.

US regulators seem to be amenable to the idea and have described a potential approval pathway for such “bespoke, personalized therapies.” Watch this space.

Gene resurrection

It was a big year for Colossal Biosciences, the biotech company hoping to “de-extinct” animals like the woolly mammoth and the dodo. In March, the company created what it called “woolly mice”—rodents with furry coats and curly whiskers akin to those of woolly mammoths.

The company made an even more dramatic claim the following month, when it announced it had created three dire wolves. These striking snow-white animals were created by making 20 genetic changes to the DNA of gray wolves based on genetic research on ancient dire wolf bones, the company said at the time.

Whether these animals can really be called dire wolves is debatable, to say the least. But the technology behind their creation is undeniably fascinating. We’re talking about the extraction and analysis of ancient DNA, which can then be introduced into cells from other, modern-day species.

Analysis of ancient DNA can reveal all sorts of fascinating insights into human ancestors and other animals. And cloning, another genetic tool used here, has applications not only in attempts to re-create dead pets but also in wildlife conservation efforts. Read more here.

Embryo scoring

IVF involves creating embryos in a lab and, typically, “scoring” them on their likelihood of successful growth before they are transferred to a person’s uterus. So far, so uncontroversial.

Recently, embryo scoring has evolved. Labs can pinch off a couple of cells from an embryo, look at its DNA, and screen for some genetic diseases. That list of diseases is increasing. And now some companies are taking things even further, offering prospective parents the opportunity to select embryos for features like height, eye color, and even IQ.

This is controversial for lots of reasons. For a start, there are many, many factors that contribute to complex traits like IQ (a score that doesn’t capture all aspects of intelligence at any rate). We don’t have a perfect understanding of those factors, or how selecting for one trait might influence another.

Some critics warn of eugenics. And others note that whichever embryo you end up choosing, you can’t control exactly how your baby will turn out (and why should you?!). Still, that hasn’t stopped Nucleus, one of the companies offering these services, from inviting potential customers to have their “best baby.” Read more here.

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

Kyle “KJ” Muldoon Jr. was born with a rare genetic disorder that left his body unable to remove toxic ammonia from his blood. He was lethargic and at risk of developing neurological disorders. The condition can be fatal. 

KJ joined a waiting list for a liver transplant. Then Rebecca Ahrens-Nicklas and Kiran Musunuru at the University of Pennsylvania offered his parents an alternative. The pair were developing potential gene-editing therapies for diseases like KJ’s. His parents signed him up.

The team set to work developing a tailored treatment using base editing—a form of CRISPR that can correct genetic “misspellings” by changing single bases, the basic units of DNA. They tested it in human cells, mice, and monkeys, and KJ received an initial low dose when he was seven months old. He later received two higher doses. Today, KJ is doing well. At an event in October, his happy parents described how he was meeting all his developmental milestones.

Others have received gene-editing therapies intended to treat conditions including sickle cell disease and a predisposition to high cholesterol. But KJ was the first to receive a personalized treatment—one that was designed just for him and will probably never be used again. 

The expense was similar to that of a liver transplant, which costs around $1 million, says Musunuru, but he thinks that will come down to a few hundred thousand dollars per treatment within the next few years.

KJ’s doctors will monitor him for years, and they can’t yet say how effective this gene-editing approach is. But they plan to launch a clinical trial to test such personalized treatments in children with similar disorders caused by “misspelled” genes that can be targeted with base editing.

They’re hopeful that approval by the US Food and Drug Administration will soon follow. Musunuru says the FDA has agreed on a trial protocol that could involve as few as five patients with at least three genetic variants. In November, FDA administrators described in the New England Journal of Medicine how the agency might approve personalized therapies like KJ’s using a new pathway.

The new year has barely begun, but the first days of 2026 have brought big news for health. On Monday, the US’s federal health agency upended its recommendations for routine childhood vaccinations—a move that health associations worry puts children at unnecessary risk of preventable disease.

There was more news from the federal government on Wednesday, when health secretary Robert F. Kennedy Jr. and his colleagues at the Departments of Health and Human Services and Agriculture unveiled new dietary guidelines for Americans. And they are causing a bit of a stir.

That’s partly because they recommend products like red meat, butter, and beef tallow—foods that have been linked to cardiovascular disease, and that nutrition experts have been recommending people limit in their diets.

These guidelines are a big deal—they influence food assistance programs and school lunches, for example. So this week let’s look at the good, the bad, and the ugly advice being dished up to Americans by their government.

The government dietary guidelines have been around since the 1980s. They are updated every five years, in a process that typically involves a team of nutrition scientists who have combed over scientific research for years. That team will first publish its findings in a scientific report, and, around a year later, the finalized Dietary Guidelines for Americans are published.

The last guidelines covered the period 2020 to 2025, and new guidelines were expected in the summer of 2025. Work had already been underway for years; the scientific report intended to inform them was published back in 2024. But the publication of the guidelines was delayed by last year’s government shutdown, Kennedy said last year. They were finally published yesterday.

Nutrition experts had been waiting with bated breath. Nutrition science has evolved slightly over the last five years, and some were expecting to see new recommendations. Research now suggests, for example, that there is no “safe” level of alcohol consumption.

We are also beginning to learn more about health risks associated with some ultraprocessed foods (although we still don’t have a good understanding of what they might be, or what even counts as “ultraprocessed”.) And some scientists were expecting to see the new guidelines factor in environmental sustainability, says Gabby Headrick, the associate director of food and nutrition policy at George Washington University’s Institute for Food Safety & Nutrition Security in Washington DC.

They didn’t.

Many of the recommendations are sensible. The guidelines recommend a diet rich in whole foods, particularly fresh fruits and vegetables. They recommend avoiding highly processed foods and added sugars. They also highlight the importance of dietary protein, whole grains, and “healthy” fats.

But not all of them are, says Headrick. The guidelines open with a “new pyramid” of foods. This inverted triangle is topped with “protein, dairy, and healthy fats” on one side and “vegetables and fruits” on the other.

There are a few problems with this image. For starters, its shape—nutrition scientists have long moved on from the food pyramids of the 1990s, says Headrick. They’re confusing and make it difficult for people to understand what the contents of their plate should look like. That’s why scientists now use an image of a plate to depict a healthy diet.

“We’ve been using MyPlate to describe the dietary guidelines in a very consumer-friendly, nutrition-education-friendly way for over the last decade now,” says Headrick. (The UK’s National Health Service takes a similar approach.)

And then there’s the content of that food pyramid. It puts a significant focus on meat and whole-fat dairy produce. The top left image—the one most viewers will probably see first—is of a steak. Smack in the middle of the pyramid is a stick of butter. That’s new. And it’s not a good thing.

While both red meat and whole-fat dairy can certainly form part of a healthy diet, nutrition scientists have long been recommending that most people try to limit their consumption of these foods. Both can be high in saturated fat, which can increase the risk of cardiovascular disease—the leading cause of death in the US. In 2015, on the basis of limited evidence, the World Health Organization classified red meat as “probably carcinogenic to humans.” 

Also concerning is the document’s definition of “healthy fats,” which includes butter and beef tallow (a MAHA favorite). Neither food is generally considered to be as healthy as olive oil, for example. While olive oil contains around two grams of saturated fat per tablespoon, a tablespoon of beef tallow has around six grams of saturated fat, and the same amount of butter contains around seven grams of saturated fat, says Headrick.

“I think these are pretty harmful dietary recommendations to be making when we have established that those specific foods likely do not have health-promoting benefits,” she adds.

Red meat is not exactly a sustainable food, and neither are dairy products. And the advice on alcohol is relatively vague, recommending that people “consume less alcohol for better overall health” (which might leave you wondering: Less than what?).

There are other questionable recommendations in the guidelines. Americans are advised to include more protein in their diets—at levels between 1.2 and 1.6 grams daily per kilo of body weight, 50% to 100% more than recommended in previous guidelines. There’s a risk that increasing protein consumption to such levels could raise a person’s intake of both calories and saturated fats to unhealthy levels, says José Ordovás, a senior nutrition scientist at Tufts University. “I would err on the low side,” he says.

Some nutrition scientists are questioning why these changes have been made. It’s not as though the new recommendations were in the 2024 scientific report. And the evidence on red meat and saturated fat hasn’t changed, says Headrick.

In reporting this piece, I contacted many contributors to the previous guidelines, and some who had led research for 2024’s scientific report. None of them agreed to comment on the new guidelines on the record. Some seemed disgruntled. One merely told me that the process by which the new guidelines had been created was “opaque.”

“These people invested a lot of their time, and they did a thorough job [over] a couple of years, identifying [relevant scientific studies],” says Ordovás. “I’m not surprised that when they see that [their] work was ignored and replaced with something [put together] quickly, that they feel a little bit disappointed,” he says.

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

At some point next month, a handful of volunteers will be injected with two experimental gene therapies as part of an unusual clinical trial. The drugs are potential longevity therapies, says Ivan Morgunov, the CEO of Unlimited Bio, the company behind the trial. His long-term goal: to achieve radical human life extension.

The 12 to 15 volunteers—who will be covering their own travel and treatment costs—will receive a series of injections in the muscles of their arms and legs. One of the therapies is designed to increase the blood supply to those muscles. The other is designed to support muscle growth. The company hopes to see improvements in strength, endurance, and recovery. It also plans to eventually trial similar therapies in the scalp (for baldness) and penis (for erectile dysfunction).

But some experts are concerned that the trial involves giving multiple gene therapies to small numbers of healthy people. It will be impossible to draw firm conclusions from such a small study, and the trial certainly won’t reveal anything about longevity, says Holly Fernandez Lynch, a lawyer and medical ethicist at the University of Pennsylvania in Philadelphia.

Unlimited Bio’s blood supply therapy is already accessible at clinics in Honduras and Mexico, says Morgunov—and the company is already getting some publicity. Khloe Kardashian tagged Unlimited Bio in a Facebook post about stem-cell treatments she and her sister Kim had received at the Eterna clinic in Mexico in August. And earlier this week, the biohacking influencer Dave Asprey posted an Instagram Reel of himself receiving one of the treatments in Mexico; it was shared with 1.3 million Instagram followers. In the video, Eterna’s CEO, Adeel Khan, says that the therapy can “help with vascular health systemically.” “I’m just upgrading my system for a little while to reduce my age and reduce my vascular risk,” Asprey said.

Genes for life

Gene therapies typically work by introducing new genetic code into the body’s cells. This code is then able to make proteins. Existing approved gene therapies have typically been developed for severe diseases in which the target proteins are either missing or mutated.

But several groups are exploring gene therapies for healthy people. One of these companies is Minicircle, which developed a gene therapy to increase production of follistatin, a protein found throughout the body that has many roles and is involved in muscle growth. The company says this treatment will increase muscle mass—and help people live longer. Minicircle is based in Próspera, a special economic zone in Honduras with its own bespoke regulatory system. Anyone can visit the local clinic and receive that therapy, for a reported price of $25,000. And many have, including the wealthy longevity influencer Bryan Johnson, who promoted the therapy in a Netflix documentary.

Unlimited Bio’s Morgunov, a Russian-Israeli computer scientist, was inspired by Minicircle’s story. He is also interested in longevity. Specifically, he’s committed to radical life extension and has said that he could be part of “the last generation throughout human history to die from old age.” He believes the biggest “bottleneck” slowing progress toward anti-aging or lifespan-extending therapies is drug regulation. So he, too, incorporated his own biotech company in Próspera.

“A company like ours couldn’t exist outside of Próspera,” says Unlimited Bio’s chief operating officer, Vladimir Leshko.

There, Morgunov and his colleagues are exploring two gene therapies. One of these is another follistatin therapy, which the team hopes will increase muscle mass. The other codes for a protein called vascular endothelial growth factor, or VEGF. This compound is known to encourage the growth of blood vessels. Morgunov and his colleagues hope the result will be increased muscle growth, enhanced muscle repair, and longer life. Neither treatment is designed to alter a recipient’s DNA, and therefore it won’t be inherited by future generations.

The combination of the two therapies could benefit healthy people and potentially help them live longer, says Leshko, a former electrical engineer and professional poker player who retrained in biomedical engineering. “We would say that it’s a preventive-slash-enhancing indication,” he says. “Potentially participants can experience faster recovery from exercise, more strength, and more endurance.”

Of the 12 to 15 volunteers who participate in the trial, half will receive only the follistatin therapy. The other half will receive both the VEGF and the follistatin therapies. The treatments will involve a series of injections throughout large muscles in the arms and legs, says Morgunov.

He is confident that the VEGF therapy is safe. It was approved in Russia over a decade ago to treat lower-limb ischemia—a condition that can cause pain, numbness, and painful ulcers in the legs and feet. Morgunov reckons, based on previously published estimates, that around 10,000 people in Russia have already had the drug, although he says he hasn’t “done deep fact-checking on that.”

Other researchers aren’t convinced.

Limited bio

VEGF is a powerful compound, says Seppo Ylä-Herttuala, a professor of molecular medicine at the University of Eastern Finland who has been studying VEGF and potential VEGF therapies for decades. He doesn’t know how many people have had VEGF gene therapy in Russia. But he does know that the safety of the therapy will depend on how much is administered and where. Previous attempts to inject the therapy into the heart, for example, have resulted in edema, a sometimes fatal buildup of fluid. Even if the therapy is injected elsewhere, VEGF can travel around the body, he says. If it gets to the eye, for example, it could cause blindness. Leshko counters that the VEGF should remain where it is injected, and any other circulation in the body, if it occurs, should be short-lived. 

And while the therapy has been approved in Russia, there’s a reason it hasn’t been approved elsewhere, says Ylä-Herttuala: The clinical trials were not as rigorous as they could have been. While “it probably works in some patients,” he says, the evidence to support the use of this therapy is weak. At any rate, he adds, VEGF will only support the growth of blood vessels—it won’t tackle aging.  “VEGF is not a longevity drug,” he says.

Leshko points to a 2021 study in mice, which suggested that a lack of VEGF activity might drive aging in the rodents. “We’re convinced it qualifies as a potential longevity drug,” he says.

There is even less data about follistatin. Minicircle, the company selling another follistatin gene therapy, has not published any rigorous clinical trial data. So far, much of the evidence for follistatin’s effects comes from research in rodents, says Ylä-Herttuala.

Clinical trials like this one should gather more information, both about the therapies and about the methods used to get those therapies into the body. Unlimited Bio’s VEGF therapy will be delivered via a circular piece of genetic code called a plasmid. Its follistatin therapy, on the other hand, will be delivered via an adeno-associated virus (AAV). Plasmid therapies are easier to make, and they have a shorter lifespan in the body—only a matter of days. They are generally considered to be safer than AAV therapies. AAV therapies, on the other hand, tend to stick around for months, says Ylä-Herttuala. And they can trigger potentially dangerous immune reactions.

It’s debatable whether healthy people should be exposed to these risks, says Fernandez Lynch. The technology “still has serious questions about its safety and effectiveness,” even for people with life-threatening diseases, she says. “If you are a healthy person, the risk of harm is more substantial because it’ll be more impactful on your life.”

But Leshko is adamant. “Over 120,000 humans die DAILY from age-related causes,” he wrote in an email. “Building ‘ethical’ barriers around ‘healthy’ human (in fact, aging human) trials is unethical.” Morgunov did not respond to a request for comment.

Some people want to take those risks anyway. In his video, the biohacker influencer Asprey—who has publicly stated that he’s “going to live to 180”—described VEGF as a “longevity compound,” and Eterna’s CEO Khan, who delivered the treatment, described it as “the ultimate upgrade.” Neither Asprey nor Khan clinic responded to requests for comment. 

Michael Gusmano, a professor of health policy at Lehigh University in Bethlehem, Pennsylvania, worries that this messaging might give trial participants unrealistic expectations about how they might benefit. There is “huge potential for therapeutic misconception when you have some kind of celebrity online influencer touting something about which there is relatively sparse scientific evidence,” he says. In reality, he adds, “the only thing you can guarantee is that [the volunteers] will be contributing to our knowledge of how this intervention works.”

“I would certainly not recommend that anyone I know enter into such a trial,” says Gusmano.

A penis project

The muscle study is only the first step. The Unlimited Bio team hopes to trial the VEGF therapy for baldness and erectile dysfunction, too. Leshko points to research in mice that links high VEGF levels to larger, denser hair follicles. He hopes to test a series of VEGF therapy injections into the scalps of volunteers. Morgunov, who is largely bald, has already started to self-experiment with the approach.

An erectile dysfunction trial may follow. “That one we think has great potential because injecting gene therapy into the penis sounds exciting,” says Leshko. A protocol for that trial has not yet been finalized, but he imagines it would involve “five to 10” injections.

Ylä-Herttuala isn’t optimistic about either approach. Hair growth is largely hormonal, he says. And injecting anything into a penis risks damaging it (although Leshko points out that a similar approach was taken by another company almost 20 years ago). Injecting a VEGF gene therapy into the penis would also risk edema there, Ylä-Herttuala adds.

And he points out that we already have some treatments for hair loss and erectile dysfunction. While they aren’t perfect, their existence does raise the bar for any potential future therapies—not only do they have to be safe and effective, but they must be safer or more effective than existing ones.

That doesn’t mean the trials will flop. No small trial can be definitive, but it could still provide some insight into how these drugs are working. It is possible that the therapies will increase muscle mass, at least, and that this could be beneficial to the healthy recipients, says Ylä-Herttuala. 

Before our call, he had taken a look at Unlimited Bio’s website, which carries the tagline “The Most Advanced Rejuvenation Solution.” “They promise a lot,” he said. “I hope it’s true.”

Correction: This story was corrected to note that half of trial volunteers volunteers receive only the follistatin therapy.

In just a couple of weeks, we’ll be bidding farewell to 2025. And what a year it has been! Artificial intelligence is being incorporated into more aspects of our lives, weight-loss drugs have expanded in scope, and there have been some real “omg” biotech stories from the fields of gene therapy, IVF, neurotech, and more.   

As always, the team at MIT Technology Review has been putting together our 2026 list of breakthrough technologies. That will be published in the new year (watch this space). In the meantime, my colleague Antonio Regalado has compiled his traditional list of the year’s worst technologies.

I’m inviting you to put your own memory to the test. Just how closely have you been paying attention to the Checkup emails that have been landing in your inbox this year?!

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

This week I’ve been thinking about babies. Healthy ones. Perfect ones. As you may have read last week, my colleague Antonio Regalado came face to face with a marketing campaign in the New York subway asking people to “have your best baby.”

The company behind that campaign, Nucleus Genomics, says it offers customers a way to select embryos for a range of traits, including height and IQ. It’s an extreme proposition, but it does seem to be growing in popularity—potentially even in the UK, where it’s illegal.

The other end of the screening spectrum is transforming too. Carrier screening, which tests would-be parents for hidden genetic mutations that might affect their children, initially involved testing for specific genes in at-risk populations.

Now, it’s open to almost everyone who can afford it. Companies will offer to test for hundreds of genes to help people make informed decisions when they try to become parents. But expanded carrier screening comes with downsides. And it isn’t for everyone.

That’s what I found earlier this week when I attended the Progress Educational Trust’s annual conference in London.

First, a bit of background. Our cells carry 23 pairs of chromosomes, each with thousands of genes. The same gene—say, one that codes for eye color—can come in different forms, or alleles. If the allele is dominant, you only need one copy to express that trait. That’s the case for the allele responsible for brown eyes. 

If the allele is recessive, the trait doesn’t show up unless you have two copies. This is the case with the allele responsible for blue eyes, for example.

Things get more serious when we consider genes that can affect a person’s risk of disease. Having a single recessive disease-causing gene typically won’t cause you any problems. But a genetic disease could show up in children who inherit the same recessive gene from both parents. There’s a 25% chance that two “carriers” will have an affected child. And those cases can come as a shock to the parents, who tend to have no symptoms and no family history of disease.

This can be especially problematic in communities with high rates of those alleles. Consider Tay-Sachs disease—a rare and fatal neurodegenerative disorder caused by a recessive genetic mutation. Around one in 25 members of the Ashkenazi Jewish population is a healthy carrier for Tay-Sachs. Screening would-be parents for those recessive genes can be helpful. Carrier screening efforts in the Jewish community, which have been running since the 1970s, have massively reduced cases of Tay-Sachs.

Expanded carrier screening takes things further. Instead of screening for certain high-risk alleles in at-risk populations, there’s an option to test for a wide array of diseases in prospective parents and egg and sperm donors. The companies offering these screens “started out with 100 genes, and now some of them go up to 2,000,” Sara Levene, genetics counsellor at Guided Genetics, said at the meeting. “It’s becoming a bit of an arms race amongst labs, to be honest.”

There are benefits to expanded carrier screening. In most cases, the results are reassuring. And if something is flagged, prospective parents have options; they can often opt for additional testing to get more information about a particular pregnancy, for example, or choose to use other donor eggs or sperm to get pregnant. But there are also downsides. For a start, the tests can’t entirely rule out the risk of genetic disease.

Earlier this week, the BBC reported news of a sperm donor who had unwittingly passed on to at least 197 children in Europe a genetic mutation that dramatically increased the risk of cancer. Some of those children have already died.

It’s a tragic case. That donor had passed screening checks. The (dominant) mutation appears to have occurred in his testes, affecting around 20% of his sperm. It wouldn’t have shown up in a screen for recessive alleles, or even a blood test.

Even recessive diseases can be influenced by many genes, some of which won’t be included in the screen. And the screens don’t account for other factors that could influence a person’s risk of disease, such as epigenetics, microbiome, or even lifestyle.

“There’s always a 3% to 4% chance [of having] a child with a medical issue regardless of the screening performed,” said Jackson Kirkman-Brown, professor of reproductive biology at the University of Birmingham, at the meeting.

The tests can also cause stress. As soon as a clinician even mentions expanded carrier screening, it adds to the mental load of the patient, said Kirkman-Brown: “We’re saying this is another piece of information you need to worry about.”

People can also feel pressured to undergo expanded carrier screening even when they are ambivalent about it, said Heidi Mertes, a medical ethicist at Ghent University. “Once the technology is there, people feel like if they don’t take this opportunity up, then they are kind of doing something wrong or missing out,” she said.

My takeaway from the presentations was that while expanded carrier screening can be useful, especially for people from populations with known genetic risks, it won’t be for everyone.

I also worry that, as with the genetic tests offered by Nucleus, its availability gives the impression that it is possible to have a “perfect” baby—even if that only means “free from disease.” The truth is that there’s a lot about reproduction that we can’t control.

The decision to undergo expanded carrier screening is a personal choice. But as Mertes noted at the meeting: “Just because you can doesn’t mean you should.”

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

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Weight-loss drugs have been back in the news this week. First, we heard that Eli Lilly, the company behind the drugs Mounjaro and Zepbound, became the first healthcare company in the world to achieve a trillion-dollar valuation.

Those two drugs, which are prescribed for diabetes and obesity respectively, are generating billions of dollars in revenue for the company. Other GLP-1 agonist drugs—a class that includes Mounjaro and Zepbound, which have the same active ingredient—have also been approved to reduce the risk of heart attack and stroke in overweight people. Many hope these apparent wonder drugs will also treat neurological disorders and potentially substance use disorders, too.

But this week we also learned that, disappointingly, GLP-1 drugs don’t seem to help people with Alzheimer’s disease. And that people who stop taking the drugs when they become pregnant can experience potentially dangerous levels of weight gain during their pregnancies. On top of that, some researchers worry that people are using the drugs postpartum to lose pregnancy weight without understanding potential risks.

All of this news should serve as a reminder that there’s a lot we still don’t know about these drugs. This week, let’s look at the enduring questions surrounding GLP-1 agonist drugs.

First a quick recap. Glucagon-like peptide-1 is a hormone made in the gut that helps regulate blood sugar levels. But we’ve learned that it also appears to have effects across the body. Receptors that GLP-1 can bind to have been found in multiple organs and throughout the brain, says Daniel Drucker, an endocrinologist at the University of Toronto who has been studying the hormone for decades.

GLP-1 agonist drugs essentially mimic the hormone’s action. Quite a few have been developed, including semaglutide, tirzepatide, liraglutide, and exenatide, which have brand names like Ozempic, Saxenda and Wegovy. Some of them are recommended for some people with diabetes.

But because these drugs also seem to suppress appetite, they have become hugely popular weight loss aids. And studies have found that many people who take them for diabetes or weight loss experience surprising side effects; that their mental health improves, for example, or that they feel less inclined to smoke or consume alcohol. Research has also found that the drugs seem to increase the growth of brain cells in lab animals.

So far, so promising. But there are a few outstanding gray areas.

Are they good for our brains?

Novo Nordisk, a competitor of Eli Lilly, manufactures GLP-1 drugs Wegovy and Saxenda. The company recently trialed an oral semaglutide in people with Alzheimer’s disease who had mild cognitive impairment or mild dementia. The placebo-controlled trial included 3808 volunteers.

Unfortunately, the company found that the drug did not appear to delay the progression of Alzheimer’s disease in the volunteers who took it.

The news came as a huge disappointment to the research community. “It was kind of crushing,” says Drucker. That’s despite the fact that, deep down, he wasn’t expecting a “clear win.” Alzheimer’s disease has proven notoriously difficult to treat, and by the time people get a diagnosis, a lot of damage has already taken place.

But he is one of many that isn’t giving up hope entirely. After all, research suggests that GLP-1 reduces inflammation in the brain and improves the health of neurons, and that it appears to improve the way brain regions communicate with each other. This all implies that GLP-1 drugs should benefit the brain, says Drucker. There’s still a chance that the drugs might help stave off Alzheimer’s in those who are still cognitively healthy.

Are they safe before, during or after pregnancy?

Other research published this week raises questions about the effects of GLP-1s taken around the time of pregnancy. At the moment, people are advised to plan to stop taking the medicines two months before they become pregnant. That’s partly because some animal studies suggest the drugs can harm the development of a fetus, but mainly because scientists haven’t studied the impact on pregnancy in humans.

Among the broader population, research suggests that many people who take GLP-1s for weight loss regain much of their lost weight once they stop taking those drugs. So perhaps it’s not surprising that a study published in JAMA earlier this week saw a similar effect in pregnant people.

The study found that people who had been taking those drugs gained around 3.3kg more than others who had not. And those who had been taking the drugs also appeared to have a slightly higher risk of gestational diabetes, blood pressure disorders and even preterm birth.

It sounds pretty worrying. But a different study published in August had the opposite finding—it noted a reduction in the risk of those outcomes among women who had taken the drugs before becoming pregnant.

If you’re wondering how to make sense of all this, you’re not the only one. No one really knows how these drugs should be used before pregnancy—or during it for that matter.

Another study out this week found that people (in Denmark) are increasingly taking GLP-1s postpartum to lose weight gained during pregnancy. Drucker tells me that, anecdotally, he gets asked about this potential use a lot.

But there’s a lot going on in a postpartum body. It’s a time of huge physical and hormonal change that can include bonding, breastfeeding and even a rewiring of the brain. We have no idea if, or how, GLP-1s might affect any of those.

How—and when—can people safely stop using them?

Yet another study out this week—you can tell GLP-1s are one of the hottest topics in medicine right now—looked at what happens when people stop taking tirzepatide (marketed as Zepbound) for their obesity.

The trial participants all took the drug for 36 weeks, at which point half continued with the drug, and half were switched to a placebo for another 52 weeks. During that first 36 weeks, the weight and heart health of the participants improved.

But by the end of the study, most of those that had switched to a placebo had regained more than 25% of the weight they had originally lost. One in four had regained more than 75% of that weight, and 9% ended up at a higher weight than when they’d started the study. Their heart health also worsened.

Does that mean that people need to take these drugs forever? Scientists don’t have the answer to that one, either. Or if taking the drugs indefinitely is safe. The answer might depend on the individual, their age or health status, or what they are using the drug for.

There are other gray areas. GLP-1s look promising for substance use disorders, but we don’t yet know how effective they might be. We don’t know the long-term effects these drugs have on children who take them. And we don’t know the long-term consequences these drugs might have for healthy-weight people who take them for weight loss.

Earlier this year, Drucker accepted a Breakthrough Prize in Life Sciences at a glitzy event in California. “All of these Hollywood celebrities were coming up to me and saying ‘thank you so much,’” he says. “A lot of these people don’t need to be on these medicines.”

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

It has started to get really wintry here in London over the last few days. The mornings are frosty, the wind is biting, and it’s already dark by the time I pick my kids up from school. The darkness in particular has got me thinking about vitamin D, a.k.a. the sunshine vitamin.

At a checkup a few years ago, a doctor told me I was deficient in vitamin D. But he wouldn’t write me a prescription for supplements, simply because, as he put it, everyone in the UK is deficient. Putting the entire population on vitamin D supplements would be too expensive for the country’s national health service, he told me.

But supplementation—whether covered by a health-care provider or not—can be important. As those of us living in the Northern Hemisphere spend fewer of our waking hours in sunlight, let’s consider the importance of vitamin D.

Yes, it is important for bone health. But recent research is also uncovering surprising new insights into how the vitamin might influence other parts of our bodies, including our immune systems and heart health.

Vitamin D was discovered just over 100 years ago, when health professionals were looking for ways to treat what was then called “the English disease.” Today, we know that rickets, a weakening of bones in children, is caused by vitamin D deficiency. And vitamin D is best known for its importance in bone health.

That’s because it helps our bodies absorb calcium. Our bones are continually being broken down and rebuilt, and they need calcium for that rebuilding process. Without enough calcium, bones can become weak and brittle. (Depressingly, rickets is still a global health issue, which is why there is global consensus that infants should receive a vitamin D supplement at least until they are one year old.)

In the decades since then, scientists have learned that vitamin D has effects beyond our bones. There’s some evidence to suggest, for example, that being deficient in vitamin D puts people at risk of high blood pressure. Daily or weekly supplements can help those individuals lower their blood pressure.

A vitamin D deficiency has also been linked to a greater risk of “cardiovascular events” like heart attacks, although it’s not clear whether supplements can reduce this risk; the evidence is pretty mixed.

Vitamin D appears to influence our immune health, too. Studies have found a link between low vitamin D levels and incidence of the common cold, for example. And other research has shown that vitamin D supplements can influence the way our genes make proteins that play important roles in the way our immune systems work.

We don’t yet know exactly how these relationships work, however. And, unfortunately, a recent study that assessed the results of 37 clinical trials found that overall, vitamin D supplements aren’t likely to stop you from getting an “acute respiratory infection.”

Other studies have linked vitamin D levels to mental health, pregnancy outcomes, and even how long people survive after a cancer diagnosis. It’s tantalizing to imagine that a cheap supplement could benefit so many aspects of our health.

But, as you might have gathered if you’ve got this far, we’re not quite there yet. The evidence on the effects of vitamin D supplementation for those various conditions is mixed at best.

In fairness to researchers, it can be difficult to run a randomized clinical trial for vitamin D supplements. That’s because most of us get the bulk of our vitamin D from sunlight. Our skin converts UVB rays into a form of the vitamin that our bodies can use. We get it in our diets, too, but not much. (The main sources are oily fish, egg yolks, mushrooms, and some fortified cereals and milk alternatives.)

The standard way to measure a person’s vitamin D status is to look at blood levels of 25-hydroxycholecalciferol (25(OH)D), which is formed when the liver metabolizes vitamin D. But not everyone can agree on what the “ideal” level is.

Even if everyone did agree on a figure, it isn’t obvious how much vitamin D a person would need to consume to reach this target, or how much sunlight exposure it would take. One complicating factor is that people respond to UV rays in different ways—a lot of that can depend on how much melanin is in your skin. Similarly, if you’re sitting down to a meal of oily fish and mushrooms and washing it down with a glass of fortified milk, it’s hard to know how much more you might need.

There is more consensus on the definition of vitamin D deficiency, though. (It’s a blood level below 30 nanomoles per liter, in case you were wondering.) And until we know more about what vitamin D is doing in our bodies, our focus should be on avoiding that.

For me, that means topping up with a supplement. The UK government advises everyone in the country to take a 10-microgram vitamin D supplement over autumn and winter. That advice doesn’t factor in my age, my blood levels, or the amount of melanin in my skin. But it’s all I’ve got for now.

Earlier this week, the UK’s science minister announced an ambitious plan: to phase out animal testing.

Testing potential skin irritants on animals will be stopped by the end of next year, according to a strategy released on Tuesday. By 2027, researchers are “expected to end” tests of the strength of Botox on mice. And drug tests in dogs and nonhuman primates will be reduced by 2030. 

The news follows similar moves by other countries. In April, the US Food and Drug Administration announced a plan to replace animal testing for monoclonal antibody therapies with “more effective, human-relevant models.” And, following a workshop in June 2024, the European Commission also began working on a “road map” to phase out animal testing for chemical safety assessments.

Animal welfare groups have been campaigning for commitments like these for decades. But a lack of alternatives has made it difficult to put a stop to animal testing. Advances in medical science and biotechnology are changing that.

Animals have been used in scientific research for thousands of years. Animal experimentation has led to many important discoveries about how the brains and bodies of animals work. And because regulators require drugs to be first tested in research animals, it has played an important role in the creation of medicines and devices for both humans and other animals.

Today, countries like the UK and the US regulate animal research and require scientists to hold multiple licenses and adhere to rules on animal housing and care. Still, millions of animals are used annually in research. Plenty of scientists don’t want to take part in animal testing. And some question whether animal research is justifiable—especially considering that around 95% of treatments that look promising in animals don’t make it to market.

In recent decades, we’ve seen dramatic advances in technologies that offer new ways to model the human body and test the effects of potential therapies, without experimenting on humans or other animals.

Take “organs on chips,” for example. Researchers have been creating miniature versions of human organs inside tiny plastic cases. These systems are designed to contain the same mix of cells you’d find in a full-grown organ and receive a supply of nutrients that keeps them alive.

Today, multiple teams have created models of livers, intestines, hearts, kidneys and even the brain. And they are already being used in research. Heart chips have been sent into space to observe how they respond to low gravity. The FDA used lung chips to assess covid-19 vaccines. Gut chips are being used to study the effects of radiation.

Some researchers are even working to connect multiple chips to create a “body on a chip”—although this has been in the works for over a decade and no one has quite managed it yet.

In the same vein, others have been working on creating model versions of organs—and even embryos—in the lab. By growing groups of cells into tiny 3D structures, scientists can study how organs develop and work, and even test drugs on them. They can even be personalized—if you take cells from someone, you should be able to model that person’s specific organs. Some researchers have even been able to create organoids of developing fetuses.

The UK government strategy mentions the promise of artificial intelligence, too. Many scientists have been quick to adopt AI as a tool to help them make sense of vast databases, and to find connections between genes, proteins and disease, for example. Others are using AI to design all-new drugs.

Those new drugs could potentially be tested on virtual humans. Not flesh-and-blood people, but digital reconstructions that live in a computer. Biomedical engineers have already created digital twins of organs. In ongoing trials, digital hearts are being used to guide surgeons on how—and where—to operate on real hearts.

When I spoke to Natalia Trayanova, the biomedical engineering professor behind this trial, she told me that her model could recommend regions of heart tissue to be burned off as part of treatment for atrial fibrillation. Her tool would normally suggest two or three regions but occasionally would recommend many more. “They just have to trust us,” she told me.

It is unlikely that we’ll completely phase out animal testing by 2030. The UK government acknowledges that animal testing is still required by lots of regulators, including the FDA, the European Medicines Agency, and the World Health Organization. And while alternatives to animal testing have come a long way, none of them perfectly capture how a living body will respond to a treatment.

At least not yet. Given all the progress that has been made in recent years, it’s not too hard to imagine a future without animal testing.

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

This week, we heard that Tom Brady had his dog cloned. The former quarterback revealed that his Junie is actually a clone of Lua, a pit bull mix that died in 2023.

Brady’s announcement follows those of celebrities like Paris Hilton and Barbra Streisand, who also famously cloned their pet dogs. But some believe there are better ways to make use of cloning technologies.

While the pampered pooches of the rich and famous may dominate this week’s headlines, cloning technologies are also being used to diversify the genetic pools of inbred species and potentially bring other animals back from the brink of extinction.

Cloning itself isn’t new. The first mammal cloned from an adult cell, Dolly the sheep, was born in the 1990s. The technology has been used in livestock breeding over the decades since.

Say you’ve got a particularly large bull, or a cow that has an especially high milk yield. Those animals are valuable. You could selectively breed for those kinds of characteristics. Or you could clone the original animals—essentially creating genetic twins.

Scientists can take some of the animals’ cells, freeze them, and store them in a biobank. That opens the option to clone them in the future. It’s possible to thaw those cells, remove the DNA-containing nuclei of the cells, and insert them into donor egg cells.

Those donor egg cells, which come from another animal of the same species, have their own nuclei removed. So it’s a case of swapping out the DNA. The resulting cell is stimulated and grown in the lab until it starts to look like an embryo. Then it is transferred to the uterus of a surrogate animal—which eventually gives birth to a clone.

There are a handful of companies offering to clone pets. Viagen, which claims to have “cloned more animals than anyone else on Earth,” will clone a dog or cat for $50,000. That’s the company that cloned Streisand’s pet dog Samantha, twice.

This week, Colossal Biosciences—the “de-extinction” company that claims to have resurrected the dire wolf and created a “woolly mouse” as a precursor to reviving the woolly mammoth—announced that it had acquired Viagen, but that Viagen will “continue to operate under its current leadership.”

Pet cloning is controversial, for a few reasons. The companies themselves point out that, while the cloned animal will be a genetic twin of the original animal, it won’t be identical. One issue is mitochondrial DNA—a tiny fraction of DNA that sits outside the nucleus and is inherited from the mother. The cloned animal may inherit some of this from the surrogate.

Mitochondrial DNA is unlikely to have much of an impact on the animal itself. More important are the many, many factors thought to shape an individual’s personality and temperament. “It’s the old nature-versus-nurture question,” says Samantha Wisely, a conservation geneticist at the University of Florida. After all, human identical twins are never carbon copies of each other. Anyone who clones a pet expecting a like-for-like reincarnation is likely to be disappointed.

And some animal welfare groups are opposed to the practice of pet cloning. People for the Ethical Treatment of Animals (PETA) described it as “a horror show,” and the UK’s Royal Society for the Prevention of Cruelty to Animals (RSPCA) says that “there is no justification for cloning animals for such trivial purposes.” 

But there are other uses for cloning technology that are arguably less trivial. Wisely has long been interested in diversifying the gene pool of the critically endangered black-footed ferret, for example.

Today, there are around 10,000 black-footed ferrets that have been captively bred from only seven individuals, says Wisely. That level of inbreeding isn’t good for any species—it tends to leave organisms at risk of poor health. They are less able to reproduce or adapt to changes in their environment.

Wisely and her colleagues had access to frozen tissue samples taken from two other ferrets. Along with colleagues at not-for-profit Revive and Restore, the team created clones of those two individuals. The first clone, Elizabeth Ann, was born in 2020. Since then, other clones have been born, and the team has started breeding the cloned animals with the descendants of the other seven ferrets, says Wisely.

The same approach has been used to clone the endangered Przewalski’s horse, using decades-old tissue samples stored by the San Diego Zoo. It’s too soon to predict the impact of these efforts. Researchers are still evaluating the cloned ferrets and their offspring to see if they behave like typical animals and could survive in the wild.

Even this practice is not without its critics. Some have pointed out that cloning alone will not save any species. After all, it doesn’t address the habitat loss or human-wildlife conflict that is responsible for the endangerment of these animals in the first place. And there will always be detractors who accuse people who clone animals of “playing God.” 

For all her involvement in cloning endangered ferrets, Wisely tells me she would not consider cloning her own pets. She currently has three rescue dogs, a rescue cat, and “geriatric chickens.” “I love them all dearly,” she says. “But there are a lot of rescue animals out there that need homes.”

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.

For those of us in the Northern Hemisphere, it’s the season of the sniffles. As the weather turns, we’re all spending more time indoors. The kids have been back at school for a couple of months. And cold germs are everywhere.

My youngest started school this year, and along with artwork and seedlings, she has also been bringing home lots of lovely bugs to share with the rest of her family. As she coughed directly into my face for what felt like the hundredth time, I started to wonder if there was anything I could do to stop this endless cycle of winter illnesses. We all got our flu jabs a month ago. Why couldn’t we get a vaccine to protect us against the common cold, too?

Scientists have been working on this for decades. It turns out that creating a cold vaccine is hard. Really hard.

But not impossible. There’s still hope. Let me explain.

Technically, colds are infections that affect your nose and throat, causing symptoms like sneezing, coughing, and generally feeling like garbage. Unlike some other infections,—covid-19, for example—they aren’t defined by the specific virus that causes them.

That’s because there are a lot of viruses that cause colds, including rhinoviruses, adenoviruses, and even seasonal coronaviruses (they don’t all cause covid!). Within those virus families, there are many different variants.

Take rhinoviruses, for example. These viruses are thought to be behind most colds. They’re human viruses—over the course of evolution, they have become perfectly adapted to infecting us, rapidly multiplying in our noses and airways to make us sick. There are around 180 rhinovirus variants, says Gary McLean, a molecular immunologist at Imperial College London in the UK.

Once you factor in the other cold-causing viruses, there are around 280 variants all told. That’s 280 suspects behind the cough that my daughter sprayed into my face. It’s going to be really hard to make a vaccine that will offer protection against all of them.

The second challenge lies in the prevalence of those variants.

Scientists tailor flu and covid vaccines to whatever strain happens to be circulating. Months before flu season starts, the World Health Organization advises countries on which strains their vaccines should protect against. Early recommendations for the Northern Hemisphere can be based on which strains seem to be dominant in the Southern Hemisphere, and vice versa.

That approach wouldn’t work for the common cold, because all those hundreds of variants are circulating all the time, says McLean.

That’s not to say that people haven’t tried to make a cold vaccine. There was a flurry of interest in the 1960s and ’70s, when scientists made valiant efforts to develop vaccines for the common cold. Sadly, they all failed. And we haven’t made much progress since then.

In 2022, a team of researchers reviewed all the research that had been published up to that year. They only identified one clinical trial—and it was conducted back in 1965.

Interest has certainly died down since then, too. Some question whether a cold vaccine is even worth the effort. After all, most colds don’t require much in the way of treatment and don’t last more than a week or two. There are many, many more dangerous viruses out there we could be focusing on.

And while cold viruses do mutate and evolve, no one really expects them to cause the next pandemic, says McLean. They’ve evolved to cause mild disease in humans—something they’ve been doing successfully for a long, long time. Flu viruses—which can cause serious illness, disability, or even death—pose a much bigger risk, so they probably deserve more attention.

But colds are still irritating, disruptive, and potentially harmful. Rhinoviruses are considered to be the leading cause of human infectious disease. They can cause pneumonia in children and older adults. And once you add up doctor visits, medication, and missed work, the economic cost of colds is pretty hefty: a 2003 study put it at $40 billion per year for the US alone.

So it’s reassuring that we needn’t abandon all hope: Some scientists are making progress! McLean and his colleagues are working on ways to prepare the immune systems of people with asthma and lung diseases to potentially protect them from cold viruses. And a team at Emory University has developed a vaccine that appears to protect monkeys from around a third of rhinoviruses.

There’s still a long way to go. Don’t expect a cold vaccine to materialize in the next five years, at least. “We’re not quite there yet,” says Michael Boeckh, an infectious-disease researcher at Fred Hutch Cancer Center in Seattle, Washington. “But will it at some point happen? Possibly.”

At the end of our Zoom call, perhaps after reading the disappointed expression on my sniffling, cold-riddled face (yes, I did end up catching my daughter’s cold), McLean told me he hoped he was “positive enough.” He admitted that he used to be more optimistic about a cold vaccine. But he hasn’t given up hope. He’s even running a trial of a potential new vaccine in people, although he wouldn’t reveal the details.

“It could be done,” he said.

This article first appeared in The Checkup, MIT Technology Review’s weekly biotech newsletter. To receive it in your inbox every Thursday, and read articles like this first, sign up here.