We’re learning more about what vitamin D does to our bodies

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.

Cloning isn’t just for celebrity pets like Tom Brady’s dog

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.

Here’s why we don’t have a cold vaccine. Yet.

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.

An AI app to measure pain is here

How are you feeling?

I’m genuinely interested in the well-being of all my treasured Checkup readers, of course. But this week I’ve also been wondering how science and technology can help answer that question—especially when it comes to pain. 
In the latest issue of MIT Technology Review magazine, Deena Mousa describes how an AI-powered smartphone app is being used to assess how much pain a person is in.

The app, and other tools like it, could help doctors and caregivers. They could be especially useful in the care of people who aren’t able to tell others how they are feeling.

But they are far from perfect. And they open up all kinds of thorny questions about how we experience, communicate, and even treat pain.

Pain can be notoriously difficult to describe, as almost everyone who has ever been asked to will know. At a recent medical visit, my doctor asked me to rank my pain on a scale from 1 to 10. I found it incredibly difficult to do. A 10, she said, meant “the worst pain imaginable,” which brought back unpleasant memories of having appendicitis.

A short while before the problem that brought me in, I’d broken my toe in two places, which had hurt like a mother—but less than appendicitis. If appendicitis was a 10, breaking a toe was an 8, I figured. If that was the case, maybe my current pain was a 6. As a pain score, it didn’t sound as bad as I actually felt. I couldn’t help wondering if I might have given a higher score if my appendix were still intact. I wondered, too, how someone else with my medical issue might score their pain.

In truth, we all experience pain in our own unique ways. Pain is subjective, and it is influenced by our past experiences, our moods, and our expectations. The way people describe their pain can vary tremendously, too.

We’ve known this for ages. In the 1940s, the anesthesiologist Henry Beecher noted that wounded soldiers were much less likely to ask for pain relief than similarly injured people in civilian hospitals. Perhaps they were putting on a brave face, or maybe they just felt lucky to be alive, given their circumstances. We have no way of knowing how much pain they were really feeling.

Given this messy picture, I can see the appeal of a simple test that can score pain and help medical professionals understand how best to treat their patients. That’s what is being offered by PainChek, the smartphone app Deena wrote about. The app works by assessing small facial movements, such as lip raises or brow pinches. A user is then required to fill a separate checklist to identify other signs of pain the patient might be displaying. It seems to work well, and it is already being used in hospitals and care settings.

But the app is judged against subjective reports of pain. It might be useful for assessing the pain of people who can’t describe it themselves—perhaps because they have dementia, for example—but it won’t add much to assessments from people who can already communicate their pain levels.

There are other complications. Say a test could spot that a person was experiencing pain. What can a doctor do with that information? Perhaps prescribe pain relief—but most of the pain-relieving drugs we have were designed to treat acute, short-term pain. If a person is grimacing from a chronic pain condition, the treatment options are more limited, says Stuart Derbyshire, a pain neuroscientist at the National University of Singapore.

The last time I spoke to Derbyshire was back in 2010, when I covered work by researchers in London who were using brain scans to measure pain. That was 15 years ago. But pain-measuring brain scanners are yet to become a routine part of clinical care.

That scoring system was also built on subjective pain reports. Those reports are, as Derbyshire puts it, “baked into the system.” It’s not ideal, but when it comes down to it, we must rely on these wobbly, malleable, and sometimes incoherent self-descriptions of pain. It’s the best we have.

Derbyshire says he doesn’t think we’ll ever have a “pain-o-meter” that can tell you what a person is truly experiencing. “Subjective report is the gold standard, and I think it always will be,” 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.

Take our quiz: How much do you know about antimicrobial resistance?

This week we had some terrifying news from the World Health Organization: Antibiotics are failing us. A growing number of bacterial infections aren’t responding to these medicines—including common ones that affect the blood, gut, and urinary tract. Get infected with one of these bugs, and there’s a fair chance antibiotics won’t help. 

The scary truth is that a growing number of harmful bacteria and fungi are becoming resistant to drugs. Just a few weeks ago, the US Centers for Disease Control and Prevention published a report finding a sharp rise in infections caused by a dangerous type of bacteria that are resistant to some of the strongest antibiotics. Now, the WHO report shows that the problem is surging around the world.

In this week’s Checkup, we’re trying something a bit different—a little quiz. You’ve probably heard about antimicrobial resistance (AMR) before, but how much do you know about microbes, antibiotics, and the scale of the problem? Here’s our attempt to put the “fun” in “fundamental threat to modern medicine.” Test your knowledge below!

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 test could reveal the health of your immune system

Attentive readers might have noticed my absence over the last couple of weeks. I’ve been trying to recover from a bout of illness.

It got me thinking about the immune system, and how little I know about my own immune health. The vast array of cells, proteins, and biomolecules that works to defend us from disease is mind-bogglingly complicated. Immunologists are still getting to grips with how it all works.

Those of us who aren’t immunologists are even more in the dark. I had my flu jab last week and have no idea how my immune system responded. Will it protect me from the flu virus this winter? Is it “stressed” from whatever other bugs it has encountered in the last few months? And since my husband had his shot at the same time, I can’t help wondering how our responses will compare. 

So I was intrigued to hear about a new test that is being developed to measure immune health. One that even gives you a score.

Writer David Ewing Duncan hoped that the test would reveal more about his health than any other he’d ever taken. He described the experience in a piece published jointly by MIT Technology Review and Aventine.

The test David took was developed by John Tsang at Yale University and his colleagues. The team wanted to work out a way of measuring how healthy a person’s immune system might be.

It’s a difficult thing to do, for several reasons. First, there’s the definition of “healthy.” I find it’s a loose concept that becomes more complicated the more you think about it. Yes, we all have a general sense of what it means to be in good health. But is it just the absence of disease? Is it about resilience? Does it have something to do with withstanding the impact of aging?

Tsang and his colleagues wanted to measure “deviation from health.” They looked at blood samples from 228 people who had immune diseases that were caused by single-gene mutations, as well as 42 other people who were free from disease. All those individuals could be considered along a health spectrum.

Another major challenge lies in trying to capture the complexity of the immune system, which involves hundreds of proteins and cells interacting in various ways. (Side note: Last year, MIT Technology Review recognized Ang Cui at Harvard University as one of our Innovators under 35 for her attempts to make sense of it all using machine learning. She created the Immune Dictionary to describe how hundreds of proteins affect immune cells—something she likens to a “periodic table” for the immune system.)

Tsang and his colleagues tackled this by running a series of tests on those blood samples. The vast scope of these tests is what sets them apart from the blood tests you might get during a visit to the doctor. The team looked at how genes were expressed by cells in the blood. They measured a range of immune cells and more than 1,300 proteins.

The team members used machine learning to find correlations between these measurements and health, allowing them to create an immune health score for each of the volunteers. They call it the immune health metric, or IHM.

When they used this approach to find the immune scores of people who had already volunteered in other studies, they found that the IHM seemed to align with other measures of health, such as how people respond to diseases, treatments, and vaccines. The study was published in the journal Nature Medicine last year.

The researchers behind it hope that a test like this could one day help identify people who are at risk of cancer and other diseases, or explain why some people respond differently to treatments or immunizations.

But the test isn’t ready for clinical use. If, like me, you’re finding yourself curious to know your own IHM, you’ll just have to wait.

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.

A pivotal meeting on vaccine guidance is underway—and former CDC leaders are alarmed

This week has been an eventful one for America’s public health agency. Two former leaders of the US Centers for Disease Control and Prevention explained the reasons for their sudden departures from the agency in a Senate hearing. And they described how CDC employees are being instructed to turn their backs on scientific evidence.

The CDC’s former director Susan Monarez and former chief medical officer Debra Houry took questions from a Senate committee on Wednesday. They painted a picture of a health agency in turmoil—and at risk of harming the people it is meant to serve.

On Thursday, an advisory CDC panel that develops vaccine guidance met for a two-day discussion on multiple childhood vaccines. During the meeting, which was underway as The Checkup went to press, members of the panel were set to discuss those vaccines and propose recommendations on their use.

Monarez worries that access to childhood vaccines is under threat—and that the public health consequences could be dire. “If vaccine protections are weakened, preventable diseases will return,” she said.

As the current secretary of health and human services, Robert F. Kennedy Jr. oversees federal health and science agencies that include the CDC, which monitors and responds to threats to public health. Part of that role involves developing vaccine recommendations.

As we’ve noted before, RFK Jr. has long been a prominent critic of vaccines. He has incorrectly linked commonly used ingredients to autism and made other incorrect statements about risks associated with various vaccines.

Still, he oversaw the recruitment of Monarez—who does not share those beliefs—to lead the agency. When she was sworn in on July 31, Monarez, who is a microbiologist and immunologist, had already been serving as acting director of the agency. She had held prominent positions at other federal agencies and departments too, including the Advanced Research Projects Agency for Health (ARPA-H) and the Biomedical Advanced Research and Development Authority (BARDA). Kennedy described her as “a public health expert with unimpeachable scientific credentials.”

His opinion seems to have changed somewhat since then. Just 29 days after Monarez took on her position, she was turfed out of the agency. And in yesterday’s hearing, she explained why.

On August 25, Kennedy asked Monarez to do two things, she said. First, he wanted her to commit to firing scientists at the agency. And second, he wanted her to “pre-commit” to approve vaccine recommendations made by the agency’s Advisory Committee on Immunization Practices (ACIP), regardless of whether there was any scientific evidence to support those recommendations, she said. “He just wanted blanket approval,” she said during her testimony. 

She refused both requests.

Monarez testified that she didn’t want to get rid of hardworking scientists who played an important role in keeping Americans safe. And she said she could not commit to approving vaccine recommendations without reviewing the scientific evidence behind them and maintain her integrity. She was sacked.

Those vaccine recommendations are currently under discussion, and scientists like Monarez are worried about how they might change. Kennedy fired all 17 members of the previous committee in June. (Monarez said she was not consulted on the firings and found out about them through media reports.)

“A clean sweep is needed to reestablish public confidence in vaccine science,” Kennedy wrote in a piece for the Wall Street Journal at the time. He went on to replace those individuals with eight new members, some of whom have been prominent vaccine critics and have spread misinformation about vaccines. One later withdrew.

That new panel met two weeks later. The meeting included a presentation about thimerosal—a chemical that Kennedy has incorrectly linked to autism, and which is no longer included in vaccines in the US—and a proposal to recommend that the MMRV vaccine (for measles, mumps, rubella, and varicella) not be offered to children under the age of four.

Earlier this week, five new committee members were named. They include individuals who have advocated against vaccine mandates and who have argued that mRNA-based covid vaccines should be removed from the market.

All 12 members are convening for a meeting that runs today and tomorrow. At that meeting, members will propose recommendations for the MMRV vaccine and vaccines for covid-19 and hepatitis B, according to an agenda published on the CDC website.

Those are the recommendations for which Monarez says she was asked to provide “blanket approval.” “My worst fear is that I would then be in a position of approving something that reduces access [to] lifesaving vaccines to children and others who need them,” she said.

That job now goes to Jim O’Neill, the deputy health secretary and acting CDC director (also a longevity enthusiast), who now holds the authority to approve those recommendations.

We don’t yet know what those recommendations will be. But if they are approved, they could reshape access to vaccines for children and vulnerable people in the US. As six former chairs of the committee wrote for STAT: “ACIP is directly linked to the Vaccines for Children program, which provides vaccines without cost to approximately 50% of children in the US, and the Affordable Care Act that requires insurance coverage for ACIP-recommended vaccines to approximately 150 million people in the US.”

Drops in vaccine uptake have already contributed to this year’s measles outbreak in the US, which is the biggest in decades. Two children have died. We are already seeing the impact of undermined trust in childhood vaccines. As Monarez put it: “The stakes are not theoretical.”

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.