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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.

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In mid-October, a mysterious object cracked the windshield of a packed Boeing 737 cruising at 36,000 feet above Utah, forcing the pilots into an emergency landing. The internet was suddenly buzzing with the prospect that the plane had been hit by a piece of space debris. We still don’t know exactly what hit the plane—likely a remnant of a weather balloon—but it turns out the speculation online wasn’t that far-fetched.

That’s because while the risk of flights being hit by space junk is still small, it is, in fact, growing. 

About three pieces of old space equipment—used rockets and defunct satellites—fall into Earth’s atmosphere every day, according to estimates by the European Space Agency. By the mid-2030s, there may be dozens. The increase is linked to the growth in the number of satellites in orbit. Currently, around 12,900 active satellites circle the planet. In a decade, there may be 100,000 of them, according to analyst estimates.

To minimize the risk of orbital collisions, operators guide old satellites to burn up in Earth’s atmosphere. But the physics of that reentry process are not well understood, and we don’t know how much material burns up and how much reaches the ground.

“The number of such landfall events is increasing,” says Richard Ocaya, a professor of physics at the University of Free State in South Africa and a coauthor of a recent paper on space debris risk. “We expect it may be increasing exponentially in the next few years.”

So far, space debris hasn’t injured anybody—in the air or on the ground. But multiple close calls have been reported in recent years. In March last year, an 0.7-kilogram chunk of metal pierced the roof of a house in Florida. The object was later confirmed to be a remnant of a battery pallet tossed out from the International Space Station. When the strike occurred, the homeowner’s 19-year-old son was resting in a next-door room.

And in February this year, a 1.5-meter-long fragment of SpaceX’s Falcon 9 rocket crashed down near a warehouse outside Poland’s fifth-largest city, Poznan. Another piece was found in a nearby forest. A month later, a 2.5-kilogram piece of a Starlink satellite dropped on a farm in the Canadian province of Saskatchewan. Other incidents have been reported in Australia and Africa. And many more may be going completely unnoticed. 

“If you were to find a bunch of burnt electronics in a forest somewhere, your first thought is not that it came from a spaceship,” says James Beck, the director of the UK-based space engineering research firm Belstead Research. He warns that we don’t fully understand the risk of space debris strikes and that it might be much higher than satellite operators want us to believe. 

For example, SpaceX, the owner of the currently largest mega-constellation, Starlink, claims that its satellites are “designed for demise” and completely burn up when they spiral from orbit and fall through the atmosphere.

But Beck, who has performed multiple wind tunnel tests using satellite mock-ups to mimic atmospheric forces, says the results of such experiments raise doubts. Some satellite components are made of durable materials such as titanium and special alloy composites that don’t melt even at the extremely high temperatures that arise during a hypersonic atmospheric descent. 

“We have done some work for some small-satellite manufacturers and basically, their major problem is that the tanks get down,” Beck says. “For larger satellites, around 800 kilos, we would expect maybe two or three objects to land.” 

It can be challenging to quantify how much of a danger space debris poses. The International Civil Aviation Organization (ICAO) told MIT Technology Review that “the rapid growth in satellite deployments presents a novel challenge” for aviation safety, one that “cannot be quantified with the same precision as more established hazards.” 

But the Federal Aviation Administration has calculated some preliminary numbers on the risk to flights: In a 2023 analysis, the agency estimated that by 2035, the risk that one plane per year will experience a disastrous space debris strike will be around 7 in 10,000. Such a collision would either destroy the aircraft immediately or lead to a rapid loss of air pressure, threatening the lives of all on board.

The casualty risk to humans on the ground will be much higher. Aaron Boley, an associate professor in astronomy and a space debris researcher at the University of British Columbia, Canada, says that if megaconstellation satellites “don’t demise entirely,” the risk of a single human death or injury caused by a space debris strike on the ground could reach around 10% per year by 2035. That would mean a better than even chance that someone on Earth would be hit by space junk about every decade. In its report, the FAA put the chances even higher with similar assumptions, estimating that “one person on the planet would be expected to be injured or killed every two years.”

Experts are starting to think about how they might incorporate space debris into their air safety processes. The German space situational awareness company Okapi Orbits, for example, in cooperation with the German Aerospace Center and the European Organization for the Safety of Air Navigation (Eurocontrol), is exploring ways to adapt air traffic control systems so that pilots and air traffic controllers can receive timely and accurate alerts about space debris threats.

But predicting the path of space debris is challenging too. In recent years, advances in AI have helped improve predictions of space objects’ trajectories in the vacuum of space, potentially reducing the risk of orbital collisions. But so far, these algorithms can’t properly account for the effects of the gradually thickening atmosphere that space junk encounters during reentry. Radar and telescope observations can help, but the exact location of the impact becomes clear with only very short notice.

“Even with high-fidelity models, there’s so many variables at play that having a very accurate reentry location is difficult,” says Njord Eggen, a data analyst at Okapi Orbits. Space debris goes around the planet every hour and a half when in low Earth orbit, he notes, “so even if you have uncertainties on the order of 10 minutes, that’s going to have drastic consequences when it comes to the location where it could impact.”

For aviation companies, the problem is not just a potential strike, as catastrophic as that would be. To avoid accidents, authorities are likely to temporarily close the airspace in at-risk regions, which creates delays and costs money. Boley and his colleagues published a paper earlier this year estimating that busy aerospace regions such as northern Europe or the northeastern United States already have about a 26% yearly chance of experiencing at least one disruption due to the reentry of a major space debris item. By the time all planned constellations are fully deployed, aerospace closures due to space debris hazards may become nearly as common as those due to bad weather.

Because current reentry predictions are unreliable, many of these closures may end up being unnecessary.

For example, when a 21-metric-ton Chinese Long March mega-rocket was falling to Earth in 2022, predictions suggested its debris could scatter across Spain and parts of France. In the end, the rocket crashed into the Pacific Ocean. But the 30-minute closure of south European airspace delayed and diverted hundreds of flights. 

In the meantime, international regulators are urging satellite operators and launch providers to deorbit large satellites and rocket bodies in a controlled way, when possible, by carefully guiding them into remote parts of the ocean using residual fuel. 

The European Space Agency estimates that only about half the rocket bodies reentering the atmosphere do so in a controlled way. 

Moreover, around 2,300 old and no-longer-controllable rocket bodies still linger in orbit, slowly spiraling toward Earth with no mechanisms for operators to safely guide them into the ocean.

“There’s enough material up there that even if we change our practices, we will still have all those rocket bodies eventually reenter,” Boley says. “Although the probability of space debris hitting an aircraft is small, the probability that the debris will spread and fall over busy airspace is not small. That’s actually quite likely.”

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“Like riding a bike” is shorthand for the remarkable way that our bodies remember how to move. Most of the time when we talk about muscle memory, we’re not talking about the muscles themselves but about the memory of a coordinated movement pattern that lives in the motor neurons, which control our muscles. 

Yet in recent years, scientists have discovered that our muscles themselves have a memory for movement and exercise.

When we move a muscle, the movement may appear to begin and end, but all these little changes are actually continuing to happen inside our muscle cells. And the more we move, as with riding a bike or other kinds of exercise, the more those cells begin to make a memory of that exercise.

When we move a muscle, the movement may appear to begin and end, but all these little changes are actually continuing to happen inside our muscle cells.

We all know from experience that a muscle gets bigger and stronger with repeated work. As the pioneering muscle scientist Adam Sharples—a professor at the Norwegian School of Sport Sciences in Oslo and a former professional rugby player in the UK—explained to me, skeletal muscle cells are unique in the human body: They’re long and skinny, like fibers, and have multiple nuclei. The fibers grow larger not by dividing but by recruiting muscle satellite cells—stem cells specific to muscle that are dormant until activated in response to stress or injury—to contribute their own nuclei and support muscle growth and regeneration. Those nuclei often stick around for a while in the muscle fibers, even after periods of inactivity, and there is evidence that they may help accelerate the return to growth once you start training again. 

Sharples’s research focuses on what’s called epigenetic muscle memory. “Epigenetic” refers to changes in gene expression that are caused by behavior and environment—the genes themselves don’t change, but the way they work does. In general, exercise switches on genes that help make muscles grow more easily. When you lift weights, for example, small molecules called methyl groups detach from the outside of certain genes, making them more likely to turn on and produce proteins that affect muscle growth (also known as hypertrophy). Those changes persist; if you start lifting weights again, you’ll add muscle mass more quickly than before.

In 2018, Sharples’s muscle lab was the first to show that human skeletal muscle has an epigenetic memory of muscle growth after exercise: Muscle cells are primed to respond more rapidly to exercise in the future, even after a monthslong (and maybe even yearslong) pause. In other words: Your muscles remember how to do it.

Subsequent studies from Sharples and others have replicated similar findings in mice and older humans, offering further supporting evidence of epigenetic muscle memory across species and into later life. Even aging muscles have the capacity to remember when you work out.

At the same time, Sharples points to intriguing new evidence that muscles also remember periods of atrophy—and that young and old muscles remember this differently. While young human muscle seems to have what he calls a “positive” memory of wasting—“in that it recovers well after a first period of atrophy and doesn’t experience greater loss in a repeated atrophy period,” he explains—aged muscle in rats seems to have a more pronounced “negative” memory of atrophy, in which it appears “more susceptible to greater loss and a more exaggerated molecular response when muscle wasting is repeated.” Basically, young muscle tends to bounce back from periods of muscle loss—“ignoring” it, in a sense—while older muscle is more sensitive to it and might be more susceptible to further loss in the future. 

Illness can also lead to this kind of “negative” muscle memory; in a study of breast cancer survivors more than a decade after diagnosis and treatment, participants showed an epigenetic muscle profile of people much older than their chronological age. But get this: After five months of aerobic exercise training, participants were able to reset the epigenetic profile of their muscle back toward that of muscle seen in an age-matched control group of healthy women.  

What this shows is that “positive” muscle memories can help counteract “negative” ones. The takeaway? Your muscles have their own kind of intelligence. The more you use them, the more they can harness it to become a lasting beneficial resource for your body in the future. 

Bonnie Tsui is the author of On Muscle: The Stuff That Moves Us and Why It Matters (Algonquin Books, 2025).

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At a press conference on Monday, President Trump announced that his administration was taking action to address “the meteoric rise in autism.” He suggested that childhood vaccines and acetaminophen, the active ingredient in Tylenol, are to blame for the increasing prevalence and advised pregnant women against taking the medicine. “Don’t take Tylenol,” he said. “Fight like hell not to take it.” 

The president’s  assertions left many scientists and health officials perplexed and dismayed. The notion that childhood vaccines cause autism has been thoroughly debunked. 

“There have been many, many studies across many, many children that have led science to rule out vaccines as a significant causal factor in autism,” says James McPartland, a child psychologist and director of the Yale Center for Brain and Mind Health in New Haven, Connecticut.

And although some studies suggest a link between Tylenol and autism, the most rigorous have failed to find a connection. 

The administration also announced that the Food and Drug Administration would work to make a medication called leucovorin available as a treatment for children with autism. Some small studies do suggest the drug has promise, but “those are some of the most preliminary treatment studies that we have,” says Matthew Lerner, a psychologist at Drexel University’s A.J. Drexel Autism Institute in Philadelphia. “This is not one I would say that the research suggests is ready for fast-tracking.” 

The press conference “alarms us researchers who committed our entire careers to better understanding autism,” said the Coalition for Autism Researchers, a group of more than 250 scientists, in a statement.

“The data cited do not support the claim that Tylenol causes autism and leucovorin is a cure, and only stoke fear and falsely suggest hope when there is no simple answer.”

There’s a lot to unpack here. Let’s begin. 

Has there been a “meteoric rise” in autism?

Not in the way the president meant. Sure, the prevalence of autism has grown, from about 1 in 500 children in 1995 to 1 in 31 today. But that’s due, in large part, to diagnostic changes. The latest iteration of the Diagnostic and Statistical Manual of Mental Illnesses, published in 2013, grouped five previously separate diagnoses into a single diagnosis of autism spectrum disorder (ASD).

That meant that more people met the criteria for an autism diagnosis. Lerner points out that there is also far more awareness of the condition today than there was several decades ago. “There’s autism representation in the media,” he says. “There are plenty of famous people in the news and finance and in business and in Hollywood who are publicly, openly autistic.”

Is Tylenol a contributor to autism? 

Some studies have found an association between the use of acetaminophen in pregnancy and autism in children. In these studies, researchers asked women about past acetaminophen use during pregnancy and then assessed whether children of the women who took the medicine were more likely to develop autism than children of women who didn’t take it. 

These kinds of epidemiological studies are tricky to interpret because they’re prone to bias. For example, women who take acetaminophen during pregnancy may do so because they have an infection, a fever, or an autoimmune disease.

“Many of these underlying reasons could themselves be causes of autism,” says Ian Douglas, an epidemiologist at the London School of Hygiene and Tropical Medicine. It’s also possible women with a higher genetic predisposition for autism have other medical conditions that make them more likely to take acetaminophen. 

Two studies attempted to account for these potential biases by looking at siblings whose mothers had used acetaminophen during only one of the pregnancies. The largest is a 2024 study that looked at nearly 2.5 million children born between 1915 and 2019 in Sweden. The researchers initially found a slightly increased risk of autism and ADHD in children of the women who took acetaminophen, but when they conducted a sibling analysis, the association disappeared.  

Rather, scientists have long known that autism is largely genetic. Twin studies suggest that 60% to 90% of autism risk can be attributed to your genes. However, environmental factors appear to play a role too. That “doesn’t necessarily mean toxins in the environment,” Lerner says. In fact, one of the strongest environmental predictors of autism is paternal age. Autism rates seem to be higher when a child’s father is older than 40.

So should someone who is pregnant  avoid Tylenol just to be safe?

No. Acetaminophen is the only over-the-counter pain reliever that is deemed safe to take during pregnancy, and women should take it if they need it. The American College of Obstetricians and Gynecologists (ACOG) supports the use of acetaminophen in pregnancy “when taken as needed, in moderation, and after consultation with a doctor.” 

“There’s no downside in not taking it,” Trump said at the press conference. But high fevers during pregnancy can be dangerous. “The conditions people use acetaminophen to treat during pregnancy are far more dangerous than any theoretical risks and can create severe morbidity and mortality for the pregnant person and the fetus,” ACOG president Steven Fleischman said in a statement.

What about this new treatment for autism? Does it work? 

The medication is called leucovorin. It’s also known as folinic acid; like folic acid, it’s a form of folate, a B vitamin found in leafy greens and legumes. The drug has been used for years to counteract the side effects of some cancer medications and as a treatment for anemia. 

Researchers have known for decades that folate plays a key role in the fetal development of the brain and spine. Women who don’t get enough folate during pregnancy have a greater risk of having babies with neural tube defects like spina bifida. Because of this, many foods are fortified with folic acid, and the CDC recommends that women take folic acid supplements during pregnancy. “If you are pregnant and you’re taking maternal prenatal vitamins, there’s a good chance it has folate already,” Lerner says.

“The idea that a significant proportion of autistic people have autism because of folate-related difficulties is not a well established or widely accepted premise,” says McPartland.

However, in the early 2000s, researchers in Germany identified a small group of children who developed neurodevelopmental symptoms because of a folate deficiency. “These kids are born pretty normal at birth,” says Edward Quadros, a biologist at SUNY Downstate Health Sciences University in Brooklyn, New York. But after a year or two, “they start developing a neurologic presentation very similar to autism,” he says. When the researchers gave these children folinic acid, some of their symptoms improved, especially in children younger than six. 

Because the children had low levels of folate in the fluid that surrounds the spine and brain but normal folate levels in the blood, the researchers posited that the problem was the transport of folate from the blood to that fluid. Research by Quadros and other scientists suggested that the deficiency was the result of an autoimmune response. Children develop antibodies against the receptors that help transport folate, and those antibodies block folate from crossing the blood-brain barrier. High doses of folinic acid, however, activate a second transporter that allows folate in, Quadros says. 

There are also plenty of individual anecdotes suggesting that leucovorin works. But the medicine has only been tested as a treatment for autism in four small trials that used different doses and measured different outcomes. The evidence that it can improve symptoms of autism is “weak,” according to the Coalition of Autism Scientists. “A much higher standard of science would be needed to determine if leucovorin is an effective and safe treatment for autism,” the researchers said in a statement.