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Science experienced many first-of-a-kind feats this year. These are the groundbreaking achievements that grabbed our attention.

Cosmic web shake-up

Glowing threads of gas, galaxies and dark matter provided the first tangible evidence that shock waves permeate the cosmic web, the large-scale structure of the universe (SN: 3/25/23, p. 14). Simulations had predicted that colliding threads generate shock waves, which catapult charged particles into the web’s magnetic fields and create a faint glow. That aura appeared in data from radio telescopes, confirming the shock waves exist. The glow also provides the first (if indirect) peek at the cosmic web’s magnetic fields.

Hats off

After more than 50 years of searching, mathematicians finally found an einstein tile (ein Stein is German for “one stone”). The shape, dubbed “the hat,” fits with its mirror image to create an infinite pattern that never repeats (SN: 4/22/23, p. 7). Soon after, researchers discovered a “vampire” einstein, a shape that doesn’t require its mirror image to create an infinite nonrepeating pattern (SN: 7/1/23, p. 9). Einstein tiles and their unique balance between order and disorder could spur new discoveries in materials science.

Fleeting debut

The first appearance of oxygen-28, a superheavy form of the element that physicists created in a particle accelerator, was much briefer than researchers had expected (SN: 10/7/23 & 10/21/23, p. 4). The isotope decayed almost immediately after forming, despite its atomic nucleus having full outer shells of protons and neutrons — a property that is typically linked with extra stability. Oxygen-28’s instability hints that something may be wrong with our understanding of the strong nuclear force, which binds protons and neutrons.

RNA retrieval

Scientists isolated and decoded RNA from an extinct creature for the first time. The fragile molecules, which help ensure that cells follow their DNA instruction manuals, were extracted from a preserved Tasmanian tiger held in a museum (SN: 11/4/23, p. 10). Researchers hope that the feat will aid efforts to bring back the wolflike marsupial, which is named after its homeland and died out in 1936.

Surviving a deep freeze

Adult corals can be safely flash-frozen and revived, researchers demonstrated, raising hopes that cryopreservation could be useful in coral conservation (SN: 9/23/23, p. 11). The key to preventing ice crystals from forming and damaging tissues is to bathe corals in a rigid metal container filled with a dehydrating solution before plunging them in liquid nitrogen. Whatever water remains in the tissues solidifies so quickly that it cannot crystallize and expand.

Neutrino cartography

A new map of the Milky Way is the first made without using light. Instead, cosmic cartographers used data from a detector in Antarctica and AI to chart nearly massless particles called neutrinos onto the galaxy’s plane. The resulting image (third image below; optical and gamma-ray versions shown for comparison) offered a rough idea of where the first known high-energy neutrinos to originate in the Milky Way were born (SN: 8/12/23, p. 13). With some refinement, the approach could pinpoint their birthplace and those of other amped-up ghostly particles.

Every letter counts

This year marked the completion of the pangenome, an effort to catalog every single letter, or building block, in humankind’s genetic instruction manual (SN: 6/3/23, p. 6). The undertaking involved compiling and comparing nearly all the DNA of 47 people to get the most comprehensive snapshot yet of human genetic diversity. A few months later, researchers added the final piece: the Y chromosome (SN: 10/7/23 & 10/21/23, p. 7). The pangenome could shed light on the molecular foundations of fertility, heart disease, Alzheimer’s disease and more.

Star eats planet

Astronomers have long suspected that stars swallow up planets, but no one had ever caught a star in the act until this year (SN: 6/3/23, p. 8). About 10,000 light-years from Earth, the sunlike star engulfed an orbiting planet that was about 10 times as massive as Jupiter. Over several days, the star grew noticeably brighter and burped a bunch of gas, suggesting it engulfed a companion star. But the relatively small amount of energy released tipped off researchers that the star had actually eaten a planet.

This year, celebrity gossip, a national shortage and eyebrow-raising clinical trials made household names of weight-loss and diabetes drugs like Ozempic, Wegovy and Mounjaro.

The buzzy drugs belong to a class of powerful medications that can manage blood sugar levels and drastically reduce body weight — a hot property that kicked them into the mainstream. This spring, even WeightWatchers got on board, acquiring a virtual clinic that offers prescriptions for the popular drugs.

The medications’ ever-expanding reach might explain why many people in the United States are having trouble filling prescriptions. From 2020 to 2022, the number of prescriptions for these drugs quadrupled — up to roughly 9 million in the final months of 2022, according to one analysis. In 2023, the U.S. Food and Drug Administration included both Ozempic and Wegovy on its drug shortages list.

And demand may continue to rocket up. Data from clinical trials and other studies suggest these drugs can improve cardiovascular health and perhaps even help treat addiction (SN: 8/30/23).

The FDA approved Ozempic for type 2 diabetes in 2017, and now new, potentially more potent and easier-to-produce versions are in the pipeline, says Susan Yanovski, a physician and nutrition specialist at the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Md. “I’ve been doing this for more than 30 years now, and I have not seen this degree of excitement.”

It’s the first time doctors have had obesity drugs that work so well, she says, approaching weight-loss levels previously seen only with bariatric surgery. But, Yanovski cautions, “it’s still early days.”

Amid the hubbub, a fresh influx of clinical trial data has opened a Pandora’s box of questions. How exactly do the drugs work? Who should take them? For how long? What’s the full range of side effects? “We’ve got a lot of research to do,” Yanovski says.

Semaglutide belongs to a powerful class of drugs

Ozempic is the brand name for the drug semaglutide; Wegovy, also semaglutide, has a higher maximum dose and is approved for weight loss. Semaglutide mimics a gut hormone, GLP-1, that’s secreted after people eat. When given a high dose weekly, people without diabetes can lose about 15 percent of their body weight, on average, after nearly 16 months. Scientists think the drug acts on the body and the brain, making people feel full and muffling food cravings.

Yet semaglutide may have an even more dramatic action — saving lives, scientists suggested November 11 in Philadelphia at the American Heart Association meeting. Weekly injections of the drug lowered the risk of heart attacks, strokes and death due to cardiovascular disease in some adults, Cleveland Clinic cardiologist A. Michael Lincoff reported (SN: 11/15/23). The trial targeted people who are overweight or obese who have high cardiovascular risk but not diabetes.

That’s important because it wasn’t clear until now that these patients would see heart benefits, says Tiffany Powell-Wiley, a cardiologist and epidemiologist at the National Heart, Lung and Blood Institute in Bethesda. The find “really opens up the number of patients that we can treat with semaglutide,” she says. Powell-Wiley notes, though, that no single drug — even a powerful one — can fix the many factors that lead to the development of obesity.

Still, pharmaceutical companies are racing to investigate new, improved relatives of semaglutide. Some of these drugs mimic multiple gut hormones rather than just one. One such molecule, tirzepatide (brand name Mounjaro), mimics both GLP-1 and the gut hormone GIP. The FDA approved tirzepatide for treating type 2 diabetes last year and for treating obesity in November, under the brand name Zepbound. The drug seems to cause even more weight loss than semaglutide, Yanovski says.

Another drug in development could one-up even tirzepatide. Retatrutide simulates three gut hormones: GLP-1, GIP and glucagon. People treated with a high dose lost an average of 24 percent of their body weight after nearly a year of treatment, a small clinical trial reported this year.

The full roster of these drugs, what they do and where they stand in the approval process makes for a dizzying array of information. But an assortment of options may pay off, Yanovski says. “We really need a variety of drugs … so that we can match the right treatment to the right patient.”

For some people, the benefits of weight-loss drugs outweigh the risks

But like any medication, Yanovski cautions, these drugs come with side effects. Semaglutide can cause nausea, diarrhea, vomiting, stomachache and constipation, among other ailments. Large amounts of rapid weight loss can also spur gallbladder disease, a complication sometimes seen after bariatric surgery. And these medications aren’t melting away only fat. When people rapidly lose lots of weight, they can also lose muscle mass, a particular concern for older patients, Yanovski says.

As these drugs roll out into larger populations of people, rare side effects not seen in clinical trials will also emerge. One recent study found that people using semaglutide or a related drug for weight loss had an increased risk of serious gastrointestinal conditions, including inflammation of the pancreas and bowel blockages, compared with people using a different type of weight-loss drug.

And patients will probably need to take these medications long term or risk gaining the weight back. “This is not a flaw in the medications; this is how medications work,” Yanovski says. If you stop taking cholesterol-lowering meds, for instance, your cholesterol may shoot up.

But the drugs’ high cost (Wegovy’s list price is about $1,350 per month and insurance coverage varies) puts even short-term use out of reach for many people. The cost can exacerbate health disparities and drive people to hunt for altered versions on the internet. Though these drugs may be cheaper, Yanovski says, they’re not FDA-approved and could be counterfeit.

She hopes to see people with obesity, particularly those with medical complications, gain better access to the approved drugs and in settings where they can be monitored by their doctors to ensure that the benefits outweigh the risks.

Those without a true need for the drugs probably should avoid them, Yanovski says. They’re “serious medications for a serious disease,” she says. “I think the buzz that these are some kind of miracle cure for obesity, or that you should take these medications just because you want to lose that stubborn 10 pounds, is overhyped.”

PHILADELPHIA ­— Ten patients enrolled in the experimental drug trial, and they were the sickest of the sick. 

All had a genetic disorder that cranks up levels of LDL cholesterol in the blood. Known as “bad cholesterol,” LDL cholesterol is infamous for clogging arteries. The patients’ disorder, called heterozygous familial hypercholesterolemia, can lead to severe heart disease at an early age — and death. 

Their arteries had been bathing in high LDL cholesterol since birth. In several patients, even typical cholesterol-lowering drugs couldn’t get the levels “even remotely under control,” says Andrew Bellinger, a cardiologist and chief scientific officer at Verve Therapeutics, a Boston-based biotechnology company. 

Now, his team has tried a new approach: a genetic medicine called VERVE-101 designed to turn off a cholesterol-raising gene. Using a kind of molecular pencil, the medicine erases one DNA letter and writes in another, inactivating the gene. A single genetic change. A single medication. A potential treatment that lasts a lifetime.

That’s the hope, anyway. Bellinger presented the results of a small clinical trial called heart-1 at the American Heart Association meeting in November. VERVE-101 successfully lowered LDL cholesterol, Bellinger reported. It’s the first time anyone has shown that a DNA spelling change made inside a person’s body could have such an effect. “We can achieve clinically meaningful LDL reductions with a single dose,” he said.

People with familial hypercholesterolemia have lifelong symptoms, so “this whole concept of ‘one and done’ is really amazing,” says Pam Taub, a cardiologist at the University of California, San Diego who was not involved with the trial. These patients must take medications their entire lives. An infused drug like VERVE-101 — designed to alter a person’s DNA — could change treatment strategy. 

Taub points out questions about VERVE-101’s safety. One trial patient had a heart attack. Another died due to cardiac arrest. But that death was not related to treatment, Bellinger said.

Moving forward, establishing VERVE-101’s safety is crucial, agreed Karol Watson, a cardiologist at the David Geffen School of Medicine at UCLA who wasn’t involved with the new work. Editing people’s DNA to lower their cholesterol “is a strategy that could be revolutionary, but we have to make sure it’s safe,” she said at the meeting. “You are changing the genome forever.”

Here’s what we know about four key aspects of the new medicine and its history.   

VERVE-101 relies on a DNA-modifying protein called a base editor  

The composition of VERVE-101 is simple. It’s just two types of RNA molecules — molecular cousins of DNA — bundled inside a bubble of fat. 

Infused into the bloodstream, the drug travels to the liver and slips into cells. One of the RNA molecules tells cells to build a protein called an adenine base editor. The other acts as a genetic GPS, guiding the editor protein to the correct stretch of DNA.

The technology is CRISPR 2.0. First generation CRISPR/Cas9 tools act like molecular scissors and can disrupt genes by snipping through DNA’s strands (SN: 8/14/19). Base editors are more like molecular pencils. They edit DNA by performing chemistry on an individual DNA letter, or base, rewriting one for another, creating a new genetic sequence (SN: 10/25/17). 

“Base editors actually change a sequence that you choose into a different sequence of your choosing,” says Howard Hughes Medical Institute investigator David Liu, a chemist at Harvard University whose team invented the technology in 2016. In the case of VERVE-101, that sequence is inside the PCSK9 gene, which encodes instructions for manufacturing a protein that raises blood cholesterol levels. Just one edit in a precise location shuts PCSK9 down.

Editing wraps up less than a week after the infusion, and the drug breaks down rapidly, Bellinger said. Both the fat bubble, called a lipid nanoparticle, and its RNA cargo degrade, and within a few weeks, VERVE-101 vanishes from the body. “The only thing that’s left is the DNA change you made to the PCSK9 gene,” he said. 

PCSK9 is a tempting target for gene-editing therapy 

PCSK9 has been a hot therapeutic target for the last decade or so, says Parag Joshi, a preventive cardiologist at UT Southwestern Medical Center in Dallas who was not part of the trial. 

Researchers knew that some people have PCSK9 mutations that switch the gene off. These people tended to have lower levels of LDL cholesterol — and drastically less heart disease, geneticist Helen Hobbs, an HHMI investigator at UT Southwestern Medical Center, and colleagues reported in 2006.

That landmark study pushed the field forward, Joshi says. Suddenly, scientists had proof that people could live healthy lives when PCSK9 was inactivated. That made it “a very attractive drug target,” Joshi says. It suggested that disabling PCSK9 would do no harm — and could even help, by lowering the risk of heart disease.  

Typically, the PCSK9 protein breaks down another protein called the LDL receptor. This receptor is one of the good guys; it keeps bad cholesterol in check by snatching it from the blood and transporting it into liver cells for disposal. Without enough LDL receptors, LDL cholesterol levels in the blood ratchet up. 

Sekar Kathiresan, a cardiologist and Verve’s CEO and cofounder puts it succinctly: PCSK9 causes disease. “If you turn it off, all you get is health.”

Today, a few existing therapies target PCSK9, including injected antibodies or an RNA-based drug that shuts down production of the protein. Patients should take a daily statin pill to lower LDL cholesterol, Joshi says. But it’s often not enough. 

And though the therapies are theoretically effective for people with familial hypercholesterolemia, Kathiresan says, “very few patients are actually on these medications.”

His team thinks that’s because the current approach is just too heavy a burden — asking patients to take daily pills or intermittent injections for decades. “That model doesn’t seem to be working,” Kathiresan says. “And that’s what we’re trying to fix.” 

Early VERVE-101 clinical trial results reveal potential benefits — and risks 

Kathiresan’s team gave a single IV infusion of VERVE-101 to 10 people with heterozygous familial hypercholesterolemia, most of whom had severe heart disease. In those who received the highest drug doses tested, blood levels of LDL cholesterol dropped sharply, by 39 to 55 percent. And the drop appears long-lasting, Bellinger said. For the patient at the highest dose, LDL cholesterol levels held steady for 180 days after VERVE-101 infused into the bloodstream. 

Bellinger called the results “pretty much what we expected and planned,” given the team’s earlier results in nonhuman primates. But the new patient data, though preliminary, places the drug on the precipice of something bigger. “This opens the door for an entirely new way to treat heart disease,” Kathiresan says.  

VERVE-101’s utility will ultimately depend on its safety. During the trial, the team spotted some potential red flags. Four patients had minor reactions to the IV infusion, including headache and mild fever. But at the heart meeting, attention hummed over something more severe. A day after the infusion, one patient had a heart attack. Five weeks after the infusion, a different patient died when their heart suddenly stopped beating. 

That incident was probably caused by the patients’ underlying heart disease, Kathiresan says. That’s the conclusion reached by an independent data safety monitoring board that investigated the cases, he says. 

The heart attack, however, may have been related to the treatment, because it happened so soon after dosing, the monitoring board determined. Kathiresan notes, though, that the patient had been experiencing chest pains prior to the study, something they didn’t mention to the study’s investigators.

These are “very, very sick patients,” says UCSD cardiologist Taub. For future trials with the drug, she thinks such patients should be excluded.

Kathiresan’s team is now planning to enroll patients with less-advanced disease. They’re also going to check for blockages in patients’ arteries, to try and avoid including people at extremely high risk of heart attack.

“This opens the door for an entirely new way to treat heart disease.”

Sekar Kathiresan, Verve Therapeutics CEO and cofounder

In 2024, the company plans to enroll more patients at the two highest doses to determine which dose to move forward. The researchers are also testing a second version of the drug, VERVE-102, which uses a different lipid nanoparticle. Depending on those results, Verve plans to move one of the drugs on to a larger clinical trial in 2025. And if successful in people with familial hypercholesterolemia, the company intends to expand to an even broader group of patients, including those without the genetic disorder.

Developing new medicines is a long road, Kathiresan says. It can take more than a decade for a drug to go from a concept to a medication that doctors can prescribe, he says. Verve started its PCSK9-editing project in 2018. Kathiresan says he hopes to have an approved medication by the end of the decade. 

VERVE-101 is one of several base editing drugs currently in clinical trials

One potential side effect of gene-editing therapies is unintentional tweaks to DNA. VERVE-101 targets PCSK9, but what if it strays to a different spot in the genome, asks Anne Goldberg, an endocrinologist at Washington University School of Medicine in St. Louis. The technology “looks really interesting,” she says, “but we need more data.”

A DNA change at the wrong spot could put people at risk of developing cancer. With VERVE-101, Bellinger said, “we think that risk is very low.” Most of the company’s work, he said, goes into demonstrating that “we do not make edits elsewhere in the genome.” 

Today’s base editors — including the one in VERVE-101 — are much improved since the early days of the technology, says Harvard’s Liu, who was not involved with the trial. They “have very high on-target editing efficiency while also having minimal off-target editing.” 

Currently, five other base-editing clinical trials targeting other diseases, like sickle-cell disease and leukemia, are ongoing. Liu is hopeful that the gene-editing agents will give patients “a completely new lease on life.” 

Bellinger said his team thinks of VERVE-101 as a one-time procedure for health, like “molecular surgery without a scalpel.” In theory, it’s possible to reverse the edit made by VERVE-101, but it’s not what he and his colleagues envision. 

For cardiologist Donald Lloyd-Jones, who was not involved with the trial, the dream is to offer people with familial hypercholesterolemia a treatment that doesn’t rely on taking a statin pill every single day. A therapy like VERVE-101 “might be something they really consider as an option,” said Lloyd-Jones, of Northwestern University Feinberg School of Medicine in Chicago.

“If we get those safety data, if we get those efficacy data,” he said at the meeting, “I think this would be a very interesting approach to a lifetime fix.”

This year’s United Nations’ annual climate summit, dubbed COP28, is making a lot of headlines — not something I would have found myself writing a few years ago.

One reason for COP’s higher profile is a growing sense of urgency to take stronger action to reduce humans’ fossil fuel emissions and mitigate the looming climate crisis. The world is nowhere near on track to meet the goals of the 2015 Paris Agreement — that is, reducing greenhouse gas emissions sufficiently to limit global warming to “well below” 2 degrees Celsius of preindustrial averages by the year 2100 (SN: 12/12/15). Meanwhile, 2023 has been the hottest year on record, people have been suffering through a barrage of extreme weather events, including heat waves, droughts and floods, and 2024 is likely to break more temperature records (SN: 12/6/23; SN: 7/19/23).

The headlines emerging from COP28 have been a mix of pleasing, frustrating and bewildering. For example: It’s good news that 198 nations have ratified the Loss and Damage Fund, a formal acknowledgment by wealthy, high-polluting nations that they should help mitigate the rising costs of climate change faced by developing nations. But it’s frustrating that the pledges by the wealthy nations so far amount to just about $725 million, less than 0.2 percent of the annual climate change–linked losses faced by developing nations.

For me, one of the biggest questions related to those headlines pertains to methane. It feels unclear whether, on balance, there’s more good or bad news when it comes to emissions of that second most important human-caused greenhouse gas.

Methane is a powerhouse climate-warming gas, with about 80 times the atmosphere-warming potential of carbon dioxide. However, methane has a saving grace: It mercifully lingers for only about a decade in the atmosphere (SN: 4/22/20). Carbon dioxide can stick around for up to 1,000 years. Cutting methane emissions can mean its atmospheric concentration drops relatively rapidly.

The Global Methane Pledge, launched two years ago at COP26, may be gaining some momentum, but it still lacks the sign-on of key big-emitting nations. Then there’s the December 1 announcement by 49 oil and gas companies that they would reduce methane leaks from their infrastructure to “near zero” by 2030, which seems like a good thing on the face of it but has also been called greenwashing (SN: 11/24/21).

And all of this policy wrangling is happening against a bizarre backdrop: a startling, puzzling, worrisome sharp increase in methane emissions over the last decade — not from humans, but from natural sources, particularly wetlands.

To help me sift through the headlines and better understand all the news that’s seeping out, I talked with Euan Nisbet, a geochemist at Royal Holloway, University of London in Egham.

Methane “is rising very fast,” Nisbet says. “So fast it looks like the Paris Agreement is going to fail.”

Countries are promising to cut methane emissions

While the rise in natural methane emissions is worrisome, about 60 percent of current methane emissions into the atmosphere still comes from human activities. Methane doesn’t just seep out of leaky oil and gas pipelines or get pumped into the air during coal combustion. Agriculture, including ruminant animals, are a big source (SN: 5/5/22). Landfills are another (SN: 11/14/19).

That’s where the Global Methane Pledge comes in, promising a 30 percent cut in humans’ emissions by 2030. The pledge was spearheaded in 2021 by the United States and the European Union, and so far, 150 nations have signed on. Most recently, Turkmenistan, which has sizable methane emissions, joined. So there’s hope: If everyone were to follow suit, it really is possible to cut global methane emissions deeply, bringing us much closer to meeting the Paris Agreement’s goals, Nisbet argues in a Dec. 8 editorial in Science.

Still, many of the world’s biggest methane emitters, including China, India, Russia, Iran and South Africa, have not signed on to the pledge. China’s methane comes in large part from its coal combustion; India’s, from coal as well as waste heaps and biomass fires. And China alone currently releases an estimated 65 million metric tons of methane per year, more than double that of the United States or India, the next two biggest emitters.

With only seven years left before the 2030 deadline, meeting the global pledge’s methane reduction goals would be steep — but, Nisbet says, not impossible.

There’s precedent for successfully making such steep cuts to methane in such a short time, he adds. During the 2000s, “there was a seven-year period where [the U.K. government] brought methane emissions down by 30 percent,” in large part by reducing emissions from landfills and gas leaks.

China has just released its own Methane Emissions Control Action Plan in November, alongside a joint commitment between China and the United States to take action on methane. That news sounds potentially promising, if not wholly reassuring, as the plan does not include a lot of concrete numbers, Nisbet says.

So, what about the oil and gas industry’s recent promise to address its leaky infrastructure? Such a promise also sounds positive on the face of it — leaky infrastructure is definitely the low-hanging fruit when it comes to reducing humans’ methane emissions to the atmosphere (SN: 2/3/22).

On the other hand, hundreds of scientific and environmental organizations have signed an open letter in response. The letter suggests that the oil and gas industry’ promise is just greenwashing, “a smokescreen to hide the reality that we need to phase out oil, gas and coal,” the letter states. Furthermore, many oil and gas companies may routinely abandon old, still-leaking wells — effectively eliminating those leaks from their company’s emissions roster without actually stopping them.

That said, addressing the leaks does have to be done, Nisbet says. “I’d love to shut down the coal industry quickly, but I’m aware of the enormous social problems that brings. It’s a very difficult thing to nuance. You can’t go cold turkey. We’ve got to wind it down in an intelligent and collaborative way. The best thing to do is to stop the crazy leaks and venting.”

Natural methane emission has been surging

Plugging the leaks as soon as possible has taken on an increasing urgency, Nisbet says, because of a stark rise in natural methane being emitted to the atmosphere. Why this rise is happening isn’t clear, but it seems to be some sort of climate change–related feedback, perhaps linked to changes in both temperature and precipitation.

That natural methane emissions bump was also not something that the architects of the Paris Agreement saw coming. Most of that rise has happened since the agreement was signed. From 1999 to 2006, atmospheric methane had spent several years in near-equilibrium — elevated due to human activities, but relatively stable. Then, in 2007, atmospheric methane concentrations began to increase. In 2013, there was a particularly sharp rise, and then again in 2020.

Much of that increase seems to have come from tropical wetlands. Over the past decade, researchers have tracked shifts in methane sources by measuring carbon-12 and carbon-13 in the gas. The ratio of those two forms of carbon in the methane varies significantly depending on the source of the gas. Fossil fuel-derived methane tends to have higher concentrations of carbon-13 relative to carbon-12; methane from wetlands or agriculture tends to be more enriched in carbon-12.

The recent spikes in natural methane are eerily reminiscent of ice core records of “glacial termination” events, times in Earth’s deep past when the world abruptly shifted from a glacial period to a period of rapid warming, Nisbet and others reported in June in Global Biogeochemical Cycles. Such glacial termination events are large-scale reorganizations of the ocean-atmosphere system, involving dramatic changes to the circulation of the global ocean, as well as to large climate patterns like the Indian Ocean Dipole (SN: 1/9/20).

“Is this comparable to the start of a termination event? It looks horribly like that,” Nisbet says. But “it may not be. It might be totally innocent.”

Right now, scientists are racing to understand what’s happening with the natural methane bump, and how exactly the increased emissions might be linked to climate change. But as we search for those answers, there is something that humans can and must do in the meantime, he says: Cut human emissions of the gas as much as possible, as fast as possible. “It’s very simple. When you’re in a hole, stop digging.”

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