For weeks, I have been watching coronavirus cases drop across the United States. At the same time, cases were heading skyward in many places in Europe, Asia and Oceania. Those surges may have peaked in some places and seem to be on a downward trajectory again, according to Our World in Data.

Much of the rise in cases has been attributed to the omicron variant’s more transmissible sibling BA.2 clawing its way to prominence. But many public health officials have pointed out that the surges coincide with relaxing of COVID-19 mitigation measures.

People around the world are shedding their masks and gathering in public. Immunity from vaccines and prior infections have helped limit deaths in wealthier countries, but the omicron siblings are very good at evading immune defenses, leading to breakthrough infections and reinfections. Even so, at the end of February, the U.S. Centers for Disease Control and Prevention posted new guidelines for masking, more than doubling the number of cases needed per 100,000 people before officials recommended a return to the face coverings (SN: 3/3/22).

Not everyone has ditched their masks. I have observed some regional trends. The majority of people I see at my grocery store and other places in my community in Maryland are still wearing masks. But on road trips to the Midwest and back, even during the height of the omicron surge, most of the faces I saw in public were bare. Meanwhile, I was wearing my N95 mask even when I was the only person doing so. I reasoned that I was protecting myself from infection as best I could. I was also protecting my loved ones and other people around me from me should I have unwittingly contracted the virus.

But I will tell you a secret. I don’t really like wearing masks. They can be hot and uncomfortable. They leave lines on my face. And sometimes masks make it hard to breathe. At the same time, I know that wearing a good quality, well-fitting mask greatly reduces the chance of testing positive for the coronavirus (SN: 2/12/21). In one study, N95 or KN95 masks reduced the chance of testing positive by 83 percent, researchers reported in the February 11 Morbidity and Mortality Weekly Report. And school districts with mask mandates had about a quarter of the number of in-school infections as districts where masks weren’t required (SN: 3/15/22).

With those data in mind, I am not ready to go barefaced. And I’m not alone. Nearly 36 percent of the 1,916 respondents to a Science News Twitter poll said that they still wear masks everywhere in public. Another 28 percent said they mask in indoor crowds, and 23 percent said they mask only where it’s mandatory. Only about 12 percent have ditched masks entirely.

Some poll respondents left comments clarifying their answers, but most people’s reasons for masking aren’t clear. Maybe they live in the parts of the country or world where transmission levels are high and hospitals are at risk of being overrun. Maybe they are parents of children too young for vaccination. Perhaps they or other loved ones are unvaccinated or have weakened immune systems that put them at risk for severe disease. Maybe, like me, they just don’t want to get sick — with anything.

Before the pandemic, I caught several colds a year and had to deal with seasonal allergies. Since I started wearing a mask, I haven’t had a single respiratory illness, though allergies still irritate my eyes and make my nose run. I’ve also got some health conditions that raise my risk of severe illness. I’m fully vaccinated and boosted, so I probably won’t die if I catch the virus that causes COVID-19, but I don’t want to test it (SN: 11/8/21). Right now, I just feel safer wearing a mask when I’m indoors in public places.

I’ve been thinking a lot about what would convince me that it was safe to go maskless. What is the number or metric that will mark the boundary of my comfort zone?

The CDC now recommends using its COVID-19 Community Levels map for determining when mask use is needed. That metric is mostly concerned with keeping hospitals and other health care systems from becoming overwhelmed. By that measure, most of the country has the green light to go maskless. I’m probably more cautious than the average person, but the levels of transmission in that metric that would trigger mask wearing — 200 or more cases per 100,000 population — seem high to me, particularly since CDC’s prior recommendations urged masking at a quarter of that level.

The metric is designed for communities, not individuals. So what numbers should I, as an individual, go by? There’s always the CDC’s COVID-19 Integrated County View that tracks case rates and test positivity rates — the percentage of tests that have a positive result. Cases in my county have been ticking up in the last few days, with 391 people having gotten COVID-19 in the last week — that’s about 37 out of every 100,000 people. That seems like relatively low odds of coming into contact with a contagious person. But those are only the cases we know about officially. There may be many more cases that were never reported as people take rapid antigen tests at home or decide not to test. There’s no way to know exactly how much COVID-19 is out there.

And the proportion of cases caused by BA.2 is on the rise, with the more infectious omicron variant accounting for about 35 percent of cases nationwide in the week ending March 19. In the mid-Atlantic states where I live, about 30 percent of cases are now caused by BA.2. But in some parts of the Northeast, that variant now causes more than half of cases. The increase is unsettling but doesn’t necessarily mean the United States will experience another wave of infections as Europe has. Or maybe we will. That uncertainty makes me uncomfortable removing my mask indoors in public right now.

Maybe in a few weeks, if there’s no new surge in infections, I’ll feel comfortable walking around in public with my nose and mouth exposed. Or maybe I’ll wait until the number of cases in my county is in single digits. I’m pretty sure there will come a day when I won’t feel the need to filter every breath, but for me, it’s not that time yet. And I truthfully can’t tell you what my magic number will be.

Here’s what I do know: Even if I do decide to have an unmasked summer, I will be strapping my mask back on if COVID-19 cases begin to rise again.

The sperm whale is an endangered species. A major reason is that the whale oil is heat-resistant and chemically and physically stable. This makes it useful for lubricating delicate machinery. The only substitute is expensive carnauba wax from the leaves of palm trees that grow only in Brazil … [but] wax from the seeds of the jojoba, an evergreen desert shrub, is nearly as good.

Update
After sperm whale oil was banned in the early 1970s, the United States sought to replenish its reserves with eco-friendly oil from jojoba seeds (SN: 5/17/75, p. 335). Jojoba oil’s chemical structure is nearly identical to that of sperm whale oil, and the shrub is native to some North American desert ecosystems, making the plant an appealing replacement. Today, jojoba shrubs are cultivated around the world on almost every continent. Jojoba oil is used in hundreds of products, including cosmetics, pharmaceuticals, adhesives and lubricants. Meanwhile, sperm whale populations have started to recover under international anti-whaling agreements (SN: 2/27/21, p. 4).

Surviving on blood alone is no picnic. But a handful of genetic tweaks may have helped vampire bats evolve to become the only mammal known to feed exclusively on the stuff.

These bats have developed a range of physiological and behavioral strategies to exist on a blood-only diet. The genetic picture behind this sanguivorous behavior, however, is still blurry. But 13 genes that the bats appear to have lost over time could underpin some of the behavior, researchers report March 25 in Science Advances.

“Sometimes losing genes in evolutionary time frames can actually be adaptive or beneficial,” says Michael Hiller, a genomicist now at the Senckenberg Society for Nature Research in Frankfurt.
Hiller and his colleagues pieced together the genetic instruction book of the common vampire bat (Desmodus rotundus) and compared it with the genomes of 26 other bat species, including six from the same family as vampire bats. The team then searched for genes in D. rotundus that had either been lost entirely or inactivated through mutations.

Of the 13 missing genes, three had been previously reported in vampire bats. These genes are associated with sweet and bitter taste receptors in other animals, meaning vampire bats probably have a diminished sense of taste — all the better for drinking blood. The other 10 lost genes are newly identified in the bats, and the researchers propose several ideas about how the absence of these genes could support a blood-rich diet.

Some of the genes help to raise levels of insulin in the body and convert ingested sugar into a form that can be stored. Given the low sugar content of blood, this processing and storage system may be less active in vampire bats and the genes probably aren’t that useful anymore. Another gene is linked in other mammals to gastric acid production, which helps break down solid food. That gene may have been lost as the vampire bat stomach evolved to mostly store and absorb fluid.

One of the other lost genes inhibits the uptake of iron in gastrointestinal cells. Blood is low in calories yet rich in iron. Vampire bats must drink up to 1.4 times their own weight during each feed, and, in doing so, ingest a potentially harmful amount of iron. Gastrointestinal cells are regularly shed in the vampire bat gut, so by losing that gene, the bats may be absorbing huge amounts of iron and quickly excreting it to avoid an overload — an idea supported by previous research.

One lost gene could even be linked to vampire bats’ remarkable cognitive abilities, the researchers suggest. Because the bats are susceptible to starvation, they share regurgitated blood and are more likely to do so with bats that previously donated to themselves (SN: 11/19/15). Vampire bats also form long-term bonds and even feed with their friends in the wild (SN: 10/31/19; SN: 9/23/21). In other animals, this gene is involved in breaking down a compound produced by nerve cells that is linked to learning and memory — traits thought to be necessary for the vampire bats’ social abilities.

“I think there are some compelling hypotheses there,” says David Liberles, an evolutionary genomicist at Temple University in Philadelphia who wasn’t involved in the study. It would be interesting to see if these genes were also lost in the other two species of vampire bats, he says, as they feed more on the blood of birds, while D. rotundus prefers to imbibe from mammals.

Whether the diet caused these changes, or vice versa, isn’t known. Either way, it was probably a gradual process over millions of years, Hiller says. “Maybe they started drinking more and more blood, and then you have time to better adapt to this very challenging diet.”

Higher and higher still, the cotton bollworm moth caterpillar climbs, its tiny body ceaselessly scaling leaf after leaf. Reaching the top of a plant, it will die, facilitating the spread of the virus that steered the insect there.

One virus behind this deadly ascent manipulates genes associated with caterpillars’ vision. As a result, the insects are more attracted to sunlight than usual, researchers report online March 8 in Molecular Ecology.

The virus involved in this caterpillar takeover is a type of baculovirus. These viruses may have been evolving with their insect hosts for 200 million to 300 million years, says Xiaoxia Liu, an entomologist at China Agricultural University in Beijing. Baculoviruses can infect more than 800 insect species, mostly the caterpillars of moths and butterflies. Once infected, the hosts exhibit “tree-top disease,” compelled to climb before dying and leaving their elevated, infected cadavers for scavengers to feast upon.
The clever trick of these viruses has been known for more than a century, Liu says. But how they turn caterpillars into zombies doomed to ascend to their own deaths wasn’t understood.

Previous research suggested that infected caterpillars exhibit greater “phototaxis,” meaning they are more attracted to light than uninfected insects. Liu and her team confirmed this effect in the laboratory using cotton bollworm moth caterpillars (Helicoverpa armigera) infected with a baculovirus called HearNPV.

The researchers compared infected and uninfected caterpillars’ positions in glass tubes surrounding a climbing mesh under an LED light. Uninfected caterpillars would wander up and down the mesh, but would return to the bottom before pupating. That behavior makes sense because in the wild, this species develops into adults underground. But infected hosts would end up dead at the top of the mesh. The higher the source of light, the higher infected hosts climbed.

The team moved to the horizontal plane to confirm that the hosts were responding to light rather than gravity, placing caterpillars in a hexagonal box with one of the side panels illuminated. By the second day after infection, host caterpillars crawled to the light about four times as often as the uninfected.

When the researchers surgically removed infected caterpillars’ eyes and put the insects in the box, the blinded insects were attracted to the light a quarter as often as unaltered infected hosts. That suggested that the virus was using a caterpillar’s vision against itself.

The team then compared how active certain genes were in various caterpillar body parts in infected and uninfected larvae. Detected mostly in the eyes, two genes for opsins, the light-sensitive proteins that are fundamental for vision, were more active after an infection with the virus, and so was another gene associated with vision called TRPL. It encodes for a channel in cell membranes involved in the conversion of light into electrical signals.

When the team used the gene-editing tool CRISPR/Cas9 to shut off the opsin genes and TRPL in infected caterpillars, the number of hosts attracted to the light in the box was cut roughly in half. Their height at death on the mesh was also reduced.

Baculoviruses appear capable of commandeering the genetic architecture of caterpillar vision, exploiting an ancient importance of light for insects, Liu says.

Light can cue crucial biological processes in insects, from directing their developmental timing, to setting their migration routes.

These viruses were already known to be master manipulators in other ways, tweaking their hosts’ sense of smell, molting patterns and the programmed death of cells, says Lorena Passarelli, a virologist at Kansas State University in Manhattan, who was not involved with the study. The new research shows that the viruses manipulate “yet another physiological host process: visual perception.”

There’s still a lot to learn about this visual hijacking, Passarelli says. It’s unknown, for instance, which of the virus’s genes are responsible for turning caterpillars into sunlight-chasing zombies in the first place.

Human language, in its many current forms, may owe an evolutionary debt to our distant ape ancestors who sounded off in groups of scattered individuals.

Wild orangutans’ social worlds mold how they communicate vocally, much as local communities shape the way people speak, researchers report March 21 in Nature Ecology & Evolution. This finding suggests that social forces began engineering an expanding inventory of communication sounds among ancient ancestors of apes and humans, laying a foundation for the evolution of language, say evolutionary psychologist Adriano Lameira, of the University of Warwick in England, and his colleagues.

Lameira’s group recorded predator-warning calls known as “kiss-squeaks” — which typically involve drawing in breath through pursed lips — of 76 orangutans from six populations living on the islands of Borneo and Sumatra, where they face survival threats (SN: 2/15/18). The team tracked the animals and estimated their population densities from 2005 through 2010, with at least five consecutive months of observations and recordings in each population. Analyses of recordings then revealed how much individuals’ kiss-squeaks changed or remained the same over time.
Orangutans in high-density populations, which up the odds of frequent social encounters, concoct many variations of kiss-squeaks, the researchers report. Novel reworkings of kiss-squeaks usually get modified further by other orangutans or drop out of use in crowded settings, they say.

In spread-out populations that reduce social mingling, these apes produce relatively few kiss-squeak variants, Lameira’s group finds. But occasional kiss-squeak tweaks tend to catch on in their original form in dispersed groups, leading to larger call repertoires than in high-density populations.

Low-density orangutan groups — featuring small clusters of animals that occasionally cross paths — might mirror the social settings of human ancestors. Ancient apes and hominids also lived in dispersed groups that could have bred a growing number of ways to communicate vocally, the researchers suspect.

Some bacteria carry tiny syringes filled with chemicals that may thin out competitors or incapacitate predators. Now, researchers have gotten up-close views of these syringes, technically known as contractile injection systems, from a type of cyanobacteria and a marine bacterium.

Figuring out how key parts of the molecular syringes work may help scientists devise their own nanomachines. Artificial injection machines could direct antibiotics against troublesome bacteria while leaving friendly microbes untouched.

Genes encoding pieces of the injection machinery are found in many bacterial species. But, “just by looking at the genes, it’s quite hard to predict how these contractile injection systems work,” says Gregor Weiss, a cellular structural biologist at ETH Zurich.
So Weiss and colleagues examined bacterial syringes using cryo-electron microscopy, in which cells are flash frozen to capture cellular structures as they typically look in nature (SN: 6/22/17).

Previously, researchers have found syringes anchored in some bacteria’s outer membranes, where the bacteria can shoot their payload into cells they bump into. Other species’ injectors squirt their contents into the environment.

But in a type of cyanobacteria called Anabaena, the syringes are in an unusual place, nestled in the membrane of the internal structure where the bacteria carry out photosynthesis, Weiss and colleagues report in the March Nature Microbiology. Buried inside the cells, “it’s hard to imagine how [the syringes] could get out and interact with the target organism,” Weiss says.
Anabaena may use its syringes against itself to trigger programmed cell death when the cyanobacteria come under stress. In the team’s experiments, ultraviolet light or high salt levels in water triggered some syringes to dump their payload. That led to the death of some Anabaena cells in the long chains that the cyanobacteria grow in, forming hollow “ghost cells.”

Ghost cells shed their outer wall and membrane, exposing unfired syringes in the inner membrane to the outside. The ghosts may act like Trojan horses, delivering their deadly payload to predators or competitors, the team hypothesizes. The researchers haven’t yet found which organisms are the probable targets of Anabaena’s syringes.

Inside a type of marine bacteria called Algoriphagus machipongonensis, the story is a bit different. Here, the syringes have a different architecture and float unmoored within the bacterial cell, ETH Zurich’s Charles Ericson and colleagues report in the March Nature Microbiology. The injectors are also found in the liquid in which the bacteria are grown in the laboratory, but how they get out of the cell is a mystery. Perhaps they are released when the bacteria die or get eaten by a predator, Ericson says.

The team also found two proteins loaded inside the Algoriphagus’ syringes, but what those proteins do isn’t known. The researchers tried genetically engineering E. coli to produce one of the proteins, but it kills the bacteria, says study coauthor Jingwei Xu, also at ETH Zurich.
Comparing the structures of syringes from various species, the researchers identified certain structures within the machines that are similar, but slightly different from species to species. Learning how those modifications change the way the injectors work may allow researchers to load different cargoes into the tubes or target the syringes against specific bacteria or other organisms. “Now we have the general blueprint,” Ericson says, “can we re-engineer it?”

More than 2,000 years ago, Hippocrates, the Greek physician often considered the father of modern medicine, identified what came to be known as the clitoris, a “little pillar” of erectile tissue near the vagina’s entrance. Aristotle then noticed that the seemingly small structure was related to sexual pleasure.

Yet it wasn’t until 2005 that urologist Helen O’Connell uncovered that the “little pillar” was just the tip of the iceberg. The internal parts of the organ reach around the vagina and go into the pelvis, extending a network of nerves deeper than anatomists ever knew.

It took millennia to uncover the clitoris’s true extent because sexism has long stymied the study of female biology, science journalist Rachel E. Gross argues in her new book, Vagina Obscura. Esteemed men of science, from Charles Darwin to Sigmund Freud, viewed men as superior to women. To be male was to be the ideal standard. To be female was to be a stunted version of a human. The vagina, the ancient Greeks concluded, was merely a penis turned inside out, the ovaries simply interior testicles.

Because men mostly considered women’s bodies for their reproductive capabilities and interactions with penises, only recently have researchers begun to truly understand the full scope of female organs and tissues, Gross shows. That includes the basic biology of what “healthy” looks like in these parts of the body and their effects on the body as a whole.

Vagina Obscura itself was born out of Gross’ frustration at not understanding her own body in the wake of a vaginal infection. After antibiotics and antifungal treatments failed due to a misdiagnosis, her gynecologist prescribed another treatment. As Gross paraphrases, the doctor told her to “shove rat poison up my vagina.” The infection, it turned out, was bacterial vaginosis, a hard-to-treat, sometimes itchy and painful condition caused by an overgrowth of bacteria that normally reside in the vagina. (The rat poison was boric acid, which is also an antiseptic. “It’s basically rat poison,” the doctor said. “You’re going to see that on the internet, so I might as well tell you now.”)
The book’s exploration of female anatomy begins from the outside in, first traversing the clitoris’s nerve-filled external nub to the vagina, ovaries and uterus. The last chapter focuses on gender affirmation surgery, detailing how physicians have transformed the field for transgender people. (Gross is up-front that words such as women and men create an artificial binary, with seemingly more objective terms like “male” and “female” not performing much better in encompassing humankind’s diversity, including intersex and transgender people.)

Throughout this tour, Gross doesn’t shy away from confronting the sexism and prejudices behind controversial ideas about female biology, such as vaginal orgasms (versus coming from the clitoris) and the existence of the G-spot (SN: 4/25/12). Both “near-mystical” concepts stem from the male perspective that sexual pleasure should be straightforward for women, if only men could hit the right spot. Nor are the more appalling offenses swept under the rug, including racism, eugenics and female genital cutting. Footnotes throughout the book detail Gross’ efforts to navigate controversial views and stigmatizing or culturally charged terminology.

To lift readers’ spirits, she finds the right spots to deliver a dose of wry humor or a pun. She also shares stories of often forgotten researchers, such as lab technician Miriam Menkin, who showed in 1944 that in vitro fertilization is possible (SN: 8/12/44). Yet Menkin’s role in describing the first instance of a human egg being fertilized in a lab dish has largely been erased from IVF’s history (SN: 6/9/21). There’s also plenty of opportunity to marvel at the power of the female body. Despite the long-held notion that a person is born with all the eggs they’ll ever have, for example, researchers are now discovering the ovary’s regenerative properties.

Studying female bodies more closely could ultimately improve quality of life. Chasing cells capable of producing more eggs might bring about discoveries that could restore the menstrual cycle in cancer patients rendered infertile by chemotherapy or make menopause less miserable. Patients with endometriosis, a painful disorder in which uterine tissue grows outside the uterus, are often dismissed and their symptoms downplayed. Some doctors even recommend getting pregnant to avoid the pain. But people shouldn’t have to suffer just because they aren’t pregnant. Researchers just haven’t asked the right questions yet about the uterus or endometriosis, Gross argues.

Vagina Obscura reinforces that female bodies are more than “walking wombs” or “baby machines.” Understanding these organs and tissues is important for keeping the people who have them healthy. It will take a lot of vagina studies to overcome centuries of neglect, Gross writes. But the book provides a glimpse into what is possible when researchers (finally) pay attention.

It was the mid-1980s, at a meeting in Switzerland, when Wally Broecker’s ears perked up. Scientist Hans Oeschger was describing an ice core drilled at a military radar station in southern Greenland. Layer by layer, the 2-kilometer-long core revealed what the climate there was like thousands of years ago. Climate shifts, inferred from the amounts of carbon dioxide and of a form of oxygen in the core, played out surprisingly quickly — within just a few decades. It seemed almost too fast to be true.

Broecker returned home, to Columbia University’s Lamont-Doherty Earth Observatory, and began wondering what could cause such dramatic shifts. Some of Oeschger’s data turned out to be incorrect, but the seed they planted in Broecker’s mind flowered — and ultimately changed the way scientists think about past and future climate.

A geochemist who studied the oceans, Broecker proposed that the shutdown of a major ocean circulation pattern, which he named the great ocean conveyor, could cause the North Atlantic climate to change abruptly. In the past, he argued, melting ice sheets released huge pulses of water into the North Atlantic, turning the water fresher and halting circulation patterns that rely on salty water. The result: a sudden atmospheric cooling that plunged the region, including Greenland, into a big chill. (In the 2004 movie The Day After Tomorrow, an overly dramatized oceanic shutdown coats the Statue of Liberty in ice.)
It was a leap of insight unprecedented for the time, when most researchers had yet to accept that climate could shift abruptly, much less ponder what might cause such shifts.

Broecker not only explained the changes seen in the Greenland ice core, he also went on to found a new field. He prodded, cajoled and brought together other scientists to study the entire climate system and how it could shift on a dime. “He was a really big thinker,” says Dorothy Peteet, a paleoclimatologist at NASA’s Goddard Institute for Space Studies in New York City who worked with Broecker for decades. “It was just his genuine curiosity about how the world worked.”

Broecker was born in 1931 into a fundamentalist family who believed the Earth was 6,000 years old, so he was not an obvious candidate to become a pathbreaking geoscientist. Because of his dyslexia, he relied on conversations and visual aids to soak up information. Throughout his life, he did not use computers, a linchpin of modern science, yet became an expert in radiocarbon dating. And, contrary to the siloing common in the sciences, he worked expansively to understand the oceans, the atmosphere, the land, and thus the entire Earth system.

By the 1970s, scientists knew that humans were pouring excess carbon dioxide into the atmosphere, through burning fossil fuels and cutting down carbon-storing forests, and that those changes were tinkering with Earth’s natural thermostat. Scientists knew that climate had changed in the past; geologic evidence over billions of years revealed hot or dry, cold or wet periods. But many scientists focused on long-term climate changes, paced by shifts in the way Earth rotates on its axis and circles the sun — both of which change the amount of sunlight the planet receives. A highly influential 1976 paper referred to these orbital shifts as the “pacemaker of the ice ages.”

Ice cores from Antarctica and Greenland changed the game. In 1969, Willi Dansgaard of the University of Copenhagen and colleagues reported results from a Greenland ice core covering the last 100,000 years. They found large, rapid fluctuations in oxygen-18 that suggested wild temperature swings. Climate could oscillate quickly, it seemed — but it took another Greenland ice core and more than a decade before Broecker had the idea that the shutdown of the great ocean conveyor system could be to blame.
Broecker proposed that such a shutdown was responsible for a known cold snap that started around 12,900 years ago. As the Earth began to emerge from its orbitally influenced ice age, water melted off the northern ice sheets and washed into the North Atlantic. Ocean circulation halted, plunging Europe into a sudden chill, he said. The period, which lasted just over a millennium, is known as the Younger Dryas after an Arctic flower that thrived during the cold snap. It was the last hurrah of the last ice age.

Evidence that an ocean conveyor shutdown could cause dramatic climate shifts soon piled up in Broecker’s favor. For instance, Peteet found evidence of rapid Younger Dryas cooling in bogs near New York City — thus establishing that the cooling was not just a European phenomenon but also extended to the other side of the Atlantic. Changes were real, widespread and fast.

By the late 1980s and early ’90s, there was enough evidence supporting abrupt climate change that two major projects — one European, one American — began to drill a pair of fresh cores into the Greenland ice sheet. Richard Alley, a geoscientist at Penn State, remembers working through the layers and documenting small climatic changes over thousands of years. “Then we hit the end of the Younger Dryas and it was like falling off a cliff,” he says. It was “a huge change after many small changes,” he says. “Breathtaking.”
The new Greenland cores cemented scientific recognition of abrupt climate change. Though the shutdown of the ocean conveyor could not explain all abrupt climate changes that had ever occurred, it showed how a single physical mechanism could trigger major planet-wide disruptions. It also opened discussions about how rapidly climate might change in the future.

Broecker, who died in 2019, spent his last decades exploring abrupt shifts that are already happening. He worked, for example, with billionaire Gary Comer, who during a yacht trip in 2001 was shocked by the shrinking of Arctic sea ice, to brainstorm new directions for climate research and climate solutions.

Broecker knew more than almost anyone about what might be coming. He often described Earth’s climate system as an angry beast that humans are poking with sticks. And one of his most famous papers was titled “Climatic change: Are we on the brink of a pronounced global warming?”

It was published in 1975.

You can never have too much ice cream, but you can have too much ice in your ice cream. Adding plant-based nanocrystals to the frozen treat could help solve that problem, researchers reported March 20 at the American Chemical Society spring meeting in San Diego.

Ice cream contains tiny ice crystals that grow bigger when natural temperature fluctuations in the freezer cause them to melt and recrystallize. Stabilizers in ice cream — typically guar gum or locust bean gum — help inhibit crystal growth, but don’t completely stop it. And once ice crystals hit 50 micrometers in diameter, ice cream takes on an unpleasant, coarse, grainy texture.

Cellulose nanocrystals, or CNCs, which are derived from wood pulp, have properties similar to the gums, says Tao Wu, a food scientist at the University of Tennessee in Knoxville. They also share similarities with antifreeze proteins, produced by some animals to help them survive subzero temperatures. Antifreeze proteins work by binding to the surface of ice crystals, inhibiting growth more effectively than gums — but they are also extremely expensive. CNCs might work similarly to antifreeze proteins but at a fraction of the cost, Wu and his colleagues thought.

An experiment with a sucrose solution — a simplified ice cream proxy — and CNCs showed that after 24 hours, the ice crystals completely stopped growing. A week later, the ice crystals remained at 25 micrometers, well beneath the threshold of ice crystal crunchiness. In a similar experiment with guar gum, ice crystals grew to 50 micrometers in just three days.
“That by itself suggests that nanocrystals are a lot more potent than the gums,” says Richard Hartel, a food engineer at the University of Wisconsin–Madison, who was not involved in the research. If CNCs do function the same way as antifreeze proteins, they’re a promising alternative to current stabilizers, he says. But that still needs to be proven.

Until that happens, you continue to have a good excuse to eat your ice cream quickly: You wouldn’t want large ice crystals to form, after all.