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Google, Microsoft, and Perplexity promote scientific racism in AI search results


AI-powered search engines are surfacing deeply racist, debunked research.

Literal Nazis

LOS ANGELES, CA – APRIL 17: Members of the National Socialist Movement (NSM) salute during a rally on near City Hall on April 17, 2010 in Los Angeles, California. Credit: David McNew via Getty

AI-infused search engines from Google, Microsoft, and Perplexity have been surfacing deeply racist and widely debunked research promoting race science and the idea that white people are genetically superior to nonwhite people.

Patrik Hermansson, a researcher with UK-based anti-racism group Hope Not Hate, was in the middle of a monthslong investigation into the resurgent race science movement when he needed to find out more information about a debunked dataset that claims IQ scores can be used to prove the superiority of the white race.

He was investigating the Human Diversity Foundation, a race science company funded by Andrew Conru, the US tech billionaire who founded Adult Friend Finder. The group, founded in 2022, was the successor to the Pioneer Fund, a group founded by US Nazi sympathizers in 1937 with the aim of promoting “race betterment” and “race realism.”

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Hermansson logged in to Google and began looking up results for the IQs of different nations. When he typed in “Pakistan IQ,” rather than getting a typical list of links, Hermansson was presented with Google’s AI-powered Overviews tool, which, confusingly to him, was on by default. It gave him a definitive answer of 80.

When he typed in “Sierra Leone IQ,” Google’s AI tool was even more specific: 45.07. The result for “Kenya IQ” was equally exact: 75.2.

Hermansson immediately recognized the numbers being fed back to him. They were being taken directly from the very study he was trying to debunk, published by one of the leaders of the movement that he was working to expose.

The results Google was serving up came from a dataset published by Richard Lynn, a University of Ulster professor who died in 2023 and was president of the Pioneer Fund for two decades.

“His influence was massive. He was the superstar and the guiding light of that movement up until his death. Almost to the very end of his life, he was a core leader of it,” Hermansson says.

A WIRED investigation confirmed Hermanssons’s findings and discovered that other AI-infused search engines—Microsoft’s Copilot and Perplexity—are also referencing Lynn’s work when queried about IQ scores in various countries. While Lynn’s flawed research has long been used by far-right extremists, white supremacists, and proponents of eugenics as evidence that the white race is superior genetically and intellectually from nonwhite races, experts now worry that its promotion through AI could help radicalize others.

“Unquestioning use of these ‘statistics’ is deeply problematic,” Rebecca Sear, director of the Center for Culture and Evolution at Brunel University London, tells WIRED. “Use of these data therefore not only spreads disinformation but also helps the political project of scientific racism—the misuse of science to promote the idea that racial hierarchies and inequalities are natural and inevitable.”

To back up her claim, Sear pointed out that Lynn’s research was cited by the white supremacist who committed the mass shooting in Buffalo, New York, in 2022.

Google’s AI Overviews were launched earlier this year as part of the company’s effort to revamp its all-powerful search tool for an online world being reshaped by artificial intelligence. For some search queries, the tool, which is only available in certain countries right now, gives an AI-generated summary of its findings. The tool pulls the information from the Internet and gives users the answers to queries without needing to click on a link.

The AI Overview answer does not always immediately say where the information is coming from, but after complaints from people about how it showed no articles, Google now puts the title for one of the links to the right of the AI summary. AI Overviews have already run into a number of issues since launching in May, forcing Google to admit it had botched the heavily hyped rollout. AI Overviews is turned on by default for search results and can’t be removed without resorting to installing third-party extensions. (“I haven’t enabled it, but it was enabled,” Hermansson, the researcher, tells WIRED. “I don’t know how that happened.”)

In the case of the IQ results, Google referred to a variety of sources, including posts on X, Facebook, and a number of obscure listicle websites, including World Population Review. In nearly all of these cases, when you click through to the source, the trail leads back to Lynn’s infamous dataset. (In some cases, while the exact numbers Lynn published are referenced, the websites do not cite Lynn as the source.)

When querying Google’s Gemini AI chatbot directly using the same terms, it provided a much more nuanced response. “It’s important to approach discussions about national IQ scores with caution,” read text that the chatbot generated in response to the query “Pakistan IQ.” The text continued: “IQ tests are designed primarily for Western cultures and can be biased against individuals from different backgrounds.”

Google tells WIRED that its systems weren’t working as intended in this case and that it is looking at ways it can improve.

“We have guardrails and policies in place to protect against low quality responses, and when we find Overviews that don’t align with our policies, we quickly take action against them,” Ned Adriance, a Google spokesperson, tells WIRED. “These Overviews violated our policies and have been removed. Our goal is for AI Overviews to provide links to high quality content so that people can click through to learn more, but for some queries there may not be a lot of high quality web content available.”

While WIRED’s tests suggest AI Overviews have now been switched off for queries about national IQs, the results still amplify the incorrect figures from Lynn’s work in what’s called a “featured snippet,” which displays some of the text from a website before the link.

Google did not respond to a question about this update.

But it’s not just Google promoting these dangerous theories. When WIRED put the same query to other AI-powered online search services, we found similar results.

Perplexity, an AI search company that has been found to make things up out of thin air, responded to a query about “Pakistan IQ” by stating that “the average IQ in Pakistan has been reported to vary significantly depending on the source.”

It then lists a number of sources, including a Reddit thread that relied on Lynn’s research and the same World Population Review site that Google’s AI Overview referenced. When asked for Sierra Leone’s IQ, Perplexity directly cited Lynn’s figure: “Sierra Leone’s average IQ is reported to be 45.07, ranking it among the lowest globally.”

Perplexity did not respond to a request for comment.

Microsoft’s Copilot chatbot, which is integrated into its Bing search engine, generated confident text—“The average IQ in Pakistan is reported to be around 80”—citing a website called IQ International, which does not reference its sources. When asked for “Sierra Leone IQ,” Copilot’s response said it was 91. The source linked in the results was a website called Brainstats.com, which references Lynn’s work. Copilot also referenced Brainstats.com work when queried about IQ in Kenya.

“Copilot answers questions by distilling information from multiple web sources into a single response,” Caitlin Roulston, a Microsoft spokesperson, tells WIRED. “Copilot provides linked citations so the user can further explore and research as they would with traditional search.”

Google added that part of the problem it faces in generating AI Overviews is that, for some very specific queries, there’s an absence of high quality information on the web—and there’s little doubt that Lynn’s work is not of high quality.

“The science underlying Lynn’s database of ‘national IQs’ is of such poor quality that it is difficult to believe the database is anything but fraudulent,” Sear said. “Lynn has never described his methodology for selecting samples into the database; many nations have IQs estimated from absurdly small and unrepresentative samples.”

Sear points to Lynn’s estimation of the IQ of Angola being based on information from just 19 people and that of Eritrea being based on samples of children living in orphanages.

“The problem with it is that the data Lynn used to generate this dataset is just bullshit, and it’s bullshit in multiple dimensions,” Rutherford said, pointing out that the Somali figure in Lynn’s dataset is based on one sample of refugees aged between 8 and 18 who were tested in a Kenyan refugee camp. He adds that the Botswana score is based on a single sample of 104 Tswana-speaking high school students aged between 7 and 20 who were tested in English.

Critics of the use of national IQ tests to promote the idea of racial superiority point out not only that the quality of the samples being collected is weak, but also that the tests themselves are typically designed for Western audiences, and so are biased before they are even administered.

“There is evidence that Lynn systematically biased the database by preferentially including samples with low IQs, while excluding those with higher IQs for African nations,” Sear added, a conclusion backed up by a preprint study from 2020.

Lynn published various versions of his national IQ dataset over the course of decades, the most recent of which, called “The Intelligence of Nations,” was published in 2019. Over the years, Lynn’s flawed work has been used by far-right and racist groups as evidence to back up claims of white superiority. The data has also been turned into a color-coded map of the world, showing sub-Saharan African countries with purportedly low IQ colored red compared to the Western nations, which are colored blue.

“This is a data visualization that you see all over [X, formerly known as Twitter], all over social media—and if you spend a lot of time in racist hangouts on the web, you just see this as an argument by racists who say, ‘Look at the data. Look at the map,’” Rutherford says.

But the blame, Rutherford believes, does not lie with the AI systems alone, but also with a scientific community that has been uncritically citing Lynn’s work for years.

“It’s actually not surprising [that AI systems are quoting it] because Lynn’s work in IQ has been accepted pretty unquestioningly from a huge area of academia, and if you look at the number of times his national IQ databases have been cited in academic works, it’s in the hundreds,” Rutherford said. “So the fault isn’t with AI. The fault is with academia.”

This story originally appeared on wired.com

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Studies of migraine’s many triggers offer paths to new therapies


One class of drugs has already found success in treating the painful, common attacks.

Displeased African American woman holding her head in pain.

For Cherise Irons, chocolate, red wine, and aged cheeses are dangerous. So are certain sounds, perfumes and other strong scents, cold weather, and thunderstorms. Stress and lack of sleep, too.

She suspects all of these things can trigger her migraine attacks, which manifest in a variety of ways: pounding pain in the back of her head, exquisite sensitivity to the slightest sound, even blackouts and partial paralysis.

Irons, 48, of Coral Springs, Florida, once worked as a school assistant principal. Now, she’s on disability due to her migraine. Irons has tried so many migraine medications she’s lost count—but none has helped for long. Even a few of the much-touted new drugs that have quelled episodes for many people with migraine have failed for Irons.

Though not all are as impaired as Irons, migraine is a surprisingly common problem, affecting 14 percent to 15 percent of people. Yet scientists and physicians remain largely in the dark about how triggers like Irons’ lead to attacks. They have made progress nonetheless: The latest drugs, inhibitors of a body signaling molecule called CGRP, have been a blessing for many. For others, not so much. And it’s not clear why.

The complexity of migraine probably has something to do with it. “It’s a very diverse condition,” says Debbie Hay, a pharmacologist at the University of Otago in Dunedin, New Zealand. “There’s still huge debate as to what the causes are, what the consequences are.”

That’s true despite decades of research and the remarkable ability of scientists to trigger migraine attacks in the lab: Giving CGRP intravenously to people who get migraines gives some of them attacks. So do nitric oxide, a natural body molecule that relaxes blood vessels, and another signaling molecule called PACAP. In mice, too, CGRP and PACAP molecules can bring on migraine-like effects.

All these molecules act as “on” switches for migraine attacks, which suggests that there must be “off” switches out there, too, says Amynah Pradhan, a neuroscientist at Washington University in St. Louis. Scientists have been actively seeking those “off” switches; the CGRP-blocking drugs were a major win in this line of research.

Despite the insights gleaned, migraine remains a tricky disease to understand and treat. For example, the steps between the molecular action of CGRP and a person experiencing a headache or other symptoms are still murky. But scientists have lots of other ideas for new drugs that might stave off migraine attacks, or stop ongoing ones.

“It’s important to have an expanded toolbox,” says Pradhan.

Deciphering migraine mechanisms

Migraine is the second most prevalent cause of disability in the world, affecting mainly women of childbearing age. A person may have one migraine attack per year, or several per week, or even ongoing symptoms.

Complicating the picture further, there’s not just one kind of migraine attack. Migraine can cause headache; nausea; sensitivity to light, sound or smell; or a panoply of other symptoms. Some people get visual auras; some don’t. Some women have migraine attacks associated with menstruation. Some people, particularly kids, have “abdominal migraine,” characterized not so much by headaches as by nausea, stomach pain, and vomiting.

Initially, the throbbing nature of the head pain led researchers to suspect that the root problem was expansion of the blood vessels within the membranes surrounding the brain, with these vessels pulsing in time with the heartbeat. But, as it turns out, the throbbing doesn’t really match up with heart rate.

Then researchers noticed that many signs that presage migraine attack, such as light sensitivity and appetite changes, are all regulated by the brain, particularly a region called the hypothalamus. The pendulum swung toward suspicion of a within-brain origin.

Today, scientists wonder if both in-brain and beyond-brain factors, including blood vessels releasing pain-causing molecules, play a role, as may other contributors such as immune cells.

What all these proposed mechanisms ultimately point to, though, is pain created not in the brain itself but in the meninges—a multilayered “plastic bag around your brain,” as described by Messoud Ashina, a neurologist at the University of Copenhagen and director of the Human Migraine Research Unit at Rigshospitalet Glostrup in Denmark. These membranes contain cerebrospinal fluid that cushions the brain and holds it in place. They also support blood vessels and nerves that feed into the brain. The brain itself cannot feel pain, but nerves in the meninges, especially the trigeminal nerve between the face and brain, can. If they’re activated, they send the brain a major “ouch” message.

Physicians and pharmacists already possess a number of anti-migraine tools — some to prevent future attacks, others to treat an attack once it’s started. Options to stop a current migraine attack in its tracks include over-the-counter painkillers, such as aspirin and ibuprofen, or prescription opioids. Triptans, developed specifically to counter migraine attacks once they’ve begun, are drugs that tighten up blood vessels via interactions with serotonin receptors.

However, scientists later recognized that constricting blood vessels is not the main way triptans relieve migraine; their action to quiet nerve signals or inflammation may be more relevant. Ditans, a newer class of migraine drugs, also act on serotonin receptors but affect only nerves, not blood vessels, and they still work.

For migraine attack prevention, pre-CGRP-era tools still in use today include antidepressants, blood pressure medications, epilepsy drugs, and injections of botulinum toxin that numb the pain-sensing nerves in the head and neck.

Most of these medicines, except triptans and ditans, weren’t designed specifically for migraine, and they often come with unpleasant side effects. It can take months for some preventive medicines to start working, and frequent use of triptans or painkillers can lead to another problem, the poorly understood “medication overuse headache.

A powerful new player

The CGRP drugs provided a major expansion to the migraine pharmacopoeia, as they can both prevent attacks from happening and stop ones that have already started. They also mark the first time that clues from basic migraine research led to an “off” switch that prevents migraine attacks from even starting.

CGRP is a small snippet of protein made in various places in the body. A messenger molecule that normally clicks into another molecule, called a receptor, on a cell’s surface, CGRP can turn on activity in the receiving cell. It’s found in pain-sensing nerve fibers that run alongside meningeal blood vessels and in the trigeminal ganglia near the base of the skull where many nerves are rooted. The molecule is a powerful blood vessel dilator. It also acts on immune cells, nerve cells, and the nerve-supporting cells called glia.

All of these features—a location in the meningeal nerve fibers with several actions that might be linked to migraine, like expanding blood vessels—pointed to CGRP being a migraine “on” switch. Further research also showed that CGRP is often found at higher levels in the body fluids of people who get migraines.

In a small 2010 study, 12 out of 14 people with migraine did report a headache after receiving intravenous CGRP; four of them also experienced aura symptoms such as vision changes. Only two out of 11 people who don’t normally get migraine attacks also developed a headache after CGRP infusion.

CGRP also caused mice to be extra sensitive to light, suggesting it could have something to do with the light sensitivity in humans, too.

The steps between CGRP in the bloodstream or meninges as a trigger and migraine symptoms like light sensitivity aren’t fully understood, though scientists do have theories. Ashina is pursuing how CGRP, PACAP, and other substances might trigger migraine attacks. These molecules all stick to receptors on the surface of cells, such as the ones in blood vessel walls. That binding kicks off a series of events inside the cell that includes generation of a substance called cyclic AMP and, ultimately, opening of channels that let potassium ions out of the cell. All that external potassium causes blood vessels to dilate—but it might also trigger nearby pain-sensing nerves, such as the trigeminal cluster, Ashina hypothesizes.

It’s a neat story, but far from proven. “We still don’t really know what CGRP does in the context of migraine,” says Greg Dussor, a neuroscientist at the University of Texas at Dallas.

In one possible model for migraine, various molecules can activate blood vessel cells to release potassium, which activates nearby neurons that send a pain signal to the brain. Various strategies that seek to interfere with this pathway, including the anti-CGRP drugs, are of great interest to migraine researchers.

In one possible model for migraine, various molecules can activate blood vessel cells to release potassium, which activates nearby neurons that send a pain signal to the brain. Various strategies that seek to interfere with this pathway, including the anti-CGRP drugs, are of great interest to migraine researchers. Credit: Knowable Magazine

Uncertainty about CGRP’s precise role in migraine hasn’t stopped progress in the clinic: There are now eight different blockers of CGRP, or its receptor, approved by the US Food and Drug Administration for migraine treatment or prevention. The American Headache Society recently released a statement saying that CGRP drugs should be considered first-line treatments for migraine. Despite CGRP’s widespread presence across the body, blocking it results in few and generally mild side effects, such as constipation.

“It’s a good drug,” says Dan Levy, a neurophysiologist at Beth Israel Deaconess Medical Center in Boston who recently described the role of the meninges in migraine for the Annual Review of Neuroscience.

Questions remain, though. One is whether, and how well, CGRP blockers work in men. Since three to four times as many women as men have migraine, the medicines were mostly tested in women. A recent review found that while CGRP blockers seem to prevent future headaches in both sexes, they haven’t been shown to stop acute migraine attacks in men as currently prescribed. (Notably, men made up less than a fifth of those included in the studies as a whole, making it more difficult to detect any low-level effects.)

More data may settle the question. Hsiangkuo Yuan, neurologist and director of clinical research at Thomas Jefferson University’s headache center in Philadelphia, says he’s been tracking the effects of CGRP blockers in his patients and hasn’t seen much difference between the sexes so far in terms of CGRP-blocking antibodies, though there may be a difference in how people respond to small molecules that block CGRP.

Access to CGRP inhibitors has also become an issue. Many insurers won’t pay for the new drugs until patients have tried and failed with a couple of other treatments first — which can take several months. This led Irons, the Florida patient, to try multiple medications that didn’t help her before she tried several CGRP blockers. In her case, one CGRP drug didn’t work at all; others worked for a time. But eventually they all failed.

Searching for new “off” switches

Her case illustrates the need for still more options to prevent or treat migraine attacks, even as the CGRP success story showed there’s hope for new medicines.

“CGRP has really paved the way,” says Andrew Russo, a neuroscientist at the University of Iowa in Iowa City who described CGRP as a new migraine target for the Annual Review of Pharmacology and Toxicology in 2015. “It’s a very exciting time for the field.”

Physicians have a number of therapies that can treat migraine — from familiar painkillers such as acetaminophen to the newer ditans and CGRP blockers. Yet, many patients still struggle to find consistent symptom relief, motivating scientists to continue to search for new medications.

Physicians have a number of therapies that can treat migraine — from familiar painkillers such as acetaminophen to the newer ditans and CGRP blockers. Yet, many patients still struggle to find consistent symptom relief, motivating scientists to continue to search for new medications. Credit: Knowable Magazine

Russo and Hay, of New Zealand, are interested in building on CGRP action with a potential novel therapy. It turns out CGRP doesn’t hit just one receptor on the surface of cells, like a key that matches only one lock. In addition to the traditional CGRP receptor, it also binds and activates the AMY1 receptor—which itself can be activated by another molecule, amylin.

AMY1 receptors are found at key sites for migraine pain, such as the trigeminal nerves. In a small study, Russo and Hay found that injecting a synthetic version of amylin creates migraine-like attacks in about 40 percent of people with migraine. The researchers also discovered that in mice, activating AMY1 causes sensitivity to touch and light.

Again, that sounds like a migraine attack “on” switch, and Russo believes there’s a good chance that researchers can develop a drug that acts as an “off” switch.

Another promising “on” switch contender is PACAP. Like CGRP, it’s a small protein and signaling molecule. PACAP also appears in the trigeminal nerves that transmit migraine pain and seems to be elevated in some people experiencing a migraine attack. In rodents, PACAP causes expansion of blood vessels, inflammation in the nervous system, and hypersensitivity to touch and light. In a little over half of people with migraine, intravenous PACAP kicked off a fresh, migraine-like attack.

But, Russo says, “PACAP is more than just a CGRP wannabe.” It appears to work at least somewhat differently. In mice, antibodies that block PACAP do nothing against the light aversion activated by CGRP, and vice versa. That suggests that PACAP and CGRP could instigate two alternate pathways to a migraine attack, and some people might be prone to one or the other route. Thus, PACAP-blocking drugs might help people who don’t get relief from CGRP blockers.

Clinical research so far hints that anti-PACAP treatments indeed might help. In 2023, the Danish pharmaceutical company Lundbeck announced results of a trial in which they dosed 237 people with an antibody to PACAP. Those who received the highest dose had, on average, six fewer migraine days in the four weeks following the treatment than they did before receiving the medication, compared to a drop by only four days in people who received a placebo.

Then there’s Ashina’s work, which unites many of the “on”-switch clues to suggest that PACAP, CGRP and other molecules all act by triggering cyclic AMP, causing blood vessel cells to spew potassium. If that’s so, then drugs that act on cyclic AMP or potassium channels might serve as “on” or “off” switches for migraine attacks.

Ashina has tested that hypothesis with cilostazol, a blood vessel dilator used in people who have poor circulation in their legs. Cilostazol boosts production of cyclic AMP and, Ashina found, it caused attacks in a majority of people with migraine.

He also tried levcromakalim, another blood vessel opener that lowers blood pressure. It’s a potassium-channel opener, and this, too, caused migraine attacks for all 16 people in the study.

To Ashina, these experiments suggest that medicines that turn off migraine-inducing pathways at or before the point of potassium release could be of benefit. There might be side effects, such as changes in blood pressure, but Ashina notes there are potassium-channel subtypes that may be limited to blood vessels in the brain. Targeting those specific channels would be safer.

“I personally really like the potassium-channel track,” says Russo. “I think if we can find drugs targeting the ion channels, the potassium channels, that will be fruitful.”

Hopeful for opioids

Russo is also upbeat about work on a new kind of opioid. Traditional opioids, whether from poppies or pharmacies, work on a receptor called mu. Along with their remarkable pain-dulling abilities, they often create side effects including constipation and itching, plus euphoria and risk for addiction.

But there’s another class of opioid receptors, called delta receptors, that don’t cause euphoria, says Pradhan, who’s investigating them. When delta-targeting opioid molecules are offered to animals, the animals won’t self-administer the drugs as they do with mu-acting opioids such as morphine, suggesting that the drugs are less pleasurable and less likely to be habit-forming.

Delta receptors appear in parts of the nervous system linked to migraine, including the trigeminal ganglia. Pradhan has found that in mice, compounds acting on the delta opioid receptor seem to relieve hypersensitivity to touch, a marker for migraine-like symptoms, as well as brain activity associated with migraine aura.

Encouraged by early evidence that these receptors can be safely targeted in people, two companies—PharmNovo in Sweden and Pennsylvania-based Trevena—are pursuing alternative opioid treatments. Migraine is one potential use for such drugs.

Thus, the evolving story of migraine is one of many types of triggers, many types of attacks, many targets, and, with time, more potential treatments.

“I don’t think there’s one molecule that fits all,” says Levy. “Hopefully, in 10, 15 years, we’ll know, for a given person, what triggers it and what can target that.”

This story originally appeared in Knowable Magazine.

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Knowable Magazine explores the real-world significance of scholarly work through a journalistic lens.

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Startup can identify deepfake video in real time

Real-time deepfakes are no longer limited to billionaires, public figures, or those who have extensive online presences. Mittal’s research at NYU, with professors Chinmay Hegde and Nasir Memon, proposes a potential challenge-based approach to blocking AI bots from video calls, where participants would have to pass a kind of video CAPTCHA test before joining.

As Reality Defender works to improve the detection accuracy of its models, Colman says that access to more data is a critical challenge to overcome—a common refrain from the current batch of AI-focused startups. He’s hopeful more partnerships will fill in these gaps, and without specifics, hints at multiple new deals likely coming next year. After ElevenLabs was tied to a deepfake voice call of US president Joe Biden, the AI-audio startup struck a deal with Reality Defender to mitigate potential misuse.

What can you do right now to protect yourself from video call scams? Just like WIRED’s core advice about avoiding fraud from AI voice calls, not getting cocky about whether you can spot video deepfakes is critical to avoid being scammed. The technology in this space continues to evolve rapidly, and any telltale signs you rely on now to spot AI deepfakes may not be as dependable with the next upgrades to underlying models.

“We don’t ask my 80-year-old mother to flag ransomware in an email,” says Colman. “Because she’s not a computer science expert.” In the future, it’s possible real-time video authentication, if AI detection continues to improve and shows to be reliably accurate, will be as taken for granted as that malware scanner quietly humming along in the background of your email inbox.

This story originally appeared on wired.com.

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sustainable-building-effort-reaches-new-heights-with-wooden-skyscrapers

Sustainable building effort reaches new heights with wooden skyscrapers


Wood offers architects an alternative to carbon-intensive steel and concrete.

At the University of Toronto, just across the street from the football stadium, workers are putting up a 14-story building with space for classrooms and faculty offices. What’s unusual is how they’re building it — by bolting together giant beams, columns, and panels made of manufactured slabs of wood.

As each wood element is delivered by flatbed, a tall crane lifts it into place and holds it in position while workers attach it with metal connectors. In its half-finished state, the building resembles flat-pack furniture in the process of being assembled.

The tower uses a new technology called mass timber. In this kind of construction, massive, manufactured wood elements that can extend more than half the length of a football field replace steel beams and concrete. Though still relatively uncommon, it is growing in popularity and beginning to pop up in skylines around the world.

A photo of a modern apartment interior with wooden beams, floor and ceiling. Windows overlook the surrounding neighborhood.

Mass timber can lend warmth and beauty to an interior. Pictured is a unit in the eight-story Carbon12 condominium in Portland, Oregon.

Mass timber can lend warmth and beauty to an interior. Pictured is a unit in the eight-story Carbon12 condominium in Portland, Oregon. Credit: KAISER + PATH

Today, the tallest mass timber building is the 25-story Ascent skyscraper in Milwaukee, completed in 2022. As of that year, there were 84 mass timber buildings eight stories or higher either built or under construction worldwide, with another 55 proposed. Seventy percent of the existing and future buildings were in Europe, about 20 percent in North America, and the rest in Australia and Asia, according to a report from the Council on Tall Buildings and Urban Habitat. When you include smaller buildings, at least 1,700 mass timber buildings had been constructed in the United States alone as of 2023.

Mass timber is an appealing alternative to energy-intensive concrete and steel, which together account for almost 15 percent of global carbon dioxide emissions. Though experts are still debating mass timber’s role in fighting climate change, many are betting it’s better for the environment than current approaches to construction. It relies on wood, after all, a renewable resource.

Mass timber also offers a different aesthetic that can make a building feel special. “People get sick and tired of steel and concrete,” says Ted Kesik, a building scientist at the University of Toronto’s Mass Timber Institute, which promotes mass timber research and development. With its warm, soothing appearance and natural variations, timber can be more visually pleasing. “People actually enjoy looking at wood.”

Same wood, stronger structure

Using wood for big buildings isn’t new, of course. Industrialization in the 18th and 19th centuries led to a demand for large factories and warehouses, which were often “brick and beam” construction—a frame of heavy wooden beams supporting exterior brick walls.

As buildings became ever taller, though, builders turned to concrete and steel for support. Wood construction became mostly limited to houses and other small buildings made from the standard-sized “dimensional” lumber you see stacked at Home Depot.

But about 30 years ago, builders in Germany and Austria began experimenting with techniques for making massive wood elements out of this readily available lumber. They used nails, dowels and glue to combine smaller pieces of wood into big, strong and solid masses that don’t require cutting down large old-growth trees.

Engineers including Julius Natterer, a German engineer based in Switzerland, pioneered new methods for building with the materials. And architects including Austria’s Hermann Kaufmann began gaining attention for mass timber projects, including the Ölzbündt apartments in Austria, completed in 1997, and Brock Commons, an 18-story student residence at the University of British Columbia, completed in 2017.

In principle, mass timber is like plywood but on a much larger scale: The smaller pieces are layered and glued together under pressure in large specialized presses. Today, beams up to 50 meters long, usually made of what’s called glue-laminated timber, or glulam, can replace steel elements. Panels up to 50 centimeters thick, typically cross-laminated timber, or CLT, replace concrete for walls and floors.

These wood composites can be surprisingly strong—stronger than steel by weight. But a mass timber element must be bulkier to achieve that same strength. As a building gets higher, the wooden supports must get thicker; at some point, they simply take up too much space. So for taller mass timber buildings, including the Ascent skyscraper, architects often turn to a combination of wood, steel and concrete.

Historically, one of the most obvious concerns with using mass timber for tall buildings was fire safety. Until recently, many building codes limited wood construction to low-rise buildings.

Though they don’t have to be completely fireproof, buildings need to resist collapse long enough to give firefighters a chance to bring the flames under control, and for occupants to get out. Materials used in conventional skyscrapers, for instance, are required to maintain their integrity in a fire for three hours or more.

To demonstrate mass timber’s fire resistance, engineers put the wood elements in gas-fired chambers and monitor their integrity. Other tests set fire to mock-ups of mass timber buildings and record the results.

These tests have gradually convinced regulators and customers that mass timber can resist burning long enough to be fire-safe. That’s partly because a layer of char tends to form early on the outside of the timber, insulating the interior from much of the fire’s heat.

Mass timber got a major stamp of approval in 2021, when the International Code Council changed the International Building Code, which serves as a model for jurisdictions around the world, to allow mass timber construction up to 18 stories tall. With this change, more and more localities are expected to update their codes to routinely allow tall mass timber buildings, rather than requiring them to get special approvals.

There are other challenges, though. “Moisture is the real problem, not fire,” says Steffen Lehmann, an architect and scholar of urban sustainability at the University of Nevada, Las Vegas.

All buildings must control moisture, but it’s absolutely crucial for mass timber. Wet wood is vulnerable to deterioration from fungus and insects like termites. Builders are careful to prevent the wood from getting wet during transportation and construction, and they deploy a comprehensive moisture management plan, including designing heat and ventilation systems to keep moisture from accumulating. For extra protection from insects, wood can be treated with chemical pesticides or surrounded by mesh or other physical barriers where it meets the ground.

Another problem is acoustics, since wood transmits sound so well. Designers use sound insulation materials, leave space between walls and install raised floors, among other methods.

Potential upsides of mass timber

Combating global warming means reducing greenhouse gas emissions from the building sector, which is responsible for 39 percent of emissions globally. Diana Ürge-Vorsatz, an environmental scientist at the Central European University in Vienna, says mass timber and other bio-based materials could be an important part of that effort.

In a 2020 paper in the Annual Review of Environment and Resources, she and colleagues cite an estimate from the lumber industry that the 18-story Brock Commons, in British Columbia, avoided the equivalent of 2,432 metric tons of CO2 emissions compared with a similar building of concrete and steel. Of those savings, 679 tons came from the fact that less greenhouse gas emissions are generated in the manufacture of wood versus concrete and steel. Another 1,753 metric tons of CO2 equivalent were locked away in the building’s wood.

“If you use bio-based material, we have a double win,” Ürge-Vorsatz says.

But a lot of the current enthusiasm over mass timber’s climate benefits is based on some big assumptions. The accounting often assumes, for instance, that any wood used in a mass timber building will be replaced by the growth of new trees, and that those new trees will take the same amount of CO2 out of the atmosphere across time. But if old-growth trees are replaced with new tree plantations, the new trees may never reach the same size as the original trees, some environmental groups argue. There are also concerns that increasing demand for wood could lead to more deforestation and less land for food production.

Studies also tend to assume that once the wood is in a building, the carbon is locked up for good. But not all the wood from a felled tree ends up in the finished product. Branches, roots and lumber mill waste may decompose or get burned. And when the building is torn down, if the wood ends up in a landfill, the carbon can find its way out in the form of methane and other emissions.

“A lot of architects are scratching their heads,” says Stephanie Carlisle, an architect and environmental researcher at the nonprofit Carbon Leadership Forum, wondering whether mass timber always has a net benefit. “Is that real?” She believes climate benefits do exist. But she says understanding the extent of those benefits will require more research.

In the meantime, mass timber is at the forefront of a whole different model of construction called integrated design. In traditional construction, an architect designs a building first and then multiple firms are hired to handle different parts of the construction, from laying the foundation, to building the frame, to installing the ventilation system, and so on.

In integrated design, says Kesik, the design phase is much more detailed and involves the various firms from the beginning. The way different components will fit and work together is figured out in advance. Exact sizes and shapes of elements are predetermined, and holes can even be pre-drilled for attachment points. That means many of the components can be manufactured off-site, often with advanced computer-controlled machinery.

A lot of architects like this because it gives them more control over the building elements. And because so much of the work is done in advance, the buildings tend to go up faster on-site — up to 40 percent faster than other buildings, Lehmann says.

Mass timber buildings tend to be manufactured more like automobiles, Kesik says, with all the separate pieces shipped to a final location for assembly. “When the mass timber building shows up on-site, it’s really just like an oversized piece of Ikea furniture,” he says. “Everything sort of goes together.”

This story originally appeared in Knowable Magazine.

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Can walls of oysters protect shores against hurricanes? Darpa wants to know.


Colonized artificial reef structures could absorb the power of storms.

picture of some shoreline

Credit: Kemter/Getty Images

On October 10, 2018, Tyndall Air Force Base on the Gulf of Mexico—a pillar of American air superiority—found itself under aerial attack. Hurricane Michael, first spotted as a Category 2 storm off the Florida coast, unexpectedly hulked up to a Category 5. Sustained winds of 155 miles per hour whipped into the base, flinging power poles, flipping F-22s, and totaling more than 200 buildings. The sole saving grace: Despite sitting on a peninsula, Tyndall avoided flood damage. Michael’s 9- to 14-foot storm surge swamped other parts of Florida. Tyndall’s main defense was luck.

That $5 billion disaster at Tyndall was just one of a mounting number of extreme-weather events that convinced the US Department of Defense that it needed new ideas to protect the 1,700 coastal bases it’s responsible for globally. As hurricanes Helene and Milton have just shown, beachfront residents face compounding threats from climate change, and the Pentagon is no exception. Rising oceans are chewing away the shore. Stronger storms are more capable of flooding land.

In response, Tyndall will later this month test a new way to protect shorelines from intensified waves and storm surges: a prototype artificial reef, designed by a team led by Rutgers University scientists. The 50-meter-wide array, made up of three chevron-shaped structures each weighing about 46,000 pounds, can take 70 percent of the oomph out of waves, according to tests. But this isn’t your grandaddy’s seawall. It’s specifically designed to be colonized by oysters, some of nature’s most effective wave-killers.

If researchers can optimize these creatures to work in tandem with new artificial structures placed at sea, they believe the resulting barriers can take 90 percent of the energy out of waves. David Bushek, who directs the Haskin Shellfish Research Laboratory at Rutgers, swears he’s not hoping for a megastorm to come and show what his team’s unit is made of. But he’s not not hoping for one. “Models are always imperfect. They’re always a replica of something,” he says. “They’re not the real thing.”

Playing defense Reefense

The project is one of three being developed under a $67.6 million program launched by the US government’s Defense Advanced Research Projects Agency, or Darpa. Cheekily called Reefense, the initiative is the Pentagon’s effort to test if “hybrid” reefs, combining manmade structures with oysters or corals, can perform as well as a good ol’ seawall. Darpa chose three research teams, all led by US universities, in 2022. After two years of intensive research and development, their prototypes are starting to go into the water, with Rutgers’ first up.

Today, the Pentagon protects its coastal assets much as civilians do: by hardening them. Common approaches involve armoring the shore with retaining walls or arranging heavy objects, like rocks or concrete blocks, in long rows. But hardscape structures come with tradeoffs. They deflect rather than absorb wave energy, so protecting one’s own shoreline means exposing someone else’s. They’re also static: As sea levels rise and storms get stronger, it’s getting easier for water to surmount these structures. This wears them down faster and demands constant, expensive repairs.

In recent decades, a new idea has emerged: using nature as infrastructure. Restoring coastal habitats like marshes and mangroves, it turns out, helps hold off waves and storms. “Instead of armoring, you’re using nature’s natural capacity to absorb wave energy,” says Donna Marie Bilkovic, a professor at the Virginia Institute for Marine Science. Darpa is particularly interested in two creatures whose numbers have been decimated by humans but which are terrific wave-breakers when allowed to thrive: oysters and corals.

Oysters are effective wave-killers because of how they grow. The bivalves pile onto each other in large, sturdy mounds. The resulting structure, unlike a smooth seawall, is replete with nooks, crannies, and convolutions. When a wave strikes, its energy gets diffused into these gaps, and further spent on the jagged, complex surfaces of the oysters. Also unlike a seawall, an oyster wall can grow. Oysters have been shown to be capable of building vertically at a rate that matches sea-level rise—which suggests they’ll retain some protective value against higher tides and stronger storms.

Today hundreds of human-tended oyster reefs, particularly on America’s Atlantic coast, use these principles to protect the shore. They take diverse approaches; some look much like natural reefs, while others have an artificial component. Some cultivate oysters for food, with coastal protection a nice co-benefit; others are built specifically to preserve shorelines. What’s missing amid all this experimentation, says Bilkovic, is systematic performance data—the kind that could validate which approaches are most effective and cost-effective. “Right now the innovation is outpacing the science,” she says. “We need to have some type of systematic monitoring of projects, so we can better understand where the techniques work the best. There just isn’t funding, frankly.”

Hybrid deployments

Rather than wait for the data needed to engineer the perfect reef, Darpa wants to rapidly innovate them through a burst of R&D. Reefense has given awardees five years to deploy hybrid reefs that take up to 90 percent of the energy out of waves, without costing significantly more than traditional solutions. The manmade component should block waves immediately. But it should be quickly enhanced by organisms that build, in months or years, a living structure that would take nature decades.

The Rutgers team has built its prototype out of 788 interlocked concrete modules, each 2 feet wide and ranging in height from 1 to 2 feet tall. They have a scalloped appearance, with shelves jutting in all directions. Internally, all these shelves are connected by holes.

A Darpa-funded team will install sea barriers, made of hundreds of concrete modules, near a Florida military base. The scalloped shape should not only dissipate wave energy but invite oysters to build their own structures.

What this means is that when a wave strikes this structure, it smashes into the internal geometry, swirls around, and exits with less energy. This effect alone weakens the wave by 70 percent, according to the US Army Corps of Engineers, which tested a scale model in a wave simulator in Mississippi. But the effect should only improve as oysters colonize the structure. Bushek and his team have tried to design the shelves with the right hardness, texture, and shading to entice them.

But the reef’s value would be diminished if, say, disease were to wipe the mollusks out. This is why Darpa has tasked Rutgers with also engineering oysters resistant to dermo, a protozoan that’s dogged Atlantic oysters for decades. Darpa prohibited them using genetic-modification techniques. But thanks to recent advances in genomics, the Rutgers team can rapidly identify individual oysters with disease-resistant traits. It exposes these oysters to dermo in a lab, and crossbreeds the survivors, producing hardier mollusks. Traditionally it takes about three years to breed a generation of oysters for better disease resistance; Bushek says his team has done it in one.

The tropics are a different story

Oysters may suit the DoD’s needs in temperate waters, but for bases in tropical climates, it’s coral that builds the best seawalls. Hawaii, for instance, enjoys the protection of “fringing” coral reefs that extend offshore for hundreds of yards in a gentle slope along the seabed. The colossal, complex, and porous character of this surface exhausts wave energy over long distances, says Ben Jones, an oceanographer for the Applied Research Laboratory at the University of Hawaii—and head of the university’s Reefense project. He said it’s not unusual to see ocean swells of 6 to 8 feet way offshore, while the water at the seashore laps gently.

A Marine base in Hawaii will test out a new approach to coastal protection inspired by local coral reefs: A forward barrier will take the first blows of the waves, and a scattering of pyramids will further weaken waves before they get to shore.

Inspired by this effect, Jones and a team of researchers are designing an array that they’ll deploy near a US Marine Corps base in Oahu whose shoreline is rapidly receding. While the final design isn’t set yet, the broad strokes are: It will feature two 50-meter-wide barriers laid in rows, backed by 20 pyramid-like obstacles. All of these are hollow, thin-walled structures with sloping profiles and lots of big holes. Waves that crash into them will lose energy by crawling up the sides, but two design aspects of the structure—the width of the holes and the thinness of the walls—will generate turbulence in the water, causing it to spin off more energy as heat.

The manmade structures in Hawaii will be studded with concrete domes meant to encourage coral colonization. Though at grave risk from global warming, coral reefs are thought to provide coastal-protection benefits worth billions of dollars.

In the team’s full vision, the units are bolstered by about a thousand small coral colonies. Jones’ group plans to cover the structures with concrete modules that are about 20 inches in diameter. These have grooves and crevices that offer perfect shelters for coral larvae. The team will initially implant them with lab-bred coral. But they’re also experimenting with enticements, like light and sound, that help attract coral larvae from the wild—the better to build a wall that nature, not the Pentagon, will tend.

A third Reefense team, led by scientists at the University of Miami, takes its inspiration from a different sort of coral. Its design has a three-tiered structure. The foundation is made of long, hexagonal logs punctured with large holes; atop it is a dense layer with smaller holes—“imagine a sponge made of concrete,” says Andrew Baker, director of the university’s Coral Reef Futures Lab and the Reefense team lead.

The team thinks these artificial components will soak up plenty of wave energy—but it’s a crest of elkhorn coral at the top that will finish the job. Native to Florida, the Bahamas, and the Caribbean, elkhorn like to build dense reefs in shallow-water areas with high-intensity waves. They don’t mind getting whacked by water because it helps them harvest food; this whacking keeps wave energy from getting to shore.

Disease has ravaged Florida’s elkhorn populations in recent decades, and now ocean heat waves are dealing further damage. But their critical condition has also motivated policymakers to pursue options to save this iconic state species—including Baker’s, which is to develop an elkhorn more rugged against disease, higher temperatures, and nastier waves. Under Reefense, Baker says, his lab has developed elkhorn with 1.5° to 2° Celsius more heat tolerance than their ancestors. They also claim to have boosted the heat thresholds of symbiotic algae—an existentially important occupant of any healthy reef—and cross-bred local elkhorn with those from Honduras, where reefs have mysteriously withstood scorching waters.

An unexpected permitting issue, though, will force the Miami team to exit Reefense in 2025, without building the test unit it hoped to deploy near a Florida naval base. The federal permitting authority wanted a pot of money set aside to uninstall the structure if needed; Darpa felt it couldn’t do that in a timely way, according to Baker. (Darpa told WIRED every Reefense project has unique permitting challenges, so the Miami team’s fate doesn’t necessarily speak to anything broader. Representatives for the other two Reefense projects said Baker’s issue hasn’t come up for them.)

Though his team’s work with Reefense is coming to a premature end, Baker says, he’s confident their innovations will get deployed elsewhere. He’s been working with Key Biscayne, an island village near Miami whose shorelines have been chewed up by storms. Roland Samimy, the village’s chief resilience and sustainability officer, says they spend millions of dollars every few years importing sand for their rapidly receding beaches. He’s eager to see if a hybrid structure, like the University of Miami design, could offer protection at far lower cost. “People are realizing their manmade structures aren’t as resilient as nature is,” he says.

Not just Darpa

By no means is Darpa the only one experimenting in these areas. Around the world, there are efforts tackling various pieces of the puzzle, like breeding coral for greater heat resistance, or combining coral and oysters with artificial reefs, or designing low-carbon concrete that makes building these structures less environmentally damaging. Bilkovic, of the Virginia Institute for Marine Science, says Reefense will be a success if it demonstrates better ways of doing things than the prevailing methods—and has the data to back this up. “I’m looking forward to seeing what their findings are,” she says. “They’re systematically assessing the effectiveness of the project. Those lessons learned can be translated to other areas, and if the techniques are effective and work well, they can easily be translated to other regions.”

As for Darpa, though the Reefense prototypes are just starting to go in the water, the work is just beginning. All of these first-generation units will be scrutinized—both by the research teams and independent government auditors—to see whether their real-world performance matches what was in the models. Reefense is scheduled to conclude with a final report to the DoD in 2027. It won’t have a “winner” per se; as the Pentagon has bases around the world, it’s likely these three projects will all produce learnings that are relevant elsewhere.

Although their client has the largest military budget in the world, the three Reefense teams have been asked to keep an eye on the economics. Darpa has asked that project costs “not greatly exceed” those of conventional solutions, and tasked government monitors with checking the teams’ math. Catherine Campbell, Reefense’s program manager at Darpa, says affordability doesn’t just make it more likely the Pentagon will employ the technology—but that civilians can, too.

“This isn’t something bespoke for the military… we need to be in line with those kinds of cost metrics [in the civilian sector],” Campbell said in an email. “And that gives it potential for commercialization.”

This story originally appeared on wired.com.

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Why a diabetes drug fell short of anticancer hopes


Studies suggested it could treat cancer, but the clinical trials were a bust.

Multi-pipettes

Pamela Goodwin has received hundreds of emails from patients asking if they should take a cheap, readily available drug, metformin, to treat their cancer.

It’s a fair question: Metformin, commonly used to treat diabetes, has been investigated for treating a range of cancer types in thousands of studies on laboratory cells, animals, and people. But Goodwin, an epidemiologist and medical oncologist treating breast cancer at the University of Toronto’s Mount Sinai Hospital, advises against it. No gold-standard trials have proved that metformin helps treat breast cancer—and her recent research suggests it doesn’t.

Metformin’s development was inspired by centuries of use of French lilac, or goat’s rue (Galega officinalis), for diabetes-like symptoms. In 1918, researchers discovered that a compound from the herb lowers blood sugar. Metformin, a chemical relative of that compound, has been a top type 2 diabetes treatment in the United States since it was approved in 1994. It’s cheap—less than a dollar per dose—and readily available, with few side effects. Today, more than 150 million people worldwide take the stuff.

Illustration of French lilac plant.

The French lilac, Galega officinalis, has been used medicinally since medieval times, including for symptoms associated with diabetes. Investigations of the plant’s chemical galegine led to the development of metformin, a related molecule synthesized in the lab. Credit: Wikimedia Commons

Metformin has a variety of effects, such as improving immune function and the body’s responses to insulin, which in turn regulates blood sugar. It can also slow growth of cancer cells in the lab. Many of these benefits seem to stem from metformin’s action in the cell’s powerhouses, the mitochondria, where it slows the production of energy and limits the generation of damaging chemicals called free radicals.

Researchers have considered metformin for treating a plethora of conditions, from glaucoma to polycystic ovary syndrome to pimples. “It really has a reputation of being a potential wonder drug,” says Michael Pollak, an oncologist and researcher at McGill University in Montreal. “There’s still a lot of work to be done on metformin.” (Pollak consults for biotechnology companies interested in metformin analogs as medicines.)

But the latest research has convinced Pollak and some others that treatment of cancers should be taken off the list.

More studies, but no proof

One of the first hints linking metformin to anticancer effects came in a short note in the British Medical Journal in 2005. Researchers analyzed medical records of almost 12,000 people from the Tayside region of Scotland who were newly diagnosed with diabetes between 1993 and 2001. Of those, more than 900 went on to develop cancer. Interestingly, those who’d taken metformin at some point during the study period were 23 percent less likely to have received a later cancer diagnosis.

This finding fueled further research on people with diabetes taking metformin and the risk for breast cancer, liver cancer, ovarian and endometrial cancer, and other types. The authors of a 2013 analysis, covering more than 1 million patients in 41 observational studies like the original one, concluded that metformin “might be associated with a significant reduction in the risk of cancer.” But such associations are not proof.

Researchers went on to explore the link in studies with cells in dishes and in lab animals, finding that metformin slowed growth of blood, breast, endometrial, lung, liver, stomach, and thyroid cancer cells. It also seemed to make cancer cells extra sensitive to chemotherapy drugs. In one mouse study, scientists grafted human breast, prostate, or lung cancer cells into the animals and treated them with either standard chemotherapy drugs, metformin, or a combination of both. The combination worked best, preventing tumor growth and prolonging relapse.

These findings made sense to researchers. Metformin treats metabolic problems in diabetes, and cancer has also been linked to metabolic issues such as obesity. Even before the 2005 British Medical Journal study, Goodwin had noticed that breast cancer patients with high insulin did worse than those with normal insulin levels.

That logic, plus the promising data, led scientists to conduct a number of randomized controlled trials—the gold-standard experiment in medicine. Researchers would enroll people with cancer and split them into two groups. One group would get standard cancer therapy plus metformin; the other group would get standard therapy plus a placebo, a pill containing no medication.

And metformin flopped, big time. While a number of studies are ongoing, trials for two types of cancer recently reported no benefit overall from metformin. In June 2024, at the American Society of Clinical Oncology meeting in Chicago, researchers reported a Canadian trial with 407 men with low-risk prostate cancer. The enrollees had been diagnosed within six months before starting the trial and had decided to monitor their cancer without starting immediate treatment. Half took metformin and half took a placebo. After biopsies at 18 and 36 months to test whether their disease had progressed, there was no difference between the two groups.

A larger British and Swiss trial including nearly 1,900 patients with newly diagnosed or relapsed prostate cancer that had spread to other body parts was reported at the European Society for Medical Oncology Congress in Barcelona, Spain, in September. This trial also found that metformin plus standard treatment, compared to standard treatment alone, did not improve overall prostate cancer survival in the study population.

A multinational study of breast cancer helmed by Goodwin also led to disappointment. The researchers enrolled more than 3,600 patients between 2010 and 2013; these patients had been diagnosed about a year before enrollment and had already undergone chemotherapy and surgery. In addition to standard cancer treatment, half received metformin and half received a placebo.

By 2016, it was clear that metformin wasn’t doing anything to enhance survival for about 1,100 participants with a particular cancer subtype. When the study wrapped in 2020, the researchers analyzed the rest of the patients, counting how many were alive and free of breast or any other form of cancer. Metformin made no difference in those results, or to survival overall, the team reported in 2022.

Fatal flaws in the research

In retrospect, researchers think they know why earlier studies oversold metformin’s potential. Many of the studies that examined medical records had a crucial flaw, says Samy Suissa, a pharmacoepidemiologist at McGill.

Here’s what happens: Researchers sift through old medical records to see if someone ever took metformin. Then they compare cancer rates among people who took the drug at any point to those who never took it. But you have to be alive to take metformin. Anyone who died, of cancer or other causes, before having a chance at a metformin prescription is left out of the calculations. This skews the results; it’s called the “immortal time bias.” It makes any drug, metformin or otherwise, look like it helps patients to survive because it can only be taken by people who are alive, says Suissa.

Plus, scientists are more likely to publish studies that show metformin is promising than ones where it makes no difference, skewing the scientific literature.

As for those studies of cells in dishes and of lab animals, many experiments used much higher doses of metformin than are used in people. Too much metformin risks a buildup of lactate, a byproduct of low oxygen metabolism that acidifies the blood and can be fatal.

Researchers still suspect metformin might treat specific subgroups of cancer. For example, the authors of the prostate cancer trial presented in Barcelona suggested that metformin might help patients whose cancer has spread to other tissues or multiple sites in their bones. And Goodwin saw a hint in her trial that it might help women whose cancers contain a certain version of a cell-growth gene called ERBB2. But it would require another trial, focused on women with that particular cancer, to prove it.

And there are now better treatments for those patients than there were more than a decade ago when Goodwin started her study, reducing the opportunity to test metformin. Goodwin doesn’t currently have the funding to follow up on this theory.

It may also be that the clinical trials recruited patients with cancers that were too far along. “I always thought we were asking too much of metformin,” says Victoria Bae-Jump, a gynecological oncologist at the University of North Carolina Lineberger Comprehensive Cancer Center in Chapel Hill. “Maybe it just needs to be earlier in the pathway of growth.” Bae-Jump is now testing metformin in women who have early-stage endometrial cancer or a precursor to it.

Others are investigating metformin for people who have precancerous lesions in their mouths. “The idea would be to keep them from progressing, or reverse the tissues to be more normal,” says Frank Ondrey, a head and neck cancer surgeon at the Masonic Cancer Center of the University of Minnesota in Minneapolis. In a small, uncontrolled study of 23 people, metformin halved lesion size in four of them. Ondrey is involved in two ongoing studies, one a randomized, controlled trial, to further test metformin in people with precancerous lesions; these should yield results within a few years.

Subdued expectations

Metformin is also being tested for other conditions such as dementia and a genetic disorder called fragile X syndrome. And perhaps the ultimate potential use for metformin is to slow aging itself. “I think it’s much easier to treat aging and prevent cancer than to treat cancer,” says Nir Barzilai, a geroscientist at Albert Einstein College of Medicine in New York and president of the nonprofit Academy for Health & Lifespan Research. Through its enhancement of insulin action and metabolism plus its minimization of free radical production, metformin influences all the key hallmarks of aging, such as problems with DNA, mitochondria and stem cells, says Barzilai.

He and colleagues are gathering funds for a randomized, controlled trial of metformin in 3,000 people age 65 through 79 who are showing signs of age-related disease already. The trial will test whether fewer people taking metformin die over six years. Barzilai, who is 68, says he is confident in metformin’s anti-aging ability and already takes the drug himself.

Others, mindful of what happened with cancer, are more circumspect. Pollak says that many of the studies in other areas of medicine are too small to prove metformin works, and Suissa notes that some of the studies finding benefits in populations taking metformin, including for longevity, have the same problems the oh-so-promising early cancer research did.

In short, Suissa says, “Don’t believe everything you hear.”

This story originally appeared in Knowable Magazine.

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Greening of Antartica shows how climate change affects the frozen continent


Plant growth is accelerating on the Antarctic Peninsula and nearby islands.

Moss and rocks cover the ground on Robert Island in Antarctica. Photographer: Isadora Romero/Bloomberg

Moss and rocks cover the ground on Robert Island in Antarctica. Photographer: Isadora Romero/Bloomberg Credit: Bloomberg via Getty

Moss and rocks cover the ground on Robert Island in Antarctica. Photographer: Isadora Romero/Bloomberg Credit: Bloomberg via Getty

When satellites first started peering down on the craggy, glaciated Antarctic Peninsula about 40 years ago, they saw only a few tiny patches of vegetation covering a total of about 8,000 square feet—less than a football field.

But since then, the Antarctic Peninsula has warmed rapidly, and a new study shows that mosses, along with some lichen, liverworts and associated algae, have colonized more than 4.6 square miles, an area nearly four times the size of New York’s Central Park.

The findings, published Friday in Nature Geoscience, based on a meticulous analysis of Landsat images from 1986 to 2021, show that the greening trend is distinct from natural variability and that it has accelerated by 30 percent since 2016, fast enough to cover nearly 75 football fields per year.

Greening at the opposite end of the planet, in the Arctic, has been widely studied and reported, said co-author Thomas Roland, a paleoecologist with the University of Exeter who collects and analyzes mud samples to study environmental and ecological change. “But the idea,” he said, “that any part of Antarctica could, in any way, be green is something that still really jars a lot of people.”

illustration of Antarctica and satellite photos

Credit: Inside Climate News

Credit: Inside Climate News

As the planet heats up, “even the coldest regions on Earth that we expect and understand to be white and black with snow, ice, and rock are starting to become greener as the planet responds to climate change,” he said.

The tenfold increase in vegetation cover since 1986 “is not huge in the global scheme of things,” Roland added, but the accelerating rate of change and the potential ecological effects are significant. “That’s the real story here,” he said. “The landscape is going to be altered partially because the existing vegetation is expanding, but it could also be altered in the future with new vegetation coming in.”

In the Arctic, vegetation is expanding on a scale that affects the albedo, or the overall reflectivity of the region, which determines the proportion of the sun’s heat energy that is absorbed by the Earth’s surface as opposed to being bounced away from the planet. But the spread of greenery has not yet changed the albedo of Antarctica on a meaningful scale because the vegetated areas are still too small to have a regional impact, said co-author Olly Bartlett, a University of Hertfordshire researcher who specializes in using satellite data to map environmental change.

“The real significance is about the ecological shift on the exposed land, the land that’s ice-free, creating an area suitable for more advanced plant life or invasive species to get a foothold,” he said.

Bartlett said Google Earth Engine enabled the scientists to process a massive amount of data from the Landsat images to meet a high standard of verification of plant growth. As a result, he added, the changes they reported may actually be conservative.

“It’s becoming easier for life to live there,” he said. “These rates of change we’re seeing made us think that perhaps we’ve captured the start of a more dramatic transformation.”

In the areas they studied, changes to the albedo could have a small local effect, Roland said, as more land free of reflective ice “can feed into a positive feedback loop that creates conditions that are more favorable for vegetation expansion as well.”

Antarctic forests at similar CO2 levels

Other research, including fossil studies, suggests that beech trees grew on Antarctica as recently as 2.5 million years ago, when carbon dioxide levels in the atmosphere were similar to today, another indicator of how unchecked greenhouse gas emissions can rapidly warm Earth’s climate.

Currently, there are only two species of flowering plants native to the Antarctic Peninsula, Antarctic hair grass, and Antarctic pearlwort. “But with a few new grass seeds here and there, or a few spores, and all of a sudden, you’ve got a very different ecosystem,” he said.

And it’s not just plants, he added. “Increasingly, we’re seeing evidence that non-native insect life is taking hold in Antarctica. And that can dramatically change things as well.”

The study shows how climate warming will shake up Antarctic ecosystems, said conservation scientist Jasmine Lee, a research fellow with the British Antarctic Survey who was not involved in the new study.

“It is clear that bank-forming mosses are expanding their range with warmer and wetter conditions, which is likely facilitating similar expansions for some of the invertebrate communities that rely on them for habitat,” she said. “At the same time, some specialist species, such as the more dry-loving mosses and invertebrates, might decline.”

She said the new study is valuable because it provides data across a broad region showing that Antarctic ecosystems are already rapidly altering and will continue to do so as climate change progresses.

“We focus a lot on how climate change is melting ice sheets and changing sea ice,” she said. “It’s good to also highlight that the terrestrial ecosystems are being impacted.”

The study shows climate impacts growing in “regions previously thought nearly immune to the accelerated warming we’re seeing today,” said climate policy expert Pam Pearson, director of the International Cryosphere Climate Initiative.

“It’s as important a signal as the loss of Antarctic sea ice over the past several years,” she said.

The new study identified vegetative changes by comparing the Landsat images at a resolution of 300-square-feet per pixel, detailed enough to accurately map vegetative growth, but it didn’t identify specific climate change factors that might be driving the expansion of plant life.

But other recent studies have documented Antarctic changes that could spur plant growth, including how some regions are affected by warm winds and by increasing amounts of rain from atmospheric rivers, as well as by declining sea ice that leads adjacent land areas to warm, all signs of rapid change in Antarctica.

Roland said their new study was in part spurred by previous research showing how fast patches of Antarctic moss were growing vertically and how microbial activity in tiny patches of soil was also accelerating.

“We’d taken these sediment cores, and done all sorts of analysis, including radiocarbon dating … showing the growth in the plants we’d sampled increasing dramatically,” he said.

Those measurements confirmed that the plants are sensitive to climate change, and as a next step, researchers wanted to know “if the plants are growing sideways at the same dramatic rate,” he said. “It’s one thing for plants to be growing upwards very fast. If they’re growing outwards, then you know you’re starting to see massive changes and massive increases in vegetation cover across the peninsula.”

With the study documenting significant horizontal expansion of vegetation, the researchers are now studying how recently deglaciated areas were first colonized by plants. About 90 percent of the glaciers on the Antarctic Peninsula have been shrinking for the past 75 years, Roland said.

“That’s just creating more and more land for this potentially rapid vegetation response,” he said. “So like Olly says, one of the things we can’t rule out is that this really does increase quite dramatically over the next few decades. Our findings raise serious concerns about the environmental future of the Antarctic Peninsula and of the continent as a whole.”

This story originally appeared on Inside Climate News.

Photo of Inside Climate News

Greening of Antartica shows how climate change affects the frozen continent Read More »

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Neo-Nazis head to encrypted SimpleX Chat app, bail on Telegram

“SimpleX, at its core, is designed to be truly distributed with no central server. This allows for enormous scalability at low cost, and also makes it virtually impossible to snoop on the network graph,” Poberezkin wrote in a company blog post published in 2022.

SimpleX’s policies expressly prohibit “sending illegal communications” and outline how SimpleX will remove such content if it is discovered. Much of the content that these terrorist groups have shared on Telegram—and are already resharing on SimpleX—has been deemed illegal in the UK, Canada, and Europe.

Argentino wrote in his analysis that discussion about moving from Telegram to platforms with better security measures began in June, with discussion of SimpleX as an option taking place in July among a number of extremist groups. Though it wasn’t until September, and the Terrorgram arrests, that the decision was made to migrate to SimpleX, the groups are already establishing themselves on the new platform.

“The groups that have migrated are already populating the platform with legacy material such as Terrorgram manuals and are actively recruiting propagandists, hackers, and graphic designers, among other desired personnel,” the ISD researchers wrote.

However, there are some downsides to the additional security provided by SimpleX, such as the fact that it is not as easy for these groups to network and therefore grow, and disseminating propaganda faces similar restrictions.

“While there is newfound enthusiasm over the migration, it remains unclear if the platform will become a central organizing hub,” ISD researchers wrote.

And Poberezkin believes that the current limitations of his technology will mean these groups will eventually abandon SimpleX.

“SimpleX is a communication network rather than a service or a platform where users can host their own servers, like in OpenWeb, so we were not aware that extremists have been using it,” says Poberezkin. “We never designed groups to be usable for more than 50 users and we’ve been really surprised to see them growing to the current sizes despite limited usability and performance. We do not think it is technically possible to create a social network of a meaningful size in the SimpleX network.”

This story originally appeared on wired.com.

Neo-Nazis head to encrypted SimpleX Chat app, bail on Telegram Read More »

why-trolls,-extremists,-and-others-spread-conspiracy-theories-they-don’t-believe

Why trolls, extremists, and others spread conspiracy theories they don’t believe


Some just want to promote conflict, cause chaos, or even just get attention.

Picture of a person using an old Mac with a paper bag over his head. The bag has the face of a troll drawn on it.

There has been a lot of research on the types of people who believe conspiracy theories, and their reasons for doing so. But there’s a wrinkle: My colleagues and I have found that there are a number of people sharing conspiracies online who don’t believe their own content.

They are opportunists. These people share conspiracy theories to promote conflict, cause chaos, recruit and radicalize potential followers, make money, harass, or even just to get attention.

There are several types of this sort of conspiracy-spreader trying to influence you.

Coaxing conspiracists—the extremists

In our chapter of a new book on extremism and conspiracies, my colleagues and I discuss evidence that certain extremist groups intentionally use conspiracy theories to entice adherents. They are looking for a so-called “gateway conspiracy” that will lure someone into talking to them, and then be vulnerable to radicalization. They try out multiple conspiracies to see what sticks.

Research shows that people with positive feelings for extremist groups are significantly more likely to knowingly share false content online. For instance, the disinformation-monitoring company Blackbird.AI tracked over 119 million COVID-19 conspiracy posts from May 2020, when activists were protesting pandemic restrictions and lockdowns in the United States. Of these, over 32 million tweets were identified as high on their manipulation index. Those posted by various extremist groups were particularly likely to carry markers of insincerity. For instance, one group, the Boogaloo Bois, generated over 610,000 tweets, of which 58 percent were intent on incitement and radicalization.

You can also just take the word of the extremists themselves. When the Boogaloo Bois militia group showed up at the Jan. 6, 2021, insurrection, for example, members stated they didn’t actually endorse the stolen election conspiracy but were there to “mess with the federal government.” Aron McKillips, a Boogaloo member arrested in 2022 as part of an FBI sting, is another example of an opportunistic conspiracist. In his own words: “I don’t believe in anything. I’m only here for the violence.”

Combative conspiracists—the disinformants

Governments love conspiracy theories. The classic example of this is the 1903 document known as the “Protocols of the Elders of Zion,” in which Russia constructed an enduring myth about Jewish plans for world domination. More recently, China used artificial intelligence to construct a fake conspiracy theory about the August 2023 Maui wildfire.

Often the behavior of the conspiracists gives them away. Years later, Russia eventually confessed to lying about AIDS in the 1980s. But even before admitting to the campaign, its agents had forged documents to support the conspiracy. Forgeries aren’t created by accident. They knew they were lying.

As for other conspiracies it hawks, Russia is famous for taking both sides in any contentious issue, spreading lies online to foment conflict and polarization. People who actually believe in a conspiracy tend to stick to a side. Meanwhile, Russians knowingly deploy what one analyst has called a “fire hose of falsehoods.”

Likewise, while Chinese officials were spreading conspiracies about American roots of the coronavirus in 2020, China’s National Health Commission was circulating internal reports tracing the source to a pangolin.

Chaos conspiracists—the trolls

In general, research has found that individuals with what scholars call a high “need for chaos” are more likely to indiscriminately share conspiracies, regardless of belief. These are the everyday trolls who share false content for a variety of reasons, none of which are benevolent. Dark personalities and dark motives are prevalent.

For instance, in the wake of the first assassination attempt on Donald Trump, a false accusation arose online about the identity of the shooter and his motivations. The person who first posted this claim knew he was making up a name and stealing a photo. The intent was apparently to harass the Italian sports blogger whose photo was stolen. This fake conspiracy was seen over 300,000 times on the social platform X and picked up by multiple other conspiracists eager to fill the information gap about the assassination attempt.

Commercial conspiracists—the profiteers

Often when I encounter a conspiracy theory I ask: “What does the sharer have to gain? Are they telling me this because they have an evidence-backed concern, or are they trying to sell me something?”

When researchers tracked down the 12 people primarily responsible for the vast majority of anti-vaccine conspiracies online, most of them had a financial investment in perpetuating these misleading narratives.

Some people who fall into this category might truly believe their conspiracy, but their first priority is finding a way to make money from it. For instance, conspiracist Alex Jones bragged that his fans would “buy anything.” Fox News and its on-air personality Tucker Carlson publicized lies about voter fraud in the 2020 election to keep viewers engaged, while behind-the-scenes communications revealed they did not endorse what they espoused.

Profit doesn’t just mean money. People can also profit from spreading conspiracies if it garners them influence or followers, or protects their reputation. Even social media companies are reluctant to combat conspiracies because they know they attract more clicks.

Common conspiracists—the attention-getters

You don’t have to be a profiteer to like some attention. Plenty of regular people share content where they doubt the veracity or know it is false.

These posts are common: Friends, family, and acquaintances share the latest conspiracy theory with “could this be true?” queries or “seems close enough to the truth” taglines. Their accompanying comments show that sharers are, at minimum, unsure about the truthfulness of the content, but they share nonetheless. Many share without even reading past a headline. Still others, approximately 7 percent to 20 percent of social media users, share despite knowing the content is false. Why?

Some claim to be sharing to inform people “just in case” it is true. But this sort of “sound the alarm” reason actually isn’t that common.

Often, folks are just looking for attention or other personal benefit. They don’t want to miss out on a hot-topic conversation. They want the likes and shares. They want to “stir the pot.” Or they just like the message and want to signal to others that they share a common belief system.

For frequent sharers, it just becomes a habit.

The dangers of spreading lies

Over time, the opportunists may end up convincing themselves. After all, they will eventually have to come to terms with why they are engaging in unethical and deceptive, if not destructive, behavior. They may have a rationale for why lying is good. Or they may convince themselves that they aren’t lying by claiming they thought the conspiracy was true all along.

It’s important to be cautious and not believe everything you read. These opportunists don’t even believe everything they write—and share. But they want you to. So be aware that the next time you share an unfounded conspiracy theory, online or offline, you could be helping an opportunist. They don’t buy it, so neither should you. Be aware before you share. Don’t be what these opportunists derogatorily refer to as “a useful idiot.”

H. Colleen Sinclair is Associate Research Professor of Social Psychology at Louisiana State University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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The Conversation is an independent source of news and views, sourced from the academic and research community. Our team of editors work with these experts to share their knowledge with the wider public. Our aim is to allow for better understanding of current affairs and complex issues, and hopefully improve the quality of public discourse on them.

Why trolls, extremists, and others spread conspiracy theories they don’t believe Read More »

toxic-chemicals-from-ohio-train-derailment-lingered-in-buildings-for-months

Toxic chemicals from Ohio train derailment lingered in buildings for months

This video screenshot released by the US National Transportation Safety Board (NTSB) shows the site of a derailed freight train in East Palestine, Ohio.

Enlarge / This video screenshot released by the US National Transportation Safety Board (NTSB) shows the site of a derailed freight train in East Palestine, Ohio.

On February 3, 2023, a train carrying chemicals jumped the tracks in East Palestine, Ohio, rupturing railcars filled with hazardous materials and fueling chemical fires at the foothills of the Appalachian Mountains.

The disaster drew global attention as the governors of Ohio and Pennsylvania urged evacuations for a mile around the site. Flames and smoke billowed from burning chemicals, and an acrid odor radiated from the derailment area as chemicals entered the air and spilled into a nearby creek.

Three days later, at the urging of the rail company Norfolk Southern, about 1 million pounds of vinyl chloride, a chemical that can be toxic to humans at high doses, was released from the damaged train cars and set aflame.

Federal investigators later concluded that the open burn and the black mushroom cloud it produced were unnecessary, but it was too late. Railcar chemicals spread into Ohio and Pennsylvania.

As environmental engineers, I and my colleagues are often asked to assist with public health decisions after disasters by government agencies and communities. After the evacuation order was lifted, community members asked for help.

In a new study, we describe the contamination we found, along with problems with the response and cleanup that, in some cases, increased the chances that people would be exposed to hazardous chemicals. It offers important lessons to better protect communities in the future.

How chemicals get into homes and water

When large amounts of chemicals are released into the environment, the air can become toxic. Chemicals can also wash into waterways and seep into the ground, contaminating groundwater and wells. Some chemicals can travel below ground into nearby buildings and make the indoor air unsafe.

A computer model shows how chemicals from the train may have spread, given wind patterns. The star on the Ohio-Pennsylvania line is the site of the derailment.

Enlarge / A computer model shows how chemicals from the train may have spread, given wind patterns. The star on the Ohio-Pennsylvania line is the site of the derailment.

Air pollution can find its way into buildings through cracks, windows, doors, and other portals. Once inside, the chemicals can penetrate home items like carpets, drapes, furniture, counters, and clothing. When the air is stirred up, those chemicals can be released again.

Evacuation order lifted, but buildings were contaminated

Three weeks after the derailment, we began investigating the safety of the area near 17 buildings in Ohio and Pennsylvania. The highest concentration of air pollution occurred in the 1-mile evacuation zone and a shelter-in-place band another mile beyond that. But the chemical plume also traveled outside these areas.

In and outside East Palestine, evidence indicated that chemicals from the railcars had entered buildings. Many residents complained about headaches, rashes, and other health symptoms after reentering the buildings.

At one building 0.2 miles away from the derailment site, the indoor air was still contaminated more than four months later.

Nine days after the derailment, sophisticated air testing by a business owner showed the building’s indoor air was contaminated with butyl acrylate and other chemicals carried by the railcars. Butyl acrylate was found above the two-week exposure level, a level at which measures should be taken to protect human health.

When rail company contractors visited the building 11 days after the wreck, their team left after just 10 minutes. They reported an “overwhelming/unpleasent odor” even though their government-approved handheld air pollution detectors detected no chemicals. This building was located directly above Sulphur Run creek, which had been heavily contaminated by the spill. Chemicals likely entered from the initial smoke plumes and also rose from the creek into the building.

Our tests weeks later revealed that railcar chemicals had even penetrated the business’s silicone wristband products on its shelves. We also detected several other chemicals that may have been associated with the spill.

Homes and businesses were mere feet from the contaminated waterways in East Palestine.

Enlarge / Homes and businesses were mere feet from the contaminated waterways in East Palestine.

Weeks after the derailment, government officials discovered that air in the East Palestine Municipal Building, about 0.7 miles away from the derailment site, was also contaminated. Airborne chemicals had entered that building through an open drain pipe from Sulphur Run.

More than a month after the evacuation order was lifted, the Ohio Environmental Protection Agency acknowledged that multiple buildings in East Palestine were being contaminated as contractors cleaned contaminated culverts under and alongside buildings. Chemicals were entering the buildings.

Toxic chemicals from Ohio train derailment lingered in buildings for months Read More »

illinois-city-plans-to-source-its-future-drinking-water-from-lake-michigan

Illinois city plans to source its future drinking water from Lake Michigan

The Great Lakes Compact —

As aquifers dry up, some Midwest communities are looking to the region’s natural resources.

Waves roll ashore along Lake Michigan in Whiting, Indiana.

Enlarge / Waves roll ashore along Lake Michigan in Whiting, Indiana.

This article originally appeared on Inside Climate News, a nonprofit, independent news organization that covers climate, energy, and the environment. It is republished with permission. Sign up for their newsletter here

The aquifer from which Joliet, Illinois, sources its drinking water is likely going to run too dry to support the city by 2030—a problem more and more communities are facing as the climate changes and groundwater declines. So Joliet eyed a huge water source 30 miles to the northeast: Lake Michigan.

It’s the second-largest of the Great Lakes, which together provide drinking water to about 10 percent of the US population, according to the National Oceanic and Atmospheric Administration’s Office for Coastal Management.

Soon, Joliet residents will join them. After years of deliberation, their city government decided last year to replace the aquifer by piping it in from Lake Michigan, buying it from the city of Chicago.

Project construction will start in 2025 with the intent to have water flowing to residents by 2030, said Theresa O’Grady, an engineering consultant working with the city of Joliet. Joliet will foot the approximately $1 billion bill for the project, including the cost to build 65 miles of piping that will transport water from Chicago to Joliet and neighboring communities.

Not just anyone can gain access to Lake Michigan’s pristine, saltless water. That’s rooted in the Great Lakes Compact, an agreement that governs how much water each state or Canadian province can withdraw from the lakes each day. With some exceptions, only municipalities located within the 295,200-square-mile basin (which includes the surface area of the lakes themselves) can get approved for a diversion to use Great Lakes drinking water.

Joliet is one of those exceptions.

“I’ve seen occasional news stories about, ‘Is Kansas suddenly going to get Lake Michigan water because Joliet got Lake Michigan water?’ We are going above and beyond to demonstrate how much we respect the privilege we have to use Lake Michigan water. We are spending hundreds of millions of dollars to be good stewards of that,” said Allison Swisher, Joliet’s director of public utilities.

In April 2023, then-Chicago Mayor Lori Lightfoot signed an agreement with Joliet and five other nearby communities to supply them with treated Lake Michigan water. Now, legal experts and other Great Lakes communities are left wondering how Joliet, located well outside of the Great Lakes basin, fits in.

The exemption in the Great Lakes Compact

The Great Lakes Region, which encompasses portions of New York, Pennsylvania, Ohio, Indiana, Illinois, Michigan, Wisconsin, and Minnesota, as well as the Canadian province of Ontario, is governed through the Great Lakes Compact, enacted in 2008.

“If you do not live in a straddling community, or you’re not a city in a straddling county, you don’t have a ticket to the dance. You can’t even ask for a Great Lakes water diversion,” said Peter Annin, director of the Mary Griggs Burke Center for Freshwater Innovation at Northland College and author of The Great Lakes Water Wars.

“With the exception of the state of Illinois,” he added.

The Chicago exemption, as it is often referred to, has roots in the 1800s, when animal waste from the city’s stockyards would flush into the Chicago River, ultimately pouring into Lake Michigan.

“That’s why Chicago embarks on this massive Panama Canal-like water diversion project, to take all that sewage and put it into this long canal, which then would connect with the Des Plaines River southwest of the city, and then the Illinois River, and then the Mississippi River,” Annin said, referring to the infamous reversal of the Chicago River. “Chicago’s solution was to flush its toilet to St. Louis.”

Every day, Chicago had the right to use billions of gallons of Lake Michigan water to divert this water and dilute the pollution downstream. The state of Wisconsin began challenging the diversion in the 1920s, arguing that Illinois’ superfluous water use was depleting water levels in the lake. In 1967, the Supreme Court sided with Illinois, and now, Chicago can do whatever it wants with its 2.1 billion gallons per day.

“So here we are today with this really kind of unbelievable Joliet water diversion proposal,” Annin said.

Illinois city plans to source its future drinking water from Lake Michigan Read More »

your-cells-are-dying-all-the-time.

Your cells are dying. All the time.

Apoptosis, necroptosis, and pyroptosis, oh my —

Some go gently into the night. Others die less prettily.

3D rendering of an NK Cell destroying a cancer cell.

Enlarge / 3D rendering of an NK Cell destroying a cancer cell.

Billions of cells die in your body every day. Some go out with a bang, others with a whimper.

They can die by accident if they’re injured or infected. Alternatively, should they outlive their natural lifespan or start to fail, they can carefully arrange for a desirable demise, with their remains neatly tidied away.

Originally, scientists thought those were the only two ways an animal cell could die, by accident or by that neat-and-tidy version. But over the past couple of decades, researchers have racked up many more novel cellular death scenarios, some specific to certain cell types or situations. Understanding this panoply of death modes could help scientists save good cells and kill bad ones, leading to treatments for infections, autoimmune diseases, and cancer.

“There’s lots and lots of different flavors here,” says Michael Overholtzer, a cell biologist at Memorial Sloan Kettering Cancer Center in New York. He estimates that there are now more than 20 different names to describe cell death varieties.

Here, Knowable Magazine profiles a handful of classic and new modes by which cells kick the bucket.

Unplanned cell death: Necrosis

Lots of bad things can happen to cells: They get injured or burned, poisoned or starved of oxygen, infected by microbes or otherwise diseased. When a cell dies by accident, it’s called necrosis.

There are several necrosis types, none of them pretty: In the case of gangrene, when cells are starved for blood, cells rot away. In other instances, dying cells liquefy, sometimes turning into yellow goop. Lung cells damaged by tuberculosis turn smushy and white — the technical name for this type, “caseous” necrosis, literally means “cheese-like.”

Any form of death other than necrosis is considered “programmed,” meaning it’s carried out intentionally by the cell because it’s damaged or has outlived its usefulness.

A good, clean death: Apoptosis

The two main categories of programmed cell death are “silent and violent,” says Thirumala-Devi Kanneganti, an immunologist at St. Jude Children’s Research Hospital in Memphis, Tennessee. Apoptosis, first named in 1972, is the original silent type: It’s a neat, clean form of cell death that doesn’t wake the immune system.

That’s handy when cells are damaged or have served out their purpose. Apoptosis allows tadpoles to discard tail cells when they become frogs, for example, or human embryos to dispose of the webbing between developing fingers.

The cell shrinks and detaches from its neighbors. Genetic material in the nucleus breaks into pieces that scrunch together, and the nucleus itself fragments. The membrane bubbles and blisters, and the cell disintegrates. Other cells gobble up the bits, keeping the tissue tidy.

In necrosis, a cell dies by accident, releasing its contents and drawing immune cells to the site of damage by creating inflammation. In apoptosis, the cell collapses in on itself and the bits are cleared away without causing damaging inflammation.

Enlarge / In necrosis, a cell dies by accident, releasing its contents and drawing immune cells to the site of damage by creating inflammation. In apoptosis, the cell collapses in on itself and the bits are cleared away without causing damaging inflammation.

Your cells are dying. All the time. Read More »