Comparing stimulation of a Venus flytrap and the mutant DYSC. Credit: Ines Kreuzer, Rainer Hedrich, Soenke Scherzer

This mutant Venus flytrap mysteriously lost its ability to “count” to 5

The town of İznik, in northwest Turkey, may not be as well-known as nearby Istanbul, but it has a history just as long and storied. Once ruled over by followers of Alexander the Great, it eventually became one of the most important urban centers in the Roman Empire, where, renamed Nicaea, it found its major claim to fame in Christian history, hosting the first and second Councils of Nicaea – the meetings which formally set out some of the foundational beliefs of the religion. 

Over the centuries since then, it’s seen earthquakes, invasions, industry, and decline, with some of the oldest and most venerated sites destroyed even in the modern era. It’s been the capital of four civilizations and has been suggested as a UNESCO World Heritage Site.

Given all this, it may be surprising that the town has only just got its own museum – but now, more than two years after the first stone was laid, the İznik Museum of Archaeology has finally been completed.

“The new museum contains quite significant movable cultural assets,” former museum director and archaeologist Taylan Sevil told the local Ihlas News Agency. “There are artifacts of many civilizations from prehistoric times to the present.”

Among those artifacts are a marble board game from the Roman era, a highly decorated sarcophagus dedicated to the Greek hero Achilles, and the sarcophagus of Alexander the Great’s general Antigonos I. But there’s another relic that’s even more intriguing: an Ancient Roman letter of mourning, found in Antigonos’s tomb, newly translated and displayed 2,500 years after it was originally composed.

“I, the sad Arete, cry out with all body and soul from the tomb of Antigonos,” the message reads. “I pull my hair out from grief and I express myself by crying. This ill luck, the death, has captured me instead of emancipating this precious man.”

It’s not known who “Arete” was – the term is not really a name, but an Ancient Greek concept describing “excellence” in some way. Depending on what or who it was applied to, it could refer to the realization of one’s full potential; moral virtue; self-restraint or justice; strength and bravery; or simply the state of being “good”. 

But whoever the message came from, it conveys an emotional story that we all go through at some point: grief at the loss of someone important to us. No wonder, then, that it’s one of the showstoppers in the new museum, which officials hope will become one of the most important in the world.

“The museum fills a huge gap here,” Sevil said. “It [will invite] people to witness world civilization.”

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It's a long stretch of road where the gauge could have been lost. Image credit: cve iv/Serban Bogdan/Shutterstock.com, edited by IFLScience

Authorities in Western Australia have warned the general population that a radioactive capsule used as a gauge in a mining operation has been lost on a stretch of road that is about 1,400 kilometers (870 miles) long. The risk to the population is considered minimal, but people need to be warned of what to do in case they see it.

The gauge is tiny. It’s 8 millimeters by 6 millimeters (0.31 inches by 0.24 inches), roughly like two hearing aid batteries stuck together. It was being taken from the town of Newman to the Northeastern suburbs of Perth. Exposure to it for a long time could cause radiation burns or radiation sickness, and if anyone finds it they should immediately alert the authorities. A concern is that the small capsule could have got stuck to a car's wheel.

The capsule was being taken to Perth for repair on January 10, and it arrived there on January 16 and was placed in a secure radiation store. The packaging was then opened on January 25, and it was then that it was discovered that the package had broken; one bolt was missing, and the capsule and all its screws likely dropped out of that hole and were potentially lost on the road between Newman and Perth.

Nuclear densitometry is not used just for mining, but also in archaeology and civil construction. It is unclear which radioactive element was used in this gauge. The Western Australian government's advice on these items mentions cobalt-60 and caesium-137. The isotope radium-226 is also used for this purpose, as it can be used up to 300-meter (984-foot) depths. Radium-226 emits mostly alpha particles, but its decay products can emit also beta particles and gamma rays. While dangerous, none of these elements can be weaponized.

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Picture the scene: a beautiful bright clear California day, the sun is shining, the sky is blue, the ocean is pink. Wait, what? Well, thanks to scientists at UC San Diego’s Scripps Institution of Oceanography and the University of Washington that's exactly what you'll get if you go down to San Diego beach in January and February. 

To study how freshwater outflows are mixing with the ocean surfzone, they've started an experiment called Plumes in Nearshore Conditions, or PiNC (see what they did there).

“I'm excited because this research hasn't been done before and it's a really unique experiment,” said Scripps coastal oceanographer Sarah Giddings, who is leading the PiNC study, in a statement.

The experiment is focused on the area around Los Peñasquitos Lagoon, located within Torrey Pines State Beach and Natural Reserve in San Diego, California. The team wants to investigate how freshwater, which is more buoyant and usually warmer than the ocean, interacts with the waves. 

That's where the pink dye comes in, by coloring the freshwater the team can track where the small freshwater plumes are meeting the saltwater surf. The environmentally safe dye will then be tracked as it progresses, both by drone and by sensors on poles situated along the sand. There’s even a jet ski fitted with a fluorometer that can measure the light emitted from the dye. Outside of the surf zone further sensors can measure salinity, temperature, the height of the waves, and the ocean currents. 

This is the first of the dye releases with two more planned for towards the end of January and early February. The researchers hope that the pink dye will be able to tell them more about how sediment, pollutants, and even larvae travel into the ocean through these freshwater outflows. 

“We're bringing together a lot of different people with different expertise, such that I think it's going to have some really great results and impacts," continued Giddings. "We will combine results from this experiment with an older field study and computer models that will allow us to make progress on understanding how these plumes spread.” 

If that's tickled you pink, learn about this bubblegum bright lake that stays pink all year round.

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Ten years after its discovery, the implications of Crispr genome editing are profound and far-reaching, and we are only getting started. This tool, adapted from a bacterial immune system, allows us to cut and edit the genetic code in any living cell to make highly targeted changes and repairs. A small number of people with genetic diseases have been helped by Crispr therapies, highlighting the potential to impact the lives of those suffering from the approximately 7,000 genetic diseases with known causes. Trials are ongoing in diseases ranging from diabetes to infectious disease.

In 2023, we will begin to benefit from new Crispr-based solutions in other areas. For instance, following on the heels of the initial clinical trial results, the first agricultural applications using Crispr have recently entered the market: A US Food and Drug Administration–approved edit to cattle genes re-creates a slick coat that is occasionally found in nature and allows cows to tolerate increasing temperatures; a Crispr-edited tomato, approved for sale in Japan, has enhanced nutritional qualities. In other crops, Crispr is being used experimentally to increase yield, reduce pesticide and water use, and protect against disease. 

The next space for Crispr innovations will be climate change, the defining fight of our times. In 2023, bold new efforts using Crispr to target climate change will begin.

First, new research aims at reducing carbon emissions from agriculture. Agriculture is responsible for about a quarter of all greenhouse gas emissions, and these mainly come from microbes found either in soil, for example in rice paddies, or in the guts of farm animals. This new research is focusing on how to use Crispr to edit these microbes or shift the composition of microbial communities to reduce or even eliminate greenhouse gas emissions.

Second, we are finding ways to improve the inherent ability of plants and microbes to capture carbon and store it in the soil. Plants “breathe in” carbon dioxide during photosynthesis and use it to make energy, but usually the carbon is cycled back into the atmosphere fairly quickly. New research aims to work with plants and soil microbes to not just capture carbon but also store it in soil for long periods of time, replacing some of the soil carbon that has been lost in vast quantities since the advent of modern agriculture. 

Third, we are developing new ways to minimize farmer inputs like fertilizers and pesticides that have high carbon costs, as well as other environmental health costs. New Crispr research aims to edit staple crops like rice so they can grow with less fertilizer. Crispr can be used to make plants resistant to common pathogens and pests, reducing the need for high-carbon-emission chemical inputs. 

Finally, we need ways to help agriculture deal with the degree of climate change that has already occurred or is inevitable. New research is using Crispr to engineer plants that can produce more food and other materials with less water and that are tolerant to temperature extremes.

A great deal of the attention surrounding Crispr has focused on the medical applications, and for good reason: The results are promising, and the personal stories are uplifting, offering hope to many who have suffered from long-neglected genetic diseases. In 2023, as Crispr moves into agriculture and climate, we will have the opportunity to radically improve human health in a holistic way that can better safeguard our society and enable millions of people around the world to flourish.

Crispr Wants to Feed the World

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String theory began over 50 years ago as a way to understand the strong nuclear force. Since then, it’s grown to become a theory of everything, capable of explaining the nature of every particle, every force, every fundamental constant, and the existence of the Universe itself. But despite decades of work, it has failed to deliver on its promise.

 

What went wrong, and where do we go from here?

Beginning threads

Like most revolutions, string theory had humble origins. It started in the 1960s as an attempt to understand the workings of the strong nuclear force, which had only recently been discovered. Quantum field theory, which had been used successfully to explain electromagnetism and the weak nuclear force, wasn’t cutting it, so physicists were eager for something new.

 

A group of physicists took a mathematical technique developed (and later abandoned) by quantum godfather Werner Heisenberg and expanded it. In that expansion, they found the first strings—mathematical structures that repeated themselves in spacetime. Unfortunately, this proto-string theory made incorrect predictions about the nature of the strong force and also had a variety of troublesome artifacts (like the existence of tachyons, particles that only traveled faster than light). Once another theory was developed to explain the strong force—the one we use today, based on quarks and gluons—string theory faded from the scene.

 

But again, like most revolutions, whispers remained through the years, keeping hopes alive. In the 1970s, physicists uncovered several remarkable properties of string theory. One, the theory could support more forces than just the strong nuclear force. The strings in string theory had enormous tension, forcing them to curl up on themselves into the smallest possible volume, something around the Planck scale. Once in place, the strings could support various vibrations, just like a taut guitar string. The different vibrations led to different manifestations of forces: one note for strong nuclear, another for electromagnetism, and so on.

 

One of the possible vibrations of the string acted like a massless spin-2 particle. This is a very special particle because that would be the quantum force carrier of the gravitational force, the holy grail of a quantized theory of gravity. The theorists at the time couldn’t believe their chalkboards: String theory naturally, elegantly included quantum gravity, and they weren’t even trying!

 

The second big deal to come out in the 1970s was the introduction of supersymmetry, which claimed that all the particles that carry forces (called bosons, a category that includes photons and gluons) were linked to a supersymmetric partner from the collection of particles that build stuff (called fermions, like electrons and quarks), and vice versa.

 

This symmetry doesn’t appear in everyday settings; it only manifests at extremely high energies. So if you were to go back in time to the earliest moments of the Big Bang or had enough funding to build a particle collider along the orbit of Jupiter, you wouldn’t just see the normal zoo of particles we’re familiar with; you'd see all their supersymmetric partners, too. These were given suitably stupid names, like selectrons, sneutrinos, squarks, photinos, and my personal (least) favorite, the wino boson.

 

By making this connection, string theory could build a bridge from the bosons to the fermions, allowing it to leap from just a theory of forces to a theory of every single particle in existence. The introduction of supersymmetry also solved the nasty problem of tachyons by replacing those troublesome particles with supersymmetric partners, which was a nice flourish.

 

At the end of the 1970s, string theory could potentially explain all the particles and all the interactions among them and provide a quantum solution to gravity.

 

One theory to rule them all, one theory to find them, one theory to bring them all, and in the stringiness bind them.

Requiem for a string: Charting the rise and fall of a theory of everything

Rocket Report: NASA validates new engine design; Chinese firm tests mini Starship

The discovery could open the door to an anti-obesity pill that targets neurons in the brain. Experiments in rats show that cells called astrocytes control a chemical pathway to the gut. However, the study suggests that continuously gorging on fatty and sugary products disrupts that link.

“Calorie intake seems to be regulated in the short-term by astrocytes. We found that a brief exposure (three to five days) of high fat/calorie diet has the greatest effect on astrocytes, triggering the normal signaling pathway to control the stomach. Over time, astrocytes seem to desensitize to the high fat food. Around 10-14 days of eating high fat/calorie diet, astrocytes seem to fail to react and the brain’s ability to regulate calorie intake seems to be lost. This disrupts the signaling to the stomach and delays how it empties,” says lead author Dr. Kirsteen Browning from Penn State College of Medicine, in a media release.

Understanding the brain’s role and the complex mechanisms that lead to gluttony may lead to therapies to treat weight gain. The CDC estimates that over 40 percent of U.S. adults are obese, raising their risk of cardiovascular disease and Type 2 diabetes.

What happens in the brain after consuming a high-fat diet?

Astrocytes initially react when someone consumes junk food, releasing chemicals called gliotransmitters. They stimulate neurons that ensure the stomach contracts correctly to fill and empty in response to food passing through the digestive system.

When something inhibits astrocytes, it disrupts the cascade. The decrease in signaling chemicals leads to a delay in digestion because the stomach doesn’t fill and empty appropriately. The vigorous investigation used behavioral observation to monitor food intake in more than 200 lab rodents fed either a normal or high-fat diet for one, three, five, or 14 days.

Study authors combined this with pharmacological and specialist genetic techniques to target distinct neural circuits. This enabled the team to specifically inhibit astrocytes in a particular region of the brainstem, the posterior part that connects to the spinal cord.

Researchers then assessed how individual neurons behaved when the rats were awake. If the same mechanism occurs in humans, drugs could safely target the mechanism, providing the treatment doesn’t affect other neural pathways.

“We have yet to find out whether the loss of astrocyte activity and the signaling mechanism is the cause of overeating or that it occurs in response to the overeating. We are eager to find out whether it is possible to reactivate the brain’s apparent lost ability to regulate calorie intake.

If this is the case, it could lead to interventions to help restore calorie regulation in humans,” Dr. Browning concludes.

The findings appear in The Journal of Physiology.

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Recent research led by the University of Queensland and the University of Göttingen examined the effects of transitioning to clean energy by connecting global resource inventories with demographic systems to uncover potential risks and benefits. The findings suggest that the increased demand for energy transition metals (ETMs) may be more disruptive to some communities than reducing thermal coal production.

The researchers determined that while ending coal production could affect at least 33.5 million people living in mine-town systems, an additional 115.7 million may be impacted by disruptions caused by energy transition metals (ETMs). The findings were published in the journal Nature Communications.

The researchers linked the location and type of resource with human settlements in order to assess interactions, dependencies, and contingencies between resources and populations – a “mine-town systems” approach. The research takes into account both sides of the energy transition by incorporating global resource inventories for coal on the one hand, and the energy transition metals on the other. Energy transition metals refer to the minerals that are required for renewable technologies to accelerate the transition to a clean energy future. These minerals and metals are essential for wind turbines, solar panels, and batteries for electric vehicles.

Dr. Kamila Svobodova, who led the study, is an Honorary Research Fellow at the University of Queensland and holds a research fellowship at the University of Göttingen. Svobodova explained: “These findings will help inform future planning and regulation of the energy transition. Our new mine-town systems approach establishes an empirical basis for examining the scale and location of demographic effects of changing energy systems.”

“The data shows an asymmetry in the distribution of risks: mine-town systems within the United States are most sensitive to coal phase-out, while systems in Australia and Canada are most sensitive to ETM phase-in. This study highlights an urgent need for more granular socio-economic data on populations living and working in affected areas, and for targeted macro-level planning in order to support a transition from coal to ETMs that is fair for local people.”

Svobodova adds: “Questions of social disruption are rarely considered at a global scale. However, in this study, we are able to deliver a global-scale model which can also be scaled down to national jurisdictions and regions which are under pressure from energy transition.”

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Vulcan Point was formed when the main caldera – or crater – of Taal Volcano filled with water, creating Main Crater Lake. Out of its turquoise waters peaks the tip of one of the volcano’s cinder cones, creating the tiny island, Vulcan Point.

Main Crater Lake itself was formed in 1911 when an eruption lowered the elevation of the island by 1-3 meters (3-10 feet). It is nestled in the caldera of Taal Volcano, which has erupted numerous times, dating back to 3580 BCE, and is the second most active volcano in the Philippines.

In January 2020, the volcano erupted again, causing Main Crater Lake to dry up and disappear, temporarily disrupting the whole island-within-a-lake-within-an-island-within-a-lake-within-an-island thing. Fortunately for Vulcan Point fans, the lake soon refilled.

Where is Vulcan Point?

Taal Volcano, and therefore Vulcan Point, are found on Luzon Island in the province of Batangas in the Philippines. The volcano is located around 50 kilometers (30 miles) south of the capital, Manila.

It is surrounded by Lake Taal, which is the only place in the world you can find tawilis, the world’s only freshwater sardine, and the freshwater Garman's sea snake.

The turducken of islands/lakes really is the gift that keeps on giving.

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So far Johnson's team has focused on the unsurprising: developing a diet and exercise regimen. If you eat and drink right and get regular exercise you will improve your overall fitness, probably more so when you've spent large sums on a team to help you stick to it. Johnson sticks to a 1,977-calorie vegan diet, and even sticks to a sleep schedule. He also takes a number of medicines and supplements.

Meanwhile, he monitors everything from his bowels and his body fat, to his nocturnal erections, Popular Mechanic reports. Adjustments to his regimen and medication are made after viewing the data.

Aging biologist and YouTuber Andrew Steele's view on Project Blueprint.

So far, Johnson claims to have seen good results, improving measures such as his blood pressure and lung capacity. 

"My new endeavor, Project Blueprint, aims to measure all 70+ organs of my body and then maximally reverse the quantified biological age of each," he writes on his website. "We have measured over 15 organs and I’ve scored 507 age reversal points. My chronological age is 44, measured biological age is 36."

He claims his GrimAge – a metric based on biomarkers in your DNA, which has been shown as a good predictor of morbidity – is 36. 

While it's good that he's getting some returns on his $2 million, so far there's nothing really out of the ordinary going on. We have known that diet, exercise and aging are linked for a long time, so it's no real surprise that living healthily made Johnson fitter, and equivalent to a younger man. So far, it seems like he's paid for a gym routine and a diet, rather than the brain, heart, lungs, penis, and rectum of an 18-year-old.

According to the team's regenerative medicine doctor, they may be looking at gene therapies, though no specifics were given. Gene therapies have shown promise in reversing aging signs in mice, with some scientists skeptical similar therapies could one day be applied to humans.

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Egypt discovers 4,300-year-old tombs in ancient burial ground

CAIRO -- Egypt on Thursday said it uncovered several 4,300-year-old tombs in Saqqara as it continues a series of discoveries in the ancient burial ground.

The tombs date back to the Fifth and Sixth dynasties of the Old Kingdom (2686-2181 B.C.), officials said in Saqqara, which lies some 19 miles south of Cairo.

Egyptian archaeologist Zahi Hawass, the director of the Egyptian excavation team, works at the site of the Step Pyramid of Djoser in Saqqara, 15 miles southwest of Cairo, Egypt, Jan. 26, 2023.

Ministry of Tourism & Antiquities

 

Egyptologist Zahi Hawass, who led the team that made the discovery in Saqqara's Gisr Al-Mudir area, said "12 beautifully carved statues" were also found as well as two deep burial shafts, one of which includes what he described as possibly the "most complete mummy found in Egypt to date."

"The most important tomb belongs to Khnumdjedef, an inspector of the officials, a supervisor of the nobles, and a priest in the pyramid complex of Unas, the last king of the fifth dynasty. The tomb is decorated with scenes of daily life," Hawass said.

Egyptian archaeologist Zahi Hawass, the director of the Egyptian excavation team, speaks during a press conference at the site of the Step Pyramid of Djoser in Saqqara, 15 miles southwest of Cairo, Egypt, Jan. 26, 2023.

Amr Nabil/AP

"The second largest tomb belonged to Meri, who held many important titles, such as keeper of the secrets and assistant of the great leader of the palace."

Another tomb featured a handful of statues of unidentified individuals, including two couples.

Egyptian antiquities workers watch recently discovered artifacts at the site of the Step Pyramid of Djoser in Saqqara, 24 kilometers (15 miles) southwest of Cairo, Egypt, Jan. 26, 2023.

Amr Nabil/AP

 

Hawass said the main highlight was the uncovering of a 15-meter-deep burial shaft where a "large rectangular limestone sarcophagus" was found at its bottom.

The mummy of a man called Hekashepes was found inside, he revealed. It is covered with gold leaf.

An Egyptian archaeologist restores antiquities after the announcement of new discoveries in Gisr el-Mudir in Saqqara, in Giza, Egypt, Jan. 26, 2023.

Mohamed Abd El Ghany/Reuters

“This mummy may be the oldest and most complete mummy found in Egypt to date,” Hawass added.

Wooden and stone statues were also uncovered in another 10-meter-deep shaft, as was a stone sarcophagus that included a mummy of a man called Fetek, according to the inscriptions found on the coffin.

Recently discovered artifacts at the site of the Step Pyramid of Djoser in Saqqara, 15 miles southwest of Cairo, Egypt, Jan. 26, 2023.

Ministry of Tourism & Antiquities

 

Egypt hopes a string of discoveries will help revive its ailing tourism industry, a key source of hard currency.

Extensive excavation efforts in Saqqara in recent years have led to several high-profile archaeological discoveries, including the unearthing of a 4,400-year-old tomb of royal priest Wahtye in 2018 and the discovery of hundreds of mummified animals and statues a year later.

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Hody Buford Childress, who died Jan. 1 at age 80, had spent 10 years secretly giving a local pharmacy $100 to help pay for prescriptions locals couldn’t afford.

And while Childress was clearly looking to do something nice for those most in need, his actions set off a ripple effect.

These waves of goodness started years ago when Childress struck up an arrangement with Brooke Walker, owner of Geraldine Drugs in Geraldine, Alabama. He came into the pharmacy at least monthly and hand her a folded-up $100 bill, asking her to apply the money to those in need, WHNT-TV reported.

It was a secret that was kept over the years and revealed this month at his funeral.

Childress told Walker to simply tell anyone who didn’t have money for prescriptions that the gift came from a person who “felt led by God to help another.”

“He said, ‘Don’t tell a soul where the money came from — if they ask, just tell them it’s a blessing from the Lord,’” Walker said.

She also shared a more detailed history of how it all began.

“He came in one day and asked if there were ever times when someone couldn’t get their medication due to financial reasons. And I told him yes — many times,” Walker told WHNT-TV. “In the beginning, I was keeping it in an envelope because I thought it was a one-time donation. Then, [Hody] returned the next month…and the next…and the next.”

When he became too sick to deliver the money, he told his daughter about the incredible effort, NPR reported.

His kids, Tania Nix and Doug Childress, told “Good Morning America, their father’s way of living and loving others inspired them.

“Daddy’s done a lot for everybody,” Doug Childress said.

Considering Childress was a “man of modest means,” as Walker proclaimed, this $100 per month gesture meant a lot to everyone, including him.

The pharmacy owner said she has seen others helped by Childress later come back to pay it forward, and she, too, plans to launch the “Hody Childress” fund to keep the good deeds flowing.

Childress’ story offers several essential reminders. Every kind deed matters and, over time, there can be a ripple effect when we step out in faith, stretch ourselves, and live out God’s mandate to love others.

He likely didn’t realize his secret would spark a long-lasting legacy, but that’s precisely what’s happening.

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In 2020, it became the most popular form of dieting in the U.S., according to the Food Information Council's Food and Health Survey, and it remains a significant part of diet culture. Proponents claim it can help with everything from weight loss to cholesterol and blood sugar management, despite some less than promising research.

So does intermittent fasting really work? It's a complicated question with an equally complicated answer, says Rachel Rodgers, an associate professor of applied psychology at Northeastern University.

Rodgers, who specializes in body image, disordered eating and health-related behaviors, spoke to Northeastern Global News about her skepticism around intermittent fasting, the issues with diets more generally and why modern food production has made eating in moderation nearly impossible. Her comments have been edited for brevity and clarity.

What is intermittent fasting?

That is an important question because what people call intermittent fasting can look quite different. There is intermittent fasting that is alternating days on which people eat ad libitum, those being called "feast days," and those where their intake is much reduced, "fast days." It can look like time restricted fasting where people will not eat for a certain amount of consecutive hours and then eat the rest of the time. It can be periodic fasting, whereby you might fast for up to 24 hours twice a week but not on alternating days. So, it really depends.

What is the professed benefit of intermittent fasting?

I'm not convinced about the benefits. In terms of the clinical literature, we really don't know that much. There are three or four clinical trials that have been conducted on these behaviors, only one of which was a really rigorous one with follow-ups where people were assessed multiple times after the end. The rest of the literature is piecemeal in terms of what the studies actually look like, what they were actually assessing.

There is evidence that different forms of intermittent fasting are associated with some decreases in weight. However, that should be placed in the context that up to 40% or 50% of the people drop out of the clinical trials [and] that it's not clear that they're actually adhering to the protocol. Any changes that we're seeing are not clearly attributable to what the intervention was actually designed to do and to measure. All that aside, there do seem to be some small reductions in weight in people who are engaging in these kinds of behaviors.

In terms of the mechanisms at work, we don't really know. Is it just that people are eating less? Is it that there are metabolic benefits? It's possible. It's a little bit unclear. The other purported health benefits are really unclear in terms of the data. Anything about health indicators is not clear at all.

Is intermittent fasting an effective, helpful form of dieting or health-related behavior?

I am personally wary of any behavior that is specifically designed to target weight rather than to help people develop a comfortable and attuned relationship to their eating behaviors in a way that is going to work for them sustainably. I'm also wary of anything that has a rule because once you get into a rules system, rules get broken and then you get into black and white thinking. You've broken the rule––everything's gone wrong. As we know, that's the basis of a binge-restriction cycle. Intermittent fasting is essentially a form of dieting, and that's something I generally find less helpful as a philosophy.

Are there any long-term effects that people need to look out for?

The problem is we don't have the data to predict that. My main concern is that it might increase peoples' reliance on rule-based patterns and, potentially, disordered eating. It could increase other mental health concerns if it becomes hard to sustain or people feel like they're failing at something. But we don't really know.

Why do you think intermittent fasting has become so popular?

At any point in time you're going to have a certain kind of dieting that becomes fashionable.

One of the marketing strengths of this particular one is that it's not so much about what you can eat but when. Sometimes that can be easier for people because we all have particular foods that we like to eat, so not being told that you can't have something, just that it's about when, can be perceived as easier.

Also, one of the things that's difficult in our society, due to an intense amount of food marketing as well as the way foods are engineered, is eating in moderation. This is not the fault of people. It's a logical result of the food environment we live in, and therefore having that 'now I can eat, now I just don't eat' [approach] avoids the difficulties in moderation.

If, as you say, intermittent fasting and other diets are not a helpful way to approach eating, what strategies or approaches do you think are more helpful?

There are other approaches to eating that I think are more helpful. These are ones that are flexible and that are based on the idea that eating will look different for every person and it might look different for each person at a different point in time. These ways of eating are much more in tune with physical cues, or hunger and satiety and being able to recognize those bodily signals. Am I hungry? Am I not hungry? What would I like to eat now? Why am I thinking I would like to eat that thing now? Am I just bored? Am I not?

There is a pattern of eating that is called intuitive eating that's really based on rejecting diet culture and being attuned to those things. Mindful eating is another approach that really focuses on enjoying the foods and paying attention in a nonjudgmental way that also gets into the idea that eating is a process rather than, "What's this going to do for me? Is it going to make me immortal? Am I going to be beautiful and shiny?"

I think the question we should be asking ourselves when it comes to intermittent fasting is, how did we come to live in a world where we need to be not eating half of the time? Because if this works, if this is the way forward, it seems kind of drastic. How did we get to a place where our food environment is so pressurizing and the foods that we're surrounded with are so dense and so difficult to eat in moderation that this is now seeming like a perfectly realistic option?

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People often think they know what causes chronic depression. Surveys indicate that more than 80% of the public blames a “chemical imbalance” in the brain. That idea is widespread in pop psychology and cited in research papers and medical textbooks. Listening to Prozac, a book that describes the life-changing value of treating depression with medications that aim to correct this imbalance, spent months on the New York Times bestseller list.

The unbalanced brain chemical in question is serotonin, an important neurotransmitter with fabled “feel-good” effects. Serotonin helps regulate systems in the brain that control everything from body temperature and sleep to sex drive and hunger. For decades, it has also been touted as the pharmaceutical MVP for fighting depression. Widely prescribed medications like Prozac (fluoxetine) are designed to treat chronic depression by raising serotonin levels.

Yet the causes of depression go far beyond serotonin deficiency. Clinical studies have repeatedly concluded that the role of serotonin in depression has been overstated. Indeed, the entire premise of the chemical-imbalance theory may be wrong, despite the relief that Prozac seems to bring to many patients.

A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form. An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them. They found no convincing evidence that lower levels of serotonin caused or were even associated with depression. People with depression didn’t reliably seem to have less serotonin activity than people without the disorder.

To evaluate the evidence that imbalances of serotonin cause depression, the psychiatric researcher Joanna Moncrieff of University College London organized a review that looked at hundreds of papers in six areas of research.

Courtesy of Joanna Moncrieff

Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. Genetic studies also seemed to rule out any connection between genes affecting serotonin levels and depression, even when the researchers tried to consider stress as a possible cofactor.

“If you were still of the opinion that it was simply a chemical imbalance of serotonin, then yeah, it’s pretty damning,” said Taylor Braund, a clinical neuroscientist and postdoctoral research fellow at the Black Dog Institute in Australia who was not involved in the new study. (“The black dog” was Winston Churchill’s term for his own dark moods, which some historians speculate were depression.)

The realization that serotonin deficits by themselves probably don’t cause depression has left scientists wondering what does. The evidence suggests that there may not be a simple answer. In fact, it’s leading neuropsychiatric researchers to rethink what depression might be.

Treating the Wrong Disease

The focus on serotonin in depression began with a tuberculosis drug. In the 1950s, doctors started prescribing iproniazid, a compound developed to target lung-dwelling Mycobacterium tuberculosis bacteria. The drug wasn’t particularly good for treating tuberculosis infections — but it did bless some patients with an unexpected and pleasant side effect. “Their lung function and everything wasn’t getting much better, but their mood tended to improve,” said Gerard Sanacora, a clinical psychiatrist and the director of the depression research program at Yale University.

Perplexed by this outcome, researchers began studying how iproniazid and related drugs worked in the brains of rats and rabbits. They discovered that the drugs blocked the animals’ body from absorbing compounds called amines — which include serotonin, a chemical that carries messages between nerve cells in the brain.

Several prominent psychologists, among them the late clinicians Alec Coppen and Joseph Schildkraut, seized on the idea that depression could be caused by a chronic deficiency of serotonin in the brain. The serotonin hypothesis of depression went on to inform decades of drug development and neuroscientific research. During the late 1980s, it led to the introduction of selective serotonin reuptake inhibitor (SSRI) drugs, like Prozac. (The drugs raise levels of serotonin activity by slowing down the neurotransmitter’s absorption by neurons.) Today, the serotonin hypothesis is still the explanation most often given to patients with depression when they’re prescribed SSRIs.

But doubts about the serotonin model were circulating by the mid-1990s. Some researchers noticed that SSRIs often fell short of expectations and didn’t improve significantly on the performance of older drugs like lithium. “The studies didn’t really stack up,” Moncrieff said.

Merrill Sherman/Quanta Magazine

By the early 2000s, few experts believed that depression is caused solely by lack of serotonin, but no one ever attempted a comprehensive evaluation of the evidence. That eventually prompted Moncrieff to organize such a study, “so that we could get a view as to whether this theory was supported or not,” she said.

She and her colleagues found that it wasn’t, but the serotonin hypothesis still has adherents. Last October — just a few months after their review appeared — a paper published online in Biological Psychiatry claimed to offer a concrete validation of the serotonin theory. Other researchers remain skeptical, however, because the study looked at only 17 volunteers. Moncrieff dismissed the results as statistically insignificant.

A Different Chemical Imbalance

Although serotonin levels don’t seem to be the primary driver of depression, SSRIs show a modest improvement over placebos in clinical trials. But the mechanism behind that improvement remains elusive. “Just because aspirin relieves a headache, [it] doesn’t mean that aspirin deficits in the body are causing headaches,” said John Krystal, a neuropharmacologist and chair of the psychiatry department at Yale University. “Fully understanding how SSRIs produce clinical change is still a work in progress.”

John Krystal, the chair of the psychiatry department at Yale University, called the effort to understand the clinical effects of SSRI drugs “a work in progress.”

Nicole Mele

Speculation about the source of that benefit has spawned alternative theories about the origins of depression.

Despite the “selective” in their name, some SSRIs change the relative concentrations of chemicals other than serotonin. Some clinical psychiatrists believe that one of the other compounds may be the true force inducing or relieving depression. For example, SSRIs increase the circulating levels of the amino acid tryptophan, a serotonin precursor which helps regulate sleep cycles. Over the last 15 years or so, this chemical has emerged as a strong candidate in its own right for staving off depression. “There’s quite good evidence from tryptophan depletion studies,” said Michael Browning, a clinical psychiatrist at the University of Oxford.

A number of tryptophan depletion studies found that about two-thirds of people who have recently recovered from a depressive episode will relapse when given diets artificially low in tryptophan. People with a family history of depression also appear vulnerable to tryptophan depletion. And tryptophan has a secondary effect of raising serotonin levels in the brain.

Recent evidence also suggests that both tryptophan and serotonin may contribute to the regulation of bacteria and other microbes growing in the gut, and chemical signals from these microbiota could affect mood. While the exact mechanisms linking the brain and gut are still poorly understood, the connection seems to influence how the brain develops. However, because most tryptophan depletion studies so far have been small, the matter is far from settled.

Other neurotransmitters like glutamate, which plays an essential role in memory formation, and GABA, which inhibits cells from sending messages to one another, may be involved in depression as well, according to Browning. It’s possible that SSRIs work by tweaking the amounts of these compounds in the brain.

Moncrieff sees the hunt for other chemical imbalances at the root of depression as akin to rebranding rather than a truly novel line of research. “I would suggest that they are still subscribing to something like the serotonin hypothesis,” she said — the idea that antidepressants work by reversing some chemical abnormality in the brain. She thinks instead that serotonin has such widespread effects in the brain that we may have trouble disentangling their direct antidepressant effect from other changes in our emotions or sensations that temporarily override feelings of anxiety and despair.

Genetic Answers

Not all theories of depression hinge on neurotransmitter deficiencies. Some look for culprits at the genetic level.

When the first roughly complete draft sequence of the human genome was announced in 2003, it was widely hailed as the foundation of a new era in medicine. In the two decades since then, researchers have identified genes that underlie a huge spectrum of disorders, including about 200 genes that have been linked to a risk of depression. (Several hundred more genes have been identified as possibly raising the risk.)

“It’s really important that people understand that there is a genetics of depression,” Krystal said. “Until very recently, only psychological and environmental factors were considered.”

Our knowledge of the genetics, however, is incomplete. Krystal noted that studies of twins suggest that genetics may account for 40% of the risk of depression. Yet the currently identified genes seem to explain only about 5%.

Moreover, simply having the genes for depression doesn’t necessarily guarantee that someone will become depressed. The genes also need to be activated in some way, by either internal or external conditions.

“There’s a false distinction that is sometimes drawn between environmental factors and genetic factors,” said Srijan Sen, a neuroscientist at the University of Michigan. “For most common traits of interest, both genetic and environmental factors play a critical role.”

Sen’s lab studies the genetic basis of depression by mapping subjects’ genomes and carefully observing how individuals with different genetic profiles respond to changes in their environment. (Recently, they have looked at stress brought on by the Covid-19 pandemic.) Different genetic variations can affect whether individuals respond to certain types of stress, such as sleep deprivation, physical or emotional abuse, and lack of social contact, by becoming depressed.

Research suggests that in the brains of people with chronic depression, the “white matter” areas that are rich in nerve fibers have fewer connections. The cause for this difference is uncertain, however. Ralph T. Hutchins/Science Source

Environmental influences like stress can also sometimes give rise to “epigenetic” changes to a genome that affect subsequent gene expression.

For example, Sen’s laboratory studies epigenetic changes in the caps on the ends of chromosomes, known as telomeres, which affect cell division. Other labs look at changes in chemical tags called methylation groups that can turn genes on or off. Epigenetic changes can sometimes even be passed down through generations. “The effects of the environment are just as biological as the effects of genes,” Sen said. “Just the source is different.”

Studies of these genes may someday help identify the form of treatment a patient would respond to best. Some genes may predispose an individual to better results from cognitive behavioral therapy, while other patients might fare better with an SSRI or therapeutic ketamine. However, it’s far too early to say which genes respond to which treatment, Sen said.

A Product of Neural Wiring

Differences in a person’s genes may predispose them to depression; so, too, may differences in the neural wiring and structure of their brain. Numerous studies have shown that individuals differ in how the neurons in their brains interconnect to form functional pathways, and that those pathways influence mental health.

Jonathan Repple and Susanne Meinert of Goethe University and their colleagues are exploring why chronically depressed people have fewer connections in their brains. Possible explanations include neuroplasticity and inflammation. Roberto Schirdewahn/WWU

In a recent conference presentation, a team led by Jonathan Repple, a psychiatry researcher at Goethe University in Frankfurt, Germany, described how they scanned the brains of acutely depressed volunteers and found that they differed structurally from those of a non-depressed control group. For example, people experiencing depression showed fewer connections within the “white matter” of the nerve fibers in their brains. (However, there is no white-matter threshold for poor mental health: Repple notes that you can’t diagnose depression by scanning someone’s brain.)

After the depressed group underwent six weeks of treatment, Repple’s team ran another round of brain scans. This time, they found that the general level of neural connectivity in the depressed patients’ brains had increased as their symptoms lessened. To get the increase, it didn’t seem to matter what kind of treatment the patients received, so long as their mood improved.

A possible explanation for this change is the phenomenon of neuroplasticity. “Neuroplasticity means that the brain actually is able to create new connections, to change its wiring,” Repple said. If depression occurs when a brain has too few interconnections or loses some, then harnessing neuroplastic effects to increase interconnectedness might help lift a person’s mood.

Chronic Inflammation

Repple warns, however, that another explanation for the effects his team observed is also possible: Perhaps the depressed patients’ brain connections were impaired by inflammation. Chronic inflammation impedes the body’s ability to heal, and in neural tissue it can gradually degrade synaptic connections. The loss of such connections is thought to contribute to mood disorders.

Good evidence supports this theory. When psychiatrists have evaluated populations of patients who have chronic inflammatory diseases like lupus and rheumatoid arthritis, they’ve found that “all of them have higher-than-average rates of depression,” said Charles Nemeroff, a neuropsychiatrist at the University of Texas, Austin. Of course, knowing that they have an incurable, degenerative condition may contribute to a patient’s depressed feelings, but the researchers suspect that the inflammation itself is also a factor.

Charles Nemeroff, a neuropsychiatrist at the University of Texas, Austin, thinks that in the future, treatments for depression will be tailored to individual patients by a more nuanced understanding of their risk factors. UT Austin Health

Medical researchers have found that inducing inflammation in certain patients can trigger depression. Interferon alpha, which is sometimes used to treat chronic hepatitis C and other conditions, causes a major inflammatory response throughout the body by flooding the immune system with proteins known as cytokines — molecules that facilitate reactions ranging from mild swelling to septic shock. The sudden influx of inflammatory cytokines leads to appetite loss, fatigue and a slowdown in mental and physical activity — all symptoms of major depression. Patients taking interferon often report feeling suddenly, sometimes severely, depressed.

If overlooked chronic inflammation is causing many people’s depression, researchers still need to determine the source of that inflammation. Autoimmune disorders, bacterial infections, high stress and certain viruses, including the virus that causes Covid-19, can all induce persistent inflammatory responses. Viral inflammation can extend directly to tissues in the brain. Devising an effective anti-inflammatory treatment for depression may depend on knowing which of these causes is at work.

It’s also unclear whether simply treating inflammation could be enough to alleviate depression. Clinicians are still trying to parse whether depression causes inflammation or inflammation leads to depression. “It’s a sort of chicken-and-egg phenomenon,” Nemeroff said.

The Umbrella Theory

Increasingly, some scientists are pushing to reframe “depression” as an umbrella term for a suite of related conditions, much as oncologists now think of “cancer” as referring to a legion of distinct but similar malignancies. And just as each cancer needs to be prevented or treated in ways relevant to its origin, treatments for depression may need to be tailored to the individual.

If there are different types of depression, they may present similar symptoms — such as fatigue, apathy, appetite changes, suicidal thoughts, and insomnia or oversleeping — but they might emerge from completely different mixes of environmental and biological factors. Chemical imbalances, genes, brain structure and inflammation could all play a role to varying degrees. “In five or 10 years, we won’t be talking about depression as a unitary thing,” Sen said.

To treat depression effectively, medical researchers may therefore need to develop a nuanced understanding of the ways it can arise. Nemeroff expects that someday the gold standard for care won’t be just one treatment — it will be a set of diagnostic tools that can determine the best therapeutic approach to an individual patient’s depression, be it cognitive behavioral therapy, lifestyle changes, neuromodulation, avoiding genetic triggers, talk therapy, medication or some combination thereof.

That prediction may frustrate some physicians and drug developers, since it’s much easier to prescribe a one-size-fits-all solution. But “appreciating the true, real complexity of depression takes us down a path that is ultimately going to be most impactful,” Krystal said. In the past, he said, clinical psychiatrists were like explorers who landed on a tiny unknown island, set up camp, and got comfortable. “And then we discovered that there’s this whole, enormous continent.”

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Have you wondered why generous people also happen to be the happiest people on this planet?

One of the most generous people I knew in my life was my grandmother.

Growing up, I was no stranger to her generous gestures and her generous endeavors.

As a person with a kind heart, she’d always be generous toward others. Her kindness touched the hearts and minds of many people she was around.

Generosity was a driving force in her life. It was a goddess that showed her a way out of dark times. And all her actions were from coming from a place of genuine love and concern for people.

She’d always put a smile on her face, and as long as others were happy, she was too.

Her relentless generosity is what made her the happiest person in the world. Investing her time and energy into others was her life’s purpose.

And you know what else is interesting about my grandmother? She’s 99 and she’s still alive, which makes me wonder if being happy all her life has helped her live a long life.

If my grandmother were to lose all of her fortunes, she would still be happy. Because the way she stayed content with herself and the world around her was by making sure that everyone around her was happy. As long as everyone was happy, she was too. It’s like her happiness depended on everyone else’s happiness.

If someone in the family was struggling, she was quick to offer her help and support.

Turns out, there is a whole science behind generosity. It’s no secret, generosity and happiness are interconnected. As research has shown, giving to others can help you feel happier and improve your life.

And it doesn’t matter what you do — whether you like giving gifts or helping people financially, generosity goes a long way.

Being generous not only makes people you’re generous towards happy — it makes you happy too. Giving to others can do wonders for your mind — and psychological well-being.

How to practice kindness

If you’re wondering how you can practice generosity, it’s not hard science.

You don’t need to move mountains to achieve a happy state. Sometimes happiness lies in simple gestures like helping someone with groceries, cooking someone a homemade meal, or sending someone a thoughtful postcard.

If you incorporate generosity into your daily life and practice it every day, you’ll see just how improved your life will be.

While being generous won’t overhaul your life and completely erase emotional scars, it can overall increase your happiness and emotional well-being.

One or two random acts of kindness won’t change your life drastically, but practicing kindness regularly over a period of time will produce a change.

Consistently practicing acts of kindness is what matters the most… and ultimately leads to noticeable life changes.

The same thing can be said about habits. Building healthy habits takes time, energy, and commitment. Likewise, practicing acts of generosity takes time.

It’s the repeated behaviors added together that will produce dramatic results.

The takeaway

If you want to make your life a little happier, practice kindness. By practicing acts of kindness over a period of time, you’ll notice your life will change for the better.

A little bit of kindness goes a long way.

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The tradition started a few years ago as a means to support South Colonie families who participate in the district’s backpack program. With rising costs, this year’s tradition continued to support even more families in need.

“Throughout the month of December our staff donates and collects food,” said Transportation Director Peter Tunny. On Saturday, Dec. 17 several members of the transportation team came together to deliver meals to local families. “It is the highlight of our year to donate a generous supply of food to our South Colonie families the weekend prior to the holiday break.”

The Board of Education invited drivers to its meeting on Tuesday, Jan. 17 to allow President Brian Casey to recognize them for their efforts.

“I want to thank the Transportation department for their continued support and generosity of our families,” said Board President Brian Casey. 

“Your kindness and efforts are recognized and very much appreciated.”

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"Escapism is an everyday phenomenon among humans, but little is known regarding its motivational underpinnings, how it affects experiences, and the psychological outcomes from it," said Dr. Frode Stenseng of the Norwegian University of Science and Technology, lead author of the paper.

Running to explore or to evade?

"Escapism is often defined as 'an activity, a form of entertainment, etc. that helps you avoid or forget unpleasant or boring things." In other words, many of our everyday activities may be interpreted as escapism," said Stenseng. "The psychological reward from escapism is reduced self-awareness, less rumination, and a relief from one's most pressing, or stressing, thoughts and emotions."

Escapism can restore perspective, or it can act as a distraction from problems that need to be tackled. Escapism which is adaptive, seeking out positive experiences, is referred to as self-expansion. Meanwhile maladaptive escapism, avoiding negative experiences, is called self-suppression. Effectively, running as exploration or as evasion.

"These two forms of escapism are stemming from two different mindsets, to promote a positive mood, or prevent a negative mood," said Stenseng.

Escapist activities used for self-expansion have more positive effects but also more long-term benefits. Self-suppression, by contrast, tends to suppress positive feelings as well as negative ones and lead to avoidance.

Self-suppression associated with exercise dependence

The team recruited 227 recreational runners, half men and half women, with widely varying running practices. They were asked to fill out questionnaires which investigated three different aspects of escapism and exercise dependence: an escapism scale which measured preference for self-expansion or self-suppression, an exercise dependence scale, and a satisfaction with life scale designed to measure the participants' subjective well-being.

The scientists found that there was very little overlap between runners who favored self-expansion and runners who preferred self-suppression modes of escapism. Self-expansion was positively related with well-being, while self-suppression was negatively related to well-being. Self-suppression and self-expansion were both linked to exercise dependence, but self-suppression was much more strongly linked to it. Neither escapism mode was linked to age, gender, or amount of time a person spent running, but both affected the relationship between well-being and exercise dependence. Whether or not a person fulfilled criteria for exercise dependence, a preference for self-expansion would still be linked to a more positive sense of their own well-being.

Although exercise dependence corrodes the potential well-being gains from exercise, it seems that perceiving lower well-being may be both a cause and an outcome of exercise dependency: the dependency might be driven by lower well-being as well as promoting it.

Similarly, experiencing positive self-expansion might be a psychological motive that promotes exercise dependence.

"More studies using longitudinal research designs are necessary to unravel more of the motivational dynamics and outcomes in escapism," said Stenseng. "But these findings may enlighten people in understanding their own motivation, and be used for therapeutical reasons for individuals striving with a maladaptive engagement in their activity."

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NASA will join a military program to develop nuclear thermal propulsion

A new wave of medicines that treat obesity have taken the world by storm and been met with applause, concern, and abuse.

These are “breakthrough drugs,” writes Eric Topol, a professor of molecular medicine at Scripps Research and one of the best known practicing scientists in the United States. “While there are many drawbacks, we shouldn’t miss such an extraordinary advance in medicine—the first real, potent, and safe treatment of obesity.” 

Novo Nordisk’s semaglutide (also known as Wegovy or Ozempic) was approved as an obesity treatment in adults back in June 2021 in the US and in early 2022 in the United Kingdom and the European Union. At the end of 2022, the US Food and Drug Administration also approved it for treating obesity in children aged 12 and up. On its heels, Eli Lilly’s tirzepatide (or Mounjaro)—approved for treating diabetes—is likely to be authorized for treating obesity in the US later this year. It’s already being prescribed off-label for that purpose. 

Developed about a decade ago, semaglutide works by stimulating the hormone GLP-1, which prompts the body to pump out more insulin (like tirzepatide, it began as a treatment for diabetes). Tirzepatide also stimulates GLP-1, along with a hormone called GIP that likewise leads to insulin secretion. Both drugs work to provide a sense of fullness. In clinical trials, the treatments—delivered by weekly injections for 15–16 months—reduced body weight substantially: On average, those receiving semaglutide lost around 15 percent of their body weight, those on tirzepatide roughly 20 percent. In conjunction with the shots, participants in both trials were supported to adhere to a reduced-calorie diet and get 150 minutes of exercise a week. 

The success—and mushrooming popularity—of these drugs brings us to a crossroads. We can make bigger bodies smaller with them, but does that mean we should? They promise to help people whose weight poses a health risk. And by shedding more light on what drives obesity, they could also chip away at harmful stereotypes that being overweight is simply a personal failing. At the same time, framing fatness as a disease to be done away with could lead to even greater stigma—as well as turbocharging society’s obsession with thinness.

Members of the fat acceptance community—a decades-old social justice movement that has sought to reclaim the word “fat”—warn that these treatments risk entrenching the fat stigma that pervades society. Celebrating these drugs is “reinforcing for the general public the idea that fat is diseased and bad, and that we should be trying to eradicate fat people,” says Tigress Osborn, the chair of the National Association to Advance Fat Acceptance (NAAFA). (People within the fat activist community prefer the term “fat,” as they view “obesity” as a medicalized term that pathologizes bigger bodies.) 

The activists fear that fat people may feel pressured to take these medications in order to access the same rights as their non-fat counterparts, rather than out of any desire to improve their health. “Is it really about health improvement when a person is experiencing daily weight stigma and feeling shamed and blamed and is looking for a solution to decrease the influence of that in their life?” says Sarah Nutter, a psychologist at the University of Victoria in Canada who specializes in weight stigma and body image. 

To go through life in a fat body means you are less likely to be hired for a job and will be paid less than non-fat people. The effects of weight discrimination—which can include poorer medical treatment, loneliness, psychological distress, and increased stress—may actually be cutting short the lives of fat people.

Deciding whether to take the drugs becomes  a “devil’s choice,” says Osborn. “Assert that I have the right to be as I am right now—or exchange that right for significantly more rights and privileges in the culture.” The fat acceptance movement instead pushes for fat people to be afforded the same rights as everybody else, regardless of size. 

Novo Nordisk’s campaign “It’s Bigger Than Me,” with actor Queen Latifah as its face, has drawn particular criticism. Through it, the company is trying to align itself with the talking points of fat acceptance—eliminating weight stigma and bias and shattering the misconception that obesity is simply a lack of willful control—while at the same time selling a drug that has the goal of making fat people smaller. “By saying that if you take away the fatness, you’re giving them the chance to thrive, you’re not—you’re just making the person smaller, and you’re selling them smallness as a gateway out of oppression,” says Marquisele Mercedes, a doctoral student in public health at Brown University.

Yet these concerns are opposed by an obvious truth: Anti-obesity drugs are effective at tackling what is a complicated condition. While the underpinnings of obesity remain elusive, a colliding consensus among researchers has landed on one irrefutable fact: Obesity is not a physical manifestation of an absence of willpower. Research has proven, repeatedly, that dieting doesn’t work to reduce weight and keep it off. Obesity is a complex, entangled mishmash of biological and environmental factors that scientists have yet to fully solve and which can’t be boiled down to the simple matter of calories in, calories out. “That concept is wrong,” says Francesco Rubino, a professor of metabolic surgery at King’s College London. “It’s not true that obesity is the consequence of too much energy.”

Having working drugs that can step in where other interventions have failed will offer important health benefits for some. Obesity raises the risk of a number of debilitating and deadly conditions, including heart disease, diabetes, high blood pressure, stroke, and certain forms of cancer. These drugs could even help solve the mystery of the root causes of weight gain, Rubino says. On top of a reduced urge to eat, people who take semaglutide appear to have a lowered impulse to partake in dopamine-fueled behaviors, like drinking booze or shopping, according to David Macklin, a doctor who has treated many patients with the drug.

But these treatments aren’t intended for the masses. They are indicated for a specific group of patients: people with a body mass index of 30 kg/m², the clinical definition of obesity, or for people who have a BMI of 27 kg/m² or higher (and so are classified as overweight) if they have another weight-related condition that threatens their health, such as high blood pressure. (It’s worth mentioning that BMI, the  diagnostic tool most commonly used globally to determine obesity, has been shown to be a flawed and discriminatory health metric.) 

Unsurprisingly though, it hasn’t taken long for people who don’t fall into these categories to start taking the drugs for aesthetic reasons. In May 2022, Australian health authorities reported a widespread shortage of semaglutide, where it is still only used to treat diabetes, due to reports of people using it for weight loss. The shortage is so great that it will last until April 2023, leaving people who have diabetes without access. In the US, semaglutide is also a scarce commodity. Production problems are partly to blame, but the shortage is thought to have been exacerbated by a flurry of attention on TikTok—#Ozempic currently has about 433.5 million views on the social media platform. Semaglutide has been described as the worst-kept secret in Hollywood. Celebrities like Elon Musk have admitted to using it to slim down, and it’s been promoted by celebrity television personality Dr Oz. It’s become so in-demand that people are mixing the drug themselves at home using the raw ingredients purchased online. 

There’s also the looming unanswered question of how long people will have to take these drugs, owing to the strong likelihood that the weight will return when they cease treatment. Research has found that patients who stopped taking semaglutide and discontinued the supporting lifestyle interventions regained about two-thirds of their lost weight within a year. Given the probable need for patients to continue taking the drug, its price is no small issue: In the US, semaglutide costs over $1,000 a month, and Medicare, the government-provided health insurance program, doesn’t cover it. As for long-term health effects, the brevity of the trials conducted so far can’t tell us much, although Ozempic’s website warns that potential side effects include thyroid tumors and pancreatitis. 

None of these concerns have done much to dampen appetite for the treatments. Novo Nordisk is projected to pull in $3.5 billion this year from its versions of semaglutide. As for Eli Lilly’s tirzepatide, it’s estimated to bring the company $25 billion in annual sales if approved as a treatment for obesity, and it is projected to be “the biggest drug ever.” If there were ever a time to reconsider whether these drugs should be embraced by the mainstream, this is that moment. 

When the writer Roxane Gay wrote about her complicated decision to get weight-reduction surgery, she noted a depressing truth: “I had to accept that I could change my body faster than this culture will change how it views, treats, and accommodates fat bodies.” With the arrival of anti-obesity drugs, it seems that the balance between accepting fat bodies and wishing to drive them out of existence is going to become even more skewed.  

The Problematic Arrival of Anti-Obesity Drugs

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Researchers look a dinosaur in its remarkably preserved face

The emergence of disease-causing bacteria that are resistant to antibiotics is often attributed to the overuse of antibiotics in people and livestock. But researchers have homed in on another potential driver of resistance: antidepressants. By studying bacteria grown in the laboratory, a team has now tracked how antidepressants can trigger drug resistance1.

“Even after a few days exposure, bacteria develop drug resistance, not only against one but multiple antibiotics,” says senior author Jianhua Guo, who works at the Australian Centre for Water and Environmental Biotechnology at the University of Queensland in Brisbane. This is both interesting and scary, he says.

Globally, antibiotic resistance is a significant public-health threat. An estimated 1.2 million people died as a direct result of it in 20192, and that number is predicted to climb.

Early clues

Guo became interested in the possible contributions of non-antibiotic drugs to antibiotic resistance in 2014 after work by his lab found more antibiotic-resistance genes circulating in domestic wastewater samples than in samples of wastewater from hospitals, where antibiotic use is higher.

Guo’s group and other teams also observed that antidepressants — which are among the most widely prescribed medicines in the world — killed or stunted the growth of certain bacteria. They provoke “an SOS response”, Guo explains, triggering cellular defence mechanisms that, in turn, make the bacteria better able to survive subsequent antibiotic treatment.

In a 2018 paper, the group reported that Escherichia coli became resistant to multiple antibiotics after being exposed to fluoxetine3, which is commonly sold as Prozac. The latest study examined 5 other antidepressants and 13 antibiotics from 6 classes of such drugs and investigated how resistance in E. coli developed.

In bacteria grown in well-oxygenated laboratory conditions, the antidepressants caused the cells to generate reactive oxygen species: toxic molecules that activated the microbe’s defence mechanisms. Most prominently, this activated the bacteria’s efflux pump systems, a general expulsion system that many bacteria use to eliminate various molecules, including antibiotics. This probably explains how the bacteria could withstand the antibiotics without having specific resistance genes.

But exposure of E. coli to antidepressants also led to an increase in the microbe’s mutation rate, and the subsequent selection of various resistance genes. Although in bacteria grown in anaerobic conditions, levels of reactive oxygen species were much lower and antibiotic resistance developed much more slowly.

Moreover, at least one antidepressant, sertraline, promoted the transfer of genes between bacterial cells, a process that can speed up the spread of resistance through a population. Such transfer can occur between different types of bacteria, allowing resistance to hop between species — including from harmless bacteria to pathogenic ones.

Growing recognition

Kiran Patil, who studies microbiome–chemical interactions at the University of Cambridge, UK, says that in the past five years there has been a growing appreciation that many non-antibiotic medicines that target human cells can also affect bacteria and contribute to antibiotic resistance. “The strength of the study is the mechanistic details,” says Patil.

Lisa Maier, who is based at the University of Tübingen in Germany and studies interactions between drugs and the microbiome, says that to understand how antidepressants can drive antibiotic resistance, researchers need to determine what molecules the drugs are targeting in the bacteria and to assess the effects of the medications on a wider variety of clinically relevant bacterial species. In 2018, Maier and her colleagues surveyed 835 medicines that did not target microbes and found 24% inhibited the growth of at least one strain of human gut bacteria4.

Patil and Maier say it is important to gather evidence to assess the real-world impact of antidepressants on resistance, such as whether antidepressants are driving the accumulation of antibiotic-resistant bacteria, particularly disease-causing ones, in people, animals or the environment.

Although significant amounts of antidepressants have been found in wastewater, reported levels tend to fall below the concentrations at which Guo’s group saw significant effects in E. coli. But concentrations of some of the antidepressants that had strong effects in this study are expected to be reached in the large intestines of people taking the drugs.

Follow-up studies

Maier says that several studies now link antidepressants and other non-antibiotic pharmaceuticals to changes in bacteria and that preliminary studies have given the “first hints” regarding how such drugs can affect the microbiomes of people taking them.

But in healthy humans, E. coli is found mainly in the large intestine, where conditions are anaerobic, meaning that the process described in the paper might not occur at the same rate in people, says Maier. Future studies should use bacterial growing conditions that model sites at which antidepressants might be acting, says Patil.

Guo says his lab is now looking at the microbiomes of mice given antidepressants. Early, unpublished data suggest that the drugs can change the animals’ gut microbiota and promote gene transfer.

But Guo and Maier caution people against stopping taking antidepressants on the basis of this research. “If you have depression, that needs to be treated in the best possible way. Then, bacteria second,” says Maier.

Although researchers and pharmaceutical companies need to quantify the contribution of non-antibiotic pharmaceuticals to antibiotic resistance, says Guo. “Non-antibiotic pharmaceuticals are a big concern that we shouldn’t overlook,” he says.

doi: https://doi.org/10.1038/d41586-023-00186-y

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They swiftly locked the entry gates at the New Delhi campus and cut off electricity in the winter chill, leaving the students to sit and watch the program on laptops and cellphones, their faces glowing beneath a blank projection screen. Then, just minutes into the viewing, which the students were holding in defiance of an order by the public university, they were attacked by a smaller group of masked men throwing stones.

“They will shut one screen, and we will open hundreds,” said Aishe Ghosh, one of the student activists who attended.

The documentary, “India: The Modi Question,” focuses on Mr. Modi’s role during Hindu-Muslim riots that tore through the state of Gujarat in 2002, when he was its chief minister. The murder of a group of Hindu pilgrims at a railway station prompted a wave of mob violence in which about 1,000 people, most of them Muslims, were killed, and perhaps 150,000 uprooted.

Mr. Modi’s critics at the time accused him of clearing the way for the carnage, or at least turning a blind eye to it. The BBC special cites an unnamed British official who wrote that the massacres bore “the hallmarks of ethnic cleansing” of Gujarat’s Muslim minority, and it reveals that a British investigation in 2002 had found Mr. Modi “directly responsible.”

“The Modi Question” was not set to air anywhere in India. But questions about whether Mr. Modi was complicit in the 2002 riots remain sensitive for the national government and his governing Bharatiya Janata Party, which point to investigations that have cleared him. Arindam Bagchi, a foreign ministry spokesman, denounced the documentary, saying it was “designed to push a particular discredited narrative” and betrayed a “colonial mind-set.”

But the government has not stopped at criticizing the documentary. It has also taken steps to make it difficult to view inside India, the latest intervention in the free flow of information by state machinery that carefully tends to the image of India’s most powerful leader in generations.

Without banning the documentary officially, India’s Ministry of Information and Broadcasting blocked segments of “The Modi Question” from appearing on YouTube, with the cooperation of the site’s parent company, Alphabet. The ministry took that action under a cluster of “I.T. rules” passed in 2021 that allow it to suppress virtually any information that appears online.

Such measures are unusual but not unprecedented — in 2015, the government blocked another BBC documentary, “India’s Daughter,” concerning a notorious rape and murder in New Delhi. (YouTube has since made it viewable.)

Twitter has been more resistant to barring content at the direction of the Indian government, but it, too, blocked posts linking to footage from “The Modi Question.”

Digital content is slippery, though. By using VPNs and trading flash drives and the like, enterprising Indians have been able to get ahold of the documentary fairly easily.

At the southernmost end of India, left-wing student groups in the state of Kerala announced that they would be staging wildcat screenings of the documentary. Local B.J.P. leaders declared that it would be tantamount to “treason” and called on Kerala’s chief minister to prevent it. Kerala’s Communist government is often hostile to the right-wing central government, however, and the attacks on the documentary seemed as likely to attract attention to it as to make it disappear.

On Wednesday, the Indian police detained student activists outside Jamia Millia Islamia, a university in New Delhi, hours before students planned to screen the documentary outside one of its gates. University officials had banned gatherings inside the campus to watch the film, and police officers in riot gear were stopping students from assembling anywhere on a long road that divides the campus.

“By doing this,” said Sanam Hussain, a student activist, “they are making this documentary more popular, and now everyone wants to watch it.”

The BBC’s broadside comes at a sensitive time for Mr. Modi’s government. Thursday is India’s Republic Day, traditionally marked by a military parade and diplomatic grandeur. Egypt’s general-turned-president, Abdel Fattah el-Sisi, a strongman who cut down the hopes for democracy that emerged during the Arab Spring, is to be this year’s guest of honor. India is also engaged in a major diplomatic push as it prepares to host the Group of 20 summit later this year.

Mr. Modi’s defenders question why, after 21 years, the Gujarat unrest is being brought up now. After the riots, Mr. Modi’s rise within the B.J.P. and national politics was thwarted temporarily, and the United States denied him an entry visa under a little-used law intended to protect religious freedom. That order was lifted by President Barack Obama in 2014, when Mr. Modi became prime minister.

By then, the rehabilitation of Mr. Modi’s image within India was almost complete. In 2012, an investigative team appointed by the country’s Supreme Court recommended that he be cleared of all charges, and in July 2022, the court upheld that judgment. Most related cases and even convictions of others have been dropped or overturned, usually for lack of evidence.

Most of the story told by the BBC documentary would be familiar to Indians who followed the news in 2002. But a few incendiary new aspects were brought to light, including the previously unreported British investigation that found that “Narendra Modi is directly responsible” for the mass killings. Jack Straw, then Britain’s foreign secretary, told investigators at the time that the episode was “a particularly egregious example of political involvement to prevent the police from doing their job, which was to protect both communities, the Hindus and the Muslims.”

The BBC said in a statement last week that the documentary was “rigorously researched according to highest editorial standards.”

The U.S. government, which is hoping to align India as a strategic partner in its rivalries with Russia and China, signaled that it wanted no part in the controversy. Ned Price, a State Department spokesman, told reporters that he was not familiar with the content of “The Modi Question” but that he was “very familiar with the shared values that enact the U.S. and India as two thriving and vibrant democracies.”

The Gujarat nightmare may be 21 years old, but in India, the wheels of justice can grind slowly. In the city of Vadodara on Tuesday, 22 Hindu men were acquitted of charges in the killings of 17 Muslims during the days of frenzy in 2002. In the meantime, eight of the 22 accused had died.

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In Xinzhou region of northern Shanxi province the coffin makers have been busy. We watched the skilled craftsmen as they carved elaborate decorations into the freshly-cut wood. Over recent months, they say, they haven't had time to stop.

One villager, a customer, told us that at times the coffins have sold out. Laughing with a dose of the black humour you find in the area, he added that those in the funeral industry had been "earning a small fortune".

There has been much debate about the real number of Covid deaths in China, after the virus ripped through its megacities.

Some 80% of the population - more than a billion people - have been infected since China scrapped restrictions in December, according to leading epidemiologist Wu Zunyou. Last weekend China reported 13,000 Covid-related deaths in less than a week, adding to the 60,000 deaths it has counted since December.

But these deaths have been in hospitals. In rural areas there are only sparse medical facilities and those who die at home are mostly not being counted.

There is not even an official estimate for the number of village deaths. But the BBC found evidence the death toll is mounting.

We visited a crematorium and they too have been busy, mourners dressed in white walking forward carrying the ceremonial box which would eventually contain the remains of a loved one.

In another village, we saw one man and woman loading huge tissue paper birds onto the back of a flatbed truck. "They're cranes. You ride the crane into the afterlife," the woman said.

As they packed up other elaborate, Buddhist images newly made from tissue paper they said they'd had an explosion in demand for their funeral decorations, two or three times what's normal.

Everyone we met in this part of Shanxi who is connected to the funeral industry told us a similar story about an increase in deaths and they all attributed it to the coronavirus.

Wang Peiwei is determined to put on a good funeral for his sister-in-law

"Some sick people are already very weak," one man said as he continued to load the truck. "Then they catch Covid, and their elderly bodies can't handle it."

We followed the truck to where the artworks were being delivered and met Wang Peiwei, whose sister-in-law had just died.

The mother-of-two in her 50s had suffered from severe diabetes for years and then she caught the coronavirus.

"After she got Covid she had a high fever, and her organs began to fail. Her immune system wasn't strong enough to make it," said Mr Wang.

The courtyard at the family house was filling up with decorations for the ceremony. Mr Wang told us there were still more images, flowers and the like to come.

Standing in front of a tent in the courtyard where her body was covered up he explained that, on the day of the funeral, 16 people would carry her coffin and bury her in accordance with tradition.

He said that, though the cost of funeral arrangements had skyrocketed because of the number of Covid deaths, they would pay the extra money in her honour.

"She was a great person. We must hold a grand event to send her off, the best we can afford," he said.

Every year, hundreds of millions of younger people go back to their hometowns at this time to celebrate the Lunar New Year. It's China's most important festival.

The villages they are returning to are now places where mostly older people live - people who are more vulnerable to Covid.

Millions of people have travelled back to their hometowns from big cities

There has been great concern that this year's Spring Festival mass migration could quickly spread the coronavirus into more remote areas, to deadly effect.

The government warned those in the cities not to go home this year if their elderly relatives had not yet been infected.

Doctor Dong Yongming, who operates a very small village clinic, thinks at least 80% of residents there had already caught Covid.

"All the villagers come to us when they're sick," he said. "We're the only clinic here."

Most who had died there had underlying diseases, he said.

In terms of managing the medicine they had as Covid hit the village, Dr Dong said they would not sell medicine to people beyond their needs.

"For example, I would only give out four Ibuprofen tablets per person," he said. "They don't need two boxes. It'll just be wasted."

However he said he believed the worst of this Covid wave was already behind them: "We haven't had any patients in recent days."

Those who die in this region are buried in the fields. Farmers then continue to plant crops and raise livestock around the mounds of their ancestors.

Driving along the road we noticed fresh mounds of earth with red flags placed on the top. A lot of them. A farmer herding goats confirmed that they were new graves.

"Families have been burying elderly people here after they die. There are just too many," he said.

Fresh graves dot the nearby fields

In his village of a few thousand, he said that more than 40 residents had died during the most recent Covid wave.

"One day someone would die, then the next day someone else. It's been non-stop over the past month," he said.

But in the countryside here, they are quite philosophical about life and death. This farmer said people would still celebrate the new year like they always have.

"My son and daughter-in-law will come back soon," he said.

I asked if locals were worried that family members returning could mean more infections.

"People shouldn't worry. No fear!" he said. "You will still become infected even if you hide. Most of us have already got it and we are fine."

He, and many others are hoping that Covid's most deadly work has already been done and that, for the time being at least, their energy can be spent on being with the living rather than burying the dead.

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HUMANITY MAY NOT exactly be winning its battle to avert climate change, but the electrification of cars has begun to look like a success story. Ten percent of new passenger vehicles sold around the world last year were electric, powered by batteries instead of gasoline—the extraction of which costs the world not only in noxious carbon emissions, but in local environmental damage to the communities on the front lines. 

Still, that revolution has its own dirty side. If the goal is to electrify everything we have now, ASAP—including millions of new trucks and SUVs with ranges similar to gas-powered models—there will be a massive increase in demand for minerals used in batteries like lithium, nickel, and cobalt. That means a lot more holes in the ground—nearly 400 new mines by 2035, according to one estimate from Benchmark Minerals—and a lot more pollution and ecological destruction along with them. It’s why a new study published today by researchers associated with UC Davis tries to map out a different path, one where decarbonization can be achieved with less harm, and perhaps faster. It starts with fewer cars.

The analysis focuses on lithium, an element found in almost every design of electric car batteries. The metal is abundant on Earth, but mining has been concentrated in a few places, such as Australia, Chile, and China. And like other forms of mining, lithium extraction is a messy business. Thea Riofrancos, a political scientist at Providence College who worked on the research project, knows what hundreds of new mines would look like on the ground. She has seen what a falling water table near a lithium mine does to drought conditions in the Atacama desert and how indigenous groups have been left out of the benefits of extraction while being put in the way of its harms. 

Riofrancos and the team looked at paths to sunset gas-powered cars, but in a way that replaces them with fewer EVs, using smaller batteries. A future with millions of long-range, hefty eSUVs isn’t the default. Still, “the goal isn’t to say, ‘No new mining, ever,” says Alissa Kendall, a professor of civil and environmental engineering at UC Davis who coauthored the research. Instead, she says the researchers found that “we can do this better” if people become less reliant on cars to get around.

The team mapped out five paths for the US, each focusing on different scenarios for lithium demand. In the first, the world keeps on the path it has laid out for itself: Cars become electric, Americans sustain their love affair with big trucks and SUVs, and the number of cars per person stays the same. Few people take public transit because, frankly, the majority of systems continue to suck. 

The other scenarios model worlds with progressively better public transit and walking and biking infrastructure. In the greenest of them, changes in housing and land use policy allow everything—homes, shops, jobs, schools—to get closer together, shrinking commutes and other routine journeys. Trains replace buses, and the share of people who own a car at all drops dramatically. In this world, fewer new electric vehicles are sold in 2050 than were sold in 2021, and those that do roll off the lot have smaller electric batteries, made up of mostly recycled materials, so every new one doesn’t need more mining to support it.

Most of the benefits come from changes that few mineral demand forecasters consider: reducing the number of miles people drive and the number of cars driven overall. This is tricky because it requires something people typically don’t love—change.

To become less car-dependent, people would have to change their habits for getting around, shift their preferences for the kinds of cars they drive, and question how many trips they take and why.

At the core of the project is the idea that, contrary to what some carmakers would like you to believe, simply replacing one kind of car with another won’t save the world from its climate change mess. Consumerism got us here; it can’t get us out.

How to break that stranglehold? The best strategy is to make people feel like they’re gaining something by taking fewer car trips, not losing, Riofrancos says. To actively want a future where cars are less important and—crucially, since many people already feel that way—believe it’s actually achievable.

That might begin to feel like a fairytale, a beautiful but unreachable goal for places in which car ownership is literally etched into the landscape through roads and parking lots. But Kendall argues that even in car-dependent places like the US, it is possible with gradual changes. “Right now, we’ve got really lousy transit all around us,” she says. “But we expect transit to be profitable. We don’t expect roads to be profitable.” 

One good option is to get people onto ebikes and into ebuses, which require a fraction of the lithium per rider needed for personal electric cars (and especially hulking electric SUVs and trucks). It’s possible some people might do that voluntarily if made aware of the impact of extracting battery materials. But governments may have to also thoughtfully wield some “sticks,” Riofrancos says.

Norway; the state of New York; and Washington, DC, have introduced higher fees for the heaviest personal cars, a move that may dissuade some people from buying the biggest SUV and truck-style EVs. In the future, car safety rules could also penalize packing extra weight into vehicles by using bigger batteries, Riofrancos says. And she suggests that regulations emulating fuel economy rules could be created to incentivize more efficient use of battery materials.

For the US, in particular, reducing car dependence and therefore battery material demand will require changes to cities’ infrastructure.  Some places have already seen success in shifting people out of cars and onto bikes or even just their feet.

A program funded by the federal government back in 2005 saw four very different US communities—Columbia, Missouri; Marin County, California; Minneapolis, Minnesota; and Sheboygan County, Wisconsin—invest a total of $100 million in walking and biking trails. A follow-up study found that the number of trips taken by bike increased 36 percent, and those taken by foot went up 14 percent. The share of driving trips went down by 3 percent. These efforts didn’t cut car use dramatically, but they demonstrated that with investment, people do change their behavior, says Kevin Mills, head of policy at the Rails-to-Trails Conservancy, a nonprofit group that oversaw the study.  

A funding bill the US Congress passed in December will build on that work by sending $45 million to active transportation projects across the nation. Groups pushing for a less car-centric world have hailed the money as a major victory while acknowledging that when it comes to offering truly connected alternatives to roads, the funding is a drop in the bucket. “We know there are billions of dollars of need,” says Mills. The plan is to help communities use the money to “plant seeds” and demonstrate residents’ overwhelming demand for non-car forms of transport, he says.

It’s only a start—and a far cry from the most radical, resource-light scenarios the report authors imagine, Riofrancos says, plans that involve cities somehow becoming much denser and bringing transit to the suburbs. But one positive development in those projections for materials demand, Riofrancos notes, is that our ability to even imagine them shows a paradigm shift in climate policy debates.

Not long ago, projecting the future of transportation was often a matter of comparing a battery-powered future to a fossil-fueled one—what would it look like if some share of cars went electric? Today, it’s a given that there will be fewer gas cars on the road tomorrow, perhaps barely any. That means people can start asking a much more interesting question: Should conventional cars be replaced at all?

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