Climate scientists say the earth's temperature has increased by an average of 0.74 deg C over the past 100 years, but warming across South Asia's Himalayas has been greater than the global averages.

Glaciers in Nepal, wedged between two major carbon polluters – India and China – melted 65 per cent faster in the last decade than in the previous one, the UN chief said in a video message after visiting the Solukhumbu region.

“I am here today to cry out from the rooftop of the world: stop the madness,” he said, calling for an end to “fossil fuel age”, with the warning that melting glaciers would mean swollen lakes and rivers sweeping away entire communities, and seas rising at record rates.

Glaciers in the Hindu-Kush Himalaya could lose up to 75 per cent of their volume by century's end due to global warming, scientists said in a report published in June this year, causing dangerous flooding and water shortages for 240 million people who live in the mountainous region.

Climbers returning from Everest have said the mountain was dryer and greyer now.

Mr Guterres, who is on a four-day visit to the country, said: “Record temperatures mean record glacier melt. Nepal has lost close to one-third of its ice in just over 30 years.”

He also urged countries to limit global temperature rise to 1.5 deg C to avert “the worst of climate chaos”.

REUTERS

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“It’s an unambiguous readout of what’s in the environment,” says Ian Wheeldon, co-lead researcher and a UC Riverside chemical engineering professor. He believes that giving plants the power to share what they’re experiencing, in a way that’s visible to the naked eye, will deepen people’s understanding of them.

The idea of using plants as environmental sentinels isn’t new. Years ago, plant biologists noticed that trinitrotoluene (TNT, an explosive) builds up in root tissues, choking plants. Researchers succeeded in growing plants that could detect TNT in the soil, but signaling that information to people was complicated. In 2016, biologists at MIT figured out how to make them glow in infrared light in front of a camera attached to a computer, which could then send an email alert.

There are lower-tech methods of confirming whether a plant was exposed to contaminants, like bringing samples back to a lab for testing, but that can be costly and time-consuming. Sensors in the field can track things like light levels, soil conditions, and moisture, but they still require a power source—which will eventually require maintenance or shut down entirely.

Getting plants to simply change colour would be much easier. “This technique is nice because you don’t need any special equipment. You just see it,” says Yunde Zhao, a professor of cell and developmental biology at the University of California, San Diego who was not involved in this project.

This study, published last week in Nature Chemical Biology, is the first to use a visible marker to detect organophosphate pesticides in plants. Sophisticated synthetic biology tools, enabling researchers to turn on gene expression in response to specific environmental triggers, already exist for biological systems like human cell lines and bacteria—single-celled organisms with short life cycles. “In plants, those tools are very limited,” says co-lead researcher and UC Riverside plant biologist Sean Cutler.

Manipulating molecular pathways in complex multicellular plants that take months to grow is much trickier than running experiments in microbes, where a scientist can make a genetic tweak and observe the consequences in a single sitting. With this project, the team aimed to scale these tools up, “building the widgets that allow us to program lots of complicated inputs and outputs in a plant system,” Cutler says.

The team engineered the plants to respond to the pesticide azinphos-ethyl, which has been banned in the European Union because of its toxicity in mammals. They did this by hijacking a hormonal pathway that plants use to signal distress.

Arabidopsis, like all plants, uses a hormone called abscisic acid, or ABA, to send alerts when it’s stressed by conditions like cold, drought, or changes in soil chemistry. ABA binds to receptors in the plant, making it close its pores to hold in more water. Cutler’s team rewired this pathway by changing the shape of the ABA receptor’s binding pocket, molding it so it can also detect and bind to azinphos-ethyl molecules.

Binding something other than ABA to an ABA receptor could trigger the plant’s stress response, but that isn’t easy for people to see without special equipment and close observation. So the researchers wanted the molecular binding to make the plant do something visibly obvious: change colour.

To make A. thaliana turn red on cue, the researchers gave the plants a gene from beets. They used a long synthetic DNA sequence developed by Zhao’s lab called RUBY, which contains instructions for making betalain, the bright red pigment that gives beets their signature colour. When exposed to this pesticide, their engineered compound acts as a sensor, activating RUBY. As a result, the plant’s leaves turn from green to deep red. “The results are just beautiful,” says Zhao.

“This paper is opening up a new capacity to reprogram plant responses,” says Stanford bioengineering professor Jenn Brophy, who was not involved in the study. But she points out that this kind of engineering gets tricky—a tiny change to a protein’s structure can change how it folds, causing it to malfunction. The team needed to make sure the ABA receptor could sense the pesticide but still be able to perform its usual job.

Cutler says his team found specific protein mutations that they harnessed to make a system where the individual pieces couldn’t interfere with the plant’s normal signaling pathways. “Part A is broken on its own, and part B is broken on its own,” he says. “But magically, when they’re together, their function is restored.”

Theoretically, one could make a plant turn red in response to any number of chemicals, not just azinphos-ethyl. Many organophosphate pesticides are chemically similar enough to bind to the same modified receptor. But making the plant respond differently to each chemical—like blue for acephate and purple for malathion—is much harder. With every additional pathway, the odds of metabolism-disrupting cross talk get higher.

The signal doesn’t necessarily have to be a visible colour change—the team has also experimented with temperature. A second receptor pathway in these engineered plants responds to diazinon, an insecticide that’s currently banned for residential use in the United States. As part of the same study, the team used diazinon to turn on the plant’s normal ABA signaling, triggering a stress-induced increase in leaf temperature that can be seen by infrared night-vision cameras, similar to what the MIT team had tried before.

The challenge now is figuring out just how many molecular switches can be engineered before things get too complicated—and creating separate pathways that all produce easily observable outputs. Wheeldon believes it will be worth the effort. Having more switches, he says, “increases the complexity of the questions you can answer and the applications you can go after.”

While these colour-changing plants still only exist in the lab, Cutler says his team hopes to “create biosensors that allow you to engineer organisms that sense all kinds of chemicals.” For example, because plants already produce ABA in response to drought; he imagines thirsty plants that could change colour overnight to call for help before they experience real damage.

Wheeldon’s research group has been studying pesticides for years—they’re used in agriculture globally, so they were an obvious first target for sensing experiments. But Cutler’s team has a long list of molecules that they’re testing now: pharmaceuticals, substances of abuse, natural plant products, and other agrochemicals.

“In the long run, I think that we will be able to create biotechnologies that can help provide the public or other specific users with information on chemicals in the environment,” says Wheeldon. “Real-time feedback about what is in the environment—for example, is the local water supply contaminated? Are bad actors using harmful chemicals in their industrial processes?”

Brophy envisions at-home applications for this technology too, for the black thumbs amongst us, like “houseplants that change colours to tell you that they need something.”

“I feel a lot of pressure to have nice plants in my office, being a professor of plant biology. But oh man, I just struggle,” she says, chuckling.

Because these plants are transgenic—meaning they contain DNA from another species—they would face a tough approval process if anyone tried to bring them to market in the US. Betalain-producing plants and A. thaliana don’t naturally cross-pollinate, so researchers would need to demonstrate that any transgenic plant they engineer won’t have any unintended effects on the environment.

It’s not impossible, though. Earlier this year, the US Department of Agriculture approved the sale of purple tomatoes, which contain snapdragon genes that boost their antioxidant content and increase shelf life. Last month, the agency gave the go-ahead to a glow-in-the-dark petunia that contains genes from bioluminescent mushrooms and will go to market next year.

With more research, plants that speak in colour may get the green light too.

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Tolullah Oni has a challenge for you. Next time you’re in a city—especially one you don’t know well—go for a long run, bike ride, or walk. See if you can tell when you enter an affluent neighborhood. You should, she says, be able to guess.

“Suddenly it’s a couple of degrees lower in hot areas. There’s a bit more shade. Separation from traffic is a bit higher. Your eyes are not streaming as much,” says Oni, the clinical director of research at the University of Cambridge and an urban epidemiologist whose research takes her to cities around the world. Invariably, when Oni reviews the streets she has passed through, her predictions are spot on. “I would go back and check, and yeah, that was a posh area.”

Not all urban areas are created equal, and this can have a big impact on a person’s health. Air quality, heat, food—these are just some of the ways your environment can influence health. Often, it is the poorest areas of a city that have the most negative impact. And with the world’s urban population set to double roughly by 2050, working out how to detect and address these inequalities is becoming more critical than ever.

Ahead of her talk at WIRED Impact in London on November 21, WIRED caught up with Oni to discuss how to maximize the positive impact that cities have on health. This interview has been edited for length and clarity.

WIRED: What made you realize the impact that cities have on health?

Tolullah Oni: My doctorate looked at HIV and tuberculosis. I had a couple of patients who had very well-controlled and well-managed HIV-TB who then died prematurely of other conditions. In particular, I had a patient who had HIV and had very good care and had a very controlled viral load. But they died, prematurely in their forties, of a stroke from uncontrolled high blood pressure.

So I started looking at the broader factors that influence health and found that most lay outside of health care—a lot lay in urban environments. So I realized we needed to understand the epidemiology of the urban context as the main propagator of diseases.

How does a city specifically help or harm someone’s health?

It’s what people eat, what they breathe, how they move. The built environment, of which transport infrastructure is part. This includes how easy it is to walk or cycle. And by easy, I mean access, but also how easy it is to do that without risking life and limb.

It’s also access to green space, which influences mental health and physical health in terms of space needed to be physically active, but it’s also infrastructure that reduces exposure to extreme heat. And also our student environment, our levels of air pollution, the risk of injury.

These are the factors that determine our health.

Haze shrouds the skyline of Brooklyn and buildings in Manhattan as seen from the Empire State Building.

Photograph: Gary Hershorn/Getty Images

A monorail train is seen passing through cityscape engulfed in smog (mixture of smoke gases and chemicals in the air) in Mumbai.

Photograph: Ashish Vaishnav/Getty Images

In this aerial view, smoke haze from fires blankets the city of Santa Cruz, Bolivia, on October 25, 2023.

Photograph: RODRIGO URZAGASTI/Getty Images

The city skyline is pictured amid high levels of air pollution in Bangkok on October 18, 2023.

Photograph: ALEX OGLE/Getty Images

Are there some cities that, broadly speaking, are “healthy”? Who sets a good example?

It’s a difficult question. Averages hide a lot. I’m always loath to say one city has others beaten.

The easiest thing to say is that maybe in places where inequality is lower, where healthy public space is much more fairly and equitably distributed, things are better.

London is a fairly good city to be physically active and to be outdoors—lots of green space—but it’s highly inequitable in terms of who has access to that. And it’s highly inequitable in terms of the quality of air that people breathe. Even in cycling infrastructure. There are some parts of London that you have to be very risk-embracing to be a cyclist.

So the big question: How do you make a city healthier?

A lot of the work I do is on identifying risks—better connecting health and climate risks to what may seem like a good thing.

For example, if you have new road infrastructure coming into cities and then growing rapidly, that’s generally a mark of development—helping people become more mobile and facilitating economic activity.

But where there weren’t big roads before, now you have big roads where cars can move very quickly. As the speed of cars increases, so does the risk of injury. Maybe people need to get from this side of the road to that side. Or it’s displacing cycling infrastructure.

Often with developers of public spaces it’s a sin of omission rather than of commission. It’s just, “We will just cut and paste and do things this way, because we’ve got a template.” Nobody’s asking for clean air, and nobody’s asking for walkability. What is rarely apparent is what the health cost is, because that cost is born in a different sector and often at a different time.

So my job is using advocacy and participatory approaches to unearth a demand for improvement—for example for clean air or walkable streets. We focus on three pathways: air quality, walkability, and food environment.

City workers take a break at lunchtime in the now redeveloped area with modern glass offices and angular structures at Aldgate in the City of London.

Photograph: Mike Kemp/Getty Images

We also work on financing. Who is financing urban infrastructure projects? How to encourage or incentivize ways of considering health impacts and designing those in.

Tell me more about participation. What’s the role of city-dwellers in making cities healthier?

In a lot of places, the urban environment is dynamic, and it’s shifting really quickly. So a lot of the work I’ve been doing is looking at building participatory infrastructure, to enable people to be part of constantly measuring what the risks are.

The aim is to be able to see the data in real time and for us to be able to use that data for research, but also for those participating to use those data for activism and advocacy. Data is only useful when it makes demands of people.

We call it “precision activism”: Can you work with people to generate their own data for tailored activism, based on data that they generate in real time? Because the activism around demanding space that is healthy and climate resilient often relies only on emotion. And while that is important, often it’s dismissible without evidence.

We know this can complement more conventional ways of collecting data. So with the example of air quality, we have shown how wearable air-quality sensors can complement static sensors. And we’re doing work looking at how we can work with the city governments, for example with more qualitative multimedia approaches, so we can understand what the contexts are—we can take geolocated photos, videos, to help us understand what the sources of health risks are.

I can wear an air-quality sensor and call for change—but I can’t build a cycle path. Who ultimately is responsible for ensuring the health of cities?

So, governments have the mandate to ensure health for all. They can’t really absolve any responsibility from that. That said, in a lot of cities it’s being built by the private sector. So government is responsible also in the legislation holding the private sector accountable.

What you often see is that the private sector will just do what it is forced to do and nothing else. But we live in an interesting era where people can vote with their wallets. These are your customers; you can alienate people. There is benefit, even when you’re thinking selfishly, to doing the right thing.

There’s been opposition to some urban health improvements recently—London’s ultra-low-emission zone, for example, or walkable “15-minute” cities. How can we convince people to support these sorts of measures?

I really didn’t think it would be possible to weaponize 15-minute cities. But there we go.

One aspect of it is making the hidden visible. It’s clear to me the convenience of getting in my car and going along and not having to change my car for years because I don’t want to.

What is not clear to me is what the cost of inaction is. Either for me or for people like me or my neighborhood. These impacts are often hidden. When I engage with cities, they say, “We can’t afford to make these changes.” And you say, “What if I told you that you’ve lost 3 percent of your GDP in one year because of this exposure. What if I told you that the proportion of people dying prematurely.” I think a really core part of it is making those connections.

Another aspect is that people don’t like things happening to them without them being involved in some way. You can’t evangelize it from top down, like “Just trust me. This is the right thing to do.” You have to understand it from where people are. What issues they face, what worries them, and actually try to bring them along with you.

And then there’s identifying what role people can play, either in what they do or advocate for.

Cities aren’t uniform. What can cities around the world teach one other?

So: intersectoral governance mechanisms. Sounds a very boring three words, but really it makes a huge difference.

What that means is, it’s often very difficult to get data to be interpretable across sectors. If you can’t show what the health outcomes are of extreme heat, for example, it’s very difficult to create momentum. In a lot of places either the exposure has not been measured, the health outcomes are not being measured, or it’s very difficult to bring them together.

The second thing is nimbleness. Particularly in cities where there are high degrees of informality. Sometimes informality in society is baked into informality in governance, which means that you’re able to adapt very quickly to changing contexts and changing realities.

Let me give you an example. In Cape Town, before the pandemic, it was quite difficult to work across sectors. But during the pandemic, one of the key responses was to move from a sectoral approach to a places approach. So rather than you being the minister of housing, you were deployed to be responsible for this entire borough. They were able to adapt.

Cape Town South Africa.Photograph: Peter Titmuss/Getty Images

That ability is going to be something that is increasingly necessary, because the climate bed that we’ve made for ourselves already means we will have these significant societal disruptions. And we have to have ways of not just running cities in peacetime, for want of a better word, but actually being able to adapt in the context of a societal disruption.

Third is vision, in terms of planning. This is something that you see very prominently in Asia and the Middle East. A kind of a long-term vision for shaping a climate-healthy and climate-resilient space, cognizant of how your demography is changing.

If you know that you will have an aging population, what is your vision, for an actual aging, older population in 30 years? You see this articulated so strongly and so ubiquitously in terms of strategy in cities in some parts of the world.

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First, we can remove emissions from our economy. This will reduce global emissions by just 1.3%, but it must be done so we share the transition burden with other countries.

Second, we can stop approving new coal and gas projects, which will raise the cost of these products and so reduce world demand for them to some extent. This would have an important demonstration effect, although the reduction in world emissions may be less than some advocates think.

Third, we can quickly pursue industries in which Australia has a clear comparative advantage in a net-zero world. Of any country, Australia is probably best placed to produce green iron and other minerals that require energy-intensive processing, as well as green transport fuels, urea for fertilizer, and polysilicon for solar panels.

Australia's huge green industry opportunity

Of these three ways, by far the least public discussion is on the third: producing energy-intensive green exports. Yet these industries could reduce world emissions by as much as 6–9%, easily Australia's largest contribution to the global effort. And it would transform our economy, turning Australia into a green energy superpower.

Australia produces almost 40% of the world's iron ore. Turning iron ore into metallic iron accounts for 7% of global emissions. Our iron ore is largely processed overseas, often using Australian coal, which can be exported cheaply.

In the net-zero world, iron ore can be reduced to iron metal using green hydrogen rather than coal. Considerable renewable energy will be needed, yet renewable energy and hydrogen are very expensive to export.

Therefore, rather than export ore, renewable energy and hydrogen, it makes economic sense to process our iron in Australia, before shipping it overseas. Doing so would reduce global emissions by around 3%.

Likewise, turning Australia's bauxite into green aluminum using low-cost renewable energy could reduce world emissions by around 1%. Making polysilicon is also energy-intensive, so again Australia is a natural home for its production. And Australian low-cost green hydrogen plus sustainable carbon from biomass are needed for making green urea and transport fuels.

From gas and coal power to clean power

Australia is the world's largest exporter of gas and coal taken together. Some analysts focus on the costs of losing this large comparative advantage as the world responds to climate change. They overlook two key points.

First, Australia has the world's best combination of wind and solar energy resources, and enormous sources of biomass for a zero-emissions chemical industry.

Second, we have abundant and much-needed minerals that require huge amounts of energy to process. The high cost of exporting renewable energy and hydrogen makes it economically logical for these industries to be located near the energy source.

In other words, more of Australia's minerals and other energy-intensive products should now be processed in Australia.

If Australia seizes this opportunity it can repeat the experience of the China resources boom of around ten years ago, but this time the opportunity can be sustained, not boom and bust, with benefits spread over more regions and people.

Some of the actions governments must take to achieve the 6–9% reduction in world emissions will also help to decarbonize our economy. We must develop the skills we need, support well-staffed government bodies to provide efficient approvals for new mines and processes, build infrastructure that will often be far from the east coast electricity grid, and maintain open trade for imports and exports.

What government must do

But we also need policy changes to give private investors assistance to bridge the current cost gap between green and black products (meaning ones made by clean or by fossil fuel energy) in these new industries, and to help early movers.

If we help companies to produce these products at scale, costs will fall as processes are streamlined and technology improves. Capital grants for early movers are an option, but more work is needed to determine the best forms of support.

Let's make a distinction between energy-intensive green products and mining. While Australia should mine the energy transition minerals the world needs—such as lithium, cobalt and rare earths—mining does not need the financial incentives just cited. Critical minerals are used in black as well as green products and Australia already has significant expertise in mining.

Some will argue Australia can wait until other countries have proven the technology and scaled up production so that the green-black price gap disappears; these new green industries will end up in Australia anyway because of our strong comparative advantage. This complacent argument has many flaws.

Australia is making decisions on its climate and economic direction now. If we do not focus on industries in which we have sustainable advantages we will end up damaging our prosperity. For example, we might pursue labor intensive industries that will be low margin and pay low wages, when other countries are better locations for them.

Second, while technology breakthroughs will be shared internationally, innovation is often about streamlining processes to suit local conditions. If we learn these lessons in Australia, we can achieve lowest-cost world production. If not, these industries could permanently locate elsewhere.

The need for speed

Most importantly, Australia needs to move now to put in place the incentives set out above. No other nation that has the capacity to make these energy intensive green products at scale seems focused on the task. If Australia does not do it, the reduction in world emissions could be seriously delayed.

Of all countries, Australia is best placed to show the world what is possible. Companies and countries using conventionally made steel today can say they want to use green iron but none is available. Let's deny them that excuse.

Once the large investment, productivity and prosperity benefits of this agenda are properly explained, all Australians will applaud it.

What's more, the level of renewable energy required by the transition will see our power prices fall to some of the lowest in the world.

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The Food and Drug Administration is warning consumers to ditch 26 over-the-counter eye drop products found at big retailers—including CVS, Rite Aid, and Target—due to a risk of infection. Consumers should not buy any of the products and should immediately stop using them if they've already purchased them.

The products include Target's branded Up&Up Dry Eye Relief Lubricant Eye Drops and Up&Up Extreme Relief Dry Eye, as well as Lubricant Eye Drops and Lubricant Gel Drops branded by CVS Health and Rite Aid. The warning also includes eye drop products branded as Rugby and Leader (both from Cardinal Health) and Velocity Pharma. A full list can be found here, as can links to report adverse events.

In an adversary posted Friday, the FDA reported that no infections or adverse events have been linked to the products so far. But the agency said it "found insanitary conditions in the manufacturing facility and positive bacterial test results from environmental sampling of critical drug production areas in the facility."

The potential for contamination is particularly concerning for products intended for the eye because the eye is considered an immune privileged site of the body. That is, innate immune responses are held back in specific locations of the body to prevent damage from inflammation—damage that, in the case of the eye, could lead to vision loss.

If pathogens from contaminated eye drops are applied directly to the eye, the resulting infection could also lead to vision loss and even blindness, the FDA warns.

On October 25, the FDA recommended that the manufacturer of the products issue a recall of all lots. The FDA noted that CVS, Rite Aid, and Target are in the process of pulling the drops, but products branded from Leader, Rugby, and Velocity may still be available for purchase online or on shelves.

The sweeping warning and recommendation for a recall of 26 products comes amid a string of eye drop contamination problems this year. Most notably, an outbreak of extremely drug-resistant bacterial infections linked to EzriCare Artificial Tears came to light at the beginning of the year. At the latest count, 81 people in 18 states were infected. Four people died in connection with the outbreak, four others required having one of their eyeballs surgically removed, and 14 other people lost vision. In March, the FDA warned of two other eye drop products, from Pharmedica and Apotex, which were not linked to the outbreak but raised concerns regarding non-sterility.

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While extreme heat currently accounts for less than 1% of cardiovascular-related deaths, the modeling analysis predicted this will change because of a projected rise in summer days that feel at least 90 degrees. This heat index, which factors in what the temperature feels like with humidity, measures extreme temperature.

Older adults and Black adults will be most vulnerable because many have underlying medical conditions or face socioeconomic barriers that can influence their health—such as not having air conditioning or living in locations that can absorb and trap heat, known as "heat islands."

"The health burdens from extreme heat will continue to grow within the next several decades," said Sameed A. Khatana, M.D., M.P.H., a study author, cardiologist, and assistant professor of medicine at the University of Pennsylvania, Philadelphia. "Due to the unequal impact of extreme heat on different populations, this is also a matter of health equity and could exacerbate health disparities that already exist."

To generate these predictions, researchers evaluated county-level data from the contiguous 48 states between May and September of 2008–2019.

More than 12 million deaths related to cardiovascular disease occurred during that time. Using environmental modeling estimates, they also found that the heat index rose to at least 90 degrees about 54 times each summer.

Researchers linked the extreme temperatures that occurred during each summer period to a national average of 1,651 annual cardiovascular deaths. Some areas, such as the South and Southwest, were affected more than others, such as the Northwest and Northeast.

Using modeling analyses to forecast environmental and population changes, the researchers looked to 2036–2065 and estimated that each summer, about 71 to 80 days will feel 90 degrees or hotter. Based on these changes, they predicted the number of annual heat-related cardiovascular deaths will increase 2.6 times for the general population—from 1,651 to 4,320. This estimate is based on greenhouse gas emissions, which trap the sun's heat, being kept to a minimum. If emissions rise significantly, deaths could more than triple, to 5,491.

For older adults and Black adults, the projections were more pronounced. Among those ages 65 and older, deaths could almost triple, increasing from 1,340 to 3,842 if greenhouse gas emissions remain steady—or to 4,894 if they don't. Among Black adults, deaths could more than triple, rising from 325 to 1,512 or 2,063.

In comparing current and future populations, the researchers accounted for multiple factors, including age, underlying health conditions, and where a person lived.

Most people adapt to extreme heat, as the body finds ways to cool itself, such as through perspiration. However, people with underlying health conditions, including diabetes and heart disease, can have different responses and face increased risks for having a heart attack, irregular heart rhythm, or stroke.

"The number of cardiovascular events due to heat affects a small proportion of adults, but this research shows how important it is for those with underlying risks to take extra steps to avoid extreme temperatures," said Lawrence J. Fine, M.D., a senior advisor in the clinical applications and prevention branch, in the Division of Cardiovascular Sciences at the National Heart, Lung, and Blood Institute (NHLBI), part of NIH.

The authors described cooling approaches that some cities are using—planting trees for shade, adding cooling centers with air conditioning, and using heat-reflective materials to pave streets or paint roofs. However, more research is necessary to understand how these approaches may impact population health.

"In addition to thinking about the impact of extreme temperatures in the U.S., this type of modeling forecast also foreshadows the impact that extreme heat could have throughout the world, especially in regions with warmer climates and that are disproportionately affected by health disparities," said Flora N. Katz, Ph.D., director of the Division of International Training and Research at the NIH Fogarty International Center.

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An ophthalmologist at Baylor College of Medicine in Houston offers some tips for easing both eye strain and headaches.

"We focus on one object, especially an object that's up close, like a computer screen or phone, for prolonged periods of time, and we don't give our eye muscles time to rest," said Dr. Masih Ahmed, an assistant professor of ophthalmology at Baylor.

"If you don't give your muscles enough time to rest, that can cause some tension of those muscles," Ahmed explained.

Dry eye can also cause eye strain, as you subconsciously blink less when reading, watching TV or working on the computer.

Follow the 20-20-20 rule when working in front of a screen, Ahmed suggested.

Take a 20-second break every 20 minutes to focus on something 20 feet away to give your eyes a rest. And use artificial tears if you have dry eyes.

Prolonged eyestrain can give you a headache. If you wear corrective lenses, make sure you have the proper prescription, he advised.

If you have an astigmatism, you won't see as sharply. This might require more focus and energy, leading to eye strain.

"You might squint more trying to get that pinhole effect for things to look clearer. Astigmatism can also make things look distorted in shape if your astigmatism is not corrected," Ahmed noted in a Baylor news release.

Get a good fit

Glasses that sit too tight on your temples can also give you a headache.

Make sure your glasses always fit well. Stronger prescription glasses are thicker on the edge. This can cause distortion for the vision on the edge of the glasses.

"Because they sit further off your eye, they may require more power of your muscles in the eye to be able to focus on close tasks whereas contact lenses sit on your eye, so that decreases the amount of focusing power that you may need," Ahmed noted.

"Contacts give you that full vision, whereas glasses stop right there and, the edge, especially thicker ones, can be tougher to see through," he explained.

Consider getting surgery like Lasik if your glasses or contacts give you pain. That can give you your best corrected vision without needing glasses or contacts.

When adults reach ages 40 to 50, the ability to focus up close diminishes. At that point, you might need reading glasses to avoid squinting and eye strain.

"When you put on reading glasses, the whole glass you're looking through is meant for that power for you to read through so that makes it a little easier because you're not having to look down through that bifocal or progressive part of the lens," Ahmed said.

Lighting is key

Lighting can also make a big difference. The room and computer screen light should be similar if you're working in front of a monitor, he said. It can be helpful to have a backlight behind your computer screen to provide a softer glow.

Your eyes can be strained by sitting in a dark room with a bright screen.

"This becomes more common as we work on computers and spend time with screens. Dry eye has increased, and eye strain symptoms have increased as well, so make sure you take frequent breaks and work in a well-lit space," Ahmed said.

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In an era where a world of information is just a few clicks away, health anxiety has taken on a new dimension. Many of us have experienced moments of worry when seemingly innocuous symptoms trigger thoughts of dire health conditions. Could that persistent headache be a sign of a brain tumour rather than just a consequence of too many late nights? Is that peculiar skin lump a harbinger of melanoma? A quick Google search often exacerbates these worries, leaving us awash in a sea of potential ailments. Fortunately, for most, these fears dissipate once the headache subsides or a reassuring word from a trusted GP alleviates concerns.

In the wake of a devastating global pandemic, there is naturally a greater concern for the health of ourselves and those around us. But for those grappling with health anxiety, this concern is not so easily overcome by rationalising or reassurance. Their fears persist and intensify, and their worry about health is frequent, severe and resistant to the soothing words of medical professionals. Temporary relief is short-lived, as fears and doubts quickly resurface or latch on to a new symptom. Their ceaseless preoccupation with health obstructs their ability to relax and savour life, compelling them to seek perpetual and expensive medical consultations, procedures and tests.

This condition used to be called hypochondriasis and it was often met with derision and misconceptions that it stemmed from attention-seeking or malingering. As our understanding of the condition has deepened, we have become more aware of the profound distress experienced by those afflicted and the incapacitating anxiety underlying their health concerns. The latest version of the Diagnostic and Statistical Manual has also replaced hypochondriasis with two related disorders: illness anxiety disorder and somatic symptom disorder.

In illness anxiety disorder, individuals harbour an overwhelming fear of contracting a severe, potentially life-threatening illness, even in the absence of any significant symptoms. For instance, in the wake of the pandemic a small percentage of the population are so afraid of getting Covid that they can’t function normally. They remain housebound, compulsively sanitise and order everything online. In contrast, those grappling with somatic symptom disorder do manifest subjectively experienced symptoms, such as back pain, breathlessness or heart palpitations, which support their belief that they have a grave illness. However, there is an excessive focus on these symptoms and a catastrophising of their meaning. Instead of attributing their real back pain to tension or their palpitations to panic, they are convinced of sinister ailments like tumours or impending heart attacks. This having been said, the first port of call is of course always to rule out a physical cause before assuming a psychological condition.

Ironically, in a cruel twist of fate, health anxiety fuels itself through the physiological symptoms of anxiety, attentional bias and the nocebo effect.

When confronted with fear, the body’s natural response is to trigger the fight-or-flight reaction, eliciting a wide array of somatic symptoms, such as elevated heart rate, shortness of breath, chest pain, sweating, nausea, diarrhoea and dizziness. These somatic responses reinforce the belief that something is seriously amiss, exacerbating anxiety and creating a feedback loop. Furthermore, once we fixate on a symptom, we develop an attentional bias, magnifying its importance and intensifying our experience of it, often neglecting other signs that we are well and healthy.

Health anxiety can also be complicated by the nocebo effect, which operates in the opposite direction of the more familiar placebo effect. It occurs when we read about the symptoms of a possible illness or the negative side effects of a medication and subsequently experience those symptoms or side effects, even when we’ve unknowingly been given a sugar pill rather than the real drug. Clearly our mind exerts a profound influence over our bodily experience.

The advent of Dr Google has had detrimental consequences for health anxiety sufferers, enabling them to delve into endless rabbit holes for every symptom and participate in forums and subreddits where they inadvertently amplify each other’s fears. While their aim is to seek reassurance, the outcome frequently involves heightened anxiety and newfound information that fuels rumination. The escalation in this trend has culminated in the coining of the term cyberchondria.

One of the challenges in treating health anxiety is persuading sufferers that their anxiety, not a physical ailment, is the root issue. While it’s essential to acknowledge the possibility of a physical ailment, and to attempt to rule this out, complete certainty can never be guaranteed. There will always be a minute chance that something has been overlooked and a dreaded illness may lurk in the shadows. Consequently, a crucial facet of treatment involves helping patients to tolerate the reality that life inherently lacks absolute certainty and we have limited control over it.

Treatment also encompasses challenging erroneous thought patterns and relying on empirical evidence for specific outcomes. For example, a vast majority of headaches do not signify brain tumours, so it makes sense to consider more benign causes unless symptoms become severe.

Nevertheless, research into death anxiety, a cornerstone of health anxiety, suggests that solely addressing the specific health-related concern, such as a headache, may fail to target underlying existential fears. In this case, the anxiety may simply shift to a different symptom. Consequently, treatment strategies that focus on an acceptance of mortality may prove more effective.

While it can be initially challenging to persuade health anxiety sufferers to seek psychological assistance, most respond well to treatment once they embrace it. Health anxiety exists on a spectrum that encompasses our ordinary apprehensions about illness and death, making it a condition we can all empathise with. Accepting uncertainty and coming to terms with our mortality is a challenge for us all, but an important one to reckon with if we wish to free ourselves from the tyranny of many forms of anxiety, including health anxiety.

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An ancient landscape that has remained hidden beneath the East Antarctic Ice Sheet (EAIS) for at least 14 million years has been revealed by a new satellite data and radar imaging study. According to the researchers, the preservation of this primordial scenery attests to the fact that the EAIS has remained relatively unchanged for eons, yet this stability could soon be threatened by an unprecedented rise in global temperatures.

The study authors used satellite data to identify undulations in the ice sheet’s surface that provided clues as to the nature of the terrain beneath. Using radio-echo sounding techniques, they were then able to image the landscape covered by the ice over an area of 32,000 square kilometers (12,355 square miles).

“The land underneath the East Antarctic Ice Sheet is less well known than the surface of Mars,” explained study author Professor Stewart Jamieson in a statement. “And that’s a problem because that landscape controls the way that ice in Antarctica flows, and it controls the way it might respond to past, present and future climate change.”

Analyzing their data, the researchers identified three river-carved upland blocks separated by deep U-shaped valleys. It’s likely that the waterways that formed this landscape flowed during and after the break-up of the Gondwana supercontinent, before the first glaciers appeared and helped erode the valleys to a depth of around 800 meters (2,625 feet).

The river valleys and highlands are situated about 350 kilometers (217 miles) from the edge of the ice sheet.

“What we find is an ancient land surface that has not been eroded by the ice sheet and instead it looks like it was created by rivers before the ice came along,” said Jamieson. “This tells us that there hasn’t been a lot of change in this particular area, which indicates that although this part of the ice sheet may have retreated during warmer times in the past, the conditions at this site likely did not change much, and that helps us understand how the ice sheet might respond to future and ongoing warming.”

In their write-up, the study authors explain that the landscape has probably been encased in ice for at least 14 million years. During this period, the warmest temperatures occurred about three million years ago in the mid-Piacenzian warm period, yet the most reliable ice sheet models suggest that the EAIS didn’t retreat as far as this river landscape.

It’s even possible that the ancient scenery formed as far back as 34 million years ago, when the EAIS first appeared following the Eocene-Oligocene transition (EOT) from warm to glacial conditions. However, it’s unclear if the ice sheet has ever retreated far enough during this period to expose and alter the three river valleys, which lie some 350 kilometers (217 miles) from the edge of the EAIS.

“The age of the land surface is uncertain, but it is likely to predate the mid-Miocene [14 million years ago] and perhaps dates from the transition from warm to glacial conditions in Antarctica following the EOT,” write the researchers. “The survival of the landscape implies a long-term stable basal thermal regime and that the ice margin is unlikely to have retreated as far inland as this locality during warm periods of the last 14 [million years].”

Moreover, these findings indicate that the temperature increase of the mid-Piacenzian warm period was insufficient to cause the EAIS to retreat as far as this ancient landscape. However, the study authors warn “we are now on course to develop atmospheric conditions similar to those that prevailed between 34 and 14 [million years ago] […] between now and 2100 under continued fossil fuel burning.”

Unless this is halted, the long-term stability of the EAIS could soon be a thing of the past.

The study is published in the journal Nature Communications.

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A new Antarctic ice sheet modeling study from scientists at UC San Diego’s Scripps Institution of Oceanography suggests that meltwater flowing out to sea from beneath Antarctic glaciers is making them lose ice faster.

The model’s simulations suggest this effect is large enough to make a meaningful contribution to global sea-level rise under high greenhouse gas emissions scenarios.

The extra ice loss caused by this meltwater flowing out to sea from beneath Antarctic glaciers is not currently accounted for in the models generating major sea-level rise projections, such as those of the Intergovernmental Panel on Climate Change (IPCC). If this process turns out to be an important driver of ice loss across the entire Antarctic ice sheet, it could mean current projections underestimate the pace of global sea-level rise in decades to come.

Implications for Coastal Communities

“Knowing when and how much global sea-level will rise is critical to the welfare of coastal communities,” said Tyler Pelle, the study’s lead author and a postdoctoral researcher at Scripps. “Millions of people live in low-lying coastal zones and we can’t adequately prepare our communities without accurate sea-level rise projections.”

An aerial view of the Denman Glacier ice tongue in East Antarctica. Credit: Jamin S. Greenbaum

 

The study, published on October 27 in Science Advances and funded by the National Science Foundation (NSF), NASA, and the Cecil H. and the Ida M. Green Foundation for Earth Sciences at the Institute of Geophysics and Planetary Physics at Scripps, modeled the retreat of two glaciers in East Antarctica through the year 2300 under different emissions scenarios and projected their contributions to sea-level rise. Unlike previous Antarctic ice sheet models, this one included the influence of this flow of meltwater from beneath glaciers out to sea, which is known as subglacial discharge.

Model Predictions and Findings

The two glaciers the study focused on, named Denman and Scott, together hold enough ice to cause nearly 1.5 meters (5 feet) of sea-level rise. In a high emissions scenario (IPCC’s SSP5-8.5 scenario, which assumes no new climate policy and features 20% higher CO2 emissions by 2100), the model found that subglacial discharge increased the sea-level rise contribution of these glaciers by 15.7%, from 19 millimeters (0.74 inches) to 22 millimeters (0.86 inches) by the year 2300.

These glaciers, which are right next to each other, sit atop a continental trench that is more than two miles deep; once their retreat reaches the trench’s steep slope, their contribution to sea-level rise is expected to accelerate dramatically. With the added influence of subglacial discharge, the model found that the glaciers retreated past this threshold about 25 years earlier than they did without it.

“I think this paper is a wake-up call for the modeling community. It shows you can’t accurately model these systems without taking this process into account,” said Jamin Greenbaum, co-author of the study and a researcher at Scripps’ Institute of Geophysics and Planetary Physics.

A key takeaway, beyond the understudied role of subglacial discharge in accelerating sea-level rise, is the importance of what humanity does in the coming decades to rein in greenhouse gas emissions, said Greenbaum. The low emissions scenario runs of the model did not show the glaciers retreating all the way into the trench and avoided the resulting runaway contributions to sea-level rise.

“If there is a doomsday story here it isn’t subglacial discharge,” said Greenbaum. “The real doomsday story is still emissions and humanity is still the one with its finger on the button.”

Understanding Subglacial Discharge

In Antarctica, subglacial meltwater is generated from melting that occurs where the ice sits on continental bedrock. The main sources of the heat melting the ice in contact with the ground are friction from the ice grinding across the bedrock and geothermal heat from Earth’s interior permeating up through the crust.

Prior research suggested that subglacial meltwater is a common feature of glaciers around the world and that it is present under several other massive Antarctic glaciers, including the infamous Thwaites Glacier in West Antarctica.

When subglacial discharge flows out to sea it is thought to accelerate melting of the glacier’s ice shelf – a long floating tongue of ice that extends out to sea beyond the last part of the glacier that is still in contact with solid ground (known as the grounding line). Subglacial discharge is thought to speed up ice shelf melting and glacial retreat by causing ocean mixing that stirs in additional ocean heat within the cavity beneath a glacier’s floating ice shelf. This enhanced ice shelf melting then causes the upstream glacier to accelerate, which can drive sea level rise.

The notion that subglacial discharge causes additional ice shelf melting is widely accepted in the scientific community, said Greenbaum. But it hasn’t been included in sea-level rise projections because many researchers weren’t sure if the process’ effect was sufficiently large to increase sea-level rise, mainly because its effects are localized around the glacier’s ice shelf.

Pelle said subglacial discharge came onto his radar in 2021 when he and his colleagues observed that East Antarctica’s Denman Glacier’s ice shelf was melting faster than expected given local ocean temperatures. Puzzlingly, Denman’s neighbor Scott Glacier’s ice shelf was melting much more slowly despite virtually identical ocean conditions.

Modeling Challenges and Future Research

To test whether subglacial discharge could reconcile the melt rates seen at the Denman and Scott ice shelves, as well as whether subglacial meltwater might accelerate sea-level rise, the team combined models for three different environments: the ice sheet, the space between the ice sheet and bedrock, and the ocean.

Once the researchers married the three models into one they ran a series of projections up to 2300 using a NASA supercomputer.

The projections featured three main scenarios: a control that featured no additional ocean warming, a low emissions pathway (SSP1-2.6), and a high emissions pathway (SSP5-8.5). For each scenario, the researchers created projections with and without the effect of present-day levels of subglacial discharge.

The model’s simulations revealed that adding in subglacial discharge reconciled the melt rates seen at Denman and Scott Glaciers. As for why Scott Glacier was melting so much slower than Denman, Pelle said the model showed that “a strong subglacial discharge channel drained across the Denman Glacier grounding line, while a weaker discharge channel drained across the Scott Glacier grounding line.” The strength of the discharge channel at Denman, Pelle explained, was behind its speedy melt.

For the control and low-emissions model runs the contributions to sea-level rise were close to zero or even slightly negative with or without subglacial discharge at 2300. But in a high emissions scenario, the model found that subglacial discharge increased the sea-level rise contribution of these glaciers from 19 millimeters (0.74 inches) to 22 millimeters (0.86 inches) in 2300.

In the high emissions scenario that included subglacial discharge, Denman and Scott Glaciers retreated into the two-mile-deep trench beneath them by 2240, about 25 years earlier than they did in the model runs without subglacial discharge. Once the grounding lines of the Denman and Scott Glaciers retreat past the lip of this trench their yearly sea-level rise contribution explodes, reaching a peak of 0.33 millimeters (0.01 inches) per year – roughly half of the present-day annual sea-level rise contribution of the entire Antarctic ice sheet.

Pelle said the trench’s steep slope is behind this explosive increase in sea-level rise contribution. As the glacier retreats down slope, its ice shelf begins losing thicker and thicker slabs of ice from its leading edge. This process of ice loss quickly outpaces ice accumulation at the ice sheet’s interior, causing further glacial retreat. Researchers refer to this process as “Marine Ice Sheet Instability,” and it can promote explosive ice loss from glaciers like Denman and Scott.

Credit: David Evans/The World

 

Researchers refer to topography such as the trench beneath Denman and Scott Glaciers as a retrograde slope and worry that it creates a positive feedback loop by which glacial retreat begets more retreat. Large areas of the West Antarctic Ice Sheet, such as Thwaites Glacier, also have retrograde slopes that, while not as dramatic as the Denman-Scott trench, contribute to fears of broader ice sheet instability.

“Subglacial meltwater has been inferred beneath most if not all Antarctic glaciers, including Thwaites, Pine Island, and Totten glaciers,” said Pelle. “All these glaciers are retreating and contributing to sea-level rise and we are showing that subglacial discharge could be accelerating their retreat. It’s urgent that we model these other glaciers so we can get a handle on the magnitude of the effect subglacial discharge is having.”

The researchers behind this study are doing just that. Pelle said they are in the process of submitting a research proposal to extend their new model to the entire Antarctic ice sheet.

Future iterations of the model may also attempt to couple the subglacial environment with the ice sheet and ocean models so that the amount of subglacial meltwater dynamically responds to these other factors. Greenbaum said that the current version of their model kept the amount of subglacial meltwater constant throughout the model runs, and that making it respond dynamically to the surrounding environment would likely make the model more true to life.

“This also means that our results are probably a conservative estimate of the effect of subglacial discharge,” said Greenbaum. “That said, we can’t yet say how much sea-level rise will be accelerated by this process – hopefully it’s not too much.”

Part of Greenbaum’s upcoming fieldwork in Antarctica, supported by NSF and NASA, aims to directly investigate the impacts of subglacial meltwater in both the East and West Antarctic ice sheets. In collaboration with the Australian Antarctic Division and the Korea Polar Research Institute, Greenbaum and his collaborators will be visiting the ice shelves of Denman and Thwaites Glaciers in East and West Antarctica, respectively, looking for direct evidence that subglacial freshwater is discharging into the ocean beneath the glaciers’ ice shelves and contributing to warming.

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Sunday, 29 October

• Who: SpaceX
• What: Falcon 9 B5
• When: 6:28 a.m. UTC
• Where: Vandenberg AFB Space Launch Complex 4
• Why: SpaceX will be using a Falcon 9 to launch 22 Starlink satellites into low Earth orbit. If you like to see satellites with your own eyes using apps like ISS Detector, this batch will be listed as Starlink Group 7-6.

• Who: SpaceX
• What: Falcon 9 B5
• When: 10:48 p.m. UTC
• Where: Space Launch Complex 40
• Why: Similarly to the previous launch, SpaceX will be launching another group of 23 Starlink satellites. This time, it’s Starlink Group 6-25. These Starlink satellites will join the Starlink constellation which provides internet for customers around the planet.

Tuesday, 31 October

• Who: CNSA
• What: Long March 4C
• When: 11:09 p.m. UTC
• Where: Taiyuan Satellite Launch Centre
• Why: It’s unknown what China is sending to space on this mission.

Thursday, 2 November

• Who: SpaceX
• What: Falcon 9 B5
• When: 10:48 p.m. UTC
• Where: Space Launch Complex 40
• Why: SpaceX will launch a Falcon 9 rocket again this time carrying 23 Starlink satellites to a low Earth orbit. This group will be known as Starlink Group 6-26 and are all painted with anti-reflective coatings to make the lives of astronomers a bit easier.

Friday, 3 November

• Who: CNSA
• What: Long March 7A
• When: 8:00 a.m. UTC
• Where: Wenchang Satellite Launch Centre
• Why: China is sending yet another unknown payload into a geosynchronous transfer orbit.

Recap

• The first launch we got last week was a Falcon 9 taking Starlink satellites to space in the Starlink 116 mission. The first stage of the rocket landed too so that it can be reused, saving SpaceX some money.
• Next up, the CNSA launched a Long March 2D rocket carrying the Yaogan 39 remote sensing satellite into its planned orbit.

• Finally, China launched the Shenzhou 17 crew spacecraft atop a Long March 2F. The spacecraft launched from Jiuquan Satellite Launch Centre carrying the astronauts Hongbo Tang, Shengjie Tang, and Xinlin Jiang to the Tiangong Space Station.

That’s all for this week, check back next time.

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October is Cholesterol Awareness Month, and a leading medical expert says increased awareness of this condition can’t come too soon. A quarter of a million volunteers have taken part in a huge testing program for blood pressure and cholesterol levels, and the results are very concerning.

Dr Avinash Hari Narayanan (MBChB), Clinical Lead at London Medical Laboratory, says: ‘27% of people taking part in Our Future Health’s new research program were found to have high blood pressure and a huge 54% were found to have high total cholesterol levels.

‘High cholesterol is a major underlying risk factor for cardiovascular disease (CVD), which is the leading cause of death worldwide, often leading to heart attacks and strokes. In England, high cholesterol leads to over 7% of all deaths and affects up to 60% of adults, according to NHS figures. Further research has revealed that, if 90% of people with CVD were identified and treated, almost 14,000 heart attacks, strokes and deaths would be prevented in three years.

‘With cholesterol levels having such a critical long-term impact on our overall health and 54% of us likely to have the condition, absolute clarity is needed in test results and interpretation. However, the UK has recently switched from the well-known and understood measurement of LDL (low-density lipoprotein), traditionally known as “bad” cholesterol, to a new measure. It’s vital that this change doesn’t confuse anyone receiving a test.

‘Previously, the focus of a cholesterol test was on our LDL (“bad”) cholesterol levels. That’s because not all cholesterol is a problem. It’s a natural fatty substance in our blood, produced in the liver and in some of the foods we eat, which helps to keep the cells in our bodies healthy. However, high LDL levels, uncontrolled, can increase our risk of heart attack and stroke.

‘Our LDL “bad” cholesterol levels used to be compared alongside our HDL (high-density lipoprotein) “good” cholesterol levels, as well as the total cholesterol level. Many people who are carefully watching their diet have become used to measuring their LDL levels over time as a key indicator of their potential health risks.

‘However, some researchers believe that measuring your “non-HDL” cholesterol levels gives a better assessment of the risk for heart disease than measuring only “bad” LDL levels. Because of this change, your “non-HDL” level is the measurement patients will probably be given now by their GPs.

‘Many people with high blood pressure will have become knowledgeable about LDL cholesterol, which makes up most of the body’s cholesterol. LDL carries cholesterol to the cells that need it. If there’s too much cholesterol for the cells to use it can build up in the artery walls, leading to disease of the arteries. In general, the higher your total and LDL cholesterol levels, the higher your risk for coronary heart disease. The former NHS guidance (still given by NHS Scotland) said LDL levels should be 3mmol/L or less.

‘However, the new non-HDL measure is very different. England’s NHS says, as a guide, your non-HDL cholesterol should be lower than 4mmol/L. That is potentially confusing, as a 4mmol/L reading of LDL would put you at a notably higher risk of cardiovascular disease.

‘So why has this change been made and are patients always clear about what their new measurements should be?

‘There are some good reasons for the change. Some heart attacks happen to people who don't have a high LDL level. Researchers found we also need to consider other parts of “bad” cholesterol, known as VLDL (Very low-density lipoproteins), IDL (Intermediate-density lipoproteins) and lipoprotein(a), a type of LDL with an added protein. Previous testing also ignored triglyceride, another type of blood fat.

‘What do these new measurements tell us? VLDLs carry triglycerides and, to a lesser degree, cholesterol to our tissues. IDLs are created when VLDLs give up their fatty acids. They’re then either removed by our liver or converted into LDL. The added protein in lipoprotein(a) makes it stickier, narrowing arteries. It is thought to be largely caused by our genes rather than diet. Finally, triglycerides are another type of blood fat. If your triglycerides are high, it can mean you’re at risk of heart disease, liver disease and diabetes. 

‘When you take the new test, as well as your new non-HDL reading, you will also be given an HDL (good cholesterol) and total cholesterol reading, which should be 5mmol/L or less. With cholesterol becoming something of a “silent epidemic”, impacting 1-in-2 people, the new, more accurate testing should be welcome. However, those used to checking their LDL “bad” cholesterols may feel confused or still wish to monitor this reading separately. Many people have monitored their LDL cholesterol levels for years, to see how diet and lifestyle are impacting their readings. Losing this continuity could potentially lead to complications.

‘Fortunately, there are some up-to-date tests that, while offering the new non-HDL measure, also continue to identify LDL “bad” cholesterol levels. For example, London Medical Laboratory’s Cholesterol Profile test is a revolutionary and convenient home-fingerprick test. It measures total cholesterol, LDL, HDL, non-HDL, triglycerides and two other key markers.

‘London Medical Laboratory’s fingerprick Cholesterol Profile test is considered the gold standard in regular testing. It is used to measure seven key biomarkers enabling people to make the positive lifestyle and dietary changes needed to improve their chances of a long and healthy life.  It can be taken at home through the post, or at one of the many drop-in clinics that offer these tests across London and nationwide in over 95 selected pharmacies and health stores.

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A new study involving 4.3 million people in the UK found that those diagnosed with atrial fibrillation (AF) had a 45% higher risk of mild cognitive impairment (MCI). MCI is an early stage of cognitive decline and can sometimes indicate the early onset of dementia-related conditions. The study suggests that factors like cardiovascular risks and other health issues may contribute to the progression from MCI to dementia in these individuals.

This research sheds light on the connection between MCI and AF diagnosis in the UK, which had not been thoroughly explored before.

Rui Providencia, MD, Ph.D., Full Professor at the Institute of Health Informatics Research at University College London and the study’s senior author, said, “Our study showed that AF was associated with a 45% increase in the risk of MCI and that cardiovascular risk factors and multi-comorbidity appear to associate with this outcome.”

Researchers used the health records of 4.3 million individuals in the UK to study the risk of mild cognitive impairment (MCI) following a diagnosis of atrial fibrillation (AF). They identified 233,833 individuals with AF and 233,747 without AF.

The study found that after an AF diagnosis, there was a 45% higher risk of MCI. Other factors linked to a greater MCI risk included older age, female gender, socioeconomic status, a history of depression, stroke, and having multiple health conditions. However, these factors did not change the connection between AF and MCI. Among people aged over 74, AF and MCI were often diagnosed when multiple health conditions like diabetes, depression, high cholesterol, and peripheral artery disease were present.

Interestingly, patients with AF who received treatment with digoxin didn’t show an increased risk of MCI. Conversely, the risk of MCI was higher in AF patients who didn’t receive oral anticoagulant therapy and those who received amiodarone treatment. Patients with AF who were treated with oral anticoagulants and amiodarone treatment did not face a higher risk of MCI.

During the study, 1,117 individuals were diagnosed with dementia after having mild cognitive impairment (MCI). Those with MCI who also had atrial fibrillation (AF) were at a higher risk of developing dementia. The risk of dementia was also associated with factors like gender, asthma, smoking, chronic kidney disease, and having multiple health conditions.

The research suggests that cardiovascular risk factors and the presence of various health issues may influence the progression from MCI to dementia. To potentially prevent cognitive decline and the development of dementia, the researchers propose integrated care for AF, which includes managing comorbidities alongside anticoagulation treatment. Further research, in the form of a clinical trial, is needed to explore this idea more deeply.

This study underscores the potential association between AF diagnosis and an elevated risk of memory decline. Understanding this link offers opportunities for more comprehensive and integrated care strategies to address cognitive deterioration in individuals with AF, potentially reducing the risk of dementia. Further exploration of these findings through a clinical trial is recommended for a deeper understanding of this complex relationship.

Journal reference:

Sheng-Chia Chung Ph.D., Martin Rossor MD, et al., Cognitive Impairment and Dementia in Atrial Fibrillation: A Population Study of 4.3 Million Individuals. JACC: Advances. DOI: 10.1016/j.jacadv.2023.100655.

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One of the most consequential places on earth is also one of its least accessible: Antarctica’s icy underbelly. The grounding line is where the terrestrial ice sheet reaches the sea and begins floating, becoming the ice shelf. As global temperatures rise, seawater is eating away at that belly, forcing the grounding line to retreat and speeding the decline of Antarctica’s glaciers. If just one of them melted entirely, it could add several feet to sea levels.

The trouble for scientists is that there are thousands of feet of ice between the surface and the glacial underside they urgently need to study. Two new papers, though, are shining light on this mysterious realm—literally so in the case of a swimming robot called Icefin. Scientists drilled a borehole into the ice with hot water, and lowered Icefin through to take video and other measurements along the grounding line. Meanwhile, another team of researchers has found that the groundwater flowing underneath ice sheets could be boosting sea level rise.

Think of the floating ice shelf as a dam that holds back the ice sheet on land. What’s really threatening Antarctic ice isn’t so much hotter air temperatures, but (relatively) warm ocean water eating away at the underside of this shelf. If the shelf weakens and splinters into icebergs, the dam will break, and the ice sheet on land will accelerate its slide into the ocean. Because Antarctic ice is thousands of feet thick, the flow of a single glacier into the sea could have an enormous impact. Thwaites—aka the Doomsday Glacier—could alone add 2 feet of sea level rise. If it tugs on neighboring glaciers as it dies, that will add another 8 feet.

The full Icefin team doing initial fieldwork before the Ross Ice Shelf study.

 Photograph: David Holland

Scientists have used satellites to measure the surface of Antarctica’s ice for decades, but that’s like asking a doctor to assess a patient’s health by only looking at their skin. New techniques, like ground-penetrating radar and robotics, are their equivalent of x-rays and MRIs—tools that let researchers make better diagnoses by peering below the surface. “By discovering new phenomena, we will now be able to produce models that are more realistic,” says University of Houston physicist Pietro Milillo, who is studying Antarctic glaciers but wasn’t involved in either of the new papers. “The hope is that this will reduce the uncertainty for sea level rise projections.”

A team led by Peter Washam, an oceanographer and climate scientist at Cornell University, used Icefin to observe a crevasse near the grounding line of the Ross Ice Shelf in West Antarctica. It was 50 meters (164 feet) tall and at most 50 meters wide. As they piloted the robot through the crevasse, it took water temperature and pressure readings and recorded video. A doppler acoustic sensor tracked particles floating in the water to determine how fast they were moving and in what direction, providing measurements of currents within the crevasse.

Icefin shows that the ice shelf’s belly is not a flat surface, like a perfectly cut ice cube. Instead, these deep crevasses undulate and are pockmarked with “scallop” formations through which seawater flows in fascinating and complex ways. “It paints this really neat picture of what we see with the ocean circulation being mirrored with the ice morphology,” says Washam, lead author of a paper describing Icefin’s adventures, which was published today in Science Advances.

“This is a groundbreaking study using state-of-the-art underwater technology to explore critical regions of Antarctica in unprecedented detail,” says British Antarctic Survey physical oceanographer Peter Davis, who wasn’t involved in the research. “Never before have we been able to observe the ice-ocean interactions occurring within a basal crevasse at an Antarctic ice shelf grounding line at such fine spatial scales.”

Icefin found that ocean currents move water through the crevasse, but dynamics within it generate more movement. Because the crevasse is 50 meters tall, the pressure at its top is less than at the opening, at the bottom. The freezing point of seawater is lower deeper in the ocean, so the further down you go, the easier it is for ice to melt. As a result, seawater in this crevasse is freezing at the top, but melting at the opening.

The cycle of melting and freezing, in turn, moves water. Melting ice produces freshwater, which is less dense than saltwater, so it rises to the top of the crevasse. But when seawater freezes at the top, it dumps its salt, which leads to downwelling. Altogether, this creates churn. “You have rising due to melting, and sinking due to freezing, all within the small 50-meter feature,” says Washam.

This is where the surface topography of the ice really matters. If the ice were flat, it could accumulate a protective layer of cold water. “It forms this barrier between the relatively warmer ocean and the cold ice,” says Alexander Robel, head of the Ice and Climate Group at Georgia Tech, who studies Antarctica’s glaciers but wasn’t involved in the research. If the ice doesn’t mix with the warmer water, it resists melting. ”It just sits there,” he says.

But as Icefin has shown, the underside of the ice shelf can be dimpled, like a golf ball. “The rougher that interface is, the more it can generate turbulence when water flows over it, and that turbulence is going to mix water,” says Robel. This jagged topography can melt faster than flatter parts of the ice shelf’s belly.

This dynamic hasn’t been adequately represented in models of Antarctic glacier melt, which could be why they are melting faster than scientists had predicted, Robel says. “There have been a number of different ideas about what could be causing this difference, but having real ground-truth observations from an actual glacier allows us to say, ‘Well, this idea is right, and this idea is wrong,’ and can help us improve those models,” says Robel—both to explain what’s already happening and to predict future changes.

Washam also thinks this dynamic might be leading to the breakup of ice shelves, because it creates crevasses that propagate upwards through the ice until pieces crack into the sea. “Their main form of mass loss—how they lose their ice into the ocean—is actually from big old icebergs breaking off, because you have these crevasses that eventually break through,” he says.

A second paper published today in Science Advances offers more troubling news from the grounding line. In this one, a team from four institutions modeled the environment underneath the Denman and Scott Glaciers in East Antarctica. These two glaciers could together add 1.5 meters (5 feet) to sea level rise if they disappeared. The modeling found long rivers of freshwater flowing from the interior of the ice sheets toward the coast, caused by geothermal heat warming the underside of the glaciers, plus the friction of all that ice grinding against the ground.

When that freshwater dumps into the ocean at the grounding line, it provides turbulence that draws relatively warm ocean water closer to the grounding line, enhancing melting. “As we thin the ice shelf, we're essentially weakening this dam,” says Scripps Institution of Oceanography glaciologist Tyler Pelle, lead author of the new paper. “This is especially important at the grounding line, just because it is that glacier’s very last contact point with the bedrock. We're essentially, at this point, thinning the most sensitive part.”

Scientists know how freshwater drives melt, but “we've never modeled how these very localized melt enhancements could drive glacial retreat on century timescales, which is what's important in terms of sea level rise,” Pelle says. The new modeling finds that such subglacial discharge could increase the sea level rise contribution of the Denman and Scott glaciers by about 16 percent by the year 2300 in scenarios of high greenhouse gas emissions. These rivers of subglacial water run beneath most Antarctic glaciers, including Thwaites. “We think that we could really be underestimating Antarctica's global contribution to sea level rise, because we're not accounting for this process,” Pelle adds.

Taken together, these papers add to our rapidly evolving understanding of the hidden processes driving the decline of Antarctica’s glaciers, and they underscore the urgent need to reduce carbon emissions. “These systems aren’t yet doomed to collapse and add meters to global sea level. It all depends on how much CO₂ we continue to add to the atmosphere and the impact of that on ocean warming,” says University of Waterloo glaciologist Christine Dow, coauthor of the groundwater paper. “It’s not too late to prevent their collapse. But, as these models show, we’re running out of time.”

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Alcohol is an ideal antiseptic

Conventional alcoholic beers have been considered immune to foodborne pathogens, given their intrinsic properties and processes that form an essential part of their manufacture. Their inherent antimicrobial properties include ethanol content, hops bitter acids, acidic pH, dissolved carbon dioxide, anaerobic conditions, and low sugar content. When combined with pasteurization, wort boiling, filtration, and refrigerated storage, cases of food poisoning from beer are rare.

Research has depicted that ethanol concentrations of 3.5% - 5% (vol) can effectively prevent the growth of most common food pathogens. While certain bacterial strains have been shown to survive even in full-strength beers, these are usually due to poor prolonged refrigeration.

In recent decades, and especially since the coronavirus disease (COVID-19) pandemic, there has been a shifting trend in consumer demand from alcoholic beer to low- (<2.5% alcohol by volume [ABV]) or non-alcoholic (<0.5% ABV) beer. This shift has been attributed to demographics, religion, social regulations, health, and consumers choosing to regulate their calorie intake.

Given their lower than 3.5% ABV, low- and non-alcoholic beers may be at risk of pathogenic growth if bacterial contamination is introduced at any step during the beverage’s production. Unfortunately, most research on the association between foodborne pathogens and beer is restricted to traditional beer, with a severe dearth of data on non-alcoholic beers.

About the study

The present study aims to investigate the impacts of ethanol concentration, storage temperature, and pH on the growth of five strains of Escherichia coli (E. coli), Salmonella enterica, and Listeria monocytigenes in low- to no alcohol-containing beers.

Non-alcoholic canned beer with baseline ethanol and pH concentrations of <0.5% and 3.65 were adjusted using O.1M sodium hydroxide (NaOH) and 99% ethanol. Final concentrations of pH 4.20, 4.50, and 4.80 and ethanol = <0.50% and 3.20% ABV in triplicate were prepared in sterile, parafilm-sealed vials. E. coli O157:H7, S. enterica, and L. monocytogenes were added to the vials, which were subsequently stored at four and 14°C for 63 days.

Periodic sampling to test for pathogen growth or die-off involved streaking beer samples on Violet Red Bile Agar (VRBA), Modified Oxford Media (OX), and Bismuth Sulfite Agar (BSA) to test for E. coli, L. monocytogenes, and S. enterica, respectively.

Statistical analyses comprised one-way analysis of variance (ANOVA) to evaluate the effects of storage temperature, ethanol content, and pH on pathogen populations.

Study findings

 E. coli and S. enterica were found to survive in low- and non-alcoholic beer at all temperatures, pH, and % ABV under study. L. monocytogenes was observed to be less resilient, with population size declining below the detection limit after a few days.

In non-alcoholic beer, pH was associated with declines in microbial population sizes across tested strains – at 4°C, pH 4.20 resulted in a 1.23 log-transformed decrease in E. coli population size, while pH 4.50 resulted in a 2.37 log reduction in S. enterica. L. monocytogenes was below the detection limit at all pH values, though lower pH was associated with more rapid population reduction. At 14°C storage conditions, E. coli and S. enterica populations were observed to grow regardless of pH. In contrast, for L. monocytogenes, higher storage temperature was found to result in more profound population declines compared to 4°C.

In low (3.20% ABV) alcohol-content beers, all microbes presented population declines at 4°C. At 14°C, E. coli and S. enterica depicted population declines but persisted at low population sizes throughout the study period. In contrast, L. monocytogenes population sizes rapidly reduced below the minimum detection limits by day 6 for pH 4.20 and 4.50 and day 10 for pH 4.80.

These findings suggest that % ABV and storage temperature are the most critical determinants of foodborne pathogen persistence and growth, trends confirmed by ANOVA analyses.

Conclusions

In the present study, researchers investigated the effects of % ABV, storage temperature, and pH on the growth and persistence of foodborne pathogens in low- and non-alcoholic beers. They inoculated pH (4.20, 4.50, and 4.80), temperature (4 and 14°C), and % ABV (<0.50 and 3.20) standardized beer with a five-strain cocktail of E. coli, S. enterica, and L. monocytogenes and monitored bacterial growth over 63 days.

Alcohol content and storage temperature were revealed to be the most significant determinants of bacterial growth, with non-alcoholic beer being far more susceptible to microbial growth than low-alcoholic beer.

“Due to the increased susceptibility to spoilage and pathogens, the formulation of those beverages must be evaluated for safety by a Process Authority. Low and non-alcoholic beers should be processed through pasteurization, to achieve commercial sterility. Sterile filtration and the addition of preservatives should be considered as additional steps to reduce this microbial risk.”

Journal reference:

Çobo, M., Charles-Vegdahl, A., Kirkpatrick, K. R., & Worobo, R. W. (2023). Survival of foodborne pathogens in low and Non-Alcoholic craft beer. Journal of Food Protection, 100183, DOI – https://doi.org/10.1016/j.jfp.2023.100183, https://www.sciencedirect.com/science/article/pii/S0362028X23068679?via%3Dihub

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Study authors from the University of Illinois Chicago discovered that individuals with Type 2 diabetes who confined their eating to an eight-hour window daily shed more weight over a period of six months than those who cut their caloric intake by 25 percent. Additionally, both groups experienced comparable reductions in long-term blood sugar levels, according to the findings published in JAMA Network Open.

“Our study shows that time-restricted eating might be an effective alternative to traditional dieting for people who can’t do the traditional diet or are burned out on it,” says senior author Krista Varady, a professor of kinesiology and nutrition, in a media release. “For many people trying to lose weight, counting time is easier than counting calories.”

The study involved 75 participants, dividing them into three groups: those adhering to the time-restricted eating guidelines, those who reduced their caloric intake, and a control group. Over the course of six months, measurements were taken of the participants’ weight, waist circumference, blood sugar levels, and other health indicators.

Participants in the time-restricted eating group reported finding the regimen easier to stick to than those in the calorie-reduction group. The researchers attribute this to the fact that individuals with diabetes are frequently advised by their doctors to reduce their caloric intake as an initial strategy. Consequently, many participants in the study may have previously attempted — and found challenging — that approach to dieting.

Notably, even though the time-restricted eating group was not explicitly instructed to decrease their caloric intake, they naturally did so by eating within a predetermined timeframe.

Type 2 diabetes can develop in anyone but is more common in individuals over the age of 25, particularly those with a family history of the condition. With the anticipated increase in the number of cases, the research team emphasizes the importance of identifying additional options for managing weight and blood sugar levels.

Why is Type 2 Diabetes so dangerous for your health?

Type 2 diabetes is a chronic condition that affects how your body turns food into energy. When you have Type 2 diabetes, your body’s cells become resistant to insulin, a hormone that helps regulate blood sugar levels. As a result, glucose (sugar) builds up in your blood.

Over time, high blood sugar can damage your nerves, blood vessels, and organs. This can lead to a number of serious health complications, including:

• Heart disease and stroke: Type 2 diabetes is a leading cause of cardiovascular disease, which includes heart disease and stroke. People with Type 2 diabetes are twice as likely to have a heart attack as people without diabetes.

• Kidney disease: Type 2 diabetes is the leading cause of kidney failure. High blood sugar can damage the tiny blood vessels in the kidneys, making it difficult for them to filter waste from the blood.

• Eye problems: Type 2 diabetes can lead to a number of eye problems, including diabetic retinopathy, glaucoma, and cataracts. Diabetic retinopathy is a common cause of blindness in adults.

• Neuropathy: Type 2 diabetes can damage the nerves in your body, leading to numbness, pain, and tingling in your hands and feet. Neuropathy can also lead to foot problems, such as ulcers and infections.

In addition to these serious health complications, Type 2 diabetes can also make it difficult to control other chronic conditions, such as high blood pressure and high cholesterol.

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A Minnesota doctor who had worked for a poison control center was charged this week in the poisoning death of his wife, who died from a lethal dose of the highly toxic gout medication, colchicine.

Connor Bowman, 30, was arrested last Friday and charged Monday with second-degree murder in the death of Betty Bowman, 32, who worked as a pharmacist at the Mayo Clinic.

In an investigation that followed her suspicious death on August 20, police learned that the two were having marital problems, including a deteriorating relationship and infidelity, and were talking about a divorce. They also learned that Connor Bowman was in debt and stood to gain $500,000 in life insurance upon his wife's demise.

Connor Bowman initially claimed Betty died of a rare hyper-inflammatory condition called hemophagocytic lymphohistiocytosis (HLH), but tests for the unusual condition were inconclusive, and a source told police that Betty was previously healthy before her rapid deterioration.

On August 21, the day after Betty's death, the medical examiner's office deemed the death suspicious and informed the Rochester, Minnesota, police. Connor Bowman told the medical examiner's office that Betty should be cremated immediately and tried to cancel the planned autopsy.

When it wasn't canceled, he questioned the toxicology testing that would be done, asking one death investigator over email for a list of everything they would test for.

The toxicology testing as part of the autopsy revealed an extremely high level of colchicine in her blood, as well as detection of the gout drug in her urine. Betty had not been diagnosed with gout, and none of her doctors had prescribed her colchicine. In retrospect, her death is a textbook case of colchicine poisoning.

A drug with a “dark side”

Colchicine is a centuries-old treatment for gout—a form of arthritis that occurs when elevated blood levels of urate form into needle-shaped crystals around joints, leading to severely painful inflammation. Colchicine, extracted from two flowering plants (Colchicum autumnale and Gloriosa superba), has weak anti-inflammatory activity, which makes it effective against gout. But it is shockingly toxic. And despite its long-standing use, the line between nontoxic and toxic doses remains unclear.

The reason is the fundamentally disruptive way colchicine works. The drug binds to the protein tubulin in cells, preventing it from forming into microtubules, which are vital structural components of cells. Microtubular networks are required for separating chromosomes during mitosis among many other functions. Thus, at sufficient doses, the drug halts all cells division, impairs protein assembly, decreases endocytotis and exocytosis, alters cell shape, and reduces cell motility.

Colchicine is rapidly absorbed in the gastrointestinal tract and equally rapidly distributed throughout all tissues in the body. Thus, with a toxic dose, the damage is systemic. And the downstream effects of demolishing microtubular function lead to multi-organ failure.

In a 2010 review published in Clinical Toxicology, an international team of researchers labeled colchicine a drug with a "dark side" and laid out the three stages of poisoning: The first is a gastrointestinal phase, the first 24 hours after the poisoning, in which damage to gastrointestinal mucosa leads to nausea, vomiting, diarrhea, abdominal discomfort. It might look like severe food poisoning or cholera. Then there's the second, multi-organ phase, from one to seven days after poisoning, in which the toxic effects spread around the body. There can be a variety of multi-organ dysfunction and metabolic derangements. Death often takes the form of faltering cardiovascular function and cardiac arrhythmia or arrest, but respiratory distress, liver failure, kidney failure, brain swelling, and secondary sepsis can also occur. For the lucky, the third phase is the recovery phase, which can last from seven to 21 days after the poisoning. In this phase, failing organs rebound, but patients might experience alopecia (hair loss) and other complications, including delirium, stupor and coma, convulsions, adrenal hemorrhage, and pancreatitis. In some rare cases, patients' skin blisters and peels off.

Betty Bowman didn't make it to the third stage. She was admitted to the hospital on August 16 with severe gastrointestinal distress and dehydration. She was treated as if she had food poisoning. The night before, she had texted a friend that she was drinking at home with Connor Bowman and, upon falling ill, thought the cause was something mixed into a large smoothie she had been given.

She did not improve with the standard treatment for food poisoning and instead rapidly deteriorated. In the four days she was hospitalized before her death on August 20, she experienced cardiac problems, fluid in her lungs, and eventually organ failure. During that time, she also had a large part of her colon removed due to the discovery of necrotic tissue.

Damning Internet history

The medical literature indicates that a lethal oral dose of colchicine is anything that exceeds 0.8 mg per kilogram. The police investigation that looked at Connor Bowman's Internet history found "on August 10, Bowman was converting [Betty's] weight to kilograms and is multiplying it by 0.8," according to the charging document. He was also shopping for liquid colchicine on August 10 and 11, visiting the GoodRX website where he searched for the drug and then Stripe, an online payment platform.

He also allegedly searched for things like "internet browsing history: can it be used in court?" and "delete amazon data police." He tried using a VPN but initially mistyped it as "bpn."

The toxicology report found 29 ng/mL of colchicine in her blood, which was drawn on August 16, the day she was admitted to the hospital and a day after drinking the suspicious smoothie. The medical examiner noted that the concentration was high given that it had been 24 hours since the dose and the drug was metabolized quickly.

Law enforcement also found a $450,000 bank deposit in Connor Bowman's home after the death.

Betty Bowman's family set up a GoFundMe page to take donations to help with, among other things, legal costs. The page notes that the family is raising funds because "As new evidence emerges, we realize Betty might have been taken from us not by natural causes."

Connor Bowman is scheduled to appear in court on November 1, and he faces up to 40 years in prison if convicted.

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Researchers may have just spotted the elusive, ephemeral nucleus of nitrogen-9 for the first time.

With seven protons and two neutrons, the lopsided atomic nucleus of nitrogen-9 pushes the limits of what can even be considered a nucleus at all. Yet signs of its existence seem to be lurking in years-old data from experiments seeking out a different unusual nucleus, researchers report in the Oct. 27 Physical Review Letters.

If follow-up studies can confirm the detection, nitrogen-9 will be the first nucleus spotted with five more protons than it can stably hold — until now, the limit was four.

“What are the limits of nuclear existence?” asks nuclear physicist Andreas Heinz of Chalmers University of Technology in Gothenburg, Sweden, who was not involved in the study. That’s what the study’s authors and physicists more generally are trying to understand, he says.

Protons and neutrons, the subatomic particles that make up atomic nuclei, are essentially glued together by the strong nuclear force (SN: 9/13/22). But the force can’t hold together nuclei that have wildly skewed ratios of protons to neutrons. Too many of either particle — especially protons, which repel each other due to their positive charge — and the nuclear bucket starts to overflow.

Beyond this overflow point, which physicists call the “drip line,” nuclei cannot fully bind their particles.

“People talk about the drip line as something like the end of the existence of nuclei,” says Marek Płoszajczak, a nuclear physicist at the Grand Accélérateur National d’Ions Lourds in Caen, France, who was not involved with the study.

But nuclei do exist beyond the drip line, if only ephemerally (SN: 11/15/21). To qualify as a nucleus, a handful of protons and neutrons need to hang out together for something like 10-22 seconds — a blink so brief that more of these moments fit in a second than seconds fit in the age of the universe. Though Heinz notes that’s a somewhat arbitrary definition based mainly on just one previous study.

Scientists searching for nuclei beyond the drip line are testing that definition. “We’re interested in how far you can go before you no longer can consider these things new nuclei,” says nuclear scientist Robert Charity of Washington University in St. Louis.

Finding a nucleus as far beyond the drip line as nitrogen-9 — five protons beyond — was surprising even for Charity’s team. Until now, scientists had only ever found isotopes up to four protons beyond the drip line.

The atoms of any given element each have a fixed number of protons. But the number of neutrons can vary, creating what are known as isotopes of that element (SN: 9/14/23). Charity and colleagues had been hunting for an isotope of oxygen, oxygen-11, by smashing high-powered beams of oxygen-13 nuclei into beryllium targets and measuring the decay products of short-lived nuclei produced in the collision.

Years after the experiment, Charity says, he noticed decay products in the data that looked like they should have crumbled away from nitrogen-9 nuclei. His theorist colleagues later confirmed that the decay products could really have come from the isotope. It lasts for about 10-21 seconds, or about 10 times as long as the minimum cutoff, Charity says.

The statistical strength of the evidence for nitrogen-9 falls right on the knife-edge of what scientists would consider a discovery. But the team really does have “strong evidence” for nitrogen-9, Heinz says. “For me, this sounds really convincing.” And, he says, the possible discovery should come as reassuring news to experimentalists looking for other isotopes beyond the drip line.

As for theorists? Płoszajczak says the new result should give them a “push” to improve their models of nuclei beyond the drip line, which are still rather limited. “These experiments show that the life of the nucleus extends far beyond the drip line.”

When it came to nitrogen-9, experiment beat theory to the punch. But better theories could make it possible to start looking for drippy nuclei on purpose, which would, in turn, make it easier to verify theories. When that happens, “we will start to have a kind of a discussion — a talk with nature,” Płoszajczak says. “Then, I think the whole field will explode. So we are just at the beginning.”

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Clinical depression is considered one of the most treatable mood disorders, but neither the condition nor the drugs used against it are fully understood. First-line SSRI treatments (selective serotonin reuptake inhibitors) likely free up more of the neurotransmitter serotonin to improve communication between neurons. But the question of how SSRIs enduringly change a person’s mood has never returned completely satisfying answers.

In fact, SSRIs often don’t work. Scientists estimate that over 30 percent of patients don’t benefit from this class of antidepressants. And even when they do, the mood effects of SSRIs take several weeks to kick in, although chemically, they achieve their goal within a day or two. (SSRIs raise the levels of serotonin in the brain by blocking a “transporter” protein that decreases serotonin levels.) “It's really been a puzzle to many people: Why this long time?” says Gitte Knudsen, a neurobiologist and neurologist at the University of Copenhagen, Denmark. “You take an antibiotic and it starts working immediately. That's not been the case with the SSRIs.”

Experts have proposed theories about what causes the delay, but to Knudsen, the most compelling involve our brains’ ability to physically readjust over time: a characteristic called neuroplasticity. In adulthood, brains rarely create new neurons, but they do sprout new interconnections between existing ones, called synapses. Essentially, they adapt by rewiring. “That's exactly what happens when we exercise and learn something,” Knudsen says. This transformation improves cognitive function and emotional processing. Knudsen thinks rewiring could also break someone free from cycles of negative rumination—a hallmark of depressive episodes.

Knudsen believes that SSRIs owe their efficacy at least in part to boosting neuroplasticity. Writing in Molecular Psychiatry earlier this month, her team showed how they had tested this theory on people, thanks to a special kind of PET scan developed in the past few years. They recruited 32 people to take the SSRI escitalopram (also known by the brand name Lexapro) or a placebo for one month. Then they asked the people to take a PET scan at the end of the trial, and used radioactive tracers to track where in the brain new synapses were forming.

The more time someone spent on the antidepressant before their brain scan, the more synaptic signals the team detected—a proxy for increased connections. “This is one of the first pieces of evidence that these drugs do take time to work, and they do work through increasing the number of synaptic contacts between nerve cells,” Knudsen says.

The finding suggests that SSRIs improve neuroplasticity during the first weeks or months of treatments, and that neuroplasticity contributes to the drugs’ benefit—and to the delay before users feel better. “It has been a paradox,” says Jonathan Roiser, a cognitive neuroscientist at University College London who was not involved in the work. Because the drugs’ chemical effects happen on a scale of days, he says, “there needed to be this extra bit of explanation about why the mood change does not happen immediately.”

“This is really important not just for general scientific understanding, but for actually improving our ability to treat patients,” says Camilla Nord, a cognitive neuroscientist at the University of Cambridge in the UK, who was not part of Knudsen’s team. “This could help us target the treatment at particular subgroups of patients—or maybe help us understand why it doesn't work in some people.”

Since SSRIs were invented about 40 years ago, neuroscientists and psychologists have wanted to know exactly how they work. Studies clarified serotonin’s role about 20 years ago by proving that when serotonin levels rise, the brain veers away from negative biases in processing emotions. But these momentary changes in perception aren’t enough to relieve symptoms. “You need a cumulative exposure to a more positive input over time to break out of the depressive state,” says Roiser. “Previously, this had been the end of the explanation.”

One theory for why there’s a lag between the start of SSRI treatment and mood change is that the brain takes weeks to recalibrate serotonin levels. Think of it as a feedback system: Initially, after an SSRI spikes a person’s serotonin levels, their brain responds by pumping the brakes on producing the neurotransmitter. Instead of maintaining a boost, their serotonin levels fall again. “It's like a thermostat,” Knudsen says. It takes a while before the brain adjusts.

“It is a fairly simplistic explanation that has helped doctors try to explain to patients why it takes time and what these drugs do,” Knudsen says. But, as a neurologist hoping to improve treatment, Knudsen wasn’t satisfied with this answer, partly because studies in rats suggested that a more complicated story was unfolding. These studies showed that in female rats given daily doses of SSRIs, new synapses formed in their visual cortex and hippocampus, brain areas linked to learning and memory. This indicated that SSRIs induce neuroplasticity.

But until about seven years ago, scientists couldn’t replicate these studies in humans, since there was no way to measure synaptic density without cutting out brain tissue. Then in 2016, researchers developed a way to detect synaptic activity in live human brains during PET scans. These scans detect light emitted by radioactive “labels” designed to stick to specific proteins. The patient receives an injection of these radioactive markers, which diffuse to the target proteins in the brain. The scan reveals a map of where exactly those proteins are.

Scientists quickly began using the PET method to study disorders like Alzheimer’s and schizophrenia, convincing Knudsen of its power for mental health studies. So her team organized a double-blind, randomized clinical trial in which healthy participants would receive a standard 20-milligram SSRI or a placebo daily. After three to five weeks, the team would collect PET scans of the synapses in each person’s neocortex and hippocampus. In this case, the labels were designed to stick to a protein at the connection between neurons. Tracing them would map out the brain’s synapses, allowing scientists to measure synaptic density.

Their hypothesis was simple: The participants who took the drug instead of the placebo would show more synaptic density. That hypothesis was wrong.

“At first glance, it seemed slightly disappointing,” Knudsen says. There was no significant difference between synapses in the drug and placebo cohorts. But an imperfection in the study became its life raft. For logistical reasons, each person’s PET scan varied from 24 to 35 days after their first drug dose. This introduced a new variable into the experiment—duration—and it let the researchers perform a new analysis.

“It was only when we started to look closer at the timing that we could see they had an increase,” Knudsen says. Participants who spent longer on the drug had more synapses than those who spent less time. And for those on the placebo, timing didn’t matter whatsoever. Knudsen thinks this means that these synaptic changes accumulate during the weeks it takes for SSRIs to ramp up.

Nord says that the Danish team’s biological explanation nicely complements the psychological theory that augmenting positive emotions has a cumulative effect on mood. “The two explanations are compatible,” says Nord, whose book The Balanced Brain: The Science of Mental Health was released in September. “They’re explaining it at different levels.”

“It's a different perspective to what's come before,” agrees Roiser. “It gives the additional weight to this idea that you need the cumulative changes over time in order to shift the environment to be more positive, which can then explain how people are then going to recover from depression.”

Neuroplasticity may be an antidote to the distressing recurring thoughts that are often present in depression. “It's almost as if the brain is fixed in an unhealthy pattern that is reinforcing itself,” Knudsen says. If rumination reinforces negative thinking, then forming new connections offers a way out, she says, “like having a reset button that makes you think differently.”

But Mark Rasenick, a neuroscientist at the University of Illinois Chicago, hesitates to draw broad conclusions based on how the healthy individuals in Knudsen’s study responded to SSRIs. Antidepressants affect mood more in a depressed person, he says: “What do they do to healthy people? The answer is not much.”

Knudsen agrees that healthy participants may respond less to the neuroplastic effects than people diagnosed with clinical depression, and she says that the project’s next phase, including participants with depression, is ongoing.

Rasenick imagines a PET study of only depressed patients, all receiving the same SSRI for the first time. Some participants won’t benefit from the drug, so this setup could compare neuroplasticity in those who benefit versus those who don’t.

In 2016, Rasenick’s team proposed another biological explanation for why the effects of antidepressants lag, when they observed that SSRIs gradually accumulate in the membrane of certain brain cells in rats. They may not have an effect until they build up to a critical level. Based on a pilot study Rasenick published last year, this facet of SSRI action may one day allow doctors to use blood tests to quickly measure whether a patient is responding to the drugs. Still, Rasenick believes that neuroplasticity is an important factor too. “To have the evidence from living human brains is critical,” he says.

PET scans are becoming an unparalleled resource for measuring wiring in human brains. “It's very rare to have the ability to do an experiment like this,” Nord says. “They're giving us a quite unusual window into the processes that are happening in this treatment.” Knudsen’s team has also used them to investigate psilocybin’s effects, and another team has studied ketamine’s. “What this paper is really showing is that you can detect these new connections being formed,” Roiser adds.

The problem is, PET scans and radioactive labels cost researchers thousands of dollars per participant. (About $4,500 per scan in this study, according to Knudsen.) Yet the benefits might pay off if they improve treatment. Nearly one in five adults in the United States have been diagnosed with clinical depression, making it “a major contributor to mortality, morbidity, disability, and economic costs,” according to the CDC.

Rosier says this new study suggests it could be beneficial to speed up synapse formation, perhaps with an accelerant drug that could complement SSRIs. “One can imagine encouraging these neuroplastic changes during antidepressant treatment, maybe making them happen faster,” Roiser says. That could help the many people who spend months trying drugs to find the one that works. But there’s still much to uncover about why depression varies from person to person, and how to predict the best treatment. (A fast-acting antidepressant that acts on the neurotransmitter GABA instead of serotonin recently earned approval to treat postpartum depression, but not for general depression.)

Knudsen likens treating depression to treating a fever. Antibiotics can’t kill every kind of bacterial infection, and they do nothing if the fever is caused by a virus. So doctors have to know the exact cause of the fever if they want to be confident about the medication they give. Neuroscientists yearn for the same grasp of the biological causes of depression. “To expect that the same kind of medication would be helpful for all patients with depression is perhaps a bit naive,” Knudsen says. “It makes a whole lot of sense to rethink what depression really is and how it should be treated.”

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The word "unprecedented" gets tossed around a lot these days, but what happened with Hurricane Otis and its impact on Acapulco on Tuesday were truly without precedent. And it was with only slight precedent anywhere in terms of how quickly it intensified.

 

Otis was the textbook definition of rapid intensification, going from a 50 mph tropical storm on Monday evening to a 165 mph category 5 hurricane last night. Through about mid-morning on Tuesday, everything was going basically as you'd expect for a modest hurricane with Otis. It may have been tracking toward a category 2 type landfall, or even a category 3 type landfall in the worst case, if you assumed the general rules of rapid intensification in this region. But Otis did not follow the rules.

 

Much like an onion, there are layers to this story that are important. First, take it from one of the more seasoned NOAA hurricane hunters—this was not what they expected when they flew their mission on Tuesday. Meteorologist Jeremy DeHart wrote on the site formerly known as Twitter, "I have arrived to a storm & been surprised by the intensity, but nothing like this. Expected a marginal hurricane, found a Cat 3! Reminiscent of the stories I've heard about flying into Patricia ('05), in the same part of the world."

 

And this was before Otis had peaked. The typical satellite-derived intensity values often used to "proxy" intensity of storms that are far away from reconnaissance flights failed in this case to grasp how intense Otis was. In other words, Otis intensified so quickly that it basically outran the ability to measure how intense it actually was.

 

Here was the raw model output for Otis from Tuesday morning. This is what general weather forecasters would use to assess what will happen with a storm's wind forecast. The dashed line is what actually occurred.

 

None of the best, most reliable tropical modeling had Otis as a hurricane, let alone a category 5 storm. To put it bluntly, this was an absolutely catastrophic forecasting failure.

 

By late Tuesday morning, the experts at the National Hurricane Center had it at 90 mph making landfall. This is well above any forecast data, and they concluded in their discussion that it seemed reasonable to potentially see further intensification adjustments upward before landfall. But even in their worst-case scenario, the NHC forecast would have still been off by probably two categories less than 18 hours before landfall. And this was using strong meteorological analysis to bias-correct the models upward, too. To their credit, they had it at 140 mph by the late afternoon advisory.

 

Interestingly, one of the tools we use to forecast the probability that a storm will rapidly intensify, SHIPS guidance, also failed. Early on Tuesday morning, it showed only about a 2–3x above normal chance that the storm would intensify from a 50 mph tropical storm to a 100–125 mph hurricane. Yes, that is above climatology, but it's not exactly impressive given what we've seen in recent years.

 

By Tuesday afternoon, those odds had increased to 5–9x above normal. But even this only showed 2x above normal odds that we'd get to 140 mph+. There were finally some hints available by mid to late morning on Tuesday, but nothing that would have offered a meaningful forecast improvement over what the NHC had (which called for 20–30 mph of intensification over 12–24 hours).

How did this happen?

The first question is why Otis did what it did. It was probably a combination of a couple of things. First, Otis was placed ideally in an environment that facilitated constructive wind shear. When we discuss wind shear, it's usually referenced in a negative sense; wind shear inhibits and destroys storms. But in occasional cases, as we've witnessed in the Gulf of Mexico with Ian, Delta, and Zeta, among many other storms in recent years, the wind shear can actually be constructive and help "vent" the system. In this case, Otis was optimally placed in the right entrance region of the jet stream.

 

Storms are aided in intensification when placed in the left front or right rear (entrance) of the jet stream. Why? In that portion of the jet stream, the winds aloft diverge, meaning they either move in opposite directions or stronger wind diverges away from weaker wind. Upper-level divergence leads to rising air. Rising air is necessary for storms to form and maintain, and thus surface pressures tend to fall in this region of the jet stream as well.

 

A conceptual model of a jet streak showing that the right entrance region (bottom left quadrant) is

supportive of upper-level divergence and surface pressure falls.

Penn State University

 

Otis wasn't exactly square in the middle of the right entrance region, but it was close. Additionally, Otis tracked right over an area of 31°C sea surface temperatures, likely warmed by a combination of El Nino and climate change.

 

This rich, warm water did not hurt matters at all.

 

So how did every reliable model we use miss this? That's for graduate students and researchers to answer in the coming years because I have no formal idea. There was something about Otis that models just could not capture and translate to rapid intensification. Human forecasters, recognizing the setup were able to mitigate some, but not all, of the under-forecast issue. Otis' smaller size may have also contributed. My hunch is also that if Otis had tracked, say, 30 or 40 miles east or west of where it was, it would not have gone off to the races like this. It was simply perfectly placed to optimize intensification.

A less sexy explanation?

Otis was almost unprecedented in the historical record. Only Hurricane Patricia in the Pacific in 2015 had a greater rate of intensification than Otis. And in the modern era, no massive storm has hit Acapulco.

 

Unprecedented outcomes are just that, and if the historical record has only one other remotely comparable event in this region, it becomes tough to expect that modeling can "capture" the concept that this would occur in this environment.

 

It feels like this was a combination of bad luck, bad timing, and bad placement. And it just so happened that a metropolitan area with over 1 million people was in the way.

 

It's easy to sit here and pontificate about this or to say that weather forecasts are often wrong. But they're not. They're often right. With hurricanes, forecasting has improved by leaps and bounds in the last 20 to 30 years. Perfect? No, but often more than acceptable. A failure like this shocks us because we aren't actually used to forecast failures of this magnitude anymore. 100 years ago? Sure, this was fairly routine. But in the 2020s, we have standards and expectations for weather forecasts, and clearly this was a shock to the system.

 

Busts like this remind us that it's an imperfect business and there is still much work to do. The work to be done to understand Otis will take time, but we will certainly see many research papers in the coming years.

 

This story originally appeared on The Eyewall.

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