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Their results elucidate that increased consumption of confectionery, butter, added sugars, butter, and milk-based desserts was associated with increased mental health symptoms. These symptoms were aggravated by reduced fresh fruit and vegetable intake.

Food and mental health

Mental health disorders are common conditions affecting more than 970 million individuals globally, with depression and anxiety representing the leading causes of disability and disease burden.

A growing body of literature on the association between diet and mental health exists, with previous studies suggesting that high single-nutrient intake, especially saturated fats and free sugars, and low dietary fiber heighten the risk of depression or anxiety.

Sweetened beverages, meat, specific fruits and vegetables, and fish have also been identified as contributing to mental health disorder risk.

Still, these studies have the critical limitation of being single-nutrient studies, thereby failing to capture the mental health effects of diets, which generally comprise a combination of multiple nutrients consumed simultaneously. The synergistic effects of multi-nutrient diets on depression and anxiety symptoms remain hitherto uncharacterized.

About the study

In the present study, researchers employed reduced rank regression (RRR), a data-driven statistical model to characterize major dietary patterns (DPs), to holistically evaluate the association between dietary habits and mental health outcomes.

They used long-term, extensive cohort data from the UK Biobank and self-reported mental health questionnaires and clinical diagnoses.

Their dataset initially comprised 502,401 participants from the UK Biobank, a prospective cohort study of consenting adults aged between 37 and 73, conducted across the UK between 2006 and 2010. Multiple rounds of participant screening excluded those with incomplete questionnaires, abnormal energy (calorific) intakes, cancers, and insufficient covariate data

The final study population comprised 157,212 individuals, of which 70,271 were diagnosed with baseline depression and 70,070 with baseline anxiety at the start of the study.

All participants were followed up on a 3–4-month schedule for an average of 7.6 years. Depression and anxiety were analyzed separately in the study to avoid one mental health cohort confounding results from the other.

Data for dietary assessment was collected using the Oxford WebQ tool, a web-based 24-hour method of collating the consumption frequency of 206 food items and 32 beverage types. Collected data was classified into 50 groups based on nutritional similarity.

Researchers focused data analyses on energy density, fiber density, saturated fatty acids, and free sugars, given the a priori hypotheses of their role in depression and anxiety.

Mental health outcomes were measured during and at the end of the study using the Patient Health Questionnaire-9 (PHQ-9) for depression and General Anxiety Disorder-7 (GAD-7) questionnaire for anxiety.

Both are self-reporting, 3-point-scale severity questionnaires, with scores of 10 or higher confirming depression or anxiety, respectively. Covariates included age (collected at study initiation), sex, ethnicity, education level, smoking, physical activity (compiled using the International Physical Activity Questionnaire [IPAQ]), hypertension, diabetes, and cardiovascular disease (CVD) history, and Townsend deprivation index. The deprivation index is a proxy for socioeconomic status compared to others living in the same postal code.

Dietary patterns were evaluated using the RRR model. Each participant was assigned a z-score, a weighted score representing adherence to each of the DPs identified by RRR analysis. Logistic regression models were used to calculate odds ratios (ORs) with adjustments incorporated for each measured covariate. Finally, sensitivity analyses were employed to verify the results’ robustness.

Study findings

The RRR model identified four DPs, named DP1–4. Of these, DP4 was found to explain only 4.3% of the variation found in the model and was excluded from further analyses. Collectively, DP1–3 were found to explain 74.1% of the variation observed (44.0%, 20.0%, and 10.1%, respectively).

Dietary pattern 1, the “high caloric diet,” was characterized by high butter and animal-fat intake and low intakes of fresh fruits and vegetables. This dietary pattern showed strong non-linear associations with depression, anxiety and correlations with sex and physical activity

Dietary pattern 2, the “high sugar, low-fat diet,” comprised a high intake of sugary beverages, and table sugar, and low butter and animal fat. This dietary pattern did not show a linear association with mental health but a non-linear U-shaped curve, indicating that extremes of adherence (very low and especially very high) to this diet are associated with depression and anxiety.

Dietary pattern 3, the “high sugar, high fat, high fiber diet,” comprised diets containing high butter, animal fats, milk-based desserts, and low alcohol and bread consumption. This pattern is non-linearly associated with depressive and anxiety symptoms, with anxiety associations strengthened for individuals aged ≥ 60 years.

“Our findings highlight the intricate relationships between overall diet pattern and symptoms of depression and anxiety. The current analysis has yielded robust findings that increased consumption of free sugars and saturated fatty acids was associated with a heightened risk of symptoms related to depression and anxiety.”

Sensitivity analyses verified that all computations employed for DP1–3 were valid and significant.

Conclusions

The study explored the multi-food dietary association between nutrient intake and depression or anxiety. The long-term (7.6 years), large cohort (157,212) study utilized the RRR model to characterize major DPs. Three major DPs were identified, named “high caloric diet,” “high sugar, low-fat diet,” and “high sugar, high fat, high fiber diet.”

Study results highlight that diets rich in butter, animal fats, confectionery, chocolate, cheese, and sugary drink may cause gut microbial alterations, thereby contributing to an increasing risk of anxiety or depression.

Lowered consumption of fiber and fresh fruits and vegetables were found to exacerbate these conditions.

“Using the RRR approach, our findings of curvilinear relation between nutrients suggest to limit intakes of chocolate and confectionery, butter and other animal fat spreads, high-fat cheese, sugar-sweetened beverages, and other sugary drinks, table sugars and preserves, and milk-based desserts. The excessive consumption of these foods may trigger systemic inflammation, increase oxidative stress, and cause alterations in gut microbiota, thereby contributing to the risk of developing symptoms of depression and anxiety.”

Journal reference:

Chen, H. et al. (2023) "The associations of dietary patterns with depressive and anxiety symptoms: a prospective study", BMC Medicine, 21(1). doi: 10.1186/s12916-023-03019-x. https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-023-03019-x#article-info

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On Thursday, 17th Aug. In 2023, ISRO announced the separation of the Lander Module, comprising the Vikram lander and the Pragyan rover, from the Propulsion Module.

Just after the separation, the Lander Imager (LI) Camera-1 captured the Moon. ISRO shared the view of the Moon on their official X (formerly Twitter handler).

It mentioned, “View from the Lander Imager (LI) Camera-1 on August 17, 2023, just after the separation of the Lander Module from the Propulsion Module.”

The officials also shared one video of the Moon captured on August 15, 2023, by Chandrayaan-3 Lander Position Detection Camera (LPDC).

< Watch the video at the source page. >

The health of the Lander Module (LM) is reported to be normal. On the other hand, the Propulsion Module will keep traveling for several months or years in its current orbit. It will conduct spectroscopic research on the Earth’s atmosphere and analyze changes in cloud polarization to find signs of extraterrestrial planets that might be habitable for us.

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Hundreds of millions of people across the globe are living amid unprecedented temperatures, with July becoming the hottest month on record. Another heatwave is building in the US Pacific north-west.

Heat is the main cause of weather-related death in the US. How does it affect the body?

“Heat stress means that the body is experiencing a deep buildup of heat – more than it can release,” said Uwe Reischl, professor in the school of public and population health at Boise State University. Depending on the severity of heat, symptoms can range from the uncomfortable to the fatal.

The ‘optimum’ body temperature

The “optimum” internal temperature at which our bodies comfortably function is about 98.6F (36.8C). While it varies slightly from person to person, the core body temperature needs to stay within a narrow range of 97-99F (36-37C) to protect organs, and for cells to function best.

When the body becomes too hot, blood vessels in the skin dilate, and sweat is released. Heat is dissipated via the evaporation of sweat, which cools the surface of the skin, liberating heat transferred from the core.

High humidity can hinder this natural cooling process. And when the heat index – a combined metric of air temperature and humidity – reaches 90F, the risk of heat-related illness starts to rise.

First, cramps and fatigue

Some of the first physical symptoms of heat-related illness are muscle cramps, which can happen all over the body.

The next stage is heat exhaustion – a more serious condition that occurs when the body still cannot get rid of excess heat. The signs can include:

• Fatigue
• Headache
• Lightheadedness
• Nausea
• Dry mouth
• Vomiting

“Not everyone is going to show the same symptoms,” said Gredia Huerta-Montañez, a pediatrician and environmental health researcher at Northeastern University. “It’s easy to ignore them, so we need to continue educating communities.”

Inside the body, the heart quickens and muscles slow

Inside the body, excess heat has a dramatic effect. The heart has to pump faster to spur more blood flow to the skin, so heat can be released. To reduce the amount of heat produced by the muscles, the body becomes sluggish and moves more slowly.

Breathing becomes heavier as the body seeks to take in more oxygen.

Urination becomes less frequent as the body seeks to retain as much fluid as it can. However, large amounts of fluid can be lost due to elevated sweat rates (which can exceed 2 liters per hour in healthy young adults), meaning dehydration can develop quickly.

Blood flow to the gastrointestinal tract and kidneys is reduced, which, if sustained for prolonged periods, can cause damage to these organs.

The most dangerous stage: heatstroke

Heatstroke is the most serious heat-related illness. When the body reaches 103F or higher, organs such as the brain, the heart, the gut and the kidneys can become damaged.

A victim of heatstroke might experience abrupt changes in cognitive function and mental state, such as confusion, hallucination and seizure. A person can fall unconscious and, in extreme cases, go into cardiac arrest.

Heatstroke is a medical emergency, and it is important to cool the person and seek help quickly.

“If you’re left with the decision, even if an ambulance is there, of ‘Do we get this person to a hospital or cool them?’, cooling should take priority,” said Robert Meade, an extreme heat researcher at the University of Ottawa.

“The longer the person stays at that elevated body temperature, all of these effects on the central nervous system like endotoxemia are just going to continue to occur.”

Endotoxemia occurs when the body becomes so hot that the gut has been starved of blood and oxygen, and the intestinal barrier starts to break down. Bacteria from the gastrointestinal tract can enter the bloodstream.

The window in which it can turn fatal is short, and even for survivors there can be long-term health complications.

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Japan—like other countries—is seeing ever-hotter summers. This July was the warmest in 100 years, with at least 53 people dying of heatstroke and almost 50,000 needing emergency medical attention.

Workman, which makes clothes for construction workers, launched a version of their fan-fitted jackets adapted for the high street in 2020 as demand grew.

The mechanism is simple—two electric, palm-sized fans powered by a rechargeable battery are fitted into the back of the jacket.

They draw in air to then deliver a breeze—at variable speeds—onto the wearer's body.

The jackets retail for 12,000 to 24,000 yen ($82-164).

"As the weather gets hotter, people who have never worn fan-equipped clothing before want to find ways to cool down... so more people are interested in buying it," Workman spokesman Yuya Suzuki told AFP.

"Just like you feel cool when you are at home with a fan, you feel cool just by wearing (the jacket) because the wind is blowing through your body all the time," he said.

Aging population at risk

Japanese summers are known to be hot and humid, but this July Tokyo really sweated.

The average temperature was 28.7 Celsius (83.7 Fahrenheit), the highest on record since 1875.

Heatstroke is particularly deadly in Japan, which has the second-oldest population in the world after Monaco.

More than 80 percent of heat-related deaths in the past five years have been among senior citizens.

"Some people die from heatstroke," said Nozomi Takai of MI Creations, a company selling neck-cooling tubes mainly to factory and warehouse workers.

"Individuals as well as companies are putting more and more effort into measures against it every year," Takai said.

The gel inside his firm's brightly colored tubes—priced at 2,500 yen—is cool enough to use after 20 minutes in the fridge.

Wearing it on the neck will "considerably cool the whole body" for about an hour, she said.

Takai's company joined an expo this year on "measures against extreme heat" in Tokyo to showcase new products that help users stay cool in the scorching heat.

At another booth, Tokyo-based company Liberta had a series of clothing including T-shirts and arm sleeves using prints that make users feel cool—especially when they sweat.

The prints use materials such as xylitol that feel cool when reacting with water and sweat, they said.

Chikuma, an Osaka-based company, has even created office jackets and dresses equipped with electric fans.

"We developed them with the idea that it could be proposed in places where casual wear is not allowed," Yosuke Yamanaka of Chikuma said.

Regular fan-fitted clothes can make the wearer look puffy, as they need to be zipped up, and cuffs are tight.

But jackets developed jointly by Chikuma, power tool maker Makita and textile giant Teijin do not need to be buttoned up, thanks to a special structure that sandwiches the fans in two layers and keeps the cool air in, Yamanaka said.

Men adopting parasols

Parasols, which are commonly associated in Japan with skin-tone-conscious women protecting against a summer tan, are now proving more popular with men too.

Komiyama Shoten, a small, luxury umbrella maker in Tokyo, began making parasols for men around 2019 after the environment ministry encouraged people to use them.

Before, many male customers thought parasols "were for women and they were embarrassed", the owner Hiroyuki Komiya said.

"Once you use it, you can't let go," he added.

On the busy streets of popular tourist destination Asakusa, Kiyoshi Miya, 42, said he decided to "use his umbrella as a parasol".

"It's like I'm always in the shade and the wind feels cool," he said.

Another visitor, Shoma Kawashima, wore a wearable fan around his neck to stay cool under the blazing sun.

"It's so hot I want to be naked," the 21-year-old said.

Gadgets are helpful, but "not a solution" to rising temperatures, he added.

© 2023 AFP

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The team used a simple oral rinse to see if levels of white blood cells—an indicator of gum inflammation—in the saliva of healthy adults could be linked to warning signs for cardiovascular disease. they found that high levels correlated with compromised flow-mediated dilation, an early indicator of poor arterial health.

"Even in young healthy adults, low levels of oral inflammatory load may have an impact on cardiovascular health—one of the leading causes of death in North America," said Dr. Trevor King of Mount Royal University, corresponding author of the study published in Frontiers in Oral Health.

Tooth care for heart health

Periodontitis is a common infection of the gums which has previously been linked to the development of cardiovascular disease: scientists suspect that inflammatory factors may enter the bloodstream through the gums and damage the vascular system. King and his colleagues set out to study currently healthy young people without diagnosed periodontal issues to determine whether lower levels of oral inflammation can be clinically relevant to cardiovascular health.

"We are starting to see more relationships between oral health and risk of cardiovascular disease," said Ker-Yung Hong, first author of the study, now studying dentistry at the University of Western Ontario. "If we are seeing that oral health may have an impact on the risk of developing cardiovascular disease even in young healthy individuals, this holistic approach can be implemented earlier on."

The team chose pulse-wave velocity, which can measure the stiffness of arteries, and flow-mediated dilation, a measure of how well arteries can dilate to allow for higher blood flow, as key indicators of cardiovascular risk. These measure arterial health directly: stiff and poorly functioning arteries raise patients' risk of cardiovascular disease.

The scientists recruited 28 non-smokers between 18 and 30, with no comorbidities or medications that could affect cardiovascular risk and no reported history of periodontal disease. They were asked to fast for six hours, except for drinking water, prior to visiting the lab.

At the lab, participants rinsed their mouths with water before rinsing their mouths with saline which was collected for analysis. Participants then laid down for 10 minutes for an electrocardiogram, and stayed lying down for another 10 minutes so that the scientists could take their blood pressure, flow-mediated dilation, and pulse-wave velocity.

"The mouth rinse test could be used at your annual checkup at the family doctors or the dentist," said Dr. Michael Glogauer of the University of Toronto, a co-author of the study. "It is easy to implement as an oral inflammation measuring tool in any clinic."

The heart of the matter

The scientists found that high white blood cells in saliva had a significant relationship to poor flow-mediated dilation, suggesting these people may be at elevated risk of cardiovascular disease. However, there was no relationship between white blood cells and pulse wave velocity, so longer-term impacts on the health of the arteries had not yet taken place.

The scientists hypothesized that inflammation from the mouth, leaking into the vascular system, impacts the ability of arteries to produce the nitric oxide that allows them to respond to changes in blood flow. Higher levels of white blood cells could have a greater impact on vascular dysfunction; the levels found in the participants are usually not considered clinically significant.

"Optimal oral hygiene is always recommended in addition to regular visits to the dentist, especially in light of this evidence," said King. "But this study was a pilot study. We are hoping to increase the study population and explore those results. We are also hoping to include more individuals with gingivitis and more advanced periodontitis to more deeply understand the impact of different levels of gingival inflammation on cardiovascular measures."

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Exercise scientists long ago debunked the notion that you need to hit 10,000 steps each day to stay healthy and live longer. Even a little movement is good, they argue, though more is better. Now, a new study underscores that people can reap significant benefits from a comparatively small number of daily steps.

Researchers analyzed 17 studies that looked at how many steps people took, typically in a weeklong period, and followed up on their health outcomes after around seven years. They concluded that a habit of walking just under 4,000 steps per day reduced the risk of dying from any cause, including from cardiovascular disease.

That translates into a 30- to 45-minute walk, or roughly two miles, although it varies from person to person, said Dr. Seth Shay Martin, a cardiologist at Johns Hopkins Medicine and an author of the study. But the more steps you take, the better off you are: Mortality risk decreased by 15 percent with every additional 1,000 steps participants took.

“It’s the best medicine we can recommend: Just going out for a walk,” said Dr. Randal Thomas, a preventive cardiology specialist at the Mayo Clinic who was not involved with the study.

The study could not definitively prove whether the steps themselves decreased the risk of developing diseases and dying, or if people who tend to be healthier anyway also get more steps in throughout the day. And because the researchers combined data across studies to determine that 4,000-step target, it may not confer the same benefit for every person, said Jennifer Heisz, an associate professor at McMaster University and the author of “Move the Body, Heal the Mind,” who was not involved in the study.

“I wouldn’t want people to look at that as a magical number, that you must be above that exact step count,” Dr. Martin said. “It’s more so that more is better.”

That principle is already well established in exercise research, said Dr. I-Min Lee, a professor of medicine at Harvard Medical School and an expert on step counts and health, who was also not involved with the study. But the new research emphasizes that fitness is not “all or nothing,” she said: Every little bit of exercise helps. The small snippets of movement built into our day — trailing from the bedroom to the bathroom, darting out to get coffee — add up and make a difference, she said.

But people who don’t consider themselves to be active, or who may struggle to exercise because of chronic conditions, may underestimate the value of the movement they get, Dr. Heisz said. Taking an extra loop around the block, or stepping out for a 10-minute walk break, can have a big impact.

People who are at the high end of the step counts in these studies are likely already exercising, whether they’re running or playing sports, Dr. Lee said; it is those who currently get few steps who could benefit most from moving more.

To incorporate that extra exercise, people can start by evaluating their baseline steps, either with a fitness tracker or a step counter built into a smartphone, and think about how to add just one walk into their day, Dr. Martin said. That can mean taking a meeting on the phone while walking instead of doing a video call, parking your car farther away or bringing your kids to the park and chasing them around, he suggested.

“People think, ‘Oh, well, this isn’t going to get me to those 10,000 steps, I’m not even close, so why bother?’” Dr. Heisz said. “It’s a discouraging thing. But saying and keeping this mantra that some is better than none, I think you really can get mental health and physical benefits from just short, brief movement breaks.”

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In 1967, the physicist John Wheeler was giving a lecture about a mysterious and startling phenomenon in deep space that the field was just beginning to understand. But it didn’t have a great name to match. Wheeler and his audience were equally tired of hearing “gravitationally completely collapsed object” over and over, so someone threw out an idea for a different name. A few weeks later, at another conference, Wheeler debuted the suggestion: black hole. And it’s perfect, isn’t it? What else would you call a dark abyss that swallows light and matter and doesn’t let go?

Decades later, black holes—invisible, impenetrable, and many light-years away—are more familiar to us than ever before. We know that supermassive versions sit at the center of most galaxies, including our own Milky Way. In 2019, we even got pictures that show a black hole as an imposing shadow against the glow of cosmic material. Scientists have detected the gravitational ripples that result when black holes smash into each other; the entire cosmos, we recently learned, might be humming with the force of such collisions. The list goes on.

But the big mystery still remains: We don’t know what lies at the center of a black hole, beyond the boundary where matter winks out of view forever. “The question is definitely answerable in that someone could fall inside the black hole and find out the answer,” Eliot Quataert, a theoretical astrophysicist at Princeton, told me in an email. “The problem is they couldn’t convey that answer to someone outside the black hole—because nothing can get out.”

Because such hands-on observation is impossible, scientists must approach the subject theoretically. The effort involves mind-bending physics calculations, endless thought experiments, and seriously entertaining the possibility that the universe is delightfully weirder than we can imagine. It also requires accepting that we’ll never truly know for sure what’s inside a black hole.

For us Earthlings, a bottomless pit more massive than the sun might be difficult to fathom. “Black holes are not solid objects, like planets or asteroids,” Shane Larson, a physics professor at Northwestern University, told me. They’re more like regions in space, seemingly empty spots made noticeable by the stars orbiting wildly around them. “It’s kind of like an open window,” Larson said: an invisible line that separates exterior from interior.

To understand why black holes scramble our understanding of cosmic forces, we need to think about their structure. If a black hole were a Ferrero Rocher chocolate ball, the first layer of chocolate and crushed hazelnuts would be the region just outside the event horizon, where gravity is still weak enough that a nearby star could safely whizz by and not fall in. Next up is a layer of crispy wafer; this is the event horizon, the point of no return. Under this layer lies smooth chocolate filling, through which trapped cosmic material is sucked toward the center. And then there’s the heart of the Ferrero candy, the whole, roasted hazelnut. This is the singularity, a tiny, concentrated point of infinite density.

Physicists believe they understand what the space beyond the event horizon—nearly all the way through the chocolate filling—should look like, based on Einstein’s theory of general relativity. If an astronaut were to fall into a black hole, she would descend, and as she went deeper, she would experience the very fabric of space-time warping all around her. The 1915 theory describes well what must occur in such an extreme environment, where gravity overwhelms all other forces in the universe. The trouble starts farther in, closer to the singularity, where “the laws of physics as we currently understand them break down,” Larson said.

Deep inside a black hole, general relativity isn’t enough to explain what’s happening; you also need a different kind of physics, quantum mechanics, which deals with the tiniest particles of the universe, atoms and their even-smaller components. “When collapsing all matter down to a point,” as a black hole does, “the size gets small enough that quantum effects become important,” James Miller-Jones, an astronomer at Curtin University, in Australia, told me in an email. Unfortunately, general relativity and quantum mechanics do not get along.

According to the principles of general relativity, once stuff goes into a black hole, it’s lost for good. You can determine some fundamental properties of the black hole, such as its mass, but not its constituent parts. In the 1970s, Stephen Hawking showed that black holes actually evaporate very slowly, emitting radiation from just outside the event horizon. This development should have been thrilling for quantum mechanics, which dictates that information can’t be destroyed. If someone took apart a completed puzzle and scattered it around your garden, you could collect the pieces and put them together again, Nicholas Warner, a physics and astronomy professor at the University of Southern California, told me. It would take some time and effort without a picture to guide you, but quantum theory says you could do it. But the particles wafting off black holes seem entirely devoid of information about the contents of their interior—a clear-cut violation of that principle. It’s as if someone had run all those puzzle pieces through a washing machine, and “they all become this gloopy, gray mess,” Warner said.

Theoretical physicists around the world are trying to reconcile the mismatch between general relativity and quantum mechanics. Warner is a member of the camp that believes that Einstein’s theory—the very principles that predicted the existence of black holes before astronomers found evidence of them—is incomplete. Other experts feel the same but say Einstein isn’t the only one to blame. “Maybe you have to change quantum mechanics too,” Daniel Harlow, a physicist at MIT, told me. Harlow and his colleagues have posited that the radiation that Hawking discovered is indeed encoded with information from the depths, and our understanding of quantum mechanics isn’t good enough yet to unscramble it.

Everyone is searching for a theory of quantum gravity that avoids any contradiction. “We don’t have one of those,” Charles Hailey, an astrophysicist at Columbia University, told me. “Not even close.” But some physicists I spoke with said the field could crack it within decades, certainly in this century. Scientists would finally know—but only in the theoretical sense, of course.

That’s the thing about black holes. We can get only so close to the truth, only experience certain kinds of knowing. Even the powerful telescopes that have shown us sparkling galaxies nearly all the way back to the Big Bang can’t help us here. “Observationally, we’re almost certainly not going to learn anything about the inside of black holes in this century,” Carl Rodriguez, a physics professor at the University of North Carolina at Chapel Hill, told me in an email. The best we can do is to study some effects of black holes. Maya Fishbach, an astrophysicist at the University of Toronto, thinks we’ll learn more by studying the invisible gravitational waves that fan out when two black holes collide and merge into one. Those waves carry with them information about the newly formed black hole, which vibrates in the aftermath of its creation like a bell. “Just like listening to a ringing bell can tell us what the bell is made of, listening to the black hole [ringing] can tell us what the black hole is made of,” Fishbach told me.

But the purest form of discovery will always remain out of reach. “If ‘know’ means a student could take a field trip, observe directly with their own senses, then come back and write a class report about what they observed, then we will never know what is inside,” Larson said. Perhaps that’s not the worst thing. “If it were easy to encounter situations like that”—environments with extreme, drag-you-into-the-abyss gravity—”it would probably be bad for us,” Harlow said. Safer to study black holes from afar, in our quiet cosmic neighborhood, where gravity is far weaker and we overcome it each day, simply by pulling back the covers and getting out of bed in the morning.

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Source:  National University of Singapore, Yong Loo Lin School of Medicine

Summary:  Medications to treat various chronic diseases may hinder the body's ability to lose heat and regulate its core temperature to optimal levels. The loss of effective thermoregulation has implications for elderly people receiving treatment for illnesses like cancer, cardiovascular, Parkinson's disease/dementia and diabetes, particularly during hot weather, according to a review by a team of scientists.

Medications to treat various chronic diseases may hinder the body's ability to lose heat and regulate its core temperature to optimal levels. The loss of effective thermoregulation has implications for elderly people receiving treatment for illnesses like cancer, cardiovascular, Parkinson's disease/dementia and diabetes, particularly during hot weather, according to a review by a team of scientists from various institutions in Singapore.

The group, led by Associate Professor Jason Lee from the Human Potential Translational Research Programme at the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine), identified and reviewed relevant research papers using keyword searches on databases such as PubMed and Google Scholar. These papers studied the associations and effects of medications on thermoregulation. The review findings were presented in a topical manner, focusing on medication classes used to treat commonly diagnosed chronic conditions (e.g., diabetes, cardiovascular disease, neurodegenerative disease, and cancer). The findings were published in Pharmacological Reviews, titled Effects of Medications on Heat Loss Capacity in Chronic Disease Patients:

Health Implications Amidst Global Warming

The findings show that medications used to treat common chronic conditions, like blood thinners, blood pressure drugs, Parkinson's disease/Alzheimer's medications, and some chemotherapy drugs, can make it harder for the human body to handle hot weather by reducing its ability to sweat or increase blood flow to the skin.

Lead author and second-year PhD candidate from the Human Potential Translational Research Programme Mr Jericho Wee said, "Rising global temperatures caused by climate change pose a significant health concern for clinical patients reliant on long-term medications and healthcare. Increasingly, we will continue to see more elderly patients, many who have multiple health conditions and are taking different types of medication concurrently to manage their chronic diseases, compounding the risk of heat-related illness and dehydration. Understanding how each medication impacts thermoregulation, in the face of warmer environments, is the crucial first step to predicting the possible health outcomes when multiple medications are taken concurrently." While previous reviews have highlighted the impacts of medications on heat, the scope of those reviews did not present the evidence in the context of the chronic diseases and ageing. The team's narrative review presents the evidence in the context of high ambient temperatures and their impact on chronic disease sufferers who are on long-term and life-long medication.

Senior author Assoc Prof Jason Lee said, "This review emphasises the importance of studying the mechanisms of altered thermoregulation in individuals with diabetes and other cardiometabolic conditions to prevent heat-induced conditions. This is most relevant in Singapore and many other countries, where we have rapidly ageing populations and rising ambient temperatures. Pharmacological and thermal physiologists should focus transdisciplinary efforts on this area of research to refine and enhance safe medication prescription guidelines to preserve the health of people who need these medications, even in hot weather."

Assoc Prof Melvin Leow, the review's co-author and Senior Consultant Endocrinologist at Tan Tock Seng Hospital said, "Physicians are often unaware of the potential harms certain drugs may cause by compromising the body's thermoregulatory control mechanisms. This is an especially important area to delve into as those with chronic diseases and older adults are susceptible to adverse health outcomes in the heat, due to their reduced thermoregulatory capacity. It is timely and prudent that scientists and doctors collaborate even closer in this important field that cuts across a wide range of medical disciplines."

The study was supported by the National Research Foundation, Prime Minister's Office, Singapore under its Campus for Research Excellence and Technological Enterprise (CREATE) Programme.

The findings, in brief:

Cancer

Patients on certain cancer medications have reported symptoms of hot flushes, such as inappropriate sweat responses and an increase in core temperature which affects quality of life. Exercise and improved fitness levels have been shown to reduce the frequency of hot flushes and improve thermoregulatory responses in other chronic conditions such as diabetes, and it remains a crucial component in maintaining the nervous and cardiovascular functions of cancer patients. However, bodily impairments and limitations caused by chemotherapy and medications may limit their ability to exercise, which perpetuates a cycle of loss in exercise capacity that is crucial to their recovery.

Cardiovascular disease

Patients who have cardiovascular diseases, such as coronary heart disease, stroke and heart failure, are more vulnerable to high heat exposure because their hearts will be working harder to deliver blood to the skin and working muscles to maintain core temperature at an optimal level whilst maintaining work output. Anti-platelet medications, such as aspirin and clopidogrel, are usually taken to prevent blood clots from forming in the blood vessels, that could lead to stroke or heart disease. Yet, these anti-platelet medications may increase core temperature, whether at rest or during exercise. These medications also reduce skin blood flow and suppress sweat responses, which means thermoregulatory responses would be less sensitive to accumulated heat, and delay in cooling itself down, which could lead to heat stroke.

Used for multiple cardiovascular conditions, such as ischemic heart disease, high blood pressure, and heart failure, beta-blockers can reduce skin blood flow during heat stress by reducing blood pressure and facilitating additional constriction of skin blood vessels. However, the findings of the effects of beta-blockers on sweat responses remain mixed, with some studies showing no changes in sweating, while others demonstrate reduced sweating. As such, greater research efforts are needed to understand how different types of beta-blockers may impact sweating.

Some studies have highlighted that the type of beta-blocker is an additional consideration. For example, non-selective beta-blockers like propranolol, widely prescribed at the population level, can result in greater impairments in thermoregulation than selective-beta-blockers that only target cardiac or peripheral tissues. Hence, non-selective beta-blockers could predispose patients to greater heat strain and heat-related illness.

Diabetes

Insulin, which is typically used to reduce high blood sugar, or hyperglycaemia, in patients with Type 1 diabetes, has been shown to impair the ability of the body to regulate heat properly. It also increases metabolic heat production at rest and during exercise, which can be fatal to the body when the accumulated heat cannot be dissipated quickly. For patients with Type 2 diabetes who consumed metformin to manage their condition, nearly 30% of patients experience diarrhoea and nausea when they are first prescribed the medication. If the fluid loss cannot be sufficiently replaced, patients, especially the elderly, are at a higher risk of dehydration, which may result in greater cardiovascular strain during exertional heat stress.

Neurocognitive diseases

Due to an internal imbalance in dopamine and acetylcholine levels, patients with neuropsychiatric diseases such as Parkinson's and Alzheimer's disease experience thermoregulatory dysfunction when their body is unable to control its temperature. However, the medications to manage these neurological conditions have been known to alter the brain's control of thermoregulation and thermoregulatory responses, such as sweating and cutaneous vasodilation, which could result in both hyperthermia and hypothermia. Anticholinergics and cholinesterase inhibitors are prescribed to improve motor and cognitive symptoms in the brain for Parkinson's Disease patients. However, these agents also alter the dopamine and acetylcholine levels, likely inducing changes in the central thermoregulatory drive that affects the central processing and integration of thermal information and numbs the instinctive responses to heat stress, while driving up the body's core temperature. This could lead to an increased risk of developing heat-related illnesses.

Dopamine replacement agents and dopamine agonists are usually prescribed to those with Parkinson's disease to increase dopamine levels to help in movement and coordination. While highly effective, these agents have been observed to significantly influence thermoregulation and impair sweat responses which are crucial for heat dissipation. It is important that the dosage of these agents is appropriately adjusted to minimise the onset of severe after-effects.

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The creative spark can flare up in anyone at any time. For the cognitive neuroscientist Evangelia Chrysikou, who grew up in Greece, creativity is almost a fundamental human instinct. We wouldn’t be where we are today as a species, spread across the globe, she says, if we couldn’t imagine what’s possible—and make it happen. For her, all creative acts fall along a spectrum of recombining what you know into something that didn’t previously exist. She offers a simple example of what you might do if you’re sitting on a chair in a room and someone attacks you. 

“You will very quickly rearrange your thinking about what the chair is, and use it as a shield, or use other items around you as a weapon,” she says.

“What I have found fascinating is, clearly we can all do it, but what are these processes? There’s something in our brain that lets us take something that, everyday, you use as a pen, and immediately reorganize it into something that has other kinds of characteristics that can serve a different purpose,” like a tiny spear. In her lab at Drexel University, she probes brain activity with fMRI machines and transcranial electrical stimulation to understand what underpins our ability to think flexibly and solve problems.

Creative acts rely on access to particular knowledge.

In a new study, she assembled a group of 20 “eminent” creators, people with “exceptionally high creativity,” and matched them with a control group—people of the same age and educational and professional background—with lesser powers of creativity. (The researchers assessed subjects’ creativity based on responses to a “creative achievement questionnaire.”) She and her colleagues from Johns Hopkins University, Columbia University, and elsewhere, wanted to find out what in the brain might explain some of the differences in creative achievement between these groups. Among other things, the researchers monitored the blood-oxygenation levels of the participants’ brains while in a resting state—while they weren’t performing any task—to compare how different the functional connections are between certain areas of the brain for each group.

Nautilus caught up with Chrysikou recently to discuss her findings.

Are there any notable differences in the brains of “eminent” creative people compared to those who are merely successful and smart?

Yes. So in this recent study, we wanted to find out whether there’s something about how the different parts of the brain talk to each other under rest, where there is no particular task to be achieved. Is there something about the connectedness of the different regions of the brain within the eminent group that differs from the non-eminent group, and how are these related to the creative success of the participants? 

The key finding was that, for the eminent creators, there was a higher connectivity, both within each hemisphere, the right and left, but particularly across them—and especially in the two key networks that many studies have identified as important for creative thinking, the default mode network and the executive control network. Past research has shown that, during most of our day-to-day activities, these two networks are antagonistic. In creative tasks, they seem to be talking a little bit more with each other. In this particular study, our results mirror this finding. For the eminent creators, there was much more dialogue between these two networks relative to the non-eminent creators. 

What about when you had the participants engage in a creativity task—were there differences there?

When the participants were completing the alternative uses task—the traditional measure for creativity, where you show people an object and you ask them in a few seconds to verbally generate an alternative use for it—the brains of eminent creators were more efficient, meaning the recruitment of brain regions was much more focused compared to the non-eminent creators, whose recruitment of brain regions was more variable, widespread, and less organized. In other words, the brain areas that support creative functions were activated and engaged in eminent creators more often and more strongly and with more specificity. This was true across the eminent creator group, whether they were famous artists, writers, or lawyers, which I think is a really cool finding.

How might you explain your findings in terms of what’s happening psychologically?

Given what we know about the default mode network, which activates strongly when we remember the past and imagine the future, and the executive control network, which activates when we carry out our plans, our finding suggests that creative acts rely on access to particular knowledge. You have memories about the world around you, about how things work, how things operate. These memories are retrieved in certain ways, depending on the context of a particular goal you have to achieve.

So the brains of highly creative people engage in this dialogue or filtering of the memory search process based on the context, the tasks that they have to accomplish, especially when they are creating something new. That memory search also helps you reinterpret the particular object. We need to do much more experimental work to be able to say, “Here is this particular kind of memory that was reorganized.” The level of resolution of the results we have is a little bit fuzzier than that. But it’s still a very interesting first step toward addressing that question of how you borrow from memory to create things that don’t exist. 

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People who adhered to the lifestyle's emphasis on rest, exercise, and socializing with friends had a lower risk of cardiovascular disease mortality.

The study is published in Mayo Clinic Proceedings.

While many studies have established the health benefits of a Mediterranean diet and lifestyle, little research has been conducted on the diet outside of its region of origin.

"This study suggests that it's possible for non-Mediterranean populations to adopt the Mediterranean diet using locally available products and to adopt the overall Mediterranean lifestyle within their own cultural contexts," said lead author Mercedes Sotos Prieto, Ramon y Cajal research fellow at La Universidad Autónoma de Madrid and adjunct assistant professor of environmental health at Harvard Chan School. "We're seeing the transferability of the lifestyle and its positive effects on health."

The researchers analyzed the habits of 110,799 members of the UK Biobank cohort, a population-based study across England, Wales, and Scotland using the Mediterranean Lifestyle (MEDLIFE) index, which is derived from a lifestyle questionnaire and diet assessments.

Participants, who were between the ages of 40 and 75, provided information about their lifestyle according to the three categories the index measures: "Mediterranean food consumption" (intake of foods part of the Mediterranean diet such as fruits and whole grains); "Mediterranean dietary habits" (adherence to habits and practices around meals, including limiting salt and drinking healthy beverages); and "physical activity, rest, and social habits and conviviality" (adherence to lifestyle habits including taking regular naps, exercising, and spending time with friends).

Each item within the three categories was then scored, with higher total scores indicating higher adherence to the Mediterranean lifestyle.

The researchers followed up nine years later to examine participants' health outcomes. Among the study population, 4,247 died from all causes; 2,401 from cancer; and 731 from cardiovascular disease.

Analyzing these results alongside MEDLIFE scores, the researchers observed an inverse association between adherence to the Mediterranean lifestyle and risk of mortality. Participants with higher MEDLIFE scores were found to have a 29% lower risk of all-cause mortality and a 28% lower risk of cancer mortality compared to those with lower MEDLIFE scores.

Adherence to each MEDLIFE category independently was associated with lower all-cause and cancer mortality risk. The "physical activity, rest, and social habits and conviviality" category was most strongly associated with these lowered risks, and additionally was associated with a lower risk of cardiovascular disease mortality.

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• Oceans absorb more than 90% of the excess heat caused by climate change.

• Oceans are hitting record high temperatures. The global average sea surface temperature hit an all-time record high of 69.73 degrees Fahrenheit on July 31, according to a data set maintained by Copernicus, the the Earth observation component of the European Union’s Space program, which goes back as far as 1979.

• Record ocean temperatures cause stronger storms, displace and kill fish populations, stress coral reef populations, turbocharge the growth of harmful algal blooms and in the long-term, cause sea level rise.

The oceans of the world absorb the overwhelming majority of the heat caused by global warming, creating serious consequences for life in and around them, including humans.

“The oceans do a lot of the work in reducing the level of warming,” Baylor Fox-Kemper, professor of earth, environmental, and planetary sciences at Brown University, told CNBC. “Over 90 percent of the excess energy on earth due to climate change is found in warmer oceans, some of it in surface oceans and some at depth.”

The oceans cover 70% of the earth’s surface, and water can absorb tremendous amounts of energy.

“Water has a huge heat capacity, which means that it takes a lot of energy to change the temperature of water,” Carlos E. Del Castillo, head of NASA’s Ocean Ecology Laboratory, told CNBC. “Do the mental experiment. Put two pots on a stove. One with water, one without. Both on high. Wait one minute. If you touch the water, you will barely feel a difference in temperature. If you touch the metal of the empty pot you will burn. This is because the heat capacity of water is way higher that that of a metal.” Castillo admitted the science is a bit more complicated that this mental thought exercise, but it helps visualize the idea of heat capacity.

That shows “why a small change in temperature in the ocean” means the oceans have been absorbing massive quantities of heat, Castillo said.

Record temperatures of 101 degrees in the ocean off the coast of Florida is one more example of the increasingly obvious effects of climate change. NASA on Monday said July was the warmest month in its record books dating back to 1880.

“The warmer ocean that we are seeing now represents a ratcheting up of the climate change signal,” Benjamin Kirtman, professor of atmospheric sciences at the University of Miami, told CNBC. “This is consistent with a continued increase in extreme weather in the climate system, that is more heat waves and marine heat waves, droughts in already dry regions, floods in already wet areas, extreme winds, and fire.”

The more greenhouse gasses we emit, the hotter the oceans will get.

“Greenhouse gas warm the entire climate system including the ocean. Put simply, the greenhouse gases serve to trap more heat, some of which is absorbed by the ocean,” Kirtman told CNBC. “So, as greenhouse gas concentrations increase, we expect the ocean to absorb more heat and warm.”

By the numbers: Record highs and big-picture trends

Daily global sea surface temperature in degrees Celsius for the ocean waters between latitude 60 degrees to the South and 60 degrees to the North, with a line for each year starting in January 1979 to July 2023. The years 2023 and 2016 are shown with thick lines. The other years are color coded by decade, with the 1970s in blue and the 2020s in brick red. The chart was made by and is shared with the courtesy of Copernicus, the the Earth observation component of the European Union’s Space program.
Copernicus

The global average sea surface temperature hit an all-time record high of 69.73 degrees Fahrenheit on July 31, according to a data set maintained by Copernicus, the the Earth observation component of the European Union’s Space program, which goes back as far as 1979. This particular data set measures temperatures at about 33 feet below the surface of the ocean.

“Global” in this data set is defined as the oceans beyond the polar region, between 60 degrees latitude south and north. Measuring sea surface temperatures in this extrapolar region is considered standard for climate monitoring, but the sea surface temperature among all ice-free oceans also reached a record-high level in July, Copernicus said.

The previous record was set in March 2016 — March is the time of year when oceans in the southern hemisphere get warmest, and because the southern hemisphere has more ocean it tends to be the hottest peak of the year, Gavin Schmidt, director of the NASA Goddard Institute for Space Studies, told CNBC.

In addition to the daily record on July 31, the monthly sea surface temperature for July was the hottest July on record, “by far,” Copernicus said. The anomaly for July, which is a measurement of the difference between what the sea surface temperature was and a long-term average for that month, was 0.92 degrees Fahrenheit, according to Copernicus.

Sea surface temperature anomalies displayed in degrees Celsius, compared to a 1991-2020 reference period, averaged over the extrapolar global ocean for the month of July from 1979 to 2023. The chart was made by and is shared with the courtesy of Copernicus, the the Earth observation component of the European Union’s Space program.
Copernicus

These record sea surface temperatures arise from multiple factors, including the El Niño weather pattern, which is currently in effect. “The particularly warm waters this year have to do with climate variations like El Niño in the Pacific and a similar pattern in the Atlantic on top of the steady ocean warming of climate change,” Fox-Kemper told CNBC.

“These climate variations occur when sea surface temperature patterns of warming and cooling self-reinforce by changing patterns of winds and precipitation that deepen the sea surface temperature changes.”

But global warming is also contributing. “It would be nearly impossible to reach these ocean temperatures without the added boost of greenhouse gasses from fossil fuel burning and other human activities,” Fox-Kemper told CNBC.

Human-caused greenhouse gas emissions are adding the equivalent of a permanent El Niño worth of heat to the climate every five to ten years, Zeke Hausfather, energy systems analyst and data scientist with a strong interest in climate science and policy and a research scientist at Berkeley Earth, told CNBC.

The recent bout of record-breaking sea surface temperatures are part of a long-term trend. “The last 10 years have been the warmest since at least the 1880s for sea surface temperature,” Castillo told CNBC.

Currently, 44 percent of the global ocean is experiencing what’s called a “marine heatwave,” according to Sarah Kapnick, chief scientist at the National Oceanic Atmospheric Administration. That’s the highest percentage of the global ocean experiencing a marine heatwave since 1991, Kapnick told CNBC via a spokesperson. A marine heatwave is defined as when the ocean temperatures are higher than 90% of the previous observations for that region at that time of year, according to NOAA.

So why does it matter that the oceans are getting hotter?

Warmer oceans make stronger storms

“The most powerful storms on earth — hurricanes and tropical and extratropical cyclones — extract much of their energy from warm, moist air near the ocean surface. Hotter seawater means warmer and moister air, which then has more energy to release leading to stronger storms,” Fox-Kemper told CNBC.

This explains why the most prevalent paths for strong storms follow warm ocean currents like the Gulf Stream and Kuroshio in the Northern Hemisphere, Fox-Kempler said.

In September, the streets of downtown Fort Myers were flooded from Hurricane Ian. This sort of damage can disrupt medical and food supply chains that can raise health risks for diabetics as well as others with chronic diseases. Itâs one of the surprising impacts from climate change that Florida and other coastal states face.
Miami Herald | Tribune News Service | Getty Images

Evaporation of water vapor from the ocean surface, which makes the moist air that drives the stronger storms, is a factor of ocean temperatures and wind speed, and the impact of ocean temperature on that equation is “highly non-linear,” Kirtman told CNBC, meaning that small changes in temperature lead to large increases in evaporation. When water vapor condenses, it releases heat into the atmosphere, which starts a positive feedback loop. “So, if the atmosphere is more moist, there is more condensational heating which intensifies the storm,” he said.

The impact of the warming sea waters on hurricane development varies depending on what region of the ocean sees the highest increase in temperature, Michael Lowry, a hurricane specialist and storm surge expert, told CNBC. The ocean temperatures in the main development region for hurricanes, like the deep tropical Atlantic south of the 20 degrees latitude, are especially critical.

“This is what seasonal hurricane outlooks like those issued by NOAA last week are keying in on,” Lowry told CNBC, referring to a hurricane forecast outlook where NOAA said the warming oceans would boost hurricane activity for the remainder of the season.

But wherever a hurricane forms, the hot oceans will strengthen it. “The extreme sea surface temperature is like dry powder when storms get going. As we say in this business, it only takes one,” Lowry said.

Fish populations will migrate or die

Fish populations depend on specific temperatures.

“All species have a preferred and a lethal temperature range. Once the upper border of the preferred temperature range is reached, they go deeper or pole-ward to cooler waters, if they can,” Rainer Froese, senior scientist at the Helmholtz Centre for Ocean Research in Germany told CNBC. “Already at the upper tolerance range, growth and reproduction are hampered. At the upper lethal range, they die.”

Fish will migrate towards colder waters, if they can. Fish that lived in Florida will be found in New York waters, and fish that lived in New York waters will migrate to Nova Scotia, according to Daniel Pauly, professor at the University of British Columbia’s Institute for the Oceans and Fisheries. “Individuals are found, especially in the summertime, to reach areas that they never reach before,” Pauly told CNBC.

Fisherman Vigfus Asbjornsson (L) sorts his catch of cod and pollack on August 16, 2021 in Hofn, Hornafjordur, Iceland. Global warming is contributing to a rise in temperatures in the waters around Iceland, which is effecting the fishing industry. Changing temperatures have a strong influence on where species of fish find habitat, leading to shifts in the fishing catch. One local fisherman also said the spawning grounds of the fish he catches are moving farther north year by year. Iceland is undergoing a strong impact from climates change, including accelerated melting of the island’s many glaciers but also new opportunities for agriculture.
Sean Gallup | Getty Images News | Getty Images

Warmer sea water is dangerous for fish for two reasons: “Warmer water contains less oxygen than cold water, but the metabolic oxygen demand of fish is higher in warm water,” Lorenz Hauser, professor at the School of Aquatic and Fishery Sciences in Seattle, told CNBC.

“Fish metabolism depends very much on water temperature, and with warmer water, fish need more food to maintain their bodies and grow,” Hauser told CNBC. “On the other hand, ecosystems change with warmer water, and there may not be sufficient prey around. This was the case with the recent stock collapse of Pacific cod in Alaska.”

While fish may have a chance to migrate if sea water changes are gradual, in a sudden ocean temperature increase like a heatwave, the fish will die, Pauly told CNBC. This is particularly true for larger fish because the surface of the gills on a fish do not grow as fast as the total weight. The bigger fish have less gill area per unit of weight in the same species, Pauly said.

“In the future, we will see massive changes in regional species composition, and lots of die-offs where species cannot escape fast enough, or where they fall prey to predators or are out-competed by species that they have not encountered before,” Froese told CNBC.

Coral reefs are dying

Coral reef populations are getting ravaged by the hot ocean temperatures. The Coral Restoration Foundation, a nonprofit coral reef restoration organization headquartered in Florida, has been taking corals out of the ocean and putting them in land-based holding tanks.

“On July 20th, Coral Restoration Foundation teams visited Sombrero Reef, a restoration site we’ve been working at for over a decade. What we found was unimaginable — 100% coral mortality,” Phanor Montoya-Maya, Restoration Program Manager at Coral Restoration Foundation, said in written statement in July. “We have also lost almost all the corals in the Looe Key Nursery in the Lower Keys.”

Javier Solar, a member of the Coral Restoration Foundation, brings up threatened coral transplants from the Florida Keys waters for safe keeping on land until the waters cool off. The threat of coral bleaching is extreme as the water temperatures hit over 90 degrees. Members of Coral Restoration Foundation work to save coral species that are threatened by extremely warm waters due to global warming in the Florida Keys. Coral that had been out planted is being removed from the ocean for safe keeping until the water cools down.
Carolyn Cole | Los Angeles Times | Getty Images

Coral reefs thrive in ocean temperatures between 73 and 84 degrees Fahrenheit, but they can survive in both higher and lower temperatures for short periods of time, Castillo told CNBC. But the hot ocean temperatures in Florida have caused “wide-spread coral bleaching,” Castillo said. Coral bleaching happens when the over stressed corals expel zooxanthellae, an algae that they need to survive.

“Although coral can survive bleaching and re-grow their zooxanthellae, these bleaching events debilitate the coral. In the case of the recent heat wave, outright coral die off were reported,” Castillo told CNBC.

Coral reefs are critical to the marine ecosystems. About a quarter of marine species depend on the coral reefs in some capacity, Castillo said.

More dangerous algae blooms

“Microorganisms like it hot,” Hans W. Paerl, professor of marine and environmental sciences at the University of North Carolina at Chapel Hill’s Institute of Marine Sciences, told CNBC. “The higher the temperature and the faster they grow, and so this really has been a boon to them.”

The organisms that can grow really quickly in hot ocean temperatures and cause harmful algae blooms include dinoflagellates and diatoms, which are also called sometimes called microalgae or red tide, and cyanobacteria, which is sometimes called blue-green algae.

In an aerial view, brownish water is visible in the waters at the Berkeley Marina as an algal bloom grows in the San Francisco Bay on August 01, 2023 in Berkeley, California. The San Francisco Regional Water Quality Control Board has warned that a toxic algae bloom in the San Francisco Bay, similar to one that occurred one year ago and killed tens of thousands of fish, has returned to the Bay.
Justin Sullivan | Getty Images News | Getty Images

Both people and animals can get sick by being exposed to these algal blooms or eating seafood contaminated with them. The severity of the sickness depends on type of algae and how long exposure lasted, according to the Centers for Disease Control and Prevention.

Algal blooms can become more intense when nitrogen and phosphorus in fertilizer runoff gets to oceans, and climate change is impacting the pace and cadence of fertilizer runoff because of the increasing severity of both rain storms and dry spells.

“When you have a major storm, it’s going to pick up more nutrients from the land and flush them into our coastal and ocean systems,” Paerl told CNBC. “If a wet period is followed by an extensive drought, then you actually enhance the growth for some of these organisms, because they like stagnant, dry conditions, as well.”

The combination of hotter waters and more fertilizer runoff will drive the algae and bacteria growth and respiration, which creates low oxygen zones that impacts fish populations and can in some instances cause “dead zones,” Paerl told CNBC. “That, of course, has huge implications for the food web, and ultimately for us, in terms of consumers of fish and shellfish.”

As the oceans warm, the blooms themselves are migrating to cooler waters where they’d never been seen before, says Christopher Gobler, professor at Stony Brooke University’s School of Marine and Atmospheric Sciences who researches Coastal ecosystem ecology, climate change, harmful algal blooms.

“Harmful algal blooms that may have never had a chance to form in the past have become dense and widespread in regions such as Alaska and northern Europe,” Gobler told CNBC. “This is highly problematic as these new occurrences can take ecosystems and communities by surprise, exposing marine life and, in some cases humans, to toxins that were regionally unknown, causing mass mortalities and/or illnesses.”

Long-term: Sea level rise

“Water expands as it gets warmer,” Gary Griggs, professor of earth and planetary sciences at the University of California in Santa Cruz, told CNBC.

Kimberly McKenna, Associate Director at Stockton University Coastal Research Center points at a graph indicating rising sea levels in Atlantic City, New Jersey on October 26, 2022. Ten years after the devastating hurricane Sandy, the seaside town of Atlantic City, on the American east coast, has fortified its famous promenade between its casinos and the Atlantic Ocean. But behind the beaches, for the inhabitants of certain neighborhoods, the flooded streets are almost part of everyday life.
Angela Weiss | Afp | Getty Images

So broadly speaking, warmer oceans will lead to sea level rise and coastal flooding risk. “As the ocean warms it expands, much like a gas, and takes up more space, hence sea level rise. Warmer oceans in the higher latitudes means less sea ice which allows the oceans to warm further,” Kirtman told CNBC. “This is known as a positive feedback.”

Generally, about two-thirds of global sea level rise is caused by ice melt from Antarctica, Greenland and continental glaciers and the other one-third from “overall temperature increase,” Griggs said. But also, the recent trend in record-high sea surface temperatures aren’t enough on their own to cause any noticeable changes in sea level, Griggs noted.

“Any large-scale increase in ocean water temperature increases sea level and the amount can be determined if you know the total volume of water affected and the amount of temperature increase by using the coefficient of thermal expansion,” Griggs told CNBC. But there are approximately 330 million cubic miles of sea water, and it takes “a lot of heat to substantially increase sea level rise.”

Economic impacts and looking ahead

Right now, it’s really too soon to measure the economic impact of these record sea surface temperatures, Judith Kildow, founder and director emeritus of the National Ocean Economics Program, told CNBC. Years of more data are needed. In some cases, people who depend on the oceans for their livelihood are adapting, Kildow said. “Fishermen are turning their boats into whale watching enterprises when they no longer can fish profitably,” Kildow told CNBC.

But there will be cascading economic impacts. “Bleached coral reefs, rising sea levels from warming, and migration of fisheries north to their normal temperatures will have an effect on the fishing industry and coastal tourism as well as the value of coastal real estate,” Kildow told CNBC. AStronger storms, driven by warming ocean waters, will cause more devastating and expensive damage if they make landfall. “Value of costal real estate will drop precipitously in a short period of time,” Kildow said.

If it sounds like a lot of bleak news, it is. Asked if there were any benefits to the warming oceans, Schmidt from NASA responded: “Slightly extended beach swimming period?”

The best way to ameliorate the whole cornucopia of negative impacts is to reduce greenhouse gas emissions.

“Of course, the key to all of this is less fossil fuel combustion,” Paerl told CNBC. It’s also important to reduce the release of other greenhouse gas like methane and nitrogen oxides, he said. “So that’s one thing we should all be doing is consuming and burning less fossil fuels.”

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Most cancers in the United States are found in people age 65 and older, but a new study shows a concerning trend: Cancer among younger Americans, particularly women, is on the rise, with gastrointestinal, endocrine and breast cancers climbing at the fastest rates.

A study published Wednesday in JAMA Network Open showed that while cancers among older adults have declined, cancers among people younger than 50 have increased slightly overall, with the largest increases among those age 30 to 39.

“This is a population that has had less focus in cancer research and their numbers are getting bigger, so it’s important to do more research to understand why this is happening,” said Paul Oberstein, director of the Gastrointestinal Medical Oncology Program at NYU Langone’s Perlmutter Cancer Center, who was not involved in the study.

If some younger people have an increased risk of cancer, as they age, the concern is that their cancer risk may propagate, Oberstein said. “If we don’t understand what’s causing this risk and we can’t do something to change it, we’re afraid that as time goes on, it’s going to become a bigger and bigger challenge.”

There is not a clear explanation why cancer is rising among younger people, but experts say there are several possible reasons behind the trend, including rising obesity rates and lifestyle factors such as drinking alcohol, smoking, sleeping poorly and being sedentary. Environmental factors, including exposure to pollutants and carcinogenic chemicals, also probably play a role.

The researchers analyzed data from more than 560,000 patients in the United States diagnosed between 2010 and 2019 with early-onset cancer — defined as cancers that affected people younger than 50.

They found that, overall, early-onset cancer diagnoses rose by nearly 1 percent during the study period to 56,468 patients, up from 56,051 patients in 2010. The trend was most pronounced in the 30-to-39 age group, with cases increasing about 19 percent.

Cancer has increased among younger Americans

Researchers analyzed data from more than 560,000 U.S. patients diagnosed between 2010 and 2019

Early-onset breast and other cancers

There were significant increases in certain types of cancer. Breast cancer, for instance, accounted for the highest number of cancer cases in younger people, and increased about 8 percent over the 10-year period, said Daniel Huang, assistant professor at the National University of Singapore and a transplant hepatologist at the National University Hospital, who is the senior author of the study.

Gastrointestinal cancers, including of the colon, appendix and bile duct, increased about 15 percent during that time — making it the fastest-growing type of cancer among younger people, he said.

The differences between men and women were striking. The number of early-onset cancers in women increased by 4.4 percent during the study period; among men the number declined by nearly 5 percent. The increases seen among younger women were probably driven by the rise in cancers of the breast and uterus.

Although the total numbers were small, the biggest increases in cancer among younger people by race were seen in Asian or Pacific Islander (32 percent) and Hispanic patients (28 percent). Cases among younger Black patients slightly declined, falling by about 5 percent. It’s not clear if the decline is meaningful or if cases are underdiagnosed.

Overall, younger people diagnosed with cancer still represent a relatively small portion of overall cancer cases, but the increases are nonetheless concerning.

“It’s an important trend, especially important if it continues, but it is a small part of what’s going on in oncology,” said Otis Brawley, an oncologist at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins.

The study did not examine cancer stages, so it’s unclear from the data whether the early-onset cancers developed earlier or were simply being diagnosed earlier in the course of the disease, experts explained.

Identifying risk factors for young cancer

Most cancer risk factors are based on studies of predominantly older adults, but studies are being designed to help understand how certain exposures in earlier life may affect cancer risk in later life, said Hyuna Sung, senior principal scientist and cancer epidemiologist at the American Cancer Society.

Studies such as the one in JAMA, she said, “motivate new studies to help identify risk factors that may be able to explain these trends.”

Other research has shown a trend toward younger diagnosis in colorectal cancer. One in five new cases of colorectal cancer in the United States occur in people younger than 55 — a rate that has about doubled over the past three decades, according to a concerning recent report from the American Cancer Society.

In 2018, the American Cancer Society updated its colorectal cancer screening guidelines, lowering the age to start screening for those at average risk from age 50 to 45.

Experts say trends such as those seen in the new study should be closely monitored as they may influence other screening recommendations, including those for breast cancer.

“As we continue to do better at identifying people who are at higher risk at younger ages, we really need to adjust our screening practices as well,” said Jennifer Litton, a breast medical oncologist at the University of Texas MD Anderson Cancer Center.

An estimated 1.9 million new cancer cases are diagnosed each year in the United States. In some cases, there are no screening tests for certain cancers, and when there are, the tests are often not recommended for young people who are at average risk.

One of the most important things people can do to minimize their risk, Brawley said, is to manage body weight, exercise, limit alcohol consumption and avoid smoking.

Source

Artist's conception of the newly found species.

Matheus Fernandes

 

It was relatively small in comparison to the giants that would follow it later in Earth’s history. With a hip height of approximately 0.3 meters (about a foot) and a length of perhaps a meter (roughly three feet), this ancient reptile existed long before the evolution of the pterosaurs most of us recognize.

 

Its most striking features are its skull and hands, two body parts that rarely survive fossilization among similar animals this old. The skull consists of a raptorial-like beak without teeth, while its forelimbs end in long fingers with scimitar-like claws. These two surprising features are among many revelations in a paper published Wednesday in Nature.

 

Venetoraptor gassenae is the name of this new species of lagerpetid, a type of pterosaur precursor that lived about 230 million years ago in Brazil. Named for the district of Vale Vêneto in the same municipality in which the fossil was found—and for the plundering it might have done with its beak and claws ("raptor" is Latin for "plunderer")—it is also named to honor Valserina Maria Bulegon Gassen. Although not a paleontologist herself, the authors note that she is “one of the main people responsible for the CAPPA/UFSM” (the Centro de Apoio à Pesquisa Paleontológica da Quarta Colônia, Universidade Federal de Santa Maria), a paleontological research support center).

 

This discovery augments an ever-growing number of dinosaur and pterosaur predecessor fossils coming out of South America. These rare finds, even with their fragmentary skulls and hands, unveil more about evolution and life during the early Triassic. But the partially articulated, well-preserved Venetoraptor is unique among such fossils; unearthing it was, according to lead author and discoverer Rodrigo Temp Müller, “one of the most exciting points of my career.”

Inspiring fear

Müller is a paleontologist at CAPPA/UFSM. He describes lagerpetids as “lightly-built animals that lived side-by-side with the first dinosaurs.” Although a fraction of the size of theropods like T.rex would evolve about 150 million years later, “their beak and claws surely [inspired] some fear to small animals” that co-existed with them.

 

It is exactly those two features that set Venetoraptor apart from other dinosaur and pterosaur precursors, as they provide evidence that these predecessors were a lot more morphologically diverse than previously understood. The beak appears to be without teeth, although they may not have been preserved. The team suggests it could have used it to eat hard fruit or tear flesh from prey. In extant birds, beaks also help with vocalization, thermoregulation, and sexual display.

 

Venetoraptor’s long hands may have helped it grab prey or even climb trees. And they indicate that the creatures walked bipedally. Not having to walk on all fours is, as interpreted by the team in the paper, “one of the main forces that drove the evolution of forelimb diversity within Ornithodira during the Late Triassic.”

 

Until 2020, it was thought that lagerpetids were closely related to dinosaurs. Evidence developed since suggests they are more closely related to pterosaurs, even if they couldn’t fly. This paper adds further evidence to support this thinking.

 

Müller noted that “at some point in evolutionary history, a common ancestor between lagerpetids and pterosaurs evolved advantages that led one of these lineages to dominate the skies.”

Crunching numbers on evolution

Co-author Martín Ezcurra is a paleontologist at the Sección Paleontología de Vertebrados, CONICET−Museo Argentino de Ciencias Naturales “Bernardino Rivadavia” in Argentina. He was also the lead author on the 2020 paper providing evidence that lagerpetids are more closely related to pterosaurs. Since 2012, he’s been steadily working on a fossil data set, one he hopes to finish in 15 years.

 

“The idea,” he told Ars, “is to have a complete data set for all these reptiles that lived between 265 million years ago to 175 million years ago, which is a very important moment [in] reptile evolution.”

 

When the initial version of this data set was published in 2016, the year after he earned his PhD, there were 81 fossils represented. In the years since, that number has almost tripled. The team used this data set to perform a number of analyses to determine where Venetoraptor fit in the evolutionary tree and how it compared to other dinosaur/pterosaur precursors.

 

Ezcurra explained that numbers are assigned to every significant aspect of each bone, such as its shape and overall morphology. “With those numbers,” he said, “we build a matrix,” essentially encoding the anatomical structure of each animal. Having these numbers makes it easier to compare new finds to known species. Currently, there are 240 species in the data set, with 900 characteristics represented by numbers.

 

“So it’s a huge data set,” he continued. “It’s more than 200,000 different observations all transformed into numbers.” And with this, the researchers could build an evolutionary tree. Even on a powerful cluster and using parallelized code, the analysis still takes hours to days.

 

Beyond building evolutionary trees, the data set also allowed researchers to track the origin and migration of species and their descendants. Ezcurra said that three pieces of information were necessary to do this: knowing where each species fits on the evolutionary tree, the geographic location of the species as indicated by fossil discoveries, and its place in geologic time.

 

Equipped with these three things, the researchers determined that lagerpetids probably originated in South America. The team also found that some later members of the lagerpetid family discovered in North America were closely related to earlier South American lagerpetids. This indicates that at some point following their origin, the lagerpetids migrated north.

 

Using yet further computer analyses designed by the researchers, the team was able “to quantify the time and how many latitudinal degrees in the globe that [dinosaurs and lagerpetids] moved at the time.” They pinpointed that dispersal to shortly after a period termed the Carnian Pluvial Event, roughly 235 million years ago, a time of high global humidity and more abundant rains.

 

Separating the north and south portions of Pangea’s single landmass was an enormous desert. With the end of the Carnian Pluvial Event, the climate—specifically within the desert—was less extreme, enabling animals to cross it into the northern sections of the world.

 

Ezcurra’s data set also enabled the team to compare the morphologies of the dinosaur and lagerpetid species to each other, which created another matrix (the “dissimilarity matrix”), which generated “a ‘morphospace’ that plots all the species in a single area” and graphs how different they were from each other. “With that plot,” Ezcurra explained, “we saw that the diversity of these dinosaurs and pterosaur precursors was actually huge. Actually bigger than that of the first dinosaurs and similar to that of the first pterosaurs. So we concluded that dinosaurs and pterosaurs originated from a pool of diversity that was considerably bigger than previously thought.”

Revisiting the Triassic

Robin Whatley is a vertebrate paleontologist and associate professor at Columbia College Chicago who was not involved in the research.

 

“This is a great example of a study by a group of paleontologists who are working from their collective knowledge to describe various aspects of a new fossil with surprising features for an animal of its age,” she told Ars. “These authors highlight the unique combination of a tall, raptor-like beak and sharp claws with extended areas for the insertion of tendons that would allow grasping abilities, features that might give Venetoraptor increased abilities for climbing or manipulating food items. While it’s not possible to know exactly how Venetoraptor was using its beak and claws, these authors find compelling evidence for ecological diversity in this early ornithodire, well before diverse beak and limb morphologies show up in closely related dinosaurs and pterosaurs.”

 

The find also reinforces the critical role of South American fossils in our developing understanding of this time. “Over the past two decades, about 30 new species have been described from Triassic beds of Brazil, including forerunners to mammals and representatives of distinct lineages of archosaurs,” Marina B. Soares, co-author and associate professor at the Federal University of Rio de Janeiro, Brazil said in a press release. “In this regard, Venetoraptor gassenae stands out as a key fossil in understanding the morphological and ecological diversity seen in the precursors of the highly successful dinosaurs and pterosaurs.”

 

Nature, 2023.  DOI: 10.1038/s41586-023-06359-z

 

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AS AN OUTBOUND packer at an Amazon warehouse in St. Peters, Missouri, Jennifer Crane has 37 seconds to assemble a cardboard box, retrieve a product from a shelf, plop it in said box, stuff it full of packing material, seal it, slap on a tracking label, and finally hoist it onto a conveyor belt. Then she has to do it all over again, for 10 hours. Last October, a case of sparkling water became her undoing.

While lifting the case, Crane says, she felt a searing pain tear down her left arm into her fingertips. She visited Amazon’s on-site first aid clinic, known as AmCare or the Wellness Center, where she says staff told her she had a small sprain and would be fine and gave her an ice pack. “I sat in there for 20 minutes until the ice pack got warm,” Crane says, by which time her shift was ending. When she got in her car to drive to work the next morning, her left hand couldn’t grip the steering wheel. Nonetheless, she says, a clinic staffer told her she needed to get back to work.

Crane, a member of a union organizing committee at her facility, pushed back, demanding to see a doctor, who prescribed work restrictions. AmCare staff plugged them into an Amazon software tool that digested the doctor’s orders and suggested a suitable alternative, less intensive job. A company safety director wrote in a 2019 email that shifting injured employees into restricted roles could cut the company’s workers’ compensation costs by keeping them in work, and also slash the number of serious injuries it had to report to the federal government, according to reporting by Reveal. Crane spent seven weeks waving a Swiffer duster around the 855,000-square-foot warehouse for 10 hours a day with her throbbing left hand slung over her shoulder for relief. When she finally got an appointment for an MRI, a doctor said she’d torn a ligament in her wrist.

Crane’s encounter with the case of sparkling water tipped her into a system developed by Amazon to manage one of the side effects of its famous logistics operation—a steady flow of injured workers. Recent OSHA investigations and WIRED interviews with 11 on-site medical representatives (OMRs) who have worked at AmCare in the last few years describe a system that can put employees at risk of further injury by keeping them working instead of referring them to appropriate medical care.

“What some companies are doing, and I think Amazon is one of them, is using their own clinics to ‘treat people’ and send them right back to the job, so that their injury doesn't have to be recordable,” says Jordan Barab, a former deputy assistant secretary at OSHA who writes a workplace safety newsletter.

Amazon spokesperson Maureen Lynch Vogel disputes this characterization, saying the company does not try to hide injuries and that employees who visit AmCare can seek outside treatment at any time. “Any suggestion that we intentionally or systematically delay or discourage employees from seeking needed medical care is false,” she says.

WIRED’s conversations with clinic staff who worked at 12 different facilities and recent OSHA citations, however, suggest that OMRs, typically emergency medical technicians, have sometimes been encouraged to steer workers toward in-house treatment. “Everything that we were doing was kind of pseudo-medical, enough to have the gloss of being medical,” says an EMT who worked in a Nevada AmCare. “When we’re in ambulances as EMTs, the entire point is to get people to definitive care. Then I get to Amazon, and it's like, ‘No, we're not getting them to a doctor.’ So what did you need me for? I'm the person who gets people to doctors.”

Inexpert Advice

AmCare staff are not qualified to diagnose and treat injuries, and although they follow protocols written with doctors’ input, they do not work under a physician’s supervision. Officially, they provide only first aid. Amazon typically hires EMTs for these roles, but it doesn’t require that they maintain their licenses. “EMTs are often hired as OMRs, but they do not operate as EMTs once hired,” Vogel of Amazon says.

OMRs typically treat employees who visit AmCare with heat, ice, or over-the-counter painkillers and handle referrals to workers’ compensation doctors. They can also refer workers to internal injury specialists, typically athletic trainers, for stretches and exercises designed to prevent further injury. Those staff and OMRs report to health and safety managers, who are not medical professionals. By limiting treatment to first aid provided by staff who don’t work under their medical licenses, Amazon avoids having to report these injuries to OSHA. Despite the “first” in first aid, AmCare staff often treat injured employees for days or weeks while they continue doing the job that injured them. OSHA says this can put employees at increased risk of developing enduring health issues.

< Watch the video at the source page. >

In April, OSHA issued Amazon the third citation in the agency’s 53-year history for medical mismanagement, finding that it seriously endangered employees’ health. That put the online retailer in the company of employers found to operate first aid clinics that put workers at risk of infection, scarring, or long-lasting injuries. Amazon had already received at least three warnings about AmCare from OSHA dating back to 2016, The Intercept reported. OSHA now found that over a six-month period, Amazon staff at a warehouse outside Albany, New York, sent at least six employees with serious injuries back to work instead of referring them to doctors, worsening their pain and potentially leading to “prolonged injuries and lifelong suffering.” The company is appealing. “We disagree with the claims in this citation,” Vogel of Amazon says, “and will continue our long-standing efforts to improve safety at our sites.”

In one instance, according to OSHA, an employee was hit in the head with a box, and blood began dripping out of their ear, a sign of a skull fracture. The employee later developed a headache, yet staff sent them back to work without calling a doctor. A week later, a 28-pound bench press bar collided with an employee’s head, causing a concussion, but staff returned the worker to their job operating heavy machinery.

Interviews with OMRs who worked at other facilities suggest that the practice of sending injured employees back to work isn’t limited to the Albany warehouse. Eight OMRs who spoke to WIRED say they faced direct pressure from managers to keep the number of workers they sent to doctors low, despite Amazon protocol requiring them to offer injured employees the option of being referred to outside medical care. Several former OMRs say that when an injured worker requested to see a doctor, they had to wait for a senior manager to interview the worker first, although Amazon says this is not part of its protocol. An OMR who worked in Maryland says that if their managers saw in the messaging system that they sent workers to the doctor on the day they were injured, “they'd be hauling ass to our office to ream us one.”

Peter Torres, who worked at AmCare in a facility in California’s Central Valley, says managers would bring up their high “day one” numbers in meetings, a count of employees sent to the doctor the same day they were injured. “It was making us look bad,” he says managers told the AmCare staff. “We needed to try to find a way to improve those numbers, which was a big shock to me.” Torres says that he had to seek permission from senior management to send employees to a doctor, and that sometimes they would try to talk workers out of going. Three other OMRs say that they heard from either managers or employees that the managers had talked workers out of seeing a doctor.

Once, a manager asked Torres to try to convince an injured employee to be treated in-house. A colleague had already decided to refer the worker to a doctor, and Torres was asked to talk the worker out of going. “Where I come from, in the emergency medical services world, that’s a big no-no. You never step on somebody else’s patient,” he says.

In the spring of 2022, a fulfillment center in Salt Lake City, Utah, was sending five to six employees to workers’ comp doctors every week, amongst the highest rates for Amazon facilities in the region, says former OMR Jed Martinez. He says that senior operations managers told staff that they needed to reduce that number to one or two per week. Managers encouraged OMRs to tell employees that there was nothing a doctor would offer that AmCare couldn’t provide, he says.

Vogel of Amazon says the managers’ behavior described by Torres, Martinez, and other OMRs violates company policy and that the company tracks “day one” numbers only to ensure its staff are providing high-quality first aid.

Many of the clinic staffers who spoke to WIRED said they tried to do their best to help employees under the limitations Amazon placed on them, and that some employees did appear to improve. But others deteriorated—especially those with repetitive stress injuries, says a former Colorado-based EMT. Amazon policy states that employees who aren’t improving should be immediately referred to an outside provider, but she saw some workers get stuck in an injury loop. “We really struggled to get those people better because they were still going out there and doing the same repetitive movement that injured them in the first place.”

Delayed Care

Amazon is fighting a growing throng of regulators, law enforcement, and politicians trying to force it to meaningfully address warehouse safety. OSHA currently has investigations open at 18 Amazon warehouses and has already issued six citations across eight facilities in 2023, including the one in April for medical mismanagement and one last month for ergonomic hazards at a New Jersey facility. It was accompanied by a warning letter alleging that AmCare employees at the warehouse failed to ensure that injured employees received proper medical care, including several employees with head injuries.

In Washington state, a trial began on July 24 after the state's occupational safety regulator said that at three Amazon warehouses the ergonomics and pace of work, combined with the company’s discipline system, elevated the risk of developing musculoskeletal disorders. The agency ordered Amazon to change its processes, but it claims to have made improvements and is pushing back on the allegations. Meanwhile, the US Department of Justice is investigating whether the company deliberately underreported injuries, and Bernie Sanders recently launched a Senate investigation into the company’s safety record. The various probes could force Amazon to revamp its processes, or haul executives before Congress.

When an Amazon worker gets injured and receives treatment through AmCare, the company expects them to continue hitting their productivity targets, although time spent visiting the clinic is not counted against them. For years, company protocol let AmCare staff treat workers for up to three weeks before they had to refer them to a doctor or close their case, although two clinic staffers say they saw patients for longer. Vogel says Amazon removed the three-week guidance in March 2022, but OSHA alleges that some employees continued to use it.

In a warning letter sent in January to the site manager of an Amazon facility in Deltona, Florida, as part of an investigation begun in July 2022, the agency said that employees reported that AmCare staff commonly presented the three-week rule as a requirement. AmCare staff in Logan Township, New Jersey, also said they could see workers for up to 21 days before issuing an outside referral, according to the July OSHA warning letter.

Three OMRs at two facilities outside Florida tell WIRED they saw colleagues tell injured employees they could not see a doctor until Amazon had treated them first. Vogel says that this would be a violation of company policy.

While on-site first aid clinics are common at large employers, the sort of prolonged, medically unsupervised treatment that Amazon offers is not, says Debbie Berkowitz, a former OSHA chief of staff and fellow at Georgetown University’s Kalmanovitz Initiative for Labor and the Working Poor. She says the practice of using on-site clinics to prevent recordable injuries became common in the meatpacking industry, which has a history of abusing its workforce. “So they’re taking a page out of a really low-road industry that treats workers as expendable,” she says.

Ongoing Investigation

As criticism of its injury problem has grown, Amazon has claimed to make improvements. The company cites steep reductions in its lost-time incident rate, the number of injuries leading to a full day or more of missed work, a marker of severity. But an analysis of OSHA data by the Strategic Organizing Center, a coalition of labor unions, found that as that figure dropped, there was a commensurate rise in injured employees who performed restricted jobs or were temporarily transferred to another role, which the SOC groups together as “light duty.”

In 2018, the majority of injured workers taken off their jobs were sent home on workers’ comp, and only one in five were reassigned to light-duty work. By 2022 those proportions had roughly flipped, with most injured workers on light duty and only one in four sent home. Over the same period, overall injuries have fluctuated, but not significantly improved, suggesting that a similar number of workers are getting injured, but Amazon is finding ways to keep them working.

The SOC analysis also found that in 2022, nearly seven out of every 100 Amazon warehouse workers were injured seriously enough to be taken off their job, more than double the rate for warehouses more generally. Amazon argues that it should instead be compared to an industry average of its own devising that has been adjusted to include three large competing retailers, which do not report most of their injuries under the warehousing category. Using that approach, Amazon’s analysis found that its total injury rate is still higher than average, but not double that figure.

Amazon’s safety report for 2022 touts a 23 percent reduction in recordable injuries for US workers between 2019 and 2022. But 2019 was a particularly high year for injuries, and total injuries dropped just 8 percent from 2017 through 2022.

After a worker is injured, getting reassigned to alternative work can spare them the pay cut that comes with being signed off work. It also potentially gives the company cover to avoid addressing the root cause, says Eric Frumin, the SOC’s director of health and safety, by improving its lost-time injury numbers without reducing injuries.

Amazon uses a piece of software that matches injured employees with jobs that fit their restrictions. A doctor specifies physical limitations for the worker, such as how much weight they can lift or whether they can bend over, which OMRs plug into the program. The software spits out a list of jobs and percentages indicating how well each job satisfies the restrictions. If a suitable job is available, Amazon will offer it to the employee, and jobs that don’t quite match a person’s restrictions can be modified.

A Wisconsin-based OMR says that his experience with the algorithm showed it sometimes underestimated a job’s rigor, especially when it came to weight limits. He says some doctors used to tour the facility to get an idea of what the jobs entailed, but those who didn’t would sometimes write restrictions that didn’t adequately protect workers from further injury. “These are highly mechanized, intensely engineered jobs. Even when the job is lifting less than 10 pounds, it's lifting less than 10 pounds 17 times a minute,” says Frumin. “That’s something doctors should know about when they're evaluating patients from Amazon.” Amazon says employees sign paperwork outlining the new job’s responsibilities and can ask the doctor involved for a different assignment if they feel it is too demanding.

In April, James Diaz was moving a 3,000-pound unit loading device at an Amazon Air hub in San Bernardino, California, when it hit him in the ankle. AmCare staff told him it didn’t look too bad, gave him some ice, and sent him back to work. “I really had to advocate for myself on the severity, and it wasn’t until a few days later that they sent me out,” he says. Amazon says that Diaz was told he could seek outside treatment, per its policy, and that he declined, but Diaz denies this and notes that he was not given workers’ comp paperwork until he escalated his case to a safety manager, in a request reviewed by WIRED. A doctor gave him a restriction against pushing and pulling, so Amazon’s software tool suggested a series of production jobs that he rotated through over a period of months. “They call it light duty, but it's not,” he says. “They still have you lifting heavy packages and boxes and throwing them around. Even standing is half my weight on my ankle.” Amazon says that Diaz has the right to decline his assignment; however, if he did, he might lose eligibility for state workers’ compensation benefits.

When a production job can’t be found for an injured worker, Amazon has created jobs that appear to contribute little to its logistics operation—like dusting, the reassignment given to Crane after she injured her wrist. Other injured employees sit at a computer for 10-hour shifts annotating images to train Amazon’s machine-learning algorithms. One worker who injured her back told WIRED this was a relief from her job lifting heavy boxes, but for others, the hours of computer work could aggravate their injuries. In 2016, Amazon began loaning injured employees out to nonprofits as part of a program called Amazon Community Together, but it eliminated that program during a round of layoffs this year.

In May, 400 workers at Amazon's STL8 facility in St. Peters, Missouri, petitioned management to improve safety. In July, 14 workers filed a complaint with federal regulators alleging unsafe working conditions at STL8. COURTESY OF MISSOURI WORKERS CENTER

While the company touts its “robust return-to-work program,” it exists at such a scale only because so many employees get injured in the first place. Even those who do make it to a doctor can emerge with long-lasting, sometimes debilitating pain. In March of last year, Willow Hart felt a disc slip in her back while retrieving items at an Amazon warehouse in Georgia. The pain came on slow and built over the next two weeks until one day the disc pinched her sciatic nerve. “I got out of bed and collapsed crying,” she says. She hasn't been able to return to her job since. The financial strain forced her to move back in with her parents, where she fell into a deep depression. “I didn’t take the whole concept of pain as a constant companion well,” she says.

Crane, the outbound packer at Amazon’s facility in St. Peters, Missouri, says that a workers’ comp doctor cleared her to return to full duty in November, even though a physical therapy exam found that her injured hand had regained only a fraction of its strength. It was right as the peak holiday season was ramping up. “It sucked. I was in pain,” she says. Overtime was mandatory, so she clocked 11-hour days, five days a week, popping pain medication to make it through her shifts and relying on her teenage kids to open jars at home. She still takes 1,200 milligrams of ibuprofen twice a day. “I've learned to try to take it before I go to work so the pain doesn't get quite so bad,” she says. Ten months after becoming injured, she still sometimes wears her brace to work.

Last month, Crane joined 13 other workers at her facility in filing a complaint with OSHA. It alleges that Amazon’s working practices lead to serious injuries and that “mistreatment” by AmCare staff has worsened employees’ job-related harms. Amazon’s Vogel says that staff surveys indicate the vast majority of workers feel safe at the facility. Three weeks ago, OSHA staff visited Amazon in St. Peters for an inspection triggered by the complaint. The agency says its investigation is ongoing.

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The 5,300-year-old mummy, nicknamed Ötzi (which rhymes with "tootsie"), is the oldest human body ever found intact.

He has fascinated the world since his body was first unearthed in Italy's Ötztal Alps in 1991. But the way most people imagine this 46-year-old man isn't necessarily accurate.

According to a study, led by researchers at Germany's Max Planck Institute, Ötzi may not be a hairy, caucasian hunter-gatherer, as previous reconstructions suggested, but a farmer with relatively dark skin and a balding head.

"The genome analysis revealed phenotypic traits such as high skin pigmentation, dark eye color, and male pattern baldness that are in stark contrast to the previous reconstructions that show a light skinned, light eyed, and quite hairy male," says evolutionary anthropologist Johannes Krause from the Max Planck Institute in Germany.

A forensic reconstruction of Iceman. (South Tyrol Museum of Archeology)

Scientists might know what Ötzi last ate and what his voice might have sounded like, but what he looked like is another matter.

The first genome study on Ötzi took place back in 2012 and found evidence that this man was closely related to present-day Sardinians. As such, it was assumed he was descended from populations of eastern hunter-gatherers and caucasian hunter-gatherers who merged in the fifth millennium.

But the new findings found no detectable ancestry of this kind. Instead, researchers uncovered "unusually high" Anatolian farmer ancestry in Ötzi's genome, higher than almost any other known population in Europe at that time.

The findings suggest Ötzi was closely related to a lineage of Neolithic farmers in Anatolia, where the country of Türkiye now sits. They later migrated to Italy but remained relatively isolated in the Alps, keeping to themselves.

Ötzi's ancestors may have started mixing with hunter-gatherers elsewhere in Europe just a few dozen generations before his birth – a relatively short time in terms of a population's evolution.

The ancestry of the Iceman, a mix of Anatolian farmer (orange) and European hunter-gatherers (green). (Wang et al., Cell Genomics, 2023)

In Ötzi's genome, researchers found evidence of an agricultural diet and skin pigmentation that is darker than that typically found across present-day European populations.

They also found risk alleles associated with male-pattern baldness. Whatever hair the hunter once had was probably black.

The findings match the appearance of the mummy itself, explains Krause, which is dark and has no hair. But previous studies assumed that this appearance was the result of being frozen for millennia, not an accurate representation of Ötzi's looks in life.

The authors of the new analysis acknowledge that "a single individual has… limited resolution in representing the population history of his time and region", but their results do match other ancient humans found in Italy.

One body found near the southern Alps, for instance, also shows high Anatolian-farmer-related ancestry in recent genome studies.

"Future studies with a denser sampling from the southern Alps will be needed to replicate our findings and show if the Iceman was an outlier or a representative of his population," the researchers conclude.

The study was published in Cell Genomics.

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Researchers from Florida Atlantic University's Charles E. Schmidt College of Science tested wristbands of various textures to determine their risk for harboring potentially harmful pathogenic bacteria. Despite being worn daily, routine cleaning of wristbands is generally overlooked or simply ignored.

For the study, researchers tested plastic, rubber, cloth, leather and metal (gold and silver) wristbands to see if there is a correlation between wristband material and the prevalence of bacteria. They investigated the hygienic state of these various types of wristbands worn by active individuals and identified the best protocols to properly disinfect them.

Using standard microbiological assays, researchers looked at bacterial counts, type of bacteria and their distribution on the wristband surfaces.

They also conducted a bacteria susceptibility assay study screening the effectiveness of three different disinfectant solutions: Lysol Disinfectant Spray; 70 percent ethanol, commonly used in hospitals and alcohol wipes; and a more natural solution, apple cider vinegar.

Results of the study, published in the journal Advances in Infectious Diseases, suggest you may want to "go for the gold" or silver the next time you purchase a wristband. Nearly all wristbands (95 percent) were contaminated. However, rubber and plastic wristbands had higher bacterial counts, while metal ones, especially gold and silver, had little to no bacteria.

"Plastic and rubber wristbands may provide a more appropriate environment for bacterial growth as porous and static surfaces tend to attract and be colonized by bacteria," said Nwadiuto Esiobu, Ph.D., senior author and a professor of biological sciences in the Charles E. Schmidt College of Science.

The most important predictor of wristband bacteria load was the texture of wristband material and activity (hygiene) of the subject at sampling time. There were no significant differences between males and females in the occurrence or distribution of the bacteria groups.

Researchers tested plastic, rubber, cloth, leather and metal (gold and silver) wristbands to determine if there is a correlation between wristband material and the prevalence of bacteria. Credit: Florida Atlantic University

Bacteria found in the study were common skin residents of the genera Staphylococcus and Pseudomonas, and intestinal organisms of the genera Escherichia, specifically E. coli. Staphylococcus spp was prevalent on 85 percent of the wristbands; researchers found Pseudomonas spp on 30 percent of the wristbands; and they found E. coli bacteria on 60 percent of the wristbands, which most commonly begins infection through fecal-oral transmission.

The gym-goer showed the highest staphylococcal counts, which emphasizes the necessity of sanitizing wristbands after engaging in rigorous activity at the gym or at home.

Staphylococcus aureus is a type of bacteria found on human skin, in the nose, armpit, groin or other areas that cause a wide variety of clinical diseases. Pseudomonas spp., commonly in the environment, can cause infections in the blood, lungs (pneumonia) or other parts of the body after surgery. Enterobacteria are a large family of bacteria including many of the more familiar pathogens such as E. coli and Salmonella.

"The quantity and taxonomy of bacteria we found on the wristbands show that there is a need for regular sanitation of these surfaces," said Esiobu. "Even at relatively low numbers these pathogens are of public health significance. Importantly, the ability of many of these bacteria to significantly affect the health of immunocompromised hosts indicates a special need for health care workers and others in hospital environments to regularly sanitize these surfaces."

Findings from the study showed that Lysol Disinfectant Spray and 70 percent ethanol were highly effective regardless of the wristband material with 99.99 percent kill rate within 30 seconds. Apple cider vinegar was not as potent and required a full two-minute exposure to reduce bacterial counts. While these common household disinfectants all proved at least somewhat effective on all materials (rubber, plastic, cloth and metal), antibacterial efficacy was significantly increased at two minutes compared to thirty seconds.

Different disinfectants, depending on their active ingredients, kill bacteria in different ways, such as by disrupting cell membrane integrity, altering or removing proteins or interfering with metabolic activities.

"Other potential forms of bacterial transmission and facilitation of infection, such as earbuds or cell phones, should be similarly studied," said Esiobu.

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The Faroe Islands, an incongruous speckling of green in the North Atlantic, are about as far away as you can hope to get on Earth from a toxic-waste dump, time zones distant from the nearest population centers (Norway to the east, Iceland to the west). Pál Weihe was born in the Faroes and has lived there for most of his life. He is a public-health authority for the nation, population around 53,000; chairman of the Faroese Medical Association and chief physician of the Department of Occupational Medicine and Public Health in the Faroese hospital system. He is also vice chairman of the Faroe Islands Art Society; a widower; a grandfather. A crumpled funeral program and half-empty juice boxes share space in the back seat of his Land Cruiser.

Despite the remoteness of his location, Weihe’s medical career has been defined by his efforts to protect the Faroese from exposure to chemicals that reach the islands from across the sea. His research clinic is a cozy two-story house on a hill just above the Tórshavn harbor. Medical textbooks in English and Danish (the Faroes are part of the Kingdom of Denmark) line the walls, hinting at the scope of this task: “Basic and Clinical Immunology”; “Klinisk Social Medicin”; “Marine Medicine Research Collection”; “Gynaekologi”; “Hunter’s Diseases of Occupations.” His colleagues are almost all women, and at 73, he is decades their elder. The slender mahogany chairs he has chosen for the conference room, made by a local carpenter, bow to the future: “They have a feminine shape,” he said, “and this is a house of women.”

On a blustery morning in early April, the house was relatively quiet because of the Easter holiday, but two staff members, Jóhanna Petursdóttir and Marita Hansen, had come in with Weihe to examine volunteers enrolled in an ongoing study that began in 1986. Back then, Weihe and a Danish professor of environmental medicine, Philippe Grandjean, recruited more than 1,000 pregnant women, and later their newborns, to study the impact of mercury from seafood on fetal and child development. The Faroese mother-infant pairs showed that exposure to the toxin in the womb, even at low levels, can cause learning and memory deficits in children, findings that led to global advisories for pregnant women to limit their fish intake. Grandjean and Weihe continued enrolling new groups whenever there was funding to do so and moved on to assessing the impacts of other pollutants.

In 2009, Grandjean happened to be reading a toxicology journal when a study caught his eye. The authors had exposed rats to one of a group of common chemicals that are classed together as “per- and polyfluoroalkyl substances,” or PFAS for short. The chemicals, many of which repel water, oil and grease and can often withstand high heat, are used in countless consumer products. They also linger in the environment. The exposure, they found, damaged the rodents’ immune system. The question was whether the same would be true in people.

Grandjean, who had never heard of PFAS, was intrigued. By then, he and Weihe were investigating whether several other persistent chemical pollutants affected how children responded to routine vaccination. So it was relatively easy to add PFAS to their study. Over the prior 23 years, they had periodically asked the children from their mother-child groups for biological samples: blood and hair trimmings. They also saved samples from the children’s mothers around the time of their birth. This biobank, a portion of which is preserved in a dozen freezers in the basement of the national hospital, served as a kind of time machine: Grandjean and Weihe were able to test for chemicals in the serum of babies who were now years and even decades older.

Around the same time, other potential health impacts of PFAS were starting to receive attention in the United States. Lawsuits filed beginning in the late ’90s raised serious concerns about a DuPont factory near Parkersburg, W.Va., that used a type of PFAS called PFOA to make Teflon. For decades, the company had dumped waste containing the chemical into the Ohio River and unlined pits on its property, polluting both the air and drinking water of tens of thousands of people. As part of a settlement, DuPont funded a study to determine if residents had been harmed by the chemicals. Its major conclusions, published online in 2012, were damning: The evidence, including blood samples and health surveys, indicated a “probable link” between PFOA and high cholesterol, ulcerative colitis, thyroid disease, testicular cancer, kidney cancer and pregnancy-induced hypertension.

Grandjean, Weihe and their colleagues published their own paper in 2012 showing that PFAS reduced the number of antibodies that children maintained after they received tetanus and diphtheria vaccinations. (Weihe was so alarmed at the apparent lack of protection for some of them that he called their parents to offer them boosters.) Between the Faroese and the Ohio Valley residents, however, there was a crucial difference. The Faroese had not been exposed to high levels of the chemicals, as the subjects in the DuPont study had; the levels of PFAS circulating in the bloodstreams of the Faroese were akin to U.S. and European averages. If such relatively small quantities of PFAS could interfere with the immune system, Weihe and Grandjean asked, what other processes might be affected? And how long might it take for those outcomes to appear? The two researchers have been seeking answers by documenting the health of the babies in their study as they move through childhood and into adulthood.

Even today, many Americans, including physicians, are unfamiliar with PFAS — perhaps in part because they used to be called PFCs, and the alphabet soup of “P” abbreviations that refer to individual variations is confusing. Among those who are aware of the chemicals, few seem concerned about their possible exposure. If practically everyone has ingested some PFAS and most of us haven’t noticed any effects, the thinking goes, how bad for us could it be?

“I’ve heard some people say, ‘Well, if everybody is exposed to PFAS, how come we aren’t all dead?’” Jamie DeWitt, a professor of pharmacology and toxicology at the Brody School of Medicine at East Carolina University, told me. In fact, she says, “People actually are dying.” DeWitt cited a report in The Lancet that calculated that about nine million people each year die from chronic diseases caused by environmental pollutants of all kinds. “We need prevention,” DeWitt says. “And that means acknowledging that environmental exposures lead to diseases.”

Confounding that acknowledgment for PFAS is the breadth of health conditions with which exposure to the chemicals has been associated: the cholesterol and cancer outcomes highlighted by the DuPont study and the decreased vaccine response demonstrated in the Faroese children, but potentially others that have yet to be proven as persuasively. Those include endocrine disruption, metabolism and immune dysfunction, liver disease, asthma, infertility and neurobehavioral issues — their diversity a potential result, as Linda Birnbaum, former director of the National Institute of Environmental Health Sciences (N.I.E.H.S.) and the National Toxicology Program put it to me, of the fact that “PFAS has a great deal of complexity.”

Many of these health problems are common and chronic. Are PFAS contributing to their development, and if so, how much? Would reducing our contact with the chemicals meaningfully improve our overall health?

The chemicals known as PFAS have been found in a dizzying array of goods, notably waterproof, stain-resistant and nonstick ones and several kinds of household cleaning products, even brussels sprouts (although data on those is limited). They are also associated with a wide variety of health problems.

Credit...Grant Cornett for The New York Times

The first variation of PFAS (pronounced pee-fas) was discovered accidentally by a DuPont researcher looking for more stable refrigerants in the 1930s, then used by scientists in the Manhattan Project during the uranium-enrichment process. Many of the chemicals also stabilized explosives and made excellent protective coatings and lubricants for electronics, reducing surface tension such that both water- and oil-based substances slid right off; some also maintained their properties under extreme heat. They were subsequently incorporated into waterproof, stain-resistant and nonstick consumer products. (The chemicals also have vital uses in medical devices, cellular networks and in the aerospace and renewable-energy industries.) The special durability of PFAS derives from their structure. There are thousands of variations, each a unique chemical, but all of them include carbon atoms bonded to fluorine atoms. Many PFAS have bonds that are so strong that no one is sure how long it takes for them to break down on their own in nature; it could be hundreds or even thousands of years. For this reason, PFAS are often referred to collectively as “forever chemicals.”

DuPont and 3M, which was manufacturing PFAS and using one in Scotchgard, began studying the potential health effects of their formulations in part as an occupational-safety measure. Initially, scientists assumed that because the first compounds were so stable and resistant to change — “inert,” in chemistry parlance — it would be impossible for them to interact with biological systems. The companies’ in-house experiments, along with other studies, quickly overturned that notion. By 1965, DuPont had indication that PFAS increased the liver and kidney weight of rats.

In the late ’70s and early ’80s, the companies were seeing alarming signals in their animal studies — in one study, monkeys exposed to extreme levels of PFAS died — and among their employees. In 1979, DuPont observed that workers who had contact with the chemicals appeared to have higher rates of abnormal liver function. In 1981, 3M researchers alerted their DuPont colleagues that pregnant rats exposed to PFAS had pups with eye irregularities; that year, an employee at a Teflon plant gave birth to a child with one nostril, a keyhole pupil and a serrated eyelid. In 1984, DuPont detected PFAS in the tap water of three communities near its West Virginia factory.

In 1998, 3M told the Environmental Protection Agency that it had tried and failed to identify members of the public without PFOS — a type of PFAS it was producing — in their blood. Two years later the company, which was the only U.S. maker of PFOS, announced that it planned to phase out its manufacture of the chemical. (3M had occasionally shared data with the E.P.A. in the 1980s; DuPont’s human and animal research wouldn’t become known until 2001, after a lawsuit forced the company to turn over documentation related to PFOA to opposing counsel, and he alerted the E.P.A. and other agencies.) In 1999, the National Health and Nutrition Examination Survey, an ongoing project run by the Centers for Disease Control and Prevention to track the health of the U.S. population, began testing for PFAS in participants and would confirm 3M’s observations: The chemicals were present in virtually everyone.

This revelation was met with a collective shrug by federal health officials and policymakers. More than two decades later, in fact, PFAS production remains largely unregulated. There are more than 12,000 variations of the chemicals, very few of which have been investigated for their potential health effects. Using data from the E.P.A. and other government agencies, the Environmental Working Group, a nonprofit research and advocacy organization, has mapped more than 41,000 places in the United States and its territories where PFAS are potentially being made, used or released: military sites, airports, landfills, wastewater-treatment plants, oil refineries. This year, the group announced that more than 2,800 domestic locations are confirmed to be contaminated with the chemicals.

PFAS can be removed from tap water, but according to the E.P.A., tap water typically accounts for only about 20 percent of a person’s overall exposure to the chemicals; we also eat them, inhale them and rub them on our skin. Testing by government agencies and watchdog groups have found PFAS in carpets, furniture, nail polish, shampoo, mascara, nonstick cookware, dental floss, raincoats, fast-food wrappers, pizza boxes, microwave popcorn bags, yoga pants, sneakers, sanitary pads, tampons, menstrual cups, bedding, upholstery, children’s pajamas, paint, vinyl flooring and artificial turf. They’re in the protective equipment used by firefighters and medical personnel. They’re in an especially effective foam for putting out fuel-based flames. They’re in dust and the household cleaning products you might use to get rid of it. They are in flamingos in the Caribbean and plovers in South Korea. They are in alligators. They are in Antarctic snow. In Europe, they’ve been discovered in organic eggs; in the United States certain states have found them in produce and meat. Last year, a study of PFAS in freshwater fish in the United States revealed median levels so elevated that eating a single serving could be equivalent to drinking PFAS-contaminated water for a month. In June, the U.S. Geological Survey reported that it had tested private wells and public water supplies and found at least one PFAS in 45 percent of the nation’s tap water.

Lately, statistics like these seem to appear ever more frequently in the news. In response to growing apprehension about the pervasiveness and toxicity of the chemicals, new regulations are in the works in the United States and the European Union. The E.P.A. has a “PFAS Strategic Roadmap,” and the White House has created a PFAS strategy team whose mission, among other goals, is “to understand and to significantly reduce the environmental and human health impacts of PFAS.” For decades, members of communities whose drinking water was found to contain significant levels of PFAS — Pease and Merrimack, in New Hampshire; the Cape Fear watershed, in North Carolina; the Great Lakes region; and many others — have been virtually alone in pressing public-health agencies to offer them both testing and, based on those results, medical guidance. Often, those agencies simply advise people worried about their exposure to consult their family physician. But chronic exposure to pollutants is not well covered in medical school. “People want to know, could this have contributed to my high cholesterol, my miscarriage, my loved one’s cancer?” Courtney Carignan, an exposure scientist and epidemiologist at Michigan State University, told me. “These are reasonable questions, and doctors are often very dismissive. They don’t have the knowledge to answer those questions.”

Last year, the National Academies of Science, Engineering and Medicine — whose publications typically reflect scientific consensus on a topic — reviewed all the studies that had been published related to the impact of the chemicals on humans. The resulting report is the first to offer three tiers of specific medical guidance based on the amount of PFAS detected in someone’s blood. Those in the middle category, it says, should pay close attention to their cholesterol and be checked for hypertensive disorders during pregnancy. Currently, this advice would apply to most of the U.S. population.

The Faroe Islands are distinguished by their precipitous cliffs, fjords and valleys. Waterfalls cascade down grassy slopes, where sheep are plentiful, and seabirds nest in crags. But the landscape is less inherently hospitable to humans. Nearly a century ago, the Danish poet Nis Petersen, who spent a year on the southernmost island, Suðuroy, wrote that a third of the male population perished outdoors, presumably succumbing to rocky or watery deaths. When the inhabitants of this dire locale discovered, sometime around the ninth century, that they could chase pilot whales into shallow bays, slaughter them and harvest their meat and blubber to avoid starvation, they interpreted the annual summer arrival of the creatures, laden with nutrients, to be “a gift from heaven,” Pál Weihe told me — “a kind of blessing.” The event, known as grindadráp, eventually became a cultural rite, rather than an act of desperation, one that persists in defiance of vigorous protests from animal-rights groups.

Moral arguments, however, were not Weihe’s concern when, as a young doctor in the 1990s, he began telling anyone who would listen that children and any women who might become pregnant should avoid eating whale meat. Roughly a decade before, while a resident in environmental and occupational medicine at Odense University Hospital in Denmark, he met Grandjean, an expert on the neurological damage caused by lead exposure. Grandjean, an enthusiastic bird-watcher with the extravagant eyebrows of a rockhopper penguin, had fond memories of banding storm petrels in the Faroes in his late teens and was familiar with the grindadráp. He had also been reading in news reports that mercury was accumulating up the marine food chain, with concentrations peaking in top predators like pilot whales.

The neurological damage that acute mercury poisoning could cause was, like the dangers of lead poisoning, well known. But it was unclear how much people should worry about low-level exposure over the long term. To answer a question like that, scientists cannot perform randomized clinical trials in a perfectly controlled setting — the kind of experiment that most convincingly demonstrates cause and effect. Recruiting hundreds of participants, randomly assigning some of them to ingest mercury at varying levels and others (the controls) to ingest a placebo and then waiting a lifetime to see what happens would be unethical and impractical.

Instead, researchers impose those controlled conditions on animals or on human cells, then compare their findings with observational studies in people. In such epidemiological studies, scientists seek out volunteers who have already been exposed to a toxin, for example, and ask about or monitor their health after the fact. But because the subjects have not been randomly assigned to experimental or control groups, it is always possible that another, related variable is influencing the outcome.

Weihe and Grandjean realized, however, that the Faroe Islands offered circumstances uniquely suited to epidemiology. Everyone’s living conditions are roughly uniform: same environment, free health care and schooling for all, similar genetic backgrounds. Moreover, after a grindadráp, whale products are distributed free to anyone who wants them, so presumably people’s mercury exposure was as random as their taste preferences.

In 1985, Weihe and Grandjean advertised in the Faroes for pregnant women willing to enroll themselves and their future child in an environmental-health study. More than 1,000 agreed to take part. When they gave birth, they surrendered samples of their hair and umbilical-cord blood and tissue. Then the researchers waited until the children entered school. Even after seven years, more than 90 percent of the women returned with their first graders — an unheard-of retention rate in epidemiology — and the children underwent neurological assessments. The tests showed that 7-year-olds whose mothers had the highest mercury concentrations when they were born were also at the highest risk for language, attention and memory deficits, among other issues. They also scored lower on I.Q. tests. Those results, published in 1997, were the basis for the E.P.A.’s estimate of how much mercury people can ingest daily without ill effects. In the Faroes, meanwhile, women heeded Weihe’s advice to avoid whale meat, and their overall mercury levels, along with those of their children, fell.

Nearly 15 years later, when Grandjean and Weihe wanted to learn more about the health impacts of PFAS, they were able to examine the frozen samples of mother-child pairs enrolled from 1997 through 2000. After checking the women’s PFAS levels at delivery, they then tested blood taken from the children after vaccinations for tetanus and diphtheria, at ages 5 and 7. They found that for each doubling of maternal PFAS levels, the children’s antibody concentration after the shots was 40 percent lower. For each doubling of PFAS among the children, their antibody concentration was 50 percent lower.

In Weihe’s clinic in April, he, Hansen and Petursdóttir were receiving teenagers from their fifth mother-infant group who were born in 2009. The first subject arrived with his mother and younger sister. He kept his eyes on his sneakers as Hansen took a clipping of his curly blond hair, tied a string around the lock and dropped it into an envelope. Then Petursdóttir beckoned him over to draw blood. She had learned to do this last year on babies from the sixth group, when they were just three months old. The stress of inserting a needle into the tiny veins of squalling infants, and the anxiety of their parents as they watch researchers try to do so, is a major obstacle in recruiting babies for studies generally. “Every day I was worrying about what to wear because I was sweating,” Petursdóttir told me. “I couldn’t wear colors.” The Kelly green turtleneck she had on that day was a hard-earned sign of confidence; she and her colleagues had gotten samples from more than 600 babies.

Weihe ushered the family into an exam room. At his direction, the boy, an avid soccer player, stood on a plate to measure swaying, first with his eyes open, then closed; held a penlike instrument in each hand, trying to keep it still; and pushed a button in response to a signal to gauge his reaction time. After he was done, Weihe emerged from the exam room. “I have told the boy and his mother that this is a completely normal young man,” he said.

“I would be surprised if he wasn’t,” his mother told me. Still, she said she appreciated the extra testing her son receives as a study participant.

Precisely where the Faroese are encountering the PFAS — and how they can, in turn, prevent further exposure — is a conundrum. There is no PFAS production on the islands, and the drinking water is already pure. The toxins must come from abroad, presumably in food and consumer products. “That means when you transform this into public-health advice it is quite difficult,” Weihe told me. “In communication before, we really emphasized what you can do.” Indeed, when women stopped eating pilot whale, it took about three months to clear the related mercury from their bodies. But expelling PFAS can take anywhere from several days to 70 years — and that presumes you can figure out how to avoid taking in more.

The sheer range of health problems that have been linked to PFAS exposure makes it hard to picture how a single type of contaminant could contribute to all of them. If you list the dizzying number of ways you might interact with the chemicals and draw a line from each of them to a list of potential outcomes, you end up with a mess of scribbles and the conclusion that everything causes everything.

Describing how PFAS act on our biology becomes even more convoluted when you factor in how many variations there are. Scientists have a decent understanding of how some of the earliest formulations, like PFOS and PFOA, behave on a cellular level. But health data on newer formulations is extremely limited. It’s safe to say that once we eat, drink, breathe or absorb PFAS molecules, some readily bind to one of our major blood proteins. (Stanford University researchers reported this property in 1956.) As blood circulates throughout the body, it delivers PFAS to our organs and other tissues. Some PFAS molecules resemble the fatty acids we burn for fuel and use as cellular building blocks, says Carla Ng, an associate professor of civil and environmental engineering at the University of Pittsburgh. Our cells thus recognize them as beneficial and bring them inside their outer membrane as they do other resources. “The things that PFAS look like,” she says, “are the things our body is used to dealing with as food and parts of ourself.”

Some PFAS appear to travel with other fatty acids to the liver, where they can accumulate in its cells and proteins. (Tests of cadavers have shown that newer formulations of the chemicals may congregate in other tissues, including the brain, but the data on them is limited.) A 2022 review by researchers at the Keck School of Medicine at the University of Southern California, along with colleagues elsewhere, found “consistent evidence” from rodent experiments and epidemiological studies that PFAS increase the risk of liver impairment, including nonalcoholic fatty liver disease. This result is particularly worrisome, because rates of the condition have soared in recent decades.

Once inside cells, PFAS have been shown to increase oxidative stress, creating structural damage that has been associated with a wide range of conditions, including cancer, diabetes and cardiovascular disease. They also can penetrate the nucleus of the cell, where our DNA resides. Perhaps most problematically, they are known to bind with at least 14 receptors. (The dioxin in Agent Orange, by comparison, binds with only one.) Those actions influence how cells express or suppress genes that, in turn, govern how cells perform fundamental functions like producing energy and storing fat. When cells aren’t working properly, they cause glitches in the organs they make up. Those impairments can unfold in various ways, depending on which receptors PFAS target, where the cells are (say, the liver or the brain) and when they encounter the chemicals — in utero, for instance, or during adulthood. As a result of the activation or deactivation of a particular receptor in a particular tissue, however, there could be numerous intermediate cellular interactions unspooling over decades, Sue Fenton, a reproductive endocrinologist at the N.I.E.H.S., told me. Rarely does any disease have a singular cause. Yet while it’s impossible to say that PFAS alone caused any one person’s illness, it is possible to estimate the burden that those chemicals, like other toxins, put on people’s bodies.

‘They are all problematic. When they’re tested, they all do the same stuff.’

The liver appears to be disproportionately impacted by PFAS, where they likely act on its cells in multiple ways. The organ produces cholesterol and has a critical role in detoxifying blood and balancing blood sugar. It helps regulate our metabolic and immune systems, as well as our estrogen and testosterone levels. That’s one theory as to why testicular cancer has been associated with PFAS exposure, demonstrated in a case study of U.S. Air Force servicemen published in July. (Bisphenol A, or BPA, a chemical found in plastics that can mimic estrogen, also binds to nuclear receptors, but to fewer of them; it does not persist in the body or the environment.)

Grandjean and Weihe suspect that PFAS may also throw off the endocrine system, which is driven by the hypothalamus region of the brain and encompasses hormone-producing organs throughout the body. Specifically, they wonder if PFAS are “obesogens,” chemicals thought to disrupt the system’s metabolism, potentially affecting the body’s ability to maintain a stable energy balance. To test this hypothesis, they plan to ask the teenagers in their study to undergo scans to measure their bone density, muscle mass and fat tissue now that they’re entering puberty. “Obesity is an epidemic,” Grandjean told me. “And we can’t explain it by lack of physical activity or changing habits.”

Body composition can be easily measured, and abnormalities in or changes to it can hint at problems that are harder to see. In March, a 20-year study by researchers who are part of the N.I.H.’s Environmental Influences on Child Health (ECHO) consortium found that increased prenatal exposure to PFAS was associated with lower birth weight, a conclusion supported by rodent studies. That could be significant, as low birth weight (less than 5.5 pounds) is strongly linked in turn to infant mortality, developmental issues and chronic conditions later in life, like heart disease, cancer and diabetes. Cells are particularly vulnerable during development. In utero and in infancy, they divide more rapidly than they can repair themselves when damaged; the insult persists like a crack in the foundation of a building — a hidden weakness that, in certain situations, might prove catastrophic. Fenton says this phenomenon may explain why the offspring of mice exposed to PFAS are more likely to develop metabolic problems and liver damage in adulthood. “Something programs them for a lifetime of disease,” she told me. “It’s something that may take years to see. We don’t have it completely figured out yet.”

Of all the organs and systems PFAS can affect, the most complicated to assess is the brain. Neurological outcomes are tricky to define and test for in people — or to observe in animal proxies — and countless variables may play a role. “Are PFAS the cause of ADHD? Do they increase the risk of autism? There is plenty of evidence to say we should be concerned,” Alan Ducatman, a clinician and professor emeritus at the West Virginia University School of Public Health, told me. “There’s not enough evidence to say we know,” he added. “But we really do need to know.”

A major obstacle to gleaning that information, however, is the fact that there are thousands of varieties of PFAS. So far, human health data exists for a tiny fraction of them. Leaders in the industries still using the chemicals argue that each PFAS formulation should be considered separately — a health outcome linked to one type doesn’t necessarily apply to another. “All PFAS are not the same, and they should not all be regulated the same way,” the American Chemistry Council, a lobbying organization, wrote in March, responding to an E.P.A. draft proposal to limit six kinds of PFAS in drinking water. To consider them individually would be virtually impossible — which might well be the point.

In 2020, Linda Birnbaum and 15 other researchers published their scientific rationale for the regulatory management of PFAS as a chemical class in the journal Environmental Science and Technology Letters. “They are all problematic,” she says. “When they’re tested, they all do the same stuff.” Scott Belcher, an associate professor of biological sciences at North Carolina State University’s Center for Environmental and Health Effects of PFAS, concurs: “I have not seen a PFAS tested for toxicity that’s not toxic.”

At this point, you may be wondering how much PFAS is inside of you. A lab can tell you how much (of some types) is in your blood — if you can afford to pay hundreds of dollars out of pocket to be tested. But there is not much you can do with the results. In 2019, the Agency for Toxic Substances and Disease Registry, a branch of the C.D.C., published “an overview of the science and guidance for clinicians” on its website. The 21-page document, however, offers scant actionable advice. “For asymptomatic individuals exposed to PFAS,” it says, “insufficient evidence exists at this time to support deviations from established standards of medical care.” The agency recommends that physicians respond to patient queries using language like this: “It is possible that PFAS contributed to your health problems, but there is no way to know if PFAS exposure has caused your illness or made it worse.” For communities with contaminated water or other significant exposures, PFAS-REACH (Research, Education and Action for Community Health) has published more specific guidance that aims to “inform patient and clinician decision making” on its website.

There are, in fact, a few ways to remove PFAS from the body, though none of them are medically approved for that purpose. Donating blood or plasma is one way. (This passes the chemicals on to someone else.) Women also tend to have lower PFAS levels than men do because they eliminate PFAS during menstruation, childbirth and nursing. Dialysis removes certain PFAS, and at least one cholesterol-lowering medication appears to do so as well.

The state of the science of PFAS has thus left physicians with concrete reasons for concern but incomplete information about how to identify patients who may be most at risk or how to help them. The most urgent questions now, says Tracey Woodruff, an author of the ECHO birth-weight study who directs the program for reproductive health and the environment at the University of California, San Francisco, are: “How do we quantify health harms? And what’s the extent of these exposures that we should be addressing?”

Defining those parameters is especially tricky when it comes to immune function. Though the Faroe Islands studies showed that PFAS exposure reduced antibody production, they couldn’t prove that fewer antibodies led to more cases of tetanus or diphtheria — perhaps those children’s immune systems still worked just fine. In 2020, many researchers raised concerns that significant exposure to PFAS might make people more susceptible to the coronavirus and, later, less protected by vaccination. By year’s end, Grandjean, who is also a research professor at the University of Rhode Island (the Faroe Islands study is part of its Sources, Transport, Exposure and Effects of PFAS program), was co-author of a paper in PLoS One that linked exposure to a PFAS called PFBA with more severe Covid-19.

Obstetricians are among the doctors most in need of solutions, because PFAS cross the placenta and are excreted in breast milk. Babies are so much smaller than grown-ups that when they ingest the milk, their PFAS levels become several times that of their mother — probably the highest they will be in their lifetime. Suppose a woman discovers that she has been heavily exposed to the chemicals: Are there steps she can take to reduce the amount she passes on to her newborn? Or to strengthen her child’s resilience against PFAS-related harm? (Breastfeeding enhances immune function.) And what about young adults born before PFOS production ended in 2002, when average levels of the chemical were six times what they are now — should they be monitoring certain aspects of their health more closely?

“When I talk to families, I try to be real,” Elizabeth Friedman, a pediatrician and the medical director of environmental health at Children’s Mercy Kansas City, in Missouri, told me. “Are there risks associated with PFAS exposure? Yes, it looks like there are. If you breastfeed, will you expose your baby? Yes, you will. Do we know that that will cause harm? Will it be more or less beneficial if you feed them formula? What’s in your tap water?” (If the drinking water is contaminated, formula mixed with it will be, too.) Science still has not come up with a cost-benefit analysis that she can use in these conversations with parents. “People don’t get answers to their questions,” says Friedman, who is also a regional director of a national network of pediatric environmental-health experts. “But they feel heard.”

Among the groups most likely to be exposed to PFAS in their drinking water are those in low-income communities or who live near military or industrial sites. Subsistence fishing and hunting, which many rural and Indigenous people rely on, increases that risk. Until very recently, the responsibility for setting public drinking-water standards for PFAS has fallen to states, local governments and tribes. In March, the E.P.A.

determined that two kinds of PFAS — PFOS and PFOA — are “likely to be carcinogenic to humans” and proposed a goal of removing them almost entirely from public drinking water. (The suggested regulations also set thresholds for four other PFAS.) The agency has stated that if approved later this year, the rule “will prevent thousands of deaths and reduce tens of thousands of serious PFAS-attributable illnesses.” But complying with the standards will be expensive. In June, 3M and DuPont (along with its sibling companies Chermours and Corteva) agreed in federal court to pay a total of $10.3 billion and $1.19 billion, respectively, for testing and cleaning up public water supplies to U.S. cities and towns. (DuPont’s legal circumstances have been complicated by corporate restructuring beginning in 2015: Its PFAS entities are now split among the three businesses, with Chermours having absorbed Teflon and other chemicals operations.) None of the companies has admitted liability. 3M has pledged to stop the production and use of all PFAS by 2025. But though reducing PFAS in tap water will reduce it in people, what exists already will simply move somewhere else — into toxic waste sites, the soil, the ocean.

The problem of PFAS pollution goes beyond drinking water: The Faroe Islands demonstrate as much. PFAS is entering the environment — plants, animals and people — through many routes. In the United States, chemical manufacturing is regulated by the E.P.A. through the Toxic Substances Control Act. Under the law, companies seeking approval for new chemicals test their own products and report the results, but failure to do so is punishable by relatively small fines. In February, the European Chemicals Agency released a proposal recommending a sweeping ban on the production and use of PFAS in the European Union, including imported products. Absent that sort of broad government regulation, however, people have few options but to try to avoid exposure to PFAS on their own.

One afternoon this spring, Grandjean, Weihe and I sat around the kitchen table in Weihe’s clinic. He was heating up lemon sole for lunch that he had cooked the previous evening for a family gathering. Grandjean, who like Weihe is 73, was recounting a formative lesson he’d learned from one of his mentors, Irving Selikoff, a physician and researcher at Mount Sinai Hospital who died in 1992. In the 1950s, Selikoff was a founder of a medical practice in Paterson, N.J., and began treating workers from a nearby asbestos plant who, over time, developed startlingly high rates of lung cancer and mesothelioma. The studies he later conducted, and the attention he drew to prior research, helped lead to the regulation of asbestos.

Grandjean recounted what he characterized as one of Selikoff’s “famous dictums”: “When you look at your tables, don’t forget that the people behind them are real, though the tears have been wiped away.”

He ran his hand across his cheek. “He had seen them,” Grandjean went on. “He said to me, ‘You may not have seen the victims, but don’t forget.’”

It’s a lesson that Grandjean has had much cause to consider since, and one, sadly, that will probably continue to resonate. The proposed E.P.A. regulations only cover six PFAS variations, and new formulations are entering the market all the time. “There are literally thousands of PFAS structures being used. We’re discovering them every day in water,” Scott Belcher, the North Carolina State biologist, told me. “If we’re putting these chemicals out into the environment before we understand how they’re working, are we experimenting on humans? That’s kind of de facto what we’re doing.”

To mitigate the harms of PFAS, companies have begun making them so that the human body expels them much faster — within days as opposed to years. But that also makes them harder to detect. These variations still last indefinitely in the environment, and there is evidence that at least some of them may be just as harmful as their predecessors: Though people eliminate them more quickly, they may also be re-exposed more frequently, which many scientists fear will make the chemicals equally detrimental. And even brief exposures to toxins during development can have irreversible consequences. Either way, the rollout of new PFAS has many researchers and advocates anxious that we’ve missed an opportunity to examine and change the systems that allowed most people on Earth to consume substances that raise such serious health concerns.

“I really think even scientists who are not involved don’t fully appreciate that there is no chemical safety testing,” Belcher says. “There is this mythical ‘they,’ that ‘they’re’ taking care of this, and it must be safe because it’s out there. That’s a common misconception about how this works.”

Weihe wishes the Faroese were less sanguine about the chemicals’ having made it all the way to them. “I must say, I would like them to be more angry and more upset and more furious,” he told me. Perhaps as they, along with the rest of us, become data points on graphs that describe the harms that result from exposure, they will be. But studying if and how a ubiquitous substance causes chronic illness is by its nature a lifetime project: Those who take it on, and those whose suffering they document, are as likely as not to be gone before any final reckoning.

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