James' World 2

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CLIMATEWIRE | EPA finalized regulations Tuesday for a fee that oil and gas companies could begin paying on excess methane emissions next year — if Republicans don’t repeal it first.

The rule guides implementation of a levy created by the 2022 climate law and is the last important climate standard of the Biden administration. It was unveiled at an event on the sidelines of this year’s U.N. climate conference in Baku, Azerbaijan, shortly before a U.S.-China methane summit.

EPA Administrator Michael Regan, who did not attend the global meeting, said in a statement that the rule is “the latest in a series of actions under President Biden’s methane strategy to improve efficiency in the oil and gas sector, support American jobs, protect clean air, and reinforce U.S. leadership on the global stage.”

EPA estimated that the levy would keep 1.2 million metric tons of methane out of the atmosphere through 2035 and deliver “up to $2 billion” in climate benefits.

Companies will begin paying the levy next year for excess emissions released in 2024. Oil and gas operators will pay $900 for each metric ton of methane that’s above a threshold enshrined in the Inflation Reduction Act. The fee, called the waste emissions charge, will climb to $1,500 a ton for 2026 and beyond. The levy reinforces EPA’s Clean Air Act rules for methane by ensuring that if operators aren’t covered by those standards — or don’t comply with them — they would pay the fee.

But President-elect Donald Trump’s victory last week throws doubt on the future of President Joe Biden’s methane policies — particularly the methane fee. Trump could direct former Rep. Lee Zeldin, a New York Republican whom Trump announced as his future EPA administrator Monday, to pare back elements of those policies or scrap them. Zeldin faces Senate confirmation.

The Biden EPA has rolled out important methane rules at each of the last three U.N. climate summits. The administration has also built its climate diplomacy around the need to curb methane — a superpollutant that’s 80 times more powerful than carbon dioxide at raising temperatures over a 20-year time horizon.

The U.S. joined the European Union in 2021 to launch the Global Methane Pledge, which has resulted in more than 150 countries promising to work together to reduce global methane at least 30 percent by 2030. The U.S. summit with China on Tuesday marks the second time the biggest two polluters are meeting to curb the potent gas.

But under Trump, EPA could quickly begin the process of pulling back and replacing Biden-era methane rules with laxer standards — including those that drive implementation of the methane fee. Because the rule is being finalized so late in Biden’s term, Republican lawmakers could invalidate it through a Congressional Review Act resolution.

But experts say those moves wouldn’t absolve Trump’s EPA from having to implement the fee.

“The law is still the law,” said one industry advocate who was granted anonymity to talk about future policies.

A CRA resolution would allow the Trump administration to craft a more industry-friendly methane fee. It could, for instance, make it easier for oil and gas operators to claim fee exemptions offered under the Inflation Reduction Act. Trump could also let operators delay paying the fee until their annual greenhouse gas reports are finalized late in the year. The Trump EPA could also allow corporations to net emissions across all assets, removing restrictions on how cleaner facilities may compensate for dirtier ones to mitigate fees.

If Trump and congressional Republicans wish to kill the methane fee, they would have to enact legislation to repeal it. Democrats and Biden moved the IRA through the annual budget process, and the GOP could potentially use the same maneuver to undo parts of it. Trade groups like the American Petroleum Institute and Independent Petroleum Association of America oppose the fee.

Rosalie Winn, an attorney with the Environmental Defense Fund, said legislation to scrap the fee “would be directly contrary to the interests of the American people.”

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As we age, the mind tends to wander forward in time, considering myriad hypotheticals of increasingly philosophical tone: Will we live a long life? And if we do, will it be a life well lived? What does living well mean, exactly?

For some, living well suggests contentment and happiness. But it is also a potential prescription against atypical brain aging and diseases like dementia.

In a 2023 paper published in Nature Aging, researchers find that managing negative emotions could protect the brain from harm in old age.

The finding came as part of the effort to understand why negative emotions, such as persistent stress and anxiety, are seemingly risk factors for neurodegenerative conditions like dementia — and what can be done to stop this outcome.

“The health of the elderly is an increasingly important public health issue with the aging of the population,” co-author Patrik Vuilleumier, a neurologist and professor at the University of Geneva, explains to Inverse. “It is important not only to live long but, even more so, to live in good physical and mental health.”

Most research so far on aging and the brain has focused on cognitive functions, says Vuilleumier, like memory, attention, and motor skills. Emotions, meanwhile, “have been relatively neglected,” he says.

Yet we know emotions influence physical and psychological health. Still, scientists aren’t quite sure how the brain switches from one emotion to another or if emotions and their effects on our body change as we age — including what the consequences of not managing negative emotions might be on our long-term health.

The effect of emotions on the brain

In an effort to answer these questions, Vuilleumier and his colleagues evaluated whether the brains of older people (over 65 years old) react to negative emotions in similar ways to those of younger people (about 25 years old). They studied participants’ ability to regulate their emotions after seeing video clips showing people in a state of emotional suffering. During the experiment, the scientists measured the participants’ brain activity using functional magnetic resonance imaging (fMRI).

The results suggest older people’s brains are more likely to show emotional inertia, which means the degree to which one’s emotional state is resistant to change. In an earlier study, the same team found that negative emotions activate certain brain regions and the brain can remain altered long after those emotions are triggered. The duration depends on the regulation capacities of each individual, Vuilleumier explains.

“We uncovered that, in general, negative emotions can trigger changes in the communication between different brain regions and these changes were found to persist longer in older subjects,” he says.

This was especially obvious when examining the connections between the amygdala and the posterior singular cortex, which are both parts of the brain that help regulate emotion and encode memories.

Changes in brain connectivity were even more pronounced in older adults, who also reported experiencing more anxiety, rumination, and negative emotions. It’s possible that these conditions may amp up the emotional inertia seen in the study.

Emotional inertia and disease

As of March 2023, the team was still analyzing the results to see if prolonged emotional inertia actually represents an increased risk for degenerative diseases like dementia. The plan is to follow the participants over several years and see what changes. Some observational studies do suggest that poor emotion regulation is linked to frequent age-related neurodegenerative conditions, though.

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This advice certainly comes from a good place. But it’s also fundamentally wrong.

This is not to say that tetanus isn’t as bad as parents promise. In North America, the Cleveland Clinic estimates, 10 percent of cases are fatal. In countries with inadequate or inaccessible medical care, the number is believed to be much higher.

Even survival takes its toll. On Friday, the U.S. Centers for Disease Control and Prevention released a new installment in its “Notes from the Field” series about an unvaccinated 6-year-old boy in Oregon who contracted tetanus after he got a cut in his forehead. The bacteria incubated inside his little body for a few days, then suddenly manifested in horrible jaw clenching and muscle spasms, heart rate, blood pressure, and body temperature irregularities. He lived, but only after 57 days in the hospital and more than $800,000 in medical bills.

But counter to what rusty nail warnings might have you believe, the disease has nothing to do with iron oxide, the chemical compound more commonly known as rust. Rather, tetanus is a product of the bacteria Clostridium tetani, which is in dirt, dust, and feces—in other words, everywhere. It can enter your body through puncture wounds, yes, but also through superficial cuts, bug bites, surgical procedures, and any other rupture to your skin. It can come from stepping on a rusty nail, or tending the soil in your garden. That’s why it’s so essential to track your booster shots: You need one every decade, not just when you rip your palm open on a rusty chain link fence. Waiting for a classic tetanus injury won’t work when anything could, in theory, be a tetanus injury.

If the bacteria enter your body and you aren’t up-to-date on your vaccinations, the tiny invaders begin to multiply rapidly. This incubation period, which lasts between three and 21 days, according to the CDC, is symptom free. But as the bacteria begin to die inside you, they form a neurotoxin that attacks the nervous system. Specifically, it inhibits the chemical GABA, which regulates muscle contractions. The result is a body-wide state of tension, from lockjaw in your face to uncontrollable arching spasms in your back to permanently-curled toes.

How rusty nails came to be so closely associated with tetanus isn’t clear. Iron oxide is basically harmless to the human body; millions of people drink water transported by rusty iron pipes with no health effects. (Bridges aren’t so lucky—rusting has buckled many an iron span.) Perhaps it’s some classic American folklore. Or, as Esther Inglis-Arkell argued on the site i09, it has something to do with the anaerobic environment in which the tetanus-causing Clostridium tetani bacteria thrives. As iron oxidizes, it eats up atmospheric oxygen, creating a low-oxygen environment for the bacteria to grow. While rust doesn’t cause tetanus, the two may have a symbiotic (and symbolic) relationship.

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Rusty nails aren’t the only threat. Photo from Deposit Photos.

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Scientists are still learning about the causes of Alzheimer’s, but most agree that many factors contribute to an individual’s risk of getting the disease. Some risk factors, such as age and genes, are inescapable. Others can be modified with lifestyle changes, such as exercise and nutrition—in one study, participants were able to reduce their risk of getting Alzheimer’s by 60 percent. Although most risk studies focus on dementia in general, here are important findings about the known risk factors as they apply to Alzheimer’s.

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Joelle Bolt

Katie Peek and Joelle Bolt; Sources: Risk factor relative importance: G. Livingston et al., The Lancet, 396, 413 (2020); normal brain aging: “Alzheimer’s Disease and Other Dementias,” Mayo Clinic, 2020

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As someone who has spent most of his professional life studying how children develop, I’m often asked by parents (especially mums) why children (especially boys) are prone to pick up the nearest stick, pencil, soft toy or even banana and turn them into weapons?

Girls certainly do this too. But research – and parents’ experience – shows you’re more likely to find boys using various objects as swords, guns or grenades to attack one another.

While some parents worry this is too violent, these actions do not mean you are raising a burgeoning psychopath. Rather, they are significant components of healthy development.

Playful aggression

Role playing is a key part of children’s play, when they pretend to be someone or something else. They can do this on their own or with others.

When they do it with others it is called “sociodramatic play”. This type of play teaches children both verbal and social skills while they interact with others.

Play fighting is one form of sociodramatic play. It can include rough and tumble play, chasing one another around, superhero play, wrestling and mock fighting. Psychologists call this “playful aggression”.

This kind of play is not about hurting anybody. Rather, it provides opportunities for children to explore their world with a sense of empowerment and control (because they set the rules) and to build relationships as they negotiate the play.

How does it work?

Imagine children are playing a battle with pillow forts and cardboard swords. This is not just a question of whose fort topples first. The game will require them to read facial expressions, express themselves and develop an awareness of power dynamics (or what researchers call “relationships hierarchies”).

Relationship hierarchies are complex, but focus on power and who is in charge. During episodes of playful aggression, this might mean taking control, giving in to someone else’s idea, or sharing power. These hierarchies allow children to make decisions about who they want to play with, who to avoid, or how to adapt their behavior to create friendships.

So relationship hierarchies play an important role in emotional and social development. They teach children how to get along with one another, how to make and play within a rule structure, and how to recognize the difference between playful and harmful behavior.

For example, other children’s reactions during the game will teach them that yelling and jumping may be considered fun. But rough pushing or deliberately breaking rules – such as turning into a killer dragon when everyone else has agreed to be tigers – is not OK and will make your friends unhappy.

Why do we see this more in boys?

You might be wondering why such behaviors seem to be more evident in boys than girls. Research shows boys (on the whole) tend to be more physical in how they play.

Their play often focuses on themes related to power and dominance and playful aggression is the perfect way to experiment with these themes.

Theories about sex differences in social play extend across many research areas including psychology, neurobiology, evolutionary psychology and anthropology. Current theories link these differences to testosterone and differences in neurochemistry.

There is some evidence to suggest boys and girls are socialized differently in relation to being physical.

However, the degree of influence is contestable, given sex differences in behavior appear very early in life and in other mammals. Perhaps the socialization process exacerbates nature – and as such, nature and nurture may be working in tandem.

The end result is still the same, with more boys than girls engaging in playful aggression.

When girls role play, it tends to focus on what researchers call “tend and befriend” or on people and nurturing. For example, games built around families or looking after pets.

But this is not to say girls can’t be aggressive. However, research suggests if girls fight, it is usually done with words to hurt someone’s feelings and children are upset with each other. It is not done for fun.

Perhaps this is why playful aggression can be difficult for some mothers to understand and appreciate.

But there is no link between playful aggression in children and being aggressive as an adult.

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While there are plenty of things that teenagers worry about, dementia isn’t normally one of them. Yet one new major Alzheimer’s drug trial is recruiting people as young as 18 to answer what may be the most pressing question facing the field: Can the ravages of the disease be prevented by identifying those on track to get it and treating them up to 10 years before they show symptoms?

The recent arrival of drugs that slow the cognitive decline of Alzheimer’s in many people is a welcome breakthrough, but so far their efficacy has only been demonstrated in people with mild symptoms. By the time patients are diagnosed, their brains have already undergone extensive changes. But growing evidence suggests that taking the drugs well before that damage has occurred could significantly slow the disease and possibly even stop it in its tracks.

“Now we have drugs that can slow the disease by 30 percent or so in people with symptoms, but that’s not good enough,” says Reisa Sperling, a neurologist who heads the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital in Boston. “We want to get to 100 percent, and that means preventing people from getting to the symptomatic stages.”

Earlier and earlier

In medicine, treating a disease when it is causing pathological changes in the body, but hasn’t yet progressed far enough to cause clinical symptoms, is known as secondary prevention. (Primary prevention is heading off a disease before there is any pathology, and tertiary prevention is managing symptomatic disease to slow the worsening of symptoms.) Secondary prevention has been essential to medicine’s triumphs in reducing the risks of death and disability for those with early heart disease or diabetes. Doctors don’t wait for someone to have a heart attack before prescribing a cholesterol-lowering statin or for someone to suffer artery or kidney damage before putting them on metformin to control blood sugar.

In 2023, the results of trials of lecanemab (brand name Leqembi) and donanemab on Alzheimer’s patients with mild cognitive impairment suggested that medicine may now have the tools to bring secondary prevention to bear on the disease. Both drugs are monoclonal antibodies that target the hardened clumps of protein called amyloid plaque that form in the brains of Alzheimer’s patients.

Although much is still unknown about the mechanisms of Alzheimer’s, there is little question now that the buildup of plaque precedes symptoms by many years. In the lecanemab and donanemab trials, the earlier patients were along the long road to plaque buildup, the better the drugs did in removing most of the plaque and slowing cognitive decline. “It’s when you remove nearly all the plaque with one of these drugs that you see the real benefits in terms of symptoms,” says Randall Bateman, a physician and professor of neurology at Washington University School of Medicine.

Because patients with even mild symptoms already have a large buildup of plaque, testing the notion that plaque-fighting drugs can be more effective earlier in the buildup process means enlisting presymptomatic patients for trials. “Studies are moving toward people who are just at the borderline for being positive for plaque and treating them to try to keep them from accumulating more of it and from having symptoms,” says Susan Abushakra, a physician and researcher who is vice president of clinical development and medical affairs at Alzheimer’s-focused biotech company Alzheon in Framingham, Mass.

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It would be hard to imagine any one person who’s had more of an impact on public health than Bill Gates. Much of the wealth he amassed as founder of Microsoft has gone to charity—according to Fortune, he is one of only five billionaires to have given away more than 20 percent of his wealth. In 2023, the Bill and Melinda Gates Foundation, which he started with his former wife, Melinda Gates, spent more than $8 billion of its more than $70-billion endowment. 

Gates has focused his philanthropy largely on some of the most intractable health problems, such as malaria, HIV/AIDS, and childhood vaccination. In recent years, he has turned to Alzheimer’s disease, starting with diagnostics and more recently expanding to proteomics and healthcare programs related to the disease. Scientific American Custom Media asked him about Alzheimer’s:

SCIENTIFIC AMERICAN CUSTOM MEDIA:
What sparked your interest in Alzheimer’s? How has your personal experience with the disease contributed to your decision to get involved?

Gates: Like many people, I have a personal connection to Alzheimer’s. My dad died from Alzheimer’s, so I understand first-hand what a cruel disease it is, and how difficult it can be to watch a loved one suffer with it. We were fortunate to have the resources to provide my dad with excellent care, and our family is grateful for the wonderful caregivers who helped him in the 13 years he lived with the disease. But for the majority of families battling Alzheimer’s, this is not an option. Caregiving most often falls to a spouse or a child, which can be overwhelming.

The financial burden of the disease is easier to quantify than the emotional cost. The lifetime cost of care for Alzheimer’s and other dementias is rapidly increasing in the U.S., Japan, Europe, and other countries. According to the Institute for Health Metrics and Evaluation, the global cost will exceed $1.6 trillion by 2050 and represent nearly one-third of all healthcare spending. Unlike those with many chronic diseases, people with Alzheimer’s incur long-term care costs as well as direct medical expenses. If you get the disease in your 60s or 70s, you might require expensive care for decades. 

As I spent time learning about Alzheimer’s and the research into it, I came to understand the challenges. The brain can’t be sampled easily or often, for example, and the blood-brain barrier is a double-edged sword—it both protects the brain and makes it harder for treatments to get in.

Even so, as I learned about all the innovation in this field, I grew optimistic about the ability to make progress toward treatment and eventually a cure. This is a frontier where we can dramatically improve human life. It’s a miracle that people are living so much longer today, but longer life expectancies alone are not enough. People should be able to enjoy their later years—and we need a breakthrough in Alzheimer’s to fulfill that. 

As someone who takes a bird’s- eye view of major health issues, how would you describe the current outlook for Alzheimer’s research and clinical practice? 

After decades of negative clinical trials and dozens of failed therapies, researchers are making progress on both diagnostics and therapeutics. 

Blood-based diagnostics are advancing rapidly—the first blood test for Alzheimer’s, PrecivityAD, was launched in late 2020. A few others have followed since, but we are looking forward to the first FDA-cleared blood tests on the horizon. Once this becomes a reality, the next hurdle will be ensuring these tests are used properly, accessible, and available to the patients that need them, and that we understand how these tests work in different patient populations.

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Tony Healey

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