‘This Year Nearly Broke Me As A Scientist’ – US Researchers Reflect On How 2025’s Science Cuts Have Changed Their Lives

Many researchers are working to advocate for science in the public sphere. John McDonnell/AP Photo

BY CARRIE MCDONOUGH, BRIAN G. HEN NING, CARA POLAND, NATHANIEL M. TRAN, RACHAEL SIRIANI AND STEPHANIE J. NAWYN

From beginning to end, 2025 was a year of devastation for scientists in the United States.

January saw the abrupt suspension of key operations across the National Institutes of Health, not only disrupting clinical trials and other in-progress studies but stalling grant reviews and other activities necessary to conduct research. Around the same time, the Trump administration issued executive orders declaring there are only two sexes and ending DEI programs. The Trump administration also removed public data and analysis tools related to health disparties, climate change and environmental justice, among other databases.

February and March saw a steep undercutting of federal support for the infrastructure crucial to conducting research as well as the withholding of federal funding from several universities.

And over the course of the following months, billions of dollars of grants supporting research projects across disciplines, institutions and states were terminated. These include funding already spent on in-progress studies that have been forced to end before completion. Federal agencies, including NASA, the Environmental Protection Agency, the National Oceanic and Atmospheric Administration and the U.S. Agency for International Development have been downsized or dismantled altogether.

The Conversation asked researchers from a range of fields to share how the Trump administration’s science funding cuts have affected them. All describe the significant losses they and their communities have experienced. But many also voice their determination to continue doing work they believe is crucial to a healthier, safer and more fair society.

Pipeline of new scientists cut off

Carrie McDonough, Associate Professor of Chemistry, Carnegie Mellon University

People are exposed to thousands of synthetic chemicals every day, but the health risks those chemicals pose are poorly understood. I was a co-investigator on a US$1.5 million grant from the EPA to develop machine-learning techniques for rapid chemical safety assessment. My lab was two months into our project when it was terminated in May because it no longer aligned with agency priorities, despite the administration’s Make America Healthy Again report specifically highlighting using AI to rapidly assess childhood chemical exposures as a focus area.

Labs like mine are usually pipelines for early-career scientists to enter federal research labs, but the uncertain future of federal research agencies has disrupted this process. I’m seeing recent graduates lose federal jobs, and countless opportunities disappear. Students who would have been the next generation of scientists helping to shape environmental regulations to protect Americans have had their careers altered forever.

I’ve been splitting my time between research, teaching and advocating for academic freedom and the economic importance of science funding because I care deeply about the scientific and academic excellence of this country and its effects on the world. I owe it to my students and the next generation to make sure people know what’s at stake.

Fewer people trained to treat addiction

Cara Poland, Associate Professor of Obstetrics, Gynecology and Reproductive Biology, Michigan State University

I run a program that has trained 20,000 health care practitioners across the U.S. on how to effectively and compassionately treat addiction in their communities. Most doctors aren’t trained to treat addiction, leaving patients without lifesaving care and leading to preventable deaths.

This work is personal: My brother died from substance use disorder. Behind every statistic is a family like mine, hoping for care that could save their loved one’s life.

With our federal funding cut by 60%, my team and I are unable to continue developing our addiction medicine curriculum and enrolling medical schools and clinicians into our program.

Meanwhile, addiction-related deaths continue to rise as the U.S. health system loses its capacity to deliver effective treatment. These setbacks ripple through hospitals and communities, perpetuating treatment gaps and deepening the addiction crisis.

Communities left to brave extreme weather alone

Brian G. Henning, Professor of Philosophy and Environmental Studies and Sciences, Gonzaga University

In 2021, a heat dome settled over the Northwest, shattering temperature records and claiming lives. Since that devastating summer, my team and I have been working with the City of Spokane to prepare for the climate challenges ahead.

We and the city were awarded a $19.9 million grant from the EPA to support projects that reduce pollution, increase community climate resilience and build capacity to address environmental and climate justice challenges.

As our work was about to begin, the Trump administration rescinded our funding in May. As a result, the five public facilities that were set to serve as hubs for community members to gather during extreme weather will be less equipped to handle power failures. Around 300 low-income households will miss out on efficient HVAC system updates. And our local economy will lose the jobs and investments these projects would have generated.

Despite this setback, the work will continue. My team and I care about our neighbors, and we remain focused on helping our community become more resilient to extreme heat and wildfires. This includes pursuing new funding to support this work. It will be smaller, slower and with fewer resources than planned, but we are not deterred.

LGBTQ+ people made invisible

Nathaniel M. Tran, Assistant Professor of Health Policy and Administration, University of Illinois Chicago

This year nearly broke me as a scientist.

Shortly after coming into office, the Trump administration began targeting research projects focusing on LGBTQ+ health for early termination. I felt demoralized after receiving termination letters from the NIH for my own project examining access to preventive services and home-based care among LGBTQ+ older adults. The disruption of publicly funded research projects wastes millions of dollars from existing contracts.

Then, news broke that the Centers for Disease Control and Prevention would no longer process or make publicly available the LGBTQ+ demographic data that public health researchers like me rely on.

But instead of becoming demoralized, I grew emboldened: I will not be erased, and I will not let the LGBTQ+ community be erased. These setbacks renewed my commitment to advancing the public’s health, guided by rigorous science, collaboration and equity.

Pediatric brain cancer research squelched

Rachael Sirianni, Professor of Neurological Surgery, UMass Chan Medical School

My lab designs new cancer treatments. We are one of only a few groups in the nation focused on treating pediatric cancer that has spread across the brain and spinal cord. This research is being crushed by the broad, destabilizing impacts of federal cuts to the NIH.

Compared to last year, I am working with around 25% of our funding and less than 50% of our staff. We cannot finish our studies, publish results or pursue new ideas. We have lost technology in development. Students and colleagues are leaving as training opportunities and hope for the future of science dries up.

I’m faced with impossible questions about what to do next. Do I use my dwindling research funds to maintain personnel who took years to train? Keep equipment running? Bet it all on one final, risky study? There are simply no good choices remaining.

Inequality in science festers

Stephanie Nawyn, Associate Professor of Sociology, Michigan State University

Many people have asked me how the termination of my National Science Foundation grant to improve work cultures in university departments has affected me, but I believe that is the wrong question. Certainly it has meant the loss of publications, summer funding for faculty and graduate students, and opportunities to make working conditions at my and my colleagues’ institutions more equitable and inclusive.

But the greatest effects will come from the widespread terminations across science as a whole, including the elimination of NSF programs dedicated to improving gender equity in science and technology. These terminations are part of a broader dismantling of science and higher education that will have cascading negative effects lasting decades.

Infrastructure for knowledge production that took years to build cannot be rebuilt overnight.

READ ORIGINAL STORY HERE

What Is Uranium Enrichment And How Is It Used For Nuclear Bombs? A Scientist Explains

Uranium ore. RHJPhtotos/Shutterstock

BY KAITLIN COOK

DECRA FELLOW, DEPARTMENT OF

NUCLEAR PHYSICS AND ACCELERATOR

APPLICATIONS, AUSTRALIAN NATIONAL

UNIVERSITY

Late last week, Israel targeted three of Iran’s key nuclear facilities – Natanz, Isfahan and Fordow, killing several Iranian nuclear scientists. The facilities are heavily fortified and largely underground, and there are conflicting reports of how much damage has been done.

Natanz and Fordow are Iran’s uranium enrichment sites, and Isfahan provides the raw materials, so any damage to these sites would limit Iran’s ability to produce nuclear weapons.

But what exactly is uranium enrichment and why does it raise concerns?

To understand what it means to “enrich” uranium, you need to know a little about uranium isotopes and about splitting the atom in a nuclear fission reaction.

What is an isotope?

All matter is made of atoms, which in turn are made up of protons, neutrons and electrons. The number of protons is what gives atoms their chemical properties, setting apart the various chemical elements.

Atoms have equal numbers of protons and electrons. Uranium has 92 protons, for example, while carbon has six. However, the same element can have different numbers of neutrons, forming versions of the element called isotopes.

This hardly matters for chemical reactions, but their nuclear reactions can be wildly different.
The difference between uranium-238 and uranium-235

When we dig uranium out of the ground, 99.27% of it is uranium-238, which has 92 protons and 146 neutrons. Only 0.72% of it is uranium-235 with 92 protons and 143 neutrons (the remaining 0.01% are other isotopes).

For nuclear power reactors or weapons, we need to change the isotope proportions. That’s because of the two main uranium isotopes, only uranium-235 can support a fission chain reaction: one neutron causes an atom to fission, which produces energy and some more neutrons, causing more fission, and so on.

This chain reaction releases a tremendous amount of energy. In a nuclear weapon, the goal is to have this chain reaction occur in a fraction of a second, producing a nuclear explosion.

In a civilian nuclear power plant, the chain reaction is controlled. Nuclear power plants currently produce 9% of the world’s power. Another vital civilian use of nuclear reactions is for producing isotopes used in nuclear medicine for the diagnosis and treatment of various diseases.

What is uranium enrichment, then?

To “enrich” uranium means taking the naturally found element and increasing the proportion of uranium-235 while removing uranium-238.

There are a few ways to do this (including new inventions from Australia), but commercially, enrichment is currently done with a centrifuge. This is also the case in Iran’s facilities.

Centrifuges exploit the fact that uranium-238 is about 1% heavier than uranium-235. They take uranium (in gas form) and use rotors to spin it at 50,000 to 70,000 rotations per minute, with the outer walls of the centrifuges moving at 400 to 500 metres per second.

This works much like a salad spinner that throws water to the sides while the salad leaves stay in the centre. The heavier uranium-238 moves to the edges of the centrifuge, leaving the uranium-235 in the middle.

This is only so effective, so the spinning process is done over and over again, building up the percentage of the uranium-235.

Most civilian nuclear reactors use “low enriched uranium” that’s been enriched to between 3% and 5%. This means that 3–5% of the total uranium in the sample is now uranium-235. That’s enough to sustain a chain reaction and make electricity.

What level of enrichment do nuclear weapons need?

To get an explosive chain reaction, uranium-235 needs to be concentrated significantly more than the levels we use in nuclear reactors for making power or medicines.

Technically, a nuclear weapon can be made with as little as 20% uranium-235 (known as “highly enriched uranium”), but the more the uranium is enriched, the smaller and lighter the weapon can be. Countries with nuclear weapons tend to use about 90% enriched, “weapons-grade” uranium.

According to the International Atomic Energy Agency (IAEA), Iran has enriched large quantities of uranium to 60%. It’s actually easier to go from an enrichment of 60% to 90% than it is to get to that initial 60%. That’s because there’s less and less uranium-238 to get rid of.

This is why Iran is considered to be at extreme risk of producing nuclear weapons, and why centrifuge technology for enrichment is kept secret.

Ultimately, the exact same centrifuge technology that produces fuel for civilian reactors can be used to produce nuclear weapons.

Inspectors from the IAEA monitor nuclear facilities worldwide to ensure countries are abiding by the rules set out in the global nuclear non-proliferation treaty. While Iran maintains it’s only enriching uranium for “peaceful purposes”, late last week the IAEA board ruled Iran was in breach of its obligations under the treaty.

READ ORIGINAL STORY HERE

H-bomb Creator Richard Garwin Was A Giant In Science, Technology And Policy

President Barack Obama presents the Presidential Medal of Freedom to Richard Garwin at the White House on Nov. 22, 2016. AP Photo/Andrew Harnik

BY MATHEW BUNN

PROFESSOR OF THE PRACTICE OF

ENERGY, NATIONAL SECURITY

AND FOREIGN POLICY,

HARVARD KENNEDY SCHOOL

Richard Garwin, who died on May 13, 2025, at the age of 97, was sometimes called “the most influential scientist you’ve never heard of.” He got his Ph.D. in physics at 21 under Enrico Fermi – a Nobel Prize winner and friend of Einstein’s – who called Garwin “the only true genius” he’d ever met.

A polymath curious about almost everything, he was one of the few people elected to the National Academy of Sciences, the National Academy of Engineering and the National Academy of Medicine for pathbreaking contributions in all of those fields. He held 47 patents and published over 500 scientific papers. A giant trove of his papers and talks can be found in the Garwin Archive at the Federation of American Scientists.

Garwin was best known for having done the engineering design for the first-ever thermonuclear explosion, turning the Teller-Ulam idea of triggering a fusion reaction with radiation pressure into a working hydrogen bomb – one with roughly 700 times the power of the Hiroshima bomb. He did that over the summer when he was 23. Over the decades that followed, he contributed to countless other military advances, including inventing key technology that enabled reconnaissance satellites.

Arms control advocate

Yet Garwin was also a longtime advocate of nuclear arms control and ultimately of nuclear disarmament. Working on nuclear deterrence and arms control, now at the Harvard Kennedy School of Government, I got to know Garwin as a tireless and effective participant in dialogues with scientists and current or former officials in Russia, China, India and elsewhere, making the case for steps to limit nuclear weapons and reduce their dangers.

Garwin was an early participant in the Pugwash Conferences on Science and World Affairs, which won the Nobel Peace Prize in 1995 for its disarmament work. He was also a founding member, in 1980, of the National Academies’ Committee on International Security and Arms Control, where he continued discussing ideas for reducing nuclear dangers with foreign colleagues throughout his life.

The deep respect that top Russian and Chinese nuclear weapons scientists had for him was palpable – even though he was often blunt in telling them where he thought their arguments were wrong. Once, at a workshop in Beijing, after listening to the leader of China’s program to develop nuclear “breeder” reactors lay out his program, Garwin started his remarks by saying, “This is a poorly designed breeder program that will fail” – and then laying out why he thought that was the case.

Because nongovernment experts have a freedom to explore ideas that government negotiators lack, these kinds of dialogues played a key role in developing the concepts that led to nuclear arms control agreements and, I would argue, contributed to ending the Cold War. As an example, one committee team that included Garwin helped convince Chinese weapons scientists that their country had no more need for nuclear tests and should sign the Comprehensive Test Ban Treaty – which it did soon after the discussion.

Only weeks before his death, he and I and others participated in a Zoom meeting with Russian nuclear weapons experts discussing what initial steps should be taken if U.S.-Russian political relations improved enough for them to resume discussions of nuclear restraint and risk reduction.

Garwin’s mind seemed to be interested in everything at once – and he had a wry sense of humor that could enliven a dry meeting. When I was directing a National Academies study about dealing with the plutonium from dismantled nuclear weapons after the Cold War, he would send an email with a penetrating insight on some issue in the study, followed by an equally long query about the parking arrangements for the meeting.

We put him in charge of assessing all the especially strange options for dealing with the plutonium. Once, while diagramming on a chalkboard the option of diluting the plutonium in the ocean, he drew the ship that would be doing the work and then began drawing many smaller vessels. Someone asked him what those were, and he said: “Oh, those are the Greenpeace boats.”

Science, technology and policy

Garwin’s unbelievable energies focused on three broad areas: fundamental science, new technologies and advising the government.

In fundamental science, he made major contributions to the detection and study of gravitational waves, and he helped to discover what physicists call parity violation in the weak nuclear force – a discovery that was one of the building blocks for what is now the standard model of the fundamental forces of the universe.

In new technologies, beyond weapons and satellites, he played a key role in the invention of touch screens, magnetic resonance imaging, laser printers and the GPS technology that enables us all to get directions on our cellphones. He was a researcher at IBM from 1952 to 1993.

Garwin advised the government on panels ranging from the President’s Science Advisory Committee, to the JASON panel of high-level defense advisers, to leading the State Department’s Arms Control and Nonproliferation Advisory Board (now called the International Security Advisory Board). He made major contributions to thinking about problems ranging from antisubmarine warfare to missile defense. He was a pungent critic of the “Star Wars” missile defense program launched in the Reagan administration, pointing out the wide range of ways enemies could defeat it more cheaply. His range was remarkable: He was called on to offer ideas for capping the blowout of the Deepwater Horizon oil rig and on managing the COVID-19 pandemic.

His curiosity was not limited to important matters. Once, as I was sitting next to him waiting for a meeting to start, he told me that if you took a Superball – a small, extremely elastic rubber ball – and bounced it diagonally on the floor so that it bounced up onto the bottom of the table, it would bounce back onto the same spot on the floor and back into your hand. I said I didn’t believe it for a minute – surely it would keep bouncing forward until it got to the other side of the table. He gave me an explanation I didn’t fully understand, involving energy of forward motion being converted to torque, and then converted into energy of backward motion.

When I got home, I received an express package from him containing an article he’d written in the American Journal of Physics, titled “Kinematics of an Ultraelastic Rough Ball,” with pages of equations explaining how this worked. The first figure in the paper is a stick-figure drawing of bouncing such a ball, with a footnote: “This was first demonstrated to me by L. W. Alverez using a Wham-O Super Ball.” Luis Alverez was a Nobel Prize winner in physics.

An honored life

Garwin’s brilliance was obvious to all who encountered him and won him wide recognition. In addition to election to all three national academies, he was awarded the National Medal of Science in 2002 by President George W. Bush. In 2016, President Barack Obama awarded him the Presidential Medal of Freedom.

Amid all this activity, Garwin was a family man. His marriage to his beloved wife, Lois, lasted over 70 years, until her death in 2018. They have three children, five grandchildren and one great-grandchild.

The advances Garwin contributed to have enhanced our understanding of the universe and benefited millions of people around the world. And as dark as nuclear dangers may seem today, the world is further from the nuclear brink than it would have been if Richard Garwin had never been born.

READ ORIGINAL STORY HERE

Being Alone Has Its Benefits − A Psychologist Fips The Script On The ‘Loneliness Epidemic’

BY VIRGINIA THOMAS

ASSISTANT PROFESSOR OF

PSYCHOLOGY, MIDDLEBURY

Over the past few years, experts have been sounding the alarm over how much time Americans spend alone.

Statistics show that we’re choosing to be solitary for more of our waking hours than ever before, tucked away at home rather than mingling in public. Increasing numbers of us are dining alone and traveling solo, and rates of living alone have nearly doubled in the past 50 years.

These trends coincided with the surgeon general’s 2023 declaration of a loneliness epidemic, leading to recent claims that the U.S. is living in an “anti-social century.”

Loneliness and isolation are indeed social problems that warrant serious attention, especially since chronic states of loneliness are linked with poor outcomes such as depression and a shortened lifespan.

But there is another side to this story, one that deserves a closer look. For some people, the shift toward aloneness represents a desire for what researchers call “positive solitude,” a state that is associated with well-being, not loneliness.

As a psychologist, I’ve spent the past decade researching why people like to be alone – and spending a fair amount of time there myself – so I’m deeply familiar with the joys of solitude. My findings join a host of others that have documented a long list of benefits gained when we choose to spend time by ourselves, ranging from opportunities to recharge our batteries and experience personal growth to making time to connect with our emotions and our creativity.

So it makes sense to me why people live alone as soon as their financial circumstances allow, and when asked why they prefer to dine solo, people say simply, “I want more me time.”

It’s also why I’m not surprised that a 2024 national survey found that 56% of Americans considered alone time essential for their mental health. Or that Costco is now selling “solitude sheds” where for around US$2,000 you can buy yourself some peace and quiet.

It’s clear there is a desire, and a market, for solitude right now in American culture. But why does this side of the story often get lost amid the warnings about social isolation?

I suspect it has to do with a collective anxiety about being alone.

The stigma of solitude

This anxiety stems in large part from our culture’s deficit view of solitude. In this type of thinking, the desire to be alone is seen as unnatural and unhealthy, something to be pitied or feared rather than valued or encouraged.

This isn’t just my own observation. A study published in February 2025 found that U.S. news headlines are 10 times more likely to frame being alone negatively than positively. This type of bias shapes people’s beliefs, with studies showing that adults and children alike have clear judgments about when it is – and importantly when it is not – acceptable for their peers to be alone.

This makes sense given that American culture holds up extraversion as the ideal – indeed as the basis for what’s normal. The hallmarks of extraversion include being sociable and assertive, as well as expressing more positive emotions and seeking more stimulation than the opposite personality – the more reserved and risk-averse introverts. Even though not all Americans are extraverts, most of us have been conditioned to cultivate that trait, and those who do reap social and professional rewards. In this cultural milieu, preferring to be alone carries stigma.

But the desire for solitude is not pathological, and it’s not just for introverts. Nor does it automatically spell social isolation and a lonely life. In fact, the data doesn’t fully support current fears of a loneliness epidemic, something scholars and journalists have recently acknowledged.

In other words, although Americans are indeed spending more time alone than previous generations did, it’s not clear that we are actually getting lonelier. And despite our fears for the eldest members of our society, research shows that older adults are happier in solitude than the loneliness narrative would lead us to believe.

Social media disrupts our solitude

However, solitude’s benefits don’t automatically appear whenever we take a break from the social world. They arrive when we are truly alone – when we intentionally carve out the time and space to connect with ourselves – not when we are alone on our devices.

My research has found that solitude’s positive effects on well-being are far less likely to materialize if the majority of our alone time is spent staring at our screens, especially when we’re passively scrolling social media.

This is where I believe the collective anxiety is well placed, especially the focus on young adults who are increasingly forgoing face-to-face social interaction in favor of a virtual life – and who may face significant distress as a result.

Social media is by definition social. It’s in the name. We cannot be truly alone when we’re on it. What’s more, it’s not the type of nourishing “me time” I suspect many people are longing for.

True solitude turns attention inward. It’s a time to slow down and reflect. A time to do as we please, not to please anyone else. A time to be emotionally available to ourselves, rather than to others. When we spend our solitude in these ways, the benefits accrue: We feel rested and rejuvenated, we gain clarity and emotional balance, we feel freer and more connected to ourselves.

But if we’re addicted to being busy, it can be hard to slow down. If we’re used to looking at a screen, it can be scary to look inside. And if we don’t have the skills to validate being alone as a normal and healthy human need, then we waste our alone time feeling guilty, weird or selfish.

The importance of reframing solitude

Americans choosing to spend more time alone is indeed a challenge to the cultural script, and the stigmatization of solitude can be difficult to change. Nevertheless, a small but growing body of research indicates that it is possible, and effective, to reframe the way we think about solitude.

For example, viewing solitude as a beneficial experience rather than a lonely one has been shown to help alleviate negative feelings about being alone, even for the participants who were severely lonely. People who perceive their time alone as “full” rather than “empty” are more likely to experience their alone time as meaningful, using it for growth-oriented purposes such as self-reflection or spiritual connection.

Even something as simple as a linguistic shift – replacing “isolation” with “me time” – causes people to view their alone time more positively and likely affects how their friends and family view it as well.

It is true that if we don’t have a community of close relationships to return to after being alone, solitude can lead to social isolation. But it’s also true that too much social interaction is taxing, and such overload negatively affects the quality of our relationships. The country’s recent gravitational pull toward more alone time may partially reflect a desire for more balance in a life that is too busy, too scheduled and, yes, too social.

Just as connection with others is essential for our well-being, so is connection with ourselves.

READ ORIGINAL STORY HERE

Machine Learning Cracked The Protein-Folding Problem And Won The 2024 Nobel Prize In Chemistry

Demis Hassabis and John Jumper at Google DeepMind on Oct. 9, 2024, after being awarded the Nobel Prize in chemistry. AP Photo/Alastair Grant

BY MARC ZIMMER

PROFESSOR OF CHEMISTRY

CONNECTICUTT COLLEGE

The 2024 Nobel Prize in chemistry recognized Demis Hassabis, John Jumper and David Baker for using machine learning to tackle one of biology’s biggest challenges: predicting the 3D shape of proteins and designing them from scratch.

This year’s award stood out because it honored research that originated at a tech company: DeepMind, an AI research startup that was acquired by Google in 2014. Most previous chemistry Nobel Prizes have gone to researchers in academia. Many laureates went on to form startup companies to further expand and commercialize their groundbreaking work – for instance, CRISPR gene-editing technology and quantum dots – but the research, from start to end, wasn’t done in the commercial sphere.

Although the Nobel Prizes in physics and chemistry are awarded separately, there is a fascinating connection between the winning research in those fields in 2024. The physics award went to two computer scientists who laid the foundations for machine learning, while the chemistry laureates were rewarded for their use of machine learning to tackle one of biology’s biggest mysteries: how proteins fold.

The 2024 Nobel Prizes underscore both the importance of this kind of artificial intelligence and how science today often crosses traditional boundaries, blending different fields to achieve groundbreaking results.

The challenge of protein folding

Proteins are the molecular machines of life. They make up a significant portion of our bodies, including muscles, enzymes, hormones, blood, hair and cartilage.

Understanding proteins’ structures is essential because their shapes determine their functions. Back in 1972, Christian Anfinsen won the Nobel Prize in chemistry for showing that the sequence of a protein’s amino acid building blocks dictates the protein’s shape, which, in turn, influences its function. If a protein folds incorrectly, it may not work properly and could lead to diseases such as Alzheimer’s, cystic fibrosis or diabetes.

A protein’s overall shape depends on the tiny interactions, the attractions and repulsions, between all the atoms in the amino acids its made of. Some want to be together, some don’t. The protein twists and folds itself into a final shape based on many thousands of these chemical interactions.

For decades, one of biology’s greatest challenges was predicting a protein’s shape based solely on its amino acid sequence. Although researchers can now predict the shape, we still don’t understand how the proteins maneuver into their specific shapes and minimize the repulsions of all the interatomic interactions in a few microseconds.

To understand how proteins work and to prevent misfolding, scientists needed a way to predict the way proteins fold, but solving this puzzle was no easy task.

In 2003, University of Washington biochemist David Baker wrote Rosetta, a computer program for designing proteins. With it he showed it was possible to reverse the protein-folding problem by designing a protein shape and then predicting the amino acid sequence needed to create it.

It was a phenomenal jump forward, but the shape chosen for the calculation was simple, and the calculations were complex. A major paradigm shift was required to routinely design novel proteins with desired structures.

A new era of machine learning

Machine learning is a type of AI where computers learn to solve problems by analyzing vast amounts of data. It’s been used in various fields, from game-playing and speech recognition to autonomous vehicles and scientific research. The idea behind machine learning is to use hidden patterns in data to answer complex questions.

This approach made a huge leap in 2010 when Demis Hassabis co-founded DeepMind, a company aiming to combine neuroscience with AI to solve real-world problems.

Hassabis, a chess prodigy at age 4, quickly made headlines with AlphaZero, an AI that taught itself to play chess at a superhuman level. In 2017, AlphaZero thoroughly beat the world’s top computer chess program, Stockfish-8. The AI’s ability to learn from its own gameplay, rather than relying on preprogrammed strategies, marked a turning point in the AI world.

Soon after, DeepMind applied similar techniques to Go, an ancient board game known for its immense complexity. In 2016, its AI program AlphaGo defeated one of the world’s top players, Lee Sedol, in a widely watched match that stunned millions.

In 2016, Hassabis shifted DeepMind’s focus to a new challenge: the protein-folding problem. Under the leadership of John Jumper, a chemist with a background in protein science, the AlphaFold project began. The team used a large database of experimentally determined protein structures to train the AI, which allowed it to learn the principles of protein folding. The result was AlphaFold2, an AI that could predict the 3D structure of proteins from their amino acid sequences with remarkable accuracy.

This was a significant scientific breakthrough. AlphaFold has since predicted the structures of over 200 million proteins – essentially all the proteins that scientists have sequenced to date. This massive database of protein structures is now freely available, accelerating research in biology, medicine and drug development.

Designer proteins to fight disease

Understanding how proteins fold and function is crucial for designing new drugs. Enzymes, a type of protein, act as catalysts in biochemical reactions and can speed up or regulate these processes. To treat diseases such as cancer or diabetes, researchers often target specific enzymes involved in disease pathways. By predicting the shape of a protein, scientists can figure out where small molecules – potential drug candidates – might bind to it, which is the first step in designing new medicines.

In 2024, DeepMind launched AlphaFold3, an upgraded version of the AlphaFold program that not only predicts protein shapes but also identifies potential binding sites for small molecules. This advance makes it easier for researchers to design drugs that precisely target the right proteins.

Google bought Deepmind for reportedly around half a billion dollars in 2014. Google DeepMind has now started a new venture, Isomorphic Labs, to collaborate with pharmaceutical companies on real-world drug development using these AlphaFold3 predictions.

For his part, David Baker has continued to make significant contributions to protein science. His team at the University of Washington developed an AI-based method called “family-wide hallucination,” which they used to design entirely new proteins from scratch. Hallucinations are new patterns – in this case, proteins – that are plausible, meaning they are a good fit with patterns in the AI’s training data. These new proteins included a light-emitting enzyme, demonstrating that machine learning can help create novel synthetic proteins. These AI tools offer new ways to design functional enzymes and other proteins that never could have evolved naturally.

AI will enable research’s next chapter

The Nobel-worthy achievements of Hassabis, Jumper and Baker show that machine learning isn’t just a tool for computer scientists – it’s now an essential part of the future of biology and medicine.

By tackling one of the toughest problems in biology, the winners of the 2024 prize have opened up new possibilities in drug discovery, personalized medicine and even our understanding of the chemistry of life itself.

READ ORIGINAL STORY HERE

MicroRNA Is The Nobel-Winning Master Regulator Of The Genome – Researchers Are Learning To Treat Disease By Harnessing How It Controls Genes

BY ANDREA KASINSKI

ASSOCIATE PROFESSOR OF BIOLOGICAL

SCIENCES, PURDUE UNIVERSITY

When Victor Ambros and Gary Ruvkun discovered a new molecule they called microRNA in the 1980s, it was a fascinating diversion from what for decades had been called the central dogma of molecular biology.

Recognized with the 2024 Nobel Prize in physiology or medicine, Ambros and Ruvkun had identified a new kind of genetic material that transformed how researchers understood gene regulation.

Like DNA, RNA is a form of genetic material made from individual nucleotides linked into chains. According to the central dogma, genetic information flows in one direction: DNA is transcribed into RNA, and RNA is translated into proteins. But in one major deviation from the central dogma, some RNAs are never translated or coded into proteins.

MicroRNA is one type of these so-called noncoding RNAs. They’re short stretches of genetic material that, rather than coding for a specific protein themselves, control the RNAs that do code for proteins. In effect, microRNAs turn particular genes on and off.

I dedicated my scientific career to understanding how RNA works, in part because research on RNA has lagged behind other macromolecules like DNA and proteins. The Nobel Prize recognition of microRNA molecules marks both their importance in biology and their promise as potential treatments for various diseases, including cancer.

MicroRNAs and disease

Scientists regard microRNAs as master regulators of the genome due to their ability to bind to and alter the expression of many protein-coding RNAs. Indeed, a single microRNA can regulate anywhere from 10 to 100 protein-coding RNAs. Rather than translating DNA to proteins, they instead can bind to protein-coding RNAs to silence genes.

The reason microRNAs can regulate such a diverse pool of RNAs stems from their ability to bind to target RNAs they don’t perfectly match up with. This means a single microRNA can often regulate a pool of targets that are all involved in similar processes in the cell, leading to an enhanced response.

Because a single microRNA can regulate multiple genes, many microRNAs can contribute to disease when they become dysfunctional.

In 2002, researchers first identified the role dysfunctional microRNAs play in disease through patients with a type of blood and bone marrow cancer called chronic lymphocytic leukemia. This cancer results from the loss of two microRNAs normally involved in blocking tumor cell growth. Since then, scientists have identified over 2,000 microRNAs in people, many of which are altered in various diseases.

The field has developed a fairly solid understanding of how microRNA dysfunction contributes to disease. Changing one microRNA can change several other genes, resulting in a plethora of alterations that can collectively reshape the cell’s physiology. For example, over half of all cancers have significantly reduced activity in a microRNA called miR-34a. Because miR-34a regulates many genes involved in preventing the growth and migration of cancer cells, losing miR-34a can increase the risk of developing cancer.

Researchers are looking into using microRNAs as therapeutics for cancer, heart disease, neurodegenerative disease and others. While results in the laboratory have been promising, bringing microRNA treatments into the clinic has met multiple challenges. Many are related to inefficient delivery into target cells and poor stability, which limit their effectiveness.

Delivering microRNA to cells

One reason why delivering microRNA treatments into cells is difficult is because microRNA treatments need to be delivered specifically to diseased cells while avoiding healthy cells. Unlike mRNA COVID-19 vaccines that are taken up by scavenging immune cells whose job is to detect foreign materials, microRNA treatments need to fool the body into thinking they aren’t foreign in order to avoid immune attack and get to their intended cells.

Scientists are studying various ways to deliver microRNA treatments to their specific target cells. One method garnering a great deal of attention relies on directly linking the microRNA to a ligand, a kind of small molecule that binds to specific proteins on the surface of cells. Compared with healthy cells, diseased cells can have a disproportionate number of some surface proteins, or receptors. So, ligands can help microRNAs home specifically to diseased cells while avoiding healthy cells. The first ligand approved by the U.S. Food and Drug Administration to deliver small RNAs like microRNAs, N-acetylgalactosamine, or GalNAc, preferentially delivers RNAs to liver cells.

Identifying ligands that can deliver small RNAs to other cells requires finding receptors expressed at high enough levels on the surface of target cells. Typically, over one million copies per cell are needed in order to achieve sufficient delivery of the drug.

One ligand that stands out is folate, also referred to as vitamin B9, a small molecule critical during periods of rapid cell growth such as fetal development. Because some tumor cells have over one million folate receptors, this ligand provides sufficient opportunity to deliver enough of a therapeutic RNA to target different types of cancer. For example, my laboratory developed a new molecule called FolamiR-34a – folate linked to miR-34a – that reduced the size of breast and lung cancer tumors in mice.

Making microRNAs more stable

One of the other challenges with using small RNAs is their poor stability, which leads to their rapid degradation. As such, RNA-based treatments are generally short-lived in the body and require frequent doses to maintain a therapeutic effect.

To overcome this challenge, researchers are modifying small RNAs in various ways. While each RNA requires a specific modification pattern, successful changes can significantly increase their stability. This reduces the need for frequent dosing, subsequently decreasing treatment burden and cost.

For example, modified GalNAc-siRNAs, another form of small RNAs, reduces dosing from every few days to once every six months in nondividing cells. My team developed folate ligands linked to modified microRNAs for cancer treatment that reduced dosing from once every other day to once a week. For diseases like cancer where cells are rapidly dividing and quickly diluting the delivered microRNA, this increase in activity is a significant advancement in the field. We anticipate this accomplishment will facilitate further development of this folate-linked microRNA as a cancer treatment in the years to come.

Many labs are working to develop treatments based on the discoveries new Nobel laureates Ambros and Ruvkun made decades ago. While there’s still considerable work to be done to overcome the hurdles associated with microRNA treatments, it’s clear that RNA shows promise as a therapeutic for many diseases.

READ ORIGINAL STORY HERE

Racism And Discrimination Lead To Faster Aging Through Brain Network Changes, New Study Finds

Locus coeruleus highlighted in blue; region of precuneus highlighted in green. Negar Fani

AUTHORS:

NEGAR FANI

ASSOCIATE PROFESSOR OF PSYCHIATRY

AND NEUROSCIENCE, EMORY UNIVERSITY

NATHANIEL HARNETT

ASSOCIATE PROFESSOR OF PSYCHIATRY

HARVARD UNIVERSITY

Racism steals time from people’s lives – possibly because of the space it occupies in the mind. In a new study published in the journal JAMA Network Open, our team showed that the toll of racism on the brain was linked to advanced aging, observed on a cellular level.

Black women who were more frequently exposed to racism showed stronger connections in brain networks involved with rumination and vigilance. We found that this, in turn, was connected to accelerated biological aging.

We are neuroscientists who use a variety of approaches, including self-reported data and biological measurements like brain scans, to answer our questions about the effects of stressors on the brain and body. We also use this data to inform the development of interventions to help people cope with this stress.

Why it matters

Aging is a natural process. However, stress can speed up the biological clock, making people more vulnerable to aging-related diseases, from cardiovascular disease to diabetes and dementia.

Epidemiological studies consistently show that Black people experience these aging-related health problems at an earlier age than white people. New studies also show focal effects of aging on the brain, indicating disparities in brain aging between Black and white populations.

Race-related stressors, including racial discrimination, affect the rate at which people age on a biological level. These experiences activate the stress response system and have been linked to greater activity in brain regions that process incoming threats. However, until now, researchers in our field have not understood how brain changes linked to racism contribute to accelerated aging.

Racial discrimination is a ubiquitous stressor that often goes unnoticed. It might look like a doctor questioning a Black patient’s pain level and not prescribing pain medication, or a teacher calling a Black child a “thug.” It is a constant stressor faced by Black people starting at an early age.

Rumination – reliving and analyzing an event on a loop – and vigilance, meaning being watchful for future threats, are possible coping responses to these stressors. But rumination and vigilance take energy, and this increased energy expenditure has a biological cost.

In our study of Black women, we found that more frequent racial discrimination was linked to more connectivity between two key regions. One, called the locus coeruleus, is a deep brain region that activates the stress response, promoting arousal and vigilance. The other is the precuneus, a key node of a brain network that engages when we think about our experiences and internalize – or suppress – our emotions.

These brain changes, in turn, were linked to accelerated cellular aging measured by an epigenetic “clock.” Epigenetics refers to changes that happen to our DNA from the environment. Epigenetic clocks assess how the environment affects our aging at a molecular level.

Higher clock values indicate that someone’s biological age is greater than their chronological age. In other words, the space that racist experiences occupy in people’s minds has a cost, which can shorten the lifespan.

What still isn’t known

Although we saw links between racism, brain connectivity changes and accelerated aging, we did not measure coping responses like rumination and vigilance in real time, meaning as people were experiencing them.

We also do not know how other factors such as neighborhood disadvantage, gender and sexuality intersect to influence accelerated aging and related health disparities.

What’s next

Our next steps are to use real-time measurement of everyday racism along with physiological measurements and neuroimaging to take a deeper dive into these research questions.

We want to know how different types of racial discrimination and coping styles influence brain and body responses. Understanding these issues better can bring more attention to prevention, such as programs that target implicit bias in physicians and teachers. It can also inform interventions like neuromodulation, which involves the use of external or internal devices to stimulate or inhibit brain activity. Neuromodulation can be used as a therapy aid to reduce stress.

The Research Brief is a short take on interesting academic work.

READ ORIGINAL STORY HERE

Even Short Trips To Space Can Change An Astronaut’s Biology − A New Set Of Studies Offers The Most Comprehensive Look At Spaceflight Health Since NASA’s Twins Study

BY SUSAN BAILEY

PROFESSOR OF RADIATION CANCER,

BIOLOGY AND ONCOLOGY,

COLORADO STATE UNIVERSITY

Only about 600 people have ever traveled to space. The vast majority of astronauts over the past six decades have been middle-aged men on short-duration missions of fewer than 20 days.

Today, with private, commercial and multinational spaceflight providers and flyers entering the market, we are witnessing a new era of human spaceflight. Missions have ranged from minutes, hours and days to months.

As humanity looks ahead to returning to the Moon over the coming decade, space exploration missions will be much longer, with many more space travelers and even space tourists. This also means that a wider diversity of people will experience the extreme environment of space – more women and people of different ethnicities, ages and health status.

Since people respond differently to the unique stressors and exposures of space, researchers in space health, like me, seek to better understand the human health effects of spaceflight. With such information, we can figure out how to help astronauts stay healthy both while they’re in space and once they return to Earth.

As part of the historic NASA Twins Study, in 2019, my colleagues and I published groundbreaking research on how one year on board the International Space Station affects the human body.

I am a radiation cancer biologist in Colorado State University’s Department of Environmental and Radiological Health Sciences. I’ve spent the past few years continuing to build on that earlier research in a series of papers recently published across the portfolio of Nature journals.

These papers are part of the Space Omics and Medical Atlas package of manuscripts, data, protocols and repositories that represent the largest collection ever assembled for aerospace medicine and space biology. Over 100 institutions from 25 countries contributed to the coordinated release of a wide range of spaceflight data.

The NASA Twins Study

NASA’s Twins Study seized on a unique research opportunity.

NASA selected astronaut Scott Kelly for the agency’s first one-year mission, during which he spent a year on board the International Space Station from 2015 into 2016. Over the same time period, his identical twin brother, Mark Kelly, a former astronaut and current U.S. senator representing Arizona, remained on Earth.

My team and I examined blood samples collected from the twin in space and his genetically matched twin back on Earth before, during and after spaceflight. We found that Scott’s telomeres – the protective caps at the ends of chromosomes, much like the plastic tip that keeps a shoelace from fraying – lengthened, quite unexpectedly, during his year in space.

When Scott returned to Earth, however, his telomeres quickly shortened. Over the following months, his telomeres recovered but were still shorter after his journey than they had been before he went to space.

As you get older, your telomeres shorten because of a variety of factors, including stress. The length of your telomeres can serve as a biological indicator of your risk for developing age-related conditions such as dementia, cardiovascular disease and cancer.

In a separate study, my team studied a cohort of 10 astronauts on six-month missions on board the International Space Station. We also had a control group of age- and sex-matched participants who stayed on the ground.

We measured telomere length before, during and after spaceflight and again found that telomeres were longer during spaceflight and then shortened upon return to Earth. Overall, the astronauts had many more short telomeres after spaceflight than they had before.

One of the other Twins Study investigators, Christopher Mason, and I conducted another telomere study – this time with twin high-altitude mountain climbers – a somewhat similar extreme environment on Earth.

We found that while climbing Mount Everest, the climbers’ telomeres were longer, and after they descended, their telomeres shortened. Their twins who remained at low altitude didn’t experience the same changes in telomere length. These results indicate that it’s not the space station’s microgravity that led to the telomere length changes we observed in the astronauts – other culprits, such as increased radiation exposure, are more likely.

Civilians in space

In our latest study, we studied telomeres from the crew on board SpaceX’s 2021 Inspiration4 mission. This mission had the first all-civilian crew, whose ages spanned four decades. All of the crew members’ telomeres lengthened during the mission, and three of the four astronauts also exhibited telomere shortening once they were back on Earth.

What’s particularly interesting about these findings is that the Inspiration4 mission lasted only three days. So, not only do scientists now have consistent and reproducible data on telomeres’ response to spaceflight, but we also know it happens quickly. These results suggest that even short trips, like a weekend getaway to space, will be associated with changes in telomere length.

Scientists still don’t totally understand the health impacts of such changes in telomere length. We’ll need more research to figure out how both long and short telomeres might affect an astronaut’s long-term health.

Telomeric RNA

In another paper, we showed that the Inspiration4 crew – as well as Scott Kelly and the high-altitude mountain climbers – exhibited increased levels of telomeric RNA, termed TERRA.

Telomeres consist of lots of repetitive DNA sequences. These are transcribed into TERRA, which contributes to telomere structure and helps them do their job.

Together with laboratory studies, these findings tell us that telomeres are being damaged during spaceflight. While there is still a lot we don’t know, we do know that telomeres are especially sensitive to oxidative stress. So, the chronic oxidative damage that astronauts experience when exposed to space radiation around the clock likely contributes to the telomeric responses we observe.

We also wrote a review article with a more futuristic perspective of how better understanding telomeres and aging might begin to inform the ability of humans to not only survive long-duration space travel but also to thrive and even colonize other planets. Doing so would require humans to reproduce in space and future generations to grow up in space. We don’t know if that’s even possible – yet.

Plant telomeres in space

My colleagues and I contributed other work to the Space Omics and Medical Atlas package, as well, including a paper published in Nature Communications. The study team, led by Texas A&M biologist Dorothy Shippen and Ohio University biologist Sarah Wyatt, found that, unlike people, plants flown in space did not have longer telomeres during their time on board the International Space Station.

The plants did, however, ramp up their production of telomerase, the enzyme that helps maintain telomere length.

As anyone who’s seen “The Martian” knows, plants will play an essential role in long-term human survival in space. This finding suggests that plants are perhaps more naturally suited to withstand the stressors of space than humans.

READ ORIGINAL STORY HERE

A Young Black Scientist Discovered A Pivotal Leprosy Treatment In The 1920s − But An Older Colleague Took The Credit

Alice Augusta Ball

BY MARK M. LAMBERT

ASSISTANT PROFESSOR OF BEHAVIORAL

MEDICINE, MEDICAL HUMANITIES,

AND BIOETHICS, DES MOINES UNIVERSITY

Hansen’s disease, also called leprosy, is treatable today – and that’s partly thanks to a curious tree and the work of a pioneering young scientist in the 1920s. Centuries prior to her discovery, sufferers had no remedy for leprosy’s debilitating symptoms or its social stigma.

This young scientist, Alice Ball, laid fundamental groundwork for the first effective leprosy treatment globally. But her legacy still prompts conversations about the marginalization of women and people of color in science today.

As a bioethicist and historian of medicine, I’ve studied Ball’s contributions to medicine, and I’m pleased to see her receive increasing recognition for her work, especially on a disease that remains stigmatized.

Who was Alice Ball?

Alice Augusta Ball, born in Seattle, Washington, in 1892, became the first woman and first African American to earn a master’s degree in science from the College of Hawaii in 1915, after completing her studies in pharmaceutical chemistry the year prior.

After she finished her master’s degree, the college hired her as a research chemist and instructor, and she became the first African American with that title in the chemistry department.

Impressed by her master’s thesis on the chemistry of the kava plant, Dr. Harry Hollmann with the Leprosy Investigation Station of the U.S. Public Health Service in Hawaii recruited Ball. At the time, leprosy was a major public health issue in Hawaii.

Doctors now understand that leprosy, also called Hansen’s disease, is minimally contagious. But in 1865, the fear and stigma associated with leprosy led authorities in Hawaii to implement a mandatory segregation policy, which ultimately isolated those with the disease on a remote peninsula on the island of Molokai. In 1910, over 600 leprosy sufferers were living in Molokai.

This policy overwhelmingly affected Native Hawaiians, who accounted for over 90% of all those exiled to Molokai.

The significance of chaulmoogra oil

Doctors had attempted to use nearly every remedy imaginable to treat leprosy, even experimenting with dangerous substances such as arsenic and strychnine. But the lone consistently effective treatment was chaulmoogra oil.

Chaulmoogra oil is derived from the seeds of the chaulmoogra tree. Health practitioners in India and Burma had been using this oil for centuries as a treatment for various skin diseases. But there were limitations with the treatment, and it had only marginal effects on leprosy.

The oil is very thick and sticky, which makes it hard to rub into the skin. The drug is also notoriously bitter, and patients who ingested it would often start vomiting. Some physicians experimented with injections of the oil, but this produced painful pustules.

The Ball Method

If researchers could harness chaulmoogra’s curative potential without the nasty side effects, the tree’s seeds could revolutionize leprosy treatment. So, Hollmann turned to Ball. In a 1922 article, Hollmann documents how the 23-year-old Ball discovered how to chemically adapt chaulmoogra into an injection that had none of the side effects.

The Ball Method, as Hollmann called her discovery, transformed chaulmoogra oil into the most effective treatment for leprosy until the introduction of sulfones in the late 1940s.

In 1920, the Ball Method successfully treated 78 patients in Honolulu. A year later, it treated 94 more, with the Public Health Service noting that the morale of all the patients drastically improved. For the first time, there was hope for a cure.

Tragically, Ball did not have the opportunity to revel in this achievement, as she passed away within a year at only 24, likely from exposure to chlorine gas in the lab.

Ball’s legacy, lost and found

Ball’s death meant she didn’t have the opportunity to publish her research. Arthur Dean, chair of the College of Hawaii’s chemistry department, took over the project.

Dean mass-produced the treatment and published a series of articles on chaulmoogra oil. He renamed Ball’s method the “Dean Method,” and he never credited Ball for her work.

Ball’s other colleagues did attempt to protect Ball’s legacy. A 1920 article in the Journal of the American Medical Association praises the Ball Method, while Hollmann clearly credits Ball in his own 1922 article.

Ball is described at length in a 1922 article in volume 15, issue 5, of Current History, an academic publication on international affairs. That feature is excerpted in a June 1941 issue of Carter G. Woodson’s “Negro History Bulletin,” referring to Ball’s achievement and untimely death.

Joseph Dutton, a well-regarded religious volunteer at the leprosy settlements on Molokai, further referenced Ball’s work in a 1932 memoir broadly published for a popular audience.

Historians such as Paul Wermager later prompted a modern reckoning with Ball’s poor treatment by Dean and others, ensuring that Ball received proper credit for her work. Following Wermager’s and others’ work, the University of Hawaii honored Ball in 2000 with a bronze plaque, affixed to the last remaining chaulmoogra tree on campus.

In 2019, the London School of Hygiene and Tropical Medicine added Ball’s name to the outside of its building. Ball’s story was even featured in a 2020 short film, “The Ball Method.”

The Ball Method represents both a scientific achievement and a history of marginalization. A young woman of color pioneered a medical treatment for a highly stigmatizing disease that disproportionately affected an already disenfranchised Indigenous population.

In 2022, then-Gov. David Ige declared Feb. 28 Alice Augusta Ball Day in Hawaii. It was only fitting that the ceremony took place on the Mānoa campus in the shade of the chaulmoogra tree.

READ ORIGINAL STORY HERE

The Hidden Risk Of Letting AI Decide – Losing The Skills To Choose For Ourselves

BY JOE ARVAI

DANA AND DAVID DORNSIFE

PROFESSOR OF PSYCHOLOGY AND

DIRECTOR OF THE WRIGLEY INSTITUTE FOR

ENVIRONMENTAL AND SUSTAINABILITY,

USC DORNSIFE COLLEGE OF LETTERS,

ARTS AND SCIENCES

As artificial intelligence creeps further into people’s daily lives, so do worries about it. At the most alarmist are concerns about AI going rogue and terminating its human masters.

But behind the calls for a pause on the development of AI is a suite of more tangible social ills. Among them are the risks AI poses to people’s privacy and dignity and the inevitable fact that, because the algorithms under AI’s hood are programmed by humans, it is just as biased and discriminatory as many of us. Throw in the lack of transparency about how AI is designed, and by whom, and it’s easy to understand why so much time these days is devoted to debating its risks as much as its potential.

But my own research as a psychologist who studies how people make decisions leads me to believe that all these risks are overshadowed by an even more corrupting, though largely invisible, threat. That is, AI is mere keystrokes away from making people even less disciplined and skilled when it comes to thoughtful decisions.

Making thoughtful decisions

The process of making thoughtful decisions involves three common sense steps that begin with taking time to understand the task or problem you’re confronted with. Ask yourself, what is it that you need to know, and what do you need to do in order to make a decision that you’ll be able to credibly and confidently defend later?

The answers to these questions hinge on actively seeking out information that both fills gaps in your knowledge and challenges your prior beliefs and assumptions. In fact, it’s this counterfactual information – alternative possibilities that emerge when people unburden themselves of certain assumptions – that ultimately equips you to defend your decisions when they are criticized.

The second step is seeking out and considering more than one option at a time. Want to improve your quality of life? Whether it’s who you vote for, the jobs you accept or the things you buy, there’s always more than one road that will get you there. Expending the effort to actively consider and rate at least a few plausible options, and in a manner that is honest about the trade-offs you are willing to make across their pros and cons, is a hallmark of a thoughtful and defensible choice.

The third step is being willing to delay closure on a decision until after you’ve done all the necessary heavy mental lifting. It’s no secret: Closure feels good because it means you’ve put a difficult or important decision behind you. But the cost of moving on prematurely can be much higher than taking the time to do your homework. If you don’t believe me, just think about all those times you let your feelings guide you, only to experience regret because you didn’t take the time to think a little harder.

Dangers of outsourcing decisions to AI

None of these three steps are terribly difficult to take. But, for most, they’re not intuitive either. Making thoughtful and defensible decisions requires practice and self-discipline. And this is where the hidden harm that AI exposes people to comes in: AI does most of its “thinking” behind the scenes and presents users with answers that are stripped of context and deliberation. Worse, AI robs people of the opportunity to practice the process of making thoughtful and defensible decisions on their own.

Consider how people approach many important decisions today. Humans are well known for being prone to a wide range of biases because we tend to be frugal when it comes to expending mental energy. This frugality leads people to like it when seemingly good or trustworthy decisions are made for them. And we are social animals who tend to value the security and acceptance of their communities more than they might value their own autonomy.

Add AI to the mix and the result is a dangerous feedback loop: The data that AI is mining to fuel its algorithms is made up of people’s biased decisions that also reflect the pressure of conformity instead of the wisdom of critical reasoning. But because people like having decisions made for them, they tend to accept these bad decisions and move on to the next one. In the end, neither we nor AI end up the wiser.

Being thoughtful in the age of AI

It would be wrongheaded to argue that AI won’t offer any benefits to society. It most likely will, especially in fields like cybersecurity, health care and finance, where complex models and massive amounts of data need to be analyzed routinely and quickly. However, most of our day-to-day decisions don’t require this kind of analytic horsepower.

But whether we asked for it or not, many of us have already received advice from – and work performed by – AI in settings ranging from entertainment and travel to schoolwork, health care and finance. And designers are hard at work on next-generation AI that will be able to automate even more of our daily decisions. And this, in my view, is dangerous.

In a world where what and how people think is already under siege thanks to the algorithms of social media, we risk putting ourselves in an even more perilous position if we allow AI to reach a level of sophistication where it can make all kinds of decisions on our behalf. Indeed, we owe it to ourselves to resist the siren’s call of AI and take back ownership of the true privilege – and responsibility – of being human: being able to think and choose for ourselves. We’ll feel better and, importantly, be better if we do.