Category: Academic Reportage

Source: The Conversation – USA (2) – By Tevis Garrett Graddy-Lovelace, Provost Associate Professor of Environment, Development and Health, American University School of International Service

The U.S. government has caused massive food waste during President Donald Trump’s second term. Policies such as immigration raids, tariff changes and temporary and permanent cuts to food assistance programs have left farmers short of workers and money, food rotting in fields and warehouses, and millions of Americans hungry. And that doesn’t even include the administration’s actual destruction of edible food.

The U.S. government estimates that more than 47 million people in America don’t have enough food to eat – even with federal and state governments spending hundreds of billions of dollars a year on programs to help them.

Yet, huge amounts of food – on average in the U.S., as much as 40% of it – rots before being eaten. That amount is equivalent to 120 billion meals a year: more than twice as many meals as would be needed to feed those 47 million hungry Americans three times a day for an entire year.

This colossal waste has enormous economic costs and renders useless all the water and resources used to grow the food. In addition, as it rots, the wasted food emits in the U.S. alone over 4 million metric tons of methane – a heat-trapping greenhouse gas.

As a scholar of wasted food, I have watched this problem worsen since Trump began his second term in January 2025. Despite this administration’s claim of streamlining the government to make its operations more efficient, a range of recent federal policies have, in fact, exacerbated food wastage.

Immigration policy

Supplying fresh foods, such as fruits, vegetables and dairy, requires skilled workers on tight timelines to ensure ripeness, freshness and high quality.

The Trump administration’s widespread efforts to arrest and deport immigrants have sent Immigration and Customs Enforcement, the Border Patrol and other agencies into hundreds of agricultural fields, meat processing plants and food production and distribution sites. Supported by billions of taxpayer dollars, they have arrested thousands of food workers and farmworkers – with lethal consequences at times.

Dozens of raids have not only violated immigrants’ human rights and torn families apart: They have jeopardized the national food supply. Farmworkers already work physically hard jobs for low wages. In legitimate fear for their lives and liberty, reports indicate that in some places 70% of people harvesting, processing and distributing food stopped showing up to work by mid-2025.

News reports have identified many instances where crops have been left to rot in abandoned fields. Even the U.S. Department of Labor declared in October 2025 that aggressive farm raids drive farmworkers into hiding, leave substantial amounts of food unharvested and thus pose a “risk of supply shock-induced food shortages.”

Foreign aid cuts

When the Trump administration all but shut down the U.S. Agency for International Development in early 2025, the agency had 500 tons of ready-to-eat, high-energy biscuits worth US$800,000, stored to distribute to starving people around the world who had been displaced by violence or natural disasters. With no staff to distribute the biscuits, they expired while sitting in a warehouse in Dubai.

Incinerating the out-of-date biscuits reportedly cost an additional $125,000.

An additional 70,000 tons of USAID food aid may also have been destroyed.

Tariffs

In the late 20th century, as globalized trade patterns grew, U.S. farmers struggled with agricultural prices below their production costs. Yet tariffs in the first Trump administration did not protect small farms.

And the tariffs imposed in early 2025, after Trump regained the White House, severed U.S. soybean trade with China for months. Meanwhile, there’s nowhere to store the mountains of soybeans. An October 2025 agreement may resume some activity, but at lower price levels and a slower pace than before, as China looks to Brazil and Argentina to meet its vast demand.

Though the soybeans were intended to feed the Chinese pig industry, not humans, the specter of waste looms both in terms of the potential spoilage of soybeans and the actual human food that could have been grown in their place.

Other efforts lead to more waste

Since taking office, the second Trump administration has taken many steps aimed at efficiency that actually boosted food waste. Mass firings of food safety personnel risks even more outbreaks of foodborne diseases, tainted imports, and agricultural pathogens – which can erupt into crises requiring mass destruction, for instance, of nearly 35,000 turkeys with bird flu in Utah.

In addition, the administration canceled a popular program that helped schools and food banks buy food from local farmers, though many of the crops had already been planted when the cancellation announcement was made. That food had to find new buyers or risk being wasted, too. And the farmers were unable to count on a key revenue source to keep their farms afloat.

Also, the administration slashed funding for the Federal Emergency Management Agency that helped food producers, restaurants and households recover from disasters – including restoring power to food-storage refrigeration.

The fall 2025 government shutdown left the government’s major food aid program, SNAP, in limbo for weeks, derailing communities’ ability to meet their basic needs. Grocers, who benefit substantially from SNAP funds, announced discounts for SNAP recipients – to help them afford food and to keep food supplies moving before they rotted. The Department of Agriculture ordered them not to, saying SNAP customers must pay the same prices as other customers.

Food waste did not start with the Trump administration. But the administration’s policies – though they claim to be seeking efficiency – have compounded voluminous waste at a time of growing need. This Thanksgiving, think about wasted food – as a problem, and as a symptom of larger problems.

American University School of International Service master’s student Laurel Levin contributed to the writing of this article.

Garrett Graddy-Lovelace received funding from the NSF Multiscale RECIPES for Sustainable Food Systems project.

– ref. As US hunger rises, Trump administration’s ‘efficiency’ goals cause massive food waste – https://theconversation.com/as-us-hunger-rises-trump-administrations-efficiency-goals-cause-massive-food-waste-270027

Source: The Conversation – USA (2) – By Stephen Siff, Associate Professor of Journalism, Miami University

As the Detroit Lions barrel toward a Thanksgiving Day game with the Green Bay Packers, some die-hard fans may be fantasizing about what it would be like to be on the field themselves: calling plays from the Lions huddle, accepting the snap from between a crouching center’s thighs, and spinning to hand off the football before the defensive linemen come crashing down.

In 1963, Lions head coach George Wilson allowed writer and Paris Review editor George Plimpton to enact that fantasy.

With a Sports Illustrated contract in hand, Plimpton convinced Lions management to allow him to enter preseason training camp at Cranbrook, the private boys school in Bloomfield Hills, Michigan. His plan was to go undercover as a rookie quarterback for a magazine article that would reach dramatic culmination when he called a series of plays in a game of professional football.

No one expected the amateur athlete to survive for long on a field with real-life Lions. But in writing about the experience, Plimpton turned off-field fandom and on-field bumbling into literary gold.

His resulting 1966 book, “Paper Lion: Confessions of a Last-String Quarterback,” became a bestseller that was praised by The New York Times as “one of the greatest books written on sports, and the most thoroughly engaging book on any subject in recent memory.”

A 1968 movie based on the book starred Alan Alda as Plimpton and members of the 1967 Lions team as themselves.

Decades before I became a journalism professor at Miami University of Ohio, I discovered Plimpton’s sportswriting from reading the paperback versions I found on my parents’ bookshelves. Plimpton was a leading member of a mid-20th-century class of literary journalists, including Tom Wolfe, Truman Capote, Gay Talese and Norman Mailer, who were becoming known for applying novelistic techniques and sometimes personal, subjective perspectives to nonfiction.

While the other literati tackled heavy topics, Plimpton’s engaging, conversational prose goofed around on the fringes of pro sports. Many of his books followed the same “participatory journalism” formula. He wrote about pitching against MLB all-stars, traveling with the PGA tour, boxing a bout against Archie Moore and playing with the Boston Bruins.

Those were just the full-length books. Other television and magazine projects had Plimpton competing in tennis and bridge; performing stand-up comedy; acting in a Western; playing with the New York Philharmonic; and attempting to be an aerialist with the circus.

However, he is best known for trying his hand quarterbacking for the Lions.

Posh writer meets the gridiron

In some ways, Plimpton seemed exactly the wrong person for this job. The possessor of a distinctively old money accent and patrician wealth and manners, he was founding editor of The Paris Review and in 1967 a mainstay of literary salons in Paris and New York. “Author, critic, interviewer, party-giver … friend of everybody, gifted, personable, energetic, bright, with-it, rich, a legend in his own time,” The New York Times gushed.

Just the kind of person whom your average football fan might enjoy seeing knocked flat.

Plimpton joined a team he described as recovering from scandal. After ending the 1962 season with an 11-3 record and a Playoff Bowl victory for third place in the NFL, the NFL commissioner’s office fined six Lions for gambling on the championship game between Green Bay and New York. More significant on field, the commissioner suspended Lions great defensive tackle and future Pro Football Hall of Famer Alex Karras for one year. Without him, the Lions would end the 1963 season 5-8-1.

Plimpton wrote his way onto the team by promising to “just hang around on the periphery of things and not bother anyone, just try to participate enough to get the feel of things.”

Wilson agreed, and Plimpton arrived at training camp a few months later with his own football, purchased from an army-navy store in Times Square, and a “mild fiction” about having played quarterback at Harvard and for the nonexistent Newfoundland Newfs.

Plimpton’s attempt at deception might raise ethical questions; however, the joke is always on him. The coaching staff seemed to have thought it would be hilarious if anyone on the team actually took the gangly 36-year-old with the nasal accent as a professional football player. It seems unlikely that anyone did.

“I never had the temerity to pretend I was something that I wasn’t,” Plimpton wrote. “The team caught on quickly enough.”

At camp, Plimpton hung around the dining hall and sat in the back of team meetings. A master of small talk, he lets the reader eavesdrop on conversations with Hall of Famers Karras, Dick “Night Train” Lane and Joe Schmidt.

Plimpton takes us with him one night to a bar frequented by coaches, where we listen in rounds of liars’ poker with Wilson, Scooter McLean and Les Bingaman. We tag along as he chats with Karras at Lindell’s A.C., the bar the player owned in downtown Detroit at the time.

Lessons in grit

At training camp, Plimpton faced the teasing of players but earned respect by facing the brutality of sport and by persisting despite the inevitability of pain. He never played football in school, beyond a beery game between Harvard Crimson and Harvard Lampoon, and did not know the basics of playing quarterback.

Several days into camp, he was allowed to participate in a play where, as quarterback, he was supposed to quickly hand off the ball to another player.

“At ‘two’ the snap back came,” Plimpton wrote. “I began to turn without the proper grip on the ball, moving too nervously, and I fumbled the ball, gaping at it, mouth ajar, as it fell and bounced twice, once away from me, then back, and rocked back and forth gaily at my feet. I flung myself on it (…) and I heard the sharp strange whack of gear, the grunts, and then a quick sudden weight whooshed the air out of me.”

The same thing happened when Plimpton was allowed to take the field in an annual intra-squad game played in Pontiac. Over his first three plays he lost 20 yards by falling down, getting knocked over by his own teammates and being literally picked from the ground by a zealous defender. On the bus ride home, Plimpton admitted to Wilson that he didn’t like being hit.

The coach gently explained that “love of physical contact” was necessary to make it in pro football.

“When kids, out in a park, chose of sides for tackle rather than touch, the guys that want to be ends and go out for the passes, or even quarterback, because they think subconsciously they can get rid of the ball before being hit, those guys don’t end up as football players,” Wilson mused. “They become great tennis players, or skiers, or high jumpers. It doesn’t mean they lack courage or competitiveness.”

“But the guys who put up their hands to be tackles or guards, or fullbacks who run not for daylight but for trouble – those are the ones who will make it as football players.”

This quality of great football players – an irrational enthusiasm for bruising physical contact – is celebrated by Plimpton in the veteran Lions who take him into their orbit. He becomes friends with Karras and offensive lineman John Gordy, in particular, and shoots the breeze on topics ranging from the NFL commissioner to Adolf Hitler.

In a subsequent book, Plimpton goes with the pair to a madcap golf tournament and starts a ridiculous business venture, suggesting the on-field madness necessary to succeed in football bleeds into off-field life as well.

But it is not Plimpton’s way to delve into the psychology of his idols. Rather, he listens as they spin tales that show how reckless the grown men who run toward trouble really are.

Stephen Siff does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

– ref. George Plimpton’s 1966 nonfiction classic ‘Paper Lion’ revealed the bruising truths of Detroit Lions training camp – https://theconversation.com/george-plimptons-1966-nonfiction-classic-paper-lion-revealed-the-bruising-truths-of-detroit-lions-training-camp-267946

Source: The Conversation – USA – By Saif Khan, Ph.D. Candidate in Biology, University of Southern California

Naloxone, also known by the brand name Narcan, is one of the most important drugs in the United States’ fight against the opioid crisis. It reverses an opioid overdose nearly instantly, restarting breathing in a person who was unresponsive moments before and on the brink of death. To bystanders witnessing it being administered, naloxone can appear almost supernatural.

Although the Food and Drug Administration approved naloxone for medical use in 1971 and for over-the-counter purchase in 2023, exactly how it works is still unclear. Researchers know naloxone acts on opioid receptors, a family of proteins responsible for the body’s response to pain. When opioids such as morphine and fentanyl bind to these receptors, they produce not only pain relief and euphoria but also dangerous side effects. Naloxone competes with opioids for access to these receptors, preventing the drugs from triggering effects in the body. How it does this at the molecular level, however, has been an ongoing question.

In our recently published research in the journal Nature, my team and I were able to provide some definitive evidence of how naloxone works by capturing images of it in action for the first time.

Biology of opioids

To better grasp how naloxone works, it’s helpful to first zoom in on the biology behind opioids.

One member of the family of opioid receptors, MOR – short for µ-opioid receptor – is a central player in regulating the body’s response to pain. It sits on the surface of neurons, mostly in the brain and spinal cord, and acts as a communication hub.

When an opioid – such as an endorphin, the body’s natural painkillers – interacts with MOR, it changes the structure of the receptor. This change in shape allows what’s called a G protein to bind to the receptor and trigger a signal to the rest of the body to reduce pain, induce pleasure, or – in the case of overdose – dangerously slow breathing and heart rate.

In everyday terms, MOR is like a lock on the outside of the cell. The G protein is the mechanism inside the lock that turns when the correct key – in this case, an endorphin or a drug like fentanyl – goes in. For decades, scientists believed that an opioid’s ability to enable this signaling cascade was linked to how effectively it reshaped the structure of the receptor – essentially, whether the lock could open wide enough for the internal mechanism of the G-protein to engage.

Yet, recent research – including our work – has revealed that the critical step to how opioids work is not how wide they open the lock but how well the mechanism works. G proteins act like a switch, releasing one molecule in exchange for another molecule that triggers the protein to send the signal that sets off opioid effects.

In essence, drugs like fentanyl, by acting on the receptor, transmit physical changes to G proteins that result in the switch flipping more rapidly. What we now see is that naloxone jams the mechanism, preventing the switch from flipping and sending the signal.

Capturing the switch

Researchers know that the effects of opioids are triggered when the G protein switch is flipped. But what does this process look like?

For years, attempts to visualize this mechanism were largely limited to two states – before the G protein binds to the µ-opioid receptor, and after the molecule was released from the G protein. The states in between were considered too unstable to isolate. My team and I wanted to capture these unseen states moment by moment as the switch flips and the molecule is released.

To do this, we used a technique called cryo-electron microscopy, which freezes molecules in motion to visualize them at near-atomic resolution. For both naloxone and the opioid drug loperamide (Imodium), we trapped the G protein bound to the opioid receptor right before it released the molecule.

We captured four distinct structural states leading up to the release of the molecule from the G protein.

The first of these, which we call the latent state, is the earliest form of the opioid receptor and G protein after they make contact. We found that both the opioid receptor and the G protein are inactive at this point. Moreover, naloxone stabilizes this latent state. What this means is that naloxone effectively jams the mechanism right at the start, preventing all subsequent steps required for activation.

In the absence of naloxone, an opioid drug promotes a transition to the remaining three states: The G-protein rotates and aligns itself with the receptor (engaged), swings open the door blocking the molecule that would trigger the switch from flipping (unlatched), and holds that door open so the molecule can be released (primed) and send the signal to carry out the drug’s effects.

To confirm that our snapshots reflect what’s really happening, we performed extensive computational simulations to watch these four states change over time. Together, these findings point to the molecular root of naloxone’s therapeutic effects: By stalling the opioid receptor and G protein at a latent state, it shuts down opioid signaling, reversing an opioid overdose within minutes.

Visualizing new drugs

Designing a new key for a lock is most successfully done when you know exactly what that lock looks like. By mapping the exact sequence of how opioids interact with opioid receptors and pinpointing where different drugs can intervene in this process, our findings provide a blueprint for engineering the next generation of opioid medicines and overdose antidotes.

For example, one of the persistent challenges with naloxone is that it must often be administered repeatedly during an overdose. This is especially the case for fentanyl overdoses, where the opioid can outcompete or outlast the effects of the treatment.

Knowing that naloxone works by stalling the µ-opioid receptor in an early, latent state suggests that molecules that can bind more tightly or more selectively to this form of the receptor could be more effective at stabilizing this inactive state and thus preventing an opioid’s effects.

By uncovering the structure of molecules involved in opioid signaling, researchers may be able to develop drugs that provide longer-lasting protection against overdose.

This research was supported by the National Institutes of Health.

– ref. How does Narcan work? Mapping how it reverses opioid overdose can provide a molecular blueprint for more effective drugs – https://theconversation.com/how-does-narcan-work-mapping-how-it-reverses-opioid-overdose-can-provide-a-molecular-blueprint-for-more-effective-drugs-269706

Source: The Conversation – USA – By Mark Louie Ramos, Assistant Research Professor of Health Policy and Administration, Penn State

Should you believe the findings of scientific studies? Amid current concerns about the public’s trust in science, old arguments are resurfacing that can sow confusion.

As a statistician involved in research for many years, I know the care that goes into designing a good study capable of coming up with meaningful results. Understanding what the results of a particular study are and are not saying can help you sift through what you see in the news or on social media.

Let me walk you through the scientific process, from investigation to publication. The research results you hear about crucially depend on the way scientists formulate the questions they’re investigating.

The scientific method and the null hypothesis

Researchers in all kinds of fields use the scientific method to investigate the questions they’re interested in.

First, a scientist formulates a new claim – what’s called a hypothesis. For example, is having some genetic mutations in BRCA genes related to a higher risk of breast cancer? Then they gather data relevant to the hypothesis and decide, based on the data, whether that initial claim was correct or not.

It’s intuitive to think that this decision is cleanly dichotomous – that the researcher decides the hypothesis is either true or false. But of course, just because you decide something doesn’t mean you’re right.

If the claim is really false but the researcher decides, based on the evidence, it’s true – a false positive – they commit what’s called a Type 1 error. If the claim is really true but the researcher fails to see that – a false-negative conclusion – then they commit a Type 2 error.

Moreover, in the real world, it gets a little messier. It’s really hard to decide about the truth or falsity of a claim just based on what’s observed.

For that reason, most scientists employ what is called the null hypothesis significance testing framework. Here’s how it works: A researcher first states a “null hypothesis,” something that’s contrary to what they want to prove. For instance, in our example the null hypothesis is that BRCA genetic mutations are not associated with increased breast cancer occurrence.

The scientist still gathers data and makes a decision, but the decision is not about whether the null is true. Instead, a researcher decides whether there’s enough evidence to reject the null hypothesis or not.

What rejecting the null does and doesn’t mean

Understanding this distinction is crucial. Rejecting the null is equivalent in practice to acting as though it is false – in the example, rejecting the null means claiming that those with some BRCA gene mutations do have a higher risk of breast cancer. Along with other evidence, such as the size of the increased risk, this outcome can justify recommending early breast cancer screening for people with the identified BRCA mutations.

But failing to reject the null hypothesis doesn’t imply that it’s true – in this case, it doesn’t mean there is no association between the BRCA mutations and breast cancer. Rather, such a result is inconclusive; there’s not enough evidence to claim there is an association. A negative result – inadequate evidence to say the null is false – does not necessarily invite the researcher to believe the null is true.

This is because null hypothesis significance testing is set up to control for Type 1 error (false positive) at a level defined in advance by the researcher but at the cost of having less control over Type 2 error (false negative).

A researcher’s chances of correctly rejecting the null if there is increased risk can depend on how much data they have, how complex the design of the study is and, most importantly, how large the effect actually is. It’s much easier to reject the null if BRCA mutations truly increase cancer risk many times than it is if the risk is only slightly elevated. A researcher can end up with a result that is not statistically significant but cannot rule out the possibility of an increased risk that is too small for the study to detect.

Which results are more often publicized

Once they have their result and the researchers want to disseminate their work, they typically do so through peer-reviewed publication. Journal publishers consider a researcher’s write-up of their study, send it out for other scientists to review, and then decide whether to publish it.

In this process, the publishers tend to favor studies that rejected their null hypothesis over those that failed to reject it. This is called positive publication bias.

It is natural for publishers to prefer studies that support new claims since they objectively carry more information than studies that failed to reject their null hypothesis. Journals want to publish something new and noteworthy.

Many sources flag this phenomenon as “bad science,” but is it really? Remember, the framework used to make decisions about scientific claims is intentionally only capable of either rejecting the null hypothesis – in other words, supporting the claim – or alternatively declaring inconclusive results.

The framework isn’t designed to be able to prove the null hypothesis. That said, researchers can reverse the design of a scientific investigation so that a previous claim becomes the null hypothesis in a new study with fresh data.

For instance, rather than a null hypothesis that there is no association between BRCA mutations and breast cancer, the null hypothesis becomes that the increased breast cancer risk from BRCA mutations is equal to or greater than some value the researcher settles on before gathering fresh data.

Rejecting the null this time would mean the increased risk is smaller than that set value, thus supporting the claim consistent with what had previously been the null hypothesis on prior data. In the example, rejecting the null means the effect of BRCA genes is small enough to be practically negligible in terms of developing breast cancer.

It’s critical for a researcher to structure their study so that what they’re interested in proving is aligned with the rejection of the null. Publishers are naturally less inclined to consider studies that failed to reject their null hypothesis, not because they do not want to publish studies that support negative statements but because null hypothesis significance testing does not actually support negative statements. Failure to reject the null just means your results are inconclusive – and may perhaps seem less newsworthy.

What positive publication bias does

So what does the practice of preferring to publish studies that reject their null hypothesis do?

While we can’t know for certain, we can see how this plays out under different circumstances. You can explore the scenarios in this app I made.

If scientists are acting in good faith, using null hypothesis significance testing appropriately, it turns out that positive publication bias on the part of scientific journal publishers will increase the proportion of true discoveries in their pages much more than it will increase the proportion of false positives.

If editors did not exercise any positive publication bias, journals would be almost entirely full of studies with inconclusive results.

Of course, if scientists are not acting in good faith and are just interested in getting published while ignoring proper use of statistical tests, that can lead to false-positive rates being as high or higher than the rate of true discoveries. But this possibility is true even without positive publication bias.

Mark Louie Ramos does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

– ref. Absence of evidence is not evidence of absence – and that affects what scientific journals choose to publish – https://theconversation.com/absence-of-evidence-is-not-evidence-of-absence-and-that-affects-what-scientific-journals-choose-to-publish-264854