Agriculture In Africa: Science And Research Can’t Make An Impact Without Investment And Good Policies

Women rice farmers in Senegal. Photo by Alvo Pavan, via Getty Images

BY PAPE ABDOULAYE SECK

CHERCHEUR ACADEMIE NATIONALE,

DES SCIENCE ET TECHNIQUES 

DU SENEGAL (ANSTS)

Agriculture is the lifeblood of Africa. More than 60% of African households depend directly or indirectly on the land for their livelihoods. And the continent has nearly 60% of the world’s uncultivated arable land.

Farming is a fragile sector, however. It has to deal with climate change, market volatility, weak infrastructure and demographic pressure. Addressing these challenges requires political commitment and investment. It also requires science, innovation and high-quality research.

I have been involved in scientific research, particularly agricultural research, for more than four decades. My roles have included researcher, member of multiple science academies, director general of the Africa Rice Center/CGIAR, and Senegal’s minister in charge of agricultural research.

Throughout these years, one criticism has repeatedly surfaced: agricultural research is often perceived as expensive while delivering little for people. This perception is widely shared and frequently echoed in political and media debates.

Based on my experience, I believe the criticism rests on a questionable assumption: that the impact of science depends exclusively on those who produce it. When innovations fail to change the world, scientists themselves are often presented as the culprits.

The reality is far more complex. The history of agricultural transformation across the world shows that research alone never changes societies. Impact follows when an agricultural ecosystem effectively connects science to producers, markets, finance, institutions and public policy.

International institutions have highlighted the difficulties many developing countries face in turning scientific knowledge into development. The reasons include weak innovation ecosystems, too little infrastructure and limited institutional coordination.

An example of what success looks like is the Green Revolution in Asia. Scientific breakthroughs improved wheat and rice varieties which transformed agriculture. It was not simply because the science was strong. There were other factors too. They included governments investing in irrigation, extension services, rural infrastructure, credit systems and market organisation.

In India and Vietnam, for example, science operated within a coherent system linking researchers, farmers, institutions and markets.

Science generates knowledge, informs policies, stimulates innovation and opens new possibilities. But it does not change societies on its own.

The missing parts

Recent decades have brought advances on a number of fronts. In seeds, irrigation, soil fertility management, climate adaptation, biotechnology, digital agriculture, agroecology and sustainable food systems.

African researchers, universities and international agricultural research centres have contributed enormously to this progress.

Rwanda and Ethiopia provide useful examples of how coordinated ecosystems can speed up change. In both, stronger links between research, extension systems, public investment and farmer support mechanisms have made a difference. They have contributed to faster uptake of new technologies. And they have led to productivity gains in several strategic crops such as maize, rice, cassava, beans and soybeans.

Another example is rice. During my years at AfricaRice, I saw major scientific advances in rice research. This included the development of New Rice for Africa varieties. ⁠ These resulted from years of scientific work combining the high productivity potential of Asian rice with the resilience of African rice, particularly its tolerance to drought, poor soils and local climatic stresses. It wasn’t easy, because the two rice species are genetically distant.

Farmers quickly took up the new varieties. Farmer incomes and food production improved in countries where governments, seed systems, extension services and development partners worked together. In Uganda, Guinea and several west African countries, coordinated programmes helped accelerate adoption among smallholder farmers.

These examples show that effective agricultural innovation will only be adopted and scaled if several conditions are met together. These include:

access to inputs and technologies

accessible financing

efficient extension services

functioning infrastructure

organised markets

coherent, predictable public policies.

Without these conditions, innovations often remain confined to research stations, pilot projects or scientific publications. Where seed systems, rural financing or market organisation are weak, good science makes little difference.

In several African countries, farmers aren’t using improved seed varieties because they can’t get certified seeds at scale. Likewise, promising innovations in irrigation, post-harvest technologies or digital agriculture have struggled because of weaknesses in infrastructure, rural credit or institutional coordination.

What’s needed

Debates on agricultural research in Africa must go beyond simplistic criticism. Agricultural research should not be viewed as a cost. Rather it is a strategic investment in food security, economic sovereignty, environmental sustainability, public health, social stability and human dignity.

Blaming science for lacking impact masks the weaknesses of broader development systems.

As Africa faces the defining challenge of the 21st century – feeding its population without destroying the planet – it would be a mistake to weaken scientific research. The continent must instead strengthen alliances between science, policy, finance, private sector actors, farmers, universities and civil society.

Across Africa, emerging innovation platforms show that when these actors work together, scientific advances can create tangible economic and social change. The challenge now is to broaden this beyond isolated successes.

In the end, the impact of science is a collective responsibility.

And science can only change the world when societies decide to give it the means to do so.

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Africa Has The World’s Greatest Genetic Diversity, Yet It’s Missing From Research: We’re Filling The Gap

Africa has the richest genetic diversity, making it crucial that its people feature in genetic databases. Jacob Wackerhausen / IStock Getty Images

BY MICHELE RAMSAY AND ANANYO CHOUDHURY

Throughout history, most of the world’s genomic research has relied on DNA data from people of European ancestry.

A genome is the full DNA code of about three billion (a thousand million) bases, including all the chromosomes. Each person has two genomes: one from their mother and the other from their father.

Well resourced environments favour European-based research generating hundreds of thousands of whole human genomes with associated health data. Yet modern humans, our species, evolved on the African continent. African populations therefore contain the deepest branches of human genetic history and the greatest genetic diversity on the planet. Yet the continent remains strikingly underrepresented in global genomic databases.

The African continent is populated by people from over 2,000 ethnolinguistic groups, yet genetic data exist for fewer than a hundred groups. This is akin to having a GPS map of a city with only 5% of the streets marked and the rest left blank.

This bias has profoundly shaped modern medicine, from disease prediction tools to ancestry testing. And it’s why researchers increasingly recognise that studying African genomes has the potential to reveal insights and health-related biological pathways never observed before.

As a team of researchers we were involved in identifying under-represented groups in nine African countries for human whole-genome sequencing. Our multidisciplinary team involved in the Assessing Genetic Diversity in Africa project (AGenDA) has worked out ethical ways to obtain, record and share genetic material and to add to global databases.

The AGenDA dataset alone is expected to uncover millions of previously unknown genetic variants and analyses are underway. These discoveries will inform research into diseases that affect populations in African and worldwide. They include diabetes, heart disease, cancer and neurological or mental health conditions.

This is only a first step. Capturing the full scope of African genomic diversity will require hundreds of thousands of genomes. The project aims to bridge some of the most obvious gaps rather than fully map the continent’s diversity.

But expanding African genomic data is not only important for Africa. It will strengthen global biomedical science.

What it takes

Modern genomic science relies on large databases of DNA sequences to understand disease risk, ancestry and human evolution. These databases underpin a wide range of scientific and medical tools. They are used in medical research, disease prediction, drug development, ancestry testing and increasingly in artificial intelligence models that analyse health data.

When a population is absent from a reference database, a library of whole genome sequences, science simply cannot detect it. Genetic algorithms work by comparing individuals to reference populations. In the absence of a specific reference population, the algorithms will assign the closest available match.

This problem becomes particularly visible in ancestry testing. This is a form of genetic testing often used to learn more about biological heritage. Because African reference data remain incomplete, people with African ancestry may receive vague or misleading results about their origins.

Without more African genomic data the assignment of specific ancestry may be incorrect. In addition, disease risk predictions would be misleading. For example it has been shown that standard doses for medications like warfarin (a blood thinner) or efavirenz (an HIV medication) could be ineffective or toxic for people who harbour specific variants that are more common in African populations.

Prior knowledge of the distribution of such variants in a population could be key to deciding the suitability of a drug for patients from that population.

Filling some of the gaps

The AGenDA project was designed to begin addressing some of the gaps in genome data and African representation. This project involved large multi-country scientific collaborations across the continent. It also required co-ordinating research across multiple ethics committees, regulatory frameworks and institutions. Scientists collaborated with research partners in Angola, the Democratic Republic of Congo, Kenya, Libya, Mauritius, Rwanda, Tunisia and Zimbabwe.

The aim was not simply to increase the number of African genomes in global databases. Instead, the team carefully selected populations to address major geographic and ethnolinguistic gaps in genomic data.

But generating large genomic databases requires careful community engagement and consent from participants to share their data. Biological samples for DNA extraction must be collected and the sequencing performed one base at a time.

We therefore built community engagement and culturally appropriate consent processes into the project from the beginning.

More than 1,000 whole genomes were sequenced from communities that had rarely been included in previous genetic studies. These included:

hunter-gatherer populations

Nilo-Saharan-speaking communities

Afro-Asiatic speakers

understudied Bantu-speaking populations

communities from north Africa and the Indian Ocean islands.

Selecting samples required careful consideration of what African diversity actually represents.

Genetic diversity does not map neatly onto modern national borders. Instead, researchers considered a range of additional factors. These included:

poorly represented geographic regions in genomic databases

major ancestral population histories

languages spoken and self-identified ethnic groups

recent patterns of migration.

In some cases, neighbouring communities may appear close due to geographic proximity but have distinct genetic histories that reflect population separations thousands of years ago.

Why studying African genomes benefits science everywhere

African genomes contain more genetic variation than populations on any other continent. This diversity provides a powerful resource for scientific discovery. When researchers study more diverse populations they are better able to achieve a number of things.

Firstly, they can identify new genetic variants.

Secondl,y they can investigate evolutionary forces, like natural selection, that have shaped the genomes of people in different parts of the world.

And thirdly, they can pinpoint variants that influence health and disease.

More inclusive genomic datasets are also essential as genomics becomes integrated with artificial intelligence systems that analyse medical data and predict health outcomes. Future medical technologies could be biased to work best for whoever is represented in the data.

Ultimately, expanding African genomic representation will help ensure that the benefits of genomic medicine are shared more equitably. At the same time, it will improve the accuracy and depth of understanding in global genetic science.

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Book Review: The Strangers Within Us

BY LINA DELZOVICH

In March 1953, a healthy 28-year-old woman donated blood at a clinic in northern England. As technicians tried to determine her blood type, they could hardly believe what they saw. The woman, identified as Mrs. McK, had both type O and type A red blood cells. The results contradicted a central paradigm of 20th century medicine, which stated that people can only have one blood type — A, B, AB, or O.

When Robert Race, a blood-type specialist in London, received the findings, he revealed that the case wasn’t unprecedented. About a decade earlier, American biologist Ray Owen stumbled on a similar phenomenon not in humans, but in cows, in which — due to the shared placental blood circulation — twin calves had two different types of blood cells.

When asked, Mrs. McK divulged that she had a twin brother who died young. Almost 30 years later, she was still carrying her twin’s cells inside her body. The revelation was so discombobulating that Race described Mrs. McK as a “chimera,” referring to a monstrous creature from Greek mythology with a head and forequarters of a lion, a goat’s head on its back, and a serpent for a tail.

This is only one of many mind-boggling and fascinating examples of cellular trickery described by French science journalist Lise Barnéoud in “Hidden Guests: Migrating Cells and How the New Science of Microchimerism Is Redefining Human Identity.” A biological phenomenon, microchimerism refers to the presence of a small number of cells from one individual within another genetically distinct individual. It most commonly occurs during pregnancy when fetal cells escape into the mother’s bloodstream or maternal cells sneak into the placenta, eventually becoming part of the embryo or fetus. Likewise, twins may exchange cells before birth, too.

The cases aren’t that rare. “Approximately 8 percent of fraternal twins and 21 percent of fraternal triplets carry blood cells from their companions in utero,” Barnéoud writes, citing a 2020 review. Similarly, fetal cells that wander outside the placenta can persist in the mother’s body for years, genomic scientist Diana Bianchi discovered decades after Mrs. McK’s case, in 1993. Bianchi and her team found male cells in the blood of six women who had given births to sons from one to 27 years earlier. Male cells are easier to spot in women because they have X and Y chromosomes in their cell nucleus while female cells have two X chromosomes, and the Y chromosome stands out. But males can carry foreign cells too.

These wandering cells can settle anywhere in the body, making up “a tiny fraction of a kidney, for example, or the entire organ,” Barnéoud reveals. Some have been known to make a home in lungs and others in livers. Moreover, “microchimeric cells can cross the blood-brain barrier and take up permanent residence in our command center,” Barnéoud writes. A 2012 study of 54 deceased women referenced in the book found that 63 percent had male cells in their brains. And one far-fetched hypothesis even posits that women may also acquire foreign cells through semen. So, “if you don’t want to wind up with a head full of cells from multiple men, you’d better use protection!” writes Barnéoud.

Microchimerism refers to the presence of a small number of cells from one individual within another genetically distinct individual. It most commonly occurs during pregnancy.

“Mothers likely carry their children’s cells within them for the rest of their lives,” according to Barnéoud. Children may be carrying their parents. If your mother’s cells sneaked in, clinging to you while you were in utero, you may still harbor them. Bianchi found that maternal cells migrated into their offspring’s thymus, thyroid, liver, skin, and spleen. “So you think your mother is always looking over your shoulder?” Barnéoud quotes Judith Hall, a pediatrician and geneticist who wrote an editorial commenting on Bianchi’s findings, as saying. “She may be in your shoulder.”

Moreover, researchers now hypothesize that even your grandmother’s cells may be lurking in your body, passed on from your mother. It seems that a lot of us may be chimeras, not only Mrs. McK.

However, Barnéoud argues that by using the term “chimeric,” scientists did a great disservice to the cells, instantly casting them as villains. Understandably, they were shocked because Mrs. McK defied the laws of immunology at the time, which stated that a healthy immune system can’t tolerate foreign cells. Eventually, chimeric cells lived up to their reputation: In the mid-1990s, scientists implicated them in autoimmune diseases, which disproportionately affect women.

Sometimes, it seems, the immune system may decide to go after them, causing increased inflammation. (Except in this case the term “autoimmune” doesn’t apply because the cells indeed are foreign and the body isn’t attacking itself.) And so “these cells became migrants, intruders, vagrants crossing the placental border and colonizing, invading, or squatting on maternal territory,” Barnéoud writes. In medicine, it seems, the concept of “us” and “them” is just as dominant as in politics and wars.

It took time to realize that the “invading” cells can come in peace — and even bring benefits. Early in this millennia, scientists learned that microchimeric cells can repair wounds by forming skin and blood vessels. They also can heal heart damage; when injected into mice after a heart attack, they find a way to the damaged heart parts and fix them. And in post-mortem findings of a child who had diabetes, researchers discovered maternal cells were producing insulin in the pancreas, decreeing that the cells were likely helping to “restore function and regenerate diseased tissue.”

And just like that, the chimeric cells “have gone from being suspicious vagrants to productive immigrants, naturalized — in the political sense of the term — to their new home,” Barnéoud quotes historian of science Aryn Martin as saying.

Told in beautiful, sometimes bordering on poetic, language with occasional snark and humor thrown in, the book upends some of the very foundations of medicine, immunology, and genetics. And, having been rooted in cutting-edge research, it rocks our philosophical concept of self. A discovery that the microbial cells in our body may outnumber our own, made us realize we’re only partially human. Now comes the second blow to our ego — we aren’t fully one-human either. “Twenty years after the microbial upheaval, another is underway: even the human half of us does not solely consist of our ‘I,’” Barnéoud’s observes.

“The idea of an entirely independent individual self-constructed from a single fertilized egg is a myth.”

Clever chapter names — “The Other in Me,” “The Other Mes” and “I’ve Got You Under My Skin” — make you question your biological composition. You can’t help but wonder where all these “others of you” came from and how they interact with one another — and yourself. Instead of a single, uniform genome defining your biological identity, you begin to see yourself as something greater than just you.

“The idea of an entirely independent individual self-constructed from a single fertilized egg is a myth,” Barnéoud concludes. That myth may bode well with the ideals of modern Western societies, where we prioritize the individual’s rights over the needs of a collective, but in this new, emerging biological reality, no human is a true individuum. We all are living communities of cells — some ours, some ancestral, some microbial — all of which are in perpetual flux that sometimes results in health and sometimes disease.

Instead of being battlegrounds of “us” and “them,” our bodies operate on never-ending negotiations, tolerating and benefiting from genetic strangers within. “We are each of us a collective in constant co-construction,” Barnéoud resolves, “and our equilibrium depends on the interactions of our constituents.”

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Vice President Dick Cheney’s Life Followed The Arc Of The Biggest Breakthroughs In Cardiovascular Medicine

BY WILLIKAM CORNWELL

ASSOCIATE PROFESSOR OF CARDIOLOGY,

UNIVERSITY OF COLORADO ANSCHULTZ

MEDICAL CAMPUS

The life and political legacy of former Vice President Dick Cheney, who died on Nov. 4, 2025, at the age of 84, has been well documented. But his decades-long battle with heart disease may be less appreciated.

Cheney benefited from almost every major advance made in cardiovascular medicine. These breakthroughs enabled him to sustain an active political career and gave him additional years of an enjoyable life after he moved away from the political spotlight.

As a cardiologist who specializes in both sports medicine and heart disease, as well as advanced heart failure and transplant cardiology, I frequently provide care for patients who, like Cheney, are supported by powerful medicines and procedures to help support heart function.

Cheney’s passing provides an opportunity to reflect on the rapid evolution in medical technology, especially in the past half-century, that improved the lifespan and overall quality of life for Cheney, as well as millions of heart patients around the world.

The formative days of cardiac medicine

Cheney suffered his first of five heart attacks at age 37, in 1978, when the standard of care mainly involved pain relief and bed rest, and when medical professionals did not yet have a clear understanding of what causes heart attacks in the first place.

Today, doctors understand that a heart attack occurs when blood flow through an artery is blocked by a blood clot called a thrombus and oxygen cannot get to the heart muscle. Imagine a kink in a hose that prevents water passing through it. When the heart muscle does not receive oxygen for a long enough period of time, the heart muscle will die and a scar will form.

In the 1960s and ’70s, however, doctors thought a thrombus was the result of – not the cause of – a heart attack.

It is now clear that the formation of a thrombus leads to a heart attack rather than the other way around. That important lesson revolutionized the way doctors like me treat patients with heart attacks.

Big and small breakthroughs

Today, we reopen arteries with stents. When stents are not available, we use powerful medications called thrombolytics, or clot-busters, to break down the thrombus. These kinds of treatments seem commonplace today, but it wasn’t until 1988 that a pivotal study showed combining aspirin and streptokinase, a clot-buster drug, improved survival after a heart attack by almost 50%.

Cheney had additional heart attacks in 1984, 1988, 2000 and 2010. Notably, all but the last were during election years, underscoring the detrimental effects of stress on heart health. His heart attack in 2000 occurred as the courts worked to determine whether Al Gore or George W. Bush – with whom Cheney would become vice president – had won the presidential election.

As technology advanced over the years, Cheney had multiple angioplasties – a procedure to open up narrowed or blocked arteries. During an angioplasty, a procedure developed in the 1980s, heart doctors would place a balloon made of flexible polymers inside an artery to open up and clear the thrombus.

While angioplasties were helpful, one of the main limitations was that the walls of the artery would quickly shrink back – known as recoiling – after the balloon was deflated.

How stents became mainstream

That limitation led to the concept of stents – devices that are now frequently used to treat heart attack patients.

Cheney’s first heart attack in 1978 occurred well before the first stents became available.

Stents started out as metal, tubelike structures that cardiologists used to open up narrowed or blocked blood vessels. The original stents, made of stainless steel, fixed the problem of blood vessels recoiling.

But over time, cardiologists found that stents become stenotic, meaning they themselves would become narrow, making it difficult for blood to flow through them. This problem was solved with the introduction of drug-eluting stents, which have a polymer that coats the metal struts of a stent and prevents stenosis from occurring.

Drug-eluting stents were a game-changer and reduced the need for repeated procedures by about 50% to 70%. Like millions of Americans, Cheney received several stents during his long battle with heart disease.

While stents are helpful, sometimes patients require a surgery called coronary artery bypass graft. Heart surgeons perform this procedure when there are blockages that angioplasty or a stent cannot fix, or when there are too many blockages in the heart arteries.

In 1988, at age 47, Cheney underwent a quadruple bypass operation to help restore blood flow to his heart following his third heart attack.

Battling heart disease

Despite the best efforts of cardiologists, many patients with heart disease, like Cheney, go on to develop heart failure.

There are two main types of heart failure. One – called heart failure with preserved ejection fraction – occurs when the left ventricle, the largest and strongest chamber of the heart, becomes stiff and unable to relax.

The other type – heart failure with reduced ejection fraction – occurs when the left ventricle becomes enlarged and weakened, and fails to pump blood efficiently.

Both types of heart failure make it difficult for the heart to adequately pump blood throughout the body. Cheney, like millions of people throughout the world, suffered from a dilated and weakened heart.

Fortunately, now there are several classes of medications used to treat the kind of heart failure that Cheney suffered from.

There are four main types of drugs that heart failure cardiologists use to manage patients with this condition, which are referred to as the “four pillars” of heart failure management. These medications work together to reduce the amount of stress placed on the heart and to create an environment that helps a weakened heart pump blood more efficiently throughout the body.

Thanks to these four medication types, millions of patients with dilated, weak hearts are living much longer with a higher quality of life and staying out of the hospital. Some of these medications are also used for patients with stiffened hearts, but there is a lot of ongoing research to better understand how to take care of patients with that kind of heart failure.

Despite the use of medications to treat dilated, weak hearts, some patients suffer from continued weakening of the heart muscle and progress to end-stage, or advanced, heart failure. When this happens, there are only two treatment options available. These options are a mechanical pump or a heart transplant.

Heart transplantation is the gold-standard, preferred treatment option for advanced heart failure that results from a dilated, weakened heart.

In 2023, there were about 4,500 heart transplants in the U.S. and about 2,200 in Europe. On average, patients live well over a decade with a heart transplant, and many will go on to live for 20 to 30 more years.

An ounce of prevention is worth a pound of cure

Benjamin Franklin famously quipped, “An ounce of prevention is worth a pound of cure.”

In an interview with “60 Minutes” in 2013, Cheney said his heart disease was the result of genetics and an unhealthy lifestyle. He admitted that he drank beer, ate fatty foods and also smoked three packs of cigarettes per day.

Millions of people across the U.S. and Europe have a lifestyle that is similar to that of Cheney’s prior to his heart transplant. While heart patients benefit from medications, stents and surgeries, preventive strategies cannot be underestimated.

Almost all major health organizations, including the American Heart Association, American Cancer Society and the Department of Health and Human Services, recommend 150 minutes per week of moderate-intensity exercise.

This recommendation translates to a brisk walk about 30 minutes per day, five days per week. This level of exercise leads to large increases in survival and preservation of overall health throughout a lifetime.

While Cheney lived through five heart attacks, the goal for patients and their doctors is to avoid the first. Scientific advances in cardiology have led to a dramatic improvement in survival and quality of life for millions of people, but preventive measures are still by far the most effective lifesaving measure.

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How New Foreign Worker Visa Fees Might Worsen Doctor Shortages In Rural America

Many physicians who aren’t U.S. citizens come to the U.S. to do medical residency programs. SDI Productions/E+ via Getty Images

BY PATRICK AGUILAR

MANAGING DIRECTOR OF HEALTH,

WASHINGTON UNIVERSITY 

IN SAINT LOUIS

There are almost 1.1 million licensed physicians in the United States. That may sound like a lot, but the country has struggled for decades to train enough physicians to meet its needs – and, in particular, to provide care in rural and underserved communities.

Foreign-born physicians have long filled that gap, reducing the overall national shortage and signing up to practice in often overlooked regions and specialties. Today, 1 in 5 doctors licensed to practice in the U.S. were born and trained in another country.

But the ability of physicians from other countries to obtain work in the U.S. may be threatened by the Trump administration’s aims of limiting foreign workers. In September, Trump issued a proclamation requiring employers sponsoring foreign-born workers through a type of work visa called an H-1B to pay a fee of US$100,000 to the government. The White House has signaled doctors may be exempt but has not clarified its position.

As a physician and professor who studies the intersection of business and medicine, I believe increasing restrictions on H-1B visas for physicians may exacerbate the physician shortage. To grasp why that is, it’s important to understand how foreign-trained doctors became such an integral part of U.S. health care – and the role they play today.

The roots of today’s physician shortage

The Association of American Medical Colleges, a trade association representing U.S. medical schools, estimates there will be a deficit of about 86,000 physicians in the country by 2036.

The roots of this shortage stretch back more than a century. In 1910, a landmark study called the Flexner Report detailed significant inconsistencies in the quality of education at American medical schools. The report resulted in the closure of over half the country’s medical schools, winnowing their numbers down from 148 to 66 over two decades.

As a result, the number of doctors in the U.S. declined until new training programs emerged. Between 1960 and 1980, 40 new medical schools launched with the help of federal funding. In 1980, a congressionally mandated assessment deemed the problem solved, but by the early 2000s, a physician shortage emerged once more. In 2006, the American Association of Medical Colleges called for raising medical school enrollment by 30%.

Growth in medical school enrollment hit that target in the late 2010s, but even so, the U.S. still lacks enough medical graduates to fill yearslong training programs, called residencies, that early-career physicians must complete to become fully qualified to practice.

Especially lacking are primary care physicians – particularly in rural areas, where there are one-third as many physicians per capita as in urban areas.

Opportunities for foreign-born doctors

Even as the U.S. built up medical school enrollment in the 1960s and 1970s, the government joined other countries such as the U.K. and Canada in creating immigration policies that drew physicians from developing countries to practice in underserved areas. Between 1970 and 1980, their numbers grew sharply, from 57,000 to 97,000.

Foreign-born and -trained physicians have remained a key pillar of the U.S. medical system. In recent years, the majority of those physicians have come from India and Pakistan. Citizens of Canada and Middle Eastern countries have added significantly to that count, as well. Most arrive in the U.S. as trainees in residency programs through one of two main visa programs.

The majority come on J-1 visas, which allow physicians to enter the U.S. for training but require them to return to their home country for at least two years when their training is complete. Those who wish to remain in the U.S. to practice must transition to an H-1B visa.

A small percentage of physicians come to the U.S. on H-1Bs from the start.

H-1B visas are employer-sponsored temporary work permits that allow foreign-born, highly skilled workers to obtain U.S. employment. Employers directly petition the government on behalf of visa applicants, certifying that a foreign worker will be paid a similar wage to U.S. workers and will not adversely affect the working conditions of Americans.

Several programs sponsor H-1B visas for physicians, though the most common requires a three-year commitment to work in an underserved area after completing their training.

Foreign physicians fill a crucial need

In 2025, foreign-trained medical graduates filled 9,700 of the nearly 40,000 training positions. Of those, roughly one-third were actually U.S. citizens who attended medical schools in other countries, with the remainder being foreign citizens seeking more training in the U.S.

After residency, these doctors frequently practice in precisely the geographic areas where the physician shortage is most severe. A nationwide survey of international medical graduates found that two-thirds practice in regions that the federal government has designated as lacking sufficient access to health care.

These doctors also occupy a disproportionate number of primary care positions. In a sample of 15,000 physicians who accepted new jobs in one year, foreign-born doctors were nine times more likely to enter primary care specialties. In 2025, 33.3% of internal medicine, 20.4% of pediatric and 17.6% of family medicine training positions were filled by physicians trained in other countries.

Who will pay?

Approximately 8,000 foreign-born physicians received H-1B visas in 2024. The new requirement of a $100,000 sponsorship fee would hit hardest for hospitals, health systems and clinics in areas of the country most significantly affected by the physician shortage.

These organizations are already under economic strain due to increasing labor costs and Medicare payments that have not kept pace with inflation. Dozens of these hospitals have closed in recent years, and many currently do not make enough money to support their operations.

On Sept. 25, 2025, 57 physician organizations cosigned a letter petitioning Homeland Security Secretary Kristi Noem to waive the new application fee for physicians.

Already, however, the new rule may be having a chilling effect. Despite years of annual growth in the number of foreign-born applicants to U.S. physician training programs, 2025 has seen a nearly 10% drop. If the new H-1B fee is applied to physicians, the number is likely to keep falling.

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Antioxidants Help Stave Off A Host Of Health Problems – But Figuring Out How Much You’re Getting Can Be Tricky

The antioxidant levels of a food can be affected by its storage time in the supermarket. d3sign/Moment via Getty Images

BY NATHANIEL JOHNSON

ASSISTANT PROFESSOR OF

NUTRITION AND DIETETICS,

UNIVERSITY OF NORTH DAKOTA

When it comes to describing what an antioxidant is, it’s all in the name: Antioxidants counter oxidants.

And that’s a good thing. Oxidants can damage the structure and function of the chemicals in your body critical to life – like the proteins and lipids within your cells, and your DNA, which stores genetic information. A special class of oxidants, free radicals, are even more reactive and dangerous.

As an assistant professor of nutrition, I’ve studied the long-standing research showing how the imbalances in antioxidants and oxidants lead to oxidative stress, which is linked to cancer, diabetes, cardiovascular disease and dementia and Alzheimer’s disease. In fact, a primary cause of aging is the damage accumulated across of a lifetime of oxidative stress.

Simply put: To help prevent oxidative stress, people need to eat foods with antioxidants and limit their exposure to oxidants, particularly free radicals.

The research: Food, not supplements

There’s no way for any of us to avoid some oxidative stress. Just metabolism – the processes in your body that keep you alive, such as breathing, digestion and maintaining body temperature – are a source of oxidants and free radicals. Inflammation, pollution and radiation are other sources.

As a result, everyone needs antioxidants. There are many different types: enzymes, minerals, vitamins and phytochemicals.

Two types of phytochemicals deserve special mention: carotenoids and flavonoids. Carotenoids are pigments, with the colors yellow, orange and red; they contain the antioxidants beta-carotene, lycopene and lutein. Some flavonoids, called anthocyanins, are pigments that give foods a blue, red or purple color.

Although your body produces some of these antioxidants, you can get them from the foods you eat, and they’re better for you than supplements.

In fact, researchers found that antioxidant supplements did not reduce deaths, and some supplements in excessive amounts contribute to oxidative stress, and may even increase the risk of dying.

It should be pointed out that in most of these studies, only one or two antioxidants were given, and often in amounts far greater than the recommended daily value. One study, for example, gave participants only vitamin A, and at an amount more than 60 times an adult’s recommended intake.

Foods rich in antioxidants

In contrast, increased antioxidant intake from whole foods is related to decreased risk of death. And although antioxidant supplementation didn’t reduce cancer rates in smokers, the antioxidants in whole foods did.

But measuring antioxidants in foods is complicated. Extensive laboratory testing is required, and too many foods exist to test them all anyway. Even individual food items that are the same exact variety of food – such as two Gala apples – can have different amounts of antioxidants. Where the food was grown and harvested, how it was processed and how it was stored during transportation and while in the supermarket are factors. The variety of the food also matters – the many different types of apples, for instance, can have different amounts of antioxidants.

Nonetheless, in 2018, researchers quantified the antioxidant content of more than 3,100 foods – the first antioxidant database. Each food’s antioxidant capacity was determined by the amount of oxidants neutralized by a given amount of food. The researchers measured this capacity in millimoles per 100 grams, or about 4 ounces.

For fruits easily found in the grocery store, the database shows blueberries have the most antioxidants – just over 9 millimoles per 4 ounces. The same serving of pomegranates and blackberries each have about 6.5 millimoles.

For common vegetables, cooked artichoke has 4.54 millimoles per 4 ounces; red kale, 4.09 millimoles; cooked red cabbage, 2.15; and orange bell pepper, 1.94.

Coffee has 2.5 millimoles per 4 ounces; green tea has 1.5; whole walnuts, just over 13; whole pecans, about 9.7; and sunflower seeds, just over 5. Herbs and spices have a lot: clove has 465 millimoles per 4 ounces; rosemary has 67; and thyme, about 64. But keep in mind that those enormous numbers are based on a quarter-pound. Still, just a normal sprinkle packs a powerful nutritional punch.

Other tips

Other ways to choose antioxidant-rich foods: Read the nutrition facts label and look for antioxidant vitamins and minerals – vitamins A, C, E, D, B2, B3 and B9, and the minerals selenium, zinc and manganese.

Just know the label has a drawback. Food producers and manufacturers are not required to list every nutrient of the food on the label. In fact, the only vitamins and minerals required by law are sodium, potassium, calcium, iron and vitamin D.

Also, focus on eating the rainbow. Colorful foods are often higher in antioxidants, like blue corn. Many darker foods are rich in antioxidants, too, like dark chocolate, black barley and dark leafy vegetables, such as kale and Swiss chard.

Although heat can degrade oxidants, that mostly occurs during the storage and transportation of the food. In some cases, cooking may increase the food’s antioxidant capacity, as with leafy green vegetables.

Keep in mind that while blueberries, red kale and pecans are great, their antioxidant profile will be different than that of other fruits, vegetables and nuts. That’s why diversity is the key: To increase the power of antioxidants, choose a variety of fresh, flavorful, colorful and, ideally, local foods.

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1 Gene, 1 Disease No More – Acknowledging The Full Complexity Of Genetics Could Improve And Personalize Medicine

A whole lot more than just one genetic mutation determines whether and how disease develops. lvcandy/DigitalVision Vectors via Getty Images

BY SANTHOSH GIRIRAJAN

PROFESSOR OF BIOCHEMISTRY,

MOLECULAR BIOLOGY AND GENOMICS,

PENN STATE

Genetic inheritance may sound straightforward: One gene causes one trait or a specific illness. When doctors use genetics, it’s usually to try to identify a disease-causing gene to help guide diagnosis and treatment. But for most health conditions, the genetics is far more complicated than how clinicians are currently looking at it in diagnosis, counseling and treatment.

Your DNA carries millions of genetic variants you inherit from your parents or develop by chance. Some are common variants, shared by many people. Others are rare variants, found in very few people or even unique to a family. Together, these variants shape who you are – from visible traits such as height or eye color to health conditions such as diabetes or heart disease.

In our newly published research in the journal Cell, my team and I found that a genetic mutation involved in neurodevelopmental and psychiatric conditions such as autism and schizophrenia is affected by multiple other genetic variants, changing how these conditions develop. Our findings support the idea that, rather than focusing on single genes, taking the whole genome into account would provide insight into how researchers understand what makes someone genetically predisposed to certain diseases and how those diseases develop.

Primary and secondary variants

Certain rare variants can cause problems on their own, such as the genetic mutations that cause sickle cell anemia and cystic fibrosis. But in many cases, whether someone actually develops symptoms of disease depends on what else is happening across the genome.

While a primary variant might trigger a disease, secondary variants can alter how that disease develops and progresses. Think of it like a song: The melody (primary variant) is the main part of the song, but the bassist and drummer (secondary variants) can change its groove and rhythm.

That’s why two people with the same genetic mutation can seem so different. One person might have severe symptoms, another person mild symptoms, and another none at all. These variations can even occur within the same family. This phenomenon, called variable expressivity, arises from differences in the secondary variants a person has. In most cases, these variants amplify the effects of the primary mutation. A higher number of secondary variants on top of a primary variant generally leads to more severe disease.

Sometimes, a primary variant and a secondary variant together can cause two different disorders in the same person, such as Prader-Willi syndrome and Pitt-Hopkins syndrome. Other times, secondary variants have no obvious effect on their own but together can tip the balance of whether and how a disease will appear, even in the absence of a primary variant. This can be seen in the development of heart disease in children.

Insights from a missing piece of a chromosome

My team and I studied a genetic change known as a 16p12.1 deletion, where a small piece of chromosome 16 is missing. Researchers have linked this mutation to developmental delay, intellectual disability and psychiatric conditions such as schizophrenia. Yet most children inherit this genetic variant from a parent who has milder symptoms, different symptoms or sometimes no symptoms at all.

To understand why this happens, we analyzed 442 individuals from 124 families carrying this genetic mutation. We found that children lacking this piece of chromosome 16 had more secondary variants elsewhere in the genome compared to their carrier parents. These secondary variants took many forms, including both small changes and large deletions, duplications and expansions of their DNA.

Each type of secondary variant was associated with different health outcomes. Some were linked to smaller head size and reduced cognitive function, while others contributed to higher rates of psychiatric or developmental symptoms. This suggests that while a 16p12.1 deletion makes the genome more sensitive to neurodevelopmental disorders, which symptoms manifest depends on which other variants are present.

The story gets even more complex when considering the fact that children not only inherit a 16p12.1 deletion from one parent but also inherit secondary variants from both parents.

My team and I found that the symptoms of the parent with this genetic mutation often match those of their spouse. For example, a parent with a 16p12.1 deletion who shows signs of anxiety or depression is more likely to have a partner who also has these symptoms. This pattern, called assortative mating, means that when parents with overlapping genetic risks have children, those risks can combine and accumulate.

Over generations, this stacking of secondary variants can lead to children who have more severe symptoms than their parents.

Biases in genetics research

One reason why scientific understanding of secondary variants has lagged is that genetic research often depends on who is recruited to participate in these studies and how researchers recruit them.

Most studies recruit patients affected with a particular disease. Families recruited from genetic clinics typically have children with severe versions of the disease. But if studies focus only on patients with the most acute symptoms, researchers may overestimate the effects of primary variants and miss the subtler role that secondary variants may play in how a disease develops.

But if researchers were to study people drawn from the general population – say, by recruiting people from a large shopping mall – some might carry the same primary variant but have far milder symptoms or none at all. This variability allows researchers to better dissect how different parts of the genome interact with each other and affect how a disease develops.

In our study, for example, we found that people with a 16p12.1 deletion who were recruited from the general population often had milder symptoms and different patterns of secondary variants compared to those who were recruited in a clinic.

Embracing complexity in genetics

Instead of a deterministic view where one mutation equals one outcome, a more complex model accounts for the fact that whether and how a disease develops depends on the interplay between different genetic variants and environment. This has implications for how genetics is used in the clinic.

Currently, a child who tests positive for a genetic variant might be diagnosed with a disease tied to that mutation. In the future, doctors might also examine the child’s broader genetic profile to better predict their developmental trajectory, psychiatric risk or response to therapies. Families could be counseled with a more realistic picture of their child’s probability of developing a disease, rather than assuming every person with the same genetic variant will share the same outcome.

The science is still emerging. Larger and more diverse datasets and models that can better capture the subtle effects of genetic variants and environmental factors are still needed. But what’s clear is that secondary variants are not secondary in importance.

By embracing this complexity, I believe genetics can move closer to its ultimate promise: not just explaining why disease happens, but predicting who is most at risk and personalizing care for each individual.

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How Does Your Immune System Stay Balanced? A Nobel Prize-Winning Answer

Regulatory T cells (red) interact with other immune cells (blue) and modulate immune responses. National Institute of Allergy and Infectious Diseases/NIH via Flickr

BY AIMEE PUGH BERNARD

ASSOCIATE PROFESSOR OF IMMUNILOGY

AND MICROBIOLOGY, UNIVERSITY OF

COLORADO ANSCHULZ MEDICAL CAMPUS

Every day, your immune system performs a delicate balancing act, defending you from thousands of pathogens that cause disease while sparing your body’s own healthy cells. This careful equilibrium is so seamless that most people don’t think about it until something goes wrong.

Autoimmune diseases such as Type 1 diabetes, lupus and rheumatoid arthritis are stark reminders of what happens when the immune system mistakes your own cells as threats it needs to attack. But how does your immune system distinguish between “self” and “nonself”?

The 2025 Nobel Prize in physiology or medicine honors three scientists – Shimon Sakaguchi, Mary Brunkow and Fred Ramsdell – whose groundbreaking discoveries revealed how your immune system maintains this delicate balance. Their work on two key components of immune tolerance – regulatory T cells and the FOXP3 gene – transformed how researchers like me understand the immune system, opening new doors for treating autoimmune diseases and cancer.

How immune tolerance works

While the immune system is designed to recognize and eliminate foreign invaders such as viruses and bacteria, it must also avoid attacking the body’s own tissues. This concept is called self-tolerance.

For decades, scientists thought self-tolerance was primarily established in the parts of the body that make immune cells, such as the thymus for T cells and the bone marrow for B cells. There, newly created immune cells that attack “self” are eliminated during development through a process called central tolerance.

However, some of these self-reactive immune cells escape this process of elimination and are released into the rest of the body. Sakaguchi’s 1995 discovery of a new class of immune cells, called regulatory T cells, or Tregs, revealed another layer of protection: peripheral tolerance. These cells act as security guards of the immune system, patrolling the body and suppressing rogue immune responses that could lead to autoimmunity.

While Sakaguchi identified the cells, Brunkow and Ramsdell in 2001 uncovered the molecular key that controls them. They found that mutations in a gene called FOXP3 caused a fatal autoimmune disorder in mice. They later showed that similar mutations in humans lead to immune dysregulation and a rare and severe autoimmune disease called IPEX syndrome, short for immunodysregulation polyendocrinopathy enteropathy X-linked syndrome. This disease results from missing or malfunctioning regulatory T cells.

In 2003, Sakaguchi confirmed that FOXP3 is essential for the development of regulatory T cells. FOXP3 codes for a type of protein called a transcription factor, meaning it helps turn on the genes necessary for regulatory T cells to develop and function. Without this protein, these cells either don’t form or fail to suppress harmful immune responses.

Harnessing the immune system for medicine

Regulatory T cells can be heroes or villains, depending on the context. When regulatory T cells don’t work, it can lead to disease. A breakdown in immune tolerance can result in autoimmune diseases, where the immune system attacks healthy tissues. Conversely, in cancer, regulatory T cells can be too effective in suppressing immune responses that might otherwise destroy tumors.

Understanding how FOXP3 and regulatory T cells work launched a new era in immunotherapies that harness the immune system to treat autoimmune diseases and cancer. For autoimmune diseases such as rheumatoid arthritis and Type 1 diabetes, researchers are exploring ways to boost the function of Tregs. For cancer, the goal is to inhibit Tregs, allowing the immune system to target tumors more aggressively.

Beyond disease treatment, this research may also improve organ transplantation, where immune tolerance is crucial to prevent rejection. Scientists are exploring how to engineer or expand Tregs to help the body accept transplanted tissues over the long term.

Continuing to unlock the secrets of immune regulation can help lead to a future where the immune system can be precisely tuned like a thermostat – whether to turn it down in autoimmunity or rev it up against cancer.

The 2025 Nobel Prize reminds us that science, at its best, doesn’t just explain the world – it changes lives.

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BOOK REVIEW: How To Do A Midlife Self Review That Actually Works

In Live to 100 and Love It!: An Easy Road Map to Longevity Stacey Colino and the editors of Prevention share a science-backed, six-step routine for redefining your identity after 60.

BY STACEY COLINO

W hen you live for several decades viewing yourself a certain way—as a colleague, as a parent, as a certain type of person—it’s understandable that self-perceptions become solidified. Consciously or not, we all have beliefs about who we are that are based on our behaviors, abilities, feelings, and personality characteristics as well as how others see us and how they respond to us. This is what psychologists call “self-concept”—a reflection of how you see yourself as a person— and it has a powerful effect on the way you act, the choices you make, the attitudes you have, and how you move through life. If you’ve always been known as a go-getter or, conversely, a low-key person, you probably assume you’ll always be that way.

And then you hit middle age, and maybe you start to feel not quite like yourself. One reason may be that your reactions, preferences, needs, values, and expectations have shifted over time, but your self-concept hasn’t kept up. “We tend to think of ourselves as static, but we do change,” says Mark Leary, Ph.D., professor emeritus in the department of psychology and neuroscience at Duke University and author of The Curse of the Self.

Update Your Self Concept

Thinking of ourselves as being one way when we have in fact changed can leave us feeling confused, out of sorts, stuck, or full of self-doubt, says Leary. Research has found that this is a common phenomenon at a certain point in life: Self-concept clarity—the extent to which someone has a clear understanding of their self and identity—increases each decade until the 60s, then begins to decline; after that, “people become less sure of their identity,” the study authors noted, perhaps partly because of shifts in their work, family, and community roles at this life stage. Rediscovering a sense of self has been rated as one of the most challenging aspects of midlife for women, according to a study involving 81 women over 23 years.

Unfortunately, harboring outdated ideas about yourself can end up holding you back from taking smart risks and embracing new challenges when doing so might lead you to feel more fulfilled. “If we’re looking at ourselves through an old lens of who we are, we take those outdated views into our future and make decisions based on that,” says Michele Patterson Ford, Ph.D., a psychologist in private practice and a senior lecturer at Dickinson College in Pennsylvania. On the other hand, updating your self-concept to reflect who and how you are now can help you pursue experiences and activities that feel satisfying and meaningful and skip or minimize those that may not suit you anymore. After doing some self-reflection, you might realize that you’ve outgrown the intense fear of public speaking you used to have and might actually enjoy giving the professional talks you’ve been invited to present. Or maybe you’ll realize that you’ve had enough of the corporate grind and what you really want to do is pursue your artistic talent. And when you have a stronger, clearer sense of who you are now, you’re likely to feel more comfortable in your own skin, maybe even happier, which is valuable in its own right. Ultimately, the goal is to make choices and changes that are in your current best interest, rather than in the best interest of you 10 or 20 years ago. So how can you figure out if you’re working with a self-concept that reflects who you are now? You dig in and do an inventory.

6-Step Self Review

Step 1: Sit down and, in writing, take stock of your current strengths, weaknesses, values, and preferences, suggests Susan Krauss Whitbourne, Ph.D., professor emerita of psychological and brain sciences at the University of Massachusetts, Amherst. Ask yourself questions like these:What are 5–10 things I am good at? These could be anything from talents to work skills to hobbies to interpersonal qualities, etc.

What are 5–10 things I struggle with? These could be daily challenges you have, things you avoid, or where you have trouble with motivation, etc.

What are 5–10 values I closely hold?These might be hard work or kindness.

What are 5–10 things I love? These can be as wide-ranging as hanging out with your dog to working in your business.

Step 2 Ask people who know you well if you’ve got the right idea. Do they think you embody these talents, values, and passions (and struggles) as much as you believe you do?

Step 3 Reflect on their answers. If everything is aligned, move on to step 4. If the answer is no, take a look at how you spend your time so you can make a concerted effort to engage in more activities that reflect the qualities and things you value. Living in a way that aligns with what you value about yourself can help solidify your self-concept, says Ford.

Step 4 Think about what was important to you 10, 20, or 30 years ago and write a letter to your younger self sharing what you’ve learned about yourself over time, how you’ve changed, and what really matters to you now.

Step 5 Stay open-minded. You might have lost some qualities you care about over time. Updating your self-concept is as much about consciously letting go of notions that no longer suit you as it is reclaiming aspects of yourself that you value.

Step 6 Rethink the terms you use or yourself. Tune in to the ways you label or describe yourself— like calling yourself an introvert or an extrovert or seeing yourself as uncreative—and assess whether these terms accurately describe your current behaviors.

Now that you have a better understanding of who you are today, ask yourself the following questions to create a path to the future:What kinds of activities make you feel fulfilled? What do you truly enjoy doing?

What have you always wanted to do or try but haven’t? Can you do it now?

Is your social circle supportive and gratifying? If not, how can you expand it?

When you imagine the future, what do you want your life to look like in five years? Ten years? Fifteen years?

What do you value most in life, and are you living in a way that’s true to those values? If not, what can you do to change that?

What nonmaterial things would you like to have more of in your life?

How would you like people to remember you when you’re gone?

If today were your last day on earth, how would you spend it?

Now think about how you can set yourself up to bring more of these valuable experiences into your life. Assess this on a practical level, as well as on financial, psychological, and emotional levels. Also, think of older people you know who have these elements in their lives. Consider seeking their advice for steps you could take to cultivate them in yours.

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Hold Up, Humans. Ants Figured Out Medicine, Farming And Engineering Long Before We Did

BY TANYA LATTY AND CHRIS R. REID

Think back to a time you helped someone move a heavy object, such as a couch. While at first the task may have appeared simple, it actually required a suite of advanced behaviours.

The job needed verbal commands for social coordination (“pivot!”) and anticipation of near-future events (moving other furniture out of the way). It also required a clear, shared vision of the final goal (which room to take the couch to).

It’s a small but satisfying example of human cooperation. But before we all get too pleased with ourselves, consider that ants – creatures with tiny brains and no capacity for speech – routinely pull off feats that rival, and sometimes exceed, our own.

Understanding ant intelligence

Earth is literally crawling with ants. Scientists estimate there are at least 20 quadrillion ants on Earth. That’s 20 followed by 15 zeros – more ants than stars in our galaxy!

These incredible insects are amongst the most successful organisms on the planet. Part of the success comes from an ability to form complex societies, ranging from a few individuals to millions. And those societies, or colonies, are remarkably co-operative.

Take, for example, ants’ abilities to move large food items. To do it, they mobilise teams of dozens – or even hundreds – of fellow workers. Together, they efficiently work together to transport the load back to the nest.

Longhorn crazy ants (Paratrechina longicornis) are even known to clear debris from a path before a heavy object arrives – seemingly anticipating its trajectory and preparing the way.

One experiment pit longhorn crazy ants against humans, all tasked with moving T-shaped objects (scaled to body size) through tight spaces. In some trials, the human teams were not permitted to speak or use gestures.

And the result? Ants performed better in larger groups compared to smaller ones, showing the clear benefits of collective action. In contrast, human performance did not improve with group size. And when communication was restricted, human performance declined as group size increased.

All this highlights how ants rely on collective intelligence, without the need for central control or sophisticated cognition.

Expert farmers

Humanity’s invention of agriculture 12,000 years ago is understandably hailed as one of our greatest achievements.

But leaf cutter ants beat us to it. These ants (from the species Atta and Acromyrmex) evolved to undertake large-scale agriculture about 55 million years ago.

These ants cut and transport fresh leaves not to eat directly, but to feed a fungus that serves as their main food source.

This evolutionary partnership allows the ants to feed colonies with populations in the millions.

Remarkably, leaf cutter ants have also evolved a form of biological pest control to protect their crops from bacteria. Some worker ants patrol the gardens, detecting infected sections of the fungus. Then they apply antibiotics produced by bacteria that live on their bodies.

What’s more, many ant species farm aphids and other sap-sucking insects.

As these farmed insects feed on plant sap, they excrete a sugary liquid the ants eagerly collect. In return, ants serve as bodyguards, defending their tiny livestock from predators such as ladybirds and lacewings.

In some species, queen ants gently carry sap-sucking insects in their jaws as they fly off to start new colonies. Fossilised ants preserved in amber suggest this behaviour evolved up to 20 million years ago, long before humans domesticated animals.

Ant medicine

Medical care may seem like a distinctly human innovation. But several ant species have evolved sophisticated ways to treat injuries.

When a Florida carpenter ant (Camponotus floridanus) is injured during a battle between colonies, its nest-mates will amputate a damaged limb to prevent infection from spreading. Ants receiving this battlefield care are more likely to survive than ants left untreated.

Some ants can also detect infection and treat infected wounds by cleaning them and applying antimicrobial secretions from specialised glands.

Master builders

Some ant species are known to literally put their bodies on the line for the colony.

Army ants (Eciton burchellii) join their bodies together to form structures. These include bridges across gaps on the forest floor, and “scaffolds” across steep terrain to prevent other ants from slipping.

Even the nest is made of hundreds of thousands of ants joined together, complete with tunnels and chambers housing the larvae and the queen. The entire structure is packed up and rebuilt each day, after the colony emigrates a few hundred metres into the forest.

Weaver ants (Oecophylla smaragdina), meanwhile, self-assemble into rope ladders to span vertical gaps.

They also form a line of workers that pull leaves together in treetops to form nests. Once the leaves are winched into place, other ants arrive with ant larvae in their jaws. Each larva produces a tiny blob of silk which the ants use to glue the leaves together.

Fire ants (Solenopsis invicta), a major pest species, owes its invasive success partly to a unique method of dispersal.

When their underground nests are flooded by rain, the ants join together into a huge raft which floats on a layer of buoyant larvae. These rafts can ride floodwaters in safety for hundreds of kilometres, until the ants reach dry land.

Lessons for humanity?

Humans rightly take pride in our greatest achievements – agriculture, medicine, engineering and building civilisations. But remarkably, ants mastered these innovations millions of years before we did.

Ants may be tiny – but by working together they can build complex societies and solve many problems. They might even teach humans a thing or two.

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Chronic Kidney Disease Often Goes Undiagnosed, But Early Detection Can Prevent Severe Outcomes

BY ELEANOR RIVERA

ASSISTANT PROFESSOR OF POPULATION

HEALTH NURSING SCIENCE,

UNIVERSITY OF ILLINOIS CHICAGO

For a disease afflicting 35.5 million people in the U.S., chronic kidney disease flies under the radar. Only half the people who have it are formally diagnosed.

The consequences of advanced chronic kidney disease are severe. When these essential organs can no longer do their job of filtering waste products from the blood, patients need intensive medical interventions that gravely diminish their quality of life.

As an assistant professor of nursing and an expert in population health, I study strategies for improving patients’ awareness of chronic kidney disease. My research shows that patients with early-stage chronic kidney disease are not getting timely information from their health care providers about how to prevent the condition from worsening.

Here’s what you need to know to keep your kidneys healthy:

What do your kidneys do, and what happens when they fail?

Kidneys have multiple functions, but their most critical and unglamorous job is filtering waste out of the body. When your kidneys are working well, they get rid of everyday by-products from your normal metabolism by creating urine. They also help keep your blood pressure stable, your electrolytes balanced and your red blood cell production pumping.

The kidneys work hard around the clock. Over time, they can become damaged by acute experiences like severe dehydration, or acquire chronic damage from years of high blood pressure or high blood sugar. Sustained damage leads to chronically impaired kidney function, which can eventually progress to kidney failure.

Kidneys that have failed stop producing urine, which prevents the body from eliminating fluids. This causes electrolytes like potassium and phosphate to build up to dangerous levels. The only effective treatments are to replace the work of the kidney with a procedure called dialysis or to receive a kidney transplant.

Kidney transplants are the gold standard treatment, and most patients can be eligible to receive them. But unless they have a willing donor, they can spend an average of five years waiting for an available kidney.

Most patients with kidney failure receive dialysis, which artificially replicates the kidneys’ job of filtering waste and removing fluid from the body. Dialysis treatment is extremely burdensome. Patients usually have to undergo the procedure multiple times per week, with each session taking several hours. And it comes with a major risk of death, disability and serious complications.

What are the risk factors of chronic kidney disease?

In the U.S., the biggest contributors to developing chronic kidney disease are high blood pressure and diabetes. Up to 40% of people with diabetes and as many as 30% of people with high blood pressure develop chronic kidney disease.

The problem is, as with high blood pressure, people with early-stage chronic kidney disease almost never experience symptoms. Clinicians can test a patient’s overall kidney function using a measure called the estimated glomerular filtration rate. Current guidelines recommend that everyone – particularly people with risk factors like high blood pressure and diabetes – get their kidney function routinely tested to ensure the condition doesn’t progress silently.

Early treatment for kidney disease often relies on managing high blood pressure and diabetes. New medications called SGLT2 inhibitors, originally developed to treat diabetes, may be able to directly protect the kidneys themselves, even in people who don’t have diabetes.

Patients with early-stage kidney disease can benefit from knowing their kidney function scores and from treatment innovations like SGLT2 inhibitors, but only if they are successfully diagnosed and can discuss treatment options during routine visits with their health care providers.

What are some barriers to early treatment?

Early treatment for chronic kidney disease often gets overlooked during routine clinical care. In fact, as many as one-third of patients with kidney failure have no record of health care treatment for their kidneys in the early stages of their disease.

Even if a diagnosis for chronic kidney disease is noted in a patient’s medical record, their provider might not discuss it with them: As few as 10% of people with the disease are aware that they have it.

That’s partly due to the constraints of the U.S. health care system. The diagnosis, treatment and monitoring of early-stage chronic kidney disease occurs mostly in the primary care setting. However, primary care visit time is limited by insurance company reimbursement policies. Especially with patients who have multiple health problems, doctors may prioritize more noticeably pressing concerns.

The result is that many clinicians put off addressing chronic kidney disease until symptoms emerge or test results worsen, often leaving early-stage patients undiagnosed and poorly informed about the disease. Research shows that people who are nonwhite, female and of lower socioeconomic status or education level are most likely to fall into this gap.

But patients are eager for this knowledge, according to a study I co-authored. I interviewed patients who had early-stage kidney disease about their experiences receiving care. In their responses, patients expressed dissatisfaction with the lack of information they received from their health care providers and voiced a strong interest in learning more about the disease.

As kidney disease progresses to the later stages, patients get treated by kidney specialists called nephrologists, who provide patients with targeted treatment and more robust education. But by the time patients progress to late-stage disease or even kidney failure, many symptoms can’t be reversed and the disease is much harder to manage.

How can patients take charge of kidney health?

People who are at risk for chronic kidney disease or who have developed early-stage disease can take several steps to minimize the chances that it will progress to kidney failure.

First, patients can ask their doctors about chronic kidney disease, especially if they have risk factors such as high blood pressure or diabetes. Studies show that patients who ask questions, make requests and raise concerns with their provider during their health care visit have better health outcomes and are more satisfied with their care.

Some specific questions to ask include “Am I at risk of developing chronic kidney disease?” and “Have I been tested for chronic kidney disease?” To help patients start these conversations at the doctor’s office, researchers are working to develop digital tools that visually represent a patient’s kidney disease test results and risks. These graphics can be incorporated into patients’ medical records to help spur conversations during a health care visit about their kidney health.

Studies show that patients with chronic kidney disease who have a formal diagnosis in their medical records receive better care in line with current treatment guidelines and experience slower disease progression. Such patients can ask, “How quickly is my chronic kidney disease progressing?” and “How can I monitor my test results?” They may also want to ask, “What is my treatment plan for my chronic kidney disease?” and “Should I be seeing a kidney specialist?”

In our research, we saw that patients with chronic kidney disease who had seen a loved one experience dialysis treatment were especially motivated to stick with their treatment to prevent kidney failure.

But even without the benefit of direct experience, the possibility of kidney failure may motivate patients to follow their health care providers’ recommendations to eat a healthy diet, get regular physical activity and take their medications as prescribed.

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