Health
As RFK Jr. Champions Chronic Disease Prevention, Key Research Is Cut
Robert F. Kennedy Jr. has spoken of an “existential threat” that he said can destroy the nation.
“We have the highest chronic disease burden of any country in the world,” Mr. Kennedy said at a hearing in January before the Senate confirmed him as the secretary of Health and Human Services.
And on Monday he is starting a tour in the Southwest to promote a program to combat chronic illness, emphasizing nutrition and lifestyle.
But since Mr. Kennedy assumed his post, key grants and contracts that directly address these diseases, including obesity, diabetes and dementia, which experts agree are among the nation’s leading health problems, are being eliminated.
These programs range in scale and expense. Researchers warn that their demise could mean lost opportunities to address an aspect of public health that Mr. Kennedy has said is his priority.
“This is a huge mistake,” said Dr. Ezekiel Emanuel, the co-director of the Healthcare Transformation Institute at the University of Pennsylvania’s Perelman School of Medicine.
Decades of Diabetes Research Discontinued
Ever since its start in 1996, the Diabetes Prevention Program has helped doctors understand this deadly chronic disease. The condition is the nation’s most expensive, affecting 38 million Americans and incurring $306 billion in one recent year in direct costs. With about 400,000 deaths in 2021, it was the eighth leading cause of death.
The program has been terminated, and the reason has little to do with its merits. Instead, it seems to be a matter of a lead researcher’s working in the wrong place at the wrong time.
The program began when doctors at 27 medical centers received funding from the National Institutes of Health for a study asking whether Type 2 diabetes could be prevented. The 3,234 participants had high risk of the disease.
The results were a huge victory. Those assigned to follow a healthy diet and exercise routine regularly reduced their chances of developing diabetes by 58 percent. Those who took metformin, a drug that lowers blood sugar, decreased their risk by 31 percent.
The program entered a new phase, led by Dr. David M. Nathan, a diabetes expert at Harvard Medical School. Researchers followed the participants to see how they fared without the constant attention and support of a clinical trial. The researchers also examined their genetics and metabolism and looked at measures of frailty and cognitive function.
Several years ago, the investigators had an idea. Some studies suggested that people with diabetes had a higher risk of dementia. But scientists didn’t know if it was vascular dementia or Alzheimer’s or what the precise risk factors were. The diabetes program could renew its focus on investigating this with its 1,700 aging participants.
The group added a new principal investigator, the dementia expert Dr. Jose A. Luchsinger. For administrative reasons, including the newfound focus on dementia, the program decided its money should flow through Dr. Luchsinger’s home institution, Columbia University, rather than through Harvard or George Washington University, where a third principal investigator works.
On March 7, the Trump administration cut $400 million in grants and contracts to Columbia, saying Jewish students were not protected from harassment during protests over the war in Gaza. The diabetes grant was among those terminated: $16 million a year that Columbia shared across 30 medical centers. The study ended abruptly.
Asked about the termination, Andrew G. Nixon, director of communications at the Department of Health and Human Services, provided a statement from the agency’s acting general counsel saying that “anti-Semitism is clearly inconsistent with the fundamental values that should inform liberal education” and that “Columbia University’s complacency is unacceptable.”
At the time their grant ended, the researchers had started advanced cognitive testing for evidence of dementia in patients, followed by brain imaging to look for amyloid, the hallmark of Alzheimer’s disease. They planned to complete the tests during the next two years.
Then, Dr. Luchsinger said, the group was going to look at blood biomarkers of amyloid and other signs of dementia, including brain inflammation. For comparison, they planned to perform the same tests on participants’ blood samples from 7 and 15 years ago.
“Very few studies have blood collected and stored going that far back,” Dr. Luchsinger said.
Now much of the work cannot begin, and the part that had started remains incomplete.
Another troubling question the researchers hoped to answer was whether metformin increases, decreases or has no effect on the risk of dementia.
“This is the largest and longest study of metformin ever,” Dr. Luchsinger said. Participants assigned to take the drug in the 1990s took it for more than 20 years.
“We thought we had the potential to put to rest this question about metformin,” Dr. Luchsinger said.
The only ways to save the program, Dr. Nathan said, are for Mr. Kennedy to agree to restore the funding at Columbia or to transfer the grant to a principal investigator at another medical center.
The study investigators are appealing to the diabetes caucus in Congress, hoping it can help make their case to the Health and Human Services.
“We hope the congressmen and senators might prevail and say: ‘This is crazy. This is chronic disease. This is what you wanted to study,’” Dr. Nathan said.
So far, there has been no change.
Include Diversity. Actually, That’s Too Much Diversity.
Compared with the Diabetes Prevention Program, a program to train pediatricians to become scientists is tiny. But pediatric researchers say that the Pediatric Scientist Development Program helps ensure that chronic childhood diseases are included in medical research.
It began 40 years ago when chairs of pediatric departments called for the creation of the program, which has been continually funded ever since by the National Institute of Child Health and Human Development.
Participants are clinicians who were trained in subspecialties like endocrinology and nephrology, practiced as clinicians and were inspired to go into research to help young patients with the diseases they had seen firsthand.
The highly competitive program pays for seven to eight pediatricians to train at university medical centers for a year, pairing them with mentors and giving them time away from the clinic to research conditions including obesity, asthma and chronic kidney disease.
In retrospect, the program’s fate was sealed in 2021 when its leaders applied for a renewal of their grant. It seemed pro forma. This was its eighth renewal.
This time, though, an external committee of grant reviewers told the investigators their proposal’s biggest weakness was a lack of diversity. The program needed to seek pediatricians who represented diverse ethnicities, economic backgrounds, states, types of research and pediatric specialties.
The critique said, for example, that “attention must be given to recruiting applicants from diverse backgrounds, including from groups that have been shown to be nationally underrepresented in the biomedical, behavioral, clinical and social sciences.”
So the program’s leaders sprinkled diversity liberally through a rewritten grant application.
“Diversity, in its broadest sense, was all over the grant,” said Dr. Sallie Permar, professor and chairwoman of pediatrics at Weill Cornell Medical College and director of the program. “It was exactly what the reviewers appreciated when we resubmitted.”
The grant was renewed in 2023. Now it is terminated. The reason? Diversity.
The termination letter, from officials in the National Institute of Child Health and Human Development, said there was no point in trying to rewrite the grant request. The inclusion of diversity made the application so out of line that “no modification of the project could align the project with agency priorities.”
Mr. Nixon, the health department spokesman, did not reply to queries about the pediatric program’s cancellation.
Participants in the program are distraught.
Dr. Sean Michael Cullen had been studying childhood obesity at Weill Cornell in New York. He has investigated why male mice fed a high-fat diet produced offspring that became fat, even when those offspring were fed a standard diet.
He hoped his findings would help predict in humans which children were at risk of obesity so pediatricians could try to intervene.
Now the funds are gone. He may seek private or philanthropic funding, but he doesn’t have any clear prospects.
Dr. Evan Rajadhyaksha is in a similar situation. He’s a childhood kidney disease specialist at Indiana University. When he was a resident, he cared for a little girl who developed kidney disease because of a condition in which some urine washes up from the bladder into the kidneys.
Dr. Rajadhyaksha has a hypothesis that vitamin D supplementation could protect children with this condition.
Now, that work has to stop. Without funding, he expects to leave research and return to clinical work.
Dr. Permar said she hadn’t given up. The program costs only $1.5 million each year, so she and her colleagues are looking for other support.
“We are asking foundations,” she said. “We are starting to ask industry — we haven’t had industry funding before. We are asking department chairs and children’s hospitals, are they willing to fund-raise?”
“We are literally looking under every couch cushion,” Dr. Permar said.
“But,” she said, federal support for the program “has been the foundation and cannot be supplanted.”
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Fatigue can stem from a variety of illnesses and life stressors, but when that exhaustion lasts for months — often following an infection — it may indicate a condition called chronic fatigue syndrome.
Approximately 3.3 million people in the United States currently have the syndrome, with about one in four people confined to their bed at some point during the illness, according to the Centers for Disease Control and Prevention.
Despite its prevalence, experts say it’s a poorly understood condition that physicians frequently miss, with past research suggesting that only about 15% of those affected are diagnosed correctly.
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What is chronic fatigue syndrome?
Formally known as myalgic encephalomyelitis (ME), chronic fatigue syndrome (CFS) is a chronic disease that causes fatigue so severe that it impairs the ability to perform daily activities.
Approximately 3.3 million people in the United States currently have the chronic fatigue syndrome, with about one in four people confined to their bed at some point during the illness. (iStock)
The National Academy of Medicine defines the syndrome as having the following three symptoms that last at least six months.
- Severe fatigue that is 1) new and 2) decreases the ability to perform activities that you did normally prior to illness
- “Malaise” that worsens after physical or mental effort that previously was well-tolerated
- Unrestful sleep
People may also experience trouble with thinking and memory (often called “brain fog”) or lightheadedness when standing up.
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There are no tests to confirm chronic fatigue, so doctors diagnose it by talking to their patients, examining them and excluding other disorders, like hypothyroidism and depression, that often share the same symptoms.
Chronic fatigue is frequently missed by physicians, with past research suggesting that only about 15% of those affected are diagnosed correctly. (iStock)
“CFS, fibromyalgia and long COVID are all related conditions with different names,” Dr. Jacob Teitelbaum, author of “From Fatigued to Fantastic” — whose research focuses on chronic fatigue syndrome — told Fox News Digital. “What these illnesses have in common is that they are immune disorders, and immune disorders predominantly affect women.”
Many genes related to immune disorders are on the X chromosome, suggesting a genetic component, the doctor added.
Causes of chronic fatigue
Chronic fatigue syndrome may be triggered by infection or other physiologic stressors, but its causes and symptoms can vary widely from person to person, according to Dr. Julia Oh, a professor in dermatology, molecular genetics and microbiology, and integrative immunobiology at the Duke University School of Medicine in North Carolina.
Teitelbaum compared the condition to a “severe energy crisis” in the body. When energy drops low enough, the “control center” in the brain — the hypothalamus, which regulates sleep, hormones, blood pressure and pulse — may not work as well.
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Although hypothalamic dysfunction can trigger dozens of other symptoms, the hallmark signs are insomnia (despite exhaustion), brain fog and widespread pain, the doctor said.
Anything that causes severe energy depletion can trigger the syndrome, including chronic life stressors, nutritional deficiencies, thyroid and stress hormone imbalances, and sleep problems.
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These triggers are usually associated with a gradual onset of CFS, but sudden onset can be caused by certain infections, with two classic ones being COVID and mononucleosis, past research has shown.
Head and neck trauma and sudden hormonal shifts after pregnancy can also trigger chronic fatigue, Teitelbaum warned.
Anything that causes severe energy depletion can trigger the syndrome, including chronic life stressors, nutritional deficiencies, thyroid and stress hormone imbalances, and sleep problems, according to one doctor. (iStock)
There aren’t currently any blood tests to uniformly diagnose the syndrome, but Dr. Oh said she is hopeful that will change in the future.
Her research team developed an experimental artificial intelligence-based tool, BioMapAI, that has been shown to identify the condition with high accuracy by analyzing stool, blood and other common lab tests, according to early research published in July in the journal Nature Medicine.
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“Instead of finding one smoking gun for the disease, our AI model uncovered a distinct biological fingerprint that was dysregulated in the patients, which spanned changes in gut bacteria, hyperactive immune cells and disrupted metabolism,” Oh told Fox News Digital.
Treatments and therapies
Given how differently chronic fatigue syndrome can affect people, there is no universally effective therapy, according to Oh.
The CDC recommends that patients with CFS work with their doctors to create a management plan based on the symptoms that most affect quality of life.
There are no tests to confirm chronic fatigue, so doctors diagnose it by evaluating symptoms and excluding other disorders.
Treatments generally include a combination of lifestyle changes, therapies and medications. Patients and their physicians should weigh the potential benefits and risks of any approach.
There are some alternative therapies that have shown to be effective for some. Teitelbaum developed a protocol called SHINE, which focuses on sleep, hormones and hypotension, infections, nutrition and exercise. Some research has shown that this approach can help to improve the quality of life for people with CFS and fibromyalgia.
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Others may find alternative treatments, like physiotherapy (physical therapy) to be helpful.
Those who experience persistent fatigue that hinders their ability to participate in regular activities or impacts their quality of life should speak with a doctor.
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Long before the Black Death killed millions across Europe in the Middle Ages, an earlier, more elusive version of the plague spread across much of Eurasia.
For years, scientists were unsure how the ancient disease managed to spread so widely during the Bronze Age, which lasted from roughly 3300 to 1200 B.C., and stick around for nearly 2,000 years, especially since it wasn’t spread by fleas like later plagues. Now, researchers say a surprising clue may help explain it, a domesticated sheep that lived more than 4,000 years ago.
Researchers found DNA from the plague bacterium Yersinia pestis in the tooth of a Bronze Age sheep discovered in what is now southern Russia, according to a study recently published in the journal Cell. It is the first known evidence that the ancient plague infected animals, not just people, and offers a missing clue about how the disease spread.
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“It was alarm bells for my team,” study co-author Taylor Hermes, a University of Arkansas archaeologist who studies ancient livestock and disease spread, said in a statement. “This was the first time we had recovered the genome from Yersinia pestis in a non-human sample.”
A domesticated sheep, likely similar to this one, lived alongside humans during the Bronze Age. (iStock)
And it was a lucky discovery, according to the researchers.
“When we test livestock DNA in ancient samples, we get a complex genetic soup of contamination,” Hermes said. “This is a large barrier … but it also gives us an opportunity to look for pathogens that infected herds and their handlers.”
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The highly technical and time-consuming work requires researchers to separate tiny, damaged fragments of ancient DNA from contamination left by soil, microbes and even modern humans. The DNA they recover from ancient animals is often broken into tiny pieces sometimes just 50 “letters” long, compared to a full human DNA strand, which contains more than 3 billion of those letters.
Animal remains are especially tough to study because they are often poorly preserved compared to human remains that were carefully buried, the researchers noted.
The finding sheds light on how the plague likely spread through close contact between people, livestock and wild animals as Bronze Age societies began keeping larger herds and traveling farther with horses. The Bronze Age saw more widespread use of bronze tools, large-scale animal herding and increased travel, conditions that may have made it easier for diseases to move between animals and humans.
When the plague returned in the Middle Ages during the 1300s, known as the Black Death, it killed an estimated one-third of Europe’s population.
The discovery was made at Arkaim, a fortified Bronze Age settlement in the Southern Ural Mountains of present-day Russia near the Kazakhstan border. (iStock)
“It had to be more than people moving,” Hermes said. “Our plague sheep gave us a breakthrough. We now see it as a dynamic between people, livestock and some still unidentified ‘natural reservoir’ for it.”
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Researchers believe sheep likely picked up the bacteria from another animal, like rodents or migratory birds, that carried it without getting sick and then passed it to humans. They say the findings highlight how many deadly diseases begin in animals and jump to humans, a risk that continues today as people move into new environments and interact more closely with wildlife and livestock.
“It’s important to have a greater respect for the forces of nature,” Hermes said.
The study is based on a single ancient sheep genome, which limits how much scientists can conclude, they noted, and more samples are needed to fully understand the spread.
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The researchers plan to study more ancient human and animal remains from the region to determine how widespread the plague was and which species may have played a role in spreading it.
Researchers (not pictured) found plague-causing Yersinia pestis DNA in the remains of a Bronze Age sheep. (iStock)
They also hope to identify the wild animal that originally carried the bacteria and better understand how human movement and livestock herding helped the disease travel across vast distances, insights that could help them better anticipate how animal-borne diseases continue to emerge.
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The research was led by scientists at the Max Planck Institute for Infection Biology, with senior authors Felix M. Key of the Max Planck Institute for Infection Biology and Christina Warinner of Harvard University and the Max Planck Institute for Geoanthropology.
The research was supported by the Max Planck Society, which has also funded follow-up work in the region.
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