Neonatal necrotizing enterocolitis (NEC) remains one of pediatrics’ most devastating intestinal disorders, and safer, mechanism-driven therapies are urgently needed. New findings suggest that tiny vesicles naturally present in human breast milk—exosomes—may offer protection by delivering a specific regulatory microRNA.
Researchers report that exosomes enriched with miR-144-5p can help restore the intestinal tight junction barrier, a key defense line that collapses during NEC. By focusing on miR-144-5p, the team moves beyond earlier observations that breast milk exosomes can reduce NEC severity and instead pinpoints a molecular cargo likely responsible for part of that benefit.
The study centers on how NEC damages epithelial integrity and promotes inflammatory signaling. Tight junction disruption is associated with increased permeability, bacterial translocation, and worsening inflammation—conditions that accelerate disease progression in vulnerable newborns. The investigators therefore examined whether miR-144-5p could counter these barrier failures in NEC contexts.
Mechanistically, the work links miR-144-5p action to the TLR4/NF-κB pathway, a well-known inflammatory axis. Toll-like receptor 4 (TLR4) senses danger-associated cues and can trigger NF-κB activation, driving transcription of pro-inflammatory mediators. In NEC, exaggerated signaling through this route contributes to tissue injury and impaired repair.
By modulating this cascade, miR-144-5p appears to dampen downstream inflammatory responses while promoting recovery of junctional structure. The paper’s data indicate that exosomal delivery is central: miRNAs packaged within vesicles can be taken up by recipient cells more efficiently than naked RNA, enabling functional gene regulation in target intestinal compartments.
Together, the results support a model in which breast milk exosomal miR-144-5p alleviates NEC by suppressing TLR4-driven NF-κB activation, thereby reducing inflammatory injury and enabling tighter regulation of epithelial junctions. If translated, such a cargo-guided approach could complement existing supportive NEC treatments.
While additional work will be required to confirm efficacy across models and to evaluate safety, the study provides a clear mechanistic roadmap: therapeutic exosomes or miRNA mimics that bias TLR4/NF-κB activity may be a promising strategy for protecting the neonatal gut.
Subject of Research: Neonatal necrotizing enterocolitis (NEC), breast milk-derived exosomes, miR-144-5p, tight junction barrier repair, TLR4/NF-κB signaling.
Article Title: Human milk exosomal-miR-144-5p alleviates neonatal necrotizing enterocolitis by regulating the TLR4/NF-κB pathway.
Article References: Chen, Z., Chen, C., Hu, X. et al. Human milk exosomal-miR-144-5p alleviates neonatal necrotizing enterocolitis by regulating the TLR4/NF-κB pathway. Pediatr Res (2026). https://doi.org/10.1038/s41390-026-05305-9
Short-chain fatty acids (SCFAs)—especially acetate, propionate, and butyrate—are produced when gut microbes ferment carbohydrates that the human body cannot digest. Over the past decade, these small molecules have moved beyond being viewed as simple fuel. Instead, they are now recognized as signalling messengers that help tune metabolism, shape immune responses, and support physiological balance across organs. A new review in Nature Metabolism brings together scattered findings to clarify how SCFAs are made, how they are processed in the body, and why they matter for health.
The article emphasizes that SCFA production is not uniform. It depends on which microbial communities inhabit the gut, which dietary substrates reach the colon, and how microbes share resources through cross-feeding. When multiple bacterial species coordinate, fermentation pathways can shift, increasing the output of particular SCFAs. In that way, the “hardware” of the microbiome and the “inputs” provided by diet jointly determine the chemical signals generated in the intestine.
After their formation, SCFAs are handled by host tissues through absorption and further metabolic conversion. The review highlights that acetate, propionate, and butyrate can influence local and systemic physiology, helping link intestinal chemistry to whole-body regulation. Their effects are therefore both immediate—through signalling pathways—and longer-lasting—through changes in gene regulation.
Mechanistically, the authors focus on receptor-mediated communication. SCFAs activate specific receptors on immune and metabolic cells, altering inflammatory tone and metabolic signalling. This receptor layer helps explain how intestinal events can reverberate in distant tissues that rely on tightly controlled energy and immune states.
Beyond receptors, SCFAs also affect epigenetics. By influencing chromatin-modifying enzymes and related regulatory networks, they can change how genes are expressed without altering DNA sequence. Such effects provide a plausible bridge between diet–microbiome interactions and sustained shifts in health trajectories.
The review further surveys tissue-specific outcomes, from effects on gut barrier function to immune regulation and metabolic homeostasis. Importantly, this heterogeneity helps reconcile why SCFAs sometimes show protective associations while other contexts yield mixed results—differences in dose, timing, microbial ecology, and host physiology can all matter.
When the evidence is assembled, the paper argues that SCFAs are strongly implicated in metabolic health and disease risk. Conditions such as obesity, insulin dysregulation, and inflammatory disorders have been linked to altered SCFA profiles, though causality remains an active area of investigation. The authors also discuss the limitations of current studies, including differences in measurement methods and confounding dietary factors.
Finally, the review evaluates translational opportunities. Rather than treating SCFAs as isolated supplements, it frames dietary and therapeutic strategies around pathways that enhance beneficial SCFA production or mimic their downstream effects. With low fibre intake becoming a public health concern worldwide, the work positions SCFAs as a key biological rationale for improving diet quality.
Overall, this Nature Metabolism review synthesizes what is known—and what is still uncertain—about SCFAs as central mediators between gut microbes and host biology. It suggests that targeting microbial fermentation and SCFA signalling could become a practical lever for metabolic disease prevention.
Subject of Research: Gut microbiota–derived short-chain fatty acids and their physiological roles Article Title: Short-chain fatty acids Article References: Dagbasi, A., Cai, M., Hirdaramani, A. et al. Short-chain fatty acids. Nat Metab (2026). https://doi.org/10.1038/s42255-026-01579-9 DOI:https://doi.org/10.1038/s42255-026-01579-9 Image Credits: AI Generated
The symptoms: The girl arrived at an emergency department after waking up with sudden, severe pain in her upper back. Within hours of the pain emerging, she developed rapidly worsening weakness in all four limbs, making it impossible for her to stand or walk.
She also reported painful tingling and loss of sensation in her hands, and doctors discovered that she had diminished reflexes and sensory changes beginning at her upper chest and moving down her body. In multiple instances at the hospital, she lost control of her bladder and bowels.
The combination of acute paralysis, severe back pain and incontinence suggested damage to the spinal cord, but the cause wasn't immediately clear, her doctors wrote in a report of the case.
What happened next: The medical team launched an extensive search for the underlying cause. An MRI of her neck and torso showed evidence of extensive inflammation or injury that stretched from her lower neck to the middle of her back. The scan also showed a small tear in one of the disks in her lower neck, with a small amount of disk material pushing outward.
However, the girl and her parents did not report any recent falls or injuries, and the MRI alone couldn't determine what had caused this apparent damage.
The girl's medical team then performed blood tests, a spinal fluid analysis and more imaging to look for signs of infections, autoimmune diseases or other inflammatory conditions that can trigger acute paralysis in children. These tests all came back negative.
While clinicians continued investigating, the girl was treated with intravenous steroids and underwent a procedure called plasmapheresis, during which blood is drawn from the patient into a machine which separates blood plasma (the liquid portion of blood) from blood cells and then returns the blood cells to the patient mixed with fresh plasma from donors. This process helps to filter out harmful antibodies and abnormal proteins that can be present in people with autoimmune or blood disorders.
Over the following days, the girl gradually regained her ability to feel, walk and control her bladder. However, repeat MRI scans showed worsening inflammation, which didn't seem to match the girl's improving condition.
The cause of the girl's symptoms was not immediately clear when she arrived at the emergency department. (Image credit: Douglas Sacha via Getty Images)
The diagnosis: Throughout her hospital stay, the medical team suspected a diagnosis of transverse myelitis, which is a rare neurological disorder that involves swelling in the spinal cord. However, as infectious and autoimmune causes became increasingly unlikely, the physicians changed their minds.
They instead concluded that the girl had experienced a spinal cord infarction, or essentially a stroke affecting the spinal cord. This blood-flow blockage was most likely caused by an exceptionally rare condition called fibrocartilaginous embolism (FCE).
In FCE, a small piece of jelly-like material from the soft center of an intervertebral disk breaks off, enters the bloodstream and blocks one of the arteries supplying the spinal cord. The resulting loss of blood flow can cause sudden paralysis, sensory loss and bowel and bladder dysfunction.
It's unknown exactly how many people experience FCE, as it's difficult to diagnose and frequently underreported. One literature review found only 30 suspected cases and 41 confirmed cases of FCE that had been documented in the U.S.
The case study notes that FCE is most common in children and young adults ages 10 to 20, and that rate also jumps up later in adulthood, around ages 40 to 60. It is slightly more common among female patients than male. While slightly younger than the most commonly affected demographic, the 8-year-old patient in this case otherwise fit this description.
FCE is difficult to diagnose because there is no definitive laboratory or imaging test for it. Instead, physicians must rule out more common causes of spinal cord injury while looking for imaging findings and clinical signs and symptoms that might fit the diagnosis of FCE.
The treatment: There isn't a specific treatment for FCE; instead, care focuses on managing the symptoms caused by the spinal stroke.
The patient was treated with corticosteroids to reduce inflammation, medications to manage pain and plasmapheresis. After a few weeks, and with extensive rehabilitation therapy, the girl regained nearly all of her strength and functional abilities. Her only lingering symptom was weakness in her hands.
What makes the case unique: The case study notes that FCE is often linked to minor trauma to the spine, such as that caused by heavy lifting or other activities that briefly increase pressure inside the spinal disks. In this case, however, the medical team was unable to identify a clear triggering event, and the girl was otherwise healthy and had no reported history of physical trauma. The girl simply woke up with symptoms, which made the diagnosis even more unexpected.
The case also highlights that, although FCE is rare and often carries a poor prognosis — as many patients experience long-term disability and some may even die from complications — meaningful recovery is also possible. The case report authors concluded that, with early recognition and supportive treatment, patients with FCE may achieve improved outcomes and a return to their normal activities.
This article is for informational purposes only and is not meant to offer medical advice.
Kakadiya, J., Lakhani, D. A., Gaddamanugu, S., Goncalves, F. G., & Mullen, A. J. (2026). Presumed fibrocartilaginous embolism causing spinal cord infarct in 8-year-old female: A case report. Radiology Case Reports.https://doi.org/10.1016/j.radcr.2026.03.047
Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!
Gun violence is a uniquely American epidemic, according to Dr. Selwyn Rogers Jr., the founding director of the University of Chicago Medicine Trauma Center.
Rogers helped found the trauma center in 2018 on Chicago's South Side, which had lacked a local adult trauma center since 1991. For nearly 30 years, people injured on the South Side had to endure long ambulance rides to access care elsewhere in the city, and lives were lost as a result.
Since founding the new trauma center, Rogers has cared for many victims of gun violence. In a new book — "Healing the Gun Violence Epidemic: Ending Violence, Rebuilding Communities, and a Trauma Surgeon's Vision for Restoring Hope" (North Atlantic Books, 2026) — he tells their stories, along with those of advocates and organizations working to confront the underlying factors that drive gun violence in the first place. The book unpacks how we got here, and what we must do next, drawing on Rogers' experience as a witness to gun violence's toll.
Live Science spoke to Rogers about his work, new book and vision for how Americans should tackle this epidemic.
Nicoletta Lanese: In the book, you trace this trajectory of how we arrived here and what the future could look like, when it seems that strong gun legislation is unlikely. To put it plainly, what gives you hope for the future as a person who sees the impacts of gun violence daily?
Dr. Selwyn Rogers Jr.: I'll start off by saying, I'm pathologically optimistic. Otherwise I couldn't do what I do as a trauma surgeon, where I see some of the worst things.
What makes me hopeful, despite the current political headwinds, are people. When I see a mother who is grieving her son, who just died from gun violence, who says to me, "I have to keep going for my other kids." That gives me hope. When I see someone who acknowledges that they used to hurt others with a firearm, who now is passionate about prevention of other people getting hurt. That brings me hope. When I see the bugged out eyes of a five-year-old Black boy looking at me in my white coat, going, "Are you a doctor?" I say, yes, I am. That brings me hope.
There are all of these moments of human connection. If we just look for them, they're all around us. That brings me hope every time.
NL: The book draws on your experience as a trauma surgeon and also highlights societal factors driving gun violence. When did you begin thinking about treatment that goes beyond the operating room?
SR: I trained in Boston at the time of the crack epidemic in the early 1990s, and Boston, like many cities in the United States, had a fair bit of penetrating trauma. (We separate trauma into "blunt" and "penetrating": "blunt" meaning events where there's no penetration of the skin by a missile or a projectile, and "penetrating" where there is some projectile that violates the skin and causes internal damage.)
During that time, I was particularly struck that those who suffered penetrating trauma disproportionately look like me. I happen to be African-American, they happened to be mostly African-American or Hispanic. They happened to be mostly male. Something about that connected with me as I wanted to be part of helping to solve that problem over the course of my career.
That brought me to Vanderbilt and Meharry Medical College in Nashville, which is where I took my first job. I earned a Master's in Public Health at Vanderbilt School of Medicine, and as part of that experience, I had to do a practicum that involved real-life work trying to understand healthcare outcome differences across a two-mile difference in space: I was at Vanderbilt, a traditional academic medical center, and Meharry Medical College's county hospital, Nashville General Hospital.
Two people could have the same exact diagnosis and have very disparate outcomes, and trying to understand those differences and how you can make a difference in that space was very informative.
NL: How do you think about those social drivers of health in relation to trauma surgery?
SR: When I was in training early on, as well as when I was a junior faculty, it was really striking to me that there were some patients who would come back again and again after traumatic injury. Thinking about how we treat other conditions that are not trauma — for example, heart disease — if I had a heart attack, blockage of my coronary blood vessels supplying my heart, I would today get a stent and get antithrombotic, antiplatelet therapy to reopen my heart. But if at the same time it was discovered that I had high cholesterol, I was overweight, I had a sedentary lifestyle, I smoked, those risk factors would also be addressed as part of my holistic recovery.
For trauma, we don't treat it that way; for the most part, we treat it as an event. Something happened, and we will take care of you.
But we don't look at all the other factors that put you at risk in the first place. And because we often don't do that, when people leave the hospital, the four walls of the emergency department or the trauma center, their risk factors haven't changed. Why would we think that they're not going to be re-injured again? So bringing that framing has been a very fundamental part of my both professional journey and my academic journey.
NL: And those paired interests eventually brought you to your role in Chicago?
SR: In many ways, I've been preparing my entire career to be in Chicago. My current role combines both my technical interest in helping people using my skills and training as a surgeon, but also the social drivers of health and healthcare disparities.
All of those things culminated in a knock on the door where the chair of the Department of Surgery at University of Chicago, said, "Hey, we have an opportunity to open a brand-new adult trauma center on the South Side of Chicago." Before that call in 2016, I did not know that there was no adult trauma center on the South Side of Chicago since 1991.
I've been here nine years now, and I love the city of Chicago. I love what I do; I love the patients I take care of; I love the community. I can't imagine doing anything else.
NL: Can you clarify what services a trauma center offers, as opposed to an emergency room?
SR: The distinction is that the emergency room, emergency ward, emergency department is a place. It's a place where people who are the most severely ill go to seek care. Now, in our healthcare system, people also seek care in the emergency department because they don't know where else to go. They may not have a primary care doctor, they may not have health insurance, so the ED becomes a place where they go.
Trauma centers offer a comprehensive system of care that can't necessarily be delivered by an emergency room alone. (Image credit: Douglas Sacha via Getty Images)
A trauma center is not that. A trauma center is a system of care incorporating operating rooms, interventional radiology, social workers, anesthesiologists, trauma surgeons, orthopedic — basically a whole team of people that surround the individual and their injuries and try to restore them to health.
For traumatically injured patients, time is critical and minutes mean life or loss of function. Let's say you fell off your bicycle and you lacerated, or cut, your brachial artery, the artery that supplies your arm. If you don't go to a trauma center within a short period of time — minutes, maybe an hour max — you will likely die from that relatively straightforward injury.
The two things that trauma centers are very good at is stopping bleeding that will lead to death, and controlling complications of trauma. Those require a coordinated set of team members to do all those things in a short period of time.
In 1991, when there was no adult trauma center on the South Side, people who were injured on the South Side of Chicago would go to other adult trauma centers throughout the city. Chicago, as you know, is a pretty big city. You can drive for an hour and still be in Chicago. It's hard for me to calculate the number of lives lost [because of the time it took to reach a trauma center].
That's exactly what happened to a kid by the name of Damien Turner. He was an 18-year-old community activist advocating for rent control and other social issues on the South Side, and unfortunately, he was shot on August 15, 2010, literally four blocks from the University of Chicago. He was transported to Northwestern, where he arrived dead. His mother said that, "If the South Side had an adult trauma center, my son would still be alive."
You can debate whether or not that may be true, but it's hard to debate the reality that time matters if you're shot and actively bleeding to death. Because Damien Turner led a youth group called Fearless Leading by the Youth, in his honor, that organization mobilized around a simple slogan: Trauma center now.
This problem of gun violence in America is not unsolvable, it's not intractable.
NL: What do you think people often get wrong about gun violence in Chicago?
SR: Chicago has an outsized influence in this country, for better or for worse, right? It's in the middle of the Midwest. It has very high visibility as the third largest city. We've had mayors and governors and presidential candidates and presidents of the United States. All those things have put a lot of spotlight on Chicago.
With this framing that Chicago has all this violence, this is all a Democratic city problem — urban blight became synonymous with Chicago, which is far from the truth. One of the things that made me write the book is to dispel those myths. But also to bring the stories to change the narrative that this problem of gun violence in America is not unsolvable, it's not intractable.
If we bring a public health lens, we can solve this problem, just like we've solved so many others.
NL: What would it mean to bring a public health lens?
SR: Going back to 2005, when I was in training in Boston, I was very struck by people who came back over and over again, injured. So we developed a violence recovery program that was hospital-based. The number of these programs have grown over the past 20 years to basically embed people with lived experiences — some of whom have been shot themselves, some of whom have been justice-involved — as credible messengers to help connect people with services, provide psychological support, and change the arc or trajectory of people's lives.
That's what I would call secondary prevention. Something has already happened; how can we lower the risk? It's no different than someone who has an opiate addiction, and we make sure that they have access to naloxone so that they don't overdose and die. That's a public health risk mitigation strategy. Having a team of credible, trusted messengers to help transition that person from injured to recovered is something that every hospital should invest in.
Ideally, we would also invest in programs to prevent people from being injured in the first place. Those are harder because they're not constrained within the four walls of an emergency department or the many, many walls of a health system. They're, if you will, societal.
I think that there is an important opportunity for surgeons in particular, plus emergency medicine, physicians, nurses, and other healthcare providers, to bring voice to the voiceless. Oftentimes, people who are injured who come into our emergency departments, they don't have the agency that a physician or nurse or other healthcare provider has. How can we bring their voice to the forefront, often realizing that people who are the closest to the problem can often be the source of some of those solutions?
Our opportunity for primary prevention that I see is that we could approach gun violence not as a criminal problem, but as a public health one, for which we need to determine risk factors, protective factors, mitigation factors to lower people's risk.
NL: What do secondary prevention programs look like for the patients?
SR: There are probably 80 or so hospital-based violence intervention programs across the country with a blueprint that's been coordinated by a nonprofit called the Health Alliance for Violence Intervention. It hires individuals who are not necessarily social workers or pastoral care (though they can be), but often people with lived experience from the community that can relate to and can connect with the person because they've either been in the situation themselves, or they're from the neighborhood, from the community.
That's the first thing, to create that trusted relationship. The next thing that happens is you're getting out of the hospital. What's your life look like afterwards? If you were on the margin and living paycheck to paycheck, and now you're not working, now you can't pay your rent. Where's the next meal gonna come from?
Turns out there's a whole host of community-based organizations that are doing great secondary prevention work. Our violence recovery team can be the connector.
We could approach gun violence not as a criminal problem, but as a public health one.
It's not like we're creating new services; there is the Supplemental Nutrition Assistance Program, there is the Victims of Crime Act, which is a fund, but people don't know about it and don't know how to access it. A violence recovery team serves as a connective tissue or bridge to those services to get people access to things that they need to keep on progressing and recovering.
There are also a number of more established secondary prevention efforts. Oftentimes, street outreach organizations like Institute for Nonviolence Chicago have credibility to interrupt those cycles of violence. And there are others, like Cure Violence, that take people with lived experience, who are justice-involved, have spent time in prison or jail, and want to do something positive.
Those people are incredibly strong proponents; they don't want their son, their brother to be injured like they were injured. Those people can be important interrupters to the cycle of violence. They know many of the people in the community that are involved, and sometimes, it's literally a conversation to prevent a retaliatory shooting.
With that framing, you take folks who have been injured, shot themselves or [who have] shot others, and you wrap around a set of services to take them from the illegal economy into the legal economy. That might involve trauma-informed care, cognitive behavioral therapy, and skills development. I think those are all things that have evolved very intentionally in the city of Chicago over the past decade.
NL: We're currently seeing social support being weakened at the federal level. Do you see that as a place for cities to step up in new ways?
SR: In Chicago, I'll give a specific example for the community violence intervention ecosystem. The civic business community have put their money where their mouth is. They've put in $100 million over the past several years; that's new funding that wasn't there before.
Holistically, no matter what's going on at the federal, state, municipal, local level, at the end of the day, it is about the human connection, right? It's about what we do for the person next to us. It's what we do for our neighbor. If your neighbor is sick and shut in, do we actually show up for our neighbor and say, "Hey, can I bring you a cup of soup?" How much does that really cost?
You don't need the federal government to do that.
This interview has been condensed and edited lightly for clarity.
"Healing the Gun Violence Epidemic"
"Healing the Gun Violence Epidemic" shares the stories of gun violence victims that Dr. Selwyn Rogers Jr. has met through his work as a trauma surgeon, as well as the lessons he's taken from bearing witness to that multifaceted trauma. Rogers explores underlying factors driving gun violence and shares insights into which policies have failed and which solutions have succeeded not just in his home of Chicago, but across the United States.
What it means: Genes contain the instructions for the various proteins that determine traits, such as eye color or blood type. An allele is a specific variant of a gene. Alleles come in pairs, one from each parent. Some are dominant, meaning that copy will override any instruction from the other allele in the pair, and some are recessive, meaning there have to be two copies of that particular allele for those instructions to translate into an observable feature. Of course, not all inheritance is as simple as dominant and recessive patterns, particularly for traits that arise from combinations of hundreds of genes.
How to use it in a sentence: We learned in grade school that alleles for brown eyes are dominant over alleles for blue eyes, leaving the kids with hazel eyes feeling lost and confused.
Can you crack our science word of the day puzzle, Chain Word?
Scientists may have found a way to rejuvenate key cells that help rebuild muscle in the body and thus preserve muscle into old age, they report in a new mouse study.
It is "really exciting stuff," Matthew Krause, a muscle physiologist at the University of Windsor in Ontario, said of the results. It could have clinical applications down the road if shown to work in humans, as well, added Krause, who was not involved in the research.
The body loses muscle with age and with chronic conditions that compromise people's mobility. To find a potential treatment for this muscle atrophy, the scientists behind the new study looked to "satellite cells." These stem cells are located around skeletal muscle fibers and play an important role in muscle regeneration.
Muscles incur microscopic damage with use, and this damage calls satellite cells into action. They proliferate to rebuild muscle fibers, by either merging into the torn muscle cells or forming new muscle cells. With age, satellite cells activate less efficiently and muscles become weak. But the new study, published July 24 in the journal Scientific Reports, suggests that it may be possible to rescue satellite cells from dormancy.
When muscles tear during exercise, a protein called hepatocyte growth factor (HGF) gets released. This is the signal that binds to receptors on satellite cells and activates them. Previously, studies from the same team showed that HGF works less well in old lab mice because its structure is chemically altered by a compound called peroxynitrite, and this makes it harder for HGF to plug into its receptor on satellite cells. This chemical alteration is known as nitration.
Peroxynitrite is produced through the reaction of unstable nitrogen and oxygen molecules, called radicals, said study co-author Ryuichi Tatsumi, a muscle physiologist at Kyushu University in Japan. These radicals are produced during normal metabolism, but their levels increase with age, he explained.
As a result, satellite cells cannot be activated efficiently to trigger muscle growth, even if the amount of HGF itself does not decline. Tatsumi and colleagues showed this in a previous study in rats.
Regular physical activity can help older adults preserve muscle, but even so, muscular tissue tends to weaken with age. (Image credit: Maskot via Getty Images)
In the new study, the scientists tested two compounds to see if they could counter this effect in lab mice. They used an experimental setup in which mice couldn't use their muscles as normal, so they weakened; such muscle disuse is known to increase HGF nitration around muscle cells.
Both of the tested compounds are known to protect proteins from damage caused by highly reactive chemicals by intercepting the reaction before it can take place. In experiments, the team treated HGF with each compound before exposing it to peroxynitrite. They found that, compared with untreated HGF, HGF treated with either compound showed substantially lower levels of nitration. This preserved its ability to activate satellite cells grown in lab dishes.
At high concentrations, one of the compounds — lipoic acid trisulfide (LASSS) — not only prevented nitration but also markedly increased HGF's ability to plug into its receptor. That suggests LASSS may chemically modify HGF in a way that could boost its effects.
To see if these observations carried over to living animals, the researchers gave lab mice LASSS in their drinking water. Although these were young mice, they were prevented from bearing weight on their hind limbs for five days, so they experienced short-term muscle disuse. Compared with untreated animals, the mice given LASSS had substantially lower HGF nitration around their muscle cells.
It's "pretty remarkable" that providing LASSS by mouth was sufficient to produce this effect, Krause said. He noted, however, that the researchers did not measure muscle atrophy or try administering LASSS to old mice to see the effects on the muscle. Longer experiments would be needed to observe those changes, he told Live Science.
The compound could also be tested in other forms of muscle wasting, Krause suggested. For example, severe chronic diseases like cancer can cause cachexia, a wasting syndrome marked by dramatic weight and muscle loss.
In general, protein nitration has been linked to several age-related disorders, including Alzheimer's disease, in which nitrated proteins accumulate in the brain. Understanding how to protect proteins from this kind of chemical damage could have implications beyond muscle biology, Tatsumi said.
However, further studies are still needed to assess the effectiveness and safety of LASSS in older animals. Experiments involving aging animals are expensive and can take a lot of time, Tatsumi said, but he is optimistic that this understanding will help address a range of age-related disorders with this same underlying biology.
"That is our big wish," he told Live Science. "I think, in the near future, we can do that."
As recently as 2019, U.S. military health researchers had concerns about testosterone levels among the troops. Their worries were not that male service members didn't have enough of the hormone, as current Defense Secretary Pete Hegseth fears. Instead, experts worried about the troops' inappropriate use of testosterone replacement therapy (TRT), the practice of using injectables or gels to increase a person's circulating testosterone.
"Out of every 1,000 male service members, almost 3 are inappropriately receiving TRT," researchers wrote in a report published on Health.mil, the military's health system website. (That report is available on the Wayback Machine.)
This could lead to harmful side effects, the report authors noted.
"Those being inappropriately treated may experience adverse effects of the medication," including obstructive sleep apnea and edema, the report continued. TRT may worsen sleep apnea and cause swelling in the limbs from water retention. "These adverse effects have the potential to impact deployability and medical readiness."
In short, supplementing testosterone unnecessarily could reduce military readiness, rather than boost it, per the report authors. Now, in a reversal of these concerns, more service members might find themselves offered TRT in the wake of a new military policy announced July 15 by the Department of Defense. It states that all active-duty and reserve service members' testosterone levels will be tested annually starting at age 30.
It is unclear how the policy might affect female service members. Live Science contacted the Department of Defense, which declined to answer questions about the expected testing protocol or criteria for offering service members TRT.
Such an initiative goes well beyond what medical organizations recommend regarding hormone screening for men, experts told Live Science. And while the screening could catch some service members who actually need treatment, the policy might also lead to overtreatment and, in turn, unwanted side effects.
"One of my big, big concerns around this is, how are these tests going to be conducted?" said Luke Cox, a lecturer in sport and exercise science at Swansea University in the U.K. who studies performance-enhancing drugs, including steroidal hormones like testosterone.
Testosterone and military readiness
Testosterone has strong cultural connections with hypermasculinity. As the primary hormone responsible for the development of male sexual characteristics, it's been associated with concepts of strength, aggression and virility. Hegseth continued this pattern by tying the hormone to military readiness in a video announcing the policy change.
"[I]t's about restoring and optimizing your natural capabilities, projecting your longevity and ensuring you have the biological foundation required to sustain the fight," Hegseth said.
That rhetoric aligns with promises made in advertisements for TRT, which pitch testosterone as a tool to "attain that higher level of living," Cox told Live Science. The clinical trial data is more circumspect, however.
In men with genuinely low circulating testosterone levels — often defined as lower than 300 nanograms per deciliter (ng/dL) — TRT does have benefits. (This 300 ng/dL threshold isn't the universal definition for "low testosterone," as not everyone below that line has troubling symptoms. We'll unpack that later.)
Much of the clearest evidence of benefit is for sexual symptoms: In a large clinical trial, men with low testosterone saw increased sexual desire and sexual activity, such as masturbating or having sex, after TRT. For men whose levels are not low, additional supplementation hasn't been shown to have a clear benefit in the bedroom.
One side effect of TRT is that it often dramatically lowers sperm count, because supplementing testosterone prompts the body to stop making it in the testes. (Image credit: SCIEPRO/SCIENCE PHOTO LIBRARY via Getty Images)
Most of this research has been done on men over age 40, because testosterone naturally declines with age. Low testosterone is rarer in younger men, although exact estimates of its prevalence vary. Estimates also vary among older age groups, but a large study called the European Male Ageing Study found that 0.1% of 40- to 49 year-olds had low testosterone, along with symptoms such as fatigue or low sexual desire. That number rose to 5.1% among those in their 70s.
In 2024, 42.8% of active-duty military members, including men and women, were 25 and younger. Only 8.3% were 41 or older. But the prevalence of low testosterone is generally on the rise, said Dr. Joshua Halpern, chief scientific officer and regional medical director at Posterity Health and a reproductive urologist at Northwestern University's Feinberg School of Medicine.
It will be very important for them and their physicians to understand the risks of treatment and the alternatives that may be more appropriate for preserving their fertility.
Dr. Joshua Halpern, Posterity Health and Northwestern University's Feinberg School of Medicine
Studies suggest that testosterone levels are lower, on average, in young men today than they were in the year 2000. Scientists have theorized that this trend may stem from increases in body mass index, as well as other factors, such as sedentary lifestyles, changing diets and exposure to environmental toxins, according to a 2020 article in Urology Times.
"While active service members are typically among the healthiest of men, and therefore at lower risk for testosterone deficiency, a significant proportion of service members could have a low testosterone number," Halpern told Live Science. "But that doesn't necessarily mean they should receive treatment."
Treating with testosterone
There is no universal testosterone level that is definitively "too low." The cutoff of 300 ng/dL is based on the point at which symptoms of low testosterone — such as fatigue, low libido and poor mood — tend to present themselves. However, some men have no problems associated with low or low-to-normal numbers.
Plus, testosterone doesn't act in isolation. In fact, some symptoms of "low T" in aging men may actually arise from low estrogen, which stems from these individuals' declining testosterone levels. That's because the male body converts a portion of its total testosterone into estrogen. The two hormones normally work together to regulate sexual desire and erectile function, while estrogen specifically regulates fat accumulation, studies suggest.
There is also a broad range of "normal," running from around 300 to 1,000 ng/dL. For that reason, the American Urological Association recommends testing only if a man is experiencing symptoms that point to low testosterone.
"Making a diagnosis of testosterone deficiency in the absence of signs and/or symptoms increases the likelihood of making a false diagnosis and reduces the potential benefit of testosterone therapy," the association's guidelines state.
Testosterone also has a complicated role in the body. It can affect mood, energy and bone health, but the hormone itself can also be affected by health conditions and lifestyle factors. Studies suggest that intense periods of physical training can temporarily suppress testosterone in military members. That finding tracks with civilian studies that have found that levels can shift dramatically based on people's recent sleep and exercise.
That's why doctors recommend two separate blood tests, both taken in the morning, before diagnosing low testosterone. This helps to ensure that a person's levels are consistently in a low range.
In some cases, it may be that the best treatment isn't TRT but rather an approach that addresses the underlying health conditions that are affecting testosterone levels. This might include assessing whether a patient has sleep apnea and treating it if they do, for example.
Meanwhile, pushing testosterone levels too high can lead to erythrocytosis, an overconcentration of red blood cells that can bring a risk of blood clots and stroke. What constitutes "too much" varies person to person. Due to some testosterone being converted into estrogen, too-high levels can also lead to unwanted side effects like breast growth in some men on TRT.
The other major side effect of TRT is that testosterone replacement shuts off the body's own production of testosterone in the testes. TRT only raises the level of testosterone circulating in the blood, not in the testes where sperm production takes place. Sensing the testosterone in the bloodstream, the brain suppresses its production in the testes, thus diminishing or stopping sperm production. This can cause infertility, and sperm production may take several years to recover after a person stops TRT.
"[F]or young service members who are found to have low testosterone, it will be very important for them and their physicians to understand the risks of treatment and the alternatives that may be more appropriate for preserving their fertility," Halpern said.
Meanwhile, a federal judge has questioned the treatment program. An ongoing lawsuit against the federal government's ban on transgender troops states that "the Armed Forces must adhere to high mental and physical health standards ... without the benefit of routine medical treatment or special provisions." The judge raised questions about how the TRT that will be offered to cis men differs from that which transgender men would use.
This article is for informational purposes only and is not meant to offer medical advice.
Redheads are a rare breed, with people who sport ginger locks making up less than 2% of the global population. With such low numbers, would it be possible for red hair to go "extinct," leaving people with natural hair hues ranging from black to blond, with nary a hint of red?
In a word, no. Experts told Live Science about how the genetics of red hair means the trait is sticking around.
"There is no evidence that redheads are going extinct," said Katerina Zorina-Lichtenwalter, a research associate at the University of Colorado Boulder's Institute for Behavioral Genetics who has studied red hair inheritance. She told Live Science that the genes responsible for red hair "are harmless, they do not interfere with reproduction and they are not linked to a disease that would prevent people from reaching reproductive age."
Nevertheless, the myth of an impending red hair extinction isn't a new one.
"The 'Is red hair becoming extinct?' question has been around for decades," Ian Jackson, a professor emeritus at the University of Edinburgh's Institute of Genetics and Cancer, told Live Science. "There have also been extinction stories about blond hair that go back to the mid-19th century."
The logic behind the supposed redhead extinction usually goes something like this: Red hair is rare; in the world's redhead hotspots in the United Kingdom and Ireland, only about 10% of the population is categorized as redheads. And red hair is a recessive trait, meaning two redhead carriers have to have get together to have redheaded children.
But these issues won't doom redheads to extinction, experts said.
First, let's look at genetics. A person needs to inherit the recessive version ofMC1R — a gene involved in pigment production — from both parents. Someone with only one copy may not have red hair at all, but they can still pass the variant to their children. So, the role of carrying red hair genes through the generations is shared by people of all hair colors, not just redheads.
Redheads celebrate Redhead Day on Sept. 4, 2016 in Breda, a city in the Netherlands. (Image credit: Brian Dowling via Getty Images)
This hidden-carrier effect is why a recessive trait can remain in a population even when it is uncommon to see. Jackson gave a simple example: If a variant is carried by half the population, only about a quarter of couples would both carry it. Among those couples, roughly one-quarter of children would inherit two copies.
For red hair to truly disappear, the relevant variants would have to be steadily removed from the gene pool. In evolutionary terms, that would usually mean people carrying these variants — or people with red hair — were having fewer children than everyone else.
"The only reason things go extinct in large populations is because you don't produce as many kids as the others, to put it in blunt terms, and I don't know that there's any evidence for that," Jonathan Rees, professor emeritus of dermatology at the University of Edinburgh, told Live Science.
Second, let's look at skin cancer risk. Rees said people with MC1R variants have a greater skin-cancer risk "somewhere in the region of two to four fold."
But skin cancer risk does not automatically equal evolutionary decline. Many skin cancers occur after people have already had children. Mortality rates for melanoma in the U.K. are the highest in people aged 90 and older, according to Cancer Research UK, after they've had more than enough time to pass on their genes.
Theoretically, before the invention of sunscreen and modern medicine, it may have been more likely for redheads to have died of skin cancer before they had children. Given that the trait has persisted, though, are there any evolutionary benefits to having red hair?
Red hair may carry surprising health advantages. For instance, recent research suggested the red‑hair pigment pheomelanin can help regulate excess cellular cysteine, which can be harmful at high concentrations.
"The vitamin D story is the one that people most often peddle," Rees said. The idea being that lighter pigmentation of the skin (and red hair being linked to lighter skin) increases the amount of vitamin D that people can make during the gloomy winters. But he added that the evidence there is lacking, especially because it can be hard to define who, exactly, is a redhead. It's a spectrum: where does red hair end and strawberry blond hair begin? That makes it hard to study without sequencing the genomes of large swathes of the population.
However, the frequency of red hair could still fluctuate. Jackson said the frequency may "go down somewhat as people become more mobile" and have children with partners from regions where MC1R variants are less common. But that would be a change in frequency, not extinction.
As long as MC1R variants persist silently in carriers — and as long as redheads are not having significantly fewer children than everyone else — the world's redheads are not about to disappear.
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