Publisher Health

New research from the University of Oklahoma has revealed how an aggressive type of breast cancer can manipulate the immune system to draw nerves into tumors, creating conditions that may help the cancer grow.
Scientists have known for years that many solid tumors contain extensive nerve networks. What has been less clear is how those nerves enter the tumor in the first place. The new study, published in Cell Death & Differentiation, provides an explanation for this process in triple-negative breast cancer, a particularly difficult form of the disease to treat.
Immune Cells Help Draw Nerves Into Tumors
The researchers discovered that tumors attract macrophages, a type of immune cell that normally helps the body fight infections and repair damaged tissue. After entering the tumor, these macrophages release brain-derived neurotrophic factor (BDNF), a protein that encourages nearby nerves to grow toward and into the cancer.
BDNF is most widely known for supporting the growth and survival of nerve cells in the brain. In breast cancer, however, the researchers found that tumors can take advantage of this same biological signal. By prompting nerve growth inside the tumor, the process may contribute to cancer progression and resistance to treatment.
“Macrophages are the critical source for drawing nerves into the tumor. Although macrophages typically play a positive role in the body, they are facilitating a negative function in this scenario of breast cancer,” said Maureen Cox, Ph.D., an assistant professor in the Department of Microbiology and Immunology at the OU College of Medicine and a research member of OU Health Stephenson Cancer Center.
Blocking the Signal Slowed Tumor Growth
The discovery could open the door to a different way of treating cancer. Instead of focusing only on destroying cancer cells, future therapies might interrupt the signaling between macrophages and the nerves that appear to support tumor growth.

Cox and her colleagues tested this strategy in mice. They used a drug that blocks BDNF signaling and found that nerves no longer grew into the tumors. Tumor growth was also significantly reduced.
“It looks really promising that we can use this drug, which is already on the market, to target BDNF,” Cox said. “We believe that the nerves are immunosuppressive, so if we can stop the nerves from growing in the first place, maybe we can boost the immune response to help fight the cancer.”
Evidence From Triple-Negative Breast Cancer Patients
The researchers also examined data from people with triple-negative breast cancer to determine whether the same biological pattern might occur in humans. Tumors containing higher levels of macrophages and BDNF were linked with poorer survival, providing evidence that the mechanism observed in mice could also be relevant to patients.
Cox and her team now want to better understand exactly how nerves contribute to tumor growth. Some evidence indicates that nerves may stimulate the formation of blood vessels, which can supply tumors with oxygen and nutrients. Other research suggests that cancer cells may move along nerves as they leave the original tumor and metastasize.
The researchers also plan to test the same intervention in high-grade ovarian cancer, another aggressive cancer that can be difficult to treat.

“Ultimately, we want to turn the anti-tumor immunity back on in cancer patients so their own immune systems can reject the tumors,” she said.
Research Support
The research was supported by the National Institute of General Medical Sciences of the NIH (award numbers P20GM103447 and P20GM103639). This project was also supported by Oklahoma’s Tobacco Settlement Endowment Trust (TSET), a primary funder of the Stephenson Cancer Center and TSET Health Promotion Research Center at the University of Oklahoma, and by the Oklahoma Shared Clinical and Translational Resources through an Institutional Development Award from the National Institute of General Medical Sciences (grant no. U54GM104938).

Ursula Quitterer calls it “Compound 10,” a chemical substance developed by her research team that could potentially slow the progression of Alzheimer’s disease.
Quitterer, Professor of Molecular Pharmacology at ETH Zurich, has so far tested the experimental treatment in mice. The results were encouraging. The nerve cell death typically associated with dementia slowed significantly, and the treated animals lived longer.
The work behind the compound began nearly 20 years ago, when Quitterer received brain tissue samples from patients treated by a doctor and colleague at Ain Shams University Hospital in Cairo. The tissue had been removed during tumor surgery from people with dementia as well as non-dementia patients.
A New Drug Target in Alzheimer’s Disease
Quitterer used those samples to investigate an enzyme called GRK2, which has long been a major focus of her research.
GRK2 plays an important regulatory role in many human cells. It helps cells respond appropriately to signals, stress, and strain. The enzyme is active in organs including the heart and the brain, where it helps support normal nerve cell function.
By analyzing the Cairo tissue samples at the molecular level and conducting experiments in mice, Quitterer and her colleagues uncovered evidence that GRK2 plays an important role in dementia. Their findings were recently published in the journal Cell Reports Medicine.

What Happens When GRK2 Stops Working
GRK2 exists in cells in two forms. One is normal and functional, while the other has been inactivated by cellular metabolism.
Quitterer’s team found unusually large amounts of the inactive form in brain tissue from people with dementia. The researchers observed the same pattern in mice, specifically in a mouse model for Alzheimer’s disease.
They also discovered that inactive GRK2 can clump together inside brain cells during dementia. These aggregates collect on mitochondria (the “powerhouses” of the cells), where they can interfere with normal function and cause damage.
“The GRK2 aggregates block the pores of the mitochondria, reducing the amount of energy they can supply and leading to a situation of stress inside the cells,” Quitterer explains.
The mouse experiments revealed another important effect. Inactive GRK2 appeared to increase production of amyloid beta, a protein fragment that is considered a main cause of Alzheimer’s.

That process can then feed back on itself. Amyloid beta places additional stress on nerve cells, and that stress encourages the formation of more inactive GRK2 and more GRK2 aggregates. The result is a vicious circle that can contribute to the progression of dementia.
Compound 10 Breaks the Harmful Cycle
To interrupt this process, Quitterer and her colleagues created several chemical compounds and tested them in cell cultures and mice.
Compound 10 stood out as particularly effective. It prevented GRK2 molecules from forming aggregates, which allowed mitochondria to function better. The researchers also saw less amyloid beta accumulating in cells, while nerve cells were better able to maintain their function and avoid dying.
The effects were not limited to the brain.
In mice, compound 10 also had a positive effect on heart function and aging processes. One visible example was that older animals developed fewer grey hairs.
An Unexpected Effect on Aging
The broader effects of compound 10 suggest that interfering with GRK2 aggregation may influence more than Alzheimer’s related processes.
In addition to protecting nerve cells and supporting mitochondrial function, the compound appeared to benefit the heart and affect some signs of aging in the mice.
These findings remain preclinical, however. Compound 10 has not yet been developed into a treatment for people.
Why Alzheimer’s Research Takes Years
The researchers have applied for a patent covering compound 10, and the basic research phase has now been completed.
“It took so long simply because everything takes so long in Alzheimer’s research,” explains Quitterer.
Because Alzheimer’s is an age-related disease, the team needed to conduct experiments using older animals. In mice, that means working with animals that are about one and a half to two years old.
Each experiment can also require roughly one and a half to two years before researchers have enough information to draw conclusions and design the next study.
“It’s all a great deal slower than in cancer research, for example.”
Quitterer and ETH Zurich are now searching for a company interested in helping move the compound toward the next stages of drug development.
A Different Approach to Treating Alzheimer’s
“Alzheimer’s is a very complex disease,” says Quitterer.
Existing medications do not cure Alzheimer’s. At best, they can delay its progression by several months.
“That’s why it’s so important that we’ve now identified a new target protein in the form of GRK2, as well as an active ingredient that operates via GRK2 and therefore via a different mechanism than existing Alzheimer’s drugs.”
Because compound 10 acts through a different biological pathway, the researchers believe it could potentially complement existing treatments rather than replace them.
Using compound 10 alongside other medications may one day help improve quality of life for people with Alzheimer’s disease.

A low dose of digoxin may help people with heart failure avoid hospitalization and reduce the risk of death, according to three studies led by UMCG cardiologists Dirk Jan van Veldhuisen, Kevin Damman, and Peter van der Meer. The researchers believe the new findings could eventually influence heart failure treatment guidelines and make this inexpensive medication available to many more patients.
Heart failure is a serious and growing health problem. More than 500,000 people in the Netherlands are estimated to have the condition, and that number is expected to increase in the years ahead. In people with heart failure, the heart cannot pump blood as effectively as it should. This can lead to severe shortness of breath, fatigue, and repeated trips to the hospital.
Digoxin Could Join the ‘Fantastic Four’
Standard heart failure care currently relies on a combination of four medications, commonly known as the ‘Fantastic Four.’ Cardiologists have long investigated whether digoxin could provide additional benefits as a fifth treatment.
Three UMCG studies now provide evidence supporting that possibility. The findings were published in publications including Nature Medicine and the Journal of the American Medical Association (JAMA) and were also presented at the ESC Heart Failure Congress in Barcelona.
Heart Failure Hospitalizations Fell by 25%
One of the studies included 1,000 people with heart failure who were treated at 43 centers across the Netherlands. Half received a low dose of digoxin in addition to their usual treatment for an average of three years, while the other half received a placebo.

Among those taking digoxin, deaths from cardiovascular disease and worsening heart failure were reduced (by 19%). However, that individual result did not reach statistical significance.
The researchers then combined the findings with data from two earlier studies in a meta-analysis, creating a much larger group of patients. With the additional data, they found that digoxin produced a meaningful and statistically significant benefit, even when patients were already taking the four standard heart failure medications.
The clearest benefit was a reduction in hospital admissions for heart failure, which fell by an average of 25%. Low-dose digoxin was also found to be safe and relatively easy to use.
Problems Increased After Digoxin Was Stopped
A third study followed approximately 600 of the original 1,000 participants who had been assigned either digoxin or placebo.
Researchers found that people who had been taking digoxin and then had to stop experienced significantly more problems during the first six weeks compared with people who had never taken the drug. Among 288 patients, 14 were hospitalized or died.

According to the researchers, this finding does not directly prove that digoxin is effective. Still, they considered the size and timing of the effect both impressive and surprising.
A Heart Failure Drug That Costs Less Than Ten Cents a Day
The researchers believe the results of the three studies could eventually lead to changes in heart failure guidelines, potentially allowing many more patients to receive digoxin.
Its low price makes the findings especially notable. Digoxin has been used in medicine for centuries and costs less than ten cents per day. By comparison, many newer heart failure medications cost several euros each day.
Why a Low Dose of Digoxin Matters
Digoxin (digitalis) is the oldest and least expensive medicine used to treat heart failure. At a low dose, the drug primarily works by reducing several harmful compensatory responses that occur when the heart is struggling. For example, digoxin suppresses stress hormones (such as adrenaline) in the blood, which can benefit the heart.
Higher doses of digoxin were commonly prescribed in the past. Those doses caused heart muscle cells to contract more strongly, but that effect ultimately proved less helpful. For a weakened heart muscle, reducing strain is preferable to forcing it to work harder.
During the past 25 to 30 years, several effective new treatments for heart failure have become available. As a result, digoxin use has steadily declined, and only about 15 percent of heart failure patients now receive it.
Earlier research had already suggested that patients given low doses of digoxin did considerably better than those receiving higher doses. Until the new UMCG research, however, randomized, prospective studies had not directly investigated and confirmed this effect.
Funding Made the Digoxin Studies Possible
Research involving older and inexpensive medications can be difficult to fund, even when those drugs have the potential to improve patient care while lowering costs.
Hartstichting therefore provided 3 million euros for this research through its collaboration with ZonMw as part of the Good Use of Medicines program.

Physical activity and healthy blood sugar levels during midlife may be linked to a significantly slower decline in thinking abilities later in life, according to new research from UT Health San Antonio, the academic health center of The University of Texas at San Antonio. The findings suggest that exercise may be especially important for Hispanic adults.
Scientists already know that cardiovascular problems in midlife can raise the risk of cognitive decline and dementia. This study is among the first to investigate how specific cardiovascular health factors may relate to cognitive aging across different ethnic groups.
Researchers analyzed 402 people from San Antonio. Of the participants, 52% were Hispanic, and the rest were non-Hispanic white. Their mean age was 57.9, and 58.5% were women.
The findings varied by ethnicity. Physical activity was particularly associated with slower cognitive decline among Hispanic participants, while lower fasting blood glucose levels were linked to slower cognitive decline among non-Hispanic white participants.
“By improving cardiovascular health through modifiable lifestyle changes, there is a potential to meaningfully alleviate the public health burden of Alzheimer’s disease and other dementias, particularly in high-risk populations,” said Claudia Satizabal, PhD, associate professor in the Department of Population Health Sciences at UT Health San Antonio and its Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases, where she leads the Population Neuroscience Core.
Satizabal is co-senior author of the study with Chen-Pin Wang, PhD, associate professor-research in the Department of Population Health Sciences. The research, titled “Longitudinal association between midlife cardiovascular health and cognitive change in a bi-ethnic cohort,” was published July 23 by Alzheimer’s & Dementia: Behavior & Socioeconomics of Aging.
All of the study authors are affiliated with either the Glenn Biggs Institute or The University of Texas Rio Grande Valley.

Cardiovascular Health and Dementia Risk
As people around the world live longer and the proportion of older adults grows, age-related conditions such as dementia are becoming increasingly common. The study notes that 6.7 million people in the United States currently have Alzheimer’s disease.
At the same time, research increasingly suggests that many risk factors for cognitive decline and dementia can be modified. Recent estimates indicate that nearly 40% of Alzheimer’s cases may be connected to such factors. Cardiovascular health, in particular, has emerged as an important influence on how the brain ages.
One widely used approach for measuring cardiovascular health is the American Heart Association’s Life’s Simple 7 (LS7) framework. It includes three behavioral factors (healthy diet, non-smoking, and physical activity) and four health factors (blood pressure, body mass index, total cholesterol and fasting blood glucose). According to the study, LS7 provides an overall measure of cardiovascular health and has also been proposed as a way to support better brain health.
Previous research has found that stronger adherence to LS7 is associated with better cognitive performance, healthier brains, and a lower risk of dementia. However, these relationships do not appear to be identical across different populations.
Hispanic older adults face a disproportionate burden of Alzheimer’s disease and related dementias. About 14% of Hispanic adults aged 65 or older have Alzheimer’s, compared with 10% of non-Hispanic white older adults. Mexican Americans, who make up the largest Hispanic population in the United States, also have particularly high rates of diabetes, obesity and dyslipidemia, conditions that can increase dementia risk.

Why South Texas Offers Important Insights
Despite these disparities, Hispanic populations remain underrepresented in Alzheimer’s research. The researchers note that this lack of representation makes it more difficult to understand how dementia risk develops over time and to identify prevention strategies that may work effectively for everyone.
To help address that gap, the UT Health San Antonio team investigated the relationship between cardiovascular health in midlife, measured through LS7 scores, and later cognitive decline among Mexican American and non-Hispanic white older adults. The participants had previously taken part in the San Antonio Heart Study (SAHS) and the San Antonio Longitudinal Study of Aging (SALSA).
The SAHS was a landmark, long-term project led by UT Health San Antonio to investigate the causes of Type 2 diabetes and heart disease. Conducted from 1979 through the 2000s, the project followed more than 5,000 people to better understand why certain ethnic populations experience higher health risks.
SALSA later grew out of that work. Also conducted by UT Health San Antonio, it became a major, long-term observational study focused on chronic diseases, healthy aging and the process through which older adults develop disabilities. Its participants had previously been enrolled in the SAHS.
“Importantly, the inclusion of both ethnic groups from the same source population and geographic setting allows for direct comparison within a shared contextual framework and strengthens our ability to identify disparities in cognitive aging and their cardiovascular correlates,” the new study notes.
Tracking Cognitive Changes Over Time
For the new analysis, researchers evaluated cardiovascular health among SAHS participants who were later enrolled in SALSA, using their LS7 scores.
Cognitive ability was measured as many as four times with the Mini-Mental State Examination, an established 11-question screening test that evaluates memory, attention and thinking skills.
The team also used generalized estimating equation models to examine how cardiovascular factors were related to changes in cognition. The statistical models accounted for age, sex, income, and education.
Researchers additionally performed sensitivity analyses to assess attrition bias. These extra statistical checks were designed to determine whether people dropping out of the study could have distorted the final results.
Exercise and Blood Sugar Show Different Links
The analysis found that engaging in any physical activity, rather than living a sedentary lifestyle, was particularly associated with slower cognitive decline among Mexican Americans.
Fasting glucose also emerged as an important factor. This measurement reflects the amount of sugar in the blood after an eight- to 12-hour fast. Among non-Hispanic white participants, fasting glucose readings of 126 milligrams per deciliter or lower were associated with a slower rate of cognitive decline.
“Our findings suggest that engaging in any level of physical activity and potentially maintaining optimal fasting blood glucose levels in midlife are associated with a significantly slower rate of cognitive decline in late life,” said Janette Vazquez, PhD, first author of the study and currently a senior postdoctoral fellow at the Glenn Biggs Institute. But since the results differed by ethnicity, further research is needed in larger samples to replicate the differences, she said.
The findings suggest that cardiovascular health during midlife could influence cognitive aging many years later, but they also indicate that the most important factors may not be the same for every population.
“The longitudinal exploration of cardiovascular health throughout life, rather than assessing it at a single time point, could also provide further insight into the trajectory phenotypes contributing to cognitive decline by ethnicity,” Vazquez said.
Participants from the study are now being invited to join the San Antonio Heart and Mind Study (SAHMS) at the Glenn Biggs Institute. Researchers hope the ongoing project will generate additional discoveries by collecting state-of-the-art brain imaging and other neurological data.

Growing older has plenty of upsides – but achy joints is not one of them.
As we age, the joints that once handled every bend and fall start to weaken. This is because the amount of cartilage, a tough but flexible kind of connective tissue, and fluid in your joints decreases over time.
This may lead some people to avoid activities such as exercise. But with the right approach, exercise can actually help protect your joints.
Let’s dive into the science.Why joints matterEach joint is cushioned by articular cartilage, a type of specialized tissue that covers the ends of bones. This cartilage protects the joints and creates a smooth surface for motion.
A thick liquid known as synovial fluid also helps lubricate your knees, hips and shoulders. It does this by reducing friction between your cartilage and joints. Synovial fluid also supplies cartilage with key nutrients.
However, cartilage isn’t very good at repairing itself. This is partly because it doesn’t have its own blood supply.

The gradual breakdown of cartilage is known as osteoarthritis, a condition which affects more than 500 million people worldwide. People with osteoarthritis often feel the most pain in weight-bearing joints such as the knees, hips and spine.How exercise impacts your jointsThe body distributes synovial fluid through motion. So exercise helps gets this fluid, and the nutrients it contains, to cartilage.
Meanwhile, muscles around your joints act as shock absorbers. So strengthening your muscles, including through exercises such as weightlifting, helps to reduce the pressure placed on your joints. Research suggests strength exercises targeting the quadriceps, a group of muscles at the front of the thigh, are particularly effective at reducing joint pain.
A landmark Cochrane review assessed all the relevant evidence looking at the effect of exercise on osteoarthritis. It found exercise reduces pain and improves function in people with knee osteoarthritis. It also showed exercise has a similar impact as anti-inflammatory drugs, but without the same side effects.
Exercise may also help maintain proprioception, the body’s ability to sense its own position and movement. However, proprioception declines with age. So as you get older, your brain is less able to register these signals and may cause your joints to bear weight unevenly. This wears down your joints quicker.
However, exercising on varied and even unstable surfaces can reduce this wear-and-tear process. It forces your ankle, knee and hip joints to quickly adjust their movements, keeping them engaged and flexible.What about low-impact exercise?

Low-impact exercise refers to exercises where you keep at least one foot on the ground, or support the body in some other way. This kind of exercise reduces the amount of weight and force placed on joints.
Examples of low-impact exercise include swimming and water aerobics. Both involve being suspended in water, which can support up to 90% of your body weight. Cycling may also be beneficial for your joints, particularly your knees.
Tai chi, a gentle form of exercise based on gentle movements and breathing techniques, is another option. Research suggests it may be as effective as physical therapy for people with knee osteoarthritis. Yoga can also help strengthen the muscles around your joints and improve your overall flexibility.
Walking deserves a special mention. Walking on uneven terrain, such as on grass, gravel or bush trails, can help maintain proprioception. One 2026 study found unstable surface training significantly improves postural control, or the ability to remain stable, in older adults.
Another systematic review found exercises which challenged participants’ balance reduced fall rates by roughly 23%. This is important, given falls are the leading cause of injury-related death in adults over 65.I’ve never done low-impact exercise. How can I start?Here are three tips to make low-impact exercise as safe and effective as possible.
1. Start small
You don’t need any fancy equipment to start. Where possible, opt to walk on uneven surfaces, such as grass, sand or gravel, instead of pavement. Even ten minutes walking across a park lawn will improve your joint movement.
You can also practise standing on one leg, for example while brushing your teeth. It’s best to start on firm ground first, aiming to stand on each leg for 30 seconds. You can then progress to standing on a folded towel or foam pad. Importantly, you should master each task or level of difficulty before advancing.
2. Use support
Safety is paramount. Always perform low-impact exercises near something you can hold for support, such as a park bench or bathroom vanity. If you’re walking for exercise, walking poles are an excellent option. Importantly, never exercise on unstable surfaces when you’re tired.
3. Get advice
No exercise is risk-free. For example, holding a yoga pose beyond your range of motion may injure your lower back, shoulders or knees. Doing deep squats or lunges with poor form can put unnecessary strain on your knee joint.
So before you start, speak to a certified exercise physiologist or physiotherapist. They can help you design a tailored exercise program.The bottom lineOur joints are subject to the inevitable wear-and-tear of age, but low-impact exercise can help. So it’s worth trying, no matter how young or old you are.

New Australian research is shedding light on why walking often becomes slower and more tiring with age. The findings suggest that the body gradually gives up some movement efficiency in favor of staying stable and upright.
Led by researchers at Flinders University and the University of Canberra, the study found that aging is associated with a “safety-first” walking strategy. This approach emphasizes stability instead of speed and energy efficiency, helping explain why older adults may fatigue more quickly and also face a greater risk of falling.
Researchers analyzed movement data from 107 healthy adults between the ages of 26 and 86. They found small but meaningful age-related differences in how the ankle and nearby muscles manage each step.
How the Ankle Changes With Age
Lead author and sport and exercise technology expert Dr. Cody Lindsay says the ankle is essential for maintaining balance while also helping propel the body forward.
“As we get older, the body starts to favor stability over efficiency,” says Dr. Lindsay, from the Flinders Caring Futures Institute.
“That helps keep us upright, but it also makes walking more of an effort.”
The researchers found that older adults are more likely to activate opposing muscles around the ankle at the same time. This pattern is known as co-contraction. It makes the ankle joint stiffer and can improve stability when the foot contacts the ground.

However, Dr. Lindsay says this comes at a cost.
“Stiffening the joint makes walking safer, but it also means the muscles are working harder without generating as much forward movement,” he says.
Older participants also generated less push-off power with each step. As a result, their strides were shorter, and their walking speeds were slower.
A Safety First Strategy for Walking
Co-author Associate Professor Maarten Immink says the findings point to a wider change in the way the body manages movement as people grow older.
“The nervous system adopts a safety-first approach, compensating for age-related changes by favoring stability over performance,” says Associate Professor Immink, Lead of the Active Lives Research Program within the Caring Futures Institute at Flinders University.

“These changes can also increase fatigue and make walking longer distances more challenging, while reducing the ability to recover from trips or slips — a key factor in falls among older adults.”
“Even gradual changes can affect confidence and independence, and people may notice they tire more quickly or feel less steady, especially on uneven ground.”
Exercise May Help Preserve Mobility
The findings also suggest possible ways to help people maintain mobility as they age.
Rather than focusing only on building strength, the researchers say exercise programs should also emphasize balance and coordination while paying attention to how different muscles work together during each step.
“For older Australians, simple actions can make a difference, including regular physical activity, balance exercises such as tai chi, lower-leg strengthening and activities that challenge coordination,” says Dr. Lindsay, from Flinders’ College of Health and Enablement.
“Staying active is one of the most important things people can do, and small, consistent exercises can help you stay confident, mobile and independent for longer.”
The researchers hope these findings can contribute to improved prevention and rehabilitation strategies designed to reduce falls and support healthy aging.

Why Gen Z women know more about periods than their mumsImage source, Getty ImagesByJasmine Ketibuah-FoleyWest of EnglandPublished16 August 2026Terms such as “cycle syncing” and “going luteal” have become part of everyday vocabulary for many young women.From periods and hormones to PMOS (polyendocrine metabolic ovarian syndrome) and fertility, a growing number say they now understand their bodies better than previous generations did.But while campaigners welcome greater awareness, questions remain about misinformation and health anxiety.We spoke to women, parents and experts about the changing conversation around menstrual health.More from Bristol’People don’t expect disabled people to have sex’Published7 days agoIn pictures: Eclipse, elephants and wedding cowPublished7 days agoMan, 90, with Parkinson’s walks 90 miles for charityPublished15 AugustImage source, Iqra WasimIqra Wasim from Fishponds in Bristol has struggled with PMOS symptoms such as painful acne since the age of 11.PMOS affects about one in eight women. It is a major cause of female infertility and symptoms can include irregular periods, excessive hair growth and weight gain.Wasim, who learned more about it through asking doctors questions and social media, said she now educates her mum, who also has PMOS, on ways to manage symptoms.”My mum was going through heavy bleeding with her PMOS and didn’t know what birth control was,” she said. “I told her about it and she thought I was talking about being sexually active, but I explained there’s so much more to the medicine – that showed the main knowledge gap between us.”My mum’s generation did have knowledge, but it only stayed between women, families or doctors and now someone can talk about their period and PMOS online and millions of women can relate to it.”Our generation is more willing to ask whether something is normal.”But I don’t think that social media is a replacement for a medical professional,” Wasim added.Caroline Herman founded ‘All Yours Period Box,

Viruses that remain in the body for years, including Epstein-Barr, cytomegalovirus (CMV), and herpes virus, are extremely common. In many people, they cause no symptoms and appear to be harmless. But growing evidence suggests that when these dormant viruses become active again, they may play a role in autoimmune diseases and other long-lasting health conditions.
Now, researchers at Boston Children’s Hospital and collaborating institutions have found that COVID 19 can reactivate certain dormant viruses in hospitalized patients. The findings come from a new Nature study involving 15 biomedical research institutions across the United States. The results provide new insight into viruses that persist in the body and could eventually help guide strategies for preventing or treating their reactivation.
Tracking Hidden Viruses During COVID-19
Physician scientist Ofer Levy, MD, PhD, director of the Precision Vaccines Program (PVP) at Boston Children’s, served as a site principal investigator for the National Institutes of Health (NIH) funded research.
The study followed 1,154 patients across 20 U.S. biomedical research hospitals and was designed to identify biomarkers associated with COVID severity and patient outcomes. Researchers used genomic sequencing to search for signs that dormant viruses had become active again. Viral infections that have long since cleared from an active state can sometimes reemerge when the body is under stress.
“This is the largest and most comprehensive biomarker study of COVID-19, in which we followed more than one thousand patients, collected more than 200,000 samples, and generated more than 1 billion data points over the course of a year for this public resource,” says Joann Diray Arce, PhD, who leads the PVP-Data Management and Analysis Core and is the lead of the study’s Clinical and Data Coordinating Center.
11 Viruses Reactivated After Hospital Admission
Within the first 40 days after patients were admitted to the hospital, the researchers identified 11 reactivated viruses. The most frequently detected included Epstein-Barr, herpes simplex 1, cytomegalovirus, and Anelloviridae viruses.

One finding stood out in particular. Reactivation of Anelloviridae, a poorly understood family of viruses that typically remains latent in about 90 percent of the population, showed a prominent association with long-term physical disability and long COVID.
“This association with long COVID is an interesting finding as millions around the world suffer from this chronic condition,” says Levy. “Having new insight as to the molecular and viral associations with long COVID could point the way to better understanding and ultimately better diagnostics and treatments.”
Inflammation May Trigger Viral Reactivation
Blood sample analysis also revealed an unexpected pattern involving Epstein-Barr and cytomegalovirus. Rather than appearing to reactivate because the immune system had been suppressed, these viruses seemed to become active in response to inflammation.
Researchers say the finding points to a surprising mechanism and challenges the prevailing idea that chronic viral reactivation occurs mainly because of immunosuppression. The results show that dormant viruses can reactivate frequently in people who appear to have functioning immune systems during severe illness, particularly when systemic inflammation is elevated.
“Although many no longer think of COVID being a problem, up to 50,000 Americans died of COVID in 2025-2026 respiratory season and some estimates suggest over 10 million U.S. adults suffer from long COVID,” says Levy. “We need to help these patients recover with the best outcomes.” He adds, “Moreover, sooner or later, there may be another coronavirus pandemic, which means we need to learn all the lessons we can from COVID-19 to be better prepared.”
Searching for Better Treatments

The researchers next plan to investigate how the immune system responds to these reactivated viruses throughout the course of COVID 19. Their goal is to identify effective treatments and determine the best timing for possible interventions.
Other Boston Children’s researchers on the study include Jing Chen, PhD, Annmarie Hoch, Al Ozonoff, PhD, Kinga Smolen, PhD, and Hanno Steen, PhD.

What’s driving men to get penis fillers, despite the risks?Image source, Getty ImagesByJames GallagherInside Health presenter, BBC Radio 4Published16 August 2026Jason didn’t want a “Coke can” – that’s the nickname for a penis that has been enlarged with so much filler it resembles a stubby drink can.”Some people go really overboard,” Jason tells me when we meet in Manchester.His procedure increased the girth of his penis by 16% – an amount he, and his partner, are really happy with. He says it has given him a “self-confidence boost”.”Everything still functions” as normal, Jason explains – just with “that extra little bit of width”.It is not clear how many men like Jason are having penis fillers. And you can’t walk down the street and get a sense of it in the way you can visibly see the popularity of lip fillers. There is little regulation and there are no official records as anybody can start offering the procedure.Penis fillers even became the topic of a bizarre conspiracy theory at the last Winter Olympics. Male ski jumpers were rumoured to be using fillers to increase the surface area of their suits so they could jump further.However, some men have ended up in A&E with a penis turning black and skin “sloughing off” after a botched procedure. And the British Association of Urological Surgeons has issued warnings to men having these procedures.So why are men doing it and what are the risks?Why are men getting penis fillers?Inside HealthListen on SoundsJames Gallagher visits a private clinic to find out about about the procedure, meets a man who has had it done, and chats to a surgeon who says he is dealing with the consequences when it goes wrong.Jason talked to us frankly, but anonymously, about his decision to have fillers.He was happy with the length of his penis but wanted a “bit more symmetry” and more girth to “get that nice, balanced look”.”If you feel like it’s a bit lacking,” Jason says, “then, why not?”He spent a year weighing up options and ruled out having a surgical procedure. He chose a type of filler – hyaluronic acid – that is temporary so he knew that even if he hated the look it would “eventually just dissolve”.Jason says he wasn’t motivated by swaggering alpha masculinity – “I don’t subscribe to ‘how big your dick is, is how big of a man you are'”. Rather, he says expectations of male beauty have shifted.”It’s not just women that need to keep up, men need to keep up as well.”It’s literally just society changing. I think the way the media portrays everything has a massive impact on everyday life now,” he says. “It’s like you can’t actually go anywhere without seeing some picture-perfect somebody.”Trawl the websites of clinics offering penis enlargement – which ask questions like “are you embarrassed by the size of your penis?” – and you can see how some tap into this.There are a variety of penis-enhancement options. There are surgical and non-surgical techniques and different materials that can be injected into the penis.Most common by far is injecting the gel-like substance hyaluronic acid – the same key ingredient used in lip fillers.Hyaluronic acid is a naturally occurring sugar molecule in the body and is known as a “moisture magnet” as it grabs hold of water.Image source, BBC/James GallagherDr Javed Hussain has been offering penis fillers for more than a year at his clinic in Prestwich, Greater Manchester.Hussain trained as a doctor before moving into cosmetic procedures, but penis fillers do not legally require any medical training to perform. He says demand is increasing. He’s treated men of all ages – some in their mid-20s, while his oldest client is aged 72.The process starts with consultations on the patient’s health, reasons for wanting to have the procedure, expectations about the results, and a discussion about the risks.On the day of the event itself, a penis is injected with hyaluronic acid three times – on the top and on either side. The hyaluronic acid filler is delivered through a cannula that enters at the base and travels along the length of the shaft.Image source, BBC/James GallagherThe filler is then massaged to give an even look, which the patient continues as home.At a cost of up to £3,500, Hussain says men can expect between 10% and 20% more girth for the next six to nine months.But there are risks. These range from relatively minor ones such as soreness, bruising and uneven filler, to serious ones including infection. These risks apply to all procedures using filler. However, there is also a risk of damaging the vital structures and blood vessels in the penis that are needed for an erection. When asked why he feels comfortable offering procedures that are concerning surgeons, Hussain says he “totally understands” why some are worried. “It comes from the right place, that nervousness,” he says, “but at the same time, more and more evidence is growing and we’re getting the results” and that “there is a benefit” to men.Hussain says he has an “immediate action plan” including drugs to quickly dissolve the filler in the event that things go wrong, and reports that “thankfully, we’ve never needed to” – although the BBC cannot independently corroborate that.But he recalls one patient who came to him for advice after treatment elsewhere, which had “really gone wrong”.He says the incorrect type of filler had been used and the “shaft of the penis was starting to become black” as the procedure had damaged the blood vessels in the penis and the skin was dying. The man was sent straight to A&E.Image source, BBC/James GallagherProf Vaibhav Modgil, an andrologist and consultant urological surgeon for the NHS in Manchester, has seen these men coming into hospital after botched procedures.”When it does happen, it can be devastating for the patient,” he says.He recalls seeing men with “skin necrosis, where an area of the skin dies off it turns very black and then it sort of sloughs off.”So, men will go in thinking, ‘Oh, it’s gonna be brilliant’, but they might come out actually being even more dissatisfied than when they went in.”Alex, who did not want his real name to be used, travelled to Germany for a different type of penis enhancement procedure.He had surgery to cut the ligament that attaches the penis to the pubic bone to make it appear longer. He also had his own fat cells harvested and injected into his penis to enlarge it.When he woke up after the procedure, he was in so much pain he couldn’t stand.”I sustained a lot of bruising and all my upper legs turned yellow,” Alex says. “I couldn’t walk properly for about a month.”Alex was treated in Modgil’s clinic where eventually he was given the all-clear. “Many people do not get that luxury,” he says. “I got off lucky.”Alex says he knows he was “never small in the first place”, but society and porn had convinced him that a bigger penis was “masculine and the best”.Image source, Getty ImagesDespite a lack of official data on the number of penile enhancement procedures, Modgil says online search trends, advertising and social media all “points to the fact that the numbers are on the up”. This has led the British Association of Urological Surgeons to issue new recommendations against these procedures.”The guidance that we’ve recently produced essentially says we cannot recommend that any of these procedures should take place because the evidence is so poor,” says Modgil.It looked at 36 studies, involving 3,750 men, but said it was still not clear what the “safety profile” of these procedures were.This is partly down to a lack of data on how fillers affect the penis long-term. But there is also concern that – just like lip fillers – you do not need any qualifications to perform the procedure.Modgil says an outright ban is “probably too severe”, but if these procedures are going to continue then the industry “massively needs regulation”.He called for a national registry to record when penis filler procedures have been performed and for long-term data to be collected so men can make an informed decision based on the risks and the benefits.Back in Manchester, Jason is happy with the results of his procedure and thinks he’ll do it again when his current fillers wear off.Inside Health was produced by Gerry Holt.More weekend picks from James GallagherI tried the UK’s ‘saltiest’ sandwich – here’s what I learnedPublished16 MayI inhaled traffic fumes to find out where air pollution goes in my bodyPublished7 FebruaryI’m watching brain surgery to see if Alzheimer’s can ever be curedPublished26 December 2025I found a bacteria-eating virus in my loo – could it save your life?Published28 June 2025

Rising levels of carbon dioxide in the atmosphere may already be influencing human biology. New research has identified long-term changes in blood chemistry that appear to track rising atmospheric CO2, raising concerns that an important blood marker could approach the upper end of its healthy range within the next several decades.
The findings may be particularly important for children and teenagers. Because their bodies are still developing, younger generations are expected to experience the greatest lifetime exposure to elevated atmospheric CO2.
Decades of Blood Data Reveal a Shift
In a study published in Air Quality, Atmosphere and Health, scientists from The Kids Research Institute Australia, Curtin University and The Australian National University (ANU) examined more than 20 years of U.S. population health data. They found persistent changes in several measures of blood chemistry that closely followed the upward trend in atmospheric CO2.
The researchers used information from the U.S. National Health and Nutrition Examination Survey (NHANES), analyzing blood test results from roughly 7,000 people at two-year intervals between 1999 and 2020.
Since 1999, average serum bicarbonate levels have increased by about 7 percent. Bicarbonate is a blood marker closely associated with carbon dioxide in the body. During the same period, average levels of calcium and phosphorus decreased.
Those biological trends occurred as atmospheric CO2 climbed from about 369 parts per million (ppm) in 2000 to more than 420 ppm today.

Study author Associate Professor Alexander Larcombe said the results indicate that the body may already be adjusting to changes in the composition of the atmosphere.
“What we’re seeing is a gradual shift in blood chemistry that mirrors the rise in atmospheric carbon dioxide, which is driving climate change,” A/Prof Larcombe said.
How the Body Responds to More CO2
Bicarbonate is essential for regulating the body’s acid-base balance. As CO2 increases, the body can retain additional bicarbonate to help keep blood pH stable. Although this response helps preserve that balance, maintaining it over long periods could have physiological effects.
“If current trends continue, modeling indicates average bicarbonate levels could approach the upper limit of today’s accepted healthy range within 50 years,” A/Prof Larcombe said
“Calcium and phosphorus levels could also reach the lower end of their healthy ranges later this century.”
Humans evolved when atmospheric CO2 concentrations were approximately 280 to 300 ppm. During the past decade, atmospheric levels have risen by an average of about 2.6 ppm each year, while 2024 alone saw an increase of 3.5 ppm.

Fellow Author Dr Phil Bierwirth, a retired environmental geoscientist affiliated with the ANU Emeritus Faculty, emphasized that the study does not establish a direct cause-and-effect relationship. However, he said the consistency of the changes across a large population warrants attention.
“I actually think that what we are seeing is because our bodies are not adapting,” Dr Bierwirth said.
“It appears we are adapted to a range of CO2 in the air that may now have been surpassed.
“The normal range maintains a delicate balance between how much CO2 is in the air, our blood pH, our breathing rate and bicarbonate levels in the blood.
“As CO2 in the air is now higher than humans have ever experienced, it appears to be building up in our bodies. Maybe we can never adapt such that it is vitally important to limit atmospheric levels of CO2.”
A Potential New Dimension of Climate Risk
The researchers say the results suggest that rising atmospheric CO2 could represent a form of climate-related risk that is different from more familiar threats such as heatwaves, extreme weather and sea-level rise.
According to A/Prof Larcombe, increasing CO2 may need to be considered not only as an environmental concern, but also as a long-term public health factor that should be monitored.
“We’re not saying people are suddenly going to become unwell when we cross a certain threshold,” he said.
“But this suggests there may be gradual physiological changes occurring at a population level, and that’s something we should be monitoring as part of future climate change policy.”
The researchers recommend monitoring the composition of the atmosphere together with biological markers across populations. Tracking both alongside established climate indicators could help scientists determine how slow environmental changes affect human biology over periods of decades.
CO2 Reduction Could Have Health Implications
Cutting CO2 emissions remains essential for limiting global warming. The findings also raise the possibility that lowering emissions could have an additional role in protecting long-term human health.
The researchers argue that potential physiological effects from rising CO2 should therefore be considered in future discussions about climate policy, alongside its established environmental consequences.
Associate Professor Larcombe is part of the Wal-yan Respiratory Research Centre, a partnership between The Kids Research Institute Australia, Perth Children’s Hospital and Perth Children’s Hospital Foundation.