Publisher Health

A new study led by a team of researchers at Moffitt Cancer Center reveals that lymphoma can accelerate the biological aging of the immune system and other tissues, providing new insight into how cancer reshapes the body beyond tumor growth.
The study, published in Cancer Cell, shows that B cell lymphoma rapidly transforms young T cells, which are key immune fighters, into a state resembling those of T cells in much older individuals. These changes included increased inflammation, impaired protein balance and altered iron regulation. The effects were not limited to immune cells. Markers of aging also appeared in the blood vessels, kidneys and intestines.
“Cancer doesn’t just grow in isolation; it has widespread effects on patients. We found that lymphoma alone, without treatment, is enough to provoke systemic signs of aging,” said John Cleveland, Ph.D., senior author and chief scientific officer at Moffitt. “This helps explain why many cancer patients experience symptoms typically associated with aging.”
The findings challenge the long-held belief that accelerated aging in cancer patients is primarily caused by treatments like chemotherapy or radiation. While those therapies are known to age cells, this study shows that the cancer itself can push immune and tissue systems into an aged state.
“Our results also suggest there may be opportunities to reverse some cancer-driven aging effects,” said Rebecca Hesterberg, Ph.D., the study’s lead author and a researcher in Moffitt’s Department of Tumor Microenvironment and Metastasis. “By understanding the biology, we can begin to think about interventions that not only treat the cancer but also protect or even restore healthy immune function.”
Researchers discovered that lymphoma-exposed T cells accumulated excess iron, making them resistant to a type of cell death called ferroptosis. They also exhibited defects in protein quality control, a hallmark of aging. Some of these changes were reversible when tumors were eliminated in animal models, pointing to new therapeutic opportunities.
With the global population aging and cancer risk rising with age, the study underscores the importance of understanding how cancer interacts with aging biology.
The research was supported by the National Institutes of Health (CA241713, CA244328, P01-CA250984, CA267032, AG063543, P30-CA076292 and CA233399), the Leukemia and Lymphoma Society and the Florida Department of Health (23L10).

Few people with high blood pressure were using salt substitutes, even though they are a simple and effective way to lower sodium intake and manage blood pressure, according to preliminary research presented at the American Heart Association’s Hypertension Scientific Sessions 2025. The meeting is the premier scientific exchange focused on recent advances in basic and clinical research on high blood pressure and its relationship to cardiac and kidney disease, stroke, obesity and genetics.
High blood pressure occurs when the force of blood flowing through the blood vessels is consistently too high. High blood pressure can lead to other serious events such as heart attack and stroke. Using data from 2017 to 2020, 122.4 million (46.7%) adults in the U.S. had high blood pressure and it contributed to more than 130,000 deaths. Too much sodium and too little potassium in the diet are risk factors for high blood pressure.
“Overall, less than 6% of all U.S. adults use salt substitutes, even though they are inexpensive and can be an effective strategy to help people control blood pressure, especially people with difficult-to-treat high blood pressure,” said lead study author Yinying Wei, M.C.N., R.D.N., L.D., and Ph.D. candidate in the departments of applied clinical research and hypertension section, cardiology division, at UT Southwestern Medical Center in Dallas. “Health care professionals can raise awareness about the safe use of salt substitutes by having conversations with their patients who have persistent or hard-to-manage high blood pressure.”
Salt substitutes are products that replace some or all of the sodium with potassium. Potassium salt tastes similar to regular salt, except when heated it can have a bitter aftertaste. Many foods contain some sodium in their natural state, however, the largest amount of sodium comes from processed and packaged foods and meals prepared at restaurants. The American Heart Association recommends consuming no more than 2,300 mg of sodium a day, with an ideal limit of less than 1,500 mg per day for most adults, especially for those with high blood pressure. For most people, cutting back by 1,000 mg a day can improve blood pressure and heart health.
This study is the first to examine long-term trends in salt substitute use among a nationally representative sample of U.S. adults. Using data from the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2020, researchers analyzed the use of products that replace salt with potassium-enriched or other alternative salts.
The investigation focused on people with high blood pressure, and an additional analysis was conducted among adults eligible to use salt substitutes, including people with normal kidney function and those not taking medications or supplements that affect blood potassium levels. Some salt substitutes contain potassium, and they can raise blood potassium to dangerous levels in people with kidney disease or those taking certain medications or potassium supplements. Excessive potassium can lead to irregular heart rhythms. People with high blood pressure who are thinking about switching from regular salt to a salt substitute should first consult with a health care professional.
The analysis found: Overall, salt substitute use among all U.S. adults remained low, peaking at 5.4% in 2013-2014 before falling to 2.5% by 2017-March 2020. Data collection for 2020 stopped before March because of the pandemic. Among adults eligible to use salt substitutes, only 2.3% to 5.1% did so. Usage was highest in people with high blood pressure whose BP was controlled with medications (3.6%-10.5%), followed by those with high blood pressure whose BP was not controlled despite medications (3.7%-7.4%). Salt substitute use remained consistently less than 5.6% among people with untreated high blood pressure and for people with normal blood pressure. Adults who ate at restaurants three or more times a week appeared less likely to use salt substitutes compared to those who ate out less often, but this difference was no longer statistically significant after accounting for age, race/ethnicity, education level and insurance status.”Salt substitute use remained uncommon over the last two decades including among people with high blood pressure,” Wei said. “Even among individuals with treated and poorly managed or untreated high blood pressure, most continued to use regular salt.”

“This study highlights an important and easy missed opportunity to improve blood pressure in the U.S. — the use of salt substitutes,” said Amit Khera, M.D., M.Sc., FAHA, an American Heart Association volunteer expert. “The fact that use of salt substitutes remains so low and has not improved in two decades is eye-opening and reminds patients and health care professionals to discuss the use of these substitutes, particularly in visits focused on high blood pressure.” Khera, who was not involved in this study, is a professor of medicine, clinical chief of cardiology and director of preventive cardiology at UT Southwestern Medical Center in Dallas.
The study has several limitations. First, information about salt substitute use was self-reported, so there may have been underreporting or misclassification. In addition, all types of salt substitutes were included in the analysis, therefore, the analysis could not specifically separate potassium-enriched salt from other types of salt substitutes. Finally, the survey data did not capture how much salt substitute the participants used.
“Future research should explore why salt substitute-use remains low by investigating potential barriers, such as taste acceptance, cost and limited awareness among both patients and clinicians,” said Wei. “These insights may help guide more targeted interventions.”
Study details, background and design: The analysis included 37,080 adults, ages 18 and older (37.9% were aged 18-39, 36.9% were aged 40-59 years, and 25.2% were aged 60 and older). 50.6% of participants were women, 10.7% of participants self-reported their race as non-Hispanic Black, and 89.3% self-reported they were from other racial and ethnic groups. Participants were categorized into four subgroups based on presence or absence of high blood pressure (≥130/80 mm Hg) and whether they were using blood pressure lowering medication: 1) high blood pressure that was treated and controlled; 2) high blood pressure that was treated and not controlled; 3) untreated high blood pressure; and 4) those with normal blood pressure. Salt types were classified as ordinary salt (iodized salt, sea salt, kosher salt), salt substitute (potassium-enriched or other salt substitute) and no salt use. An additional analysis was conducted on a subgroup of individuals eligible to use salt substitutes — those with healthy kidney function (estimated glomerular filtration rate ≥ 60) and not taking medications or supplements that affect blood potassium levels. The frequency of eating at restaurants to assess its influence on salt substitute use was also evaluated. All analyses incorporated NHANES sampling weights and complex survey design.Research Highlights: Despite their effectiveness in lowering sodium intake and managing blood pressure, salt substitutes were rarely used by people with high blood pressure, according to a review of almost 20 years of U.S. health survey data. Researchers recommend increasing awareness of salt substitutes as a strategy to help effectively treat blood pressure, especially for individuals with difficult-to-treat or treatment-resistant high blood pressure. The study is supported by a grant from the National Institutes of Health. Note: The study featured in this news release is a research abstract. Abstracts presented at American Heart Association’s scientific meetings are not peer-reviewed, and the findings are considered preliminary until published as a full manuscript in a peer-reviewed scientific journal.

Researchers led by Hiroshi Ohno at the RIKEN Center for Integrative Medical Sciences (IMS) in Japan have discovered why smoking tobacco helps people suffering from ulcerative colitis, a chronic disease typified by inflammation of the large intestine. Published in the scientific journal Gut, the study shows that smoking produces metabolites that encourage bacteria from the mouth to grow in the large intestines where they trigger an immune response. These findings imply that protection against ulcerative colitis can be achieved through prebiotics like hydroquinone or probiotic therapy with bacteria like Streptococcus mitis, thus eliminating the need to smoke and all the associated risks for other diseases.
Inflammatory bowel disease comes in two main varieties, Crohn’s disease and ulcerative colitis. Although both cause chronic abdominal pain, diarrhea, fatigue and weight loss, their causes and the exact type and location of the inflammation differ. Along with these differences is a mystery that has puzzled doctors and scientists for over 40 years; smoking increases the risk of Crohn’s disease but somehow protects against ulcerative colitis. As both diseases are related to gut inflammation — which is an immune response — and gut immunity depends in part on the types of bacteria in the gut, Ohno and his team at RIKEN IMS set out to investigate whether the differential effects of smoking on these diseases can be explained by gut bacteria.
The researchers used a combination of human clinical data and experiments with mice to reach their conclusions. Among those with ulcerative colitis, they found that smokers had certain bacteria usually found in the mouth, such as Streptococcus, growing in the gut, specifically in the colonic mucosa that cover the inner lining of the intestines. This phenomenon did not occur in ex-smokers. Thus, while these bacteria normally pass all the way through the digestive system as we swallow saliva throughout the day, smoking somehow allows them to settle down in the gut mucosa.
The next question was why? The researchers also examined gut metabolites — small substances produced in the gut when food is broken down and processed by the body and gut bacteria. They found that levels of several gut metabolites were higher in smokers with ulcerative colitis than in ex-smokers with colitis. In mice, the researchers found that one of these metabolites, called hydroquinone, promoted the growth of Streptococcus in the gut mucosa. So, smoking-related metabolites like hydroquinone allow mouth bacteria like Streptococcus to flourish in the mucus layer that covers the inner lining of the intestines. But how do these bacteria help reduce inflammation? And why don’t they help in Crohn’s disease?
The researchers then went back to the oral bacteria that they had discovered was growing in the gut mucosa of smokers with ulcerative colitis, and isolated 10 strains from the saliva of smokers. When they treated mouse models of Crohn’s disease and ulcerative colitis with each of these 10 strains for five days, they found that giving the mice Streptococcusmitis had almost the same effect as smoking. Inflammation was reduced in mice with ulcerative colitis and exacerbated in mice with Crohn’s disease.
Analysis showed that S. mitis triggered the emergence of helper Th1 cells, which are an important part of the gut’s immune response to invaders. In Crohn’s disease this likely worsens the condition because the original inflammation is actually caused by these same helper Th1 cells. But in colitis, the Th1 cells fight against an initial Th2-immune response, and this ends up reducing inflammation.
As smoking poses high risks for cancer, heart disease, and many other illnesses, it is not a sustainable treatment for ulcerative colitis. “Our results indicate the relocation of bacteria from the mouth to the gut, particularly those of the Streptococcus genus, and the subsequent immune response in the gut, is the mechanism through which smoking helps protect against the disease,” says Ohno. “Logically, direct treatment with this kind of bacteria, or indirect treatment with hydroquinone, is thus likely to mimic the beneficial effects of smoking but avoid all the negative effects.”

Two ambulance workers have been arrested over the deaths of six adults, police have said.The investigation was launched in 2023 and last year a man in his 30s, from West Wiltshire, was arrested on suspicion of six counts of gross negligence manslaughter and four counts of ill-treatment or wilful neglect by a care worker.A 59-year-old woman was also arrested on suspicion of gross negligence manslaughter in March this year. Police have only released details of the investigation and arrests now.The two South Western Ambulance Service workers have been released on bail, Wiltshire Police said.”We can confirm a major investigation is under way relating to several adult deaths in and around Wiltshire,” said Det Ch Insp Phil Walker from the force’s major crime team.”Our focus is on supporting the families and loved ones of those who have died,” he added.Det Ch Insp Walker said the investigation has been ongoing since an initial report in 2023. The man in his 30s was arrested in June 2024.”Detailed inquiries have been undertaken since to ascertain the facts,” he added.A spokesperson for the ambulance service said it started an internal investigation as soon as it became aware of concerns and had since been “working closely” with police.The service said the two workers were “immediately relieved of all duties, including the treatment of patients,” adding one of the individuals is no longer employed by the trust.”We would like to reassure people that this is an isolated situation and there is no ongoing risk to patients. Please continue to call 999 in a life-threatening emergency,” the spokesperson added.According to the Crown Prosecution Service, the offence of gross negligence manslaughter requires the breach of an existing duty of care, which gives rise to a serious and obvious risk of death.South Western Ambulance Service was most recently inspected by health watchdog the Care Quality Commission in 2022 and was rated as “good”, having made improvements since previous inspections.The trust was rated as “outstanding” for care and “good” for its response times, effectiveness and leadership.Its emergency and urgent care services was rated as requiring improvement.

Mayo Clinic researchers have pinpointed how excessive alcohol consumption contributes to fatty liver disease, a condition that affects more than one in three people in the U.S. Also known as Metabolic Dysfunction Associated Steatotic Liver Disease, it is a long-lasting disease that can lead to type 2 diabetes and even liver cancer. Excessive alcohol can contribute to this fatty disease as well — and Mayo Clinic researchers recently discovered a reason why.
The researchers found that exposure to excessive alcohol alters an important enzyme that recycles damaged proteins.
How the liver works
The liver is the primary filter for everything you ingest. Liver cells, or hepatocytes, support this organ’s giant job by releasing dozens of various proteins while collecting, sorting, degrading and recycling nearly everything that passes through this massive, sieve-like organ. Fat coming from the gut, for example, is absorbed then stored in hepatocytes as lipid droplets, which are globular structures that store fat. The body can use these lipid droplets as an energy source, especially during periods of fasting. However, too many lipid droplets can lead to fatty liver disease.
The researchers found the key lies with an important enzyme called the valosin-containing protein (VCP). VCP plays a role in many important processes including recycling unwanted proteins and is found in cells throughout the body.
“We were surprised to see VCP removing a specific protein from the surface of the lipid droplet. When that particular protein called HSD17β13 accumulates, the fat content in liver cells balloons and contributes to fatty liver disease,” says Mark McNiven, Ph.D., senior author on the study, which was published and highlighted in the Journal of Cell Biology.
In people without fatty liver disease, the enzyme, VCP, appears to keep the protein, HSD17β13, in check to prevent lipid droplets from over-accumulating in the liver cells.

However, the researchers found that exposure to excessive alcohol removes VCP almost completely from the lipid droplet surface, allowing HSD17β13 to significantly accumulate.
The researchers also saw and captured the elaborate recycling mechanism of VCP. They witnessed VCP working with a chaperone protein to deliver damaged proteins to an organelle called a lysosome, which then broke apart the unwanted proteins.
“It was astounding to see this. We tried several experiments to confirm what we were seeing, and every result indicated VCP directs the HSD17β13 protein from the lipid droplet to the lysosome,” says Sandhya Sen, Ph.D., a Mayo Clinic research fellow and lead author of the study.
Their findings mean HSD17β13 is a target for potential new therapies to prevent or treat fatty liver disease, says Dr. McNiven.
“This study increases our understanding of the biology of lipid droplets, the central culprit of fatty liver, and how the hepatocyte works in an effort to reduce its fat content,” Dr. McNiven says. “It also could help predict which patients are prone to the detrimental effect of excessive alcohol consumption on their liver if this cellular system is compromised.”
The research is part of a larger effort at Mayo Clinic called the Precure initiative focused on developing tools that empower clinicians to predict and intercept biological processes before they evolve into disease or progress into complex, hard-to-treat conditions.
Review the study for a complete list of authors, disclosures and funding.

Alcohol-associated liver disease (ALD) is a major cause of liver transplantation and death worldwide, and its impact is only growing. In 2022, the annual cost of ALD in the United States was $31 billion. By 2040, this number could be as high as $66 billion. ALD has limited therapeutic options, so scientists are looking for new ways to target the molecular biology of ALD to help prevent its occurrence or reduce its severity.
Now, scientists at University of California San Diego School of Medicine have found that chronic alcohol use impairs the production of a key cellular signaling protein that helps keep gut bacteria within the gut. Without this guardrail in place, bacteria from the gut can more easily migrate to the liver, exacerbating liver damage caused by alcohol. Targeting this mechanism with existing drugs could provide one approach to minimizing the liver damage from alcohol use and reducing the burden of ALD.
Studying a combination of human liver biopsies and mouse models of ALD, the researchers found: Chronic alcohol use reduced the expression of muscarinic acetylcholine receptor M4 (mAChR4), a key cellular communication protein in the gut. Reduced mAChR4 expression hindered the formation of goblet cell-associated antigen passages (GAPs), specialized structures that teach the immune system to promote antimicrobial immunity, thereby preventing harmful bacteria from migrating to the liver. Restoring mAChR4 function, either by chemically activating mAChR4 or by targeting related signaling pathways allowed GAPs to form and conferred resistance to ALD.While the researchers focused on the role of mAChR4 in the gut, this cellular signaling protein is also known to play a critical role in sections of the brain that regulate habits, learning and addiction. This treatment approach may also have wider implications for alcohol-related disorders, because the expression of mAChR4 is known to be lower in the brains of patients with alcohol use disorder (AUD). Drugs that target mAChR4 are currently in clinical trials for schizophrenia, and the researchers suggest that these drugs could be readily repurposed for ALD and AUD. However, further research is required to demonstrate this potential.
The study, published in the journal Nature, was led by Cristina Llorente, Ph.D., Michael Karin, Ph.D., and Bernd Schnabl, M.D., at UC San Diego School of Medicine. The study was funded, in part, by the National Institutes of Health (grants R01 AA029106, R21 AA030654, P30 AR073761, D34 HP31027, P50 AA011999) and the American Association for the Study of Liver Diseases (award 8998GA). Bernd Schnabl has consulted for Ferring Research Institute, HOST Therabiomics, Intercept Pharmaceuticals, Mabwell Therapeutics, Patara Pharmaceuticals, Surrozen, and Takeda. He is also the founder of Nterica Bio.

Wildfires burning across Canada and the Western United States are spewing smoke over millions of Americans – the latest examples of ashy haze becoming a regular experience, with health impacts far greater than scientists previously estimated.
Although wildfires have long been part of life in the Western U.S., warmer, drier conditions are fueling bigger blazes that occur more often and for longer. Smoke from these blazes is spreading farther and lingering longer than in the past. In a Sept. 18 study in Nature, Stanford University researchers estimate that continued global warming could lead to about 30,000 additional deaths each year nationwide by 2050, as climate-driven increases in fire activity generate more smoke pollution across North America.
“There’s a broad understanding that wildfire activity and wildfire smoke exposure are changing quickly. This is a lived experience, unfortunately, for folks on the West Coast over the last decade and folks on the East Coast in the last few years,” said senior study author Marshall Burke, a professor of environmental social sciences in the Stanford Doerr School of Sustainability. “Our paper puts some numbers on what that change in exposure means for health outcomes, both now and in the future as the climate warms.”
The researchers found no U.S. community is safe from smoke exposure. When monetized, deaths related to wildfire smoke could reach $608 billion in annual damages by 2050 under a business-as-usual emissions scenario where global temperatures rise about 2 degrees Celsius above pre-industrial levels. That estimated toll surpasses current estimates of economic costs from all other climate-driven damages in the U.S. combined, including temperature-related deaths, agricultural losses, and storm damage.
“What we see, and this is consistent with what others find, is a nationwide increase in wildfire smoke,” said lead study author Minghao Qiu, an assistant professor at Stony Brook University who worked on the study as a postdoctoral researcher in Burke’s lab. “There are larger increases on the West Coast, but there’s also long-range transport of wildfire smoke across the country, including massive recent smoke events in the Eastern and Midwestern U.S. from Canadian fires.”
Uniquely dangerous pollution
Deaths from wildfire smoke result from inhaling a complex mix of chemicals. Wildfires can expose large numbers of people to these toxic pollutants for days or weeks at a time, contributing to deaths up to three years after the initial exposure, according to the new study.

Within wildfire smoke pollution, researchers often focus on fine particulate matter, known as PM2.5, which penetrates the lungs and enters the bloodstream. While the health effects of PM2.5 from other sources are well studied, less is known about the specific dangers of PM2.5 from wildfire smoke. Some recent research shows that wildfire smoke can contain a range of toxic chemicals harmful to human health. Qiu, Burke, and colleagues used U.S. death records to assess these additional risks from smoke.
The researchers combined county-level data on all recorded U.S. deaths from 2006 to 2019 with measurements of ground-level smoke emissions, wind variation, and the movement of airborne particulate matter, using machine learning to predict how wildfire emissions changes in one area affected smoke concentrations in another. They linked changes in smoke concentrations to variation in historical mortality and used global climate models to project future fire activity, smoke levels, and health impacts under different warming scenarios through 2050.
The results show that excess deaths from smoke PM2.5 exposure under a business-as-usual emissions scenario could increase more than 70% to 70,000 per year from roughly 40,000 annual deaths attributed to smoke from 2011 to 2020. The largest projected increases in annual smoke exposure deaths occur in California (5,060 additional deaths), New York (1,810), Washington (1,730), Texas (1,700), and Pennsylvania (1,600).
Understanding climate impacts
By quantifying economic damage from smoke-related deaths, the findings uncover a hidden tax on families and businesses. The researchers found that even if the world cuts emissions rapidly enough to stabilize global temperatures below 2 C by the end of the century, deaths from climate-driven smoke exposure in the U.S. alone would likely still exceed 60,000 per year by 2050.
“If you look at the leading climate impact assessment tools that are used to inform policy, none of them incorporate how changes in climate could influence wildfire smoke and related human mortality,” Qiu said. “Our study shows climate models are missing a huge part of the climate impacts in the U.S. – it’s like leaving the main character out of a movie.”
A shared burden

Actions by public health officials and communities can mitigate this growing threat. For example, investing in better indoor air filtration can help reduce exposure for vulnerable individuals or communities. Prescribed burns or other fuels management approaches can help to reduce the severity of wildfires and resulting smoke waves.
“Our understanding of who is vulnerable to this exposure is much broader than we thought,” Burke said. “It’s pregnant people, it’s kids in schools, it’s anyone with asthma, it’s people with cancer. We look at one specific health outcome in this study – mortality – and unfortunately find a shared burden of exposure for individuals across the U.S.”
Burke is also a professor (by courtesy) of Earth system science; deputy director at the Center on Food Security and the Environment; and a senior fellow with the Stanford Institute for Economic Policy Research (SIEPR), the Woods Institute for the Environment, and the Freeman Spogli Institute for International Studies.
Additional Stanford co-authors include Jessica Li, a research data analyst at the Center on Food Security and the Environment; Renzhi Jing, a postdoctoral researcher in primary care and population policy; Makoto Kelp, a postdoctoral researcher in Earth system science; Jeff Wen, a PhD student in Earth system science; Mathew Kiang, assistant professor of epidemiology and population health; Sam Heft-Neal, a senior research scholar at the Center on Food Security and the Environment; and Noah Diffenbaugh, the Kara J Foundation Professor and Kimmelman Family Senior Fellow. Other study co-authors are from the University of California, San Diego, the University of Washington, Princeton University, the National Oceanic and Atmospheric Administration, and the National Bureau of Economic Research.
This research was supported by the Keck Foundation, Stanford’s Center for Innovation in Global Health, Stony Brook University, the Harvard University Center for the Environment, and the Stanford Research Computing Center.

2 hours agoShareSaveJames DiamondSomerset, WilitonShareSaveBBCA pharmacy chain has serious questions to answer over allegations of financial mismanagement, according to MP Sadik Al Hassan.Staff at Jhoots Pharmacies run by Sarbjit Jhooty are owed £670,000 in unpaid wages, according to union Pharmacists Defence Association. There are about 150 Jhoots Pharmacies across the UK, of which 129 are run by Sarbjit.Mr Al Hassan said the situation was “shocking”, with patients left struggling to get prescriptions as Jhoots branches were regularly and unexpectedly closed, or open with low stock.Sarbjit said he was working to return things to normal “as swiftly as possible” while NHS representatives said they were working to resolve issues.The Pharmacists Defence Association said the £670,000 unpaid wage bill related to locum staff who worked for Jhoots branches across the UK.Unlike permanent employees, locum staff operate in a freelance capacity and usually provide short-term cover.One former Jhoots worker claims to be owned several thousand pounds after working at a branch in Somerset.She asked to be kept anonymous, fearing speaking publicly may impact her claim for payment, and said: “[In] January they just seemed to stop paying us.”She said she spoke to Sarbjit about the issues, and he referred her to HR. However, her emails to the department went unanswered.”It’s been horrendous,” she said. “We’ve all fallen behind with all our bills, people have mortgages, car payments to pay.”It’s affected us greatly, even down to being able to send my child to school with a packed lunch for the day. I wasn’t able to provide at points, having to borrow money off family members.”It’s affected my mental health quite heavily.”She said issues at the pharmacy also meant staff had to deal with “angry customers”.”They weren’t getting their medication,” she explained. “Or they were being promised it and then it was being given to other patients, so then we were having to reorder the stock. It wasn’t pleasant.”‘Unsafe’In Wiltshire, Swindon South MP Heidi Alexander is promoting a petition calling on Jhoots’ bosses to act after a branch in the town had regularly been closed.She said there had been “repeated closures, no pharmacists, unanswered calls, empty shelves”.”This isn’t just inconvenient. When people are unwell, it’s unsafe,” she added.In Fishponds, Bristol, one branch was closed with a sign on the door blaming a lack of pharmacists.Similarly in Somerset, a poster in the window of the closed Jhoots Pharmacy in Williton reads “no pharmacist today”. Residents there told the BBC it had been consistently shut for three to four weeks.”It’s impacted everybody around here,” said one resident, who said it had particularly impacted the older generation who had found it “very hard” to get their prescriptions.Residents in Portishead have also seen a “massive decline” in the availability of pharmacy services, according to Mr Al Hassan.The North Somerset MP, who used to be a pharmacist, said the situation was “unacceptable”.”Jhoots are unreliably open, they don’t necessarily have common items of stock available for prescriptions and now one of them [in Portishead], on the Thursday before the last bank holiday, shuttered their doors and never reopened,” he added.Jhoots managementAcross the UK there are 153 Jhoots pharmacies registered with the General Pharmaceutical Council. All are owned, at least in part, by either Sarbjit or Manjit Jhooty. Manjit, who owns more than 20 Jhoots branches through his companies Pasab and Jhoots Healthcare, said the trading name Jhoots was used by several, independent companies which each had their own management structure and procedures.He said his branches remained “fully functional and continue to deliver services to the communities they serve”.The allegations in this article relate to pharmacies managed by Sarbjit, who confirmed he operated independently from Manjit.”While we share the name, Jhoots Pharmacy is an entirely separate and independent pharmacy,” Sarbjit said.He admitted there had been issues at his pharmacies, and blamed “workforce and recruitment challenges” which he said had been a problem in the South West “for many years”.”We are actively engaging with staff, local partners, and wider stakeholders to address these pressures and ensure that patient care and community services are supported in the long term,” he added.Sarbjit did not respond to the BBC’s request for comment on allegations Jhoots staff had not been paid.An NHS issue?Mr Al Hassan is due to meet Jhoots bosses this month, but he said the NHS also needed to get a handle on the issues.He said the health service could grant and take away NHS work from pharmacies and called on Jhoots to surrender its NHS contracts in his constituency.”Even though that Jhoots [in Portishead] is closed, it still counts as having a pharmacy contract in the area,” he explained.”In 2023, Jhoots bought another 40-odd pharmacies that were closing.”They were allowed to do that despite their history of poor abilities to open their pharmacy or contract compliance.”This level of contract management puts the entire reputation of pharmacy at risk, to allow an operator like this to continue,” he continued. When approached for comment, NHS England directed the BBC to various NHS Integrated Care Boards in the South West which are responsible for managing pharmaceutical contracts on a local level. In very similar statements, spokespeople for the care boards in North Somerset, Somerset and Swindon said they recognised the concern caused when pharmacies closed. They added they were “committed” to ensuring residents had access to alternative provision.All said they could take formal action against pharmacies in breach of their contracts “where necessary”.Related internet links

The production and use of over 400 million tons of plastic each year has polluted beaches, rivers, and even the deepest parts of the ocean, reaching depths of up to 11,000 meters. In addition to visible environmental impacts, plastic contributes to climate change. It is estimated that plastic production generates 1.8 billion tons of greenhouse gases per year. Scientific evidence also suggests that using plastic materials in everyday life has impacted human health.
A large number of plastic particles detach from curtains, furniture, clothing, and other plastic objects. These particles remain suspended in the air, dissolve in drinking water, adhere to food, and can be inhaled, ingested, or come into contact with people’s skin. Consequently, scientists have found microplastics in blood, the brain, the placenta, breast milk, and human bones.
A study linked to a research project supported by FAPESP and published in the journal Osteoporosis International reviewed 62 scientific articles and found that microplastics have also been harming bone health in various ways. One notable example is their ability to impair the function of bone marrow stem cells by promoting the formation of osteoclasts, which are multinucleated cells that degrade tissue through a process known as bone resorption.
“The potential impact of microplastics on bones is the subject of scientific studies and isn’t negligible. For example, in vitro studies with bone tissue cells have shown that microplastics impair cell viability, accelerate cell aging, and alter cell differentiation, in addition to promoting inflammation,” says Rodrigo Bueno de Oliveira, coordinator of the Laboratory for Mineral and Bone Studies in Nephrology (LEMON) at the Faculty of Medical Sciences of the State University of Campinas (FCM-UNICAMP), in the state of São Paulo, Brazil.
Oliveira reports that studies on animals have found that accelerated osteoclast senescence can compromise bone microstructure, causing dysplasia. This can lead to bone weakening, deformities, and potentially pathological fractures. “In this study, the adverse effects observed culminated, worryingly, in the interruption of the animals’ skeletal growth,” says the researcher.
Oliveira further explains that, although the effects of these particles on bone mechanics are not yet fully understood, the data suggest that the presence of the material in the bloodstream, for example, may compromise bone health. “Most strikingly, a significant body of research suggests that microplastics can reach deep into bone tissue, such as bone marrow, and potentially cause disturbances in its metabolism,” he says.
Connection
Not surprisingly, Oliveira’s team is starting a research project to verify in practice what seems perfectly possible in theory: the relationship between exposure to microplastics and the worsening of metabolic bone diseases. Using animal models, the scientists will study the impact of microplastics on the strength of rodent femurs.
According to the International Osteoporosis Foundation (IOF), the prevalence of osteoporosis-related fractures is increasing worldwide due to the aging population. It is estimated that there will be a 32% increase in osteoporosis-related fractures by 2050.
“Improving quality of life and reducing the risk of bone complications, such as fractures, is a priority in healthcare. We already know that practices such as physical exercise, a balanced diet, and pharmacological treatments contribute significantly to this. However, although osteometabolic diseases are relatively well understood, there’s a gap in our knowledge regarding the influence of microplastics on the development of these diseases. Therefore, one of our goals is to generate evidence suggesting that microplastics could be a potential controllable environmental cause to explain, for example, the increase in the projected number of bone fractures,” says Oliveira.

Micro- and nanoplastics prevalent in the environment routinely enter the human body through water we drink, foods we eat, and even the air we breathe. Those plastic particles infiltrate all systems of the body, including the brain, where they can accumulate and trigger Alzheimer’s-like conditions, according to a new study by researchers in the University of Rhode Island College of Pharmacy.
After a previous study that showed how microplastics can infiltrate all systems of the body — including the blood-brain barrier, which protects the brain from harmful substances as small as viruses and bacteria — URI pharmacy assistant professor Jaime Ross expanded the study to determine the brain health impacts of the plastic toxins. Her findings indicate that the accumulation of micro- and nanoplastics in the brain can lead to cognitive decline and even Alzheimer’s disease, especially in those who carry genetic risk factors.
Ross’ latest study, published recently in the journal Environmental Research Communications, examined mice that had been genetically modified to include the naturally occurring gene APOE4, a strong indicator of Alzheimer’s risk making people 3.5 times more likely to develop the disease than those who carry the APOE3 variant of the gene that is passed from parents to offspring.
“In these mice, like in people, it’s not a guarantee that you’re going to see any changes in cognition. You could have identical twins both carrying APOE4, one totally cognitively healthy, and the other could develop Alzheimer’s disease,” Ross said. “So that tells us there’s something about lifestyle, something about the environment going on. There are modifiable factors we’re studying related to Alzheimer’s-diet, exercise, vitamins, and especially environmental toxins like microplastics. If you carry the APOE4, and you happen to consume a lot of microplastics, will this contribute to Alzheimer’s disease?”
To find out, Ross and her team exposed two groups of mice — one with the APOE4 variant and one with APOE3 — to micro- and nanoplastics in their drinking water over a period of three weeks. The tiny particles from polystyrene — among the most abundant plastics in the world, found in Styrofoam take-out containers, plastic cups and more — infiltrated the mice’ organs, including the brain, as expected. The research included a control group from each APOE designation did not receive microplastic exposure.
Ross’ team then ran the mice through a series of tests to examine their cognitive ability, beginning with an open-field test, in which researchers put a mouse in a chamber and allow it to explore at will for 90 minutes. Ordinarily, a mouse will hug the walls, naturally attempting to hide from potential predators. However, after microplastic exposure, the APOE4 mice — especially the male mice — tended to wander more in the middle of the chamber and spend time in open space, leaving themselves vulnerable to predators.
To test their ability to recognize novel objects, Ross placed mice in an open chamber with two distinct objects. After having time to explore the objects, the mice were removed and returned later, this time with one of the objects replaced with a different shape. The female mice with APOE4 and microplastic exposure were slow to recognize the novel objects, if they did at all, a sign of cognitive decline affecting memory.

“In the first test, you can see the males are spending more time and resting more in the center of the arena. In females, we saw changes in novel object recognition,” Ross said. “In human Alzheimer’s patients, men tend to experience more changes in apathy; they care less. Women experience more changes in memory. So the memory and the apathy connection are pretty clear: When you expose animals that are carrying the largest known risk factor in humans for developing Alzheimer’s disease to micro- and nanopastics, lo and behold, their behavior changes in a sex-dependent manner similar to the sex-dependent differences we see with Alzheimer’s patients.”
The results are concerning enough to warrant further study into the cognitive decline caused by exposure to micro- and nanoplastics, which are among the most prominent environmental toxins to which people are routinely exposed. (A separate URI study released in 2023 revealed of the extent to which microplastics accumulate in the environment, shockingly finding that the top two inches of the floor of Narragansett Bay contain more than 1,000 tons of microplastics.)
Ross is continuing to expand her research into the topic and encourages others to do so, in the hope of leading to better regulation of the toxins. The Microplastics Safety Act, introduced in the U.S. House of Representatives in July would direct the U.S. Food and Drug Administration to study the human health impacts of microplastics in food and water, specifically focusing on vulnerabilities for children, the endocrine and reproductive systems, and links to cancer and chronic illnesses.
“There has not been a lot of money spent on the human health impacts of microplastics,” Ross said, noting she is in regular discussion with the Rhode Island Congressional delegation about the need for regulation. “It’s interesting that what we’re seeing in mice is similar to what we’re seeing in the real world. We want to encourage further research into the scourge of micro- and nanoplastics.”