Publisher Health

Men with early, curable stages of prostate cancer are missing opportunities to have their cancer detected because national guidelines and media health campaigns focus on urinary symptoms despite a lack of scientific evidence, say experts at the University of Cambridge.
Prostate cancer is the most common type of cancer in men. According to Cancer Research UK, over 52,000 men are diagnosed with prostate cancer each year and there are more than 12,000 deaths.
Over three-quarters (78%) of men diagnosed with the disease survive for over ten years, but this proportion has barely changed over the past decade in the UK, largely because the disease is detected at a relatively late stage. In England, for example, nearly half of all prostate cancers are picked up at stage three of four (stage four being the latest stage).
Despite no evidence of a link between urinary symptoms and prostate cancer, national guidelines, health advice and public health campaigns continue to promote this link. In a review published today in BMC Medicine, Cambridge researchers argue that not only is this unhelpful, but it may even deter men from coming forward for early testing and detection of a potentially treatable cancer.
“When most people think of the symptoms of prostate cancer, they think of problems with peeing or needing to pee more frequently, particularly during the night,” said Vincent Gnanapragasam, Professor of Urology at the University of Cambridge and an Honorary Consultant Urologist at Addenbrooke’s Hospital, Cambridge. “This misperception has lasted for decades, despite very little evidence, and it’s potentially preventing us picking up cases at an early stage.”
Prostate enlargement can cause the urinary problems often included in public health messaging, but evidence suggests that this is rarely due to malignant prostate tumours. Rather, research suggests that the prostate is smaller in cases of prostate cancer. A recent study — the UK PROTECT trial — even went as far as to say that a lack of urinary symptoms may in fact be an indicator of a higher likelihood of cancer.

The Department of Health and Human Services delayed asking the manufacturer to process the bulk vaccine the government already owned into vials.WASHINGTON — The shortage of vaccines to combat a fast-growing monkeypox outbreak was caused in part because the Department of Health and Human Services failed early on to ask that bulk stocks of the vaccine it already owned be bottled for distribution, according to multiple administration officials familiar with the matter.By the time the federal government placed its orders, the vaccine’s Denmark-based manufacturer, Bavarian Nordic, had booked other clients and was unable to do the work for months, officials said — even though the federal government had invested well over $1 billion in the vaccine’s development.The government is now distributing about 1.1 million doses, less than a third of the 3.5 million that health officials now estimate are needed to fight the outbreak. It does not expect the next delivery, of half a million doses, until October. Most of the other 5.5 million doses the United States has ordered are not scheduled to be delivered until next year, according to the federal health agency.To speed up deliveries, the government is scrambling to find another firm to take over some of the bottling, capping and labeling of frozen bulk vaccine that is being stored in large plastic bags at Bavarian Nordic’s headquarters outside Copenhagen. Because that final manufacturing phase, known as fill and finish, is highly specialized, experts estimate it will take another company at least three months to gear up. Negotiations are ongoing with Grand River Aseptic Manufacturing, a Michigan factory that has helped produce Covid-19 vaccines, to bottle 2.5 million of the doses now on order, hopefully shaving months off the timetable, according to people familiar with the situation.Health and Human Services officials so miscalculated the need that on May 23, they allowed Bavarian Nordic to deliver about 215,000 fully finished doses that the federal government had already bought to European countries instead of holding them for the United States.At the time, the nation had only eight confirmed monkeypox cases, agency officials said. And it could not have used those doses immediately because the Food and Drug Administration had not yet certified the plant where the vaccine, Jynneos, was poured into vials.But it could now. Some states are trying to stretch out doses by giving recipients only one shot of the two-dose vaccine. California, Illinois and New York have declared public health emergencies. In New York City, every available slot for a monkeypox shot is taken.Lawrence O. Gostin, a former adviser to the Centers for Disease Control and Prevention who has consulted with the White House about monkeypox, said the government’s response has been hobbled by “the same kinds of bureaucratic delays and forgetfulness and dropping the ball that we did during the Covid pandemic.”The obstacles to filling and finishing vials follow other missteps that have limited vaccine supply. The United States once had some 20 million doses in a national stockpile but failed to replenish them as they expired, letting the supply dwindle to almost nothing. It had 372,000 doses ready to go in Denmark but waited weeks after the first case was identified in mid-May before requesting the delivery of most of those doses. Another roughly 786,000 doses were held up by an F.D.A. inspection of the manufacturer’s new fill-and-finish plant but have now been shipped.The government also owns the equivalent of about 16.5 million doses of bulk vaccine produced and stored by Bavarian Nordic. But by the time the health agency ordered 500,000 doses worth to be vialed on June 10, other countries with outbreaks had submitted their own orders and the earliest delivery date was October.Another order for 110,000 doses for European nations soon followed. When the United States came back with two more orders of 2.5 million doses each — announced July 1 and July 15 — the bulk could only be delivered next year.Xavier Becerra, who oversees both the C.D.C. and the Food and Drug Administration, has been under attack for months for what critics describe as his hands-off approach to public health crises.Pete Marovich for The New York TimesMr. Gostin, who now directs the O’Neill Institute for National and Global Health Law at Georgetown University, predicted that President Biden’s decision to appoint two new monkeypox response coordinators would help “light a fire” under federal health agencies. The White House announced Tuesday that Robert Fenton, an administrator at the Federal Emergency Management Agency, and Dr. Demetre Daskalakis, a C.D.C. official, will lead the response.Mr. Gostin said the nation’s public health agencies have been “kind of asleep at the wheel on this,” and the new coordinators should help with “unblocking all of the obstacles to procuring and delivering vaccines and drugs, which has been deeply frustrating.”Two senior federal officials, who requested anonymity in order to speak frankly, said Mr. Biden is upset by the vaccine shortage. His administration has often touted its success delivering hundreds of millions of coronavirus shots to Americans, and is stung by criticism that a lack of foresight and management has left gay men — the prime risk group for monkeypox — unprotected.Some critics blame a failure of leadership at the Health and Human Services Department, saying the department’s secretary, Xavier Becerra, has taken a hands-off approach to an increasingly serious situation. His department not only oversees both the C.D.C. and the Food and Drug Administration, but also runs the Biomedical Advanced Research and Development Authority, or BARDA, which helps develop and buys vaccines, tests and treatments to protect against highly contagious viruses, bioterrorism and other hazards.During a press call on monkeypox last week, Mr. Becerra said his department is doing all it can to ensure that “we not only stay ahead of this virus but that we end this outbreak.” He noted that he had recently elevated the agency’s Office of Strategic Preparedness and Response so it can respond more quickly to public health emergencies.Sarah Lovenheim, his spokeswoman, said in a statement: “Our response has accelerated to meet evolving needs on the ground, and it will keep accelerating. We will use every lever possible to continue allocating doses ahead of timelines, as possible.”So far, according to the C.D.C.,6,326 cases of monkeypox have been reported. For now, the virus is spreading almost entirely among gay and bisexual men, and those with multiple or anonymous partners are considered especially at risk. Mr. Becerra noted that while more than a million Americans have died of Covid-19, no one in the United States has died of monkeypox.The official case count is widely considered an underestimate. Not only is testing limited, but public health officials like Dr. Joseph Kanter, the top medical official in Louisiana, said that monkeypox can be hard to diagnose. “It can be one or two solitary lesions, so if it’s not on a clinician’s radar,” he said, it can be missed.With too few doses, health officials apparently plan to rely heavily on the “test and trace” strategy that figured heavily in the early stages of the Covid pandemic. As the pandemic escalated, the sheer torrent of cases overwhelmed the ability of health officials to contact people who might have been infected by someone who had tested positive for the coronavirus. Once Covid vaccines became available, they became the cornerstone of the administration’s pandemic response.Working on a monkeypox vaccine at a laboratory near Munich on Tuesday.Lukas Barth/ReutersThrough early June, Health and Human Services officials appeared firmly convinced that the United States had more than enough supply of the monkeypox vaccine, called Jynneos, to handle what appeared to be a handful of cases.Bavarian Nordic was able to develop the vaccine, which also works against smallpox, largely thanks to the federal government’s backing, which surpassed $1 billion in 2014 and is now edging toward $2 billion. Dawn O’Connell, the federal health agency’s assistant secretary for preparedness and response, told reporters in early June: “The world has Jynneos because we invested in it.”The company opened a new $75 million fill-and-finish plant in 2021 that is now bottling as many as 200,000 to 300,000 doses a week. At the time, the United States was counting on Jynneos to protect against smallpox, not monkeypox, and the government had a large stockpile of another effective smallpox vaccine. No F.D.A. inspection was scheduled until after the monkeypox outbreak, and it did not conclude until July 27.In early June, Health and Human Services officials agreed to essentially loan back about 215,000 finished doses of vaccine to Bavarian Nordic so the firm could supply them to European countries that were suffering outbreaks.“It didn’t make sense while we were waiting for F.D.A. to get the inspection done — which is coming — that we sit on doses that our international colleagues in Europe could actually use,” Ms. O’Connell said on June 10. Now the government is trying reschedule delivery of those doses for later this year, a company spokesman said.The final stage of putting the liquid vaccine into vials accounts for a substantial share of the cost of vaccine production. Some federal officials say the health department was slow to submit its orders for that work because officials at BARDA argued they were short on funds.When the demand for vaccines became an outcry, though, the agency found the money to pay for five million more doses to be vialed. Officials are now contemplating shifting half the work to another firm that may be able to finish and fill doses more than twice as fast.Some experts say it can take as long as six to nine months for a plant to gear up to handle a vaccine like Jynneos, which contains a live virus in a weakened state. Carlo de Notaristefani, who oversaw coronavirus vaccine manufacturing for the federal government until last year, said that such factories must operate at a high “biological safety level,” including a fully enclosed, segregated manufacturing line.But he and other experts said it should be possible to streamline the transfer of Bavarian Nordic’s process so another plant could be ready in about three months. A company spokesperson said Bavarian Nordic agreed to pay $10 million of the cost of such a transfer after federal officials said they did not have the budget for it.Kitty Bennett

A Purdue University chemical engineer has improved upon traditional methods to produce off-the-shelf human immune cells that show strong antitumor activity, according to a paper published in the peer-reviewed journal Cell Reports.
Xiaoping Bao, a Purdue University assistant professor from the Davidson School of Chemical Engineering, said CAR-neutrophils, or chimeric antigen receptor neutrophils, and engraftable HSCs, or hematopoietic stem cells, are effective types of therapies for blood diseases and cancer. Neutrophils are the most abundant white cell blood type and effectively cross physiological barriers to infiltrate solid tumors. HSCs are specific progenitor cells that will replenish all blood lineages, including neutrophils, throughout life.
“These cells are not readily available for broad clinical or research use because of the difficulty to expand ex vivo to a sufficient number required for infusion after isolation from donors,” Bao said. “Primary neutrophils especially are resistant to genetic modification and have a short half-life.”
Bao has developed a patent-pending method to mass-produce CAR-neutrophils from human pluripotent stem cells (hPSCs), that is, cells that self-renew and are able to become any type of human cell. The chimeric antigen receptor constructs were engineered to express on the surface of the hPSCs, which were directed into functional CAR-neutrophils through a novel, chemically defined protocol.
The method was created in collaboration with Qing Deng at Purdue’s Department of Biological Sciences, Hal E. Broxmeyer, now deceased, at Indiana University School of Medicine, and Xiaojun Lian at the Pennsylvania State University.
“We developed a robust protocol for massive production of de novo neutrophils from human pluripotent stem cells,” Bao said. “These hPSC-derived neutrophils displayed superior and specific antitumor activities against glioblastoma after engineering with chimeric antigen receptors.”
Bao disclosed the innovation to the Purdue Research Foundation Office of Technology Commercialization, which has applied for an international patent under the Patent Cooperation Treaty system of the World Intellectual Property Organization. The innovation has been optioned to an Indiana-headquartered life sciences company.
“We will also work with Dr. Timothy Bentley, professor of neurology and neurosurgery,and his team at the Purdue College of Veterinary Medicine to run clinical trials in pet dogs with spontaneous glioma,” Bao said.
This research project was partially supported by the Davidson School of Chemical Engineering and College of Engineering Startup Funds, Purdue Center for Cancer Research, Showalter Research Trust and federal grants from the National Science Foundation and National Institute of General Medical Sciences.
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Materials provided by Purdue University. Original written by Steve Martin. Note: Content may be edited for style and length.

A new large study led by researchers atthe American Cancer Society (ACS) shows older age and smoking are the two most important risk factors associated with a relative and absolute five-year risk of developing any cancer. The findings also demonstrate that in addition to age and smoking history, clinicians should consider excess body fatness, family history of any cancer, and several other factors that may help patients determine if they may benefit from enhanced cancer screening or prevention interventions. The data was published today in the journal Cancer.
“Single cancer type-specific screening recommendations are based on risk factors for that specific type of cancer,” said Dr. Alpa Patel, senior vice president, population science at the American Cancer Society and lead author of the study. “Our findings are encouraging as we are working to define subgroups in the general population who could benefit from enhanced cancer screening and prevention.”
For this study, researchers analyzed two ACS prospective cohort studies, Cancer Prevention Study-II Nutrition Cohort and Cancer Prevention Study-3 to identify the risk factors associated with greater than two-percent absolute risk of any cancer within five years. The authors studied 429,991 participants in the United States with no prior personal history of cancer and followed for cancer for up to five years. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals for association. Using these HRs, individualized Coherent Absolute Risk Estimation was used to calculate absolute risks by age.
The results showed 15,226 invasive cancers were diagnosed among participants within five-years of enrollment. The multivariable-adjusted relative risk of any cancer was strongest for current smokers compared with never smokers. In men, alcohol intake, family history of cancer, red meat consumption, and physical inactivity were also associated with risk. In women, body mass index (BMI), type 2 diabetes, hysterectomy, parity, family history of cancer, hypertension, tubal ligation, and physical inactivity were associated with cancer risk. Absolute five-year risk exceeded two-percent among nearly all persons greater than 50 years old and among some persons less than 50 years old including current or former smokers (less than 30 years since quitting) and long-term nonsmokers with a BMI greater than 25 or a first-degree family history of cancer. The absolute five-year risk was as high as 29% in men and 25% in women.
“As we consider the possibility that future tests may be able to identify several types of cancer, we need to begin understanding who is most at risk for developing any type of cancer,” said Patel. “These types of data are not widely available, but necessary to inform future screening options, such as blood-based multi-cancer early detection tests that could help save lives.”
Other ACS study authors include: Emily Deubler, Dr. Lauren Teras, and Cari Lichtman. Dr. Christina Clarke-Dur is senior author of the paper and represents Grail, LLC, a subsidiary of Illumina, Inc., which provided funding support for the research.
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Materials provided by American Cancer Society. Note: Content may be edited for style and length.

Two years ago, University of Alabama at Birmingham researchers and colleagues reported that reductive stress — an imbalance in the normal oxidation/reduction, or redox, homeostasis — caused pathological changes associated with heart failure in a mouse model. This was a follow-up to their 2018 clinical study that found about one in six heart failure patients shows reductive stress.
Now they have extended their description of changes caused by reductive stress to describe changes in the proteome of heart cells in mice, disclosing a likely proteome signature for reductive stress cardiomyopathy. A proteome is the complement of proteins expressed in a cell or tissue.
Using tandem mass spectrometry, researchers led by Rajasekaran Namakkal-Soorappan, Ph.D., associate professor in the UAB Department of Pathology, Division of Molecular and Cellular Pathology, looked at differential protein expression between control hearts and reductive-stress hearts in a mouse model of chronic reductive stress.
They found about 560 proteins were differentially expressed, and 32 proteins were significantly altered — 20 being upregulated and 12 downregulated. The reductive stress mouse model is caused by a constitutively active NRF2, the redox sensor that maintains redox homeostasis in cells.
Through gene ontology and pathway analysis, the researchers found that the majority of the differentially expressed proteins are involved in stress-related pathways such as antioxidants, NADPH, protein quality control and others. Proteins involved in mitochondrial respiration, lipophagy and cardiac rhythm were dramatically decreased in the reductive stress hearts.
The most significantly changed subset of proteins was in the glutathione family. Glutathione is an antioxidant, active in redox homeostasis, that can exist in a reduced or oxidized form.
Surprisingly, the levels of about half of 104 altered proteins were found not to correlate with levels of their messenger RNAs, the gene message that is read by ribosomes to make a protein. The reason for this asynchrony is not known.
In association with the altered proteome, the reductive stress mice displayed pathological cardiac remodeling. This cardiomyopathy makes it harder for the heart to pump blood, and it can lead to heart failure. The researchers also found post-translational modifications such as oxidation, N-ethylmaleimide, methionine loss and acetylation in the reductive stress hearts.
“Under reductive stress, we observed downregulation of several myocardial adaptation or rescue pathways and upregulation of pathophysiological processes, which are associated with reductive stress cardiomyopathy over time,” Namakkal-Soorappan said. “Thus, our results provide a rationale to develop personalized antioxidant therapeutic strategies to avoid reductive stress-mediated proteome alterations in humans.”
Co-authors with Namakkal-Soorappan are Sini Sunny, Arun Jyothidasan and Steven Pogwizd, UAB Department of Pathology; Cynthia L. David and Krishna Parsawar, the University of Arizona; Arul Veerappan, New York University School of Medicine; and Dean P. Jones, Emory University.
In research publications, Namakkal-Soorappan lists his name as Namakkal S. Rajasekaran. The UAB Department of Pathology is part of the Marnix E. Heersink School of Medicine.
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Materials provided by University of Alabama at Birmingham. Original written by Jeff Hansen. Note: Content may be edited for style and length.

It’s sunburn season. Many of us have experienced the pain and peeling that comes from unprotected time in the sun, but we may not focus on a remarkable and vital part of the process: the regeneration of skin as the damaged tissue is replaced with new.
Even without sunburn, the outer layer of skin, the epidermis, is constantly turning over to replace dead or damaged cells throughout our lifetime. This epidermal layer provides an essential barrier for the human body, reducing water loss and combating environmental threats. Scientists are working to identify the molecular mechanisms controlling skin epidermal regeneration, but much remains poorly understood.
Now a Northwestern University research team has identified a molecular switch, through a protein called CDK9, that plays an early and critical role in the skin stem cell differentiation process. This switch is “off” in the stem cells. When the switch is turned on, a specific group of genes is immediately activated to trigger downstream gene regulators, allowing the skin cells to progressively gain barrier function. The findings have relevance for improved understanding of cancer and wound healing, in addition to the fundamental understanding of skin regeneration.
“Skin stem cells need to continuously make decisions, to either make more copies of themselves — a process known as self-renewal — or to switch their fate towards differentiation. A delicate balance between these two decisions is crucial to maintain the integrity of skin and its barrier function,” said Xiaomin Bao, a stem cell biologist at Northwestern who supervised the research. “We have discovered the switch bound to selected genomic regions inside the stem cells, ready to trigger the cell fate switch of initiating the stem cell’s movement towards differentiation.”
Bao is an assistant professor of molecular biosciences in the Weinberg College of Arts and Sciences and an assistant professor of dermatology at Northwestern University Feinberg School of Medicine. Her lab studies the fundamental biology of the process of skin stem cell differentiation.
The study was published recently by the journal Nature Communications.
Discovery of the switch
The integrity of skin epidermis relies on subsets of skin stem cells to continuously self-renew or differentiate, compensating for daily wear and tear. The differentiation process involves significant changes from more than 6,000 genes, ceasing stem cell proliferation while activating barrier-function genes.
Integrating genomics, genetics and pharmacological inhibition to human skin models, Bao and her team identified that the kinase activity switch of the protein CDK9 plays a key role in the decision of cells to initiate differentiation and progressively acquire the barrier function of the tissue. The kinase activity is off in the stem cell state, and the rapid-response genes directly controlled by the kinase are suppressed. When the kinase activity is on, the rapid-response genes are activated, which subsequently induce the downstream effectors, a group of transcription factors that can further drive the expression of barrier-function genes.
CDK9 (cyclin-dependent kinase 9) plays crucial roles in modulating gene expression at the step of “transcription,” a process of copying specific DNA regions to RNA, before RNA can serve as templates for synthesizing new proteins. In the stem cell state, CDK9 is maintained in the “off” state when bound together with the proteins AFF1 and HEXIM1 on DNA, awaiting specific cellular signals such as the activation of protein kinase C signaling. Once the signaling is activated, this is sufficient to switch CDK9 from the inactive to the active state, allowing the rapid synthesis of RNA from the genomic regions directly bound by CDK9, the researchers found.
The switch is a quick one. “All the components are poised for action deep inside the stem cells,” Bao said. When the stem cell receives specific external signals, the response inside the nucleus is very fast, with activated CDK9 quickly causing rapid-response genes such as ATF3 to be expressed within as short as one hour. The expression of ATF3 potently induces several downstream transcription factors to rewire the cell fate towards differentiation. This quick switch for gene activation is also built upon the pre-recruitment of RNA-synthesis machinery together with CDK9 to the rapid-response genes, before the signaling is activated.
“We are probing the unknown,” Bao said. “Stem cell regulation is fundamental for sustaining the integrity of human tissue. We have found a key mechanism initiating the fate switch of skin stem cell towards differentiation, an integral process of regeneration. Learning more about the fundamental molecular mechanisms can help in the understanding of many different human diseases.”
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Materials provided by Northwestern University. Original written by Megan Fellman. Note: Content may be edited for style and length.

Why do some people with amyloid plaques in their brains associated with Alzheimer’s disease show no signs of the disease, while others with the same amount of plaque have clear memory and thinking problems? Researchers looked at genetic and life course factors that may help create a “cognitive reserve” that provides a buffer against the disease in a study published in the August 3, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology.
They found that factors such as taking part in clubs, religious groups, sports or artistic activities, along with educational attainment by age 26, occupation and reading ability, may affect the brain’s cognitive reserve. The study suggests that continuing to learn over a lifetime may help protect the brain, which is true even for people who have lower scores on cognitive tests in childhood. Previous studies have shown that people with low scores in childhood are more likely to have a steeper cognitive decline in old age than people with high scores.
“These results are exciting because they indicate that cognitive ability is subject to factors throughout our lifetime and taking part in an intellectually, socially and physically active lifestyle may help ward off cognitive decline and dementia,” said study author Dorina Cadar, PhD, Brighton and Sussex Medical School in the United Kingdom. “It’s heartening to find that building up one’s cognitive reserve may offset the negative influence of low childhood cognition for people who might not have benefited from an enriching childhood and offer stronger mental resilience until later in life.”
The study involved 1,184 people who were born in 1946 in the United Kingdom. They took cognitive tests when they were eight years old and again when they were 69 years old. A cognitive reserve index combined people’s education level at age 26, participation in enriching leisure activities at age 43 and occupation up to age 53. Their reading ability at age 53 was also tested as a measure of overall lifelong learning separate from education and occupation.
The cognitive test participants took at age 69 has a maximum total score of 100. The average score for this group was 92, with the lowest score being 53 and the highest score being 100.
The researchers found that higher childhood cognitive skills, a higher cognitive reserve index and higher reading ability were all associated with higher scores on the cognitive test at age 69. Researchers found that for every unit increase in childhood test scores, the old-age cognitive test score increased by 0.10 points on average. For every unit increase in the cognitive reserve index, cognitive scores increased by 0.07 points on average, and for every unit increase in reading ability, cognitive scores increased by 0.22 points on average.
People with a bachelor’s degree or other higher education qualifications scored 1.22 points more on average than those with no formal education. People who engaged in six or more leisure activities such as adult education classes, clubs, volunteer work, social activities and gardening scored 1.53 points more on average than people who engaged in up to four leisure activities. Those with a professional or intermediate level job scored 1.5 points more on average than those with partly skilled or unskilled occupations.
The study also found that for people with a higher cognitive reserve index and reading ability, their scores on cognitive tests did not decline as rapidly as people with lower scores, regardless of their test scores at age eight.
Michal Schnaider Beeri, PhD, of Icahn School of Medicine at Mount Sinai in New York, who wrote an editorial accompanying the study, said, “From a public health and societal perspective, there may be broad, long-term benefits in investing in high education, widening opportunities for leisure activities and providing cognitive challenging activities for people, especially those working in less skilled occupations.”
A limitation of the study is that the people who remained involved in the study until age 69 may be more likely to be healthier, have better overall thinking skills and be more socially advantaged than those who did not complete the study, so the results may not reflect the general population.
The study was supported by the U.K. Alzheimer’s Society, U.K. Medical Research Council, U.S. National Institute on Aging and U.K. Economic and Social Research Council.
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Materials provided by American Academy of Neurology. Note: Content may be edited for style and length.

A new study explores the use of music-listening to relieve acute pain, finding that people who were given the impression that they had control over the music they heard experienced more pain relief than people who were not given such control. Dr. Claire Howlin of Queen Mary University of London, U.K., and colleagues from University College Dublin, Ireland, present these findings in the open-access journal PLOS ONE on August 3, 2022.
Music listening can be used for pain relief, especially for chronic pain, i.e., pain lasting more than 12 weeks. However, the underlying mechanisms of these benefits are unclear, especially for acute pain, i.e., pain lasting less than 12 weeks. Basic musical features, such as tempo or energy, seem to be less important for pain relief; instead, feeling able to make decisions about the music may be key for pain relief. However, previous work has largely focused on findings from lab-based samples that did not explore real-world, pre-existing acute pain.
To improve understanding, Howlin and colleagues asked 286 adults experiencing real-world acute pain to rate their pain before and after listening to a music track. The track was specially composed in two different versions of varying complexity. Participants were randomly assigned to hear either the low- or high-complexity version, and some were randomly selected to be given the impression that they had some control over the musical qualities of the track, although they heard the same track regardless of their choice.
The researchers found that participants who felt they had control over the music experienced greater relief in the intensity of their pain than participants who were not given such an impression. In questionnaires, participants reported enjoying both versions of the track, but no links were found between music complexity and amount of pain relief. Additionally, participants who engage more actively with music in their everyday life experienced even greater pain-relief benefits from having a sense of control over the track used in this study.
These findings suggest that choice and engagement with music are important for optimizing its pain-relief potential. Future research could further explore the relationship between music choice and subsequent engagement, as well as strategies for boosting engagement to improve pain relief.
The authors add: “Now we know that the act of choosing music is an important part of the wellbeing benefits that we see from music listening. It’s likely that people listen more closely, or more carefully when they choose the music themselves.”
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Materials provided by PLOS. Note: Content may be edited for style and length.

Blood pressure should be measured in both arms and the higher reading should be adopted to improve hypertension diagnosis and management, according to a new study.
The research, led by University of Exeter, analysed data from 53,172 participants in 23 studies worldwide to examine the implications of choosing the higher or lower arm pressure.
The study, published in Hypertension, found that using the higher arm blood pressure reading reclassified 12 per cent of people as having hypertension, who would have fallen below the threshold for diagnosis if the lower reading arm was used.
Although International guidelines advise checking blood pressure in both arms, the practice is currently not widely adopted in clinics.
Study lead Dr Christopher Clark, from the University of Exeter, said: “High blood pressure is a global issue and poor management can be fatal. This study shows that failure to measure both arms and use the higher reading arm will not only result in underdiagnosis and undertreatment of high blood pressure but also under-estimation of cardiovascular risks for millions of people worldwide.”
The team found that using the higher arm measurement compared to using the lower arm resulted in reclassification of 6572 (12.4%) of participants’ systolic blood pressures from below to above 130 mm Hg, and 6339 (11.9%) from below to above 140 mm Hg, moving them above commonly used diagnostic thresholds for hypertension.
Dr Clark continued: “It’s impossible to predict the best arm for blood pressure measurement as some people have a higher reading in their left arm compared to right and equal numbers have the opposite. Therefore, it’s important to check both arms as detecting high blood pressure correctly is a vital step towards giving the right treatment to the right people.”
“Our study now provides the first evidence that the higher reading arm blood pressure is the better predictor of future cardiovascular risk.”
The study also revealed that higher arm blood pressure readings better predicted all-cause mortality, cardiovascular mortality, and cardiovascular events, compared to the lower arm reading. The authors stressed the importance of assessing both arms in the diagnosis and management of hypertension and cardiovascular diseases.
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Materials provided by University of Exeter. Note: Content may be edited for style and length.

The genes involved in coronary heart disease, the most common form of heart disease, appear to be nearly the same for everyone, according to a VA study.
Roughly one-third to one-half of everyone’s chances for developing this type of heart disease are rooted in their genes. This genetic risk seems to be the same across all major racial and ethnic backgrounds, including people of European, African, Japanese, and Indigenous ancestries, the VA study found.
“Some groups, such as African Americans, are more likely to suffer from heart disease, and our findings indicate that’s not because they have a higher genetic risk for the disease,” says study author Dr. Catherine Tcheandjieu, a genetic epidemiologist at the VA Palo Alto Health Care System and University of California San Francisco. “It confirms that other factors are responsible for more heart disease in those populations, such as access to health care and different lived experiences,” she adds.
The genetic study — the largest to date on heart disease — was published August 1, 2022, in Nature Medicine. It looked at nearly a quarter of a million cases of coronary heart disease, including more than 100,000 U.S. Veterans with the disease.
Coronary artery disease is the leading cause of death in the United States, responsible for one in every five deaths. It occurs when major blood vessels to the heart muscle become narrowed or blocked, which can lead to heart attack.
The study was led by investigators at the Palo Alto VA and involved researchers from several other VAs across the nation.