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Prenatal exposure to air pollution increases the risk of severe respiratory distress in newborn babies, according to new research conducted at the Penn State College of Medicine in collaboration with the Maternal-Infant Research on Environmental Chemicals (MIREC) Study led by Health Canada. The risk increases with exposure specifically to fine particulate matter (PM2.5) and nitrogen dioxide (NO2), which occur in wildfire and cigarette smoke and vehicle emissions, among other sources.
The findings, which published on Jan. 25 in the journal Environmental Health Perspectives, reveal a better understanding of infant respiratory distress, the leading cause of admission in neonatal intensive care units and death among newborns worldwide.
“Mothers’ exposure to air pollution while pregnantis known to be associated with adverse long-term respiratory issues, such as asthma, in their children,” said Chintan K. Gandhi, assistant professor of pediatrics at Penn State and corresponding author of the paper. “However, what we didn’t know is that maternal exposure to air pollution could cause babies to suffer severe respiratory distress soon after birth.”
To conduct their study, the researchersanalyzed data from the MIREC Study, a multi-year study that examined the exposures of 2,001 pregnant women from 10 Canadian cities to environmental chemicals, including PM2.5 and NO2. The MIREC Study team estimated the women’s exposures to PM2.5 and NO2 beginning three months prior to pregnancy through the end of the third trimester by using models based on satellite information and ground-level air quality monitoring devices.
The MIREC team found that during the study period, the women were exposed to PM2.5 concentrations ranging from 1.47 to 23.71 micrograms per cubic meter of air (μg/m3), with a median of 8.81 μg/m3, and NO2 concentrations ranging from 1.72 to 53.10 parts per billion (ppb), with a median of 18.02 ppb. To provide context, the U.S. Environmental Protection Agency provides standards for maximum annual exposures of 9.0 to 10.0 µg/m3 for PM2.5 and 53 ppb for NO2.
However, Gandhi said, “There really is no safe level of air pollution.”
Using data from the MIREC study, the team led by Penn State researchers examined associations between the mothers’ exposure to air pollution and physician-diagnosed respiratory distress in newborns. The examination extended beyond diagnosis to encompass the severity of respiratory distress, quantified by the necessity for oxygen, mechanical ventilation and systemic antibiotics in the infants.

“This nuanced approach provides a comprehensive understanding of the intricate relationship between maternal air pollution exposure and the varying degrees of respiratory distress observed in newborns,” Gandhi said.
Key findings from the collaborative research include: Increased risk of severe respiratory distress: Babies born to mothers exposed to higher levels of PM2.5 were more likely to experience severe respiratory distress, requiring interventions such as assisted ventilation and systemic antibiotics. Consistent associations across pregnancy stages: The association between PM2.5 exposure and severe respiratory distress remained consistent whether the exposure occurred during the pre-pregnancy stage or at any stage during pregnancy. NO2 exposure and systemic antibiotics: NO2 exposure in mothers was associated with an increased need for systemic antibiotics among babies.Gandhi highlighted a crucial observation in the study, noting that the incidence of respiratory stress in babies remained consistent across various levels of air pollution exposure. However, the significant revelation emerged in the escalation of severe respiratory stress with increasing levels of exposure.
“We found that the more air pollution mothers were exposed to, the greater the chances that their babies would suffer severe respiratory distress,” he said.
While the team did not investigate the specific mechanism through which pollutants are transmitted from mother to child, Gandhi pointed to previous research indicating heightened inflammatory markers in mothers exposed to air pollution. These markers, detected through blood tests in the same cohort of mothers, underscore a potential pathway for the impact of air pollution on maternal health and its subsequent influence on newborns, he said.
“Our findings hold substantial importance as they suggest that preventing death and illness in babies due to respiratory distress is plausible through the reduction or elimination of air pollution,” Gandhi said. “It is imperative for policymakers to grasp the gravity of this situation.”
Other authors on the paper include Markey Johnson, research scientist, Health Canada; Lauren Mazur, graduate student, Penn State; Mandy Fisher, senior epidemiologist, Health Canada; William Fraser, professor, Universite de Sherbrooke; Liu Sun, scientific evaluator, Health Canada; and Perry Hystad, associate professor, Oregon State University.
The MIREC study was funded by Health Canada’s Chemicals Management Plan, the Ontario Ministry of the Environment and the Canadian Institute for Health Research.

Published15 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, SCIENCE PHOTO LIBRARYBy Michelle RobertsDigital health editorAn uncommon medical treatment withdrawn in the mid-1980s may have caused some very rare cases of Alzheimer’s, scientists believe. The team at University College London has been studying five cases linked to injections of human growth hormone that came from deceased donors. The findings do not mean Alzheimer’s is infectious – you cannot catch it from contact with people who have it. But it might be “seeded” or transmitted into the brain by certain procedures. The researchers say all of the people in their study had been treated as a child with cadaver-derived human growth hormone, or c-hGH, that was contaminated with brain proteins that are seen in Alzheimer’s disease.There is no suggestion it can be passed on in day-to-day life or during routine medical or social care. There is no ongoing public health risk because growth hormone treatment is now made synthetically.The c-hGH was used to treat at least 1,848 people in the UK between 1959 and 1985.Its use was stopped when experts recognised that some batches were contaminated with a different type of infectious protein which had caused a rare and fatal brain condition called Creutzfeldt-Jakob disease (CJD) in some people.The latest findings in Nature Medicine suggest Alzheimer’s-related amyloid protein might be spread accidentally during medical and surgical procedures in the same way as CJD.The researchers stress that the circumstances are highly unusual – there have been no reported cases of Alzheimer’s acquired from any other medical or surgical procedures. And as c-hGH treatment is no longer used, there is no risk of any new transmission via this route. Lead author Prof John Collinge, director of the UCL Institute of Prion Diseases, said: “There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care. “The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins.”Dr Richard Oakley, associate director of research and innovation at Alzheimer’s Society, said: “There is no cause for concern for the health of the general population.”Prof Bart De Strooper, from the UK Dementia Research Institute at UCL, said: “No-one should reconsider or forego any medical procedure, especially for blood transfusion or neurosurgery, which saves many lives worldwide every year.”The Nature Medicine study reports on eight people referred to UCLH’s National Prion Clinic at the National Hospital for Neurology and Neurosurgery in London, who had all been treated with c-hGH in childhood, often over several years.Five of them had symptoms of dementia, and either had already been diagnosed with Alzheimer’s disease or would otherwise meet the diagnostic criteria for this condition.Another person met criteria for mild cognitive impairment.These people were between 38 and 55 years old when they started having neurological symptoms. Researchers say the unusually young age at which these patients developed symptoms suggests they did not have the usual Alzheimer’s which is associated with old age. More on this story’Transmittable Alzheimer’s’ concept raisedPublished9 September 2015NHS exploring Alzheimer’s disease blood testsPublished9 November 2023

Published21 hours agoShareclose panelShare pageCopy linkAbout sharingA former miner whose teeth fell out has said he is “thrilled” to finally get an NHS dental appointment after suffering seven months of agony.David Creamer, from Rotherham, said he had been “living on painkillers and soup” since June after being unable to get the dental treatment he needed.Mr Creamer said he contacted 16 NHS dentists but could not be seen.Eventually he opted for private consultation and was told he needed all his teeth removing at a cost of £5,000.Mr Creamer has now been offered an NHS dentist in Rotherham after his plight was highlighted on BBC Radio Sheffield.The 62-year-old lost a crown in June while eating a sandwich in Blackpool, and five of his teeth fell out.His GP prescribed painkillers and anti-inflammatory medication but Mr Creamer said he was told he needed to be referred by an NHS dentist in order to be seen at a dental hospital.Eventually, Mr Creamer said, he paid for a private consultation and was told all his teeth other than two or three at the back had decayed and were “unsaveable”.They needed extracting by a dental surgeon, followed by several weeks of healing and then denture fitting, he was told.But Mr Creamer said that as he was on benefits, he could not afford the £5,274 bill for the work.Eddie Crouch, chair of the British Dental Association (BDA), said hundreds of people nationwide needed hospital care because of a lack of dental surgeries.He said 12,000 people were struggling to find an NHS dentist.Mr Crouch saId: “It isn’t about extra money but about [working] to prevent these problems… otherwise people like Dave turn up in other areas of the health service which costs more in the long run.”The BDA said government had allowed NHS dentistry to “fall off a cliff” and “promised ring fences are torn down around a budget that’d already been cut to the bone”.A Department of Health and Social Care spokesperson said: “Access to dentistry is improving – last year 1.7 million more adults and some 800,000 more children saw an NHS dentist – and we have also announced plans to increase dental training places by 40%.”We invest £3bn each year to deliver NHS dentistry and we are also taking preventative measures, such as expanding water fluoridation schemes to reduce the number of children experiencing tooth decay.”We want every adult and child who needs an NHS dentist to get one regardless of where in England they live. We have already taken steps to improve access and incentivise practices to deliver more NHS dental care, and will set out new measures in our Dental Recovery Plan in due course.”Mr Creamer said he was “over the moon” that he had now been offered an appointment and would finally be free from pain, but “disgusted” and “astounded” that he had to go to the media first.Follow BBC Yorkshire on Facebook, Twitter and Instagram. Send your story ideas to yorkslincs.news@bbc.co.uk.Related Internet LinksBritish Dental AssociationDepartment of Health and Social CareNHS: DentistryThe BBC is not responsible for the content of external sites.

Five cases of Alzheimer’s disease are believed to have arisen as a result of medical treatments decades earlier, reports a team of UCL and UCLH researchers.
Alzheimer’s disease is caused by the amyloid-beta protein, and is usually a sporadic condition of late adult life, or more rarely an inherited condition that occurs due to a faulty gene. The new Nature Medicine paper provides the first evidence of Alzheimer’s disease in living people that appears to have been medically acquired and due to transmission of the amyloid-beta protein.
The people described in the paper had all been treated as children with a type of human growth hormone extracted from pituitary glands from deceased individuals (cadaver-derived human growth hormone or c-hGH). This was used to treat at least 1,848 people in the UK between 1959 and 1985, and used for various causes of short stature. It was withdrawn in 1985 after it was recognised that some c-hGH batches were contaminated with prions (infectious proteins) which had caused Creutzfeldt-Jakob disease (CJD) in some people. c-hGH was then replaced with synthetic growth hormone that did not carry the risk of transmitting CJD.
These researchers previously reported that some patients with CJD due to c-hGH treatment (called iatrogenic CJD) also had prematurely developed deposits of the amyloid-beta protein in their brains.* The scientists went on to show in a 2018 paper that archived samples of c-hGH were contaminated with amyloid-beta protein and, despite having been stored for decades, transmitted amyloid-beta pathology to laboratory mice when it was injected.** They suggested that individuals exposed to contaminated c-hGH, who did not succumb to CJD and lived longer, might eventually develop Alzheimer’s disease.
This latest paper reports on eight people referred to UCLH’s National Prion Clinic at the National Hospital for Neurology and Neurosurgery in London, who had all been treated with c-hGH in childhood, often over several years.
Five of these people had symptoms of dementia, and either had already been diagnosed with Alzheimer’s disease or would otherwise meet the diagnostic criteria for this condition; another person met criteria for mild cognitive impairment. These people were between 38 and 55 years old when they started having neurological symptoms. Biomarker analyses supported the diagnoses of Alzheimer’s disease in two patients with the diagnosis, and was suggestive of Alzheimer’s in one other person; an autopsy analysis showed Alzheimer’s pathology in another patient.
The unusually young age at which these patients developed symptoms suggests they did not have the usual sporadic Alzheimer’s which is associated with old age. In the five patients in whom samples were available for genetic testing, the team ruled out inherited Alzheimer’s disease.

As c-hGH treatment is no longer used, there is no risk of any new transmission via this route. There have been no reported cases of Alzheimer’s acquired from any other medical or surgical procedures. There is no suggestion that amyloid-beta can be passed on in day-to-day life or during routine medical or social care.
However, the researchers caution that their findings highlight the importance of reviewing measures to ensure there is no risk of accidental transmission of amyloid-beta via other medical or surgical procedures which have been implicated in accidental transmission of CJD.
The lead author of the research, Professor John Collinge, Director of the UCL Institute of Prion Diseases and a consultant neurologist at UCLH, said: “There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care. The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins.
“However, the recognition of transmission of amyloid-beta pathology in these rare situations should lead us to review measures to prevent accidental transmission via other medical or surgical procedures, in order to prevent such cases occurring in future.
“Importantly, our findings also suggest that Alzheimer’s and some other neurological conditions share similar disease processes to CJD, and this may have important implications for understanding and treating Alzheimer’s disease in the future.”
Co-author Professor Jonathan Schott (UCL Queen Square Institute of Neurology, honorary consultant neurologist at UCLH, and Chief Medical Officer at Alzheimer’s Research UK) said: “It is important to stress that the circumstances through which we believe these individuals tragically developed Alzheimer’s are highly unusual, and to reinforce that there is no risk that the disease can be spread between individuals or in routine medical care. These findings do, however, provide potentially valuable insights into disease mechanisms, and pave the way for further research which we hope will further our understanding of the causes of more typical, late onset Alzheimer’s disease.”
First author Dr Gargi Banerjee (UCL Institute of Prion Diseases) said: “We have found that it is possible for amyloid-beta pathology to be transmitted and contribute to the development of Alzheimer’s disease. This transmission occurred following treatment with a now obsolete form of growth hormone, and involved repeated treatments with contaminated material, often over several years. There is no indication that Alzheimer’s disease can be acquired from close contact, or during the provision of routine care.”
The study was supported by the Medical Research Council, the National Institute for Health and Care Research (NIHR), the NIHR UCLH Biomedical Research Centre, Alzheimer’s Research UK, and the Stroke Association.

Clinical research led by Indiana University School of Medicine investigators and their collaborators in Uganda has revealed that hydroxyurea significantly reduces infections in children with sickle cell anemia. Their latest findings enhance strong evidence of hydroxyurea’s effectiveness and could ultimately reduce death in children in Africa, the continent most burdened by the disease.
The group’s research, recently published in the journal Blood, revealed that hydroxyurea treatment resulted in a remarkable 60% reduction in severe or invasive infections, including malaria, bacteremia, respiratory tract infections and gastroenteritis, among Ugandan children with sickle cell anemia.
“Our investigation provides powerful justifications for hydroxyurea’s use in children with sickle cell anemia in Africa,” said Dr. Chandy John, the Ryan White Professor of Pediatrics at IU School of Medicine and co-lead investigator of the latest study. “Given the high rates of infection in this region, we hope our evidence will encourage ministries of health to continue supporting and expanding access to hydroxyurea for young patients who can greatly benefit from the treatment.”
Sickle cell anemia is a genetic blood disorder that alters the structure of red blood cells and affects oxygen distribution throughout the body, increasing susceptibility to serious health complications and life-threatening infections. According to the World Health Organization, more than 300,000 children worldwide are born with sickle cell disease each year, with a high prevalence found in African countries.
While hydroxyurea has had U.S. Food and Drug Administration approval as a sickle cell disease treatment for children since 2017, its accessibility and acceptance in Africa have been comparatively limited. As hydroxyurea has become more recognized in African countries for its effectiveness in treating sickle-cell-related complications, John and his colleagues noticed a knowledge gap about the treatment’s effect on infections. This led the research group to incorporate hydroxyurea treatment and analysis into their established clinical trial, Zinc for Infection Prevention in Sickle Cell Anemia.
During the study, the researchers examined the effects of hydroxyurea on 117 children in Uganda and focused on a range of infections. After hydroxyurea treatment, results showed a substantial decrease in the incidence of these infections. Additionally, eight of the nine deaths that occurred in the trial were children whose parents declined hydroxyurea treatment. The only death in a child on hydroxyurea treatment occurred four days after starting treatment, providing insufficient time for hydroxyurea to have an effect.
Of the five children for whom a cause of death was known, all five died of infectious causes. The high death rate in the study, despite expert clinical care by study personnel, provides further evidence of the urgent need for additional interventions to decrease mortality in children with sickle cell disease in Africa.
“Infections commonly precede other complications related to sickle cell anemia and often result in hospitalizations that can lead to death,” said Dr. Ruth Namazzi, site principal investigator, first author on the study and a lecturer in the Department of Pediatrics and Child Health at Makerere University in Uganda. “We believe incorporating hydroxyurea treatment as the standard of care for sickle cell anemia across Africa will not only reduce infections but will more importantly save countless lives.”
Additional IU researchers who contributed to the study include Caitlin Bond, Andrea Conroy, Dibyadyuti Datta and Michael Goings. They collaborated with Namazzi; Dr. Robert Opoka of Global Health Uganda; Dr. Abner Tagoola of Jinja Regional Referral Hospital; Jeong Hoon Jang of Yonsei University; and Dr. Russell E. Ware of Cincinnati Children’s Hospital Medical Center.

A new qualitative study highlights the negative interpersonal and psychological consequences associated with “yo-yo dieting,” also known as weight cycling. The work underscores how toxic yo-yo dieting can be and how difficult it can be for people to break the cycle.
“Yo-yo dieting — unintentionally gaining weight and dieting to lose weight only to gain it back and restart the cycle — is a prevalent part of American culture, with fad diets and lose-weight-quick plans or drugs normalized as people pursue beauty ideals,” says Lynsey Romo, corresponding author of a paper on the study and an associate professor of communication at North Carolina State University.
“Based on what we learned through this study, as well as the existing research, we recommend that most people avoid dieting, unless it is medically necessary. Our study also offers insights into how people can combat insidious aspects of weight cycling and challenge the cycle.”
For the study, researchers conducted in-depth interviews with 36 adults — 13 men and 23 women — who had experienced weight cycling where they lost and regained more than 11 pounds. The goal was to learn more about why and how people entered the yo-yo dieting cycle and how, if at all, they were able to get out of it.
All the study participants reported wanting to lose weight due to social stigma related to their weight, and/or because they were comparing their weight to that of celebrities or peers.
“Overwhelmingly, participants did not start dieting for health reasons, but because they felt social pressure to lose weight,” Romo says.
The study participants also reported engaging in a variety of weight-loss strategies, which resulted in initial weight loss, but eventual regain.

Regaining the weight led people to feel shame and further internalize stigma associated with weight — leaving study participants feeling worse about themselves than they did before they began dieting. This, in turn, often led people to engage in increasingly extreme behaviors to try to lose weight again.
“For instance, many participants engaged in disordered weight management behaviors, such as binge or emotional eating, restricting food and calories, memorizing calorie counts, being stressed about what they were eating and the number on the scale, falling back on quick fixes (such as low-carb diets or diet drugs), overexercising, and avoiding social events with food to drop pounds fast,” says Romo. “Inevitably, these diet behaviors became unsustainable, and participants regained weight, often more than they had initially lost.”
“Almost all of the study participants became obsessed with their weight,” says Katelin Mueller, co-author of the study and graduate student at NC State. “Weight loss became a focal point for their lives, to the point that it distracted them from spending time with friends, family, and colleagues and reducing weight-gain temptations such as drinking and overeating.”
“Participants referred to the experience as an addiction or a vicious cycle,” Romo says. “Individuals who were able to understand and address their toxic dieting behaviors were more successful at breaking the cycle. Strategies people used to combat these toxic behaviors included focusing on their health rather than the number on the scale, as well as exercising for fun, rather than counting the number of calories they burned.
“Participants who were more successful at challenging the cycle were also able to embrace healthy eating behaviors — such as eating a varied diet and eating when they were hungry — rather than treating eating as something that needs to be closely monitored, controlled or punished.”
However, the researchers found the vast majority of study participants stuck in the cycle.
“The combination of ingrained thought patterns, societal expectations, toxic diet culture, and pervasive weight stigma make it difficult for people to completely exit the cycle, even when they really want to,” Romo says.
“Ultimately, this study tells us that weight cycling is a negative practice that can cause people real harm,” Romo says. “Our findings suggest that it can be damaging for people to begin dieting unless it is medically necessary. Dieting to meet some perceived societal standard inadvertently set participants up for years of shame, body dissatisfaction, unhappiness, stress, social comparisons, and weight-related preoccupation. Once a diet has begun, it is very difficult for many people to avoid a lifelong struggle with their weight.”

Calcium ions are essential for cells, but can be toxic in higher concentrations. A team of researchers has now designed and prepared a combination drug that kills tumor cells by modulating the calcium influx into the cell. An external calcium source is not necessary because only the calcium ions already present in the tumor tissue are used, according to the study published in the journal Angewandte Chemie.
Biological cells need calcium ions, among other things, for the proper functioning of the mitochondria, the powerhouses of the cells. However, if there is too much calcium, the mitochondrial processes become unbalanced and the cell suffocates. A research group led by Juyoung Yoon of Ewha Womens University in Seoul, South Korea, together with teams from China, has now taken advantage of this process and developed a synergistic antitumor drug that can open calcium channels and thus trigger a deadly calcium storm inside the tumor cell.
The researchers targeted two channels, the first one in the outer membrane, and the other was a calcium channel in the endoplasmic reticulum, a cell organelle that also stores calcium ions. The channel located in the outer membrane opens when it is exposed to a large amount of reactive oxygen species (ROS), while the channel in the endoplasmic reticulum is activated by nitric oxide molecules.
To generate the ROS that open the outer membrane calcium channel, the researchers used the dye indocyanine green. This bioactive agent can be activated by irradiation with near-infrared light, which not only triggers reactions that lead to ROS, but it also heats up the environment. The team explains that the high local temperature activates the other active agent, BNN-6, to release nitric oxide molecules that open the channel in the endoplasmic reticulum.
Following successful trials in tumor cell lines, the team tested an injectable formulation in tumor-implanted mice. To create a biocompatible combined drug, the researchers loaded the active ingredients into tiny modified porous silica beads that are not harmful to the body, but can be recognized by tumor cells and transported into the cell. After injecting the beads into the bloodstream of the mice, the researchers observed that the drug accumulated in the tumor. Exposure to near-infrared light successfully triggered the mechanism of action, and the tumor disappeared after a few days in mice that received the preparation.
The authors emphasize that this ion influx approach may also be useful in related biomedical research areas where a similar mechanism could activate ion channels different from calcium in order to find new therapeutic approaches.

A University of Houston optometry researcher is warning against the use of low-level red light (LLRL) therapy as a method to control myopia, or nearsightedness, especially in children. Over the last few years, LLRL has emerged as a viable myopia treatment after studies reported the treatment as effective and responsible for significant reduction in myopia progression. The company behind one of the devices reports that it is already being used to address myopia in over 100,000 pediatric patients.
But the excitement over its results as a myopia treatment may have come too soon, ahead of its proven safety.
“Based on measurements in our laboratory, it is recommended that clinicians strongly reconsider the use of LLRL therapy for myopia in children until safety standards can be confirmed,” report Lisa Ostrin, associate professor at the UH College of Optometry in The College of Optometrists journal.
Ostrin reports the therapy can put the retina at risk of photochemical and thermal damage. “The safety profiles of red-light laser devices for myopia have not been fully investigated,” she said.
For LLRL therapy, children are instructed to look into a red light-emitting instrument for three minutes, twice a day, five days a week, for the duration of the treatment period, which could last years.
“We found that the red-light instruments for myopia exceed safety limits,” said Ostrin, whose research characterizes the laser output and determines the thermal and photochemical maximum permissible exposure (MPE) of LLRL devices. “For both LLRL devices evaluated here, three minutes of continuous viewing approached or surpassed the luminance dose MPE, putting the retina at risk of photochemical damage.”
Ostrin examined two different LLRL devices, and while both instruments were confirmed to be Class-1 laser products, as defined by International Electrotechnical Commission standards, according to Ostrin they are unsafe to view continuously for the required treatment duration of three minutes.
Class-1 lasers are low-powered devices that are considered safe from all potential hazards when viewed accidentally and briefly. Examples of Class-1 lasers are laser printers, CD players and digital video disc (DVD) devices. Class-1 lasers are not meant to be viewed directly for extended periods.
“Thermal ocular injury from a laser can occur with exposures at any wavelength when the temperature change of the retina is greater than 10°C, resulting in the denaturation of proteins. With thermal damage, the lesion size is typically less than the size of the beam diameter, and the resultant scotomas are permanent.” said Ostrin.

Engaging in music throughout your life is associated with better brain health in older age, according to a new study published by experts at the University of Exeter.
Scientists working on PROTECT, an online study open to people aged 40 and over, reviewed data from more than a thousand adults over the age of 40 to see the effect of playing a musical instrument — or singing in a choir — on brain health. Over 25000 people have signed up for the PROTECT study, which has been running for 10 years.
The team reviewed participants’ musical experience and lifetime exposure to music, alongside results of cognitive testing, to determine whether musicality helps to keep the brain sharp in later life.
The findings show that playing a musical instrument, particularly the piano, is linked to improved memory and the ability to solve complex tasks — known as executive function. Continuing to play into later life provides even greater benefit. The work also suggests that singing was also linked to better brain health, although this may also be due to the social factors of being part of a choir or group.
Anne Corbett, Professor of Dementia Research at the University of Exeter said: “A number of studies have looked at the effect of music on brain health. Our PROTECT study has given us a unique opportunity to explore the relationship between cognitive performance and music in a large cohort of older adults. Overall, we think that being musical could be a way of harnessing the brain’s agility and resilience, known as cognitive reserve.”
“Although more research is needed to investigate this relationship, our findings indicate that promoting musical education would be a valuable part of public health initiatives to promote a protective lifestyle for brain health, as would encouraging older adults to return to music in later life. There is considerable evidence for the benefit of music group activities for individuals with dementia, and this approach could be extended as part of a healthy ageing package for older adults to enable them to proactively reduce their risk and to promote brain health.”
Stuart Douglas, a 78-year-old accordion player from Cornwall, has played the instrument throughout his life and now plays with the Cober Valley Accordion Band as well as the Cornish Division of the Royal Scottish Country Dance Society. He said: “I learnt to play the accordion as a boy living in a mining village in Fife and carried on throughout my career in the police force and beyond. These days I still play regularly, and playing in the band also keeps my calendar full, as we often perform in public. We regularly play at memory cafes so have seen the effect that our music has on people with memory loss, and as older musicians ourselves we have no doubt that continuing with music into older age has played an important role in keeping our brains healthy.”
This study is supported by the National Institute for Health and Care Research (NIHR) Applied Research Collaboration South West Peninsula (PenARC) and NIHR Exeter Biomedical Research Centre.

The number of people with obesity has nearly tripled since 1975, resulting in a worldwide epidemic. While lifestyle factors like diet and exercise play a role in the development and progression of obesity, scientists have come to understand that obesity is also associated with intrinsic metabolic abnormalities. Now, researchers from University of California San Diego School of Medicine have shed new light on how obesity affects our mitochondria, the all-important energy-producing structures of our cells.
In a study published January 29, 2023 in Nature Metabolism, the researchers found that when mice were fed a high-fat diet, mitochondria within their fat cells broke apart into smaller mitochondria with reduced capacity for burning fat. Further, they discovered that this process is controlled by a single gene. By deleting this gene from the mice, they were able to protect them from excess weight gain, even when they ate the same high-fat diet as other mice.
“Caloric overload from overeating can lead to weight gain and also triggers a metabolic cascade that reduces energy burning, making obesity even worse,” said Alan Saltiel, PhD, professor in the Department of Medicine at UC San Diego School of Medicine. “The gene we identified is a critical part of that transition from healthy weight to obesity.”
Obesity, which affects more than 40% of adults in the United States, occurs when the body accumulates too much fat, which is primarily stored in adipose tissue. Adipose tissue normally provides important mechanical benefits by cushioning vital organs and providing insulation. It also has important metabolic functions, such as releasing hormones and other cellular signaling molecules that instruct other tissues to burn or store energy.
In the case of caloric imbalances like obesity, the ability of fat cells to burn energy starts to fail, which is one reason why it can be difficult for people with obesity to lose weight. How these metabolic abnormalities start is among the biggest mysteries surrounding obesity.
To answer this question, the researchers fed mice a high-fat diet and measured the impact of this diet on their fat cells’ mitochondria, structures within cells that help burn fat. They discovered an unusual phenomenon. After consuming a high-fat diet, mitochondria in parts of the mice’s adipose tissue underwent fragmentation, splitting into many smaller, ineffective mitochondria that burned less fat.
In addition to discovering this metabolic effect, they also discovered that it is driven by the activity of single molecule, called RaIA. RaIA has many functions, including helping break down mitochondria when they malfunction. The new research suggests that when this molecule is overactive, it interferes with the normal functioning of mitochondria, triggering the metabolic issues associated with obesity.

“In essence, chronic activation of RaIA appears to play a critical role in suppressing energy expenditure in obese adipose tissue,” said Saltiel. “By understanding this mechanism, we’re one step closer to developing targeted therapies that could address weight gain and associated metabolic dysfunctions by increasing fat burning.”
By deleting the gene associated with RaIA, the researchers were able to protect the mice against diet-induced weight gain. Delving deeper into the biochemistry at play, the researchers found that some of the proteins affected by RaIA in mice are analogous to human proteins that are associated with obesity and insulin resistance, suggesting that similar mechanisms may be driving human obesity.
“The direct comparison between the fundamental biology we’ve discovered and real clinical outcomes underscores the relevance of the findings to humans and suggests we may be able to help treat or prevent obesity by targeting the RaIA pathway with new therapies,” said Saltiel “We’re only just beginning to understand the complex metabolism of this disease, but the future possibilities are exciting.”
Co-authors of the study include: Wenmin Xia, Preethi Veeragandham, Yu Cao Yayun Xu, Torrey Rhyne, Jiaxin Qian, Ying Jones,Chao-Wei Hung, Zichen Wang, Hiroyuki Hakozaki and Johannes Schoneberg at UC San Diego, Peng Zhao at University of Texas Health Science Center, Hui Gao and Mikael Ryden at Karolinska Institute, Christopher Liddle, Ruth Yu, Michael Downes, Ronald Evans and Jianfeng Huang at Salk Institute for Biological Studies,Martin Wabitsch at Ulm University Medical Center and Shannon Reilly at Weill Medical College of Cornell University.
This study was funded, in part, by the National Institutes of Health (Grants P30DK063491, R01DK122804, R01DK124496, R01DK125820 and R01DK128796).