Heart disease is the leading cause of death among men, and being a father may put men at an even greater risk of poor heart health later in life, reports a new study from scientists at Northwestern University and Ann & Robert H. Lurie Children’s Hospital of Chicago.
The study of 2,814 men between the ages of 45 and 84 found cardiovascular health in older age was worse for fathers compared to nonfathers. Study participants’ heart health was rated based on their diet, physical activity, smoking habits, weight, blood pressure, and level of lipids and glucose in their blood.
“The changes in heart health we found suggest that the added responsibility of childcare and the stress of transitioning to fatherhood may make it difficult for men to maintain a healthy lifestyle, such as a healthy diet and exercise,” said corresponding author Dr. John James Parker, an internist, pediatrician and assistant professor of pediatrics and general internal medicine at Northwestern University Feinberg School of Medicine.
“We really need to study fathers as a unique population and track men’s health outcomes as they become fathers. Cardiovascular health is especially important since the health behaviors and factors are all modifiable.”
The study was published as a peer-reviewed preprint earlier this month in the journal AJPM Focus with a more finalized version publishing soon.
Fathers have worse heart health but lower death rates
Despite fathers in the study having worse hearth health in older age, the study found they actually have lower rates of death than nonfathers. Parker said this conflicting association could be because fathers may have a more robust social support system, and social connectedness has been linked with lower mortality.

“Fathers may also be more likely to have someone as their future caretaker (i.e., their children) to help them attend medical appointments and manage medications and treatments as they get older,” Parker said. “We also found that fathers had lower rates of depressive symptoms than nonfathers, so mental health may be contributing to the lower age-adjusted death rates in fathers.”
The study included men who self-identified as Black, Chinese, Hispanic or White, and the age-adjusted rate of death for all Black fathers was lower than for Black nonfathers, the only racial and ethnic subgroup with this association.
“Fatherhood may be protective for Black men,”Parker said. “Maybe becoming a father helps promote a healthy lifestyle for Black men. Studying this association further could have important public health implications.”
Previous studies that evaluated fatherhood, cardiovascular health, cardiovascular disease and mortality have not included racially and ethnically diverse populations and lacked comprehensive cardiovascular health evaluation. This study is novel because it included men from the Multi-Ethnic Study of Atherosclerosis (MESA).
This study also examined influence of the age men transition to fatherhood on heart health and disease outcomes. Interestingly, men who became at younger ages (25 years old and younger) — especially Black and Hispanic men — had worse heart health and high death rates and may benefit from focused clinical and public health attention.
“If you’re under 25, you may be less financially stable, your brain may be less mature, and, especially for racial and ethnic minorities, you may have lower-paying jobs with fewer benefits and limited leave policies,” Parker said. “All of this can make it harder to focus on your health. There are a lot of public health interventions for young mothers, but no one has ever really looked at young fathers in this way.”
‘A father’s health has a major influence on their family’

Since most men in the U.S. are fathers, identifying some of the explanations for the associations among health, disease and fatherhood could have important health implications for men, especially for men of color, the scientists said.
“A lot of times we focus on the health of mothers and children, and we don’t even think of fathers, but their health has a major influence on their family,” said Parker, citing previous research that found higher obesity rates among partners if their spouse was obese. “To improve the health of families, we need to consider the multi-directional relationship among mothers, fathers, other caregivers and children.”
The study also found a higher smoking rate among fathers, which Parker said is surprising because other studies have shown many fathers quit smoking when they have kids.
“This study looked at older fathers, so it’s possible men might quit smoking when they become fathers but then later, maybe they become more stressed and take up the habit again,” Parker said. “Either way, we should look at what’s happening with smoking rates because smoking is a leading cause of preventative death and if a father is smoking it will influence their families as well.”
The scientists defined study participants’ cardiovascular health using the American Heart Association Life’s Essential 8 scores (excluding sleep). Men were categorized as either fathers (82% study participants) or nonfathers based on an interview in which participants were asked to list any children’s ages and medical conditions. Men who did not list any children were categorized as nonfathers.
Other Northwestern study authors include Dr. Craig Garfield, Clarissa Simon, Laura Colangelo and Norrina Allen.

OAK BROOK, Ill. – Low-level light therapy appears to affect healing in the brains of people who suffered significant brain injuries, according to a study published today in Radiology, a journal of the Radiological Society of North America (RSNA).
Lights of different wavelengths have been studied for years for their wound-healing properties. Researchers at Massachusetts General Hospital (MGH) conducted low-level light therapy on 38 patients who had suffered moderate traumatic brain injury, an injury to the head serious enough to alter cognition and/or be visible on a brain scan. Patients received light therapy within 72 hours of their injuries through a helmet that emits near-infrared light.
“The skull is quite transparent to near-infrared light,” said study co-lead author Rajiv Gupta, M.D., Ph.D., from the Department of Radiology at MGH. “Once you put the helmet on, your whole brain is bathing in this light.”
The researchers used an imaging technique called functional MRI to gauge the effects of the light therapy. They focused on the brain’s resting-state functional connectivity, the communication between brain regions that occurs when a person is at rest and not engaged in a specific task. The researchers compared MRI results during three recovery phases: the acute phase of within one week after injury, the subacute phase of two to three weeks post-injury and the late-subacute phase of three months after injury.
Of the 38 patients in the trial, 21 did not receive light therapy while wearing the helmet. This was done to serve as a control to minimize bias due to patient characteristics and to avoid potential placebo effects.
Patients who received low-level light therapy showed a greater change in resting-state connectivity in seven brain region pairs during the acute-to-subacute recovery phase compared to the control participants.
“There was increased connectivity in those receiving light treatment, primarily within the first two weeks,” said study coauthor Nathaniel Mercaldo, Ph.D., a statistician with MGH. “We were unable to detect differences in connectivity between the two treatment groups long term, so although the treatment appears to increase the brain connectivity initially, its long-term effects are still to be determined.”
The precise mechanism of the light therapy’s effects on the brain is also still to be determined. Previous research points to the alteration of an enzyme in the cell’s mitochondria (often referred to as the “powerhouse” of a cell), Dr. Gupta said. This leads to more production of adenosine triphosphate, a molecule that stores and transfers energy in the cells. Light therapy has also been linked with blood vessel dilation and anti-inflammatory effects.

“There is still a lot of work to be done to understand the exact physiological mechanism behind these effects,” said study coauthor Suk-tak Chan, Ph.D., a biomedical engineer at MGH.
While connectivity increased for the light therapy-treated patients during the acute to subacute phases, there was no evidence of a difference in clinical outcomes between the treated and control participants. Additional studies with larger cohorts of patients and correlative imaging beyond three months may help determine the therapeutic role of light in traumatic brain injury.
The researchers expect the role of light therapy to expand as more study results come in. The 810-nanometer-wavelength light used in the study is already employed in various therapeutic applications. It’s safe, easy to administer and does not require surgery or medications. The helmet’s portability means it can be delivered in settings outside of the hospital. It may have applications in treating many other neurological conditions, according to Dr. Gupta.
“There are lots of disorders of connectivity, mostly in psychiatry, where this intervention may have a role,” he said. “PTSD, depression, autism: these are all promising areas for light therapy.”###
“Effects of Low-Level Light Therapy on Resting-State Connectivity Following Moderate Traumatic Brain Injury: Secondary Analyses of a Double-blinded, Placebo-controlled Study.” Collaborating with Drs. Gupta, Mercaldo and Chan were Maria G. Figueiro Longo, M.D., Jonathan Welt, M.D., Arman Avesta, M.D., Jarone Lee, M.D., Michael H. Lev, M.D., Eva-Maria Ratai, Ph.D., Michael R. Wenke, B.S., Blair A. Parry, B.A., Lynn Drake, M.D., Richard R. Anderson, M.D., Terry Rauch, Ph.D., Ramon Diaz-Arrastia, M.D., Kenneth K. Kwong, Ph.D., Michael Hamblin, Ph.D., and Benjamin Vakoc, Ph.D. 
Radiology is edited by Linda Moy, M.D., New York University, New York, N.Y., and owned and published by the Radiological Society of North America, Inc. (https://pubs.rsna.org/journal/radiology)
RSNA is an association of radiologists, radiation oncologists, medical physicists and related scientists promoting excellence in patient care and health care delivery through education, research and technologic innovation. The Society is based in Oak Brook, Illinois. (RSNA.org)
For patient-friendly information on brain MRI, visit RadiologyInfo.org.

A data analytics firm that helps insurers collect big fees while leaving some patients with unpaid bills has been summoned to explain its business model.The chairmen of two Senate committees overseeing health policy, concerned about companies “padding their own profits” at the expense of patients, are looking into the practices of a data analytics firm that works with big insurers to cut payments to medical providers.The firm, MultiPlan, recommends what it says are fair payments for medical care, but the firm and the insurers can collect higher fees when payouts are lower. This business model could “result in an improper conflict of interest,” the chairmen of the two committees, Ron Wyden of Oregon and Bernie Sanders of Vermont, wrote in a letter to the firm’s chief executive that was released on Tuesday.The senators called on MultiPlan to meet with the committees’ staffs to discuss an investigation last month by The New York Times that found the firm’s pricing tools could leave patients with unexpectedly large bills when they see doctors outside their health plans’ networks.“Our committees are engaged in ongoing legislative work to put a stop to practices by plan service providers that drive up health care costs for consumers while padding their own profits,” the letter to Travis Dalton, the MultiPlan chief executive, said.In a statement, MultiPlan said it was working with the Senate committees “to address their questions and explain the cost and complexity patients can face” when choosing high-priced care outside their networks. “We are committed to helping make health care transparent, fair and affordable for all,” the statement said.The committees’ inquiry reflects growing scrutiny of the New York-based firm, which has largely remained out of the limelight even as it has staked out a dominant position in a lucrative corner of health care.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A baby’s exposure to air pollution while in the womb is associated with the development of certain mental health problems once the infant reaches adolescence, new research has found. The University of Bristol-led study, published in JAMA Network Open today [28 May], examined the long-term mental health impact of early-life exposure to air and noise pollution.
Growing evidence suggests air pollution, which comprises toxic gases and particulate matter, might contribute to the onset of mental health problems. It is thought that pollution could negatively affect mental health via numerous pathways, including by compromising the blood-brain barrier, promoting neuroinflammation and oxidative stress, and directly entering the brain and damaging tissue.
Despite youth being a key period for the onset of these problems, until now, relatively few studies have investigated the associations of air and noise exposure during early life with mental health.
In this new study, researchers sought to examine the long-term impact of air and noise pollution exposure during pregnancy, early childhood and adolescence on three common mental health problems: psychotic experiences (including hallucinations, such as hearing or seeing things that others cannot, and delusions, such as having very paranoid thoughts), depression and anxiety.
To investigate this, the team used data from over 9,000 participants from Bristol’s Children of the 90s birth cohort study (also known as the Avon Longitudinal Study of Parents and Children), which recruited over 14,000 pregnant women from the Bristol area between 1991 and 1992, and has followed the lives of the women, the children and their partners ever since.
By linking participants’ early childhood data with their mental health reports at the ages of 13, 18 and 24 years, researchers were able to use this to map against outdoor air and noise pollution in South West England at different time points.
Researchers found that relatively small increases in fine particulate matter during pregnancy and childhood were associated with more psychotic experiences and depression symptoms many years later in teenage years and early-adulthood. These associations persisted after considering many related risk factors, such as family psychiatric history, socioeconomic status, and other area-level factors such as population density, deprivation, greenspace and social fragmentation.

The team found that every 0.72 micrograms per cubic meter increase in fine particulate matter (PM2.5) during pregnancy and childhood was associated with an 11 per cent increased odds and 9 per cent increased odds for psychotic experiences, respectively; while exposure in pregnancy was associated with a 10 per cent increased odds for depression. In contrast, higher noise pollution exposure in childhood and teenage years was subsequently associated with more anxiety symptoms.
Dr Joanne Newbury, Sir Henry Wellcome Postdoctoral Research Fellow in the University’s Bristol Medical School: Population Health Sciences (PHS) and the study’s lead author, said: “Childhood, adolescence, and early adulthood are critical periods for the development of psychiatric disorders: worldwide, nearly two-thirds of those affected become unwell by the age of 25. Our findings add to a growing body of evidence — from different populations, locations, and using different study designs — suggesting a detrimental impact of air pollution (and potentially noise pollution) on mental health.
“This is a major concern, because air pollution is now such a common exposure, and rates of mental health problems are increasing globally. Given that pollution is also a preventable exposure, interventions to reduce exposure, such as low emissions zones, could potentially improve mental health. Targeted interventions for vulnerable groups including pregnant women and children could also provide an opportunity for more rapid reductions in exposure.
“It is important to emphasise that these findings, by themselves, do not prove a causal association. However, other recent studies have shown that low emissions zones appear to have a positive impact on mental health.”
The research, which involved researchers from King’s College London, University College London and Cardiff University, was funded by the University of Bristol, Wellcome, Economic and Social Research Council (ESRC), Medical Research Council (MRC), National Institute for Health and Care Research (NIHR), and the Natural Environment Research Council (NERC).

A University of Saskatchewan (USask) research team’s discovery of the additional health benefits of an appetite-suppressing protein has doubled the potential for scientists to find new avenues for treating obesity and metabolic disorders in animals and people.
The researchers’ findings, which were recently published in Nature Communications Biology, highlight their discovery of the lipid-lowering effects of nesfatin-1-like peptide (NLP). This newly identified peptide — or small protein — is a close relative of nesfatin-1 (NESF-1), which regulates feed intake and body weight.
“We found that both NESF-1 and NLP lower lipid (fat) accumulation in human liver cells,” said research team member Dr. Suraj Unniappan (PhD), the university’s Centennial Enhancement Chair in Comparative Endocrinology and a professor at the Western College of Veterinary Medicine (WCVM). The collaborative study involved researchers at the WCVM and USask College of Medicine.
While the lipid-lowering effect of nesfatin-1 was previously reported, Unniappan said identifying NLP and understanding its lipid-lowering capabilities in human cells represent new advancements in the field of endocrinology.
“We are far away from bringing these findings to bedside,” said Unniappan. “But we now have additional multiple targets available that could be explored for lipid disease treatment and therapeutic advancements.”
The research team’s discovery is hopeful news since there’s a lack of new therapies for many metabolic diseases — including non-alcoholic fatty liver disease (recently renamed as metabolic dysfunction-associated steatotic liver disease or MAFLD), which affects about 20 per cent of Canadians. A hormone-based drug was approved in the United States in March 2024, but so far, there are no drugs currently available in Canada exclusively for treating this disease.
Typical treatment plans for both humans and animals suffering from metabolic disease generally consist of diet and exercise changes to gradually lower body weight and reduce fat accumulation.

Unniappan and his research team have been at the forefront of nesfatin-1 research. Discovered in 2006 by a group of researchers in Japan, nesfatin-1 was initially recognized for its ability to suppress food intake.
The USask team went a step further than previous studies and successfully verified that genetic disruption of NLP leads to changes in genes involved in lipid metabolism in mice.
“We found that if you disrupt the gene that is the source of that protein [NLP] naturally present in these animals, then that actually leads to changes in lipid metabolism-associated genes,” said Unniappan.
Discovering such results — that administering NLP reduces lipid levels, while disrupting its production alters lipid metabolism — reinforces its pivotal role in metabolic regulation.
Unniappan and Dr. Atefeh Nasri (PhD), who completed her doctoral program at USask in 2023 and is now a post-doctoral fellow at Dalhousie University, collaborated with Dr. Scott Widenmaier (PhD), an assistant professor of anatomy, physiology and pharmacology, and an expert in metabolic disease at the USask College of Medicine. The team’s fourth member was undergraduate student Mateh Kowaluk.
Unniappan hopes that this new research can pave the way for further exploration of treatment options. He plans to work with collaborators to extend this research to more complex animal models — including rodents — and eventually studying larger animals such as cats and dogs. Like humans, these species also suffer from obesity and related metabolic disorders.
“It’s beautiful to know the same peptide can achieve so many meritorious health effects, that in combination have the potential to help both human and animal patients,” said Unniappan.
This research was supported by the Canadian Institutes of Health Research (CIHR) and the USask Centennial Enhancement Chair in Comparative Endocrinology.

Thousands of Australians struggle with serious mental health conditions. But when the recommended treatment involves antipsychotic medications, the side effects are excess kilos, which only adds weight to an already complex diagnosis.
Now, world first research from the University of South Australia shows that antipsychotics can be reformulated with a strategically engineered coating that not only mitigates unwanted weight gain but also boosts serotonin levels by more than 250%.
Funded by the Hospital Research Foundation (THRF) Group, researchers specifically tested Lurasidone, a drug used in the treatment of schizophrenia and bipolar depression, finding that the new coatings target the gut microbiome to improve drug absorption by 8-fold, while concurrently overcoming common side effects such as weight gain.
The coatings are created from tiny core-shell particles made from the dietary fibre, inulin, and bioactive medium chain triglycerides. The inulin shell boosts the gut microbiome by providing an energy source for gut bacteria, while the medium chain triglycerides facilitate drug absorption into the bloodstream.
It’s a breakthrough discovery that has the potential to change the lives of millions of people worldwide.
Lead researcher UniSA’s Dr Paul Joyce says microbiota-targeting microcapsules have the potential to improve treatment outcomes of mental health medications.
“Most patients suffering from schizophrenia or bipolar disorder are prescribed a range of antipsychotic medications, which trigger significant adverse effects by disrupting the gut microbiome — the microbial ecosystem that naturally colonises the gut,” Dr Joyce says.

“The most notable side effect is weight gain, with many patients often seeing increases of between 10-15% of their body weight after just three months of treatment.
“Because the gut microbiome plays a major role in regulating overall health, especially mood and cognition, the detrimental impact of these medications on the microbiome often makes them counterproductive.
“Instead of improving mood and cognition, the medication leads to a cascading cycle of poor mental and metabolic health as patients now struggle with excess weight and mental health issues.
“To make matters worse, most antipsychotics need to be consumed with food to maximise their effect. Yet for a very vulnerable patient population, ensuring this happens is challenging, with most patients gaining suboptimal drug levels.
“Clearly, new strategies are needed to eliminate side effects and the need for these medications to be taken with food — and that’s exactly what we’ve achieved with the drug Lurasidone.
“This research shows that when antipsychotic drugs are formulated with our new smart core-shell microparticles, drug absorption increases, mitigating the need for the medication to be consumed with food, while also boosting the diversity and abundance of the gut microbiome to overcome common side effects, such as weight gain.
“Importantly, because we are not developing new drugs, rather reformulating them, the new therapies can be fast-tracked for clinical use, so we could expect them within the next few years rather than the 10-15 years needed for new drug molecules to be approved by regulatory bodies.”
Next steps are to test the efficacy of these re-formulated therapies within human patients, with longer term goals being to extend these technologies across all mental health therapies, including anti-depressants, to mitigate any adverse effects.

In a study led by Jan Korbel at the European Molecular Biology Laboratory (EMBL) and Ashley Sanders at the Berlin Institute for Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB), researchers have found that approximately one in 40 human bone marrow cells carry massive chromosomal alterations — copy number variations and chromosomal rearrangements, for example — without causing any apparent disease or abnormality. In addition, cell samples from people over the age of 60 tended to have higher numbers of cells with such genomic alterations, suggesting a previously unidentified mechanism that may contribute to ageing-related diseases. The study was published in the journal Nature Genetics.
“The study highlights that we are all mosaics,” said Korbel, who is Senior Scientist in the Genome Biology Unit and Head of Data Science at EMBL Heidelberg. “Even so-called normal cells carry all sorts of genetic mutations. Ultimately, this means that there are more genetic differences between individual cells in our bodies than between different human beings.”
Both Korbel and Sanders, Group Leader at the Max Delbrück Center study how genetic structural variation — deletions, duplications, inversions, and translocations of large sections of the human genome — contributes to the development of disease. In the cancer field, it is well known that genetic mutations can cause cells to grow out of control and lead to the formation of a tumour, explained Sanders. “We are applying similar concepts to understand how non-cancerous diseases develop,” she added.
The discovery was enabled by a single-cell sequencing technology called Strand-seq, a unique DNA sequencing technique that can reveal subtle details of genomes in single cells that are too difficult to detect with other methods. Sanders is a pioneer in the development of this technology. As part of her doctoral research, she helped develop the Strand-seq protocol, which she later honed with colleagues while working as postdoctoral fellow in Korbel’s lab.
Strand-seq enables researchers to detect structural variants in individual cells with better precision and resolution than any other sequencing technology allows, Sanders said. The technology has ushered in an entirely new understanding of genetic mutations and is now being widely used to characterise genomes and to help translate findings into clinical research.
“We are just recognising that contrary to what we learned in textbooks, every cell in our body doesn’t have the exact same DNA,” she said.
Genetic mosaicism is common
The study represents the first time anyone has used Strand-seq technology to study mutations in the DNA of healthy people. The researchers included biological samples from a range of age groups — from newborn to 92-years-old — and found mutations in blood stem cells, which are located in the bone marrow, in 84% of the study participants, indicating that large genetic mutations are very common.

“It’s just amazing how much heterogeneity there is in our genomes that has gone undetected so far,” said Sanders. “What this means in terms of how we define normal human ageing and how this can impact the types of diseases we get is really an important question for the field.”
The study also found that in people over the age of 60, bone marrow cells carrying genetic alterations tended to be more abundant, with populations of specific genetic variants, or sub-clones, more common than others. The frequent presence of these sub-clones suggests a possible connection to ageing.
But whether the mechanisms that keep sub-clones from proliferating in check break down as we age, or whether the expansion of sub-clones itself contributes to diseases of ageing is not known, said Korbel. “In the future, our single cell studies should give us clearer insights into how these mutations that previously went unnoticed affect our health and potentially contribute to how we age.”

Greater use of pharmacists to treat minor illnesses could potentially save millions of dollars in health care costs, according to new research led by Washington State University. The findings also indicate a way to improve healthcare access by expanding availability of pharmacists’ clinical services including prescribing medications, amid an ongoing shortage of primary care providers.
The study found that care for a range of minor health issues — including urinary tract infections, shingles, animal bites and headaches — costs an average of about $278 less when treated in pharmacies compared to patients with similar conditions treated at “traditional sites” of primary care, urgent care or emergency room settings. Follow-ups with pharmacy patients showed that almost all their illnesses had resolved after the initial visit with a pharmacist.
Notably, if all of the illnesses in the three-year study that were treated at a traditional site of care had been treated by community pharmacists, it would have saved an estimated $23 million in health care expenses.
“The findings show that pharmacists, especially in the outpatient community setting, are a viable solution to part of our patient access to care problem in our state and country,” said lead author Julie Akers, a WSU pharmacy researcher. “Pharmacists are trained and qualified to do this work, and unfortunately in many settings, highly underutilized. And they could have a huge impact on how fast patients access care, which can minimize the complexity and the progression of their condition.”
For this study, published in the journal ClinicoEconomics and Outcomes Research, Akers’ research team analyzed data of nearly 500 patients who received care from 175 pharmacists at 46 pharmacies across the state of Washington from 2016 to 2019. The team also followed up with the patients 30 days after their pharmacy visits to assess treatment effectiveness. They then compared these cases with insurance data of patients from the same time period with conditions of the same type and level who had sought care at a doctor’s office, urgent care facility or emergency room.
The researchers found that for almost every minor illness in the study, pharmacy care was not only effective but cost much less, sometimes dramatically so. For instance, the study found that for an uncomplicated case of urinary tract infection, normally treated with antibiotics, a first visit to an emergency room cost on average $963, a primary care physician’s office, $121 — at the pharmacy, the average was $30.
The study was conducted by a team of pharmacy researchers in coordination with an advisory board of physicians. The findings highlight the advantages of expanding the physician-pharmacist collaboration that allows some pharmacists to directly prescribe medications.

Washington state was the first in the nation to enact the “prescribing authority” in 1979 which enables a licensed prescriber such as a physician to delegate a pharmacist to prescribe and administer certain drugs.
As part of their education, pharmacists are trained in clinical evaluation of common illnesses, and as Akers pointed out, they already regularly make recommendations for conditions that can be treated with over-the-counter medications. The prescribing authority allows them to take their current practice to the next level if over-the-counter medicines are not enough.
Pharmacists also often refer patients to different providers for conditions that are complex, need further testing or cannot be resolved through medication alone. For less serious conditions, this study shows that pharmacists with prescribing authority can help fill a gap in care, especially in rural areas or at times of the day when there are few options available, Akers said.
“We’ve seen over time, more and more patients struggle to get access to care,” she said. “Over the past couple of decades, we’ve seen inappropriate use of urgent cares and emergency departments for things that really didn’t need go to that level of service.”
There is more work to do to be able to expand this treatment at pharmacies, Akers added. This includes creating greater public awareness, so people expect this type of service at pharmacies as they now do with vaccinations. Pharmacies also need to address the financial sustainability of providing these expanded patient care services, and Akers hopes the team’s next project will involve helping pharmacies transition to medical billing, which could greatly increase access to care for patients without the ability to pay out of pocket for care.
The current study was supported by a grant from the National Association of Chain Drug Stores Foundation. Additional co-authors include Jennifer Miller, Linda MacLean, Bidisha Mandal and Clark Hogan of WSU as well as Brandy Seignemartin of Idaho State University.

An international research group led by researchers from the University of Turku and Turku University Hospital in Finland has succeeded in identifying the probable origin of stuttering in the brain.
Stuttering is a speech rhythm disorder characterised by involuntary repetitions, prolongations or pauses in speech that prevent typical speech production. Approximately 5-10% of young children stutter, and an estimated 1% continue to stutter into adulthood. A severe stutter can have a profound negative impact on the life of the individual affected.
“Stuttering was once considered a psychological disorder. However, with further research, it is now understood to be a brain disorder related to the regulation of speech production,” says Professor of Neurology Juho Joutsa from the University of Turku.
Stuttering may also be acquired as a result of certain neurological diseases, such as Parkinson’s disease or a stroke. However, the neurobiological mechanisms of stuttering are not yet fully understood, and where it originates in the brain remains uncertain. The findings from brain imaging studies are partly contradictory, and it is challenging to determine which changes are the root cause of stuttering and which are merely associated phenomena.
Stuttering localised in the same brain network regardless of its cause
Researchers from Finland, New Zealand, the United States and Canada developed a new research design that could provide a solution to this problem. The study included individuals who had suffered a stroke, some of whom developed a stutter immediately after it. The researchers discovered that although the strokes were located in different parts of the brain, they all localised to the same brain network, unlike the strokes that did not cause stuttering.
In addition to people who had suffered a stroke, the researchers used magnetic resonance imaging (MRI) to scan the brains of 20 individuals with developmental stuttering. In these individuals, the stuttering was associated with structural changes in the nodes of the brain network originally identified in relation to causal stroke lesions — the greater the changes, the more severe the stuttering. This finding suggests that stuttering is caused by a common brain network, regardless of the aetiology (developmental or neurological).
The key nodes of the network identified by the researchers were putamen, amygdala and claustrum located deep within the brain, and the connections between them.
“These findings explain well-known features of stuttering, such as the motor difficulties in speech production and the significant variability in stuttering severity across emotional states. As major nuclei in the brain, the putamen regulates motor function and the amygdala regulates emotions. The claustrum, in turn, acts as a node for several brain networks and relays information between them,” explains Joutsa.
The results of the study provide a unique insight into the neurobiological basis of stuttering. Locating stuttering in the brain opens up new possibilities for medical treatment. Researchers hope that in the future, stuttering could be effectively treated, for example, with brain stimulation that can be targeted specifically to the now identified brain network.

Binge-eating disorder is the most prevalent eating disorder in the United States, but previous studies have presented conflicting views of the disorder’s duration and the likelihood of relapse. A new five-year study led by investigators from McLean Hospital, a member of the Mass General Brigham healthcare system, showed that 61 percent and 45 percent of individuals still experienced binge-eating disorder 2.5 and 5 years after their initial diagnoses, respectively. These results contradict previous prospective studies that documented faster remission times, according to the authors.
“The big takeaway is that binge-eating disorder does improve with time, but for many people it lasts years,” said first author Kristin Javaras, DPhil, PhD, assistant psychologist in the Division of Women’s Mental Health at McLean. “As a clinician, oftentimes the clients I work with report many, many years of binge-eating disorder, which felt very discordant with studies that suggested that it was a transient disorder. It’s very important to understand how long binge-eating disorder lasts and how likely people are to relapse so that we can better provide better care.”
The results were published May 28 in Psychological Medicine, [JR1] published by Cambridge University Press.
Binge-eating disorder, which is estimated to impact somewhere between 1 percent and 3 percent of U.S. adults, is characterized by episodes during which people feel a loss of control over their eating. The average age of onset is 25 years.
While previous retrospective studies, which rely on people’s sometimes-faulty memories, have reported that binge-eating disorder lasts seven to sixteen years on average, prospective studies tracking individuals with the disorder over time have suggested that many individuals with the disorder enter remission within a much smaller timeframe — from one to two years.
However, the researchers noted that most previous prospective studies had limitations, including a small sample size (