Category: 8. Health

Cardiac MRI shows the effects of air pollution on the heart — and the findings aren’t good, according to a study published July 1 in Radiology.

The research adds to growing evidence that air pollution is a cardiovascular risk factor, contributing to residual risk not accounted for by typical clinical predictors such as smoking or hypertension, the RSNA noted in a statement.

“Even modest increases in air pollution levels appear to have measurable effects on the heart,” said senior author Kate Hanneman, MD, of the University of Toronto in Canada. “Our study suggests that air quality may play a significant role in changes to heart structure, potentially setting the stage for future cardiovascular disease.”

Heart disease is the main cause of death around the world, the investigators noted. Although prior work has indicated that poor air quality contributes to cardiovascular disease, changes in the heart resulting from exposure to air pollution have remained unclear, they explained, observing that fine particulate matter in the air may contribute to diffuse myocardial fibrosis, a form of scarring in the heart muscle that can precede heart failure. (“Fine particulate matter” can include vehicle exhaust, industrial emissions and wildfire smoke, and particles are small enough to enter the bloodstream through the lungs.)

With Hanneman, a team led by Jacques Du Plessis, MD, also of the University of Toronto, explored the relationship between long-term exposure to fine particulate matter with 2.5-µm or smaller aerodynamic diameter (PM2.5) and the extent of diffuse myocardial fibrosis quantified with cardiac MRI native T1 mapping z scores (used to assess myocardial tissue characteristics; score expressed as zero, positive, and negative, with positive scores indicating potential abnormality).

The study included a total of 694 patients who underwent cardiac MRI between January 2018 and December 2022. Of these, 493 had dilated cardiomyopathy and 201 had normal findings. Du Plessis’ team quantified diffuse myocardial fibrosis and assessed patients’ residence-specific ambient PM2.5 concentration (the mean of daily exposure concentration in the year before cardiac MR imaging using measurements from the nearest air quality monitoring station).

The group reported the following:

• In multivariable models, each 1-µg/m3 increase in one-year mean PM2.5 exposure was associated with a 0.3 higher native T1 z score in patients with dilated cardiomyopathy (p < 0.001) and 0.27 higher native T1 z score in controls (p = 0.02).
   
• For absolute values, each 1-µg/m3 increase in one-year mean PM2.5 exposure was associated with 9.1 msec higher native T1 at 1.5-tesla imaging (p = 0.01) and 12.1 msec higher native T1 at 3-tesla imaging (p < 0.001). (An elevated native T1 typically indicates abnormal changes in the myocardial tissue composition.)
   
• The largest effect sizes for the association of PM2.5 exposure with native T1 z scores were in women (p < 0.001), smokers (p = 0.04), and patients with hypertension (p = 0.004).

Images from cardiac MRI native T1 mapping show that higher long-term exposure to fine particulate air pollution is associated with higher extent of myocardial fibrosis. Images and caption courtesy of the RSNA.

Overall, higher long-term exposure to fine particulate air pollution was connected to higher levels of myocardial fibrosis in both the patients with cardiomyopathy and the controls, suggesting that “myocardial fibrosis may be an underlying mechanism by which air pollution leads to cardiovascular complications,” the authors wrote.  

How can clinicians gauge a patient’s cardiac health in relation to poor air quality? Neighborhood data can help, according to Hanneman.

“A simple way to estimate someone’s exposure to air pollution is by looking at air quality data for the neighborhood they live in — information that is publicly available in many areas,” she told AuntMinnie. “Some health providers may ask about environmental exposures during routine visits. For people who want a more detailed assessment, portable air monitors are available that provide real-time air quality data.”

In any case, the effects of air pollution on lung health can be mitigated both on individual and societal levels, Hanneman noted.

“On a personal level, people can take steps like limiting outdoor activity on days when air quality is poor and using indoor air purifiers to reduce exposure,” she said. “On a broader scale, public health efforts include improving air quality standards, reducing emissions from traffic and industry, and addressing sources such as wildfire smoke to improve air quality for everyone.”

In an accompanying commentary, Davis Vigneault, MD, DPhil, of Stanford University emphasized the role radiology can play in tackling the problem of air pollution exposure and heart disease risk.

“The study … suggests several interesting avenues for future research, including the investigation of particulate pollution components, related co-pollutants, and at-risk subgroups,” he noted. “Moreover, [the] work sets an important example of how imaging research may be used beyond the diagnosis of an individual patient to guide public policy interventions to improve health outcomes more broadly.”

The complete study can be found here.

A new study examines the economic impact of Salmonella Dublin across Danish dairy farms over a 10-year period.

The infectious and multi-resistant cattle disease Salmonella Dublin can be fatal to both humans and animals and causes significant losses for farmers. Although Denmark has attempted to eradicate the disease since 2008, it has not yet succeeded.

The new study points to possible reasons—and the necessary solutions.

While we’ve all heard of salmonella in chickens, salmonella in cows is likely unknown to many. Nevertheless, Salmonella Dublin is a disease that has been present in cattle herds for decades—in Denmark as well as many other countries. And it is on the rise globally.

It causes pneumonia and blood poisoning and kills many thousands of calves and cows every year.

Although Salmonella Dublin infects humans far less frequently than the more regular salmonella, there is every reason to take it seriously: it is significantly more dangerous and kills up to 12% of those who become infected. At the same time, it is often resistant to antibiotics. Infection can occur through contact with animals as well as through unpasteurized dairy products and undercooked meat.

Still, Denmark has not managed to eradicate the disease—despite a national eradication plan launched in 2008, which set out to completely eliminate the disease. Today, the infection rate is estimated to be around 5% of Danish cattle herds, down from 20-25% in 2008.

In contrast, the infection has increased in recent years to about 18% of herds in the United States and as much as 60% in the United Kingdom.

“Salmonella Dublin is not just a serious threat in the barn. Globally, it is a potential public health risk that is likely to grow as antibiotic resistance spreads. This is a bacterium that kills people every year, and it is high time we do more to combat it,” says Dagim Belay, assistant professor at the food and resource economics department at the University of Copenhagen.

“Denmark has made great progress in the fight against this disease—so why have we not yet reached the goal? One possible reason is that farmers may not have a strong enough incentive to fight it. However, our research shows that the consequences are not only a matter of health—there are also hidden financial losses associated with infection,” says Jakob Vesterlund Olsen from the food and resource economics department.

The study shows that Salmonella Dublin leads to increased calf mortality, lower milk yield, higher medication costs, and more veterinary treatments.

“The tricky thing about Salmonella Dublin is that it often flies under the radar. Many herds are infected without visible symptoms, meaning both the disease and the economic losses can develop gradually without being noticed. Infection reduces productivity and weakens the animals year after year—and the financial losses accumulate over time,” says Belay.

Cattle farms with high levels of infection face average additional annual costs of around EUR 11,300 (about $13,307 USD. But even herds with low levels of infection face financial losses. A typical herd of 200 dairy cows with low-level infection incurs extra variable costs of approximately EUR 6,700 (about $7,891 USD) per year.

“Our estimates are conservative. They are based on data from a Danish system that already has a control program—unlike most other countries. If similar estimates were made in the UK or the US, the economic costs would be significantly higher,” says Belay.

The researchers highlight a key problem in how Danish authorities currently monitor Salmonella Dublin. The Danish Veterinary and Food Administration measures the level of antibodies against the bacterium in the farm’s milk tank, and if the antibody level is below a certain threshold, the herd is deemed salmonella-free.

“Threshold-based regulation has been instrumental in helping Denmark substantially reduce the prevalence of Salmonella Dublin to its current low level. But the current threshold is rather arbitrarily set. And our data shows that production losses already occur at infection levels well below that threshold,” says Olsen.

“So, it is also crucial to give farmers stronger incentives to eradicate the problem. For example, by offering subsidies to farmers who invest in prevention, early detection, and control measures, or by introducing a discounted milk price for milk from chronically infected herds,” says Belay.

Finally, the researchers urge authorities to provide targeted information to cattle producers about the hidden costs of Salmonella Dublin and about effective control strategies.

The study appears in the journal Agricultural Economics.

Source: University of Copenhagen

Researchers using cardiac MRI have found that long-term exposure to air pollution is associated with early signs of heart damage, according to a study that was published today in Radiology, a journal of the Radiological Society of North America (RSNA). The research indicates that fine particulate matter in the air may contribute to diffuse myocardial fibrosis, a form of scarring in the heart muscle that can precede heart failure.

Cardiovascular disease is the leading cause of death worldwide. There is a large body of evidence linking poor air quality with cardiovascular disease. However, the underlying changes in the heart resulting from air pollution exposure are unclear.

We know that if you’re exposed to air pollution, you’re at higher risk of cardiac disease, including higher risk of having a heart attack. We wanted to understand what drives this increased risk at the tissue level.”

Kate Hanneman, M.D., M.P.H., study’s senior author, Department of Medical Imaging at the Temerty Faculty of Medicine, University of Toronto and University Health Network in Toronto

Dr. Hanneman and colleagues used cardiac MRI, a noninvasive imaging technique, to quantify myocardial fibrosis and assess its association with long-term exposure to particles known as PM_2.5. At 2.5 micrometers in diameter or less, PM_2.5 particles are small enough to enter the bloodstream through the lungs. Common sources include vehicle exhaust, industrial emissions and wildfire smoke.

The researchers wanted to evaluate the effects of air pollution on both healthy people and those with heart disease, so the study group included 201 healthy controls and 493 patients with dilated cardiomyopathy, a disease that makes it more difficult for the heart to pump blood.

Higher long-term exposure to fine particulate air pollution was linked with higher levels of myocardial fibrosis in both the patients with cardiomyopathy and the controls, suggesting that myocardial fibrosis may be an underlying mechanism by which air pollution leads to cardiovascular complications. The largest effects were seen in women, smokers and patients with hypertension.

The study adds to growing evidence that air pollution is a cardiovascular risk factor, contributing to residual risk not accounted for by conventional clinical predictors such as smoking or hypertension.

“Even modest increases in air pollution levels appear to have measurable effects on the heart,” Dr. Hanneman said. “Our study suggests that air quality may play a significant role in changes to heart structure, potentially setting the stage for future cardiovascular disease.”

Knowing a patient’s long-term air pollution exposure history could help refine heart disease risk assessment and address the health inequities that air pollution contributes to both in level of exposure and effect. For instance, Dr. Hanneman said, if an individual works outside in an area with poor air quality, healthcare providers could incorporate that exposure history into heart disease risk assessment.

The air pollution exposure levels of the patients in the study were below many of the global air quality guidelines, reinforcing that there are no safe exposure limits.

“Public health measures are needed to further reduce long-term air pollution exposure,” Dr. Hanneman said. “There have been improvements in air quality over the past decade, both in Canada and the United States, but we still have a long way to go.”

In addition to illuminating the links between air pollution and myocardial fibrosis, the study highlights the important role that radiologists will play in research and clinical developments going forward.

“Medical imaging can be used as a tool to understand environmental effects on a patient’s health,” Dr. Hanneman said. “As radiologists, we have a tremendous opportunity to use imaging to identify and quantify some of the health effects of environmental exposures in various organ systems.”

GABA, or gamma-aminobutyric acid, is an amino acid functioning as the principal inhibitory neurotransmitter that can act on the brain to slow or stop the reception of certain signals to the brain, leading to a calmer and more relaxed state. Low GABA levels in the brain have been associated with neurological disorders and diseases like depression, Alzheimer’s or epilepsy. Recently, there has been a push towards understanding more about the gut’s influence on mood, behavior and mental health, as well as what foods might fuel or hinder a healthy mind. Researchers set to work on determining whether brain GABA levels can be increased through dietary additions with the aim of modulating the gut bacteria present in an individual to bypass the blood-brain barrier, a barrier in which it is not proven yet GABA can pass through.

Results were published in npj Science of Food in April 2025.

The relationship between the gut and brain is not necessarily a newly established one, but one that is gaining more attention and influence in how science looks at treating the body more holistically. The two systems communicate effectively, but researchers wanted to know the answer of just how directly these two systems can pass information: can an increase in gut-derived GABA directly cause an increase in the levels of brain GABA?

Researchers confirmed a direct association between gut GABA, brain GABA and the gut microbiota through trials on mice. There are still no solid results on whether or not gut microbiota-derived GABA can cross the blood-brain barrier and directly increase brain GABA. However, further studies do indicate a potential for other pathways to cause an increase in brain GABA elevation, such as stimulation through the Vagus nerve or hormonal pathways.

Our study suggests that prebiotics have the ability to prevent or treat those brain diseases by increasing brain GABA levels via promoting gut GABA production through modulating gut microbiota.”

Thunatchaporn Kumrungsee, study corresponding author, associate professor at Hiroshima University’s Graduate School of Integrated Sciences for Life

In trials done on mice, researchers found the fructo-oligosaccarides (FOS), non-digestible oligosaccharides, and Aspergillus-derived enzymes, lipase and protease, as prebiotics that have shown effective in elevation brain GABA through the influence on the gut. FOS appeared to have a significant increase on the mice’s brain GABA in both the cortex and hippocampus, both sites where GABA acts to reduce excitability and induce a sense of calmness. Additionally, FOS and enzyme supplementation also raised homocarnosine levels in the hippocampus.

“Food factors such as prebiotics and fungi-derived enzymes with prebiotic-liked effects have an ability to increase brain GABA and homocarnosine, a GABA-containing brain-specific peptide, which can possibly in turn enhance brain health through gut microbiota modulation,” said Kumrungsee.

Homocarnosine appears to also be linked to some of the same brain diseases, with a previous study by Kumrungsee indicating homocarnosine-deficient mice were more prone to exhibiting depression-like behaviors and instances of hyperactivity.

Despite a lack of confirmed data on an increase in GABA in the brain derived directly from gut microbiota, there is good reason to believe prebiotic consumption might increase the brain’s GABA levels, as shown in the study. Researchers still need to unravel the mechanism by which the gut might influence the brain and what pathway might be responsible. Once clarified, the next goal is to figure out if the prebiotic treatment used in the study can be further employed for the treatment of GABA-related diseases, like epilepsy or depression.

Jason D. Braga, Norihisa Kato, Noriyuki Yanaka and Thanutchaporn Kumrungsee of the Program of Food and AgriLife Science at Hiroshima University with Jason D. Braga also of the Institute of Food Science and Technology at Cavite State University, Yongshou Yang of the School of Life Sciences at Anhui University, Kyoichi Nishio, Masasumi Okada, Manabu Kuroda and Shotaro Yamaguchi of Amano Enzyme Inc. and Thunatchaporn Kumrungsee of Smart Agriculture at Hiroshima University contributed to this research.

This research was made possible by the Japanese Society of Functional Fermented Foods and Enzyme Supplements, the Danone Institute of Japan Foundation research grant, the Japanese Ministry of Education, Culture, Sports, Science and Technology, and Amano Enzyme Inc.

A new study has identified early-pregnancy gut microbiota signatures associated with the development of gestational diabetes mellitus, a metabolic disorder that carries substantial risks to both maternal and fetal health. The study, published in the American Society for Microbiology journal Microbiology Spectrum, provides new avenues for gestational diabetes prevention and management.

Gestational diabetes is a prevalent metabolic disorder characterized by abnormal glucose metabolism, primarily in the mid to late stages of pregnancy. Early intervention for gestational diabetes can substantially reduce complications for both mother and baby. Gestational diabetes significantly increases the risk of maternal complications such as gestational hypertension, polyhydramnios, and cesarean delivery, while also posing long-term health risks for the fetus, including asphyxia at birth and increased susceptibility to obesity and diabetes in adulthood.

In the new study, researchers from The Second Hospital, Southern Medical University, and the Third Affiliated Hospital of Guangzhou Medical University, all in Guangzhou, China, set out to identify gut microbiota dysbiosis that is strongly linked to the onset and progression of gestational diabetes that may serve as a critical early-warning biomarker. The scientists analyzed the fecal microbiota of 61 pregnant women during their first trimester of pregnancy using 16S rRNA sequencing. They then correlated these microbial profiles with oral glucose tolerance test results at 24-28 weeks of gestation and clinical delivery outcomes.

The researchers discovered that there were significant differences in gut microbiota composition between those with gestational diabetes and women who had healthy pregnancies. Based on their findings, the researchers developed an early diagnostic model for gestational diabetes, based on genus-level markers, with high diagnostic precision.

“These findings suggest that microbiota-based tools could enable early, non-invasive detection of gestational diabetes mellitus, offering new opportunities for prevention and personalized management,” write the study authors. “This research highlights the role of the gut microbiome in pregnancy and has important implications for improving maternal and fetal health outcomes.”

While glucose, or sugar, is a well-known fuel for the brain, Weill Cornell Medicine researchers have demonstrated that electrical activity in synapses—the junctions between neurons where communication occurs—can lead to the use of lipid or fat droplets as an energy source.

The study, published July 1 in Nature Metabolism, challenges “the long-standing dogma that the brain doesn’t burn fat,” said principal investigator Dr. Timothy A. Ryan, professor of biochemistry and of biochemistry in anesthesiology, and the Tri-Institutional Professor in the Department of Biochemistry at Weill Cornell Medicine. 

The paper’s lead author, Dr. Mukesh Kumar, a postdoctoral associate in biochemistry at Weill Cornell Medicine who has been studying the cell biology of fat droplets, suggested that it makes sense that fat may play a role as an energy source in the brain like it does with other metabolically demanding tissues, such as muscle.

The research team was particularly intrigued by the DDHD2 gene, which encodes a lipase, or enzyme that helps break down fat. Mutations in DDHD2 are linked to a type of hereditary spastic paraplegia, a neurological condition that causes progressive stiffness and weakness in the legs, in addition to cognitive deficits.

Prior research by other investigators has demonstrated that blocking this enzyme in mice causes a build-up of triglycerides—or fat droplets that store energy—throughout the brain.  “To me, this was evidence that maybe the reason we claim the brain doesn’t burn fat is because we never see the fat stores,” Dr. Ryan said. 

Research demonstrates lipids have an important role

The current study explored whether the lipid droplets that build up in the absence of DDHD2 are used as fuel by the brain, particularly when glucose isn’t present, Dr. Ryan said.

Dr. Kumar found that when a synapse contains a lipid droplet filled with triglycerides in mice without DDHD2, neurons can break down this fat into fatty acids and send it to the mitochondria—the cell’s energy factories—so they can produce adenosine triphosphate (ATP), the energy the cell needs to function.

The process of being able to use the fat is controlled by the electrical activity of the neurons, and I was shocked by this finding. If the neuron is busy, it drives this consumption. If it’s at rest, the process isn’t happening.”  

Dr. Timothy A. Ryan, professor of biochemistry and of biochemistry in anesthesiology

In another study, researchers injected a small molecule into mice to block the enzyme carnitine palmitoyltransferase 1 (CPT1), which helps transport fatty acids into the mitochondria for energy production. Blocking CPT1 prevented the brain from using fat droplets, which then led to torpor, a hibernation-like state, in which the body temperature rapidly plummets and the heartbeat slows. “This response convinced us that that there’s an ongoing need for the brain to use these lipid droplets,” Dr. Ryan said.

Implications for future research

This research may encourage the further investigation of neurodegenerative conditions and the role of lipids in the brain. Glucose fluctuations or low levels of glucose can occur with aging or neurological disease, but fatty acids broken down from lipid droplets may help to maintain the brain’s energy, Dr. Kumar said. “We don’t know where this research will go in terms of neurodegenerative conditions, but some evidence suggests that accumulation of fat droplets in the neurons may occur in Parkinson’s disease,” he said.

Researchers also need to better understand the interplay between glucose and lipids in the brain, Dr. Ryan said. “By learning more about these molecular details, we hope to ultimately unlock explanations for neurodegeneration, which would give us opportunities for finding ways to protect the brain.”

This research was supported in part by the National Institute of Neurological Disorders and Stroke and the National Cancer Institute, both part of the National Institutes of Health, through grant numbers NS036942, NS11739 and F31CA278383. Additional support was provided by Aligning Science Across Parkinson’s through grant number ASAP-000580.

Schoolchildren born late in the year are at greater risk of developing mental health problems compared with their older peers, according to a new study.

A recent study by the Norwegian University of Science and Technology (NTNU) has found that children born in October, November or December are statistically more often identified as having a mental health diagnosis than their classmates born earlier in the year. The findings apply to both boys and girls, and regardless of whether they were born full term or prematurely.

Extensive research material

The researchers have followed over one million Norwegians aged 4 to 17 years (all born between 1991 and 2012) through Norwegian health registries.

The aim of the study was to identify what are known as ‘relative age effects’. In other words, whether children and adolescents born late in the year are more frequently diagnosed with mental health disorders than their peers born early in the year (January, February and March).

Our findings show that the youngest members of a school class tend to be diagnosed with a mental illness more frequently than the oldest.

This is most obvious with regard to ADHD, where we saw an increase in incidence of 20-80 per cent for the youngest class members, depending on whether the children were born full term or prematurely.”

Christine Strand Bachmann, a PhD research fellow at the Norwegian University of Science and Technology (NTNU’s) Department of Public Health and Nursing

The researchers found the same trend for ‘other neuropsychiatric disorders’. These include delayed developments in areas such as language, academic skills and motor skills.

The study has been published in BMJ Peadiatrics Open.

Additional risks for premature girls

In addition, the youngest premature girls were at a significantly greater risk of being diagnosed with emotional disorders, such as anxiety, depression and adaptation disorders, compared with the oldest premature girls in the same year group.

“We know that children and adolescents born prematurely are already more vulnerable to poor mental and social health compared with children and young people born full term. For those born prematurely, the risks associated with being born late in the year comes in addition to this vulnerability.

“We believe that these findings, which show an increase in the number of psychological diagnoses for the youngest class members, can partly be linked to the way in which we organize our education system. The school system is unable to adequately provide for children with normal, but more immature behaviour. Possible solutions include flexible school start dates or additional support.”

In addition to being a researcher at NTNU, Christine Strand Bachmann is also a consultant at the Neonatal Intensive Care Unit, Children and Adolescent Medicine Department, St. Olavs Hospital.

In a large community-based study, researchers at Fatty Acid Research Institute observed weak but statistically significant inverse associations between several types of inflammatory biomarkers with omega-6 fatty acids.

“Chronic inflammation is recognized as an important risk factor for a variety of health disorders,” said Fatty Acid Research Institute’s president William Harris and his colleagues.

“Omega-6 fatty acids, particularly linoleic (LA) and arachidonic acid (AA), have been shown to be either pro- or anti-inflammatory, and researchers have advocated both for and against reducing their dietary intake.”

The authors relied on data from the Framingham Offspring Study, a well-known research cohort from the Boston area.

The Framingham Offspring Study is a landmark longitudinal research initiative that follows the children of participants in the original Framingham Heart Study to investigate genetic and lifestyle factors influencing cardiovascular and metabolic health.

Launched in 1971, it has provided decades of valuable insights into chronic disease risk and prevention.

The cohort’s rigor and continuity make it one of the most trusted sources for understanding long-term health trajectories.

This was a cross-sectional study, meaning that the LA and AA levels were measured in the same blood samples as the 10 inflammation-related biomarkers in 2,700 individuals.

The relationships between the levels of these two omega-6 fatty acids and 10 separate blood/urine biomarkers of inflammation and oxidative stress were statistically evaluated.

After adjusting (controlling statistically) for multiple other potentially confounding factors (age, race, sex, smoking, blood lipid levels, blood pressure, body weight, etc.), the researchers found that higher LA levels were associated with statistically significantly lower levels of five of the 10 biomarkers, and in no case was higher LA related to higher levels of any biomarker.

For AA, higher levels were linked with lower concentrations of four markers, and, like LA, there were no statistically significant associations with higher levels of inflammation/oxidation.

“These new data show clearly that people who have the highest levels of LA (and AA) in their blood are in a less inflammatory state than people with lower levels,” Dr. Harris said.

“This finding is exactly the opposite of what one would expect if omega-6 fatty acids were ‘proinflammatory’ — in fact, they appear to be anti-inflammatory.”

“In the flurry of news stories about the harms of seed oils — the primary sources of LA in the diet — many voices are calling for reducing Americans’ intakes of LA.”

“This is not a science-based recommendation, and this study — in addition to many more — point in precisely the opposite direction: instead of lowering LA intakes, raising intakes appears to be a healthier recommendation.”

“These findings contradict a narrative, not previous research findings.”

“There are many studies in the medical literature that are consistent with our findings here.”

The study was published June 22 in the journal Nutrients.

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Heidi T.M. Lai et al. 2025. Red Blood Cell Omega-6 Fatty Acids and Biomarkers of Inflammation in the Framingham Offspring Study. Nutrients 17 (13): 2076; doi: 10.3390/nu17132076