Category: 8. Health

Cardiovascular disease (CVD) remains the leading cause of death and disability for adults in the U.S. Recent projections from the American Heart Association suggest that by 2050, more than 45 million American adults will have clinical CVD and more than 184 million will have hypertension. As a result, inflation-adjusted direct health care costs related to CVD risk factors are projected to triple between 2020 and 2050, to $1.34 trillion annually, and direct costs related to clinical CVD conditions are projected to rise from $393 billion to $1.49 trillion. Thus, understanding early-life determinants of cardiovascular health behaviors and health factors are of particular interest.

In the first prospective study of social determinants from birth, and how they impact young adult cardiovascular health, researchers from Boston University Chobanian & Avedisian School of Medicine and colleagues are investigating the upstream causes of cardiovascular disease – the factors that drive poor diet, a sedentary lifestyle, nicotine exposure, poor sleep, obesity, and adverse blood cholesterol, blood pressure and blood glucose levels. Known as the Future of Families Cardiovascular Health Among Young Adults (FF-CHAYA) Study, a new paper describes the rationale, study design, methods and characteristics of the FF-CHAYA cohort, a novel longitudinal study designed to examine associations of childhood social determinants with young adult cardiovascular health and early arterial injury.

In recent years, social determinants of health (SDoH) have received significant attention as upstream societal and structural factors that drive the propensity for beneficial or adverse health outcomes. While data on SDoH among middle-aged adults is increasingly available, as are longitudinal associations with downstream health outcomes, investigations examining the full array of SDoH in children and prospective associations with health outcomes is rare.”

Donald Lloyd-Jones, MD, ScM, corresponding author, professor of medicine at Boston University Chobanian & Avedisian School of Medicine and director of the Framingham Heart Study

Using the largest and longest running study of a representative group of children born between 1998-2000, the researchers examined more than 2,000 young adults (average age 23 years) from 22 cities across the U.S. who had been followed since birth. Families provided information on socioeconomic status, neighborhood conditions, environmental exposures, schools, behavior and other psychosocial factors up to seven times during early life. As young adults, all participants answered detailed questions about health status and health behaviors, and three-quarters of them had in-person examinations with checks on height, weight, body shape, blood pressure and blood drawn for clinical measures. Those same young adults also underwent sophisticated ultrasound imaging of the carotid arteries in the neck to look for signs of early arterial injury. The researchers are now linking their detailed sociological data with state-of-the-art, quantitative measures of cardiovascular health in young adulthood.

According to the researchers, detailing childhood social determinants helps target those factors that drive poor cardiovascular health across the life course. “Ultimately we hope it will guide pediatricians, family practitioners and even public health policy makers to those things that will launch children into better lifelong health trajectories,” adds Lloyd-Jones.

These findings appear online in the Journal of the American Heart Association.

Funding for this study was provided by grant R01 HL149869 from the National Heart, Lung, and Blood Institute and supported by institutional funding from Princeton University and Northwestern University Feinberg School of Medicine.

There was no benefit to modulating the intensity of antiplatelet therapy compared with standard antiplatelet therapy in high-risk patients who had undergone complex stenting procedures, according to late-breaking research presented in a Hot Line session today at ESC Congress 2025.

Dual antiplatelet therapy (DAPT) consisting of aspirin plus a P2Y12 receptor inhibitor, such as clopidogrel, is generally given to patients after coronary stenting (percutaneous coronary intervention [PCI]) to prevent ischemic events, such as heart attacks (myocardial infarction). Principal Investigator, Professor Duk-Woo Park from Asan Medical Center, Seoul, South Korea, explained why the TAILORED-CHIP trial was carried out: “The optimal antiplatelet therapy is not well established for patients who have undergone complex PCI procedures and are at high risk of ischaemic events. We hypothesized that modulating the intensity of antiplatelet therapy over time, i.e. stronger inhibition in the early phase to reduce ischaemic events and weaker inhibition in the later phase to mitigate bleeding, may be beneficial in this high-risk population. The TAILORED-CHIP trial was designed to study whether early escalation with low-dose ticagrelor plus aspirin and late de-escalation with clopidogrel alone would be better than standard clopidogrel plus aspirin.”

The open-label randomized TAILORED-CHIP trial was conducted at 24 sites in South Korea. Patients with high-risk anatomical or clinical characteristics undergoing complex PCI were enrolled and were randomized 1:1 to receive tailored antiplatelet strategy consisting of early escalation (low-dose ticagrelor at 60 mg twice daily plus aspirin for 6 months) then late de-escalation (clopidogrel monotherapy for 6 months) or standard DAPT (clopidogrel plus aspirin for 12 months).

The primary outcome was net adverse clinical events, defined as a composite of death from any cause, myocardial infarction, stroke, stent thrombosis, unplanned urgent revascularization and clinically relevant bleeding (BARC type 2, 3, or 5) at 12 months. Prespecified secondary outcomes included major ischemic and clinically relevant bleeding events.

In total, 2,018 patients were enrolled. The mean age was 64.0 years and 17.1% were women. Most patients (93.7%) had PCI conducted in at least two major heart vessels during the same procedure.

At 12 months, the primary of outcome of net adverse clinical events was not significantly different between the groups, occurring in 10.5% of patients assigned to tailored antiplatelet therapy and in 8.8% of patients assigned to standard DAPT (hazard ratio [HR] 1.19; 95% confidence interval [CI] 0.90 to 1.58; p=0.21).

There was no significant difference in the incidence of major ischaemic events at 12 months between the tailored-therapy and DAPT groups (3.9% vs. 5.0%, respectively; HR 0.78; 95% CI 0.52 to 1.19; p=0.25). However, the incidence of clinically relevant bleeding at 12 months was significantly higher in the tailored-therapy group (7.2%) compared with the DAPT group (4.8%; absolute difference 2.45%; 95% CI 0.37% to 4.53%; p=0.002). The incidence of major bleeding was similar in the tailored-therapy group (1.7%) and the DAPT group (1.5%; absolute difference 0.21%; 95% CI −0.89% to 1.31%; p=0.70).

Summarizing the findings, Professor Park said: “Our results suggest that a tailored strategy in patients undergoing complex high-risk PCI does not provide a net clinical benefit. We observed an increase in bleeding complications without a significant reduction in ischaemic events. This challenges the notion that ‘more is better’ even in carefully selected patients at high ischemic risk undergoing complex PCI procedures. Standard 12-month DAPT remains appropriate.”

Fine-particulate air pollution can drive devastating forms of dementia by triggering the formation of toxic clumps of protein that destroy nerve cells as they spread through the brain, research suggests.

Exposure to the airborne particles causes proteins in the brain to misfold into the clumps, which are hallmarks of Lewy body dementia, the second most common form of dementia after Alzheimer’s disease.

The finding has “profound implications” for preventing the neurodegenerative disorder, which affects millions worldwide, with scientists calling for a concerted effort to improve air quality by cutting emissions from industrial activity and vehicle exhausts, improving wildfire management and reducing wood burning in homes.

“Unlike age or genetics, this is something we can change,” said Dr Xiaobo Mao, a neurologist at Johns Hopkins University in the US and the study’s lead investigator. “The most direct implication is that clean air policies are brain health policies.”

The researchers began by analysing hospital records of the 56.5 million US Medicare patients. They looked at those who were admitted for the first time between 2000 and 2014 with the protein damage. Armed with the patients’ zip codes, the scientists estimated their long-term exposure to PM2.5 pollution, airborne particles that are smaller than 2.5 thousandths of a millimetre. These can be inhaled deep into the lungs and are found in the bloodstream, brain and other organs.

They found that long-term exposure to PM2.5 raised the risk of Lewy body dementia, but had less of an impact on rates of another neurodegenerative brain disease that is not driven by the toxic proteins.

Lewy bodies are made from a protein called alpha-synuclein. The protein is crucial for healthy brain functioning, but can misfold in various ways to produce different kinds of harmful Lewy bodies. These can kill nerve cells and cause devastating disease by spreading through the brain.

To see if air pollution could trigger Lewy bodies, the team exposed mice to PM2.5 pollution every other day for 10 months. Some were normal mice, but others were genetically modified to prevent them making alpha-synuclein. The results were striking: in normal mice, nerve cells died off, leading to brain shrinkage and cognitive decline. The genetically modified mice were largely unaffected.

Further work in mice showed that PM2.5 pollution drove the formation of aggressive, resilient and toxic clumps of alpha-synuclein clumps that looked very similar to Lewy bodies in humans. Although the work is in mice, the findings are considered compelling evidence.

“Putting the two together, to me, indicates that there’s a pretty strong association with air pollution causing Lewy body dementia. We think it’s a very important driving factor for dementia,” said Ted Dawson, a senior author on the study and a professor in neurodegenerative diseases at Johns Hopkins. “There needs to be a concerted effort to keep our air clean.”

The work, published in Science, builds on previous studies that have found PM2.5s in people’s brains where damage has been linked to Alzheimer’s disease and reductions in intelligence.

“Our findings have profound implications for prevention because they identify air pollution as a modifiable risk factor for Lewy body dementia,” Mao told the Guardian. “By lowering our collective exposure to air pollution, we can potentially reduce the risk of developing these devastating neurodegenerative conditions on a population-wide scale.”

Last year, researchers at University College London and the Francis Crick Institute in London launched a project called Rapid, for Role of Air Pollution in Dementia, to investigate how the air we breathe may harm the brain.

“This is an important and compelling study that deepens our understanding of how air pollution can drive neurodegenerative disease,” said Prof Charles Swanton, a co-leader of the Rapid project and deputy clinical director at the Crick.

“By linking fine-particulate matter exposure to the biology of Lewy body dementia, it provides a mechanistic bridge between environmental exposure and disease pathology. More broadly, the work underscores the urgent need to understand and mitigate the impact of air pollution on dementia and disease risk more broadly, given its enormous and growing public health burden.”

After a cat located in San Fransisco, California, tested positive for H5N1 highly pathogenic avian influenza (H5N1), the FDA, state and local public health and agriculture partners, and federal partners suggest that after further testing, there a link between the strain detected in the cat and certain lots of RAWR Raw Cat Food Chicken Eats, a product the cat ate prior to falling ill.

According to the FDA, the San Francisco Department Public Health (SFDPH) was notified a cat ate Lot CC 25 093 before becoming ill with H5N1 and euthanized.¹ An initial PCR testing of the open product was conducted and detected H5N1. Subsequent whole genome sequencing (WGS) of a diagnostic sample from the cat and the open sample from Lot CCS 25 093 were performed by the USDA National Veterinary Service Laboratories.

The FDA then collected and tested 2 retail samples of the same RAWR Chicken Eats product with a different lot number (CC 25 077) and Sell By Date (09/18/26), each testing positive for Influenza A Virus, and a WFS performed on one sample was also positive for H5N1.¹ WGS results also indicated that H5N1 from all 3 samples were within the same WGS cluster, indicating relatedness. This cluster involves a virus lineage that was detected from around November to December 2024, and is no longer circulating, supporting that the infected cat became ill from eating the Lot CCS 25 093 of the Chicken Eats product.¹

RELATED: Additional cat food company announces recall over H5N1 concerns

NVSL testing of the cat, Lot CCS 25 093, and Lot CCS 25 077 identified the H5N1 as genotype B3.13. This genotype virus was found in other brands of raw poultry-based pet foods before that were associated with the illness or death of cats.¹

The RAWR Raw Cat Food Chicken Eats, Sell by 09/18/26, and RAWR Cat Food Chicken Eats, Sell by 10/03/26, are sold in 2.5-pound resealable frozen plastic bags that have 40 1 ounce sliders in them in retail stores nationwide and online. The bags are white and yellow with black lettering, and have the lot code CCS 25 077 and CCS 25 093 printed in the center of the back of each bag.

At this time, the FDA is not aware of any human cases of HPAI contracted through exposure to contaminated food.

H5N1 in dogs and cats

The H5N1 virus can result in illness and death in birds and mammals such as domesticated cats and large felids as well as dogs. For dogs however, their cases usually present with mild clinical signs and low mortality in comparison to cats. Currently, there are no known dogs with highly pathogenic avian influenza in the United Sates, but other countries have seen fatal cases. There is a list of animals that have tested positive for the virus on the USDA’s APHIS website.

Animals who have weak immune systems or are very old or young are especially at risk of contracting the virus. Animals with the virus typical present with the following signs, according to the American Veterinary Medical Association²:

• Discharge from the eyes and nose
• Difficulty breathing
• Fever
• Lethargy
• Low appetite
• Neurologic signs such as blindness, incoordination, seizures, and tremors
• Reddened or inflamed eyes.

While there have been no identified cases of H5N1 infections among anyone handling raw pet food products, humans are still at risk of being infected if an active virus gets into their eyes, nose, our mouth. Because of this, it is crucial for people to wash their hands after handling any pet food products as well as sanitize contact surfaces.

References

1. FDA Notifies Pet Owners That Tests Show H5N1 Contamination in Certain Lots of RAWR Raw Cat Food Chicken Eats. News release. US Food and Drug Administration. September 3, 2025. Accessed September 4, 2025. https://www.fda.gov/animal-veterinary/cvm-updates/fda-notifies-pet-owners-tests-show-h5n1-contamination-certain-lots-rawr-raw-cat-food-chicken-eats?utm_medium=email&utm_source=govdelivery
2. American Veterinary Medical Association. Avian influenza in companion animals. American Veterinary Medical Association. Published 2025. https://www.avma.org/resources-tools/animal-health-and-welfare/animal-health/avian-influenza/avian-influenza-companion-animals

Bipolar disorder (BD) is a chronic mental health condition characterized by recurrent episodes of depression and mania. It poses a substantial burden on global health, with an increasing incidence. Despite its prevalence, there exists a significant gap in understanding the underlying neuropathological mechanisms. Although mitochondrial dysfunction has been implicated in BD, the specific brain region damaged is not yet fully understood. A deeper understanding is essential for advancing research efforts and developing better therapeutic strategies.

In an effort to bridge the knowledge gap, a team of researchers in Japan investigated the thalamus and medial temporal regions of the brain-areas involved in mood regulation and cognitive function. The research team, led by Professor Tadafumi Kato from the Department of Psychiatry and Behavioral Science, Juntendo University Graduate School of Medicine, Japan, and Dr. Akito Nagakura from Tokyo Metropolitan Matsuzawa Hospital, Japan, set out with a vision to change the trajectory of BD research. Their findings were published in Psychiatry and Clinical Neurosciences on September 2, 2025.

“Although animal models have pointed to the involvement of the paraventricular thalamic nucleus in the pathophysiology of BD, neuropathological knowledge is limited. In particular, we aimed to investigate whether the accumulation of certain neurodegenerative proteins, previously associated with neurological diseases, might play a role in the pathology of BD,” says Prof. Kato.

The research involved an analysis of postmortem brain tissue, specifically the paraventricular thalamus and medial temporal regions, which were studied in detail. The postmortem tissues were subjected to immunohistochemical analyses using antibodies targeting key neurodegenerative markers, including phosphorylated tau, amyloid β, α-synuclein, and TDP-43. Additionally, markers of granulovacuolar degeneration (GVD), such as CHMP2B and CK-1δ, were investigated. This comprehensive approach enabled an efficient assessment of the expression and distribution of multiple proteins that are commonly associated with neurodegenerative diseases.

The findings revealed significantly higher neurofibrillary tangle (NFT) stages in patients with BD, along with argyrophilic grain pathology. Both are related to tau proteins that accumulate in brain cells and are commonly associated with aging. These findings replicated a greater burden of tau-related pathology in BD, as suggested by previous postmortem brain and neuroimaging studies, possibly linked to the age of onset.

More importantly, the presence of CHMP2B-positive GVD in the paraventricular thalamus in about half of the BD cases was an observation not previously reported.

Together, these insights highlight the potential role of neurodegenerative protein accumulation and dysfunctional paraventricular thalamus in the underlying biology of BD.

Overall, the findings add to a growing body of evidence that suggests that BD is a brain-based disease. By uncovering specific protein pathologies, such as CHMP2B-positive GVD, and tau accumulation in key brain regions, the research strengthens the biological understanding of BD beyond simply clinical symptoms.

As the understanding of underlying brain changes improves, there is a growing need for early detection, personalized treatment strategies, and therapies that address the root mechanisms.

“Our study, by demonstrating the presence of CHMP2B-positive GVD in the paraventricular thalamus and increased NFT stages in patients with BD, may pave the way for the development of new diagnostic tools and targeted therapies,” concludes Prof. Kato.