Category: 8. Health

Prediabetes affects a third of people in the United States and most of them will develop Type 2 diabetes, yet effective dietary intervention strategies remain limited. Pistachios have shown promise in improving markers of diet quality, yet little is known about how they influence the gut microbiome – a key player in glucose regulation and inflammation.

A new study led by Kristina Petersen, associate professor of nutritional sciences at Penn State, determined that nighttime pistachio consumption affects gut bacteria in adults with prediabetes. Though the potential therapeutic implications of the findings remain unclear, according to Petersen, they may prove significant for people who are working to improve their metabolic health.

The findings, published in the journal Current Developments in Nutrition, suggested that replacing a traditional carbohydrate-based bedtime snack with pistachios may reshape the gut microbiome. A previous study by these researchers demonstrated that pistachios have a similar effect on blood glucose as 15 to 30 grams of carbohydrates.

“A common dietary recommendation for individuals with prediabetes is to consume a nighttime snack consisting of 15 to 30 grams of carbohydrates to help regulate overnight and morning blood glucose levels,” said Terrence Riley, lead author of this research who earned his doctorate in nutritional sciences at Penn State and currently works as a postdoctoral research fellow at Louisiana State University. “As an example, you could eat one or two slices of whole grain bread.”

Researchers observed that consuming about two ounces of pistachios each night for 12 weeks resulted in significantly different stool microbial community profiles compared to those who consumed the recommended 15 to 30 grams of a carbohydrate snack. Specific bacterial groups, including Roseburia and members of the Lachnospiraceae family – known as “good” bacteria that produces beneficial short-chain fatty acids like butyrate – were more abundant following the pistachio condition.

According to Petersen, butyrate serves as a primary energy source for colon cells, helps maintain the gut barrier and supports anti-inflammatory processes. 

Pistachios seem to be able to meaningfully shift the gut microbial landscape in adults with prediabetes especially when consumed as a nighttime snack. These microbiome changes may offer other long-term health benefits – potentially helping to slow the development of Type 2 diabetes or to reduce systemic inflammation – which we hope to explore in future research.”

Kristina Petersen, associate professor of nutritional sciences, Penn State

The study involved 51 adults with prediabetes and was conducted over two 12-week periods separated by a break, so the effects of the first part of the trial would not affect the second part. By the end of the study, all participants received both treatments. Stool samples were collected and analyzed using 16S rRNA gene sequencing, a technique that can help classify bacteria based on their genetic makeup.

Petersen noted that participants who ate pistachios also experienced reductions in several bacterial groups that have been linked to less favorable metabolic outcomes.

“Levels of Blautia hydrogenotrophica – a bacterium that helps produce compounds that can build up in the blood and harm kidney and heart health – were lower after pistachio consumption,” Petersen said. “Levels of Eubacterium flavonifractor, which breaks down beneficial antioxidant compounds from foods like pistachios, also decreased.”

Petersen added that the strength of this study is the design used – a randomized crossover clinical trial, in which all participants receive both treatments in a randomized order. By including all participants in the pistachio group and the standard care group, the study helped the researchers better understand how specific foods like pistachios can influence the gut microbiome.

While the study demonstrated shifts in gut bacteria, it remains unclear whether these changes directly translate to improvements in health – a question that requires further research, Petersen said.

Jordan Bisanz, assistant professor of biochemistry and molecular biology at Penn State; Penny Kris-Etherton, retired professor of nutritional sciences at Penn State; Justin Wright of Wright Labs, LLC; and Regina Lamendella, Jeremy Chen See and Khushi Kanani of Juniata College all contributed to this research.

The study was funded by the American Pistachio Growers, Penn State’s Clinical and Translational Science Institute through the National Center for Advancing Translational Sciences of the National Institutes of Health, and additional support from Juniata College and the U.S. National Science Foundation. It is registered at ClinicalTrials.gov (NCT04056208).

A new study led by researchers at the University of Rochester Medical Center (URMC) found that early-life exposure to antibiotics can impair an infant’s developing immune system, and that a naturally occurring metabolite may hold the key to reversing that damage. 

Published in Cell, the study uncovered how antibiotic exposure during pregnancy and infancy may permanently weaken the immune system’s ability to fight respiratory infections like the flu. By analyzing both mouse models and human infant lung tissue, the researchers discovered that early antibiotics disrupt the gut microbiome’s ability to produce inosine, a molecule that serves as an important signal for developing immune cells. 

By supplementing inosine in mice, however, the researchers were able to correct the immune system issues caused by antibiotics. The finding opens the door to potential therapeutic strategies to bolster immune memory in vulnerable infants. 

Think of inosine as a molecular messenger. It travels from the gut to developing immune cells, telling them how to mature properly and prepare for future infections.”

Hitesh Deshmukh, MD, PhD, senior author, chief of the Division of Neonatology at UR Medicine Golisano Children’s Hospital (GCH) 

The project was part of a long-term R35-funded NIH initiative – which are distributed to experienced investigators to study long-term projects – to investigate how early-life exposures shape lifelong disease risk, including asthma and chronic lung disease.

“We know that antibiotics can be lifesaving for infants, but they also disrupt the microbiome during a critical window of immune development,” said Deshmukh. “Our study identifies one way that disruption affects lung immunity, and more importantly, a way to potentially fix it.” 

The disruption ultimately affects the formation of tissue-resident memory T cells, a specialized population of immune cells that reside in the lungs and provide long-term protection against viral infections. Without these cells, infants may remain vulnerable to severe respiratory illness well into adulthood. 

“We’ve discovered that the gut microbiome acts as a teacher for the developing immune system,” Deshmukh explained. “When antibiotics disrupt this natural education process, it’s like removing key chapters from a textbook: the immune system never learns crucial lessons about fighting respiratory infections.” 

The study compared infant mice exposed to common antibiotics (ampicillin, gentamicin, and vancomycin-the same ones frequently used in pregnant women and newborns) with those that maintained their natural gut bacteria. The following differences were found: 

• Antibiotic-exposed infant mice had significantly reduced populations of protective CD8+ T cells in their lungs 

• These mice showed impaired ability to form tissue-resident memory cells, specialized immune cells that live in the lungs and provide rapid protection against reinfection 

• The immune deficits persisted into adulthood, suggesting permanent changes to immune development 

Using lung samples from an NIH-funded biobank run by URMC (BRINDL biobank), the team confirmed that similar immune deficits were present in human infants exposed to antibiotics. These infants not only showed fewer memory T cells but also demonstrated gene expression patterns similar to older adults, who are also at greater risk for respiratory infections. 

Most importantly, supplementing antibiotic-exposed mice with inosine largely restored their ability to develop functional memory T cells and mount effective immune responses, offering a promising future avenue for potential therapies. 

“This suggests we might be able to protect at-risk infants through targeted supplementation,” said Deshmukh. “While much more research is needed before this approach could be applied clinically, it gives us a path forward.” 

The findings could influence future research on how to design interventions-including dietary supplements, metabolite therapies, or microbiome-supportive strategies-to help newborns develop stronger immune memory without relying solely on antibiotics or risky probiotics. The study also underscores the importance of balancing the life-saving benefits of antibiotics with careful stewardship, particularly during sensitive windows of immune development. 

Deshmukh credits GCH neonatologist Gloria Pryhuber, MD, as instrumental in the research. Pryhuber’s BRINDL biobank of infant lung samples, collected through a 15-year NIH-funded effort, allowed the team to test their findings in human cells. 

“This paper wouldn’t have been possible without Dr. Pryhuber’s generosity and expertise,” Deshmukh said. “The ability to compare our mouse model results to human cells was absolutely critical. It was one of the main reasons I came to Rochester (from Cincinnati Children’s Hospital) -to collaborate with her.” 

A new study shows that starting blood thinners just days after a stroke is not only safe—it significantly lowers the chance of another stroke.

The findings could help change how doctors treat stroke patients worldwide.

The new study in The Lancet finds that starting blood thinners within four days of an ischemic stroke caused by atrial fibrillation can significantly lower the risk of a second stroke—without increasing the risk of brain bleeding.

The findings offer the most definitive evidence to date on a question that has long challenged clinicians: How soon is too soon to begin blood-thinning therapy after stroke?

The study, called CATALYST, analyzed data from more than 5,400 patients across four major randomized clinical trials. Steven Warach, professor of neurology at Dell Medical School at The University of Texas at Austin, served as the US principal investigator and coauthor of the study. He also led the US-based START trial, one of the four studies included in the meta-analysis, which was published earlier this year in JAMA Neurology.

“For decades, clinicians have been uncertain when to safely start anticoagulation after stroke,” says Warach.

“This study provides the clearest evidence yet that in most cases, it’s not only safe to start earlier—it’s better for patients.”

Atrial fibrillation, an irregular heartbeat that increases stroke risk, causes about 1 in 3 ischemic strokes. Although direct oral anticoagulants (DOACs) are highly effective in preventing future strokes, the best time to start them after an initial stroke has remained controversial, with many physicians waiting one to two weeks to begin treatment.

By pooling individual patient data from all high-quality trials available, the CATALYST analysis offers a more reliable answer.

Key findings

• Starting DOACs within four days of stroke onset cut the risk of a second stroke by nearly one-third.
• No added risk of brain bleeding or other major complications.
• Benefits observed across a broad range of patients, regardless of stroke severity or prior treatment.
• Suggests earlier DOAC use should become the new standard of care.
• Potential to shorten hospital stays and improve global outcomes.

“This gives clinicians the clarity they’ve been waiting for—and gives patients a better chance at recovery,” says Warach. “It’s a major step forward in evidence-based stroke care.”

Source: University of Texas at Austin

Specialty

Please chooseI’m not a medical professional.Allergy and ImmunologyAnatomyAnesthesiologyBiostatisticsCardiac/Thoracic/Vascular SurgeryCardiologyCritical CareDentistryDermatologyDiabetes and EndocrinologyEmergency MedicineEpidemiology and Public HealthFamily MedicineForensic MedicineGastroenterologyGeneral PracticeGeneticsGeriatricsHealth PolicyHematologyHIV/AIDSHospital-based MedicineI’m not a medical professional.Infectious DiseaseIntegrative/Complementary MedicineInternal MedicineInternal Medicine-PediatricsMedical Education and SimulationMedical PhysicsMedical StudentNephrologyNeurological SurgeryNeurologyNuclear MedicineNutritionObstetrics and GynecologyOccupational HealthOncologyOphthalmologyOptometryOral MedicineOrthopaedicsOsteopathic MedicineOtolaryngologyPain ManagementPalliative CarePathologyPediatricsPediatric SurgeryPharmacologyPhysical Medicine and RehabilitationPlastic SurgeryPodiatryPreventive MedicinePsychiatryPsychologyPulmonologyRadiation OncologyRadiologyRheumatologySubstance Use and AddictionSurgeryTherapeuticsTraumaUrologyMiscellaneous

CONFERENCE REPORTER

Patients with bipolar disorder face an average diagnostic delay of 10 years. This gap can lead to misdirected treatments, worsening symptoms, and life altering consequences, but the delay is partly due to the disorder’s complex and often difficult to quantify presentation. Focusing on patient symptom insight, clinician investigation, and new tests with potential to measure this disorder may provide better care for patients suffering from bipolar disorder.

At the 2025 Southern California Psychiatry Conference, clinicians Kellogg, Trinh, and Hanaie presented their lecture “Empowering Clinicians to Identify and Treat Bipolar Disease Earlier in the Disease Course,” where they addressed the persistent challenges in diagnosing bipolar disorder and promising new therapeutic options.¹

Kellogg outlined what he sees as the three core diagnostic challenges for bipolar: patient factors (like expressing their emotions), clinician challenges (like hearing and recognizing subtle symptoms), and the absence of definitive lab tests. For the patient, they may not “fully grasp the terms or concepts used in diagnostic criteria…when asked about their symptoms, making it hard to provide accurate descriptions,” Kellogg explained. The patient’s struggle with recognizing manic symptoms, a dominance of depressive episodes, lack of emotional insight, overlapping symptoms with other disorders, and psychosis also contribute to the complexity clinicians face in diagnosing. Providers, Kellogg said, must navigate the subtleties of early onset symptoms, family history (importantly mood disorders and suicidality), and any insights gained from antidepressant misadventures in which the patient reacted notably to a medication. In bipolar patients, antidepressants can also induce hypomania or prove ineffective, signaling an incorrect diagnosis of major depressive disorder. This factor makes it all the more difficult to identify a correct bipolar diagnosis. High rates of psychiatric and medical comorbidities—including anxiety, substance use disorders, migraines, thyroid dysfunction, and type 2 diabetes—further complicate the diagnostic process.²

With the potential benefits of developing lab-based diagnostic tools, there are unfortunately no definitive blood tests for bipolar disorder currently. However, new research focuses in on RNA biomarkers, RNA editing, artificial intelligence applications, genetic mutations in thyroid pathways, and ceramide-based metabolite profiling. These techniques, Kellog noted, are showing promise and may provide new biological markers for identifying the disorder. Kellogg concluded by underscoring the severe consequences of undiagnosed bipolar disorder, which can lead to impaired relationships, academic and employment issues, and legal or financial problems; diagnosing earlier on in the disease course and preventing these outcomes may become easier with new diagnosis techniques.

Dr Trinh continued with a focus on the treatment landscape, drawing from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD) trials conducted from 1998 to 2005. This landmark study explored treatment efficacy, relapse prevention, and long-term quality of life through randomized, collaborative care models and longitudinal tracking. Trinh pointed out the study’s result that 58% of participants achieved recovery, but 49% relapsed within two years.

Trinh emphasized the value of non-pharmacological approaches such as psychoeducation, cognitive behavioral therapy, interpersonal and social rhythm therapy, family focused therapy, and lifestyle modifications. In terms of prescription changes from the STEP-BD study, the addition of antidepressants offered no significant benefit over mood stabilizers alone in preventing depressive relapse. For treatment resistant cases, Trinh highlighted combination therapy, electroconvulsive therapy, clozapine, and investigational treatments like ketamine and transcranial magnetic stimulation. Trinh also pointed to recent FDA approvals for acute mania and mixed episodes (including iloperidone, olanzapine, and cariprazine), as well as newer agents for bipolar depression such as lumateperone and lurasidone.

References

1. Kellogg J, Trinh L, Hanaie J. Empowering clinicians to identify and treat bipolar disease earlier in the disease course. Conference Proceedings of the Southern California Psychiatry Conference. July 2025;11-12. Huntington Beach, CA.

2. Goldman ML, Mangurian C, Corbeil T, et al. Medical comorbid diagnoses among adult psychiatric inpatients. Gen Hosp Psychiatry. 2020;66:16-23.

At the Society of NeuroInterventional Surgery’s (SNIS) 22nd Annual Meeting today, researchers presented findings about how pregnancy can worsen the rupture risk for brain arteriovenous malformations, abnormal connections between arteries and veins whose rupture can result in serious brain injury or death.

During pregnancy, hormonal shifts and the increased demand on the heart to pump a higher volume of blood can place added strain on both the body and the brain. Researchers at the University of Mississippi Medical Center in Jackson recently investigated whether these physical changes can aggravate health issues for pregnant women with three brain conditions that are prone to rupturing and causing serious brain injury: arteriovenous malformations (abnormal tangles of blood vessels that disrupt blood flow), brain aneurysms (bulges in weakened brain arteries that can cause stroke if ruptured), and cavernous malformations (unusually shaped blood vessels that can cause brain bleeding if ruptured).

In the study, “Rupture Risk of Intracranial Vascular Malformations During Pregnancy: A Systematic Review and Meta-analysis,” the research team reviewed 5,609 journal articles from multiple academic databases that discussed pregnant women with these conditions, ultimately choosing 15 to statistically analyze. They then used data from the articles to group patients by whether they experienced a rupture. The scientists found that while pregnancy didn’t seem to make a major difference in rupture rates for women with brain aneurysms and cavernous malformations, pregnant women with arteriovenous malformations were much more likely to experience ruptures than non-pregnant women with the same condition.

These findings show that we still have much to learn about how pregnancy affects the brain. We need more research into these effects and their potential causes so that doctors can more precisely target how to treat pregnant women with these and other serious health conditions.” 

Evan Bowen, medical student, University of Mississippi Medical Center

Most men who are treated for prostate cancer according to modern guidelines have good survival rates and the majority of these men will die of causes other than prostate cancer. This is revealed in a new study from Uppsala University published in the Journal of the National Comprehensive Cancer Network.

“We were surprised by how much life expectancy affected the prognosis. This shows the importance of a thorough assessment of the general health of a man with newly diagnosed prostate cancer. The patient’s life expectancy has a substantial impact on the choice of appropriate treatment strategy,” says Marcus Westerberg, researcher at the Department of Surgical Sciences at Uppsala University, who led the study.

In prostate cancer, the disease progression often takes decades and the risk of dying from prostate cancer therefore depends on both the characteristics of the cancer and life expectancy based on the man’s age and other diseases at the time of diagnosis. Recommendations in guidelines and care programmes are therefore also based on both cancer characteristics and life expectancy. This means that the recommended initial treatment can range from active monitoring for low-risk cancer to combinations of local and systemic treatment for high-risk cancer.

High average age at disease onset

As the average age at diagnosis of prostate cancer is often high and the cancer often progresses very slowly, it is particularly important to know the long-term risk of death from prostate cancer in order to choose the best treatment for patients. Previously, not much has been known about this.

We wanted to fill that knowledge gap, so we looked at outcomes up to 30 years after the men were diagnosed. In all cases, we had information about the characteristics of the cancer, treatment and the patient’s life expectancy based on age and comorbidity.”

Marcus Westerberg, Researcher, Department of Surgical Sciences, Uppsala University

The researchers used data from the Prostate Cancer Database Sweden (PCBase), which contains information from the National Prostate Cancer Register (NPCR) and other health data registers. They focused on men who had received the recommended treatment for prostate cancer that had not spread in the body. Using statistical modelling, the researchers estimated the lifetime risk of dying from prostate cancer and other causes.

11 per cent risk of dying of cancer

For men with low-risk cancer and short life expectancy (less than 10 years), the risk of dying from prostate cancer was 11 per cent and the risk of dying from other causes was 89 per cent within 30 years of diagnosis.

For men with high-risk cancer (e.g. stage T3, PSA 30 ng/ml and Gleason score 8) and long life expectancy (over 15 years), the risk of dying from prostate cancer was 34 per cent and the risk of dying from other causes was 55 per cent within 30 years of diagnosis.

“We hope that our results will be used to provide a realistic picture of the prognosis for men with prostate cancer. Our study shows that most men who receive the recommended treatment have a good prognosis,” Westerberg concludes.

Life expectancy was based on age and comorbidity. Examples of low-risk cancers are stage T1, PSA 5 ng/ml and Gleason score 6. Examples of high-risk cancers are stage T3, PSA 30 ng/ml and Gleason score 8.

 

A new research paper was published in Volume 16 of Oncotarget on June 25, 2025, titled “Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer.”

In this study, researchers led by Shailender S. Chauhan and Noel A. Warfel from the University of Arizona discovered that prostate cancer cells survive treatment by storing fats in tiny cellular compartments when oxygen levels are low. This process makes the cancer cells less vulnerable to a type of cell death known as ferroptosis. The findings provide new insight into why prostate tumors often resist therapies and suggest potential strategies to improve treatment outcomes.

This study focused on ferroptosis, a form of programmed cell death that relies on iron and lipid oxidation to destroy cancer cells. Researchers tested prostate cancer cells under normal and low oxygen conditions and found that hypoxia, or reduced oxygen levels, allowed cancer cells to build up lipid droplets (LD). These structures act as storage units for fats, shielding cancer cells from oxidative damage and preventing ferroptosis from occurring.

The researchers found that this adaptation of prostate cancer cells made them less sensitive to ferroptosis-inducing drugs like Erastin and RSL3, even when these drugs were combined for a stronger effect. The team also reported that hypoxia caused significant changes in lipid metabolism, decreasing the availability of specific fatty acids that normally promote ferroptosis. 

“Transcriptomic analysis revealed that hypoxia significantly reduced the expression of genes related to incorporating polyunsaturated fatty acids into phospholipids (ACSL4, LPCAT3), and parallel lipidomic analysis demonstrated that hypoxia significantly decreased the levels of the ferroptosis-prone lipid class, phosphatidylethanolamine (PE) and increased production of neutral lipid species, cholesteryl ester (ChE (22:5)) and triglycerides (TG(48:1), TG:(50:4), and TG(58:4)).”

This research highlights the importance of the tumor microenvironment, particularly oxygen levels, in shaping how cancer cells respond to therapy. By altering their metabolism and storing lipids, prostate tumors may evade treatments designed to trigger ferroptosis. These findings underscore the need to develop new strategies targeting LD dynamics or lipid metabolism to overcome this resistance.

Understanding how prostate cancer (Pca) adapts to survive in hypoxic conditions offers a potential avenue for improving therapies. For example, preventing lipid accumulation in cancer cells or releasing stored fats may restore their sensitivity to ferroptosis and improve the effectiveness of current therapies. This approach could have broader implications for treating other solid tumors that share similar metabolic features.

A stroke occurs when blood flow is cut off to the brain, either by a burst blood vessel (hemorrhagic) or a blockage (ischemic). Both types of stroke are considered an emergency and require immediate medical attention.

To identify symptoms of a stroke, remember to BE FAST:

B – balance may be affected

E – eyesight may become blurry or someone may experience double vision

F – facial dropping can occur

A – arms and legs may feel loss of sensation or grip

S – slurred speech

T – time to call 911

If you experience one or more of these symptoms, getting medical care within four hours is essential to help mitigate lasting effects like aphasia and movement issues. Women are more likely to develop blood clots, leading to an increased risk of stroke.

Risk factors for stroke include high blood pressure, high cholesterol, lack of exercise, poor diet, excessive alcohol consumption, smoking, and diabetes. If you’re at risk, lifestyle changes like increasing movement, limiting alcohol and smoking, and eating a DASH diet for hypertension.

The Primary Stroke Center at GBMC has one of the highest stroke survival rates for inpatient stay, 1 month post-discharge and 6 months post-discharge in Maryland. Learn more here.