Category: 8. Health
-
Profiling an invisible hazard: Equipping sites to work with hydrogen
The Flame 1750 H2 detector can pick up a 1m flame at a distance of up to 40m within 5 seconds, according to Dräger. While hydrogen has advantages that explain its ongoing use as a putative green replacement for many other fuels, it does present a quite distinct set of safety challenges. But it seems the risks can be mitigated with sufficient awareness, and the deployment of appropriate technologies and best practices, as Envirotec discovered in conversation with industrial safety and gas detection expert Dräger. The firm assists organisations to work safely with hydrogen, and to equip their sites accordingly. Gas detection systems are a key ingredient.
Hydrogen’s particular strength is with its versatility as a means to store, transport and distribute energy over large distances and between sectors – indeed, it’s the only at-scale technology able to do so. It can be produced wherever renewable energy such as wind or solar is generated, and then transported to where it is required. This is the ideal, at least.
There are certainly similarities between hydrogen and methane, and some of the existing infrastructure for natural gas can be repurposed for it. Both are explosive, for one thing. But there are key differences in terms of their properties and the specific risks they present. Adam Pope, Marketing Manager and Gas Detection Lead with Dräger suggests this is not always apparent to operators and staff who have worked with natural gas or LPG. “They’ll maybe have some idea about the Hindenburg disaster,” he muses, referencing the 1937 calamity that drew a line under an earlier era’s exploration of hydrogen as a fuel, but they’ll often be unfamiliar with hydrogen’s special challenges, and the necessary risk-mitigation strategies.
For one thing, hydrogen’s flame characteristics are quite distinct from other common fuels, in that it is difficult to detect with the naked eye in daylight (although it can be seen in darker conditions). It also emits very little heat – so you can’t feel it until you are in very close proximity.
One way it can be detected is by the electromagnetic radiation emitted when it burns – a signature that can be picked up by certain classes of detector.
Some of the key risk factors specific to hydrogen are listed in the side panel (“Hydrogen risk factors”, see end of article). Its flammability and propensity to leak from structures place a premium on high-integrity storage. And leak detection is a vital element of safeguarding.
These risk factors will obviously be unfamiliar where hydrogen is a recent add-on to an organisation’s core expertise. For example, at a wind or solar energy site where the operators have opted to produce hydrogen via electrolysis.
Points of vulnerability in the value chain are explored in an ebook from Dräger.1 Even where existing infrastructure can be adapted there will be vital new ideas to grasp. For example, existing gas pipelines, where suitable, will require new monitoring and maintenance regimes.
The ebook explains that “the probability of safety incidents increases when people are involved”. The document adds: “When heavy machines such as trucks are moved around, even minor bumps need to be taken seriously as they increase the risk of leakage.”
Profiling a site
Gaining a full picture of a site’s risks is a vital precursor to designing mitigation measures – and requires an individualised risk assessment, something Dräger’s literature recommends “before joining the hydrogen economy”. There is no standard risk profile, seemingly, and the risks manifest in different ways in each site.Fire and gas mapping is one service the group introduces at this early stage, says Adam Pope, which will result in a colour-coded 3d map of a site intended to afford a clear understanding of the different risks, and of where leaked gases will travel in different circumstances.
Fixed gas and flame detection is the primary means to protect a site from explosion risk, by alerting operators to the presence of a leak, so that premises can be evacuated and processes can potentially be shut down.
A range of different technologies is used here, each with different strengths and weaknesses. Best practice involves a mix of technologies, as Adam explains.
Three layers of protection
Point detectors are the core technology for gas detection and form the foundation of most safety systems, he says. These will be located anywhere there is a danger that gas can accumulate, such as in confined spaces. The downside is that the gas must be able to make contact with the detector or it might be missed.The choice of sensor technology is crucial here. As Adam points out, the infrared sensors used to detect hydrocarbons are completely blind to hydrogen. Instead, catalytic bead (CatEx) sensors, or electrochemical (EC) sensors, can be used here. CatEx sensors offer a robust way to detect hydrogen up to the explosive limit (i.e., below 100% LEL, the Lower Explosion Level), providing a fast response time. EC sensors are typically used where lower (ppm) concentration levels of hydrogen are to be detected, and also offer a fast response time and high accuracy.
An earlier warning of leakage is available with ultrasonic detectors, to be deployed as an additional layer of detection where appropriate. These exploit the fact that hydrogen’s small molecule size results in a high-frequency noise, wherever there’s a leak. The acoustic sensor can detect leaks occurring up to 7 – 15 m away from the leak source, and deliver an on/off signal that can be used to trigger an alarm or automatic shutdown of equipment.
Ultrasonic detectors are good for outdoor locations, where the wind might otherwise carry hydrogen away from point detectors.
The relative invisibility of hydrogen flames means an additional layer of detection can sometimes be appropriate for a site, in the form of hydrogen flame detectors. Two technologies appear to stand out: UV/IR detectors, and 3IR.2 A traditional option for detecting hydrocarbon fires is a UV/IR detector, employing one ultraviolet and one infrared sensor, and providing a swift response time but with some potential for false alarms, particularly when trying to detect hydrogen.
To assist with hydrogen detection specifically, Dräger has adopted a technology called “3IR” – so-named for its use of three separate IR sensors, and this is incorporated in the company’s Flame 1750 H₂ detector. The 3IR technology produces a low rate of false alarms and a fast response – as Adam says, it can detect a 1m flame at a distance of up to 40m, within 5 seconds. It also provides a wide field of detection in comparison to UV/IR. A case study explores the details of these claims, which is also the focus of a recent white paper.
Dräger’s flame-detection technology partner Micropack conducted the analysis and used HazMap3D software to model a complex industrial installation, and to indicate the detection coverage available with ten Dräger Flame 1750 H2 detectors. A colour-coded analysis displayed the detected fire-risk areas in green, and blind spots in red. And this seemingly showed that it provided 64% coverage, with 36% of the target areas remaining outside the flame detector’s range or obstructed. In comparison, twenty UV/IR flame detectors in the same installation achieved only 44% coverage, leaving 56% unprotected. The conclusion? 3IR technology reduces cost and increases coverage.
Multichannel approach
Unlike hydrocarbon combustion, which is typically detected through CO₂ emissions, hydrogen flames are primarily identified by the presence of water vapour — a difference that appears central to this detection method. The 3IR detector focuses on the 2–4 µm region of the electromagnetic spectrum, where hydrogen’s characteristic spectral features are found. Each of the three separate IR sensors focuses on a specific region of this band: One focuses on the area where combustion signatures are strongest, and the other two provide reference channels, to help distinguish any detected hydrogen flame signature from other potential heat sources in the vicinity. By a continuous comparison of the three signals, the detector is able to filter out sources of false positives such as welding equipment or sunlight.A variety of issues come into play when safeguarding a site that uses or stores hydrogen in any way. When conducting a risk assessment, Dräger advises on issues such as the placement and choice of gas and flame detectors, in addition to matters such as suitable storage locations for hydrogen, and working out where any gas will go if it escapes.
Safeguarding a site may also involve integrating gas and flame detectors with an internal alarm management system, and other systems that can, for example, shut down processes that might carry an explosion risk when combined with hydrogen.
Dräger provides an end-to-end service which also incorporates third-party products such as alarms, “to create a seamless safety infrastructure”.
While the landscape of risks might be unfamiliar to many at this point – or the world is in the process of getting familiar with them – a consistent message from Dräger seems to be that all the risks can be managed. With awareness of the appropriate safeguards, selection of the right technologies, and putting best-practice into action, this promising clean energy source can become as routine as any other form of fuel.
Notes
[1] “Hydrogen: How to meet the safety challenges.” Ebook available from Dräger. https://www.draeger.com/Content/Documents/Content/hydrogen-safety-challenges-ebk-11064-en-master.pdf.
[2] “Detecting the Invisible: Understanding hydrogen flames and choosing the right detector”, PDF, available from Dräger.Hydrogen risk factors – SIDE PANEL
The universe’s lightest element presents its own unique set of risk factors, some of which are listed here.- Explosion risk: While hydrogen is not explosive on its own, it becomes highly explosive when mixed with air in certain concentrations. It also has a relatively low ignition energy. After production, hydrogen will tend to be compressed to prepare it for storage or transport, and this adds to the explosion risk. It also produces a much bigger explosion than natural gas, with around 7x the explosion velocity.
- Leak risk: With its small molecule size, and low viscosity, hydrogen leaks more readily than other fuels such as methane. A container that is “air-tight” for methane, might not necessarily be “air-tight” for hydrogen. This also means pipelines and other structures have to be engineered to hydrogen-ready specifications, and it will be important to ensure there are regular inspections of things like joints in pipelines.
- Threat to structures: The small size of molecules also accounts for hydrogen’s ability to embrittle structures, by permeating their interior. To protect against this, storage tanks tend to be made of stainless steel or composites.
- Forms gas pockets: Its lightness is one important difference with methane, and the fact of hydrogen’s being lighter than air means leaks are not so easily detected at ground level, even when dangerous amounts might be accumulating beneath a nearby ceiling, as Dräger’s literature explains. The placement of gas detectors should reflect this.
- Odourless: Hydrogen is odourless, like methane. An odourant marker is added to the latter (most commonly a particular blend of mercaptans), to get around this nasal invisibility. Such a possibility is being investigated and trialled with hydrogen, but the results are still awaited.
Continue Reading
-
MRI May Aid Early Pancreatic Cancer Detection in Diabetes
TOPLINE:
MRI-based screening in patients older than 50 years with new-onset or deteriorating diabetes detected stage IB pancreatic cancer in a patient with deteriorating diabetes, highlighting the need for targeted screening in this high-risk population.
METHODOLOGY:
- New-onset diabetes in patients older than 50 years was found to increase the risk for pancreatic cancer by six- to eight-fold, and recent evidence suggests that the deterioration of diabetes in individuals with stable, long-standing disease may also be an indicator of subclinical pancreatic cancer.
- Researchers conducted the PANDOME study to evaluate the effectiveness and safety of MRI-based screening for the early detection of pancreatic cancer in patients with new-onset diabetes (n = 97; median age, 61 years; 63.9% women) or deteriorating diabetes (n = 12; median age, 68 years; 58.3% women).
- New-onset diabetes was defined as elevated A1c levels within the past 12 months, whereas deteriorating diabetes was defined as long-standing diabetes (> 2 years) with a > 2% increase in A1c levels over the past 6 months not linked to weight gain or diabetes medication noncompliance.
- All patients underwent MRI/cholangiopancreatography, blood biobanking, and anxiety/depression monitoring; MRI results were scored as normal, benign-abnormal, suspicious, or incidental findings.
TAKEAWAY:
- Compared with patients with new-onset diabetes, those with deteriorating diabetes had significantly higher A1c levels (P = .02), greater weight loss (P = .0038), and increased insulin requirements (P < .0001).
- Among 109 participants, more than 50% had small cystic lesions with an average size of 6 mm, prompting seven endoscopic ultrasound procedures — four of which required biopsies. Of the four pancreatic biopsies performed, one revealed stage IB pancreatic ductal adenocarcinoma in a patient with deteriorating diabetes.
- Extra-pancreatic incidental findings were detected in 8.2% of cases, with two requiring biopsies, revealing one new diagnosis of follicular lymphoma and one diagnosis of recurrent lymphoma.
- According to the Enriching New-Onset Diabetes for Pancreatic Cancer score — where a high-risk score predicts a 3.6% probability of pancreatic cancer within 3 years — the deteriorating diabetes group had a higher proportion of high-risk individuals than the new-onset diabetes group (75% vs 35.6%).
IN PRACTICE:
“Preliminary results from the PANDOME study support further MRI-based PC [pancreatic cancer] screening research efforts in individuals with NOD [new-onset diabetes] and DD [deteriorating diabetes],” the authors concluded.
SOURCE:
This study was led by Richard Frank, MD, Division of Hematology/Oncology, Nuvance Health, Norwalk, Connecticut. It was published online in The Journal of Clinical Endocrinology & Metabolism.
LIMITATIONS:
T his study faced challenges with low accrual rates due to healthcare network realignments and high declination rates by potential participants. Selection bias potentially led to lower detection rates, as most participants were referred by primary care physicians or endocrinologists. Moreover, the majority of participants were White individuals (83%), despite higher pancreatic cancer risk among Black populations, limiting generalizability.
DISCLOSURES:
This study received support from a Tribute to Pamela/The Naughton Family Fund, the Rallye for Pancreatic Cancer, Pacific Crest Trail for Pancreatic Cancer, and the Glenn W. Bailey Foundation. The authors declared no conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Continue Reading
-
Anti-ageing skincare trend millennials retinol social media influence dermatologists advice
The skincare industry has seen a major shift from a 3-step cleansing routines to prioritising anti-ageing products.
Previously, products specifically reserved for older age groups like retinol (a derivative of vitamin A) are now found in the beauty drawers of millennials and Gen Z.
But what is driving this trend? Is it an educated choice based on skincare science or just a byproduct of changing beauty standards and skincare attitude? Although these products promise long-term gains, they also require careful usage and guidance to truly be effective and safe.
CULTURAL, SOCIAL MEDIA INFLUENCES
Society’s obsession with “youthful” and “glowing” skin has created an environment where proactive skincare is celebrated.
With Instagram, healthcare routines have transformed into a content-creation ritual, a habit showcased to the public rather than solely for personal upkeep.
Social media influencers tirelessly promote and disseminate “anti-ageing” tricks, alongside endless viral transformation highlights and product suggestion videos.
Society’s obsession with “youthful” and “glowing” skin has created an environment where proactive skincare is celebrated. (Photo: Getty Images) “I started using anti-ageing products like retinol at around 19, although I don’t use them very often. I was influenced mostly by social media and the people around me who were starting to focus on skincare,” said 21-year-old Maria, who thinks that anti-ageing products could delay her wrinkles.
The idea of “preventive care” has become popular online, not just with dermatologists but also among lifestyle creators.
Preventing wrinkles, fine lines and dullness before they appear is now seen by many as responsible self-care.
Beauty brands have cleverly promoted anti-ageing products as crucial youthful investments, appealing even to individuals showing no signs of ageing.
Terms such as “prevention,” “repair,” and “anti-pollution” position these products as indispensable for the urban youth.
Dr. Amit Bhasin, dermatologist and founder of PrivLux Skin & Wellness Clinic, explains, “This trend is driven by marketing pressure, where beautiful packaging, viral ads, or celebrity-endorsed brands (often without any research or dermatological backing) convince people to start treatments that may not be safe for them.”
When he asks a patient why they purchased a certain product, the reply comes swift: ‘Because I loved the packaging’ or ‘I saw someone famous using it.’
“This kind of impulsive buying, based on aesthetic appeal rather than science, is worrying,” he adds.
Dermatologist Dr. Kiran Sethi, founder of Isya Aesthetics, agrees: “People fall for marketing, that’s why marketing exists. It works. That’s why doctors are needed to sift through the news.”
WHEN SHOULD YOU START AN ANTI-AGEING SKINCARE ROUTINE?
While many young adults turn to anti-ageing products thinking they will improve their skin texture, not everyone is aware of how their skin actually functions at that age.
Skin in 20s is already naturally rich in collagen, the primary building block of the skin, and tends to have faster cell turnover, which is why dermatologists often recommend a minimal, protective routine instead of jumping into active-heavy formulas.
“You are still net positive in collagen until the age of 25 and then the decrease is about 1% a year. But visible ageing typically happens in your 30s. I think we can consider anti-aging products after the age of 30,” Dr. Sethi points out.
Aarushi, 27, started using retinol a few months ago after relocating from London to India. She noticed early signs of comedonal acne and neck lines and wanted to act early.
“To fix these issues, I did some online research, then consulted my mother’s dermatologist and bought a famous K-beauty cream, not recommended by the doctor,” she says.
She uses it two to three times a week, only at night, and has had a relatively smooth experience so far.
“Thankfully I haven’t felt any negative effects until now. To be honest, I haven’t seen any changes in my neckline, but I have seen a huge difference in my acne. My acne has reduced quite a bit since I started using retinol,” she says.
On the other hand, not everyone had professional input before starting. Maria, for instance, admitted, “I didn’t consult a dermatologist beforehand, so I wasn’t fully aware of the potential side effects or how to use it properly.”
While many young adults turn to anti-ageing products thinking they will improve their skin texture, not everyone is aware of how their skin actually functions at that age, say experts. (Photo: Getty Images) Saleha, 28, also reflected on her past use. “I saw people online discussing how retinols help reverse ageing and get rid of fine lines and wrinkles, so that fueled most of my insecurities back then.”
But over time, her approach changed. “Honestly, I’ve never been consistent with it, and it’s totally overhyped. Ageing is natural, we as women have been influenced by society and social media to look a certain way which isn’t ideal.”
CAUTION IS NECESSARY
Many dermatologists now say that overloading on actives at a young age may do more harm than good.
“I see the consequences every day in my clinic, chemical burns, severe pigmentation, skin thinning, or post-inflammatory hyperpigmentation (PIH), all because they self-medicated with actives like retinol without understanding how to use the,” Dr. Bhasin warns.
Dr. Sethi adds that many young people power pack and combine a significant number of actives with rollers and guashas, and get barrier damage resulting in sensitive, rosacea-prone and irritated skin.
“Overdoing it will do the opposite of the goal of great skin. Signs of overuse include red, inflamed, dry, acne-prone and sensitive skin,” she says.
LESS IS MORE
Dermatologists repeatedly emphasise that in your 20s, less is more.
Building a strong foundation with cleanser, moisturiser and sunscreen is more effective than experimenting with powerful actives without supervision.
Introduce retinol later, when its actually needed, doctor says.
For young people, focus on simplistic skincare routines with protective sunblock and antioxidative care to prevent environmental damage.
Other ways to strike a balance is by maintaining a healthy lifestyle like having a balanced diet, getting regular sleep and managing stress.
While the anti-ageing products can be beneficial, their use should be thoughtful and tailored to individual needs.
(Article by Arima Singh)
– Ends
Continue Reading
-
Vaginal microbiome fights back against stubborn BV infections
New research reveals how the vaginal microbiome can sabotage antibiotic treatment, explaining why bacterial vaginosis keeps coming back, and what it will take to finally stop it.
Study: Vaginal pharmacomicrobiomics modulates risk of persistent and recurrent bacterial vaginosis. Image credit: Kateryna Kon/Shutterstock.com
Scientists have reviewed the available literature to document the effect of vaginal microbiome-drug interactions on the efficacy of antibiotics against recurrent bacterial vaginosis (BV). This review has been published in Npj Biofilms and Microbiomes.
Bacterial vaginosis: Prevalence, symptoms, and diagnosis
BV is a common infection occurring in women of reproductive age causing discomfort and pain in the vagina. Although the majority of BV patients experience no symptoms, some women may have a prominent vaginal discharge with a fishy odor, along with burning and itching sensation.
BV is characterized by vaginal bacterial dysbiosis, particularly a loss of Lactobacillus, which may pose severe health threats. For instance, it increases the risk of sexually transmitted infection (STI), pelvic inflammatory disease, preterm birth, and preeclampsia in pregnant women.
Global prevalence of BV varies significantly. A recent survey estimated that approximately 30% of US women of reproductive age have BV, and this number increases to more than 50% in sub-Saharan African women.
Since no single causative agent of BV is known, it is diagnosed using the Nugent Score. It is also diagnosed clinically through nucleic acid amplification tests (NAATs) or by identifying the presence of at least three Amsel criteria, including a pH greater than 4.5, characteristic homogeneous milk-like vaginal discharge, a fishy odor, and 20% clue cells.
However, the authors emphasize that routine screening for asymptomatic BV is not generally recommended, as treatment may not significantly reduce adverse pregnancy outcomes.
High recurrence rate of bacterial vaginosis
Although antibiotic therapy, such as metronidazole, tinidazole, or clindamycin, is recommended to treat BV, a high recurrence rate within one to six months of treatment has been recorded in approximately 20% to 70% of women.
Key contributing factors, rather than a single cause, to high BV recurrence rates are the persistence of protective bacterial biofilm, and antibiotic resistance within the bacterial biofilm and vaginal canal. Other factors that contribute to this recurrence include non-adherence to multidose therapy, continual exchange of pathogenic bacterial vaginosis-associated bacteria (BVAB) between sexual partners pre or post treatment, and inability to restore optimal levels of Lactobacillus in the vaginal microbiome.
How vaginal pharmacomicrobiomics affect the efficacy of antibiotic therapy?
Pharmacomicrobiomics involves the interaction between drugs and microbes, which is crucial for enhancing the scope of precision medicine. It focuses on understanding how microbiome variations affect drug disposition, toxicity, and efficacy. The microbiome present in various anatomic sites, such as the mouth, gut, skin, lungs, and vagina, may either improve or hinder the efficacy of drugs.
Overexpression of a DNA repair protein (RecA) in Bacteroides fragilis, a common gut and vaginal commensal bacterium, elevates resistance to metronidazole. Previous studies have indicated that oral metronidazole only temporarily reinstates healthy vaginal microbiota in patients with recurrent BV. A higher prevalence of Prevotella before treatment and Gardnerella post-treatment has been associated with enhanced risk of BV recurrence.
Many scientists have hypothesized that vaginal microbial dysbiosis is associated with modifications in drug disposition, activity, and toxicity, which contributes to antibiotic resistance and adverse reproductive outcome due to genital infection. For instance, the metabolism of the anti-HIV drug, tenofovir (TFV), by Gardnerella vaginalis has been linked to reduced HIV prevention efficacy. TFV reduced HIV incidence by only 18% in African women with G. vaginalis-dominated (BV-like) microbiota and 61% in women with Lactobacillus-dominant microbiota.
Host-specific and drug-specific factors determine the systematic distribution of drugs in different body parts. Multiple studies have shown that a dysbiotic female genital tract causes BV to increase the local pH by trapping ions that reduce the effectiveness of tenofovir disoproxil fumarate (TDF). It also promotes alterations in other factors essential for the drug compound to migrate across the female genital tract compartment to treat BV.
Previous studies have also shown that T-cell uptake of TFV is influenced by alterations in vaginal microbiota and pH, contributing to the drug’s inconsistent efficacy in BV-positive individuals. An abundance of specific microbes, such as Lactobacillus, may alter the movement of drugs across the genital tract by modifying local drug transporters in a pH-dependent or independent manner. Bacteroides and Prevotella are two common BVAB highly resistant to metronidazole by altering pyruvate fermentation.
The importance of vaginal pH on drug efficacy has also been shown in labor induction for term or preterm birth. It has been speculated that vaginal microbiota could indirectly influence the effectiveness of drugs by altering host drug metabolism and producing bacterial metabolites that compete with the drug receptor.
Reproductive hormones directly regulate the composition and abundance of the vaginal microbiome during the menstrual cycle and pregnancy, which may influence how drugs are absorbed and metabolized, particularly when using vaginal inserts or pessaries.
Transporters recognize and export various antibiotics, including β-lactams, macrolides, and aminoglycosides, to their target sites. Multiple studies have shown that G. vaginalis, a renowned BVAB, upregulates efflux pumps and ABC transporters, which significantly contribute to bacterial colonization and infection of host tissues and multidrug resistance by actively eliminating various antibiotics and metabolites from bacterial cells.
The authors hypothesize that transport proteins expressed on vaginal epithelial cells and bacteria may be exchanged via extracellular vesicles. This speculative but plausible mechanism could further contribute to resistance and drug clearance. In addition to resistance, transporter proteins may influence how efficiently antibiotics reach and accumulate in vaginal tissues, potentially explaining some cases of treatment failure due to insufficient local drug exposure.
Conclusions
The current study hypothesized that the efficacy of recommended antibiotics for treating BV is reduced by vaginal microbiota-associated factors including pH and metabolism, leading to antibiotic resistance. Therefore, to improve therapeutic outcomes and decrease the incidence of persistent and recurrent BV, it is essential to consider the vaginal microbiome-drug interactions and efficacy of antibiotics against recurrent BV.
The authors emphasize exploring novel strategies to enhance treatment, including probiotics, prebiotics, postbiotics, and bacteriophage therapies. They also suggest investigating the potential of transporter/enzyme inhibitors and new drug delivery systems to improve local drug exposure in the vaginal tract.
They conclude that future research should leverage experimental models such as vaginal organ-on-chip systems and personalized metagenomic profiling to better understand these interactions and guide individualized treatment approaches.
Download your PDF copy now!
Journal reference:
- Amabebe, E. et al. (2025) Vaginal pharmacomicrobiomics modulates risk of persistent and recurrent bacterial vaginosis. Npj Biofilms and Microbiomes. 11(1), 1-12. https://doi.org/10.1038/s41522-025-00748-0. https://www.nature.com/articles/s41522-025-00748-0
Continue Reading
-
Certain Plant-Based Foods May Cut Crohn’s Disease Risk
TOPLINE:
A high combined intake of fruits, vegetables, legumes, and potatoes was associated with a reduced risk for Crohn’s disease — driven largely by specific foods such as apples or pears, bananas, mushrooms, and onions or garlic. Alternatively, a high intake of potatoes was associated with an increased risk for ulcerative colitis.
METHODOLOGY:
- The International Organization for the Study of Inflammatory Bowel Disease recommends eating more fruits and vegetables for their fiber benefits, but current guidelines do not distinguish between subcategories despite their differing compositions and potential effects on inflammatory bowel disease (IBD) risk.
- Researchers analyzed data of 341,519 participants without IBD (mean age, 52.1 years; 70% women) from a popular European cohort to evaluate how consumption of individual fruits, vegetables, legumes, and potatoes influenced the risk for Crohn’s disease and ulcerative colitis.
- At baseline, validated food frequency questionnaires were used to assess dietary intake of fruits, vegetables, legumes, and potatoes (including other tubers).
- Participants in the lowest vs highest quartiles had median daily intakes of 291.6 vs 840.9 g/d of combined fruits, vegetables, legumes, and potatoes; 17.0 vs 100.3 g/d of apples/pears; 6.6 vs 14.0 g/d of bananas; 2.1 vs 6.2 g/d of mushrooms; 4.1 vs 11.9 g/d of onions or garlic; and 64.7 vs 82.1 g/d of potatoes.
TAKEAWAY:
- The median follow-up period was 13.4 years, during which 149 participants developed Crohn’s disease and 379 developed ulcerative colitis.
- A higher combined intake of fruits, vegetables, legumes, and potatoes was associated with a lower risk of developing Crohn’s disease (highest vs lowest quartile; adjusted hazard ratio [aHR], 0.44; 95% CI, 0.26-0.76) but not ulcerative colitis (aHR, 1.07; 95% CI, 0.76-1.50).
- A subsequent post hoc analysis showed that the pooled intake of apples or pears, bananas, mushrooms, and onions or garlic was linked to a comparable risk reduction for Crohn’s disease as total fruit, vegetable, legume, and potato intake (highest vs lowest quartile; pooled aHR, 0.58; 95% CI, 0.33-1.02).
- However, a higher intake of potatoes was associated with a higher risk of developing ulcerative colitis (highest vs lowest quartile; aHR, 1.51; 95% CI, 1.05-2.17).
IN PRACTICE:
“In conclusion, we found that high combined intake of fruits, vegetables, legumes, and potatoes is associated with a lower risk of developing CD but not UC. This was particularly apparent for apple/pear, banana, mushrooms, and onion/garlic intakes. A higher risk of UC was observed for a higher intake of potatoes,” the authors of the study wrote.
SOURCE:
This study was led by Antoine Meyer, MD, PhD, Université Paris-Saclay, Villejuif, France. It was published online in the American Journal of Gastroenterology.
LIMITATIONS:
This study relied on food frequency questionnaires measured only at baseline, which may not have fully captured dietary changes over time. The mostly older, female population may not have represented the broader European or younger populations. As with all observational studies, residual confounding from unmeasured factors could not be ruled out.
DISCLOSURES:
The cohort was supported by the International Agency for Research on Cancer, the Department of Epidemiology and Biostatistics, School of Public Health, and other sources. Some authors declared receiving speaker fees, grants, consulting fees, and travel support from various pharmaceutical companies.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Continue Reading
-
PM vows to eradicate polio from Pakistan – RADIO PAKISTAN
- PM vows to eradicate polio from Pakistan RADIO PAKISTAN
- New polio case from KP takes tally to 14 Dawn
- Pakistan records one more poliovirus case; countrywide tally reaches 14 The Hindu
- Pakistan: Over 60,000 polio vaccine refusals reported during April campaign, says report ANI News
- Pakistan reports 14th polio case in 2025 Samaa TV
Continue Reading
-
Cardiometabolic heart failure with preserved ejection fraction: from molecular signatures to personalized treatment | Cardiovascular Diabetology
Tan YT, Wenzelburger F, Lee E, Heatlie G, Leyva F, Patel K, et al. The pathophysiology of heart failure with normal ejection fraction: exercise echocardiography reveals complex abnormalities of both systolic and diastolic ventricular function involving torsion, untwist, and longitudinal motion. J Am Coll Cardiol. 2009;54(1):36–46.
Google Scholar
Rosch S, Kresoja KP, Besler C, Fengler K, Schöber AR, von Roeder M, et al. Characteristics of heart failure with preserved ejection fraction across the range of left ventricular ejection fraction. Circulation. 2022;146(7):506–18.
Google Scholar
Pecchia B, Samuel R, Shah V, Newman E, Gibson GT. Mechanisms ofexercise intolerance in heart failure with preserved ejection fraction (HFpEF). Heart Fail Rev. 2025. https://doi.org/10.1007/s10741-025-10504-3.
Google Scholar
Miranda JJ, Barrientos-Gutiérrez T, Corvalan C, Hyder AA, Lazo-Porras M, Oni T, et al. Understanding the rise of cardiometabolic diseases in low- and middle-income countries. Nat Med. 2019;25(11):1667–79.
Google Scholar
Shahim B, Kapelios CJ, Savarese G, Lund LH. Global public health burden of heart failure: an updated review. Card Fail Rev. 2023;9: e11.
Google Scholar
Campbell P, Rutten FH, Lee MM, Hawkins NM, Petrie MC. Heart failure with preserved ejection fraction: everything the clinician needs to know. Lancet. 2024;403(10431):1083–92.
Google Scholar
Samson R, Jaiswal A, Ennezat PV, Cassidy M, Le Jemtel TH. Clinical phenotypes in heart failure with preserved ejection fraction. J Am Heart Assoc. 2016;5(1): e002477.
Google Scholar
Wong ND, Sattar N. Cardiovascular risk in diabetes mellitus: epidemiology, assessment and prevention. Nat Rev Cardiol. 2023;20(10):685–95.
Google Scholar
Lopez-Jimenez F, Almahmeed W, Bays H, Cuevas A, Di Angelantonio E, le Roux CW, et al. Obesity and cardiovascular disease: mechanistic insights and management strategies. A joint position paper by the world heart federation and world obesity federation. Eur J Prev Cardiol. 2022;29(17):2218–37.
Google Scholar
Kenchaiah S, Chesebro JH. The epidemiologic association between obesity and heart failure. Am Coll Cardiol Ext Learn. 2017;49(8):4–6.
Google Scholar
Hong Y, Gao Z, Wei H, Wei Y, Qiu Z, Xiao J, et al. Bi-directional association of body size and composition with heart failure: a Mendelian randomization study. Int J Cardiol. 2024;407: 132069.
Google Scholar
Kosiborod MN, Abildstrøm SZ, Borlaug BA, Butler J, Rasmussen S, Davies M, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069–84.
Google Scholar
Kramer CM, Borlaug BA, Zile MR, Ruff D, DiMaria JM, Menon V,et al. Tirzepatide reduces LV mass and paracardiac adipose tissue in obesity-related heart failure: SUMMIT CMR substudy. J Am Coll Cardiol. 2025;85(7):699–706.
Google Scholar
Hullon D, Subeh GK, Volkova Y, Janiec K, Trach A, Mnevets R. The role of glucagon-like peptide-1 receptor (GLP-1R) agonists in enhancing endothelial function: a potential avenue for improving heart failure with preserved ejection fraction (HFpEF). Cardiovasc Diabetol. 2025;24(1):70.
Google Scholar
Hall JL, Terzic A. Heart failure transcriptome. Circ Cardiovasc Genet. 2011;4(5):469–71.
Google Scholar
Alpert MA, Karthikeyan K, Abdullah O, Ghadban R. Obesity and cardiac remodeling in adults: mechanisms and clinical implications. Prog Cardiovasc Dis. 2018;61(2):114–23.
Google Scholar
Mishra S, Kass DA. Cellular and molecular pathobiology of heart failure with preserved ejection fraction. Nat Rev Cardiol. 2021;18(6):400–23.
Google Scholar
Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1789–858.
Walters GWM, Yeo JL, Bilak JM, Pepper C, Gulsin GS, Freeman SC, et al. The effectiveness of lifestyle interventions in heart failure with preserved ejection fraction: a systematic review and network meta-analysis. J Card Fail. 2024;30(8):994–1009.
Google Scholar
Carbone S, Lavie CJ. Disparate effects of obesity on survival and hospitalizations in heart failure with preserved ejection fraction. Int J Obes (Lond). 2020;44(7):1543–5.
Google Scholar
Hamo CE, DeJong C, Hartshorne-Evans N, Lund LH, Shah SJ, Solomon S, et al. Heart failure with preserved ejection fraction. Nat Rev Dis Primers. 2024;10(1):55.
Google Scholar
Khan MS, Fonarow GC, Khan H, Greene SJ, Anker SD, Gheorghiade M, et al. Renin-angiotensin blockade in heart failure with preserved ejection fraction: a systematic review and meta-analysis. ESC Heart Fail. 2017;4(4):402–8.
Google Scholar
Castiglione V, Gentile F, Ghionzoli N, Chiriacò M, Panichella G, Aimo A, et al. Pathophysiological rationale and clinical evidence for neurohormonal modulation in heart failure with preserved ejection fraction. Card Fail Rev. 2023;9: e09.
Google Scholar
Lund LH,Benson L, Dahlström U, Edner M. Association between use of renin-angiotensin system antagonists and mortality in patients with heart failure and preserved ejection fraction. JAMA. 2012;308(20):2108–17.
Google Scholar
Nassif ME, Windsor SL, Borlaug BA, Kitzman DW, Shah SJ, Tang F, et al. The SGLT2 inhibitor dapagliflozin in heart failure with preserved ejection fraction: a multicenter randomized trial. Nat Med. 2021;27(11):1954–60.
Google Scholar
Anker SD, Butler J, Filippatos G, Ferreira JP, Bocchi E, Böhm M, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451–61.
Google Scholar
Peikert A, Bart BA, Vaduganathan M, Claggett BL, Kulac IJ, Kosiborod MN, et al. Contemporary use and implications of beta-blockers in patients with HFmrEF or HFpEF: the DELIVER trial. JACC Heart Fail. 2024;12(4):631–44.
Google Scholar
Salah HM, Fudim M, Al’Aref SJ, Khan MS, Almarzooq ZI, Devabhaktuni SR, et al. Meta-analysis of efficacy of sacubitril/valsartan in heart failure with preserved ejection fraction. Am J Cardiol. 2021;145:165–8.
Google Scholar
Thangaraj PM, Oikonomou EK, Dhingra LS, Aminorroaya A, Jayaram R, Suchard MA, et al. Computational phenomapping of randomized clinical trial participants to enable assessment of their real-world representativeness and personalized inference. Circ Cardiovasc Qual Outcomes. 2025. https://doi.org/10.1161/CIRCOUTCOMES.124.011306.
Google Scholar
Bozkurt B, Ezekowitz J. Substance and substrate: LVEF and sex subgroup analyses of PARAGON-HF and PARADIGM-HF trials. Circulation. 2020;141(5):362–6.
Google Scholar
Solomon SD, McMurray JJV, Anand IS, Ge J, Lam CSP, Maggioni AP, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609–20.
Google Scholar
Solomon SD, McMurray JJV, Vaduganathan M, Claggett B, Jhund PS, Desai AS, et al. Finerenone in Heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2024;391(16):1475–85.
Google Scholar
Stoicescu L, Crişan D, Morgovan C, Avram L, Ghibu S. Heart failure with preserved ejection fraction: the pathophysiological mechanisms behind the clinical phenotypes and the therapeutic approach. Int J Mol Sci.2024;25(2):794.
Google Scholar
Patel R, Wadid M, Makwana B, Kumar A, Khadke S, Bhatti A, et al. GLP-1 receptor agonists among patients with overweight or obesity, diabetes, and HFpEF on SGLT2 inhibitors. JACC Heart Fail. 2024;12(11):1814–26.
Google Scholar
Lam CSP, Gamble GD, Ling LH, Sim D, Leong KTG, Yeo PSD, et al. Mortality associated with heart failure with preserved vs. reduced ejection fraction in a prospective international multi-ethnic cohort study. Eur Heart J. 2018;39(20):1770–80.
Google Scholar
Prausmüller S, Weidenhammer A, Heitzinger G, Spinka G, Goliasch G, Arfsten H, et al. Obesity in heart failure with preserved ejection fraction with and without diabetes: risk factor or innocent bystander? Eur J Prev Cardiol. 2023;30(12):1247–54.
Google Scholar
Borlaug BA, Sharma K, Shah SJ, Ho JE. Heart failure with preserved ejection fraction. JACC. 2023;81(18):1810–34.
Google Scholar
Savji N, Meijers WC, Bartz TM, Bhambhani V, Cushman M, Nayor M, et al. The Association of obesity and cardiometabolic traits with incident HFpEF and HFrEF. JACC Heart Fail. 2018;6(8):701–9.
Google Scholar
Li C, Xu MM, Wang K, Adler AJ, Vella AT, Zhou B. Macrophage polarization and meta-inflammation. Transl Res. 2018;191:29–44.
Google Scholar
Girona J, Soler O, Samino S, Junza A, Martínez-Micaelo N, García-Altares M, et al. Lipidomics reveals myocardial lipid composition in a murine model of insulin resistance induced by a high-fat diet. Int J Mol Sci. 2024;25(5):2702.
Google Scholar
Geng J, Zhang X, Guo Y, Wen H, Guo D, Liang Q, et al. Moderate-intensity interval exercise exacerbates cardiac lipotoxicity in high-fat, high-calories diet-fed mice. Nat Commun. 2025;16(1):613.
Google Scholar
Oishi Y, Manabe I. Organ system crosstalk in cardiometabolic disease in the age of multimorbidity. Front Cardiovasc Med. 2020;7:64.
Google Scholar
Atzemian N, Mohammed S, Di Venanzio L, Gorica E, Costantino S, Ruschitzka F, et al. Cardiometabolic disease management: influences from epigenetics. Epigenomics. 2025;17:463.
Google Scholar
Schleh MW, Caslin HL, Garcia JN, Mashayekhi M, Srivastava G, Bradley AB, et al. Metaflammation in obesity and its therapeutic targeting. Sci Transl Med. 2023;15(723):eadf9382.
Google Scholar
Zhang H, Zhou W, Wang X, Men H, Wang J, Xu J, et al. Exacerbation by knocking-out metallothionein gene of obesity-induced cardiac remodeling is associated with the activation of CARD9 signaling. Int J Biol Sci. 2025;21(3):1032–46.
Google Scholar
Kersten S. The impact of fasting on adipose tissue metabolism. Biochim Biophys Acta Mol Cell Biol Lipids. 2023;1868(3): 159262.
Google Scholar
Lu J, Zhao J, Meng H, Zhang X. Adipose Tissue-resident immune cells in obesity and type 2 diabetes. Front Immunol. 2019;10:1173.
Google Scholar
Barcia Durán JG, Das D, Gildea M, Amadori L, Gourvest M, Kaur R, et al. Immune checkpoint landscape of human atherosclerosis and influence of cardiometabolic factors. Nat Cardiovasc Res. 2024;3(12):1482–502.
Google Scholar
Baloglu I, Turkmen K, Selcuk NY, Tonbul HZ, Ozcicek A, Hamur H, et al. The relationship between visceral adiposity index and epicardial adipose tissue in patients with type 2 diabetes mellitus. Exp Clin Endocrinol Diabetes. 2021;129(5):390–5.
Google Scholar
Li C, Liu X, Adhikari BK, Chen L, Liu W, Wang Y, et al. The role of epicardial adipose tissue dysfunction in cardiovascular diseases: an overview of pathophysiology, evaluation, and management. Front Endocrinol (Lausanne). 2023;14:1167952.
Google Scholar
Villasante Fricke AC, Iacobellis G. Epicardial adipose tissue: clinical biomarker of cardio-metabolic risk. Int J Mol Sci. 2019;20(23):5989.
Google Scholar
van Woerden G, Gorter TM, Westenbrink BD, Willems TP, van Veldhuisen DJ, Rienstra M. Epicardial fat in heart failure patients with mid-range and preserved ejection fraction. Eur J Heart Fail. 2018;20(11):1559–66.
Google Scholar
Janssen-Telders C, Eringa EC, de Groot JR, de Man FS, Handoko ML. The role of epicardial adipose tissue remodelling in heart failure with preserved ejection fraction. Cardiovasc Res. 2025. https://doi.org/10.1093/cvr/cvaf056.
Google Scholar
Zhou Y, Wei Y, Wang L, Wang X, Du X, Sun Z, et al. Decreased adiponectin and increased inflammation expression in epicardial adipose tissue in coronary artery disease. Cardiovasc Diabetol. 2011;10:2.
Google Scholar
Venteclef N, Guglielmi V, Balse E, Gaborit B, Cotillard A, Atassi F, et al. Human epicardial adipose tissue induces fibrosis of the atrial myocardium through the secretion of adipo-fibrokines. Eur Heart J. 2015;36(13):795–805a.
Google Scholar
Basurto Acevedo L, Barrera Hernández S, Fernández Muñoz MJ, Saucedo García RP, Rodríguez Luna AK, Martínez MC. An increase in epicardial fat in women is associated with thrombotic risk. Clin Investig Arterioscler. 2018;30(3):112–7.
Google Scholar
Agra RM, Teijeira-Fernández E, Pascual-Figal D, Jesús SM, Fernández-Trasancos Á, Sierra J, et al. Differential behavior between S100A9 and adiponectin in coronary artery disease. Plasma Epicardial Fat Life Sci. 2014;100(2):147–51.
Google Scholar
Whitman J, Kozaily E, Michos ED, Silverman DN, Fudim M, Mentz RJ, et al. Epicardial fat in heart failure and preserved ejection fraction: novel insights and future perspectives. Curr Heart Fail Rep. 2025;22(1):13.
Google Scholar
van Woerden G, van Veldhuisen DJ, Westenbrink BD, de Boer RA, Rienstra M, Gorter TM. Connecting epicardial adipose tissue and heart failure with preserved ejection fraction: mechanisms, management and modern perspectives. Eur J Heart Fail. 2022;24(12):2238–50.
Google Scholar
Pugliese NR, Paneni F, Mazzola M, De Biase N, Del Punta L, Gargani L, et al. Impact of epicardial adipose tissue on cardiovascular haemodynamics, metabolic profile, and prognosis in heart failure. Eur J Heart Fail. 2021;23(11):1858–71.
Google Scholar
Yen CH, Lin JL, Sung KT, Su CH, Huang WH, Chen YY, et al. Association of free fatty acid binding protein with central aortic stiffness, myocardial dysfunction and preserved ejection fraction heart failure. Sci Rep. 2021;11(1):16501.
Google Scholar
Sun Q, Güven B, Wagg CS, Almeida de Oliveira A, Silver H, Zhang L, et al. Mitochondrial fatty acid oxidation is the major source of cardiac adenosine triphosphate production in heart failure with preserved ejection fraction. Cardiovasc Res. 2024;120(4):360–71.
Google Scholar
Lamounier-Zepter V, Look C, Alvarez J, Christ T, Ravens U, Schunck W-H, et al. Adipocyte fatty acid-binding protein suppresses cardiomyocyte contraction. Circ Res. 2009;105(4):326–34.
Google Scholar
Schulze PC, Drosatos K, Goldberg IJ. Lipid use and misuse by the heart. Circ Res. 2016;118(11):1736–51.
Google Scholar
D’Arcy MS. Mitophagy in health and disease. Molecular mechanisms, regulatory pathways, and therapeutic implications. Apoptosis. 2024;29(9–10):1415–28.
Google Scholar
Castillo EC, Vázquez-Garza E, Yee-Trejo D, García-Rivas G, Torre-Amione G. What is the role of the inflammation in the pathogenesis of heart failure? Curr Cardiol Rep. 2020;22(11):139.
Google Scholar
Tsampasian V, Swift AJ, Assadi H, Chowdhary A, Swoboda P, Sammut E, et al. Myocardial inflammation and energetics by cardiac MRI: a review of emerging techniques. BMC Med Imaging. 2021;21(1):164.
Google Scholar
AbouEzzeddine OF, Kemp BJ, Borlaug BA, Mullan BP, Behfar A, Pislaru SV, et al. Myocardial energetics in heart failure with preserved ejection fraction. Circ Heart Fail. 2019;12(10):e006240.
Google Scholar
Mihalik SJ, Goodpaster BH, Kelley DE, Chace DH, Vockley J, Toledo FG, et al. Increased levels of plasma acylcarnitines in obesity and type 2 diabetes and identification of a marker of glucolipotoxicity. Obesity (Silver Spring). 2010;18(9):1695–700.
Google Scholar
Tourki B, Halade GV. Heart failure syndrome with preserved ejection fraction is a metabolic cluster of non-resolving inflammation in obesity. Front Cardiovasc Med. 2021;8: 695952.
Google Scholar
Packer M, Kitzman DW. Obesity-related heart failure with a preserved ejection fraction: the mechanistic rationale for combining inhibitors of aldosterone, neprilysin, and sodium-glucose cotransporter-2. JACC Heart Fail. 2018;6(8):633–9.
Google Scholar
Mohammed SA, Ambrosini S, Lüscher T, Paneni F, Costantino S. Epigenetic control of mitochondrial function in the vasculature. Front Cardiovasc Med. 2020;7:28.
Google Scholar
Liu H, Huang Y, Zhao Y, Kang GJ, Feng F, Wang X, et al. Inflammatory macrophage interleukin-1β mediates high-fat diet-induced heart failure with preserved ejection fraction. JACC Basic Transl Sci. 2023;8(2):174–85.
Google Scholar
Smolgovsky S, Bayer AL, Kaur K, Sanders E, Aronovitz M, Filipp ME, et al. Impaired T cell IRE1α/XBP1 signaling directs inflammation in experimental heart failure with preserved ejection fraction. J Clin Invest. 2023. https://doi.org/10.1172/JCI171874.
Google Scholar
Herold J, Kalucka J. Angiogenesis in adipose tissue: the interplay between adipose and endothelial cells. Front Physiol. 2020;11: 624903.
Google Scholar
Ong SG, Lee WH, Theodorou L, Kodo K, Lim SY, Shukla DH, et al. HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore. Cardiovasc Res. 2014;104(1):24–36.
Google Scholar
Fusaru AM, Pisoschi CG, Bold A, Taisescu C, Stănescu R, Hîncu M, et al. Hypoxia induced VEGF synthesis in visceral adipose depots of obese diabetic patients. Rom J Morphol Embryol. 2012;53(4):903–9.
Google Scholar
Glennon-Alty L, Hackett AP, Chapman EA, Wright HL. Neutrophils and redox stress in the pathogenesis of autoimmune disease. Free Radic Biol Med. 2018;125:25–35.
Google Scholar
Medina-Leyte DJ, Zepeda-García O, Domínguez-Pérez M, González-Garrido A, Villarreal-Molina T, Jacobo-Albavera L. Endothelial dysfunction, inflammation and coronary artery disease: potential biomarkers and promising therapeutical approaches. Int J Mol Sci. 2021;22(8):3850.
Google Scholar
Saavedra-Alvarez A, Pereyra KV, Toledo C, Iturriaga R, Del Rio R. Vascular dysfunction in HFpEF: potential role in the development, maintenance, and progression of the disease. Front Cardiovasc Med. 2022;9:1070935.
Google Scholar
Momot K, Wojciechowska M, Krauz K, Czarzasta K, Puchalska L, Zarębiński M, et al. Endoplasmic reticulum stress and expression of nitric oxide synthases in heart failure with preserved and with reduced ejection fraction—pilot study. Cardiol J. 2024;31(6):885–94.
Google Scholar
Bilak JM, Alam U, Miller CA, McCann GP, Arnold JR, Kanagala P. Microvascular dysfunction in heart failure with preserved ejection fraction: pathophysiology, assessment, prevalence and prognosis. Card Fail Rev. 2022;8: e24.
Google Scholar
Wijnen M, Duschek EJJ, Boom H, van Vliet M. The effects of antidiabetic agents on heart failure. Neth Heart J. 2022;30(2):65–75.
Google Scholar
Hsu CN, Hsuan CF, Liao D, Chang JK, Chang AJ, Hee SW, et al. Anti-diabetic therapy and heart failure: recent advances in clinical evidence and molecular mechanism. Life (Basel). 2023;13(4):1024.
Google Scholar
Yoshida Y, Shimizu I, Minamino T. Capillaries as a therapeutic target for heart failure. J Atheroscler Thromb. 2022;29(7):971–88.
Google Scholar
Wang T, Tian J, Jin Y. VCAM1 expression in the myocardium is associated with the risk of heart failure and immune cell infiltration in myocardium. Sci Rep. 2021;11(1):19488.
Google Scholar
Ristagno G, Fumagalli F, Bottazzi B, Mantovani A, Olivari D, Novelli D, et al. Pentraxin 3 in cardiovascular disease. Front Immunol. 2019;10:823.
Google Scholar
Gogiraju R, Bochenek ML, Schäfer K. Angiogenic endothelial cell signaling in cardiac hypertrophy and heart failure. Front Cardiovasc Med. 2019;6:20.
Google Scholar
Kolijn D, Kovács Á, Herwig M, Lódi M, Sieme M, Alhaj A, et al. Enhanced cardiomyocyte function in hypertensive rats with diastolic dysfunction and human heart failure patients after acute treatment with soluble guanylyl cyclase (sGC) activator. Front Physiol. 2020;11:345.
Google Scholar
Kansakar S, Guragain A, Verma D, Sharma P, Dhungana B, Bhattarai B, et al. Soluble guanylate cyclase stimulators in heart failure. Cureus. 2021;13(9): e17781.
Google Scholar
Cho JG, Lee A, Chang W, Lee MS, Kim J. Endothelial to mesenchymal transition represents a key link in the interaction between inflammation and endothelialdysfunction. Front Immunol. 2018;9:294.
Google Scholar
Shen J, Liang J, Rejiepu M, Ma Z, Zhao J, Li J, et al. Analysis of immunoinfiltration and EndoMT based on TGF-β signaling pathway-related genes in acute myocardial infarction. Sci Rep. 2024;14(1):5183.
Google Scholar
Zhang L, He J, Wang J, Liu J, Chen Z, Deng B, et al. Knockout RAGE alleviates cardiac fibrosis through repressing endothelial-to-mesenchymal transition (EndMT) mediated by autophagy. Cell Death Dis. 2021;12(5):470.
Google Scholar
Valero-Muñoz M, Oh A, Faudoa E, Bretón-Romero R, El Adili F, Bujor A, et al. Endothelial-mesenchymal transition in heart failure with a preserved ejection fraction: insights into the cardiorenal syndrome. Circ Heart Fail. 2021;14(9): e008372.
Google Scholar
Zhang Y, Zhu Z, Wang T, Dong Y, Fan Y, Sun D. TGF-β1-containing exosomes from cardiac microvascular endothelial cells mediate cardiac fibroblast activation under high glucose conditions. Biochem Cell Biol. 2021;99(6):693–9.
Google Scholar
Singh V, Kaur R, Kumari P, Pasricha C, Singh R. ICAM-1 and VCAM-1: gatekeepers in various inflammatory and cardiovascular disorders. Clin Chim Acta. 2023;548: 117487.
Google Scholar
Li C, He J, Zhong X, Gan H, Xia Y. CX3CL1/CX3CR1 axis contributes to angiotensin II-induced vascular smooth muscle cell proliferation and inflammatory cytokine production. Inflammation. 2018;41(3):824–34.
Google Scholar
Zuo L, Prather ER, Stetskiv M, Garrison DE, Meade JR, Peace TI, et al. Inflammaging and oxidative stress in human diseases: from molecular mechanisms to novel treatments. Int J Mol Sci. 2019;20(18):4472.
Google Scholar
Béland S, Désy O, El Fekih R, Marcoux M, Thivierge MP, Desgagné JS, et al. Expression of class II human leukocyte antigens on human endothelial cells shows high interindividual and intersubclass heterogeneity. J Am Soc Nephrol. 2023;34(5):846–56.
Google Scholar
Yap C, Mieremet A, de Vries CJM, Micha D, de Waard V. Six shades of vascular smooth muscle cells illuminated by KLF4 (Krüppel-Like Factor 4). Arterioscler Thromb Vasc Biol. 2021;41(11):2693–707.
Google Scholar
Chen R, McVey DG, Shen D, Huang X, Ye S. Phenotypic switching of vascular smooth muscle cells in atherosclerosis. J Am Heart Assoc. 2023;12(20): e031121.
Google Scholar
Li N, Cao Y, Li Y, Zhang K, Zhang L, Luo Q, et al. Predictive value of epicardial adipose tissue volume for early detection of left ventricular dysfunction in patients suspected of coronary artery disease. Clin Radiol. 2025;81: 106760.
Google Scholar
Zurek M, Aavik E, Mallick R, Ylä-Herttuala S. Epigenetic regulation of vascular smooth muscle cell phenotype switching in atherosclerotic artery remodeling: a mini-review. Front Genet. 2021;12: 719456.
Google Scholar
Elia L, Quintavalle M, Zhang J, Contu R, Cossu L, Latronico MV, et al. The knockout of miR-143 and -145 alters smooth muscle cell maintenance and vascular homeostasis in mice: correlates with human disease. Cell Death Differ. 2009;16(12):1590–8.
Google Scholar
Costantino S, Libby P, Kishore R, Tardif JC, El-Osta A, Paneni F. Epigenetics and precision medicine in cardiovascular patients: from basic concepts to the clinical arena. Eur Heart J. 2018;39(47):4150–8.
Google Scholar
Hamdani N, Costantino S, Mügge A, Lebeche D, Tschöpe C, Thum T, et al. Leveraging clinical epigenetics in heart failure with preserved ejection fraction: a call for individualized therapies. Eur Heart J. 2021;42(20):1940–58.
Google Scholar
Benincasa G, Pepin ME, Russo V, Cacciatore F, D’Alto M, Argiento P, et al. High-resolution DNA methylation changes reveal biomarkers of heart failure with preserved ejection fraction versus reduced ejection fraction. Basic Res Cardiol. 2025;120(2):347–61.
Google Scholar
Gilsbach R, Preissl S, Grüning BA, Schnick T, Burger L, Benes V, et al. Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease. Nat Commun. 2014;5:5288.
Google Scholar
Xu X, Tan X, Tampe B, Nyamsuren G, Liu X, Maier LS, et al. Epigenetic balance of aberrant Rasal1 promoter methylation and hydroxymethylation regulates cardiac fibrosis. Cardiovasc Res. 2015;105(3):279–91.
Google Scholar
Tao H, Yang JJ, Chen ZW, Xu SS, Zhou X, Zhan HY, et al. DNMT3A silencing RASSF1A promotes cardiac fibrosis through upregulation of ERK1/2. Toxicology. 2014;323:42–50.
Google Scholar
Cheng W, Li X, Liu D, Cui C, Wang X. Endothelial-to-mesenchymal transition: role in cardiac fibrosis. J Cardiovasc Pharmacol Ther. 2021;26(1):3–11.
Google Scholar
Ford TJ, Corcoran D, Padmanabhan S, Aman A, Rocchiccioli P, Good R, et al. Genetic dysregulation of endothelin-1 is implicated in coronary microvascular dysfunction. Eur Heart J. 2020;41(34):3239–52.
Google Scholar
Bain CR, Ziemann M, Kaspi A, Khan AW, Taylor R, Trahair H, et al. DNA methylation patterns from peripheral blood separate coronary artery disease patients with and without heart failure. ESC Heart Fail. 2020;7(5):2468–78.
Google Scholar
Landim-Vieira M, Childers MC, Wacker AL, Garcia MR, He H, Singh R, et al. Post-translational modification patterns on β-myosin heavy chain are altered in ischemic and nonischemic human hearts. Elife. 2022. https://doi.org/10.7554/eLife.74919.
Google Scholar
Funamoto M, Imanishi M, Tsuchiya K, Ikeda Y. Roles of histone acetylation sites in cardiac hypertrophy and heart failure. Front Cardiovasc Med. 2023;10:1133611.
Google Scholar
Atzemian N, Dovrolis N, Ragia G, Portokallidou K, Kolios G, Manolopoulos VG. Beyond the rhythm: in silico identification of key genes and therapeutic targets in atrial fibrillation. Biomedicines. 2023;11(10):2632.
Google Scholar
Mengozzi A, Costantino S, Paneni F, Duranti E, Nannipieri M, Mancini R, et al. Targeting SIRT1 Rescues age- and obesity-induced microvascular dysfunction in ex vivo human vessels. Circ Res. 2022;131(6):476–91.
Google Scholar
Zhang Y, Mi SL, Hu N, Doser TA, Sun A, Ge J, et al. Mitochondrial aldehyde dehydrogenase 2 accentuates aging-induced cardiac remodeling and contractile dysfunction: role of AMPK, Sirt1, and mitochondrial function. Free Radic Biol Med. 2014;71:208–20.
Google Scholar
Costantino S, Mengozzi A, Velagapudi S, Mohammed SA, Gorica E, Akhmedov A, et al. Treatment with recombinant Sirt1 rewires the cardiac lipidome and rescues diabetes-related metabolic cardiomyopathy. Cardiovasc Diabetol. 2023;22(1):312.
Google Scholar
Costantino S, Mohammed SA, Ambrosini S, Telesca M, Mengozzi A, Walavalkar K, et al. Chromatin rewiring by SETD2 drives lipotoxic injury in cardiometabolic HFpEF. Circ Res. 2025.
Patel BM, Raghunathan S, Porwal U. Cardioprotective effects of magnesium valproate in type 2 diabetes mellitus. Eur J Pharmacol. 2014;728:128–34.
Google Scholar
Zhu W, Trivedi CM, Zhou D, Yuan L, Lu MM, Epstein JA. Inpp5f is a polyphosphoinositide phosphatase that regulates cardiac hypertrophic responsiveness. Circ Res. 2009;105(12):1240–7.
Google Scholar
Nomura Y, Nakano M, Woo Sung H, Han M, Pandey D. Inhibition of HDAC6 activity protects against endothelial dysfunction and Atherogenesis in vivo: a role for HDAC6 neddylation. Front Physiol. 2021;12: 675724.
Google Scholar
Mohammed SA, Gorica E, Albiero M, Karsai G, Mengozzi A, Caravaggi CM, et al. Targeting SETD7 rescues diabetes-induced impairment of angiogenic response by transcriptional repression of semaphorin 3G. Diabetes. 2025. https://doi.org/10.2337/db24-0997.
Google Scholar
Miranda JB, Lunardon G, Lima VM, de Oliveira ST, Lino CA, Jensen L, et al. Set7 deletion prevents glucose intolerance and improves the recovery of cardiac function after ischemia and reperfusion in obese female mice. Cell Physiol Biochem. 2022;56(3):293–309.
Google Scholar
Roh J, Hill JA, Singh A, Valero-Muñoz M, Sam F. Heart failure with preserved ejection fraction: heterogeneous syndrome. Diverse Preclin Models Circ Res. 2022;130(12):1906–25.
Google Scholar
Zakeri R, Cowie MR. Heart failure with preserved ejection fraction: controversies, challenges and future directions. Heart. 2018;104(5):377–84.
Google Scholar
Shah SJ. Precision medicine for heart failure with preserved ejection fraction: an overview. J Cardiovasc Transl Res. 2017;10(3):233–44.
Google Scholar
Strianese O, Rizzo F,Ciccarelli M, Galasso G, D’Agostino Y, Salvati A, et al. Precision and personalized medicine: how genomic approach improves the management of cardiovascular and neurodegenerative disease. Genes (Basel). 2020;11(7):747.
Google Scholar
Gorica E, Mohammed SA, Ambrosini S, Calderone V, Costantino S, Paneni F. Epi-drugs in heart failure. Front Cardiovasc Med. 2022;9: 923014.
Google Scholar
Lu J, Qian S, Sun Z. Targeting histone deacetylase in cardiac diseases. Front Physiol. 2024;15:1405569.
Google Scholar
Gordon JW, Shaw JA, Kirshenbaum LA. Multiple facets of NF-κB in the heart: to be or not to NF-κB. Circ Res. 2011;108(9):1122–32.
Google Scholar
Yang J, He J, Ismail M, Tweeten S, Zeng F, Gao L, et al. HDAC inhibition induces autophagy and mitochondrial biogenesis to maintain mitochondrial homeostasis during cardiac ischemia/reperfusion injury. J Mol Cell Cardiol. 2019;130:36–48.
Google Scholar
Khurana I, Maxwell S, Royce S, Mathiyalagan P, Karagiannis T, Mazarakis N, et al. SAHA attenuates Takotsubo-like myocardial injury by targeting an epigenetic Ac/Dc axis. Signal Transduct Target Ther. 2021;6(1):159.
Google Scholar
Tsujikawa LM, Fu L, Das S, Halliday C, Rakai BD, Stotz SC, et al. Apabetalone (RVX-208) reduces vascular inflammation in vitro and in CVD patients by a BET-dependent epigenetic mechanism. Clin Epigenet. 2019;11(1):102.
Jahagirdar R, Zhang H, Azhar S, Tobin J, Attwell S, Yu R, et al. A novel BET bromodomain inhibitor, RVX-208, shows reduction of atherosclerosis in hyperlipidemic ApoE deficient mice. Atherosclerosis. 2014;236(1):91–100.
Google Scholar
Duan Q, McMahon S, Anand P, Shah H, Thomas S, Salunga HT, et al. BET bromodomain inhibition suppresses innate inflammatory and profibrotic transcriptional networks in heart failure. Sci Transl Med. 2017;9(390):eaah5084.
Google Scholar
Nicholls SJ, Schwartz GG, Buhr KA, Ginsberg HN, Johansson JO, Kalantar-Zadeh K, et al. Apabetalone and hospitalization for heart failure in patients following an acute coronary syndrome: a prespecified analysis of the BETonMACE study. Cardiovasc Diabetol. 2021;20(1):13.
Google Scholar
Chistiakov DA, Orekhov AN, Bobryshev YV. Cardiac-specific miRNA in cardiogenesis, heart function, and cardiac pathology (with focus on myocardial infarction). J Mol Cell Cardiol. 2016;94:107–21.
Google Scholar
Foinquinos A, Batkai S, Genschel C, Viereck J, Rump S, Gyöngyösi M, et al. Preclinical development of a miR-132 inhibitor for heart failure treatment. Nat Commun. 2020;11(1):633.
Google Scholar
Batkai S, Genschel C, Viereck J, Rump S, Bär C, Borchert T, et al. CDR132L improves systolic and diastolic function in a large animal model of chronic heart failure. Eur Heart J. 2021;42(2):192–201.
Google Scholar
van Rooij E, Sutherland LB, Thatcher JE, DiMaio JM, Naseem RH, Marshall WS, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci U S A. 2008;105(35):13027–32.
Google Scholar
Han Y, Xie H, Liu Y, Gao P, Yang X, Shen Z. Effect of metformin on all-cause and cardiovascular mortality in patients with coronary artery diseases: a systematic review and an updated meta-analysis. Cardiovasc Diabetol. 2019;18(1):96.
Google Scholar
Dies RM, Jackson CN, Flanagan CJ, Sinnathamby ES, Spillers NJ, Potharaju P, et al. The evolving role of vericiguat in patients with chronic heart failure. Cureus. 2023;15(12): e49782.
Google Scholar
Di Fusco SA, Alonzo A, Aimo A, Matteucci A, Intravaia RCM, Aquilani S, et al. ANMCO position paper on vericiguat use in heart failure: from evidence to place in therapy. Eur Heart J Suppl. 2023;25(Suppl D):D278–86.
Google Scholar
Chen C, Lv J, Liu C. Vericiguat in patients with heart failure across the spectrum of left ventricular ejection fraction: a patient-level, pooled meta-analysis of VITALITY-HFpEF and VICTORIA. Front Endocrinol (Lausanne). 2024;15:1335531.
Google Scholar
Van Tassell BW, Buckley LF, Carbone S, Trankle CR, Canada JM, Dixon DL, et al. Interleukin-1 blockade in heart failure with preserved ejection fraction: rationale and design of the diastolic heart failure anakinra response trial 2 (D-HART2). Clin Cardiol. 2017;40(9):626–32.
Google Scholar
Van Tassell BW, Trankle CR, Canada JM, Carbone S, Buckley L, Kadariya D, et al. IL-1 blockade in patients with heart failure with preserved ejection fraction. Circ Heart Fail. 2018;11(8): e005036.
Google Scholar
Alogna A, Koepp KE, Sabbah M, Espindola Netto JM, Jensen MD, Kirkland JL, et al. Interleukin-6 in patients with heart failure and preserved ejection fraction. JACC Heart Fail. 2023;11(11):1549–61.
Google Scholar
Chia YC, Kieneker LM, van Hassel G, Binnenmars SH, Nolte IM, van Zanden JJ, et al. Interleukin 6 and development of heart failure with preserved ejection fraction in the general population. J Am Heart Assoc. 2021;10(11): e018549.
Google Scholar
Petrie M, Borlaug B, Buchholtz K, Ducharme A, Hvelplund A, Ping CLS, et al. HERMES: effects of ziltivekimab versus placebo on morbidity and mortality in patients with heart failure with mildly reduced or preserved ejection fraction and systemic inflammation. J Cardiac Fail. 2024;30(1):126.
Michaëlsson E, Lund LH, Hage C, Shah SJ, Voors AA, Saraste A, et al. Myeloperoxidase inhibition reverses biomarker profiles associated with clinical outcomes in HFpEF. JACC Heart Fail. 2023;11(7):775–87.
Google Scholar
Vacca A, Wang R, Nambiar N, Capone F, Farrelly C, Mostafa A, et al. Lifestyle interventions in cardiometabolic HFpEF: dietary and exercise modalities. Heart Fail Rev. 2024. https://doi.org/10.1007/s10741-024-10439-1.
Google Scholar
La Gerche A, Howden EJ, Haykowsky MJ, Lewis GD, Levine BD, Kovacic JC. Heart failure with preserved ejection fraction as an exercise deficiency syndrome: JACC focus seminar 2/4. J Am Coll Cardiol. 2022;80(12):1177–91.
Google Scholar
Kitzman DW, Brubaker P, Morgan T, Haykowsky M, Hundley G, Kraus WE, et al. Effect of caloric restriction or aerobic exercise training on peak oxygen consumption and quality of life in obese older patients with heart failure with preserved ejection fraction: a randomized clinical trial. JAMA. 2016;315(1):36–46.
Google Scholar
Diab A, Dastmalchi LN, Gulati M, Michos ED. A heart-healthy diet for cardiovascular disease prevention: where are we now? Vasc Health Risk Manag. 2023;19:237–53.
Google Scholar
Zielinski MR, Gibbons AJ. Neuroinflammation, Sleep, and circadian rhythms. Front Cell Infect Microbiol. 2022;12: 853096.
Google Scholar
Wiech P, Würzburger L, Rossi VA, Caselli S, Schmied CM, Niederseer D. Hypertensive response to exercise, hypertension and heart failure with preserved ejection fraction (HFpEF)-a continuum of disease? Wien Klin Wochenschr. 2023;135(23–24):685–95.
Google Scholar
Lee VYJ, Houston L, Perkovic A, Barraclough JY, Sweeting A, Yu J, et al. The effect of weight loss through lifestyle interventions in patients with heart failure with preserved ejection fraction-A systematic review and meta-analysis of randomised controlled trials. Heart Lung Circ. 2024;33(2):197–208.
Google Scholar
Billingsley HE, Carbone S, Driggin E, Kitzman DW, Hummel SL. Dietary interventions in heart failure with preserved ejection fraction: a scoping review. JACC Adv. 2025;4(1): 101465.
Google Scholar
Continue Reading
-
Cervical Cancer Risk Overlooked After Age 65
TOPLINE:
Analysis of over 2.1 million women in China revealed that those aged 65 years or older vs those younger than 65 years had significantly higher rates of high-risk human papillomavirus (hr-HPV) infection (13.67% vs 8.08%) and cervical cancer (0.092% vs 0.01%) although most guidelines recommend discontinuing screening for women aged 65 years or older with a normal screening history.
METHODOLOGY:
- Researchers conducted a retrospective analysis of cervical cancer screening data from Shenzhen, China (2017-2023), to assess hr-HPV distribution and cervical intraepithelial neoplasia grade 2 or worse (CIN2+) prevalence in women aged 65 years or older vs those younger than 65 years.
- Data collection encompassed 628 healthcare facilities, including 496 community health centers, 94 hospitals, 11 maternal and child health hospitals, and 27 other medical facilities.
- Clinical records included demographic information, cytology results, HPV testing covering 14 hr-HPV genotypes (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68), and colposcopy/biopsy outcomes.
- Analysis included 2,152,766 complete records from an initial collection of 2,580,829, yielding an 83.4% data validity rate.
TAKEAWAY:
- Analysis of 2,152,766 records revealed that women aged 65 years or older (n = 17,420; 0.81%) vs those younger than 65 years showed higher hr-HPV prevalence (13.67% vs 8.08%), CIN2+ detection rate (0.333% vs 0.155%), and cancer rate (0.092% vs 0.01%; P for all < .001).
- Single, double, and triple hr-HPV infections were found in 10.56%, 2.32%, and 0.57% of women aged 65 years or older, with CIN2+ detection rates of 2.01%, 2.73%, and 4.04%, respectively, all exceeding rates in those younger than 65 years (P < .001).
- A significant dose-response relationship emerged between hr-HPV infections and CIN2+ risk in women aged 65 years or older (P for trend < .001), with odds ratios being 55.86 (95% CI, 21.81-143.07), 65.95 (95% CI, 22.63-192.18), and 85.45 (95% CI, 24.15-302.35) for single, double, and triple infections, respectively.
IN PRACTICE:
“Currently, there is a significant global gap in cervical cancer prevention for older women, and urgent action is needed. First, screening and early diagnosis for women aged ≥ 65 should be strengthened, including affordable screening services and age-appropriate technologies to detect and treat precancerous lesions. Additionally, community engagement, health education, and media campaigns can raise awareness of cervical cancer risks and prevention among older women, encouraging active participation in screening programs,” authors of the study wrote.
SOURCE:
The study was led by Zichen Ye, He Wang, and Yingyu Zhong, who served as joint first authors. It was published online in Gynecology and Obstetrics Clinical Medicine.
LIMITATIONS:
The study faced several limitations despite using high-quality, large-sample, real-world cervical cancer screening data collected over 7 years in Shenzhen. Because women aged 65 years or older were not included in the national target screening population, participants may have had symptoms or concerns, introducing potential selection bias. The low number of hr-HPV infections in this age group led to some results trending toward extremes, affecting result stability. Additionally, data from a single region in China limited generalizability to other populations. The researchers could not obtain specific information about the types of cytologic detection products and HPV genotyping products used, which may have affected result precision and comparability.
DISCLOSURES:
The study was supported by the Sanming Project of Medicine in Shenzhen (SZSM202211032). The authors reported having no relevant conflicts of interest.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Continue Reading
