Category: 8. Health

  • Impact of Diabetes on Coronary Angiographic Findings in ST-Elevation Myocardial Infarction Patients: A Comparative Study

    Impact of Diabetes on Coronary Angiographic Findings in ST-Elevation Myocardial Infarction Patients: A Comparative Study


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  • AIC ‘aware’ of suspected botulism cases which reports claim have left ‘hundreds of cows’ dead | Farm News

    AIC ‘aware’ of suspected botulism cases which reports claim have left ‘hundreds of cows’ dead | Farm News

    All material is copyright Farmers Guardian Limited. Farmers Guardian and Farmersguardian.com are registered trademarks of Farmers Guardian Limited, Unit 4 Fulwood Park, Caxton Road, Fulwood, Preston, England, PR2 9NZ. Farmers Guardian Limited is registered in England and Wales with company registration number 07931451. Part of Arc network, www.arc-network.com.

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  • Good vibrations could revolutionize assisted reproductive technology

    Good vibrations could revolutionize assisted reproductive technology

    In the quest to address infertility, Cornell researchers have developed a groundbreaking device that could simplify and automate oocyte cumulus removal, a critical step in assisted reproductive technologies. 

    Their vibration-powered chip not only simplifies a complex procedure but also extends it to areas of the world lacking skilled embryologists or well-funded labs, reducing overall costs. This offers hope to millions of couples struggling with infertility – and makes fertility treatments more accessible worldwide.

    “This platform is a potential game-changer,” said Alireza Abbaspourrad, associate professor of food chemistry and ingredient technology in food science in the College of Agriculture and Life Sciences (CALS). “It reduces the need for skilled technicians, minimizes contamination risks and ensures consistent results – all while being portable and cost-effective.”

    He is co-author of “On-Chip Oocyte Cumulus Removal using Vibration Induced Flow,” published Sept. 5 in the journal Lab on a Chip.

    Doctors treating infertility need to do a critical step: gently separate protective cumulus cells from oocytes, the developing egg cells. The process, known as cumulus removal (CR), is essential for evaluating oocyte maturity before spermatozoon injection, or ensuring successful fertilization after insemination in vitro fertilization (IVF). 

    Traditionally, CR relies on manual pipetting: by flushing the single oocyte repeatedly with a micropipette, cumulus cells are detached from the oocyte. However, the technique demands precision, expertise and significant time. Errors can lead to damaged oocytes or failed fertilization, making the procedure a delicate and labor-intensive task.

    The team’s innovation: a disposable, open-surface chip that uses vibrations, which they call vibration-induced flow, to automate CR. The chip features a spiral array of micropillars that create a whirling flow when vibrated, separating smaller cumulus cells from larger oocytes.

    “The process is fast, efficient, noninvasive and more consistent, while reducing manual labor and preserving embryo development outcomes,” said Amirhossein Favakeh, a doctoral candidate in Abbaspourrad’s lab and a co-author of the study. “The oocytes remain safely in the loading chamber, while the cumulus cells are swept into an adjacent collection well.”

    The researchers tested the device on mouse oocytes, which share genetic similarities with human eggs. They optimized the system by adjusting vibration power, exposure time and enzyme concentration. They found that the platform could denude up to 23 oocytes simultaneously without any loss or damage. Even freeze-thawed oocytes, which are typically more fragile, were successfully processed.

    To ensure the safety of the technique, the team compared fertilization and embryo development rates between oocytes denuded manually and those treated with vibration induced flow. The results were nearly identical: fertilization rates were 90.7% for manual pipetting and 93.1% for vibration induced flow, while the rate of formation of blastocysts, balls of cells formed early in a pregnancy, were 50.0% and 43.1%, respectively.

    “This shows that our method doesn’t compromise the developmental potential of the oocytes,” Abbaspourrad said.

    The implications of this technology extend far beyond fertility clinics. The chip’s ability to separate particles of different sizes could be applied to other biomedical fields, such as cancer cell isolation or microfluidic research. Its low cost and ease of use make it particularly appealing for regions with limited access to advanced medical facilities.

    Favakeh said this approach has the potential to democratize access to fertility treatment by reducing the reliance on expensive equipment and highly trained embryologists, which might allow these procedures to be brought to underserved areas.

    “Ordinarily, the whole process is costly and delicate; clinics invest a lot of time in training and it is very dependent on human resources,” Abbaspourrad said. “With this, you don’t need a highly trained human to do it. And what is really important is there is almost no chance of damaging or losing the cell.”

    The team plans to expand their research to include human oocytes and explore applications in intracytoplasmic sperm injection, in which CR is performed prior to fertilization. They also aim to refine the chip’s design for broader use in cell manipulation and sorting.

    For now, the Cornell scientists are celebrating a major step forward in assisted reproductive technologies, they said.

    This is a small device with a big impact, Abbaspourrad said.

    “Replacing tedious manual methods with a simple vibration-based chip improves the speed, safety and consistency of oocyte preparation,” he said, “making fertility treatments more accessible and reliable.”

    Co-authors include Amir Mokhtare, a postdoctoral fellow in Abbaspourrad’s lab; Yi Athena Ren, assistant professor of reproductive biology in animal science (CALS); and Hanxue Zhang, a postdoctoral associate in Ren’s lab.

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  • Smoking May Drive Pancreatic Cancer Progression, Study Finds

    Smoking May Drive Pancreatic Cancer Progression, Study Finds

    A study from the University of Michigan’s Rogel Cancer Center revealed a previously unknown biological pathway explaining why smoking not only increases the risk of pancreatic cancer but also accelerates its progression. The findings, published in Cancer Discovery, illuminate how toxins from cigarettes trigger immune-mediated mechanisms that drive tumor growth and spread.1

    Person holding cigarette | Image Credit: © methaphum – stock.adobe.com

    Pancreatic Cancer

    Pancreatic cancer is notoriously aggressive, ranking among the deadliest cancers due to late diagnosis and poor response to therapy. Known risk factors include chronic pancreatitis, obesity, diabetes, family history, and especially smoking, which has long been associated with both increased incidence and poorer outcomes. However, the precise molecular basis by which smoking exacerbates disease progression has been largely misunderstood.1,2

    Smoking’s role in cancer development is well established, with tobacco-related carcinogens broadly implicated in various tumor types. For pancreatic cancer specifically, smoking has been linked to roughly 20% of cases, and heavy smokers face worse survival outcomes than non-smokers. This new study deepens clinical understanding by uncovering the immune system’s role in amplifying the tumor-promoting effects of cigarette toxins.3

    The Study

    The researchers administered a chemical carcinogen commonly found in cigarette smoke to mice bearing pancreatic tumors, aiming to assess its effects on the immune landscape, particularly IL-22, a cytokine previously implicated in tumor microenvironments. In doing so, they discovered an immune mechanism that magnifies tumor aggression.1,2

    “It dramatically changed the way the tumors behave. They grew much bigger, they metastasized throughout the body. It was really quite dramatic,” Timothy L. Frankel, MD, co-director of the Rogel and Blondy Center for Pancreatic Cancer and Maud T. Lane Professor of Surgical Oncology at Michigan Medicine, and senior study author, said in a news release.2

    Study Methods

    The experimental approach involved treating tumor-bearing mice with a smoke-related chemical ligand. Researchers observed tumor behavior in both immunocompetent mice and those lacking functioning immune systems. This comparison revealed that the carcinogen’s effects hinged on immune activity. They then investigated immune cell populations and identified regulatory T cells (Tregs) that produce IL-22 and suppress anti-tumor immunity. Depletion of Tregs in mice neutralized the tumor-accelerating impact of the chemical. The team validated these findings using human immune cells and tissue samples from patients, comparing immune profiles of smokers versus non-smokers with pancreatic cancer.1,2

    Findings

    The researchers discovered that a chemical carcinogen from cigarette smoke fueled rapid tumor growth and metastasis in mice—but only when the immune system was intact. A subset of regulatory T cells proved to be key drivers, simultaneously releasing IL-22 and suppressing anti-tumor immune responses. When these T cells were eliminated, the carcinogen’s tumor-promoting effects disappeared entirely.1,2

    “These T-regulatory cells have the ability to both make IL22 but also massively suppress any anti-tumor immunity. It’s a two-pronged attack. When we eliminated all the Treg cells from these mice, we reversed the entire ability of the cigarette chemical to let the tumor grow,” Frankel said.2

    Human validation revealed that smokers with pancreatic cancer exhibited higher levels of these IL-22–producing Tregs compared with non-smokers. The team also demonstrated that a pharmacological inhibitor targeting the chemical’s signaling could shrink tumors—highlighting therapeutic potential.1,2

    “If we are able to inhibit the super suppressive cells, we might also unlock natural anti-tumor immunity,” Frankel explained. “This could be even further activated by current immunotherapies, which do not work well in pancreatic cancer because of the immunosuppressive environment.”2

    Conclusion

    This study offers compelling insight into how smoking amplifies pancreatic cancer risk and lethality through immune modulation. By identifying IL-22–producing T-regs as potent facilitators of tumor growth—especially in response to tobacco-related carcinogens—it opens avenues for targeted treatments and risk-tailored approaches. Inhibiting this pathway could not only slow disease progression but also enhance the efficacy of existing immunotherapies, which have so far struggled in pancreatic cancer due to its immunosuppressive environment.

    “There’s a potential that we need to treat smokers who develop pancreatic cancer differently,” Frankel said. “We may also need to screen smokers more closely for pancreatic cancer development. There is not a great screening mechanism, but people who smoke should be educated about symptoms to look out for and consider referrals to a high-risk clinic.”2

    REFERENCES
    1. Griffith B, Kadiyala P, McGue J, et al. Aryl hydrocarbon receptor ligands drive pancreatic cancer initiation and progression through pro-tumorigenic T cell polarization. Cancer Discov. September 4, 2025. Doi:10.1158/2159-8290.CD-25-0377
    2. Study shows how smoking drives pancreatic cancer. News Release. September 4, 2025. Accessed September 5, 2025. https://www.eurekalert.org/news-releases/1096775
    3. Yuan C, Morales-Oyarvide V, Babic A, et al. Cigarette smoking and pancreatic cancer survival. J Clin Oncol. March 30, 2017. doi: 10.1200/JCO.2016.71.2026

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  • Passive Smoke Exposure in Prepubescent Males Affects Lung Function in Children, Grandchildren

    Passive Smoke Exposure in Prepubescent Males Affects Lung Function in Children, Grandchildren

    A new study has found that paternal prepubertal passive smoke exposure was associated with impaired lung function trajectories in offspring.1

    “Recently, there has been increasing interest in intergenerational transmission of exposure to risk factors. Some emerging evidence has suggested maternal passive smoke exposure during their own intrauterine life as a risk factor for childhood asthma in their offspring. Active paternal smoking before age 15 years (prepuberty) increased the risk of childhood asthma and early lung function deficits in their offspring. The association between active paternal prepubertal smoking and asthma even persisted into adulthood in their offspring,” Jiacheng Liu, PhD candidate, Allergy and Lung Health Unit, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Victoria, Australia, and colleagues wrote.1 “Our preliminary analysis extended from active smoking to passive smoke exposure during paternal prepuberty and identified an association between this paternal smoke exposure and childhood asthma in their offspring.2 Thus, we hypothesized that the intergenerational association of passive smoke exposure before paternal completing puberty might persist well into offspring adulthood, impairing their lifetime lung function trajectory.”

    Liu and colleagues analyzed data from 890 father-offspring pairs from the Tasmanian Longitudinal Health Study. The offspring were probands in the original cohort in TAHS who underwent spirometry at 6 time points from ages 7 to 53 years. Lung function trajectories, including forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC) and FEV1/FVC), were previously derived using group-based trajectory modeling. Fathers reported their own passive smoke exposure prior to age 15. The investigators used multinomial logistic regressions to assess associations between paternal prepubertal passive smoke exposure and lung function trajectories in offspring. They also assessed active paternal smoking, offspring passive smoke exposure and respiratory illnesses during childhood, and subsequent active smoking, as potential mediations and interactions.

    Liu and colleagues found that paternal prepubertal passive smoke exposure was associated with below average FEV1 (adjusted multinomial OR [aMOR], 1.56; 95% CI, 1.05-2.31) and early low-rapid decline FEV1/FVC trajectories (aMOR, 2.30; 95% CI, 1.07-4.94) in offspring. Furthermore, offspring exposed to childhood passive smoke had an augmented association with below average FEV1 trajectory (aMOR, 2.36; 95% CI, 1.34-4.13; P = .003).1

    For the link between paternal prepubertal passive smoke exposure and offspring below-average FEV1 trajectory, active paternal smoking, active offspring smoking, and childhood passive smoke exposure contributed 13.7% (95% CI, 7.7%–59.5%), 13.4% (95% CI, 7.6%–52.4%), and 10.9% (95% CI, 6.0%–47.4%), respectively. Other mediators of offspring asthma/wheeze, bronchitis, and pneumonia/pleurisy showed a limited effect, with each contributing ≤2.0%, while preterm birth, low birth weight, and childhood food allergy showed no mediation. Overall, all mediators explained 14.1% of the total effect.1

    For the association with early low–rapid decline FEV1/FVC trajectory, offspring asthma/wheeze accounted for 14.8% (95% CI, 7.6%–73.7%), with childhood passive smoke exposure and active paternal smoking contributing 12.4% (95% CI, 6.4%–57.7%) and 11.3% (95% CI, 6.0%–53.5%), respectively. Other mediators contributed <7%. Collectively, all mediators explained 10.1% of the total effect.1

    “In conclusion, this study revealed that paternal prepubertal passive smoke exposure was associated with impaired pre-COPD lung function trajectories across the first 6 decades of their offspring’s lives, including the below average FEV1 and early low-rapid decline FEV1/FVC trajectories. These findings suggest that smoking may adversely affect lung function not only in smokers but also in their children and grandchildren. The association of such paternal exposure was augmented when offspring were also exposed to passive smoke during childhood, highlighting an opportunity for intervention. Fathers exposed to tobacco smoke during prepuberty may still reduce risk for future generations by avoiding smoking around their children. The weaker associations observed for other impaired lung function trajectories should be interpreted with caution,” Liu and colleagues said.2

    References
    1. Liu J, Perret JL, Lodge CJ, et al. Paternal prepubertal passive smoke exposure is related to impaired lung function trajectories from childhood to middle age in their offspring. Thorax Published online September 2, 2025. doi: 10.1136/thorax-2024-222482.
    2. Liu J, Bowatte G, Pham J, et al. Pre-pubertal smoke exposure of fathers and increased risk of offspring asthma: a possible transgenerational effect. Eur Respir J. 2022;60: 2200257. doi:10.1183/13993003.00257-2022

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  • Respiratory Variability as a Potential Biomarker of Disease Impact, An

    Respiratory Variability as a Potential Biomarker of Disease Impact, An

    Oscar FC van den Bosch,1,&ast; Johan PA van Lennep,2,&ast; Ricardo Alvarez-Jimenez,1 Henriët van Middendorp,2 Andrea WM Evers,2 Monique AH Steegers,1 Patrick Schober,1 Stephan A Loer1

    1Department of Anesthesiology, Amsterdam UMC, Location Vrije Universiteit, Amsterdam, The Netherlands; 2Institute of Psychology, Leiden University, Leiden, The Netherlands

    Correspondence: Oscar FC van den Bosch, Department of Anesthesiology, Amsterdam UMC, Location Vrije Universiteit, ZH 6F 003, De Boelelaan 1117, Amsterdam, 1081 HV, The Netherlands, Email [email protected]

    Purpose: Fibromyalgia is a complex multisystem disorder characterized by generalized chronic pain. While its etiology remains largely unclear, neuroinflammation, chronic stress, and autonomic dysregulation may play significant roles. Resultantly, respiratory patterns could serve as both a biomarker and a therapeutic target in fibromyalgia. We hypothesized that fibromyalgia impact, anxiety, depression, pain intensity, and pain sensitivity are associated with reduced respiratory variability.
    Patients and methods: In this observational study, twenty-three female participants with fibromyalgia completed the Revised Fibromyalgia Impact Questionnaire (FIQR) and Hospital Anxiety and Depression Scale (HADS). Chronic pain intensity was assessed using a numerical rating scale. Pain sensitivity was measured using pain pressure thresholds, wind-up pain, and aftersensations. Respiratory rate, respiratory rate variability, and tidal volume variability were measured noninvasively using a thoracic bioimpedance electrode during restful waiting.
    Results: No association was observed of respiratory variability with fibromyalgia impact, anxiety, chronic pain intensity, wind-up pain, and aftersensations. Higher depression scores were associated with lower tidal volume variability (r = − 0.45, 95% CI: − 0.04 to − 0.73, p = 0.033). Additionally, higher pain pressure thresholds correlated with lower respiratory rate variability (R = − 0.43, 95% CI: − 0.02 to − 0.72, p = 0.039) and tidal volume variability (R = − 0.47, 95% CI: − 0.07 to − 0.74, p = 0.023).
    Conclusion: While no direct association was found between respiratory variability and overall fibromyalgia impact, respiratory variability was associated with depression and pain sensitivity, both of which influence quality of life. These findings suggest that respiratory variability may have potential as a biomarker reflecting specific symptom dimensions of fibromyalgia. Further research is warranted.

    Keywords: chronic pain, fibromyalgia, respiration, variability, pain sensitivity, biomarker

    Introduction

    Fibromyalgia is a complex disorder characterized by chronic, widespread nociplastic pain, with clinical features suggestive of central sensitization mechanisms.1 While its etiology remains largely unclear, systemic factors such as neuroinflammation, chronic stress, and autonomic dysregulation have been proposed to play significant roles.2 Despite its profound impact on quality of life, treatment options for fibromyalgia remain limited. Emerging therapeutic approaches are predominantly non-pharmacological, with breathing exercises showing particular promise.3,4 The potential benefit of breathing exercises may be linked to the connection between respiration, inflammation, and autonomic dysregulation.5–7 Consequently, respiratory patterns could serve as both a biomarker and a therapeutic target in fibromyalgia.

    The respiratory pattern in healthy subjects naturally varies over time, showing consistent fluctuations in rate, rhythm, and depth.8,9 These fluctuations reflect the body’s adjustment to changing needs in internal and external environments and result from various physiological inputs and chemical feedback loops.10,11 More specifically, the respiratory centers receive and process multiple signals from different parts of the body, including central and peripheral chemoreceptors, pulmonary stretch receptors, and joint receptors, as well as from brain regions responsible for processing emotions. Notably, anxiety and depression are common in fibromyalgia patients and can influence their respiratory patterns.

    Pain and breathing are closely linked bidirectionally. Acute pain typically triggers an increase in respiration, including an increase in inspiratory flow, respiratory rate, and tidal volume; however, the effects on respiratory variability are still not fully understood.12 Chronic pain is associated with hyperventilation, which tends to decrease when pain is alleviated.13 Conversely, voluntary control of breathing can significantly impact the perception of pain. For instance, slow, deep breathing has analgesic effects and enhances parasympathetic (vagal) activity;14 however, this effect is less pronounced in individuals with chronic pain.15

    Given the complex interplay between pain and breathing, we hypothesized that disease impact, anxiety, depression, and pain sensitivity are related to reduced spontaneous variability in respiratory parameters of patients with fibromyalgia. If such a relationship exists, respiratory variability analysis could be a promising diagnostic tool. Moreover, the application of specific breathing techniques might beneficially affect chronic pain-related symptoms. Our aim was to examine the relationships between respiratory variability and disease impact, anxiety, depression, and pain sensitivity in patients with fibromyalgia.

    Methods

    Study Setting

    This exploratory study was a pre-planned sub-study of a larger randomized controlled trial which aimed to investigate the effects of pharmacological conditioning with s-ketamine on pain hypersensitivity in patients with fibromyalgia. The study was approved by the Medical Ethics Committee of Leiden University (The Netherlands) on 14 September 2022 (reference NL73444.058.21) and was prospectively registered in the EudraCT database (reference 2019-004812-73). The study complies with the Declaration of Helsinki. All participants provided written informed consent. This study was conducted between March 2023 and March 2024 and adhered to the Strengthening the Reporting of Observational Studies in Epidemiology statement. The study was conducted at Amsterdam UMC, location VUmc, a university hospital in the Netherlands. Regarding data sharing, the deidentified participant data is available from the corresponding author upon reasonable request.

    Funding

    The Dutch Arthritis Society (ReumaNL) and the NWO Stevin grant, both awarded to A. Evers, the Department of Health, Medical and Neuropsychology, Leiden University, and the Department of Anesthesiology, Amsterdam UMC, location Vrije Universiteit, provided funding.

    Patient Population

    Women (18–75 years) with chronic pain due to fibromyalgia, diagnosed by a rheumatologist, were eligible for inclusion in this study.16 Participants were recruited via outpatient clinics, patient organizations, and online advertisements via social media. Potential participants were excluded if they had a medical diagnosis other than fibromyalgia that could explain their chronic pain symptoms. Severe psychiatric comorbidities unrelated to the symptoms of fibromyalgia, including current or previous dependence on strong analgesics, alcohol, or drugs, were exclusion criteria. Additional exclusion criteria included caffeine use within 12 hours before the trial, cardiac or respiratory comorbidity, a body mass index > 35 kg/m2, and pregnancy or breastfeeding. Recorded patient characteristics included age, height, weight, educational level, and concomitant medical conditions.

    Outcomes

    The overall impact of fibromyalgia was assessed using the revised Fibromyalgia Impact Questionnaire (FIQR), which evaluates disease burden across three domains: function, overall impact, and symptoms.17 The total score is calculated by summing individual item responses and is normalized to a 0–100 scale, where higher scores reflect a greater disease burden. The presence and severity of anxiety and depression were assessed using the Hospital Anxiety and Depression Scale (HADS). The two subscales for anxiety and depression both range from 0–23, where higher scores reflect more severe symptoms.

    Baseline chronic pain intensity was quantified using a numerical rating scale (NRS; 0–10).

    Pain sensitivity was assessed using three quantitative sensory tests: pain thresholds (PPTs), wind-up pain, and aftersensation.18,19 The quantitative sensory tests were performed with a handheld analogue algometer capable of exerting a force of up to 10 kg (Force Dial; Wagner Instruments, Greenwich, CT, USA). Pressure stimuli were applied to the thenar muscles of the dominant hand and ipsilateral tibialis anterior. The PPTs were examined by applying three different pressure stimuli (kg force) to three neighboring sites on the hand and lower leg. The pressures required to elicit the first moment of pain were averaged to calculate the mean pressure threshold in kilograms force.19 The mean pressure thresholds were calculated for each body site. Wind-up pain was measured using temporal summation, determined by applying pressure pain at the pain threshold level, while participants were asked to rate the first, fifth, and tenth stimuli on an NRS scale.19 A single temporal summation (wind-up pain) score was obtained by subtracting the first from the tenth (last) stimulus. After-sensations were determined by asking participants to rate late pain (on the NRS) 15s after the tenth summation stimulus on the hand and lower leg and subtracting this pain score from the tenth stimulus.

    Respiratory Variability

    Respiratory measurements were performed using an impedance-based, non-invasive respiratory volume monitor (ExSpiron, Respiratory Motion, Waltham, MA, USA) with a thoracic electrode. This monitor continuously measures respiratory rate and changes in tidal volume with clinically appropriate accuracy.20 The measured values were stored in internal memory as averages over 60-second periods. All baseline measurements were taken during 30 minutes of restful waiting. We calculated the quantitative variability of breathing parameters (ie, respiratory rate, tidal volume, and minute ventilation) over the 30-min period using the coefficient of variation, defined as the ratio between the standard deviation and mean of a time series.10

    Statistical Analysis

    As this was an exploratory study and no prior data were available in this specific context, no formal sample size calculation could be conducted. The findings may serve as a basis for estimating appropriate sample sizes in future, adequately powered studies. Data were analyzed using R software (2021, R Core Team, Vienna, Austria). Numerical data were assessed using histograms and Q-Q plots, and subsequently tested for non-normality using the Shapiro–Wilk test. Normally distributed data were described as mean (standard deviation), whereas non-normally distributed data were presented as medians (interquartile ranges). To examine correlations between respiratory variability and other variables, Spearman’s rank correlation with a 95% confidence interval and significance level (p-value) were calculated.21 Statistical significance was defined as p < 0.05.22

    Results

    We recruited 54 participants; 14 declined participation, 12 did not meet eligibility criteria, and respiratory data were incompletely captured or stored in 5 cases. Consequently, data from 23 patients with chronic pain due to fibromyalgia were included in the final analysis. The patient characteristics and baseline pain assessments are presented in Table 1. We analyzed 1,380 measurements of respiratory rate and tidal volume.

    Table 1 Baseline Characteristics

    The mean respiratory rate was 15.5 ± 2.3 breaths/min (mean ± SD), mean variability of the respiratory rate was 0.201 ± 0.039 (mean ± SD), and mean variability of tidal volume was 0.233 ± 0.081 (mean ± SD). The median fibromyalgia disease impact score (FIQR) was 42 (interquartile range: 34–59; range: 13–77), indicating a mild to severe disease impact. The median anxiety score (HADS) was 6 (interquartile range: 6–8; range: 1–14), indicating normal to borderline abnormal (mild) anxiety. The median depression score (HADS) was 6 (interquartile range: 4.5 to 10.5; range: 1–15), indicating normal to borderline abnormal (mild) depression. The median chronic pain intensity (NRS) was 4 (interquartile range: 2.5 to 5.0; range, 1–8), indicating mild to moderate chronic pain intensity. Fibromyalgia disease impact (FIQR score) correlated with pain intensity (r = 0.48, 95% confidence interval: 0.04–0.76, p = 0.034) but not with anxiety or depression scores.

    No association was found between the respiratory variability parameters and the impact of fibromyalgia (Figure 1A–C).

    Figure 1 Correlations between respiratory variability and fibromyalgia impact in women with fibromyalgia syndrome. Respiratory parameters were measured during 30 min of restful waiting. Variabilities in the respiratory rate and tidal volume were calculated as coefficients of variation. The fibromyalgia impact was measured using the Revised Fibromyalgia Impact Questionnaire (FIQR). (A) Mean respiratory rate, (B) Variability of respiratory rate, (C) Variability of tidal volume. R: Spearman’s rank correlation coefficient.

    The associations between anxiety and depression (HADS scores) and respiratory variability are shown in Figures 2A–C and 3A–C. We observed a negative association between the HADS score for depression and variability in tidal volume (r = −0.45, 95% confidence interval: −0.04 to −0.73, p = 0.033) but not the variability in respiratory rate. We found no association between anxiety and respiratory variability.

    Figure 2 Correlations between anxiety and respiratory variability in women with fibromyalgia syndrome. Anxiety was assessed using the Hospital Anxiety and Depression Scale (Hads). Respiratory parameters were measured during 30 min of restful waiting. Variabilities in the respiratory rate and tidal volume were calculated as coefficients of variation. (A) Mean respiratory rate, (B) Variability of respiratory rate, (C) Variability of tidal volume. R: Spearman’s rank correlation coefficient.

    Figure 3 Correlations between depression and respiratory variability in women with fibromyalgia syndrome. Depression was assessed using the Hospital Anxiety and Depression Scale (Hads). Respiratory parameters were measured during 30 min of restful waiting. Variabilities in the respiratory rate and tidal volume were calculated as coefficients of variation. (A) Mean respiratory rate, (B) Variability of respiratory rate, (C) Variability of tidal volume. R: Spearman’s rank correlation coefficient.

    The associations between chronic pain intensity and respiratory variability are shown in Figure 4A–C. No association was observed between pain intensity and respiratory variability.

    Figure 4 Correlations between chronic pain intensity and respiratory variability in women with fibromyalgia syndrome. Chronic pain intensity was measured using the Numerical Rating Scale (NRS). Respiratory parameters were measured during 30 min of restful waiting. Variabilities in the respiratory rate and tidal volume were calculated as coefficients of variation. (A) Mean respiratory rate, (B) Variability of respiratory rate, (C) Variability of tidal volume. R: Spearman’s rank correlation coefficient.

    The associations between pain sensitivity, measured by PPTs, and respiratory variability are shown in Figure 5A–C. We observed a negative association between the PPT and variability in both respiratory rate (r = −0.43, 95% confidence interval: −0.03 to −0.72, p = 0.039) and tidal volume (r = −0.47, 95% confidence interval: −0.07 to −0.74, p = 0.023). We found no associations of respiratory variability with the other pain sensitivity measures.

    Figure 5 Correlations between pain pressure thresholds and respiratory variability in women with fibromyalgia syndrome. The pain pressure threshold (kg) was defined as the mean pressure needed to evoke pain in three tests at the thenar muscle of the dominant hand and ipsilateral tibialis anterior muscle. Respiratory parameters were measured during 30 min of restful waiting. Variabilities in the respiratory rate and tidal volume were calculated as coefficients of variation. (A) Mean respiratory rate, (B) Variability of respiratory rate, (C) Variability of tidal volume. R: Spearman’s rank correlation coefficient.

    Discussion

    This is the first exploratory study to quantify respiratory variability in patients with fibromyalgia. We tested the hypothesis that variability in respiratory parameters, specifically respiratory rate and tidal volume, is associated with the impact of fibromyalgia on quality of life, anxiety, depression, pain intensity, and pain sensitivity. We found no association of respiratory parameters with fibromyalgia disease impact (FIQR), anxiety, chronic pain intensity, wind-up pain, and aftersensations; however, we observed an association between depression and respiratory variability, as well as between PPTs and variability in both respiratory rate and tidal volume. Patients with a decreased pain threshold, which may indicate central sensitization, exhibited higher variability in both respiratory rate and tidal volume. While the exact pathophysiology of increased pain sensitivity in fibromyalgia remains unknown,23,24 emerging evidence suggests a central rather than peripheral nervous system origin.25–28 Because of this likely central origin, we believe that fibromyalgia may affect breathing variability.

    Previous studies have examined spontaneous breath-to-breath variations in breathing parameters of healthy individuals, using similar non-invasive respiratory monitoring during restful waiting and expressing respiratory variability as the coefficient of variation.29,30 However, differences in the duration of respiratory measurements across studies limit direct comparisons. Despite these methodological differences, respiratory rate variability was lower in healthy individuals studied by Vlemincx et al29 (0.164 ± 0.072) than in fibromyalgia patients in the present study (0.201 ± 0.039). Although this comparison remains speculative, it suggests that respiratory rate variability is elevated in chronic pain conditions and may be further increased in patients with heightened pain sensitivity.

    Consistent with broader fibromyalgia studies,31,32 our cohort showed mild-moderate symptom burden, though respiratory variability patterns did not align with disease impact scores. Regarding the mechanisms explaining the association between fibromyalgia, pain sensitivity, and respiratory variability, we believe that neuroinflammation and autonomic dysregulation are two potential pathways. Recent evidence indicates that inflammation plays a significant role in the etiology of fibromyalgia.2 Pro-inflammatory cytokines such as IL-1, IL-6, IL-8, IL-17, and TNF-a are elevated in patients with fibromyalgia compared to healthy controls and have also been associated in some studies with symptoms such as pain, anxiety, and fatigue.33–35 Furthermore, positron emission tomography (PET) scans reveal increased activation of glial cells in the brains of patients with fibromyalgia, indicating ongoing neuroinflammation.36 Inflammation may influence respiratory plasticity as it reduces the adaptive capabilities of respiratory control.5 The second proposed mechanism is autonomic dysregulation, as there is a disruption in the balance between the sympathetic and parasympathetic nervous systems in fibromyalgia patients.37 This disruption could also be reflected in altered respiratory variability.7 Conversely, modifying respiratory variability through targeted breathing exercises may, in turn, influence fibromyalgia symptoms, presenting a potential therapeutic approach.

    These findings show that patients with heightened somatic symptom burden and pain sensitivity displayed greater respiratory rate variability, which may reflect altered central control of respiration. In general, low or absent respiratory variability implies a rigid regulation of breathing, reflecting poorer reactivity to input into the respiratory center. By contrast, increased respiratory variability associated with heightened pain sensitivity may indicate a dysregulated respiratory system characterized by an exaggerated response to stimuli.

    Our findings on respiratory variability contribute to the body of research on the relation between pain and respiration. We demonstrated that pain sensitivity and chronic pain intensity have different associations with respiration, as pain pressure thresholds but not chronic pain intensity were inversely correlated with variability of respiratory rate and tidal volume. Prior studies have consistently shown an increase in minute ventilation in response to tonic sustained pain stimuli.38–42 This increase in total ventilatory output is a result of increased tidal volume,38,39,41 respiratory rate,42 or both.40 Sudden, short-lasting pain stimuli result in increased inspiratory flow.43–45 Chronic pain also causes hyperventilation, but this could partly be attributed to the influence of anxiety, panic, and a sense of uncontrollability rather than the direct effect of actual painful stimuli.46,47

    Regarding the relation between chronic pain and variability of other vital functions, recent studies have reported that chronic pain in fibromyalgia is also associated with heart rate variability (HRV). This association is likely influenced by the relation between the low- and high-frequency components of HRV and the sympathetic and parasympathetic branches of the autonomic nervous system. Chronic pain may affect the autonomic nervous system in general and the sympathetic nervous system activity in particular.48,49 Elevated sympathetic and reduced parasympathetic cardiac modulation have been observed in patients with fibromyalgia.50 Consistent with these findings, HRV has been associated with quality of life, physical function, and perceived stress.51 Regarding the underlying mechanism, the observed decrease in HRV in fibromyalgia is unlikely to be due to deconditioning alone, as reduced HRV is less evident in patients with chronic fatigue syndrome, who are presumably less active and fit than patients with fibromyalgia.52 Instead, it is speculated that the lack of an autonomic response to stressors may contribute to deficits in pain inhibition in fibromyalgia.52,53 Further studies are needed to explore whether the relationship between pain sensitivity and respiratory variability is mediated by the autonomic nervous system.

    This study raises the question of whether respiratory variability could aid in the diagnosis, classification, and follow-up of chronic pain. A recent study addressed the potential applications of machine learning algorithms to automatically detect and monitor pain using respiratory and cardiovascular measurements.54 Another intriguing question for future studies is whether therapeutic interventions aimed at decreasing breathing variability may also decrease pain sensitivity and thus potentially improve chronic pain states. Two previous studies have shown favorable results of hyperventilatory breathing exercises on pain thresholds. In the first study, participants engaged in deep, forceful breathing while receiving electrical stimuli. Those who performed the breathing exercises exhibited higher pain thresholds than those in the control group who did not receive such instructions.4 In the second study, participants performed a series of thirty deep, forceful breaths. Similarly, using standardized electrical stimuli, the authors observed significantly higher pain thresholds in participants who performed the breathing exercises compared to the control group.3 These findings suggest that targeted breathing interventions may modulate pain sensitivity, and we propose that respiratory variability is a specific topic of interest. Future key experiments include longitudinal follow-up of respiratory measurements in patients with fibromyalgia to explore whether changes in symptom load over time are consistently associated with alterations in respiratory variability.

    Regarding the limitations of our study, we focused exclusively on patients with fibromyalgia, a condition in which identifying a clear biological substrate is complex. Therefore, our results relate to this specific pain syndrome. However, we expect similar effects on respiratory patterns in other patients with central sensitization due to chronic pain. In addition, participants with high PPTs were exposed to more intense pressure stimuli, which – theoretically – could have independently contributed to the observed decrease in respiratory variability. However, this seems unlikely as respiratory variability was assessed over a longer period of 30 minutes. Of note, participants in this study had normal to borderline abnormal scores on the HADS anxiety and depression subscales, which limits the ability to extrapolate our findings to individuals with clinically significant affective symptoms. The HADS is a screening tool rather than a diagnostic instrument. Nonetheless, our results suggest that respiratory patterns may be sensitive to subtle affective states, even in the absence of overt psychopathology. The sample size was relatively small (n = 23), and no formal power analysis was conducted, as this was an exploratory investigation. As such, the findings should be interpreted with caution and considered hypothesis-generating rather than confirmatory. While the risk of type I error from multiple comparisons exists, this is generally considered acceptable within the context of exploratory research.22 It should be noted that PPT is not a specific marker of central pain sensitivity, as it may also be influenced by peripheral nociceptive mechanisms. Lastly, concomitant medications (eg, antidepressants, analgesics) were not controlled for and may confound respiratory or symptom measures.

    Conclusion

    In conclusion, this exploratory study aimed to investigate the association between fibromyalgia and respiratory variability. Contrary to our hypothesis, we found no association between fibromyalgia disease impact and chronic pain intensity on respiratory variability. However, in patients with fibromyalgia, respiratory variability decreases with mildly increased depression scores, but not with anxiety. Also, respiratory variability increases with decreasing patient’s pain pressure threshold, which may be a surrogate marker for central sensitization, suggesting a possible link between central sensitization and respiratory variability. Further studies should examine the potential benefits of respiratory variability for the diagnosis, monitoring, and treatment of fibromyalgia.

    Funding

    The Dutch Arthritis Society (ReumaNL) and the NWO Stevin grant, both awarded to A. Evers, the Department of Health, Medical and Neuropsychology, Leiden University, and the Department of Anesthesiology, Amsterdam UMC, location Vrije Universiteit, provided funding.

    Disclosure

    The author(s) report no conflicts of interest in this work.

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  • Infection Preventionists Call for Recognition, Balance, and Collaboration

    Infection Preventionists Call for Recognition, Balance, and Collaboration

    In this installment of the conversation with Infection Control Today®(ICT®), authors of the study, “Quantifying the Progressing Landscape of Infection Preventionists: A Survey-Based Analysis of Workload and Resource Needs” shared the key takeaways from their study.

    The authors are Brenna Doran, PhD, MA, who specializes in hospital epidemiology and infection prevention at the University of California, San Francisco, and is a coach and consultant in infection prevention; Jessica Swain, MBA, MLT, director of infection prevention and control at Dartmouth Health in Lebanon, New Hampshire; and Shanina Knighton, an associate professor at Case Western Reserve University School of Nursing and senior nurse scientist at MetroHealth System in Cleveland, Ohio.

    “Infection prevention is one of the cornerstones of patient and staff safety,” the panel emphasized, but too often the professionals behind this work feel unseen. Doran began by stating, “We want IPs to know that we see them, that we really value and recognize their dedication, their passion, their work.”

    Reflecting on the COVID-19 pandemic, Doran recalled, “We worked days, we worked evenings, we worked weekends, we worked holidays, we were on call. And again, we came together. We coalesced around the same mission.” Yet, long hours were not new. “We were working more hours even before COVID-19 happened. This overarching discordance…we wanted to publish this manuscript to look at how many hours IPs work, the expectations that organizations have, and what our expectations are of each other.”

    The consequences of unrelenting workloads are serious. “We’re seeing people leave the IP field…IPs that are leaving due to burnout,” Doran explained. “If your marketing program is you’re going to work 45 [to] 50 hours a week, only get paid 40… It’s going to be really hard to not only keep the IPs that you have but also bring in that fresh generation.”

    For leadership, the message is equally clear. Knighton stressed, “Infection prevention is not an expense, it’s an investment. Every dollar spent on preventing infections has a significant impact on treatment costs, legal risk, and reputational damage.” They added, “IPs cannot do it alone…ensuring that we have a hospital-wide culture of infection prevention” is essential.

    Swain echoed this, stating, “Although we’re not revenue-generating, we are cost-saving. From the boards all the way down, there needs to be recognition of the impact that your infection preventionist and your infection prevention programs have on your organization as a whole.”

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  • Mitochondrial antioxidant found to drive breast cancer metastasis

    Mitochondrial antioxidant found to drive breast cancer metastasis

    The mitochondria may be the powerhouse of the cell, but mounting evidence suggests this organelle is also a driving force behind cancer. Now, new evidence points to the mitochondrial metabolite glutathione, highlighting its central role in helping breast cancer cells break away from the primary tumor, travel through the body, and take root in other tissues.

    The findings are among the first to link a specific mitochondrial metabolite to metastasis, with strong implications for the study of cancer at the cellular level. “We hope that our work will bring more attention to how organelles and their metabolites are relevant to cancer biology,” says Kivanç Birsoy, head of the Laboratory of Metabolic Regulation and Genetics at Rockefeller.

    A mysterious connection with metastasis

    The vast majority of cancer deaths are due to its spread, rather than complications from the original tumor. Knowing that metastasis lies at the heart of cancer mortality, researchers have spent decades trying to identify—and defeat—the specific factors that enable rogue cells to break away from the primary tumor and colonize the rest of the body.

    Metabolites play a key role, with prior studies having shown that the metabolites lactate, pyruvate, glutamine, and serine each support distinct stages of metastasis. And since mitochondria within the cancer cell are responsible for not only generating energy but also providing metabolites, it is unsurprising that a handful of recent studies have linked mitochondrial activity to metastasis in breast, renal, and pancreatic cancers.

    However, researchers had been unable to identify the precise mechanisms at play. “Mitochondria have thousands of metabolites, and it’s been difficult to determine which are important to tumor formation and growth, and which initiate metastasis,” says Birsoy.

    Cells under stress

    In their study, Birsoy and colleagues utilized an innovative strategy that involved protein tagging able to distinguish primary tumor cells and from those that had migrated from the breast to the lung. The team, led by graduate fellow Nicole DelGaudio and postdoctoral fellow Hsi-wen Yeh, then analyzed the metabolites in these organelles to reveal how mitochondrial metabolites shift when cancer cells colonize new sites.

    “These techniques allowed us to, in an unbiased manner, see the difference between what’s essential in metastasis and what’s essential in the primary tumor,” DelGaudio says.

    Among thousands of mitochondrial compounds, one stood out: glutathione. A major antioxidant involved in reducing oxidative stress, enhancing metabolic detoxification, and regulating the immune system, glutathione levels were found to have skyrocketed in metastatic cancer cells that invaded the lung. To further confirm the findings, the team used a spatial metabolomics technique that allowed them to visualize the distribution of glutathione directly within lung tissues.

    They then shifted their focus toward mitochondrial membrane proteins, screening for transporters that stood out as essential for metastatic cells growing in the lung. Once again, a clear frontrunner emerged: SLC25A39, the mitochondrial glutathione transporter. The findings closed the loop, linking a metabolite and its transporter to metastasis by demonstrating that mitochondrial glutathione import via the SLC25A39 transporter is essential for cancer spread.

    Birsoy and colleagues also found how mitochondrial glutathione drives cancer spread: not by acting as an antioxidant—an effect ruled out through multiple experiments—but by signaling to activate ATF4, a transcription factor that helps cancer cells survive in low-oxygen conditions. This also pinpointed when glutathione is specifically required: during the early steps of metastatic colonization, when cancer cells adapt rapidly to the stressful environment of a new tissue.

    A familiar culprit

    This work builds on recent significant work from the Birsoy lab. In 2021, his team was the first to demonstrate that SLC25A39 is the transporter that brings glutathione into the mitochondria; in 2023, they showed that SLC25A39 is not only a transporter but a dynamic sensor that regulates the amount of glutathione in the mitochondria and adjusts those levels accordingly. So when this metabolite and its mitochondrial transporter showed up in cancer screenings, Birsoy knew where to take his experiments next.

    “Because we found this transporter earlier and knew how to block the entry of glutathione, we already had the tools necessary to investigate its role in cancer metastasis,” he says.

    The findings may have clinical implications—especially since the team also found that breast cancer samples from patients whose disease had spread to the lung showed elevated SLC25A39, and that higher SLC25A39 expression was strongly correlated with poorer overall survival in breast cancer patients. One day, a small molecule that targets this metabolite by blocking its transporter could potentially forestall breast cancer metastasis, with fewer side-effects than sweeping therapies that target more general cellular processes.

    In the short-term, however, the paper emphasizes the importance of nailing down just how metabolites within different compartments operate within our cells.

    “We’re trying to make our knowledge of metabolism more precise,” Birsoy says. “It’s not just about some metabolite levels going up and others going down. We need to look at the organelles, the precise compartments, to understand how metabolites influence human health.”


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  • Dapagliflozin Fails to Lower Cardiovascular Risk in Patients with HF

    Dapagliflozin Fails to Lower Cardiovascular Risk in Patients with HF

    David Berg, MD, MPH | Image Credit: Brigham and Women’s Hospital

    Dapagliflozin, an SGLT2 inhibitor, did not significantly reduce short-term risk of cardiovascular death or worsening heart failure (HF) in patients admitted with HF, according to results from the DAPA ACT HF-TIMI 68 trial.1

    Presented as late-breaking research at the European Society of Cardiology Congress 2025 in Madrid, the trial involved the administration of dapagliflozin to patients currently hospitalized for HF. Despite the lack of significant cardiovascular death risk reduction, the trial did exhibit positive effects when data were combined.1

    HF is the leading cardiovascular reason for hospital admission worldwide, with rates increasing dramatically over the last 10 years. Patients hospitalized for HF also have a high risk of death and other adverse outcomes in the early post-discharge period. Previous clinical trials have suggested that initiating and optimizing disease-modifying chronic heart failure therapies, including beta-blockers and mineralocorticoid receptor antagonists, in the early post-discharge period may improve both short- and long-term outcomes.2

    “However, there are limited data on initiating sodium-glucose cotransporter-2 inhibitors in patients hospitalized for HF,” David Berg, MD, MPH, investigator in the TIMI Study Group at Brigham and Women’s Hospital and principal investigator of DAPA ACT, said in a statement. “We designed the trial to test the hypothesis that in-hospital initiation of the SGLT2i, dapagliflozin, as compared with placebo, could safely and effectively decrease the early risk of cardiovascular death or worsening HF among patients hospitalized for HF.”1

    The trial was a double-blind, placebo-controlled, randomized trial conducted at 210 sites in the USA, Canada, Poland, Hungary, and the Czech Republic. For inclusion, patients had to be ≥18 years of age and be hospitalized with a primary diagnosis of HF, including signs and symptoms of fluid overload, as well as elevated natriuretic peptide levels during index hospitalization.1

    A total of 2401 patients were included in the study and randomly assigned in a 1:1 ratio to dapagliflozin 10 mg daily or placebo at least 24 hours and no later than 14 days after hospital admission and as early as possible following initial stabilization. The median age was 69 years, and 33.9% of patients were women. Investigators noted a primary efficacy outcome composite of cardiovascular death or worsening HF over the first 2 months.1

    Ultimately, the primary outcome occurred in 10.9% of patients assigned to dapagliflozin and 12.7% of patients in the placebo group (hazard ratio [HR], 0.86; 95% CI, 0.68-1.08; P = .20). Cardiovascular death occurred in 2.5% of patients with dapagliflozin and 3.1% with placebo (HR, 0.78; 95% CI, 0.48-1.27), and a worsening HF event occurred in 9.4% and 10.3% of patients, respectively (HR, 0.91; 95% CI, 0.71-1.18).1

    All-cause mortality occurred in 3% of patients receiving dapagliflozin and 4.5% receiving placebo (HR, 0.66; 95% CI, 0.43-1). Rates of symptomatic hypotension were 3.6% and 2.2%, respectively, and rates of worsening kidney function were 5.9% and 4.7%, respectively.1

    A prespecified meta-analysis was conducted, including 2 other SGLT2i trials – specifically, empagliflozin and sotagliflozin – to assess in-hospital initiation in a total of 3527 patients hospitalized for HF. SGLT2is reduced early risks of cardiovascular death or worsening HF (HR, 0.71; 95% CI, 0.54-0.93; P = .012) and all-cause mortality (HR, 0.57; 95% CI, 0.41-0.8; P = .001).1

    “In-hospital initiation of dapagliflozin did not significantly reduce the risk of cardiovascular death or worsening HF over the first 2 months in DAPA ACT HF-TIMI 68,” Berg said. “However, the totality of trial data suggests that in-hospital initiation of an SGLT2i reduces the early risk of cardiovascular death or worsening HF and all-cause mortality.”1

    References
    1. 1: European Society of Cardiology. Evidence appears supportive for the initiation of SGLT2 inhibitors in patients hospitalized for heart failure. August 30, 2025. Accessed September 4, 2025. https://www.escardio.org/The-ESC/Press-Office/Press-releases/Evidence-appears-supportive-for-the-initiation-of-SGLT2-inhibitors-in-patients-hospitalised-for-heart-failure
    2. 2: Berg DD, Patel SM, Haller PM, et al. Dapagliflozin in Patients Hospitalized for Heart Failure: Primary Results of the DAPA ACT HF-TIMI 68 Randomized Clinical Trial and Meta-Analysis of Sodium-Glucose Cotransporter-2 Inhibitors in Patients Hospitalized for Heart Failure. Circulation. Published online August 29, 2025. doi:10.1161/CIRCULATIONAHA.125.076575

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  • Researchers note spike in kidney deaths related to blood pressure

    Researchers note spike in kidney deaths related to blood pressure

    Deaths from blood-pressure-driven kidney disease have increased dramatically during the past quarter-century, according to a new study.

    Deaths from high blood pressure-related kidney disease increased by nearly half in the U.S. over the past 25 years, researchers reported Thursday at an American Heart Association meeting in Baltimore.

    The highest death rates were among Black Americans, followed by Hispanic people, results show.

    “Despite national efforts to reduce health inequalities, Black individuals still had over three times the death rate compared to other groups of people,” researcher Dr. Joiven Nyongbella said in a news release. He’s an internal medicine resident at Wayne State University/Henry Ford Rochester Hospital in Detroit.

    High blood pressure is a known risk factor for kidney damage, according to the AHA. It can damage the blood vessels in and around the kidneys, contributing to scarring of the organs.

    For the new study, researchers looked at death certificate data from 1999 to 2023 maintained by the U.S. Centers for Disease Control and Prevention.

    Results showed a 48% increase in deaths from kidney disease related to high blood pressure.

    Men and Black or Hispanic adults had rates that were even higher than average, researchers found.

    “High blood pressure isn’t just about strokes or heart attacks — it’s also a major cause of kidney disease and death, especially in Black and Hispanic communities,” Nyongbella said.

    Overall, the death rate rose from 3.3 deaths per 100,000 people in 1999 to 4.9 per 100,000 in 2023.

    Researchers also found that:

    Men had a higher death rate than women, 4.5 versus 3.7 deaths per 100,000.

    Black adults had the highest death rate at nearly 10.4 per 1000,000.

    Hispanic adults had a 15% higher death rate compared to non-Hispanic people, 4.5 versus just under 4 per 100,000.

    “The message is simple: Check your blood pressure, treat it early and don’t ignore it, because it can quietly lead to life-threatening kidney problems,” Nyongbella said.

    Findings presented at medical meetings should be considered preliminary until published in a peer-reviewed journal.

    More information

    The American Heart Association has more on high blood pressure and your kidneys.

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