Aging-US
Aging-US Podcast
Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.
Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity
Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity
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Mar 23, 2025 • 5min
Montelukast Improves Retinal Health in Aging Mice
BUFFALO, NY — March 25, 2025 — A new #research paper was #published in Aging (Aging-US) on January 31, 2025, in Volume 17, Issue 2, titled “Cysteinyl leukotriene receptor 1 modulates retinal immune cells, vascularity and proteolytic activity in aged mice.”
The study, led by first author and corresponding author Andreas Koller from the University Hospital of the Paracelsus Medical University, found that blocking an inflammatory receptor called CysLTR1 in the retinas of aging mice improved retinal health. These findings suggest a new approach to slowing age-related vision loss and protecting eye health in older adults.
Age-related vision problems are a growing concern worldwide, and inflammation plays a key role in damaging the retina over time. The retina is the part of the eye that captures light and sends visual signals to the brain, making it vital for clear eyesight. In this study, scientists focused on the CysLTR1 receptor, which is known to promote inflammation and is found in high amounts in the retina. They explored whether blocking this receptor could reduce the harmful effects of aging in the eye.
To achieve this, researchers treated aged mice with montelukast (MTK), a drug commonly used for asthma, which specifically blocks CysLTR1. The oral treatment lasted eight weeks and results were compared with both untreated aged mice and healthy young mice. After treatment, the older mice showed major improvements in retinal health.
One key finding was a reduction in immune cells called microglia, which tend to increase with age and contribute to chronic inflammation in the retina. With CysLTR1 blocked, the number of these immune cells dropped significantly, suggesting reduced retinal inflammation. Lower inflammation is linked to a lower risk of age-related eye diseases like macular degeneration.
“The reduction in immune cells caused by Cysltr1 suppression may dampen neuroinflammation, a known promoter of tissue aging.”
Another important result was the restoration of blood vessel function. The tiny blood vessels in the retina had narrowed in aging mice, reducing blood flow and oxygen supply to the eye. MTK treatment increased the diameter of these vessels, improving circulation and possibly helping the retina work more efficiently.
The study also indicated that blocking CysLTR1 helped boost the retina’s natural ability to clear out waste proteins. As we age, this cleaning process slows down, allowing harmful material to build up in the eye. After treatment, the aged mice had stronger proteasome activity—the system responsible for breaking down cellular waste—and fewer signs of waste accumulation.
Importantly, the treatment did not harm retinal nerve cells, which are essential for vision. This evidence indicates that the therapy was not only effective but also safe.
While more research is needed to confirm these results in humans, this study highlights the potential of repurposing MTK to protect against age-related vision decline. Because it is already an approved drug, testing it for age-related eye diseases like macular degeneration or diabetic retinopathy could move forward more quickly. Blocking inflammation and supporting the eye’s natural cleaning systems may be a promising new way to preserve healthy vision in aging populations.
DOI - https://doi.org/10.18632/aging.206193
Corresponding author - Andreas Koller - a.koller@salk.at
Video short - https://www.youtube.com/watch?v=ngnrPJzHlpI
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Mar 19, 2025 • 1h 4min
Longevity & Aging Series (S3, E2): Dr. Julia Sidorova
In this installment of the Longevity & Aging Series, Dr. Julia Sidorova from the Department of Laboratory Medicine and Pathology at the University of Washington (Seattle, WA) joined host Dr. Evgeniy Galimov to discuss her co-authored research paper from Volume 16, Issue 20 of Aging (Aging-US), titled “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.”
DOI - https://doi.org/10.18632/aging.206132
Corresponding Author - Julia M. Sidorova - julias@uw.edu
Video interview - https://www.youtube.com/watch?v=3yn8O-JA6GE
Abstract
Werner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it.
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Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats
About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)
Please visit our website at https://www.Aging-US.com and connect with us:
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Mar 18, 2025 • 6min
How Environmental Chemicals May Accelerate Biological Aging
Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity.
Understanding How Scientists Measure Aging at the DNA Level
Aging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person’s actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers.
The Study: Investigating the Impact of Environmental Pollutants on Aging
A research team led by first author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, conducted an exposome-wide association study to examine how different environmental pollutants affect epigenetic aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they analyzed blood and urine samples from 2,346 adults aged 50 to 84. The study measured 64 environmental chemicals, including heavy metals, pesticides, plastics, and tobacco-related compounds, to identify potential links to accelerated aging. The study titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey,” was published in Aging on February 11, 2025.
Full blog - https://aging-us.org/2025/03/how-environmental-chemicals-may-accelerate-biological-aging/
Paper DOI - https://doi.org/10.18632/aging.206201
Corresponding author - Andres Cardenas - andresca@stanford.edu
Video short - https://www.youtube.com/watch?v=WcL-K399a7M
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Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics
About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)
Please visit our website at https://www.Aging-US.com and connect with us:
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Mar 16, 2025 • 4min
Influence of Age, Sex, and Mitochondrial Haplotype on Gut Microbiome in Rats
BUFFALO, NY — March 19, 2025 — A new #research paper was #published in Aging (Aging-US) on February 27, 2025, in Volume 17, Issue 2, titled “Age, sex, and mitochondrial-haplotype influence gut microbiome composition and metabolites in a genetically diverse rat model.”
The research team, led by first author Hoang Van M. Nguyen and corresponding author Archana Unnikrishnan from the University of Oklahoma Health Sciences, studied how aging affects gut bacteria in a special group of rats generated to have genetic diversity similar to humans. Their research found that both biological sex and mitochondrial DNA—the small set of genes inherited only from mothers—play a key role in how gut bacteria change over time.
The gut microbiome, a collection of bacteria in the intestines, affects digestion, metabolism, and even brain function. As people age, these bacteria shift, and some of these changes are linked to diseases like Alzheimer’s, Parkinson’s, and metabolic disorders. However, most studies have looked at either men or women without comparing differences between sexes, and few have explored how mitochondrial DNA might influence these changes.
To better understand these factors, researchers analyzed fecal samples from the genetically diverse rats to assess gut bacteria composition and metabolic byproducts. The results showed that aging affects gut bacteria differently in males and females. More bacterial species changed with age in female rats than in males, and only a few changes were consistent across both sexes. These findings suggest that men and women may experience aging differently at the microbial level, which could impact nutrition and disease risk.
“Five microbial species changed significantly with age in male rats compared to nine microbial species in female rats. Only three of these microbes changed with age in both male and female rats.”
Another key discovery was that mitochondrial DNA influences how gut bacteria evolve with age. These effects were different in males and females, suggesting a deeper connection between mitochondrial function and gut health, with potential implications for personalized medicine and aging research.
In addition to studying bacteria, the researchers analyzed metabolic compounds such as short-chain fatty acids and bile acids, which help with digestion. They found that aging altered these compounds based on both sex and mitochondrial DNA. For example, older female rats had higher levels of short-chain fatty acids in their feces, possibly due to differences in nutrient absorption.
This study highlights new factors that shape the gut microbiome in aging populations. Understanding how biological sex and mitochondrial DNA influence these changes could lead to targeted approaches for maintaining gut health and preventing age-related diseases. These findings reinforce the importance of personalized health strategies that consider both genetic and biological differences.
DOI - https://doi.org/10.18632/aging.206211
Corresponding author - Archana Unnikrishnan - archana-unnikrishnan@ouhsc.edu
Video short - https://www.youtube.com/watch?v=RtsqRi2_uAI
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About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
Please visit our website at https://www.Aging-US.com and connect with us:
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Mar 15, 2025 • 4min
Breast Cancer Treatments Linked to Accelerated Aging in Survivors
BUFFALO, NY — March 18, 2025 — A new #research paper was #published by Aging (Aging-US) on March 7, 2025, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors.”
Led by first author Cong Wang and corresponding author Xiao-Ou Shu from Vanderbilt University, this study examines how breast cancer and its treatments contribute to accelerated aging in survivors. Their study revealed that breast cancer patients show signs of faster biological aging compared to cancer-free individuals, with long-term effects lasting up to ten years post-diagnosis. This finding raises concerns about the potential lasting impact of cancer therapies on aging and overall health.
Breast cancer is one of the most common cancers in women worldwide, with improved treatments leading to longer survival rates. However, emerging evidence suggests that these treatments may also accelerate aging. The study used Phenotypic Age Acceleration (PAA), a biological marker that estimates a person’s aging rate based on blood tests. Researchers compared data from 1,264 breast cancer patients and 429 cancer-free controls. The results indicated that breast cancer survivors had significantly higher PAA at diagnosis and continued to show signs of accelerated aging up to ten years later.
“This is the first large study with 10 years of follow-up to evaluate PAA among BC survivors.”
The study found that tumor severity played a role in aging acceleration. Women with advanced-stage (Stage III/IV) or high-grade tumors showed the highest levels of aging acceleration. Additionally, treatments such as chemotherapy and endocrine therapy were linked to increased biological aging. One year after diagnosis, chemotherapy was associated with the most significant rise in PAA, while endocrine therapy had long-term effects, increasing aging markers even ten years after treatment.
Interestingly, not all cancer treatments had the same effect. Surgery and radiation therapy were associated with lower aging acceleration over time. These findings suggest that systemic therapies, which affect the whole body, may contribute more to aging-related changes than localized treatments.
The findings highlight the need for ongoing monitoring of breast cancer survivors beyond their initial recovery. Understanding how cancer treatments influence aging can help improve post-treatment care and potentially lead to strategies that reduce these effects. Further research is needed to explore whether lifestyle changes, medications, or other interventions could slow down aging in cancer survivors.
As the number of breast cancer survivors continues to grow, addressing the long-term health consequences of cancer treatment is crucial. This study provides valuable insights into how different factors contribute to accelerated aging, helping to shape future research and healthcare approaches for breast cancer survivors.
DOI - https://doi.org/10.18632/aging.206218
Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org
Video short - https://www.youtube.com/watch?v=cfuyzVyDeHY
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About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
Please visit our website at https://www.Aging-US.com and connect with us:
Facebook - https://www.facebook.com/AgingUS/
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Mar 12, 2025 • 2min
Aging (Aging-US) to Participate at the AACR Annual Meeting 2025
BUFFALO, NY — March 17, 2025 — Impact Journals (Aging’s publisher) is pleased to announce its participation as an exhibitor at theAmerican Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois.
This 2025 AACR Annual Meeting theme, “Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact,” highlights significant advancements and groundbreaking discoveries in cancer research. Aging closely aligns with this mission, dedicated to disseminating impactful scientific research at the intersection of oncology and gerontology.
Visit Booth 2815 to meet directly with members of the Aging team, explore the latest research publications, and discuss opportunities for collaboration and manuscript submissions. Aging, supported by its publisher Impact Journals, remains dedicated to promoting innovation, collaboration, and advancing scientific knowledge in aging-related cancer research.
About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)
Please visit our website at https://www.Aging-US.com and connect with us:
Facebook - https://www.facebook.com/AgingUS/
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LinkedIn - https://www.linkedin.com/company/aging/
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Mar 9, 2025 • 5min
Long-Lived Families Show Lower Risk for Peripheral Artery Disease
BUFFALO, NY — March 12, 2025 — A new #research paper was #published in Aging (Aging-US) on February 25, 2025, Volume 17, Issue 2, titled “Epidemiology and genetic determination of measures of peripheral vascular health in the Long Life Family Study.”
Researchers from multiple institutions, led by first author and corresponding author Deidra R. Fricke from the University of Pittsburgh, studied the genetic and lifestyle factors that influence peripheral artery disease (PAD), a condition that restricts blood flow to the legs. Their findings suggest that people from families with exceptional longevity have a lower risk of PAD, possibly due to inherited genetic traits or healthier lifestyle habits.
Peripheral artery disease is a common but often undiagnosed condition that affects millions worldwide. It increases the risk of heart disease, stroke, and mobility issues. This study conducted using data from the Long Life Family Study (LLFS), found that individuals from long-lived families have significantly better vascular health than the general population.
“Peripheral artery disease (PAD) is a major contributor to morbidity in older adults.”
The researchers analyzed over 3,000 participants, including 1,090 long-lived individuals, their 1,554 children, and 362 spouses. Among the oldest participants (average age 89), about 18% had PAD. However, among their children (average age 60), only 1% had PAD—far lower than the expected 12% found in other studies. This finding suggests that certain protective factors, whether genetic or lifestyle-related, help maintain healthier arteries in these families.
In the study, key risk factors for PAD were identified, including aging, high blood pressure, smoking, and hypertension medication use. Interestingly, unlike in other studies, high cholesterol and diabetes were not major risk factors in this group. This data further supports the idea that long-lived families may have genetic protective factors that contribute to better vascular health.
In addition to lifestyle factors, the study found four genomic regions linked to PAD risk. Three of these were new discoveries, while the fourth was similar but not identical to previously published findings. These genetic markers may help scientists better understand why some individuals are more likely to develop PAD and how to prevent it.
“We identified four genomic sites that may harbor variants associated with protection from PAD.”
This research highlights the value of studying long-lived families to unlock the secrets of healthy aging and vascular health. Understanding what helps them maintain better artery function could lead to new strategies for preventing PAD, heart disease, and other age-related conditions.
Paper DOI: https://doi.org/10.18632/aging.206204
Corresponding author: Deidra R. Fricke — der94@pitt.edu
Keywords: aging, ankle-brachial index, peripheral arterial disease, heritability, genomewide linkage analysis, genomewide association study
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About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)
Please visit our website at https://www.Aging-US.com and connect with us:
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/
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Mar 9, 2025 • 5min
Platelet-Rich Plasma May Support Ovarian Function in Women with Poor Ovarian Response
BUFFALO, NY — March 10, 2025 — A new #research paper was #published in Aging (Aging-US) on February 18, 2025, Volume 17, Issue 2, titled “Transcriptomic landscape of cumulus cells from patients <38 years old with a history of poor ovarian response (POR) treated with platelet-rich plasma (PRP).”
Researchers from IVIRMA New Jersey, Yale School of Medicine, Yale University, and Acibadem Mehmet Ali Aydinlar University studied how a treatment called platelet-rich plasma (PRP) might help women with poor ovarian response. Their results suggest that PRP may enhance ovarian rejuvenation and improve egg quality, potentially increasing pregnancy success rates for women undergoing in vitro fertilization (IVF).
Diminished ovarian reserve is a major challenge in fertility treatments, affecting many women undergoing IVF. It is associated with fewer collected eggs and lower pregnancy success rates. Some studies have explored PRP—a concentration of growth factors derived from a patient’s own blood—as a potential treatment to rejuvenate ovarian function. However, the biological effects of PRP treatment at the molecular level remain unclear.
In this study, the research team, led by first author Leah M. Roberts and corresponding author Emre Seli, analyzed cumulus cells, specialized cells that surround the egg, using RNA sequencing technology. Samples were collected from women aged 18 to 37 with poor ovarian response, who either received PRP therapy or standard treatment before IVF.
The results showed significant differences in gene expression between the two groups. PRP-treated samples exhibited increased activity in genes related to metabolism, cell survival, and communication between cells, all of which are crucial for egg development and fertility. One key finding was that PRP influenced carbohydrate metabolism in cumulus cells. This is essential, as cumulus cells provide energy to the developing egg, and previous research has linked metabolic health to embryo quality. PRP also appeared to regulate pathways related to cell proliferation and programmed cell death, suggesting it may help support egg survival.
“Our findings indicate that PRP treatment regulates certain pathways that could contribute to follicular activation and oocyte maturation.”
Although PRP has been used in medicine for wound healing and tissue repair, its role in fertility treatment is still under investigation. Some clinical trials have shown improved ovarian reserve markers after PRP treatment, while others have not found a direct benefit for pregnancy rates. This study sheds light on how PRP affects cumulus cells, offering valuable insights into its potential for improving fertility treatments.
The researchers hope that further studies will help refine PRP treatments, determine the best protocols, and identify which patients may benefit the most. By understanding the molecular effects of PRP on ovarian cells, scientists may develop targeted fertility therapies to support women facing infertility due to diminished ovarian reserve.
DOI - https://doi.org/10.18632/aging.206202
Corresponding author - Emre Seli - emre.seli@yale.edu
Video short - https://www.youtube.com/watch?v=3Zc_0tr0S84
About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
Please visit our website at https://www.Aging-US.com and connect with us:
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
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YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
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MEDIA@IMPACTJOURNALS.COM

Mar 5, 2025 • 7min
How Radiation Therapy Affects Tumors: Glioblastoma vs. Low-Grade Gliomas
Radiation therapy or radiotherapy, is a common treatment for cancer, but its effectiveness differs across patients. A recent study published as the cover for Volume 17, Issue 2 of Aging explored why this happens. The findings provide valuable insights, particularly for brain cancers like glioblastoma (GBM) and low-grade gliomas (LGG).
Understanding Glioblastoma and Low-Grade Gliomas
Glioblastoma and LGG are both brain tumors, but they behave in very different ways. GBM is highly aggressive, with most patients surviving only 12 to 18 months, even with surgery, chemotherapy, and radiation therapy. LGG, on the other hand, grows more slowly, and many patients live for decades with proper care.
Despite their differences, LGG and GBM are biologically linked. Some LGG tumors eventually transform into GBM, making early treatment decisions critical. Given radiation therapy’s effectiveness in GBM, it has often been assumed that LGG patients would also benefit from it. However, a new study titled “Variability in radiotherapy outcomes across cancer types: a comparative study of glioblastoma multiforme and low-grade gliomas” challenges this assumption.
Full blog - https://aging-us.org/2025/03/how-radiation-therapy-affects-tumors-glioblastoma-vs-low-grade-gliomas/
Paper DOI - https://doi.org/10.18632/aging.206212
Corresponding author - Morten Scheibye-Knudsen - mscheibye@sund.ku.dk
Video short - https://www.youtube.com/watch?v=j91rzDJHXTE
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Keywords - aging, cancer, biomarkers, radiotherapy, GBM, LGG, survival
About Aging-US
The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.
The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)
Please visit our website at https://www.Aging-US.com and connect with us:
Facebook - https://www.facebook.com/AgingUS/
X - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/@AgingJournal
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/
Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc
MEDIA@IMPACTJOURNALS.COM

Mar 2, 2025 • 4min
Toxic Environmental Pollutants Linked to Faster Aging and Health Risks in U.S. Adults
BUFFALO, NY — March 5, 2025 — A new #research paper was #published in Aging (Aging-US) on February 11, 2025, Volume 17, Issue 2, titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey.”
First author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, and colleagues from other U.S. institutions, studied how exposure to harmful chemicals in the environment affects aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they discovered that cadmium, lead, and cotinine are linked to faster biological aging, a process that can increase the risk of age-related diseases.
The study analyzed data from 2,346 U.S. adults aged 50 to 84 who participated in a national health survey. Researchers tested their blood and urine for 64 different chemicals, including metals, pesticides, and industrial pollutants. They assessed how these exposures influenced eight different epigenetic aging markers—biological clocks that measure how fast a person’s body is aging at the DNA level.
"We harnessed data from the National Health and Nutrition Examination Survey 1999-2000 and 2001-2002 cycles to examine exposome-wide associations between environmental exposures and epigenetic aging."
The strongest effects were linked to cadmium, a toxic metal found in cigarette smoke and some foods. People with higher levels of cadmium in their blood showed signs of accelerated aging. Higher levels of cotinine, a chemical related to tobacco exposure, were also linked to increased biological age, reinforcing the harmful effects of smoking. Additionally, lead exposure, a heavy metal found in old paint and contaminated water, was also associated with faster aging.
The researchers also found that some pollutants, including a type of PCB (PCB118) and a type of dioxin (HpCDD), were linked to slower biological aging. However, it is unclear if this fact is beneficial, as past research shows that slower aging in some cases can still be linked to health risks.
This study is one of the largest to investigate how pollution affects the aging process. Unlike previous research that focused on only a few chemicals, it examined a wide range of pollutants in a diverse group of people. The findings suggest that everyday exposure to toxic substances can speed up aging at the cellular level, increasing the risk of age-related diseases.
In summary, these findings raise concerns about how widespread environmental contaminants may accelerate aging and contribute to chronic diseases such as heart disease, cancer, and cognitive decline. Reducing exposure to toxic substances like cadmium and lead—found in cigarettes, polluted air, and contaminated food—could help slow biological aging and improve long-term health. These insights highlight the need for stronger environmental health policies to protect individuals from premature aging and disease.
DOI - https://doi.org/10.18632/aging.206201
Corresponding author - Andres Cardenas - andresca@stanford.edu
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