BUFFALO, NY- January 20, 2025 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) on December 5, 2024, Volume 16, Issue 22, titled “DNA-methylation age and accelerated epigenetic aging in blood as a tumor marker for predicting breast cancer susceptibility.”

Researchers Su Yon Jung, Herbert Yu, Youping Deng, and Matteo Pellegrini from the University of California, Los Angeles and University of Hawaii Cancer Center have found that a simple blood test could help predict breast cancer (BC) risk in older women. Their study focuses on epigenetic aging, a process that reflects how fast the body’s cells age based on DNA methylation changes (DNAm).

Breast cancer is one of the most common cancers worldwide, with the risk increasing significantly after menopause. The researchers analyzed blood samples from postmenopausal, non-Hispanic white women. They discovered that those with an “older” biological age had a significantly higher risk of being diagnosed with breast cancer. The risk was even greater in women who had their ovaries removed before natural menopause, likely due to reduced estrogen levels, a hormone that plays a key role in aging and breast health.

“Of note, in women with bilateral oophorectomy before natural menopause experiencing shorter lifetime estrogen exposure than those with natural menopause, epigenetic age accel substantially influenced BC development, independent of obesity status and exogeneous estrogen use.”

The study also found that lifestyle factors influence epigenetic aging and breast cancer risk. Women with obesity experienced faster biological aging, which increased their risk of developing cancer. Meanwhile, hormone replacement therapy had varying effects depending on the type and duration of treatment.

Early detection of breast cancer is crucial for effective treatment and survival. Traditional risk assessments—such as age, family history, and lifestyle habits—may not provide the full picture. This study suggests that adding a blood test to measure biological aging could help clinicians identify high-risk women earlier and offer personalized prevention strategies.

With further research, this blood test could become a routine screening tool in women’s health check-ups. It may empower women to take proactive steps to reduce their breast cancer risk through healthy lifestyle choices, including maintaining a balanced diet, staying physically active, and considering appropriate hormone therapies under medical supervision.

In conclusion, further studies are needed to validate these findings and explore their applicability to a broader population of women. However, this research presents a promising, non-invasive, and cost-effective approach to predicting breast cancer risk.

DOI - https://doi.org/10.18632/aging.206169

Corresponding author - Su Yon Jung - sjung@sonnet.ucla.edu

Video short - https://www.youtube.com/watch?v=g1tHojirvI8

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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.)

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Aging (Aging-US)

Epigenetic Aging and DNA-Methylation as Tumor Markers for Breast Cancer

BUFFALO, NY—February 12, 2025 — A new #research paper was #published in Aging (Aging-US) on January 3, 2025, in Volume 17, Issue 1, titled “Characterization of DNA methylation clock algorithms applied to diverse tissue types.”

Researchers Mark Richardson, Courtney Brandt, Niyati Jain, James L. Li, Kathryn Demanelis, Farzana Jasmine, Muhammad G. Kibriya, Lin Tong, and Brandon L. Pierce from the University of Chicago and University of Pittsburgh, studied how biological aging is measured using DNA. Their study found that while commonly used “DNA methylation clocks” work well for blood samples, they may be less reliable for other tissues like the lungs, colon, and kidneys.

DNA methylation clocks are widely used in forensic science, epigenetics and longevity research to estimate a person’s biological age based on chemical changes in DNA. These epigenetic clocks help scientists predict age-related diseases and assess how lifestyle factors, such as smoking, impact aging. Most were originally developed using blood samples, and their effectiveness in other tissues remains unclear. This study tested eight different DNA methylation clocks across nine human tissue types, including the lungs, prostate, ovaries, skeletal muscle, and kidneys. The researchers analyzed data from 973 tissue samples collected through the Genotype-Tissue Expression (GTEx) project.

Their analysis revealed significant differences in biological age estimates across tissues. While blood samples provided the most reliable results, other tissues showed noticeable variations. For example, testis and ovary tissues appeared younger than expected, while lung and colon tissues appeared older. 

“These differences across tissue types were most apparent for clocks trained using DNAm from blood only (e.g., Hannum), but also present for clocks trained on multiple tissue types (e.g., Horvath, a clock designed for pan-tissue age prediction.”
 
These findings suggest that aging may not occur at the same rate in every organ, and that standard DNA methylation clocks may not always give accurate biological age estimates outside of blood samples. The authors suggest that new, organ-specific epigenetic clocks may be needed to improve biological age prediction. Creating tissue-specific aging clocks could also improve medical diagnostics, age-related disease prevention, and health monitoring.

The researchers emphasize that larger studies with more tissue-specific DNA methylation data are needed to refine these aging clocks. By improving these tools, scientists can better understand how aging affects different organs and develop more reliable methods for measuring biological age. These advancements could lead to better predictions of age-related diseases and new strategies for healthy aging.

DOI - https://doi.org/10.18632/aging.206182

Corresponding author - Brandon L. Pierce - brandonpierce@uchicago.edu

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DNA Methylation Clocks May Require Tissue-Specific Adjustments for Accurate Aging Estimates

It’s very difficult (often impossible) to completely avoid many of the environmental toxins that can cause harm - like air pollution and forever chemicals that contaminate our water and food supply. But Drs. Bob and Rosalind Wright at Mount Sinai have a hopeful solution to this dilemma. They are pioneering the study of “resiliency factors,” not just “risk factors,” that can offset the risks of harmful exposures. It’s a fresh and welcome take on exposomics that I am very excited to share with you. For instance - did you know that omega-3 intake during pregnancy can protect against the development of asthma in the child, even if the child is exposed to known risk factors for asthma? Or that positive relationships (ones that create a sensitive, positive, caregiving environment) have been shown to potentially mitigate the effects of environmental toxins? As a practitioner, I am always looking to empower patients with real solutions to the health challenges we inevitably face and I hope you enjoy this conversation as much as I did. ~DrKF

Check out the show notes at https://www.drkarafitzgerald.com/fxmed-podcast/ for the full list of links and resources.


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Dr. Rosalind J. Wright, MD, MPH and Robert O. Wright, MD, MPH
Icahn School of Medicine at Mount Sinai https://icahn.mssm.edu/

Dr. O. Robert Wright is the Ethel H. Wise Chair of Environmental Medicine at Mount Sinai and co-founder of the Institute for Exposomic Research. His research links environmental exposures, like those tracked in the PROGRESS cohort, with the developmental origins of diseases.

Dr. Rosalind J. Wright is Dean for Public Health at Icahn School of Medicine and Co-Director of the Institute for Climate Change, Environmental Health, and Exposomics. A pioneer in environmental health, she studies how early-life exposures influence chronic diseases and has been NIH-funded for over 23 years. She also mentors the next generation of clinical scientists.


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A Fresh Take on Exposomics: Resiliency Factors That Offset Environmental Risks

BUFFALO, NY – February 14, 2025 – A new #review was #published in Oncotarget, Volume 16, on February 12, 2025, titled “SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.”

Authors Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, and Antonin Marchais from the Gustave Roussy Cancer Campus analyzed recent studies on a gene called SETDB1, which may play a key role in osteosarcoma, a type of bone cancer that mostly affects teenagers and young adults. Their review highlights how SETDB1 helps cancer cells grow, resist treatment, and avoid the immune system. Because of this, blocking SETDB1 could be a promising new way to treat osteosarcoma.

Osteosarcoma is a fast-growing bone cancer that is usually treated with surgery and chemotherapy. However, if the cancer spreads or returns, treatment options are very limited. Scientists are searching for new ways to stop this disease, and recent studies have found that osteosarcoma cells often have extra copies of the SETDB1 gene. This seems to make the cancer more aggressive and harder to treat.

“Whole exome sequencing of osteosarcoma samples from both diagnosis and relapses has highlighted several factors, including SETDB1, that are amplified in the most aggressive forms of the disease.”

SETDB1 is involved in epigenetics, meaning it affects how genes are turned on and off without changing the DNA itself. The review explains that SETDB1 helps tumors hide from the immune system, making it difficult for the body to fight the cancer naturally. The researchers believe that blocking SETDB1 could help the immune system recognize and attack osteosarcoma cells. Some experimental drugs that target SETDB1 are already being tested in the lab.

The review also describes how SETDB1 influences key cancer pathways, such as Wnt signaling, which helps cancer cells grow, and epithelial-mesenchymal transition (EMT), a process that allows cancer to spread. The authors suggest that combining SETDB1-blocking drugs with immunotherapy or radiation could be an effective new strategy for treating osteosarcoma.

Another key finding is that SETDB1 may help cancer cells become resistant to chemotherapy, making treatment less effective. This means that drugs targeting SETDB1 could not only slow cancer growth but also make existing treatments work better.

While more research is needed, this review brings attention to SETDB1 as a potential treatment target. Scientists hope that a deeper understanding of SETDB1 will lead to new therapies that improve survival rates for osteosarcoma patients.

DOI - https://doi.org/10.18632/oncotarget.28688

Correspondence to - Antonin Marchais - antonin.marchais@gustaveroussy.fr, and Maria Eugenia Marques Da Costa - jenny.marquescosta@gustaveroussy.fr

Video short - https://www.youtube.com/watch?v=f9WgaDoEubs

About Oncotarget 

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Oncotarget is indexed and archived by PubMed/Medline, PubMed Central, Scopus, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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SETDB1 Amplification Identified as a Potential Target for New Osteosarcoma Treatment

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

Video short - https://www.youtube.com/watch?v=WcL-K399a7M

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Toxic Environmental Pollutants Linked to Faster Aging and Health Risks in U.S. Adults

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.)

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How Environmental Chemicals May Accelerate Biological Aging

This week The Bklyn Combine is joined by some of our sisters to discuss who our real opps are  as well as generational trauma, the reordering of the world, and much more.

We are the Brooklyn Combine, a non-profit community organization. We work with schools, community organizations, and dedicated city officials to help provide mentorship, critical education, leadership, and social support programs to youth and young adults in low-income and underserved communities.

Music: 
1. Slow by Navy Blue
2. Guess It's All Over by Mndsgn
3. Love To The World Prayer by L.T.D.
4. Black Panta by Lee "Scratch" Perry and The Upsetters 

Episode 4 Combine Cast Members: Cheshire Boone, Amy Obonaga, Yessica Urraca, Mali X, Kenji Summers, Jazz Joseph, Divensley Charles, Kenneth J. Montgomery, and Phillip Shung.

Productive Radicalism

BUFFALO, NY — April 16, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 12, 2025, titled “DNA methylation entropy is a biomarker for aging.”

Researchers Jonathan Chan, Liudmilla Rubbi, and Matteo Pellegrini from the University of California, Los Angeles, led a study that discovered a new way to measure changes in DNA that can help predict a person’s age. This method focuses on how random certain chemical tags on DNA become over time. The team compared this new measurement, called methylation entropy, to existing methods and found it performed just as well—or even better. These findings support the idea that changes in our epigenetic information are closely linked to aging and could offer new tools for studying age-related diseases.

The study focused on DNA methylation, a process where chemical marks are added to DNA and help control which genes are turned on or off. Scientists have traditionally measured average methylation levels to estimate biological age using “epigenetic clocks.” This study, however, takes a different approach. The researchers used buccal swabs (cells from inside the cheek) from 100 individuals between ages 7 and 84 and applied targeted bisulfite sequencing techniques to measure methylation entropy across 3,000 regions of the genome.

Entropy in this context reflects how disordered or varied the methylation patterns are at certain sites on the DNA. The researchers discovered that as people age, the entropy of methylation at many locations changes in a reproducible way. Sometimes it increases, reflecting more random patterns, and sometimes it decreases, showing more uniformity. These shifts are not always tied to how much methylation is happening, which suggests entropy provides new information beyond what traditional methods can offer.

To test how well this new metric could predict age, the team used both statistical and machine learning models. They found that methylation entropy predicted age as accurately as traditional methods, and the best results came from combining entropy with other measurements like average methylation and a method called CHALM. These combined models were able to estimate age with an average error of just five years.

"[...] methylation entropy is measuring different properties of a locus compared to mean methylation and CHALM, and that loci can become both more or less disordered with age, independently of whether the methylation is increasing or decreasing with age."

This research supports the growing theory that aging is partly caused by a gradual loss of epigenetic information—the biological “instructions” that help keep our cells working properly. This insight also connects with recent studies suggesting that restoring this lost information might reverse some signs of aging. While more research is needed to study methylation entropy in other tissues, this work points to a more precise and powerful way to measure biological aging, which could influence the future of aging-related treatments and therapies.

Read the full paper: DOI: https://doi.org/10.18632/aging.206220

Corresponding author: Matteo Pellegrini - matteope@gmail.com

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Keywords: entropy, DNA methylation, aging, epigenetics, epigenetic clocks

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DNA Methylation Entropy: A New Way to Track and Predict Aging

BUFFALO, NY — April 21, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 14, 2025, titled “Effects of a natural ingredients-based intervention targeting the hallmarks of aging on epigenetic clocks, physical function, and body composition: a single-arm clinical trial.”

A team of researchers, led by first authors Natalia Carreras-Gallo and Rita Dargham, and corresponding author Varun B. Dwaraka from TruDiagnostic, studied how a natural anti-aging supplement called the Cel System might influence the aging process. They found that participants who took the supplement for one year showed a reduction in biological age, along with improved muscle strength and body composition. The study highlights the potential of lifestyle and nutritional supplements to support healthy aging.

“The Cel System supplement range was formulated to target pathways associated with the Hallmarks of Aging when combining Cel1, Cel2, and Cel3 formulas.”

Cel System is a natural supplement made from a mix of plant compounds, vitamins, and antioxidants designed to target the biological mechanisms associated with aging. Over the course of a year, 51 adults between the ages of 54 and 84 participated in the clinical trial. The group included 26 men and 25 women. Researchers tracked changes in biological age using DNA-based tests known as epigenetic clocks, along with physical performance and body composition metrics. Participants were also encouraged to walk for 10 minutes and practice mindfulness for five minutes daily.

Results showed that participants experienced improvements in grip strength, lower body mobility, and reductions in body weight, waist circumference, and body mass index. These physical gains were supported by slower biological aging, as measured by multiple epigenetic clocks. In addition, the supplement appeared to reduce stem cell turnover, a key marker of aging at the cellular level.

The study also reported changes in immune cell composition, suggesting that the supplement may help regulate immune function as people age. Biomarkers associated with liver function also shifted, pointing to potential improvements in organ health. However, levels of inflammation markers did not significantly change.

Analysis of methylation chemical marks on DNA revealed that the supplement influenced gene activity related to stress response, brain function, and cell communication. These molecular-level changes may help explain the broader benefits seen in physical and biological aging measures.

Although this was a pilot study without a control group, the findings suggest that the Cel System supplement shows potential for reducing signs of aging and improving overall health. The authors suggest future randomized controlled trials with larger sample sizes to confirm these results and explore the supplement’s long-term effects on longevity.

This study adds to growing evidence that targeted natural supplements may slow biological aging and extend healthspan. By combining epigenetic analysis with real-world health data, the findings offer new insight into how nutraceuticals, like Cel System, could promote long-term health and resilience.

Paper: DOI: https://doi.org/10.18632/aging.206221

Corresponding author: Varun B. Dwaraka – varun.dwaraka@trudiagnostic.com

Keywords: aging, epigenetic age change, physiological age change, epigenetic biomarker proxies, hallmarks of aging, nutraceutical longevity interventions

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Natural Supplement May Decrease Biological Aging and Improve Muscle Strength

BUFFALO, NY — April 23, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 3, on March 18, 2025, titled “Epigenetic and accelerated age in captive olive baboons (Papio anubis), and relationships with walking speed and fine motor performance.”

In this study, led by Sarah J. Neal from The University of Texas MD Anderson Cancer Center, researchers examined how the epigenetic age of baboons—a measure of biological aging based on DNA methylation—compared to their actual age (chronological age) and whether it related to signs of aging like slower walking or reduced hand coordination. While many baboons showed a mismatch between their epigenetic and chronological ages, these differences did not consistently align with physical performance measures.

Researchers analyzed blood samples from 140 captive olive baboons (Papio anubis) to determine whether these primates, like humans, show signs of “age acceleration”—a condition where epigenetic age surpasses chronological age. The results revealed that about a quarter of the baboons exhibited accelerated aging, while another quarter showed signs of slower aging, known as “age deceleration.” 

“We found that epigenetic age was strongly correlated with chronological age, and that approximately 27% of the sample showed age acceleration and 28% showed age deceleration."

The scientists then investigated whether these differences were reflected in physical indicators such as walking speed or fine motor skills. To do this, researchers measured walking speed by tracking how quickly baboons moved between points in their enclosures and assessed fine motor skills using a simple task that involved picking up small objects.

Older baboons did tend to walk more slowly and perform worse on tasks requiring dexterity, patterns also seen in aging humans. However, these changes were more closely related to chronological age than epigenetic age. Two different methods were used to measure the gap between epigenetic and chronological age. Each method produced slightly different outcomes, highlighting the complexity of defining age acceleration. In one analysis, the oldest baboons appeared to age more slowly epigenetically, possibly reflecting selective survival, where only the healthiest individuals live into old age.

This research is among the first to classify baboons based on their epigenetic aging rate and investigate how this links to real-world signs of aging. Although the findings did not provide clear evidence that epigenetic age acceleration leads to physical decline, they point to the importance of DNA methylation as a biomarker in aging research. Because baboons share many biological similarities with humans, these findings help refine how researchers measure aging and assess potential early warning signs of decline. Continued studies in baboons and other primates may improve our understanding of how epigenetic aging influences health and longevity—and could help develop better tools for predicting age-related decline in humans.

DOI - https://doi.org/10.18632/aging.206223

Corresponding author - Sarah Neal - SJNeal@MDAnderson.org

Video short - https://www.youtube.com/watch?v=EFfRMFbAMqk

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Epigenetic Aging Detected in Baboons, But Physical Decline Not Clearly Linked

Depression and alcohol dependence are often seen as personal struggles—but decades of study by Scripps Research professor Cindy Ehlers reveal a much bigger picture. In this episode of Science Changing Life, Ehlers breaks down how biology, culture and trauma interact to shape mental health outcomes.

Learn how her work is paving the way for more effective interventions, and how new strategies—like culturally grounded prevention programs and digital tools—can reduce harm in high-risk communities.

//

Ehlers lab: ⁠https://www.scripps.edu/ehlers/index.html⁠ 
Scripps Research Magazine: ⁠https://magazine.scripps.edu⁠ 


Wired for risk: Cindy Ehlers on the science of addiction and mental health

BUFFALO, NY — May 20, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 4, on April 17, 2025, titled “Dietary associations with reduced epigenetic age: a secondary data analysis of the methylation diet and lifestyle study.”

In this study, researchers led by first author Jamie L. Villanueva from the University of Washington and the National University of Natural Medicine, along with corresponding author Ryan Bradley from the National University of Natural Medicine and University of California, investigated how diet influences epigenetic aging. They found that certain plant-based foods containing natural compounds called methyl adaptogens were associated with a decrease in epigenetic age. This effect was measured using DNA methylation, a marker that reflects how the body ages at the cellular level. The findings suggest that targeted food choices may help slow the aging process.

Epigenetic age refers to how old a person’s cells appear biologically, rather than their actual age in years. DNA methylation patterns, which are chemical tags on DNA, can indicate whether someone is aging faster or slower than expected. For this study, researchers used Horvath’s epigenetic clock, a widely accepted tool, to measure changes in epigenetic age.

The analysis included healthy men aged 50 to 72 who had previously completed an eight-week program featuring a plant-based, nutrient-rich diet, along with guidance on exercise, sleep, and stress management. Researchers focused on individual dietary differences to understand why some participants experienced greater improvements in epigenetic age than others.

The study found that those who ate higher amounts of methyl adaptogen foods—including turmeric, rosemary, garlic, berries, green tea, and oolong tea—experienced greater reductions in epigenetic age. These benefits remained significant even after accounting for weight changes and participants’ starting epigenetic age, suggesting that the foods themselves had a direct impact on aging markers.

“In hierarchical linear regression, foods investigated as polyphenolic modulators of DNA methylation (green tea, oolong tea, turmeric, rosemary, garlic, berries) categorized in the original study as methyl adaptogens showed significant linear associations with epigenetic age change (B = -1.21, CI = [-2.80, -0.08]), after controlling for baseline epigenetic age acceleration and weight changes.”

The natural compounds in methyl adaptogen foods are known to influence how genes behave by affecting DNA methylation. Previous studies have shown that these compounds may support healthy aging and help lower the risk of conditions such as heart disease and cognitive decline.

While this study involved a relatively small group of middle-aged men, it adds knowledge to growing global research showing that diets rich in polyphenols—found in vegetables, fruits, and teas—are associated with slower aging. These findings support earlier results from studies on Mediterranean and traditional Japanese diets, both known for their health benefits.

Future research should include larger and more diverse populations and use updated epigenetic aging tools to confirm these results. Based on current evidence, this study highlights a practical, food-based strategy that may help reduce epigenetic aging and support long-term health.

DOI - https://doi.org/10.18632/aging.206240

Corresponding author - Ryan Bradley - rbradley@nunm.edu

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Green Tea, Turmeric, and Berries May Help Reverse Epigenetic Aging in Men

In a world where we are living longer but not always healthier, scientists are searching for ways to add life to our years, not just years to our lives. A recent study published in Aging (Aging-US), Volume 17, Issue 4, led by researchers at the National University of Natural Medicine, suggests that certain common foods, already known for their health benefits, might also help slow or even reverse epigenetic or biological aging. These foods, rich in specific plant compounds, appear to influence our DNA in ways that may slow down the body’s epigenetic clock.

Full blog - https://aging-us.org/2025/05/study-identifies-foods-that-may-reverse-biological-age-and-promote-healthy-aging-in-men/

Paper DOI - https://doi.org/10.18632/aging.206240

Corresponding author - Ryan Bradley - rbradley@nunm.edu

Video short - https://www.youtube.com/watch?v=T6I33AIAIFM

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Keywords - aging, epigenetics, DNA methylation, diet, biological clock

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Study Identifies Foods That May Reverse Biological Age and Promote Healthy Aging in Men

BUFFALO, NY — June 4, 2025 — A new #editorial was #published in Aging (Aging-US) Volume 17, Issue 5, on May 29, 2025, titled “Rethinking healthcare through aging biology.”

In this scientific editorial, Aging (Aging-US) Editor-in-Chief Marco Demaria from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG) and the University of Groningen (RUG), advocates for healthcare reform that addresses the biological drivers of aging rather than individual chronic conditions. The article proposes that targeting the root causes of age-related diseases through aging biology could revolutionize preventive care, extend healthspan, and reduce long-term healthcare costs. This proactive approach aligns with a growing body of aging research focused on improving healthy longevity.

Dr. Demaria explains that today’s disease-focused model is inadequate for aging populations, who often suffer from multimorbidity—the presence of multiple chronic illnesses like cancer, heart disease, and type 2 diabetes. These overlapping conditions, rooted in common aging mechanisms, overwhelm healthcare systems and lead to complex treatments with limited success. The editorial suggests that identifying and intervening in the biological aging process could prevent such diseases before they emerge.

In the editorial, Dr. Demaria outlines three healthcare paradigms. The first is the existing system, which reacts to disease after symptoms appear. The second involves intervening once age-related damage begins, using new tools such as senolytics, which eliminate harmful senescent cells, and rapalogs, which regulate cellular metabolism. The third and most forward-looking model focuses on preventing aging-related damage before it starts. This strategy supports lifelong biological balance and seeks to avoid early molecular decline through continuous health maintenance.

Prevention is key in this model. Lifestyle choices—such as exercise, a healthy diet, quality sleep, and stress reduction—play a vital role in slowing the aging process. Dr. Demaria also points to the promise of biological age diagnostics—tools or tests that estimate a person’s biological age—which allow people to track their physiological aging and adopt personalized interventions. Additionally, optimizing maternal nutrition and early-life health can contribute to lifelong disease prevention.

To support this shift, the editorial calls for major changes in medical education. Physicians must be trained in geroscience, healthspan optimization, and personalized preventive care. This knowledge will prepare future clinicians not just to treat disease, but to delay or prevent it altogether. Collaboration among healthcare providers, researchers, and policymakers will be essential for building this new system.

​​“The third paradigm—preventing aging-related damage—demands a systemic shift toward predictive and preventative research, with an emphasis on multi-omic data, lifestyle interventions, and early-life interventions.”

By redefining medicine around the science of aging, Dr. Demaria’s editorial highlights the path toward healthier aging, longer life expectancy, and a more sustainable healthcare future.

DOI - https://doi.org/10.18632/aging.206262

Corresponding author - Marco Demaria - m.demaria@umcg.nl

Video short - https://www.youtube.com/watch?v=xR-16cjHnQY

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New Vision for Healthcare Focuses on Preventing Aging-Related Diseases

In this very special episode, I have the privilege of turning the tables on Dr. Kara Fitzgerald as we celebrate 10 years of the New Frontiers podcast. I’ve been honored to walk alongside Kara on much of this journey—as a colleague, a collaborator, a mentee, and a friend—and it’s been incredible to witness the evolution of both her work and the field itself.

Together, we reflect on the stories, science, and people who have shaped this podcast—and the remarkable growth of epigenetics, personalized medicine, and functional medicine along the way. From early conversations around methylation and aging to hosting pioneers like Dr. Jeff Bland, Dr. Sidney Baker, and Dr. Charles Serhan, New Frontiers has become a living archive of how this field has moved forward.

As we talked about during the conversation: “Everybody is a piece of this ecosystem, and everybody has their role... It’s really cool to be part of that community.” This episode is a celebration of that collective journey—and a look at where we’re headed next. ~Romilly Hodges MS CNS

Check out the show notes at https://www.drkarafitzgerald.com/fxmed-podcast/ for the full list of links and resources.

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10 Year Anniversary: What I Learned After 200+ Conversations with the Best Minds in FxMed

Recent discoveries in #aging research reveal a powerful insight: the biological changes that lead to chronic #diseases begin far earlier than most people realize—often in midlife, well before symptoms appear. This early phase offers a valuable opportunity for prevention. As highlighted in a recent editorial by Marco Demaria, Editor-in-Chief of Aging and a researcher at the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen, and the University of Groningen (RUG), the aging process itself – not just the diseases it produces – can and should be a primary focus of healthcare. 

The Problem with Traditional Medicine

While modern healthcare has extended lifespan and improved treatment for many diseases, it tends to be insufficient in addressing the complex needs of aging populations. Older individuals frequently experience multiple chronic conditions simultaneously, such as cardiovascular disease, diabetes, cancer, and neurodegenerative disorders. This state of multimorbidity complicates care, increases the use of multiple medications, and reduces quality of life. The dominant traditional healthcare system, which typically begins only after symptoms appear, is costly and insufficient for addressing the interconnected nature of these conditions.

A New Model for Healthcare: Insights from the Editorial

In his recent editorial, “Rethinking healthcare through aging biology,” published in Aging Volume 17, Issue 5, Dr. Demaria outlines a shift from disease-specific treatment to targeting the biological mechanisms of aging itself, a more integrated and forward-looking approach. He presents three evolving healthcare models.

Full blog - https://aging-us.org/2025/06/a-new-vision-for-healthcare-addressing-aging-before-disease-begins/

Paper DOI - https://doi.org/10.18632/aging.206262

Corresponding author - Marco Demaria - m.demaria@umcg.nl

Video short - https://www.youtube.com/watch?v=xR-16cjHnQY

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Keywords - aging, healthcare, senolytics, epigenetics, medical education

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A New Vision for Healthcare: Addressing Aging Before Disease Begins

Dr. Andres Cardenas, from the Department of Epidemiology and Population Health at Stanford University, joins host Dr. Evgeniy Galimov to discuss a research paper he co-authored in Volume 17, Issue 2 of Aging (Aging-US), titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the National Health and Nutrition Examination Survey.”

DOI - https://doi.org/10.18632/aging.206201

Corresponding author - Andres Cardenas - andresca@stanford.edu

Video interview - https://www.youtube.com/watch?v=A1I6qoVwkfM

Longevity & Aging Series - https://www.aging-us.com/longevity

Abstract

Epigenetic clocks can serve as pivotal biomarkers linking environmental exposures with biological aging. However, research on the influence of environmental exposures on epigenetic aging has largely been limited to a small number of chemicals and specific populations. 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. A total of 8 epigenetic aging biomarkers were obtained from whole blood in 2,346 participants ranging from 50-84 years of age. A total of 64 environmental exposures including phthalates, metals, pesticides, dioxins, and polychlorinated biphenyls (PCBs) were measured in blood and urine. Associations between log2-transformed/standardized exposure measures and epigenetic age acceleration (EAA) were assessed using survey-weighted generalized linear regression. A 1 standard deviation (SD) increase in log2 serum cadmium levels was associated with higher GrimAge acceleration (beta = 1.23 years, p = 3.63e-06), higher GrimAge2 acceleration (beta = 1.27 years, p = 1.62e-05), and higher DunedinPoAm (beta = 0.02, p = 2.34e-05). A 1 SD increase in log2 serum cotinine levels was associated with higher GrimAge2 acceleration (beta = 1.40 years, p = 6.53e-04) and higher DunedinPoAm (beta = 0.03, p = 6.31e-04). Associations between cadmium and EAA across several clocks persisted in sensitivity models adjusted for serum cotinine levels, and other associations involving lead, dioxins, and PCBs were identified. Several environmental exposures are associated with epigenetic aging in a nationally representative US adult population, with particularly strong associations related to cadmium and cotinine across several epigenetic clocks.

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Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics

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Longevity & Aging Series (S3, E5): Dr. Andres Cardenas

BUFFALO, NY — July 30, 2025 — A new #research paper was #published in Aging (Aging-US) on July 23, 2025, titled “Second generation DNA methylation age predicts cognitive change in midlife: the moderating role of childhood socioeconomic status.”

In this study, led by Sophie A. Bell and Eric Turkheimer from the University of Virginia, researchers investigated how biological aging, measured through DNA methylation, is connected to changes in thinking skills during midlife and whether childhood socioeconomic status influences this relationship. 

Biological age provides a picture of how the body is aging that goes beyond simply counting years. In this study, researchers used both first- and second-generation DNA methylation clocks—tools that track chemical changes in DNA as markers of aging. GrimAge and PhenoAge, the second-generation clocks designed to reflect broader health and aging processes, were more accurate at predicting long-term changes in Intelligence Quotient (IQ) than the first-generation models that only estimated chronological age. The study analyzed 287 participants from the Louisville Twin Study, which is a long-term project that has followed twins from childhood into midlife.

“DNAmAge was estimated with five commonly used algorithms, or epigenetic clocks (Horvath, Horvath Skin and Blood, GrimAge, and PhenoAge).”

The results showed that twins with more rapid epigenetic aging had a larger drop in IQ scores. This pattern remained even after considering genetic background and early family environment, made possible by the twin-based design. Importantly, the relationship was strongest in twins who had grown up in families with lower socioeconomic status. This finding suggests that early-life disadvantage may make individuals more vulnerable to the effects of biological aging on brain health.

This research adds knowledge to earlier work showing that childhood poverty can influence long-term health. It also highlights the value of second-generation epigenetic clocks as early indicators of brain aging. Unlike the first generation of clocks, these newer tools capture broader biological changes such as inflammation, disease risk, and behaviors like smoking.

Although smoking partly explained the results because it strongly influences DNA methylation, it did not fully account for the association between accelerated biological aging and cognitive decline. This suggests that both life experiences and lifestyle factors shape body and brain aging.

By combining decades of developmental data with a genetically informed twin design, the study provides new evidence that biological aging, especially when shaped by childhood adversity, is a key factor in midlife cognitive decline. These findings may inform early health strategies that consider both social and biological risks and support the use of second-generation methylation clocks to predict age-related cognitive changes.

DOI - https://doi.org/10.18632/aging.206284

Corresponding authors - Sophie A. Bell - bvf7pa@virginia.edu, and Eric Turkheimer - ent3c@virginia.edu

Video short - https://www.youtube.com/watch?v=vopDdS1olXw

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Study in Twins Links Childhood Environment to Epigenetic Aging and Cognitive Decline

Cereno Scientific CEO Sten Sörensen discusses how his company is repurposing a 60-year-old epilepsy drug as a potential game-changer for pulmonary arterial hypertension and idiopathic pulmonary fibrosis. Learn about their promising Phase IIa results that showed improved heart function and reduced mortality risk, the FDA fast track designation they recently received, and their strategy for advancing two rare disease programs toward pivotal trials. A fascinating look at drug repurposing, epigenetic modulation, and the challenges of developing therapies for high unmet need patient populations.

Cereno Scientific Turns To Old Drug For Rare Cardiopulmonary Diseases

Citeline places biopharma and medical device professionals, and those who focus on these industries, at the forefront of knowledge and insight, by providing the perfect combination of news and information together with penetrating insight and analysis. Citeline is a leader in the field of healthcare industry information.

Welcome to New Frontiers in Functional Medicine, Longevity & Epigenetics™ where I interview the best minds in functional medicine to discuss the science and research behind medicine, longevity, epigenetics, and so much more. Expect thought-provoking ideas, new research, lots of clinical pearls for practitioners, and step-change information for clinicians and patients. Join us! ~DrKF  

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Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

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

The award-winning Science Changing Life podcast offers an inside look into how Scripps Research scientists are solving the most pressing mysteries in human health and disease. Join hosts Lauren Fish and Melissa Suran, PhD, as they speak with world-class scientists at the forefronts of immunology, infectious disease, artificial intelligence, personalized medicine, neuroscience and much more. 

Science Changing Life gives listeners a glimpse into the people behind the science, their motivations, paths to discovery, and how they’re changing the world. 

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A podcast coming from the planet of Brooklyn that examines critical thought and community, while searching for solutions to some of our most challenging issues.

New tracks tagged #epigenetics