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Plant-Based Dietary Patterns Are Associated With Slower Biological Aging

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“The present study found that dietary patterns higher in plant foods and lower in animal products were consistently associated with decelerated DNA methylation-derived aging biomarkers, specifically GrimAge2 and PhenoAge.”

As people live longer, maintaining good health is becoming just as important as extending lifespan. While chronological age simply reflects the number of years a person has lived, biological age measures how well the body is functioning and may better predict future health. Researchers have increasingly focused on lifestyle factors that may slow biological aging, and diet has emerged as one of the most promising.

A research paper published in Volume 18 of Aging titled “Plant-based dietary patterns are associated with slower epigenetic aging,” investigated whether diets emphasizing plant foods are associated with slower biological aging as measured by DNA methylation-based epigenetic clocks.

Looking Beyond Chronological Age

Not everyone ages at the same rate. While two individuals may share the same chronological age, one may remain healthier and more resilient than the other because their biological age is lower.

One of the most widely used approaches involves measuring DNA methylation, a natural chemical modification of DNA that changes throughout life. These patterns can be analyzed using so-called epigenetic clocks, including GrimAge2, PhenoAge, and HannumAge, which have been shown to predict future risks of chronic disease, disability, and mortality more accurately than chronological age alone.

Previous studies have suggested that healthy dietary patterns may help slow epigenetic aging. However, it remained unclear whether plant-based diets in people who do not necessarily follow vegetarian or vegan lifestyles are associated with these biological aging markers.

Comparing Different Types of Plant-Based Diets

To investigate this question, the researchers analyzed data from two large U.S. population studies: the Atherosclerosis Risk in Communities (ARIC) Study and the National Health and Nutrition Examination Survey (NHANES). Together, the analysis included more than 4,800 middle-aged and older adults.

Rather than simply comparing vegetarians with non-vegetarians, the investigators evaluated four different plant-based dietary patterns:

  • Overall Plant-Based Diet Index (PDI), which rewards greater intake of plant foods and lower intake of animal foods.
  • Provegetarian Diet Index, which emphasizes relatively higher consumption of plant foods while reducing animal products.
  • Healthy Plant-Based Diet Index (healthy PDI), which favors nutrient-rich foods such as fruits, vegetables, whole grains, legumes, and nuts.
  • Unhealthy Plant-Based Diet Index (unhealthy PDI), which reflects greater intake of refined grains, sugary foods, and other less nutritious plant-derived foods.

The researchers then examined whether these dietary patterns were associated with three widely used measures of epigenetic aging after accounting for age, lifestyle, socioeconomic factors, smoking, alcohol use, physical activity, and other potential confounding variables.

Healthier Plant-Based Diets Were Linked to Slower Epigenetic Aging

The study found that greater adherence to overall plant-based diets, provegetarian diets, and healthy plant-based diets was consistently associated with slower biological aging.

Participants with higher scores for the overall plant-based diet and provegetarian diet showed slower GrimAge2 and PhenoAge acceleration. Higher adherence to the overall plant-based diet was also associated with slower HannumAge. Healthy plant-based diets were linked to slower GrimAge2, although the associations with the other epigenetic clocks were less consistent.

In contrast, unhealthy plant-based diets showed no significant association with any of the biological aging measures.

These findings suggest that the quality of plant foods matters. Simply consuming fewer animal products may not be enough if the diet relies heavily on refined carbohydrates, added sugars, and other less nutritious plant-based foods.

How Diet Influences Biological Aging

Although this study was not designed to identify the underlying biological mechanisms, the authors discuss several possibilities.

Plant-based diets are typically rich in dietary fiber, vitamins, minerals, antioxidants, and other bioactive compounds that are thought to help reduce oxidative stress and chronic inflammation, two processes believed to contribute to biological aging. These diets have also been associated with improved blood pressure, healthier cholesterol levels, better glucose regulation, and reduced risk of cardiovascular disease.

Over time, these favorable metabolic effects may influence DNA methylation patterns, resulting in slower progression of biological aging as measured by epigenetic clocks.

The researchers also note that plant-based diets are not all alike. Diets centered on whole, minimally processed plant foods appear to offer greater health benefits than those dominated by refined grains, sugary beverages, and highly processed plant-derived products.

What Makes This Study Different?

Unlike many previous studies that focused on vegetarian or vegan diets, this investigation evaluated plant-based eating patterns in a largely non-vegetarian population.

This distinction is important because many people adopt diets that increase plant food consumption without completely eliminating animal products. The findings suggest that even moderate shifts toward healthier plant-based eating patterns may be associated with measurable differences in biological aging.

Another strength of the study is its use of two large, independent U.S. cohorts and multiple validated epigenetic aging measures, increasing confidence that the observed associations were consistent across different populations.

Looking Ahead

The authors conclude that dietary patterns emphasizing healthy plant foods and limiting animal products are associated with slower epigenetic aging. While the study cannot establish cause and effect, it adds to growing evidence that long-term dietary habits may influence biological processes linked to aging and future health.

Additional research, including long-term intervention studies, will be needed to determine whether adopting healthier plant-based diets can directly slow biological aging over time. As scientists continue exploring the relationship between nutrition and longevity, this study suggests that everyday food choices may play an important role in promoting healthier aging at the molecular level.

Click here to read the full research paper published in Aging.

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EDITORS’ CHOICE: Plant-based dietary patterns are associated with slower epigenetic aging

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Each month, we will highlight a paper published in Aging-US chosen as the “Editors’ Choice.” These selections are handpicked by our editors and accompanied by a brief summary, showcasing research with significant impact and novel insights in aging and age-related diseases.

In this study, titled “Plant-based dietary patterns are associated with slower epigenetic aging,” the researchers examined whether plant-based dietary patterns are linked to biological aging in large, diverse U.S. populations. Using data from the Atherosclerosis Risk in Communities (ARIC) Study and National Health and Nutrition Examination Survey (NHANES), they analyzed several versions of plant-based diet scores that reflect higher intake of plant foods and lower intake of animal products, as well as distinctions between healthy and less healthy plant-based foods. They then compared these dietary patterns with DNA methylation-based “epigenetic clocks,” which estimate biological age, including GrimAge2, PhenoAge, and HannumAge.

The results showed that greater adherence to overall plant-based diets, provegetarian diets, and especially healthy plant-based diets was consistently associated with slower epigenetic aging, meaning participants appeared biologically younger than their chronological age. In contrast, diets higher in less healthy plant-based foods did not show the same benefits.

The findings suggest that diets emphasizing whole plant foods and limiting animal products may help slow biological aging at the molecular level.

Click here to read the full research paper published in Aging-US.

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Rooted in Chinese Medicine: Zicao’s Anti-Cancer Effects on Lung Cancer

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In this new study, researchers investigated a plant used in traditional Chinese medicine and its anti-cancer effects in non-small cell lung cancer (NSCLC).

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Traditional Chinese medicine has long been explored for its potential in treating various diseases, including cancer. Lithospermum erythrorhizon, or purple gromwell, is a mysterious plant native to East Asia, and its dried root is often referred to as Zicao. Acetylshikonin, a compound derived from Zicao, has shown promise in exhibiting a variety of anti-cancer properties. While the effects of acetylshikonin on lung cancer are not yet fully understood, recent research has shed light on its potential as a therapeutic agent. 

In a new study, researchers Shih-Sen Lin, Tsung-Ming Chang, Augusta I-Chin Wei, Chiang-Wen Lee, Zih-Chan Lin, Yao-Chang Chiang, Miao-Ching Chi, and Ju-Fang Liu from Shin Kong Wu Ho-Su Memorial Hospital, Chang Gung Memorial Hospital, Chang Gung University of Science and Technology, Ming Chi University of Technology, Taipei Medical University, and China Medical University aimed to explore the mechanisms underlying acetylshikonin-induced cell death in non-small cell lung cancer (NSCLC). On December 19, 2023, their research paper was published in Aging’s Volume 15, Issue 24, entitled, “Acetylshikonin induces necroptosis via the RIPK1/RIPK3-dependent pathway in lung cancer.”

“This study explored the mechanisms underlying acetylshikonin-induced cell death in non-small cell lung cancer (NSCLC).”

Acetylshikonin and Cell Viability Reduction

In this study, researchers investigated the effects of acetylshikonin on the viability of NSCLC cells. The researchers treated H1299 and A549 cells with varying concentrations of acetylshikonin and assessed cell viability using a cell counting kit-8 (CCK-8) assay. The results showed that acetylshikonin significantly reduced cell viability in a dose-dependent manner. The IC50 values for H1299 and A549 cells were determined to be 2.34 μM and 3.26 μM, respectively. These findings suggest that acetylshikonin has the potential to effectively reduce the viability of lung cancer cells without causing significant damage to normal cells.

Cell Death Induction by Acetylshikonin

To further investigate the effects of acetylshikonin on NSCLC cells, the team examined the morphological changes associated with cell death. They observed that acetylshikonin treatment led to chromatin condensation, cell shrinkage, and the formation of cell debris, indicating cell death. Additionally, Annexin V/propidium iodide (PI) staining demonstrated an increase in the population of cells positive for Annexin V and PI, suggesting the induction of both apoptotic and necrotic cell death. Further analysis revealed that acetylshikonin increased membrane permeability, as evidenced by the uptake of PI by the cells. These findings indicate that acetylshikonin promotes cell death in NSCLC cells, potentially through necrotic pathways.

Acetylshikonin and Cell Cycle Arrest

In addition to its effects on cell viability and cell death, acetylshikonin was found to induce cell cycle arrest in NSCLC cells. The researchers examined the cell cycle progression of H1299 and A549 cells treated with acetylshikonin. Flow cytometry analysis revealed an increase in the proportion of cells in the subG1 and G2/M phases, indicating DNA fragmentation and cell cycle arrest in the G2/M phase. Western blot analysis further confirmed these findings by showing a decrease in the expression of cell cycle regulatory proteins, CDK1 and cyclin B1, in acetylshikonin-treated cells. These results suggest that acetylshikonin exerts its anti-cancer effects by inducing cell cycle arrest, thereby inhibiting cancer cell proliferation.

Oxidative Stress and Mitochondrial Dysfunction

The team also investigated the involvement of oxidative stress and mitochondrial dysfunction in acetylshikonin-induced cell death. Acetylshikonin treatment was found to increase intracellular reactive oxygen species (ROS) levels in NSCLC cells. This increase in ROS was associated with a decrease in mitochondrial membrane potential (MMP), indicating mitochondrial dysfunction. These findings suggest that acetylshikonin induces oxidative stress and disrupts mitochondrial function in NSCLC cells, potentially contributing to cell death.

Lipid Peroxidation and GPX4 Expression

The researchers explored the role of lipid peroxidation and the expression of glutathione peroxidase 4 (GPX4) in acetylshikonin-induced cell death. They observed that acetylshikonin treatment caused lipid peroxidation, as evidenced by the quenching of red fluorescence in BODIPY™ 581/591 C11-stained cells. This lipid peroxidation was associated with a decrease in GPX4 expression. GPX4 is an enzyme involved in maintaining cellular homeostasis and protecting against oxidative stress. The downregulation of GPX4 in NSCLC cells treated with acetylshikonin suggests a potential mechanism for inducing cell death.

Necroptosis Pathway Activation by Acetylshikonin

The team further investigated the mechanism by which acetylshikonin induces cell death in NSCLC cells. They found that acetylshikonin promoted the phosphorylation of receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like kinase (MLKL). These proteins are key players in the necroptosis signaling pathway. Immunofluorescence staining showed an increase in MLKL phosphorylation in acetylshikonin-treated cells, while Western blot analysis confirmed the activation of RIPK1, RIPK3, and MLKL. Importantly, pretreatment with RIPK1 inhibitors reversed the phosphorylation of MLKL and significantly attenuated cell death induced by acetylshikonin, suggesting that the activation of the RIPK1/RIPK3/MLKL cascade is involved in the necroptotic cell death pathway triggered by acetylshikonin.

Conclusion

In conclusion, acetylshikonin exhibits promising anti-cancer effects in NSCLC cells. It reduces cell viability, induces cell death, and promotes cell cycle arrest in the G2/M phase. Acetylshikonin also increases membrane permeability and activates the necroptosis signaling pathway through the phosphorylation of RIPK1, RIPK3, and MLKL. Furthermore, acetylshikonin induces oxidative stress, disrupts mitochondrial function, and promotes lipid peroxidation. These findings suggest that acetylshikonin holds potential as a therapeutic agent for the treatment of lung cancer. Further research is warranted to explore the clinical applications of acetylshikonin and its potential synergistic effects with existing lung cancer therapies.

“We determined that even low doses of acetylshikonin reduced the viability of lung cancer cells without significantly affecting normal cells. When used to treat lung cancer, acetylshikonin was shown to promote cell death and arrest cell cycle progression in the G2/M phase.”

Click here to read the full research paper published in Aging.

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Aging is an open-access, traditional, peer-reviewed journal that has published high-impact papers in all fields of aging research since 2009. All papers are available to readers (at no cost and free of subscription barriers) in bi-monthly issues at Aging-US.com.

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For media inquiries, please contact [email protected].

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