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Can epigenetic clock acceleration be linked to cancer? Searching for causality
Genetically predicted GrimAge acceleration increased the risk of colorectal cancer in males and females.
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Epigenetic clocks are a measure of biological aging obtained from the DNA methylation (DNAmeth) data. DNAmeth is correlated with chronological and biological aging at specific cytosine-phosphate-guanine (CPG) sites. The literature suggests that accelerated biological aging, compared to chronological age, increases the risk of the early development of age-related disorders like cancer.
Examples of first-generation epigenetic clocks are the HannumAge and the HorvathAge. The former is trained to evaluate age-related CPG sites found in blood, while the latter assesses CPGs found in several tissue and cell types. Second-generation epigenetic clocks, like GrimAge, and PhenoAge, assess mortality-related CPGs in addition to clinical biomarkers and plasma proteins. This means that first-generation epigenetic clocks are more equipped to predict chronological age, while second-generation ones can predict health and lifespan.
Evidence suggesting the relationship between epigenetic clock acceleration and cancer is still being explored. Research in this area is cluttered by factors like reverse causation (cancer influences epigenetic changes, not the other way around) and confounding (unmeasured confounders of the association between epigenetic acceleration and cancer development). In addition to the previous, lack of consensus between epigenetic clocks, which could be attributed to differences in their algorithm, is also among the challenges. Mendelian randomization (a method that uses measured genetic variants to determine the association between a risk factor and an outcome) is required to overcome the confounding factors. Using the said technique, Berstein et al. employed the abovementioned epigenetic clocks to examine the effects of accelerated epigenetic aging on multiple cancers using data from several international genetic consortia, like the UK biobank, FinnGen, and others.
The study revealed no strong evidence of causality between epigenetic age acceleration and breast cancer, ovarian cancer, prostate cancer, or lung cancer. However, results suggest that genetically predicted GrimAge acceleration increased the risk of colorectal cancer in males and females, detecting evidence of causality. Additional findings highlighted that genetically predicted GrimAge and HorvathAge acceleration might decrease the risk of prostate cancer and act as a protective factor against lung cancer, respectively.
The authors concluded that GrimAge acceleration might increase the risk of colorectal cancer, while results for other epigenetic clocks were less consistent, requiring further investigation.
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Epigenetic clocks are a measure of biological aging obtained from the DNA methylation (DNAmeth) data. DNAmeth is correlated with chronological and biological aging at specific cytosine-phosphate-guanine (CPG) sites. The literature suggests that accelerated biological aging, compared to chronological age, increases the risk of the early development of age-related disorders like cancer.
Examples of first-generation epigenetic clocks are the HannumAge and the HorvathAge. The former is trained to evaluate age-related CPG sites found in blood, while the latter assesses CPGs found in several tissue and cell types. Second-generation epigenetic clocks, like GrimAge, and PhenoAge, assess mortality-related CPGs in addition to clinical biomarkers and plasma proteins. This means that first-generation epigenetic clocks are more equipped to predict chronological age, while second-generation ones can predict health and lifespan.
Evidence suggesting the relationship between epigenetic clock acceleration and cancer is still being explored. Research in this area is cluttered by factors like reverse causation (cancer influences epigenetic changes, not the other way around) and confounding (unmeasured confounders of the association between epigenetic acceleration and cancer development). In addition to the previous, lack of consensus between epigenetic clocks, which could be attributed to differences in their algorithm, is also among the challenges. Mendelian randomization (a method that uses measured genetic variants to determine the association between a risk factor and an outcome) is required to overcome the confounding factors. Using the said technique, Berstein et al. employed the abovementioned epigenetic clocks to examine the effects of accelerated epigenetic aging on multiple cancers using data from several international genetic consortia, like the UK biobank, FinnGen, and others.
The study revealed no strong evidence of causality between epigenetic age acceleration and breast cancer, ovarian cancer, prostate cancer, or lung cancer. However, results suggest that genetically predicted GrimAge acceleration increased the risk of colorectal cancer in males and females, detecting evidence of causality. Additional findings highlighted that genetically predicted GrimAge and HorvathAge acceleration might decrease the risk of prostate cancer and act as a protective factor against lung cancer, respectively.
The authors concluded that GrimAge acceleration might increase the risk of colorectal cancer, while results for other epigenetic clocks were less consistent, requiring further investigation.
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
Quality Garant
Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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