Epigenetic age acceleration predicts cancer, cardiovascular, and all-cause mortality in a German case cohort
Background Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand s...
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| Vydáno v: | Clinical epigenetics Ročník 8; číslo 1; s. 64 |
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| Hlavní autoři: | , , , , , |
| Médium: | Journal Article |
| Jazyk: | angličtina |
| Vydáno: |
London
BioMed Central
03.06.2016
BioMed Central Ltd Springer Nature B.V |
| Témata: | |
| ISSN: | 1868-7075, 1868-7083, 1868-7083, 1868-7075 |
| On-line přístup: | Získat plný text |
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| Abstract | Background
Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality.
Results
DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age (Δ
age
) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of Δ
age
with cancer, cardiovascular, and all-cause mortality. Hazard ratios for Δ
age
(per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10–1.38) for all-cause mortality, 1.22 (95 % CI 1.03–1.45) for cancer mortality, and 1.19 (95 % CI 0.98–1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for Δ
age
calculated using the epigenetic clock developed by Hannum.
Conclusions
These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. |
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| AbstractList | Background
Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality.
Results
DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age (Δ
age
) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of Δ
age
with cancer, cardiovascular, and all-cause mortality. Hazard ratios for Δ
age
(per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10–1.38) for all-cause mortality, 1.22 (95 % CI 1.03–1.45) for cancer mortality, and 1.19 (95 % CI 0.98–1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for Δ
age
calculated using the epigenetic clock developed by Hannum.
Conclusions
These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. Background Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality. Results DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age (Δage) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of Δage with cancer, cardiovascular, and all-cause mortality. Hazard ratios for Δage (per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10-1.38) for all-cause mortality, 1.22 (95 % CI 1.03-1.45) for cancer mortality, and 1.19 (95 % CI 0.98-1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for Δage calculated using the epigenetic clock developed by Hannum. Conclusions These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality.BACKGROUNDPrevious studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality.DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age (Δage) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of Δage with cancer, cardiovascular, and all-cause mortality. Hazard ratios for Δage (per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10-1.38) for all-cause mortality, 1.22 (95 % CI 1.03-1.45) for cancer mortality, and 1.19 (95 % CI 0.98-1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for Δage calculated using the epigenetic clock developed by Hannum.RESULTSDNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age (Δage) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of Δage with cancer, cardiovascular, and all-cause mortality. Hazard ratios for Δage (per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10-1.38) for all-cause mortality, 1.22 (95 % CI 1.03-1.45) for cancer mortality, and 1.19 (95 % CI 0.98-1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for Δage calculated using the epigenetic clock developed by Hannum.These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging.CONCLUSIONSThese results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality. DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age ([DELA].sub.age) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of [DELA].sub.age with cancer, cardiovascular, and all-cause mortality. Hazard ratios for [DELA].sub.age (per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10-1.38) for all-cause mortality, 1.22 (95 % CI 1.03-1.45) for cancer mortality, and 1.19 (95 % CI 0.98-1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for [DELA].sub.age calculated using the epigenetic clock developed by Hannum. These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. Background Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality. Results DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age ([DELA].sub.age) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of [DELA].sub.age with cancer, cardiovascular, and all-cause mortality. Hazard ratios for [DELA].sub.age (per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10-1.38) for all-cause mortality, 1.22 (95 % CI 1.03-1.45) for cancer mortality, and 1.19 (95 % CI 0.98-1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for [DELA].sub.age calculated using the epigenetic clock developed by Hannum. Conclusions These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. Keywords: DNA methylation age, Epigenetic clock, Epigenetic age acceleration, Mortality risk Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the difference between DNA methylation and chronological ages as a marker of healthy aging. The goal of this study was to confirm and expand such observations by investigating whether different concepts of the epigenetic clocks in a population-based cohort are associated with cancer, cardiovascular, and all-cause mortality. DNA methylation age was estimated in a cohort of 1863 older people, and the difference between age predicted by DNA methylation and chronological age (Δage) was calculated. A case-cohort design and weighted proportional Cox hazard models were used to estimate associations of Δage with cancer, cardiovascular, and all-cause mortality. Hazard ratios for Δage (per 5 years) calculated using the epigenetic clock developed by Horvath were 1.23 (95 % CI 1.10-1.38) for all-cause mortality, 1.22 (95 % CI 1.03-1.45) for cancer mortality, and 1.19 (95 % CI 0.98-1.43) for cardiovascular mortality after adjustment for batch effects, age, sex, educational level, history of chronic diseases, hypertension, smoking status, body mass index, and leucocyte distribution. Associations were similar but weaker for Δage calculated using the epigenetic clock developed by Hannum. These results show that age acceleration in terms of the difference between age predicted by DNA methylation and chronological age is an independent predictor of all-cause and cause-specific mortality and may be useful as a general marker of healthy aging. |
| ArticleNumber | 64 |
| Audience | Academic |
| Author | Saum, Kai-Uwe Holleczek, Bernd Zhang, Yan Mons, Ute Perna, Laura Brenner, Hermann |
| Author_xml | – sequence: 1 givenname: Laura surname: Perna fullname: Perna, Laura email: l.perna@dkfz-heidelberg.de organization: Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ) – sequence: 2 givenname: Yan surname: Zhang fullname: Zhang, Yan organization: Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ) – sequence: 3 givenname: Ute surname: Mons fullname: Mons, Ute organization: Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ) – sequence: 4 givenname: Bernd surname: Holleczek fullname: Holleczek, Bernd organization: Saarland Cancer Registry – sequence: 5 givenname: Kai-Uwe surname: Saum fullname: Saum, Kai-Uwe organization: Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ) – sequence: 6 givenname: Hermann surname: Brenner fullname: Brenner, Hermann organization: Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Network Aging Research (NAR), University of Heidelberg |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27274774$$D View this record in MEDLINE/PubMed |
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| Keywords | Epigenetic clock DNA methylation age Mortality risk Epigenetic age acceleration |
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| Snippet | Background
Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested... Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested the... Background Previous studies have developed models predicting methylation age from DNA methylation in blood and other tissues (epigenetic clock) and suggested... |
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| StartPage | 64 |
| SubjectTerms | Aged Aging Aging (Biology) Aging - genetics Biomedical and Life Sciences Biomedicine Biorhythms Blood - metabolism Cardiovascular Diseases - genetics Cause of Death Cohort Studies development Disease susceptibility Epigenesis, Genetic Epigenetic inheritance Female Gene Function Genetic aspects Health aspects Human Genetics Humans imprinting and reproductive epigenetics Leukocyte Count Male Middle Aged Mortality Neoplasms - genetics Proportional Hazards Models Risk Factors |
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| Title | Epigenetic age acceleration predicts cancer, cardiovascular, and all-cause mortality in a German case cohort |
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