This 2022 human study investigated tissue-specific epigenetic clock measurements: “We used DNA methylation data representing 11 human tissues (adipose, blood, bone marrow, heart, kidney, liver, lung, lymph node, muscle, spleen, and pituitary gland) to quantify the extent to which epigenetic age acceleration (EAA) in one tissue correlates with EAA in another tissue. Epigenetic age was … Continue reading Are blood epigenetic clock measurements optimal?
Two epigenetic clock papers, starting with a 2022 rodent study: “We tested performance of new pan-tissue and liver-specific epigenetic mouse clocks, evaluating how these related to metabolic states, genotype-dependent life expectancy, and methylome entropy. Entropy, a measure of noise and information loss, increases as a function of time and age. In context of the methylome, … Continue reading Epigenetic clocks and entropy
This 2021 human twin study used four epigenetic clocks: “We examined the mediating role of lifestyle factors on the association between sex and biological aging in younger and older adults. The Finnish Twin Cohort (FTC) includes three large cohort studies: The older FTC includes twins born before 1958; Finntwin16 includes twins born in 1975-1979; and … Continue reading Epigenetic clocks vs. individual choices
2021’s busiest researcher took time out this month to update progress on epigenetic clocks: Hallmarks of aging aren’t all associated with epigenetic aging. Interventions that increase cellular lifespan aren’t all associated with epigenetic aging. Many of his authored or coauthored 2021 papers developed human / mammalian species relative-age epigenetic clocks. Relative-age epigenetic clocks better predict … Continue reading Epigenetic clocks so far in 2021
Another excellent blog post by Josh Mitteldorf, A New Approach to Methylation Clocks, that curated the same study: “The Levine/Horvath PhenoAge epigenetic clock was calibrated using a combination of metabolic factors that correlate with health, including inflammation, DNA transcription, DNA repair, and mitochondrial activity. Evolution is not an engineer. Living things are not constructed out … Continue reading Part 2 of Improving epigenetic clocks’ signal-to-noise ratio
This 2021 computational study investigated several methods of improving epigenetic clock reliability: “Epigenetic clocks are widely used aging biomarkers calculated from DNA methylation data. Unfortunately, measurements for individual CpGs can be surprisingly unreliable due to technical noise, and this may limit the utility of epigenetic clocks. Noise produces deviations up to 3 to 9 years … Continue reading Improving epigenetic clocks’ signal-to-noise ratio
This 2021 study subject was bats: “Exceptionally long-lived species, including many bats, rarely show overt signs of aging, making it difficult to determine why species differ in lifespan. Here, we use DNA methylation (DNAm) profiles from 712 known-age bats, representing 26 species, to identify epigenetic changes associated with age and longevity. Hypermethylated age- and longevity-associated … Continue reading A bat epigenetic clock
This 2020 Norwegian study investigated current epigenetic clock technology: “Epigenetic clocks are based on CpGs from the Illumina HumanMethylation450 BeadChip (450 K) which has been replaced by the latest platform, Illumina MethylationEPIC BeadChip (EPIC). EPIC is a major improvement over its predecessor, 450 K (> 450,000 CpGs), in terms of number of probes (> 850,000 CpGs) and genomic coverage … Continue reading Epigenetic clock technology
This 2020 review by a Hong Kong company’s researchers compared and contrasted measures of biological age: “More than a dozen aging clocks use molecular features to predict an organism’s age, each of them utilizing different data types and training procedures. We offer a detailed comparison of existing mouse and human aging clocks, discuss their technological … Continue reading Linear thinking about biological age clocks
The founder of the PhenoAge epigenetic clock methodology authored this 2020 article: “The Ge[r]oscience paradigm suggests that targeting the aging process could delay or prevent the risk of multiple major age-related diseases. We need clinically valid measures of the underlying biological process and/or classification criteria for what it means to be biologically, rather than chronologically, … Continue reading Do epigenetic clocks measure causes or effects?
This 2019 Stanford human study developed an aging clock using blood plasma proteins: “We measured 2,925 plasma proteins from 4,331 young adults to nonagenarians [18 – 95] and developed a novel bioinformatics approach which uncovered profound non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh, … Continue reading A blood plasma aging clock
This 2019 worldwide review of epigenetic clocks was a semi-anonymous mishmash of opinions, facts, hypotheses, unwarranted extrapolations, and beliefs. Diversity of viewpoints among the 21 coauthors wasn’t evident. 1. Citations of coauthors’ works seemed excessive, and they apologized for omissions. However: Challenge 5 was titled “Single-cell analysis of aging changes and disease” and Table 1 … Continue reading An epigenetic clock review by committee
This 2019 UK human study conducted a meta-analysis of genome-wide association studies of two epigenetic clocks using 13,493 European-ancestry individuals aged between ten and 98 years: “Horvath-EAA, described in previous publications as ‘intrinsic’ epigenetic age acceleration (IEAA), can be interpreted as a measure of cell-intrinsic ageing that exhibits preservation across multiple tissues, appears unrelated to … Continue reading A GWAS meta-analysis of two epigenetic clocks
This 2019 review of epigenetic clocks by Washington cancer researchers ignored the elephant in the room: Their epigenetic drift paradigm is generally inapplicable to humans because the vast majority of our cells don’t divide/proliferate. They repeatedly returned to an argument for randomness as a cause for aging and disease: “A time-dependent stochastic event process, like … Continue reading A strawman argument against epigenetic clocks
This 2019 UK/Canada/Germany human study investigated thirteen developmental disorders to identify genes that changed aspects of the epigenetic clock: “Sotos syndrome accelerates epigenetic aging [+7.64 years]. Sotos syndrome is caused by loss-of-function mutations in the NSD1 gene, which encodes a histone H3 lysine 36 (H3K36) methyltransferase. This leads to a phenotype which can include: Prenatal and … Continue reading Developmental disorders and the epigenetic clock