This genome-wide association study using mass spectrometry-based proteomics identifies and replicates novel protein quantitative trait loci (pQTLs), highlights biases from affinity-based methods, and demonstrates the broader potential of MS platforms to uncover new drug discovery targets.

Using blood DNA methylation with machine learning, we built 11 system-specific epigenetic clocks (Heart, Lung, Kidney, etc.) plus a unified Systems Age. These scores predict system-level aging, mortality and disease, revealing distinct aging subtypes for personalized care.

Simulating DNAm drift in >22k blood samples shows stochastic change explains 66–75 % of Horvath clock accuracy, 90 % for Zhang, but 63 % for PhenoAge, implying true aging reflects non-stochastic biology. Male, severe COVID-19 and smoker accelerations stem from these non-random effects.

In an 8-week twin study, only the vegan diet cut epigenetic age: lower PC GrimAge, PC PhenoAge, DunedinPACE and reduced aging in inflammation, heart, hormone, liver and metabolic systems. Omnivores didn’t shift, underscoring plant-based diets’ anti-aging edge.

WGBS of germ-layer tissues and gametes mapped 1,488 hemi-methylated candidate imprint control regions, including 19/25 known. 332 showed near-complete parent-specific methylation and 65 % overlapped CTCF/DNase sites. This draft imprintome opens paths to study imprinting errors in disease.

Methylation of specific HERV and LINE-1 loci forms potent epigenetic clocks across tissues and species. These clocks reset with reprogramming, accelerate in HIV-1, respond to therapy, and track brain organoid age, tying retroelement control to aging.

In 86 adult spinal-deformity patients, blood epigenetic clocks—especially DunedinPACE—tied faster biological aging to greater frailty (EFS, ASD-FI), worse disability (ODI, SRS-22) and more 90-day complications, suggesting biological age can refine surgical risk prediction.

22,819-probe Human Imprintome array profiles 1,088 of 1,488 candidate ICRs, filling gaps left by standard Infinium chips at lower cost. Methylation concordance: R² 0.569 vs WGBS, 0.796 vs EPIC v2; replication ICC 0.80–0.95. Delivers reliable, scalable ICR analysis.

From ~30k biobank records, researchers derived EMRAge, a lab-based biological age tied to mortality. DNA-methylation (DNAmEMRAge) and multi-omics (OMICmAge) versions outperform existing clocks in two cohorts (n=3,451; 12,666), linking aging biology across epigenome, proteome and metabolome.

Phase-I: 19 adults on dasatinib + quercetin (DQ) for 6 months showed faster epigenetic/mitotic aging and shorter telomeres. Adding fisetin (DQF) for 6 mo in 19 subjects blunted age acceleration and shifted immune-cell mix, hinting fisetin may counter DQ’s pro-aging epigenetic effects.

ARDD 2021 (Aug 30–Sep 3) drew 130 onsite and 1,800 online participants. Seventy-five talks covered aging mechanisms, modulating interventions, AI-driven discovery and research standards; a new longevity workshop linked scientists with clinicians.

Eleven trained men did squat + leg extensions to failure at 80 % vs 30 % 1-RM. The 30 % load yielded far more reps but matched volume. Both sessions cut global DNA methylation 3–6 h post-exercise, with a larger drop trending after 30 %, hinting low-load RT drives stronger muscle hypomethylation.

In 11 trained men, a single squat + leg-extension bout to failure at 80 % or 30 % 1-RM (matched volume) reshaped promoter methylation of ~46 hypertrophy genes; the heavier load yielded distinct hypomethylation patterns, revealing load-specific epigenetic drivers of muscle adaptation.

Blood DNA methylation tracked pre/post mild COVID-19 (n=21) found 756 CpG shifts and age-split clock shifts: PhenoAge/GrimAge rose in >50 yr, fell in younger adults. In 36 others, Moderna vaccine cut Horvath age by ~3.9 yr (>50). Epigenetic clocks could monitor infection and vaccine effects.

In 11 trained men, squats/leg extensions to failure at 30 % or 80 % 1-RM altered hypertrophy-related gene expression similarly: 32/58 mRNAs shifted 3 h, 17 at 6 h, with myostatin-pathway genes most affected. p70S6K and follistatin proteins rose, highlighting load-independent myostatin regulation.

In 11 trained men, squats/leg extensions to failure at 30 % or 80 % 1-RM (volume-matched) triggered similar muscle DNA-methylation and mRNA shifts—major at 3 h, fewer at 6 h—engaging focal-adhesion, MAPK and PI3K-Akt pathways alike, showing load doesn’t dictate early epigenetic response.

In 1,044 HELIX kids, a prenatal exposome combo—low dairy, non-smoker cotinine, low facility richness, ample greenspace—defined Environment E1. There, girls (not boys) showed sharply lower obesity and neurodevelopment-delay risk, echoed by DNA-methylation shifts.

In 12 mid-aged adults, 12-wk NAD3 (wasabi extract + theacrine + copper niacin) shifted 64 PBMC mRNAs, curbed CpG hypermethylation, and prevented the placebo-linked drop in sirtuin activity, paralleling higher NAD+/NADH. NAD3 may preserve DNA structure and sirtuin function, pending larger trials.

Prospective study of 43 adult spinal-deformity patients: blood epigenetic clocks and telomere length were compared with frailty, comorbidities, disability, and 90-day complications. Epigenetic age linked to CCI, ASD-FI; shorter telomeres predicted post-op complications, enhancing risk tools.

Blood DNA-methylation study (86 BD, 39 matched controls) shows bipolar patients age faster per DunedinPACE. Faster pace is largely mediated by DNAm surrogates of metabolic, anthropometric and inflammatory traits; within BD, worse metabolic profiles track higher aging pace.

Hefty alcohol and tobacco use tweaks hundreds of gene “switches”; 66 alcohol-linked changes largely explain its boost to high blood pressure, while marijuana shows little effect.

Researchers created and validated a DNAm reference for 12 blood immune cells, then profiled 23,053 samples. Sex, age, smoking, obesity, exercise and sleep altered cell fractions; more naïve CD4+ T and NK cells predicted lower all-cause mortality.

In 94 patients ≥60 y with blood cancers, T-cell PhenoAge topped healthy controls, highest in acute leukemia. Greater epigenetic age tied to poorer ECOG, IADL loss and comorbidities, while hypomethylating therapy lowered PhenoAge, hinting reversibility.

In 83 spinal-deformity patients, faster epigenetic aging (DunedinPACE, PhenoAge, GrimAge) tracked with greater frailty/disability, while shorter telomeres flagged 90-day complications—supporting biological-age markers to refine surgical risk.

New EPICv2 methylation array boosts enhancer coverage, works with diverse ancestries and as little as 1 ng DNA, and still delivers accurate, reproducible data. It supports clocks, deconvolution, trait CpGs, and maps DNMT/SETD2 mutation signatures, providing a versatile tool for epigenetic studies.