⏳Longevity Signals📈
June 3, 2025
Note: This is not medical advice. Please consult your physician before making changes to your health routine.
🩺 Longevity + Treatments 💪
The TALENTs trial indicates that nucleotide supplementation in older adults can delay biological aging, evidenced by a reduction in median DNA methylation age, and improve insulin sensitivity without severe adverse effects.
A randomized, placebo-controlled trial shows long-term therapeutic plasma exchange (TPE) is safe and effective in improving biological age markers. Particularly, biweekly TPE combined with intravenous immunoglobulin (TPE-IVIG) reversed age-related immune decline and modulated proteins linked to chronic inflammation, suggesting potential in slowing epigenetic biologic clocks.
Higher sleep scores, reflecting healthier sleep patterns, are associated with slower DNA methylation age acceleration, particularly in older adults. This slowed aging process could partially explain the link between healthier sleep patterns and lower all-cause mortality risk.
A recent clinical trial shows that oral semaglutide significantly reduces cardiovascular events risk in individuals with type 2 diabetes, atherosclerotic cardiovascular disease, and/or chronic kidney disease. The oral form’s effectiveness is consistent with injectable semaglutide, yet more research is needed.
KETO-CTA study findings, that a subset of people on keto diets may be shielded from atherosclerosis progression despite high LDL-C levels, challenged longstanding evidence linking higher LDL-C to coronary disease. The study, however, has been criticized for unclear presentation of primary endpoint data.
🧬 Longevity + Science 🧪
A Mendelian randomization study reveals significant causal associations between blood cell traits (eosinophil counts, mean corpuscular volume, and lymphocyte counts) and aging indicators (frailty index, telomere length, and epigenetic aging clocks). Monitoring these traits can provide valuable insights for assessing age-related health risks and promoting healthy aging.
Epigenetic aging, specifically DNAmPhenoAge and DNAmGrimAge, predicted progression from normal aging to Alzheimer’s disease (AD), cognitive decline, cortical thinning, and white matter disease burden. This suggests blood-based second-generation epigenetic clocks can predict AD risk and pathophysiology.
Biological age (PhenoAge) and the Clinical Frailty Scale (CFS) measured at ICU admission independently predict hospital mortality, with notable interaction in non-frail patients. Both factors are significant predictors of health outcomes in critically ill patients.
Age-related accumulation of mitochondrial DNA mutations in human blood is a two-step process, according to an analysis of whole genome sequences from approximately 750,000 individuals. Individual cells first randomly accumulate low-level ‘cryptic’ mtDNA mutations. Then, as a cell clone proliferates, these mutations are carried along and become detectable in whole blood.
Gene duplication in immune-related families is associated with extended lifespan in mammals. Notably, mammals with larger brain sizes relative to body mass, like bats and whales, have significant gene family size expansions related to immune system functions, indicating an evolutionary link between these traits.
💡Featured Article 🌟
The study explores the predictive power of DNA methylation age, derived from peripheral blood, in forecasting the progression to Alzheimer’s disease (AD), as well as its association with white matter disease burden and cortical atrophy. Using longitudinal modeling and structural neuroimaging, the researchers tested the hypothesis that accelerated epigenetic aging could predict the progression of AD. They utilized two second-generation epigenetic clocks, DNAmPhenoAge and DNAmGrimAge, to assess their predictive capabilities. Key findings indicate that these epigenetic clocks can predict the transition from cognitively normal aging to mild cognitive impairment (MCI) or AD, as well as poorer longitudinal cognitive outcomes. The study also found a strong association between epigenetic age and cortical thinning in regions relevant to AD, alongside an increased burden of white matter disease. These results contrast with previous cross-sectional studies that suggested limited applicability of blood-based epigenetic clocks in AD prediction. The study highlights the importance of longitudinal analyses and the use of whole-brain neuroimaging biomarkers, which may provide more sensitive and accurate assessments of disease risk and progression than cross-sectional studies. The findings suggest that second-generation epigenetic clocks could serve as promising predictors of AD risk and pathophysiology, potentially offering a new avenue for early intervention and treatment strategies.
This study underscores the potential utility of monitoring epigenetic age as a biomarker for cognitive decline and AD risk. By integrating these epigenetic clocks into personal health assessments, individuals may gain insights into their biological aging processes and the potential onset of neurodegenerative diseases. This approach could inform personalized interventions aimed at mitigating cognitive decline and extending healthy lifespan. Overall, the study advocates for further research using longitudinal and biomarker data, paired with validated epigenetic clocks, to enhance our understanding of the relationship between epigenetic aging and neurodegenerative diseases.
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