Telomere length is a specific biomarker that measures the span of the repetitive DNA sequences and associated proteins that cap the ends of eukaryotic chromosomes, functioning to protect the genetic material during cell division. As cells divide, telomeres naturally shorten, and their length is considered a primary indicator of cellular age and replicative senescence. Clinically, telomere length is correlated with biological aging and the risk of age-related diseases.
Origin
The concept originates from molecular biology and genetics, stemming from the Nobel Prize-winning work on the structure and protective function of telomeres in the 1970s and 80s. Its relevance to human health and longevity was solidified by studies linking shorter telomeres to increased morbidity and mortality. The mechanism of telomere maintenance is intrinsically linked to cellular metabolism and oxidative stress, placing it at the intersection of genetics and hormonal health.
Mechanism
The primary mechanism of telomere shortening is the “end-replication problem,” where DNA polymerase cannot fully replicate the very ends of the linear chromosome during cell division. Telomerase, a specialized reverse transcriptase enzyme, can counteract this by adding new repetitive sequences to the telomere ends, but its activity often declines with age. Hormones and lifestyle factors can influence the activity of telomerase and the rate of oxidative damage, thus modulating the rate of telomere attrition and cellular aging.
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Improved endocrine function from stress reduction manifests as normalized HPA axis rhythms, balanced sex hormones, enhanced thyroid function, and reduced allostatic load.
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