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The Genetic Program of Aging
Published in Shamim I. Ahmad, Aging: Exploring a Complex Phenomenon, 2017
Xiufang Wang, Huanling Zhang, Libo Su, Zhanjun Lv
Allsopp et al. (1992) put forward evidence to support the theory that telomere shortening is related to aging. Three possible hypotheses by which cell aging due to telomere shortening have been proposed. The first hypothesis suggests that telomeres are characterized by heterochromatin. After the telomere length is shortened, it will attack the nearby DNA and thus affect the expression of genes that are related to growth regulation. It has been proved that gene transferation near telomere DNA has been inhibited in low-level eukaryotes. The second hypothesis argues that the total loss of telomere DNA produces a damaging signal, which will induce growth inhibition and DNA damage via activation of p53 gene expression and PI3-kinase-like kinase activation (Karlseder et al., 1999; di Fagagna et al., 2003; Greenberg, 2005). The third hypothesis suggests that it is not the damaging signal but the shortened telomere itself that activates p53 and causes permanent growth suppression. P53 is the key mediator of the response to dysfunctional telomere (Artandi and DePinho, 2010).
The Stress System
Published in Len Wisneski, The Scientific Basis of Integrative Health, 2017
Furthermore, Epel and colleagues based their claims on studies that used averaged telomere shortening across adulthood years, ages 20–95. While telomere shortening has been associated with syndromes or conditions with symptoms of premature aging (e.g., dyskeratosis congenita, Werner syndrome, or Alzheimer disease), as well as with various other disease states (e.g., cancer, neurological, cardiovascular, infectious, as well as chronic stress), there is no solid evidence that telomere shortening causes such diseases or expedites the aging process itself. Obviously, telomere shortening is not the only arbitrator of senescence. Thus, diseases associated with premature aging must have additional mechanisms that influence telomerase synthesis and/or coordinate a dynamic confluence of telomere and nontelomere-related actions (Green and Mayeux, 2006). In addition, as already stated, both the protein and DNA components of telomere capping are part of dynamic process. So, particularly in the instance of chronic caregiver stress (especially if other disease-specific factors are not also in play), it is theoretically possible that the stress could be ameliorated by the resolution of the source of the stress and/or the individual's active participation in relaxation modalities and behaviors, which over time could result in telomere lengthening and increased telomerase expression.
Introduction to Telomere Biology
Published in Sara C. Zapico, Mechanisms Linking Aging, Diseases and Biological Age Estimation, 2017
Celia de Frutos, Pablo Bermejo-Álvarez
Telomere protective role depends on its length and secondary structure. An excessive telomere shortening has been proved to result in chromosome instability. The fourth generation of telomerase null mice lacks detectable telomere repeats and presents aneuploidy and chromosomal abnormalities, including terminal fusions (Blasco et al. 1997). However, telomere length is not the only factor determining cellular proliferative potential (O’Sullivan and Karlseder 2010) and it is unclear the minimum telomere length required for telomere protection. Telomeres may lose the protective ability from cellular activities such as nucleases or DNA-break repairing proteins, even in telomeres of a normal length; functional alterations in shelterin complex cause telomere-associated senescence independently of telomere length (Karlseder et al. 2002, Martinez and Blasco 2010).
Ergothioneine Mitigates Telomere Shortening under Oxidative Stress Conditions
Published in Journal of Dietary Supplements, 2022
Priscilla Samuel, Menelaos Tsapekos, Nuria de Pedro, Ann G. Liu, J. Casey Lippmeier, Steven Chen
Literature to date suggests that lifestyle modifications and changes to diet can potentially decelerate telomere shortening. A comprehensive lifestyle intervention consisting of a low-fat, plant-based diet, moderate exercise, stress management (yoga, meditation, breathing techniques), and social support increased telomerase activity in peripheral mononuclear blood cells over three months and relative telomere length over 5 years (Ornish et al. 2008; Ornish et al. 2013). Another study showed that supplementation with omega-3 polyunsaturated fatty acids reduced oxidative stress markers, and telomere length increased with decreasing omega-6:omega-3 ratio (Kiecolt-Glaser et al. 2013). Further, a recent systematic review which examined the effects of nutrition on telomere health found that certain nutrients such as vitamins C, D, beta-carotene, omega-3s, dietary fiber, fruits and vegetable intakes, as well as healthy dietary patterns such as the Mediterranean diet may have positive and protective effects on telomere length (Galie et al. 2020). Though some of the clinical studies have been small, they provide a growing body of evidence that specific nutrients, healthy diets, and interventions to reduce stress (both oxidative and psychological) can be effective for preserving telomere length in humans.
Maternal neglect results in reduced telomerase activity and increased oxidative load in rats
Published in Stress, 2021
Devrim Sarıbal, Aslı Kireçtepe Aydın, Mahmut Alp Kılıç, Faariah Shakil, Mustafa Balkaya
Telomere shortening is considered a hallmark of aging, as telomere length reflects mitotic potential and age is a primary predictor of telomere length. However, numerous environmental factors such as poverty, smoking, alcohol use, obesity, and a sedentary lifestyle have been shown to affect telomere length (Barrett et al., 2015). Social factors such as marital status, social support, social conflicts, isolation have been associated with telomere length as well. Significant environmental factors that accelerate aging are adverse social conditions and chronic psychological stress. Accordingly, a growing body of evidence from human studies links stress exposure to reduced telomere length. Stressful life events, particularly the ones during early childhood, are associated with telomere attrition and predict greater telomere shortening with age (Oliveira et al., 2016; Rentscher et al., 2020). Similarly, exposure to violence or being a caregiver for chronically ill patients leads to reductions in telomere length (Oliveira et al., 2016). Nevertheless, the effects of stress on telomerase activity is grossly understudied (de Punder et al., 2019). Rodent studies on the topic are very limited and report conflicting results. Therefore, establishing animal models that mimic the phenotype observed in humans is crucial for studying the effects of stress on telomere shortening and associated diseases.
Association between nutrient intake and telomere length in Japanese female university students
Published in Biomarkers, 2021
Yuki Mizuno, Shoko Konishi, Chiho Goto, Jun Yoshinaga, Mikie Hidaka, Hideki Imai
Although the association between nutrient intake and telomere length is supported by a potential biological mechanism relating to oxidative stress, the studies describing those mechanisms are limited. Nutrients with antioxidative effect can modify the balance between oxidative stress and antioxidative response that has been suggested to affect telomere length (Furumoto et al. 1998, Saretzki and Von Zglinicki 2002). With respect to vitamins, its antioxidative properties have been well-known from the findings in a number of previous reports (Sies et al. 1992, Sies and Stahl 1995, Driskell and Wolinsky 2009). Telomere shortening is supposed to be caused by the effects of reactive oxygen species because its G-rich structure is chemically sensitive to oxidative stress (von Zglinicki 2002). β-carotene, one of the carotenoids that are precursors of vitamin A and functions as vitamin A in human body after ingestion, is one of the nutrients with antioxidant properties. A previous in vitro study demonstrated that β-carotene reduces oxidative stress in mononuclear cells of subjects with Alzheimer’s disease (de Oliveira et al. 2012). Indeed, a previous study reported that increasing levels of blood carotenoid were significantly associated with longer leucocyte telomeres in adults (Min and Min 2017). Thus, high intake of vitamin A-rich food may play a role in protecting telomeres and regulating telomere length through the potential biological mechanism relating to the balance between oxidative stress and antioxidative effects.