The DOI matches its Crossref record; 52 of the 53 references it cites were found in a registry or an index.
How “Reversible” Is Telomeric Aging?
Abstract
A critical question in human health is the malleability of telomere length. Telomere length, sampled at one point during adult life, is predictive of certain types of cancer and other immune and metabolic-related diseases. We now know from basic studies that the telomere/telomerase maintenance system plays a causal role in accelerating biologic aging and promoting disease processes. One can develop short telomeres for a multitude of reasons. Historical factors such as genetics, prenatal conditions, and early adversity, contribute to adult telomere length; however, current stress and lifestyle are also associated. If these modifiable predictors are causal factors in telomere shortening, there is a tremendous opportunity to improve maintenance and possibly even lengthen telomeres with behavioral interventions. This minireview discusses our current understanding of telomere lengthening and questions facing the field. Several small-scale stress reduction/wellness studies show promising findings, suggesting that cell aging can be slowed or reversed in vivo over short periods. Moreover, possible mechanisms are discussed, that take into account actual telomeric lengthening, such as that which occurs through telomerase-mediated elongation, or mechanisms resulting in "pseudo-telomeric lengthening" as might occur from changes in cell type distribution. There is a strong need for more translational clinical to bench research to address mechanistic questions in experimental models. In addition, well-designed intervention research that examines both telomeres and potential mediators of change can further enhance our understanding of malleability, mechanism, and clinical implications of telomere lengthening. Cancer Prev Res; 5(10); 1163-8. ©2012 AACR.
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In the citing paper
“Some individuals maintain and may even lengthen average LTL for some periods (Epel, 2012; Muezzinler et al., 2013).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Epel, 2012
In the citing paper
“The reasons for this are unknown, but relatively long telomeres tend to shorten over time, and relatively short telomeres tend to lengthen over time, possibly due to the preferential recruitment of reparative mechanisms such as telomerase activity (TA) (Epel, 2012).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Epel, 2012
In the citing paper
“Important caveats must be considered in interpreting LTL (Aviv et al., 2006; Epel, 2012), e.g., (a) distinguishing between telomere shortening in the individual leukocyte vs. “apparent” telomere shortening when examining average LTL, due to a re-distribution of leukocyte cell types having different telomere lengths, such as naïve vs. memory T cells;”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Epel, 2012
In the citing paper
“Nonetheless, several studies reported “dose-response” relationships, with greater improvement in mental well-being or sense of purpose in life or greater adherence to the behavioral intervention, associating with larger increases in PBMC basal TA (Epel, 2012; Jacobs et al., 2011).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Epel, 2012
In the citing paper
“These studies have generally found intervention-associated increases in PBMC basal TA (Epel, 2012; Epel et al., 2009b; Epel, 2009; Jacobs et al., 2011; Lengacher et al., 2014; Ornish et al., 2008; Schutte and Malouff, 2014b; Starkweather et al., 2014).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Epel, 2012
In the citing paper
“In an otherwise concerning picture, findings that certain positive lifestyle changes are correlated with lowered degrees of cell aging (as indexed by LTL and/or PBMC basal TA) (Epel, 2009; Epel, 2012; Hoge et al., 2013; Puterman et al., 2010; Puterman et al., 2015) provide some encouragement, although many of the studies were small-scale, open-label or inadequately controlled.”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Epel, 2012
Citations
Cites
Hemann, M. T., Strong, M. A., Hao, L.-Y., & Greider, C. W. (2001) · Cell · doi:10.1016/s0092-8674(01)00504-9 · Cited by 1,219
Alternative lengthening of telomeres: models, mechanisms and implications
Cesare, A. J., & Reddel, R. R. (2010) · Nature Reviews Genetics · doi:10.1038/nrg2763 · Cited by 1,107
Dhabhar, F. S., & McEwen, B. S. (1997) · Brain Behavior and Immunity · doi:10.1006/brbi.1997.0508 · Cited by 1,014
Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice
Jaskelioff, M., Muller, F. L., Paik, J.-H., Thomas, E., Jiang, S., Adams, A. C., Sahin, E., Kost-Alimova, M., Protopopov, A., Cadiñanos, J., et al. (2011) · Nature · doi:10.1038/nature09603 · Cited by 857 · cited 1×
“In animal models, dramatically replenishing telomerase activity increases telomere length and induces a reversal of clinical aging (51).”
BackgroundRufer, N., Brümmendorf, T. H., Kolvraa, S., Bischoff, C., Christensen, K., Wadsworth, L., Schulzer, M., & Lansdorp, P. M. (1999) · The Journal of Experimental Medicine · doi:10.1084/jem.190.2.157 · Cited by 709
Dhabhar, F. S., Malarkey, W. B., Neri, E., & McEwen, B. S. (2012) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2012.05.008 · Cited by 589 · cited 1×
“window into the system—on their way to the battle stations, the target tissue, such as skin and the gastrointestinal tract (42).”
BackgroundShalev, I., Moffitt, T. E., Sugden, K., Williams, B., Houts, R. M., Danese, A., Mill, J., Arseneault, L., & Caspi, A. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.32 · Cited by 489
Cell aging in relation to stress arousal and cardiovascular disease risk factors
Epel, E. S., Lin, J., Wilhelm, F. H., Wolkowitz, O. M., Cawthon, R., Adler, N. E., Dolbier, C., Mendes, W. B., & Blackburn, E. H. (2006) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2005.08.011 · Cited by 450
Intensive meditation training, immune cell telomerase activity, and psychological mediators
Jacobs, T. L., Epel, E. S., Lin, J., Blackburn, E. H., Wolkowitz, O. M., Bridwell, D. A., Zanesco, A. P., Aichele, S. R., Sahdra, B. K., MacLean, K. A., et al. (2011) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2010.09.010 · Cited by 432 · cited 1×
“Finally, a 3-month trial of intensive concentrative and compassion-oriented meditation found30%significantly higher telomerase activity as compared with the waitlist control group (28).”
BackgroundIncreased telomerase activity and comprehensive lifestyle changes: a pilot study
Ornish, D., Lin, J., Daubenmier, J., Weidner, G., Epel, E., Kemp, C., Magbanua, M. J. M., Marlin, R., Yglecias, L., Carroll, P. R., et al. (2008) · The Lancet Oncology · doi:10.1016/s1470-2045(08)70234-1 · Cited by 430
Self-citation
Research works printed but not linked: 3
- Epel, 2009, The rate of leukocyte telomere shortening predicts mortality from cardiovascular diseases in elderly men, Aging, 81
- Puterman, An intricate dance: life experience, multisystem resiliency, and rate of telomere decline through the lifespan, Social Psychol Compass
- Glaser, 1994, Stress-associated immune modulation and its implications for reactivation of latent herpes viruses
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Items 101–102 of 102
Sunzeri, F. (2026) · Springer eBooks · doi:10.1007/978-3-032-14465-2_26
Sunzeri, F. (2026) · Springer eBooks · doi:10.1007/978-3-032-14465-2_1
Metadata
- Authors
- Epel, E.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Epel, Elissa
- ORCID
- Epel, Elissa
- Venue
- Cancer Prevention Research
- Published
- 2012-10-01
- Volume
- 5
- Issue
- 10
- Pages
- 1163-1168
- ISSN
- 1940-6207 (ISSN-L)
- 1940-6215
- OpenAlex
- W2099763564
- Cited by
- 103
- References
- 53
- Citations by year
- 2026: 4 · 2025: 2 · 2024: 5 · 2023: 8 · 2022: 5 · 2021: 4 · 2020: 10 · 2019: 10 · 2018: 7 · 2017: 11 · 2016: 12 · 2015: 6 · 2014: 11 · 2013: 7 · 2012: 1
- FWCI
- 0.86
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Prevention Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG030424)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- telomere length, telomere elongation, telomerase, biological aging, telomere shortening, stress reduction, lifestyle intervention, cell type distribution, cancer risk, modifiable risk factors
- MeSH terms
- Adult, Aging, Humans, Telomere Homeostasis, Telomere Shortening
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