Epitalon Induces Telomere Elongation in Human:
– Epithalon Peptide Induces Telomerase Activity and Telomere Elongation in Human Somatic Cells Buy on Springer 39.95USD
Published in Bulletin of Experimental Biology and Medicine. June 2003, Volume 135, Issue 6, pp 590-592
Abstract: Addition of Epithalon peptide in telomerase-negative human fetal fibroblast culture induced expression of the catalytical subunit, enzymatic activity of telomerase, and telomere elongation, which can be due to reactivation of telomerase gene in somatic cells and indicates the possibility of prolonging life span of a cell population and of the whole organism.
– Peptide Promotes Overcoming of the Division Limit in Human Somatic Cell Buy on Springer 39.95USD
Published in Bulletin of Experimental Biology and Medicine. May 2004, Volume 137, Issue 5, pp 503-506
Abstract: We previously showed that treatment of normal human diploid cells with Epithalon (Ala-Glu-Asp-Gly) induced expression of telomerase catalytic subunit, its enzymatic activity, and elongation of telomeres. Here we studied the effect of this peptide on proliferative potential of human fetal fibroblasts. Primary pulmonary fibroblasts derived from a 24-week fetus lost the proliferative potential at the 34th passage. The mean size of telomeres in these cells was appreciably lower than during early passages (passage 10). Addition of Epithalon to aging cells in culture induced elongation of telomeres to the size comparable to their length during early passages. Peptide-treated cells with elongated telomeres made 10 extra divisions (44 passages) in comparison with the control and continued dividing. Hence, Epithalon prolonged the vital cycle of normal human cells due to overcoming the Heyflick limit.
# Publications by Pr. Khavinson concerning Epithalon and Anti-Aging: Complete list
- Article from 2003 : “Epithalon Peptide Induces Telomerase Activity and Telomere Elongation in Human Somatic Cells”, Buy at springer.com
- Article from 2009 : “Peptide Regulation of Aging: 35-Year Research Experience” Buy at springer.com. Version visible online www.khavinson.ru/peptide-regulation-of-ageing
- Article from 2011 : “Morphofunctional fundamentals for peptide regulation of aging”,Buy on springer.com
- Article from 2002 : “Pineal-regulating tetrapeptide epitalon improves eye retina condition in retinitis pigmentosa”, Free on khavinson.ru
- Article from 2002 : “Effect of Epitalon on Interleukin-1ß Signal Transduction and the Reaction of Thymocyte Blast Transformation Under Stress”, Free on khavinson.ru
- Article from 2001 : “Epitalon stimulates melatonin production and restores circadian rhythm of cortisol in old rhesus monkeys”, Free on khavinson.ru
- Article from 2001 : “Synthetic tetrapeptide epitalon restores disturbed neuroendocrine regulation in senescent monkeys”, Free on khavinson.ru
- Article from 2003 : “Epitalon and colon carcinogenesis in rats: Proliferative activity and apoptosis in colon tumors and mucosa”, Free on khavinson.ru
- Article from 2003 : “Effect of Epitalon on biomarkers of aging, life span and spontaneous tumor incidence in female Swiss-derived SHR mice”, Free on khavinson.ru
- Article from 2003 : “Effect of Epithalon in Campbell Rats of Various Ages”, Free on khavinson.ru
- Article from 2002 : “Epitalon influences pineal secretion in stress-exposed rats in the daytime”, Free on khavinson.ru
- Article from 2000 : “Regulating Effect of Epithalone on Gastric Endocrine Cells in Pinealectomized Rats”, Free on khavinson.ru
- Article from 2000 : “Effect of epitalon on the lifespan increase in Drosophila melanogaster”, Free on khavinson.ru
- Article from 2000 : “Effect of Epithalone on the Age-Specific Changes in the Time Course of Lipid Peroxidation in Drosophila melanogaster”, Free on khavinson.ru
- 144 pages book: “Peptides and Aging”, 54 USD
- 104 pages book: “The interrelation between life span and peptide regulation of gene activity”, 139 USD
- 578 pages book: “The Pineal Gland and Cancer: Neuroimmunoendocrine Mechanisms in Malignancy”, 195 USD
- 336 pages book: “Modulating Aging and Longevity”, 175 Euros
- free PDF: “Institut of Gerontology and Bioregualtion of St Petersburg”,
After Telomerase Activation They Live 24% Longer!
Article pulished in The EMBO Scientific Publications; full article for free here.
RESULTS: Based on this notion, we tested the effects of a telomerase gene therapy in adult (1 year of age) and old (2 years of age) mice. Treatment of both groups of mice with an AAV of wide tropism expressing mouse telomerase (mTERT) demonstrated remarkable beneficial effects on health and fitness, improving several molecular biomarkers of aging. Moreover, telomerase-treated mice did not develop more neoplasias comparing to their control littermates, suggesting that the known tumorigenic activity of telomerase is severely decreased when expressed in adult or old organisms. Finally, re-introduction of mTERT in both 1- and 2-year old mice increased significantly its median lifespan (24 and 13%, respectively). These beneficial effects were not observed with a reporter virus (eGFP) or a catalytically inactive TERT (TERT-DN) demonstrating the strict dependency of an active telomerase complex.
The rate of increase of short telomeres predicts longevity in mammals.
Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Research Center, Melchor Fernández Almagro 3, E-28029 Madrid, Spain.
Full PDF, Open Access on Cell Press
Abstract: Aberrantly short telomeres result in decreased longevity in both humans and mice with defective telomere maintenance. Normal populations of humans and mice present high interindividual variation in telomere length, but it is unknown whether this is associated with their lifespan potential. To address this issue, we performed a longitudinal telomere length study along the lifespan of wild-type and transgenic telomerase reverse transcriptase mice. We found that mouse telomeres shorten ~100 times faster than human telomeres. Importantly, the rate of increase in the percentage of short telomeres, rather than the rate of telomere shortening per month, was a significant predictor of lifespan in both mouse cohorts, and those individuals who showed a higher rate of increase in the percentage of short telomeres were also the ones with a shorter lifespan. These findings demonstrate that short telomeres have a direct impact on longevity in mammals, and they highlight the importance of performing longitudinal telomere studies to predict longevity.
Copyright © 2012 The Authors. Published by Elsevier Inc. All rights reserved.
Partial reversal of aging achieved in mice.
Control of telomerase gene appears to control process
In a report posted online by the journal Nature in advance of print publication, researchers led by Ronald A. DePinho, a Harvard Medical School (HMS) professor of genetics, said they achieved the milestone in aging science by engineering mice with a controllable telomerase gene. The telomerase enzyme maintains the protective caps called telomeres that shield the ends of chromosomes.
Extracts from: Wall Street Journal
“Aging ills reversed in mice”
“These mice were equivalent to 80-year-old humans and were about to pass away,” says Ronald DePinho, co-author of the paper and a scientist at Dana-Farber Cancer Institute in Boston. After the experiment, “they were the physiological equivalent of young adults.”
The experiment focused on telomerase, an enzyme that makes small units of DNA that seal the tips of chromosomes. These DNA units, known as telomeres, act like the plastic caps at the ends of a shoelace, preventing the chromosomes from fraying and the genes inside them from unraveling. In 2009, three U.S. scientists won the Nobel Prize in medicine for illuminating the mysteries of telomerase.
As people age, low levels of telomerase are linked to the erosion of telomeres. Dr. DePinho and his colleagues wanted to see if by reactivating telomerase in mice they could halt—or possibly reverse—the shortening of telomeres, and thus turn back the clock on some aspects of aging.
One month later, the treated mice showed surprising signs of rejuvenation. Overall, their telomeres had lengthened and the levels of telomerase had increased. This woke up the dormant brain stem cells, producing new neurons. The spleen, testes and brain grew in size.
In addition, key organs started to function better. The treated mice regained their sense of smell. The male animals’ once-depleted testes produced new sperm cells, and their mates gave birth to larger litters. The treated animals went on to have a typical lifespan, though they didn’t live longer than normal mice.
The reversals of age-related decline seen in the animals “justify exploration of telomere rejuvenation strategies for age-associated diseases,” the paper concludes.
Statistically, people with longer telomeres in their blood cells have an increased number of healthy years beyond the age of 60, Dr. DePinho said. And those over 60 with the shortest telomeres have higher rates of diabetes, cardiovascular disease and Alzheimer’s.
Extracts from: The Harvard Gazette
Researchers led by Ronald A. DePinho (above), a Harvard Medical School professor of genetics, say their work shows for the first time a dramatic reversal of many aspects of age-related degeneration in mice, a milestone in aging science achieved by engineering mice with a controllable telomerase gene.
With ageing in humans, low levels of telomerase are associated with progressive erosion of telomeres, which can then contribute to tissue degeneration and functional decline in the elderly. By creating mice with a telomerase switch, the researchers were able to generate prematurely aged mice. The switch has allowed scientists to determine whether the reactivation of telomerase in the animals would restore telomeres and mitigate the signs and symptoms of aging.
The work showed a dramatic reversal of many aspects of aging, including reversal of brain disease and infertility.
Telomere loss created a cascade of signals that cause the cessation of cell division or self-destruction, stem cells are retiring, the organes atrophy, and brain cells die.
Genetic variation in human telomerase is associated with telomere length in Ashkenazi centenarians Full article on NCBI.
Proc Natl Acad Sci U S A. 2010 January 26; 107(Suppl 1): 1710–1717.
Published online 2009 November 13. doi: 10.1073/pnas.0906191106
Abstract: Telomere length in humans is emerging as a biomarker of aging because its shortening is associated with aging-related diseases and early mortality.
However, genetic mechanisms responsible for these associations are not known. Here, in a cohort of Ashkenazi Jewish centenarians, their offspring, and offspring-matched controls, we studied the inheritance and maintenance of telomere length and variations in two major genes associated with telomerase enzyme activity, hTERT and hTERC.
We demonstrated that centenarians and their offspring maintain longer telomeres compared with controls with advancing age and that longer telomeres are associated with protection from age-related diseases, better cognitive function, and lipid profiles of healthy aging.
Sequence analysis of hTERT and hTERC showed overrepresentation of synonymous and intronic mutations among centenarians relative to controls. Moreover, we identified a common hTERT haplotype that is associated with both exceptional longevity and longer telomere length.
Thus, variations in human telomerase gene that are associated with better maintenance of telomere length may confer healthy aging and exceptional longevity in humans.
A role for sister telomere cohesion in telomere elongation by telomerase Full article on PMC.
Cell Cycle. 2012 January 1; 11(1): 19–25.
Published online 2012 January 1. doi: 10.4161/cc.11.1.18633
Abstract: Telomere length homeostasis is achieved by a balance of telomere shortening caused by DNA replication and nucleolytic attack and telomere lengthening by telomerase.
The importance of telomere length maintenance to human health is best illustrated by dyskeratosis congenita (DC), a disease of telomere shortening caused by mutations in telomerase subunits. DC patients suffer stem cell depletion and die of bone marrow stem cell failure.
Recently a new class of particularly severe DC patients was found to harbor mutations in the shelterin subunit TIN2. The DC-TIN2 mutations were clustered in small domain of unknown function.
In a recently published study we showed that the DC mutation cluster in TIN2 harbored a binding site for heterochromatin protein 1 (HP1) and, further, that HP1 binding to TIN2 was required for sister telomere cohesion in S phase and for telomere length maintenance by telomerase.
We briefly review and discuss the implications of our findings in this Extra View and present some new data that may shed light on how sister telomere cohesion could influence telomere elongation by telomerase.
Introduction: Human telomeres are comprised of double-stranded TTAGGG repeats that run out as a single stranded overhang to the 3′ end of the chromosome and a six-subunit complex called shelterin. Due to the end replication problem and nucleolytic processing, telomeres shorten with each round of cell division.
This shortening functions as a molecular clock inducing cells to cease division and senesce.[2,3] Shortening can be counteracted by telomerase, a specialized reverse transcriptase that adds telomere repeats to chromosome ends.[4,5]
In humans, telomerase is expressed in the germ line and during embryogenesis but is repressed for the most part in the human soma. Hence, the stock of telomeres that an individual possesses at birth must suffice over their lifetime.
Defects in telomere maintenance can have severe consequences for human health, as evidenced by the genetic disease dyskeratosis congenita (DC). DC is caused by mutations in telomerase subunits, resulting in very short telomeres in highly proliferating tissues.[8,9] DC patients suffer stem cell depletion and die of bone marrow stem cell failure.
Understanding how telomerase functions in the germ line and during embryogenesis will be crucial to understanding the mechanism of disease in DC and the role of telomerase in human health.
– 1. de Lange T. Shelterin: the protein complex that shapes and safeguards human telomeres. Genes Dev. 2005;19:2100–2110. doi: 10.1101/gad.1346005. [PubMed]
– 2. Harley CB, Futcher AB, Greider CW. Telomeres shorten during ageing of human fibroblasts. Nature. 1990;345:458–460. doi: 10.1038/345458a0. [PubMed]
– 3. Hastie ND, Dempster M, Dunlop MG, Thompson AM, Green DK, Allshire RC. Telomere reduction in human colorectal carcinoma and with ageing. Nature. 1990;346:866–868. doi: 10.1038/346866a0. [PubMed]
– 4. Greider CW, Blackburn EH. Identification of a specific telomere terminal transferase activity in Tetrahymena extracts. Cell. 1985;43:405–413. doi: 10.1016/0092-8674(85)90170-9. [PubMed]
– 5. Greider CW, Blackburn EH. The telomere terminal transferase of Tetrahymena is a ribonucleoprotein enzyme with two kinds of primer specificity. Cell. 1987;51:887–898. doi: 10.1016/0092-8674(87)90576-9. [PubMed]
– 6. Wright WE, Piatyszek MA, Rainey WR, Byrd W, Shay JW. Telomerase activity in human germline and embryonic tissues and cells. Dev Genet. 1996;18:173–179. doi: 10.1002/(SICI)1520-6408(1996)18:2<173::AIDDVG10>3.0.CO;2-3. [PubMed]
– 7. Bessler M, Wilson DB, Mason PJ. Dyskeratosis congenita. FEBS Lett. 2010;584:3831–3838. doi: 10.1016/j.febslet.2010.05.019. [PMC free article]
– 8. Alter BP, Baerlocher GM, Savage SA, Chanock SJ, Weksler BB, Willner JP, et al. Very short telomere length by flow fluorescence in situ hybridization identifies patients with dyskeratosis congenita. Blood. 2007;110:1439–1447. doi: 10.1182/blood-2007-02-075598. [PMC free article]
– 9. Gadalla SM, Cawthon R, Giri N, Alter BP, Savage SA. Telomere length in blood, buccal cells, and fibroblasts from patients with inherited bone marrow failure syndromes.Aging (Albany NY) 2010;2:867–874. [PMC free article]
Antioxidant properties of geroprotective peptides of the pineal gland. Buy on PUBMED.
Arch Gerontol Geriatr. 2007;44 Suppl 1:213-6.
Abstract: It was shown that peptide preparations from the pineal gland (epithalamin and epitalon) possess antioxidant properties exceeding in some cases the effects of the well-known scavenger of reactive oxygen species (ROS), the melatonin, which is also produced by the pineal gland.
The methods used in our experiments in old rats included determination of total antioxidant and antiradical activities, as well as those of antioxidant enzymes (superoxide dismutase=SOD, glutathione peroxidase, glutathione-S-transferase, etc.) in blood serum, liver and brain.
It has been revealed that epithalamin (polipeptide preparation from bovine brain) and its active fragment, epitalon (Ala-Glu-Asp-Gly) along with their ability to stimulate melatonin production, have an antioxidant mechanism that is quite different from the action of melatonin.
Epithalamin can be more beneficial than melatonin because the former not only produces direct antioxidant effects, but also is able to stimulate the expression of SOD, ceruloplasmin and other antioxidant enzymes. The possibility of oxidation chains by their interaction with different ROS by means of binding of transition metals (Fe(2+)) cannot also be excluded.
Thus, the results of our experiments testify that the pineal gland peptides enhance the antioxidant defense system, which can contribute to their geroprotective properties.
The role of pineal gland in breast cancer development. Buy on PUBMED.
Crit Rev Oncol Hematol. 2003 Jun;46(3):221-34.
Abstract: The role of the modulation of the pineal gland function in development of breast cancer is discussed in this review.
An inhibition of the pineal function with pinealectomy or with the exposure to the constant light regimen stimulates mammary carcinogenesis, whereas the light deprivation inhibits the carcinogenesis. Epidemiological observations on increased risk of breast cancer in night shift workers, flight attendants, radio and telegraph operators and on decreased risk in blind women are in accordance with the results of experiments in rodents.
Treatment with pineal indole hormone melatonin inhibits mammary carcinogenesis in pinealectomized rats, in animals kept at the standard light/dark regimen (LD) or at the constant illumination (LL) regimen.
Pineal peptide preparation Epithalamin and synthetic tetrapeptide Epitalon (Ala-Glu-Asp-Gly) are potent inhibitors of mammary carcinogenesis in rodents and might be useful in the prevention of breast cancer in women at risk.
Inhibitory effect of peptide Epitalon on colon carcinogenesis induced by 1,2-dimethylhydrazine in rats. Buy on PUBMED.
Cancer Lett. 2002 Sep 8;183(1):1-8.
Abstract: The effect of synthetic pineal peptide Epitalon (Ala-Glu-Asp-Gly) on colon carcinogenesis was firstly studied in rats. Eighty 2-month-old outbred male LIO rats were subdivided into four groups and were weekly exposed to five subcutaneous injections of 1,2-dimethylhydrazine (DMH) at a single dose of 21 mg/kg body weight.
Additionally, 5 days a week, some of the rats were given subcutaneous injections of saline at a dose of 0.1 ml during the whole experiment (group 1, control) or Epitalon at a single dose of 1 microg during the whole experiment (group 2), Epitalon after termination of carcinogen injections (group 3) or during the period of DMH exposure (group 4).
Colon carcinomas developed in 90-100% of DMH-treated rats. The number of total colon tumors per rat was 4.1; 2.7; 3.7; 2.9 in groups 1, 2, 3, 4, respectively (the difference in groups 2 and 4 compared with group 1 is significant).
In rats from group 2, colon tumors were smaller than in control animals. In group 2, the incidence, as well the multiplicity of tumors in ascending and descending colon, were significantly decreased in comparison with group 1.
In group 4, the mean number of tumors per rat was significantly decreased, too. A trend to decrease the number of tumors in the rectum in rats from groups 2, 3 and 4, treated with Epitalon was found.
Epitalon inhibited also the development of tumors in jejunum and ileum. Thus, our results demonstrated an inhibitory effect of Epitalon on chemically induced bowel carcinogenesis in rats.
Melatonin as antioxidant, geroprotector and anticarcinogen. Buy on PUBMED.
Biochim Biophys Acta. 2006 May-Jun;1757(5-6):573-89. Epub 2006 Apr 17.
Abstract: The effect of the pineal indole hormone melatonin on the life span of mice, rats and fruit flies has been studied using various approaches. It has been observed that in female CBA, SHR, SAM and transgenic HER-2/neu mice long-term administration of melatonin was followed by an increase in the mean life span. In rats, melatonin treatment increased survival of male and female rats.
In D. melanogaster, supplementation of melatonin to nutrient medium during developmental stages produced contradictory results, but and increase in the longevity of fruit flies has been observed when melatonin was added to food throughout the life span.
In mice and rats, melatonin is a potent antioxidant both in vitro and in vivo. Melatonin alone turned out neither toxic nor mutagenic in the Ames test and revealed clastogenic activity at high concentration in the COMET assay. Melatonin has inhibited mutagenesis and clastogenic effect of a number of indirect chemical mutagens.
Melatonin inhibits the development of spontaneous and 7-12-dimethlbenz(a)anthracene (DMBA)- or N-nitrosomethylurea-induced mammary carcinogenesis in rodents; colon carcinogenesis induced by 1,2-dimethylhydrazine in rats, N-diethylnitrosamine-induced hepatocarcinogenesis in rats, DMBA-induced carcinogenesis of the uterine cervix and vagina in mice; benzo(a)pyrene-induced soft tissue carcinogenesis and lung carcinogenesis induced by urethan in mice.
To identify molecular events regulated by melatonin, gene expression profiles were studied in the heart and brain of melatonin-treated CBA mice using cDNA gene expression arrays (15,247 and 16,897 cDNA clone sets, respectively).
It was shown that genes controlling the cell cycle, cell/organism defense, protein expression and transport are the primary effectors for melatonin. Melatonin also increased the expression of some mitochondrial genes (16S, cytochrome c oxidases 1 and 3 (COX1 and COX3), and NADH dehydrogenases 1 and 4 (ND1 and ND4)), which agrees with its ability to inhibit free radical processes.
Of great interest is the effect of melatonin upon the expression of a large number of genes related to calcium exchange, such as Cul5, Dcamkl1 and Kcnn4; a significant effect of melatonin on the expression of some oncogenesis-related genes was also detected.
Thus, we believe that melatonin may be used for the prevention of premature aging and carcinogenesis.
Telomere length in early life predicts lifespan Free .PDF.
Edited by Cynthia Kenyon, University of California, San Francisco, CA, and approved November 29, 2011.
Abstract: The attrition of telomeres, the ends of eukaryote chromosomes, is thought to play an important role in cell deterioration with advancing age. The observed variation in telomere length among individuals of the same age is therefore thought to be related to variation in potential longevity.
Studies of this relationship are hampered by the time scale over which individuals need to be followed, particularly in long-lived species where lifespan variation is greatest. So far, data are based either on simple comparisons of telomere length among different age classes or on individuals whose telomere length is measured at most twice and whose subsequent survival is monitored for only a short proportion of the typical lifespan. Both approaches are subject to bias.
Key studies, in which telomere length is tracked from early in life, and actual lifespan recorded, have been lacking. We measured telomere length in zebra ?nches (n=99) from the nestling stage and at various points thereafter, and recorded their natural lifespan (which varied from less than 1 to almost 9 y). We found telomere length at 25 d to be a very strong predictor of realized lifespan (P < 0.001); those individuals living longest had relatively long telomeres at all points at which they were measured. Reproduction increased adult telomere loss, but this effect appeared transient and did not influence survival.
Our results provide the strongest evidence available of the relationship between telomere length and lifespan and emphasize the importance of understanding factors that determine early life telomere length.
Physical Activity, Sedentary Behavior, and Leukocyte Telomere Length in Women Free .PDF.
Mengmeng Du, Jennifer Prescott, Peter Kraft, Jiali Han, Edward Giovannucci, Susan E. Hankinson, and Immaculata De Vivo
Abstract: Leukocyte telomere length (LTL) is a potential indicator of cellular aging; however, its relation to physical activity and sedentary behavior is unclear.
The authors examined cross-sectionally associations among activity, sedentary behavior, and LTL among 7,813 women aged 43–70 years in the Nurses’ Health Study. Participants self-reported activity by questionnaire in 1988 and 1992 and sedentary behavior in 1992. Telomere length in peripheral blood leukocytes, collected in 1989–1990, was measured by quantitative polymerase chain reaction. The least-squares mean telomere length (z-score) was calculated after adjustment for age and other potential confounders. For total activity, moderately or highly active women had a 0.07-standard deviation (SD) increase in LTL (2-sidedPtrend¼0.02) compared with those least active.
Greater moderate- or vigorous-intensity activity was also associated with increased LTL (SD ¼ 0.11 for 2–4 vs. <1 hour/week and 0.04 for 7 vs. <1 hour/week; 2-sided Ptrend ¼ 0.02). Specifically, calisthenics or aerobics was associated with increased LTL (SD ¼ 0.10 for 2.5 vs. 0 hours/week; 2-sided Ptrend ¼ 0.04). Associations remained after adjusment for body mass index. Other specific activities and sitting were unassociated with LTL.
Although associations were modest, these findings suggest that even moderate amounts of activity may be associated with longer telomeres, warranting further investigation in large prospective studies.
Telomere length, cigarette smoking, and bladder cancer risk in men and women. Free on PMC.
Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):815-9.
Abstract: Truncated telomeres are among the defining characteristics of most carcinomas. Given the role of telomeres in tumorigenesis, we reasoned that constitutionally short telomeres might be associated with an increased risk of bladder cancer. Using quantitative real-time PCR, we measured relative telomere length in bladder cancer cases and healthy controls and evaluated the association between telomere length, cigarette smoking, and bladder cancer risk in a case-control study nested within the Health Professionals Follow-up Study and a case-control study nested within the Nurses’ Health Study.
Telomeres were significantly shorter in bladder cancer cases (n = 184) than in controls (n = 192). The mean relative telomere length in cases was 0.23 (SD, 0.16) versus 0.27 (SD, 0.15) in controls (P = 0.001). The adjusted odds ratio for bladder cancer was 1.88 (95% confidence interval, 1.05, 3.36) for individuals in the quartile with the shortest telomeres as compared with individuals in the quartile with the longest telomeres (P(trend) = 0.006).
We observed a statistically significant difference in telomere length among men and women (P < 0.001); however, the interaction between gender, telomere length, and bladder cancer risk was not significant.
We also observed a significant difference in telomere length across categories of pack-years of smoking (P = 0.01). These findings suggest that truncated telomeres are associated with an increased risk of bladder cancer.
Associations between Rotating Night Shifts, Sleep Duration, and Telomere Length in Women Free on PMC.
PLoS One. 2011; 6(8): e23462. Published online 2011 August 10. doi: 10.1371/journal.pone.0023462
Background: Telomere length has been proposed as a marker of aging. However, our knowledge of lifestyle risk factors determining telomere length is limited.
Methods: We evaluated the associations between years of rotating night shifts, self-reported sleep duration, and telomere length in 4,117 female participants from the Nurses’ Health Study. Telomere length in peripheral blood leukocytes was determined by Real-Time PCR assay. Information on rotating night shifts and sleep duration was collected via questionnaires prior to blood collection. We used multivariable linear regression to investigate the associations between rotating night shifts, sleep duration, and telomere length.
Results: Compared with women in the category (9 hours), those in the lowest category of sleep duration (<6 hours) had a 0.12 unit decrease in z score after adjustment for age, BMI and cigarette smoking (equivalent to 9-year telomere attrition, P for trend =0.05). Significant positive association between sleep duration and telomere length was seen among women under age of 50 (P for trend =0.004), but not among those over 50 (P for trend =0.33) (P for interaction =0.005). In addition, we observed that women with a longer history of rotating night shifts tended to have shorter telomere length, but this relation was not statistically significant (P for trend =0.36).
Conclusion: We found that sleep duration was positively associated with telomere length among women under 50 years old. Further research is needed to confirm the observed associations.
Relative Telomere Length and Cognitive Decline in the Nurses’ Health Study Free on PMC.
Neurosci Lett. Author manuscript; available in PMC 2012 March 29.
Abstract: Telomeres are short DNA repeats on the ends of mammalian chromosomes, which can undergo incomplete replication leading to gradual shortening with each cell cycle.
Age and oxidative stress are contributors to telomere shortening; thus, telomere length may be a composite measure of biologic aging, and a potential predictor of health status in older adults.
We evaluated whether relative telomere length (the proportion of telomere repeat copy number to single gene copy number, using a real-time PCR method) predicts cognitive decline measured ten years later among ~2,000 older participants in the Nurses’ Health Study (NHS). Mixed linear regression was used to evaluate mean differences in cognitive decline according to telomere length. After adjustment for potential confounders, we found that decreasing telomere length was associated with more cognitive decline, although associations were modest (e.g. for a global score, averaging all six tests in our cognitive battery, mean difference=0.03 standard units per SD increase in telomere length; p=0.04).
The magnitude of these estimates was similar to the differences we find in this cohort for women one year apart in age (e.g. the differences that we observe between women who are 73 versus 74 years of age); thus, our results suggest that telomere length is not a particularly powerful marker of impending cognitive decline.
Synthetic drugs with anti-ageing effects. Buy on PUBMED.
G.H.G. Khalsa College of Pharmacy, Gurusar Sadhar, Ludhiana 141104, India.
Abstract: Although ageing is a natural wear and tear phenomenon, it can at least be postponed or prevented by certain approaches. Some chemicals that are present in the diet or in dietary supplements have been documented to have anti-ageing effects. Recently, a number of synthetic drugs used for other therapeutic indications have been shown to have anti-ageing potential.
Herbals in the control of ageing. Buy on PUBMED.
G.H.G. Khalsa College of Pharmacy, Gurusar Sadhar, Ludhiana 141104, India.
Abstract: The significance of herbals and herbal products is gaining worldwide recognition. The concept of complementary or alternative medicine is becoming much more widely accepted, and there is an increasing belief in the efficacy of herbal remedies. Recently, the role of herbal drugs, herbal products and certain phytochemicals in the control of ageing has been documented using modern scientific approaches. This review pulls together such studies and critiques the efficacy and value of herbal medicines in the control of the ageing process.