Laut einer US-Studie verkürzt auch normaler Militärdienst die Telomere im Vergleich zur restlichen Bevölkerung, wobei die Befunde vielleicht nur durch die Personen erklärt werden, die wirklich an Kampfmissionen beteiligt waren. Man kann also sagen, Krieg verkürzt das Leben auch wenn man ihn überlebt und nicht gefangen genommen wurde?
Telomere Shortening and Accelerated Aging in US Military Veterans Abstract:
ZitatA growing body of literature on military personnel and veterans’ health suggests that prior military service may be associated with exposures that increase the risk of cardiovascular disease (CVD), which may differ by race/ethnicity. This study examined the hypothesis that differential telomere shortening, a measure of cellular aging, by race/ethnicity may explain prior findings of differential CVD risk in racial/ethnic groups with military service. Data from the first two continuous waves of the National Health and Nutrition Examination Survey (NHANES), administered from 1999–2002 were analyzed. Mean telomere length in base pairs was analyzed with multivariable adjusted linear regression with complex sample design, stratified by sex. The unadjusted mean telomere length was 225.8 base shorter for individuals with prior military service. The mean telomere length for men was 47.2 (95% CI: −92.9, −1.5; p < 0.05) base pairs shorter for men with military service after adjustment for demographic, socioeconomic, and behavioral variables, but did not differ significantly in women with and without prior military service. The interaction between military service and race/ethnicity was not significant for men or women. The results suggest that military service may contribute to accelerated aging as a result of health damaging exposures, such as combat, injury, and environmental contaminants, though other unmeasured confounders could also potentially explain the results.
Wohl auch ein Grund, warum die Lebenserwartung und gesunde Lebensspanne nach den 40er Jahren gestiegen ist (bei den Generationen die weder den ersten noch den zweiten Weltkrieg miterlebten).
Ich kann mir schon aufgrund meiner geringen militärischen Erfahrungen vorstellen, dass Militärdienst auch ohne Kampfhandlungen zum beschleunigten Altern beiträgt. Schon psychosomatisch. Beteligung an direkten Kampfhandlungen sicher extrem.
Zitat von parcel im Beitrag #153Der Text wird leider immer falsch wiedergeben
Diese Studie? Am besten vergleicht man die Sterbealter als Telomerlängen. Dann sieht man ja. Nach Rassen oder Geschlecht zu sortieren ist politisch nicht korrekt
Telomere Length Is Longer In Women with Late Maternal Age Abstract:
ZitatObjective: Maternal age at birth of last child has been associated with maternal longevity. The aim of this study was to determine whether elderly women with a history of late maternal age at last childbirth had a longer leukocyte telomere length compared with those with maternal age at last childbirth of 29 years or less.
Methods: A nested case control study was conducted utilizing data from the Long Life Family Study. Three hundred and eighty-seven women who gave birth to at least 1 child and lived to the top 5th percentile of their birth cohort, or died before the top 5th percentile of their birth cohort died, but were at least 70 years old, were studied. Logistic regression models using generalized estimating equations were used to determine the association between tertiles of telomere length and maternal age at last childbirth, adjusting for covariates.
Results: Age at birth of the last child was significantly associated with leukocyte telomere length. Compared with women who gave birth to their last child before the age of 29, women who were past the age of 33 when they had their last child were 2–3 times more likely to have leukocyte telomere length in the second and third tertiles than in the first tertile. Conclusion: These findings show an association between longer leukocyte telomere length and a later maternal age at birth of last child, suggesting that extended maternal age at last childbirth may be a marker for longevity.
Also bei den GI würde ich behaupten, sind automatisch viele andere negative Aspekte des Lebensstills dabei, welche die Lebenserwartung und die Telomere verkürzen, und daher betrachte ich diese Untersuchung skeptisch. In meine Jugend kannten wir viele GI aus der nahen Kaserne über die Disko, Kneipen etc. In der USA wird gesagt, das nur der Abschaum zum Militär geht als einfacher Soldat der sonst gar keine andere Chance hat, und die anderen drücken sich, wie z.B. Donald Trump. Und die GI Mannschaftler hier waren wirklich unterste Stufe, also massiver Alkoholkunsum, Drogenkonsum, Raucher, häufig geschieden und heftigste Streits mit der Partnerin, Fastfood und nix Bio oder Vegetarier und alles negative was man sich vorstellen kann. Aber körperlich fit. Und das war noch vor dem Irakkrieg bei GI ohne Traumatisierung durch Kampfeinsatz. Für mich sagt die Untersuchung daher eher aus, das die unterste Unterschicht einen sehr ungesunden Lebensstil hat und dieser die Telomere verkürzt.
Zitat von Aluhut im Beitrag #156Also bei den GI würde ich behaupten, sind automatisch viele andere negative Aspekte des Lebensstills dabei, welche die Lebenserwartung und die Telomere verkürzen, und daher betrachte ich diese Untersuchung skeptisch. In meine Jugend kannten wir viele GI aus der nahen Kaserne über die Disko, Kneipen etc. In der USA wird gesagt, das nur der Abschaum zum Militär geht als einfacher Soldat der sonst gar keine andere Chance hat, und die anderen drücken sich, wie z.B. Donald Trump. Und die GI Mannschaftler hier waren wirklich unterste Stufe, also massiver Alkoholkunsum, Drogenkonsum, Raucher, häufig geschieden und heftigste Streits mit der Partnerin, Fastfood und nix Bio oder Vegetarier und alles negative was man sich vorstellen kann. Aber körperlich fit. Und das war noch vor dem Irakkrieg bei GI ohne Traumatisierung durch Kampfeinsatz. Für mich sagt die Untersuchung daher eher aus, das die unterste Unterschicht einen sehr ungesunden Lebensstil hat und dieser die Telomere verkürzt.
Die Wissenschaftler haben aber auch versucht die GI`s mit Zivilisten zu vergleichen, die den möglichst gleichen Risikofaktoren ausgesetzt sind.
ZitatBased on the evidences collected it can be suggested that chronic moderate intensity aerobic exercise in a lifelong practice shows beneficial effects in a dose-response manner in cancer prevention in a novel way by modulating telomeres through epigenetic mechanism.
Meditation and vacation effects have an impact on disease-associated molecular phenotypes Abstract:
ZitatMeditation is becoming increasingly practiced, especially for stress-related medical conditions. Meditation may improve cellular health; however, studies have not separated out effects of meditation from vacation-like effects in a residential randomized controlled trial. We recruited healthy women non-meditators to live at a resort for 6 days and randomized to either meditation retreat or relaxing on-site, with both groups compared with ‘regular meditators’ already enrolled in the retreat. Blood drawn at baseline and post intervention was assessed for transcriptome-wide expression patterns and aging-related biomarkers. Highly significant gene expression changes were detected across all groups (the ‘vacation effect’) that could accurately predict (96% accuracy) between baseline and post-intervention states and were characterized by improved regulation of stress response, immune function and amyloid beta (Aβ) metabolism. Although a smaller set of genes was affected, regular meditators showed post-intervention differences in a gene network characterized by lower regulation of protein synthesis and viral genome activity. Changes in well-being were assessed post intervention relative to baseline, as well as 1 and 10 months later. All groups showed equivalently large immediate post-intervention improvements in well-being, but novice meditators showed greater maintenance of lower distress over time compared with those in the vacation arm. Regular meditators showed a trend toward increased telomerase activity compared with randomized women, who showed increased plasma Aβ42/Aβ40 ratios and tumor necrosis factor alpha (TNF-α) levels. This highly controlled residential study showed large salutary changes in gene expression networks due to the vacation effect, common to all groups. For those already trained in the practice of meditation, a retreat appears to provide additional benefits to cellular health beyond the vacation effect.
Introduction:
ZitatAncient practices such as yoga and meditation have long been thought to combat stress and promote longevity, although empirical evidence for effects on aging processes under highly controlled experimental conditions is lacking. Further, it is inherently difficult to assess effects of meditation apart from simple relaxation. Advances in the understanding of the biological bases of aging enable better assessment of acute effects of salutary interventions on biomarkers of aging. For example, impaired regulatory systems leading to systemic inflammation, and excessive stress responsivity, are related to biological aging1 and may partly underlie pathogenesis of cardiovascular2, 3 and Alzheimer’s4, 5 diseases (AD). More recent systems biology approaches have identified gene regulatory networks associated with a diversity of biological processes, including immune and stress responses, and objectively linked them with disease or salutary states.6, 7
Integrated systems biology approaches can identify gene regulatory networks, such as immune, stress and other regulatory responses, and link them with physiologic states.6 This bioinformatics approach provides an unbiased view of the immune system profile, and can be linked to changes in environmental conditions.7 These network approaches, while often applied to identifying disease profiles, can be used to identify salutary states as well, such as that which might result from intensive meditation. In addition to high-dimensional molecular data such as gene networks, blood-based biomarkers can provide an integrated overview that indexes biological aging. Telomere length predicts both cellular health and disease in rodent models and humans.8 Shorter telomeres predict onset of cardiometabolic diseases of aging.9 Chronic stress is associated with higher inflammation, shorter telomeres, and lower activity levels of telomerase, the cellular enzyme that elongates telomeric DNA.10, 11 Levels of amyloid beta (Aβ) proteins circulating in the blood appear to be stress-related in rodent models12 and may be affected by stress reduction, and greater Aβ42/Aβ40 ratios are associated with lower risk of dementia.13
Various types of meditation have been shown to improve well-being among different populations such as physicians and the general public.14, 15, 16 Preliminary evidence suggests that meditation-based interventions may slow cellular aging rates by increasing telomerase activity, but many such studies lacked an active control group.17, 18 Recent randomized trials in breast cancer suggest that long-term intensive meditation interventions might have positive effects on telomerase activity. One found that mindfulness-based and supportive expressive therapies were associated with telomere maintenance, compared with a ‘treatment as usual’ control group.19 A second study found that mindfulness-based stress reduction was associated with increases in telomerase after 3 months.20 Long-term mind–body interventions, including tai chi, yoga and meditation, have been associated with gene expression (GE) changes associated with inflammatory pathways21, 22 as reviewed elsewhere.23, 24
Short-term interventions have examined changes after one session of meditation or yoga. One study compared GE changes in experienced versus novice meditators after one session. They found changes in both groups in inflammation, energy metabolism, mitochondrial function and telomere maintenance, but experienced meditators had greater changes.25 Another study comparing experienced meditators to novices after 8 hours of meditation examined GE changes specific to epigenetic regulatory enzymes. Changes were found only in the experienced meditators.26 Another study found threefold changes in GE in the immune cells after yoga versus a control movement program.27 These studies suggest that there are greater changes in experienced meditators than in novices after one bout. However, none of these studies examined people in more controlled residential vacation settings, where larger changes can occur in periods as short as a week. One limitation to meditation studies is that short-term relaxation as a control condition may not lead to the powerful changes that prolonged vacation could. No studies we are aware of have examined how a meditation retreat may affect GE above and beyond a relaxing vacation. Further, none of these previous studies took a systems biology approach by examining covariation across GE patterns (versus specific gene pathways).
Here we examined how exposure to a short-term intensive residential meditation retreat affected biomarkers of aging and more general regulatory networks defining a wide array of biological processes. A residential retreat provides intensive daily exposure in a controlled environment but has the added ‘vacation’ effect of taking people away from the demands of their daily lives, which alone might affect regulation of stress pathways. Therefore, it is critical to compare the effects of a meditation retreat with an active randomized control group. Because regular meditators may have differences in brain function and structure, as suggested by meta-analyses,28 and greater changes in GE than novices, after meditation,25 we also recruited a third comparison group of experienced meditators. Our design allowed us to study the effects of meditation independent of the vacation effect, as well as to compare the effects of acute intensive meditation in regular meditators versus those newly trained in meditation.
Discussion:
ZitatAfter 1 week at a resort, participants felt greater vitality and decreased distress, regardless of whether they were in the resort group or in an intensive meditation/yoga retreat. The randomized group immersed in meditation and yoga for the first time exhibited more sustained well-being up to 1 month later, compared with the resort group on mindfulness. Ten months later; the novices maintained a clinically meaningful improvement in depressive symptoms compared with the vacation group. Thus, we found both a short-term vacation effect for everyone and a significant benefit of learning meditation on longer-term mood.
A thematic examination of the coexpression modules enriched for relaxation effect genes showed a suppression of correlated networks regulating stress responses, inflammation and wound healing. A parsimonious interpretation of these data is that, while on vacation, genes that are normally needed for dealing with stress, wound healing and injury are downregulated. Among the genes that were downregulated after resort/treat were MME and FOXO3, both known stress-related genes. Psychological stress and glucorticoids have been shown to increase FOXO3 in animal studies,36, 37, 38 whereas low levels of FOXO3 in mice actually prevent the behavioral stress response in mice, serving an antidepressant effect.39 We believe our study is the first documentation that a stress reduction intervention can reduce FOXO3 expression.
A number of downregulated pathways in the regular meditator group versus the other groups defined the meditation effect, including regulation of protein synthesis and trafficking, viral expression and viral infectious cycle. Following a period of intensive meditation, genes involved with the infectious cycle may get downregulated along with related host genes regulating protein synthesis, an explanation that is supported by other stress reduction interventions that have shown increased innate antiviral activity, such as upregulated Type 1 interferon activity.40 Shorter telomeres in population-based studies have been predictive of earlier onset of chronic diseases of aging, including diabetes,41 cardiovascular disease9 and certain cancers.42
Changes in biomarkers during the retreat suggested salutary improvements in regular meditators compared with other groups. Regular meditators had lower telomerase at baseline, but also showed a significant increase in peripheral blood mononuclear cell telomerase activity post treatment that was not observed in the other two groups. Theoretically, a sustained increase could stabilize or even lengthen telomeres over time, as shown in a previous study where intensive lifestyle intervention led to higher telomerase activity after 4 months, and longer telomeres after 5 years, with such changes associated with better adherence.43, 44
There were also changes in the levels of plasma Aβ levels by study group. The regular meditator group started off with a higher plasma Aβ42/Aβ40 ratio, and this ratio did not change from pre- to post-intervention. Over the four days, plasma Aβ40 levels significantly decreased in the novice meditator group, accompanied by a significant increase in the Aβ42/Aβ40 ratio. A growing number of human studies suggest that a low plasma Aβ42/Aβ40 ratio is a risk factor for major depression,45, 46 dementia47 and higher mortality.48 The Framingham Study also showed that increased plasma Aβ42:Aβ40 ratios are associated with decreased risk of AD and dementia.13 Thus, the higher Aβ42/Aβ40 ratio observed in regular meditators at baseline and the increase in this ratio from pre- to post intervention in the novice meditator and vacation groups may be salutary to brain health.
The increase in the Aβ42/Aβ40 ratio (driven by a decrease in plasma Aβ40 levels) could also be related to the observed decrease in expression of CLU as part of the relaxation effect (P=0.00045). CLU is a confirmed AD gene from genome-wide association study, and encodes apolipoprotein J, which has been shown to chaperone re-entry of Aβ into the brain following export of the peptide from the brain into the blood.49 Interestingly, genes encoding two peptidases known to degrade Aβ were also decreased in expression in blood pre–post intervention as part of the vacation effect: MME (P=0.00019) and ECE1 (P=0.0037). These data may reflect that there was less need for these peptidases, perhaps owing to lower plasma Aβ40 levels. Finally, expression of the known early-onset familial AD gene, PSEN1, was also decreased as part of the relaxation effect. PSEN1 encodes the γ-secretase needed to produce the Aβ peptide.
The vacation group showed a statistically significant increase in circulating TNF-α compared with the regular meditators, and a marginally significant increase when compared with novice meditators. Reasons for this increase could include those in the vacation group having an acute stress-related inflammation response to the blood draw, overexposure to sun or some other exposure that can lead to acute physical stress such as exercise. All participants ate a healthy ayurvedic diet, which is thought to be anti-inflammatory.
One of the most comprehensive reviews on the effects of mindfulness meditation on immune parameters was recently conducted across 20 randomized clinical trials.23 Three of these studies found decreased NF-KB and no strong evidence for changes in interleukin inflammatory markers (interleukin-6) or TNF-α, but some evidence for a decrease in CRP and increases in telomerase. Our findings are consistent with this review. We also did not find decreases in circulating inflammatory cytokines but rather slight increases, particularly in the vacation group. We did not find a decrease in NF-KB specifically; however, we did find suppression in large gene networks known to be related to inflammatory processes. We found a trend for increases in telomerase activity in the regular meditator group.
Our study has several limitations. The changes in biomarkers and GE patterns appear salutary; however, no studies have tracked these markers to see how well they predict disease or longevity in a healthy sample. The sample size is relatively small and powered only to detect medium-to-large effects. Replication of these findings with larger controlled studies will be necessary. In addition, comparing regular meditators to non-meditators is somewhat problematic, given regular meditators likely differ on many lifestyle factors that make such comparisons complicated. For example, diet, exercise regimen and stress-reduction activities such as meditation likely differ between these groups and may not only lead to baseline differences in molecular and higher-order systems, but may prime such systems to respond differentially to resort and meditation interventions. In addition, the meditation arm of this study was not strictly sitting meditation, but also included yoga postures and self-reflection exercises and lectures. Further, whereas our design did attempt to control for the vacation effect, we did not randomize regular meditators to the vacation and meditation arms, making it difficult to interpret the changes observed in the regular meditators, given they were compared with a control group comprising non-meditators. A balanced design that included randomization of regular meditators as well as non-meditators would be useful in future studies to better localize the effects driving the expression changes. Despite these limitations, our study provides a strong distinction between beneficial effects of short-term relaxation typical of a vacation versus acute intensive meditation.
In summary, our results point to both a significant ‘vacation effect’ that benefitted all groups, and a suppression of stress-related responses and immune function related to acute-phase wound healing and inflammation. We also identified a ‘meditation effect’ within the regular meditator group, characterized by a distinct network of genes with cellular functions that may be relevant to healthy aging, and this network was associated with increased expression of a number of telomere maintenance pathway genes and an increase in measured telomerase enzymatic activity. This study provides a strong distinction between beneficial effects of short-term relaxation typical of a vacation versus acute intensive meditation for regular meditators. Future studies expanding upon these results will be critical for further understanding lifestyle acute adaptations capable of promoting stress reduction and overall health and well-being.
Ich habe diese Krankheit zum Glück nicht. Aber wie schaut das bei einer Robusten Mäuselinie aus. Wenn man damit alte Mäuse impft? Ich bin kein Eugeniker aber Robust ist schon wichtig....sowohl körperlich als auch psychisch. Steven Hawkins ist ein Idol, trotz mangelndem Markus Rührl! Fakt wäre Höhe Fortpflanzungszahl und sehr starke Auslese. Irgendwie brutal
Aerobes Ausdauertraining und die Aerobe Kapazität haben deutlichen Einfluss auf die Telomerase-Aktivität und die Telomerlängen!
Kommentar Prometheus: Bei mir die bislang einzige Maßnahme, die messbaren Erfolg hat, im Gegensatz zu diversen hier im Forum diskutierten Supplementen!
Sauerstoff ist auch ein Signalmolekül und das aerobe Training hat deshalb eine sehr positive Wirkung auf den Körper. So nehmen Leistungssportler beim Training bis zu der zehnfachen Menge Sauerstoff im Vergleich zum Ruhezustand auf. Mängel von Mikronährstoffen sollten trotzdem aufgefüllt werden, damit der Körper die optimale Leistungsfähigkeit behalten kann (siehe auch Liste der Laborwerte von Dr. Strunz).
ZitatThe Relationship Between Vitamin D and Telomere/Telomerase: A Comprehensive Review (...) Recent studies suggest that micronutrients, such as vitamin D, folate and vitamin B12, are involved in telomere biology and cellular aging. In particular, vitamin D is important for a range of vital cellular processes including cellular differentiation, proliferation and apoptosis. As a result of the multiple functions of vitamin D it has been speculated that vitamin D might play a role in telomere biology and genomic stability. In this study, our main goal is investigating the relationship between telomerase enzyme and vitamin D. Findings of this study suggest that higher vitamin D concentrations, which are easily modifiable through nutritional supplementation, are associated with longer LTL, which underscores the potentially beneficial effects of this hormone on aging and age-related diseases. Vitamin D may reduce telomere shortening through anti-inflammatory and anti-cell proliferation mechanisms.
ZitatThe effect of maternal vitamin C intake on fetal telomere length (...) Our study shows a positive association between maternal vitamin C intake and fetal telomere length.
ZitatMaternal Vitamin D and Newborn Telomere Length (...) To conclude, vitamin D intake (diet + supplements), specifically during the first trimester of pregnancy, is an important factor associated with TL at birth.
ZitatMaternal diet and offspring telomere length: a systematic review (...) Seven studies were extracted and evaluated. (...) Higher circulating maternal folate and 25-hydroxyvitamin D3 concentrations, along with higher maternal dietary caffeine intakes, were associated with longer offspring telomere length, whereas higher dietary intake of carbohydrate, folate, n-3 polyunsaturated fatty acids, vitamin C, or sodium was not.
Conclusion: The limited but suggestive evidence highlights the need for further research to be conducted in this area, particularly longitudinal studies involving larger cohorts of pregnant women.
ZitatAssociation between nutrient intake and telomere length in Japanese female university students (...) Vitamin A intake was positively associated with telomere length (...) after adjusting for covariates (age, BMI, passive smoking, and drinking).
Conclusions: Our findings suggest that variation in vitamin A intake might influence telomere attrition in healthy individuals.
ZitatOptimism and telomere length among African American adults in the Jackson Heart Study (...) Optimism was not associated with leukocyte telomere length among African American adults.
ZitatTelomere Length in Healthy Adults Is Positively Associated With Polyunsaturated Fatty Acids, Including Arachidonic Acid, and Negatively With Saturated Fatty Acids Lymphocyte telomere length (LTL) is a biomarker of aging (...) Our results indicate that the majority of saturated fatty acids and monounsaturated fatty acids are negatively associated with LTL, whereas polyunsaturated fatty acids are positively associated with LTL. Multiple regression analysis revealed that arachidonic acid (C20:4n-6) is significantly, independently, positively correlated with LTL (β = 0.262; p = .000). The significant association of fatty acids, particularly C20:4n-6, with telomere length warrants further research.
ZitatPim1 maintains telomere length in mouse cardiomyocytes by inhibiting TGFβ signalling (...) Pim1 is a cardioprotective kinase that antagonizes the aging phenotype of cardiomyocytes and delays cellular senescence by maintaining telomere length(...) Pim1 maintains telomere lengths in cardiomyocytes by inhibiting phosphorylation of the TGFβ pathway downstream effectors Smad2 and Smad3, which prevents repression of telomerase reverse transcriptase. Findings from this study demonstrate a novel mechanism of telomere length maintenance and provide a potential target for preserving cardiac function.
ZitatScientists find way to increase length of human telomeres
(...) To increase telomere length, the team used a modified type of ribonucleic acid (RNA) that contained the coding sequence of TERT.
(...)introducing as few as three applications of the modified RNA (called modified TERT mRNA) to human cells over a few days increased telomere length by up to 10%.
Die TERT-Promotor-Region muss stark methyliert sein, damit es zu einer Telomerase-Expression kommt. In Krebszellen wird das oft durch Promotor-Mutationen umgangen:
Optimierte Formel für Telomererhaltung Verbindet die Testsubstanzen, die Verkürzung der Telomere verlangsamen. Verwendet zur Verlängerung der Lebenserwartung.
Optimierte Formel für Telomererhaltung Verbindet die Testsubstanzen, die Verkürzung der Telomere verlangsamen. Verwendet zur Verlängerung der Lebenserwartung.
Ein eleganter Weg, bei dem Epigenetik im Zellkern dafür nicht umgeschrieben werden muss, was im Prinzip sicherer ist. Dafür möglicherweise Risiken durch den Vektor oder Nanolipide. Ich bin überrascht, wie nah wir auf einmal solchen "Zukunftsszenarien" sind!
"senescence-mediated aging is clearly distinct from epigenetic aging [84]. By stimulation of telomerase to lengthen telomeres, cells bypass replicative senescence and fortunately rejuvenate. This longer lifespan ironically allows more time for the inherent processes of epigenetic aging to occur [84]."
Fazit der Studie: Kein erhöhtes Hautkrebsrisiko durch Telomeraseaktivierung. Dabei muss man allerdings berücksichtigen, dass die Studie mit Geld von TA Sciences finanziert wurde. Die Autoren schreiben:
"TA Sciences did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. [...] None of the authors have any competing or commercial interests that would in any way bias this study."