Longevity (immoratality) = building immunity against demise or mortality. Clues to the longevity of an intervention can be found in the following lines of evidence.

1. Telomere length restoration and telomerase activity enhancment.

2. Dampening or dousing of ageing accelerating inflammaging destruction a component of IAcODcIM complex.

3. Epigenetic adaptive influences

4. Pain threshold elevation helping evaded the anti-survival impact of chronic pain.

5. Improved neurogenesis/neuroplasticity of upregulation of NESDAC

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Healthspan

CNN US life expectancy is still on the decline WHY ? How much damage COVID19 will inflict?

Interpreting Telomere Length and Telomerase Activity as a marker of healthspan and longevity.

Several facts need to be borne in mind before hurrying to start crediting any intervention from gene therapy, enzyme, drug or lifestyle intervention as an intervention that would prolong healthspan and longevity (life expectancy). Healthspan prolongation and longevity are fairly strong end points but interpose problems with data interpretation which gets minimized if actual demise of the participants is the chosen end point instead of longevity markers like inflammatory agent levels, telomerase levels (activity) or telomere length. While plenty of comfort can be taken that the interventions having a positive effect on these are markers of health and longevity it is naïve to start to attribute positive outcome directly to the interventions without scrutiny. The most validated therefore credible five (5) determinants of healthspan duration and longevity are 1) being slender (BMI <30), 2) being sociable and staying mentally-socially active (which subsumes being extrovert, outgoing and optimist), 3) a predominantly plant based diet with sparing meat consumption but some fish consumption, 4) non-smoking and 5) physical activity exceeding 150 minutes per week. Health benefits of all other interventions remain suspect. It is a safe statement that all longevity enhancers also help with retention of youthful look through a rejuvenation effect.

A December 2010 TIME Health article Explaining Why Meditators May Live Longer by Maia Szalavitz canvasses the research on telomere and telomerase in the context of meditation as an intervention should be interpreted with caution because the meditation as intervention might have a small or negligible role in the positive outcomes.

An overview of Telomere and Telomerase.

Telomere is the name given to the part of the tips of the chromosomes the base pair pattern of which is unique and designed to serve a special purpose of staring the splitting of the DNA during cell division which is essential part of maintenance of the tissues; and these two special purposes are compared to the plastic aglets at the tips of shoelaces, which explains their purpose of prevention of the fraying of the chromosome which is a design defect inserted by nature to program death into the DNA. Telomeres shortening through loss of base-pair is an intentional design defect left there by nature but also gracefully blessed with a limited ability to repair it through the enzyme telomerase. Longevity enhancing effect of the enzyme telomerase is attributed to its ability to repairing the telomere segment of chromosome that DNA is made up of. Excessive telomerase causes the cell division to get out of control that turns the cell into a cancer cell with ability to keep dividing relentlessly such that the cell becomes immortal and invasive. Rate of functional incapacitation of the trace amounts of telomerase normally present in the cells is one of the factors that determines the speed of telomere shortening and paucity of telomerase leads to morbidogenically accelerated telomeric attrition (MATA) that predisposes to the aging related diseases. As the chromosome becomes more and more defective and malformed, cell division needed to replace the dying cells becomes progressively sloppier and eventually at point as the telomeres disintegrate cell can no longer divide because the machinery for the start of splitting of the chromosome that rests in the telomere goes missing. Aging retardation behaviours work through amplifying the chromosomal integrity retention capacity of telomerase as this enzyme mitigates and during the first half of life effectively prevents the cellular aging. Normally the levels of telomerase drop shapely after age 49 when cell death becomes rampant and most troublingly in the muscle cells leading to age related sarcopenia whereby muscle starts to get replaced with fat at the rate of a pound a year. In conclusion it can be firmly stated that maintaining healthy and ample length telomere is a desirable objective and the five established longevity drivers are linked to it, unless there is an anomalous unexplained lengthening of telomeres that is not associated with lonevity.

Does meditation prolong healthspan and life?

Do meditators live long because they meditate or those with sharp foccusers ( sharp foxers) choose to meditate but have higher quality genes that bestow them with superior focus. Poor foccussers (poor foxers) tend to stay away from and fail with meditation and are predisposed to premature death. A December 2010 TIME Health article Explaining Why Meditators May Live Longer by Maia Szalavitz canvasses the research on telomere and telomerase in the context of meditation as an intervention should be interpreted with caution because the meditation as intervention might have a small or negligible role in the positive outcomes. At current state if sucience it is impossibkle to confidently (over 95% confidence) state that meditation would prolong life especially because it is not yet determined how protracted and how many hours worth of meditation must have been practiced to bring about positive outcome with certainty.

Hoge et al’s paper Loving-Kindness Meditation practice associated with longer telomeres in women published in Brain, Behavior, and Immunity Aug 2013, Vol 32,: 159-163, reported that mitigating he stress tends to produce longer telomeres. Altruistic acts that focus on the well-being of others, such as volunteering and caregiving, boost wellness and longevity. The found that individuals experienced in Kindness Loving Meditation (KLM), a practice derived from the Buddhist tradition which utilizes a focus on unselfish kindness and warmth towards all people, tended to positively impact telomeres a biomarker associated with longevity. While merely dozen test subjects were evaluated with two dozen controls, the study leans towards anecdotal evidence but in the overall context findings are impressive enough that practice of KLM is well worth adoption given that there is really no downside to it.

Need of extreme caution of extrapolation of subhuman longevity research to human longevity.

While there does exist rodent data from Harvard researchers, who found that boosting levels of telomerase reversed signs of aging, restoring graying fur and fertility, increasing brain size and sharpening scent perception, it is unsafe to predict that same would follow in humans. Replacement of deficient enzymes or cofactors can work very differently from supplementing them when there is no serious deficiency of the substance in the body. For example, administration of neostigmine that mimics acetylcholine offers copious temporary strength to muscles of a patient with myasthenia gravis but giving neostigmine to a normal human adult fails to improve his muscle power.

Davidson et al published Alterations in brain and immune function produced by mindfulness meditation. in Psychosomatic Medicine 2003 Jul-Aug;65(4):564-70. The underlying changes in biological processes that are associated with reported changes in mental and physical health in response to meditation have not been systematically explored. We performed a randomized, controlled study on the effects on brain and immune function of a well-known and widely used 8-week clinical training program in mindfulness meditation applied in a work environment with healthy employees. We measured brain electrical activity before and immediately after, and then 4 months after an 8-week training program in mindfulness meditation. Twenty-five subjects were tested in the meditation group. A wait-list control group (N = 16) was tested at the same points in time as the meditators. At the end of the 8-week period, subjects in both groups were vaccinated with influenza vaccine. We report for the first time significant increases in left-sided anterior activation, a pattern previously associated with positive affect, in the meditators compared with the nonmeditators. We also found significant increases in antibody titers to influenza vaccine among subjects in the meditation compared with those in the wait-list control group. Finally, the magnitude of increase in left-sided activation predicted the magnitude of antibody titer rise to the vaccine. These findings demonstrate that a short program in mindfulness meditation produces demonstrable effects on brain and immune function. These findings suggest that meditation may change brain and immune function in positive ways and underscore the need for additional research.

Jaskelioff et al did published Telomerase reactivation reverses tissue degeneration in aged telomerase deficient mice in Nature. Jan 2011 6; 469(7328): 102–106. doi: 10.1038/nature09603 An ageing world population has fueled interest in regenerative remedies that may stem declining organ function and maintain fitness. Unanswered is whether elimination of intrinsic instigators driving age-associated degeneration can reverse, as opposed to simply arrest, various afflictions of the aged. Such instigators include progressively damaged genomes. Telomerase deficient mice have served as a model system to study the adverse cellular and organismal consequences of wide-spread endogenous DNA damage signaling activation in vivo. Telomere loss and uncapping provokes progressive tissue atrophy, stem cell depletion, organ system failure, and impaired tissue injury responses. Here, we sought to determine whether entrenched multi-system degeneration in adult mice with severe telomere dysfunction can be halted or possibly reversed by reactivation of endogenous telomerase activity. To this end, we engineered a knock-in allele encoding a 4-hydroxytamoxifen (4-OHT)-inducible telomerase reverse transcriptase-Estrogen Receptor (TERT-ER) under transcriptional control of the endogenous TERT promoter. Homozygous TERT-ER mice display short dysfunctional telomeres and sustain increased DNA damage signaling and classical degenerative phenotypes upon successive generational matings and advancing age. Telomerase reactivation in such late generation TERT-ER mice extends telomeres, reduces DNA damage signaling and associated cellular checkpoint responses, allows resumption of proliferation in quiescent cultures, and eliminates degenerative phenotypes across multiple organs including testes, spleens and intestines. Notably, somatic telomerase reactivation reversed neurodegeneration with restoration of proliferating Sox2+ neural progenitors, DCX+ newborn neurons, and Olig2+ oligodendrocyte populations. Consistent with the integral role of SVZ neural progenitors in generation and maintenance of olfactory bulb interneurons, this wave of telomerase-dependent neurogenesis resulted in alleviation of hyposmia and recovery of innate olfactory avoidance responses. Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease risk1, and the dramatic reversal of systemic degenerative phenotypes in adult mice observed here support the development of regenerative strategies designed to restore telomere integrity.

Any interention that lowers the risk of autoimmune dieases would prevent being affected by these 88 diseases.