Does Malformed Lamin A Produce Enough Cellular Senescence to Contribute Meaningfully to the Progression of Aging?

Progeria is one of the better known accelerated aging conditions. It isn't actually accelerated aging, but rather one specific runaway form of cell damage that gives rise to general dysfunction in cells throughout the body. Since degenerative aging is also a matter of general dysfunction in cells throughout the body, there is some overlap in the observed results, even though the root causes are completely different. So progeria patients appear, superficially at least, to be prematurely aged, and die from heart disease early in life.

The cause of progeria was discovered to be a mutation in the Lamin A (LMNA) gene, resulting in a malformed protein now called progerin. This protein is an important structural component of the cell nucleus. If it doesn't function correctly, the nucleus becomes misshapen, and near all processes involving nuclear DNA maintenance and gene expression - the production of needed proteins at the right time from their genetic blueprints - cease to work correctly. The cell becomes dysfunctional. When near all cells are in this state, the prognosis for the individual is dire. Interestingly, in the years since this discovery, it has become clear that progerin is also present in small amounts in genetically normal older individuals. There is some debate over whether or not this is important in the progression of aging. Does it cause enough damage, or is it insignificant in comparison to other harmful processes?

In this context, we can consider cellular senescence, a mechanism closely connected to DNA damage, by which a small number of problem cells can cause outsized amounts of harm. Another possibility is damage to stem cells, as they are also small in number but highly influential on tissue function. Cells become senescent in response to internal damage, including that produced by progerin, and then either self-destruct or linger to secrete a potent mix of inflammatory and other signals. It is these signals, the senescence-associated secretory phenotype, that allows a comparatively small number of cells to produce comparatively large problems. It is known that senescent cells are important in many age-related conditions, particular those with a strong inflammatory component. Is generation of progerin significant as a cause of cellular senescence in normal aging, however? In this open access paper, researchers consider some of the mechanisms involved.

GATA4-dependent regulation of the secretory phenotype via MCP-1 underlies lamin A-mediated human mesenchymal stem cell aging

The LMNA gene encodes lamin and lamin C, which are major components of the nuclear lamina. Mutations in the LMNA gene have been implicated in premature aging disorders, including Hutchinson-Gilford progeria syndrome (HGPS). HGPS is caused by splicing defect and consequent generation of progerin, mutant-truncated lamin protein. Cells of HGPS patients exhibit an abnormal nuclear structure, increased DNA damage and premature senescence. In addition to the effects of progerin, accumulation of prelamin A, precursor of lamin A, induces defects in nuclear structures. ZMPSTE24 is an enzyme that produces mature lamin by cleavage of amino acids in prelamin A.

Zmpste24 knock-out mice have been widely used to study the mechanisms of aging and progeria. Depletion of Zmpste24 causes premature senescence in mice, including decreases in life span and bone density. Increased prelamin expression caused by ZMPSTE24 deficiency causes defective DNA repair. Zmpste24 knock-out mice have been extensively studied because of their impaired DNA damage response (DDR). Lamin also functions as a structural barrier to DDR. Altogether, these findings indicate that defects in the nuclear structure induced by progerin or prelamin lead to the accumulation of DNA damage, which results in accelerated aging.

It has been reported that exogenous expression of progerin in human mesenchymal stem cells (hMSCs) can impair their differentiation potential. Furthermore, production of induced pluripotent stem cells (iPSCs) from HGPS patients has revealed that the progerin expression levels are the highest in MSCs, vascular smooth muscle cells, and fibroblasts. These results indicate that MSCs are a specific target cell type of progerin-induced senescence. Like progerin, excessive accumulation of prelamin induces premature senescence in MSCs, including wrinkled nuclei. Downregulation of ZMPSTE24 in hMSCs also induces the senescence phenotype. These investigations imply that both progerin and prelamin can induce senescence in hMSCs with change in nuclear morphology.

Senescent cells secrete a group of factors that induce senescence in neighboring cells, a phenomenon termed senescence-associated secretory phenotype (SASP). The secreted inflammatory factors propagate senescence and recruit immune cells to senescent tissues by the generation of a pro-inflammatory environment. Among the factors reported to regulate the SASP, GATA4 has been recently identified as a regulator of senescence and inflammation. GATA4 is expressed during oncogene- and irradiation-induced senescence in fibroblasts in response to DNA damage. During the process of cellular senescence, GATA4 has a regulatory role in the SASP of fibroblasts. Because GATA4-dependent cellular senescence is closely associated with DDR, the role of GATA4 in other senescence models and other cell types may reveal a new mechanism.

Senescent hMSCs also induce senescence in neighboring cells. Monocyte chemoattractant protein-1 (MCP-1) secreted from senescent human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) induces premature senescence in neighboring cells. Insulin-like growth factor binding proteins are also produced by senescent hMSCs, and they trigger senescence in adjacent normal cells. These studies investigated the mechanisms of the SASP by inducing senescence in hMSCs through prolonged passaging. However, cellular senescence of MSCs can be regulated by various factors other than passaging. In our previous report, we have demonstrated that depletion of ZMPSTE24 and introduction of progerin induce premature senescence in hUCB-MSCs. It remains to be determined whether defective lamin triggers paracrine senescence via inflammatory factors in hMSCs.

In this study, we identified that paracrine senescence is triggered in senescent hMSCs with abnormal nuclear structures by increasing the expression of MCP-1 and that inhibition of MCP-1 decreases the SASP. Furthermore, we found that GATA4 mediates the senescence of hMSCs induced by defective lamin A. We assessed whether down-regulation of GATA4 disturbs the progerin- or prelamin A-dependent senescence phenotype. Elucidating how GATA4 regulates senescence in hMSCs with nuclear defects may aid in understanding the etiology of complex aging disorders. We show that inhibition of GATA4 expression protects hMSCs from cellular senescence, implying unique therapeutic opportunity against progeroid syndromes and physiological aging.


Hi there,

I believe that Hutchison Gilforld's Progeria Syndrome is accelerated aging because of chromosomal problems, thus nucleus problems; regular aging experiences the same 'end result' just slower. Both have histone loss (H3 histone deacetylation) in nucleus, thus chromosome decompacting and uncoiling (loosening); which means compromised transcription and acceleration of dysfunction - HGPS people lose chromosomal telomere length 10x faster, they show SASP and replicarive senescence entry much quicker. Same thing for mice who despite tall telomeres have 100x faster telomeres shortening rate than regular healthy humans. Dogs replicate Exactly humans with HGPS, they lose 10x faster telomeres than humans, dogs never live much beyond 20 years old (a dog ages 5-10 times faster than healthy humans, in general you multiply by x7 your dog's age to obtain its equivalent age in human years)). It is not a coincidence, telomere rate of shortening equals longevity because telomeres are the cell cycle counters that are working with DNA methyl epiclock. They are cell replicative senescence entry counters. The total number of short telomeres predicts better mortality than telomeres length - although Rate/Speed of telomeres loss is a predictor (of acceleration) of aging process. Normal humans lose 50 base pairs per year in TTAGGG, while HGPS progeria people lose 500 base pairs; dogs too. They live as long as HGPS people (20y). While mice lose 5000 base pairs a year, they thus live only 2 years.

This has also been demonstrated in Myotis myotis little brown bats whom have higher telomeres all life than their short-lived bats counterparts. These long-lived bats live 40+ years, while the short-lived, live 20 years.

All these animals have longer lifespan through preservation of telomeres size longer. Telomerase and alternative lenghtening of telomeres (ALT, WRN helicase, Rad52, ku67, POT, Shelterin, TRF1) explain this, Telomerase is shunted away from the nucleus to the mitochondria during oxidative stress in aging; in order to mitigate mitochondrial ROS elevation, mtDNA deletions, and restore mitochondrial function - it has a dual role besides telomere elongation. Both in nucleus and mitochondria. When Telomerase transport to mitochondria is abrogated, there is higher cell DNA damage and senescence entry. Nucleus is 10 times better protected since Telomerase is housed there and nucleus is farther
From The Source OF Regular Mammal Aging :

mitochondrial ROS. Super oxide radical -> H2O2 -> MDA TBARS carbonyls 4HNE acrolein AGEs prostane 8oxodG bp-deletion..

And the only element standing in its way is the redox, mitochondrial redox buffer. Cytoplasm redox buffer and nuclear redox buffer. But the one that matters the most for cell survival is the mitochondrial one, the source of 'damage creation' lies there.

Because mitochondrial ROS rate is the Cause of oxidative stress in aging and diseases.

I really mitoSENS solves ATP loss with aging due to oxidized redox cell environment.

From 0 tp 40 years old, the plasma redox is roughly -140 mV, then +7 mv/decade rise, until at 70-85 years old, it is -110 mV.
At that high mV current the cell is a continuous oxidative stress state. It is why humans end up dying at 122 years old MLSP.

iF oxidative stress is controlled the cell can restore telomeres With or Without telomerase (this has been shown).
The reason for that is because it has been demonstrated in a study where telomerase was abrogated and The redox was rapidly oxidizing, also upon oxidizing redox there is 80% loss of hTERT catalytic subunit activity. They communicate and work in tandem, Always (telomerase enzyme has redox cysteine residue). This why eternal animals like hydras or ultra long-lived bowhead whales/Greenland sharks or Iceland mollusc bivalves live 525 years.. All of them maintain Telomere size and redox.

Just a 2 cent.

Posted by: CANanonymity at May 26th, 2018 12:08 AM

PS: I saw the video of Mrs. Elizabeth Parrish BioViva CEO, and clearly, she almost seem had a face botoxcollagen rejuvenation.
She looks like 20 years old glowing skin, yet she is 46 years old - her hTERT telomerase therapy on herself worked (this is akin to Astragalus TA65 cycloastragenol activating hTERT transcript). She has skin that very few women have at this age, plump like a teen's. This is measurable via ECM collagen levels or by image gradient subsurface scattering (SSS) on skin light ray depth scattering. Her skin fibroblast, and every organ in her body, where rejuvenated - Age Reversed, the junk she already had may not be gone or were diluted somehow during cycling but she is Epigenetically younger, like coming back to a younger you.

The danger of cancer is Weaker by Longer Telomeres in her blood leukocytes - this was demonstrated in mice where TgTERT mice had LESS tumor load if Taller Telomeres. A younger epigenetic profile often means immunity rejuvenation, thus cancer destruction. No cancer cell can survive epigenetic reprogramming, telomerase is capable of this epigenetic reprogramming somehow by talking with the DNA epigenetic clock.

Taller Telomere = anti-inflammation, powerful immunity cancer cell scavenging, extreme lifespan by no replicate senescence
Short telomeres = inflammation, acceleration aging, weak immunity cancer cell killling, SASP, high deletions/mutation load

Posted by: CANanonymity at May 26th, 2018 12:55 AM

PPS: I just want to mention that what is important is Not the having tallest telomeres
but to Maintain telomeres length tall - Enough.

This study shows that tall telomeres/excess telomerase is a double edge sword
as it accelerates the DNA methyl clock age. It is paradoxical to find acceleration of DNA epigenetic age with higher leukocyte telomeres length. The best explanation I found for this is that telomeres act as '''rate of stress/living and growth'' determinants. More telomerase and telomeres size means more activity, more growth and cell division acceleration ->
double edge sword, you risk Faster depletion of telomeres simply because of acceleration growth/cell cycling. In other words, you risk 'using up' your telomeres faster Despite being Taller. This is exactly what happens to mice, Huge telomeres 40 KB, they used them up in no time despite 40 KB long. Humans have smaller telomeres and live much longer.
The trick : Stable Zone, Maintain Telomeres in Safe Zone Neither Too Tall Neither Too Small. Sporadic hTERT therapy each 10 years prevents DNA epigenetic clock aging - While preserving Adequate Telomere Size.

GWAS Of Epigenetic Aging Rates Reveal A Critical [epigenetic clock age acceleration] Role Of TERT

Posted by: CANanonymity at May 26th, 2018 2:39 AM

CANanonymity do you have a view on TA 65 or the like ?

Posted by: Antipodean at May 27th, 2018 3:47 AM

@CANanonymity: Thanks for your excellent encyclopedic purview of telomere biology and aging. Also, nice to see the regenerative progress made by Liz Parrish... she may be the first human to reach 150, as she is already 20 years ahead of the LEV curve and knows the ins and outs of rejuvenation science! I wanted to make a comment on the LNNA gene and its role in controlling progerin. The LMNA SNP rs915179 allele G has been shown in a number of studies to markedly suppress progerin in cells (Miook CHO, 2014, Genetic maintenance and human longevity. Possibly we could experiment and see if introduction of this SNP with the G allele could help cure progeria. Also, perhaps we could use CRISPR technology to infuse the gene SNP in humans who do not have the G allele. I happen to be homozygous for the G allele, while Sebstiani (2013) has pointed out that a male and female aged 114 both were heterozygous for the G allele.

Posted by: Biotechy Marcks at May 27th, 2018 9:13 AM

Hmm, Liz Parrish is not that old so with fasting , some supplements and exercice she could genuinely look considerably younger, especially if she started from a bad point. And measured increase in the telomeres length is within the margin of error. But I have to admit it to her that she is eating her own dog food, so if there is deception is is involuntary.

As far as I understood she lengthens the telomeres within the blood but not the whole body. While it can help we don't know how much exactly. We know from the experiments with rodents that having conjointed blood system of a younger clone helps. But it also comes with double of pancreas, kidney, liver and immune systems. And yet we don't witness immoral mice.
A lot of old people could live 10-15 years longer of they were attached to such backup systems...

So if this treatment really works it could add a few years to the life expectancy. Very hard to proove thought...

Posted by: Cuberat at May 27th, 2018 9:33 AM

The article also demonstrates that GATA4 gene plays an important role in progerin expression and progeroid disease. Thus, genetically, it is important to know which GATA4 gene SNP's are important in the senescence function. It has been determined by Sebastiani 2012 Plos one, Genetic signatures of exceptional longevity in humans; that GATA4 gene is a longevity gene. The active SNP in enhancing longevity is rs804283 G/T alleles. I have the TT alleles, which is the ancestral type, and probably the good allele of this GATA4 SNP rs804283. Use of this gene SNP in treatment of progeroid disease, or treating humans that do not have the good alleles of the GATA4 gene, could possibly use CRISPR technology in the future for better life extension.

Posted by: Biotechy Marcks at May 27th, 2018 11:43 AM

Hi all, thanks for the comments.

TA65 purified concentrated cycloastragenol is too expensive (25,000$), astragalus root with high % astragalosides is alternative
TA65 does not extend mean or maximum lifespan of female mice (because already optimized by estrogenic receptors activate telomerase in female while male have extra conversion step of testosterone to estrogen by aromatase (handicapping step). It's why male mice obtain benefit from TERT telomerase thrrapy - by having less telomerase to begin with than females. And why, females being already optimized for longevity - it is redundant in them thus no effect))). Although the TA65 was done for 4 moths only from older age and thus needs to be done Whole life; in that case females will live longer too.

Another study showed mean and maximum lifespan extension in TgTERT mice, about a CR effect of 20-50% lifespan extension and the number of surviving mice that were very old (3 years or more) was much higher with TgTERT than control
It starts to resemble the longevity effects of growth hormone KO mice and Ames Dwarf mice living 4 or 5 years when combined with calorie restriction. In fact, TgTERT mice hhave much better WBGD (whole body glucose disposal) rate and lower fasting/post-prandial blood glucose levels. Thus, are insulin sensitive and avoid diabetes T2/hyperinsulinemia. This the CR-IGF-mTOR-SIR/DAF/FOXO-HGHs endocrine axis regulating senescence.


Just a 2 cent.

Posted by: CANanonymity at May 27th, 2018 1:47 PM


When you compare these mice, you have to compare them to a much bigger thhing.
That near equvalent but with large longevity difference is Another rodent;

The NMR- Naked Mole Rat, not so naked anymore, we know it lives 35 years. Pretty extraordinary - but we can do better,
a Damara Mole Rat (NMR cousin) is different and lives 8-10 years, and even better, a Peromyscus Leucopus little white footed mouse lives an extraordinary 10 years Too. What does this tells us?

TgTERT mice are not living 35, 10, 9, 8 years like these same other long lived rodents. Telomerase/TERT does not stop telomeres loss and damage accrual despite More Telomerase/TERT activity to offset this telomeres shortening.

Then What does? (allow a Mole Rat to live 10 to 40 years)

Telomere size preservation (Telomerase/TERT can't stop telomeres shortening - a Problem)).

Only 1 thing left, redox.

Posted by: CANanonymity at May 27th, 2018 2:15 PM

Posted by: CANanonymity at May 27th, 2018 1:47 PM: Another study showed mean and maximum lifespan extension in TgTERT mice, about a CR effect of 20-50% lifespan extension and the number of surviving mice that were very old (3 years or more) was much higher with TgTERT than control

Neither that study nor any other reports an increase in maximum lifespan in TgTERT mice, or mice with otherwise-supraphysiologically-activated telomerase. The authors of the cited study review the literature and note that while TgTERT alleviates some aging phenotypes, "constitutive telomerase expression in several independent Tert-transgenic mouse models resulted in increased incidence of spontaneous tumors;" positing this as the likely reason for a lack of effect of TgTERT in increasing lifespan, they combined TgTERT with enhanced expression of the tumor suppressor geness p53, p16, and p19ARF, which are virtually immune to cancer but have limited regenerative potential. Adding TgTERT to these cancer-resistant controls increases lifespan compared to this background, but they still live no longer than normal, otherwise healthy, well-husbanded aging mice (standard median LS >800 d, maximum (as tenth-decile survivorship) ≈1100 d).

By the way, your "2ç" has become devalued; I suggest discontinuing it, as Canada did the penny a decade ago.

Posted by: Michael at May 27th, 2018 4:31 PM

Hi Michael, thank you greatly for this precision.

It's strange, telomerase is really all over the place. It's important yet has deleterious effects at the same time. It really is an antagonistic pleiotropic element. Compensating for rapid telomeres loss during growth phase in early age where there is dramatic telomeres loss before puberty; and the has growth settles down in adulthood telomeres shortening speed slows down and therw is a long plateau of telomeres slowly trickling down over decades. Telomerase activity post puberty/adult reproduction arrival sees it slow down to nothing. There is no need to elongate telomeres post-puberty since their shortening speed slows down/plateaus. Reduced developmental growth and slowed metabolism after that adulthood entry period.

As such, antagonistic, when telomerase is activated it creates a form of demethylation, and why DNA epigenetic methyl clock accelerates when telomerase is called to lengthen telomeres. It's a negative (on lifespan) compensatory mechanism to spur growth and in the same stroke, mutation/tumor growth whom highjack it. Catch 22, like everything else in the body.

Telomeres must be maintained yet telomerase was made to lengthen them - with a cost (body growth/cell growth /proliferation making rapid resource exhaustion (as seen in early childhood losing rapid telomeres because of them 'growing up' fast in that early life period))) .

All this to say, if we somehow epigenetically reprogramm cancer cells to autokill (cancer shows accelerate epigenetic aging) maybe then Telomerase/TERT will be more viable alternative with low cancer risks in regular mouse and.. people.

But, as I wrote earlier and you said, Telomerase/TERT does not stop the telomeres shortening process, it just abates a little if even. In the end, aging damages end up making sure telomeres continue shortening anyways. And, thus, more and more short telomeres accumulate, until too many and it's the end.

I was wondering what makes these mice live 3, 4 years while other ones reach 10, 30 years. Of course, DNA repair, stem cell function or membrane lipid peroxidizability reduction (although mitochondria PI DBI are not correlate of MLSP anymore) are some of the mechanism explanation but oftenly their weight is not that strong in terms of explanation of such divergent lifespans (and why every lifespan extension therapy as failed to make more than 50% extension in a mouse). It's a combination of things for sure. But they all share adequate-size telomeres preservation, the lowest rate of telomeres loss possible or no telomeres loss at all. The AdG mitochondria ROS theory is source. The downstream of that in terms of damage is what matters, the oxidative stress to/in various critical proteins and enzymes, including mtDNA lesions creating mtDNA deletions (which create ATP dwindling levels over time)) explain this better.
Just a CAD nickel.

Posted by: CANanonymity at May 27th, 2018 5:58 PM

@CAD nickel: We should study just why the naked mole rat lives 10 times longer than most rat species. Do they have better DNA repair mechanisms? After all, they live in secluded underground nests where they would be more protected from many forms of radiation that surface dwelling rats are exposed to. At any rate, if we could only solve the problem of how they live so long, we should be able to apply it to humans for an 8 to 10 time life extension. That would be incredible!!

Posted by: Biotechy Marcks at May 28th, 2018 8:25 AM

Hi Biotechy, thanks for asking, just my 2cs.

NMRs are quite the outliers, like humans or bats, they should live 1/4th or less of their maximum lifespan (from their body/mass size). I think it's definitely a combination of things that mole rats living this long. Like in NMRs:

-As you said, they live in constant darkness and hypoxia burrowed in subterranean conducts they carved themselves with their rabbit/beaver-like twin fangs. This 24/7 total darkness renders them 99% blind (Blind Damara Mole Rat) with mini eyes (useless can't see) and plump but wrinkly skin, plus albino darkness-caused due to absence of light (and need of it for UV rays to skin D3 cholacalciferol production) by turning translucent and skin melanin pigment void (albinos). This hypoxia means they have strong vascular function, can function in low O2/enough mitochondria ATP even so thus mitochondria OXPHOS kinetic, better HIF1 levels (Hypoxia Inducible Factor-1 preserving mitochondria respiration and endothelial vascular function.
Also higher HSF and HSPs (Heat Shock Factor (which activates HIF-1) and being Heat Shock factor it activates HSPs Heat Shock Proteins/Chaperones. In other words, preserved stress response through upregulation of protein folding or refolding of unfolded denatured proteins, while increasing Chaperone docking of junk to proteasome/autophagosome/mitophagosome/ lysosome. Plus, low O2 hypoxia means lower O2 availability - lower ROS possible simply by less ambient O2 % available.
I.e. ROS: Reactive *Oxygen* Species, ROS are O2-based/formed from. Less O2.. Less O2 Available to make ROS.
Lower ROS, especially mitochondrial ROS means longevity extension because ROS are the source for all the downstream damages that age an animal; faster or slower depending on the accumulation rate of said damages over time.

- NMRs have protracted brain development and it is continuously plastizing/remodelling into their puberty like humans (they have Late puberty like humans, in their teen years (13-15 years before sexual reproduction entry. Late puberty and sexual reproduction capability means slowed development growth (Retarded Aging/Sexual Maturing and Prolonged Neoteny)). Long-lived animals all show this feature of Late puberty onset correlating to long lifespan. Animals that invest and relocate all resources towards Very Early Puberty/Sexual Reproduction with high offspring output live very short lives, while, inversely, animals who relocate these resources towards own somatic tissue maintenance (instead of sexual capability/by post poning puberty) live very long lifespans.

-NMRs have 10 times less DHA in their mitochondrial membranes, which means a lower Peroxidizability Index then mice, they thus live 10 times longer (DHA Polyunsaturate 22:6 Omega3 is x320 times more peroxidizable than monounsaturate/saturate, it creates Havoc when ROS attack it, it is highly susceptible and renders membrane more fluid/watery/faster kinectic but more 'fragile' by its long chain (it's why brain IQ and cognition is dependent on neuron mitochondria DHA levels - low DHA means lower IQ because slower neuronal firing by slower mitochondria membrane kinetic (less fluid membrane, more viscous waxy/more compact and riigid membrane - slow like a tank. To think your thoughts and act/react/reflex move, it needs to be Fast, Very, neuron count on a fluidizer like DHA, or EPA. Fluidizer yes, but very fragile, 320x more fragile and producing volatile far reaching lipid peroxidation chains 'end products'. Just like AGEs (Advanced Glycation End-Products), here they are ALEs (Advanced Lipoxidation End-Products). Or, more specifically, Advanced Lipoperoxidation End-Products.
Humans also show low levels of liver mitochondrial DHA but not in their brain. It's why they are protected, likewise in NMR.
But studies on mitochondria membrane peroxidation have been refuted, and now it is clear that it is more correlative than causative. But low mitochondria peroxidation is very important but not major determinant once thought.

-That brings us to the biggest determinant, redox (epigenetic age preservation and telomeres preservation are very important too). The redox is missing element. NMRs have very high levels of oxidative stress,more than in a mouse. As studies showed they 'tolerate' pain very well and just deal with it. The element missing from these studies - is For All the Timeline.
Young NMRs experience this oxidative stress but then at puberty like Humans this stops.
NMRs Maintain same redox milieu over 20 years, unlike mice whom see a rapid downfall of its redox milieu over 2 years.
It means NMRs cells become oxidative stress resistant with age while mice lose this capability fast. The damages they incur becomes fatal for the mice cells. Humans, Centenarians especially who live up to 110 years old, show this precise feature.
And not just Centenarians, animals whom Double, Triple, QUAD-Centenarians (400+ years) and more show also this feature.

Posted by: CANanonymity at May 28th, 2018 8:06 PM

I was thinking lower body temperature in long-lived mammals may be beneficial to extended lifespan. Older humans, for example, often have a lower metabolism rate, often further decreased by thyroid hormone deficiency in the elderly, especially women. Not sure what the NMR body temp and metabolism is compared to above ground dwelling rat species.

Posted by: Biotechy Marcks at May 29th, 2018 10:41 AM

"PS: I saw the video of Mrs. Elizabeth Parrish BioViva CEO, and clearly, she almost seem had a face botoxcollagen rejuvenation.
She looks like 20 years old glowing skin, yet she is 46 years old - her hTERT telomerase therapy on herself worked (this is akin to Astragalus TA65 cycloastragenol activating hTERT transcript). She has skin that very few women have at this age, plump like a teen's. This is measurable via ECM collagen levels or by image gradient subsurface scattering (SSS) on skin light ray depth scattering. Her skin fibroblast, and every organ in her body, where rejuvenated - Age Reversed, the junk she already had may not be gone or were diluted somehow during cycling but she is Epigenetically younger, like coming back to a younger you."

^uhh no this definitely isn't true, she doesn't look much younger than her age

Posted by: InquilineKea (Alex K Chen) at May 26th, 2021 9:48 PM
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