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Nugenics "Elixir"

aging reversal epigenetics dna methylation clock heterochronic parabiosis programmed aging

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#61 VP.

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Posted 18 May 2020 - 04:05 PM

If "plasma fraction" is inadequate to describe the work on Elixir, would here reside the main difference with previous work e.g. by Wyss-Coray team at Alkahest? Just wonder.

https://www.longevit...asma-therapies/

I know they found "significant" results with just a herbal formula years ago. It's possible Alkahest has found many of the same constituents as Harold but they are going the slow single disease FDA  route. 

 

Thank you Patricio. Yes 45 would be too young for proposed trial. We would like to see significant reversal. But let us see what protocol is designed by Harold. We have had 3 major trials: First one on 10 natural extracts. Each one selected to upregulate a key known repair system whose efficiency goes down with aging. We have had very encouraging results with that but it wont quantify as systemic compared with Elixir. We followed this with 2 trials of Elixir: single dose 30 days and repeat dose 155 days. You have the result of that. Although I cant disclose about ElixirI will say this: Harold came up with brilliant work due to which hopefully we wont have scaling issues and prices will remain reasonable.

 

https://joshmitteldo...rough/#comments

Edited by VP., 18 May 2020 - 04:08 PM.


#62 VP.

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Posted 18 May 2020 - 04:09 PM

Other companies are searching the same area. https://www.theguard...nts-mice-plasma

 

I have no idea how Harold leapfrogged such well funded labs. 



#63 p75213

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Posted 18 May 2020 - 07:07 PM

If it's good enough for David Sinclair it's good enough for me.

https://mobile.twitt...912928695857152

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#64 Mind

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Posted 18 May 2020 - 07:27 PM

The formula is not being released yet. That does not automatically mean it is a scam. If they are trying to build a company and a fortune based upon this formulation, then they need to keep it secret at this point.


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#65 VP.

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Posted 19 May 2020 - 02:01 PM

Prof Katcher is doing an AMA on Reddit: https://www.reddit.c...th_rats_plasma/

Harold has decided to do the AMA after publication of the study. 


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#66 albedo

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Posted 21 May 2020 - 07:57 AM

Dr. Oliver Medvedik will discuss the study in the LEAF Journal Club on May 21st, 1:00 PM EDT, live on Facebook.

https://www.lifespan...ic-age-in-rats/


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#67 albedo

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Posted 23 May 2020 - 05:09 PM

I think informative from Akshai:

 

"...we have three products developed: natural extracts mix, young plasma fractions: Elixir and powerful anti aging molecule: gel and transdermal patch. We have completed pre-clinical trials in all three..."

 

https://joshmitteldo...rough/#comments


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#68 albedo

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Posted 25 May 2020 - 05:06 PM

Dr. Oliver Medvedik will discuss the study in the LEAF Journal Club on May 21st, 1:00 PM EDT, live on Facebook.

https://www.lifespan...ic-age-in-rats/

Recorded session:

https://www.lifespan...ic-age-in-rats/

 



#69 albedo

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Posted 26 May 2020 - 03:50 PM

 

In case you missed, there were quite harsh comments by Didier Coeurnelle, mainly wrt the lifespan study which I understand is in progress.

While waiting for that, here is a potentially contradictory study posted on Josh's blog and Harold Katcher's reply:

 

"...in addition, this is still somehow in contradiction with

https://onlinelibrar...111/acel.12897"

 

"...Yes, that’s a question that has been bothering me since Amy Wagers post-doc, Shane Mayack and her papers were retracted from Nature and Blood. What Shane, who said she was innocent of everything, but made a mistake on which illustrations she used (one used previously), showed(she said) that blood cells weren’t affected by the rejuvenating factors in the blood (heterochronic parabiosis) but instead were rejuvenated (after a time) by bone marrow stromal cells. So, that was always a worry of mine – but the rats showed no ill effects at any time, I really don’t know about how good their immune systems were as we never challenged them, what I do know is that the chronic inflammation due to aging (present in all terrestrial vertebrates) disappeared. So, if nothing else, I can definitively say that chronic inflammation due to aging can be reversed with factors present in young blood. Hey, it’s a beginning and with great potential to end the diseases of aging, many of which have an inflammatory component..." (Harold Katcher)

https://joshmitteldo...rough/#comments

 

 

 



#70 rodentman

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Posted 26 May 2020 - 04:38 PM

 

In case you missed, there were quite harsh comments by Didier Coeurnelle, mainly wrt the lifespan study which I understand is in progress.

While waiting for that, here is a potentially contradictory study posted on Josh's blog and Harold Katcher's reply:

 

"...in addition, this is still somehow in contradiction with

https://onlinelibrar...111/acel.12897"

 

"...Yes, that’s a question that has been bothering me since Amy Wagers post-doc, Shane Mayack and her papers were retracted from Nature and Blood. What Shane, who said she was innocent of everything, but made a mistake on which illustrations she used (one used previously), showed(she said) that blood cells weren’t affected by the rejuvenating factors in the blood (heterochronic parabiosis) but instead were rejuvenated (after a time) by bone marrow stromal cells. So, that was always a worry of mine – but the rats showed no ill effects at any time, I really don’t know about how good their immune systems were as we never challenged them, what I do know is that the chronic inflammation due to aging (present in all terrestrial vertebrates) disappeared. So, if nothing else, I can definitively say that chronic inflammation due to aging can be reversed with factors present in young blood. Hey, it’s a beginning and with great potential to end the diseases of aging, many of which have an inflammatory component..." (Harold Katcher)

https://joshmitteldo...rough/#comments

 

 

 

 

 

Thanks for keeping us updated on all this. 

 

I don't understand why there are some who dismiss the entire study due to the fact that there wasn't a life-span study; especially in light of the lock-down.  Obviously a life-span study will be included, just as a full peer-review of everything will be on the horizon.  And it's extremely hard to believe that S. Horvath would co-author a scam, or a very poorly setup experiment, that consistently came up with inaccurate data.


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#71 p75213

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Posted 26 May 2020 - 07:44 PM

I couldn't listen to that. Just too many ums and arhs. I mean nearly every 2nd word. Very frustrating.
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#72 albedo

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Posted 01 June 2020 - 08:02 PM

This presentation by Steven Braithwaite, CSO of Alkahest, seems to me hinting to a serious competitive approach (which is great!) maybe for some of the end-points:


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#73 albedo

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Posted 02 June 2020 - 08:16 PM

This presentation by Steven Braithwaite, CSO of Alkahest, seems to me hinting to a serious competitive approach (which is great!) maybe for some of the end-points:

 

... quite acknowledged by Akshay in Josh's blog:

"Thank you Josh. We are quite excited by the potential potency and economy of our therapeutic for reversal of aging but Alkahest is run by really smart people, they have already raised $50 million and have quietly made multiple products reach Phase II with FDA. They are doing all the right things for commercializing their technologies. Their focus seems to be on individual diseases of aging especially neurodegenerative diseases rather than aging itself which may be driven by FDA. I admire how well they seem to have progressed."

 



#74 Engadin

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Posted 08 June 2020 - 10:13 AM

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S O U R C E :   Josh Mitteldorf's "Aging Matters" blog

 

 

 

 

 

 

There is great promise in 2020 that we might be able to make our bodies young without having to explicitly repair molecular damage, but just by changing the signaling environment.
 
Do we need to add signals that say “young” or remove signals that say “old”?
 
Does infusion of biochemical signals from young blood plasma rejuvenate tissues of an old animal? Or are there dissolved signal proteins in old animals that must be removed?
 
For a decade, Irena and Mike Conboy have been telling us removal of bad actors is more important. But just last month, Harold Katcher reported spectacular success by infusing a plasma fraction while taking away nothing. Then, last week, the Conboys came back with a demonstration of the rejuvenating power of simple dilution. [Link to their new paper]
 
 
Dilution procedure
 
They simply replaced half of the blood plasma in 2-year-old mice with a saline solution containing 5% albumin. What is albumin? Blood plasma is chock full of dissolved proteins, about 10% by weight. About half of these are termed albumin. Albumin is the generic portion. It doesn’t change through the lifetime. It doesn’t carry information by itself. But albumin transports nutrients and minerals through the body.
 
The Conboys took care to show that albumin has no rejuvenation power on its own, and had nothing to do with their experimental results. Rather, they had to replenish albumin in diluting blood, because the animals would be sickened if half their albumin were removed. Replacing the albumin in a transfusion is akin to replacing the volume of water or maintaining the salinity.
 
In preparation for this experiment, the Conboys have invested years in miniaturizing the technology for blood transfusions, so that mice can be subjected to the same procedures that are commonplace in human hospitals.
 
 
Dose-Response
 
The Conboy lab replaced 50% of mouse blood plasma. They got spectacular results with a single treatment, based on a lucky guess. They have not yet experimented with 30% or 70%. They don’t know yet how long the treatment will last and how long it needs to be repeated.
 
 
Evidence of rejuvenation
 
As with previous papers from the Conboy lab, the group focused on repair and stem cell activity as evidence of a more youthful state. Three separate tissue samples were taken from liver, muscle, and brain.
 
“Muscle repair was improved, fibrosis was attenuated, and inhibition of myogenic proliferation was switched to enhancement; liver adiposity and fibrosis were reduced; and hippocampal neurogenesis was increased.”
 
  • They measured nerve growth factors in the brain, and detected a more robust response, typical of young mice
  • They lacerated muscles and showed repair rates typical of much younger animals
  • They examined microscope slides of liver tissue, and showed that it is less fatty and striated than is typical of older mice

 

 

Attached File  img.png   153.95KB   0 downloads

 

Figure 2. Rejuvenation of adult myogenesis, and albumin-independent effects of TPE. One day after the NBE, muscle was injured at two sites per TA by cardiotoxin; 5 days later muscle was isolated and cryosectioned at 10 µm. (A) Representative H&E and eMyHC IF images of the injury site. Scale bar = 50 µm. (B) Regenerative index: the number of centrally nucleated myofibers per total nuclei. OO vs.ONBE p = 0.000001, YY vs ONBE non-significant p = 0.4014; Fibrotic index: white devoid of myofibers areas. OO vs ONBE p = 0.000048, YY vs YNBE non-significant p = 0.1712. Minimal Feret diameter of eMyHC+ myofibers is normalized to the mean of YY [9]. OO vs. ONBE p=3.04346E-05, YY vs. YNBE p=0.009. Data-points are TA injury sites of 4-5 YNBE and 5 ONBE animals. Young and Old levels (detailed in Supplementary Figure 1) are dashed lines. Representative images for YY versus YNBE cohorts are shown in Supplementary Figure 6. © Automated microscopy quantification of HSA dose response, as fold difference in BrdU+ cells from OPTI-MEM alone (0 HSA). There was no enhancement of myogenic proliferation at 1-16% HSA. N=6. (D) Meta-Express quantification of BrdU+ cells by automated high throughput microscopy for myoblasts cultured with 4% PreTPE versus PostTPE serum and (E) for these cells cultured with 4% of each: PreTPE serum + HSA or PostTPE serum + HSA. Significant increase in BrdU positive cells is detected in every subject 1, 2, 3, and 4 for TPE-treated serum (p=0.011, <0.0001, <0.0001, 0.0039, respectively), as well as for TPE-treated serum when 4%HSA is present (p<0.0001, <0.0001, <0.0001, =0.009 respectively). N=6. (F) Scatter plot with Means and SEM of all Pre-TPE, Post-TPE, +/- HSA cohorts shows significant improvement in proliferation in Pre TPE as compared to and Post TPE cohorts (p*=0.033), as well as Pre+HSA and Post+HSA cohorts (p*=0.0116). In contrast, no significant change was observed when comparing Pre with Pre+HSA (p=0.744) or Post with Post+HSA (p=0.9733). N=4 subjects X 6 independent assays for each, at each condition. (G) Representative BrdU IF and Hoechst staining in sub-regions of one of the 9 sites that were captured by the automated microscopy. Blood serum from old individuals diminished myogenic cell proliferation with very few BrdU+ cells being visible (illustrated by one positive cell in Pre-TPE and arrowhead pointing to the corresponding nucleus); TPE abrogated this inhibition but HSA did not have a discernable effect.

 

 

 

What’s missing? They did not test any measures of physical or cognitive performance at the level of the organism.

 

  • Evidence of behavioral changes (learning and memory, endurance, strength)
  • Inflammatory markers
  • Blood lipids
  • Methylation clock (Horvath, UCLA) or proteomic clock (Lehallier, Stanford)
 
Some of this is planned for future research. Mike and Irina plan to submit tissue samples for analysis by the Horvath mouse methylation clock.
 
 
Clock?
 
I am a committed enthusiast for the methylation and proteomic clocks that are the best surrogates we have for aging. These technologies can tell us whether anti-aging interventions have been effective without having to wait for animals (or humans) to die before reporting results. But the Conboys still regard these technologies as unproven, and they bristle at the word “clock”.  The closest they come is to catalog the entire proteome of treated mice, comparing it to untreated young and old mice.
 
Multi-dimensional t-SNE analyses and Heatmapping of these data revealed that the ONBE proteome became significantly different from OO and regained some similarities to the YY proteome. Supplementary Figure 4 confirms the statistical significance of this comparative proteomics through Power Analysis, and shows the YY vs. OO Heatmap, where the age-specific differences are less pronounced than those between OO vs. ONBE, again emphasizing the robust effect of NBE on the molecular composition of the systemic milieu.
 
Translation: As controls, they had mice that underwent plasma exchange with mice of similar age. YY were young, positive controls, and OO were old, negative controls. Treated mice were ONBE=”Old—Neutral Blood Exchange”. Rather than relying on “clock” algorithms that compute an age from the proteome, they compared the entire proteomes of test animals with those of old and young animals, and foud that they resembled the young animals more closely.
 
 
Aging and epigenetics
 
I was an early advocate of the theory that aging is driven primarily by changes in epigenetics. Other proponents include Johnson, Rando, and Horvath. This theory is now mainstream, though its acceptance is far from universal. (The main reason people have difficulty with the idea is the question, “why would the body evolve to destroy itself?” I present a comprehensive answer in my popular book and my academic book.)
 
On the face of it, the new Conboy result is powerful evidence for the epigenetic theory. They have shown that there are proteins in the blood that actively retard growth and healing. Remove half theses proteins and the animals are able to grow youthful tissues and to heal better. The obvious conclusion is that, with age, there are signaling changes in the blood that weaken the animal and inhibit repair.
 
There are, however, other ways to interpret the changes. Aubrey de Grey has said (personal communication)
 
“When everything in the blood except the cells and the albumin is replaced by water, the body will definitely respond by synthesising and secreting everything that it detects a shortage of, whereas the bad stuff will not be so rapidly replaced, since by and large it was only there in the first place as a result of impaired excretion/degradation.”
 
The Conboys don’t embrace the programmed aging perspective, but neither is their understanding of what they see the same as Aubrey’s. The way Irina explained it to me is that the age of the biological of the body is simply a measure of how much damage has accumulated, but that cycles of epigenetics and catalysis are self-reinforcing.
 
“Epigenetic, mRNA, and protein are steps of one process, regulation of gene expression. And none of these steps are permanent they all actively and constantly respond to cell environment &mdash; tissue and systemic milieu…With aging there is a drift which is re-calibrated by a number of rejuvenation approaches…When an auto-inductive age-elevated ligand is diluted, it cannot activate its own receptor and induce its own mRNA, so ligand levels diminish to their younger states for prolonged time.”
 
The Conboys theorize that these harmful proteins are part of a positive feedback loop, in other words, a cycle that is self-sustaining
 
epigenetic state ⇒ gene expression ⇒ translation to circulating proteins ⇒ feedback that alters the epigenetic state.
 
With age, the body has slipped into a dysfunctional, self-sustaining cycle, and with the shock of disruption, they are able to nudge it back into a more robust and youthful cycle, also self-sustaining.
 
 
Attached File  img (1).png   190.76KB   0 downloads
 
Figure 6. Model of the dilution effect in resetting of circulatory proteome. System: A induces itself (A, red), and C (blue); A represses B (green), C represses A. A dilution of an age-elevated protein (A, at D1: initial dilution event), breaks the autoinduction and diminishes the levels of A (event 1, red arrow); the secondary target of A (B, at event 2 green arrow), then becomes de-repressed and elevated (B induces B is postulated); the attenuator of A (C, at event 3 blue arrow), has a time-delay (TD) of being diminished, as it is intracellular and was not immediately diluted, and some protein levels persist even after the lower induction of C by A. C decreases (no longer induced by A), and a re-boot of A results in the re-induction of C by A (event 4 blue arrow) leading to the secondary decrease of A signaling intensity/autoinduction, and a secondary upward wave of B (events 5 red arrow and 6 green arrow, respectively). alpha = 0.01, kc = 0.01, beta = 0.05, epsilon = 0.1, ka = 0.1. Protein removal rates from system: removalA = 0.01, removalB = 0.1, removalC = 0.01, Initial values: initialA = 1000, initialB = 400, initialC. = 700.
 

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#75 Harkijn

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Posted 10 June 2020 - 08:37 AM

Yes, it is important to go to Josh' site. Not just for the article but also for the fascinating discussions by a number of knowledgeable scientists! One of the contributors is once again dr. Harold Katcher.


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#76 rodentman

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Posted 14 June 2020 - 06:56 AM

Man, I just love Josh, and the way he breaks things down, and compares Katcher and Conboy's work.  Very fascinating stuff.


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#77 Engadin

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Posted 14 June 2020 - 06:01 PM

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Dr. Harold Katcher has been a pioneer in the field of cancer research, in the development of modern aspects of gene hunting and sequencing. He carries expertise in bioinformatics, chronobiology, and biotechnology and is currently working in the capacity of Chief Technical Officer at Nugenics Research Pvt Ltd. exploring in anti-aging modalities.

 
They recently released a paper online on #biorxiv regarding their breakthrough research on Human Age Reversal using Young Blood #plasma, the paper’s authors include recognized Longevity academician Steve Horvath.
 
Dr Katcher spoke about how & why he moved from cancer research to Human Longevity, his research & results of 54% age reversal in Rats, his partner #akshaysanghavi, the future road map/timelines on how & when this might be commercially available.
 
 
 

 

 

 

 

 

 

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#78 rodentman

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Posted 14 June 2020 - 09:15 PM

Thanks.   Interesting video.    Boy, he sounds very convinced that this is a complete cure for aging.

 

He says that after rat trials, he will do dog trials, based on the ease of getting revenue from pet-lovers... and after that, human trials.  He's trying to rush it as much as possible, but this will probably be at least a couple years from now.

 

He also said treatment on rats 'peaked' at about 1 month.... and continued for 3 months to be at that YOUNG stage, and then he redid the treatment, with the same result.   I am not exactly sure if this means that after 3 months, the benefit 'wore-off', and the rats' biological age returned to the chronological age... or that after the 3 months... the rats started aging at a regular rate, but at the younger age.


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#79 QuestforLife

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Posted 15 June 2020 - 09:38 AM

Thanks.   Interesting video.    Boy, he sounds very convinced that this is a complete cure for aging.

 

He says that after rat trials, he will do dog trials, based on the ease of getting revenue from pet-lovers... and after that, human trials.  He's trying to rush it as much as possible, but this will probably be at least a couple years from now.

 

He also said treatment on rats 'peaked' at about 1 month.... and continued for 3 months to be at that YOUNG stage, and then he redid the treatment, with the same result.   I am not exactly sure if this means that after 3 months, the benefit 'wore-off', and the rats' biological age returned to the chronological age... or that after the 3 months... the rats started aging at a regular rate, but at the younger age.

 

Its all shown in the paper. Biomarker values improved rapidly to young or near young levels and then declined slowly. For example IL-6 declined from old to young levels in about a week and declined about half way back to old levels in about 3 months. A repeat of the protocol once again restored the biomarkers to young levels (was actually slightly better second time).  I am assuming a repeat protocol for humans would be years apart. But we need more data (and lifespan studies) before we'll know for sure.  


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#80 Mind

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Posted 15 June 2020 - 11:36 AM

It is a great result, but of course, the return to older biomarker levels (to some degree), would say to me that this treatment might not be getting to the root cause of aging (damage) exactly. There is still the question of getting rid of glucosepane, lipofuscin, A-beta, and other garbage. Changing peptide and hormone levels does not get rid of this "junk" as far as I am aware. HGH, other hormones, and peptides, have been used for decades and they improve certain biological functions, but none have truly rejuvenated anyone.


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#81 Engadin

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Posted 15 June 2020 - 12:01 PM

Changing peptide and hormone levels does not get rid of this "junk" as far as I am aware. HGH, other hormones, and peptides, have been used for decades and they improve certain biological functions, but none have truly rejuvenated anyone.

 

 

Akshay answers, though vaguely to some extent and basing it on deep level auto/mitophagy, the 'debris question' here:

 

Attached File  Clipboard01.jpg   58.42KB   8 downloads

 

 

 

 

 

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#82 rodentman

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Posted 15 June 2020 - 06:50 PM

It is a great result, but of course, the return to older biomarker levels (to some degree), would say to me that this treatment might not be getting to the root cause of aging (damage) exactly. There is still the question of getting rid of glucosepane, lipofuscin, A-beta, and other garbage. Changing peptide and hormone levels does not get rid of this "junk" as far as I am aware. HGH, other hormones, and peptides, have been used for decades and they improve certain biological functions, but none have truly rejuvenated anyone.

 

The philosophy behind this, as well as other research that comes from parabiosis isn't that the root cause of aging is cell-damage.  instead, Katcher, Conboy, Wager and others believe that cell-damage is the affect of a central aging mechanism.  This has been a major debate over the last few decades, and researchers like Aubrey De Gray argue that while upstream aging mechanisms do exist... they are too complex to tackle.
 
Dr Katcher, and others believe that the root cause is far more simple, and is basically a central aging clock, which keeps its own time and transmits signals (coordinating methylation states) throughout the body using the proper concentration/dillution of specific blood factors. There is speculation that the clock may reside in the hypothalamus, but who knows.   
 
So based upon what I am reading from his paper, Dr. Katcher hasn't truly 'reset' the central aging clock, but has learned to mimic it's signals as if it were half it's age.  This is still incredibly monumental, and could 'theoretically' postpone aging for a really long time and significantly improve our 'healthspan' but it's not a true 'resetting' of the age.
 
One assumption that I am not 100% sold on, is that this 'therapy' will only need to be done every 5 years... based on scaling up the data from rats.  Maybe someone else can clarify this, but just because a rat ages 20x faster doesn't necessarily mean that rats' blood factors will return to pre-therapeutic concentrations 20x faster than humans??
 
I wouldn't be surprised if this isn't the case.  I've had my own experience with blood factor manipulation using GDF-11, and from everything I've seen, the benefits don't 'stick', and if you discontinue the therapy, things seem to return to normal after a couple months.  Katcher has said that this therapy is 'upstream' of GDF-11,  so I suppose the more upstream, the longer it might take  for the 'independant clock' to revert everything back to pre-therapeutic levels, but who knows.
 
I guess we will know more, when they do the therapy on dogs,

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#83 Engadin

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Posted 16 June 2020 - 02:29 PM

Here is a thread into the paper via the Nrf2 path. Encouraging for those (I do for what it matters) trying to increase intake of sulforaphane:

https://surfaceyourr...d-sulforaphane/

 

 

Here a pretty easy to follow procedure to increase sulphorafane's bioavailability in broccoli sprouts by 3,5 times:

 

 

 

 

 

 

.


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#84 Harkijn

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Posted 16 June 2020 - 02:58 PM

Thanks for this Engadin! Readers who have joined Longecity in the last few years may not know that there are several SFN threads full of background and tips. This is one of them:

https://www.longecit...-the-sirtulins/


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#85 Mind

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Posted 16 June 2020 - 04:58 PM

Akshay answers, though vaguely to some extent and basing it on deep level auto/mitophagy, the 'debris question' here:

 

attachicon.gif Clipboard01.jpg

 

 

 

 

 

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Thanks for sharing this. Akshay seems to be saying that autophagy can get rid of metabolic waste (stuff that is thought to be indigestible/unbreakable), just that the process of autophagy "ages" just like everything else in the body. I am not sold on this. I would be more sold on a theory that resetting an "aging clock" would upregulate beneficial apoptosis. Basically....cells that are burdened with too much indigestible junk or virtually unbreakable crosslinks would be ejected from the body, only leaving the healthy/better-functioning cells behind.


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#86 p75213

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Posted 17 June 2020 - 08:40 AM

Moringin is also a potent activator of nrf2.

In the same way that glucoraphanin + myrosinase enzyme = sulforaphane. Glucomoringin + myrosinase enzyme = moringin.

Glucosinolate + myrosinase enzyme = isothiocyanate.


Edited by p75213, 17 June 2020 - 08:44 AM.

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#87 Avatar of Horus

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Posted 20 June 2020 - 08:43 AM

An update on this here:

Reversing age: dual species measurement of epigenetic age with a single clock

https://www.longecit...a-single-clock/


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#88 Raphy

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Posted 25 June 2020 - 06:38 PM

I believe this will prove a major breakthrough, as Josh does. Ever since the first studies showing epigenetic reset reverses multiple hallmarks of aging, the SENS model didn't make sense.

But so far epigenetic reset looked to be very hard. But if this plasma fraction is easy to produce, this will be tremendous.

#89 kurt9

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Posted 25 June 2020 - 07:46 PM

I believe this will prove a major breakthrough, as Josh does. Ever since the first studies showing epigenetic reset reverses multiple hallmarks of aging, the SENS model didn't make sense.

But so far epigenetic reset looked to be very hard. But if this plasma fraction is easy to produce, this will be tremendous.

 

Aubrey de Grey is involved with AgeX, founded by Michael West, which is working on invivo cellular reprogramming. This is tacit recognition that epigenetic reprogramming is the way to go here. 


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#90 albedo

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Posted 26 June 2020 - 10:44 AM

Well agreed Kurt9.

Also, the publication is still on BioRxiv but peer-review processes normally take time mostly when claims are important.







Also tagged with one or more of these keywords: aging reversal, epigenetics, dna methylation clock, heterochronic parabiosis, programmed aging

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