Not a very strong argument for your position LoL!
The elastin problem has been studied extensively and is very well understood by people much smarter than me. We know how elastin is lost, we know how long it takes to run out of it, we know it’s not replaceable systemically, those are scientific facts. As far as how elastin affects lifespan, it’s pretty simple logic, we die without it. Period, end of story.
So until there is a solution to the elasitin problem, human lifespan is rate limited to 120 years by this one factor. You can disagree with that all you want but you have not brought anything to the discussion that changes the established facts on elastin.
There are many other factors that limit how long humans can live, elastin is probably the hardest one to solve. When this problem is solved, this may allow for life to be longer than 120 years. Until then increasing health span is the only thing we can do.
I hope you do reach the century mark, it’s a good goal.
In the mid 90’s I was at a SNF in the SeaTac area, taking pictures of bedsores and saw a “leader board” with 6 people 100 and up, the oldest was 104. This was a Japanese only facility and very well run. The staff were very proud of their centenarians. I got to meet 2 of them.
I’ve been in over 200 SNF’s and had never seen a “leader board” like that. It was very cool 
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Dr.Bart
#570
I don’t have a position on max age limit. Some scientists don’t believe there is a limit. There is as scant evidence for 140 as there is for 120.
In medieval England life expectancy was 31 years, once you made it to 25 then average became about 51 years old. The records were very poor back then but living in to 80’s was rare. Maximal lifespan was probably around 90. Now 600 years later, same place average age is 80’s and maximal lifespan recorded was 115. So that’s about 25-30 year shift. All mostly due to proper nutrition and sanitation.
What makes you think that we achieved maximal life span in 21 century when medicine is still in its toddler stage? We cannot cure most diseases, we can only manage or lessen the impact of most of them.
The elastin problem has been studied extensively and is very well understood by people much smarter than me. We know how elastin is lost, we know how long it takes to run out of it, we know it’s not replaceable systemically, those are scientific facts.
I am NOT discounting your research of the elastin pathophysiology but I would be careful with this dogmatic approach. Science is full of dogmas and myths that were disproven. We used to think neurons cannot regenerate once they are set in place in humans. There may be simple a solution for the elastin problem that we maybe already have implemented. Just like sanitation prevented millions of deaths or fluoride increased dental health. Again, unless you have a controlled human study, you cannot be certain.
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JuanDaw
#571
From Neo’s post 41 at the thread below:
(Bryan) “My speed of aging has also reduced even further to a .64 - a new personal best, and lower than 99% of 20-year-olds.”
Compare that to .69 with Omega 3 alone, at 1g/day.
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I’ve been taking 1gm+ of Omega 3 a day for 20 years. With my first DNAm test 5 years ago my “age” was 8 years younger. Maybe that was something that helped me be lower than “average”?
Over the last 4 yeas my DNAm results did start changing when I started our senolytic program 5 years ago and as I’ve added more "things’ it has continued to improve.
My biggest improvement in the DunedinPACE happened when I started GLP1-R’s nearly 2 years ago.
That is also when all my other blood tests became the best I’ve had in 15 years.
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Neo
#573
Just fyi that he is now sub 0.5
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JuanDaw
#574
Not that I put any value in aging clocks. But the figures show that substantial improvement by that measure, may be achieved with more economical interventions. The paper Nick Norwitz cites states:
Omega-3 alone slowed the DNAm clocks PhenoAge, GrimAge2 and DunedinPACE, and all three treatments had additive benefits on PhenoAge.
Will have to wade through the paper for the figure with respect to “additive benefits” of Omega 3, plus Vit D, plus exercise. I do take 2,000 iu of Vit D. My Omega 3 intake comes from sardines.
The longevity benefit of Omega 3 was also discussed in the thread below.
The paper cited in the thread is linked below.
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I think that if you are on this forum you are not going to hit the average age of 81, you are going to hit the average age of affluent Americans which is 92.
Add in Rapamycin, SGLT2IS, Omega 3s, etc… I think 100 is a very realizable goal. After 100 it gets dicey fast.
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What we know is that elastin requires cells with higher efficiency to generate the right elastin splices. It is also possible to adjust splicing.
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Neo
#577
Does that impact the half life or the creation of new elastin?
It affects the creation of new elastin.
Neo
#579
@John_Hemming Interesting, I thought our bodies basically do not create new elastic past puberty. How meaningful is the ability to create new elastin as we age even with optimal splicing?
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Its like maintaining any protein. There are systems of homeostasis. The problem with splicing is that it is driven by the acetylation of splicing factors and the histone hence insufficient acetyl-CoA will cause splicing problems.
I do an easy test on this each week when I do my blood test by varying the acetyl-CoA levels in my cells systemically that results in different speeds of repair of the venepuncture.
You can see some photos on this web page (which is part of a poster I presented at a conference in the UK last year).
https://citrate.science/2024poster/poster.html
I am not aware of anyone else experimenting in the same way as I am with directly trying to control acetyl-CoA levels. (although other people are working with me).
One thing I have learnt from the experimentation is that the timing of energy levels matters. There is at some point a signal to repair the insult. If the acetyl-CoA level are high enough at this point then it repairs rapidly. Increasing them later probably does make things better, but the repair is still a lot slower.
You can see that with the fact that I have two venepuncture insults in the same elbow and the later one repairs more rapidly than the earlier one simply because of increased acetyl-CoA levels at the right time.
Jjazz
#581
Where are you guys getting the 0.69 number? In the Nature paper, Omega 3 reduced Dunedin Pace by 0.17, not 0.31.
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JuanDaw
#582
Nick’s vid at 7:20. Seems Nick was referring to the upper limit.
DunedinPACE d = −0.17 (−0.04 to −0.31)
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I’m looking at this and just thinking that they’re kinda all over the place. And none of them address whether Omega 3 is actually slowing the pace of aging, or it’s just gaming the system by directly affecting something measured by the tests. I still don’t put a huge amount of value in these clocks, but I think they’ll get better over time.
That said, since both Omega 3 and Vitamin D are safe, cheap and common, they are no-brainers to supplement IMO.
I also note that in the paper, 30% of the participants had Vitamin D levels of <30ng/ml, which is deficient.
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Neo
#584
Gents, I’m confused now
@Steve_Combi says roughly: Elastin is fundamentally different and we do not really grow any new
John says roughly: it’s like any other protein, if we fix the splicing we will grow new, healthy elastin
What are your thoughts on the other persons perceptive?
I think we need to fix the splicing. That is essentially fixing aging. However, I think I know what aging is. It relates to the efficiency of mitochondria which drives cytosolic acetyl-CoA levels which drives splicing.
Hence if you fix aging there is no issue with elastin.
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@Neo I’d suggest that reading all the papers I’ve provided as a reference would be the first place to start and then compare that to the papers that have been provided that support the other side of this discussion.
juliogf
#588
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