I find this Vaika study on dogs very interesting because its focused on former sled dogs (perhaps equivalent to extreme athletes in human terms). Seems like a lot of interesting things could be learned the study…
Yes - I spoke with Sergio a bit at the Longevity Meetup the night before the conference. I think they are getting close to clinical trials.
While “cellular rejuvenation” sounds like it would be a game changer… I wonder on the exact effect of what they are doing regarding aging skin. You have to be skeptical about these types of claims… so many people and companies have made similar claims in the past without the results to back them up.
Perhaps some dermatologists here can comment on this slide (below). While the improvement over and above Retin-A (Renova) is substantial, I don’t see any comparison to young skin (which is what I’d want to see it compared to, not just old/control/untreated skin.
The absolute increase shown in this slide below doesn’t seem that fantastic; perhaps 50% more than just Retin-A (which while helpful, is not a game changer in skin rejuvenation).
The insulin/insulin-like growth factor-1 (IGF-1) pathway drives an evolutionarily conserved network that regulates lifespan and longevity. Individuals with Laron syndrome who carry mutations in the growth hormone receptor (GHR ) gene that lead to severe congenital IGF-1 deficiency with decreased insulin/IGF-1 signaling (IIS) exhibit reduced prevalence rates of acne, diabetes and cancer. Western diet with high intake of hyperglycemic carbohydrates and insulinotropic dairy over-stimulates IIS. The reduction of IIS in Laron subjects unmasks the potential role of persistent hyperactive IIS mediated by Western diet in the development of diseases of civilization and offers a rational perspective for dietary adjustments with less insulinotropic diets like the Paleolithic diet.
RapAdmin, Whoa! That appears to be the heart of the matter. Yes, the Western diet of highly refined carbohydrates and sugars is a highly addictive problem. Even I am addicted, but I try to keep it under control.
Interesting. It does seem that he’s a little cagey on the efficacy of the treatments at this point. Although, he’s not a biologist. Lots of analogies, but not a lot of substance. I’ve watched a few talks with Prof Sebastiano and he seems very confident in the technology. As you mentioned a comparison with young skin would be a good metric to judge. I was wondering after watching the video if a limitation-at least at the moment-might be that the ‘safe’ window only confers a mild rejuvenation affect. I guess we’ll find out. All that being said though, the fact that they are so close to clinical trails still sounds like a huge step forward. I’ll be curious to see what kind of data they release in January.
When considering the overall clock scores, rather than the individual CpGs that comprise them, we get a slightly different picture. As shown in Figure Figure2,2, Horvath1 exhibits the strongest age correlation across pooled tissues and cells (r = 0.94), which is not entirely surprising given that it was trained to do just that. This is followed by Horvath2 (r = 0.85), which was the only other age predictor trained on more than one tissue type. While it is often misstated that the clocks developed using DNAm from whole blood do not “work” in other tissue and cell types, we found that the clocks by Hannum, Levine, Lin, and Weidner also exhibit fairly robust multi‐tissue age correlations (r = 0.68, 0.53, 0.67, and 0.46, respectively). Further, the reduced correlations appear to be due to tissue differences in the slope and intercept, rather than a lack of age correlations within tissues (Figure S3). This does not suggest that epigenetic changes are tissue‐specific, but perhaps that tissues have innate differences in vulnerability to epigenetic changes that manifest as differences in the rate of epigenetic aging as a function of chronological age. Interestingly, age slopes in these clocks appear to be most distinct when comparing brain to other tissues—with brain showing a much slower increase in epigenetic age over chronological age.
They’re robust but they’re also not strong correlations.