alphadecay
Thank you for this!
Question about the foam cell formation, is this a given event across the board? Or is there some specific mechanism driving the oxidation?
There’s a term for individuals, typical of lean mass and lower BMI, that have an alternate response to a ketogenic diet. As I’m aware, people that are overweight and have some undesirable lipid levels can see improvements after taking on a ketogenic diet, but for some reason other people with more “healthy” phenotype have a worsening of biomarkers.
What are your thoughts on this?
I have yet to give those papers a thorough read, but the follistatin one made me think of another version of gene therapy where the clinicians claim their plasmid vector of transfer allows all changes to be reversed.
https://minicircle.io/wp-content/uploads/2024/04/fstpreprint.pdf
My genomics knowledge is certainly lacking, but what are your thoughts on viral vs. plasmid derived gene therapies?
Thank you! Hmmm I am excited about the possibility for these therapies, especially in the scope of modular adjustments turning genes on and off without more permanent/unwanted changes. Time will tell.
Back to your initial post. I am intrigued by the TERT and follistatin, would love to see this study replicated. The other paper you mentioned with the multi use cocktail was also compelling, but I thought it was odd they didn’t include a longevity specific arm. I suppose that wasn’t the scope of their intended study, seems like pretty low hanging fruit though. I don’t wanna get too cynical, but I wonder if they DID try a longevity side and things didn’t work out too well? Either way, that should definitely be a follow up study.
Thaaaanks!!
Forgive my ignorance, but aren’t the shorter lived strains functioning under genetic pressures in order to be short lived? From a research perspective this makes sense as conducting studies through end-of-life would be even more exhaustive if longer lived strains were used. Outside longevity it would be better to use short lived models. I guess my main thought, in terms on longevity, is that any intervention would undoubtedly help a short lived strain, because it would essentially be undoing years of genetic constraints that caused them to be short lived in the first place.
It seems that there is an invisible, yet squishy ceiling on lifespan up to a certain age with interventions, but then a much firmer boundary past a point. Shorter lived mice blow through the first boundary, which seems a given to me, and their lifespan total is comparable to long lived mice. But that initial bump in lifespan seems more of an undoing of our own meddling than a marker of efficacy.
ITP is the best!
I know you’re aware, but for those of you out of the loop, the NIA actively takes submissions for all testing interventions. https://www.nia.nih.gov/research/dab/interventions-testing-program-itp/application-instructions
You, yes you, can follow these instructions and submit your own ideas for the testing program. Crowd sourcing at its finest.
Vacuum the rug