From the Sheekey Science Show. A great channel to watch as she is a postdoc focusing on senescent cell research.
The video mentions something i had never heard before. That lomgevity has been linked to cap independent translation. Rapamycin and other longevity hacks block cap dependent translation forcing cells to use the independent version. This is related to GPLD1.
So, it seems that cap independent translation is involved in diet longevity, genetic longevity and the results of the big longevity drugs like rapamycin. Is this the key factor? Should we just always be using cap independent translation in order to live longer?
Another new Richard Miller interview:
Will check this out tomorrow. Thanks for sharing RapAdmin
Special protein and (?) enzyme, made by the liver, called GPLD1.What it does is they are special proteins in the service (?) of most cells that are tied to the plasmin (?) rated cell by a sugar postate (?) xxxx So, GPLD1 creates that anchor. So it can fill a lot of proteins that used to be attached cells, and puts it into the plasma.
Now we donāt know what it does to the cells, we donāt know what proteins xxx the whole thing is mysterious. But there was a paper published a couple of years ago by NAVU Lab, with two really fascinating findings.
One thing they found, is that if you exercise, GPLD1 goes up. Everybody knows exercise is good for you. And then they found that if you over-express GPLD1 in mice, your brain got good. That is, cognition got good, and also, a protein called BDNF (brain-derived neurotrophic factor) that maintains xxx cells that are stress-resistant. That went up too. So that was a clue, that the way that exercise is good for you, is that it turned on GPLD1, and that did good things to your brain.
And we read that paper, and what Jin (?) did was look at all our slow-aging mice. And it turned out, that GPLD1 was up, in the liver, the fat, and the plasma, of all four of our mutant mice, all of our drug-treated mice, and calorically-restricted mice, and for the drugs that are sex-specific, in some tissues, it is sex-specific for GPLD1. And the reason I got into this is, that it turns out, and Jinna Li (Xinna Li) discovered this as well, is that GPLD1 is a cap independent protein.
25:27 to 27:10 of the Elizabeth Sheekey video.
Donāt like videos; I prefer transcripts. Since there is none, made this, for other people like me.
Paper referred to, is below:
18:39 to 18:51. of the Joe Cohen video.
Increase in longevity from drugs or supplements, rapamycin (29%) Caloric restriction, 40%.
Yes - but to get that level you have to start caloric restriction very early in life - in childhood I believe (you canāt start at mid-life and expect anything like that percent increase). And of course (and Iāve tried) very few people can do the intense levels of calorie restriction that provides the biggest lifespan benefit.
21:51 to 21:59 (of Cohen video)
I weigh 180 pounds. If I was gonna do calorie-restriction, I would have to lose 60 pounds, and keep it off for my entire life.
22:34 to 23:32 (of Cohen video)
What we need to know, if how it works. What things are modified by caloric restriction, that for instance, are also modified by rapamycin, and 17-alpha-estradiol, and modified by these anti-aging genes. This is sort of, the obsession of my lab now. Weāve made a list of thirteen things modified by caloric restriction, and also modified by eight kinds of slow-aging mice. And this way, weāre sort of, hundred of things that caloric restriction does, weāve found thirteen, so far, that, are also modified by anti-aging genes, anti-aging drugs, those, we hope, or are arguing, you know, Iām making a pitch here. Those thirteen things are the way it works. Now we wanna know, for instance, what drugs, or supplements, can people take, that turn those thirteen things off. That might be a good way of finding out what drugs or supplements are the ones that actually have some plausibility as anti-aging drugs in people.