I have done a video about the experiment I have been running. At the moment it is unlisted, but I will link it below if anyone is interested.
I don’t really reference Rapamycin although I am taking it infrequently. I think what I am doing is compatible with Rapamycin in that the different approaches combine positively, but most of what I do does not relate to Rapamycin.
At this point, I have to believe that Rapamycin saving cells from senescence plays into it’s longevity factors. It truly is a wonder drug.
According to a recent study from the University of California, San Francisco, not all senescent cells are detrimental “zombies” that need to be eliminated to avoid age-related diseases. Instead, some of them are embedded in young, healthy tissues and promote normal recovery from damage.
Scientists have now seen these cells in action in lung tissue as well as other organs that serve as barriers in the body, such as the small intestine, colon, and skin. When they employed drugs known as senolytics to eliminate these cells, lung tissue damage healed more slowly.
I think zombie cells should be made to work and function as part of the entity. In that sense they cease to be senescent.
Thanks Rap Admin for sharing this article/study. Really makes one think before taking meds to eliminate Senescent cells. As you know, I’ve been on the fence regarding this program and readings like these may keep me on the fence.
See article below, discussing senolytics and senomorphics. Article lists rapamycin, metformin, resveratrol, stains, even acarbose and 17 estradiol as senomorphics.
Another HMG-CoA reductase inhibitor simvastatin was also shown to decrease SASP expression in senescent human fibroblasts and suppress the cell non-autonomous cancer-promoting effect of SASPs in breast cancer cells.
Several naturally occurring flavonoids, particularly apigenin and kaempferol, were demonstrated to significantly inhibit SASP production in bleomycin-induced senescent BJ fibroblasts.
Likewise, lifespan extension and other beneficial health effects of acarbose and 17-α-oestradiol have been reported, but whether it is related to its senomorphic activity remains unclear [[183]]. Two Ca2+ channel blockers, loperamide and niguldipine, and dopamine antagonist fluspirilene also displayed a senomorphic effect on primary MEFs; however, only a single concentration was tested
John_Hemming, your video doesn’t explain what you did. Will you share your protocol?
Procyanidin C1 is also a senomorphic at low doses. Since the amount of Procyanidin C1 in grape seed extract is unknown (mixed cyanidins), GSE may function as a senomorphic.
PCC1 blocks the SASP expression when used at low concentrations. Importantly, it selectively kills senescent cells upon application at higher concentrations, mainly by enhancing production of reactive oxygen species (ROS) and disturbing mitochondrial membrane potential, processes accompanied by upregulation of Bcl-2 family pro-apoptotic factors Puma and Noxa in senescent cells.
Procyanidin C1 is in grape seed extract (GSE)
FWIW I take pterostilben{1,000mg]and GSE{800mg] together, every day.
pterostilben 250mg, 4 capsules {1,000mg total]
GSE 400mg, 2 capsules {800mg total]
Thanks for this Juan. I googled for procyanidin C1 and discovered my Aronia berries have it as well. Also in the same article it says they have alpha glucosidase inhibitor:
It says they have it in the bark too and since we had to mow them all down this fall I have a mountain of bark down there. Haven’t seen any recipes on how to harvest that though.
I put a couple cups of frozen berries in my morning smoothie maybe twice a week. Also have 2 daughters that eat them, but they are a hard sell. People are interested until they try them.
Pycnogenol (pine bark extract) has procyanidin C1 too.
You have to mow the bushes every 6 years or so. For one thing they get too big for the picking machine, but also the yield gets worse over time:
This is just one pile. So if anybody wants to try aronia bark it can be had very cheap here.
This is what they look like after being mowed off.
I can see why they are grown. There are many positive attributes here and they’re relatively cheap.
Thanks for the tip. I ordered Aronia powder months ago, after some research (not related to senomorphics). on cyanidins. I put them in coffee. I have to find it somewhere among my supplements and start again.
That’s a gold mine. They can be ground and made into a tincture.
Where is “here”? Iowa?
Yes, about 30 miles east of Sioux City out in the sticks. FREE.
I don’t have any idea how to process the bark. Would you just peel it off and grind to powder? I’ve never seen the product for sale anywhere.
Mostly what is done is juice, it’s sold in HyVee. I suppose the powder is what’s left over after the juice. Probably the good stuff. I didn’t know it had alpha glucosidase, and still don’t know how much.
Sorry. I have no engineering background. Am sure it can be mechanized. Maybe we should ask desertshores.
Interesting in senolytics
a biotechnology/biohacking CEO says that clearance is more effective when you’re younger
Ryan Smith TruDiagnostic reports that using too much of the blunt-edge kind can increase epigenetic age…
When you say blunt edge, are you referring to fisetin, dastanib, etc…?
Researchers are investigating medicines that selectively kill decrepit cells to promote healthy aging — but more work is needed before declaring them a fountain of youth
One of their targets is decrepit cells that build up in tissues as people age. These “senescent” cells have reached a point — due to damage, stress or just time — when they stop dividing, but don’t die. While senescent cells typically make up only a small fraction of the overall cell population, they accounted for up to 36 percent of cells in some organs in aging mice, one study showed. And they don’t just sit there quietly. Senescent cells can release a slew of compounds that create a toxic, inflamed environment that primes tissues for chronic illness. Senescent cells have been linked to diabetes, stroke, osteoporosis and several other conditions of aging.
These noxious cells, along with the idea that getting rid of them could mitigate chronic illnesses and the discomforts of aging, are getting serious attention. The US National Institutes of Health is investing $125 million in a new research effort, called SenNet, that aims to identify and map senescent cells in the human body as well as in mice over the natural lifespan. And the National Institute on Aging has put up more than $3 million over four years for the Translational Geroscience Network multicenter team led by Kirkland that is running preliminary clinical trials of potential antiaging treatments. Drugs that kill senescent cells — called senolytics — are among the top candidates. Small-scale trials of these are already underway in people with conditions including Alzheimer’s, osteoarthritis and kidney disease.
But he and others sound a note of caution as well, and some scientists think the field’s potential has been overblown. “There’s a lot of hype,” says Varga. “I do have, I would say, a very healthy skepticism.” He warns his patients of the many unknowns and tells them that trying senolytic supplementation on their own could be dangerous.
