LEAF

These guys do some neat things like this roadmap and their main news site is really quite interesting too over at :https://www.leafscience.org/

What is the "third" drug in this combo, the article says: ".. growth hormone and two diabetes medications". So far only the DHEA and Metformin has been discussed and I have no access to the source article.. any takes? edit-1: the answer is that the nature.com article got it wrong and other net sources parroted that article, https://www.leafscience.org/study-results-suggest-human-aging-can-be-r… is more accurate overview: there is no third drug involved. edit-2: scratch edit-1, HGH was obviously the primary growth hormone given and for some reason DHEA was counted as an anti-diabetic rather than a hormone (it is both) together with Metformin. Now I would just like to know the dosages involved!

People are actually very motivated to contribute to science, here's an example of research involving pets and extending their healthspan across aging: http://dogagingproject.com Phase I clinical trial: https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/28374166/ Phase II is in progress. Interview with Matt Kaeberlein from the project: https://www.leafscience.org/dr-matt-kaeberlein-the-dog-aging-project/

I am a layman so I could be totally misinterpreting things, but based on existing research it seems like the most effective method would be to filter out or suppress the production of VCAM1 which is apparently a protein that is associated with aging effects. It will be interesting to see how the research develops over the next couple decades. https://www.leafscience.org/the-fountain-of-youth-could-be-closer-to-h…

> what is a good way to get into longevity research/research support The Longevity Investor Network [1] might be of interest. (Disclaimer: I have donated, and actively consider investing, through them.) [1] https://www.leafscience.org/longevity-investor-network/

Looking up details of the study design, the molecule in question, β-Hydroxybutyrate, was tested in vitro on human tissue, and in vivo only on mice, so, as usual, wait patiently to see if there is any confirmation in, say, a large-scale study of a human population. The researchers tested the efficacy of β-hydroxybutyrate against cellular senescence in vitro on human umbilical vein endothelial cells and human aortic smooth muscle cells, and they observed the beneficial effects of this molecule in vivo: by injecting β-hydroxybutyrate into fasting mice, the scientists were able to alleviate the senescence of the animals’ aortae. https://www.leafscience.org/molecule-appears-to-have-anti-aging-effect…

Please note: facial recognition is learned, not innate. https://www.leafscience.org/visual-recognition/ Thanks.

Safe, yes, but I think "promising" is more aimed at the investors than a reflection of reality. Both Alkahest and Ambrosia's results are essentially ambiguous, which reflects the equally ambiguous animal data for plasma transfusion. This isn't going to stop other people from trying analogous things. The Conboys are trying apheresis to strip out harmful factors from old blood ( https://www.leafscience.org/conboy-interview/ ), which seems to me unlikely to move the needle either, and other groups are trying to identify and deliver signals from young blood. What all of these things have in common is that they are failing to address root causes. Why does signaling change in old blood and tissues? Because the cells that generate that signaling are either damaged or reacting to damage. Trying to force the signaling to be more youthful has very definite limits - it might compensate a little for one consequence of the damage, but that damage is still there, still producing all of the other problems that it causes. The "change the signaling" approach requires the research community to map every single one of potentially hundreds or thousands of individual changes, then understand which are relevant, and then run individual projects for each one. It just won't happen - look at the cancer research community for a guide as to how slowly that sort of scenario progresses. The plausible outer limits of signaling adjustment are probably indicated by the effects of first generation stem…