This is a respectful request to Turnbuckle to present his idea on (how to prevent) aging, as he sees it. The reason I am making this request is that Turnbuckle has not only presented a great deal of ideas and scientific data regarding how he sees the basic forces behind the aging process, but has also made a lot of progress in putting these into an applicable protocol.
However, there has been so much discussion on the minutia of all this -and Turnbuckle kindly addressed so many of the comments and questions- that I believe it is impossible to go through the many threads he has started or contributed to and their enormous content to get a clear picture of how he sees the bigger picture. And it would be a tremendous waste to have such knowledge diffuse through the many pages and thus essentially disappear.
So, Turnbuckle, can you please explain briefly how you see the main drivers of aging and how we can realistically intervene in this process?
I understand that you believe mitochondrial dysfunction -as a result of the accumulation of dysfunctional mitochondria- is a major driver of aging. However, you also place a great deal of importance on the reduced ability / willingness of stem cells to come in and replace the damaged cells. And already, this gets pretty complicated, because we have mitochondria in stem cells as well as non-stem cells of the body and their dynamics are different. Then there is a significant interplay between the whole mitochondrial dysfunction of cells, and their ability to enter apoptosis; and without the old and potentially senescent old cells getting removed, bringing in new and fresh cells will only do a limited amount of good. Finally there is the whole discussion of how different stem cells act and some degree of distinction must be made between the various types. Are we making sweeping generalizations about all stem cell types or do we approach niche stem cells Very Small Embryonic Like Stem Cells and the several others stem cells differently? Do we run the risk of depleting all of these types or does such risk apply to only some types? Are their actions all driven primarily by their mitochondrial health and so on.....
The above are the loose ends I am unable to tie up merely by reading your posts -even though I feel that you have largely answered them. Hence a summary would be tremendously useful for the community.
Thank you so very much in advance...
