I have worked on an actionable theory of aging with an empiricist mind so far - why should I worry about how the procedure work but to work on them as black boxes, alleviating missing information and known side effects. However, I have reached the limit and I need to have a theory of aging to proceed. The first thing is to build only the needed parts. What I am thinking is remove some proteins from the plasma, and then replace it, hoping the removed proteins will extend age. I will not try this on self, test it on mice first. How? Not simple now but let us see how that is done. Assume it is done. What then? Whatever I plan has to yield testing on mice but should work on human cell or on yeast first.
Goal is protein removal machine as adjunct to TPE machine some day. Filtering will be done by adding some chemicals to the plasma drawn.
Why not work with blood direct?
I think that cells (red, White) and platelets are likely sensitive to chemicals, far more than plasma. If the filtration is done, it will likely be on plasma.
Why focus on first and why?
CD38 and apoptosis prevention boosters. Cancer cells ignore apoptosis signals. Even senescent cells. In fact, senolysis is a brand-new method to deal with cancers and may work for aging too. The reason I am not hopeful is that the signals may be cell-specific. For cancers, depending on kind, the signal may be specific. It means targeted chemotherapy is needed specific to cancers. On the other hand, many cancers can share the signal.
Does not that talk imply an aging theory?
Yes it does! While purposely ambiguous on some matters, must admit a theory application sometimes. My current theory is some antagonist pleiotropy (All evil chemicals had youth-useful purpose) NAD+ resilience (fix, not robust against). What that means is that bio-events have two parts - damage up to a maximum, period measured by robustness and recovery period of resilience.
Where do they come from?
Robustness is largely species specific. Resilience is by specified groups of species. Similar species share resilience (I assume similar to break in DNA). That is because of my belief that resilience is a much harder property to arise by evolution! The hardest stress that a cell handles is DNA break. Unfixed cells become senescent. All life have the same break fix mechanism - never invented again by nature in a billion years. That is why animals share common methylation that happens at about the same rate. It is amazing that methylations are like annual rings in trees!
Why not expect age-extension at once but after some time?
It is my deep conviction that all best current modern medicine is dealing with the specific hallmark of aging determining the chemical fixes to specific problems found in increasingly precise chemistry. Lost in the trees are forest management ideas ignored. The fixed buggy tree is better for a while and attacked by another bug. If we assume that trees have the strength to fight bugs, a better approach is while the current problems are being fixed, simultaneous effort is being made to strengthen the immunity of trees, hopefully helping in the current problem and against subsequent infestations. Now the problem referred to. There are a small finite number of resilience chemicals. Apply them all and you solve many problems. Even if you don't fix any, those present in blood flower in dilute blood and regain strength. Eventually, all the bad ones are known and can be filtered out. No regrowth is stunted by the plasma The expected regrowth is not needed. Looks like 0ne week between procedure can be reduced to next day if all the bad chemicals were known and then the filtered same plasma is used. Not clear what is sped up by a week buys? CD38 is different as it is known bad with no known good things - it arises as an evil chemical byproduct of resilience, and hence can be filtered out. Slowly the list of evil be identified but never needed,
What is the assumption in above?
We assumed that the evil chemicals did not grow-in NB but good did. That is known true for every blood protein because this assumption is needed to explain AMBAR results. None of the oldies died while the clinical trial proceeded. In fact just boosts I have in mind comes from general TPE side effects and likely not nullify anti-aging parts of TPE. Too many protein fixes might. Protein subtraction might.
