126 ppm rapamycin is published as making mice live 60% longer, it is my perception that I read this has to do with reducing mTOR activity, notably though mice with mTOR -/- genes, which I pereceive as meaning they have zero mTOR receptors live 20% longer;
It seems possible that at mammals with mTOR receptors the mammals might also be making previously unstudied slightly hormesis-like chemicals that cause other changes at the body to compensate or emeliorate for having mTOR receptors, and possibly
reducing the activity of things (networks) connected to mTOR receptor activation; those slightly hormetic like ameliorators persist at the mammals when rapamycin causes the 60% greater mouse lifespan yet at the -/- mtor mice are minimally there ( genes
that produce the ameliorating chemicals) as they do not need to be. Finding those physiochemicals, likely proteins, receptor proteins or material at the cytoplasm then adminstering them to mammals as separate longevity chemicals as drugs could have the
40% longevity increase that could be linked to 60% increased longevity mice (minus) 20% at mice with no mTOR receptors; At humans, production of these chemicals, proteins, or peptides could be endogenous with germline gene modification or also gene
therapy; The possibly attainable 40% greater longevity from other mTOR receptor presence ameliators might even have different tissue or cyte localizations, potentially concentrating longevising effects, or finding areas to bring up to the body tissue
longevity increasing median, which would cause greater youthfulness of phenotype as well as greater longevity; looking at all the mRNA that rapamycin causes the production of, and comparing it to the mRNA that the mTOR -/- mice when adminstered
rapamycin make could find the ameliator 40% greater longevity genes and chemicals, just administering rapamycin to the mTOR -/- mice could find the 40% longevity mTOR ameliorating chemicals, genes, and proteins or peptides from mass characterizations at
all the proteins and peptides produced at the mammals.

Moving a math distribution of longevizing drug effects with bulk-effect different longevity drugs, and comparing that to a conctenated tissue and cyte approach; is there published research on the distribution of phenotypic and genotypic youthification of
form (variously somatic form or things like telomeres or mRNA expression profiles) at different cytes and tissues, It is possible an equation, computer model, or predictive AI would be much better, although one way to think of this is like a histogram;
if the histogram has a normal distribution then 32% of tissues and cytes are high longevity responders, 68% are at the first standard deviation; broad-group differences in distribution shape, and addressing which cytes and tissues are at what standard
deviation could be a programmatic way to find composite longevity drug combinations that cause a chemical that causes the phenotypic or also genotypic central standard deviation of one drug to be at the 2nd standard deviation of longevization with
another drug; this bulk mathematical effect complements the other idea of finding things like: one thing functions at adipose tissue, one thing works at neurons, another thing works at the cardiovascular system, another works on preventing cancer then
assembling a multitissue multicyte addressing multidrug blend; both have value, it is just that addressing entire distributions to move up an entire standard deviation of longevity increase could be accomplished with particularly larger affordability,
and simplicity.

Numerous math approaches, or groups of drugs/activities/genetic enhancements could be numerically modelled or equation limned to find the component groups that most functionally cause longevizing distribution standard deviation shifts, overlays, and
complementary groups; Receptor based, like AMPK and less mTOR, ILGF-1, and possibly receptors activated from published as causing 25-27% greater mouse longevity royal jelly chemicals or proteins, could be a standard deviation described group; then a
completely different chemical group of nonreceptor longevity increasing drugs could be another distribution group, like senolytics; a third group could be what I read about that might be called “mortality reducers” epithalon combined with thymosin
causes four times fewer people to have mortality events after six years, preventing, curing, or also genetically precluding loneliness reduces mortality 26%, I perceive there are other mortality reducers; another producible group that could actually
cause standard deviation overlap and movement of more things to second deviation or higher of greater longevity effects is to just make lipophilic and hydrophilic variations on the most effective longevity drugs; a hydrophilic and lipophilic version of
the rapamycin molecule and other receptor molecules, a lipophilic and hydrophilic version of senolytics, a lipophilic and hydrophilic version of 17 alpha estradiol, a lipophilic and hydrophilic version of the 25-27% greater longevity royal jelly proteins
or other chemicals; Also possibly lipophilic and hydrophilic and lymphatic system versions of what might be non-receptor longevity drugs like spermidine, immunizations, and NMN, could each modify the distributional histogram of effectiveness, which might
be a normal distribution at any one group of longevity drugs that could combine to move as many tissues and cytes as possible to produce an almost three-phase power like graph with all three phases being at the second deviation (upper 32%) of higher of
longevity effect.

A three of four drug blend that shifts entire distributions could have, perhaps based on the math of drug combination alone, many fewer numerically predictable side effects or contraindications than a 400 tissue or 400 cell type multihundred drug
composite. Then again, if each of the 400 drugs or gene products individually causes greater longevity and wellness, then their harmlessness might be kind of definitionally adequate, sort of, if it makes you live longer, and makes you weller, its
harmlessness is definitionally adequate. Note though that testing and time to commercialization could be much quicker with 10 highest effect longevity drugs times 6 variations (lipophilic, hydrophilic, halogenated and ethynylized, depot form, lymphatic
area, gene based, ) than testing and time to commercialization of a multihundred drug form. Notably though there are numerous opportunities for tremendous benefit from individual drugs as well, gene therapy or also germline modification to produce
longevity and mortality reducing peptides (epithalon with thymosin 4 times mortality reduction)

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)

126 ppm rapamycin is published as making mice live 60% longer, it is my perception that I read this has to do with reducing mTOR activity, notably though mice with mTOR -/- genes, which I pereceive as meaning they have zero mTOR receptors live 20% longer;
It seems possible that at mammals with mTOR receptors the mammals might also be making previously unstudied slightly hormesis-like chemicals that cause other changes at the body to compensate or emeliorate for having mTOR receptors, and possibly
reducing the activity of things (networks) connected to mTOR receptor activation; those slightly hormetic like ameliorators persist at the mammals when rapamycin causes the 60% greater mouse lifespan yet at the -/- mtor mice are minimally there ( genes
that produce the ameliorating chemicals) as they do not need to be. Finding those physiochemicals, likely proteins, receptor proteins or material at the cytoplasm then adminstering them to mammals as separate longevity chemicals as drugs could have the
40% longevity increase that could be linked to 60% increased longevity mice (minus) 20% at mice with no mTOR receptors; At humans, production of these chemicals, proteins, or peptides could be endogenous with germline gene modification or also gene
therapy; The possibly attainable 40% greater longevity from other mTOR receptor presence ameliators might even have different tissue or cyte localizations, potentially concentrating longevising effects, or finding areas to bring up to the body tissue
longevity increasing median, which would cause greater youthfulness of phenotype as well as greater longevity; looking at all the mRNA that rapamycin causes the production of, and comparing it to the mRNA that the mTOR -/- mice when adminstered
rapamycin make could find the ameliator 40% greater longevity genes and chemicals, just administering rapamycin to the mTOR -/- mice could find the 40% longevity mTOR ameliorating chemicals, genes, and proteins or peptides from mass characterizations at
all the proteins and peptides produced at the mammals.

Moving a math distribution of longevizing drug effects with bulk-effect different longevity drugs, and comparing that to a conctenated tissue and cyte approach; is there published research on the distribution of phenotypic and genotypic youthification of
form (variously somatic form or things like telomeres or mRNA expression profiles) at different cytes and tissues, It is possible an equation, computer model, or predictive AI would be much better, although one way to think of this is like a histogram;
if the histogram has a normal distribution then 32% of tissues and cytes are high longevity responders, 68% are at the first standard deviation; broad-group differences in distribution shape, and addressing which cytes and tissues are at what standard
deviation could be a programmatic way to find composite longevity drug combinations that cause a chemical that causes the phenotypic or also genotypic central standard deviation of one drug to be at the 2nd standard deviation of longevization with
another drug; this bulk mathematical effect complements the other idea of finding things like: one thing functions at adipose tissue, one thing works at neurons, another thing works at the cardiovascular system, another works on preventing cancer then
assembling a multitissue multicyte addressing multidrug blend; both have value, it is just that addressing entire distributions to move up an entire standard deviation of longevity increase could be accomplished with particularly larger affordability,
and simplicity.

Numerous math approaches, or groups of drugs/activities/genetic enhancements could be numerically modelled or equation limned to find the component groups that most functionally cause longevizing distribution standard deviation shifts, overlays, and
complementary groups; Receptor based, like AMPK and less mTOR, ILGF-1, and possibly receptors activated from published as causing 25-27% greater mouse longevity royal jelly chemicals or proteins, could be a standard deviation described group; then a
completely different chemical group of nonreceptor longevity increasing drugs could be another distribution group, like senolytics; a third group could be what I read about that might be called “mortality reducers” epithalon combined with thymosin
causes four times fewer people to have mortality events after six years, preventing, curing, or also genetically precluding loneliness reduces mortality 26%, I perceive there are other mortality reducers; another producible group that could actually
cause standard deviation overlap and movement of more things to second deviation or higher of greater longevity effects is to just make lipophilic and hydrophilic variations on the most effective longevity drugs; a hydrophilic and lipophilic version of
the rapamycin molecule and other receptor molecules, a lipophilic and hydrophilic version of senolytics, a lipophilic and hydrophilic version of 17 alpha estradiol, a lipophilic and hydrophilic version of the 25-27% greater longevity royal jelly proteins
or other chemicals; Also possibly lipophilic and hydrophilic and lymphatic system versions of what might be non-receptor longevity drugs like spermidine, immunizations, and NMN, could each modify the distributional histogram of effectiveness, which might
be a normal distribution at any one group of longevity drugs that could combine to move as many tissues and cytes as possible to produce an almost three-phase power like graph with all three phases being at the second deviation (upper 32%) of higher of
longevity effect.

A three of four drug blend that shifts entire distributions could have, perhaps based on the math of drug combination alone, many fewer numerically predictable side effects or contraindications than a 400 tissue or 400 cell type multihundred drug
composite. Then again, if each of the 400 drugs or gene products individually causes greater longevity and wellness, then their harmlessness might be kind of definitionally adequate, sort of, if it makes you live longer, and makes you weller, its
harmlessness is definitionally adequate. Note though that testing and time to commercialization could be much quicker with 10 highest effect longevity drugs times 6 variations (lipophilic, hydrophilic, halogenated and ethynylized, depot form, lymphatic
area, gene based, ) than testing and time to commercialization of a multihundred drug form. Notably though there are numerous opportunities for tremendous benefit from individual drugs as well, gene therapy or also germline modification to produce
longevity and mortality reducing peptides (epithalon with thymosin 4 times mortality reduction)

--- SoupGate-Win32 v1.05
* Origin: fsxNet Usenet Gateway (21:1/5)