I think a mathematican would be able to come up with an equation and a number to communicate divergence from species similars and convergence on high longevity;



Doing the 100 bowls thing on endoliths, or plants, finds chemicals that are common between high longevity organisms, that took some mathematically less predictable paths, to develop a shared trait, which produces chemicals and has genes that can be
tested on other species to find out if the trend



There could be a 100 bowl convergence with three layers being outside a mathematically predicted form; three data points, i think i heard, can make a trend, and at 100 bowls of two or three organisms, the divergence from other organisms at the same bowl,
and the convergence on specific chemicals and genes among the high longevity bowl organisms, suggests that if there is a third thing then the longevity trends will have greater predictive ablity for specific chemicals and genes (gene versions); one
possible approach to making three data areas to make a trend from is to put a mid-longevity specied in each of the 100 bowls and find out if any of them are shared any of the chemicals (or gemes) that the highest longevity longevity animals comverge on







then the actual chemical and kind of cytochemical and tissue chemical network that the organisms with the greatest longevity at each bowl have, notably where this shared convergence on cytocommunication network form diverges from the similar species in
the same bowl;



I read 60% of the human genome is shared with the banana, so if there is a human tissue chemical, made from a gene that is the same as that of a 3650 day tree, and there is an alternate version of that chemical and gene produced at the kings holly, then
that is a human and tree shared chemical with what may be a much greater longevity version; yeast and mice could be utilized to find out if putting the king’s holly homologous gene at a mammal causes greater longevity;



senolytic dasatinib with quercetin treatment, 190 days compared with 140 days greater longevity from start of treatment, about 35% greater longevity, “20-month-old male mice treated with D+Q”, “For all dasatinib+quercetin (D+Q) treatments, D (5mg/
kg, drug/body weight) and Q (50mg/kg) were administrated by oral gavage in 100-150 μL 10% PEG400. For treating 20-month-old mice, D+Q was delivered either once monthly or every 2 weeks, with essentially identical effects.once every 2 weeks (bi-weekly)
for 4 months.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6082705/



so that is 350 mg for a 70 kg human, 8 times, or 4 times at monthly 2.8 grams, mouse dose compensation factor changes that to 233 mg for all 8 doses.



The quercetin is 2.91 grams per dose, so 8 doses is 23.3 grams



At roayl jelly amking mice live midway between 24 and 26% longer 500 ppm at ad libitum food mixed with 9 parts trehalose was used, at mice that is 25 g a day human dose, or using mouse compendation factor that is 2.09 g/ad libitum feeding, the 50 ppm/ad
libitum feeding was almost identicallly longevizing (112 weeks compared with 110 weeks high dose) and is 250 mg ad libitum feeding human dose, or 2.08 mg ad libitum feeding human dose with mouse compensation dose



That suggests enteric coated 20 grams of trehalose and royal jelly could be effective as an oral dose, coadministered with 2.08 grams royal jelly enteric capsule dose with food



That compares with 60 mg/kg of food at precis of paper, and at medium dose that is 60 mg/kg or 4.2 grams per 24 hours, or 420 mg per 24/hours at a 70 Kh human, without mouse comepensation factor the high dose is 25 gram ad libitum with trehalose and 2.09
grams with mouse compensation factor; note this does not function with high dose medium dose order or magnitude difference



The very large dose, based on mice eating 1/6 of their body mass a day, then calculating a dose on a human eating



Highest high mouse dose is 4.2 grams a day ad libitum with food, lowest high mouse dose is 350 mg, highest medium mouse dose is 420 mg ad libitum, lowest medium mouse dose is 42 mg



most of the mutants with long lifespan had mutations in the age1 gene [4]. This gene turned out to be the catalytic subunit of class-I phosphatidylinositol 3-kinase

(PI3K).



Sirtuins, epigenetics of sirutins, sirtuin supplements. it is possible endoliths like million year lifespan endoliths have novel sirtuin effecting chemicals



Mammals possess seven sirtuins (SIRT1–7) that occupy different subcellular compartments such as the nucleus (SIRT1, -2, -6, -7), cytoplasm (SIRT1 and SIRT2) and the mitochondria (SIRT3, -4 and -5).



sitruins are deacetylases, SIRT6 is shown in previous studies to be a critical epigenetic regulator of glucose metabolism, it is possible that other things that upregulate or are actual deacetylases, including non epigenetic deacetylases could be
longevity or healthspan drugs, screening a library of molecules that do about the same thing as SIRT6 could find a longevity hieghtening epigenetic drug that is more effective than SIRT6, sirt6 is linked to aging, temoleres and inflammation



SIRT like resveratrol-mimicking drugs such as SRT1720 could extend the lifespan of obese mice by 44%. However, “feeding chow infused with the highest dose of SRT1720 beginning at one year of age increased mean lifespan by 18%, and maximum lifespan by 5%
, as compared to other short-lived obese, diabetic mice; however, treated animals still lived substantially shorter lives than normal-weight mice fed normal chow with no drug.[2] In a later study, SRT1720 increased mean lifespan of obese, diabetic mice
by 21.7%, similar to the earlier study, but there was no effect on maximum lifespan in this study.[3] In normal-weight mice fed a standard rodent diet, SRT1720 increased mean lifespan by just 8.8%, and again had no effect on maximum lifespan.[3]”



43% greater maximumn lifespan from GDF15 is published “Female hNAG-1 mice (mice expressing hNAG-1/hGDF15) have significantly increased mean and median life spans in two transgenic lines. The effect is stronger in mice on high fat diet than on low fat
diet. hNAG-1 mice display reduced body and adipose tissue weight, lowered serum IGF-1, insulin and glucose levels, improved insulin sensitivity, and increased oxygen utilization, oxidative metabolism and energy expenditure.

% change in avg or median lifespan

Female mean lifespan is up to 43% higher.”



The RNA microRNA 17 that increases longevity could be a longevity drug immediately with online ordering and enteric coated capsules or possibly snortable form, or both









microRNA 17

Mus musculus

Pro-Longevity

16%



Gdf15

growth differentiation factor 15

Mus musculus

Pro-Longevity

43%

A list of longevity increasing genes is at http://genomics.senescence.info/genes/search.php?search=&show=4&sort=1&organism=Mus+musculus&long_influence=pro&lifespan_effect=increase&search=&page=1Mir17 Growth/differentiation factor 15 (GDF15)

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