Banishing lonliness with a 1000 year functional depot injection or possibly as a combined effect with another drug could cause 26% less mortality, ““Imagine a condition that makes a person irritable, depressed and self-centred, and is associated with
a 26 per cent increase in the risk of premature mortality,” Cacioppo and her late husband, John Cacioppo, wrote in The Lancet last year. Around a third of people in industrialized countries report feeling lonely, one in 12 severely so” https://
nationalpost.com/health/all-the-lonely-people Notably the steriodal hormone pregnenolone has been researched as an anti-loneliness drug, and as a sex steroid like molecule could have ethynylization as well as halogenation as effective dose multipliers;
the first page of a search engine suggests 10 times greater effect per dose, if ethynylization is 8 times greater dose efficacy then 80 times fewer micrograms per dose could be possible; at .625 mg as a daily estrogen dose, and 300-800 nanogram/24 hours
at ethynylized estrogens or possibly progesterones (progestins), the fluorinated version could be active at 30-80 nanograms/24 hours, or a .333 gram depot injection providing 365,000 to one million gradually diffused 1microgram to 100 nanogram doses at a
one office visit dose treatment for loneliness, a 1000 to 10,000 year duration of loneliness reduction if pregnenolone has a ethynyl and fluoro dose amplified form. If a lymphatic system applied depot form of ethynylated halogenated progesterone is
possible that approximately quadruples physiological availability from omitting first pass metabolism; if a blood brain barrier passing moeity is a possible modification as well a two to ten times greater availability at the CNS, a possible location of
feelings of loneliness could be possible, so 80 nanograms /4 /2 is 10 nanograms per 24 hour dose, permitting an approximately 40 milligram 1000 year duration depot injection dose. Notably, if it is possible to make an oral depot version of a drug,
possibly from antibodies linked to palmitates, with the antibodies specific to lymphatic epithelia, then at 10% efficiency compared with an injected depot a 400 mg depot producing oral dose with 1000 year depot functionality of a ethynyl
fluoropregnenlolone could be possible; gene therapy or also germline gene therapy to produce more pregnenolone, or shift to personality genetics that is absent feelings of lonliness; also noting that the big five personality test trait areas are about 50%
heritable, and that a new personality test where, like the minnesota multiphasic personality inventory the questions were correlated, winnowed, and enhanced to be predictive, it is possible a 97-99% genetically predictable paper question or also
software psychology test with completely fresh new traits that could also be called themes could be constructed. If some percentage of these traits or themes that are 97-99% genetically predictable are the kinds of things people would change to improve
their well being, efficacy, ability, and prosociality, reduce or prevent loneliness, while maintaining or expanding creativity and initiative then those are rapidly eugenics addressable traits and themes that could also be gene therapy opportunities.

Addressing loneliness with depot drugs or causing greater plasma levels from less pregnenolone metabolism, whichever is more physiologically beneficial could reduce mortality 26%. It is unknown if numerous species of mammals along with humans experience
loneliness, gene drive could banish loneliness at perhaps all mammals; the effect on frequency of mating and the number of progeny is unknown, but imaginably increases among all mammals that experience an absence of loneliness.

Moieties that cause higher physiological availability and physiological activity at a particular mg (or mcg or ng) dose; I read that halogenated drugs are less metabolized at the liver with things like CYP enzymes, that gives longer plasma duration, as
well as possibly omits first pass metabolism, causing, imaginably, 90% or higher amounts of the drug to remain fucntional at the circulatory system; It could be that there is a kind of drug visiting and detaching from receptors many times, as well as
what I previously thought that halogenated drugs glom on to receptors and have long residence intervals from their high electronegativity glomming and staying on a receptor; also it is possible that halogenated drugs, as well as other drugs, which get
some of their durability from plasma from glomming to albumins, globulins, or other plasma proteins could have versions that glom to plasma proteins twice as avidly, or perhaps are absent any plasma protein glomming; a fluorodrug without plams protein
glomming might go almost completely unmetabolized at the liver, yet have a tissue available dose 7-9 times higher from an oral or other dosing; alternately, double duration plasma protein glomming

screen a library: radiolabelled or fluorophore labelled halogenated drugs, a few thousand, million, billion, or at a 300mm integrated circuit wafer with 1 trillion wells

Rapamycin, with like a trifluoro (methyl group like with three fluorines) that has 16 day or longer plasma half life, different plasma protein glomming could be an even more effective enhanced human longevity drug, from persisting at the circulatory
system longer; noting the mice that lived 60% longer from 126 ppm rapamycin had frequent meals but, I perceive I may have read, 9 minute rapamycin plasma half life, and I might have read human plasma half life of rapamycin might be .9 hours while
wikipedia says 57-63 hours; higher plasma protein glomming of a rapamycin; wikipedia says rapamycin is 92% protein glommed, there is some possible greater sustained rapamycin longevity effect there that could be produced and be beneficial; wikipedia
says, “ Since albumin is alkalotic, acidic and neutral drugs will primarily bind to albumin.”; Although a trained professional would know much more, the longest plasma half life of a drug I am aware of is norfluoxetine, 16 days, 384 hours; perhaps
the chemistry of such drugs (trifluoride like a methyl) could be used to produce even more beneficial, possibly even more longevizing variations of rapamycin, noting the mice were likely eating food perhaps every few minutes at the 126 ppm enteric coated
rapamycin dose; At the rapamycin molecule I read that a /\/\/\/\ with numerous \=/=\=/=\=/ is thought to be the mTOR active part of rapamycin, and it has a methyl on it that if replaced with a trifluoro methyl like moeity could cause the ten times
greater plasma half life. It is different than other things I have read, but wikipedia says ascorbic acid has a circulatory system half life of 83 days, with an eleimination constant of 4 months, that suggests something as simple as screening a variety
of locations of an ascorbic acid moeity could make a 3 month dose of a longevity producing rapamycin varaint; also I perceive I read that rapamycin’s oral absorption has to do with rapamycin’s nonsensitivity to pH, a rapamycin ascorbic acid version
could have higher effective drug absorption at a particular mg or ppm at food dose;

Longevity drug: 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)

Mass screening of longevity drug candidates with vertebrates: Fish: some fish (a goby) have median lifespans of 60 days, others like guppies, 2 years; A fish listed online is .55 inch (1.4 cm), Danionella, “When the genus was first described, these
fish were classified as the smallest adult vertebrates to inhabit freshwater”; Other fish in the .75 inch to 1 inch size are described at https://www.myaquariumclub.com/nano-fish-for-small-aquariums-5134.html; Some fish may have greater cognitive
ability than some other fish, “Dwarf puffers are one of the few species of fish that interact with their environment and owner. They will happily greet you as you approach the tank, and can even learn to be hand fed.”; another consideration for mass
screening of longevity molecules and longevity genetics and wellness molecules and wellness genetics at vertebrates is absence of aggression; it is possible that at a communal growth tank frequent fish-fish interaction of a nonpleasant nature could
affect physiology, actual physical integrity, and even the effects of stress on longevity;

Mass screening the fish: at 1 second per fish, a 3d printed 100 fish hydrosorter processes 1 million vertebrate fish for longevity drug efficacy at 10,000 seconds or 167 minutes (2.8 hours); A different engineering version: noting tube lengths, even with
green light causing many fish to prefer forward travel, at 10 seconds per fish, and a 1000 fish (32 times 32 grid) hydrosorter process it is also 2.8 hours to characterize and label 1 million fish; 117 days screens 1 billion fish.

engineering, chemistry, computer ic, computer fab, longevity, longevity technology, treon, treon verdery, physics, lasers, laser, emiconductor, dimension, math, IT, IL, pattern resonance, time travel, chronotechnology, circile, eric the circle, cartoon,
healthspan, youthspan, cpi, manufacturing, fiscal, money, software, petroleum, archive at deviantart com user treonsebastia

All technologies, ideas, and inventions of Treon Sebastian Verdery are public domain at JUly 8,2023AD and previously, as well as after that date

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