That makes me think that royal jelly with 2 oz of cheese is better.,

[Treon Verdery]

lecithin is one way to emulsify oil, also, putting royal jelly at an existing food emulsion, like liquid nondairy creamer, could be possible, “Many popular food items are emulsions, including mayonnaise, salad dressings, sauces such as Hollandaise, chocolate, and ice cream. Lecithin, a blend of naturally occurring phospholipids, is widely used in the food industry to promote o/w emulsions.”





https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2701654/











A wellness healthspan and possibly longevity drug or genetic modification: “Histone acetylation can be transient and must be maintained by enzymatic activity. Histone acetyltransferases (HATs) transfer the acetyl group (COCH3) from acetyl co-enzyme A to lysine residues”;



HDACinhibitors, favor acetylation, and cause various organisms to live about 22% longer, and ill mice to live 20 weeks rather than 8 (days? weeks?), the thing is though is that keeping a genome acetylated an optimal amount, could vary for numerous reasons, it is possible some humans have SNPs or gene copy numbers that strongly support rapid, full, all-tissue histone acetylation, whereas other humans might have different SNPs or copy numbers; histone acetyltransferase is an enzyme; at various things though 2019 normal humans vary 100% or more (IQ of 200, age at first ovulation, height), it is possible then that acetylation drugs or supplements, gene therapy, or germline gene modification could optimize the amount of histone acetylation that occurs, There could be a gene test to diagnose genetic variation like SNPs or copy number variations at the histone area acetylation enzyme, “The histone acetylation and deacetylation occurs on the lysine residues in the N-terminal tail as part of gene regulation. The mediating enzyme is often histone acetyltransferase”



Also, although not at the histone area, about half of people have varied acetylation ability, “There are three types of N-acetyletransferases. These are labelled A, B and C. These have been extensively studied in yeast. Each subtype is specific for its substrates. These NATs Genetic determines activities of NAT that again regulate drug metabolism. Nearly 20% of Asians have an isozyme that results in slower N-acetylation of drugs, while 50% of Whites”



The reactions are mediated by N-alpha-acetyltransferases (NATs), a sub-family of the GNAT superfamily of acetyltransferases. This superfamily includes histone acetyl transferases. These NATs transfer the acetyl group from acetyl-coenzyme A to the amine group.



Testing an acetyl group drug on mice: So a drug or supplement that causes more histone acetylation could be a water soluble variation on Cellulose triacetate, (triacetate, CTA or TAC) is a chemical compound produced from cellulose and a source of acetate esters, typically acetic anhydride. Triacetate is commonly used for the creation of fibres and film base. It is chemically similar to cellulose acetate. Its distinguishing characteristic is that in triacetate, at least "92 percent of the hydroxyl groups are acetylated." Notably perhaps the cellulose could be replaced with ribose, NMN, NR, or anything with active transport at the exterior cytomemebrane as well as possibly having a nuclear membrane transport peptide on it. triacetylglucose is also online, glucose pentaacetate, “GPA is completely absorbed and extensively utilized by the rat. Absorption of GPA from the gastrointestinal tract is rapid and almost complete in 4 hours.”

possibly with a nuclear memebrane transport peptide attached to it, glucose pentaacetate could heighten histone acetylation





I read that HDACinhibitors cause greater longevity, this, “Many acetylation markers on histones decrease with age, including bulk histone 4 acetylation levels and histone 3 acetylation at lysine residues 18, 27, and 56, which is thought to facilitate the aging process (Feser & Tyler, 2011). Therefore, the effects of an HDAC inhibitor, which prevents HDACs from removing acetyl groups further, have the potential to directly reverse or prevent these age‐related changes.” to my perception that suggests that cumulative modification of and from chromatin accessibility modulators occurs, noting that wikipedia mentioned 1/2 day, 24 hour HDACinhibitor activation spans, and to my perception, a paper on 10HDA as a longevity and phenotype producing HDACinhibitor noted 72 hour spans, that suggests a new kind of chromatin acetylation longevity increasing technology, an acetylator that works to modify multimonth, multidecade cumulative effects of HDACs or other chromatin accessibility modulators that are nonbeneficial to longevity, wellness, as well as healthspan, I have no idea how this works, other than fetuses remove about 90% of their epigenetic sturcturalization during development and perhaps this physiochemical effect could be caused to happen again, beneficially, at persons who have previously experienced puberty, with optimal acetylation as an immediate physiological activity once the epigenetic 90% movement to nonepigenetic form occurs; Another possibility is that a harmless drug that causes a genome to sequentially make say, one molecule, of every protein at its genome causes the entire genome to be sequentially processed, and while it is being processed a beneficial chromatin accessibility modifying modulator (like, from what I read about longevity epigenetics an acetylator) is around at sufficient amounts to modify the entire epigenetics of the entire, one gene at a time, processed genome; it is possible that something like mitosis could be genetically enhanced with gene therapy or germline gene modification to cause young phenotype (like 4 years or 14 years old) chromatin epigenetics, notably longevity, wellness and healthspan optimized acetylation (or also other beneficial chromatin accessibility modulator chemistries, like phosphorylation and others) amounts, That way, depending on the tissue, epigenetics would be reoptimized to be at a chronological 4 year old body or 14 year old body forms at most body cytes and tissues many many times repeatedly, and at a kind of continuous (some of any tissue or organ is likely mitotic at any particular moment) remodelling; Another way to cause change to gradually accumulated epigenetic nonoptimality is to possibly do a computer modelled algorithmic administration, possibly simultaneous, of different various chromatin accessibility modulators with nuclear envelope transport peptides on them, so like algorithmically, perhaps HDACinhibitors with nuclear envelope tranport peptides would have 40 times the activity as HDAC that had been apportioned as being around, but at 1/40th the usual amount, causing some sites that are HDAC beneficial to the organisms longevity, wellness and healthspan (SIRT HDAC possibly) to be HDAC-modified to be remodelled along with the HDACinhibitor modified areas; I do not have any idea how the algorithmic amounts times activities at genome location autosorting could work, although it is possible a new kind of enzyme that rather than methylating, acetylating, deacetylating, phosphorylating, or some other thing, puts tags, to be replaced with things like acetyl groups at a next pass/cycle on the genome, I think I read that basically physiochemicals put acetyls and methyls on lysine amino acids, perhaps there is some other thing that has a lighter, readily replaceable attachability to a lysine, like a PO4, or a poly PO4, or even a somehow physiologically harmless vinyl (bigger than a methyl, perhaps eentsier than an acetyl), then again, restarting it like a fetus’ 90% epigenetic renewed rewritable space every time there is a mitosis or even a quantitatively measured as beneficial and harmless to the progeny meiosis event could be more physiochemically engineerable, and composed of the reuse of other, preexisting, working, beneficial, physiological mechanisms and processes;



It is kind of physiochemically reminiscent of SENS, but perhaps there could be a youthotransferrent, kind of like an upgrade the neighbors, as compared with a senolytic that finds and terminates a nonbeneficial cyte; if some way of measuring that a particular cyte was far above the median as to youthful phenotype, while supporting of organismal longevity, wellness, and healthspan, as well as fully functional at local area physiochemistry, then its chromatin accessibility modulation, perhaps epigenetics, could be copied to neighboring cytes; peptide HDACinhibitors exist, so it is possible cyto efflux transport utilizing chromatin accessibility modulator optimization (like HDACinhibitors) peptides of a variety of forms and effects could exist, and visit the neighbors, spreading a chromatin accessibility modultion form similar or much like the far above median cyte;



At a paper I read https://www.embopress.org/doi/full/10.15252/emmm.201809854 that even though mirochondria are absent having histones HDACinhibitors cause more benficial mitochondrtial function, They could screen a library of acetylators or HDACinhibitors linked to localization molecules that cause preferential concentration at mitochondria to make and find mitochondrial epigenetic optimizers of longevity, wellness, and healthspan, they could then also quantify the beneficial effects



really primitive, but heat shock proteins cause greater longevity when the organism makes more of them, could 1-5 grams of HSP, enteric coated, to pass the stomach, have an effect on longevity; is it possible that an HSP, linked to an active transport moeity, could get rapid transport and movement to the cytes’ cytoplasm at numerous tissues; They could test this on mice to find out if eating enteric coated HSP, like eating chondrotoin, cartilidge, omega-3s, MSM causes physiological, longevity, wellness, and healthspan benefit



I read that getting rid of HDAC genetically causes mice to be nonalive, notably though hdacinhibitors cause greater longevity, at humans, as well as mice, are there HDAC, methylation, as well as a variety of other chromatin accessibility modulators (phosphorylation and others) SNPs (or gene copy number variations) that cause greater organisms longevity, wellness, and healthspan? Have human supercentenarians been characterized this way yet? Gene therapy as well as germline gene engineering could heighten longevity, wellness, and healthspan with optimized as well as new amino acid sequence SNPs (or possibly also different numbers of gene copies) at chromatin accessibility modulators



I perceive I read that when fetuses or possibly zygotes develop they automatically do a thing where they erase near 90%, it might have been 93% of their epigenetic molecular tagging, like removing methyls, acetyls, possibly like another 7-9 other chromatin accessability modulators like phosphorylators, so what I am thinking about as a wellness, healthspan, and, there is a chance, longevity technology is do some human zygotes do this a lot more than others, and what are the genotypic and phenotypic effects? If a normal human with some genome and SNPs (or gene copy number variations) erases 97% of their epigenetics as a zygote, and another normal human erases 93% of their epigenetics, which human is more optimally aligned to penotypically realize greater wellness, healthspan, and longevity? If this does occur, and at numerous things some humans are sometimes double or half of other humans while still being socially capable or thought of as conceptually fine (double height, IQ 200, first ovulation twice as early or at double usual chronological span, other things) is there any benefit to SNPs (or possibly some normal variation on number of gene copies) that strongly or lightly erase epigenetics at zygotes? It is possible that at some physical and interpersonal environments, removal of the epigenetics of previous ancestor’s reactions to stress, absence of stress, gourmand plentitude and prosperity, or perhaps athletic longevity focused protein reduced Keto longevity dieting could be beneficial, while at other ancestry occurences the person with the more epigenetic erasing SNPs (or gene copy number variation effects) might be physiologically skipping a multigenerational trend of epigenetic benefit, so what is better? It is possible that the epigenetics of a highly beneficial epigenetic environment can be purposefully duplicated, basically programmed, bringing preferred patterns of chromatin accessibility modulation (tagging) to all persons, humans, people, that is homo sapiens to create the greatest longevity, healthspan, wellness, and happiness; they coulkd find the 93% and 97% epigenetic zygote epigentic erasing at mice, and figure out which mice benefitted more, and what SNPs (or gene copy number variations) caused the mice to benefit



Do plants have epigenetic new sprout epigenetic blankness-production, if they do, would it be agriculturally beneficial to give plants a beneficial epigenetics, if they do not, would it be beneficial to cause epigenetic refreshing at plants to cause a benficial high genetic response to the environment rather than an ancestor plant’s responses to a different less growth benefitting environment; like the idea that epigenetic blankness or continuity could be bred to be higher or less at mammals it seems possible epigenetic trend or a fresh response could be created at plants on purpose to be beneficial



Longevity technology: have the identical acetylation and methylation (and other chromatin beneficial effects) you had at 7 years old, or a software model of your acetylation at 7 years old, have the 7 year old acetylation amounts all your life with custom chromatin accessibility modulators; this suggests that HDACinhibitors may cause longevity effects from making acetylation amounts similar to those at a younger phenotype, among a variety of possible mechanisms;

“The exact means by which HDAC inhibitors extend lifespan has not been fully resolved; however, a number of possible mechanisms can be envisioned. One possible scenario is that HDAC inhibitors reverse the natural age-related changes occurring in the histone acetylation landscape. This is the most simple explanation for their benefits, supported by the observation that many acetylation marks on histones generally decrease with age and in certain age-related diseases. A second possible mechanism of HDAC inhibitors is that they may affect histones and nucleosomes to directly activate transcription of pro-longevity genes. This is supported by observations that an endogenous HDAC inhibitor, β-hydroxybutyrate (BHB), can increase acetylation in the promoter of the pro-longevity transcription factor FOXO3a resulting in its increased expression, and indeed, BHB's lifespan extending effects depend on HDAC genes.

A third possible mechanism through which HDAC inhibitors may increase lifespan is through hormesis. In this scenario, while high doses of HDAC inhibitors may be toxic, low doses would elicit activation of protective genes to regain homeostasis, ultimately improving function. This is supported by observations that flies treated with HDAC inhibitors show upregulation of heat shock protein chaperones, a class of genes that are usually upregulated under stress. A fourth possibility is that HDAC inhibitors may regulate lifespan by modifying the acetylation state of non-histone proteins, activating signaling cascades that promote longevity independent of histone modifications.

Longevity causing immunization technology, longevity drug: It is possible that at the circulatory system there are circulating chemicals or physiochemicals or even chemicals that people are externally expoosed to that cause nonbeneficial methylation, the deacytlation of histones, or other nonbeneficial chromatin availability modulating things which are deleterious to longevity, wellness and healthspan immunizing against these circulating HDACish, methylationish, and otherwise deleterious chromatin availability modulators is quantifiably measurable as to any effect it has on greater longevity, wellness, and healthspan; this could be a beneficial immunization at children causing greater well being, healthspan and longevity even if immunized before elementary school; Notably the effect of the immunization on rodent and nonhuman primate progeny at more than 2 generations of progeny, female bonobos can get pregnant after 2190 24 hour spans (6 years), so 2 generations of bonobos could be as rapid as 7 years from the first sexually capable female bonobos longevity immunization; the longevity immunization would be studied to verify it was harmless and possibly beneficial to fetuses, pregnancies, babies and the people they grow into; Notably though some HDAC inhibitors are measured as actually causing change at the migration of (fetal) neural crest cytes, suggesting that some kinds of HDAC, methylation, or other chromatin accessibility modulation physiochemistry active immunizations might be better after completing having children, or, that immunizing against chromatin accessibility modulations that are simultaneously deleterious to any possible fetus and mother both are beneficial to make immunizations at;

I read that numerous HDACinhibitors cause greater longevity, is there a different thing, which could also be beneficial, that is a demethylation, that demethylates a histone, they could make a database of where this benefits longevity, wellness, and healthspan;

New fungal based longevity drug: There could be a fungal product similar to 90DA that is a longevity drug that also causes growth at fungi that could be a different chemical to quantify as to longevity effects, a chemical much like 90DA is utilized to grow fungi, “Provided is a method for the use of 10-oxo-trans-8-decenoic acid (ODA) as a fungal growth hormone to stimulate mycelial growth of cultivated mushrooms. A species of cultivated mushroom is selected and grown in a solid or liquid growth medium which has been supplemented with ODA to a concentration of 10-7M to about 10-4M. After culturing the mushroom the mycelium of cultivated mushroom is harvested. In addition to a method of using ODA, a method for the hormonal stimulation of fruiting in cultivated mushrooms is also disclosed. The ODA in this method is added to the casing layer of the compost which is mixed with mushroom spawn.” the 10 oxo-trans-8-decenoic acid chemical is slightly different than “9-oxodec-2-enoic acid”; they could grow a bunch of fungal mycelium, concentrate and separate a number of differing 10 C enoic acids, and see if any of the different ones they find have greater longevity effects on c elegans than 10HDA and 90DA and then test the fungal decanoic acids on mice to find out if the mouse longevity increase is larger than the published 25(27%) from royal jelly; patent: https://pubchem.ncbi.nlm.nih.gov/patent/US5681738#section=Patent-Title



molecules that are similar to 90DA are visually nifty at https://www.chemsrc.com/en/cas/334-20-3_1091822.html These could be screened as a library for longevity drugs, notably as compared with a 10 C decanoic acid, malonic acid has fewer C, is kind of well known, and looks kind of like 10HDA and 90DA, with fewer C at the alkane part, I perceive wikipedia communicates that malonic acid has something to do with valproate another HDAC inhibitor, possibly some variant on malonic acid could be a longevity drug or multiply beneficial HDACinhibitor