From Dmitry Kats PhD, MPH + PureBulk, Inc.
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Conceptual Framework
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The "science," safety, & clinical utility of GPR109A (as a blend & individual parts) are well-established in the clinical & research literature.
Unfortunately, until now there was no clear understanding or dissemination of this info, and so a layperson has no reason even to imagine that the etiologies & pathologies of all disease/aging represent simply the myriads of manifestations & evolutions of individuals' & populations' generationally engrained pellagra unraveling along not addressing diet's growing insufficiencies in what happens to be three identified nutrients (flush niacin, folic acid, and N-acetylglutamine) to prevent, counter, or reverse it. Indeed pellagra is beyond its Google images. Just as those pictures resemble being struck by lightning, even more excess energy is alternatively accrued into the body just not all at once but over "life" into death.
On top of the "clinician hat" Dr. Kats committed to putting on to prospectively track reports from millions for >3.5 years, all steps leading to GPR109A -- characterized by its distinct fusion of the three nutrients into a compact, convenient, efficient package -- concordantly required commitment to meticulous review & synthesis of the entire body of clinical & research literature peer-review published into top-tier medical/science journals since 1900.
GPR109A
GPR109A is the name given to the G protein-coupled receptor expressed in all tissue responsible for quite favorable, call-them anti-aging roles. On the surface, GPR109A serves as a master accountant of each of our cells' favorability for the thermodynamics and kinetics involved in how energy can metabolize (often such a process is called "redox balance").
Beyond -- contingent on adequate supply of niacin (i.e., unmodified, crystalline, immediate release nicotinic acid), the exogenous ligand of its GPR109A receptor, meant to be orally supplemented at high-enough doses, as well as folic acid + N-acetylglutamine -- GPR109A activation, the magnitude of which is reflected in the level of expression of the receptor, which signals to niacin how much is needed to bind to it, is designed to promote energy expenditure and in this way counter energy accumulating into the body over the destruction (acutely or prolonged) to the organism who continues to depart further away from fulfilling the requirements of these three to continue to support the syntheses of ATP & all organic intermediates (including all "micronutrients") as well as even the proper metabolism of all macronutrients), to sustain biological function forward, a process colloquially termed "aging."
In essence, by facilitating an exergonic reaction in where niacin is the initial reactant that leads to the syntheses of much bigger products, i.e., niacin biosynthesizing to nicotinamide adenine dinucleotide (NAD+ & NAD-phosphate (NADP+)), which is catalyzed at the last step (from nicotinic acid adenine dinucleotide) by (free) l-glutamine (correctly supplied exogenously via the heat-stable N-acetylglutamine) -- and last-but-not-least mandates sufficient folic acid alongside -- leads to a release/transfer of usable energy then coupled to utilize for ATP & other reactions whilst that for which exists no requirement to invest or make up (e.g., the additional calories from diet needed to make up for the extra work output for exercising).
Could activation of the GPR109A receptor by niacin, catalyzed by sufficient levels of folic acid + N-acetylglutamine, mimics engagement in physical activity, especially since both activities often result in the "flush" sensation (if respectively intense/long- and high-enough dose)? Well, in fact this flush represents the feeling of the transfer of the potential energy gained as byproduct of the exergonic reaction niacin drives, into being coupled to be used to accelerate biosynthesis of ATP & intermediates while also to counter, denature (e.g., xenobiotics through T/NK cells / proper autophagy through the endolysosomal GPR109A/CD38/NAADP pathway) and ultimately provide a proton motive force to drive the release of additional energy across & within cells (e.g., cellular debris from reactive oxygen & nitrogen species, pathogens, toxins, heavy metals, esterified cholesterol, and what ultimately literally boils down to inflammation (i.e., excess kinetic heat energy) out the body (see here). And more importantly, a more accurate depiction would be that exercise tries to mimic such niacin-GPR109A activation but does so considerably less efficiently and more laboriously while requiring output of work -- in order to put formulations of stored excess energy (like triglycerides in the liver e or esterified cholesterol in blood) into motion to release the potential energy contained in their prior-to-that idle bonds -- which must be recouped via calories from diet. Herein, GPR109A simultaneously activates signaling pathways to increase breakdown of glycogen and fatty acids, which can thereafter be used for any ATP-requiring processes. Through these mechanisms, dynamic regulation of the GPR109A receptor with adequate supply of these three nutrients (+ sufficient calories from diet & clean water) has further been shown to favorably enable increased expression of relevant energy transfer- and clock-regulating genes.
Overall, GPR109A plays the focal role for promotion of the fine-tuning of energy metabolism to sustain thermodynamic equilibrium (or steady state) of the transfer of energy in, out, and ubiquitously through a system connected to, in this case, an infinite exterior world system. Among many reasons, including in attempts to improve energy levels, reduce inflammation, and protect + recover cells from damage, the GPR109A receptor remains the most sought-after target in pharmaceutical development of new treatments for just about every clinical condition/disease/disorder possible. Despite artificial attempts to modulate the receptor and generate call-'em "altered thus toxic & worthless niacin" analogues & derivatives, big pharma & biotech have not uncovered the needed other components with niacin (or their "fake niacins") to instill promotion of GPR109A expression for niacin, especially after the fact of unaddressed or too voluminous of niacin deficiency when here the receptor is downregulated as cells fail further, impeding niacin to enter intracellularly and so to process as efficiently & seamlessly.
GPR109A finally puts all that's needed (& in stoichiometrically appropriate amounts) together into ON3. It may take some time to realize how quintessential of an advancement this product represents, but we now truly may have all the time in the world to enjoy until others catch on!
NIACIN
N-ACETYLGLUTAMINE
FOLIC ACID
Niacin is innately responsible for the coenzyme, NAD+ in virtually all cells of the body. When NAD+ levels are high, cells are able to produce more energy and sustain homeostasis. Accordingly, NAD+ levels decline and dysregulate along every single pathology while over "aging" into ultimately complete exhaustion in supply (in concordance with folate and available glutamine/glutamate metabolism). Niacin (i.e., immediate release, unmodified crystalline nicotinic acid, to be specific) is what innately exogenously activates the GPR109A receptor directly. The bread and butter behind niacin's prowess as the primary most essential compound in existence stems from its unique ability -- in connection to how much the GPR109A receptor expresses for it -- to turn into bigger molecules, NAD+/NADP+ to provide proton motive force and redox balance to re-balance the biochemistry through cells to open up the alleys for more efficient metabolism of ATP and everything on the way without using as much substrates. Virtually every single reaction of the interior networkings of each cell (namely their mitochondria) are dependent on continued levels of force in the reactants as well as coenzymes + substrates needed to continue whatever needs to be continued to be moved along forward. As the body accumulates more excess energy, without accordingly more niacin-GPR109A fueling forward, requirements to process the then even more needed ATP to support the host w/ more accumulating excess energy, as well as for the coenzymes, NAD+/NADP+ from niacin, and the substrates involved that convert along with their metabolisms forward, clog up, ultimately leading to inability to continue the bioenergetics through cells into systematic dysfunction.
FOLIC ACID
N-ACETYLGLUTAMINE
FOLIC ACID
Folic acid is the only actual bioavailable molecule of vitamin B9 aka folate, most especially for those with the talked-about MTHFR mutations, which entail needing more of these three in total to power -- via more needed NAD+/NADP+ -- that more needed folic acid, instead of Merck's "methylfolate." Along with DNA & RNA, which additionally entail the others, folic acid is integrally involved in the regulation of energy metabolism. This special molecule also aids niacin-to-NAD+/NADP+ synthesis by -- along with N-acetylglutamine provided -- re-opening or accelerating the first enzymatic conversion of nicotinic acid to nicotinic acid mononucleotide, which indirectly helps niacin to activate GPR109A. Over unaddressed or too voluminous of niacin deficiency, as folate (& available glutamine) stores deplete over trying to support rescue or "salvage" mechanisms for once niacin is & remains insufficient: folic acid for its methyl- group to clear extra nitrogen that the salvage precursors of NAD+ (e.g., niacinamide aka nicotinamide) must then release to turn into niacin (or its metabolites) as the only way to synthesize de novo nuclear NAD+ necessary to be made over these situations for the host to survive in lieu of enough niacin, and meanwhile, l-glutamine to catalyze the last conversion (from nicotinic acid adenine dinucleotide to NAD+).
N-ACETYLGLUTAMINE
N-ACETYLGLUTAMINE
More helpful information to come!
N-acetylglutamine represents not only the proper form of how to deliver glutamine to the body, especially orally, exogenously, but it appears -- along w/ folic acid, -- to be the mysterious "liver factor," the necessary final component clinching restoration of GPR109A expression that downregulates along the unaddressed niacin + folic acid + N-acetylglutamine deficiency. With this, leading to sufficient N-acetylglutamate synthesis teams up with folic acid metabolism to efficiently escort (sufficient, i.e., WELL beyond diet) niacin down to NAD+ from the first step of its proper biosynthesis (i.e., nicotinic acid to nicotinic acid mononucleotide). If all three precursors are adequately supplied, free l-glutamine (not supplemented but provided from N-acetylglutamine with enough of the other two precursors, niacin and folic acid) is released to catalyze the final conversion of nicotinic acid adenine dinucleotide to NAD+/NADP+.
Oh, you didn't know?
More helpful information to come!
Oh, you didn't know?
Folic Acid has been recommended for pregnant and expecting mother not only as it's safe for all ages but b/c it's mandatory!
Like a holy trinity
More helpful information to come!
Oh, you didn't know?
The three in unison at appropriate amounts dynamically fuel equilibrium of biochemical reactions responsible for homeostasis
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The three molecules comprising the GPR109A product are each from by far the best independent manufacturer & supplier, PureBulk. Often providing the compounds used experimentally in published microbiology studies, the highest standard of purity is the hallmark of PureBulk.
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