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nickandcarol posted an update
The Pure Bulk niacin seemed to be talking ages to arrive so we started to take some Solgar flush niacin we had at home with the Jarrow glutamine. Felt good to get going on the protocol. The Pure Bulk did finally arrive a few days ago, and it was really interesting to feel the difference. Much smoother in comparison to the Solgar version. We are both doing this, and again interesting to compare how we are responding. I am able to increase my dose each day as I am enjoying the experience. Nick, after his couple of months on NMN, is a little slower to settle down and is still finding it a little uncomfortable. Not so much that he is put off though.
I have just been reading about the additions we could add in in the early doses. We did both notice feeling cold during the flush. Having shivers. That seems to have passed now. We had strong prickling with the Solgar stuff, but now very little with PB.
How much would you suggest increasing the doses by? I have been adding 100mg to the dose each day or so, if it feels right. Is there a level that would be good to stay at for a while – eg 1g niacin – or more? What are we looking for when we have reached a good amount?
Also, Dmitry, I have heard, in one talk, you allude to some kind of ‘sabotage’ of the food supply to reduce the niacin contained in it. Have you written or talked about this anywhere that you could point me too?
With working in the natural food world, I am very aware how our diet has been changed with industrial processed foods, pesticides, herbicides etc… etc… etc. I wondered what aspects you have seen and were meaning in relation to niacin?
Moving away from a diet rich in animal foods has been encouraged for many years as a so called ‘healthy option’ and surely this is not good for the niacin levels. I am watching now as the onslaught increases in the media – saturated animal fat has been vilified for years, eggs are now causing blood clots (apparently!) and we need our meat to be created by an industrial process in a factory (yuk!) rather than animals naturally grazing the pastures, because that is better for the environment (as if!) … and on it goes..
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I am confused – this other individual is STILL doing NMN?!?!?!
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Wondering why they have brain damage (from NMN = nicotinamdie mononucleotide) too, aren’t they?? I dare you to check the Reddit forums after searching NMN headache or NR headache too … enjoy the other disease-driving like cancer, kidney/liver disease, and CVD too … thanks, @NaturallyFTW on twitter, bioharma shill with fake pic who also pushes Paxlovid, IVM, and HCQ to helpless masses after “she” more than 2 years ago was cured with flush niacin
“By inducing intra-axonal Ca2+ increase through a pathway requiring the action of the pro-axon death protein SARM1, accumulation of nicotinamide mononucleotide is, indeed, responsible for loss of axonal integrity [90]. The pro-degenerative action of nicotinamide mononucleotide has also been documented during vincristine-induced degeneration in dorsal root ganglion axons [91]. Accordingly, increased activity of nicotinamide/nicotinic acid-mononucleotide-adenylyltransferase (NMNAT) 1–3 protects axons from degeneration, by either limiting nicotinamide mononucleotide levels or activating SIRT1 [92][93].”
https://encyclopedia.pub/entry/19529
“Our proposed model of Wallerian degeneration predicts that axonal integrity is lost as a consequence of the accumulation of the pro-degenerative molecule NMN (Di Stefano et al., 2014), whose levels in axons are normally limited by the NAD-biosynthetic enzyme NMNAT2 (Gilley and Coleman, 2010). Here, using pharmacological and genetic experimental approaches in in vitro mammalian primary neurons and an in vivo vertebrate model organism, we show that NMN initiates a Ca2+-mediated execution program of axon degeneration after injury, which requires the presence of the recently identified pro-axon death protein SARM1.”
https://www.cell.com/cell-reports/fulltext/S2211-1247(15)01347-9?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124715013479%3Fshowall%3Dtrue“These results indicate that NAPRT is essential for NA to increase cellular NAD levels and, thus, to prevent oxidative stress of the cells. Kinetic analyses revealed that NAPRT, but not Nam phosphoribosyltransferase (NamPRT, also known as pre-B-cell colony-enhancing factor or visfatin), is insensitive to the physiological concentration of NAD. Together, we conclude that NA elevates cellular NAD levels through NAPRT function and, thus, protects the cells against stress, partly due to lack of feedback inhibition of NAPRT but not NamPRT by NAD. The ability of NA to increase cellular NAD contents may account for some of the clinically observed effects of the vitamin and further implies a novel application of the vitamin to treat diseases such as those associated with the depletion of cellular NAD pools.”
“In conclusion, our findings indicate that NA is a better substrate for elevating cellular NAD levels than Nam in human cells with endogenous NAPRT and that elevating NAD levels via the NA pathway protects the cells against injury such as by oxidative stress. Our findings, thus, document critical roles of the NA pathway in modulating cellular NAD levels and cell functions in human cells. Our current study will not only deepen the understanding of mechanisms regulating cellular NAD biosynthesis in humans but will also provide some insights into the clinical relevance of NA.”
https://jbc.org/article/S0021-9258(18)80941-3/fulltext
and
https://nature.com/articles/s41392-020-00311-7How long have they known that in humans and all higher order animals above rodents, only flush niacin (and certainly NOT the disease-driving salvage NAD+ precursors like niacinamide aka nicotinamide or NMN (nicotinamide mononucleotide) or NR (nicotinamide riboside), which are similar to niacin only in mice, which have only one NAD+ biosynthesis pathway other than tryptophan’s) are capable of fueling NAD+ biosynthesis (& beyond – like redox and NAADP+ autophagic anti-inflammation through GPR109A), powered by equimolar glutamine???
Oh yea – since 1958 officially in publication (albeit Krehl pointed it out many times before):
Biosynthesis of diphosphopyridine nucleotide. I. Identification of intermediates
https://jbc.org/article/S0021-9258(18)64789-1/pdf
How long have they continued to “ignore” this fact, flush niacin + glutamine, and instead push disease-driving salvage NAD+ precursors like NMN or NR for $100-300/month!?!?
“NAD+ has a vital role in protecting the human body against viral infections. NAD+ levels go down as people age due to a decline in NAD+ synthesis. NAD+ therapy, therefore, has been suggested to manage COVID-19 and its risk of mortality. This might turn over a new page on managing this disease, especially in third-world nations w/ limited infrastructure & facilities”
NAD+ DEFICIENCY MAY CAUSE MORTALITY AMONG COVID-19 PATIENTS
https://yuniquemedical.com/nicotinamide-adenine-dinucleotide/
“mitochondrial muscle disease leads to low NAD+ levels in both blood and muscle. Importantly, they show that treatment with niacin, a vitamin B3 form and an NAD+ precursor, improves NAD+ levels, disease signs, and muscle metabolism in patients, also improving muscle strength and performance. These results indicate that NAD+ depletion occurs in human diseases, and its repletion is a potential therapy for mitochondrial myopathies”
Niacin Cures Systemic NAD+ Deficiency and Improves Muscle Performance in Adult-Onset Mitochondrial Myopathy
https://cell.com/cell-metabolism/fulltext/S1550-4131(20)30190-X?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS155041312030190X%3Fshowall%3Dtrue
“niacin administered intravenously to those subjected to hemorrhagic injury (HI) in the absence of fluid resuscitation resulted in a significantly prolonged duration of survival. However, treatment with similar doses of nicotinamide mononucleotide (NMN), a precursor to NAD+ that does not bind
@GPR109A
, did not extend survival following HI”
“even at 5-fold higher dose, NMN was unable to increase survival rate to the level observed in niacin treated”
Deficiency of metabolite sensing receptor HCA2 impairs the salutary effect of niacin in hemorrhagic shock
https://sciencedirect.com/science/article/pii/S0925443919300092
“This finding may provide a rationale for the observation that the increased levels of Na [nicotinic acid aka “flush” niacin], but not Nm [niacinamide aka nicotinamide, or any other salvage NAD+ precursors], in circulation leads to the increase in the NAD cellular pool, emphasizing the different roles of these two forms in nutrition and signaling in mammals (for a review, see Bogan and
@CharlesMBrenner
).”
Genomics and Enzymology of NAD Biosynthesis
https://sciencedirect.com/science/article/pii/B9780080453828001386
“This study showed that the Preiss-Handler Pathway is the most efficient NAD+ production system in human cells. In conclusion, NA [nicotinic acid aka “flush” niacin] is essential nutrition for the maintenance of physiological conditions in humans”
“decrease in NAD+ level in 6 h after treatment with NAM [niacinamide aka nicotinamide]… NAM supplementation causes a slight decrease in cellular NAD+ level to some extent… NMN [nicotinamide mononucleotide] supplementation in the medium did not up-regulate NAD+ levels”
“NAD+ level was up-regulated by the supplementation of NA [nicotinic acid aka “flush” niacin] and NAMN [nicotinic acid mononucleotide], which indicates that the Preiss-Handler pathway is the active one in human cells”
“Niacin was revealed to increase NAD+ levels, which potentially leads to functions of anti-aging mechanisms”
Supplementation of nicotinic acid and its derivatives up-regulates cellular NAD+ level rather than nicotinamide derivatives in humans
https://researchsquare.com/article/rs-2481861/v1
“Inhibition of the NAD synthetase activity in the cell nucleus decreased the overall cellular NAD+ concentration, leading to cellular senescence. Accordingly, acetylation-dependent H2AX dynamics and homologous recombination repair were suppressed, leading to increased tumorigenesis. Our findings have revealed the importance of de novo NAD+ production in the cell nucleus for protection against the decreased DNA repair capacity caused by cellular senescence and thus against tumorigenesis.”
Impact of Nuclear De Novo NAD+ Synthesis via Histone Dynamics on DNA Repair during Cellular Senescence To Prevent Tumorigenesis
https://journals.asm.org/doi/abs/10.1128/mcb.00379-22?af=R
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but again, I’m just one of the good deli Jew kikes to y’all, right? Not a real scientist disseminating to you the real science -
No he stopped as soon as we heard you talking about 1 month ago.
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So I would start hitting at least 1 g 1.187 g doses, even higher .. .even 2.5 – 3 g doses … this is typical in the beginning with not enough juice … you will see that this goes away quickly … and also are you using clean distilled water?
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Ah, ok. Up to 900mg 1080mg today. Doing this 2 x a day at the moment. No have been using Berkey filtered (not fluoridated) water. We have a distiller at our shop, so we will bring that home if that would be better. Also have Qlarivia deuterium depleted water available if you think that may have any added improvement?
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naaa do NOT use that deuterium bullshit please … coldish distilled clean in a blender with some ice will be the best way … go up higher with dose, and enjoy…
You must understand that 6 year old obese children and 5 year old girls have been rightfully administered daily doses of 2 grams of flush niacin and 5 grams of glutamine, respectively, in the first case, to even get therapeutic benefits going for the little fat kids (by the NIH, themselves administered a year or so before COVID, mind you)…
“Dose-finding study of nondiabetic children age 6-12y with BMI≥95th percentile given niacin 250mg q2h × 3 doses (n=2), 500mg q2h × 3 doses (n=5), or 500mg q1h × 4 doses (n=5).
Participants
8 boys and 4 girls (age 9.7±1.8y; BMI 26.4±3.1kg/m2; BMIz 2.2±.25) were studied.
Main Outcome
Suppression of serum FFA below 0.2 mEq/L. GH [growth hormone]; insulin, and glucose were also measured serially.
Results
FFA decreased as the dose and frequency of niacin increased (p=.01). Niacin 500mg q1h 4 doses suppressed FFA <0.2 mEq/L and significantly increased GH (p =.04). Adverse effects were flushing/warmth (100%), tingling (60%), and GI complaints (20-40%).“
…
“A 5-year-old, previously healthy female presented with diffuse erythroderma (Figure 1). Rashes appeared 4 months prior, associated with pruritus. She had inadequate relief despite moisturization, topical and oral glucocorticoids. On exam, she had diffuse erythroderma (40% BSA) and bilateral supraclavicular and axillary lymphadenopathy. Serum IgE was significantly elevated – 45,850 IU/mL (ref. ≤ 90 IU/mL), she had increased eosinophils (1.69k/uL [0-0.8k/uL) and total CD4+ and memory (CD4+CD45RO+) T cells (1153 cells/uL [100-510cells/uL). Due to lymphadenopathy and family history of childhood leukemia in maternal aunt, she had a T-cell clonality assay by PCR which was unremarkable. Targeted primary immunodeficiency genetics panel (obtained for her hyper-IgE phenotype) was negative for pathogenic variants. Skin biopsy showed spongiotic dermatitis with staphylococcal impetiginization. She was treated with 10 days of oral cephalexin without significant improvement. She started oral glutamine 5g daily with continued skin moisturization. Two months later, she had only mild erythema of the shins, with decreased IgE 30,982 IU/mL and resolution of adenopathy.”
ORAL GLUTAMINE SUPPLEMENTATION FOR REFRACTORY ECZEMA AND ERYTHRODERMA WITH A HYPER-IGE PHENOTYPE
https://www.sciencedirect.com/science/article/abs/pii/S1081120622016428
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Both of you have yet to eclipse into even 1 gram flush niacin + 1.187 g glutamine territory doses. Please do not be deterred.
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