Newcomers Club
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Reply To: Poor Methylation – Niacin detox
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You got it! The difference in the pathways… the EVOLUTION of the species (and many others’), please see here (https://hom3ostasis.com/2022/11/homo-sapien-vs-hom3ostasien/) is precisely what sets flush niacin (catalyzed by equimolar glutamine) apart from everything else.
Whereas various articles are confirming the unique, distinct powers of the Preissler-Handler pathway of flush niacin (nicotinic acid, immediate release) to NAD+, such as:
“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://www.jbc.org/article/S0021-9258(18)80941-3/fulltext
and
https://www.nature.com/articles/s41392-020-00311-7and
“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
“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 to 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 Brenner).”
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
… and glutamine’s role:
“Therefore, NAD+ boosters would be effective for the prevention of COVID-19 or immediately after the infection with SARS-CoV-2″
“the glutamine supply for both the de novo synthesis and Preiss-Handler pathways is indispensable for NAD+ synthesis”
Comorbidity-associated glutamine deficiency is a predisposition to severe COVID-19
https://nature.com/articles/s41418-021-00892-y
“pharmacological interventions to enhance NAD levels via niacin will boost innate immunity to coronaviruses”
Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity
https://jbc.org/article/S0021-9258(17)50676-6/fulltext
“Hospitalization time was 10.4 ± 1.9 days in Covid-19 without L-Glutamine group and 8.9 ± 1.8 days in Covid-19 with L-Glutamine group (p = .005). In Covid-19 without the L-Glutamine group, four patients require the ICU though no one in the other group required that (p = .038)”
“adding enteral glutamine to the normal nutrition in the early period of Covid-19 infection will shorten the length of hospital stay and reduce the need for ICU”
Effect of oral l-Glutamine supplementation on Covid-19 treatment
https://clinicalnutritionopenscience.com/article/S2352-9393(20)30016-6/fulltext
“Reduced glutamine in COVID 19 may have adverse consequences for the patients’ prognosis. In COVID19 patients, depleted glutamine levels might be trigger differentiation of myofibroblasts from fibroblasts and increase abnormal collagen synthesis and fibrosis in the lungs”
“Enteral or parenteral administration of glutamine will correct the duration and pathophysiology of the patients’ stay in hospital and intensive care.”
Glutamine-Driven Metabolic Adaptation to COVID-19 Infection
https://link.springer.com/article/10.1007/s12291-022-01037-9
“NaAD+ accelerates the kcat/Km of the Qns1 glutaminase active site by ∼50-fold with a reversible substrate dissociation constant (Ks) that is 24-fold lower than the Km of Qns1 for NaAD+ to NAD+ product formation. Whereas this mode of regulation reduces the glutamine to NAD+ efficiency at low NaAD+ levels, it effectively reduces the waste of glutamine on an absolute basis in the absence of NaAD+. Moreover, at high NaAD+ levels, Qns1 achieves maximal glutamine to NAD+ efficiency and becomes strictly limited by glutamine levels to produce NAD”
Glutamine-dependent NAD+ Synthetase
https://sciencedirect.com/science/article/pii/S0021925820705235
“sickle cells have a higher level of active transport and utilization of glutamine, an amino that is required for NAD+ synthesis. (3) They then demonstrated that L-glutamine administration modestly increases NAD+ levels in sickle cells but more significantly increases the redox potential defined by the ratio of NADH to the sum of NADH plus NAD+. (4) This change in NAD redox potential appears to decrease theirsensitivity to oxidative stress. Glutamine may have additional beneficial effects by facilitating protein and glutathione synthesis.
L-Glutamine facilitates NAD+ synthesis as the substrate for the glutaminase activity of NAD synthetase, which uses the ammonia it releases from glutamine to convert nicotinic acid adenine dinucleotide to nicotinamide adenine dinucleotide”
A New Step in the Treatment of Sickle Cell Disease
https://pubs.acs.org/doi/10.1021/acs.biochem.7b00785
FDA approved L-glutamine powder for the treatment of sickle cell disease
Niacin to Improve Blood Flow in People With Sickle Cell Disease
https://clinicaltrials.gov/ct2/show/NCT00508989
“SCD [sickle cell disease] are at greater risk of severe illness & death from respiratory (lung) infections, including COVID-19, than people w/o SCD.
In 2020, there were 1,023 SCD-related deaths reported in the USA.
Rate of sickle cell disease-related death appears higher during the COVID-19 pandemic
“Given their young average age (28.6 years), these rates are striking.”
People w/ sickle cell disease who developed COVID have high rates of hospitalization, intensive care unit admission, & death
https://cdc.gov/ncbddd/sicklecell/features/scd-and-covid-19.html
… despite these corroborated truths of flush niacin, catalyzed by equimolar glutamine, being the only way to actually promote the creation of larger molecule, NAD+ & beyond (which counter inflammation, oxidative stress, pathogens, any foreign particles) and all intermediates along through our cells, with synergy from the calories of macronutrients from food and of course catalyzed all by water, they have known this for a generation 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 nicotinamide mononucleotide or nicotinamide riboside, which are similar to niacin only in inbred rodents, 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 (then later confirmed by me/the synthesis of the pre-existing research, powered equimolar glutamine)….
Biosynthesis of diphosphopyridine nucleotide. I. Identification of intermediates https://jbc.org/article/S0021-9258(18)64789-1/pdf
What I am ultimately trying to tell you is that this is the highest form of the health science advanced to human application. You should not be concerned about safety here or freaking out over the flush (it may be a bit trippy the first time only given the novelty), which in itself is this anti-inflammatory clearance of all this gunk, inflammation, oxidative stress that continues to bother you aggregating into your cells by way of this unaddressed continued, compounding lack of flush niacin + glutamine.
This predestined and planned cause, continued, compounding lacking flush niacin + glutamine (especially when we don’t address, obfuscate it and further aggravate it via putting other stuff in our body no matter Rx, OTC, or other so-called “nutrients” beyond well-balanced diet + clean water), driving the etiology and further the pathology of clinical conditions + diseases, and aging itself, has been something that continues to plague higher-order civilization species, since even before they were conceived, for many generations:
“supplementation with high-dose niacin before & during pregnancy prevents disease”
“embryo death & defects were specifically due to deficit of niacin-NAD in embryos; niacin supplementation prevented the disruption of embryogenesis”
NAD Deficiency, Congenital Malformations, and Niacin Supplementation
https://nejm.org/doi/full/10.1056/NEJMoa1616361
–
“Niacin levels were initially low in infants and rose toward normal values during treatment”
Blood Levels of Water-Soluble Vitamins in Pediatric Patients on Total Parenteral Nutrition Using a Multiple Vitamin Preparation
https://aspenjournals.onlinelibrary.wiley.com/doi/abs/10.1177/0148607189013002176
–
“the advice by Palawaththa et al. [1]: suggesting niacin supplementation to women of reproductive age aspiring to pregnancy is valid. In view of the above rationale, it deserves special attention for women for which higher risk is suspected [10].”
Can niacin supplementation prevent congenital malformations associated with maternal use of proton pump inhibitors?
https://link.springer.com/article/10.1007/s00394-022-03060-1
^ Response to the letter to editor: Can niacin supplementation prevent congenital malformations associated with maternal use of proton pump inhibitors?
https://link.springer.com/article/10.1007/s00394-022-03061-0
—
“A striking similarity among studies is that the concentration of glutamate and glutamine consistently increases with progressing lactation”
“glutamic acid (the prevalent FAA) and glutamine increased approximately 2.5 and 20 times, respectively, with progressing lactation, representing more than 50% of total FAAs at 3 months. The content of essential FAAs was also stable, so the change in total FAA content was almost entirely due to the changes in glutamic acid and glutamine. Accordingly, a healthy 1-month-old, 4-kg breast-fed infant supplied with 600 mL human milk per day would ingest approximately 120 mg of free glutamine and glutamic acid (which is more than 0.05 mg/mL human milk per kilogram body weight). This per kilogram body weight supply remains unchanged in a hypothetical 3-month old, 6-kg infant fed 800 mL human milk.”
Free Glutamine and Glutamic Acid Increase in Human Milk Through a Three-Month Lactation Period
–
“only the levels of glutamate & glutamine were different between the two groups. While the level of glutamate was increased, the level of glutamine was decreased”
“decreased level of glutamine has been reported before in ALL children with autism”
Increased Glutamate and Homocysteine and Decreased Glutamine Levels in Autism: A Review and Strategies for Future Studies of Amino Acids in Autism
https://hindawi.com/journals/dm/20
“late-life restoration of NAD+ levels rescues female reproductive function in mammals”
NAD+ Repletion Rescues Female Fertility during Reproductive Aging
^ And for the fellas:
“We therefore developed a transgenic mouse model of acquired niacin dependency (ANDY), in which NAD+ levels can be experimentally lowered using a niacin-deficient, chemically defined diet. Using ANDY mice, this report demonstrates for the first time that decreasing bodywide NAD+ levels in young adult mice, including in the testes, to levels that match or exceed the natural NAD+ decline observed in old mice, results in the disruption of spermatogenesis with small testis sizes and reduced sperm counts. ANDY mice are dependent on dietary vitamin B3 (niacin) for NAD+ synthesis, similar to humans.
NAD+-deficiency the animals develop on a niacin-free diet is reversed by niacin supplementation. Providing niacin to NAD+-depleted ANDY mice fully rescued spermatogenesis and restored normal testis weight in the animals.”
“ANDY mice with hACMSD overexpression reproducibly become NAD+-deficient in various tissues over the course of 6 weeks on a defined diet that is devoid of niacin (ND diet), but not on a control diet that is chemically identical to ND but supplemented with 30 mg/kg nicotinic acid”
Low NAD+ Levels Are Associated With a Decline of Spermatogenesis in Transgenic ANDY and Aging Mice
https://frontiersin.org/articles/10.3389/fendo.2022.896356/full
“niacin alone could improve the erectile function of patients with dyslipidemia suffering from ED [erectile dysfunction]. The effect is clinically significant in patients with moderate to severe ED. Because of the close relationship between ED and dyslipidemia, niacin might be an important therapy for managing both conditions”
Effect of Niacin on Erectile Function in Men Suffering Erectile Dysfunction and Dyslipidemia
https://academic.oup.com/jsm/article/8/10/2883/6980073
“In normal rats, obvious increase in serum testosterone especially in NL group associated with improved antioxidant status of testicular tissue was observed. In diabetic rats, niacin resulted in higher testicular weight/body weight and improved some histological parameters without affecting blood glucose, testosterone and sperm count. Testicular MDA content decreased. In conclusion, niacin especially at 800 mg/kg diet improves serum testosterone levels and antioxidant status of testes in normal rats”
Effect of pharmacological doses of niacin on testicular structure and function in normal and diabetic rats
https://onlinelibrary.wiley.com/doi/10.1111/and.13142
“Such conditions, disorders, and diseases pathologically manifested by ensuing inflammation (i.e., downstream kinetic (heat) energy) can be hypothesized as being governed by an underlying thermodynamic or bio-energetic (i.e., based on balancing of energy transfer into, out, and through the body) mechanism [42-45], which niacin—empowered and catalyzed by equimolar glutamine (with synergy further available upon combining equimolar glucose (from raw sugar/sucrose))—works to modulate back towards a state of http://HOM3OSTASIS.com, reflected in terms of health and longevity. Implications from the relevant findings of this research ultimately pave the way for not an ambitious promise, but rather an established projection, for major mitigation and even potential eradication of COVID-19, while further opening the opportunity for revolutionary advancement to drive public health forward.”
Sufficient Niacin Supply: The Missing Puzzle Piece to COVID-19, and beyond?
https://preprints.org/manuscript/202101.0180
…
Niacin Inhibits Apoptosis and Rescues Premature Ovarian Failure
https://pubmed.ncbi.nlm.nih.gov/30415247/
Chronic niacin administration ameliorates ovulation, histological changes in the ovary and adiponectin concentrations in a rat model of polycystic ovary syndrome
https://pubmed.ncbi.nlm.nih.gov/33751926/
Polycystic Ovary Syndrome and Niacin
Lack of flush niacin (nicotinic acid) is associated with premature ovarian failure, according to yet another (brand new) paper hitting the presses!
https://obgyn.onlinelibrary.wiley.com/doi/10.1111/jog.15554
Keeping diet with only 15 mg nicotinic acid these days, when a puppy’s deficiency of 20% back in 1946 was 25 mg nicotinic acid, is quite telling, no? On top of adding all the garbage to the environment and into our mouths since as they continue “racing to find answers”…
Flush niacin actually independently predicts all health outcomes accounted for all lifestyle factors including diet type & exercise even… For instance:
https://jnnp.bmj.com/content/75/8/1093
https://bmccancer.biomedcentral.com/articles/10.1186/s12885-022-10265-4
https://nature.com/articles/s41598-018-38002-7
“This meta-analysis involved 2,110 patients with T2DM from 8 RCTs across a wide range of patients’ characteristics. The results of this study suggested that niacin supplementation significantly reduced TC, TG, & LDL, and increased the level of HDL.”
Effectiveness of niacin supplementation for patients with type 2 diabetes
A meta-analysis of randomized controlled trials
“Niacin use significantly increased HDL-C by 29% and 29% and decreased triglycerides by 23% and 28% and LDL-C by 8% and 9%, respectively, in participants with and without diabetes.”
Effect of Niacin on Lipid and Lipoprotein Levels and Glycemic Control in Patients With Diabetes and Peripheral Arterial Disease
The ADMIT Study: A Randomized Trial
https://jamanetwork.com/journals/jama/fullarticle/193064
“niacin therapy had typical effects on routine clinical lipids (HDL-C + 16%, q < 0.01; LDL-C − 20%, q < 0.01; and triglyceride − 15%, q = 0.1)”
Effect of niacin monotherapy on high density lipoprotein composition and function
https://lipidworld.biomedcentral.com/articles/10.1186/s12944-020-01350-3
“niacin retains an FDA-approved indication as monotherapy for treating dyslipidemia, a main risk factor for cardiovascular events and myocardial infarction”
“Stratified meta-analysis showed an association of niacin monotherapy with reduction of some cardiovascular events among patients WITHOUT statins (acute coronary syndrome: relative risk, 0.68; 95% CI, 0.58-0.96; stroke: 0.69; 95% CI, 0.59-0.94; revascularization: 0.51; 95% CI, 0.37-0.72). These results were mainly derived from 2 trials conducted in the 1970s and 1980s”
Assessment of the Role of Niacin in Managing Cardiovascular Disease Outcomes
A Systematic Review and Meta-analysis
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2730481
“Our study concludes that lipid-modifying dosages of niacin can be safely used in patients with diabetes and that niacin should be used for patients with diabetes to sufficiently correct hypertriglyceridemia or low HDL-C levels.”
Effect of niacin on lipid and lipoprotein levels and glycemic control in patients with diabetes and peripheral arterial disease: the ADMIT study: A randomized trial. Arterial Disease Multiple Intervention Trial.
“concluded from many clinical trials using statins, lowering LDL-C alone is no longer regarded to be sufficient to treat CVD
comprehensive lipid management, in which raising HDL is an important target, a new standard. Niacin is UNSURPASSED in raising HDL”
Niacin Increases HDL by Reducing Hepatic Expression and Plasma Levels of Cholesteryl Ester Transfer Protein
https://ahajournals.org/doi/10.1161/atvbaha.108.171363
“link is supported in humans by epidemiological data demonstrating a correlation between intake of NAD+ precursor niacin (nicotinic acid) & vascular health, & LDL. In fact, niacin is an FDA-approved therapy for reducing LDL, ApoB, TG, and for raising HDL”
NAD+ in COVID-19 and viral infections
https://cell.com/trends/immunology/fulltext/S1471-4906(22)00025-4
High triglyceride to HDL-cholesterol ratio as a biochemical marker of severe outcomes in COVID-19 patients
https://clinicalnutritionespen.com/article/S2405-4577(21)00162-5/fulltext
Low HDL and high triglycerides predict COVID-19 severity
https://nature.com/articles/s41598-021-86747-5
Triglyceride/High-Density Lipoprotein Cholesterol Ratio is Associated with the Mortality of COVID-19
High-density lipoproteins may play a crucial role in COVID-19
https://virologyj.biomedcentral.com/articles/10.1186/s12985-022-01865-4
HDL cholesterol levels and susceptibility to COVID-19
https://thelancet.com/journals/ebiom/article/PIIS2352-3964(22)00347-4/fulltext
Causal Inference for Genetically Determined Levels of High-Density Lipoprotein Cholesterol and Risk of Infectious Disease
https://ahajournals.org/doi/10.1161/ATVBAHA.119.313381
The Triglyceride to High-density Lipoprotein Cholesterol Ratio, an Estimate of Insulin Resistance, is Associated with Incident Coronary Heart Disease. The Atherosclerosis Risk in Communities (ARIC) Study
https://ahajournals.org/doi/10.1161/circ.133.suppl_1.mp37
“In our study, high niacin intake during lifestyle intervention was associated with a larger reduction of liver fat content without affecting insulin sensitivity”
“Among 58 subjects with nonalcoholic fatty liver disease (NAFLD) at baseline, NAFLD resolved in 23 subjects during the lifestyle intervention. For one standard deviation increase in niacin intake, the odds ratio for resolution of NAFLD was 1.77 (95% CI, 1.00–3.43). High niacin intake may have a favorable effect on the reduction of liver fat during lifestyle intervention”
Niacin Intake Predicts the Decrease of Liver Fat Content During a Lifestyle Intervention
https://nature.com/articles/s41598-018-38002-7
“None of the patients taking IR [immediate release aka ‘flush’] niacin developed hepatoxic effects, while 12 (52%) of the 23 patients taking SR niacin did. —The SR [sustained release, altered] form of niacin is hepatotoxic and should be restricted from use. … The IR niacin is preferred for the management of hypercholesterolemia”
A Comparison of the Efficacy and Toxic Effects of Sustained- vs Immediate-Release Niacin in Hypercholesterolemic Patients
https://jamanetwork.com/journals/jama/fullarticle/366299
“pharmacologic (high-dose) niacin offers a potential treatment for liver cirrhosis, the clinical manifestation of liver fibrosis. This study offers a clue that niacin may reverse fibrosis resulting from other causes of cirrhosis including viral, alcohol, chemicals, etc.”
“this study shows for the first time that NIACIN:
* reverses preexisting collagen deposition in liver fibrosis associated w/ NASH
* prevents & reverses collagen deposition induced by oxidative stress in non-fibrotic stellate cells
* should be repurposed as an effective drug for clinical treatment of patients with NASH-fibrosis or liver cirrhosis
* has known efficacy for reversing steatohepatitis and steatosis (which can also result in liver cirrhosis)
* in patients with fibrotic NASH or liver cirrhosis is suggested as a cost-effective therapy for a major unmet need in clinical medicine.”
Niacin regresses collagen content in human hepatic stellate cells from liver transplant donors with fibrotic non-alcoholic steatohepatitis (NASH)
https://ncbi.nlm.nih.gov/pmc/articles/PMC9274597/
“Participants in an open label study at Kaiser Permanente in San Francisco received an average of 3000mg a day. After a mean duration of one year, 81% of patients had experienced reductions in intra-abdominal fat as measured by a single slice abdominal CT scan (the method agreed to provide an objective measure of changes in body fat). The average reduction in those who experienced improvement was 27%, and the degree of fat loss was significantly associated with the degree of increase in HDL cholesterol (niacin is given to people with elevated cholesterol to increase levels of good HDL cholesterol), and a reduced Total Cholesterol/HDL cholesterol ratio.”
Niacin reduces abdominal fat: pilot study
https://aidsmap.com/news/feb-2002/niacin-reduces-abdominal-fat-pilot-study
“Here, we demonstrated that oral supplementation of niacin resulted in a significant reduction in body weight and fat mass without affecting food intake in highfat diet-fed”
“Additionally, we demonstrated that niacin treatment stimulated thermogenesis in brown adipose tissue by induction of thermogenic genes via GPR109A”
“GPR109A deficient animals display obesity”
“niacin exhibited a markedly decrease in HOMA-IR values, suggesting the beneficial role of niacin in insulin sensitivity”
Niacin Fine-Tunes Energy Homeostasis Through Canonical GPR109A Signaling
https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3237699
“The findings suggest that niacin exerts beneficial effect on adiposity, glucose tolerance and insulin sensitivity, and plasma lipids, and that it specifically modulates the level of serum adiponectin under obese condition.”
Niacin improves adiponectin secretion, glucose tolerance and insulin sensitivity in diet-induced obese
https://sciencedirect.com/science/article/pii/S2314808X15000615
“Our research demonstrated that intake of niacin prevents the prevalence rate of cardiovascular disease by inhibiting low HDL-cholesterol and hyperglycemia”
“In conclusion, all the results from this research show the highest prevalence rate of cardiovascular diseases from physiological factors: hypertension, waist size, low HDL-cholesterol, and the nutrient that was related to the abnormal rate of physiological factors was niacin.”
Relationship of Niacin with Cardiovascular Disease
http://kjcls.org/journal/view.html?doi=10.15324/kjcls.2019.51.4.484
“The findings reveal that macrophage GPR109a deficiency accelerates the development of T1D [Type 1 Diabetes]. Activation of GPR109a on macrophage by nicotinic acid may provide a new strategy for preventing or treating T1D.”
GPR109a Regulates Phenotypic and Functional Alterations in Macrophages and the Progression of Type 1 Diabetes
https://onlinelibrary.wiley.com/doi/10.1002/mnfr.202200300
….
Now as for say sensitivities like dermatological ones (the most sensitive), and note this is still flush niacin solo underpowered:
In this one trial, it’s not on just acne, but really bad acne that could be considered a dermatitis-like condition (very similar features regardless: https://www.mdpi.com/2227-9059/10/10/2523)
“Acne lesion on the face, back, chest and back neck (Acne Keloidalis Nuchae) of the body are healed by niacin treatment.
Improvement in the niacin group was more than 80% after 12 weeks’ treatment.
Response of the acne lesions to niacin was superior to that of nicotinamide and this difference was statistically significant (P＜0.01).
Improvement in the niacin group increased rapidly, and it was significantly higher than in the nicotinamide group for several weeks (P＜0.01) (Table 1,Figure 1).
Improvement in the niacin group was significantly higher than in the nicotinamide group over different treatment periods (P＜0.01) (Table 1).
The number of successful cases in the niacin group was significantly higher than in the nicotinamide group after 12 weeks of treatment (Table 1).”
again, the sudden death too… alllll niacin (and with that glutamine) deficiency
https://emedicine.medscape.com/article/1095845-overview
https://pubmed.ncbi.nlm.nih.gov/10453439/
https://www.researchsquare.com/article/rs-2481861/v1
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577345/
https://www.nature.com/articles/3700491
There are many more.