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A SAMPLE OF TOP PAPERS PUBLISHED ON FLUSH NIACIN + GLUTAMINE’S BENEFITS FOR GUT / INTESTINAL / GASTRIC / LIVER / KIDNEY / VISCERAL HEALTH:
GUT/INTESTINAL/GASTRIC
“A study showed that niacin supplementation was found to suppress colitis and colon cancer through the activation of GPR109A [97].”
Role of NAD+ in regulating cellular and metabolic signaling pathway
https://www.sciencedirect.com/science/article/pii/S2212877821000351
Niacin ameliorates ulcerative colitis via prostaglandin D2‐mediated D prostanoid receptor 1 activation
https://www.embopress.org/doi/full/10.15252/emmm.201606987
Real Niacin – improves IBD/IBS (and likely CFS/FM)
https://cfsremission.com/2017/04/15/real-niacin-improves-ibdibs-and-likely-cfsfm/Effect of Niacin on Inflammation and Angiogenesis in a Murine Model of Ulcerative Colitis
https://www.nature.com/articles/s41598-017-07280-yImpacts of Dietary Protein and Niacin Deficiency on Reproduction Performance, Body Growth, and Gut Microbiota of Female Hamsters (Tscherskia triton) and Their Offspring
https://journals.asm.org/doi/10.1128/spectrum.00157-22Niacin Improves Intestinal Health through Up-Regulation of AQPs Expression Induced by GPR109A
https://www.mdpi.com/1422-0067/23/15/8332/htmEffects of niacin on intestinal epithelial Barrier, intestinal Immunity, and microbial community in weaned piglets challenged by PDCoV
https://www.sciencedirect.com/science/article/pii/S1567576922005380?via%3DihubEffect of Different Levels of Niacin on Serum Biochemical Parameters, Antioxidant Status, Cytokine Levels, Inflammatory Gene Expression and Colonic Microbial Composition in Weaned Piglets
https://www.mdpi.com/2076-2615/12/21/3018/htm“Taken together, the bioinformatics and computational findings highlight antivirus, anti-inflammation and immunity-modulation as key targets/pathways of niacin treatment in CRC &/or COVID-19.
Further, niacin may be used clinically to treat CRC &/or COVID-19, based on the identified BPs (pharmacological functions) and signaling pathways (therapeutic mechanisms).”
Network Pharmacology and bioinformatics analyses identify intersection genes of niacin and COVID-19 as potent therapeutic targets
https://academic.oup.com/bib/article/22/2/1279/5964187Low-Dose Niacin Supplementation Improves Motor Function in US Veterans with Parkinson’s Disease: A Single-Center, Randomized, Placebo-Controlled Trial
https://www.mdpi.com/2227-9059/9/12/1881Randomized controlled trial of niacin on gut microbiome and quality of life in people with Parkinson’s
https://krex.k-state.edu/handle/2097/42457“The nicotinic acid GPR109A receptor regulated the structure of the gut microbiota & that the microbial populations were different between WT and Gpr109a- mice. Bacteroidetes & Firmicutes. These findings indicate that GPR109A regulates the gut microbiota”
G Protein-Coupled Receptor 109A and Host Microbiota Modulate Intestinal Epithelial Integrity During Sepsis
https://www.frontiersin.org/articles/10.3389/fimmu.2018.02079/fullGPR109A controls neutrophil extracellular traps formation and improve early sepsis by regulating ROS/PAD4/Cit-H3 signal axis | Experimental Hematology & Oncology
https://ehoonline.biomedcentral.com/articles/10.1186/s40164-023-00376-4Dietary niacin supplementation ameliorates ethanol‐induced liver injury in rats through sealing the leaky gut
https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.26.1_supplement.lb765Prolonged niacin treatment leads to increased adipose tissue PUFA synthesis and anti-inflammatory lipid and oxylipin plasma profile
https://www.jlr.org/article/S0022-2275(20)36693-1/fulltext^ Supplementing with these stupid omegas (or anything else but flush niacin + glutamine) WILL be harmful:
Attenuation of niacin-induced prostaglandin D2 generation by omega-3 fatty acids in THP-1 macrophages and Langerhans dendritic cells
https://www.dovepress.com/attenuation-of-niacin-induced-prostaglandin-d2-generation-by-omega-3-f-peer-reviewed-fulltext-article-JIRDietary deficiencies of iron and niacin in the aetiology of symptomatic gallstones – data from a UK prospective cohort study (EPIC-Norfolk) using 7-day food diaries
https://gut.bmj.com/content/60/Suppl_1/A38.2Pellagra, a re-emerging disease causes gastrointestinal bleeding
https://gut.bmj.com/content/71/Suppl_2/A124—
Dietary Glutamine Affects Mucosal Functions in Rats with Mild DSS-Induced Colitis
https://academic.oup.com/jn/article/137/8/1931/4664946l-Glutamine and Physical Exercise Prevent Intestinal Inflammation and Oxidative Stress Without Improving Gastric Dysmotility in Rats with Ulcerative Colitis
https://link.springer.com/article/10.1007/s10753-020-01361-3l-Glutamine Attenuates DSS-Induced Colitis via Induction of MAPK Phosphatase-1
https://www.mdpi.com/2072-6643/10/3/288“addition of glutamine preserves mucosal immune response and may limit the adverse effects.”
Artificial Nutrition and Intestinal Mucosal Barrier Functionality
https://www.karger.com/Article/FullText/353603—
And especially for anyone with alcohol or substance use issues and worrying about recovery of intestines, stomach, digestive tract, viscera, etc… please know that the lack of adequate supplementation of ONLY, NOTHING ELSE, flush niacin + glutamine (AND I REALLY WANT TO STRESS TO GET THE PURE BULK PRODUCTS) in equimolar amounts (i.e., 1:1.187 mass ratio per https://www.hom3ostasis.com/Protocol), especially with toxic alcohol &/or substances using them up more over the life course, is precisely why you have damage in the first place. It would be best to stay abstinent from such toxins especially over therapy, like the founder of Alcoholics Anonymous, Bill W, himself, was able to do only with “high”- (i.e., needed) dose flush niacin (w/o even powered by glutamine), and what he died for. Please read the below thoroughly:
Alcoholics Anonymous Founder Bill Wilson’s Long-Lost Treatment Paradigm
https://www.psychotherapy.net/blog/title/alcoholics-anonymous-founder-bill-wilson-s-long-lost-treatment-paradigm^ The same is true–the further depletion of already-depleted flush niacin + glutamine into further disease, disability, and dependence–for every toxic substance, especially those that give you some kind of buzz like drugs or difference in psyche like (anti-)”antidepressants”:
Niacin mitigates blood-brain barrier tight junctional proteins dysregulation and cerebral inflammation in ketamine rat model of psychosis: Role of GPR109A receptor
https://pubmed.ncbi.nlm.nih.gov/35690118/Sobriety and Satiety: Is NAD+ the Answer?
https://www.mdpi.com/2076-3921/9/5/425
Antidepressants may lead to a decrease in niacin and NAD in patients with poor dietary intake
https://www.sciencedirect.com/science/article/abs/pii/S0306987714004617?via%3Dihub^ How benzos mess up flush niacin + glutamine too:
Supplements Accelerate Benzodiazepine Withdrawal: A Case Report and Biochemical Rationale
https://riordanclinic.org/2014/03/supplements-accelerate-benzodiazepine-withdrawal-a-case-report-and-biochemical-rationale/Diazepam-induced loss of inhibitory synapses mediated by PLCδ/ Ca [2+]/calcineurin signalling downstream of GABAA receptors
https://www.nature.com/articles/s41380-018-0100-y…
LIVER
“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/
Glutamine, fatty liver disease and aging
https://www.aging-us.com/article/202666/pdf“The homeostasis of the most important nitrogen-containing intermediates, ammonia and glutamine, is a tightly regulated process in which the gut-liver axis plays a central role. Several studies revealed that nitrogen metabolism is altered in Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD), a consensus-driven novel nomenclature for Non-Alcoholic Fatty Liver Disease (NAFLD), the most common chronic liver disease worldwide. Both increased ammonia production by gut microbiota and decreased ammonia hepatic removal due to impaired hepatic urea cycle activity or disrupted glutamine synthetase activity may contribute to hepatic ammonia accumulation underlying steatosis, which can eventually progress to hyperammonemia in more advanced stages of steatohepatitis and overt liver fibrosis. Furthermore, our group recently showed that augmented hepatic ammoniagenesis via increased glutaminase activity and overexpression of the high activity glutaminase 1 isoenzyme occurs in Fatty Liver Disease.
Understanding gut-liver axis nitrogen metabolism in Fatty Liver Disease
https://www.frontiersin.org/articles/10.3389/fendo.2022.1058101/full
Free and dipeptide forms of L-glutamine supplementation attenuate parameters of oxidative stress and nonalcoholic fatty liver disease (NAFLD), and improve glucose metabolism in insulin resistant
https://www.endocrine-abstracts.org/ea/0056/ea0056p579
Glutamine treatments attenuate alcoholic liver disease
https://spandidos-publications.com/10.3892/etm.2019.8123…
KIDNEYS
“These effects of niacin on itching were attributed to its anti-inflammatory reaction, anti-xerosis, & mast-cell stabilizing effects.”
“confirmed that niacin is an effective drug in dialysis patients. Niacin may be considered safe, low-cost therapy”
The efficacy and safety of niacin on hyperphosphatemia in ESRD patients undergoing hemodialysis: randomized controlled trial
https://ejim.springeropen.com/articles/10.1186/s43162-021-00080-xEffect of niacin on phosphorus, calcium, parathormone and vitamin D levels in hemodialysis patients; a double-blinded randomized clinical trial
https://jnephropharmacology.com/Article/npj-10569“Results: Serum cystatin C level and creatinine significantly elevated (p≤ 0.05) in the second group (control group)(subjects who didnt receive vitamin B3 supplement from baseline while those who receive vitamin B3 supplement show stable serum cystatin C and creatinine level.
Conclusion: vitamin B3 (niacin) has a beneficial role in renal protection after cardiac surgery.”
Role of vitamin B3 in the prevention of acute kidney injury post-cardiac surgery through measurement of serum Cystatin C and Creatinine
https://jptcp.com/index.php/jptcp/article/view/1096–
“The biochemical pathway for glutamine conversion to glucose in hepatocytes and renal tubular cells involves deamination to glutamate, transamination to α-ketoglutarate and conversion to oxaloacetate, a Krebs cycle intermediate, that enters the common gluconeogenic pathway. Unlike gluconeogenesis from other substrates (lactate, alanine, pyruvate), glutamine gluconeogenesis is unique in that it represents an exergonic reaction with a net yield of 8 mol ATP per mol glucose synthesized, provided there is aerobic oxidation of nicotinamide adenine dinucleotide (NADH) and flavin adenine dinucleotide (FADH)”
Role of glutamine in human carbohydrate metabolism in kidney
https://sciencedirect.com/science/article/pii/S0085253815460260….
There are SO many more papers, but I thought I would just share a few for now above…
