Why does nicotinic acid help autoimmune conditions?
Nobody fully knows. This site collects and organizes the evidence.
110 curated research summaries · 11 pathway syntheses · queryable knowledge graph
Mechanistic threads
Nicotinic Acid and the GPR109A Receptor
hypothesisHow nicotinic acid activates GPR109A to promote regulatory T cells and suppress inflammation.
40 studiesNAD+ Deficiency as a Driver of Autoimmune Disease
hypothesisNAD+ as master regulator: how depletion through the Preiss-Handler pathway connects to immune dysfunction.
41 studiesButyrate, GPR109A, and the Gut-Immune Circuit
hypothesisHow dysbiosis reduces butyrate, impairs GPR109A signaling, and how niacin bypasses the broken microbiome.
15 studiesWhy Nicotinic Acid Helps Autoimmune Conditions
hypothesisConnecting the threads: GPR109A + NAD+ → specific autoimmune conditions.
10 studiesThe Subclinical Pellagra Hypothesis
speculativePellagra's 4 Ds map to the exact conditions in these studies. The RDA prevents overt pellagra, not optimal function.
18 studiesForm, dose, and practice
Nicotinic Acid vs. Niacinamide vs. NR vs. NMN: Why Form Matters
establishedOnly nicotinic acid activates GPR109A. The form determines the mechanism.
11 studiesVitamin or Drug? The Dose-Response Problem
dataRDA is 14-18mg. Therapeutic range is 100-1000x that. The pharmacological implications.
33 studiesThe Niacin Flush: Signal, Not Side Effect
hypothesisPGD2-mediated, GPR109A-dependent. Flush intensity correlates with inflammatory state.
7 studiesSourcing and trust
Not All Nicotinic Acid Is Created Equal
dataManufacturing methods, pharmaceutical grading, and COA interpretation for gram-scale use.
0 studiesWhat the Evidence Doesn't Show
dataHepatotoxicity, AIM-HIGH, negative studies. Including them makes the positive evidence credible.
1 studiesWhy Your Doctor Doesn't Know About This
establishedOff-patent economics, the flush barrier, cholesterol framing, and the AIM-HIGH chilling effect.
2 studies