Why does nicotinic acid help autoimmune conditions?
Nobody fully knows. This site collects and organizes the evidence.
110 curated studies · 11 pathway syntheses · queryable knowledge graph
Mechanistic threads
Nicotinic Acid and the GPR109A Receptor
hypothesis40How nicotinic acid activates GPR109A to promote regulatory T cells and suppress inflammation.
NAD+ Deficiency as a Driver of Autoimmune Disease
hypothesis41NAD+ as master regulator: how depletion through the Preiss-Handler pathway connects to immune dysfunction.
Butyrate, GPR109A, and the Gut-Immune Circuit
hypothesis15How dysbiosis reduces butyrate, impairs GPR109A signaling, and how niacin bypasses the broken microbiome.
Why Nicotinic Acid Helps Autoimmune Conditions
hypothesis10Connecting the threads: GPR109A + NAD+ → specific autoimmune conditions.
The Subclinical Pellagra Hypothesis
speculative18Pellagra's 4 Ds map to the exact conditions in these studies. The RDA prevents overt pellagra, not optimal function.
Form, dose, and practice
Nicotinic Acid vs. Niacinamide vs. NR vs. NMN: Why Form Matters
established11Only nicotinic acid activates GPR109A. The form determines the mechanism.
Vitamin or Drug? The Dose-Response Problem
data33RDA is 14-18mg. Therapeutic range is 100-1000x that. The pharmacological implications.
The Niacin Flush: Signal, Not Side Effect
hypothesis7PGD2-mediated, GPR109A-dependent. Flush intensity correlates with inflammatory state.
Sourcing and trust
Not All Nicotinic Acid Is Created Equal
data0Manufacturing methods, pharmaceutical grading, and COA interpretation for gram-scale use.
What the Evidence Doesn't Show
data1Hepatotoxicity, AIM-HIGH, negative studies. Including them makes the positive evidence credible.
Why Your Doctor Doesn't Know About This
established2Off-patent economics, the flush barrier, cholesterol framing, and the AIM-HIGH chilling effect.