Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (739 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has pellagra-curative, vasodilating, and antilipemic properties.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: 3-Pyridinecarboxylic Acid; 3 Pyridinecarboxylic Acid; Nicotinic Acid; Nicotinate; Enduracin; Induracin; Nicobid; Nicamin.
Where it fits in the MeSH classification
- Broader topics
- Nicotinic Acids
Related concepts
- Pellagra-
Research landscape
PubMed indexes 11,379 records tagged with the MeSH heading “Niacin” (counts retrieved 2026-10-31). 611 of them (5.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 8,222 records.
Reviews account for 768 records (6.7%) and meta-analyses for 46. Randomized controlled trials number 364 (3.2%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 8,222 |
| 2000-2009 | 1,203 |
| 2010-2019 | 1,343 |
| 2020 onward | 611 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 768 | 6.7% |
| Meta-analyses | 46 | 0.4% |
| Randomized controlled trials | 364 | 3.2% |
Method: PubMed query "Niacin"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Niacin in the Central Nervous System: An Update of Biological Aspects and Clinical Applications | 2019 | Review article Design not recorded in structured metadata | 172 | cc by PMID 30813414 · DOI · PMC6412771 |
| Association between Dietary Niacin Intake and Migraine among American Adults: National Health and Nutrition Examination Survey | 2022 | Research article Design not recorded in structured metadata | 143 | cc by PMID 35893904 · DOI · PMC9330821 |
| Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system | 2020 | Research article Design not recorded in structured metadata | 127 | cc by PMID 32030468 · DOI · PMC7181452 |
| N-Terminal protein sequencing by nicotinic acid derivatization and MS analysis | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42581109 · DOI · PMC13658373 |
Niacin in the Central Nervous System: An Update of Biological Aspects and Clinical Applications [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Niacin (also known as "vitamin B₃" or "vitamin PP") includes two vitamers (nicotinic acid and nicotinamide) giving rise to the coenzymatic forms nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP).
- Closing excerpt
- Here, we will overview available literature data on the neuroprotective role of niacin and its derivatives, especially focusing especially on its involvement in neurodegenerative diseases (Alzheimer's, Parkinson's, and Huntington's diseases), as well as in other neuropathological conditions (ischemic and traumatic injuries, headache and psychiatric disorders).
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (136 words)
Niacin (also known as "vitamin B₃" or "vitamin PP") includes two vitamers (nicotinic acid and nicotinamide) giving rise to the coenzymatic forms nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). The two coenzymes are required for oxidative reactions crucial for energy production, but they are also substrates for enzymes involved in non-redox signaling pathways, thus regulating biological functions, including gene expression, cell cycle progression, DNA repair and cell death. In the central nervous system, vitamin B₃ has long been recognized as a key mediator of neuronal development and survival. Here, we will overview available literature data on the neuroprotective role of niacin and its derivatives, especially focusing especially on its involvement in neurodegenerative diseases (Alzheimer's, Parkinson's, and Huntington's diseases), as well as in other neuropathological conditions (ischemic and traumatic injuries, headache and psychiatric disorders).
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30813414 · DOI · PMC6412771
Association between Dietary Niacin Intake and Migraine among American Adults: National Health and Nutrition Examination Survey [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Migraine is related to brain energy deficiency.
- Closing excerpt
- 0 mg/day.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (202 words)
Migraine is related to brain energy deficiency. Niacin is a required coenzyme in mitochondrial energy metabolism. However, the relationship between dietary niacin and migraines remains uncertain. We aimed to evaluate the relationship between dietary niacin and migraine. This study used cross-sectional data from people over 20 years old who took part in the National Health and Nutrition Examination Survey between 1999 and 2004, collecting details on their severe headaches or migraines, dietary niacin intake, and several other essential variables. There were 10,246 participants, with 20.1% (2064/10,246) who experienced migraines. Compared with individuals with lower niacin consumption Q1 (≤12.3 mg/day), the adjusted OR values for dietary niacin intake and migraine in Q2 (12.4−18.3 mg/day), Q3 (18.4−26.2 mg/day), and Q4 (≥26.3 mg/day) were 0.83 (95% CI: 0.72−0.97, p = 0.019), 0.74 (95% CI: 0.63−0.87, p < 0.001), and 0.72 (95% CI: 0.58−0.88, p = 0.001), respectively. The association between dietary niacin intake and migraine exhibited an L-shaped curve (nonlinear, p = 0.011). The OR of developing migraine was 0.975 (95% CI: 0.956−0.994, p = 0.011) in participants with niacin intake < 21.0 mg/day. The link between dietary niacin intake and migraine in US adults is L-shaped, with an inflection point of roughly 21.0 mg/day.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35893904 · DOI · PMC9330821
Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Remyelination following CNS demyelination restores rapid signal propagation and protects axons; however, its efficiency declines with increasing age.
- Closing excerpt
- Niacin represents a safe and translationally amenable regenerative therapy for chronic demyelinating diseases such as multiple sclerosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (232 words)
Remyelination following CNS demyelination restores rapid signal propagation and protects axons; however, its efficiency declines with increasing age. Both intrinsic changes in the oligodendrocyte progenitor cell population and extrinsic factors in the lesion microenvironment of older subjects contribute to this decline. Microglia and monocyte-derived macrophages are critical for successful remyelination, releasing growth factors and clearing inhibitory myelin debris. Several studies have implicated delayed recruitment of macrophages/microglia into lesions as a key contributor to the decline in remyelination observed in older subjects. Here we show that the decreased expression of the scavenger receptor CD36 of aging mouse microglia and human microglia in culture underlies their reduced phagocytic activity. Overexpression of CD36 in cultured microglia rescues the deficit in phagocytosis of myelin debris. By screening for clinically approved agents that stimulate macrophages/microglia, we have found that niacin (vitamin B3) upregulates CD36 expression and enhances myelin phagocytosis by microglia in culture. This increase in myelin phagocytosis is mediated through the niacin receptor (hydroxycarboxylic acid receptor 2). Genetic fate mapping and multiphoton live imaging show that systemic treatment of 9-12-month-old demyelinated mice with therapeutically relevant doses of niacin promotes myelin debris clearance in lesions by both peripherally derived macrophages and microglia. This is accompanied by enhancement of oligodendrocyte progenitor cell numbers and by improved remyelination in the treated mice. Niacin represents a safe and translationally amenable regenerative therapy for chronic demyelinating diseases such as multiple sclerosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32030468 · DOI · PMC7181452
N-Terminal protein sequencing by nicotinic acid derivatization and MS analysis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Most MS-based workflows for N-terminal protein sequence analysis rely on the modification of primary amines at the protein N-terminus and lysine residues, in many cases through dimethylation.
- Closing excerpt
- Protocols for the nicotinoylation of proteins in solution or in gel using this reagent were optimized and successfully applied to various test proteins.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (169 words)
Most MS-based workflows for N-terminal protein sequence analysis rely on the modification of primary amines at the protein N-terminus and lysine residues, in many cases through dimethylation. However, incomplete dimethyl labeling and undesired side reactions have been reported previously and were also observed in our experiments. In this study, we evaluated alternative methods for N-terminal protein derivatization. For reductive dimethylation, the highly toxic reducing agent sodium cyanoborohydride was successfully replaced by pyridine borane. In addition, several single-reagent labeling methods were applied to model proteins and compared to the dimethylation workflow. Criteria for the selection of suitable reagents were completeness and selectivity of the protein derivatization reaction, the detection sensitivity for modified peptides by mass spectrometry, and the absence of undesirable side reactions. Comparative analyses demonstrated that the chemical derivatization of free amines by nicotinic acid N-hydroxysuccinimide ester is a particularly promising approach for N-terminal protein sequencing. Protocols for the nicotinoylation of proteins in solution or in gel using this reagent were optimized and successfully applied to various test proteins.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42581109 · DOI · PMC13658373
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review [5]
- Research article Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients [6]
- Research article Efficacy and safety of high-density lipoprotein cholesterol-increasing compounds: a meta-analysis of randomized controlled trials [7]
- Research article Mechanism of action of niacin [8]
- Research article Meta-analysis of the relationship between non-high-density lipoprotein cholesterol reduction and coronary heart disease risk [9]
- Research article Safety considerations with niacin therapy [10]
References
- Gasperi V, Sibilano M, Savini I, Catani MV. Niacin in the Central Nervous System: An Update of Biological Aspects and Clinical Applications. . 2019. PMID 30813414 · DOI · PMC6412771
- Liu H, Wang L, Chen C, Dong Z, Yu S. Association between Dietary Niacin Intake and Migraine among American Adults: National Health and Nutrition Examination Survey. . 2022. PMID 35893904 · DOI · PMC9330821
- Rawji KS, Young AMH, Ghosh T, Michaels NJ, Mirzaei R, Kappen J, et al.. Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system. . 2020. PMID 32030468 · DOI · PMC7181452
- Gehrig P, Wüthrich S, Chesnov S, Schlapbach R, Nanni P. N-Terminal protein sequencing by nicotinic acid derivatization and MS analysis. . 2026. PMID 42581109 · DOI · PMC13658373
- Carlson LA. Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J Intern Med. 2005. PMID 16018787 · DOI
- Keene D, Price C, Shun-Shin MJ, Francis DP. Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients. BMJ. 2014. PMID 25038074 · DOI · PMC4103514
- Birjmohun RS, Hutten BA, Kastelein JJ, Stroes ES. Efficacy and safety of high-density lipoprotein cholesterol-increasing compounds: a meta-analysis of randomized controlled trials. J Am Coll Cardiol. 2005. PMID 15653014 · DOI
- Kamanna VS, Kashyap ML. Mechanism of action of niacin. Am J Cardiol. 2008. PMID 18375237 · DOI
- Robinson JG, Wang S, Smith BJ, Jacobson TA. Meta-analysis of the relationship between non-high-density lipoprotein cholesterol reduction and coronary heart disease risk. J Am Coll Cardiol. 2009. PMID 19161879 · DOI
- Guyton JR, Bays HE. Safety considerations with niacin therapy. Am J Cardiol. 2007. PMID 17368274 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.