Niacin on Blood Glucose and CVD Risks, A Summary of Decades of Research

The following research summarizes decades of clinical  studies on niacin and its impact on blood sugar and cardiovascular disease risks. Niacin lowers blood lipids and reduces cardiovascular disease risks, although it also appears to slightly increase fasting blood sugar levels. We can reduce the effect of niacin on glucose by following a low-carb diet. I also need to point out that elevated blood sugar is only a marker, what really matters is the beneficial effect of niacin on cardiovascular health. The fact that niacin reduces the risk of cardiovascular disease risks is what really ultimately  matters.

Niacin is a precursor to NAD+, a molecule that is essential in over 50% of our biochemical reactions.  NAD+ decline is observed in aging and many chronic diseases.  I personally take large dose niacin daily.

In this clinical study of more than 500 human subjects, published in Diabetes Care in 2018, the authors concluded that niacin (NA), but not niacinamide, significantly increased Bacteroides abundance in humans. In the absence of systemic side effects, these favorable microbiome changes induced by microencapsulated sustained-release NA were associated with improvements in systemic insulin sensitivity and biomarkers of metabolic inflammation. [1]

In this 2016 paper published in the journal Heart, the authors concluded: In a meta-analysis of 11 trials of 26 340 nondiabetic participants between 1975 and 2014, regardless of background statin or combined laropiprant therapy , niacin treatment was associated with a moderately increased risk of diabetes. [2]

In this 2013 paper in the American Journal of Cardiology, the authors analyzed a total of 407 subjects with established vascular disease but not diagnosed with DM who participated in the FATS, HATS, AFREGS and CPC clinical studies. Authors’ conclusions: 3-year niacin use in subjects with normoglycemia at baseline was associated with increased blood glucose levels and the risk of developing impaired fasting glucose, but not diabetes, and was associated with a significantly lower incidence of coronary artery disease Associated stenosis progression and major cardiovascular events. [3]

The 18 years (1990-2007) of niacin clinical studies in the literature were summarized in a 2008 analysis of “consensus guidelines” published in the Mayo Clinic Proceedings. Authors’ main conclusions: Niacin is the most effective drug for raising HDL-C, while also lowering triglycerides and LDL-cholesterol; high-dose niacin significantly reduces cardiovascular events and atherosclerosis progression. [4]

  1. Fangmann D, Theismann EM, Türk K, Schulte DM, Relling I, Hartmann K, Keppler JK, Knipp JR, Rehman A, Heinsen FA, Franke A, Lenk L, Freitag-Wolf S, Appel E, Gorb S, Brenner C, Seegert D, Waetzig GH, Rosenstiel P, Schreiber S, Schwarz K, Laudes M. Targeted Microbiome Intervention by Microencapsulated Delayed-Release Niacin Beneficially Affects Insulin Sensitivity in Humans. Diabetes Care. 2018 Mar;41(3):398-405. doi: 10.2337/dc17-1967. Epub 2017 Dec 6. PMID: 29212824.
  2. Goldie C, Taylor AJ, Nguyen P, McCoy C, Zhao XQ, Preiss D. Niacin therapy and the risk of new-onset diabetes: a meta-analysis of randomised controlled trials. Heart. 2016 Feb;102(3):198-203. doi: 10.1136/heartjnl-2015-308055. Epub 2015 Sep 14. PMID: 26370223.
  3. Phan BA, Muñoz L, Shadzi P, Isquith D, Triller M, Brown BG, Zhao XQ. Effects of niacin on glucose levels, coronary stenosis progression, and clinical events in subjects with normal baseline glucose levels (<100 mg/dl): a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), HDL-Atherosclerosis Treatment Study (HATS), Armed Forces Regression Study (AFREGS), and Carotid Plaque Composition by MRI during lipid-lowering (CPC) study. Am J Cardiol. 2013 Feb 1;111(3):352-5. doi: 10.1016/j.amjcard.2012.09.034. Epub 2012 Nov 17. PMID: 23168285
  4. Goldberg RB, Jacobson TA. Effects of niacin on glucose control in patients with dyslipidemia. Mayo Clin Proc. 2008 Apr;83(4):470-8. doi: 10.4065/83.4.470. PMID: 18380993.


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