Too much vitamin B3 could harm your heart

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Niacin, also known as vitamin B3, is used as both a dietary supplement and to fortify our flour and cereals, and might be linked to an increased risk of heart disease, say international researchers who sampled the blood of over 4300 people. They say that two by-products of B3 breaking down in our bodies are associated with an increased risk of heart disease, and in their tests on humans and mice, they found one of these breakdown products helped increase the amount of pro-inflammation proteins in the lining of our blood vessels. While this study cannot prove directly that niacin causes heart disease, the team recommend larger studies to explore the link.

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From: Springer Nature

Excess amounts of breakdown products of the essential micronutrient niacin, also known as vitamin B3, may be linked to an increased risk of mortality, heart attacks and stroke, according to a study reported in Nature Medicine this week.

Niacin is used both as a dietary supplement and to fortify flour and cereal. Research has previously shown that niacin can lower levels of low-density lipoprotein cholesterol; however, the vitamin seemingly does not have the expected effects on decreasing cardiovascular disease risk — the so-called ‘niacin paradox.’ This paper provides a potential explanation for this paradox by showing that a breakdown product of niacin may promote inflammation in blood vessels.

In an analysis of plasma samples from 4,325 people in three patient cohorts that include both men and women from the United States and Europe, Stanley Hazen and colleagues found that two breakdown products of niacin — the metabolites N1-methyl-2-pyridone-5-carboxamide (2PY) and N1-methyl-4-pyridone-3- carboxamide (4PY) — are associated with an increased risk of cardiovascular disease. In subsequent human genetic and mouse studies, the authors showed that this increased risk may be mediated by the ability of one of these breakdown products (4PY) to increase the abundance of the pro-inflammatory protein VCAM-1 in the endothelial cells that line blood vessels.

Given these initial findings, Hazen and colleagues note that further work in larger studies is needed to explore the links between niacin and its breakdown products and cardiovascular disease.

Journal/
conference:
Nature Medicine
Research:Paper
Organisation/s: Lerner Research Institute, Cleveland, OH, USA
Funder: This work was supported by grants from the National Institutes of Health (NIH) (both the National Heart, Lung, and Blood Institute and the Office of Dietary Supplements: R01HL103866 and P01HL147823, S.L.H.); R01HL133169, R01HL148110, R01HL168493 and U54HL170326 (H.A.); Pilot Project Programs of the USC Center for Genetic Epidemiology and Southern California Environmental Health Sciences Center (P30ES007048) (J.A.H.); and the Deutsche Forschungsgemeinschaft (WI 5229/1-1) (M.W.). M.F. was supported, in part, by NIH training grants T32 HL134622 and T32 GM007250. A.H. is a participant in the BIH-Charité Advanced Clinician Scientist Program funded by Charité – Universitätsmedizin Berlin and the Berlin Institute of Health. The LipidCardio study (U.L. and I.D.) was partially supported by Sanofi-Aventis Deutschland GmbH. We also gratefully acknowledge the UK Biobank Resource for providing access to their data under application number 33307.
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