Niacin for Cholesterol: Why Raising HDL Didn’t Prevent Heart Attacks

Niacin raised HDL cholesterol more than any other available treatment. Two large randomized trials tested whether that prevented heart attacks — and found no benefit, alongside real harm.

Medical Disclaimer: This content is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Information is based on current medical literature and clinical guidelines but may not apply to your specific situation. Individual responses vary based on personal medical history and concurrent conditions. Always consult qualified healthcare providers for medical decisions. Never delay seeking medical care based on content you’ve read. If experiencing a medical emergency, seek immediate medical attention.

These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not to replace medical care.

In brief: Niacin raises HDL cholesterol — the “good” kind — more than any other available treatment, and for years it was prescribed on the assumption that doing so would protect the heart. That assumption was tested directly in more than 28,000 people across two large randomized trials. Niacin improved every cholesterol measure as expected but did not reduce heart attacks or strokes, and in the larger trial it caused measurable harm, including more new diabetes, serious infections, and bleeding. Major guidelines no longer recommend it for routine cardiovascular prevention, and one formulation was withdrawn from the European market. Niacin is not a supplement still awaiting evidence; it has been tested, and the results were negative.

Changed Every Number, Changed No Outcomes

Most supplements in this series share a problem: they move a biomarker, and no one has run the trial that would show whether that translates into fewer heart attacks. Niacin is the opposite case. The trial was run — twice, in more than 28,000 people — and the answer came back.

Niacin raises HDL cholesterol by 20 to 35%, a bigger move than any other treatment can produce, and it lowers triglycerides, LDL, and lipoprotein(a) as well. On paper that is a near-perfect lipid panel. For decades that logic drove millions of prescriptions, on the seemingly reasonable assumption that a number so strongly tied to heart disease must be worth changing. When the assumption was finally tested directly, niacin changed every number the hypothesis predicted and prevented none of the events the numbers were supposed to predict — and, in the larger trial, it caused measurable harm. Niacin is the starkest example in this series of a treatment that improved the lab report without helping the patient.

Find Your Situation

This table maps what the evidence supports for specific profiles; each row is examined below.

The Hypothesis That Made Sense

The reasoning was clean, and for a long time it looked airtight. Low HDL cholesterol predicts heart attacks; in observational data, each 1 mg/dL of higher HDL tracked with roughly 2 to 3% lower cardiovascular risk. (17) Niacin raises HDL more than anything available, so it should prevent heart attacks. That simple chain of logic drove prescribing for decades.

The flaw was not the biology. It was treating correlation plus a plausible mechanism as if it were proof. Decades of observational data, a coherent biological story, and a dramatic biomarker effect all pointed the same way; the one missing piece was the only one that ultimately settles the question — a randomized trial measuring the events the treatment was meant to prevent. Niacin belongs in the same company as the reversals Article 1 examined: B vitamins for homocysteine, antioxidant vitamins, the antiarrhythmic drugs in CAST, and hormone replacement in WHI. Each made biological sense, moved its marker the right way, and failed — or harmed — when finally tested. Niacin is the version most people have personally encountered, because the prescription was so common.

What Niacin Does to Lipids

Niacin is vitamin B3 (nicotinic acid), but its lipid effects appear only at doses far above anything nutritional. The recommended daily intake is about 14 to 16 mg; the doses used to alter lipids run from 1,000 to 3,000 mg — roughly a hundredfold higher. At nutritional doses niacin does nothing measurable to cholesterol. At these doses it is not acting as a vitamin; it is acting as a drug, and that distinction runs through the whole story.

At pharmacological doses, niacin raises HDL by 20 to 35% — the largest HDL increase any therapy produces, and its original selling point. It also lowers triglycerides by 20 to 50%, LDL by 10 to 20%, and lipoprotein(a) by 20 to 30% — and it remains one of the few agents that lowers Lp(a), a genetically set risk factor statins don’t touch. Whether lowering Lp(a) with niacin prevents events has never been shown, a point that matters for the narrow role niacin still retains. The mechanism spans several pathways: niacin curbs the liver’s output of VLDL (the triglyceride-rich precursors to LDL introduced in Article 4), reduces fatty-acid release from fat tissue, and slows HDL clearance. (7)

On paper, that comprehensive improvement looks like an ideal cardiovascular drug. That appearance is exactly what made the trial results so instructive: a lipid panel can improve in every direction while the disease underneath does not change at all. Niacin did not fail because it was weak — it failed despite being one of the most powerful lipid-modifying agents ever made. The failure was never about potency; it was about the target.

Why Raising HDL Didn’t Prevent Disease

Before the trials, the observational case looked overwhelming: higher HDL tracked with fewer events across populations, consistently enough to shape guidelines. But a correlation that strong can still be reporting something other than cause — and here it was. Low HDL travels with insulin resistance, inflammation, and visceral fat, the metabolic state that actually drives cardiovascular disease. HDL was largely reading that state, not creating protection. This is precisely the marker-versus-target distinction Article 3 was built around, and two independent lines of evidence exposed it.

The first is genetic. Mendelian randomization uses inherited gene variants as a natural experiment: if HDL were truly protective, people born with genetically higher HDL should have fewer heart attacks. A landmark 2012 Lancet analysis across more than 100,000 people tested exactly this, using a variant that raises HDL without disturbing LDL or triglycerides — and found no reduction in heart attacks, even though the genetic HDL increase predicted a 13% lower risk if HDL were causal. (3) The contrast with LDL is decisive: gene variants that lower LDL from birth do protect against heart disease, consistently. Inherited differences in HDL therefore behave as a marker of metabolic health rather than a cause of cardiovascular protection.

The second line is mechanistic, and it explains why raising the number didn’t help. HDL particles are functionally diverse: some efficiently pull cholesterol out of artery walls and return it to the liver (reverse cholesterol transport), and some do this poorly. Niacin raises the number of HDL particles without reliably improving how well they perform that job, so the particle count rises while the cholesterol-clearing work does not. Raising the HDL number need not change the disease the number was tracking.

The Trials: AIM-HIGH and HPS2-THRIVE

Two large randomized trials tested niacin in exactly the patients expected to benefit, on top of effective statin therapy.

AIM-HIGH (2011) enrolled 3,414 patients with established cardiovascular disease, low HDL, and high triglycerides — the textbook profile for HDL-raising therapy — all already on a statin, and added extended-release niacin (1,500 to 2,000 mg) or placebo. (1) The lipids moved as predicted: HDL rose 25% (from a median of 35 to 42 mg/dL), triglycerides fell 29%, LDL fell 12%. The events did not. After a mean of three years the trial was stopped early for futility, with cardiovascular events in 16.4% of the niacin group versus 16.2% on placebo (hazard ratio 1.02) — and a small, unexpected uptick in ischemic stroke in the niacin arm. (1) For every 100 patients given niacin on top of a statin, essentially the same number had events as on the statin alone.

HPS2-THRIVE (2014) was far larger: 25,673 patients with established vascular disease, all on effective statin therapy with a mean LDL of about 63 mg/dL, randomized to extended-release niacin combined with laropiprant (an anti-flushing agent) or placebo, and followed about four years. (2) Again the lipids moved — HDL up about 6 mg/dL, LDL down about 10 mg/dL — and again the events did not: major vascular events occurred in 13.2% of the niacin group versus 13.7% on placebo (rate ratio 0.96, 95% CI 0.90–1.03, P=0.29). This time the trial was large enough to see what smaller studies had missed: niacin caused harm.

The infection signal was not a fluke of one trial: AIM-HIGH independently showed more serious infections with niacin (8.1% vs 5.8%). (1) HPS2-THRIVE also recorded a small, non-significant 9% increase in death. (2) The results led directly to the withdrawal of extended-release niacin/laropiprant from the European market and to the manufacturer halting the product. (2) Adding niacin to a statin, in other words, improved the cholesterol panel and made patients no less likely to have a heart attack — while making them measurably more likely to develop diabetes, bleed, or be hospitalized for infection.

The Whole Drug Class Tested the Same Idea — and Mostly Failed the Same Way

Niacin’s failure could have been specific to niacin. So it is worth knowing that an entire separate drug class, built solely to raise HDL through a different mechanism, was put through the same test.

CETP inhibitors block an enzyme that shuttles cholesterol between lipoprotein particles, raising HDL substantially. Four large outcome trials followed. Torcetrapib (ILLUMINATE, 2007, ~15,000 patients) increased deaths and was halted — partly through off-target effects on blood pressure. (8) Dalcetrapib (dal-OUTCOMES, 2012, ~16,000) raised HDL about 30% with no effect on LDL — the cleanest test of HDL-raising alone — and reduced no events. (9) Evacetrapib (ACCELERATE, 2017, ~12,000) doubled HDL and lowered LDL by about a quarter, and still reduced no events. (11)

The fourth trial is the one that matters most for honesty. Anacetrapib (REVEAL, 2017, 30,449 patients) did modestly reduce major coronary events — by 9% (rate ratio 0.91, 95% CI 0.85–0.97). (12) But the trial investigators and subsequent analyses attributed that benefit to its lowering of LDL and non-HDL cholesterol, not to its large HDL increase. The lone success in the class came through the LDL pathway, not the HDL one — which is the rule, not the exception to it.

Put together: two niacin trials and four CETP trials — roughly 100,000 patients across five different HDL-raising drugs — plus the natural experiment of genetics in another 100,000. Every intervention raised HDL. Not one reduced cardiovascular events through HDL raising; the single positive trial worked by lowering LDL instead. This is no longer a hypothesis being adjudicated. The HDL-raising strategy has been tested about as thoroughly as any idea in modern cardiology, and it has not held up.

Where Guidelines Stand

For most supplements in this series, guidelines are silent — the products were never tested to the standard guidelines require. Niacin is the rare exception that had a place and lost it. For years, raising HDL with niacin was a recognized adjunctive lipid strategy, written into earlier guidance. The 2018 ACC/AHA cholesterol guideline removed it — not as a routine refresh but as a direct response to AIM-HIGH and HPS2-THRIVE — and current US and European guidelines do not recommend niacin for routine cardiovascular prevention, directing add-on therapy instead to agents with outcome evidence, such as ezetimibe and PCSK9 inhibitors. (5) The European Medicines Agency withdrew extended-release niacin/laropiprant from the market after HPS2-THRIVE. (2) In the United States, the FDA followed in 2016, withdrawing approval of the two niacin–statin combination products, Advicor and Simcor, after concluding that the evidence no longer supported the idea that raising HDL or lowering triglycerides in statin-treated patients reduces cardiovascular risk. (15) This is the only supplement in the series that held a guideline indication and had it taken away — a firmer verdict than never having had one. The removal is not an absence of evidence; it is the presence of evidence that the earlier recommendation was wrong.

The Case Some Specialists Still Make — and Its Limits

For evenhandedness, the contrary view deserves a fair hearing. A minority of lipid specialists argue niacin was retired too quickly. (6) Their strongest evidence is the Coronary Drug Project, the original niacin outcome trial: among 1,119 men who had survived a heart attack, niacin — given in the 1960s and 70s, before statins existed — significantly reduced nonfatal recurrent heart attacks compared with placebo (8.9% versus 12.2%), and a follow-up nine years after the trial ended found 11% fewer deaths among the men who had taken it. (13,14) They add that the modern trials gave niacin only to patients already at very low LDL on statins, leaving little room for further benefit, and that niacin’s unusual ability to lower Lp(a) keeps it relevant where options are few. The argument is not unreasonable, and it is why niacin has not disappeared entirely.

None of this overturns the conclusion for the question most people face. The Coronary Drug Project’s within-trial benefit was limited to nonfatal heart attacks; niacin did not reduce mortality during the trial itself, and the 11% mortality difference emerged only in an exploratory analysis years after the drug was stopped, in men who had no statin lowering their LDL to begin with. (13,14) The question today is different — whether niacin adds benefit on top of modern statin therapy — and in over 28,000 patients across two trials, the answer was no, with harm. (1,2) The “it might still work off statins” line is untested in the population where decisions are actually made. And the Lp(a) rationale runs into the same wall that defines this article: niacin lowers Lp(a), but no trial has shown that lowering Lp(a) with niacin prevents events. That leaves two genuinely narrow situations, both specialist-managed, not self-directed. In severe hypertriglyceridemia above roughly 500 mg/dL — where the immediate risk is pancreatitis, not just cardiovascular events — aggressive triglyceride lowering is warranted on its own terms, and niacin’s triglyceride effect can contribute when fibrates and prescription omega-3 are inadequate or not tolerated. And in very high Lp(a) with established disease, a few specialists consider niacin as a temporary measure while purpose-built Lp(a) therapies advance. Those investigational agents — the RNA-based drugs pelacarsen and olpasiran — lower Lp(a) by roughly 80% or more, far beyond niacin, and their cardiovascular outcome trials are expected to report in 2026; until they do, whether lowering Lp(a) reduces events remains unproven for any agent. Both niacin situations involve specialist oversight, monitoring for diabetes and liver toxicity, and explicit awareness that the cardiovascular benefit is unproven.

Safety: What the Large Trials Revealed

Niacin’s full risk profile only became clear once trials grew large enough to detect it. (4)

The most important signal is metabolic. Niacin worsens insulin resistance and raises blood glucose; HPS2-THRIVE found a 32% relative increase in new diabetes (HR 1.32) — about 13 extra cases per 1,000 over four years — and worse control among those who already had diabetes. (2,10) Because low HDL and insulin resistance travel together, the people most likely to be offered niacin are often the very people most exposed to this harm.

Beyond glucose: niacin can inflame the liver, particularly in sustained-release form, so liver function warrants monitoring at these doses; the over-the-counter sustained-release products are a poor middle ground, trading a little less flushing for retained liver risk without clinical supervision. (4) Niacin raises uric acid and can precipitate gout. (4) Combined with a statin it adds to muscle-related risk — relevant because the population historically considered for niacin is already on a statin. (2,10) And HPS2-THRIVE surfaced the harms no one had expected: a 38% relative increase in serious bleeding and a 22% relative increase in serious infections, neither anticipated from the smaller, earlier studies. (2,10)

Recent work may help explain why a drug that improved the lipid panel so thoroughly delivered so little. A 2024 analysis identified a terminal breakdown product of niacin, called 4PY, that forms when the body processes excess niacin; higher blood levels of it tracked with more cardiovascular events across several cohorts, and in laboratory models 4PY directly drove inflammation in blood-vessel walls. (16) This is association and mechanism rather than an outcome trial, and it should be read as an emerging hypothesis, not settled fact — but it offers a biologically plausible account of niacin’s long-standing paradox: a treatment that lowers LDL yet yields less benefit than that lowering predicts, as if an offsetting harm were at work.

The Forms, and the “No-Flush” Problem

Niacin’s tolerability is its other practical obstacle, and it doubles as a guide to which products do anything at all. Within 30 to 60 minutes of a pharmacological dose, most people flush intensely — warmth, redness, and itching across the face and upper body, like a sunburn from the inside. It is caused by a release of prostaglandins (which is why aspirin, which blocks that pathway, blunts it). It eases somewhat with continued use but rarely disappears, and roughly 20 to 40% of people stop niacin within the first year largely because of it.

That flush is also a tell. The product marketed as the gentle alternative — “no-flush” niacin, or inositol hexanicotinate — doesn’t flush because it doesn’t engage niacin’s pathways; in clinical studies it does not lower LDL or raise HDL. It is, on lipids, inactive: the absence of flushing is not a feature but a signal that nothing pharmacological is happening. This is the exact product-versus-label gap Article 2 mapped — the bottle says “niacin,” but the molecule inside doesn’t behave like the niacin the trials studied.

The practical reading: a niacin product that doesn’t cause flushing isn’t affecting your lipids, and a dose kept deliberately low to avoid flushing isn’t either. Pharmacological niacin requires flushing doses — and even at those doses, two large trials found no cardiovascular benefit in statin-treated patients, alongside measurable harm. (1,2)

Two Example Patients

Both are composites — not real individuals — built from the populations and trials reviewed here, meant to show how the evidence applies, not to direct any reader’s decision.

Patient A is 64, started on extended-release niacin twelve years ago for low HDL, on a statin, with an HbA1c of 6.1% (prediabetes), no cardiovascular events, refilling the niacin without active review since his original prescriber retired; he read about HPS2-THRIVE and asks his physician about it. His situation sits close to the profile the evidence treats least favorably: the indication he started on — raising HDL for protection — is no longer supported, (1,2,5) and his prediabetes places him squarely in the group most exposed to niacin’s diabetes signal. (2) Whether to continue is a question for him and his physician, ideally with a follow-up lipid panel and HbA1c to document the change; if niacin is stopped, the lipid numbers will drift back — HDL down, LDL and triglycerides up — and the trials indicate those reversals do not translate into worse outcomes, because the lipid movement was not producing protection to begin with. (1,2)

Patient B is 58, with a heart attack five years ago, on a statin and ezetimibe with LDL of 58 mg/dL, recently found to have an Lp(a) of 220 nmol/L (very high), under a lipidologist’s care and weighing niacin as a temporary bridge toward an Lp(a)-lowering trial. Hers is the narrow, specialist-managed exception. Niacin lowers Lp(a) by 20 to 30%, but whether that lowering reduces her risk has not been shown, and her specialist has framed it in exactly those terms; the purpose-built Lp(a) therapies in late-stage trials are designed to produce the outcome data niacin lacks. For her, any use of niacin is a bridge under specialist oversight, with monitoring for diabetes and liver function and explicit awareness that the benefit is unproven. The product is the same as Patient A’s. The situations, and what the evidence supports, are not.

Common Misconceptions

“Higher HDL is always better.” Not as a target. Genetically elevated HDL does not protect against heart disease, (3) and pharmacologically elevated HDL did not protect either, across two niacin trials and four CETP trials. (1,2,8,9,11,12) HDL is a marker of metabolic health, not a lever to pull.

“No-flush niacin is gentler niacin.” It isn’t niacin in any pharmacological sense. It doesn’t flush because it doesn’t do what niacin does; it is an inactive product whose appeal depends on the absence of an effect.

“Niacin is a vitamin, so it must be safe.” At nutritional doses (14 to 16 mg) it is a vitamin and is safe. At lipid doses (1,000 to 3,000 mg) it is a drug, with drug-level effects and drug-level harms — more diabetes, bleeding, infection, and liver risk. (2,4) The word “vitamin” on the label doesn’t change the pharmacology of a hundredfold-higher dose.

“My HDL is low, so I should raise it.” Low HDL is a signal, not a target. Guidelines and the trial evidence point toward treating the underlying metabolic state — the insulin resistance, weight, and inactivity that produce a low HDL — rather than pushing the number up directly.

“Niacin must do something if it changes lipids so dramatically.” That exact intuition is what two large randomized trials tested, and the answer was no. (1,2) A dramatic change in the lipid panel is not the same as cardiovascular protection, and niacin is the most thoroughly tested proof of that point.

“The trials only studied statin-treated patients, so niacin might still help people not on statins.” This has been raised, but it is untested in modern practice, where decisions are made about adding therapy on top of a statin. In that setting — over 28,000 patients, two large trials — niacin added no benefit and caused harm. (1,2)

The Bottom Line

Niacin is one of cardiovascular medicine’s most instructive lessons. The hypothesis was reasonable, the biology real, the observational data consistent across decades, the prescriptions written in the millions. Then it was tested properly, in more than 28,000 patients — and it failed, not neutrally but with harm: more diabetes, more serious infection and bleeding, more myopathy, no fewer heart attacks. (1,2,10) The lipid effects were genuine. The protection was not.

The arc across Articles 4 through 8 is now complete. Omega-3 has one formulation with an FDA cardiovascular drug approval. CoQ10 has one positive heart-failure trial, never replicated. Plant sterols and soluble fiber carry biomarker-based health claims with no outcome trials of their own — though fiber’s pathway has drug-class validation through cholestyramine. Niacin is unlike all of them: it was tested directly, at full scale, in the right patients, and the result was negative. Of every supplement in the series so far, niacin has the most cardiovascular outcome evidence — and that evidence says no.

The hypothesis was generated from a biomarker correlation, tested in large randomized trials, and revised in the guidelines once the results were in. (5) Many people started niacin years ago in good faith, on evidence that has since been overturned, which is why any individual change is a conversation with the prescribing clinician rather than a decision made from an article — and why, on a complex regimen, stopping abruptly on one’s own is not advisable. The broader point is concrete: a large change in a cholesterol number is not the same as protection from a heart attack, and niacin is the clearest demonstration of that distinction in cardiovascular medicine. When a product promises cardiovascular benefit on the strength of a number alone, niacin is the reason that promise needs direct proof.

Article 9 turns to red yeast rice — a supplement that contains a chemically identical version of a prescription statin, can lower LDL substantially, and carries the same risks as the drug it came from, but without the dose consistency or oversight that a prescription provides.

Key Terms

AIM-HIGH. A randomized trial of 3,414 patients, stopped early for futility, showing no cardiovascular benefit from adding niacin to a statin despite meaningful lipid changes.

CETP (cholesteryl ester transfer protein). An enzyme that moves cholesterol between lipoprotein particles. Drugs blocking it raise HDL substantially; across four large trials, only the one that also lowered LDL meaningfully reduced events — and through that LDL effect, not HDL.

HDL (high-density lipoprotein). Often called “good cholesterol.” Higher HDL correlates with lower risk in observational data, but raising it pharmacologically has not reduced events. The correlation reflects metabolic health; it does not establish cause.

HMG-CoA reductase. The rate-limiting enzyme in cholesterol synthesis that statins block to lower LDL — a different mechanism from niacin’s HDL effect.

HPS2-THRIVE. A randomized trial of 25,673 patients showing no cardiovascular benefit and significant harm from adding niacin to a statin; results led to the European market withdrawal of extended-release niacin/laropiprant.

Inositol hexanicotinate (“no-flush niacin”). A form that does not flush and does not meaningfully affect HDL or LDL — pharmacologically inactive at lipid endpoints.

Lipoprotein(a) [Lp(a)]. A genetically determined particle that raises cardiovascular risk independently of LDL and does not respond to statins. Niacin lowers it, but whether that lowering prevents events is unproven.

Mendelian randomization. A method using inherited gene variants as natural experiments to test causation. Variants raising HDL from birth do not protect against heart disease, indicating HDL is a marker rather than a cause.

Niacin (vitamin B3, nicotinic acid). A B vitamin that, at doses roughly a hundredfold above nutritional needs, substantially alters lipids. At nutritional doses it has no meaningful lipid effect.

Niacin flush. Intense prostaglandin-mediated flushing and itching — the main tolerability barrier. Its absence in “no-flush” products signals absence of lipid activity, not better tolerability.

Reverse cholesterol transport. HDL’s proposed protective job: extracting cholesterol from artery walls and returning it to the liver. Niacin raises HDL particle numbers without reliably improving how well they perform this.

Surrogate endpoint. A measurable stand-in (such as HDL level) for a clinical outcome (such as a heart attack). The niacin trials are cardiovascular medicine’s clearest demonstration that improving a surrogate need not improve outcomes.

VLDL (very-low-density lipoprotein). Triglyceride-rich particles made by the liver and converted to LDL; niacin reduces their production, part of how it changes lipids.

References

1. AIM-HIGH Investigators. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011;365(24):2255–2267.
2. HPS2-THRIVE Collaborative Group. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med. 2014;371(3):203–212.
3. Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet. 2012;380(9841):572–580.
4. Guyton JR, Bays HE. Safety considerations with niacin therapy. Am J Cardiol. 2007;99(6A):22C–31C.
5. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC guideline on the management of blood cholesterol. J Am Coll Cardiol. 2019;73(24):e285–e350.
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10. HPS2-THRIVE Collaborative Group. Serious adverse effects of extended-release niacin/laropiprant: results from HPS2-THRIVE. Am Heart J. 2019;217:55–66.
11. Lincoff AM, Nicholls SJ, Riesmeyer JS, et al. Evacetrapib and cardiovascular outcomes in high-risk vascular disease (ACCELERATE). N Engl J Med. 2017;376(20):1933–1942.
12. HPS3/TIMI55–REVEAL Collaborative Group; Bowman L, Hopewell JC, Chen F, et al. Effects of anacetrapib in patients with atherosclerotic vascular disease. N Engl J Med. 2017;377(13):1217–1227.
13. Coronary Drug Project Research Group. Clofibrate and niacin in coronary heart disease. JAMA. 1975;231(4):360–381.
14. Canner PL, Berge KG, Wenger NK, et al. Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin. J Am Coll Cardiol. 1986;8(6):1245–1255.
15. AbbVie Inc.; Withdrawal of Approval of New Drug Applications for ADVICOR and SIMCOR. 81 Fed. Reg. 22608 (April 18, 2016).
16. Ferrell M, Wang Z, Anderson JT, et al. A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. Nat Med. 2024;30(2):424–434.
17. Gordon DJ, Probstfield JL, Garrison RJ, et al. High-density lipoprotein cholesterol and cardiovascular disease: four prospective American studies. Circulation. 1989;79(1):8–15.

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