Why Niacin Is No Longer Used for Heart Disease

Niacin, Cholesterol, and the Hard Lessons of Cardiovascular Outcomes

For decades, niacin (vitamin B3) was widely promoted as a treatment for cholesterol problems and cardiovascular disease. The logic seemed straightforward: niacin improves lipid numbers—lowering LDL cholesterol and triglycerides while significantly raising HDL cholesterol—so it must protect the heart.

Today, we know that logic was flawed.

Despite improving cholesterol measurements, niacin does not reduce heart attacks, strokes, or mortality. Worse, it can cause meaningful harm. As a result, niacin is no longer recommended in modern cardiovascular guidelines.

This article explains why.

The Niacin Myth: “Fix Your Lipids, Fix Your Heart”

One of the most persistent claims online is that niacin can fix cholesterol and improve heart health.

Niacin is a naturally occurring B vitamin, and at pharmacologic doses it can:

• Lower LDL-C
• Lower non-HDL-C
• Lower LDL particle number (LDL-P)
• Lower apolipoprotein B (apoB)
• Raise HDL-C

The assumption is that these changes must reduce cardiovascular risk.

They don’t.

Niacin Improves Lab Numbers — Not Patient Outcomes

Yes, niacin reliably raises HDL cholesterol and lowers LDL cholesterol.

But across multiple large human outcomes trials:

• Not a single heart attack was prevented
• Not a single stroke was prevented
• No reduction in cardiovascular or all-cause mortality
• No lives were saved

In cardiology, outcomes—not theories or surrogate markers—determine whether a treatment works.

Niacin Failed Every Major Cardiovascular Outcomes Trial

Niacin has been rigorously tested. The results were consistent—and disappointing.

Coronary Drug Project (1975)

One of the earliest large randomized trials:

• After 5 years, mortality was higher in the niacin group
• Death rates: 21.2% with niacin vs 20.9% with placebo

Even in the pre-statin era, niacin failed to demonstrate benefit.

AIM-HIGH Trial (2011)

Studied niacin added to statin therapy in patients with:

• Low HDL-C
• High triglycerides
• Established atherosclerotic cardiovascular disease (ASCVD)

Results:

• No reduction in cardiovascular events
• Higher stroke rates in the niacin group (absolute numbers were low but concerning)
• Trial stopped early for futility

HPS2-THRIVE Trial (2014)

The definitive trial.

Over 25,000 high-risk patients were randomized to niacin plus statin therapy versus statin alone.

Results:

• No reduction in heart attacks
• No reduction in strokes
• No reduction in mortality
• Significant increases in serious adverse events, including diabetes, infection, bleeding, and liver toxicity

At that point, the evidence was unequivocal.

Surrogate Markers Don’t Save Lives

Niacin’s rise and fall underscores a critical lesson in medicine:

Improving lab values does not guarantee improved health.

Small angiographic or surrogate-endpoint studies once suggested benefit. But when hard outcomes were tested, niacin failed.

That is why:

• Niacin is not recommended in any contemporary ASCVD guideline
• FDA approval for niacin–statin combinations was withdrawn
• No professional cardiovascular society endorses its routine use
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Niacin Can Cause Metabolic and Systemic Harm

Niacin is not a benign vitamin at pharmacologic doses.

One particularly telling adverse effect is acanthosis nigricans:

• Darkening and thickening of skin folds (neck, axillae)
• A finding pathognomonic for insulin resistance
• Strongly associated with type 2 diabetes

If acanthosis nigricans is present, metabolic injury has already occurred.

Additional documented adverse effects include:

• Severe flushing and itching
• Rash
• Gastric ulcers
• Hepatotoxicity
• Cardiac arrhythmias
• Worsening glycemic control and new-onset diabetes

In large trials, patients taking niacin were far more likely to discontinue therapy due to side effects.

Niacin Can Make HDL Dysfunctional

Niacin also exposed a fundamental flaw in the long-held “HDL hypothesis.”

While niacin raises HDL-C levels, it has been shown to adversely alter the proteome of HDL particles, rendering them dysfunctional.

This means:

• HDL cholesterol levels may increase
• HDL function may worsen
• Dysfunctional HDL may become more atherogenic, not protective

This helps explain why raising HDL-C with niacin did not improve cardiovascular outcomes.

📖 Reference:
https://www.ahajournals.org/doi/10.1161/ATVBAHA.121.316278

What Happened to Niaspan?

To reduce flushing seen with immediate-release niacin, extended-release niacin (Niaspan) was developed and later acquired by Abbott.

For a time, it was widely prescribed.

Then:

• AIM-HIGH failed
• HPS2-THRIVE failed
• Niacin was removed from guidelines
• Insurance coverage disappeared

Although Niaspan technically remains available, no third-party payer covers it, and it has no meaningful role in modern cardiovascular care.

Believe Outcomes Over Surrogate Endpoints

A landmark editorial in Circulation summarized niacin’s failure succinctly:

“Niacin: Time to Believe Outcomes Over Surrogate Outcomes — If Not Now, When?”

📖 Full article:
https://www.ahajournals.org/doi/full/10.1161/CIRCOUTCOMES.116.003094

This principle now defines evidence-based cardiology.

Final Clinical Bottom Line

Niacin:

• Improves cholesterol numbers
• Does not prevent heart attacks or strokes
• Does not reduce mortality
• Increases metabolic and systemic risk
• Increases inflammation
• Has failed every modern cardiovascular outcomes trial

That is why niacin is no longer recommended for the prevention or treatment of cardiovascular disease.

Modern cardiology is outcomes-driven—and niacin simply does not meet that standard.