Niacin dosage and evidence
Written by Aaron CuhaReviewed Sep 2026
The short answer
Niacin is the only NAD-pathway product ever tested against real heart outcomes, in 25,673 people in HPS2-THRIVE and 3,414 in AIM-HIGH.
Evidence grade for Niacin: Strong. The rule: at least two finished studies in people, and at least 1,000 people who took it. The sum on this page: 2 completed trials, 29,087 people given it. A grade counts how much has been done to people, not whether it works.
- People given it
- 29,087
- Human studies
- 2
- Found nothing
- 0
Dose
Approved medicine. No human dose established for unlabelled uses
Labeled amounts sit on the prescribing information. This page records what trials measured, not a personal dose.
Slow-release nicotinic acid is an FDA-approved prescription cholesterol drug in the United States. But doctors mostly stopped using it after two large studies, AIM-HIGH and HPS2-THRIVE. Lower-dose nicotinic acid is also sold over the counter as a supplement. The mix of slow-release niacin and laropiprant tested in HPS2-THRIVE was pulled from sale worldwide after that study reported.
7 effects reported, 5 unwanted, 2 wanted, by people using it, not a trial
Goal pages: Ageing and longevity, Heart and circulation
In plain English
In plain English, from Aaron
This is how I would explain it to a friend. The evidence, with the numbers, is further down the page.
Niacin is the acid form of vitamin B3. It raises good cholesterol and lowers bad cholesterol and blood fats. It also makes your skin flush hot and red. It is sold as a supplement and was once a big prescription heart drug.
What people take it for
- Better cholesterol numbers.
- Preventing heart attacks.
- Raising NAD for longevity.
What studies in people showed
Two huge studies tested it on top of a statin. In 25,673 people, heart attacks and strokes came out about the same: 13.2 percent on niacin and 13.7 percent on a dummy pill. It also caused extra diabetes, infections and bleeding. In 3,414 people, it was 16.4 percent against 16.2 percent, and the study was stopped early. The cholesterol numbers moved just as hoped. The patients got no benefit. An old study from before statins found fewer deaths 15 years later. That was seen by watching afterwards, not by the study itself.
What people report
Reports, not study results
The good
- The flush eases for most people over weeks to months.
- Taking it with food, aspirin beforehand, and skipping alcohol and hot showers around the dose all help with the flush.
The bad
- The flush is a hot, itchy blush that lasts under about twenty minutes. For some people it never eases.
- Some people describe severe reactions, scary enough to start threads about.
- Liver strain is the main worry, mostly tied to slow-release forms.
- Blood sugar can rise a little.
- Flush-free forms are widely described as doing nothing.
Where these come from: Niacin threads on LongeCity and a heart health thread on ExcelMale, as collected for this page. The heart numbers are from the studies on this page.
My bottom line
Better numbers, no fewer heart attacks, and real harm in the biggest study. If your cholesterol needs work, get your blood work and talk to your doctor. Do not self-dose grams of this.
An opinion, not a finding. I am a coach, not a doctor.
What it has been measured to do
Measured in people
Goals Niacin has been tested for in people, biggest studies first. We count only what the studies on this page say, so the real numbers may be higher.
- Cholesterol and blood fats29,087 people · 2 studies
- Heart attacks and strokes9,503 people · 2 studies · 1 found nothing
- Living longer8,341 people · 1 study · 1 found nothing
What people using it report
Real people telling you what happened to them. Nobody checked it, and the people who post are not a fair sample, so it cannot prove anything works. It is still the best guide on this page to what people actually do with Niacin, what they expect, and what goes wrong. The full account, including the negative reports, is below.
33 of the 36 indexed goals have no study of any kind behind Niacin
No study in people, animals or cells on this page reports a result for these. That does not prove Niacin does nothing for them. It does mean anything you have heard about Niacin and one of these did not come from a study cited here.
Show full evidence
What is Niacin?
Niacin is the only NAD-pathway product ever tested against real heart outcomes, in 25,673 people in HPS2-THRIVE and 3,414 in AIM-HIGH. It moved every blood fat it was meant to move. It prevented no heart attacks or strokes in either study. In HPS2-THRIVE it caused extra serious side effects, including infections and bleeding.
If you want to see why a moving blood number is not proof, study this one. Nothing else sold for longevity has been tested this hard against outcomes that matter. The answer came back twice.
Nicotinic acid, usually called niacin, raises good cholesterol. It lowers triglycerides and bad cholesterol too. It does this reliably, and doctors have known that since the 1950s. For decades it was the standard answer to low good cholesterol. The thinking was that good cholesterol protects, so raising it should protect.
AIM-HIGH tested that in 3,414 people who already had heart and artery disease. All were on simvastatin, plus ezetimibe if needed. They took slow-release niacin at 1500 to 2000 mg a day, or a dummy pill. Niacin raised good cholesterol from 35 to 42 mg/dL on average. It dropped triglycerides from 164 to 122 mg/dL and bad cholesterol from 74 to 62 mg/dL. The study was stopped after about 3 years because it clearly was not working. Heart attacks, strokes and related events hit 16.4 percent on niacin and 16.2 percent on the dummy pill.
HPS2-THRIVE was seven times bigger. 25,673 adults with artery disease, all on a statin, took 2 g of slow-release niacin with 40 mg of laropiprant, or a dummy pill, for about 3.9 years. Laropiprant was added only to stop the flushing. Bad cholesterol was 10 mg/dL lower and good cholesterol 6 mg/dL higher on niacin. Major heart and artery events hit 13.2 percent on niacin and 13.7 percent on the dummy pill. That gap was too small to mean anything.
Then comes the part that usually gets left out. Niacin with laropiprant caused extra harm. Out of every hundred people, it added 3.7 serious upsets in blood sugar control, 1.3 new cases of diabetes, 1.0 serious stomach problems, 0.7 muscle and joint problems and 0.3 skin problems. And, unexpectedly, 1.4 infections and 0.7 bleeds. A drug that raises good cholesterol beautifully, prevents nothing, and causes serious harm in big numbers is the most useful lesson in this whole field.
How does Niacin work?
Niacin gets turned into NAD by its own route, called the Preiss-Handler pathway, not the NAMPT recycling route. That is why it is a strong NAD booster. A 2026 study in people suggested gut bacteria may turn NR and NMN into niacin, and that this may be how those two pricey products work at all. Niacin's effect on blood fats is separate. It mainly slows the release of fat from fat cells and slows fat-making in the liver. So less fat flows to the liver, and the liver sends out fewer fat-carrying particles. The flush is a third, separate action. Niacin switches on a receptor called GPR109A on immune cells in the skin. They release chemicals called prostaglandins that open up the skin's blood vessels. Work in mice with genes switched off proved each link in that chain. The laropiprant in HPS2-THRIVE blocked one of those prostaglandins to stop the flush. It stopped the flush and did nothing for the outcomes.
What have studies in people found about Niacin?
By far the biggest body of human evidence of anything in the NAD pathway. On the outcomes that matter, it is overwhelmingly negative. About 29,000 people took part in two modern studies. Both found nothing, and one found overall harm.
- HPS2-THRIVE, 25,673 people, about 3.9 years: major heart and artery events hit 13.2 percent on niacin and 13.7 percent on the dummy pill. Too close to call.
- HPS2-THRIVE harms, per hundred people: 3.7 more serious blood sugar upsets in diabetes, 1.3 more new cases of diabetes, 1.4 more infections and 0.7 more bleeds. All clearly more than chance would explain.
- Coronary Drug Project, 8,341 men, before statins existed: 15 years later, 52.0 percent of the niacin group had died, against 58.2 percent on the dummy pill. That is 11 percent fewer deaths. It was seen nearly 9 years after the drug stopped, by watching afterwards.
- AIM-HIGH, 3,414 people, about 3 years, stopped early because it was going nowhere: heart attacks, strokes and related events hit 16.4 percent on niacin and 16.2 percent on the dummy pill.
- In both modern studies the blood fats moved exactly as expected. Good cholesterol up, triglycerides down, bad cholesterol down. The numbers worked perfectly and the patients got no benefit.
- Niacin is a strong NAD booster by its own route. A 2026 study in people suggested it may be the real way NR and NMN raise NAD in the body.
What this does not tell you: AIM-HIGH and HPS2-THRIVE both added niacin on top of a statin that was already working. So they answer whether niacin adds anything to modern treatment, and the answer is no. They do not test niacin on its own in someone untreated. That hardly ever happens in real care anymore anyway. The HPS2-THRIVE harms came from niacin combined with laropiprant, so laropiprant cannot be fully ruled out as part of the cause. But the harms fit what niacin is already known to do to blood sugar. The 4PY work comes from watching people, and it does not prove that taking niacin causes heart events.
What do people who took Niacin report?
This is what real people say happened to them, good and bad. Nobody measured it. A report cannot tell a real effect from the lift people get just from expecting it to work, from a diet or training change made at the same time, or from what was really in the vial. We still put it near the top. It is the next best thing to a study in people: what happens when real people use it, including what goes wrong.
- Two things dominate: the flush, and the split between preparations.
- Immediate release is described as flushing reliably, with people starting around 250 to 500 mg and some describing gram amounts continued for years. The flush is described as a hot itchy blush lasting under about twenty minutes, and most people report it easing over weeks to months, although threads exist from people for whom it never did.
- Management tactics repeat across threads: taking it with food, water immediately after, aspirin beforehand, and avoiding alcohol and hot showers around the dose.
- Severe reactions are described, alarming enough that people started threads about them, and the pattern in the replies is others saying they have had milder versions of the same thing.
- The liver is the concern raised most seriously, and the distinction people draw is between sustained release preparations, which are the ones they associate with toxicity, and short exposure from immediate release, which they treat as lower risk. Transient enzyme elevation at higher intakes is discussed as expected rather than surprising.
- A small rise in blood sugar is mentioned, usually described as settling over months, with people managing diabetes told to involve a clinician.
- Flush free preparations are widely described as doing nothing, and at least one long-term high dose user reports years of use without the change in blood fats he was taking it for.
Sources: Niacin threads in the LongeCity supplements forum and a heart health thread on ExcelMale, found by site-restricted search, September 2026. Nothing above is attributed to any specific post and no post is reproduced.
The state of the research
This is the worked example the rest of the NAD pathway should be read against.
Niacin raises good cholesterol. In every study that simply watches people, higher good cholesterol goes with lower heart risk. So raising it ought to cut risk. For three decades that idea was treated as close enough to proven that niacin sat in the guidelines because of it. Then two large studies with a dummy pill group tested the idea head on. Both found that the blood fats changed exactly as expected, and heart events did not change at all. The bigger study found that patients were actually harmed.
Every product on this pathway is sold on the same kind of reasoning. Blood NAD falls with age. Blood NAD goes with good health. So raising blood NAD should help. That reasoning has never been tested against a real health outcome for any NAD booster. The one time the same kind of reasoning was tested at scale in this exact vitamin family, it failed twice and caused overall harm once.
The 4PY finding adds a further twist. When the body has more niacin than it needs, it breaks it down into end products. People with more of those end products had more heart events, and more of a marker of inflamed blood vessels. Gene data backs up the link. That does not prove niacin supplements cause heart events. But it is a clear, testable idea that more of this vitamin than the body needs is not harmless.
Almost all consumer writing about this pathway blends three kinds of claim into one. Keeping them apart is most of the work. A blood marker claim says a product raises NAD in the blood. That is easy to show, and for several of these products it is simply true. A middle claim says it moves something between a blood marker and a symptom, such as how stiff the arteries are. A health claim says a person walks further, remembers more, gets fewer cancers or lives longer. A product can be solid on the first kind and have nothing at all on the third. That is where most of this pathway sits. No published study in people of any NAD booster has shown a real health benefit, with one exception on this list. That exception is nicotinamide in skin cancer. It works by helping sun-damaged skin repair its DNA, not through anything to do with ageing.
The evidence, in charts
Fig. 1a · how many people
38,590people, across 4 studies in people cited here
| Study | People | Share |
|---|---|---|
| HPS2-THRIVE, New England Journal of Medicine 2014 | 25,673 | 67% |
| Journal of the American College of Cardiology 1986 | 8,341 | 22% |
| AIM-HIGH, New England Journal of Medicine 2011 | 3,414 | 9% |
| Nature Medicine 2024 | 1,162 | 3% |
One study holds 67% of these people, so the total rests more on one study than its size suggests. Counts are the number of people each study on this page says it signed up. That includes studies that only watched people and gave nobody the compound. 1 more study in people gives no headcount and is not counted here. Studies still signing people up are left out, and only studies cited on this page are counted.
Fig. 1b · evidence mix
5 of 6 sources here are studies in people. The rest is not.
- Study in people · done in people583%
- Animal study · done in animals117%
Counted from the list of sources on this page. It counts only what we cite, so there may be more studies out there. A review counts once, however many studies it sums up.
Fig. 2 · evidence over time
The studies cover 6 different years, 1986 to 2024, counted from the list of sources on this page.
Fig. 3 · legal status at a glance
US
Approved
UK
Not approved
AU
Prescription
CA
Prescription
Approved in 1 of 4, by prescription in 2, not approved in 1. This is what the law says, not a verdict on the science. See Legal status below for the full text and any notes.
Fig. 5 · what the molecule is
- Kind of compound
- Supplement
- Molecule weight
- 123.1 Da
- Half-life
- Stated in words, not a numbersee the exact wording below
- Chain length
- None on file
Half-life as stated on file: Under an hour for immediate-release nicotinic acid. Extended-release formulations were built specifically to stretch that out and blunt the flush, and the dose is not interchangeable between forms.
No amino acid sequence is on file for Niacin, which is expected: a supplement is not built from amino acids.
The studies we cite
- Study in people2011Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy
Niacin improved the blood numbers and did nothing for patients already on a statin. 3,414 people with established artery disease took slow release niacin or a dummy pill on top of their statin. Good cholesterol rose, triglycerides fell and bad cholesterol fell. Heart attacks, strokes and cardiac deaths came out identical, about 16 in every hundred in each group. The trial was stopped after about three years because it was clearly going nowhere. Funded by a government institute and by Abbott.
AIM-HIGH, NCT00120289. 3,414 patients with established atherosclerotic cardiovascular disease and LDL below 70 mg/dL, randomised to extended-release niacin 1500 to 2000 mg daily (n=1718) or placebo (n=1696), all on simvastatin plus ezetimibe as needed. Stopped after a mean of 3 years for lack of efficacy. Niacin raised median HDL from 35 to 42 mg/dL, lowered triglycerides from 164 to 122 mg/dL and lowered LDL from 74 to 62 mg/dL. The primary composite endpoint occurred in 282 niacin patients (16.4 percent) and 274 placebo patients (16.2 percent), hazard ratio 1.02 (95 percent CI 0.87 to 1.21, P=0.79). Funded by the National Heart, Lung, and Blood Institute and Abbott Laboratories.
- Study in people2014Effects of extended-release niacin with laropiprant in high-risk patients
Niacin failed on top of a statin and it harmed people. 25,673 adults with vascular disease took niacin with laropiprant or a dummy pill for close to four years. Cholesterol numbers moved the right way. Major vascular events did not, at about 13 in every hundred in each group. Treatment caused extra diabetes, extra serious blood sugar upsets, and extra stomach, muscle and skin problems, plus unexpected extra infections and bleeding. A trial this size would have found a benefit if there was one. Funded by Merck among others.
HPS2-THRIVE, NCT00461630. 25,673 adults with vascular disease on statin-based therapy randomised to 2 g extended-release niacin with 40 mg laropiprant or placebo for a median of 3.9 years. LDL was 10 mg/dL lower and HDL 6 mg/dL higher on treatment. Major vascular events occurred in 13.2 percent versus 13.7 percent, rate ratio 0.96 (95 percent CI 0.90 to 1.03, P=0.29). Treatment caused absolute excesses in serious disturbances of diabetes control (3.7 percentage points, P<0.001), new diabetes diagnoses (1.3 points, P<0.001), serious gastrointestinal events (1.0 point), musculoskeletal events (0.7 point), skin events (0.3 point), and unexpectedly infection (1.4 points) and bleeding (0.7 points). Funded by Merck and others.
- Study in people2013HPS2-THRIVE randomized placebo-controlled trial in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment
This is the design paper, and it matters because of who was left out. Before the main trial began, everyone went through a trial run and anyone who could not tolerate slow release niacin was dropped. The people who made it in were already the ones who could handle the drug. The extra harms reported a year later happened even in that hand picked group. The paper also sets out the muscle and liver checks and the reasons people stopped taking it.
The design and tolerability paper, published a year before the main result. It documents the pre-randomisation run-in used to exclude people who could not tolerate extended-release niacin, which means the main trial population was already enriched for tolerance and the adverse event excess reported later occurred despite that enrichment. Also reports the pre-specified muscle and liver outcomes and the reasons participants stopped study treatment.
- Study in people1986Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin
This is the study niacin's reputation rests on, and it is weaker than the reputation. 8,341 men who had already had a heart attack were treated between 1966 and 1975, long before statins existed. During the trial, niacin slightly cut repeat heart attacks and did not cut deaths at all. Fifteen years later, almost nine years after everyone had stopped, about 52 in every hundred niacin men had died against 58 on the dummy. That gap was found by watching afterwards, not by the trial itself.
The historical result that kept niacin in the guidelines for thirty years, and it is weaker than its reputation. In the Coronary Drug Project, 8,341 men aged 30 to 64 with a previous myocardial infarction were treated between 1966 and 1975. Niacin modestly reduced definite non-fatal recurrent myocardial infarction but did not reduce total mortality during the trial. At a mean follow-up of 15 years, nearly 9 years after the drug was stopped, all-cause mortality was 52.0 percent on niacin versus 58.2 percent on placebo, 11 percent lower, P=0.0004. This is a post-trial observational mortality difference in a pre-statin population, not a result obtained on top of modern therapy, and both AIM-HIGH and HPS2-THRIVE tested niacin on top of modern therapy and found nothing.
- Study in people2024A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk
A waste product of excess niacin is linked to more heart trouble, which would explain why taking more does not help. Researchers measured blood chemicals in over four thousand heart patients across three separate groups. People carrying the most of two niacin waste products had roughly twice the risk of a heart attack, stroke or cardiac death over three years. A gene tied to those chemicals also tracked with a marker of inflamed blood vessels. Nobody was given anything here, so this is a strong suspicion and not proof.
Observational metabolomics rather than a trial, and it proposes a mechanism for why more niacin might be actively unhelpful. In a discovery cohort of 1,162 stable cardiac patients and validation cohorts of 2,331 US and 832 European patients, serum levels of the terminal metabolites of excess niacin, 2PY and 4PY, were associated with increased 3-year risk of major adverse cardiovascular events: for 4PY, adjusted hazard ratios of 1.89 (95 percent CI 1.26 to 2.84) and 1.99 (1.26 to 3.14). A genetic variant associated with both metabolites was also associated with soluble VCAM-1 in a meta-analysis of about 106,000 people. This is association plus a mechanistic hypothesis, not causal proof in humans.
- Animal study2005GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing
In mice. Mice missing the flush receptor did not flush when given niacin. Mice missing certain other enzymes and receptors flushed less or not at all. Giving the receptor-less mice bone marrow from normal mice brought the flush back. That showed the receptor sits on immune cells in the skin.
Mouse knockout work establishing the flush mechanism. Mice lacking PUMA-G, the mouse orthologue of human GPR109A, did not flush in response to nicotinic acid. Flushing was also abolished in mice lacking cyclooxygenase type 1 and reduced in mice lacking prostaglandin D2 and E2 receptors, and transplanting wild-type bone marrow into PUMA-G-deficient mice restored the flush, locating the receptor on immune cells in skin.
Common questions
Has Niacin been tested in people?
Yes. 29,087 people given it across 2 completed trials cited here, 0 of which found nothing. Niacin is the only NAD-pathway product ever tested against real heart outcomes, in 25,673 people in HPS2-THRIVE and 3,414 in AIM-HIGH.
What is the Niacin dosage?
Approved medicine. No human dose established for unlabelled uses. Labeled amounts sit on the prescribing information. This page records what trials measured, not a personal dose. Slow-release nicotinic acid is an FDA-approved prescription cholesterol drug in the United States. But doctors mostly stopped using it after two large studies, AIM-HIGH and HPS2-THRIVE. Lower-dose nicotinic acid is also sold over the counter as a supplement. The mix of slow-release niacin and laropiprant tested in HPS2-THRIVE was pulled from sale worldwide after that study reported.
Is Niacin FDA-approved?
Slow-release nicotinic acid is an FDA-approved prescription cholesterol drug in the United States. But doctors mostly stopped using it after two large studies, AIM-HIGH and HPS2-THRIVE. Lower-dose nicotinic acid is also sold over the counter as a supplement. The mix of slow-release niacin and laropiprant tested in HPS2-THRIVE was pulled from sale worldwide after that study reported.
Did niacin fail, or did the trials fail?
The studies were large and well run, one paid for independently and the other by industry, and they agreed. AIM-HIGH put 3,414 patients on niacin or a dummy pill and was stopped because it was going nowhere. HPS2-THRIVE put 25,673 people on niacin or a dummy pill for about 3.9 years. Both saw the blood fats change as expected. Neither saw fewer heart events. The usual defence is that the AIM-HIGH dummy pill held a little niacin to copy the flush. That does not explain HPS2-THRIVE, which was seven times bigger and used a true dummy pill.
Is niacin dangerous?
In HPS2-THRIVE, slow-release niacin with laropiprant caused extra serious harm. Out of every hundred people, it added 3.7 upsets in blood sugar control, 1.3 new cases of diabetes, 1.4 serious infections and 0.7 bleeds, compared with the dummy pill. That was in people already screened in a trial run to make sure they could handle the drug. Separately, high-dose niacin has long been linked to raised liver enzymes and worse blood sugar control. This is not a harmless vitamin at gram doses.
Why does niacin cause flushing and can I avoid it?
Niacin switches on a receptor called GPR109A on immune cells in the skin. They release prostaglandins, chemicals that open up the skin's blood vessels. Work in mice proved each step. Flush-free products either use nicotinamide, which does not touch the receptor and also does not change blood fats, or use slow-release forms that are absorbed more slowly. HPS2-THRIVE blocked the flush with laropiprant and still found no benefit. So avoiding the flush is about comfort, not about whether it works.
Is niacin a better NAD booster than NMN or NR?
It gets turned into NAD by its own route, and it is a strong NAD booster. A 2026 study in people went further. It suggested gut bacteria turn NR and NMN into niacin, which would make the cheap acid the real active route for the pricey products. That is an open idea, not settled fact. What is settled is this. Being a strong NAD booster did not lead to any health benefit across about 29,000 people in studies with a dummy pill group.
Should I take niacin for longevity?
There is no evidence from studies that it helps anyone live longer or stay healthy longer. Two large studies show it does not prevent heart events on top of a statin. One of them showed overall harm, including extra infections, bleeding and new diabetes. Any dose at or above what it takes to fix a shortage should be a medical decision.