Is natto better than statins?

No — natto and statins are not treating the same problem, and the evidence behind them is not remotely comparable.

Statins have been tested in trials involving more than 170,000 people, where each 1.0 mmol/L reduction in LDL cholesterol cut major vascular events by 21%. The largest and longest trial of nattokinase, by contrast, followed 265 adults for three years and found no measurable effect on arterial plaque. Both facts matter. Neither makes natto a replacement.

Table of Contents

1. The short answer: different jobs, different evidence
2. What statins actually do
3. What natto and nattokinase actually do
4. The plaque question: what the largest trial found
5. Does natto lower cholesterol?
6. Where the natto evidence is genuinely encouraging
7. Risks specific to natto that statin users should know
8. BioAbsorb Nattokinase — an honest position
9. Frequently Asked Questions
10. Conclusion

The short answer: different jobs, different evidence

The question assumes natto and statins are competing for the same role. They aren't. Statins are LDL-lowering drugs. They block an enzyme in the liver's cholesterol production pathway, which lowers circulating LDL, which slows the build-up of plaque in artery walls. That is a lipid mechanism.

Nattokinase — the enzyme in natto that gets all the attention — is a fibrinolytic. It breaks down fibrin, the protein scaffold that holds a blood clot together. That is a clotting mechanism. Clotting and cholesterol are both involved in cardiovascular disease, but they are separate processes, and improving one does not substitute for the other.

So asking whether natto is "better" than statins is a bit like asking whether a smoke alarm is better than a fire door. Both belong in the same building. Neither does the other's job. The more useful questions are what each one is actually evidenced to do, and how confident we can be in that evidence.

What statins actually do

Statins have one of the largest evidence bases in modern medicine. The Cholesterol Treatment Trialists' Collaboration pooled individual patient data from 26 randomised trials covering 170,000 participants and found that each 1.0 mmol/L reduction in LDL cholesterol reduced major vascular events by 21% [2], with no evidence of a threshold below which the benefit stopped.

A later analysis extending to 27 trials and 175,000 participants found the benefit held even in people at low baseline risk, where each 1 mmol/L reduction prevented roughly 11 major vascular events per 1,000 people over five years [3]. A separate meta-analysis spanning 52 studies and 327,037 patients across multiple drug classes found a 19% relative risk reduction per 1 mmol/L [8], confirming that the benefit tracks the LDL reduction itself rather than any particular drug. The effect is similar in men and women at equivalent cardiovascular risk [9].

These are hard clinical endpoints — heart attacks, strokes, deaths — not surrogate markers. That distinction matters enormously when comparing against supplement research, which almost entirely reports surrogate markers instead.

Statins are not without problems. Adherence is poor: a meta-analysis of 67 studies found only 49% of patients were still adherent at one year [12] in real-world observational data, and a cohort of 22,340 older adults found 44.7% discontinued within the first year [13]. A 2026 review put first-year discontinuation across studies at anywhere from 0.8% to 70.5%, with roughly 40% failing to reach optimal adherence [14]. That is a real problem — but it is a problem of people not taking an effective drug, not evidence that the drug doesn't work.

What natto and nattokinase actually do

It helps to separate two things that get used interchangeably. Natto is a whole food: soybeans fermented with Bacillus subtilis, eaten mainly in Japan. It contains protein, fibre, isoflavones, an unusually high concentration of vitamin K2, and the enzyme nattokinase. A nattokinase supplement is an isolated extract of that one enzyme — no K2, no fibre, no isoflavones. If you want the full picture on the food itself, see our guide to what natto is.

Nattokinase's documented action is fibrinolytic. It degrades fibrin directly and inhibits plasminogen activator inhibitor-1, which is the brake on your body's own clot-clearing system. That is a coherent, well-described mechanism. What it is not is a cholesterol mechanism, and no amount of enthusiasm changes that.

This distinction is where most "natto versus statins" content goes wrong. It borrows the epidemiology of the food, applies it to the isolated enzyme, and then compares the result to a drug class measured on completely different endpoints.

The plaque question: what the largest trial found

If natto were going to compete with statins, it would need to slow plaque. It doesn't, at the doses most people take.

The Nattokinase Atherothrombotic Prevention Study is the largest and longest randomised trial of the enzyme conducted to date. Researchers at the University of Southern California randomised 265 adults with a median age of 65.3 years — none with clinical cardiovascular disease — to either 2,000 FU of nattokinase daily or a matching placebo, then tracked carotid artery intima-media thickness and arterial stiffness by ultrasound every six months. After a median of three years, the rate of change in both measures did not significantly differ between groups [1]. The authors also reported no significant effect on blood pressure or on any laboratory measure taken.

A separate retrospective observational study of 1,062 participants reached a compatible conclusion at moderate doses, finding nattokinase ineffective for both lipid-lowering and atherosclerosis progression at 3,600 FU per day [5], with benefits appearing only at 10,800 FU — three times the standard dose and well above what most products supply. Being observational rather than randomised, and conducted with authors affiliated to a nattokinase manufacturer, it carries less weight than the trial above.

We have covered this evidence in more depth in our article on whether nattokinase reduces arterial plaque. The honest summary is that at 2,000 FU, over three years, in a properly powered randomised trial, it did not.

Does natto lower cholesterol?

This is where the comparison gets genuinely interesting, because there is a trial showing a natto supplement lowering LDL — and reading the methods section explains a great deal.

A four-month randomised, double-blind, placebo-controlled trial of 113 patients with dyslipidaemia found that a nattokinase-monascus supplement produced significant reductions in total cholesterol, LDL cholesterol, and non-HDL cholesterol, with LDL-C falling by 0.43 mmol/L versus placebo [4]. Carotid intima-media thickness, notably, did not change.

The supplement contained nattokinase at 2,500 FU — and 7 mg of lovastatin derived from red yeast rice [4]. Lovastatin is a statin. It was the first statin ever approved. So the natto product that lowered cholesterol in a randomised trial did so with a statin in the capsule.

The same pattern shows up elsewhere. A trial in patients with stable coronary artery disease reporting lipid-lowering, antihypertensive and antithrombotic effects [11] also used nattokinase combined with red yeast rice rather than nattokinase alone. Nattokinase on its own has not demonstrated a meaningful lipid effect at standard doses.

If you are taking a natto-based product specifically for cholesterol, it is worth checking whether what you are actually taking is a statin under a different name — at an unregulated dose, without monitoring.

Where the natto evidence is genuinely encouraging

None of the above means natto is useless. The population data is real and it is specific.

The Takayama Study followed 13,355 men and 15,724 women aged 35 and over for 16 years, recording 1,678 cardiovascular deaths. Participants in the highest quartile of natto intake had a 25% lower risk of death from cardiovascular disease [6] compared with the lowest quartile, and a 32% lower risk of stroke death [6]. The detail that makes this compelling is what showed no association: total soy protein and soy isoflavone intake from other soy foods were not linked to reduced cardiovascular mortality. Whatever is happening appears to be specific to natto rather than to soy generally.

This is observational data, so it cannot establish cause, and people who eat natto regularly may differ in other ways. But it is a large, long, well-conducted cohort, and it is a reasonable basis for interest.

Blood pressure is the other area with positive controlled data. A randomised, double-blind, placebo-controlled trial in 86 adults with untreated systolic pressure of 130–159 mmHg found that 2,000 FU daily for eight weeks produced a net systolic reduction of 5.55 mmHg and a diastolic reduction of 2.84 mmHg [7]. Note the population: people who already had elevated blood pressure. NAPS enrolled healthy low-risk adults and found nothing, which is consistent rather than contradictory — there was less room to move. Our article on nattokinase and blood pressure works through the pooled trial data in detail.

A 3–5 mmHg systolic reduction is modest but not trivial. It is also not a substitute for antihypertensive medication, and it says nothing about cholesterol.

Risks specific to natto that statin users should know

Anyone considering natto as part of a cardiovascular plan needs to know two things that rarely appear in enthusiastic coverage.

First, vitamin K2. Natto is by a wide margin the richest dietary source of menaquinone-7, and MK-7 directly counteracts warfarin by reactivating the clotting factors warfarin suppresses. This is not a subtle interaction. Researchers developing a specially modified low-MK-7 natto reported that standard natto must be avoided by warfarin-dependent patients [10], and only their reduced-K2 version — engineered to yield roughly a fifth of normal MK-7 content — left INR values unchanged across a seven-day ingestion test. Many people on statins are also on anticoagulants. If that is you, natto the food is a genuine hazard — which is a different question from the isolated enzyme, covered in our article on whether K2 and nattokinase are the same thing.

Second, bleeding risk. Nattokinase is fibrinolytic by design. Combined with anticoagulants, antiplatelets, or aspirin, that effect stacks. Our guide to nattokinase side effects covers who should avoid it entirely.

And the point that matters most: stopping a prescribed statin to take a supplement instead is a decision with measurable consequences. The trial evidence above describes what statins prevent. Nothing in the nattokinase literature justifies giving that up. If side effects are the reason you want off a statin, that is a conversation with your prescriber — there are several drug classes and dosing strategies — not a reason to self-substitute.

BioAbsorb Nattokinase — an honest position

We sell a nattokinase supplement, so it is worth being direct about what we think it is for.

BioAbsorb Nattokinase Enzyme delivers 100 mg providing 2,000 FU of enzyme activity per capsule — the dose used in the blood pressure trial above [7] and in the NAPS trial. It is not a cholesterol product, and we don't position it as one. The evidence does not support that, and we would rather say so than sell against the data.

A few things we do think are worth knowing. The enzyme is delivered in DRcaps delayed-release vegetarian capsules, which protect it from stomach acid without the phthalates and plasticizers used in conventional enteric coatings. The formulation is deliberately free of vitamin K2 — relevant given everything above about MK-7 and anticoagulants, and useful for anyone already supplementing K2 separately. It is non-GMO, free of gluten, nuts, eggs, dairy, fish, shellfish and all animal products, and manufactured in a GMP-certified facility in Canada. Every batch is third-party tested for enzyme activity, heavy metals, gluten and microbial contaminants.

It is a fibrinolytic enzyme taken as one capsule daily on an empty stomach, for people interested in circulation and clotting support alongside — not instead of — whatever their doctor has prescribed. If you would rather get nattokinase from food, our article on nattokinase food sources covers how much natto that actually takes.

Frequently Asked Questions

Can I take nattokinase instead of my statin?

No. Statins reduce heart attacks and strokes on hard clinical endpoints across trials involving 175,000 participants [3], while nattokinase has no comparable outcome data and no demonstrated cholesterol effect at standard doses. Never stop a prescribed statin without talking to the doctor who prescribed it.

Can I take nattokinase alongside a statin?

Many people do, but this is a question for your prescriber rather than a supplement label — particularly if you also take an anticoagulant, antiplatelet or aspirin, where the combined effect on bleeding risk is the relevant concern.

Does eating natto lower cholesterol?

There is no good evidence that natto or isolated nattokinase lowers LDL cholesterol at typical intakes. The randomised trial that showed a 0.43 mmol/L LDL reduction [4] used a product containing 7 mg of lovastatin from red yeast rice.

Why do the natto studies look so positive if the big trial was negative?

Most positive findings come from observational cohorts like the Takayama Study [6], which show association rather than cause, or from trials combining nattokinase with other active compounds. The randomised evidence for the isolated enzyme at standard doses is considerably thinner.

Is natto safe if I take warfarin?

No. Natto's very high MK-7 content can substantially reduce warfarin's effect, and researchers describe standard natto as something warfarin-dependent patients must avoid [10]. Speak to your anticoagulation clinic before changing anything.

What is nattokinase actually good for, then?

The best-supported effect is a modest blood pressure reduction — the largest controlled trial recorded a net systolic drop of 5.55 mmHg [7] in people with early-stage hypertension — alongside a well-described fibrinolytic mechanism. That is a supportive role, not a replacement for cardiovascular medication.

Conclusion

Natto is not better than statins, because it is not doing what statins do — and the largest randomised trial of nattokinase, at 2,000 FU over three years in 265 adults, found no effect on plaque progression. What the enzyme does have is a coherent fibrinolytic mechanism and modest, repeatable blood pressure data. If that is the role you are looking to fill alongside your existing care, BioAbsorb Nattokinase Enzyme supplies the 2,000 FU dose used in the clinical literature — and it is worth discussing with your doctor first.

Research References

1. Nattokinase atherothrombotic prevention study: A randomized controlled trial. Clinical Hemorheology and Microcirculation, Vol. 78, No. 4 (2021), pp. 339–353. Randomised 265 adults to 2,000 FU nattokinase or placebo for a median of three years and found no significant difference in carotid intima-media thickness, arterial stiffness, blood pressure or any laboratory measure — the primary basis for this article's position on plaque.
2. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. The Lancet, Vol. 376, No. 9753 (2010), pp. 1670–1681. Established that each 1.0 mmol/L reduction in LDL cholesterol reduces major vascular events by 21%, the benchmark against which supplement evidence is compared here.
3. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. The Lancet, Vol. 380 (2012), pp. 581–590. Found the benefit persists in low-risk populations, preventing roughly 11 major vascular events per 1,000 people over five years per 1 mmol/L.
4. The Effect of Nattokinase-Monascus Supplements on Dyslipidemia: A Four-Month Randomized, Double-Blind, Placebo-Controlled Clinical Trial. Nutrients, Vol. 15, No. 19 (2023), Article 4239. Reported a 0.43 mmol/L LDL-C reduction using a supplement that contained 7 mg of lovastatin from red yeast rice alongside nattokinase at 2,500 FU.
5. Effective management of atherosclerosis progress and hyperlipidemia with nattokinase: A clinical study with 1,062 participants. Frontiers in Cardiovascular Medicine, Vol. 9 (2022), 964977. Retrospective observational study; found nattokinase ineffective for lipid-lowering and atherosclerosis progression at 3,600 FU per day, with benefit only at 10,800 FU. See also the published corrigendum, Frontiers in Cardiovascular Medicine, Vol. 9 (2022), 1076420.
6. Dietary soy and natto intake and cardiovascular disease mortality in Japanese adults: the Takayama study. The American Journal of Clinical Nutrition, Vol. 105, No. 2 (2017), pp. 426–431. Followed 29,079 adults for 16 years; highest natto intake quartile showed a hazard ratio of 0.75 for cardiovascular mortality and 0.68 for total stroke mortality, with no equivalent association for soy protein or isoflavones.
7. Effects of nattokinase on blood pressure: a randomized, controlled trial. Hypertension Research, Vol. 31, No. 8 (2008), pp. 1583–1588. Found net reductions of 5.55 mmHg systolic and 2.84 mmHg diastolic after eight weeks at 2,000 FU in adults with untreated pre-hypertension or stage 1 hypertension.
8. Intensive LDL cholesterol-lowering treatment beyond current recommendations for the prevention of major vascular events: a systematic review and meta-analysis of randomised trials including 327,037 participants. The Lancet Diabetes & Endocrinology, Vol. 8, No. 1 (2020), pp. 36–49. Found a 19% relative risk reduction in major vascular events per 1 mmol/L LDL reduction across lipid-lowering therapies.
9. Efficacy and safety of LDL-lowering therapy among men and women: meta-analysis of individual data from 174,000 participants in 27 randomised trials. The Lancet (2015). Found statin therapy similarly effective in men and women at equivalent cardiovascular risk.
10. First Clinical Trial of a Newly Developed, Low Menaquinone-7, Fermented Soybean Natto in Warfarin-Dependent Patients. Journal of Medicinal Food (2021). Confirmed that standard natto must be avoided by warfarin-dependent patients; a mutant strain yielding 19–24% of normal MK-7 content left INR unchanged in 10 warfarin-dependent patients across a seven-day ingestion test.
11. Lipid-lowering, antihypertensive, and antithrombotic effects of nattokinase combined with red yeast rice in patients with stable coronary artery disease. Frontiers in Nutrition, Vol. 11 (2024), 1380727. A further example of positive lipid findings arising from nattokinase combined with red yeast rice rather than nattokinase alone.
12. Proportion and risk indicators of nonadherence to statin therapy: a meta-analysis. Canadian Journal of Cardiology, Vol. 28, No. 5 (2012), pp. 574–580. Pooled 67 studies and found only 49.0% of patients adherent to statins at one year in observational data.
13. Predictors of first-year nonadherence and discontinuation of statins among older adults: a retrospective cohort study (2018). [journal details not confirmed] Followed 22,340 adults aged 65 and over; 44.7% discontinued statin therapy within the first year.
14. Discontinuation of statin therapy — an updated review. Current Opinion in Cardiology, Vol. 41, No. 4 (2026), pp. 291–297. Reported first-year discontinuation rates ranging from 0.8% to 70.5%, with approximately 40% of patients failing to achieve optimal adherence.

About the Author

David Kimbell is a health writer, digital entrepreneur and former aerospace engineer, based in Ottawa, Canada. He loves translating complex science into clear, actionable guidance for consumers seeking evidence-based solutions.

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Important Disclaimers

Medical Disclaimer: This article provides educational information only and is not intended as medical advice. Always consult with a qualified healthcare provider before starting any new supplement, especially if you have existing health conditions, take medications, or are pregnant or nursing.

FDA/Health Canada Statement: These statements have not been evaluated by the Food and Drug Administration or Health Canada. This product is not intended to diagnose, treat, cure, or prevent any disease.