Plant Compounds for Cardiovascular Health

Centuries of use. No proof of cardiovascular benefit.

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.

Safety note: Several plant compounds in this article carry documented interaction risks. Garlic, ginkgo, and curcumin can increase bleeding risk in people taking anticoagulant or antiplatelet drugs. Hawthorn can interact with digoxin and other cardiac medications. High-dose green tea extract has been linked to liver injury in safety reviews. Any plant-compound supplement is worth disclosing to every prescriber, because the interaction is often the part the prescriber cannot see.

In brief: Dietary patterns rich in plant compounds — Mediterranean-style and DASH eating — reduce cardiovascular events or blood pressure in randomized trials, but supplements that extract individual plant compounds from those patterns have not shown equivalent benefit in any large cardiovascular outcome trial. (8,9,10) Garlic modestly lowers blood pressure in hypertension and hawthorn improves heart failure symptoms, but neither has been shown to reduce cardiovascular events. (1,2,3,4) The two largest outcome trials in this category — SPICE for hawthorn and COSMOS for cocoa flavanols — both reported null primary endpoints, though COSMOS showed a positive secondary signal for cardiovascular death that its authors described as warranting further study. (4,8) Curcumin is poorly absorbed, high-dose green tea extract carries a documented liver-injury signal, and resveratrol’s animal findings have not translated to humans. (7,11,12) Across these compounds the pattern is consistent: laboratory activity and modest biomarker effects, but no cardiovascular outcome evidence.

Where the Evidence Stands

For the plant compounds in this article, none has randomized outcome-trial evidence for cardiovascular event prevention. Garlic lowers blood pressure modestly in people with hypertension, with no outcome trial. (1,2) Hawthorn improves heart failure symptoms and exercise tolerance, but its one large outcome trial was null, and it carries a caution for cardiac-drug interactions. (3,4) Curcumin, green tea extract, and resveratrol have no cardiovascular outcome evidence, with green tea carrying a caution for liver injury at high doses. (5,6,7,11) For cocoa flavanols, the largest trial missed its primary endpoint but produced a secondary signal that has not been confirmed. (8) The only direct outcome evidence belongs to the dietary pattern these compounds come from, not the extracted capsule. (9) This describes what the trials found; it is information for a conversation with a clinician, not a basis for self-directed treatment.

Find Your Situation

The Pattern That Runs Through This Category

Every major plant compound marketed for cardiovascular health shares the same evidence profile, and naming the profile makes each individual compound easier to read.

First, documented biological activity in laboratory studies and short-term human trials. The mechanisms are usually real — antioxidant effects, anti-inflammatory pathways, blood-vessel relaxation, lipid changes. Second, modest effects on cardiovascular risk markers in some human trials: blood-pressure reductions in the single digits of mmHg, LDL changes of a few mg/dL, near the lower bound of clinical significance. Third, an absence of large randomized trials with cardiovascular events as the endpoint. The two largest trials that directly tested cardiovascular outcomes — SPICE for hawthorn and COSMOS for cocoa flavanols — both reported null primary endpoints. (4,8) Fourth, the food-supplement distinction: the dietary patterns that contain these compounds reduce cardiovascular events or blood pressure in randomized data, while the extracted supplements have not demonstrated equivalent benefit. (9,10)

This pattern reflects something about how plant compounds appear to work in the body — embedded in a complex food matrix at natural concentrations, as part of dietary patterns that influence several aspects of cardiometabolic health at once. The capsule extracts one compound at a higher dose. The food delivers hundreds of interacting components, plus the displacement of whatever less healthy food the meal replaced.

Garlic

Garlic has been used medicinally across cultures for thousands of years and remains one of the most popular cardiovascular supplements. Its active compounds are sulfur-containing molecules, particularly allicin (formed when raw garlic is crushed) and its derivatives, which have antioxidant, antiplatelet, and lipid-modifying effects in laboratory studies.

Blood pressure. Meta-analyses consistently show that garlic supplementation modestly lowers blood pressure in people with hypertension. Pooled estimates from the Ried analyses are on the order of 8 mmHg systolic and 5 mmHg diastolic in people with hypertension, with smaller or absent effects in people with normal blood pressure. (1,2) This is a real, reproducible effect on a risk marker. Its magnitude is modest, and it sits alongside — not in place of — antihypertensive medication when that is indicated.

Cholesterol. Earlier meta-analyses suggested LDL reductions of several percent. More recent analyses with stricter quality standards show minimal or inconsistent effects. (1) The cholesterol claims made for garlic supplements are weaker than the blood-pressure claims.

Cardiovascular outcomes. No large randomized trial has tested whether garlic supplementation prevents heart attacks, strokes, or cardiovascular death.

Formulation matters. Fresh garlic, garlic powder, garlic oil, and aged garlic extract contain different compounds in different amounts. Most of the positive blood-pressure research uses aged garlic extract standardized to S-allyl cysteine. (1,2) Results from one formulation do not necessarily transfer to another — a practical limit on how far the evidence reaches.

Safety. Generally well tolerated; gastrointestinal upset and garlic odor are the main tolerability issues. Garlic’s antiplatelet activity can add to bleeding risk in people taking anticoagulant or antiplatelet drugs, which is the reason to disclose it. (14)

Hawthorn

Hawthorn (Crataegus species) has been used in European traditional medicine for cardiac complaints for centuries, and the standardized extract WS 1442 is a registered phytopharmaceutical — a plant-derived product with regulatory recognition as a medicinal product in Germany — for early-stage heart failure. Its active compounds are flavonoids and procyanidins with antioxidant and vasodilatory properties.

Heart failure symptoms. A Cochrane review identified 14 trials; the 10 with data suitable for pooling (855 patients with chronic heart failure) showed that hawthorn extract improved symptoms — shortness of breath and fatigue — along with exercise tolerance and maximal workload compared with placebo. (3) The effects were modest but statistically significant. Hawthorn does something measurable for how patients feel.

The SPICE trial — the critical anchor. SPICE randomized 2,681 patients with NYHA Class II–III heart failure and reduced ejection fraction (LVEF ≤35%), all on guideline-directed therapy, to hawthorn extract WS 1442 (900 mg/day) or placebo for 24 months. The primary outcome — time to first cardiac event, a composite of cardiac death, non-fatal myocardial infarction, and hospitalization for heart-failure progression — showed no significant difference between groups (event rates 27.9% vs 28.9%; hazard ratio 0.95, 95% CI 0.82–1.10, P=0.476). (4) A non-significant trend toward reduced cardiac mortality was reported (HR 0.89, 95% CI 0.73–1.09), and a pre-specified subgroup with less severely reduced ejection fraction (LVEF ≥25%) showed a reduction in sudden cardiac death (HR 0.59, 95% CI 0.37–0.94). The primary endpoint was null, and WS 1442 was safe when added to optimal heart-failure medication.

This is symptomatic benefit without demonstrated disease modification. Hawthorn may help some patients feel better without protecting them from heart-failure progression — a profile shared by several symptomatic heart-failure treatments. That makes it a possible adjunct for symptomatic support in mild heart failure, considered alongside a clinician, rather than a treatment that changes cardiovascular outcomes.

Safety. Generally well tolerated. It may interact with digoxin and other cardiac medications, and it is not a replacement for the therapies that carry outcome evidence in heart failure — ACE inhibitors or ARBs, beta-blockers, mineralocorticoid-receptor antagonists, and SGLT2 inhibitors.

Curcumin

Curcumin is the active compound in turmeric and one of the most heavily marketed supplements of the past decade. It inhibits several inflammatory pathways, has antioxidant activity, and improves measures of blood-vessel function in laboratory studies. The cardiovascular case for curcumin resembles the antioxidant hypothesis examined in Article 17: inflammation contributes to atherosclerosis, curcumin is anti-inflammatory, therefore curcumin should reduce cardiovascular disease. The mechanism is real; the leap to clinical benefit is the unproven step.

Human trial evidence. Some small trials report improved blood-vessel function with curcumin. A meta-analysis of seven trials (649 patients) in people with cardiovascular risk factors found that curcumin significantly reduced LDL cholesterol and triglycerides, with the effect concentrated in higher-risk groups such as those with metabolic syndrome or diabetes; the trials were small and the authors called for more rigorous study. (5) Blood-pressure effects are limited. No randomized trial has tested whether curcumin prevents heart attacks, strokes, or cardiovascular death.

The absorption problem. Curcumin is poorly absorbed. After oral dosing, plasma concentrations remain in the low nanomolar range even after gram-level doses, because most of an oral dose is poorly absorbed, rapidly metabolized in the gut and liver, and quickly eliminated. (12) Whether the anti-inflammatory effects seen in cell culture occur in human arterial walls at the concentrations standard supplementation produces is therefore uncertain. Enhanced formulations — with piperine (black-pepper extract), liposomal delivery, or nanoparticles — raise absorption substantially but have less clinical trial data and higher cost. Piperine’s absorption-boosting effect is also a practical consideration: it raises the systemic dose of curcumin reaching the bloodstream — the dose that matters for both effect and interaction risk.

Safety. Generally safe at typical doses; gastrointestinal upset is the most common complaint. Curcumin can increase bleeding risk in people on anticoagulant or antiplatelet therapy (14), and high doses have been linked to liver-enzyme elevation in some reports.

Green Tea Extract

Green tea consumption is associated with lower cardiovascular risk in observational studies, particularly across Asian populations. The active compounds — catechins, chiefly EGCG (epigallocatechin gallate) — have antioxidant, anti-inflammatory, and lipid-modifying properties in laboratory research.

Human trial evidence. A meta-analysis of 20 trials found a significant but small reduction in systolic blood pressure (about 2 mmHg), no significant effect on diastolic blood pressure, and significant reductions in LDL and total cholesterol (on the order of 7 mg/dL LDL) with green tea or its extract. (6) The effects on these risk markers are real but small, and there is no cardiovascular outcome trial.

Why the food-supplement distinction matters here. Green tea as a beverage is linked to reduced cardiovascular risk in populations where tea drinking is culturally embedded — populations that also differ in diet, activity, body weight, and many other factors. Whether a green tea extract supplement reproduces any of that has not been demonstrated.

The liver-injury signal. High-dose green tea extract carries a documented hepatotoxicity signal that distinguishes it from most compounds in this category. In its 2018 scientific opinion, the European Food Safety Authority concluded that catechins from traditionally prepared green tea infusions are generally safe, but that EGCG taken as a supplement at doses at or above 800 mg/day has been shown in clinical trials to raise serum liver transaminases, a marker of liver injury. (11) The injury appears to be largely idiosyncratic — it does not occur in everyone and is not strictly dose-predictable — and the reports cluster around concentrated extracts rather than around the beverage. (11) Following this evidence, the European Union amended its food regulation to limit EGCG in supplements. The beverage carries no comparable signal; the concentrated extract is where the risk reports concentrate. Neither has cardiovascular outcome evidence.

Resveratrol

Resveratrol received enormous attention as the proposed explanation for the “French paradox” — the observation that French populations had relatively low cardiovascular disease despite high saturated-fat intake. It is a polyphenol found in grape skins, red wine, berries, and peanuts that activates certain longevity-related proteins, extends lifespan in some model organisms, and improves metabolic measures in mice on high-fat diets.

Human evidence. Multiple trials have tested resveratrol across cardiovascular risk factors, and meta-analyses show inconsistent effects on blood pressure, lipids, and glucose, often unrelated to dose; where positive signals appear, they are small and not consistently reproduced. (7) No trial has tested whether resveratrol prevents cardiovascular events.

The dose problem. A glass of red wine contains roughly 1–2 mg of resveratrol, while standard supplements contain 100–500 mg. (7) A resveratrol-based explanation of the French paradox would require daily wine consumption no human could plausibly sustain. The paradox is more plausibly explained by overall dietary patterns, portion sizes, and other wine polyphenols than by any single extracted compound. (9)

The animal-to-human gap. The metabolic improvements seen in mice on high-fat diets have been among the least reproducible findings in supplement research when tested in humans, and the doses needed to replicate mouse outcomes in people would be pharmacologically implausible. (7)

Cocoa Flavanols and the COSMOS Trial

Cocoa flavanols deserve specific attention because, unlike most compounds in this article, they have been tested in a large randomized cardiovascular outcome trial.

COSMOS, published in 2022, was the cocoa arm of a 2×2 factorial trial that randomized 21,442 older adults (women aged ≥65, men aged ≥60) to a cocoa-extract supplement (500 mg cocoa flavanols per day, including 80 mg epicatechin) or placebo, with a separate multivitamin comparison. (8) Over a median 3.6 years, the primary endpoint — a composite of total cardiovascular events — was not significantly reduced (hazard ratio 0.90, 95% CI 0.78–1.02, P=0.11). Among the secondary endpoints, cardiovascular death was lower in the cocoa group (HR 0.73, 95% CI 0.54–0.98, a 27% relative reduction), while myocardial infarction, stroke, coronary revascularization, and all-cause mortality showed neutral or non-significant results. A pre-specified per-protocol analysis, restricted to participants who took the supplement consistently, supported a lower rate of total cardiovascular events (HR 0.85, 95% CI 0.72–0.99). There were no safety concerns. The investigators concluded that the findings warranted further study.

The evidence here is mixed, and an honest reading requires holding both sides. The primary endpoint was null. The cardiovascular-death finding was statistically significant but was one of several secondary endpoints, and when many endpoints are tested, some can cross the significance threshold by chance. The per-protocol signal — a lower event rate among the participants who took the supplement consistently — is the kind of finding that can reflect a real effect diluted by non-adherence, or can reflect the generally healthier behavior of people who take any supplement faithfully. On its own, it cannot substitute for a positive primary endpoint. By the standard this series applies to every other supplement — the same standard that classified niacin’s HDL effect, vitamin D’s biomarker effect, and B-vitamins’ homocysteine effect as insufficient for outcome claims — COSMOS does not establish cocoa flavanol supplementation as proven cardiovascular prevention.

Cocoa flavanols have the strongest plant-compound outcome evidence to date. That evidence is not yet sufficient, and the trial’s authors said as much.

Other Plant Compounds

Grape seed extract contains procyanidins with antioxidant properties and has shown modest blood-pressure reductions in some small trials. There is no cardiovascular outcome data.

Olive leaf extract contains oleuropein, with limited evidence for modest blood-pressure reduction. It is mechanistically related to the olive oil used in Mediterranean-diet trials, but the supplement has not been tested for cardiovascular outcomes the way the dietary pattern has. (9)

Ginkgo biloba is marketed for circulation and cognition. Large randomized dementia-prevention trials were negative. (13) Bleeding risk in combination with anticoagulant or antiplatelet drugs is a documented concern, and cardiovascular outcome data are limited. (14)

Pomegranate polyphenols have shown possible effects on blood pressure and atherosclerosis markers in small studies. The evidence is preliminary and not from outcome trials.

The common thread across these is the same as for the better-studied compounds: biological plausibility, occasional modest marker effects, and no cardiovascular outcome evidence.

The Evidence at a Glance

The shape of the table is the article’s thesis. Modest biomarker effects across compounds, no outcome benefit at any compound’s primary endpoint, and one entry — the dietary pattern that contains these compounds — with proven cardiovascular outcome benefit.

Why the Food-Supplement Gap Persists

The gap between food and supplement is consistent enough across compounds to demand an explanation, and several plausible ones overlap.

The dose changes the chemistry: a compound that is mildly active at the concentration found in food can behave differently when extracted and concentrated. The food matrix matters: fiber, fats, and co-occurring compounds alter absorption and effect. Bioavailability varies dramatically, and for some compounds, such as curcumin, very little of an oral dose reaches the bloodstream. (12) Dietary patterns also work through several mechanisms at once, only some of which involve the compounds that get measured.

The simplest explanation may be the most important: the measured compounds may not be the active ingredient. The cardiovascular benefit of a dietary pattern may come less from its antioxidant or anti-inflammatory molecules than from the whole pattern — fiber, the displacement of less healthy foods, monounsaturated fats, low intake of refined carbohydrate — none of which a capsule reproduces. Which explanation dominates is not settled. The empirical pattern is: the dietary patterns reduce events or blood pressure in randomized trials, and the isolated supplements have not been shown to. (9,10)

Two Patients, Same Supplement Aisle, Different Answers

Both profiles below are composites built from the populations studied in the trials this article reviews.

Patient A is a 71-year-old woman with NYHA Class II heart failure and reduced ejection fraction (LVEF 30%), on guideline-directed therapy — an ACE inhibitor, a beta-blocker, an SGLT2 inhibitor, and a low-dose diuretic. She has read about hawthorn and asks her cardiologist whether to add it. She is functioning reasonably well but still gets short of breath on hills.

The conversation has two parts. The Cochrane review shows modest symptomatic improvement with hawthorn on top of standard care — better shortness of breath, fatigue, and exercise tolerance. (3) That symptomatic effect is what she is asking about. The SPICE trial showed no reduction in cardiac events at 24 months on its primary endpoint. (4) That is what hawthorn has not been shown to do: change the trajectory of the disease. If she and her cardiologist decide to add hawthorn for symptomatic support, the evidence-based expectation is some improvement in day-to-day symptoms, no demonstrated improvement in survival or hospitalization risk, and a need to monitor for interactions with her cardiac medications. The reasonable framing is symptomatic adjunct, not disease-modifying therapy — and the therapies that modify her heart-failure trajectory are the ACE inhibitor, beta-blocker, and SGLT2 inhibitor, which carry the outcome evidence.

Patient B is a 56-year-old man on warfarin for atrial fibrillation and a daily aspirin after a coronary stent. His INR has been stable for two years. After reading about turmeric’s anti-inflammatory effects, he started a high-potency curcumin supplement (500 mg twice daily, with piperine for absorption) to “reduce inflammation in his arteries.” His next INR came back elevated, with a small bruise on his forearm he had not noticed before.

The interaction is the immediate issue, and the cardiovascular rationale for the supplement is the deeper one. Curcumin has antiplatelet activity and, taken with warfarin or antiplatelet drugs, can increase bleeding risk; turmeric and curcumin have been linked to a raised INR in people on warfarin in published reports. (14) The piperine he is taking to improve absorption raises the systemic dose reaching his bloodstream. He is on dual antithrombotic therapy, a setting where any added bleeding risk matters. Beyond the interaction, the supplement is being taken for a cardiovascular indication — reducing arterial inflammation — that no randomized outcome trial supports. The evidence-based step is to bring this to his cardiologist promptly, to discuss stopping the curcumin and rechecking the INR, and to address the underlying inflammation question directly: the interventions with cardiovascular outcome evidence are different ones — statin therapy, which has anti-inflammatory effects independent of LDL lowering, and the dietary pattern this article keeps pointing toward. (9)

Common Misconceptions

“Plants are natural, so plant-compound supplements must be safe.” Not categorically. High-dose green tea extract has been linked to liver injury. (11) Garlic, ginkgo, and curcumin can increase bleeding risk in people on blood thinners. (14) Hawthorn can interact with cardiac medications. (4) The food and the concentrated extract are different exposures, and the safety profile differs accordingly.

“Centuries of traditional use prove these supplements work.” Centuries of use indicate that these plants are generally safe to consume as foods or traditional preparations. They do not establish that modern supplement formulations — concentrated extracts at high doses, often standardized to specific compounds the traditional preparations did not isolate — prevent cardiovascular events. The two are different exposures at different doses.

“Garlic supplements are as good as eating garlic.” Both lower blood pressure modestly in people with hypertension. (1,2) Eating garlic delivers the compound within a food context — alongside other ingredients in a Mediterranean-style or otherwise plant-rich diet that has cardiovascular outcome evidence. (9) A garlic supplement delivers an extracted compound without that context. It may produce a similar blood-pressure effect; it does not deliver the dietary pattern that randomized trials show reduces cardiovascular events.

“Curcumin’s anti-inflammatory effects must reduce cardiovascular disease.” This is the same logic that failed for antioxidant vitamins (Article 17). The mechanism is real; whether anti-inflammatory effects at the doses and concentrations achievable with oral supplementation translate into cardiovascular event reduction has not been tested in any large outcome trial. The absorption problem — plasma concentrations stay in the low nanomolar range even after gram doses — makes the leap from laboratory mechanism to clinical effect particularly uncertain. (12)

“COSMOS proved cocoa flavanols prevent heart disease.” It did not. The primary endpoint was null. (8) The cardiovascular-death finding was statistically significant but was one of several secondary endpoints, and some secondary endpoints can cross the significance threshold by chance. The authors concluded the findings warranted further study rather than that the question was settled. Cocoa flavanols have the strongest plant-compound outcome evidence to date, and that evidence is not yet sufficient.

“Resveratrol explains the French paradox.” Almost certainly not. A glass of red wine contains roughly 1–2 mg of resveratrol; supplements contain 100–500 mg. (7) The doses that produce effects in mice would require implausible wine consumption in humans. The paradox is better explained by overall dietary patterns, portion sizes, and other wine components than by any single extracted compound. (9)

“Plant-compound supplements can replace dietary changes.” They have not been shown to. The cardiovascular benefit of plant-rich dietary patterns appears to come from the whole pattern — fiber, displacement of less healthy foods, multiple compounds at natural concentrations — none of which a capsule reproduces. Adding a supplement to an unchanged diet is not the same intervention as changing the diet. (9,10)

The Bottom Line

Plant compounds occupy the most frustrating category in supplement medicine: more biologically interesting than most, better supported by observational data than most, and still unproven by the outcome-trial standard cardiovascular medicine requires. Each compound has traditional use, laboratory evidence of biological activity, and some human data showing modest effects on risk markers. None has been shown to prevent heart attacks, strokes, or cardiovascular death in a large randomized trial, and the two largest trials that tested cardiovascular outcomes — SPICE for hawthorn and COSMOS for cocoa flavanols — both reported null primary endpoints. (4,8) Major cardiovascular guidelines — including the 2019 ACC/AHA primary-prevention guideline and the 2022 AHA/ACC/HFSA heart-failure guideline — do not include plant-compound supplements among recommended interventions for event prevention; they point instead to dietary patterns, risk-factor control, and proven pharmacotherapy, the interventions that carry outcome evidence. (9)

The dietary evidence is real: fruits, vegetables, nuts, olive oil, and whole grains, eaten as part of the patterns tested in randomized trials, reduce cardiovascular events or blood pressure. (9,10) Centuries of use indicate these compounds are generally safe to consume. They have not shown that the supplements prevent heart attacks.

Key Terms

Allicin: The main bioactive compound formed when raw garlic is crushed. Responsible for garlic’s characteristic odor and many of its biological effects, including antiplatelet activity and a modest antihypertensive effect.

Bioavailability: The proportion of an oral dose that reaches the bloodstream. Curcumin’s bioavailability is very low — plasma concentrations remain in the low nanomolar range even after gram-level doses — which limits how much reaches target tissues.

Catechins: Polyphenol compounds concentrated in green tea, chiefly EGCG (epigallocatechin gallate). They have antioxidant properties in laboratory research; high-dose extracts carry a liver-injury signal.

EGCG (epigallocatechin gallate): The principal catechin in green tea. Beneficial in laboratory studies, but associated with elevated liver transaminases when taken as a supplement at doses at or above 800 mg/day.

Phytopharmaceutical: A plant-derived medicinal product with formal regulatory recognition as a registered drug in some jurisdictions, particularly Germany. Hawthorn extract WS 1442 holds this status for early-stage heart failure.

Procyanidins: Flavonoid compounds in hawthorn, cocoa, and grape seed extract with antioxidant and vasodilatory properties; they contribute to hawthorn’s symptomatic effects in heart failure.

Resveratrol: A polyphenol in grape skins and red wine. Promising animal data have not reproduced in human trials, and poor bioavailability limits its effects.

References

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3. Pittler MH, Guo R, Ernst E. Hawthorn extract for treating chronic heart failure. Cochrane Database Syst Rev. 2008;(1):CD005312.
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9. Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet supplemented with extra-virgin olive oil or nuts. N Engl J Med. 2018;378(25):e34. (PREDIMED)
10. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. N Engl J Med. 2001;344(1):3–10.
11. EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS). Scientific opinion on the safety of green tea catechins. EFSA J. 2018;16(4):e05239.
12. Anand P, Kunnumakkara AB, Newman RA, Aggarwal BB. Bioavailability of curcumin: problems and promises. Mol Pharm. 2007;4(6):807–818.
13. DeKosky ST, Williamson JD, Fitzpatrick AL, et al. Ginkgo biloba for prevention of dementia: a randomized controlled trial (Ginkgo Evaluation of Memory Study). JAMA. 2008;300(19):2253–2262.
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