Piracetam: The Drug That Invented the Word “Nootropic” — Does It Meet Its Own Standard?

Reviewed by the NootropicsJet editorial team · Published: [19-03-2017] · Last updated: [25-08-2026]

Written from primary and regulatory sources: the Giurgea & Salama 1977 criteria paper, the Cochrane review record for CD001011, the UK Summary of Product Characteristics for Nootropil, the FDA’s 11 May 2026 evaluation of Semax-related bulk drug substances, and the 2019 JAMA Internal Medicine analysis of US piracetam supplements. Claims that could not be traced to a source were cut rather than hedged.

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Piracetam is the compound the word “nootropic” was invented for. That makes it a useful test case: the word came with a written definition, and we can check the drug against it.

This article covers where the definition came from, what its original wording actually said, what more than fifty years of controlled human research found and in whom, why the mechanism is still uncharacterized, and where piracetam stands legally in four jurisdictions. By the end you should be able to judge for yourself whether the prototype meets the standard it created.

Key takeaways

• The word was coined in 1972. The formal criteria came in 1977, co-authored with Mihai Salama — and the paper lists six features, lettered (a) to (f), not the four or five that circulate online.
• The one that disappears most reliably from consumer summaries is (c), facilitation of interhemispheric transfer of information — a specific, measurable claim that gets dropped because it does not fit the modern usage.
• Giurgea’s own 1982 retrospective defined a nootropic by “a particular efficiency in restoring deficient higher nervous activity.” In May 2026, the FDA — finding no ICD-10 code and no professional society guidelines for the term — reached for a medical dictionary that says the same thing. Forty-four years apart, originator and regulator both anchored the word to deficit, not enhancement.
• Cochrane pooled 24 studies and 11,959 participants. Global impression of change was the only outcome poolable at all, from four studies — and no benefit appeared on any specific measure of cognitive function.
• The licensed product’s own label states the mechanism is unknown. Not “debated” — unknown, in a document revised in July 2025.
• Piracetam is not a lawful dietary supplement ingredient in the US, is a prescription medicine across the EU and UK, and is Schedule 4 in Australia. Online availability is not evidence of legality anywhere.

What is piracetam?

Piracetam is 2-oxo-1-pyrrolidine acetamide, a cyclic derivative of the inhibitory neurotransmitter GABA that does not act at GABA receptors. Corneliu Giurgea and colleagues synthesized it at the Belgian firm UCB in 1964; it reached the European market as Nootropil around 1971.

Its awkwardness was the point. It was not a stimulant. It was not a sedative. It did not interfere with autonomic function, and it produced none of the behavioral signatures that let a pharmacologist sort a new molecule into an existing drawer. It sits under ATC code N06BX03 — a class the WHO literally labels “nootropics,” a category that exists because of this compound. In the United States, the only drug sharing its structural core with an FDA approval is levetiracetam, an antiepileptic.

Where the word “nootropic” came from

Giurgea coined the term in 1972, in Vers une pharmacologie de l’activité intégrative du cerveau. Tentative du concept nootrope en psychopharmacologie (Actualités Pharmacologiques, 25th series, pages 115–156, Masson). He returned to it the following year in English, in Conditional Reflex 8:108–115.

The word is built from the Greek noos, mind, and tropein, toward — a drug that acts toward the mind. He was not naming a market segment. He was naming a pharmacological vacancy: a compound that acted on cortical integrative function without acting like anything else in the psychopharmacology cabinet.

The 1977 criteria: what Giurgea and Salama actually wrote

Almost every consumer article credits “Giurgea’s five criteria, 1972.” Two errors sit in that phrase. The term is 1972; the criteria are 1977, published with Mihai Salama in Progress in Neuro-Psychopharmacology 1(3–4):235–247, from UCB’s own neuropharmacological research department in Brussels.

The paper’s abstract enumerates the nootropic profile in six lettered features:

(a) enhancement of learning acquisition; (b) resistance to impairing agents; (c) facilitation of interhemispheric transfer of information; (d) enhanced resistance to brain “aggressions”; (e) increased tonic, cortico-subcortical “control”; and (f) absence of usual pharmacological effects of neuro-psychotropic drugs.

Six, in the authors’ own lettering, framed by an opening claim that nootropics “selectively improve efficiency of higher telencephalic integrative activities.”

Consumer summaries typically give four or five. The item that disappears most reliably is (c) — and its disappearance is not cosmetic. Interhemispheric transfer is a specific, measurable claim about corpus callosum function; Giurgea and Moyersoons had reported transcallosal evoked-response effects in cats, and it is the kind of assertion that can be tested and failed.

The telencephalic-selectivity framing goes the same way. It is the clause that excludes stimulants by construction: a drug that acts on cortex without touching reticular or limbic structures. Strip out the specific, testable elements and you are left with a list that reads like a description of any cognitive enhancer — which is precisely how the modern consumer category uses it.

If you want the wider frame, our guide to nootropics as a drug class sets out how the term drifted from this definition to today’s usage.

The field never settled on one definition

This was contested at the time. Vladimir Skondia published a competing and more mechanistic set of criteria in 1979 (Clinical Therapeutics 2:316–332), built around cerebral metabolic activity rather than learning and memory; contemporaries described his mechanistic requirements as the more controversial list. A decade later, Poschel was still writing a rough consensus — improves some aspect of cognitive performance, most readily under disturbed neural metabolism, minimal side effects at high doses, crosses the blood-brain barrier — in the 1988 Handbook of Psychopharmacology, explicitly noting that complete agreement among pharmacologists had not been reached.

Sixteen years after the word was coined, nobody could agree on what it meant. That is the foundation the consumer category is built on.

The definition was never about healthy people

This is the part that gets lost.

In his 1982 retrospective (Drug Development Research 2:441–446), Giurgea characterized a nootropic by direct functional activation of higher integrative brain mechanisms, telencephalic functional selectivity, and “a particular efficiency in restoring deficient higher nervous activity.”

Restoring. The model systems behind the criteria were hypoxia, electroconvulsive shock and chemically induced amnesia — damaged brains, not rested ones.

Forty-four years later, a regulator arrived at the same place from the opposite direction. Evaluating semax-related bulk drug substances, the FDA noted that the substances had also been nominated for use as a “nootropic.” Its assessment: the term has no ICD-10 code, and no professional society treatment guidelines could be found for it. So the agency fell back on Dorland’s Medical Dictionary, 29th edition, which defines nootropic as “having positive effects on organically impaired cognition or nervous system function” — and folded the nootropic claim into its evaluation for cerebral ischemia (FDA, Evaluation of Semax-Related Bulk Drug Substances, 11 May 2026, footnote 3).

The originator in 1982 and the regulator in 2026 describe the same object: restoration of a deficit. Neither describes enhancement in a healthy brain. The entire consumer nootropics market sits inside that gap, and piracetam is where the gap opens.

How does piracetam work?

The most honest answer available is the one printed on the licensed product. Section 5.1 of the UK Summary of Product Characteristics for Nootropil, in text revised in July 2025, states: “Piracetam’s mode of action in cortical myoclonus is as yet unknown.” Sixty-one years after synthesis, in a regulatory document that has every incentive to say something more.

What exists instead is a set of candidate mechanisms, none established as the operative one in humans.

Membrane fluidity. Piracetam appears to bind the polar head groups of membrane phospholipids and increase fluidity — and in the work most often cited, it did so in aged mouse, rat and human brain membranes while having no effect at all in young ones (Müller et al., 1997, Biochemical Pharmacology). Mechanistically plausible, and it fits the deficit-restoration pattern; not demonstrated as the mechanism of any clinical effect in humans.

AMPA modulation. Piracetam is a weak positive allosteric modulator of AMPA receptors. The complication is that it shows very low or no affinity for any specific receptor type, which is unusual for a compound whose activity is attributed to receptor modulation. Reports also exist for NMDA and cholinergic facilitation, corticosteroid-related mechanisms, and membrane depolarization sensitive to both AMPA/kainate and GABA-A blockade. A candidate list this long and this weakly constrained is a symptom, not an explanation.

What actually is reproducible in humans is hemorheological. Per the SPC: in healthy volunteers, piracetam up to 9.6 g reduced plasma fibrinogen and von Willebrand factor levels by 30–40% versus pre-treatment and increased bleeding time; doses up to 12 g produced dose-dependent reductions in platelet aggregation.

So what does that mean for you? The best-documented thing piracetam reliably does in a healthy adult body, at the doses people actually take, is change blood. Not cognition. That is a mechanism–implication mismatch worth sitting with, and it drives the interaction warnings later in this article.

Why piracetam requires gram doses

The absence of a high-affinity target has a direct practical consequence: potency. If a compound acts by nudging bulk membrane properties rather than occupying a receptor with nanomolar affinity, you need a great deal of it.

The pharmacokinetics amplify this. Oral bioavailability is close to 100%, peak plasma levels arrive within about 1.5 hours, volume of distribution is 0.7 L/kg, no metabolite of piracetam has ever been identified, roughly 90% of the dose is excreted unchanged in urine, and plasma half-life is about 5 hours in young adult men. Absorbed almost completely, transformed not at all, cleared quickly by the kidneys.

The licensed dosing reflects this. For its one UK indication, the SPC specifies a starting dose of 7.2 g per day, escalating to a maximum of 24 g per day, divided into two or three doses. For comparison, European formulations for cognitive indications come as 800 mg and 1,200 mg tablets with usual daily doses of 2,400–4,800 mg, renally adjusted.

Those are regulatory facts about a prescription medicine, not a protocol. We do not publish piracetam dosing guidance, and the renal adjustment table in the SPC exists precisely because getting this wrong matters.

What the controlled human evidence actually shows

Almost the entire controlled literature sits in diagnosed patient populations: dementia, cognitive impairment, post-stroke, cortical myoclonus. A benefit measured in an impaired system does not transfer to a healthy adult, and nothing below should be read as though it does.

The reference point is the Cochrane review Piracetam for dementia or cognitive impairment (Flicker & Grimley Evans, CD001011). It included 24 studies with 11,959 participants in total.

Read what happened next, because it is the most misreported result in this literature. Many of the studies were of cross-over design with first-phase data unavailable or unextractable. Global impression of change was the only outcome for which pooling of data was possible at all — and that pooling involved only four studies. There was significant heterogeneity between them (Chi² = 19.17, df = 3, P < 0.001). The odds ratio for improvement on that measure was 3.43 (95% CI 2.32–5.07); using a fixed-effect model, 3.55 (95% CI 2.45–5.16).

That 3.55 is the number everyone quotes. Almost nobody says what it was measured on.

Global impression of change is a clinician’s overall rating of whether a patient seems better. And the review is explicit about the rest: although effects were found on global impression of change, no benefit was shown by any of the more specific measures of cognitive function. The reviewers’ conclusion, verbatim: published evidence does not support the use of piracetam in the treatment of people with dementia or cognitive impairment.

There is a competing analysis, and the asymmetry between them is documented rather than inferred. Waegemans and colleagues (2002, Dementia and Geriatric Cognitive Disorders) pooled nineteen double-blind placebo-controlled studies on the same global-change outcome, reported a significant odds ratio and a favorable number needed to treat, and described the result as compelling evidence for global efficacy in older subjects with cognitive impairment.

Nineteen studies against Cochrane’s four. The explanation is in Cochrane’s own methods: the pharmaceutical company marketing piracetam did not release the results of several unpublished trials. Two analyses of overlapping literature, opposite conclusions, and one side with access to data the other could not see. Most coverage cites whichever one suits it.

The one place a regulator has been persuaded is narrow. In the UK, piracetam is licensed solely for myoclonus of cortical origin, in adults, in combination with other anti-myoclonic therapies — and NICE guidance on the epilepsies lists it among options when adjunctive treatment is ineffective or not tolerated. Cortical myoclonus is not a cognitive indication.

Is there any evidence in healthy adults?

Direct answer: there is a small, old, methodologically limited body of work, and no modern, adequately powered, pre-registered randomized trial of piracetam for cognitive enhancement in healthy adults. That absence is the single most decision-relevant fact in this article.

What does exist:

• Dimond & Brouwers, 1976 (Psychopharmacology 49:307–309) reported increased verbal memory performance in healthy volunteers — a small study, in the era before modern trial standards, by a group that had a stake in the concept.
• A 1979 double-blind crossover trial in the same journal studied 16 male dyslexic adults alongside 14 matched student volunteers over 21 days. Verbal learning rose 15.0% in the dyslexic group and 8.6% in the students, over and above their placebo increase. Note the shape: the effect was roughly twice as large in the impaired group. That is the deficit-restoration pattern showing up inside a single trial.
• Wesnes et al., 1990 (Journal of Psychopharmacology 4:219–232) used a scopolamine model in 26 healthy volunteers across seven double-blind treatments including piracetam 2,400 mg orally. Aniracetam 1,500 mg significantly antagonized the scopolamine-induced decrements. Among the other active treatments, some effects were no better than chance would produce and were described by the authors as questionable.

That is the healthy-adult evidence base: two studies from the 1970s and one 1990 challenge model. Our nootropic stack guide for studying reaches the same conclusion from the student-use angle, and nothing here contradicts it.

The choline heuristic: convention, not finding

Anyone who has spent an hour in a nootropics forum has met the rule: take choline with your piracetam or you will get a headache. It is presented as pharmacology. Its actual provenance is worth knowing.

The animal work is real. Bartus and colleagues (1981, Neurobiology of Aging) gave aged Fischer 344 rats vehicle, choline, piracetam, or the combination on a one-trial passive avoidance task. The combination outperformed either alone. Aged rats, passive avoidance, 1981.

The combination was then tested in humans. Growdon, Corkin, Huff and Rosen (1986, Neurobiology of Aging 7:269–276) administered piracetam alone and with phosphatidylcholine to 18 patients with Alzheimer’s disease across three double-blind crossover protocols and a replication, at piracetam doses from 2.4 to 9.9 g/day with phosphatidylcholine at 18 g/day. Plasma choline rose as expected. Piracetam, alone or with phosphatidylcholine, did not significantly affect cognition in the group as a whole, and did not improve test performance in any single patient.

So: the synergy is an aged-rodent finding, the human test of the same combination was null, and the specific headache-prevention claim has no controlled human trial behind it that we could locate. Treat it as a community convention with a plausible-sounding rationale — which is what it is.

If you are interested in the choline compounds themselves on their own merits, that is a separate question covered in our comparison of citicoline and alpha-GPC.

Is piracetam legal? US, EU, UK and Australia

Regulatory status is the most perishable material in this article. Verify current status in your own jurisdiction before acting on anything here.

United States. Piracetam has no FDA-approved use. A new dietary ingredient notification was submitted and unsuccessful in 2003–04; the agency has stated that piracetam is not permitted to be sold as a dietary supplement and issued a warning letter on that basis in 2012, with further enforcement letters since — including one to Peak Nootropics in February 2019.

Enforcement has been limited, and the consequences are measurable. Cohen, Zakharevich and Gerona (2019, JAMA Internal Medicine) identified 14 brands, analyzed 10 samples from 5 brands, and found piracetam in 8 samples from 4 brands. Content ranged from 831 to 1,542 mg per recommended serving and from 85% to 118% of the labeled amount. Following label directions, a consumer could take 831 mg to 11,283 mg per day depending on brand — against European prescription practice of 2,400–4,800 mg/day for cognitive indications, renally adjusted.

European Union. Piracetam is a nationally authorized medicine in numerous member states rather than a centrally approved one — the EMA handles it through periodic safety update single assessments across a long list of national marketing authorizations. It is a prescription medicine, not a permitted food supplement ingredient.

United Kingdom. Prescription-only. Nootropil holds a UK marketing authorization solely for adjunctive treatment of cortical myoclonus in adults. Supply outside that route also engages the Psychoactive Substances Act 2016, under which most UK retailers withdrew racetams from sale.

Australia. Schedule 4 under the Poisons Standard — prescription-only. Supply without a prescription is unlawful.

Online availability is not evidence of legality. A vendor that ships to your address has demonstrated logistics, not compliance. In the US specifically, the 2019 JAMA data show that products sold in open defiance of a fifteen-year-old FDA position also carried label doses more than double the highest routine European prescription.

Safety, side effects, interactions and who should avoid this

The following is drawn from the UK SPC, whose safety profile derives from double-blind placebo-controlled trials including more than 3,000 subjects receiving piracetam.

Adverse reactions. Common: nervousness, hyperkinesia, weight increase. Uncommon: somnolence, depression, asthenia. Reported without established frequency: agitation, anxiety, confusion, hallucination, ataxia, impaired balance, aggravated epilepsy, headache, insomnia, vertigo, and gastrointestinal effects. In clinical studies at 1.6–15 g/day, hyperkinesia, somnolence, nervousness and depression were each reported more often on piracetam than on placebo.

Contraindications. Hypersensitivity to piracetam or other pyrrolidone derivatives. Severe renal impairment (creatinine clearance below 20 mL/min). Cerebral haemorrhage. Huntington’s chorea. End-stage renal disease is an absolute contraindication in the dosing table.

Bleeding risk — the interaction that matters most. Because of piracetam’s effect on platelet aggregation, the label advises caution in severe haemorrhage, gastrointestinal ulcer, disorders of haemostasis, prior haemorrhagic stroke, major surgery including dental surgery, and anyone taking anticoagulants or antiplatelet drugs, explicitly including low-dose aspirin. This is a drug-class warning, not a treatment plan; anyone on these medications needs to discuss it with their prescriber rather than act on an article.

Renal clearance. Roughly 90% of a dose leaves unchanged in urine, so clearance tracks creatinine clearance directly. Renal function is not an abstraction here — it is the entire elimination route.

Other interactions. Confusion, irritability and sleep disturbance have been reported with concomitant thyroid extract (T3 + T4). Metabolic drug interactions are considered unlikely given minimal CYP involvement.

Discontinuation. In myoclonic patients, abrupt discontinuation may induce myoclonic or generalized seizures; the label specifies a taper.

Who should not use this. Pregnancy — piracetam crosses the placenta, with newborn levels 70–90% of maternal. Breastfeeding — it is excreted in human breast milk. Under-18s — the UK indication is for adults, and there is no basis for use in minors outside specialist care. Anyone with renal impairment, a bleeding disorder, on anticoagulants or antiplatelets, or taking prescription medication of any kind. For anything specific to your situation, speak to a doctor or pharmacist — this article cannot do that job.

What we still don’t know

• The mechanism. Not underspecified. Unknown, per the current label.
• Whether the global-impression signal reflects anything patients or families would perceive, given that every specific cognitive measure in the same review showed no benefit.
• What was in the unpublished company trials that the manufacturer-affiliated meta-analysis could pool and the Cochrane reviewers could not see.
• Whether piracetam does anything measurable in a healthy, rested adult brain. This has never been properly tested to modern standards, and the absence has persisted for half a century.
• The safety profile at the doses US supplement labels direct — the SPC’s safety database reflects supervised prescription use with renal monitoring, not unsupervised 11 g/day.

The bottom line

Against its own 1977 criteria, piracetam scores partially at best: the interhemispheric-transfer and brain-resistance items have supporting experimental work, the learning-acquisition item rests on a thin and dated human literature, and the telencephalic-selectivity claim cannot be evaluated because nobody knows what the drug does.

Against the standard the word was supposed to set, the answer is cleaner. Giurgea defined a nootropic by its efficiency in restoring deficient higher nervous activity. On that definition, piracetam is a plausible candidate that a systematic review still judged inadequately supported — and, crucially, the definition itself never promised anything to a healthy adult. The 2026 FDA document reaching for a dictionary that says “organically impaired” is the same conclusion arriving from the regulatory side.

Who this is not for: anyone who is healthy and looking for a cognitive edge, because the evidence for that use does not exist. Anyone on anticoagulant or antiplatelet therapy. Anyone with reduced renal function. Anyone pregnant or breastfeeding. Anyone under 18. And anyone in the US, UK or Australia who assumed that a working checkout page meant a lawful product.

Piracetam’s real importance is historical and conceptual: it is the compound that forced pharmacology to invent a category, and the clearest available illustration of how far that category has drifted from the thing it named. If you want to see how the same deficit-versus-enhancement gap plays out in a compound people reach for by symptom rather than by mechanism, our article on nootropics and brain fog is the natural next read.

Frequently asked questions

Does piracetam work in healthy people? There is no modern, adequately powered, pre-registered randomized trial of piracetam for cognitive enhancement in healthy adults. The healthy-volunteer evidence consists of two small 1970s studies and a 1990 scopolamine-challenge study in 26 volunteers. In the one trial testing both groups, the effect in dyslexic adults was roughly double that in matched students.

What is piracetam’s mechanism of action? Officially unknown. The UK Summary of Product Characteristics, revised July 2025, states that piracetam’s mode of action in cortical myoclonus is as yet unknown. Candidate mechanisms include restoration of membrane fluidity in aged but not young brain membranes, and weak positive allosteric modulation of AMPA receptors — neither established as the operative mechanism in humans. Its best-documented human effects are on platelets and blood viscosity.

Is piracetam legal? It depends on jurisdiction, and this changes. In the US it has no approved use and cannot lawfully be sold as a dietary supplement, though enforcement is limited. In the EU it is a nationally authorized prescription medicine. In the UK it is prescription-only, licensed solely for cortical myoclonus. In Australia it is Schedule 4, prescription-only. Availability online is not evidence of legality.

What did the Cochrane review conclude about piracetam? That published evidence does not support its use in people with dementia or cognitive impairment. Of 24 included studies and 11,959 participants, global impression of change was the only outcome that could be pooled at all — from four studies. Effects appeared there, but no benefit was shown by any of the more specific measures of cognitive function.

Why do people take choline with piracetam? Because of a community convention that traces to a 1981 study in aged rats, where choline plus piracetam outperformed either alone on a passive-avoidance task. When the combination was tested in humans — 18 Alzheimer’s patients, piracetam 2.4–9.9 g/day with phosphatidylcholine 18 g/day — it did not significantly affect cognition in the group or improve performance in any individual patient. The headache-prevention claim specifically has no controlled human trial behind it.

Why are piracetam doses measured in grams? Because it has no high-affinity molecular target. Its proposed actions involve bulk membrane properties and weak allosteric modulation, which require far higher concentrations than receptor occupancy would. Its pharmacokinetics compound this: near-100% bioavailability, no known metabolite, about 90% excreted unchanged in urine, and a plasma half-life around 5 hours. The UK label for cortical myoclonus starts at 7.2 g/day.

Who invented the word “nootropic”? Corneliu Giurgea, the Romanian psychologist and chemist who synthesized piracetam at UCB in 1964. He coined the term in 1972 from the Greek noos (mind) and tropein (toward). The formal criteria came five years later, in a 1977 paper co-authored with Mihai Salama, which lists six defining features of the nootropic profile.

Who should avoid piracetam entirely? Per the UK label: anyone with hypersensitivity to pyrrolidone derivatives, severe renal impairment (creatinine clearance under 20 mL/min), cerebral haemorrhage, or Huntington’s chorea. Caution also applies to anyone on anticoagulants or antiplatelets including low-dose aspirin, anyone with a bleeding or haemostatic disorder, anyone facing surgery, pregnant or breastfeeding women, and under-18s.

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References

1. Giurgea C, Salama M. Nootropic drugs. Progress in Neuro-Psychopharmacology. 1977;1(3–4):235–247. doi:10.1016/0364-7722(77)90046-7
2. Giurgea C. Vers une pharmacologie de l’activité intégrative du cerveau. Tentative du concept nootrope en psychopharmacologie. Actualités Pharmacologiques, 25e série:115–156. Masson, 1972.
3. Giurgea CE. The nootropic concept and its prospective implications. Drug Development Research. 1982;2:441–446.
4. Flicker L, Grimley Evans J. Piracetam for dementia or cognitive impairment. Cochrane Database of Systematic Reviews. Art. No.: CD001011. doi:10.1002/14651858.CD001011
5. Waegemans T, Wilsher CR, Danniau A, et al. Clinical efficacy of piracetam in cognitive impairment: a meta-analysis. Dementia and Geriatric Cognitive Disorders. 2002;13(4):217–224.
6. Growdon JH, Corkin S, Huff FJ, Rosen TJ. Piracetam combined with lecithin in the treatment of Alzheimer’s disease. Neurobiology of Aging. 1986;7(4):269–276.
7. Cohen PA, Zakharevich I, Gerona R. Presence of piracetam in cognitive enhancement dietary supplements. JAMA Internal Medicine. 2019.
8. Nootropil 1200 mg Film-Coated Tablets — Summary of Product Characteristics, text revised July 2025.
9. U.S. Food and Drug Administration. Evaluation of Semax-Related Bulk Drug Substances, 11 May 2026.
10. Skondia V. Criteria for clinical development and classification of nootropic drugs. Clinical Therapeutics. 1979;2:316–332.

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This article is pharmacology and regulatory education, not medical advice. Piracetam is a prescription medicine in several jurisdictions and is not a lawful dietary supplement ingredient in the United States. Nothing here is intended to diagnose, treat, cure or prevent any disease. Talk to a qualified healthcare professional before making decisions about any medication or supplement, particularly if you are pregnant, breastfeeding, under 18, have kidney or bleeding disorders, or take prescription medication.