KAVA KAVA 300mg 60 caps

Specialized botanical preparation for adults (21+) — traditional anxiolytic extract from the root of Piper methysticum. It is NOT a dietary supplement in the EU or Polish legal sense (EFSA ban since 2002, GIS recommendation to withdraw it from circulation as a dietary supplement). It is not a medicinal product nor a food product. Intended exclusively for adults, for independent risk assessment, after reviewing the full safety and legal status section below.

Kava originates from the islands of Polynesia and Micronesia, where the beverage made from the ground root of Piper methysticum has served a ceremonial and social function for over 3000 years — in Vanuatu, Fiji and Tonga. Ethnobotany describes it as a calming agent that facilitates conversation and relaxation without loss of mental clarity — unlike alcohol. Modern pharmacology has confirmed that this effect is attributable to a group of lipophilic lactones called kavalactones, and the Cochrane meta-analysis (Pittler & Ernst 2003) demonstrated a statistically significant reduction in anxiety compared with placebo.

The Pro-Body preparation is supplied in a format of 60 HPMC capsules of 300 mg of standardized root extract Piper methysticum (standardized to 30% kavalactones, ≥98% HPLC), exclusively from the root — without leaves and stems, which are a source of the most hepatotoxic alkaloid, flavokavain B. This distinction is a central element of the safety profile, and we return to it in the section devoted to the liver.

The activity of kava is based on a group of six main kavalactones (kavalactones, kavapyrones): kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin and desmethoxyyangonin. These are lipophilic compounds that readily cross the blood-brain barrier and together are responsible for the anxiolytic, muscle-relaxant and mildly sedative action of the extract. Standardization to 30% kavalactones means that each 300 mg capsule provides approximately 60–90 mg of total kavalactones.

Chemotype profile — that is, the proportion of the individual kavalactones — differs between kava varieties and influences the character of action. Lebot and colleagues (2014) described how the composition of kavalactones and the presence of flavokavins (accompanying compounds with a cytotoxic profile) depend on the cultivar and the part of the plant. This is not a botanical detail for collectors: it is precisely the chemotype differences and the choice of raw material that explain why the traditional aqueous beverage from the root in the Pacific islands did not generate an epidemic of liver failure, whereas some Western ethanol-acetone extracts — indeed — did.

Aware adults reach for kava for one main reason: a traditional, botanical anxiolytic profile with a mechanism different from benzodiazepines, without the classic addictive potential of the latter. The same theme of calming psychological tension links kava with a broader group of mood-modulating compounds — among anxiolytic peptides for improving well-being a reduction of anxiety without the addictive profile of benzodiazepines is also sought.

A study by Sarris and colleagues (2013) demonstrated that a standardized kava extract reduced symptoms of generalized anxiety to a degree comparable with reference drugs — at the same time this analysis noted a signal of elevated liver enzymes in some of the subjects, which upholds the requirement to monitor liver function tests.

Kava (kava kava, Piper methysticum G. Forst.) is a perennial plant of the pepper family (Piperaceae), cultivated exclusively vegetatively on the islands of the South Pacific. The species name methysticum comes from the Greek for “intoxicating” — it refers to the psychoactive action of the root.

• Common name: kava, kava kava, awa, yaqona, sakau
• Botanical name: Piper methysticum G. Forst. (Piperaceae)
• Raw material part: exclusively root and rhizome (NOT leaves, NOT stems — associated with hepatotoxic flavokavain B)
• Active compounds: kavalactones (6 main: kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin, desmethoxyyangonin)
• CAS number: 9000-38-8 (kava extract)
• Standardization: 30% kavalactones (with a different batch standardization — protocol correction in accordance with the COA)
• Supplied form: hard HPMC capsule (vegan), 300 mg of root extract per capsule, 60 capsules; extract ≥98% HPLC
• Origin: Polynesia and Micronesia (Vanuatu, Fiji, Tonga, Samoa); tradition of use over 3000 years

Tradition vs Western extract: the difference in preparation method is pharmacologically significant. The traditional beverage is produced by aqueous maceration of fresh or dried root (an emulsion of kavalactones in water). Western extracts often used organic solvents (ethanol, acetone), which extract a different profile of compounds from the raw material — including more flavokavins. Singh (1992) in his review of kava ethnopharmacology described in detail the composition and pharmacology of the traditional aqueous preparation.

Kavalactones act through five parallel axes, and the anxiolytic profile is the resultant of several of them. Unlike benzodiazepines, kava does not bind to the classic benzodiazepine site of the GABA-A receptor — and this explains the different subjective profile (calming without the impairment of cognitive function typical of benzodiazepines at moderate doses).

Five axes of kavalactone action:

1. Allosteric modulation of the GABA-A receptor (site ≠ benzodiazepine) — kavain and dihydrokavain enhance inhibitory GABAergic conduction by binding to an allosteric site distinct from the benzodiazepine one. This is the main axis of anxiolysis. In the study by Sarris and colleagues (2013), the effect of reducing generalized anxiety was comparable with reference drugs of the buspirone and oxazepam class — with a different binding mechanism.
2. Weak MAO-B inhibition — yangonin exhibits weak inhibition of monoamine oxidase type B, which may raise the availability of monoamines (dopamine) and contribute to a mood-improvement component. The activity is weak compared with classic MAO inhibitors.
3. Weak inhibition of noradrenaline reuptake — affects noradrenergic transmission; the mechanism contributes to the profile of mood and arousal regulation.
4. Antagonism of T- and L-type calcium channels — kavalactones block voltage-gated Ca²⁺ channels, which accounts for the muscle-relaxant and anticonvulsant component (anticonvulsant properties described in preclinical models).
5. Anti-inflammatory and analgesic action — inhibition of cyclooxygenase COX-2; contributes to local anesthetic action (the characteristic numbness of the tongue after the traditional beverage) as well as analgesic action.

Practical picture: an aware adult describes the effect as a calming of psychological tension and muscular relaxation, with retained mental alertness — unlike the benzodiazepine “fog”. The action appears relatively quickly (lipophilic kavalactones cross the blood-brain barrier well and efficiently) and persists for several hours. The botanical mechanism of kava thereby differs from peptide anxiolytic tools — the synthetic tuftsin analog Selank modulates primarily serotonergic and GABAergic pathways as well as BDNF expression, offering a complementary approach to reducing tension without binding to kavalactones.

• Absorption: kavalactones are lipophilic and are well absorbed from the gastrointestinal tract; bioavailability increases in the presence of fat in a meal
• CNS penetration: high (low molecular mass, lipophilicity)
• Duration of action: a perceptible effect usually 30–60 min after administration, persisting for several hours
• Metabolism: hepatic, with the participation of P450 cytochromes — kavalactones inhibit among others CYP1A2, CYP2D6, CYP3A4, CYP2C9 and CYP2C19, which constitutes the mechanistic basis both of drug interactions and of part of the hepatotoxic risk (accumulation of substrates, reduction of glutathione)
• Elimination: metabolites excreted mainly in the urine
• Receptor profile: no classic affinity for the benzodiazepine site — lower addiction potential than benzodiazepines, but NOT zero risk of tolerance with frequent administration

The inhibition of a broad spectrum of P450 isoenzymes is the reason why kava is one of the plants with the highest potential for drug interactions — every drug metabolized through these pathways (from anticoagulants, through antidepressants, to some statins) may have an altered concentration.

This is not a treatment regimen. The values below are the convention for use of a traditional botanical preparation by aware adults, for independent risk assessment. The first attempt is always at the minimum dose, for assessment of individual tolerance.

• Starting dose (tolerance assessment): 1 capsule (300 mg of extract ≈ 60–90 mg of kavalactones)
• Standard dose: 1–2 capsules
• Maximum dose: 3 capsules per day (do not exceed)
• Frequency: at most 2–3 times per week — never daily. Daily, chronic administration increases the burden on the liver and the hepatotoxic risk
• Cycle duration: 4–6 weeks, after which a mandatory break
• With a meal: administration with a small amount of fat improves the absorption of kavalactones
• Time of day: on account of the calming profile — preferentially in the evening; not before driving vehicles or operating machinery

Plan your cycle around your real needs and your research schedule — kava is not a preparation “for permanent” or “for every day” use. The rarer and shorter the administration, the lower the burden on the liver. If the main goal is improving the quality of nocturnal rest, it is worth considering tools with a better-documented safety profile — e.g. dedicated peptides for sleep — instead of escalating exposure to kava.

Monitoring of liver function is not a just-in-case recommendation here — it is a condition of responsible use.

• Before starting the cycle: perform a panel of liver function tests — ALT (AlAT), AST (AspAT), GGTP, ALP (alkaline phosphatase), bilirubin. A result outside the norm = do not start the cycle
• After completing the cycle: repeat the same panel. An increase in enzymes (especially ALT/AST above 2–3 times the upper limit of normal) = discontinue and consult a physician
• During the cycle: at any symptoms on the part of the liver (jaundice, dark urine, pain in the right hypochondrium, nausea, anorexia, extreme fatigue) — discontinue immediately, regardless of the testing schedule
• For repeated cycles: consider a control panel also in the middle of a longer cycle

The Sarris (2013) study, despite a favorable efficacy profile, noted in some of the subjects a transient increase in GGTP — this is the concrete reason why we check liver enzymes before and after, and not “if something happens”.

Kava (Piper methysticum) is a traditional botanical anxiolytic of the Pacific with an over 3000-year history, whose activity is based on six kavalactones acting through five axes — with allosteric modulation of GABA-A (outside the benzodiazepine site) as the core of anxiolysis. The Cochrane meta-analysis (Pittler & Ernst 2003) and the Sarris (2013) RCT confirm efficacy in reducing anxiety comparable with reference drugs.

The other side of the equation is the documented risk of severe liver damage (~80 cases, 11 transplants, 4 deaths in the years 1990–2002), probably linked to flavokavain B from leaves and stems and to extraction with organic solvents. The Pro-Body preparation is an extract exclusively from the root, standardized to 30% kavalactones, with mandatory flavokavain B screening, ≥98% HPLC and a COA for every batch.

Status: EFSA/GIS/BfR ban as a dietary supplement — a preparation for aware adults (21+) with an absolute requirement of liver function tests before and after the cycle and zero alcohol and hepatotoxic drugs.

1. Sarris J, Stough C, Bousman CA, Wahid ZT, Murray G, Teschke R, et al. (2013). Kava in the treatment of generalized anxiety disorder: a double-blind, randomized, placebo-controlled study. PubMed
2. Pittler MH, Ernst E (2003). Kava extract for treating anxiety. PubMed
3. Teschke R, Sarris J, Lebot V (2011). Kava hepatotoxicity solution: a six-point plan for new kava standardization. PubMed
4. Singh YN (1992). Kava: an overview. PubMed
5. Lebot V, Do TK, Legendre L (2014). Detection of flavokavins (A, B, C) in cultivars of kava (Piper methysticum) using high performance thin layer chromatography (HPTLC). PubMed