Kava vs Kratom vs Kanna: A Side-by-Side Comparison
Three plants often sold in the same kind of shop, with almost nothing in common chemically or legally.
Kava, kratom and kanna get grouped together because they are sold in similar places and marketed with similar words. Underneath, they are three separate plants from three regions with different compounds, different proposed mechanisms and very different regulatory histories. This post puts the three in one place, fairly and with sources. For a deeper dive on any pair, see kanna vs kratom and kanna vs kava.
Kava (Piper methysticum) is a South Pacific root whose kavalactones enhanced GABA-A receptors in a lab study [1][7]. Kratom (Mitragyna speciosa) is a Southeast Asian tree whose alkaloids act on opioid receptors [3][4]. Kanna (Sceletium tortuosum) is a South African succulent with serotonin-transporter and PDE4 activity in lab work [8]. Each has a different safety record.
What are the main differences between kava, kratom and kanna?
Everything differs: species, region, compounds, targets, and the kind of caution attached to each.
| Kava | Kratom | Kanna | |
|---|---|---|---|
| Species | Piper methysticum [1] | Mitragyna speciosa [4] | Sceletium tortuosum [9] |
| Plant family and type | Pepper family [1] | Coffee family tree [4] | Succulent [9] |
| Region | South Pacific [1] | Southeast Asia [4] | South Africa [9] |
| Key compounds | Kavalactones, e.g. kavain [7] | Mitragynine, 7-hydroxymitragynine [4] | Mesembrine-type alkaloids [9] |
| Proposed mechanism | GABA-A receptor enhancement by kavain, lab study [7] | Mu-opioid receptor activity, plus other receptors [3][4] | Serotonin transporter and PDE4, lab studies [8] |
| Traditional use | Ceremonial and medicinal beverages [1] | Chewed or brewed as a stimulant by laborers; opium substitute [4] | Chewed, smoked or fermented [9][11] |
| Main safety flag | Rare liver injury; avoid with alcohol and sedatives [1][2] | FDA consumer warning; dependence and withdrawal; adverse events [3][5] | Possible serotonergic drug interactions; pregnancy data lacking [10] |
| FDA status | 2002 consumer advisory [2] | No approved uses; not lawfully marketed as a supplement [5] | Not approved or reviewed [10] |
| Human research | See NCCIH summary [1] | Observational and case data; FDA says a human abuse-potential study has not been conducted [5] | Small trials in healthy volunteers, mostly one extract [11][12] |
Where does each plant come from?
Three different regions, three different traditions, no shared ancestry.
NCCIH says kava is native to the South Pacific and belongs to the pepper family [1]. The DEA places kratom in the coffee family and describes it as a tropical tree indigenous to Thailand, Malaysia, Myanmar and other parts of Southeast Asia, historically used as a stimulant by laborers and as a stand-in when opium was unavailable [4]. Kanna is a succulent endemic to South Africa with a documented history as a chewed or smoked plant among the San and Khoikhoi peoples [9][11]. More at what is kanna.
How is each of the three proposed to work?
Each is proposed to act on a different system, and for kava and kanna the evidence is mostly lab work.
- Kava. A 2016 PLoS One study found that kavain, the best-known kavalactone, positively modulated GABA-A receptors, and the effect was not blocked by flumazenil. The authors called it the first experimental evidence of a direct kavalactone interaction with these receptors. It is one compound in a lab setting, not a full explanation of the plant [7].
- Kratom. NIDA says mitragynine breaks down into 7-OH and that both activate mu-opioid receptors, with effects that only partially resemble opioids like heroin or oxycodone [3]. The FDA says 7-OH has substantially greater mu-opioid potency than mitragynine and that mitragynine also acts on serotonin, dopamine, norepinephrine and kappa opioid receptors [5].
- Kanna. A standardized extract blocked the serotonin transporter and inhibited PDE4 in a 2011 study, with mesembrine the most potent alkaloid at the transporter [8]. A later cell study suggested a monoamine-releasing action may be involved, so this is unsettled [13].
The practical point is that "these are all mood plants" hides real differences. Kratom's principal alkaloids activate opioid receptors; the kanna and kava studies cited here examined other targets [3][4][7][8].
What are the safety flags for each plant?
Kratom has the most formal warnings, kava has a specific liver advisory, and kanna has the thinnest record, which is its own kind of caution.
Kava
NCCIH states that kava products have been linked to "rare cases of liver injury, some of which have been serious or even fatal." It advises against using kava with other sedating substances such as benzodiazepines or alcohol, lists digestive upset, headache and dizziness as possible side effects, and notes possible special risks in pregnancy and breastfeeding [1]. The FDA issued a consumer advisory on March 25, 2002, after case reports of severe liver injury. CDC's MMWR described 11 patients with liver failure who received transplants after using kava products, and noted that extra caution might be warranted for people with existing liver disease or risk for it [2].
Kratom
The FDA says it has warned consumers not to use kratom because of risk of serious adverse events, including liver toxicity, seizures and substance use disorder, and that deaths have been reported in rare cases, usually involving other drugs. It also cites neonatal abstinence syndrome and contamination with Salmonella or heavy metals [5]. NIDA says people may experience mild to moderate withdrawal after stopping regular use, and that fatal overdose from kratom alone is "extremely rare" [3]. A CDC report found kratom on postmortem toxicology in 152 of 27,338 overdose deaths (0.56%) across 27 states from July 2016 to December 2017, with kratom the only substance detected in 7 and fentanyl listed as a cause in 65.1% of the kratom-positive group [14].
Kanna
In the one 3-month safety trial, 37 healthy adults taking 8 mg or 25 mg of Zembrin daily showed no differences from placebo in vital signs, ECG or bloodwork [12]. WebMD lists headache and upset stomach as common side effects and flags possible interactions with SSRIs, SNRIs, MAOIs, tricyclics, antipsychotics, triptans and St. John's wort. It also says pregnancy and breastfeeding data are lacking [10]. Details: is kanna safe.
What is the legal status of kava, kratom and kanna?
None is a federally scheduled controlled substance in the sources we reviewed, but kratom's 7-OH component is the subject of active federal action.
The DEA's fact sheet says kratom is not a controlled substance under the Controlled Substances Act [4], while the FDA says it is not lawfully marketed as a dietary supplement or food additive [5]. On July 29, 2025, the FDA recommended a scheduling action for certain 7-hydroxymitragynine products, stating it was not focused on natural kratom leaf [15]. On October 14, 2026, the DEA published a notice of intent to issue a temporary scheduling order placing 7-OH and mitragynine pseudoindoxyl in Schedule I, with the order to be published on or after November 13, 2026. It is a notice, not a final order [6]. The proposed control would apply above thresholds set in the notice, based on how much 7-OH and mitragynine pseudoindoxyl a product contains per gram or milliliter, and on the ratio of mitragynine to those compounds; see the notice for the exact definitions. The notice says neither HHS nor DEA has found these substances safe below the threshold [6]. It also withdraws the DEA's earlier July 2026 notice of intent, which used a different threshold, and says a separate August 26, 2026 temporary order already places mitragynine pseudoindoxyl in Schedule I [6]. The notice does not schedule mitragynine or kratom leaf itself [6]. The status has been changing during 2026, so check the Federal Register for current rules.
Kava is sold as a dietary supplement and served at kava bars [1]. Kanna is sold as a supplement ingredient too; see is kanna legal for what we could and could not confirm. Local rules can differ for all three.
How do these plants show up in drinks?
Kava appears as traditional root beverages and in canned blends, kanna in newer functional drinks, and kratom mostly as powders, capsules and shots.
Several canned drinks blend kava and kanna, which our kanna vs kava page lays out with the amounts each brand states. We did not review kratom beverages for this post, and given the FDA's position that kratom is not lawfully marketed as a supplement or food additive [5], we are not covering them. For kanna-only options, our kanna drink ranking lists kanna per can, price and ingredients, and a short mention for transparency: kannadrinks.com is published by Psilly Goose, whose Silly drink is kanna and lion's mane with no kava, listed on our ranking alongside competitors.
How should you think about choosing between them?
Start with the caution list that applies to you, not the marketing words.
- Take sedating medicines or drink alcohol? Kava's guidance against combining it with those is the one to read [1].
- Take an SSRI, SNRI, MAOI, triptan or similar? Kanna's interaction caution is the one that matters [10].
- Concerned about dependence or regulatory change? Kratom carries the most formal warnings of the three [5].
- Pregnant or nursing? Talk to a doctor about any of them. Kava and kanna both have limited pregnancy data [1][10], and the FDA cites neonatal abstinence syndrome for kratom [5].
None of this is medical advice, and none of the three is approved by the FDA for any use. If you or someone you know is struggling with substance use, SAMHSA's National Helpline is free and confidential at 1-800-662-4357 (samhsa.gov). To read about kanna's own research base, see what studies show about kanna.
This page is general information, not medical advice. These statements have not been evaluated by the FDA. Kanna products are not intended for any disease or health condition.
References
- National Center for Complementary and Integrative Health. Kava. nccih.nih.gov
- Centers for Disease Control and Prevention. Hepatic toxicity possibly associated with kava-containing products, United States, Germany, and Switzerland, 1999 to 2002 (describes the FDA consumer advisory of March 25, 2002). MMWR. cdc.gov
- National Institute on Drug Abuse. Kratom. nida.nih.gov
- Drug Enforcement Administration, Diversion Control Division. Kratom (Mitragyna speciosa), October 2025. deadiversion.usdoj.gov
- U.S. Food and Drug Administration. FDA and Kratom (page current as of December 2025). fda.gov
- Drug Enforcement Administration. Schedules of Controlled Substances: Temporary Placement of 7-Hydroxymitragynine and Mitragynine Pseudoindoxyl in Schedule I (notice of intent; Docket DEA-1570). Federal Register, October 14, 2026 (document 2026-20943). govinfo.gov
- Chua HC, et al. Kavain, the major constituent of the anxiolytic kava extract, potentiates GABAA receptors: functional characteristics and molecular mechanism. PLoS One 2016;11(6):e0157700. PubMed Central
- Harvey AL, et al. Pharmacological actions of the South African medicinal and functional food plant Sceletium tortuosum and its principal alkaloids. J Ethnopharmacol 2011;137(3):1124-9. PubMed
- Olatunji TL, et al. Sceletium tortuosum: a review on its phytochemistry, pharmacokinetics, biological and clinical activities. J Ethnopharmacol 2021;280:114476. PubMed
- WebMD. Sceletium: Uses, side effects, interactions. webmd.com
- Terburg D, et al. Acute effects of Sceletium tortuosum (Zembrin), a dual 5-HT reuptake and PDE4 inhibitor, in the human amygdala and its connection to the hypothalamus. Neuropsychopharmacology 2013;38(13):2708-16. PubMed
- Nell H, et al. A randomized, double-blind, parallel-group, placebo-controlled trial of Extract Sceletium tortuosum (Zembrin) in healthy adults. J Altern Complement Med 2013;19(11):898-904. PubMed
- Coetzee DD, et al. Effects of a high-mesembrine Sceletium extract on monoamine transporters (cell study). J Ethnopharmacol 2016;177:111-6. PubMed
- O'Malley Olsen E, et al. Notes from the Field: Unintentional drug overdose deaths with kratom detected, 27 states, July 2016 to December 2017. MMWR 2019;68(14). cdc.gov
- U.S. Food and Drug Administration. FDA takes steps to restrict 7-OH opioid products threatening American consumers (July 29, 2025). fda.gov
Frequently asked questions
What is the difference between kava, kratom and kanna?
They are three unrelated plants. Kava is Piper methysticum from the South Pacific [1], kratom is Mitragyna speciosa from Southeast Asia [4], and kanna is Sceletium tortuosum from South Africa [9]. Each has different active compounds, a different proposed mechanism and a different safety record.
Which of the three has the most safety warnings?
Kratom carries the most formal federal warnings: the FDA has warned consumers not to use it [5]. Kava has an FDA consumer advisory about rare liver injury from 2002 [2]. Kanna has no comparable warning in what we reviewed, but it is far less studied [10].
Are kava, kratom and kanna legal?
None of the three is a federally scheduled controlled substance in the sources we reviewed [5][10]. The FDA says kratom is not lawfully marketed as a dietary supplement [5], and the DEA published an October 2026 notice of intent (not a final order) to temporarily schedule 7-OH above a threshold [6]. Local rules vary.
Which one acts on opioid receptors?
Kratom's principal alkaloids activate mu-opioid receptors [3][4]. The kava and kanna studies cited here examined other targets: kavain enhanced GABA-A receptors in a lab study [7], and kanna's proposed targets are the serotonin transporter and PDE4 [8].
Can you combine kava, kratom and kanna?
We found no studies of any combination that includes kanna. Each has its own caution list, including sedatives and alcohol for kava [1] and serotonergic medicines for kanna [10]. Talk to a doctor before combining plant products. See is kanna safe.