Kanna is a succulent plant native to South Africa, known scientifically as Sceletium tortuosum, that has been used for centuries as a mood-enhancing and stress-relieving botanical. It works primarily by increasing serotonin activity in the brain, similar in mechanism (though not in strength) to some prescription antidepressants. Today it’s sold widely as a dietary supplement in the United States, with over 40 products listed in the National Institutes of Health Dietary Supplements Label Database.
The Plant and Its Origins
Kanna is a low-growing succulent in the ice plant family, native to the dry regions of South Africa. Its Afrikaans name, “kougoed,” translates roughly to “chewable thing,” which describes exactly how indigenous peoples traditionally consumed it. The San and Khoikhoi peoples of southern Africa have likely used kanna for millennia as a traditional medicine and social aid, chewing the dried or fermented plant material and swallowing the saliva. It served practical purposes during long hunts, suppressing hunger and thirst while reducing fatigue.
Beyond its use as a stimulant for endurance, kanna held a broader role in traditional medicine. It was used as a pain reliever (particularly for toothaches and mouth pain), a sedative, and a digestive aid. Women used it during pregnancy for nausea and constipation, and after childbirth for recovery. An oil made from the plant mixed with sheep fat was even applied to relieve colic in babies. Much of this traditional knowledge has declined over the past three centuries due to colonization and cultural disruption.
How Kanna Works in the Brain
Kanna contains a family of alkaloids, with mesembrine being the most important. These compounds act on the brain through two distinct pathways. First, they block the reuptake of serotonin, meaning they allow more serotonin to remain active between nerve cells. This is the same basic mechanism used by SSRI antidepressants like fluoxetine and sertraline. Second, kanna’s alkaloids inhibit an enzyme called PDE4, which plays a role in inflammation and signaling within brain cells.
This dual action appears to be what gives kanna its particular profile of effects. A brain imaging study using a standardized kanna extract showed that it reduced activity in the brain’s threat-response circuitry, specifically the amygdala and its connections to the stress-regulation center. In plain terms, the brain’s alarm system became less reactive to perceived threats, which researchers interpreted as a potential mechanism for reducing anxiety.
Why Fermentation Matters
Traditionally, kanna was fermented before use, and modern research suggests this wasn’t arbitrary. Fermentation significantly changes the plant’s chemical makeup. The process converts mesembrenone (a less potent compound) into mesembrine (the primary active compound). In laboratory analysis, mesembrine content jumped from nearly undetectable levels to concentrations between 7.4 and 20.8 micrograms per milliliter after fermentation, while mesembrenone levels dropped correspondingly. Total alkaloid content also increased. So the ancestral practice of fermenting kanna before chewing it was, in effect, a form of potency enhancement.
Today, kanna is available in many forms beyond the traditional chew: capsules, teas, tinctures, powders, and even snuff. Most commercial supplements use standardized extracts rather than raw plant material, which allows for more consistent dosing of the active compounds.
What Clinical Trials Have Found
The most studied standardized extract of kanna is sold under the brand name Zembrin. In a randomized, placebo-controlled trial, 25 mg of this extract taken daily for three weeks produced measurable improvements in cognitive performance. Participants showed significantly better executive function (the higher-order thinking skills like working memory, attention control, and response inhibition) and cognitive flexibility (the ability to shift between tasks or mental strategies). The effect sizes were large, at 1.47 and 1.49 respectively, meaning the differences between the kanna and placebo groups were substantial, not subtle.
The same study found positive changes in mood and sleep quality. Participants in the kanna group reported uplifted spirits and better coping with stress. Scores on a standard depression rating scale improved by about 27% in the kanna group compared to roughly 14% in the placebo group, though this particular difference didn’t reach statistical significance due to the small sample size. Improvements were also noted in subcategories including irritability, anxiety, drowsiness, memory problems, and confusion.
Safety and Side Effects
In clinical testing, kanna has shown a reassuring safety profile at typical supplement doses. In a three-month study, both 8 mg and 25 mg daily doses of standardized extract were well tolerated. The most common adverse events actually occurred more frequently in the placebo group than in the groups taking kanna. No treatment-related adverse effects were observed in animal toxicity studies either.
That said, computer modeling of mesembrine’s toxicological profile has flagged moderate potential for effects on the respiratory and kidney systems at higher exposures, along with low-to-moderate potential for heart-related effects. These predictions haven’t materialized in human trials at standard doses, but they do suggest that more isn’t necessarily better.
Interactions With Other Substances
Because kanna acts as a serotonin reuptake inhibitor, the most serious safety concern is combining it with other substances that raise serotonin levels. This combination can potentially trigger serotonin toxicity, a condition where excess serotonin causes symptoms ranging from agitation and rapid heartbeat to, in severe cases, dangerous spikes in body temperature and seizures.
Substances that raise serotonin and could interact with kanna include:
- SSRI and SNRI antidepressants (the most commonly prescribed antidepressants)
- MAO inhibitors, both as antidepressants and in less obvious forms like the antibiotic linezolid
- Tricyclic antidepressants, particularly clomipramine and imipramine
- Certain pain medications like tramadol, methadone, and fentanyl (though morphine, codeine, oxycodone, and buprenorphine do not carry this risk)
- MDMA (ecstasy) and amphetamines, which cause serotonin release
- St. John’s wort and dextromethorphan (a common cough suppressant)
If you take any medication that affects serotonin, combining it with kanna is a risk that should not be taken lightly.
Regulatory Status in the U.S.
Kanna is legal in the United States and sold as a dietary supplement. In February 2011, a specific standardized extract of the plant received GRAS (Generally Recognized As Safe) status, and products containing it entered the U.S. market the following year. This means the FDA has not objected to its use as a food ingredient at specified levels, though GRAS status is not the same as FDA approval as a drug. Kanna is not currently found in any prescription or over-the-counter drug products in the U.S., aside from minor use in some homeopathic formulations. It occupies the same regulatory space as other herbal supplements like ashwagandha or valerian root.