All compounds

Kratom

Also sold as Mitragyna speciosa, ketum, biak-biak, mitragynine. Plant leaf containing mitragynine and 7-hydroxymitragynine, partial μ-opioid receptor agonists.

Works as advertised, real trade-offs (2 of 5)

Kratom leaf does what people take it for and is a genuinely different proposition from heroin or oxycodone — but it produces real opioid-type dependence, and the concentrated 7-hydroxymitragynine products now sold in the same shops are a far more dangerous thing wearing the same name.

What it is

Kratom is the leaf of Mitragyna speciosa, a tree in the coffee family native to Thailand, Malaysia and Indonesia, where the leaves have been chewed and brewed by agricultural workers for a very long time. In the West it arrives as a green powder, as capsules, or as a liquid “shot” sold at petrol stations and smoke shops.

Its main active alkaloid is mitragynine. A minor alkaloid, 7-hydroxymitragynine, is far more potent at the opioid receptor and is present in the natural leaf only in trace amounts.

Its legal status is genuinely chaotic. It is federally legal in the United States but banned in several states and municipalities; it is banned in Thailand for decades and then legalised again; it is controlled in much of Europe, Australia and the UK. It has never been approved as a medicine anywhere. No pharmaceutical company developed it and none abandoned it, which is why it does not have the tidy backstory that cardarine or tianeptine does.

The single most important thing on this page is a distinction, not a warning. “Kratom” now refers to two quite different products sold side by side:

• Leaf kratom — the ground leaf, or a modest extract of it, where the pharmacology is dominated by mitragynine.
• Concentrated 7-hydroxymitragynine products — tablets and shots, often branded and sold at the counter, containing amounts of 7-OH that do not occur in any leaf.

Nearly everything reassuring in the literature is about the first. A growing amount of what is alarming is about the second. Treating them as one substance is the main way people get hurt, and it is what most writing on this subject does.

What it actually does

Mitragynine is a partial agonist at the μ-opioid receptor, with a signalling profile that differs from morphine or oxycodone — it appears to engage the receptor without recruiting the pathway most associated with respiratory depression. That pharmacological difference is the reason kratom does not kill people the way conventional opioids do, and it is a real difference rather than an advocacy talking point.

What people get from it: pain relief, relief from opioid withdrawal, and at lower amounts a stimulant-like lift — alertness and sociability rather than sedation. That dual character is unusual and is a large part of the appeal.

The use case that deserves to be stated plainly, because most writing on kratom avoids it: a substantial number of people use kratom to stay off heroin, fentanyl or prescription opioids, and for them it is working. Survey after survey finds this population. Someone who has substituted kratom for fentanyl has not made a lateral move; they have made an enormous reduction in their risk of dying. Any page that tells that person kratom is simply dangerous is giving them advice that would kill them if they took it.

That is a different question from whether someone with no opioid history should start.

What the evidence actually shows

On pharmacology: solid. The receptor activity of mitragynine and 7-OH is well characterised in the laboratory, and the partial-agonist, differently-biased profile is a real finding, not a marketing claim.

On dependence: consistent and clear. Regular use produces tolerance and physical dependence, and stopping produces an opioid-type withdrawal — aching, runny nose, sweating, gooseflesh, restlessness, insomnia, irritability. Reviews of the literature and large user surveys agree on this. It is generally described as milder and shorter than withdrawal from heroin or methadone, but “milder than heroin withdrawal” is a low bar and people find it genuinely hard.

On deaths: this is where careful reading matters. Deaths with kratom detected in the body are documented. When those cases are examined, the overwhelming majority also involve other substances — commonly fentanyl, benzodiazepines, alcohol or other opioids. Cases where kratom appears to be the sole agent exist but are rare. The honest summary is that kratom contributes to deaths in combination far more than it causes them alone.

On liver injury: a real, uncommon signal. Adverse-event reporting includes a recognisable pattern of cholestatic liver injury — jaundice, itching, dark urine, pale stools — typically appearing after weeks of regular use and typically resolving after stopping. It is not common, but it is specific enough to be worth recognising.

On the 7-OH products: the evidence base is new and the direction is not ambiguous. Reviews published in the last couple of years describe the shift from a plant preparation to concentrated 7-OH products as a distinct public-health problem, with higher abuse potential and more severe dependence than the leaf.

What nobody knows: what happens over decades, and how many regular users become dependent. There has never been a controlled trial of kratom as a treatment for anything, so nobody can tell you how it compares to buprenorphine for the purpose most people are actually using it for.

The risk profile

Works as advertised, real trade-offs (2 of 5) — It does the thing people take it for, and it costs something specific and known.

What going wrong looks like from the inside

There are two distinct ways this goes wrong, and they feel completely different.

The slow one is dependence, and it is easy to miss because kratom is legal, cheap and sold openly. It starts as something you take for a specific reason — pain, or getting through a shift, or the tail end of an opioid habit. Then the morning dose stops being optional. You notice that you feel flat and achy if you are late with it, and that taking it fixes that, and you file this under “it helps” rather than “I am now taking it to stop feeling withdrawal.” The tell is that the reason changes: you began taking it for something, and at some point you are taking it to feel normal. People often cross that line while still describing kratom as a supplement, because the shop it comes from does not feel like a place where you develop a dependence.

The fast one belongs to the concentrated products. Somebody who has used leaf kratom uneventfully for years buys a 7-OH tablet or shot from the same counter, treats it as the same substance, and it is not. The reports describe far quicker escalation, much harder withdrawal, and people who were entirely stable on leaf finding themselves in trouble within weeks. If you take one practical thing from this page: check what you are buying, and treat anything advertising its 7-hydroxymitragynine content as a different drug.

The liver signal is worth knowing by name because it is recognisable and it is the one thing here that can become serious quietly. If your skin or the whites of your eyes look yellow, if you are itching all over without a rash, if your urine goes dark or your stools go pale — stop and get a liver panel. That combination is not a normal kratom side effect and it is not something to wait out.

Interactions and combinations

Kratom is an opioid agonist, and the rules for opioids apply even though the packaging does not look like it.

The dangerous combinations are other central nervous system depressants: benzodiazepines, alcohol, gabapentin or pregabalin, other opioids, and sedating sleep medication. This is the combination that shows up in the death data. Kratom’s more favourable respiratory profile is a real advantage on its own and is not a licence to combine it — the protection it offers is relative, and it does not extend to whatever else is in the mix.

Kratom is metabolised through the CYP450 system, and mitragynine both is a substrate and inhibits some of those enzymes. In practice this means it can raise levels of other drugs you take, and some common medicines can raise levels of kratom. There have been serious interactions reported, including with some antidepressants and with quetiapine. If you take prescription medication regularly, this is worth raising with a pharmacist, who will answer the question without any of the awkwardness of raising it elsewhere.

One specific interaction matters more than the rest: if you are on buprenorphine or methadone, or considering starting, tell the prescriber about the kratom. Kratom’s receptor activity interacts directly with how those treatments are started, and getting the sequence wrong can precipitate a sharp withdrawal.

If you’re already using it

If kratom is working for you and it is keeping you away from something considerably more dangerous, we are not going to tell you to stop. That would be worse advice than the marketing.

Things worth doing:

Know what you are actually taking. Leaf or 7-OH concentrate. If a product advertises potency, treat it as a different drug from the powder you may have used for years.

Be honest with yourself about the direction of travel. Not “how much” but “why” — for pain and function, or to avoid feeling ill. If the second one is true, that is dependence, and it is much easier to address early.

Do not combine it with sedatives, and if you are prescribed one, say that you take kratom.

Tell any doctor treating you. It will not show on a standard drug screen. If you end up in hospital, staff who do not know can misread an opioid withdrawal or a drug interaction badly.

If you want to stop, stopping kratom covers what to expect and how to find help. Kratom withdrawal is unpleasant but — unlike phenibut — it is not usually medically dangerous, which changes the options considerably.

If you have been using this regularly and want to stop: read this first. Stopping abruptly is the part that goes wrong.

This page has not yet been reviewed by a clinician. It was written from the published literature and every claim is cited, but no named medical professional has checked it. We say so here rather than let a missing byline read as an implicit one.

Last reviewed 7 September 2026. Found something wrong? Corrections are published, not silently edited.