Also known as

Herbal speedball, biak-biak, ketum, kahuam, ithang, thom, thang, kakuam, biak


Stimulant, sedative


Kratom is a tropical tree (Mitragyna speciosa) native to Southeast Asia, with leaves that contain psychoactive (mind-altering) opioid compounds. The tree's bitter leaves are consumed for mood-uplifting effects and pain relief and as an aphrodisiac.

Kratom is not currently an illegal substance and has been easy to order on the Internet in recent years. It is sometimes sold as a green powder in packets labelled 'not for human consumption'. It is also sometimes sold as an extract or gum.

In recent years, some people have used kratom as an herbal alternative to medical treatment in attempts to control withdrawal symptoms and cravings caused by addiction to other opioids or to other addictive substances such as alcohol. There is no scientific evidence that kratom is effective or safe for this purpose (see "Medication-Assisted Treatment") [1].

The leaves of the tree Mitragyna speciosa are oval or ovate-lanceolate and dark green in colour and can grow to 180 mm long and 100 mm wide. The veins of the leaves are either greenish-white or red - the former is reputed to be more potent. The average weight of a fresh and a dried leaf is about 1.7 and 0.43 g respectively. The yellow and globular flowers of the tree bear up to 120 florets. The fruit is a capsule containing numerous small flat seeds.

Kratom products are usually supplied as crushed or powdered dried leaves that are light to dark green in colour. Powdery, greenish or beige-brown kratom preparations fortified with extracts from other leaves are also available. Stable, paste-like extracts and dark brown kratom resin can be made by partially or fully boiling down the water from aqueous kratom leaf suspensions. Tinctures and capsules, filled with powdered kratom, are also available [2].

Kratom is a tree native to Southeast Asia (Thailand, Malaysia, Indonesia, Borneo, etc.). Its botanical name is Mitragyna speciosa. Kratom is in the same family as the coffee tree (Rubiaceae). The leaves of kratom have been used as an herbal drug from time immemorial by peoples of Southeast Asia. It is used in folk medicine as a stimulant (at low doses), sedative (at high doses), recreational drug, pain killer, medicine for diarrhea, and treatment for opiate addiction. Many people report that kratom is an effective treatment for arthritis, restless legs syndrome (RLS), and fibromyalgia [3].

Kratom (also known as Mitragyna speciosa) is a tree from Indonesia whose leaves produce a psychoactive effect. The leaf of the kratom tree is known to produce a full spectrum of typical opioid effects which can range from stimulation to sedation, and even both in some cases. It is commonly used as a substitute for opioid painkillers, a sleep aid and as a recreational drug.

There are a variety of strains of kratom; some of which have a much stronger opioid characteristic, causing sedation, while others are considered similar to a pleasant caffeine stimulation. As a general rule, kratom tends to produce more stimulating effects at lower doses, but becomes increasingly more sedating as the dosage is increased [4].


Kratom appeared on the global drug market only recently, thus there is no information on the extent of its use outside South East Asia.

In Thailand, the National Household Surveys provide information on drug use prevalence in that country. The 2007 Survey (26,633 respondents aged 12 - 65 years) indicated that the lifetime, past year and past 30 days prevalences for kratom were 2.32%, 0.81% and 0.57%, respectively. These figures, with the exception of lifetime use, were significantly higher than those for cannabis making kratom the most widely used illicit drug in the country. Also in Thailand, lifetime, past year and past 30-days prevalence studies among 13- to 16-year-old high-school students (n = 8 708--12,148) in 2002, 2003 and 2004 showed an increase in the lifetime use of kratom (from 3.97% to 9.43%) and cannabis (from 4.44% to 6.75%), while a slight decrease was noted for the use of amphetamines (2.79% to 2.32%). Past year and past 30-days prevalence use data followed similar trends.

A recent roadside survey involving 1,635 motor vehicle drivers in Thailand revealed the use of kratom by 0.9% of the drivers, a prevalence close to that of cannabis (1.1%) but much lower than that of amphetamines (1.8%).Internet surveys conducted by the EMCDDA in 2008 indicated that kratom was one of the most widely offered 'legal highs' in 44% of the investigated 27 European online shops along with Salvia divinorum (74%), Hawaiian Baby Woodrose seeds (48%), Spice smoking mixtures (37%), and stimulant-containing capsules (59%). A more extensive EMCDDA Internet survey in July 2011 showed that kratom was the most widely offered product with 128 out of 631 (or 20%) of online retailers shipping it to the EU. An Internet snapshot carried out in the UK in April 2009 showed that among the 346 unique products offered by 39 shops kratom (n = 30) was second only to Salvia divinorum (n = 44) [2].

Street price

Prices vary between countries and depend on the type and amount of the product purchased. According to the EMCDDA Internet surveys conducted in 2008, the prices of 'Kratom 15X' extracts ranged from EUR 2.1 to 10.3 per gram in the sampled European countries. In 2011, a follow-up EMCDDA snapshot of 314 online shops found that prices ranged from EUR 6 to 15 per 10 gram of dried kratom and EUR 7 to 8 per gram of 'Kratom 15X' extract [2].

Why take it?

Sought after effects

  • simultaneous stimulation and sedation,
  • feelings of empathy,
  • feelings of euphoria,
  • aphrodisiac qualities for some people,
  • vivid waking dreams,
  • increases sociability and talkativeness [5].

Undesired effects

  • mild depression during and/or after,
  • increase in (perceived) body temperature (feel hot and sweaty),
  • desire to repeat experience more frequently than intended, can lead to addiction,
  • tolerance building quickly after a few days in a row of repeated use, tolerance to effects reduces with a one to three days of abstinence,
  • psychosis,
  • convulsions,
  • hallucinations [5].

How long do its effects last?

Onset of effects

- oral - 10 - 40 minutes [6], 15 - 45 minutes [4], 5 - 15 minutes [5].


- oral - 1 - 2 hours [4].


- oral - 3 - 6 hours [4].

Duration of effects

- oral - 2 - 5 hours [6], [4], [5].


- oral - 6 - 48 hours [6], 3 - 6 hours [5].


Kratom preparations contain several phytochemicals in varying ratios rendering their proper pharmacological evaluation difficult. Human clinical studies are scarce.

In general, the effects of kratom in humans are dose-dependent - small doses produce 'cocaine-like' stimulation while larger dosages cause 'morphine-like' sedative-narcotic effects.

After taking a few grams of dried leaves, the invigorating effects and euphoria are felt within 10 minutes and last for one to one and a half hours. Kratom users report increased work capacity, alertness, sociability and sometimes heightened sexual desire. The pupils are usually normal or very slightly contracted; blushing may be noted. In one of the few human clinical experiments, a 50 mg oral dose of mitragynine produced motor excitement, followed by giddiness, loss of motor coordination (positive Romberg's test), and tremors of the extremities and face. For regular kratom users, loss of weight, tiredness, constipation, and hyperpigmentation of the cheek may be notable side-effects. The pharmacological mechanism responsible for stimulant activity is unclear.

Kratom taken in large, sedating doses corresponding to 10 - 25 g of dried leaves may initially produce sweating, dizziness, nausea and dysphoria but these effects are shortly superseded with calmness, euphoria and a dreamlike state that last for up to six hours. Contracted pupils (miosis) are noted.

Mitragynine and 7-hydroxymitragynine, the two alkaloids mainly responsible for the effects of kratom, are selective and full agonists of the μ-subtype opioid receptor (MOR). The receptor agonist effect of kratom alkaloids is antagonised by the opioid receptor antagonist naloxone. In addition, 5-HT2a and postsynaptic α2-adrenergic receptors, as well as neuronal Ca2+ channels are also involved in the unique pharmacological and behavioural activity of mitragynine.

In animal studies, the antinociceptive and cough-suppressant effects of mitragynine were comparable to those of codeine. In mice, 7-hydroxymitragynine was several times more potent analgesic than morphine even upon oral administration.

Kratom is slightly toxic to animals. Mice chronically treated with 7-hydroxymitragynine developed tolerance, cross-tolerance to morphine and withdrawal signs that could be precipitated by naloxone administration.

The metabolism of mitragynine in humans occurs via hydrolysis of the side-chain ester, O-demethylation of the methoxy groups, oxidative and/or reductive transformations, and the formation of glucuronide and sulfate conjugates. In a man who fatally overdosed propylhexedrine and kratom, the postmortem mitragynine concentrations ranged from 0.01 mg/kg to 1.20 mg/l [2].

More than 20 alkaloids in kratom have been identified in the laboratory, including those responsible for the majority of the pain-relieving action, the indole alkaloid mitragynine. Mitragynine is classified as a kappa-opioid receptor agonist and is roughly 13 times more potent than morphine. Mitragynine, structurally similar to yohimbine, is thought to be responsible for the opioid-like effects.

Kratom, due to its opioid-like action, has been used for treatment of pain and opioid withdrawal but structurally it is not the same as the common opioids morphine or codeine. Animal studies suggest that the primary mitragynine pharmacologic action occurs at the mu and delta-opioid receptors, as well as serotonergic and noradrenergic pathways in the spinal cord. Stimulation at post-synaptic alpha-2 adrenergic receptors, and receptor blocking at 5-hydroxytryptamine 2A may also occur. Additional animals studies show that these opioid-receptor effects are reversible with the opioid antagonist naloxone.

Time to peak concentration in animal studies is reported to be 1.26 hours, and elimination half-life is 3.85 hours [7].

Kratom behaves as an opioid receptor agonist similar in function to morphine and other opiates, although its pharmacological action and subjective effects differ significantly from those of traditional opiates [8].

Opioids exert their effects by binding to and activating the opioid receptors. They structurally mimic endogenous endorphins which are naturally found within the body and also work upon the opioid receptor system. The way in which opioids structurally mimic these natural endorphins results in their euphoria, pain relief and anxiolytic effects. This is because endorphins are responsible for reducing pain, causing sedation, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or general excitement.

One of the primary pharmacological differences between kratom and traditional opiates is that at lower dosages, mitragynine alkaloids preferentially bind to delta opioid receptors, while opiates such as morphine and heroin preferentially bind to μ-opioid receptors.

At higher doses, however, mitragynine increasingly acts upon μ-opioid in a similar manner to traditional opioids. This is speculated to be one of the reasons that kratom has a stimulating effect at lower doses and sedating effects at higher doses [9]. Unlike most other opioids, kratom also presents affinity for the κ-opioid [10], norepinephrine and serotonin [11] receptor systems where it functions as an agonist. Its action on norepinephrine and serotonin also likely contributes to kratom's stimulating properties.

Alongside of this, kratom also contains alkaloids (rhynchophylline and mitraphylline) which function as NMDA receptor antagonists [12]. This may be responsible for the mild dissociating effects which occur at heavy doses [4].

The pharmacological effects of kratom on humans are not well studied. Its metabolic half-life, protein binding, and elimination characteristics are all unknown. Kratom behaves as a μ-opioid receptor agonist, similar to opiates like morphine, although its effects differ significantly from those of opiates.

Mitragynine is a partial agonist of the mu- and delta-opioid receptors. This may account for its apparent efficacy in treating opiate withdrawal. Because kratom acts as both a stimulant and a sedative, secondary alkaloids may be pharmacologically important [5].

Lethal dosage

The lethal dosage of kratom is unknown but thought to be far above the active dosage. The precise dosage likely depends on a variety of factors including strain, potency, tolerance and method of consumption. It is unlikely that one could ingest a lethal dosage of kratom powder as the nausea will force one to vomit at around 8 - 9 grams; however, it could be possible to ingest a lethal dosage of a kratom if purer forms such as a resin or pure alkaloids are used [4].


Kratom has a low toxicity relative to dose [4].


Tolerance to many of the effects of kratom develops with prolonged and repeated use. The rate at which this occurs develops at different rates for different effects, with tolerance to the constipation-inducing effects developing particularly slowly for instance. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Kratom presents cross-tolerance with all other opioids, meaning that after the consumption of kratom all opioids will have a reduced effect [4].

Mechanism of action

Two compounds in kratom leaves, mitragynine and 7-hydroxymitragynine, interact with opioid receptors in the brain, producing sedation, pleasure, and decreased pain, especially when users consume large amounts of the plant. However, there can be uncomfortable and sometimes dangerous side-effects.

Mitragynine may also interact with other receptor systems in the brain to produce stimulant effects. When kratom is taken in small amounts, users report increased energy, sociability, and alertness instead of sedation [1].

Mode of use

Some people chew kratom leaves or brew the dried or powdered leaves as a tea. Sometimes the leaves are smoked or eaten in food [1].

In its native region, kratom leaves are often chewed fresh (usually after removing the stringy central vein). Dried leaves can also be chewed, but since they are a bit tough, most people prefer to crush them up or powder them so that they can be swallowed easily. Powdered kratom can be mixed with water and then drunk. This method is quick and easy. It can also be mixed with other liquids, such as fruit juice, milk, or kefir. Chocolate milk works especially well for masking the taste. Powdered kratom can also be made into a paste that can easily be swallowed with water. The powder can also be mixed with applesauce or yogurt. It can also be put into capsules. Dried kratom leaves are often made into a tea that is strained and then drunk. Kratom can be smoked, but doing so is impractical because the amount of leaf that constitutes a typical dose is too much to be smoked easily. A resin-like extract can be prepared by evaporating the water from kratom tea. This can be stored for later use. Small pellets of this extract can be swallowed, or it can be dissolved in hot water and consumed as a tea. Some people like to mix kratom tea with ordinary black tea, or other herbal teas, before it is consumed. This is done to make it more palatable. Sugar or honey can be added to sweeten it [3].

The leaves are crushed and then smoked, brewed with tea, or placed into gel capsules [13].


Reported health effects of kratom use include -

  • sensitivity to sunburn,
  • nausea,
  • itching,
  • sweating,
  • dry mouth,
  • constipation,
  • increased urination,
  • loss of appetite [1], [13].

Psychotic symptoms have been reported in some users.

Kratom by itself is not associated with fatal overdose, but commercial forms of the drug are sometimes laced with other compounds that have caused deaths [1].

Long-term effects

  • anorexia,
  • weight loss,
  • insomnia,
  • dry mouth,
  • frequent urination,
  • constipation [13],
  • loss of appetite,
  • darkening of the skin colour of the face,
  • bowel obstruction [4].

Physical effects

  • physical euphoria,
  • pupil constriction,
  • stimulation,
  • appetite suppression,
  • cough suppression,
  • orgasm suppression,
  • pain relief,
  • constipation,
  • difficulty urinating,
  • itchiness,
  • nausea [4].

Cognitive effects

  • cognitive euphoria,
  • dream potentiation,
  • motivation enhancement,
  • thought acceleration,
  • anxiety suppression,
  • decreased libido [4].

Visual effects

  • acuity suppression,
  • double vision,
  • visual disconnection,
  • internal hallucinations [4].

Positive effects

  • simultaneous stimulation and sedation,
  • feelings of empathy,
  • feelings of euphoria,
  • aphrodisiac qualities for some people,
  • vivid waking dreams,
  • useful with physical labour,
  • low doses can result in a lasting 'glow' in some people, feeling better than normal the next day,
  • increases sociability and talkativeness [5].

Neutral effects

  • relatively short duration,
  • change in ability to focus eyes,
  • analgesia [5].

Negative effects

  • very bitter taste,
  • dizziness, nausea and/or vomiting at higher doses,
  • mild depression during and/or after,
  • increase in (perceived) body temperature (feel hot and sweaty),
  • hangover similar to alcohol, including headaches and sometimes nausea (at higher doses),
  • desire to repeat experience more frequently than intended, can lead to addiction,
  • tolerance building quickly after a few days in a row of repeated use, tolerance to effects reduces with a one to three days of abstinence,
  • psychosis,
  • convulsions,
  • hallucinations,
  • confusion (rare),
  • loss of appetite, and weight loss (chronic use),
  • constipation (chronic use),
  • darkening of the skin colour of the face (chronic use) [5].


  • sedation,
  • nausea,
  • sweating,
  • dry mouth,
  • increased urination,
  • loss of appetite,
  • itching,
  • constipation,
  • dizziness,
  • confusion [14].


Like other opioid drugs, kratom may cause dependence (feeling physical withdrawal symptoms when not taking the drug), and some users have reported becoming addicted to kratom [1].

Dangerous interactions


  • Ketamine - Both substances bring a risk of vomiting and unconsciousness. If the user falls unconscious while under the influence there is a severe risk of vomit aspiration if they are not placed in the recovery position.
  • MXE - This combination can potentiate the effects of the opioid
  • DXM - CNS depression, difficult breathing, heart issues, hepatoxic, just very unsafe combination all around. Additionally if one takes dxm, their tolerance of opiates goes down slightly, thus causing additional synergistic effects.
  • Cocaine - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
  • Alcohol - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. Place affected patients in the recovery position to prevent vomit aspiration from excess. Memory blackouts are likely.
  • GHB/GBL - The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position.
  • Tramadol - Concomitant use of tramadol increases the seizure risk in patients taking other opioids. These agents are often individually epileptogenic and may have additive effects on seizure threshold during coadministration. Central nervous system- and/or respiratory-depressant effects may be additively or synergistically present.
  • Benzodiazepines - Central nervous system and/or respiratory-depressant effects may be additively or synergistically present. The two substances potentiate each other strongly and unpredictably, very rapidly leading to unconsciousness. While unconscious, vomit aspiration is a risk if not placed in the recovery position Blackouts/memory loss likely [6].


  • PCP - PCP can reduce opioid tolerance, increasing the risk of overdose.
  • N2O - Both substances potentiate the ataxia and sedation caused by the other and can lead to unexpected loss of consciousness at high doses. While unconscious, vomit aspiration is a risk if not placed in the recovery position. Memory blackouts are likely.
  • Amphetamines - Stimulants increase respiration rate allowing a higher dose of opiates. If the stimulant wears off first then the opiate may overcome the patient and cause respiratory arrest.
  • MAOIs - Co-administration of monoamine oxidase inhibitors (MAOIs) with certain opioids has been associated with rare reports of severe and fatal adverse reactions. There appear to be two types of interaction, an excitatory and a depressive one. Symptoms of the excitatory reaction may include agitation, headache, diaphoresis, hyperpyrexia, flushing, shivering, myoclonus, rigidity, tremor, diarrhoea, hypertension, tachycardia, seizures, and coma. Death has occurred in some cases [6].


Regular kratom use may produce dependence. The withdrawal symptoms in humans are relatively mild and typically diminish within a week [2].

  • craving,
  • weakness,
  • lethargy,
  • anxiety,
  • restlessness,
  • rhinorrhea,
  • myalgia,
  • nausea,
  • sweating,
  • muscle pain,
  • jerky limb movements,
  • tremor,
  • sleep disturbances,
  • hallucinations [2],
  • irritability,
  • hostility,
  • aggression,
  • emotional changes,
  • runny nose [1].

Drug testing

Kratom use is not detected by typical drug screening tests, but its metabolites can be detected by more specialised testing [6].

Mixing with other drugs

The consumption of kratom concomitantly with other drugs can provoke serious side-effects. In fact, adverse drug interactions involving kratom tea taken with carisoprodol, modafinil, propylhexedrine or Datura stramonium have been reported. A fatal case in the United States involved a blend of kratom, fentanyl, diphenhydramine, caffeine and morphine sold as a herbal drug [2].

Harm reduction

  • Do not drive or operate heavy machinery.
  • Do not combine with opioids.
  • Do not combine with benzodiazapines.
  • Do not combine with any other CNS depressant [5].


Treatment, if needed, may include dihydrocodeine-lofexidine combination, non-steroidal antiinflammatory agents, antidepressants and/or anxiolytics [2].


Kratom appears to have been used in Thailand for centuries, recreationally and as an antidiarrhetic. Its use as an opiate substitute in Malaysia was reported in the nineteenth century. Peasants have used it to counteract the tedium of physical labor, similar to the use of coca in South America. The chemistry of its alkaloids was investigated in the 1920's, and mitragynine was isolated in 1923. Kratom leaves became part of the ethnobotanical trade in the United States and Europe in mid 2000. In the early 2000's, stories about the use of kratom to reduce opiod withdrawal effects began circulating on web forums [5].


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