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Kratom (''Mitragyna speciosa'' Korth., Rubiaceae) is a tropical tree native to Southeast Asia whose leaves contain over 40 indole alkaloids. Its dominant constituent, mitragynine, is a G-protein-biased partial agonist at the μ-opioid that also engages α₂-adrenergic receptors.[1] Mitragynine produces its principal effects by partially activating opioid and adrenergic pathways, generating a dose-dependent spectrum from mild stimulation to opioid-like sedation.

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minlowmodhigh
Acute
Chronic
Physical
Psych.
Withdrawal
Buildupmoderate
Full reset10 days
Cross-tol.opioids
Absolute4 entries
Pre-existing liver diseasePregnancy and lactationConcurrent opioid useConcurrent CNS depressants
Relative4 entries
Respiratory compromiseHistory of psychosisRenal impairmentCYP3A4 substrates with narrow therapeutic index
Dosage varies by body weight, tolerance & metabolism · Not medical advice · Terms

First described by Pieter Willem Korthals in 1841,[2] kratom was used for centuries as a work aid and folk medicine in Thailand and Peninsular Malaysia.[3] The plant entered Western markets around 2005–2010 and became a focus of regulatory debate after the US DEA proposed — then withdrew — Schedule I classification in 2016.

Subjective effects include stimulation, mood elevation, analgesia, sedation, and euphoria, shifting from functional energy at lower doses to opioid-like warmth and cognitive slowing at higher doses.[4] The defining quality is a dual adrenergic-opioid character absent from conventional opioids, though preparation type and alkaloid content — which varies more than 50-fold across commercial products — profoundly shape the experience.[5] Common unsought effects include nausea, constipation, and pupil constriction.

Prolonged use carries clinically significant opioid-type dependence risk, with a withdrawal marked by myalgia, insomnia, anxiety, and irritability.[6] Hepatotoxicity — predominantly cholestatic — has been documented at a median latency of roughly three weeks.[7] The principal contemporary safety concern is the divergence between botanical leaf and commercially enriched 7-Hydroxymitragynine products, which carry substantially greater respiratory depression and dependence risk;[8] no formal human dose-finding trials have been completed, and long-term safety data remain limited to observational studies and case reports.

History[edit]

Traditional and historical use

''Mitragyna speciosa'' was first described by the Dutch botanist Pieter Willem Korthals in 1841 during surveys of the Dutch East Indies.[2] Korthals named the genus for the resemblance of its stipules to a bishop's mitre; earlier European accounts of leaf chewing in Peninsular Malaysia appear in the work of Low, dating to 1836.[3][9]

Kratom — กระท่อม (krathom) in Thai, ketum in Malay — has been used in southern Thailand and the Malay Peninsula for centuries as a traditional work aid and folk remedy.[3][10] Farm laborers chewed fresh leaves daily to combat fatigue during manual work, functioning analogously to coca leaf use in South America.[3] As opium became expensive or restricted, kratom served as a cheaper substitute for managing pain, cough, diarrhea, and eventually opioid withdrawal.[11][12] In some communities, kratom tea was offered to guests as a social gesture, paralleling kava hospitality in Pacific island cultures.[10]

Western discovery and research

Kratom products appeared in Western retail and online markets around 2005–2010, marketed as a legal opioid alternative and a self-treatment for opioid withdrawal.[3] Prozialeck, Jivan, and Andurkar published the first widely cited English-language pharmacology review in 2012,[11] and Kruegel and Grundmann followed in 2018 with a comprehensive neuropharmacology review characterizing the G-protein-biased opioid agonism of kratom alkaloids.[1] By 2025, hundreds of peer-reviewed publications had addressed the plant's pharmacology, toxicity, and abuse liability.

Modern era

Thailand banned kratom in 1943 under the Kratom Act B.E. 2486 — paradoxically, while simultaneously profiting from opium taxation — and classified it as a Category 5 narcotic in 1979.[13] On August 24, 2021, Thailand reversed course, removing kratom from its narcotics list.[13]

In the United States, the DEA published a notice of intent on August 31, 2016 to temporarily place mitragynine and 7-hydroxymitragynine into Schedule I.[14] The agency withdrew the notice on October 13, 2016 — the first such withdrawal in DEA history — following approximately 142,000 public comments opposing scheduling.[15]

Botanical Overview[edit]

Mitragyna speciosa Korth. belongs to the family Rubiaceae — the coffee family — making it a distant botanical relative of Coffea (coffee) and Psychotria (the genus containing the ayahuasca admixture Psychotria viridis). The genus Mitragyna contains roughly ten species of trees distributed across tropical Africa and Asia; M. speciosa is the only member widely used for its psychoactive properties.

Kratom is native to a broad swath of tropical Southeast Asia, from southern Indochina through the Malay Peninsula, Sumatra, Borneo, and as far east as New Guinea.[3] It thrives in lowland tropical forest with heavy rainfall, rich alluvial soils, and partial to full sun. Wild populations grow along riverbanks and in swamp margins. Today it is widely cultivated in Thailand, Indonesia, and Malaysia, with Indonesia the dominant source for international commerce.

The tree reaches 15–25 meters at maturity with a straight trunk and broadly spreading crown. Leaves are the pharmacologically relevant organ: large (up to 20 cm long), glossy, ovate, with prominent pinnate venation. Leaf vein color — red, green, or white — is the primary commercial cultivar marker, though the relationship between vein color and alkaloid profile is inconsistent and poorly validated in peer-reviewed literature.citation needed Flowers are deep yellow, globular, and clustered in heads, giving rise to the genus name (mitra = mitre, for the shape of the stipules).

For psychoactive use, leaves are harvested at maturity when alkaloid content is highest. Traditional preparation involves chewing fresh leaves with the tough central vein removed. For commercial sale, leaves are dried, powdered, and sometimes further extracted. Drying method, leaf maturity, and post-harvest processing all influence final alkaloid concentration.

Alkaloid Profile[edit]

Kratom leaf contains over 40 identified indole alkaloids, but its pharmacology is dominated by two: mitragynine and its hepatic metabolite 7-Hydroxymitragynine.

Mitragynine constitutes approximately 66% of total alkaloid content[17] and typically represents 0.5–1.5% of dry leaf weight. It acts as a partial agonist at μ-opioid receptors with G-protein-biased signaling and simultaneously engages α₂-adrenergic receptors.[1] This dual mechanism is proposed to explain the stimulant character at low doses (adrenergic dominance) and opioid-like sedation at higher doses (μ-opioid dominance).

7-Hydroxymitragynine occurs at trace levels in unprocessed leaf but is also produced in vivo through hepatic CYP3A4 metabolism of mitragynine.[18] It binds μ-opioid receptors with roughly 13-fold greater potency than mitragynine and acts as a full agonist without significant α₂-adrenergic activity.[19][20] Commercially enriched extracts contain dramatically higher 7-hydroxymitragynine concentrations than botanical leaf, producing a fundamentally different pharmacological and risk profile.[8]

Minor alkaloids include speciogynine and speciociliatine (both diastereomers of mitragynine, each approximately 6–7% of total alkaloid content) and paynantheine (roughly 9%). These accumulate in plasma with repeated daily dosing[21] but their individual contributions to subjective effects remain poorly characterized — most evidence is in vitro.

Alkaloid concentrations vary enormously across commercial products. A survey of retail kratom found mitragynine content ranging from 0.7% to 38.7% w/w — a greater-than-50-fold difference.[5] Growing conditions, leaf maturity at harvest, drying method, and post-harvest extraction all contribute to this variability. Vein color (red, green, white) is marketed as a reliable potency indicator but lacks consistent peer-reviewed validation.citation needed

Neuroscience[edit]

Where it acts

Kratom's mixed pharmacology explains its unusual dose-dependent character. Mitragynine partially activates μ-opioid receptors with G-protein-biased signaling — meaning it does not significantly recruit β-arrestin-2 — and simultaneously agonizes α₂-adrenergic receptors.[1][22] At lower doses, adrenergic stimulation predominates, producing alertness and energy; at higher doses, opioid receptor engagement overtakes it, producing sedation and analgesia. Kratom alkaloids additionally interact with serotonergic, dopaminergic, and noradrenergic systems, contributing to mood elevation and, during withdrawal, affective disturbance.[23][24]

What it changes

The G-protein-biased agonism of mitragynine is proposed to preserve analgesic efficacy while reducing β-arrestin-2-mediated adverse effects such as respiratory depression and rapid tolerance.[22] However, respiratory depression risk is reduced rather than eliminated, particularly with concentrated 7-hydroxymitragynine preparations.[25] Chronic use leads to opioid-receptor adaptation and tolerance, with documented cross-tolerance to classical opioids.[26] Cognitive effects with sustained use are attributed to disruption of neuroplasticity across opioid, serotonergic, and adrenergic systems.[27]

Subjective Effects[edit]

Summary

Kratom's experiential character is defined by a dose-dependent inversion: at lower doses, a warm, sociable stimulation with mood elevation and enhanced focus; at higher doses, opioid-like analgesia, bodily heaviness, and cognitive slowing. The stimulant range carries a quality distinct from caffeine — attributed to concurrent adrenergic and partial opioid receptor activity — while the sedative range approaches the analgesic warmth of codeine. Preparation type is the primary modifier: leaf powder tea produces a gentler arc than concentrated extracts, which compress onset and amplify peak intensity. Set, setting, and individual opioid tolerance strongly shape the experience.

Pharmacologically, kratom occupies a position between stimulant plants and classical opioids. Its low-dose profile resembles coca leaf — functional energy with mood lift — while its higher-dose profile approaches mild opioid analgesia, distinguished by reduced respiratory depression risk and a dual adrenergic-opioid quality absent from conventional opioids. Enriched 7-hydroxymitragynine products produce a qualitatively different experience dominated by full μ-opioid agonism, closer to classical opioid character than to traditional leaf preparations.

Preparations[edit]

Fresh leaf (chewed)

Fresh leaf is the traditional Southeast Asian preparation. Leaves are plucked, the tough central vein is removed, and the remaining lamina is chewed and held in the cheek. Onset occurs within 5–10 minutes; effects last 1–2 hours. Typical traditional use involves 1–3 leaves per session.[3] Fresh leaf is rarely available outside cultivation regions.

Dried leaf powder (oral — toss-and-wash or mixed)

Dried leaf powder is the most common commercial preparation worldwide. Users swallow measured powder directly with water ("toss and wash") or mix it into juice, yogurt, or a smoothie. Onset is 20–40 minutes; total duration 3–5 hours.[4] Dose ranges are preparation-specific:

  • Threshold: 1–2 g
  • Common (stimulant range): 2–4 g
  • Common (sedative range): 4–6 g
  • Strong: 6–8 g

Alkaloid content varies more than 50-fold across commercial products,[5] making batch-specific dose calibration essential.

Tea (oral, aqueous decoction)

Kratom tea is prepared by simmering dried leaf powder or crushed leaf in water for 15–30 minutes and straining the plant material. Onset is slightly faster than powder (15–30 minutes) due to pre-extraction of alkaloids into solution; duration is comparable at 3–5 hours. Dose ranges parallel dried powder by weight of starting material. Tea produces a somewhat smoother onset curve with less gastrointestinal irritation than raw powder, as insoluble plant fiber is removed.

Capsules (oral)

Capsules contain pre-measured dried leaf powder, typically 0.5–1 g per capsule. Onset is delayed (30–60 minutes) due to capsule dissolution. Duration and dose ranges are equivalent to powder. Capsules reduce taste aversion but make dose titration less flexible.

Extracts and concentrated products

Extracts — sold as resins, tinctures, and liquid "shots" — concentrate kratom alkaloids well beyond natural leaf levels. These products carry the highest risk of any kratom preparation. Commercial extracts marketed as botanical kratom may contain dramatically enriched 7-hydroxymitragynine concentrations, producing a fundamentally different pharmacological profile from leaf.[8] Onset is rapid (10–20 minutes for liquid extracts); duration varies by concentration. Dose equivalence between extracts and leaf powder is unreliable — labeling is frequently inaccurate, and no standardized potency system exists. Start at half or less of the dose a user would take in powder form and titrate cautiously.

Per-preparation dose tiers, timelines, and bioavailability data are in the Dose · by preparation card on this page.

Safety[edit]

Harm
Acute toxicity
Low
Chronic toxicity
Moderate
Withdrawal
Moderate
Tolerance buildup
moderate
Tolerance reset
10 days
Dependence
Physical
High
Psychological
High
Compulsive redosing
Moderate
Dose escalation
Moderate
Cross-tol.
opioids
Risk Shape
TOXPHYPSYWDRREDTOL

Toxicity

No human lethal dose has been established for mitragynine or any kratom preparation. Animal studies document hepatic, renal, pulmonary, and CNS toxicity at high doses.[28] Acute toxicity from traditional leaf doses is considered low; chronic toxicity data are limited but raise concerns for liver and cognitive function.[28]

Kratom is a documented cause of drug-induced liver injury (DILI) with a predominantly cholestatic pattern.[7] A comprehensive review found a median latency of 20.6 days from first use to symptom onset (range 2–49 days), with jaundice, pruritus, and dark urine as common presenting features.[7] Causality assessment concluded that kratom "likely causes liver injury based on totality of evidence".[7] Individual cases have demonstrated cholestatic injury mimicking primary biliary cholangitis.[29]

Published fatalities attributed in whole or part to kratom involve polydrug exposures in nearly all cases. Nine deaths in Sweden resulted from "Krypton" — kratom powder adulterated with O-desmethyltramadol.[16] A fatal case involving hydromorphone and kratom attributed death to hydromorphone toxicity with mitragynine as a contributing factor.[30] A 26-year-old male died of cardiorespiratory failure following suspected kratom use, though polydrug exposure was not fully excluded.[31] No deaths attributed solely to botanical kratom appear in published Southeast Asian literature.[9]

Contaminant and adulterant risk is a distinct safety concern for commercial kratom products:

  • Synthetic opioid adulterants: O-desmethyltramadol was documented in "Krypton" products (9 fatalities);[16] semi-synthetic 7-hydroxymitragynine enrichment appears in products marketed as botanical kratom[8]
  • Microbial contamination: FDA Import Alert 54-15 cites Salmonella contamination risk as a basis for detaining imported products[32]citation needed
  • Heavy metals: Lead, cadmium, and other heavy metal contamination is a theoretical concern for dried botanical products; no published validated surveys specific to kratom products were identifiedcitation needed
  • Labeling inaccuracy: Mitragynine content ranges 0.7–38.7% w/w across commercial products[5]

No ISO/IEC-accredited mandatory federal testing program exists for commercial kratom products in the United States. Some US states implementing Kratom Consumer Protection Act (KCPA) frameworks require testing and labeling standards.

Psychological Risks

Higher doses and concentrated 7-hydroxymitragynine products are associated with anxiety, irritability, and — in rare documented cases — psychosis.[26] Chronic kratom use may adversely affect cognitive performance through disruption of neuroplasticity via opioid, serotonergic, and adrenergic receptor interactions.[27] Epigenetic mechanisms have been implicated in withdrawal-associated cognitive impairment in animal models.[33] Kratom use patterns meeting DSM-5 substance use disorder criteria have been documented, with dose frequency showing a stronger association with dependence severity than dose amount.[34]

Tolerance & Dependence

Tolerance develops with prolonged use through μ-opioid mechanisms. Cross-tolerance with classical opioids is documented; buprenorphine can precipitate withdrawal in kratom-dependent individuals, confirming clinically significant opioid cross-tolerance.[26] The mitragynine half-life is approximately 23 hours;[35] specific tolerance recovery timelines have not been validated in published studies.

Physical dependence liability is high.[6] In studies of 150–170 regular Malaysian kratom tea users, cessation produced mild anxiety (70%), mild depression (81%), moderate pain intensity (84%), moderate pain interference (70%), and sleep problems (46%).[36][37] Severity was dose-dependent — users consuming ≥4 glasses daily had higher odds of more severe depression, pain interference, and sleep problems.[37] Withdrawal was characterized as "relatively mild" compared to classical opioid analgesic withdrawal in these studies.[37]

Severe withdrawal from concentrated 7-hydroxymitragynine products — including psychosis and respiratory compromise requiring intubation — has been documented in case reports.[26]

Withdrawal from botanical kratom leaf at moderate doses is generally manageable without medical intervention.[37] Low-dose sublingual buprenorphine has achieved complete kratom abstinence within 3 weeks in documented cases.[38] Reducing use frequency — rather than dose alone — may be a key harm reduction strategy, given that frequency shows a stronger association with dependence severity than dose amount.[34]

Recovery resources, crisis lines, and support pathways → View all

Drug Interactions

Kratom is both a CYP enzyme substrate and inhibitor/inducer, creating complex herb–drug interaction liability.

CYP3A4 inhibition is the best-characterized mechanism: a single 2 g dose of kratom tea increased midazolam AUC by 1.39× (90% CI: 1.23–1.57) and Cmax by 1.50× in 12 healthy adults.[39] PBPK modeling predicts mitragynine increases midazolam exposure 2.2–2.7× with co-administration.[40] Drugs extensively metabolized by CYP3A4 — including many opioids (oxycodone, fentanyl), benzodiazepines (midazolam, alprazolam), immunosuppressants (cyclosporine, tacrolimus), and statins — may reach toxic levels with concurrent kratom use.

CYP2D6 inhibition is demonstrated in vitro[41] but was not clinically significant at a 2 g kratom dose.[39] Significance at higher doses remains uncharacterized.

PXR-mediated enzyme induction with repeated kratom use (CYP3A4, CYP1A2, P-glycoprotein; 3–6-fold activation)[42] creates a paradoxical combination of acute CYP inhibition and chronic CYP induction, potentially reducing efficacy of co-administered drugs during sustained use.

Pharmacodynamic synergy with opioids and CNS depressants is the highest-risk interaction class. Fatal outcomes have been documented with kratom and hydromorphone[30] and kratom products adulterated with O-desmethyltramadol.[16] Combinations with alcohol, GHB/GBL, benzodiazepines, or ketamine carry pharmacodynamically plausible risk of additive CNS and respiratory depression.safety citation needed

Contraindications

Pregnancy: Contraindicated. Neonatal abstinence syndrome has been documented with kratom use during pregnancy;[43] teratogenicity is unknown. The opioid-like mechanism warrants avoidance during pregnancy and lactation.[44]

Hepatic impairment: Contraindicated. Kratom is a documented cause of drug-induced liver injury and may worsen pre-existing hepatic conditions.[7]

Concurrent opioid use: Contraindicated. Additive μ-opioid receptor agonism with documented fatal outcomes in polydrug contexts.[30][16]

Concurrent CYP3A4 substrates with narrow therapeutic index: Relative contraindication. Kratom inhibits intestinal CYP3A at typical oral doses, potentially elevating co-administered drug concentrations to toxic levels.[39]

Psychiatric history (psychosis): Relative contraindication for concentrated 7-hydroxymitragynine products, which have been associated with psychotic symptoms during withdrawal.[26]

Renal impairment: Relative contraindication. Renal impairment was present as a contributing factor in a documented fatal kratom-polydrug case;[30] the large volume of distribution (38 L/kg) suggests altered accumulation with impaired clearance.[35]

Harm Reduction[edit]

Forms & Identification

Reagent ResultsNot recorded+ add reagent results
AppearanceNot recorded+ add appearance
Red FlagsNot recorded+ add red flags

Lab testing matters more for kratom than for most botanical preparations because alkaloid content varies more than 50-fold across commercial products[5] and because some products marketed as botanical kratom contain enriched 7-hydroxymitragynine at concentrations far exceeding natural leaf levels.[8] A Certificate of Analysis (COA) from an ISO-accredited laboratory confirms mitragynine and 7-hydroxymitragynine concentrations, screens for heavy metals and microbial contaminants, and verifies absence of synthetic adulterants. Products sold without a COA should be treated as unverified. In US states that have enacted Kratom Consumer Protection Act (KCPA) frameworks, testing and labeling are mandatory — products from KCPA-regulated vendors carry greater reliability than unregulated sources.

Full identification analysis →

Guidelines

  • Start low, go slow. Begin with 1–2 g of dried leaf powder and wait at least 60 minutes before redosing. For extracts, start at half or less of an equivalent powder dose and titrate cautiously.
  • Use lab-tested products. Purchase from vendors who provide a current COA from an ISO-accredited laboratory. Verify that 7-hydroxymitragynine content is consistent with botanical leaf (typically <0.1% of dry weight) — substantially higher concentrations indicate enrichment.
  • Track dose and frequency. Dose frequency is a stronger predictor of dependence severity than dose amount.[34] Limit use to 2–3 days per week when possible to reduce dependence risk.
  • Avoid combinations. Never combine kratom with opioids, benzodiazepines, alcohol, or other CNS depressants — additive respiratory depression risk is the highest-severity interaction class.[30][16]
  • Hydrate and eat. Kratom suppresses appetite and can cause dehydration. Maintain fluid and food intake, especially with daily use.
  • Store securely. Keep all kratom products away from children and pets. Label stored powder and extracts clearly.

Set & Setting

Kratom's opioid-class pharmacology makes context especially important. Daily use in workplace settings carries impairment risk at higher doses — sedation, cognitive slowing, and impaired reaction time are dose-dependent effects. Users who take kratom for functional stimulation should be aware that the line between stimulant and sedative dosing is narrow and varies by batch. Driving or operating machinery after higher doses carries risk comparable to mild opioid impairment. Social or solitary use at sedating doses should occur in a safe, stable environment.

Aftercare & integration. After higher-dose kratom use, expect a period of low energy and mild mood dip lasting several hours as effects recede — this is a normal pharmacological rebound effect, not a medical concern. Hydrate thoroughly; kratom is mildly diuretic and appetite-suppressing, so fluid and electrolyte replenishment (water, broth, potassium-rich foods) supports recovery. If using kratom daily, monitor for constipation — a common opioid-class side effect — and maintain dietary fiber intake. Next-day grogginess is more likely with evening dosing of sedating doses; plan accordingly.

Recovery & Support

Kratom dependence is an opioid-class physical dependence. For users wanting to reduce or stop use:

  • Gradual taper is the first-line approach. Reduce dose by 0.5 g every 2–3 days, or reduce frequency by one session per week. Frequency reduction may be more effective than dose reduction alone.[34]
  • Medical support: Low-dose sublingual buprenorphine has achieved complete kratom abstinence within 3 weeks in documented cases.[38] Consult a physician experienced in opioid use disorder treatment.
  • Withdrawal management: Botanical kratom withdrawal is generally mild compared to classical opioid withdrawal — myalgia, insomnia, anxiety, and irritability are common symptoms.[6][37] Withdrawal from concentrated 7-hydroxymitragynine products can be significantly more severe.[26]
  • SAMHSA National Helpline: 1-800-662-4357 (free, confidential, 24/7). Provides referrals to local treatment facilities, support groups, and community-based organizations.
  • Support communities: Online peer-support forums provide lived-experience guidance, though advice should be verified against clinical sources.

Recovery resources, crisis lines, and support pathways → View all

Emergency Response

Recognizing an emergency: Slow or stopped breathing, blue or gray lips, unresponsiveness, pinpoint pupils, or seizures after kratom use — especially with concentrated extracts or in combination with other substances — constitute a medical emergency. Treat suspected kratom overdose as an opioid overdose.

Immediate steps:

  • 1. Call emergency services immediately (911 in the US).
  • 2. If the person is not breathing or breathing very slowly, administer naloxone if available — kratom's μ-opioid agonism is naloxone-reversible.
  • 3. Place the person in the recovery position (on their side) to prevent aspiration.
  • 4. Stay with the person until emergency responders arrive.
  • 5. Do not induce vomiting.

What to tell the dispatcher: Name the substance (kratom — specify if extract or powder), approximate amount and time of last dose, any other substances taken, and current symptoms. Good Samaritan laws in many US jurisdictions provide legal protection for individuals reporting overdoses.

Naloxone: Naloxone reverses μ-opioid agonism from both mitragynine and 7-hydroxymitragynine. It is available over the counter in the United States. Anyone using kratom extracts regularly should keep naloxone accessible.

references

  1. [1] 
    ^abcdKruegel AC, Grundmann O (2017) The medicinal chemistry and neuropharmacology of kratom: A preliminary discussion of a promising medicinal plant and analysis of its potential for abuse — Neuropharmacology doi:10.1016/j.neuropharm.2017.08.026
  2. [2] 
    ^abRoyal Botanic Gardens Kew (2024) Mitragyna speciosa Korth. - Plants of the World Online (POWO), Kew Link
  3. [3] 
    ^abcdefgCinosi E, Martinotti G, Simonato P, Singh D, Demetrovics Z, et al. (2015) Following the Roots of Kratom (Mitragyna speciosa): The Evolution of an Enhancer from a Traditional Use to Increase Work and Productivity in Southeast Asia to a Recreational Psychoactive Drug in Western Countries — BioMed Research International doi:10.1155/2015/968786
  4. [4] 
    ^abSmith KE, Rogers JM, Dunn KE, Grundmann O, McCurdy CR, Schriefer D, Epstein DH (2022) Searching for a Signal: Self-Reported Kratom Dose-Effect Relationships Among a Sample of US Adults With Regular Kratom Use Histories — Frontiers in Pharmacology doi:10.3389/fphar.2022.765917
  5. [5] 
    ^abcdeSharma A, Kamble SH, Leon F et al. (2019) Simultaneous quantification of ten key Kratom alkaloids in Mitragyna speciosa leaf extracts and commercial products by ultra-performance liquid chromatography-tandem mass spectrometry — Drug Testing and Analysis doi:10.1002/dta.2604
  6. [6] 
    ^abcSingh D, Muller CP, Vicknasingam BK (2014) Kratom (Mitragyna speciosa) dependence, withdrawal symptoms and craving in regular users — Drug and Alcohol Dependence doi:10.1016/j.drugalcdep.2014.03.017