dangerous

BANNED

Do Not Use

Kratom

Prohibited by FDA (Import Alert 54-15), Alabama, Arkansas, Indiana, Rhode Island, Vermont, Wisconsin, Louisiana (SB 154)

warningCDC documented 91 overdose deaths involving kratom (2016-2017). Most cases involved other substances, but kratom was the sole toxicological finding in some fatalities.

Kratom

OPIOID

Also known as: Mitragyna speciosa, Ketum, Kakuam, Thang, Biak-Biak, Thom

What is Kratom?

Kratom (Mitragyna speciosa) is a tropical evergreen tree native to Southeast Asia whose leaves contain alkaloids that act on opioid receptors. The two primary alkaloids—mitragynine and 7-hydroxymitragynine (7-OH)—produce dose-dependent effects: stimulation at low doses (1-5g) and sedation/analgesia at higher doses (5-15g). While marketed as a 'natural' alternative to opioids, kratom produces physiological dependence with a documented withdrawal syndrome. The FDA maintains Import Alert 54-15 and has not approved kratom for any medical use.

Why is Kratom Banned?

States ban kratom due to: (1) Opioid-like addiction and withdrawal potential; (2) 91+ documented deaths involving kratom; (3) Contamination issues including the 2018 Salmonella outbreak; (4) Lack of quality control and standardization; (5) FDA's determination that kratom products are adulterated/misbranded; (6) Emerging evidence of seizure risk with concentrated 7-OH products.

Banned by FDA (Import Alert 54-15)Banned by AlabamaBanned by ArkansasBanned by IndianaBanned by Rhode IslandBanned by VermontBanned by WisconsinBanned by Louisiana (SB 154)

Health Risks & Side Effects

warningCommon Side Effects

  • arrow_rightOpioid-like withdrawal syndrome (muscle aches, insomnia, RLS)
  • arrow_rightNausea, vomiting, and constipation
  • arrow_rightSeizures (especially with high doses or 7-OH products)
  • arrow_rightLiver toxicity (rare but documented)
  • arrow_rightRapid tolerance development requiring dose escalation
  • arrow_rightAnxiety, irritability, and mood swings

blockContraindications

  • arrow_rightHistory of opioid use disorder
  • arrow_rightLiver disease or elevated liver enzymes
  • arrow_rightPregnancy or breastfeeding
  • arrow_rightConcurrent use of CNS depressants (benzos, alcohol, opioids)
  • arrow_rightHistory of seizures
  • arrow_rightMAO inhibitor use

How Does Kratom Work?

Mitragynine is a partial agonist at mu-opioid receptors with additional activity at kappa, delta opioid receptors, alpha-2 adrenergic receptors, and serotonergic systems. 7-hydroxymitragynine is approximately 22x more potent at mu-opioid receptors. This multi-receptor activity explains kratom's unique combination of stimulant (low dose) and sedative (high dose) effects, as well as its complex withdrawal presentation combining opioid-like and stimulant-like features.

History

Traditional use in Thailand and Malaysia for centuries as a labor aid and folk medicine. Thailand banned kratom in 1943 due to interference with opium tax revenue, then decriminalized it in 2021. In the US, kratom gained popularity in the 2010s as an alternative to prescription opioids. The DEA attempted emergency Schedule I classification in 2016 but withdrew after unprecedented public backlash. Multiple contamination outbreaks, overdose deaths, and wrongful death lawsuits have driven increasing state-level regulation.

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articleWhat is Kratom?

Kratom (Mitragyna speciosa) is a tropical evergreen tree in the coffee family native to Southeast Asia, primarily Thailand, Malaysia, Indonesia, and Myanmar. The leaves contain over 40 alkaloids, with the two most pharmacologically significant being mitragynine (66% of alkaloid content) and 7-hydroxymitragynine (7-OH).

Kratom produces dose-dependent effects:

  • Low doses (1-5g): Stimulation, increased energy, alertness, and sociability—similar to coffee
  • Moderate doses (5-10g): Analgesic effects, mild euphoria, reduced anxiety
  • High doses (10-15g+): Sedation, opioid-like effects, pain relief, potential for nausea

This biphasic action results from mitragynine's complex pharmacology: at low concentrations it activates adrenergic receptors (stimulation), while at higher concentrations mu-opioid receptor activity predominates (sedation/analgesia).

Common Forms:

  • Powder: Dried, crushed leaves—most common form
  • Capsules: Measured powder doses for convenience
  • Extracts: Concentrated products with elevated 7-OH levels—higher addiction and seizure risk
  • Shots/Drinks: Liquid extracts often sold at gas stations

While kratom has been used traditionally in Southeast Asia for centuries, its modern Western use as an opioid alternative has raised significant safety concerns, leading to FDA import alerts and state-level bans.

articleKratom Withdrawal: Timeline & The 10% Taper Protocol

Never quit kratom cold turkey if you have significant dependence. Abrupt cessation causes uncomfortable withdrawal symptoms that peak around days 3-4.

Withdrawal Timeline

PhaseDurationSymptoms
Early Withdrawal6-12 hoursMild irritability, anxiety, muscle aches, sweating, runny nose
Acute Withdrawal24-72 hoursPeak physical symptoms, intense muscle pain, severe GI distress, insomnia, RLS
Subacute PhaseDays 4-7Gradual symptom reduction, lingering fatigue, reduced psychological intensity
Late Withdrawal1-2 weeksMost physical symptoms resolved, psychological symptoms may persist
PAWSWeeks to monthsMood instability, anxiety, depression, cravings, cognitive effects

The 10% Weekly Reduction Protocol

The evidence-based tapering approach involves reducing total daily dose by 10% every 7 days:

  1. Establish baseline: Measure and record your exact daily intake using a digital scale (0.1g accuracy)
  2. Calculate reduction: Multiply daily dose by 0.9 for your new weekly target
  3. Divide doses: Split daily amount across your normal dosing schedule
  4. Hold if needed: If symptoms emerge, hold current dose until stable before continuing
  5. Slower at low doses: Below 5g/day, consider 5% reductions every 1-2 weeks

Example 20g/day taper: Week 1: 18g → Week 2: 16.2g → Week 3: 14.6g → Week 4: 13.1g... continuing until cessation

Supportive Supplements

  • Magnesium glycinate (400-800mg/day): Reduces RLS and muscle tension
  • Vitamin C sodium ascorbate (megadose protocol): 5,000-25,000mg/day in divided doses during acute phase
  • Black seed oil (1-2 tsp/day): May reduce cravings and anxiety
  • L-theanine (200-400mg/day): For sleep and relaxation
  • Ashwagandha (300-600mg/day): Cortisol modulation and stress reduction

articleSafety Concerns & Side Effects

Documented Deaths

The CDC documented 91 overdose deaths involving kratom from 2016-2017. While most cases involved polysubstance use, kratom was identified as a contributing factor. A 2025 Neurology study identified 113 kratom-induced seizures from Poison Control data (2011-2017), with risk elevated in concentrated 7-OH products.

Serious Adverse Events

  • Seizures: Increasing reports, especially with extract products. Standard urinalysis does not detect kratom; diagnosis often delayed 4+ days.
  • Hepatotoxicity: Rare but documented liver injury in chronic users requiring hospitalization.
  • Cardiac events: Case reports of tachycardia and arrhythmia at high doses.
  • Respiratory depression: Possible when combined with other CNS depressants.

Common Side Effects

SystemEffects
GastrointestinalNausea, vomiting, constipation, appetite suppression
NeurologicalDizziness, tremor, seizures (high dose), cognitive impairment
PsychologicalAnxiety, irritability, depression, insomnia
PhysicalDry mouth, sweating, weight loss, tolerance escalation

Drug Interactions

Kratom inhibits CYP2D6 and CYP3A4 enzymes, potentially increasing levels of medications metabolized by these pathways. Dangerous combinations include:

  • Opioids (respiratory depression risk)
  • Benzodiazepines (enhanced sedation)
  • Alcohol (CNS depression)
  • MAO inhibitors (hypertensive crisis potential)
  • Antidepressants (serotonin syndrome risk with some SSRIs)

Contamination Issues

The 2018 Salmonella outbreak infected 199 people across 41 states. Testing has also found kratom products contaminated with heavy metals, E. coli, and even synthetic opioids. The lack of FDA oversight means product quality varies dramatically.

help_outlineFrequently Asked Questions

Kratom is fully banned in 7 states: Alabama, Arkansas, Indiana, Louisiana (as of Aug 1, 2025), Rhode Island, Vermont, and Wisconsin. It's legal with age restrictions (typically 21+) in 15+ KCPA states including Arizona, Florida, Georgia, and Texas. In remaining states, it's legal but unregulated. Check your specific state law before purchasing.
Acute kratom withdrawal symptoms typically last 4-10 days, with peak intensity around days 3-4. Physical symptoms (muscle aches, GI issues, RLS) usually resolve within 7-10 days. Psychological symptoms (anxiety, depression, cravings) may persist for weeks in Post-Acute Withdrawal Syndrome (PAWS). Duration depends on dose, frequency, and individual metabolism.
Standard 5-panel and 12-panel drug tests do NOT detect kratom. However, specialized tests for mitragynine exist and are increasingly used by probation offices, pain management clinics, and some employers. Kratom is detectable in urine for 5-7 days, blood for 24-48 hours, and hair for up to 90 days.
There are no documented deaths solely from kratom withdrawal. Unlike alcohol or benzodiazepine withdrawal, kratom withdrawal does not typically cause seizures. However, severe dehydration from vomiting/diarrhea is a risk, and psychological distress including suicidal ideation has been reported. Medical supervision is recommended for heavy users.
The safest approach is a gradual taper: reduce your dose by 10% every 7 days until cessation. Use a digital scale for accuracy. Supportive supplements (magnesium, vitamin C, black seed oil) can help manage symptoms. For heavy users (>20g/day) or those with complications, medical supervision with potential buprenorphine bridge therapy may be appropriate.
Kratom is classified as an 'atypical opioid.' Its primary alkaloids (mitragynine, 7-hydroxymitragynine) act on mu-opioid receptors like traditional opioids, but with additional activity at adrenergic, serotonergic, and other receptors. This creates both opioid-like effects (pain relief, sedation, withdrawal) and unique properties (stimulation at low doses). It produces physiological dependence and withdrawal similar to opioids.
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Research articles and educational resources

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Overview

From Wikipedia, the free encyclopediaschedule13 min read
Kratom illustration

Mitragyna speciosa

Mitragyna speciosa is a tropical evergreen tree of the Rubiaceae family native to Southeast Asia. It is indigenous to Cambodia, Thailand, Indonesia, Malaysia, Myanmar, and Papua New Guinea, where its dark green, glossy leaves, known as kratom, have been used in herbal medicine since at least the 19th century. They have also historically been consumed via chewing, smoking, and as a tea. Kratom has opioid-like properties and some stimulant-like effects.

science

Scientific Research

From PubMed • 3 peer-reviewed studies

Kratom (Mitragyna speciosa): Friend or Foe?

The primary care companion for CNS disorders2020Sethi Roopa, Hoang Nguyen et al.

Increased use of the opioid-related plant kratom as an alternative treatment for opioid withdrawal symptoms has raised concerns regarding its potential for abuse and severe adverse effects. A review of the literature was performed to characterize kratom's pharmacology, clinical efficacy, and adverse effects to increase understanding and evaluate potential use as an alternative treatment for opioid dependence. Kratom use initiated as self-medication for an opioid use disorder or pain syndrome in the absence of effective alternatives is associated with a risk of kratom dependence, withdrawal, and life-threatening toxicity. The potential for a serious adverse reaction should discourage unregulated use of kratom products.

Biased Opioid Ligands.

Molecules (Basel, Switzerland)2021Faouzi Abdelfattah, Varga Balazs R et al.

Achieving effective pain management is one of the major challenges associated with modern day medicine. Opioids, such as morphine, have been the reference treatment for moderate to severe acute pain not excluding chronic pain modalities. Opioids act through the opioid receptors, the family of G-protein coupled receptors (GPCRs) that mediate pain relief through both the central and peripheral nervous systems. Four types of opioid receptors have been described, including the μ-opioid receptor (MOR), κ-opioid receptor (KOR), δ-opioid receptor (DOR), and the nociceptin opioid peptide receptor (NOP receptor). Despite the proven success of opioids in treating pain, there are still some inherent limitations. All clinically approved MOR analgesics are associated with adverse effects, which include tolerance, dependence, addiction, constipation, and respiratory depression. On the other hand, KOR selective analgesics have found limited clinical utility because they cause sedation, anxiety, dysphoria, and hallucinations. DOR agonists have also been investigated but they have a tendency to cause convulsions. Ligands targeting NOP receptor have been reported in the preclinical literature to be useful as spinal analgesics and as entities against substance abuse disorders while mixed MOR/NOP receptor agonists are useful as analgesics. Ultimately, the goal of opioid-related drug development has always been to design and synthesize derivatives that are equally or more potent than morphine but most importantly are devoid of the dangerous residual side effects and abuse potential. One proposed strategy is to take advantage of biased agonism, in which distinct downstream pathways can be activated by different molecules working through the exact same receptor. It has been proposed that ligands not recruiting β-arrestin 2 or showing a preference for activating a specific G-protein mediated signal transduction pathway will function as safer analgesic across all opioid subtypes. This review will focus on the design and the pharmacological outcomes of biased ligands at the opioid receptors, aiming at achieving functional selectivity.

The pharmacology and toxicology of kratom: from traditional herb to drug of abuse.

International journal of legal medicine2016Warner Marcus L, Kaufman Nellie C et al.

Mitragyna speciosa (Rubiaceae), commonly known as kratom, is a tropical tree with a long history of traditional use in parts of Africa and Southeast Asia. In recent years, kratom has gained popularity for use as a recreational drug across the globe. Relatively new to the illicit market and used in a manner different from its traditional applications, preparations of kratom are touted by many as a safe and legal psychoactive product that improves mood, relieves pain, and may provide benefits in opiate addiction. Available literature was reviewed for M. speciosa via PubMed, Google Scholar, CINAHL, and EBSCO to summarize its traditional uses, phytochemical composition, pharmacology and toxicology of proposed active constituents, and potential for misuse and abuse. Research has demonstrated that both stimulant and sedative dose-dependent effects do exist, but a growing concern for the drug's effects and safety of use has resulted in national and international attention primarily due to an increase in hospital visits and deaths in several countries that are said to have been caused by extracts of the plant. The main active alkaloid substances in kratom, mitragynine and 7-hydroxymitragynine, present with a range of CNS stimulant and depressant effects mediated primarily through monoaminergic and opioid receptors. Recently, Palm Beach County, located in the southeastern corridor of Florida, has considered regulating kratom due to public safety concerns following the death of a young adult. At the local, state, and even federal levels, governments are now being confronted with the task of determining the safety and the possible regulation of kratom extracts. There are currently no standard analytical screening techniques for mitragynine and its metabolites following ingestion limiting its detection to more sophisticated techniques like liquid chromatography-mass spectrometry to determine kratom use. The growing concern of the abuse potential of kratom requires careful evaluation of its benefits and potential toxicities.

Data sourced from Wikipedia and PubMed