⚠️ Ibogaine has a narrow therapeutic window and documented cardiac fatality risk at multiple dose levels — including doses previously considered safe. No ibogaine dosing protocol should be self-administered. All protocols described here require pre-treatment cardiac screening (12-lead ECG, QTc interval measurement), metabolic panels, and on-site medical supervision with resuscitation capability.

Ibogaine Dosing Protocols: Flood Dose, Booster, and Microdose

Ibogaine is administered under several distinct dosing frameworks, each with different therapeutic goals, durations, risk profiles, and monitoring requirements. Understanding the pharmacological basis of each protocol is essential for any provider, patient, or researcher evaluating ibogaine treatment. This page covers the three primary protocols — flood dose, booster dose, and microdose — along with the safety infrastructure each demands.

Pharmacological Baseline: Why Dosing Is So Complex

Ibogaine's complexity stems from its multi-target pharmacology and variable metabolism. It acts on opioid receptors, NMDA receptors, sigma-2 receptors, and serotonin transporters simultaneously (Koenig & Bhargava, 2019). Its primary active metabolite, noribogaine, has a half-life of 24–72 hours — far longer than ibogaine itself (half-life approximately 4–7 hours) — meaning effects continue long after the acute experience ends.

Critically, ibogaine and noribogaine both prolong the cardiac QTc interval (the corrected measure of ventricular repolarization). A QTc above 500 ms is associated with potentially fatal arrhythmias, including Torsades de Pointes. Multiple documented fatalities have occurred across all major dose categories (Litjens & Brunt, 2016). Dose alone does not determine safety — individual pharmacogenomics (particularly CYP2D6 enzyme activity), underlying cardiac pathology, concurrent substances, and electrolyte status are all critical variables.

Pre-Treatment Screening: Required Before Any Protocol

Conservative clinical guidance — including protocols used at licensed facilities in Mexico, Canada, and Portugal — requires the following before any ibogaine administration:

  • 12-lead ECG with QTc measurement (contraindicated if QTc >450 ms in men, >470 ms in women per most clinical protocols; some facilities use >440 ms as a hard cutoff)
  • Complete metabolic panel including potassium, magnesium, and calcium (hypokalemia and hypomagnesemia independently prolong QTc)
  • Liver function tests (ibogaine is hepatically metabolized; hepatic impairment raises plasma levels unpredictably)
  • Complete blood count
  • CYP2D6 genotyping (recommended by Mash et al., 2018; poor metabolizers accumulate ibogaine at higher concentrations)
  • Full substance use history and washout confirmation (see contraindications below)
  • Psychiatric evaluation ruling out active psychosis, severe bipolar I with recent mania, and suicidal ideation with plan
  • Pregnancy test where applicable (ibogaine is absolutely contraindicated in pregnancy)

Protocol 1: Flood Dose

Definition and Range

A flood dose is the primary clinical protocol used for opioid use disorder (OUD) interruption, addiction treatment, and intensive psychotherapeutic purposes. It is designed to produce a full psychedelic experience lasting approximately 24–36 hours.

Typical flood dose ranges cited in peer-reviewed literature and clinical protocols:

  • 10–25 mg/kg body weight of ibogaine hydrochloride (HCl) — the most commonly administered salt form
  • Most clinical programs report a working range of 12–18 mg/kg for OUD treatment (Mash et al., 2018; Brown & Alper, 2018)
  • Total ibogaine alkaloid (TA) extract dosing varies significantly due to differing alkaloid concentrations — TA is not interchangeable with HCl at a 1:1 ratio

What a Flood Dose Session Involves

The acute experience is divided into three phases commonly described in clinical literature (Noller et al., 2018):

  1. Acute/oneiric phase (0–8 hours): Intense visionary experience, ataxia, nystagmus, bradycardia, nausea. Patients must be supine or reclined with fall-risk precautions.
  2. Evaluative phase (8–20 hours): Visions reduce; cognitive and introspective processing intensifies. Patients remain significantly impaired.
  3. Residual stimulation phase (20–36+ hours): Alertness, insomnia, continued emotional processing. QTc remains elevated throughout.

Cardiac Monitoring Requirements During Flood Dose

The Global Ibogaine Therapist Alliance (GITA) clinical guidelines and peer-reviewed protocols specify:

  • Continuous cardiac telemetry monitoring for a minimum of 24 hours post-dose
  • Crash cart and defibrillation equipment on-site
  • Clinician or nurse present continuously during peak phase (0–12 hours)
  • IV access established prior to dosing
  • Magnesium sulfate IV available for QTc management
  • No patient ambulation without supervision (ataxia creates fall risk)

Flood Dose Contraindications

⚠️ The following are absolute contraindications to flood-dose ibogaine. Administering a flood dose in the presence of any of these conditions has been associated with documented fatalities.

  • QTc prolongation at baseline (>450 ms men / >470 ms women)
  • Structural heart disease: hypertrophic cardiomyopathy, congenital heart defects, prior myocardial infarction
  • Congenital long QT syndrome (any variant)
  • Current use of QT-prolonging medications — including but not limited to: methadone, certain antidepressants (SSRIs, TCAs), antipsychotics (haloperidol, quetiapine, ziprasidone), fluoroquinolone antibiotics, azithromycin, ondansetron, and antiarrhythmics
  • Opioids on board at time of dosing: Full opioid agonists (heroin, oxycodone, fentanyl, methadone) must be cleared before dosing. Methadone requires particular caution due to its own QTc-prolonging effects and long half-life — most protocols require a transition to short-acting opioids and a minimum washout. Fentanyl's high lipophilicity and variable elimination requires extended clearance time.
  • Buprenorphine (suboxone/subutex): High-dose buprenorphine significantly attenuates ibogaine's effects on opioid receptors; most protocols require tapering to ≤2–4 mg/day and a 24–72 hour washout minimum, though this is debated
  • Serotonergic medications: SSRIs, SNRIs, MAOIs, tramadol, lithium — risk of serotonin syndrome; consult facility-specific washout timelines
  • Stimulants (cocaine, methamphetamine, Adderall): cardiac strain risk in combination
  • Severe hepatic impairment
  • Active psychosis or recent manic episode
  • Pregnancy
  • Uncorrected electrolyte abnormalities (hypokalemia, hypomagnesemia)

Consequences of Ignoring Flood Dose Safety Protocols

A 2012 systematic review of ibogaine-related fatalities (Litjens & Brunt, 2016) identified 19 deaths with probable ibogaine causation. Common contributing factors included: pre-existing cardiac conditions not identified by screening, concurrent opioid use, QT-prolonging co-medications, and absence of cardiac monitoring. A 2021 retrospective review of a Mexican clinic cohort (Mash et al., 2018) documented QTc prolongation exceeding 500 ms in a subset of patients even after standard screening — underscoring that screening reduces but does not eliminate risk.

Protocol 2: Booster Dose

Definition and Range

Booster doses are sub-flood administrations given after an initial flood dose to extend or reinforce therapeutic effects. They are not a standalone treatment for OUD interruption.

  • Typically 1–5 mg/kg ibogaine HCl, administered 24–72 hours after the flood dose
  • Some protocols use boosters at one-quarter to one-half the flood dose
  • Effect duration is shorter (4–12 hours) with less intense visionary content

Clinical Use Cases

  • Re-emergence of withdrawal symptoms in opioid-dependent patients post-flood
  • Deepening of unresolved psychological material from the flood experience
  • Some trauma-focused protocols use sequential sessions with booster-range doses

Safety Considerations Specific to Booster Doses

⚠️ Booster doses carry a compounded cardiac risk: noribogaine from the flood dose is still active during a booster session. QTc should be re-measured before any booster is administered. Noribogaine's 24–72 hour half-life means cumulative QTc prolongation is a documented risk.

  • QTc must be re-checked via ECG before booster administration — do not assume it has normalized
  • Electrolytes should be re-assessed, as the post-flood period involves metabolic changes including poor oral intake
  • Cardiac monitoring during booster is required at the same standard as flood dose
  • Minimum interval between flood and booster varies by protocol; no established universal standard exists — the more conservative guidance requires QTc return to <450 ms before proceeding
  • Cumulative total dose across flood + booster combinations should be tracked; some protocols cap total session dosing at 25 mg/kg HCl equivalent

Protocol 3: Microdose

Definition and Range

Ibogaine microdosing involves sub-perceptual or mildly perceptual doses taken on a repeated schedule, typically for ongoing mood, cognition, or addiction maintenance purposes. It does not produce the full psychedelic experience of a flood dose.

  • Common microdose ranges: 1–5 mg total dose (not per kg — total milligrams) or approximately 0.02–0.08 mg/kg
  • Some protocols use slightly higher ranges up to 50–100 mg total, which may produce mild perceptual effects and should not be considered truly sub-perceptual
  • Schedules vary widely: daily, every-other-day, or 2–3 times per week
  • Noribogaine-specific microdosing is a separate investigational area with its own pharmacokinetic profile

Claimed and Investigated Uses

Anecdotal reports and limited clinical observation suggest microdosing ibogaine may reduce opioid and stimulant cravings between flood sessions, support mood stabilization, and reduce neuroinflammation markers. Formal clinical trial data for ibogaine microdosing specifically is currently limited; most ibogaine clinical evidence pertains to flood-dose protocols (Brown & Alper, 2018).

Safety Considerations Specific to Microdosing

⚠️ Microdosing is frequently assumed to be safe because doses are low. This assumption is unsupported and potentially dangerous. Cumulative noribogaine accumulation from frequent dosing, drug interactions, and cardiac effects at low doses are all documented or plausible concerns with inadequate long-term data.

  • Cumulative noribogaine accumulation: Daily microdosing creates noribogaine buildup due to its long half-life. The cardiac implications of chronic low-level noribogaine exposure are not fully characterized in humans (Koenig & Bhargava, 2019).
  • Baseline cardiac screening is still required before microdose protocols — QTc prolongation contraindications apply regardless of dose level
  • Drug interactions remain relevant at microdose levels, particularly with serotonergic medications and QT-prolonging agents
  • Hepatotoxicity risk with chronic use: Ibogaine is metabolized hepatically via CYP2D6 and CYP3A4. Chronic low-dose exposure in the context of hepatic vulnerability (including heavy alcohol use, hepatitis C) has not been adequately studied
  • No established safe microdose schedule exists in peer-reviewed literature — protocols in use are largely practitioner-derived
  • Self-administered ibogaine microdosing without medical oversight removes the safety net that even low-probability cardiac events require

Ibogaine HCl vs. Total Alkaloid (TA) Extract vs. Root Bark: Dosing Is Not Interchangeable

Three primary forms of ibogaine are used clinically and in ceremonial contexts. They are pharmacologically non-equivalent and dose conversions are not straightforward:

  • Ibogaine HCl (hydrochloride salt): Pharmaceutical-grade purified compound. Dose-by-weight calculations (mg/kg) are based on this form in most clinical literature. Most predictable pharmacokinetics.
  • Total alkaloid (TA) extract: Contains ibogaine plus other iboga alkaloids (voacangine, ibogamine, tabernanthine). Alkaloid profile and concentration vary by source. Equivalent ibogaine-HCl dosing requires knowing the ibogaine percentage in the extract — typically 40–85% depending on preparation. Other alkaloids may have additive cardiac effects.
  • Root bark (Tabernanthe iboga): Most variable. Ibogaine content in root bark ranges approximately 1–6% by weight. Ceremonial use in Bwiti tradition uses root bark with cultural and ritual context that includes experienced oversight. Clinical dose calculations from root bark are unreliable without laboratory assay of the specific batch.

Facilities using TA extract or root bark should obtain independent alkaloid quantification to establish ibogaine-equivalent dosing before administration.

Drug Interactions: Specific Named Substances

The following interactions are clinically significant across all ibogaine dose protocols:

  • Methadone + ibogaine: Additive QTc prolongation. Multiple documented fatalities. Methadone must be discontinued and adequate washout confirmed before any ibogaine protocol.
  • SSRIs/SNRIs + ibogaine: Risk of serotonin syndrome; ibogaine inhibits serotonin reuptake. Most protocols require tapering SSRIs over 2–4 weeks prior. Abrupt discontinuation also carries psychiatric risk — taper must be medically supervised.
  • MAOIs + ibogaine: Contraindicated. Severe serotonin syndrome risk. Irreversible MAOIs (phenelzine, tranylcypromine) require minimum 14-day washout; moclobemide (reversible) minimum 24–48 hours.
  • Benzodiazepines: May be held on standby by clinical teams to manage seizures but are not administered prophylactically. Pre-existing benzo dependence complicates safety picture — withdrawal seizures can occur if benzos are abruptly stopped for ibogaine preparation.
  • Lithium: Lowers seizure threshold in combination with ibogaine; generally contraindicated.
  • Stimulants (cocaine, amphetamines): Cardiac strain risk; must be cleared before dosing.
  • Cannabis: Some protocols permit prior cannabis use; others require 48-hour abstinence due to potential cardiac and anxiety interactions during acute phase. Follow facility-specific guidance.
  • Alcohol: Acute intoxication is an absolute contraindication to dosing. Alcohol dependence complicates electrolyte status (magnesium depletion).

After the Session: Post-Dose Safety Window

Ibogaine's risk period does not end when the acute experience ends. Key post-dose safety parameters include:

  • Cardiac monitoring for minimum 24–36 hours post-flood dose (GITA guidelines)
  • No driving or operating machinery for minimum 48–72 hours due to residual ataxia and cognitive impairment
  • Hydration and electrolyte restoration — nausea and vomiting during the flood phase can cause significant fluid and electrolyte loss
  • No introduction of opioids, stimulants, or QT-prolonging medications until noribogaine has cleared (conservative estimate: 7 days)
  • Psychological support: The 72-hour post-session period is associated with both profound positive shifts and — in a smaller subset — destabilization; on-site or readily accessible mental health support is a clinical standard in responsible protocols
  • Sleep: Ibogaine-induced insomnia (stimulant phase) lasting 24–48 hours post-dose is common; melatonin is used by some facilities and is generally considered low-risk. Avoid prescribing sedatives with QTc implications (quetiapine, some antidepressants) in this window.

Frequently Asked Questions

A flood dose (typically 10–25 mg/kg ibogaine HCl) is a full psychedelic dose designed to produce a complete 24–36 hour experience for addiction interruption or deep psychological work. A booster dose (typically 1–5 mg/kg) is a supplementary administration given after a flood, either to address returning withdrawal symptoms or extend therapeutic processing. Administering a booster-range dose as a standalone without prior flood context is not a standard clinical protocol and carries the same cardiac monitoring requirements. Neither should be self-administered. The key safety distinction is that noribogaine from a flood dose is still active during a booster session, requiring a fresh ECG before proceeding.
Low dose does not mean no risk with ibogaine. Several concerns apply specifically to microdosing: (1) Noribogaine, ibogaine's active metabolite, has a half-life of 24–72 hours. Daily or frequent microdosing causes cumulative noribogaine accumulation, and the cardiac implications of chronic low-level noribogaine exposure are not well-characterized in humans. (2) Drug interactions — particularly with serotonergic medications and QT-prolonging drugs — remain pharmacologically active at microdose levels. (3) Baseline cardiac contraindications (QTc prolongation, structural heart disease) are not dose-dependent; they apply to all ibogaine exposure. Anyone considering a microdose protocol still requires pre-treatment cardiac screening and should not combine ibogaine with contraindicated medications regardless of dose.
Methadone and ibogaine together represent one of the highest-risk combinations in this field — both independently prolong the QTc interval, and their combination is associated with multiple documented fatalities. There is no universally agreed-upon transition protocol, but the conservative clinical approach used at supervised facilities involves: (1) supervised tapering of methadone to the lowest tolerable dose, (2) transition to a short-acting opioid such as morphine, (3) adequate washout of the short-acting opioid before ibogaine administration. The methadone-to-ibogaine transition requires individualized medical management over weeks and must not be rushed. Confirm that any facility you approach has specific, documented experience with methadone-maintained patients and can provide your ECG and metabolic panel data in writing. Do not abruptly stop methadone — withdrawal is medically serious and potentially life-threatening.
Minimum standards for a responsible ibogaine facility include: (1) A required pre-treatment 12-lead ECG with documented QTc values — if a facility does not require this, do not proceed. (2) Continuous cardiac telemetry monitoring during the flood dose for at least 24 hours. (3) On-site crash cart and defibrillation equipment, and a clinician (physician or nurse) physically present during the acute phase. (4) A documented medication and substance use review with specific washout requirements communicated to you in advance. (5) They should be able to tell you exactly which form of ibogaine they use (HCl, TA, or root bark), the dose range in mg/kg of ibogaine HCl equivalent, and the batch/source of their ibogaine. Red flags include: no ECG required, dosing based only on body weight without medical history review, no on-site medical professional, or pressure to proceed quickly without complete screening.
Not without a medically supervised taper completed before treatment. Combining SSRIs with ibogaine carries a risk of serotonin syndrome, a potentially life-threatening condition involving agitation, hyperthermia, autonomic instability, and neuromuscular abnormalities. Ibogaine inhibits the serotonin transporter (SERT), and combining it with SSRIs creates additive serotonin activity. Most clinical protocols require tapering SSRIs over 2–4 weeks prior to an ibogaine session. Additionally, some SSRIs (particularly citalopram and escitalopram) are themselves QT-prolonging agents, adding a cardiac risk layer. Abruptly stopping SSRIs is not recommended — it causes discontinuation syndrome and can trigger rebound depression. Any SSRI taper must be supervised by a prescribing clinician, ideally one who is coordinating with the ibogaine treatment team.
There is no approved ibogaine-specific reversal agent. Once a dose is administered, ibogaine and noribogaine must be metabolically cleared, a process that takes days. This is a core reason why dosing precision and medical supervision are non-negotiable. If a cardiac arrhythmia develops, it is managed with standard emergency cardiac protocols — defibrillation, IV magnesium sulfate, and advanced cardiac life support (ACLS). Seizures may be managed with benzodiazepines. Severe overdose with respiratory depression has been managed supportively. The absence of a reversal agent means that errors in dosing, undetected contraindications, or equipment failures can be fatal without immediate on-site emergency capability. This also underscores why self-administration, even with sourced pharmaceutical-grade ibogaine HCl, carries risks that cannot be mitigated at home.

Sources

  • Brown, T.K., & Alper, K. (2018). Treatment of opioid use disorder with ibogaine: detoxification and drug use outcomes. American Journal of Drug and Alcohol Abuse, 44(1), 24–36.
  • Global Ibogaine Therapist Alliance (GITA). Clinical Guidelines for Ibogaine-Assisted Detoxification. Currently available at gitamaps.org.
  • Koenig, X., & Bhargava, A. (2019). Potential and dangers of ibogaine as a new pharmacological approach in opioid use disorders. Frontiers in Pharmacology, 10, 697.
  • Litjens, R.P.W., & Brunt, T.M. (2016). How toxic is ibogaine? Clinical Toxicology, 54(4), 297–302.
  • Mash, D.C., Duque, L., Page, B., & Allen-Ferdinand, K. (2018). Ibogaine detoxification transitions opioid and cocaine abusers between dependence and abstinence. Frontiers in Pharmacology, 9, 529.
  • Noller, G.E., Frampton, C.M., & Yazar-Klosinski, B. (2018). Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study. American Journal of Drug and Alcohol Abuse, 44(1), 37–46.
  • Schep, L.J., et al. (2016). Ibogaine fatalities — a cause for concern. Clinical Toxicology, 54(6), 479–483.

Informational only. Not medical advice. Ibogaine is Schedule I in the US. Consult qualified professionals before considering treatment.