What is best for your patient? Have you considered psychedelics?

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Dr. Weeks’ Comment: Every day, indeed, every moment of every day, we have the opportunity to stand on principle and to respond to fear tactics and compulsion with warm hearted compassion and love. It is somewhat thrilling. Tried it recently??

“Unjust laws exist; shall we be content to obey them, or shall we endeavor to amend them, and obey them until we have succeeded, or shall we transgress them at once? Men generally, under such a government as this, think that they ought to wait until they have persuaded the majority to alter them. They think that, if they should resist, the remedy would be worse than the evil. But it is the fault of the government itself that the remedy is worse than the evil. It makes it worse. Why is it not more apt to anticipate and provide for reform? Why does it not cherish its wise minority? Why does it cry and resist before it is hurt? Why does it not encourage its citizens to be on the alert to point out its faults, and do better than it would have them?” – Henry David Thoreau, Civil Disobedience

“An individual who breaks a law that conscience tells him is unjust, and who willingly accepts the penalty of imprisonment in order to arouse the conscience of the community over its injustice, is in reality expressing the highest respect for the law” – Martin Luther King, Jr.

“An unjust law is itself a species of violence. Arrest for its breach is more so. Now the law of nonviolence says that violence should be resisted not by counter-violence but by nonviolence. This I do by breaking the law and by peacefully submitting to arrest and imprisonment.” – Mahatma Gandhi

“One has not only a legal, but a moral responsibility to obey just laws. Conversely, one has a moral responsibility to disobey unjust laws.” – Martin Luther King, Jr.

Now we admire Dr. Fernando Vega, MD, a compassionate and principled medical doctor, who courageously puts the well-being of his patients above his own. Here is a powerful and academically astute white paper that Dr. Vega presented to the Washington state medical board explaining the importance of his work and why the law has to change as regards to categorization of psychedelic medications as illegal, schedule 1 substances. In response, the Washington state medical board suspended Dr. Vega’s license. Read his paper below and share with your doctor.

 

The Hazards and Benefits of Psychedelic Medicine (v5.8)x

For presentation to the Washington State Medical Disciplinary Board, Fernando Vega, MD © 2025

This revised version incorporates recent advances in the scientific literature and insights gained through increased clinical experience.

Abstract

The re-emergence of psychedelic therapy in clinical research and practice has opened new avenues for treating individuals with treatment-resistant psychiatric conditions. This article presents the clinical reflections of a board-certified family physician drawing on more than 600 video-documented sessions involving psychedelic substances over seven years. The subjects undergoing the sessions include other physicians of multiple specialties as well as psychiatrists and psychoanalytically trained therapists. The discussion explores the therapeutic potential and associated risks of three primary classes of psychedelics: phenethylamines, tryptamines, and ibogaine, and offers practical strategies for medical risk mitigation and integrative care. The article advocates for patient-centered models that emphasize safety, preparation, and long-term integration.

Introduction

Psychedelics are increasingly recognized as promising interventions for post-traumatic stress disorder (PTSD), depression, addiction, and existential distress. The three major classes of psychedelic substances include phenethylamines (e.g., MDMA), tryptamines (e.g., psilocybin, DMT), and the atypical indole alkaloid, ibogaine. Each class carries a distinct therapeutic profile and risk spectrum, both physiological and psychological, that must be thoughtfully navigated in clinical practice.

Phenethylamines

MDMA (3,4-methylenedioxymethamphetamine), a prototypical phenethylamine, has demonstrated efficacy in the treatment of PTSD (Mithoefer et al., 2011). Its hallmark effects include increased empathy, emotional openness, and interpersonal trust, all of which facilitate therapeutic breakthroughs.

The physiological effects of 3,4-methylenedioxymethamphetamine (MDMA) are primarily attributable to its potent sympathomimetic activity. Common physiological responses include increased heart rate, elevated systolic and diastolic blood pressure, enhanced myocardial oxygen demand, hyperreflexia, mydriasis, hyperthermia, and diaphoresis. MDMA administration also induces elevations in plasma cortisol and prolactin concentrations. Other commonly used phenethylamines with similar characteristics are MDA, 2-CB, and  mescaline (peyote, San Pedro), the latter two being more classic serotonergic phenethylamines.

In certain cases, these physiological effects may become exaggerated, resulting in complications such as cardiac arrhythmias, myocardial ischemia, severe hyperthermia, or seizures. Under controlled clinical conditions, such reactions are uncommon and are generally well managed through appropriate monitoring and supportive interventions. In contrast, recreational use, often characterized by uncontrolled dosing, concomitant substance use, dehydration, and prolonged exertion, is associated with a substantially higher and less predictable risk profile.

Phenethylamines and serotonin syndrome

The principal physiological safety concern in MDMA-assisted therapy is the potential for serotonin toxicity (serotonin syndrome), particularly in individuals concurrently using monoamine oxidase inhibitors (MAOIs) or selective serotonin reuptake inhibitors (SSRIs).

Although doses up to 2 mg/kg have been administered safely, consistent with regimens reported by some underground practitioners, MDMA exhibits non-linear pharmacokinetics. Consequently, plasma concentrations and physiological responses may increase disproportionately at higher doses, complicating risk assessment and emphasizing the need for careful titration and monitoring in all therapeutic settings. In my practice I have seen many patients with MDMA stories unrelated to my sessions. One such anecdote reports a 88 kg young man (K.K.) who 18 years prior:

Took 1.7 grams (19 mg/kg) in college in 2007 before he realized the scale was off and read 0.2 grams. He was in and out of a coma for 18 hours at home by himself. He didn’t have a good care. Followed by terrible short-term memory loss for one year. Fully recovered short-term memory. Repeat use of MDMA resulted in a non-response since then. Antidepressants also have no effect on him.

Immediate management of serotonin syndrome includes the administration of a benzodiazepine to control agitation and muscle rigidity, thereby reducing excessive muscular activity and preventing hyperthermia. External cooling measures should be implemented as needed, particularly when body temperature exceeds 39.5°C to 40.0°C. If symptoms are not adequately controlled with supportive therapy alone, cyproheptadine, a serotonin 5-HT₂A receptor antagonist, may be administered to further reduce serotonergic activity. (Boyer et al, NEJM, 2005)

Cytochrome P450 2D6 inhibitors including many SSRIs and antipsychotics can significantly elevate plasma levels of MDMA (de la Torre et al., 2012), further increasing the risk of adverse effects. Common drugs that inhibit CYPD2D6 are:

Strong Inhibitors

  • Paroxetine
  • Fluoxetine
  • Quinidine
  • Methadone (in higher doses)
  • Propafenone
  • Terbinafine
  • Chlorpromazine

Moderate Inhibitors

  • Cinacalcet
  • Duloxetine
  • Fluvoxamine
  • Mirabegron
  • Fluphenazine
  • Haldoperidol
  • Clozapine

Weak Inhibitors

  • Cimetidine
  • Sertraline
  • Ritonavir
  • Desvenlafaxine
  • Escitalopram
  • Celecoxib
  • Cobazam

Although SSRIs can inhibit CYP2D6 enzymes, the primary concern with concomitant use is not metabolic inhibition but rather the blunting of MDMA’s psychological effects while potentially preserving or augmenting its peripheral physiologic effects. At clinical or typical recreational doses, MDMA is associated with a significant risk of serotonin syndrome primarily when combined with monoamine oxidase inhibitors (MAOIs), whereas this risk is substantially lower with SSRIs.

Clonus, a hallmark feature of serotonin syndrome, is commonly observed at standard therapeutic doses of MDMA and serves in my practice as an indicator of pharmacologic/physiologic intensity rather than toxicity.

Routine monitoring during sessions includes continuous assessment of cardiac rhythm, respiratory patterns, and neurological signs such as clonus, saccadic eye movements, and diaphoresis. Additional physiological parameters, such as blood pressure and temperature, are assessed when clinically indicated. These metrics help determine the pharmacologic depth of the experience, as distinct from its psychological depth.

Psychological risks include acute anxiety and dissociation, particularly in individuals with rigid ego structures or untreated personality disorders. I have found that minimizing verbal interaction and encouraging an inward-focused orientation enables patients to access what often becomes the essential core of the experience. In my view, the long-term benefits of MDMA therapy are more closely associated with the depth of subjective experience than with the pharmacologic action alone.

In my clinical practice, a phenethylamine, typically MDMA, is often followed within the same session by the administration of tryptamines, specifically psilocybin and 5-MeO-DMT. This sequencing is based on findings from the Multidisciplinary Association for Psychedelic Studies (MAPS), which indicate that therapeutic outcomes in psychedelic-assisted therapy are strongly correlated with the intensity of the mystical experience, as measured by the Mystical Experience Questionnaire (MEQ).

In cases where patients present with strongly defended psychological organization or demonstrate resistance to psychological breakthrough, ketamine may be used as an adjunct to facilitate access to deeper emotional or transpersonal material. Although most participants approach these medicines with the intention of yielding fully to the experience, individuals with more deeply ingrained defense patterns may find it more difficult to relinquish control. This challenge is particularly pronounced among individuals with personality disorders, which are often rooted in early and deeper, pre-verbal trauma that impairs one’s capacity to trust, let go, and integrate the experience.

Practically speaking, combining these medicines increases the likelihood of a transformative experience. As many practitioners have observed, not every MDMA session reaches the depth necessary for significant psychological breakthroughs. The addition of psilocybin or 5-MeO-DMT appears to enhance that potential.

5-MeO-DMT, a powerful and fast-acting tryptamine, often induces deeply transformative experiences, whether used alone or in combination with a phenethylamine. However, outcomes can vary widely. Each person’s experience is unique. Some individuals have only a minimal response, which can feel disappointing when accompanied by high expectations. For others, the experience of ego dissolution can initially be unsettling or even frightening. Yet for those who fully surrender to it, the temporary “death” of the ego often gives rise to an overwhelming sense of joy, renewal, and rebirth.

The following links feature patient accounts describing their experiences with MDMA after undergoing sessions that are sometimes combine phenethylamines with tryptamines

Rachel, 40 years old 7:08

Josephine, 23 year-old cowgirl with PTSD 6:19

Gabe, 24 year-old cowboy 5:24

Greg, 77 years old 4:44

John, 68 years old 4:02

Ron, 71 years old w/ketamine 5:24

 

 

Tryptamines

Tryptamines such as psilocybin, LSD, and DMT act primarily as selective agonists at the 5-HT₂A receptor. Unlike MDMA, they do not significantly inhibit presynaptic serotonin or dopamine transporters (SERT or DAT), resulting in a lower risk of serotonin syndrome and fewer transporter-mediated drug–drug interactions (Nichols, 2016). Beyond acute receptor effects, psilocybin has been shown to induce activity-dependent rewiring of large-scale cortical networks, leading to durable changes in brain connectivity that may underlie sustained therapeutic effects (Jiang et al., 2026). Emerging evidence further suggests that 5-HT₂A agonists exert neuroimmune modulatory effects (Thuery, 2025).

Tryptamines are generally safe from a cardiovascular perspective as well, but can induce profound psychological phenomena, including ego dissolution, awe, and acute fear. When supported and integrated appropriately, these experiences often catalyze lasting therapeutic transformation (Carhart-Harris et al., 2018). While caution is warranted in patients with schizophrenia or bipolar disorder, the incidence of psychedelic-induced psychosis remains lower than that associated with cannabis (Leweke & Koethe, 2008). Anecdotal reports from underground practitioners also challenge the notion of absolute contraindication in such populations, though these cases remain under documented in the literature.

Reports of “ego dissolution” occur most frequently with the tryptamines. This experience is often described as a loss of ordinary self-boundaries and a sense of merging with a broader, universal awareness. Although the term can sound unsettling to those unfamiliar with it, individuals who undergo such experiences commonly describe a subsequent sense of peace, psychological renewal, and personal transformation, often likening it to rebirth. Many also report a lasting reduction, or even complete resolution of the fear of death. A recurring reflection is that the former sense of self comes to feel diminished or incomplete relative to a more expansive identity that emerges afterward. Informally, personal conversations with friends or acquaintances frequently reveal subtle but meaningful differences between those who have had psychedelic experiences earlier in life and those who have not.

The following links feature patients describing their experiences with repeated use of tryptamines in a therapeutic setting:

Irina, 39 years old 22:24

Ibogaine

Ibogaine is pharmacologically distinct from both phenethylamines and tryptamines and presents greater medical complexity than classical serotonergic psychedelics. Unlike substances such as psilocybin or LSD, ibogaine and its primary metabolite, noribogaine, have relatively low affinity for the 5-HT₂A receptor and do not function as high-potency 5-HT₂A agonists. In contrast, ibogaine exhibits agonist activity at μ-, κ-, and σ-2 opioid receptors and antagonizes NMDA/glutamate receptors as well as nicotinic acetylcholine (α3β4 nACh) receptors. In addition, ibogaine exerts broad modulatory effects across multiple neurotransmitter systems, including serotonergic, dopaminergic, and glutamatergic pathways (Alper, 2001). This complex, multi-target pharmacology underlies its diverse therapeutic applications. Ibogaine and noribogaine have been most extensively studied for their potential roles in the treatment of substance use disorders (SUD), post-traumatic stress disorder (PTSD), traumatic brain injury (TBI), and other neuropsychiatric and neurologic conditions.

Ibogaine and Substance Use Disorders

One of ibogaine’s most frequently reported therapeutic effects is a marked reduction, and in many cases elimination, of substance cravings. Mechanistically, this effect is thought to involve modulation of dopaminergic reward pathways, thereby disrupting conditioned reinforcement and cue-driven craving (Mash, 2008). Clinically, individuals with opioid, cannabis, kratom, or alcohol use disorders commonly report partial and often complete relief from craving following treatment, with this effect sometimes persisting for months. Importantly, a reduction in craving does not equate to elimination of pharmacologic risk: individuals may be at increased risk of overdose if prior dosing is resumed after a period of reduced use, and diminished craving for alcohol does not preclude the ability to consume alcohol. These observations underscore that ibogaine’s effects on craving do not obviate the need for careful patient education, ongoing monitoring, and risk-management strategies.

Ibogaine and PTSD

Ibogaine’s effects on post-traumatic stress disorder share only limited similarities with those of classical serotonergic psychedelics. One overlapping feature is the reported capacity to access deeper aspects of subjective experience and to gain alternative perspectives that allow reframing of previously triggering events. Traumatic experiences are understood to be encoded not only cognitively but also in somatic and autonomic patterns. In animals, traumatic activation is often discharged through spontaneous shaking or trembling, a response thought to prevent the persistence of trauma (Levine, 1997). In the context of ibogaine treatment, patients commonly report a distinct internal quivering or tremor, particularly in the core of the body, which may reflect autonomic discharge of stress-related activation. Others describe this sensation metaphorically as akin to tuning hundreds of strings, with the body itself serving as the instrument.

The psychoactive state induced by ibogaine is highly introspective and is often described by patients as a lucid, dream-like experience that facilitates autobiographical recall, emotional processing, and psychological insight. Notably, patients frequently report preservation of ego structure and a sustained sense of volition throughout the experience. In practical terms, individuals describe remaining aware of who they are and where they are during the session, which is often perceived as allowing a more gradual and controlled approach to psychological exploration.

Ibogaine and Traumatic Brain Injury

 

In an open-label study of 30 veterans with traumatic brain injury treated with ibogaine co-administered with magnesium, researchers observed sustained improvements in neuropsychiatric symptoms and cognitive function, suggesting potential relevance for the treatment of TBI-related sequelae (Cherian, 2025). A secondary analysis summarizing the Nature Mental Health findings reported that alterations in brain rhythms following ibogaine treatment correlated with improvements in executive function and reductions in PTSD and anxiety symptoms among veterans with TBI. Additional summaries have described changes in cortical oscillatory activity, including increased slower-frequency rhythms such as theta and reduced signal complexity, findings that were associated with improvements in cognition and emotional regulation.

 

Ibogaine and Neurodegenerative Disorders

Beyond its psychotropic and anti-addictive effects, ibogaine has been shown in preclinical models to upregulate glial cell line–derived neurotrophic factor (GDNF), a key mediator of dopaminergic neuron survival and synaptic plasticity (Marton, 2024). This neurotrophic effect has prompted interest in ibogaine’s potential relevance to neurodegenerative disorders. Emerging clinical observations include case reports describing radiologic and clinical improvements, such as reduced demyelinating lesion burden in patients with multiple sclerosis (Chen, 2025), as well as sustained improvements in motor, cognitive, and psychiatric symptoms in patients with Parkinson’s disease (Erny, 2026; Mindscape, 2025). These observations parallel established evidence demonstrating the role of GDNF in supporting dopaminergic neurons in vitro and in vivo (Peterson, 2008).

While molecular and preclinical findings suggest a plausible neurotrophic and neuroprotective mechanism, it is early clinical observations, rather than mechanistic certainty, that have prompted further inquiry. In this context, symptomatic improvements are best understood as clinical signals that may reflect upstream modulation of neurotrophic, neuroplastic, and neuroprotective systems, warranting further systematic investigation.

Ibogaine and Neuropsychiatric Disorders

Ibogaine has also been explored for potential therapeutic relevance in patients with co-occurring severe mental illness, including major depressive disorder, bipolar disorder (Nunes, 2020), and schizophrenia. The peer-reviewed literature includes a documented case of ibogaine-associated psychosis in a patient with schizophrenia, as well as review articles noting potential psychiatric effects of ibogaine in populations with severe mental illness. These findings underscore the importance of careful assessment and the exclusion of psychotic disorders in research and clinical protocols.

Early observational studies and case series have described reductions in substance use, improvements in mood regulation, and decreases in depressive symptoms following ibogaine administration; however, randomized controlled trials remain limited and underpowered, and definitive efficacy has not been established (Cherian, 2024).

Ibogaine in a Family Medicine Practice

In my clinical practice, common patient-reported indications for ibogaine use include depression, anxiety, post-traumatic stress disorder, traumatic brain injury, substance use disorders, and neurodegenerative conditions such as Parkinson’s disease and multiple sclerosis. A substantial subset of patients also presents with a primary intention of psychospiritual exploration. These individuals describe ibogaine as a tool for examining subjective, symbolic, or existential dimensions of experience. Such motivations are patient-initiated and reflect personal meaning-making rather than medical claims.

Following ibogaine sessions, some patients have reported subjective changes in cognition, behavior, and sleep. These reports include a perceived reduction in intrusive or competing thoughts commonly associated with attention-deficit/hyperactivity disorder (ADHD), improved punctuality, improved sleep quality, and more regular diurnal sleep–wake cycling. Some patients describe these changes phenomenologically as the emergence of “a space between the trigger and the reaction,” characterized by a brief temporal delay between a stimulus and their behavioral or emotional response. Patients report that this delay allows for greater conscious choice and reduced reactivity.

These observations are based exclusively on patient self-report, including reports from individuals I have known for more than 20 years, and have not been independently verified through objective neurocognitive testing, physiological measurements, or other quantitative assessment tools. Patients with greater baseline somatic and interoceptive awareness appear more likely to notice and articulate subtle changes following treatment, a pattern that likely reflects individual differences in self-awareness rather than measured differences in treatment response.

Ibogaine Risk

Ibogaine inhibits various cardiac voltage-gated ion channels including human ether-a-go-go related gene (hERG) potassium, Nav1.5 sodium, Cav1.2 calcium channels. Ibogaine’s principal medical risk arises from its ability to block the hERG (KCNH2) potassium channel, a key determinant of ventricular repolarization. Inhibition of this channel slows potassium efflux during phase 3 of the cardiac action potential, resulting in QT interval prolongation and an associated risk of torsades de pointes (TdP). TdP is a polymorphic ventricular tachyarrhythmia characterized by transient episodes that can degenerate into ventricular fibrillation.

Approximately 30 ibogaine-associated deaths have been reported in the published medical literature. I have reviewed each of these cases in detail. In the majority, death occurred in the setting of polypharmacy, concurrent substance use, electrolyte abnormalities, or significant underlying medical comorbidities. In cases not attributable to overdose or clear alternative causes, the available evidence most commonly implicates malignant ventricular arrhythmia as the proximate mechanism of death. Reports of near-fatal events in the literature support ventricular arrhythmia as the primary pathophysiologic concern associated with ibogaine exposure, particularly in the setting of QT prolongation (Steinberg & Deyell, 2018; Mestre et al., 2024).

The most concerning published case is a report from Puerto Rico (Mestre et al., 2024), in which a patient without known structural heart disease developed torsade de pointes following a reported dose of approximately 2 mg/kg, with persistent QT prolongation lasting eight days. This duration of QT abnormality is notably longer than that observed in most reported ibogaine exposures. In my practice, a typical dose of 10 mg/kg has usually results in QTc normalization within 24 hours.

From a pharmacologic perspective, this presentation represents an extreme outlier relative to available dosing and time-course data. An analogy would be observing torsade de pointes persisting for a full week after a single low dose of ondansetron, when thousands of patients receiving substantially higher cumulative doses demonstrate QT normalization within hours. Such an event would prompt careful evaluation for idiosyncratic susceptibility, metabolic impairment, electrolyte disturbance, or unrecognized confounding factors, rather than being interpreted as representative of typical drug behavior.

Importantly, the cardiotoxic profile of ibogaine is not uniquely hazardous when compared with several commonly prescribed medications that also block hERG channels (e.g., methadone, haloperidol, ondansetron, and macrolides). With appropriate screening, monitoring, and adherence to established safety parameters, the risks can be responsibly mitigated. (Schwartz, NEJM, 2025)

Standard precautions prior to using ibogaine include assessing for congenital or acquired long QT syndrome, reviewing medications that may prolong the QT interval, correcting electrolyte abnormalities, and evaluating for underlying cardiac disease. Although familial screening most commonly identifies pathogenic variants in the hERG (KCNH2) channel, a range of additional potassium and sodium channel gene abnormalities associated with inherited long QT syndromes may also be detected, as described in the following (Schwartz, NEJM 2025):

There are at around ten ion channels involved in the cardiac myocyte action potential. Those of most significance in the ventricular action potential and prolongation of the QT interval are:

Current Gene(s) AP Phase Syndrome Key Drugs That Block
IKr KCNH2 (hERG) Phase 3 LQT2 Methadone, sotalol, haloperidol, TCAs, SSRIs, macrolides, ibogaine
IKs KCNQ1/KCNE1 Phase 3 LQT1 Amiodarone, propofol,
Ito KCND3 Phase 1 Brugada phenotypes Quinidine
IK1 KCNJ2 Phase 4/late 3 LQT7 Chloroquine, amiodarone

Three genes account for ~90% of confirmed cases:

  • KCNQ1 (LQT1) → ↓ IKs
  • KCNH2 (LQT2) → ↓ Ikr
  • SCN5A (LQT3) → ↑ late Ina

Although the prevalence has been estimated at roughly 1 in 2,000, underdiagnosis and reporting gaps suggest the true prevalence is likely higher (Schwartz 2025).

TdP is more common in those with structural heart diseases, including heart failure, myocardial infarction and left ventricular hypertrophy, as well as those with congenital LQTS, which may be concealed. Other risk factors include advanced age, female gender, alcoholic liver disease, recent conversion from atrial fibrillation, hypokalemia, hypomagnesaemia, hypocalcemia and digoxin or diuretic therapy.

Other modifiable factors in prevention of TdP include pharmacokinetics of the different drugs involved. Examples of potential pharmacokinetic interactions affecting drugs that prolong the QT interval, inhibit cytochrome P450 (CYP) inhibitors, or both:

CYP isoform affected
CYP1A2 CYP2D6 CYP3A4
QT prolonging drugs Haloperidol Amitriptyline Macrolides
Amitriptyline Haloperidol Citalopram/escitalopram
Imipramine Imipramine Amiodarone
Quinidine Cisapride
Haloperidol
Quinidine
Pimozide
Methadone
CYP inhibitors Fluoroquinolones Ritonavir Protease inhibitors
Cimetidine Fluoxetine/paroxetine Imidazole fungicides
Amiodarone Amiodarone Diltiazem
Grapefruit juice Quinidine SSRIs
Methadone Erythromycin
Grapefruit juice

A 2025 Stanford University study, published in Nature, involving 30 Special Operations veterans receiving ibogaine-magnesium therapy reported significant reductions in PTSD, depression, suicidality, and addiction severity. While 40% had QTc intervals > 500 ms, no adverse cardiac events were observed (Stanford Veterans Psychedelic Initiative, 2025).

A study by Knuijver et al. (2021) found that 50% of individuals receiving ibogaine therapy developed QTc intervals exceeding 500 milliseconds, a threshold associated with increased arrhythmic risk. By comparison, in my own early clinical dataset of more than 50 full-dose ibogaine sessions conducted under continuous medical supervision and cardiac monitoring, only one subject exhibited a QTc > 500 ms at 24 hours post-administration, and another showed a transient shortening of the QT interval using intermittent 12 lead ECGs.

The use of appropriate equipment is essential when studying the QT interval in patients receiving ibogaine. In our initial series of 40 patients, continuous cardiac monitors were employed. However, frequent 12-lead ECGs were still required to accurately assess QT interval changes because our monitors at that time did not provide real-time QT interval readings.

The monitors initially used to determine QT intervals:

  • Our usual office ECG is a Schiller device using the Minnesota Code–based analysis combined with Schiller’s proprietary interpretation software called SCHILLER ECG Interpretation Program (often referred to as ETM – ECG True Interpretation Module).

On the other hand,

  • Our Phillips IntelliVue monitors, which provide real time QT intervals Algorithm uses: Philips bedside monitors (e.g., IntelliVue MX450, MX700, MX800) use the Philips DXL 12-lead ECG Algorithm (developed from earlier Hewlett-Packard algorithms).

To compare the two:

Feature Schiller (ETM) Philips IntelliVue (DXL)
Core algorithm ETM, CSE-validated, Minnesota Code basis DXL algorithm, Hewlett-Packard lineage
Primary use Resting ECG carts (12-lead, office/hospital) Bedside continuous monitoring (plus 12-lead on some models)
Validation International CSE database AHA/IEC/CSE databases
     
     

Continuous, multi‑lead cardiac monitoring has yielded QTc measurements that more closely mirror values reported in the published literature, including a higher observed frequency of QTc intervals exceeding 500 ms. Relative to intermittent 12‑lead electrocardiograms (ECGs), continuous telemetry is inherently more sensitive to short‑lived fluctuations in ventricular repolarization because it captures transient changes that may not be present at the specific time a scheduled ECG is obtained.

In our observations during ibogaine use, QTc prolongation and repolarization morphology changes, including T‑wave flattening, notching, and Tpeak–Tend prolongation and can fluctuate over minutes. When QTc was measured simultaneously using a standard 12‑lead ECG and a Philips IntelliVue continuous monitoring system (DXL algorithm), substantial inter‑device differences were observed, with occasional discrepancies reaching up to 400 ms. In some cases, differences of this magnitude persisted over 24‑hour monitoring periods. These discrepancies remained despite adjustments to lead selection, electrode positioning, and the vector axis used by the IntelliVue system to derive QT for calculation.

Several factors may contribute to this degree of variability. First, signal acquisition differs by modality: 12‑lead ECGs include precordial leads, whereas many bedside monitoring systems derive signals primarily from limb‑lead vectors. Additional variability arises from differences in automated QT‑detection algorithms and in how those algorithms handle abnormal or low‑amplitude T‑wave morphology. Heart‑rate correction can further amplify divergence. Many standard ECG systems report QTc using Bazett’s formula (QTcB = QT/√RR), which is strongly heart‑rate dependent and can introduce systematic error at heart‑rate extremes. In contrast, continuous monitoring systems may apply alternative correction methods (e.g., Fridericia’s formula, QTcF = QT/RR^(1/3)) or proprietary adjustments. During the sinus bradycardia commonly observed with ibogaine, QTc estimates may differ meaningfully depending on the correction method used, the RR sampling approach, and the degree of moment‑to‑moment heart‑rate variability captured by continuous monitoring.

Measurement algorithms also differ in how they define the end of the T wave, particularly when T waves are flattened, biphasic, or notched. Even small differences in end‑of‑T placement—on the order of 1 mm on paper at 25 mm/s—correspond to ~40 ms of QT measurement variance. When combined with differences in correction formulas and RR sampling, these factors can generate large QTc discrepancies across devices without necessarily indicating true physiologic instability.

Given the known variability of automated QTc assessment, especially in the presence of repolarization morphology changes, QTc interpretation should be anchored in clinical correlation and expert review rather than reliance on a single numerical threshold. With continued prospective monitoring and systematic comparison against published datasets, our objective is to more precisely characterize the magnitude, temporal pattern, and clinical significance of QTc changes that should prompt intervention, including thresholds for electrolyte repletion, magnesium administration, escalation of monitoring, or discontinuation of therapy.

We have also used the wireless Wearlinq device during ibogaine sessions and observed an even higher apparent rate of QTc prolongation, with a larger proportion of readings exceeding 500–600 ms. Wearlinq derives six leads via a patch approximately 6 cm across the precordium, which may enhance T‑wave signal capture in that region. This configuration, together with device‑specific algorithms, likely contributes to the higher apparent frequency and amplitude of QTc prolongation detected by this system. Its continuous, multi‑lead recordings are particularly valuable for post‑session review and for characterizing transient QTc excursions that intermittent 12‑lead ECGs are unlikely to capture.

It is also important to recognize that QT interval measurements can vary by more than 50 ms even when recordings are taken only minutes apart. Flattened or low‑amplitude T waves further limit accuracy for both automated algorithms and cardiologist over‑reads, reinforcing the need for cautious clinical judgment. From a manual measurement standpoint, the difference between a QT interval of 480 ms (often treated as an upper‑range value) and 520 ms (a range associated with increased concern) is only one small box (1 mm) at 25 mm/s. Discriminating within this narrow margin is challenging even for experienced clinicians, underscoring the practical limits of manual QT measurement precision.

In our full‑dose ibogaine sessions, the following ECG changes have been consistently observed:

  1. Sinus bradycardia
  2. QTc prolongation
  3. Flattened T waves
  4. Notched T waves
  5. Prolonged Tpeak–Tend interval

By 24 hours, the majority of patients with these morphologic changes and QT intervals have returned to normal ranges, although some may exhibit persistent T-wave flattening for an additional 12 hours. I hope to continue mapping these changes over longer time frames as part of my ongoing personal research.

Early observations supported by existing medical literature and thousands of sessions conducted legally in other countries indicate that a screening ECG, basic laboratory testing, comprehensive medication review, and thorough history and physical examination provide adequate screening to ensure a safe ibogaine session. Prospective studies will be required to confirm these findings.

It is also noteworthy that numerous underground ibogaine providers operate in North America. I have personally interviewed and worked alongside with six such practitioners in Canada and the United States. Many report having treated several hundred participants each, most using traditional Bwiti methods with raw iboga bark or total extract, and all performing at least a baseline ECG prior to administration. None of these practitioners have reported serious complications or fatalities among their participants.

By contrast, there is limited publicly available information regarding the reported death of an American tourist at a retreat center in Costa Rica in 2024. The existing reports are sparse and lack sufficient clinical detail to accurately characterize the circumstances or contributing factors surrounding the event.

Conversations with individuals familiar with the situation suggest that an intravenous line could not be established and that the individual collapsed in the shower approximately twelve hours into the ceremony. However, without formal medical documentation or investigative findings, definitive conclusions cannot be drawn.

Risk Mitigation

To mitigate potential risks, I obtain ibogaine from a pharmacist in Texas. For additional verification, I have utilized King County Public Health’s Robert Clewis Center, where samples are analyzed using Fourier Transform Infrared Spectroscopy (FTIR), followed by confirmatory gas chromatography–mass spectrometry (GC–MS) at a reference laboratory. In the past, I have also coordinated independent mass spectrometry testing through patients with scientific expertise.

My pre-screening protocol includes a resting ECG for all patients and, when clinically indicated, a treadmill stress test to help identify latent or familial long QT syndromes. Any electrolyte abnormalities are corrected in advance, and intravenous magnesium is routinely administered as part of the monitoring protocol.

Genetic testing for cytochrome P450 isoform activity has not yet proven clinically useful for safety screening, though it may have future value in predicting variables such as treatment intensity or duration of the clinical course.

My clinical background includes experience in ECG interpretation and treadmill stress testing, skills I developed while also serving as a compensated physician for cardiac diagnostics at Providence Hospital in Seattle during the 1980s under the supervision of the director, James Clifton, MD. Earlier, during my residency in the 1970s—before “Do Not Resuscitate” orders became standard practice, I gained substantial experience in emergency resuscitation, routinely managing cardiac arrests, performing endotracheal intubations, and placing central lines as part of daily duties.

In addition to my clinical work, I have worked with practitioners from the Bwiti tradition, the lineage from which the ceremonial use of iboga originates. Some of these practitioners have participated in sessions I facilitated in my clinic, where they experienced purified ibogaine HCl, as their traditional practice typically involves the use of raw iboga bark. We also engage in regular weekly consultations that include detailed case discussions.

 

Microdosing Ibogaine

Microdosed ibogaine appears to have meaningful therapeutic potential, although the current body of peer-reviewed evidence remains limited. Early reports suggest possible benefit in bipolar-spectrum conditions (Fernandes-Nascimento MH). In my clinical practice, several patients with long-standing insomnia have reported dramatic improvement with microdoses in the range of 4–18 mg. Others have described reductions in anxiety, depressed mood, and emotional reactivity to previously triggering situations.

In addition, early clinical observations from my practice, along with non–peer-reviewed reports, suggest that sub-psychedelic “mini-doses” of ibogaine (approximately 150–300 mg) may lead to noticeable improvement in Parkinson’s disease symptoms within days of initiating treatment (Ermy, 2026), (Mindscape, 2023). A related dosing approach has also been described in a successful case report involving methadone detoxification using repeated low doses of ibogaine (Wilkins, 2016).

As with all therapeutic interventions, patient responses are heterogeneous, and not all individuals derive benefit. Any trial use of ibogaine should therefore be time-limited and carefully monitored. Recommended safeguards include informed consent; baseline and follow-up ECGs with QT/QTc assessment; electrolyte monitoring; and thorough medication review to identify QT-prolonging agents or CYP-mediated drug interactions. Clear stop criteria and appropriate integration support are also advised.

The following links feature patients describing their experiences with ibogaine in a therapeutic setting:

Susan, 44, years old, describes common features of an ibogaine journey 6:40

Logan, 34 years old describe the first legal administration of ibogaine in the U.S. 4:43

Michael, 40 years old describes his ibogaine session 6:50

Michael, 56 years old, ibogaine + ketamine, one month later, 2:19

Ian, 48 years old, after 3 ibogaine sessions, 8:22

Andrea, 43 years old with Multiple Sclerosis, 13:07

(Andrea returned to work after 10 years of not working because of fatigue)

Matthew, 72 years old with alcoholism and brain trauma 21:18

Integration

One of ibogaine’s most profound effects is the ability to witness one’s life story with clarity and without judgment. For many individuals, the experience is more psycho-spiritual than pharmacologic. While ibogaine is particularly effective in reducing or eliminating physical cravings associated with addiction, its long-term benefits are significantly enhanced when the experience is followed by structured integration involving family, community, and therapeutic support.

This principle holds across all psychedelic therapies: integration is essential for translating acute experiences into lasting change. Although a single session may initiate a neurobiological “reset” and interrupt maladaptive patterns, sustained recovery and personal growth depend on consistent relational and behavioral reinforcement. Ongoing therapy, family involvement, and a supportive community are critical components in ensuring meaningful and durable outcomes.

The Spiritual Dimension

Therapeutic outcomes are often correlated with Mystical Experience Questionnaire (MEQ) scores, which measure the depth of mystical or transcendent states. In clinical and experiential settings, individuals—particularly religious scholars—frequently describe a renewed understanding of their spiritual traditions following psychedelic sessions. Across many faiths, spontaneous experiences akin to satori, samadhi, bodhi, epiphany, or noetic insights have been reported. While such states are not exclusive to psychedelics, they are often catalyzed within the psychedelic context.

In a landmark study conducted by researchers at Johns Hopkins University and New York University, high-dose psilocybin was administered to 24 religious leaders representing Christian, Jewish, Buddhist, and Muslim traditions. Remarkably, 96% of participants described the experience as one of the five most spiritually significant moments of their lives. Many reported profound encounters with a divine presence, a deepening of their faith and vocation, and a greater sense of unity and interreligious understanding. (Griffiths et al, 2019)

The following are videos of this example:

Ashley, 57 years old, Buddhist Scholar, 1 1/2 years later, 3:57

Brenda, 78 years old

 

Integration and Psychospiritual Healing

The result of a psychospiritual journey, whether initiated through psychedelics, breathwork, meditation, psychotherapy, or even spontaneous experiences such as a near-death event, often transforms the way an individual perceives their life. These experiences have the potential to dissolve long-held narratives of limitation or suffering, allowing for a broader, more integrated understanding of the self. What was once viewed as broken or pathological is often recontextualized as a meaningful part of the human story.

At the boundaries of the conventional diagnosis-and-treatment model lie conditions such as compulsions, anorexia nervosa, anxiety, insomnia, fear of death, alcoholism, opiate addiction, and chronic low self-esteem. Though diverse in their presentation, these patterns most often stem from unresolved trauma and early adverse experiences that fragment the sense of self. Here, we examine the emotional roots of disease. Psychedelics, when used skillfully and within a supportive therapeutic framework, can help individuals access and integrate these underlying wounds. Rather than rejecting or suppressing painful memories, the individual learns to accept them as integral aspects of their lived experience, transforming trauma into a source of insight and strength.

Integration is the process through which these experiences are woven back into daily life, transforming moments of revelation into enduring change. By embracing all aspects of life, both joyful and painful, creative and destructive, one begins to recover a sense of wholeness. This expanded awareness nurtures compassion, authenticity, and resilience, qualities that form the foundation of sustained healing. From a platform of therapy and self-examination, the use of psychedelics allow for a piercing of the veil, in further exploration of ones own nature.

Many of my midlife patients have grieved the loss of the activities that once defined their sense of vitality—playing basketball, skiing, or engaging in sex with youthful energy. I remind them that real vitality and happiness are not rooted primarily in physical capability. It comes from the ability to inhabit the present moment, to live authentically and without apology, and to cultivate meaningful connections that nourish the soul.

When one lives from this place of alignment, life itself becomes richer and more fulfilling. The later years, often seen as a period of decline, becomes instead a time of deep integration and renewal, a return to the essence of one’s being and a realization of true holistic healing. Freed from the compulsions of ego and performance, one discovers that what once felt like loss is, in truth, an expansion into greater wholeness, presence, and peace. In this sense, these truly become the best years of your life.

The psychedelic experience, particularly when the ego remains intact or becomes reengaged during the return from the altered state, is simultaneously personal and universal. It can facilitate reconnection with a deeper sense of self that exists beneath habitual personality structures and conditioned patterns of behavior. In accessing this underlying core, individuals may rediscover aspects of their own essential nature and also recognizing that this same fundamental humanity is shared by others. Hence, healing of their community is realized.

Professional Collaboration and Practice Context

Over the past two years, I have hosted monthly meetings in my home with licensed therapists and physicians to discuss clinical experiences and share knowledge related to psychedelic-assisted therapy. I have also participated in two additional case-review groups focused on psychedelic medicine and have stayed in regular contact with physicians who used MDMA therapeutically in the 1980s, prior to its reclassification. Their historical insight has helped inform my clinical approach.

I have met with medical directors and providers from major ibogaine clinics in Mexico, as well as one in Bolivia, to discuss treatment protocols and safety standards. Through these relationships, I may be invited to assist in establishing ibogaine treatment sessions in Florida. I am also in the early planning stages of developing an ibogaine laboratory for Jim Grimsby, PhD, a neuroscientist and the head of psychedelic research at the Neuroscience Institute at the University of Colorado, Denver. Given Colorado’s more progressive regulatory stance toward psychedelic medicine, I intend to apply for medical licensure there to continue expanding this work.

At present, I travel to Texas on a monthly basis to participate in the provision of these services within a church-affiliated setting in which the substances are treated as sacraments. All participants are managed using standardized clinical protocols and receive appropriate medical monitoring throughout. In Washington, options are being evaluated for a comparable ecclesiastical framework to contextualize the sacramental use of ibogaine, with the goal of maintaining alignment with applicable legal and regulatory standards.

Conclusion

Psychedelic-assisted therapy presents both potential therapeutic benefits and recognized medical and psychological risks. With careful patient selection, medical oversight, and structured integration support, these treatments can be administered in a manner that prioritizes safety and professional responsibility. As clinical research continues to expand, there is increasing recognition of a potential role for physician involvement in the development and oversight of psychedelic care protocols. Based on my experience conducting over 600 video documented sessions, I believe I can offer valuable clinical insights that may inform ongoing academic and regulatory efforts to evaluate the role of psychedelic therapies within evidence-based medical practice.

MDMA (Phenethylamines)

  • de la Torre R, Farré M, Roset PN, Pizarro N, Abanades S, Segura M, et al. Pharmacology of MDMA in humans. Br J Pharmacol. 2012;166(1):276–294.
  • Rietjens, S. J., Hondebrink, L., Westerink, R. H. S., & Meulenbelt, J. (2012). Pharmacokinetics and pharmacodynamics of 3,4-methylenedioxymethamphetamine (MDMA): Interindividual differences due to polymorphisms and drug–drug interactions. Critical Reviews in Toxicology, 42(10), 854–876.
  • Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352(11):1112-1120. doi:10.1056/NEJMra041867
  • Hyatt K, Tormoehlen L. MDMA (Ecstasy) intoxication and serotonin syndrome. Curr Psychiatry Rep. 2014;16(5):453. https://doi.org/10.1007/s11920-014-0453-0
  • Mithoefer MC, Wagner MT, Mithoefer AT, Jerome L, Doblin R. The safety and efficacy of ±3,4-methylenedioxymethamphetamine-assisted psychotherapy in subjects with chronic, treatment-resistant PTSD: The first randomized controlled pilot study. J Psychopharmacol. 2011;25(4):439. https://doi.org/10.1177/0269881110378371
  • Parrott AC. MDMA, serotonergic neurotoxicity, and the diverse functional deficits of recreational “Ecstasy” users. Neurosci Biobehav Rev. 2013;37(8):1466–1484.
  • Zeifman, Hannes, Co-use of MDMA with psilocybin/LSD may buffer against challenging experiences and enhance positive experiences. Nature, 22 August 2023

 

Psilocybin / MEQ (mystical experience)

  • Griffiths RR, Richards WA, McCann U, Jesse R. Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance. Psychopharmacology (Berl). 2006;187(3):268-283. doi:10.1007/s00213-006-0457-5.
  • Griffiths RR, Richards WA, Johnson MW, McCann UD, Jesse R. Mystical-type experiences occasioned by psilocybin mediate the attribution of personal meaning and spiritual significance 14 months later. J Psychopharmacol. 2008;22(6):621-632.doi:10.1177/0269881108094300.
  • Griffiths, R. R., Hurwitz, E. S., Davis, A. K., Johnson, M. W., & Jesse, R. (2019).Psilocybin occasioned mystical-type experiences among religious leaders and produced increases in measures of well-being and prosocial behavior.Journal of Psychopharmacology, 33(11), 1353–1368. https://doi.org/10.1177/0269881119883813
  • Roseman L, Nutt DJ, Carhart-Harris RL. Quality of acute psychedelic experience predicts therapeutic efficacy of psilocybin for treatment-resistant depression. Front Pharmacol. 2018;8:974. doi:10.3389/fphar.2017.00974.
  • Ko K, Knight G, Rucker JJ, Cleare AJ. Psychedelics, mystical experience, and therapeutic efficacy: a systematic review. Front Psychiatry. 2022;13:917199. doi:10.3389/fpsyt.2022.917199. PMCID: PMC9340494.

Tryptamines / 5HT2A agonists

  • Thuery G, Sheridan C, Iusan P, et al. Narrating the psychoneuroimmunomodulatory properties of serotonin 5-HT2A receptor psychedelics from a transdiagnostic perspective. Acta Neuropsychiatrica. 2025;37:e77. doi:10.1017/neu.2025.10030
  • Jiang et al., Psilocybin triggers an activity-dependent rewiring of large-scale cortical networks, Cell (2026), https://doi.org/10.1016/j.cell.2025.11.009

 

5-MeO-DMT (naturalistic / MEQ)

  • Davis AK, So S, Lancelotta R, Barsuglia JP, Griffiths RR. 5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT) used in a naturalistic group setting is associated with unintended improvements in depression and anxiety. Am J Drug Alcohol Abuse. 2019;45(2):161-169. doi:10.1080/00952990.2018.1545024. PMCID: PMC6430661.
  • Davis AK, Barsuglia JP, Lancelotta R, Grant RM, Renn E. The epidemiology of 5-MeO-DMT use: benefits, consequences, patterns of use, subjective effects, and reasons for consumption. J Psychopharmacol. 2018;32(7):779-792. doi:10.1177/0269881118769063.
  • Barsuglia JP, Davis AK, Palmer R, et al. Intensity of mystical experiences occasioned by 5-MeO-DMT and comparison with a prior psilocybin study. Front Psychol. 2018;9:2459. doi:10.3389/fpsyg.2018.02459. (Reports ~75% “complete mystical experience.”)

 

5-MeO-DMT

  • Reckweg JT, Korbutt C, Hutten NRPW, et al. Safety, tolerability, pharmacokinetics, and pharmacodynamics of vaporized 5-MeO-DMT (GH001) in healthy volunteers: a randomized dose-escalation trial. Front Pharmacol. 2021;12:732843. doi:10.3389/fphar.2021.732843.
  • Reckweg JT, van Leeuwen CJ, Henquet C, et al. A phase 1/2 trial to assess safety and efficacy of a vaporized 5-MeO-DMT formulation (GH001) in patients with treatment-resistant depression. Front Psychiatry. 2023;14:1133414. doi:10.3389/fpsyt.2023.1133414. PMCID: PMC10319409.

 

Ibogaine

  • Alper KR. Ibogaine: a review. The Alkaloids: Chemistry and Biology. 2001;56:1–38.
  • Antonio T, Childers SR, Rothman RB, et al. Effect of iboga alkaloids on µ-opioid receptor coupled G-protein activation. PLOS ONE. 2013. DOI: 10.1371/journal.pone.0077262
  • Koenig X, Hilber K. The anti-addiction drug ibogaine and the heart: a delicate relation. Molecules. 2015;20(2):2208–2228.
  • Cherian KN, Keynan JN, Anker L, et al. Magnesium–ibogaine therapy in veterans with traumatic brain injuries. Nat Med. 2024;30:373–381
  • Cherian K, Shinozuka K, Tabaac BJ, Arenas A, Beutler BD, Evans VD, Fasano C, Muir OS. Psychedelic Therapy: A Primer for Primary Care Clinicians-Ibogaine. Am J Ther. 2024 Mar-Apr 01;31(2):e133-e140
  • Litjens RPW, Brunt TM. How toxic is ibogaine? Clin Toxicol (Phila). 2016;54(4):297–302.
  • Corkery JM. Ibogaine as a treatment for substance misuse: Potential benefits and practical dangers. In: Progress in Brain Research. Vol 242. Elsevier; 2018.
  • Barsuglia JP, Polanco M, Palmer R, Malcolm BJ, Kelmendi B, Calvey T. Sequential administration of ibogaine and 5-MeO-DMT in alcohol use disorder: case report SPECT study and theoretical rationale. In: Progress in Brain Research. Vol 242. Elsevier; 2018.
  • Kargbo RB. Ibogaine and analogs as therapeutics for neurological and psychiatric disorders. ACS Med Chem Lett. 2022;13(6):888–890.
  • Dickinson JE, Inzunza JAD, Perez-Villa L, Millar TG, Pushparaj AP. Ibogaine reduced severe neuropathic pain in brachial plexus nerve root avulsion: case report. Front Pain Res. 2023;4:1256396.
  • Chen, David & Domínguez, José & Uzeta, Juan & Pushparaj, Abhiram & Dickinson, Jonathan. 2025. Case report: Significant lesion reduction and neural structural changes following ibogaine treatments for multiple sclerosis. Frontiers in Immunology. 16. 10.3389/fimmu.2025.1535782.
  • MindScape Retreat. Ibogaine 14-Day Therapy for Parkinson’s Disease: Case Study of 30 Patients at MindScape Retreat. MindScape Retreat Holistic Healing and Wellness Center; Cozumel, Mexico. Accessed October 24, 2025.
  • Peterson AL, Nutt JG. Treatment of Parkinson’s disease with trophic factors. Neurotherapeutics. 2008;5(2):270-280. doi:10.1016/j.nurt.2008.02.003
  • Wilkins C, dos Santos RG, Solà J, Aixalà M, Cura P, Moreno E. Detoxification from methadone using low, repeated, and increasing doses of ibogaine: A case report. J Psychoactive Drugs. 2017;49(2):175-181.
  • He DY, McGough NN, Ravindranathan A, et al. Glial cell line-derived neurotrophic factor mediates the desirable actions of the anti-addiction drug ibogaine against alcohol consumption. J Neurosci. 2005;25(3):619-628. doi:10.1523/JNEUROSCI.3959-04.2005
  • Marton S, González B, Rodríguez-Bottero S, et al. Ibogaine Administration Modifies GDNF and BDNF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits. Front Pharmacol. 2019;10:193. Published 2019 Mar 5. oi:10.3389/fphar.2019.00193
  • Marton S, Hargitai J, Karádi Z, et al. Ibogaine modifies the expression of neurotrophic factors in dopaminergic brain regions. Front Pharmacol. 2019;10:468
  • Entheoscience (2017, September 21). Entheo-science: Patient D – How ibogaine has helped my Parkinson’s disease 1/2

    . YouTube. https://www.youtube.com/watch?v=6Nb5OYgRt2o.

  • Erny, T., Cano Montenegro, E. Y., Barth, J., & Noller, G. (2026). Ibogaine for the treatment of Parkinson’s disease: A case report. Journal of Psychedelic Studies. Advance online publication. https://doi.org/10.1556/2054.2025.00478
  • Levine, P. A. (2010). In an unspoken voice: How the body releases trauma and restoresgoodness. North Atlantic Books
  • Nunes JM, Barbosa IG, Lafer B. Ibogaine microdosing in a patient with bipolar depression: a case report. Braz J Psychiatry. 2022;44(4):462-463. doi:10.47626/1516-4446-2021-2359

Ibogaine Adverse Events:

  • Papadodima SA, et al., 2013 Death due to consumption of ibogaine: case report— A report of sudden death 5–12 hours after ingestion of ibogaine (in a “Tabernanthe iboga” preparation) during self-administered detoxification.
  • Meisner JA, et al., 2016 Ibogaine‑associated cardiac arrest and death: case report and review of the literature— Describes a 40-year-old man who self-administered 4 g ibogaine plus additional uncharacterized boosters, leading to asystole, brain death and subsequent fatality.
  • Tico Times, March 31 2025 Media report: Costa Rica Retreat Under Scrutiny After Tragic Fatal Heart Attack— U.S. tourist died August 2024 at an iboga/retreat clinic in Costa Rica, death attributed to “fatal heart attack” during ibogaine ceremony.
  • Younis A, Shaoulian E, Femia G, et al. QTc dynamics following cardioversion for persistent atrial fibrillation: a potential increase in torsades de pointes risk. Front Cardiovasc Med. 2022;9:881446. doi:10.3389/fcvm.2022.881446
  • Thomas SHL, Behr ER. Pharmacological treatment of acquired QT prolongation and torsades de pointes: clinical perspective. Br J Clin Pharmacol. 2016;81(2):420-427. doi:10.1111/bcp.12726
  • Hildyard C, Macklin P, Prendergast B, Bashir Y. QT prolongation and torsades depointes from ibogaine toxicity: a case. J Emerg Med. 2016;50(2):e83–e87
  • Paling FP, Andrews LM, Valk GD, Blom HJ. Life-threatening complications of ibogaine:three case reports. Neth J Med. 2012 Nov;70(9):422-4. PMID: 23123541.
  • Mestre D, Paula A, Gil FP, Vaz J. Multiple episodes of cardiac arrest induced by treatment with ibogaine: a case report. Cureus. 2024;16(6):e63487.
  • Schwartz PJ, Crotti L. Long QT Syndrome. New England Journal of Medicine.2025;393:2023–2034
  • Steinberg C, Deyell MW. Cardiac arrest after ibogaine intoxication. J Arrhythmia.2018;34(4):455–457. doi:10.1002/joa3.12061
  • Lamothe SM, Guo J, Li W, Yang T, Zhang S. The human ether-a-go-go-related gene (hERG) potassium channel represents an unusual target for protease-mediated damage. J Biol Chem. 2016;291(39):20387–20401.

 

 

 

Potassium Channels

  • Grant AO. Cardiac ion channels. Circ Arrhythm Electrophysiol. 2009;2(2):185-194.doi:10.1161/CIRCEP.108.789081
  • Nerbonne JM, Kass RS. Molecular physiology of cardiac repolarization. Physiol Rev.2005;85(4):1205-1253. doi:10.1152/physrev.00002.2005
  • Vandenberg JI, Perry MD, Perrin MJ, Mann SA, Ke Y, Hill AP. hERG K⁺ channels: structure, function, and clinical significance. Physiol Rev. 2012;92(3):1393-1478. doi:10.1152/physrev.00036.2011
  • Koenig X, Kovar M, Rubi L, et al. Anti-addiction drug ibogaine inhibits voltage-gated ionic currents: a study to assess the drug’s cardiac ion channel profile. Toxicol Appl Pharmacol. 2013;273(2):259-268. doi:10.1016/j.taap.2013.05.012

 

Cardiac Monitoring

  • Couderc JP, et al. Detection of Drug-Induced QT Prolongation Using Continuous Electrocardiography in Hospitalized Patients. J Electrocardiol. 2011;44(6):634–639.
  • Vandael E, et al. Risk Factors for QT Prolongation: A Systematic Review of the Evidence. Int J Clin Pharm. 2017;39(1):16–25.
  • Charbit B, et al. Frequency and Clinical Relevance of Transient QTc Prolongation Detected by Continuous Monitoring. Eur Heart J. 2018;39(Suppl):ehy565.
  • Koenig X, Hilber K. The anti-addiction drug ibogaine and the heart: a delicate relation. Molecules. 2015;20(2):2208–2228.
  • Knuijver M, et al. Cardiac monitoring of ibogaine therapy and QTc prolongation incidence. Drug Alcohol Depend. 2021;218:108405.

 

 

 

 

Author’s Note:

The phenethylamines, particularly MDMA, can help open a pathway back to one’s essence. By “essence,” I mean the self we are born with—the part that inspires a mother’s love the moment she first holds her child, and the part naturally shared with other children in play. This essence is often most deeply known by our family and childhood companions.

As life unfolds, we take on rules, schooling, jobs, cars, and houses. These are the domain of the ego, the structure that allows us to meet responsibilities and navigate the world. While the ego is necessary, over time we tend to identify primarily with it, leaving our essence less visible in daily life.

In therapeutic sessions, reconnecting with essence often feels like remembering something familiar rather than discovering something new. Afterward, ordinary every-day consciousness is infused with a wider perspective—one that reaches beyond personal suffering to encompass a sense of shared humanity. With this expanded view, challenges like anxiety, relationship struggles, or emotional pain can be met with greater clarity and healing potential.

This journey often unfolds as encounters with younger parts of ourselves. Each meeting feels like a joyful reunion, even when past trauma surfaces. From here, the mature ego can step forward as a caretaker, offering protection and compassion to these more vulnerable selves. For some, the journey may extend all the way back to birth or even conception; for others, it may involve ancestral exploration, where inherited patterns are brought into harmony with individual purpose.

To support this inner process, I offer a few guidelines. Keep conversation to a minimum, as using words tend to pull attention outward. I often suggest the use of an image of a river: Imagine yourself in a boat drifting downstream toward your essence—toward your intuition and deeper knowing. Stay connected to the flow by anchoring attention on body sensations and the music in your headphones.

Along the way, you may notice familiar figures—family members, mentors, friends, partners, even children, appearing on the banks, inviting you to engage. Acknowledge them gently and promise to return later, while continuing downstream. If inner imagery such as a door or a cave appears, allow yourself to enter and follow what arises. In about an hour or so you will know when you meet your essence, and then you can turn around and greet those people.

There are clearly many other approaches in MDMA therapy. Among the most popular is Internal Family Systems (IFS) where a trained therapist uses different parts of one’s self and acknowledges our essential nature of calm, clarity, compassion, and connectedness. Yet others involve more somatic perspective, involving the physical body as a source of wisdom and memory to access

Tryptamines often open the door to an expanded, transpersonal, or “cosmic” perspective, frequently accompanied by a profound dissolution of the ego. For individuals who rely heavily on control, this loss of self-boundaries can initially provoke anxiety or fear. This highlights the clinical importance of careful attention to set and setting: preparing the patient psychologically, creating a supportive therapeutic environment, and maintaining a strong sense of safety and containment.

From this vantage point, the cosmic perspective offers a deeper understanding of how the self relates to the larger world. In this realm, many encounter experiences of “death” — not as an end, but as a transformative passage — through which the fear of death itself is often diminished or released.

Ibogaine possesses a unique therapeutic profile among psychedelic compounds. Its effects are often described as a “life review”—a sequence of vivid, autobiographical visions unfolding in a coherent, narrative-like manner. Unlike MDMA and other agents, ibogaine typically preserves ego integrity, allowing individuals to observe and reflect on their experiences from a stable and continuous sense of self. In many cases, there appears to be an element of volition; participants may even choose which periods or themes of their life to revisit, or, even choose to defer to another time. There is no loss of identity or forgetting of self during the session, therefore there is not the fear that the ego experiences that usually inhibits self-examination.

The content of these visions frequently centers on ego-relevant themes, creating opportunities to revisit unresolved conflicts and trauma with greater compassion and insight. This process can foster psychological resolution and clarify the emotional or behavioral patterns that interfere with daily well-being. As these obstacles become more accessible, patients often find themselves able to adopt a structured, stepwise approach to long-term recovery and integration. Where therapists can be more involved in MDMA sessions, the events or time course during an ibogaine session does not lend itself to much discourse.

Effective aftercare is essential. When cravings are reduced or eliminated, patients often experience a psychological and behavioral void. This space must be intentionally filled with structured support, integration practices, and meaningful engagement in daily life. Without this scaffolding, individuals remain at elevated risk for relapse, driven not by the return of cravings themselves, but by boredom, loss of structure, or the absence of healthier coping strategies and sources of purpose.

 

Note:

This paper is based on my own clinical experience and research. Language has been refined with the assistance of ChatGPT only to improve clarity and readability. All content was reviewed and approved by the author to ensure accuracy and integrity.

 

 

 

 

 

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