Who is ibogaine not suitable for?

The clearest guide to who should not take ibogaine comes from the studies themselves. Researchers publish the criteria that disqualified people from taking part, and those lists were written by teams who had to justify every inclusion to an ethics committee [1].

Why published exclusions are the best guide

A provider's screening list is a commercial document. A study's exclusion criteria are a scientific one, written before anyone was dosed and published alongside the results.

That difference matters when comparing what different sources say. A clinic has an interest in a wider list of eligible people. A research team has an interest in nobody being harmed on record.

The Dutch hospital study of fourteen patients is the most useful source here, because its criteria were specific and numerical rather than general [1]. The Stanford study of thirty veterans adds a second set from a different population [4].

Neither list is a substitute for assessment by a clinician who has seen the person. They describe the categories that disqualify, not whether any particular individual falls into one.

Heart conditions and the baseline EKG

The heart is the first filter, because ibogaine's best-documented effect is cardiac.

The Dutch team excluded anyone whose baseline corrected QT interval was above 450 milliseconds in men or 470 milliseconds in women [1]. Those thresholds exist because ibogaine adds to whatever the interval already is.

The arithmetic is unforgiving. In that cohort, the maximum prolongation averaged 95 milliseconds [1]. Someone starting at 450 and gaining an average increase lands near 545, well past the point where the risk of a dangerous rhythm climbs. Someone starting at 400 lands near 495.

A baseline reading is therefore not a formality. It determines how much room a person has before the drug uses it up.

Existing heart disease widens the exclusion further. A review of ibogaine-related deaths notes that most involved pre-existing cardiac conditions, other drugs taken alongside, or the absence of monitoring [2]. The first of those three is the one screening can identify in advance.

A family history of sudden unexplained death before middle age is worth raising with a clinician, since inherited rhythm disorders can be present without symptoms and lengthen the interval from the start.

Blood results that rule treatment out

Blood chemistry affects the heart directly, which is why bloodwork sits beside the EKG rather than behind it.

Potassium outside the range of 3.5 to 5.0 millimoles per litre was an exclusion in the Dutch study [1]. Low potassium lengthens the QT interval on its own, so a person with it is starting from a worse position than their EKG alone suggests.

This is more relevant in this population than it might appear. Vomiting is common during ibogaine treatment, and poor nutrition, diuretics and some patterns of substance use all lower potassium. A level that is acceptable on the morning of treatment can fall during it.

Magnesium matters for the same reason, which is part of why it appears in treatment protocols. The Stanford study gave magnesium alongside ibogaine from the start [4], and the Dutch team gave it when the interval passed 500 milliseconds [1].

Medications that conflict

Two separate problems arise here, and they are often confused with one another.

The first is additive. Any drug that lengthens the QT interval adds to what ibogaine does, so the Dutch team excluded people taking them [1]. That category is broad and includes some antidepressants, antipsychotics, antibiotics, antifungals and anti-nausea drugs. The list is long enough that a full medication review is the only reliable way through it.

The second is metabolic. Ibogaine is broken down mainly by the liver enzyme CYP2D6, so drugs that inhibit that enzyme raise ibogaine levels from an unchanged dose [2]. The Dutch team excluded those too [1].

Methadone sits in that second category. It inhibits CYP2D6 and is likely to impair ibogaine metabolism [2], which is awkward because methadone maintenance is common among the people most interested in ibogaine. It is one reason protocols switch people to short-acting opioids beforehand rather than dosing them on methadone.

CYP2D6 handles roughly thirty per cent of drugs in current use [2], so the interaction question is not a rare one. Some widely used antidepressants are among the inhibitors.

Liver and kidney function

Severe liver or kidney dysfunction was an exclusion in the Dutch study [1], for a reason that follows from the metabolism.

The liver converts ibogaine to noribogaine and the kidneys handle elimination. Impairment at either step means the drug and its metabolite stay longer at higher levels, which extends the cardiac exposure rather than changing its nature.

Hepatitis C is common in people with a history of injecting drug use, and liver function in that group cannot be assumed from appearance or age. It is a bloodwork question rather than an interview question.

Psychiatric history

The psychiatric exclusions are less numerically precise than the cardiac ones, and that reflects genuine uncertainty rather than carelessness.

Ibogaine produces an intense altered state lasting many hours. In the Dutch cohort, patients reported closed-eye visuals and vivid memories, and one reported visual hallucinations [1]. A person with a psychotic disorder, or at high risk of one, is generally excluded from studies of compounds that produce such states.

The Dutch authors also noted reports in the literature and in online forums of longer-lasting disturbing behavioural changes after ibogaine, while being explicit that they did not observe or verify these [1]. Recording an unverified signal rather than omitting it is the correct handling of it, and it is a reason the psychiatric assessment is not a formality.

Active suicidality, recent psychiatric hospitalisation and unstable bipolar disorder appear as exclusions across psychedelic research more broadly. The honest position is that ibogaine-specific evidence on these is thin.

Pregnancy and other exclusions

Pregnancy and breastfeeding are standard exclusions in this literature, and the reason is absence of data rather than evidence of harm. No study has examined ibogaine in pregnancy, and none is likely to.

Age limits appear in most protocols at both ends. The Stanford cohort were veterans with traumatic brain injuries, a group defined by its exposure rather than its age [4], while the Dutch cohort had a median age of 48 [3].

Being unable to consent, or being under pressure from family or a court to undergo treatment, disqualifies a person for reasons that have nothing to do with physiology and are no less binding.

What thorough screening looks like

Screening is a sequence rather than a single appointment, and the order of the steps is part of what makes it work.

It starts with history. A full account of cardiac events in the family, previous fainting episodes, current and recent medications including anything bought without a prescription, and an honest picture of substance use. Each of those changes what the later tests mean.

Then the EKG, read against the thresholds above rather than filed as a formality. A single tracing taken on a calm morning is a starting point; some protocols repeat it, because a person's interval varies through the day.

Then bloodwork, covering potassium and magnesium, liver enzymes and kidney function. These are the results that decide whether the heart is starting from a normal position and whether the drug will clear at a typical rate.

Then a medication review conducted against a reference list rather than from memory, since the number of drugs that lengthen the QT interval or inhibit CYP2D6 is too large to hold in one's head.

Then a psychiatric assessment, and a conversation about what the experience involves and how long it lasts.

A process that skips any of these is not a faster version of the same thing. Each step rules out a different category of harm, and none of them substitutes for another. A provider who performs an EKG but no bloodwork has checked the starting position without checking what will move it.

Several questions are worth putting to any provider directly. Who reads the EKG, and what are the thresholds for declining someone. What bloodwork is required, and how recent must it be. Who reviews the medication list. What happens if the QT interval passes 500 milliseconds during treatment, and what equipment and staff are present at that moment. How long monitoring continues afterwards, and on what basis the decision to end it is made.

Answers that are specific and numerical suggest a process that exists. Answers that are reassuring and general suggest one that does not.

The grey areas

Several questions have no clean answer, and a provider who gives one is overstating what is known.

CYP2D6 genotype is the clearest example. Clearance varied more than tenfold across genotype groups in one cohort [3], and the enzyme is non-functional in roughly five to ten per cent of people of European descent [2]. Whether a poor metaboliser should be excluded outright, dosed differently, or monitored for longer has not been settled.

Weight-based dosing is a second. Both main cohorts used milligrams per kilogram [1][4], but body weight does not predict clearance nearly as well as genotype does [3].

Prior ibogaine exposure is a third. Whether a second treatment carries the same cardiac profile as the first has not been studied systematically, though repeat treatment appears in the outcome literature.

A twelve-month New Zealand follow-up recorded one death during treatment alongside its positive outcomes [5]. Screening criteria exist because of cases like that one, and their existence does not promise that careful screening prevents every one.

Where the research goes next

The exclusion lists in use today were assembled from cardiac pharmacology and from case reports of deaths. They are reasonable, and they are not validated.

Three questions would sharpen them. Whether genotype-guided dosing produces safer exposure than weight-based dosing. Whether any psychiatric history predicts a bad outcome, as opposed to being excluded out of caution. And whether the cardiac thresholds now in use are at the right numbers rather than approximately right ones.

Until then, the practical position is that the published exclusions are a floor rather than a ceiling, and that a provider who screens less thoroughly than a research team is not offering a more accessible version of the same thing. The eligibility page sets out the questions a person can work through before speaking to anyone.

Frequently asked questions

What heart conditions rule out ibogaine?

A baseline corrected QT interval above 450 milliseconds in men or 470 in women was an exclusion in the Dutch hospital study [1]. Existing heart disease features in most reported deaths [2].

Can someone on methadone take ibogaine?

Methadone inhibits CYP2D6 and is likely to impair ibogaine metabolism [2]. Study protocols switch people to a short-acting opioid beforehand rather than dosing on methadone [1].

Do antidepressants rule ibogaine out?

It depends on which one. Some lengthen the QT interval and some inhibit CYP2D6, and both categories were exclusions in the Dutch study [1]. This is a question for a clinician with the full medication list.

Is there an age limit for ibogaine?

Protocols generally set limits at both ends, though the numbers vary between them. The Dutch cohort had a median age of 48 [3]. Age matters mainly through what tends to accompany it, such as cardiac changes and a longer medication list, rather than on its own.

Does passing screening mean treatment is safe?

No. Half the patients in that screened, hospital-monitored cohort still passed a QT interval of 500 milliseconds [1]. Screening lowers the risk and does not remove it.