Noller et al. 2018: New Zealand Oral Ibogaine Observational Outcomes — Including One Death During Treatment

Definition box

Definition: Noller, Frampton & Yazar-Klosinski (2018) in *The American Journal of Drug and Alcohol Abuse* (doi: 10.1080/00952990.2017.1310218) is a twelve-month observational study of n=14 adults (50% female) receiving legal oral ibogaine treatment for opioid dependence in New Zealand. Primary outcome was Addiction Severity Index-Lite (ASI-Lite); secondary measures included Beck Depression Inventory-II (BDI-II) and Subjective Opioid Withdrawal Scale (SOWS). Completers with full interview series (n=8) showed significant reductions in ASI-Lite drug-use composite and BDI-II scores at 12 months; SOWS fell acutely after treatment in all 14. One patient enrolled in the study died during treatment—a fact the paper states and that this page discusses honestly. This is not a randomized controlled trial, not FDA approval evidence, and not proof of physician-supervised IV ibogaine infusion (psychoactive intravenous ibogaine). Most published clinical ibogaine literature is oral. Cardiac QTc risk remains central. Ibogaine is U.S. Schedule I and not FDA-approved.

Quotable answer (59 words)

Noller and colleagues’ 2018 New Zealand observational study of 14 people treated with oral ibogaine for opioid dependence reported 12-month ASI and depression improvements in completers—and one death during treatment. It is not an RCT and not evidence for psychoactive IV ibogaine infusion. Cardiac risk and monitoring culture still matter. Ibogaine is not FDA-approved.

Why this paper-spoke exists

Noller 2018 is frequently cited for “durable NZ outcomes” while the enrolled fatality is sometimes omitted in marketing. Honest paper-spokes name both the ASI/BDI signals and the death. Searchers comparing Brown & Alper 2018, Mash 2018, and this NZ cohort need route labels and risk literacy—not cure rates.

Related: /blog/brown-alper-2018-ibogaine-oud · /blog/mash-2018-ibogaine-detox-frontiers · /blog/ibogaine-mortality-cardiac-risk · Oral vs IV: /blog/ibogaine-oral-vs-iv · Entity: /what-is-ibogaine-infusion.

What was studied

| Feature | Accurate description | |---------|----------------------| | Citation | Noller G.E., Frampton C.M., Yazar-Klosinski B. *Am J Drug Alcohol Abuse*. 2018;44(1):37–46. doi 10.1080/00952990.2017.1310218 | | Design | Prospective observational 12-month follow-up | | N | 14 participants (50% female) with opioid dependence | | Setting | New Zealand — ibogaine legally available; two treatment providers | | Psychoactive route | Oral ibogaine (single treatment episode as described) | | Primary outcome | Addiction Severity Index-Lite (ASI-Lite) composites over 12 months | | Secondary | BDI-II (depression); SOWS (acute opioid withdrawal) | | Completers | n=8 with all interviews; n=4 partial data; 1 death during treatment | | What it is not | RCT; IV-psychoactive ibogaine proof; FDA package; license to skip screening |

Readers should open the primary paper for exact composites, provider context, coronial discussion, and limitation language.

Methods (plain language)

Adults seeking legal ibogaine treatment for opioid dependence in New Zealand were followed observationally after a single ibogaine treatment episode delivered by either of two providers. Researchers scored addiction severity with ASI-Lite across baseline and scheduled follow-ups through 12 months, tracked depression with BDI-II, and measured acute withdrawal with SOWS before and immediately after treatment.

Plain-language design features:

1. No randomization / no placebo control.
2. Small N — 14 enrolled; only 8 completed the full interview series.
3. Legal NZ context differs from U.S. Schedule I reality; legality ≠ cardiac safety.
4. Provider heterogeneity — two treatment providers; monitoring intensity can vary.
5. Self-selected treatment seekers; results do not generalize to all OUD patients.
6. Mortality captured — one enrolled participant died during treatment and must remain in any honest synopsis.

Key findings (no hype)

As reported by the authors:

• Among participants completing all interviews (n=8), Friedman tests showed a significant reduction in ASI-Lite drug-use composite from baseline to 12 months (p = 0.002).
• BDI-II depression scores also fell significantly from baseline to 12-month follow-up (p < 0.001) in completers.
• SOWS scores for all participants (n=14) showed significant acute reductions after treatment (p = 0.015).
• Participants with partial data (n=4) also showed reductions in ASI-Lite drug-use scores and family/social problem domains (as reported).
• Authors framed outcomes as opioid cessation or sustained reduced use over 12 months in this small cohort—observational, not RCT-proven cure rates.
• One patient enrolled in the study died during treatment. Subsequent New Zealand Health and Disability Commissioner and coronial processes (discussed in the paper’s context) involved duty-of-care and monitoring concerns; the coroner noted the death was very likely related to ibogaine even without clear post-mortem cardiac pathology defining a single mechanism.

Honest reading: durable *observed* ASI/BDI trajectories in a tiny NZ completer subset are scientifically interesting and motivate safer, better-monitored research. They are not population “success rates,” not proof that unsupervised or under-monitored treatment is safe, and not evidence for psychoactive IV ibogaine.

The death: discuss honestly

YMYL pages that cite Noller without the fatality mislead patients and families.

| Point | Accurate framing | |-------|------------------| | Fact | One enrolled participant died during treatment | | Design implication | Outcome analyses on survivors/completers do not erase treatment-period mortality | | Investigations | NZ HDC / coronial context described duty-of-care failures (monitoring/informed consent concerns in public record discussed by authors) | | Mechanism certainty | Absence of a single definitive post-mortem cardiac lesion does not equal “ibogaine-safe”; coroner still linked death as likely ibogaine-related | | Clinical takeaway | Continuous monitoring, ECG/electrolytes, and medical readiness are non-negotiable—not optional spa add-ons | | Marketing misuse | “NZ study proves safe long-term detox” is false |

See also: /blog/ibogaine-mortality-cardiac-risk, /blog/ibogaine-telemetry-acls-monitoring, /safety-and-screening.

Limits and confounders

| Limit | Why it matters | |-------|----------------| | Observational / no RCT control | Cannot prove causality vs expectancy, setting, or concurrent supports | | Tiny completer N (8/14) | Completers may differ systematically from dropouts | | Enrolled death | Efficacy narratives that ignore mortality are incomplete | | Self-report / interview outcomes | Underreporting of use possible | | Provider / setting variability | Legal NZ ≠ uniform ICU-grade cardiac protocol | | Selection effects | Motivated NZ patients ≠ all OUD populations | | Route | Oral — does not validate psychoactive IV | | Cardiac literature still applies | Knuijver 2021 QTc data and fatality reviews remain relevant |

Systematic reviews (Köck 2022; Mosca 2023) already stress limited RCTs and cardiotoxicity/mortality concerns across clinical ibogaine literature.

Route honesty: oral ≠ psychoactive IV

Noller 2018 reflects oral ibogaine in a New Zealand treatment context. That is chemically and pharmacokinetically different from this site’s entity: IV ibogaine infusion as psychoactive intravenous delivery under physician supervision.

Support IVs (fluids, magnesium, antiemetics) used in some modern programs are not the same as psychoactive IV ibogaine (/blog/electrolytes-support-iv-vs-psychoactive-iv, /blog/magnesium-ibogaine-cardiac-protocol).

Clinics that cite “the New Zealand 12-month IV study” should be asked in writing: Was the psychoactive dose oral or intravenous?

Cardiac / YMYL context

Ibogaine has been associated with QTc prolongation and, in some contexts, fatal arrhythmias. Knuijver et al. (*Addiction* 2021) documented mean QTc prolongation of about +95 ms after oral 10 mg/kg, with 50% of subjects exceeding 500 ms, in a monitored university setting—with no TdP in that small sample, which does not prove safety at scale.

Noller’s enrolled death is a reminder that observational outcome papers and safety papers must be read together. Anyone considering any ibogaine exposure needs ECG/electrolyte diligence and continuous monitoring culture—not ASI-statistic shopping (/safety-and-screening, /blog/ibogaine-ecg-pre-infusion-checklist).

What this does NOT prove for IV ibogaine infusion brand

| Claim | Status | |-------|--------| | “NZ proves year-long cure rates for IV ibogaine” | False — oral observational; small completer subset | | “Safe because ASI improved” | False — one enrolled death; scores ≠ cardiac safety | | “RCT-proven OUD treatment” | False — observational | | “FDA-cleared detox” | False — U.S. Schedule I; not FDA-approved | | Cite as adjacent oral literature with labels? | Yes — if design/route/N/death labeled |

U.S. access context remains Schedule I / not FDA. Provisional Mexico programs on this site ≠ U.S. FDA clinics (/blog/is-ibogaine-legal-us, /blog/ibogaine-mexico-medical-vs-tourism).

Soft CTA

If Noller’s ASI signals—and the death—prompted serious interest in physician-supervised IV ibogaine infusion, begin with cardiac and evidence-gap literacy: /safety-and-screening. Then request a confidential screening consult via /apply—not after “NZ cure” marketing that erases mortality.

FAQ

What did Noller et al. 2018 study? A 12-month observational follow-up of 14 people receiving legal oral ibogaine for opioid dependence in New Zealand, with ASI-Lite, BDI-II, and SOWS measures.

What were the main outcome signals? Completers (n=8) showed significant ASI-Lite drug-use and BDI-II reductions at 12 months; SOWS fell acutely after treatment in all 14.

Did anyone die? Yes. One patient enrolled in the study died during treatment. Honest summaries must include that fact.

Was this a randomized controlled trial? No. Observational design without a randomized control arm.

Does this prove IV ibogaine infusion works? No. Route was oral; design was observational; N was small; a treatment-period death occurred.

Does New Zealand legality mean ibogaine is safe? No. Legal availability is not a cardiac-safety certificate. QTc risk and monitoring requirements remain.

Is ibogaine FDA-approved for OUD? No. Schedule I in the United States; not FDA-approved.

Where can I read adjacent papers? /blog/brown-alper-2018-ibogaine-oud, /blog/mash-2018-ibogaine-detox-frontiers, /blog/knuijver-2021-ibogaine-qtc-safety, /blog/kock-2022-ibogaine-systematic-review.

Medical disclaimer

Educational research synopsis only—not medical, psychiatric, or legal advice, and not a guarantee of outcomes. Ibogaine can prolong the QTc interval and has been associated with serious cardiac events including torsades de pointes and death in some contexts. This page discusses a published enrolled death in Noller 2018 honestly. Ibogaine is Schedule I in the United States and is not FDA-approved for any indication. Provisional Mexico programs discussed on this site are not U.S. FDA clinics. Soft CTAs: /safety-and-screening, /apply.

Noller 2018 is oral observational NZ literature—not psychoactive IV ibogaine proof.

Sources (selected)

1. Noller G.E., Frampton C.M., Yazar-Klosinski B. Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study. *Am J Drug Alcohol Abuse*. 2018. doi: 10.1080/00952990.2017.1310218.
2. Brown T.K., Alper K. *Am J Drug Alcohol Abuse*. 2018. doi: 10.1080/00952990.2017.1320802.
3. Mash D.C. et al. *Front Pharmacol*. 2018. doi: 10.3389/fphar.2018.00529.
4. Knuijver T. et al. *Addiction*. 2021. doi: 10.1111/add.15448.
5. Köck P. et al. *J Subst Abuse Treat*. 2022. doi: 10.1016/j.jsat.2021.108717.
6. Mosca A. et al. *Curr Neuropharmacol*. 2023. doi: 10.2174/1570159X21666221017085612.
7. 21 CFR 1308.11 — ibogaine Schedule I (United States).