It's been almost six years since I did a bunch of reading on the topic, but the conclusion that I came to at the time was that there A) there was no reliable repository of data on ibogaine deaths and B) that protocols other than flood dosing did not prevent arrhythmia or sudden cardiac arrest. Those deaths still occurred in clinical settings where professional informed medical assistance was close at hand.
Methadone is another drug with a risk of QT prolongation (and an arguably comparable safety record on its own,) and dehydration during detox from many drugs can aggravate arrhythmia due to ion balance disruptions. Heavy alcohol use can do the same; gotta have those electrolytes.
It may be that flood dosing is riskier. It may be that microdosing, or gradual multi-day workups to peak plasma levels like
ICEERS.org's protocol may be safer, but I could not be certain. Deaths still occurred regardless. One surprising detail iirc was that deaths often occurred days after the peak, and so may have been caused by noribogaine or other metabolite. Some have suggested that T-wave morphology changes may be responsible, and once the T-wave has returned to normal that the patient is no longer likely to need monitoring. Some clinicians advocate for genetic testing prior to make sure that the patient does not have the cytochrome P450 2d6 phenotype, or at least that their dosage be adjusted, especially for those with an extreme case. Apparently, ibogaine causes T-wave flattening severe enough that it would normally indicate ACLS (advanced cardiac life support) interventions, but with ibogaine the protocol below recommends to just monitor and watch for other arrhythmias. Also, the anti-arrhythmic med amiodarone should not be used, because it also prolongs QT.
There's a lot more information
here. I'll include an excerpt below:
Basic Pharmacodynamics
In addition to the psychological effects noted in the previous section, ibogaine presents some powerful physiological effects, including ataxia, tremor, nausea, vomiting, slowed breathing, heightened sensitivity to sensory stimuli, as well as bradycardia, hypotension and other changes to heart rhythms or blood pressure, including QT interval prolongation and t-wave morphology changes. As a result, unless necessary, patients generally prefer to be lying comfortably without a lot of agitation or movement.
Ibogaine’s physiological effects, particularly its cardiac effects, can present significant and potentially life threatening risk factors even within the therapeutic dose range in patients that have certain pre-existing heart conditions, electrolyte imbalance, or who are detoxifying from alcohol or benzodiazepines (Alper 2012).
The QT interval prolongation associated with ibogaine may have several causes. The primary factor is changes to the way that cardiac cells utilize potassium to repolarize their electrical charge. This repolarization reserve is also affected by bradycardia and the blockage of the hERG channel, which modulates the bioavailability of potassium. As addressed later, this presents concerns in patients who are hypo or hyperkolemic.
Other factors also play a role in depleting repolarization reserves and causing QT prolongation. These include low levels of magnesium; other QT prolonging medications, foods and supplements; withdrawal from cocaine, alcohol, or amphetamines; and many of the risk factors outlined in Chapter 2.
In many cases, during the acute period of ibogaine metabolism, bizarre t-wave morphology may be noted. These changes may include flattening of the t-wave, biphasic t-waves, and initial decrease in the anterior slope of the t-wave. These changes have been postulated to be attributed to changes in intercellular potassium exchange caused by blockage of the hERG channel (Thurner 2013, Alper 2015).
Ibogaine is metabolized via liver enzyme CYP450-2D6 into its primary metabolite, noribogaine. There may be clinically significant variability in the initial phases of ibogaine’s effects based on a patients CYP2D6 metabolism phenotype, particularly at the extreme ends of the spectrum for poor and ultra-rapid metabolizers (Glue 2015).
Ibogaine is also known to cause a level of restlessness and sleeplessness in the days following administration in some cases. This is especially the case for patients who use benzodiazepines or other sleep inducing medications.
Seizures under the influence of ibogaine can induce lethal arrhythmias, and have led to fatalities as well as permanent injury. Ibogaine itself has not been known to induce seizures, however, this is a concern in regards to withdrawals from alcohol or benzodiazepines, as well as for epileptics.
Clinical Pharmacokinetics
Ibogaine saturation peaks at 2 hours after administration and has a half-life of up to 7 hours in human plasma (Koenig 2015). It is metabolized into noribogaine, which, it is believed, is stored in fat tissue and released over the course of the following weeks or months. Noribogaine possesses some of the same effects as ibogaine, which may account for the prolonged reported benefits.
In those patients who experience t-wave changes they generally last between 12-14 hours, but can persist for as long as 24 hours. Cardiac concerns decrease after t-wave stabilizes.
Some adverse events have been reported as late as 76 hours after administration (Alper 2012), however the factors in these instances generally can be addressed with proper screening and preparation.
bluelight.org
) would always say that ondansetron would totally eliminate any bodyload and nausea while not impacting the trip at all. And I want to even say he used to say it made the trip better, but that might just have been due to lack of bodyload. It always used to sound so appealing to me back then, because I used to get pretty bad bodyloads. Nowadays though, I basically don't ever get nausea or bodyloads, which is ironic because now I have ready access to ondansetron (my girlfriend got prescribed it and never uses it).
