Stimulants are a broad classification of psychoactive substances that induce temporary enhancements in cognitive or physical functions. However, use can present significant cardiac effects that can lead to “varying degrees of tachycardia, vasoconstriction, unpredictable blood pressure effects, and arrhythmias, depending on the dose taken and the presence or absence of coexisting cardiovascular disease” (Ghuran 2000).
In lower doses ibogaine itself acts as a stimulant, and if taken in conjunction with various stimulants, ibogaine can amplify their effects.
In addition to these general concerns, many specific stimulants present their own unique risks, which are further discussed here along with recommendations for how to minimize these risks prior to treatment. If there are doubts about compliance during intake or at any point during the treatment, a urine screen and any relevant cardiac tests should be re-administered.
Even after the terminating use for the periods described below, patients who have been using stimulants chronically may may have higher instance of arrhythmias due to hyper excitable heart. Particular attention should be paid to the cardiac status throughout the treatment process.
Crack & Cocaine
In addition to the general stimulant considerations, crack and cocaine are known to block the hERG channel and lead to QT prolongation (Karle 2002).
Ibogaine has been shown to potentiate the effects of cocaine by sensitizing receptors that mediate its effects (Szumlinksi 2000).
Methamphetamine is known to prolong the QT interval even though it does not interact with the hERG channel or any other known cardiac channel (Haning 2007), as well as to affect CYP2D6 metabolism. Ibogaine has been shown to potentiate the effects of methamphetamine by sensitizing receptors that mediate its effects (Szumlinski 2000).
It is recommended that patients cease consumption of prescription stimulants, including methylphenidate (Ritalin) and amphetamine/dextroamphetamine (Adderall), for at least five days prior to administration of ibogaine.
Caffeine inhibits the metabolism of melatonin (Härtter 2003), which may alter the circadian rhythm. Caffeine has also been shown to induce hypokalemia (low potassium) (Tajima 2010), and may contribute to QT prolongation.
It is recommended that patients cease consumption of caffeine for at least 5 days prior to administration of ibogaine.