Changa

Uncontrolled hypertension, Recent myocardial infarction, Unstable angina, Heart failure

IV DMT produces dose-dependent cardiovascular stimulation including elevated heart rate and blood pressure. While smoked Changa PK data are absent, cardiovascular autonomic effects are expected given DMT's sympathomimetic activity. Individuals with uncontrolled cardiovascular disease should avoid use.

Case reports describe seizures with combinations of lithium and classical psychedelics. The mechanism remains unclear but the association is consistent across multiple reports. Given Changa's additional MAOI component, the risk may be compounded.

Schizophrenia, Schizoaffective disorder, Psychotic spectrum disorders (personal or family history)

Classical psychedelics acting at 5-HT2A receptors may precipitate or exacerbate psychotic episodes in predisposed individuals. This is a class-level contraindication for all serotonergic psychedelics including Changa. No Changa-specific data exist.

Reduced hepatic CYP2D6 activity from liver impairment may prolong plasma exposure to DMT and harmine following smoked Changa. This is a mechanism-based concern; no clinical data specific to Changa or smoked DMT in hepatically impaired populations exist.

Approximately 5–10% of Caucasian populations are CYP2D6 poor metabolizers. Given that CYP2D6 is the primary metabolic enzyme for smoked DMT (Riba 2015), these individuals may experience prolonged and intensified effects from Changa. This pharmacogenomic consideration is mechanism-based but has not been studied for any smoked DMT preparation.

Ayahuasca (DMT + β-carboline MAOIs) administered at 4–8× human-equivalent doses in rats caused maternal deaths, embryolethality, and fetal anomalies. Although these are supratherapeutic doses in an animal model, the mechanism — serotonergic teratogenicity and MAO-mediated catecholaminergic disruption — is conservatively extrapolated to Changa, which contains the same active constituents delivered via inhalation.

Fluoxetine, Paroxetine, Sertraline, Citalopram, Escitalopram, Venlafaxine, Duloxetine, Desvenlafaxine

Concurrent use of SSRIs or SNRIs with Changa risks serotonin syndrome through both pharmacodynamic serotonergic potentiation and pharmacokinetic elevation of DMT/harmine plasma concentrations. PBPK modelling confirms that CYP2D6-inhibiting SSRIs markedly increase exposure to both DMT and harmine. This is the most clinically significant drug interaction for Changa.

Phenelzine, Tranylcypromine, Selegiline, Isocarboxazid

Combining Changa with irreversible MAOIs is potentially life-threatening. The β-carboline reversible MAO-A inhibitors in Changa compound with irreversible MAO inhibition to produce dangerous serotonergic and catecholaminergic accumulation. No case reports specific to Changa exist, but the mechanism is well-established pharmacologically.

Tramadol combines serotonin reuptake inhibition with seizure threshold reduction. When combined with Changa's MAO-A inhibiting β-carbolines, both serotonin syndrome and seizure risk are elevated through independent mechanisms.

Sumatriptan, Rizatriptan, Zolmitriptan, Eletriptan, Naratriptan, Almotriptan, Frovatriptan

Triptans are serotonergic agonists that carry additive serotonergic risk when combined with MAOI-containing preparations such as Changa. The combination may precipitate serotonin syndrome.