The term “telepathine” regularly pops up in conversations about ayahuasca, DMT, and plant remedies such as Banisteriopsis caapi. The name sounds mysterious and is sometimes linked to “telepathy,” but that is primarily historical usage and not a proven property. In practice, telepathine usually refers to harmine, a substance from the group of β-carbolines. The main reason harmine is so relevant is pharmacological: it acts primarily as reversible MAO-A inhibitor.
In this article, we calmly explain what telepathine (harmine) is, what MAO-A does in the body, why harmine plays such a major role in DMT, why the situation is different with psilocybin, and what risks are associated with combinations, with special attention to mdma. This is general information and not individual medical advice. We also make no statements regarding “safe use” in the sense of guarantees, as interactions depend on the person, dose, context, and health.
What exactly is telepathine (harmine)?
“Telepathine” is an older, historical name used in early descriptions of ayahuasca. Nowadays, it is usually harmine This is what is meant. Harmine is a β-carboline found in various plants, including Banisteriopsis caapi (an important component in ayahuasca) and Peganum harmala (Syrian rue). In older literature, you may also encounter names such as banisterine or yageine, but in a modern context, “harmine” is the most commonly used term.
The distinction between language and evidence is important. The word “telepathine” originated in part from interpretations of subjective experiences. This does not mean that telepathy has been proven as an effect. What can be described accurately, however, are the pharmacological properties of harmine and related β-carbolines.
MAO-A explained: why this enzyme is so important
MAO stands for monoamine oxidase. This is an enzyme in the body involved in the breakdown of various substances, including certain neurotransmitters and (plant) alkaloids. There are roughly two variants: MAO-A and MAO-B. Harmine primarily inhibits MAO-A, and that is relevant because MAO-A can play an important role in the breakdown of various monoamines.
If MAO-A is temporarily inhibited, certain substances cannot be broken down as quickly. This can have an intended effect (for example, with DMT, where it enables its oral action), but it can also lead to interaction risks when other agents or medication are present simultaneously. “Reversible” means that the inhibition is in principle reversible, but this does not automatically make combinations risk-free. Timing, dosage, and individual sensitivity remain decisive.
Telepathine (harmine) and DMT: why ayahuasca works orally
DMT (N,N-Dimethyltryptamine) is usually barely active upon oral ingestion because it is rapidly broken down in the gastrointestinal tract and liver, partly by MAO-A. The core function of harmine (and often harmaline) in ayahuasca is that these substances MAO-A brakes, whereby DMT can remain available longer when taken orally. As a result, the effect can last much longer and manifest differently than when DMT is inhaled.
This is one of the clearest examples of how an MAO-A inhibitor can drastically alter the effects of a tryptamine. This involves not only “enhancement,” but also enabling a completely different route of administration and duration of the experience. In this sense, harmine is not merely an “auxiliary,” but a determining factor in the pharmacological profile of ayahuasca.
Telepathine (harmine) and psilocybin: less necessary, but possibly influential
With psilocybin, the situation is different. Psilocybin is naturally orally active and is converted into psilocin in the body. Psilocin is subsequently metabolized via multiple routes, whereby glucuronidation plays an important role. There are indications that MAO-A can also contribute to degradation processes, but its role appears in any case to be less “all-determining” than with DMT.
This means that harmine in combination with psilocybin or psilocin can theoretically influence the duration or intensity, but it is likely not a prerequisite for making the substance “effective.” Combinations are referred to as “psilohuasca” in some circles. It is important to note here that there much less clinical substantiation research into the effects and risks of such combinations is more extensive than research into the standalone use of psilocybin. Less evidence does not automatically mean “dangerous,” but it does mean that predictability is lower.
In practical terms, people taking MAO-A inhibition in combination with tryptamines sometimes report an experience that feels more intense, longer, or more physical. At the same time, nausea, emotional intensity, and unpredictability may increase. These are general observations; they are not the same for everyone and are not always easy to verify.
Harmine is also active herself: not just an 'amplifier'‘
Harmine is sometimes discussed as if it merely “opens the gate” for DMT. But harmine also has own pharmacological activity. Research with pure harmine examines, among other things, pharmacokinetics (how the body absorbs and breaks down the substance) and pharmacodynamics (what the substance does in the body). This does not mean that combinations with psychedelics are automatically safe, but it does nuance the view that harmine is purely a passive addition.
Precisely because harmine itself can have effects, a combination can turn out differently subjectively and physically than someone expects based on “DMT” or “psilocybin” alone. This is one of the reasons why combinations bring more uncertainty.
Safety and interactions: why MAO-A inhibition requires extra alertness
The most important harm-reduction message regarding harmine is: MAO-A inhibition can interact strongly with other substances.. This applies not only to psychedelics, but also to various medications and recreational substances. Especially combinations with serotonergic or stimulating substances receive a lot of attention because they can theoretically and practically increase the risk of harmful reactions.
Examples of agents and medications often cited as high-risk combinations with MAO-A inhibitors are: SSRIs and SNRIs (antidepressants), tramadol, dextromethorphan, linezolid (an antibiotic with MAO-inhibiting properties), amphetamines, and mdma. This list is not exhaustive, and interactions may also depend on dosage, time between intakes, individual sensitivity, and underlying health.
An additional complication is that “plant extracts” or “concoctions” can vary in strength. As a result, the degree of MAO-A inhibition can be difficult to predict. Confusion can also arise regarding exactly what is contained in a product (for example, harmine versus harmaline versus other alkaloids). Uncertainty about composition inherently increases the risk, because it is more difficult to estimate what the combination does in the body.
MDMA risks in combination with MAO-A inhibition
MDMA acts via the serotonin system, among others, and also has stimulating properties. In combination with MAO-A inhibition, this can be particularly risky because MAO-A is involved in the breakdown of monoamines and because serotonergic load may increase. The exact risk is difficult to quantify in general terms, but harm reduction sources generally warn against this combination due to the possibility of serious side effects.
It is important to emphasize that this is not about moral judgments, but about pharmacology and risk management. If someone wants to use MDMA in a therapeutic context: MDMA sessions can currently only be discussed within scientific research or in practice via harm reduction.. In both cases, the theme of interactions, medical screening, and avoiding risk combinations is a recurring point of attention. This is not a guarantee of safety, but it is a reason why serious guidance frameworks place a strong emphasis on preparation and contraindications.
What does this mean for therapy, trauma, and counseling?
Regarding trauma and therapy, there is growing interest in substance-assisted pathways, including MDMA in a research context. At the same time, people are also coming into contact with ayahuasca, “psilohuasca,” or other combinations outside of research in which MAO-A inhibition plays a role. The key distinction here is that scientific research works with standardized dosages, selection criteria, and monitoring, whereas experiences outside of it often involve more variation and uncertainty.
A careful approach usually means building knowledge, soberly weighing risks, and not experimenting with combinations known to pose an interaction risk. It is also sensible to remain critical of your own sources of information: anecdotal evidence can be valuable as a perspective, but it is not proof and is not automatically transferable to your situation.
Anyone wishing to explore guidance or a session within a framework where harm reduction is explicitly included can read more about how this is approached in practice. On this source page you will find the context of the question about telepathine (harmine) and the combination with DMT and psilocybin, including the key points regarding MAO-A and interactions.
Conclusion
In current practice, Telepathine is primarily a historical name for harmine, a β-carboline primarily known as reversible MAO-A inhibitor. With DMT, this is crucial because MAO-A inhibition enables oral activity and prolongs the experience. With psilocybin, harmine is not necessary for oral action, but it may potentially influence intensity and duration, while simultaneously increasing unpredictability.
The biggest security issue lies in interactions. MAO-A inhibition can make combinations with serotonergic or stimulant agents, including MDMA, riskier. If you would like to explore a supervised approach within a harm-reduction framework, you can register via Sign up for MDMA session. MDMA sessions can currently only be discussed within scientific research or in practice via harm reduction, and it is advisable to take the topic of interactions and contraindications seriously if you are interested in this subject.
