In einer Megaanalyse von Nature Medicine aus dem Jahr 2026 wurde anhand von mehr als 500 Gehirnscans untersucht, wie DMT und andere Psychedelika die Gehirnkonnektivität neu verknüpfen. Nun möchte ein Forschungsteam des Albert Einstein College of Medicine herausfinden, ob die DMT-Produktion Ihres Gehirns auf einer niedrigeren Ebene dasselbe bewirkt

This post blends legitimate neuroscience with a fairly enthusiastic dose of speculation. The first part is broadly sound: modern neuroimaging studies using psychedelics such as LSD, psilocybin, DMT, mescaline, and ayahuasca do show changes in large-scale brain connectivity. A recurring finding is that networks which are normally relatively compartmentalised begin communicating more freely, while structures such as the default mode network, which is associated with internally directed thought and self-referential processing, become less rigidly organised. That part is well supported.

Where what the author is saying becomes much less certain is the leap from externally administered DMT to the brain’s own naturally occurring DMT. Those are not equivalent situations. Exogenous DMT, taken as a drug, produces pharmacological concentrations that strongly activate serotonin receptors, particularly 5-HT2A receptors, which are heavily implicated in psychedelic effects. Endogenous DMT, assuming it does have a normal physiological role, appears to exist in vastly smaller quantities. Biology is not simply “same molecule equals same effect, just less of it.” Dose, receptor occupancy, metabolism, location of production, timing, and local concentration all matter enormously. A trace amount of a signalling molecule can be profoundly important, but equally it may have a very different role entirely from what happens when the system is pharmacologically flooded.

It is true that humans appear capable of synthesising DMT. The enzymatic machinery required, particularly indolethylamine N-methyltransferase (INMT), has been identified in human tissues, and trace DMT has been reported in cerebrospinal fluid and elsewhere. But that only tells us the molecule exists. It does not tell us what it is doing, whether it acts as a significant neurotransmitter, whether its concentrations ever rise enough to meaningfully alter conscious experience, or whether it has some entirely different biochemical role. Detecting a compound is not the same as proving functional importance.

The suggestion that people with different endogenous DMT production might show measurably different baseline brain architectures is scientifically interesting, but currently speculative. Brain connectivity is influenced by an enormous number of variables: genetics, development, age, sleep quality, stress hormones, inflammation, medications, psychiatric state, stimulant use, and even ordinary day-to-day fluctuations in arousal. Isolating endogenous DMT as a causal factor among all of that would be extremely difficult. Even if a correlation were found, correlation is not causation. A distinct brain connectivity pattern associated with some biomarker does not automatically mean DMT created that pattern.

A fair summary would be to say the psychedelic neuroimaging research is real and genuinely interesting. The idea that endogenous DMT might play some subtle role in brain function is a legitimate research question. But the authors framing overstates what is currently known. It is firmly in “interesting hypothesis under investigation,” not “established mechanism explaining normal consciousness.”