Soon after the discovery of endogenous DMT in
humans, psychiatric researchers began to report
correlations between increased levels of DMT in
human fluids and schizophrenia [11–15]. It was
suggested that excess DMT biosynthesis may promote psychotic symptoms. This proposal (which
is sometimes known as the ‘‘transmethylation
hypothesis,’’ because it involves methylated
amines) attracted interest in the 1960s and
1970s. In more recent years, the transmethylation
hypothesis has been eclipsed by the dopamine
hypothesis of schizophrenia, wherein psychotic
symptoms are related to excessive activity in certain dopaminergic circuits in the brain. Recent
biochemical and genetic characterization of a
new family of receptors, the trace amine (TA)
receptors, found in mammalian central and
peripheral nervous tissues, has renewed interest
in a potential role for trace amines in psychosis
[16].
[........]
[11] Murray RM, Oon MC, Rodnight R, Birley JL, Smith A.
Increased excretion of dimethyltryptamine and certain
features of psychosis: a possible association. Arch Gen
Psychiat 1979;36:644–9.
[12] Lipinski JF, Mandel LR, Ahn HS, Vanden Heuvel WJ, Walker
RW. Blood dimethyltryptamine concentrations in psychotic
disorders. Biol Psychiat 1974;9:89–91.
[13] Checkley SA, Murray RM, Oon MC, Rodnight R, Birley JL. A
longitudinal study of urinary excretion of N,N-dimethyltryptamine in psychotic patients. Br J Psychiat
1980;137:236–9.
[14] Rodnight R, Murray RM, Oon MC, Brockington IF, Nicholls P,
Birley JL. Urinary dimethyltryptamine and psychiatric
symptomatology and classification. Psychol Med
1976;6:649–57.
[15] Tanimukai H, Ginther R, Spaide J, Bueno JR, Himwich HE.
Detection of psychotomimetic N,N-dimethylated indoleamines in the urine of four schizophrenic patients. Br J
Psychiat 1970;117:421–30.
