I have an advanced pharmacology textbook kicking around which explains the metabolic pathway of endogenous DMT. I can't be bothered to rummage for it now, but I will tell you this:
Endogenous DMT has been known for a long time, way before Strassman's '90s research/trials. Decades even. You need to read some books, there's not much on the net. But I will post a bunch of citations and links...
Literature
Steven A. Barker, John A. Monti, Samuel T. Christian, "N,N-Dimethyltryptamine: An Endogenous Hallucinogen," International Review of Neurobiology 22 (1981): 83-110.
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Tryptamine (Try), 5-methoxytryptamine (5MeOT), N-methyltryptamine (N-Met), 5-methoxy-N,N-dimethyltryptamine (5MeODMT) and N,N-dimethyltryptamine (DMT) are metabolites of the neurotransmitter 5-hydroxytryptamine (5HT). The cisternal cerebrospinal fluid (CSF) is probably a suitable biological material for investigating the problem of indolamine metabolism in schizophrenic patients. As part of a biological research programme on schizophrenia we have investigated concentrations of cisternal CSF indolamines in a group of acute paranoid patients in comparison with psychiatrically healthy controls. The concentrations of indolamines in the cisternal CSF reveal that psychotomimetic indolamines like 5MeODMT, 5MeOT and DMT and the indolamines N-Met and Try are present in psychological and pathological states. The patients suffering from acute paranoid schizophrenia have high or very high levels of the investigated indolamines in comparison with healthy controls, but there are significant individual differences in the group of these patients. The search for correlations between the level of a single indolamine and individual psychopathological symptoms could provide more specific information for diagnosis or treatment.
Uebelhack R; Franke L; Seidel K, "Methylated and unmethylated indolamine in the cisternal fluid in acute endogenous psychoses," Biomedica biochimica acta 1983;42(10):1343-6.
http://tinyurl.com/cqdu5j
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The sigma-1 receptor is widely distributed in the central nervous system and periphery. Originally mischaracterized as an opioid receptor, the sigma-1 receptor binds a vast number of synthetic compounds but does not bind opioid peptides; it is currently considered an orphan receptor. The sigma-1 receptor pharmacophore includes an alkylamine core, also found in the endogenous compound N,N-dimethyltryptamine (DMT). DMT acts as a hallucinogen, but its receptor target has been unclear. DMT bound to sigma-1 receptors and inhibited voltage-gated sodium ion (Na+) channels in both native cardiac myocytes and heterologous cells that express sigma-1 receptors. DMT induced hypermobility in wild-type mice but not in sigma-1 receptor knockout mice. These biochemical, physiological, and behavioral experiments indicate that DMT is an endogenous agonist for the sigma-1 receptor.
1 Department of Pharmacology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.
2 Department of Physiology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.
3 Pharmaceutical Research Laboratory, Department of Chemistry, Isfahan University of Technology, Isfahan 84156, IR Iran.
Dominique Fontanilla, Molly Johannessen, Abdol R. Hajipour, Nicholas V. Cozzi, Meyer B. Jackson, Arnold E. Ruoho, "The Hallucinogen N,N-Dimethyltryptamine (DMT) Is an Endogenous Sigma-1 Receptor Regulator," Science 13 February 2009: Vol. 323. no. 5916, pp. 934 - 937
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Abstract: N,N-dimethyltryptamine (DMT) is a hallucinogen found endogenously in human brain that is commonly recognized to target the 5-hydroxytryptamine 2A receptor or the trace amine–associated receptor to exert its psychedelic effect. DMT has been recently shown to bind sigma-1 receptors, which are ligand-regulated molecular chaperones whose function includes inhibiting various voltage-sensitive ion channels. Thus, it is possible that the psychedelic action of DMT might be mediated in part through sigma-1 receptors. Here, we present a hypothetical signaling scheme that might be triggered by the binding of DMT to sigma-1 receptors.
T.-P. Su, T. Hayashi, D. B. Vaupel, When the Endogenous Hallucinogenic Trace Amine N,N-Dimethyltryptamine Meets the Sigma-1 Receptor. Sci. Signal. 2, pe12 (2009).
http://stke.sciencemag.org/cgi/content/abstract/2/61/pe12
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The presence of the potent hallucinogenic psychoactive chemical N,N-dimethyltryptamine (DMT) in the human body has puzzled scientists for decades. Endogenous DMT was investigated in the 1960s and 1970s and it was proposed that DMT was involved in psychosis and schizophrenia. This hypothesis developed from comparisons of the blood and urine of schizophrenic and control subjects. However, much of this research proved inconclusive and conventional thinking has since held that trace levels of DMT, and other endogenous psychoactive tryptamines, are insignificant metabolic byproducts. The recent discovery of a G-protein-coupled, human trace amine receptor has triggered a reappraisal of the role of compounds present in limited concentrations in biological systems. Interestingly enough, DMT and other psychoactive tryptamine hallucinogens elicit a robust response at the trace amine receptor. While it is currently accepted that serotonin 5-HT(2A) receptors play a pivotal role in the activity of hallucinogenic/psychedelic compounds, we propose that the effects induced by exogenous DMT administration, especially at low doses, are due in part to activity at the trace amine receptor. Furthermore, we suggest that endogenous DMT interacts with the TA receptor to produce a calm and relaxed mental state, which may suppress, rather than promote, symptoms of psychosis. This hypothesis may help explain the inconsistency in the early analysis of endogenous DMT in humans. Finally, we propose that amphetamine action at the TA receptor may contribute to the calming effects of amphetamine and related drugs, especially at low doses.
Jacob MS, Presti DE. Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200, USA. "Endogenous psychoactive tryptamines reconsidered: an anxiolytic role for dimethyltryptamine," Med Hypotheses. 2005;64(5):930-7.
http://www.ncbi.nlm.nih.gov/pubmed/15780487?log$=activity
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Abstract The hallucinogenic substance Nprime,Nprime-dimethyltryptamine and its precursor N-methyltryptamine were found in 24-h speciments of urine from 19 normal human subjects; the mean excretion rates were 386 ng 24 h-1 and 856 ng 24 h-1 respectively. The urinary excretion of both compounds was unrelated to age, sex, urinary volume, or creatinine, nor was any consistent diurnal pattern observed. Rates for the mono and dimethylated compounds were not correlated. Diet and the intestinal flora were excluded as a source of urinary dimethyltryptamine. Administration to 4 subjects of sufficient ammonium chloride to increase the H ion concentration of the urine caused a transient increase in dimethyltryptamine excretion but no consistent increase in the rate for N-methyltryptamine. Acidification of the urine did not appear to be the determining factor in this result since in one subject the same drop in urinary pH was achieved by feeding methionine without any increase in dimethyltryptamine axcretion.
Michael C. H. Oon, Robin M. Murray, Richard Rodnight, Marion P. Murphy and James L. T. Birley, "Factors affecting the urinary excretion of endogenously formed dimethyltryptamine in normal human subjects," Psychopharmacology, Volume 54, Number 2 / January, 1977, 171-175.
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That should be enough for you to chew on for a while.
