Quote:Based on my experience, and I am not condoning this I am only reporting my experience from the past when I used to do this kind of stuff, but based on my experience with injecting a well known and highly addictive dopamine reuptake transporter inhibitor, I found that a massive dopamine increase seems subjectively more like what I would expect schizophrenia to feel like. I found that that activity created, for me, lots of delusional and paranoid thinking along with auditory hallucinations while serotonergic hallucinogens feel subjectively much different.
I agree with that and actually so does the paper. There argument was that in the initial stages of schizophrenia serotonin seems to play an important role. Perhaps even destabilizing other systems in the brain to create the kinds of dopamine havoc that gets damaged later on.
Quote:Keep in mind, it's rare to find something a phenomena in the mind or body that is caused by a single chemical or stimulus. Diseases can have multiple causes, and may be caused by interactions between chemicals and bodily systems. Schizophrenia may have multiple unique causes, or may be a result of a confluence of scenarios.
Yep this is entirely true. No one thinks schizophrenia or psychosis has one single cause anymore. The only mental illness that appears to have one single cause is huntingtons disease. A single gene defect. Most other mental illnesses have many factors both genetic and environmental.
Quote:There are many conflicting reports regarding elevated levels of DMT in schizophrenic patients.
More accurate assays with greater resolution will appear soon and will hopefully clear up some of this confusion.
Spectroscopy based or enzyme based?
One study I would love to see done is this:
NMR and LC-MS/GC-MS based metabolomic approach. Analysis of the urine, cerebrospinal fluid, and blood of schizoprhenic patients in different stages of the disease. Get people who are relatives of those with the disease, people who are prone to the disease, people who are experience first episode psychosis, people who are medicated yet still psychotic, people who are medicated but symptoms have decreased markedly, people who have stopped taking medication and had a remission and of course healthy controls with no history of mental illness in themselves or family. Couple this with fMRI, multivariant data analysis and bam you might be able to unravel some of the early metabolic changes taking place both during the development of psychosis and after its wreaked its havoc as well as what happens when the drugs work.
It would also be interesting to follow a few patients from their initial first episode psychosis and their progression after being medicated.
I would love to work on such a study from the analytical side.