PCP, LSD, Ketamine and ….  have been used as models for the state of schizophrenia, the problem with that models is very simplified, that the person with schizophrenia usually don’t have them in their blood.

However there is a substance that can cause some of the phenomenological effects of Schizophrenia – personality changes, paranoia, mania and alternations in the transient receptor potential – TRPV secondary to environmental exposure. This effect has been known since the late 1800.  To make a complex story very short, we present the CAC-Hålet theory about-

The etiology of Schizophrenia in 3 very easy steps

1/ There is a substance known to cause some of the symptoms in Schizophrenia

2/The group of persons with Schizophrenia does have it, other usually don’t

3/ There might be a connection with, the reactive phase of Schizophrenia etiology and the substance.

The Substance is: Carbon Disulfide or CS2

Since  Carbon disulfide is a known neurotoxin one might think that we just have to remove the external source of CS2 exposure in order to eliminate the problem. But the source is not external it is internal. And this endogenous production of Carbon Disulfide is continuously taken it’s toll on the system. I conclude that Carbon Disulfide could be a reactive factor that trigger but don’t predispose for the etiology of Schizophrenia.

Ref:

Clin Pathol 1993;46:861-864
Increased pentane and carbon disulfide in the
breath of patients with schizophrenia

A part of the CAC-hålet theory is now moving to GDNF – BDNF from The Etiology of Schizophrenia @ Co2reactivity.