I find this whole line of research interesting, and I look forward to seeing replication studies. I would quibble with the use of NAMI mothers as sources of information in Torrey et al (2000) on two grounds. Firstly, I don’t believe they are representative of the population in question; i.e. mothers of individuals who have been assigned a diagnosis of schizophrenia. Secondly, NAMI is an avid supporter of the bio-psychiatric position (and indeed derives a large share of its funding from pharmaceutical companies). I consider it extremely likely that the 264 mothers who were questioned were familiar with the “schizophrenia germ” hypothesis and would have been highly motivated to provide the “correct” answers. I’m not suggesting, of course, that they were deliberately lying, but simply stating the well-known fact that motivated respondents are not always reliable.

I also have a quibble with Torrey and Yolken (2003). This is a meta-analysis of 19 studies conducted in various countries between 1953 and 2003 and purports to show an increased incidence of antibodies in “schizophrenics” compared with controls. Setting aside definitional difficulties, I was struck by the fact that the controls in the US study (Boronow et al 2002) had only a 7% incidence of antibodies. The McConkey press release (2009) quotes a prevalence in the US of 22%. Even though the Boronow controls were matched to the “schizophrenic” sample, this discrepancy seems very large. One would expect the controls’ incidence to be close to the general population.

The implications of this body of research are more complicated. I have said elsewhere in my posts that neurological damage/malfunction can have an obvious effect on people’s behavior, and that when such a neurological issue is identified and described, it needs to be given a name and treated (if treatment is possible ) by neurologists. This, in my view, has nothing to do with the so-called “mental disorders.”

An additional consideration is the causal connection between physiology and behavior. If, for instance, you see a man starting to eat, you might conclude that he was hungry, and that the hunger mechanism (physiology) was the proximate cause of the eating (behavior). Life, however, is more complex than this. One man on becoming hungry might sit at this table and shout: “How about some lunch, woman?” Another goes to his kitchen and starts cooking. A third goes to his orchard and plucks some fruit. A fourth goes to a store and steals a cooked chicken. A fifth goes to McDonalds, etc., etc., etc.. And whilst the physiological hunger mechanism explains the eating, we must look to behavioral science to explain (or at least try to explain) the enormous variation in the way this drive is expressed.

The analogy to “schizophrenia” is that infection with toxoplasma gondii may impair neurological functioning in some general way, but it is quite a reach to suggest that cysts in the brain cause a person to say that she is the queen and deserves to be afforded special honor and privilege.

In my view, the brain, like any organ, is subject to a variety of assaults. Some of these impact the individual’s overall coping ability and render more likely the experience of failure. From profound feelings of failure in early adulthood to paranoid and grandiose speech is an understandable step, and I believe that this is the most fruitful way to conceptualize these issues. Of course failure can occur without neurological damage of any kind – hence the neurological heterogeneity of the “schizophrenia” population.

The fundamental principle underlying the DSM system is that unusual/disturbing behaviors are caused by mental disorders/illnesses. In my view this proposition is analogous to the notion that crop failures are caused by witchcraft. The issue is not whether Mrs. Jones is or is not a witch. The issue is that there are no witches. It is not possible to cause crops to fail by chanting curses or whatever. And there are no mental disorders. “Mental disorder” and “mental illness” are anachronistic pre-scientific terms similar to phlogiston. A century of behavioral science has demonstrated clearly that disturbing/unusual behavior is the product of the individual’s reinforcement history and the stimulus properties of the present situation (as is “normal” behavior). As long as “schizophrenia” is defined behaviorally, we should focus on behavioral explanations rather than vague pre-scientific pseudo-explanations.

Overriding this notion, of course, is the obvious fact that an organism can only perform actions of which it is physically capable. A person who has lost his eyes can’t be taught visual discrimination skills. Similarly, brain damage/malfunctions represent limits for general learning, though it is my experience that individuals in this latter category are often capable of acquiring far more skills than is often imagined.

The sad fact is that relatively little attention has been afforded to teaching the individuals concerned the skills they need to begin to find some sense of success and mastery. Indeed, the bio-psychiatric position for the past forty years has been that their position is intrinsically hopeless; that the best they can do is eat the pills, and the most they can look forward to is tardive dyskinesia. Big pharma is raking in the money and the psychiatrists, psychologists, and mental health centers are walking in perfect step to the corporate drumbeat.

The tragedy of the Webster et all (2006) study is that for all its elegance and achievement, it will be used by the bio-psychiatric/big pharma lobby to promote their dehumanizing agenda, which includes legally enforced drugging and leaves people in the same state of wretchedness and failure.

So – as always – a single question takes us in many directions. I greatly appreciate your interest and your taking the time to write. Best wishes.