Rapunzel: I just wrote a paper that explores genetic and experiential causes of differences in the brain, and effects or symptoms associated with those differences. The genetic factors that I looked at were "Schizotaxia" - a set of schizophrenic-like symptoms, including negative symptoms but no positive symptoms, observed in first-degree relatives of people with schizophrenia

Do you have a source? I ask because I was reading the work of Dr. Jonathon Leo of late and this has raised some questions in my mind about the validity of research in which the back story is unknown, i.e.,

<blockquote>The three methods most frequently cited in support of genetic factors in schizophrenia are family studies, twin studies, and adoption studies. Kandel says that all three of these methodologies support the role of genetics in schizophrenia. In this article, we examine the data that Kandel presents for each of these approaches and we will also point out the problems with each approach.

...

Kandel presents a table claiming that 14% of the biological relatives were diagnosed with schizophrenia, while only 3.4% of the control relatives were so diagnosed (Kandel, 2000, table 60-1, p. 1194). If this evidence is valid, and if the study is otherwise methodologically sound, it makes a strong case for the role of genes in schizophrenia. In Kandel’s words, “In addition to documenting the importance of genetic factors in schizophrenia, these studies of adoptees in whom schizophrenia developed showed that rearing does not play a major role in the disease” (p. 1194). But is the evidence valid?

Problem #1: The widening of the schizophrenia spectrum. The only way that Kety et al. could diagnose 14% of the biological relatives with schizophrenia was to greatly broaden the definition of schizophrenia to include diagnoses such as “latent schizophrenia,” “uncertain latent schizophrenia,” and “inadequate personality.” Kandel claims that these categories are “thought to be a mild form of the disease, a nonpsychotic condition related to schizophrenia” (p. 1194). But why should these cases be included in the overall totals when there is little evidence that chronic schizophrenia and the spectrum disorders are genetically related (Joseph, 2001a)? Kandel also claims, on the basis of family studies, that “odd” people are found among the relatives of people diagnosed with schizophrenia: “they are socially isolated, have poor rapport with people, ramble in their speech, tend to be suspicious, have eccentric beliefs, and engage in magical thinking” (p. 1194). The claim that “odd” people are found among the relatives of people diagnosed with schizophrenia means little, and was often made on basis of non-blind diagnoses by investigators devoted to the genetic position. In addition, it could just as easily be the result of the negative psychological and social environments experienced by family members. The fallacy here is that correlation is seen as being directly related to genetic causation, when there is little evidence to support this view.

If one limits the comparison to cases of chronic schizophrenia among the Kety et al. 1975 biological relatives, one is left with 5 cases of chronic schizophrenia among the 173 biological relatives of index adoptees (2.9%) and zero cases of chronic schizophrenia among the 174 biological relatives of control adoptees. Yet, 5 cases of chronic schizophrenia out of a group of 173 individuals (2.9%) is not much higher then the general population rate of 1% (Joseph, 2001b).

Source: Medical students are taught it’s all in the genes, but are they hearing the whole story?</blockquote>

<hr width=100% size=2>

Rapunzel: It's impossible at this point to say what causes what.

Fortunately, it's not impossible to say that full recovery is a very good possibility, regardless of the (unknown) cause.