Michael O’Donovan and Kenneth Kendler, eminences in psychiatric genetics for good reason, look at the implications of recent (early) progress in identifying the dispersed genetic roots of schizophrenia. For ease of reading, I’ve inserted a few paragraph breaks in their long paragraph, which is the last of 9 points they make about recent findings. The money quote’s in the last graf.
Throughout much of its history, modern psychiatry has sought to ground its categorical diagnostic approaches in basic biological findings. One such effort was to locate the “gene for” schizophrenia. It is now widely agreed that no such gene exists. Rather, the genetic vulnerability to this tragic disease is widely distributed across the genome in a way that resembles the multifactorial threshold models so popular for years in statistical genetics.
This has 2 noteworthy implications.
First, the old divisions between psychiatric genetic epidemiologists (who studied families, twins, and adoptions) and molecular geneticists—where the former did “just statistics” and the latter studied “real genes”—should crumble. Indeed, the twin researchers, using multifactorial threshold models, probably had a more accurate genetic model of psychiatric illness than molecular researchers doing linkage and candidate gene association analysis, who typically assumed single-locus models of relatively large effect. Statistical and molecular tools will need to be fully integrated in the years ahead.
Second, and more profoundly, while there is surely a discrete phenomenological state of psychosis that clinicians can agree about reliably, there is no such dichotomy at the level of genetic risk. All of us carry schizophrenia risk variants, and the vast majority of us carry quite a lot of them. With respect to genetic risk, there is no “them” and “us,” only subtle shades of gray.
This is sort of what I believe, we all have the light switch in there some where. Only for some of us, the switch is large and easy to turn on. For others, the switch is small and might never activate.
Biological psychiatry talks about gene for schizophrenia and do not find it,
while you talk about switch !
Some large and turn on,some small never activate
To find the cause of sz,to be objective is better than to be subjective
No, what they are saying now is that it’s not ONE switch, it’s damage to many sites on many different genes. The only thing they agree on is that if you get psychosis, you’ve got SOMETHING. But the negative symptoms (and associated gene markers) also occur in siblings and other relatives, for example. They just don’t attract much notice, unless you have that final switch for psychosis. It’s also possible to have lots of positive but no negative or hardly any negatives (MortimerMouse springs to mind, Jayne, too).
It seems that with DSM5 at least one positive symptom is required. I wonder how those who presented with exclusively negative symptoms in DSM IV would now be rediagnosed, or would they now be seen as not having an illness?
Symptom criteria changes:
Schizophrenia: Criterion A lists the five key symptoms of psychotic disorders: 1) delusions, 2) hallucinations, 3) disorganized speech, 4) disorganized or catatonic behavior, and 5) negative symptoms. In DSM-IV 2 of these 5 symptoms were required. However, only 1 of the 5 symptoms was required if delusions were bizarre or if hallucinations included a running commentary on a person’s thoughts/behavior, and/or two or more voices conversing. This exception has been removed for lack of specificity and poor reliability. This change makes intuitive sense. The notion of what constitutes “bizarre” is rather vague, and its removal reduces cultural bias. In DSM-5, two of these five symptoms are required AND at least one symptom must be one of the first three (delusions, hallucinations, disorganized speech).