So I keep reading lately that weed is the "trigger" for schizophrenia. I believe that to be mainly drug war propaganda.
Research follows.
It was revealed in a study published in November 2004, in the British Journal of Psychiatry, that prenatal exposure to painkillers (the medical term is "analgesics" - such as Aspirin) is linked to as much as a 500% greater probability of the children developing schizophrenia in later life.
Research has already identified a link between pre-natal/birth complications and increased risk of developing schizophrenia in offspring, particularly for those who may carry genetic susceptibility. Some studies have suggested that maternal-fetal Rh incompatibility, which arises when a mother with Rh negative blood type produces antibodies against the Rh proteins in her Rh-positive fetus's blood, may be a specific complication that can increase risk of schizophrenia, possibly by increasing risk of hypoxia (oxygen shortage) to the developing fetal brain.
Hollister et al (1996) found a 2-fold increased rate (2.1% prevalence) of schizophrenia in a retrospective study of RH incompatible infants, as compared to an expected rate of 0.8% schizophrenia in RH-compatible subjects. This 2-fold risk was recently replicated by Insel et al (2005); however, their calculated risk was only stastically significant for male babies.
Other authors who have studied this relationship (Kraft et al, 2004) point out that the risk increases with number of births, as a woman who is Rh negative will start producing antibodies during the first exposure (pregnancy with an Rh-positive fetus), but will only build up sufficient antibody numbers for an immune response against subsequent Rh-positive fetuses. These authors, re-analyzing data collected by a previous study, found: "[the]relative risk of schizophrenia in the second- and later-born RHD MFG-incompatible children is 1.7, consistent with earlier estimates."
--risk higher for male babies
--incompatibility risk (and therefore schizophrenia risk) increases in the later, of a series, of births (Kraft et al 2004).
--risk seems to be caused be "adverse prenatal environment" rather than a close association/linkage between RHD gene locus and any gene implicated in schizophrenia onset (Palmer et al 2002).
Recent epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia. In animals, infections with Toxoplasma gondii can alter behavior and neurotransmitter function. In humans, acute infection with the cat virus "T. gondii" can produce psychotic symptoms similar to those displayed by persons with schizophrenia. Two other studies found that exposure to cats in childhood was a risk factor for the development of schizophrenia, but one that is nevertheless easily avoided.
That is all...
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