A hypothesis re madness.

Before we go there, some observations.

  1. E. Fuller Torrey documented a marked increase in madness during the industrial revolution in the Northwestern USA, that appeared to follow a power law.
  2. In some places, such as Wales, the number of people with psychosis appears to be dropping, to the point that maternal units are closing
  3. However, the number of people presenting with distress and variations of psychosis is increasing, and the clinical load across both psychiatric and general medical acute wards is up — across New Zealand
  4. The correlation of gross malnutrition with children developing psychosis was well documented in two birth cohorts — 1944 in the Netherlands, and 1957-60 in China

Now the hypothesis. Schizophrenia is triggered in the fetus of a mother who has a diet deficient in polyunsaturated fats.

The paper is open, I’ve stripped the references.

Schizophrenia Spectrum Disorders are now accepted as a neurodevelopmental disorders. Some etiopathogenic origins of these disorders have been found as early as the prenatal period. Early life and prenatal stress have been implicated as potential risk factors for development of later in life psychotic events both in human and in animal studies. Gestational DHA deficiency has been shown to potentially contribute to the etiopathogenesis of SSD. Indeed, prenatal DHA deficiency has been linked to alteration in neurotransmission, such as alteration in dopaminergic system functioning, and neurocognitive impairments , with deficits in cortical maturation and attention . These events have also been reported in schizophrenic patients. In addition, postmortem studies in schizophrenic patients indicated modification in the expression of genes responsible for regulating the biosynthesis of fatty acids at PFC levels. Moreover, chronic antipsychotic treatments can also upregulate PUFA levels in red blood cell of patients with psychosis . Lowered rate of conversion of EPA into DHA has also been observed in schizophrenia . It was reported that disturbances in PUFA metabolism occurs very early in antipsychotic naive patients.

I have a few difficulties with the paper. They seem to list every psychiatric disorder and show evidence for their hypothesis: it is very hard to undo what was done in the womb, and, although there are some trials of fish oil in psychosis, they results are not consistent.

I’d like to see some testable predictions. These are, to date, lacking. The next step is to define them.

One thought on “A hypothesis re madness.

  1. Given the central role in nervous system tissue that the entire gamut of Fatty Acids cover, it’s not a bad conjecture for the relationship to exist. Functionally, schizophrenia is the inability for the brain to handle segmentation properly, as the inhibition system isn’t capable of keeping up. This will, during development & early childhood, produce low-level inflammation and further degradation of the processes.

    Malnutrition, in either the Mother or early childhood, really does cause massive problems.

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