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Posted (edited)

The study below summaries the findings regarding the prevention of schiophrenia or psychosis in prodromal subjects. I provide quotes of what I found most relevant. It looks as though omega-3 fatty acid treatment was more effective at delaying transition to psychosis in prodromal individuals, but IMO it's likely partially or wholly due to better patient adherence to a side-effect free regime. Furthermore, it treats a wider range of disorders and with fewer side effects, which might make it preferable when the diagnosis is uncertain.

 

Early signs, diagnosis, and therapeutics of the prodromal phase of schizophrenia and related psychotic disorders (Larson, Walker, Compton, 2011)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930984/

 

The following experiments were conducted on prodromal patients, the prodrome being described earlier in the paper.

 

In one texperiment using risperidone:

The results indicated that of the 31 participants receiving medication and enriched psychosocial intervention, three (9.7%) transitioned to a psychotic disorder over the 6-month period of the active treatment phase of the study. By contrast, of the 28 participants receiving standard supportive psychosocial treatment, ten (35.7%) converted to a psychotic disorder (results significant, p < 0.05). At the 12-month follow-up (during which no treatment was administered over the second 6-month period), three more of the participants in the experimental group had converted while no additional control participants converted.

In a later, better designed experiment using olanzapine:

After the first year of treatment, five out of 31 (16.1%) of the olanzapine-treated group converted to psychosis. Furthermore, there was a trend toward improvement in mean positive symptoms. By contrast, 11 out of 29 (37.9%) of the placebo-administered group converted.

The results from these studies suggest that intervention may delay conversion to psychosis and ameliorate symptoms during the active phase of treatment but there is no evidence of lasting effects after treatment cessation. Of concern is recent evidence that long-term use of even low doses of antipsychotic medication can cause sensitization of dopamine receptors in the brain. This has been suggested to possibly lead to supersensitivity psychosis or rapid-onset psychosis following cessation of antipsychotic medication [96].

There is evidence that 1–3 g/day of EPA or 10 g/day of fish oil (mix of EPA and DHA) may be beneficial in the treatment of symptoms of schizophrenia, depression, bipolar disorder, autism, attention-deficit/hyperactivity disorder, dyslexia and dyspraxia [115-118].

[...]

After 12 weeks, one of the 38 (2.6%) participants in the treatment group and eight of the 38 (21.1%) in the placebo group had converted to a psychotic disorder.

Here is other published research that I haven't read yet.

 

Treatment implications of the schizophrenia prodrome (2011)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136161/

 

Omega-3 fatty acids and schizophrenia: evidences and recommendations. (2013)

http://www.ncbi.nlm.nih.gov/pubmed/24424237

 

Prediction and prevention of the first psychotic episode: new directions and opportunities (2014)

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3974689/

Edited by MonDie
  • 3 months later...
Posted (edited)

I don't want to turn this thread into a blog, but I did read through all of the studies. I did not find a lot more information related to omega-3 as a potential treatment. The lattermost experiment wherein researchers administer a form of omega-3 called ethyl-eicosapentaenoate with or without co-administering vitamins E+C turns out to be the study that did not find positive effects. Apparently "levels of PUFA [poly unsaturated fatty acid] at baseline are bimodally distributed, defining two clinically distinct types of schizophrenia (low and high PUFA groups)." Surprisingly, it was the low PUFA patients who showed more evidence of adverse effects. I found these quotes interesting after reading the rat study.

 

A Randomized Placebo-controlled Trial of an Omega-3 Fatty Acid and Vitamins E+C in Schizophrenia (2013)

 

Patients eating more seafood, as in Norway, will probably benefit less from added EPA.

It was conducted in Norway.

 

Oxidative stress raises blood pressure, partly by cerebral regulation. There is evidence from rodent experiments and clinical trials that vitamins E and C may either reduce or increase blood pressure. In our study, EPA causes a non-significant increase in systolic blood pressure in the low PUFA patients only, in contrast to the antihypertensive effect found in several clinical studies.

 

 

 

The Antipsychotic Effects of Omega-3 Fatty Acids in Rats (2015)

 

RESULTS:

This study shows that omega-3 fatty acids, "similar to antipsychotics," reversed the psychotic like effects, increase of oxidants and decrease of antioxidants that are composed experimentally in rats.

CONCLUSIONS:

The application of omega-3 fatty acids has antipsychotic effects and causes an oxidative imbalance. This study adds new evidence to the current literature regarding the possible antipsychotic effects of omega-3 fatty acids.

 

 


 

It is also interesting that the fish oil study used a sample of UHR subjects, many of whom go on to develop mood disorders.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3974689/table/t1-tcrm-10-241/

Omega-3 also has benefits for depressed patients,. Furthermore, the same paper notes that researchers have observed a reduction of symptoms in UHR patients with the administration of antidepressants, ending the section with "an unexpectedly high incidence of depression with psychotic features was observed in UHR individuals receiving antipsychotic therapy".

Edited by MonDie

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