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A recent study published in Schizophrenia Research evaluated the effect of supplementation with omega-3 fatty acids, as an adjunct to standard pharmacotherapy, on the severity of schizophrenia symptoms, using changes in niacin skin flush response (NSFR) as a potential stratification marker to identify participants who might receive the most benefit. This open-label randomized pilot study included 99 people with schizophrenia and 30 healthy controls. All participants with schizophrenia received (and maintained) standard pharmacotherapy, while 2/3 also received omega-3 fatty acid supplementation at a daily dose of 1512 mg EPA, 1134 mg DHA, and an additional 204 mg of unspecified omega-3s during a 21-day trial period. Symptom severity was established by experienced psychiatrists using the Positive and Negative Syndrome Scale (PANSS), and NSFR was measured by an Integrated Niacin Skin Response Test Device at baseline and post-intervention.
Omega-3 therapy for schizophrenia has been a promising candidate to address the lipid peroxidation and dysregulated inflammation observed, with multiple mechanisms speculated for its effectiveness. As described in a recent meta-analysis, blunting of the NSFR occurs more often among people with schizophrenia, and the authors of the recent trial speculated that this blunting may point to impaired lipid metabolism, which might be mitigated with omega-3 supplementation. For example, the NSFR depends on phospholipase A2 (PLA2)-mediated mobilization of arachidonic acid as well as prostaglandin synthesis by cyclooxygenase (COX) to produce cutaneous microvascular dilation. Impairment of this dilation has been observed not only among people with several forms of schizophrenia, but also among those with bipolar disorder, suggesting that impaired lipid metabolism may be a common contributing factor.
There were three main findings from this recent study: first, the participants with schizophrenia did have a blunted NSFR compared to controls, consistent with previous studies. Second, omega-3 supplementation did provide a greater short-term increase in NSFR than pharmacotherapy alone. Lastly, there appeared to be a meaningful response pattern. Those participants with a blunted NSFR had a more pronounced improvement in PANSS after receiving omega-3s (P < 0.001). This did not occur in the control group, nor did it occur among those receiving omega-3s without a blunted NSFR. While this was an open-label and exploratory trial, it does suggest that the NSFR may not only identify a dysfunctional lipid homeostasis among some people with schizophrenia, but that omega-3 supplementation may at least partly mitigate symptoms among those with this metabolic dysfunction.
Lastly, it’s worth also pointing out the results of a Mendelian randomization (MR) meta-analysis published recently in Nutrition Reviews. This analysis predicted that lower genetically predicted omega-3 levels are causally related not only to schizophrenia, but to a number of mental disorders, including obsessive-compulsive disorder, bipolar disorder, and major depressive disorder, while a higher ratio of omega-6 to omega-3s is generally associated with greater risk.
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