Abstract
Background Cognitive impairments are well-established features of psychotic disorders and are present when individuals are at ultra-high risk for psychosis. However, few interventions target cognitive functioning in this population. Aims To investigate whether omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation improves cognitive functioning among individuals at ultra-high risk for psychosis. Method Data (N = 225) from an international, multi-site, randomised controlled trial (NEURAPRO) were analysed. Participants were given omega-3 supplementation (eicosapentaenoic acid and docosahexaenoic acid) or placebo over 6 months. Cognitive functioning was assessed with the Brief Assessment of Cognition in Schizophrenia (BACS). Mixed two-way analyses of variance were computed to compare the change in cognitive performance between omega-3 supplementation and placebo over 6 months. An additional biomarker analysis explored whether change in erythrocyte n-3 PUFA levels predicted change in cognitive performance. Results The placebo group showed a modest greater improvement over time than the omega-3 supplementation group for motor speed (ηp2 = 0.09) and BACS composite score (ηp2 = 0.21). After repeating the analyses without individuals who transitioned, motor speed was no longer significant (ηp2 = 0.02), but the composite score remained significant (ηp2 = 0.02). Change in erythrocyte n-3 PUFA levels did not predict change in cognitive performance over 6 months. Conclusions We found no evidence to support the use of omega-3 supplementation to improve cognitive functioning in ultra-high risk individuals. The biomarker analysis suggests that this finding is unlikely to be attributed to poor adherence or consumption of non-trial n-3 PUFAs.
| Originalsprog | Engelsk |
|---|---|
| Artikelnummer | e165 |
| Tidsskrift | BJPsych Open |
| Vol/bind | 8 |
| Udgave nummer | 5 |
| ISSN | 2056-4724 |
| DOI | |
| Status | Udgivet - 2022 |
Bibliografisk note
Funding Information:This work was supported by grant 07TGF-1102 from the Stanley Medical Research Institute, grant 566529 from the National Health and Medical Research Council of Australia (NHMRC) Australia Program (to P.D.M., I.B.H., A.R.Y. and G.P.A.) and a grant from the Colonial Foundation. K.A. was supported by a Career Development Fellowship from the NHMRC (1141207) and a Dame Kate Campbell Fellowship from The University of Melbourne; G.P.A. and A.R.Y. were supported by NHMRC Senior Research Fellowships 1080963 and 566593 respectively; B.N. was supported by NHMRC Career Development Fellowship 1027532; and P.D.M. was supported by NHMRC Senior Principal Research Fellowship 1060996.
Publisher Copyright:
Copyright © 2022 The Author(s). Published by Cambridge University Press on behalf of the Royal College of Psychiatrists.
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