Omega-3 fatty acids for the treatment of dementia
Burckhardt M, Herke M, Wustmann T, Watzke S, Langer G, Fink A
The Cochrane database of systematic reviews · 91 citas
Etiquetas de revisión
Financiación no declaradaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Revisión sistemática (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2016-04-11 · Cochrane Database Syst Rev · vol. 2016 · número 4 · pág. CD009002
- Editorial
- Elsevier BV
- Citado
- 180 citas · más que el 100% de estudios similares · 16.7× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 113 trabajos
- Acceso
- Lectura gratuita
- Áreas de investigación
- Fatty Acid Research and Health · Seaweed-derived Bioactive Compounds · Neurological Disorders and Treatments
- Palabras clave
- Dementia, Vascular dementia, Dementia with Lewy bodies, Medicine, Frontotemporal dementia, Polyunsaturated fatty acid, Disease, Psychiatry, Bioinformatics, Internal medicine, Biology, Fatty acid, Biochemistry
- MeSH
- humans, alzheimer disease, fatty acids, omega-3, cognition, randomized controlled trials as topic
6 autores
- Marion Burckhardt🇩🇪Martin Luther University Halle-Wittenberg
- Max Herke🇩🇪Martin Luther University Halle-Wittenberg
- Tobias Wustmann🇩🇪Martin Luther University Halle-Wittenberg
- Stefan Watzke🇩🇪Martin Luther University Halle-Wittenberg
- Gero Langer🇩🇪Martin Luther University Halle-Wittenberg
- Astrid Maria Fink🇩🇪Martin Luther University Halle-Wittenberg
Resumen
El texto original del estudio, en el idioma en que se publicó.
Background
Omega-3 polyunsaturated fatty acids (omega-3 PUFAs) from fish and plant sources are commonly considered as a promising non-medical alternative to improve brain functions and slow down the progression of dementia. This assumption is mostly based on findings of preclinical studies and epidemiological research. Resulting explanatory models aim at the role omega-3 PUFAs play in the development and integrity of the brain's neurons, their protective antioxidative effect on cell membranes and potential neurochemical mechanisms directly related to Alzheimer-specific pathology. Epidemiological research also found evidence of malnutrition in people with dementia. Considering this and the fact that omega-3 PUFA cannot be synthesised by humans, omega-3 PUFAs might be a promising treatment option for dementia.
Objectives
To assess the efficacy and safety of omega-3 polyunsaturated fatty acid (PUFA) supplementation for the treatment of people with dementia.
Search methods
We searched the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), MEDLINE, EMBASE, PsycINFO, CINAHL, ClinicalTrials.gov and the World Health Organization (WHO) portal/ICTRP on 10 December 2015. We contacted manufacturers of omega-3 supplements and scanned reference lists of landmark papers and included articles.
Selection criteria
We included randomised controlled trials (RCTs) in which omega-3 PUFA in the form of supplements or enriched diets were administered to people with Alzheimer's disease (AD), vascular dementia (VaD), dementia with Lewy bodies (DLB), Parkinson's disease dementia (PDD) or frontotemporal dementia (FTD).
Data collection and analysis
The primary outcome measures of interest were changes in global and specific cognitive functions, functional performance, dementia severity and adverse effects. Two review authors independently selected studies, extracted data and assessed the quality of trials according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the quality of the evidence using the GRADE approach. We received unpublished data from the trial authors and collected adverse effects information from the published articles. We conducted meta-analyses for available outcome measures at six months.
Main results
We included three comparable randomised, placebo-controlled trials investigating omega-3 PUFA supplements in 632 participants with mild to moderate AD over six, 12 and 18 months. We found no studies investigating other types of dementia. All trials were of high methodological quality. The overall quality of evidence for most of the outcomes was high.There was no evidence of a benefit from omega-3 PUFAs on cognitive function when measured at six months with the Alzheimer's Disease Assessment Scale - Cognitive subscale (standardised mean difference (SMD) -0.02, 95% confidence interval (CI) -0.19 to 0.15; 566 participants; 3 studies; high quality evidence) or Mini-Mental State Examination (mean difference (MD) 0.18, 95% CI -1.05 to 1.41; 202 participants; 2 studies; high quality evidence) or on activities of daily living (SMD -0.02, 95% CI -0.19 to 0.16; 544 participants; 2 studies; high quality evidence). There was also no effect at six months of treatment on severity of dementia measured with the Clinical Dementia Rating - Sum of Boxes (MD -0.00, 95% CI -0.58 to 0.57; 542 participants; 2 studies; high quality evidence) or on quality of life measured with the Quality of Life Alzheimer's Disease scale (MD -0.10, 95% CI -1.28 to 1.08; 322 participants; 1 study; high quality evidence). There was no difference at six months on mental health measured with the Montgomery-Åsberg Depression Rating Scale (MD -0.10, 95% CI -0.74 to 0.54; 178 participants: 1 study; high quality of evidence) or the Neuropsychiatric Inventory (SMD 0.10, 95% CI -0.07 to 0.27; 543 participants; 2 studies; high quality of evidence). One very small study showed a benefit for omega-3 PUFAs in instrumental activities of daily living after 12 months of treatment (MD -3.50, 95% CI -4.30 to -2.70; 22 participants; moderate quality evidence). The included studies did not measure specific cognitive function. The studies did not report adverse events well. Two studies stated that all adverse events were mild and that they did not differ in overall frequency between omega-3 PUFA and placebo groups. Data from one study showed no difference between groups in frequency of any adverse event (risk ratio (RR) 1.02, 95% CI 0.95 to 1.10; 402 participants; 1 study; moderate quality evidence) or any serious adverse event (RR 1.05, 95% CI 0.78 to 1.41; 402 participants; 1 study; high quality evidence) at 18 months of treatment.
Authors' conclusions
We found no convincing evidence for the efficacy of omega-3 PUFA supplements in the treatment of mild to moderate AD. This result was consistent for all outcomes relevant for people with dementia. Adverse effects of omega-3 PUFAs seemed to be low, but based on the evidence synthesised in this review, we cannot make a final statement on tolerability. The effects on other populations remain unclear.
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