In people with mild to moderate Alzheimer’s disease, regular omega-3 supplements do not appear harmful but have no beneficial effect as a treatment for dementia when compared with a placebo. More research is required to determine the effect of omega-3 supplementation in people with other types and severity of dementia, including those who are nutritionally deplete.


You work in long-term residential care and note that several residents with dementia are taking regular omega-3 supplements in the belief that this improves brain function and slows the progression of dementia symptoms. Foods rich in omega-3 fats such as oily fish are important for a healthy balanced diet but you are unsure of the safety and benefits of omega-3 supplementation for treating dementia. You decide to review the evidence.


Is omega-3 supplementation – over and above usual diet – a safe and effective option for treating cognitive and functional decline in people with dementia?


PubMed- Clinical queries (Therapy/Narrow): omega-3 AND dementia


Burckhardt M, Herke M, Wustmann T, Watzke S, Langer G, Fink A (2016). Omega-3 fatty acids for the treatment of dementia. Cochrane Database Syst Rev. 4:Cd009002.


A Cochrane systematic review assessing the efficacy and safety of omega-3 polyunsaturated fatty acid (PUFA) supplementation for the treatment of people with dementia. Inclusion criteria were:

Type of study: Randomised controlled trials (RCTs) comparing omega-3 PUFA (either as a supplement or an enriched diet) with placebo. Studies were to include people with dementia diagnosed using accepted diagnostic criteria. Dementia could be at any stage or severity. Studies investigating only dietary advice, or not specifying the intake of omega-3 PUFA, were excluded.

Types of intervention: 

  • Dietary supplements of any dose of omega-3 PUFA capsules versus placebo. Omega-3 PUFA was to be the main active ingredient of supplementation and given regularly (at least weekly) for at least 26 weeks.
  • Diets enriched with omega-3 PUFAs in specific portions versus usual diet.


Primary outcomes: changes in global and specific cognitive function, functional outcomes {e.g. activities of daily living (ADL)}, overall dementia severity and adverse effects.

Secondary outcomes: quality of life (QoL), compliance with the intervention, symptoms associated with dementia (e.g. mood changes), entry to institutional care, hospital admissions, and mortality.


Search strategy: Reviewers searched ALOIS, the specialised register of the Cochrane Dementia and Cognitive Improvement Group up to December 2015 to locate eligible studies. This register holds dementia research identified from major healthcare databases {MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), CINAHL, PsycINFO and Lilacs}, international trial registers, and sources of grey literature. In addition, major healthcare databases were searched separately, manufacturers of omega-3 products contacted, and conference abstracts and reference lists of included studies reviewed. No language restrictions applied.

Review process: Two reviewers independently examined titles/abstracts and then full text to identify relevant studies. Two reviewers also independently extracted data, performed or checked data entry, and assessed study quality. Discussion or involvement of a third person resolved differences in opinion.

Quality assessment: The Cochrane Collaboration tool was used to assess risk of bias in included trials. The tool looks at random sequence generation, allocation concealment, blinding of participants, personnel and outcome assessment, incomplete outcome data, selective reporting and potential bias from industry involvement.

Overall validity: A high-quality review involving high-quality studies.


After the removal of duplicates, 2332 articles were screened, of which 31 full-text articles were considered for inclusion. Three RCTs involving 632 participants were included in this review. All participants had Alzheimer’s disease (AD) of mild to moderate severity. Trials involved similar doses of omega-3 PUFA supplements (between 1.75 and 2.3 g/day). Trial duration varied and was for either six, 12 or 18 months. At  six months, there was no significant difference between those taking omega-3 PUFAs and those receiving placebo for changes in cognitive function, changes in functional outcome measures (activities of daily living – ADL) or overall dementia severity (see table). There were also no significant differences between groups for QoL and mental health symptoms. Non-significant results were observed regardless of the dose and duration of supplement intake. Tolerability was poorly reported in the included studies, although serious adverse events appeared to be uncommon.


  • Participants were similar at baseline for relevant characteristics including use of AD medication, dietary intake of omega-3 and MMSE score. Increased serum fatty acid levels in the omega-3 supplement but not the placebo groups indicated good compliance with the intervention.
  • Study quality was high and all outcomes were measured using validated tools. Non-significant improvement in cognition with omega-3 supplements was considered too small to be clinically significant.
  • A significant improvement in instrumental ADL (ability to live independently) observed in one very small pilot study requires confirmation with further research.

Reviewer: Cynthia Wensley RN, MHSc. Honorary Professional Teaching Fellow, the University of Auckland and PhD Candidate, Deakin University, Melbourne


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