Lim W S, Gammack J K, Van Niekerk J, Dangour A D
Department of Geriatric Medicine, Tan Tock Seng Hospital, 11 Jalan Tan Tock Seng, Singapore, Singapore, 308433.
Cochrane Database Syst Rev. 2006 Jan 25(1):CD005379. doi: 10.1002/14651858.CD005379.pub2.
Accruing evidence from observational and epidemiological studies suggests an inverse relationship between dietary intake of omega 3 polyunsaturated fatty acid (PUFA) and risk of dementia. Postulated mechanisms that might qualify omega 3 PUFA as an interventional target for the primary prevention of dementia include its anti-atherogenic, anti-inflammatory, anti-oxidant, anti-amyloid and neuroprotective properties.
To review the evidence that omega 3 PUFA supplementation prevents cognitive impairment and dementia in cognitively intact elderly persons.
The Cochrane Dementia and Cognitive Improvement Group's (CDCIG) Specialized register, MEDLINE, EMBASE,CINAHL PsycINFO, AMED AND CENTRAL and several ongoing trials databases were searched on 5 and 6 October 2005. The CDCIG Register is updated regularly and contains records from all major medical databases and many ongoing trials databases.
In order to be selected, trials needed to be randomized, placebo-controlled, doubled blinded, of minimum study duration of 6 months, involved persons aged 60 years and above without pre-existing dementia at study onset, and employed cognitive endpoints.
Reviewers, working independently, were to select, quality assess and extract relevant data where appropriate and possible. In comparing intervention with placebo, the pooled odds ratios or weighted mean differences and standardized mean difference were to be estimated.
There were no randomized trials found in the search that met the selection criteria. Results of two clinical trials are expected in 2008.
AUTHORS' CONCLUSIONS: There is a growing body of evidence from biological, observational and epidemiological studies that suggests a protective effect of omega 3 PUFA against dementia. However, until data from randomized trials become available for analysis, there is no good evidence to support the use of dietary or supplemental omega 3 PUFA for the prevention of cognitive impairment or dementia.
观察性研究和流行病学研究积累的证据表明,ω-3多不饱和脂肪酸(PUFA)的膳食摄入量与痴呆风险之间存在负相关。可能使ω-3多不饱和脂肪酸成为痴呆一级预防干预靶点的假定机制包括其抗动脉粥样硬化、抗炎、抗氧化、抗淀粉样蛋白和神经保护特性。
综述ω-3多不饱和脂肪酸补充剂预防认知功能完好的老年人认知障碍和痴呆的证据。
于2005年10月5日和6日检索了Cochrane痴呆与认知改善小组(CDCIG)的专业注册库、MEDLINE、EMBASE、CINAHL、PsycINFO、AMED和CENTRAL以及几个正在进行的试验数据库。CDCIG注册库定期更新,包含所有主要医学数据库和许多正在进行的试验数据库的记录。
为了被选中,试验需要是随机、安慰剂对照、双盲的,最短研究持续时间为6个月,纳入60岁及以上、研究开始时无痴呆病史的人群,并采用认知终点。
评审人员独立工作,在适当且可能的情况下选择、评估质量并提取相关数据。在比较干预组与安慰剂组时,应估计合并比值比或加权平均差以及标准化平均差。
检索中未发现符合入选标准的随机试验。两项临床试验的结果预计于2008年公布。
来自生物学、观察性研究和流行病学研究的证据越来越多,表明ω-3多不饱和脂肪酸对痴呆具有保护作用。然而,在随机试验的数据可用于分析之前,没有充分的证据支持使用膳食或补充ω-3多不饱和脂肪酸来预防认知障碍或痴呆。