Eating Fish Linked to Slower Memory Decline


Higher fish intake was linked to significantly decreased rate of episodic memory decline. More details in this study.


Eating more fish may be linked to lower rates of memory decline, according to a study published in the American Journal of Epidemiology.1

“In this pooled analysis including selected participants from five large cohorts of older subjects in studies from Europe and North America, we found that increasing intake of fish was modestly associated with slower rates of cognitive decline, in particular episodic memory decline– an early marker of AD risk,” wrote first author Cecilia Samieri, PhD, of the University of Bordeaux, France, and colleagues.

Because the study was so large-it included data from almost 24,000 people-it could identify modest associations that smaller studies have not been able to find.

The authors pointed out that even such modest effects may have a large public health impact. For example, one study has estimated that delaying AD onset by just year could decrease the prevalence of AD worldwide by over 9 million through 2050.2

An increasing body of evidence has suggested that consuming fish may slow cognitive decline and decrease the risk of AD. Fish are an excellent source of long-chain omega-3 polyunsaturated fatty acids (PUFAs). Many AD genes, like APOE, CLU and CR1, involve lipid metabolism or inflammation, and long-chain omega-3 PUFAs may act through these pathways. Fish also contain vitamin D and selenium, which are potentially neuroprotective.

To evaluate the issue, researchers pooled data from the French Three-City study and four US studies (Nurses’ Health Study, Women’s Health Study, Chicago Health and Aging Project and Rusk Memory and Aging Project).  The analysis included data from 23,688 adults with a mean age of 71.9-82.2 years. Participants were followed for a median of 3.9 to 9.1 years.

Participants completed food frequency questionnaires before their initial cognitive assessment, and had repeat cognitive assessments every 4 to 9 years. They also provided data on APOE gene type and other genetic mutations related to AD.

Researchers separated fish intake into the following categories: <1 serving/week, 1 serving/week, 2-3 servings/week, ≥ 4 servings/week.

Key results:

. Higher fish intake linked to slower decline in global cognition and memory (Ptrend≤ 0.031)

. Higher fish intake linked to significantly decreased rate of episodic memory decline (ptrend = 0.024)

≥4 servings/week linked to lower rates of memory decline vs <1 serving/week: -0.018 standard units lower, equivalent to four years of aging

. Results unchanged after adjusting for vascular conditions, BMI, and depression

. No evidence that consuming more fish affects APOE4 and 13 other AD genes

The lack of an association between fish consumption and AD genes likely indicates that the effect of fish on cognition is similar regardless of genetic predisposition to AD, the authors explained.

They also mentioned several potential limitations. Due to small numbers of minority participants in the five pooled studies, the study included data only from Caucasian participants. Also, 88% of participants were female with generally high education levels. So the results may not generalize to men and other populations.

Take Home Points

. Large pooled analysis of five studies in Europe and North America found that higher levels of fish consumption were linked to slower rates of global cognitive and memory decline

. People who ate ≥4 servings/week had similar memory decline as people who were four years younger, compared to people who ate <1 serving/week

. No evidence that consuming more fish affects APOE4 and 13 other AD genes


1. Samieri C, Morris MC, Bennett DA, et al. Fish intake, genetic predisposition to alzheimer's disease and decline in global cognition and memory in five cohorts of older persons. Am J Epidemiol. 2017; Oct 19. doi: 10.1093/aje/kwx330.

2. Brookmeyer R, Johnson E, Ziegler-Graham K, et al. Forecasting the global burden of Alzheimer's disease. Alzheimers Dement. 2007;3:186-191.

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