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Lower dietary intake of long‐chain polyunsaturated fatty acids predict cognitive decline (124.4)
Author(s) -
Scott Tammy,
Lichtenstein Alice,
Tucker Katherine
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.124.4
Subject(s) - polyunsaturated fatty acid , eicosapentaenoic acid , cognitive decline , arachidonic acid , docosahexaenoic acid , medicine , demographics , cohort , fatty acid , chemistry , demography , biochemistry , dementia , disease , sociology , enzyme
Docosahexanoic acid (DHA) and arachidonic acid (AA) are the predominant long‐chain fatty acids (LC‐PUFA) in the brain and are important for maintaining neuronal membrane fluidity, signaling, and modulation of inflammation. The primary source for both DHA and AA, as well as for DHA’s precursor eicosapentaenoic acid (EPA), is from dietary intake. Our objective was to assess whether lower dietary intake of DHA, EPA, or AA were risk factors for cognitive decline in the Boston Puerto Rican Health Study cohort (n=733; mean age = 57y, SD ± 7.5). Cognitive testing was conducted at baseline and two‐year follow‐up; composite scores for executive function and memory were derived. Cognitive decline was defined as 蠅 1 SD decrease in score. Baseline LC‐PUFA intake was determined through food frequency questionnaire. Statistical models were adjusted for baseline cognitive scores, demographics, lifestyle variables, health co‐morbidities and energy and fat intake. Quintiles of DHA, EPA, AA, and combined DHA+EPA intake were calculated. Results showed that being in the lowest four quintiles of DHA (<=.195 g), EPA (<=.101 g), AA (<.217 g), or combined intake (<=.30 g) was predictive of executive function decline over two years [OR=1.88 (95% CI 1.05‐3.37); OR=2.08 (95% CI 1.13‐3.81); OR=2.42 (95% CI 1.15‐5.10); OR=2.21(95% CI 1.21‐4.06), p<0.05; respectively]. Lower baseline DHA, EPA or AA were not predictive of memory decline. Grant Funding Source : Supported by: USDA agreement No. 58‐1950‐0‐014 and NIH grants P01 AG023394 and P50 HL105185