Fatty Acids and Cognitive Decline in Women
Objectives: To prospectively assess effects of select dietary fats on cognitive decline.
Design: Prospective observational; 3-year follow-up.
Setting: Northwestern University.
Participants: Four hundred eighty-two women aged 60 and older who participated in the Women's Health Initiative (WHI) Observational Study or in the control group of the WHI Diet Modification arm.
Measurements: Dietary intake from a validated food frequency questionnaire (FFQ) administered twice (mean 2.7 years apart) before baseline cognitive assessment (mean 2.9 years after second FFQ) was averaged. Testing of memory, vision, executive function, language, and attention was performed twice, 3 years apart. A global Z-score was created for both time points by averaging all Z-scores for each participant, and global cognitive change was defined as the difference between follow-up and baseline Z-scores.
Results: Median intake of saturated fat (SFA), trans-fat, (TFA), dietary cholesterol (DC), and monounsaturated fat (MUFA) was 18.53, 3.45, 0.201, and 19.39 g/d, respectively. There were no associations between degree of cognitive decline and intake of SFA (P=.69), TFA (P=.54), or DC (P=.64) after adjusting for baseline cognition, total energy intake, age, education, reading ability, apolipoprotein E ε4 allele, body mass index, estrogen and beta-blocker use, and intake of caffeine and other fatty acids. In contrast, MUFA intake was associated with lower cognitive decline in fully adjusted linear regression models, with mean decline (standard error) of 0.21 (0.05) in the lowest and 0.05 (0.05) in the highest quartiles (P=.02). This effect of MUFA intake was primarily in the visual and memory domains (P=.03 for both).
Conclusion: Greater intake of SFA, TFA, and DC was not associated with cognitive decline, whereas greater MUFA intake was associated with less cognitive decline.
Cognitive impairment is a common disorder in elderly persons. Age-related cognitive decline (ARCD) encompasses deterioration in several domains, including memory performance, executive function, and speed of cognitive processing. The causes of cognitive decline are unknown, but previous studies have linked it to cardiovascular disease (CVD) and cardiovascular risk factors such as diabetes mellitus and abnormal blood pressure. Few modifiable risk factors for ARCD have been established, but given its association with CVD, plausibly include dietary fatty acids, which have strong established roles in the etiology of CVD.
Previous prospective studies of intake of dietary saturated fatty acid (SFA), trans-unsaturated fatty acid (TFA), and mono-unsaturated fatty acid (MUFA) have had variable associations with cognitive decline, with most suggesting deleterious effects of SFA and TFA. Few studies of fatty acids and cognitive decline have measured individual components of cognitive function beyond the standard Mini-Mental State Examination, and only one had multiple assessments of diet. Thus, it remains unclear whether different fats have different effects on specific elements of cognitive function.
An association between higher dietary Ω3, but not Ω6, fatty acid intake and less cognitive decline in older women has been reported, but the corresponding associations with other fatty acids were not assessed. Given the established deleterious relationships between SFA and TFA and CVD and the beneficial relationship between MUFA and CVD, it was hypothesized that they would have similar relationships with cognitive decline. This study examined the prospective associations between these fatty acids and cognitive decline in a population of older women using comprehensive neuropsychiatric testing for multiple domains of cognitive decline.
Abstract and Introduction
Abstract
Objectives: To prospectively assess effects of select dietary fats on cognitive decline.
Design: Prospective observational; 3-year follow-up.
Setting: Northwestern University.
Participants: Four hundred eighty-two women aged 60 and older who participated in the Women's Health Initiative (WHI) Observational Study or in the control group of the WHI Diet Modification arm.
Measurements: Dietary intake from a validated food frequency questionnaire (FFQ) administered twice (mean 2.7 years apart) before baseline cognitive assessment (mean 2.9 years after second FFQ) was averaged. Testing of memory, vision, executive function, language, and attention was performed twice, 3 years apart. A global Z-score was created for both time points by averaging all Z-scores for each participant, and global cognitive change was defined as the difference between follow-up and baseline Z-scores.
Results: Median intake of saturated fat (SFA), trans-fat, (TFA), dietary cholesterol (DC), and monounsaturated fat (MUFA) was 18.53, 3.45, 0.201, and 19.39 g/d, respectively. There were no associations between degree of cognitive decline and intake of SFA (P=.69), TFA (P=.54), or DC (P=.64) after adjusting for baseline cognition, total energy intake, age, education, reading ability, apolipoprotein E ε4 allele, body mass index, estrogen and beta-blocker use, and intake of caffeine and other fatty acids. In contrast, MUFA intake was associated with lower cognitive decline in fully adjusted linear regression models, with mean decline (standard error) of 0.21 (0.05) in the lowest and 0.05 (0.05) in the highest quartiles (P=.02). This effect of MUFA intake was primarily in the visual and memory domains (P=.03 for both).
Conclusion: Greater intake of SFA, TFA, and DC was not associated with cognitive decline, whereas greater MUFA intake was associated with less cognitive decline.
Introduction
Cognitive impairment is a common disorder in elderly persons. Age-related cognitive decline (ARCD) encompasses deterioration in several domains, including memory performance, executive function, and speed of cognitive processing. The causes of cognitive decline are unknown, but previous studies have linked it to cardiovascular disease (CVD) and cardiovascular risk factors such as diabetes mellitus and abnormal blood pressure. Few modifiable risk factors for ARCD have been established, but given its association with CVD, plausibly include dietary fatty acids, which have strong established roles in the etiology of CVD.
Previous prospective studies of intake of dietary saturated fatty acid (SFA), trans-unsaturated fatty acid (TFA), and mono-unsaturated fatty acid (MUFA) have had variable associations with cognitive decline, with most suggesting deleterious effects of SFA and TFA. Few studies of fatty acids and cognitive decline have measured individual components of cognitive function beyond the standard Mini-Mental State Examination, and only one had multiple assessments of diet. Thus, it remains unclear whether different fats have different effects on specific elements of cognitive function.
An association between higher dietary Ω3, but not Ω6, fatty acid intake and less cognitive decline in older women has been reported, but the corresponding associations with other fatty acids were not assessed. Given the established deleterious relationships between SFA and TFA and CVD and the beneficial relationship between MUFA and CVD, it was hypothesized that they would have similar relationships with cognitive decline. This study examined the prospective associations between these fatty acids and cognitive decline in a population of older women using comprehensive neuropsychiatric testing for multiple domains of cognitive decline.
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