In this study of community-dwelling older women, higher saturated fat intake was associated with a poorer 4-year trajectory of global cognition and verbal memory. By contrast, higher MUFA intake was related to better global cognitive and verbal memory trajectory. The magnitude of relations found for extreme fat quintiles and cognitive change were equivalent to ~6 years of aging. Regarding worst global cognitive or verbal memory 4-year change, there was a 60–70% higher risk comparing the highest vs. lowest SFA quintiles, but a 40–50% lower risk comparing the highest vs. lowest MUFA quintiles. There were no associations of PUFA, trans fat or total fat with cognitive change.
The results regarding SFA are similar to those from prior large-scale studies38–40
that examined “bad” fats with comparable methodology (e.g., adjusting for presence of other fats). For example, Morris et al.38
observed that increasing SFA (p-trend=0.04) and trans
fat intakes (p-trend=0.07) were linearly associated with faster global cognitive decline over 5.6 years among 2,560 age-65+ participants. Similarly, among 1,486 older women of the Nurses’ Health Study with type 2 diabetes, higher SFA and trans
intakes were associated with worse cognitive decline.40
Finally, Eskelinen et al.39
reported a 2-fold elevated risk of MCI (mild cognitive impairment) among 1,341 participants with high vs. low mid-life SFA intake; although the analysis was cross-sectional, the 21-year interval between diet assessment (mean age=50 years) and cognitive examination may have approximated prospective development of MCI. Regarding our null findings for trans
fats, a potential explanation is their narrower distribution among these generally healthy women, compared to that in other cohorts38, 40
. Although trans
fat intake can be quite high among Americans,41
the median percentage of energy from trans
fat in the highest quintile for our cohort was 1.8%.
There are limited data available from larger-scale prospective studies regarding “good” fats. Solfrizzi et al.42, 43
identified significant relations of higher MUFA and PUFA intakes to better cognitive aging. Devore et al.40
observed inverse associations of higher MUFA consumption (p-trend=0.06) and higher intake of PUFA relative to SFA (p-trend=0.03) with global cognitive change among older diabetic women. Navqi et al. found significantly less 3-year memory decline among 482 Women’s Health Initiative participants in the highest vs. lowest MUFA intake quartiles (SFA and trans
fat were not significantly related to cognitive change; associations for PUFAs were not reported)44
. Morris et al.38
did not find significant associations of MUFA or PUFA with global cognitive decline, but estimates suggested inverse relations. Vercambre and colleagues37
reported inverse relations of MUFA and PUFA to 5-year global cognitive decline among 2,551 women with CVD or risk factors – but only among the oldest (73–91 years). Variability in study designs may partly explain inconsistency in findings. For example, investigators used different methods for defining fat types (e.g., total PUFA, PUFA from spreads45
, linolenic acid (n-6 PUFA) only46
), may address different sub-groups (e.g., those with diabetes40
), or may not account for other fat types – as is recommended by experts in the field.38
Finally, unsaturated fats may be more susceptible to random misclassification when using only a one-time or a lower-precision diet instrument.
Strengths of this study include its prospective design, large sample, well-validated FFQ, availability of numerous health and lifestyle covariates, high follow-up and focus on late-life cognitive change. Limitations should also be considered. First, repeated diet assessments were not available – increasing random measurement error, which could attenuate associations. Second, reverse causation is possible; however, there was a 5-year lag between the FFQ and initial cognitive assessment, and it seems unlikely that many women had substantial cognitive impairment at study entry, as all WHS participants had successfully completed a pre-randomization run-in phase that scrutinized compliance to assigned treatment. Third, generalizability of findings among these mostly Caucasian women is an issue. Although it seems unlikely that basic biological relations would differ greatly, further research on dietary fat and cognition among racial/ethnic minorities and men is needed. Lastly, residual confounding is possible, and the data should be interpreted with appropriate caution.
In conclusion, these data suggest that elevated SFA intake is related to worse late-life cognitive trajectory, and increased MUFA intake is related to better cognitive aging. Thus, decreasing SFA and increasing MUFA merit further consideration in promoting healthy cognitive aging, and dietary patterns that incorporate higher intake of “good” fats (e.g., Mediterranean)47
should be further addressed in cognitive aging research. Findings from this large-scale prospective study help to address the identified need for an expanded, stronger evidence base on dietary factors and cognitive decline.17, 48