Dietary Fats and Cognitive Status in Italian Middle-Old Adults

Abstract

The increase in life expectancy led to a significant rise in the prevalence of age-related neurological diseases, such as cognitive impairment, dementia, and Alzheimer’s disease. Although genetics certainly play a role, nutrition emerged as a key factor in maintaining optimal cognitive function among older adults. Therefore, the study aimed to investigate whether specific categories and subcategories of dietary fats, based on carbon-chain length, are associated with cognitive status in a cohort of 883 Italian participants over the age of 50. Methods: The intake of total, single class of dietary fat, such as saturated fatty acids (SFA), monounsaturated fatty acid (MUFA), and polyunsaturated fatty acid (PUFA), and also single fatty acids grouped according to carbon-chain length, were evaluated by food frequency questionnaires (FFQs). Cognitive health was assessed using the short portable mental status questionnaire (SPMSQ). Results: After adjustment for potential confounding factors subjects with a moderate consumption of both short-chain SFA (for Q2 vs. Q1, OR = 0.23, 95% CI: 0.08, 0.66) and middle-chain SFA specifically lauric acid (C12:0) intake (for Q2 vs. Q1, OR = 0.27, 95% CI: 0.09, 0.77) were less likely to suffer from cognitive impairment. Among single MUFAs, erucic acid (C22:1) intake resulted in an inverse association, in a linear way, with cognitive impairment (for Q4 vs. Q1, OR = 0.04, 95% CI: 0.00, 0.39). Conversely, moderate intake of linoleic acid (C18:2) was associated with cognitive impairment (Q3 vs. Q1, OR = 4.59, 95% CI: 1.51, 13.94). Regarding other PUFAs, individuals consuming moderate intake alpha linolenic acid (C18:3) were less likely to have cognitive impairment (for Q3 vs. Q1, OR = 0.19, 95% CI: 0.06, 0.64). Conclusions: Total SFA intake appeared to be inversely associated with cognitive impairment. Regarding specific subtypes of fatty acids, the results mostly referred to short- and middle-chain SFA. Further studies are needed to validate the results of the present study.

Erucic acid ameliorates the lipopolysaccharide‐induced memory deficit in rats through inhibited inflammation cytokines expression/caspase 3/NF‐κB pathways

“…[5,11] It has been found that erucic acid is an antioxidant and anti-inflammatory ligand that leads to improved cognitive parameters. [5,12] The effects of erucic acid as a peroxisome proliferator-activated receptor delta (PPAR-δ) ligand have been investigated in rotenone-induced PD model in zebrafish. [13] Erucic acid mediated modulation of membrane composition is associated with complex changes in lipid homeostasis that may affect amyloidogenic processing, providing an important target for lipid-based AD therapies.…”

The shift in the fatty acid composition of the circulating lipidome in Alzheimer's disease

“…Although no data are available concerning the AD‐related alterations of EA in CSF, evidence reveals changes of EA in plasma free FAs and phospholipids from AD and MCI patients 28 . Higher plasma levels of EA were associated with a poorer executive function in elderly people with a parental history of AD, 56 and its consumption was inversely associated with cognitive impairment 57 . Interestingly, in human brain EA content is highly conserved across 13 different brain regions during the ageing process, 58 except in hippocampus, which is a region affected during the initial stages of the disease 59 .…”

“… 28 Higher plasma levels of EA were associated with a poorer executive function in elderly people with a parental history of AD, 56 and its consumption was inversely associated with cognitive impairment. 57 Interestingly, in human brain EA content is highly conserved across 13 different brain regions during the ageing process, 58 except in hippocampus, which is a region affected during the initial stages of the disease. 59 Since EA crosses the blood‐brain barrier (BBB), 60 these results suggest a possible role of EA in the progression of AD that could be expressed in CSF.…”

Exploring the chain mediating roles of frailty and depressive symptoms in the relationship between pain and cognitive function among nursing home older adults

“…The inclusion criteria were as follows: (1) aged 60 and older; (2) living in the nursing home for at least 1 month; and (3) able to communicate. The exclusion criteria included serious psychological impairment or end‐stage illness according to the medical record or participating in other studies or severe cognitive impairment (the Short Portable Mental Status Questionnaire, eight or more errors) 22 . The face‐to‐face interview was conducted by well‐trained researchers in the participants' own room.…”