Abstract
ObjectiveUnhealthy lifestyles have a considerable impact on the incidence of dementia. Skipping breakfast disturbs energy homeostasis and impairs brain function. In this study, we investigated the association between breakfast skipping and cognitive performance among community-dwelling adults. MethodsWe recruited 859 community-dwelling adults aged ≥60 years from January 1 to December 31, 2021. Participants’ sociodemographic information and breakfast skipping habits were self-reported. Participants were followed up for 36 months and cognitive function was assessed using the Mini-Mental State Examination (MMSE) with an interval of 18 months. Trajectories of cognitive change were compared between individuals with and without breakfast skipping. To reduce the risk of bias owing to unmatched sample sizes between the groups, we conducted 1:1 propensity score matching (PSM) based on age, sex, education level, and ApoE genotype. ResultsAt baseline and 18-month follow-up, no difference was found in MMSE scores between participants with and without breakfast skipping. However, those who habitually skipped breakfast had significantly lower MMSE scores than those who did not at 36-month follow-up. Individuals with habitual breakfast skipping had a steeper rate of cognitive decline than those without habitual breakfast skipping during follow-up. Breakfast skipping was a risk factor for longitudinal cognitive decline, defined as a decrease in MMSE scores of ≥3, adjusted for age, sex, education, body mass index, ApoE ε4 carrier status, hypertension, diabetes, and hyperlipidemia. At the last follow-up, participants who habitually skipped breakfast had significantly higher levels of ptau181 and NfL than those who did not. In the PSM cohort, similar findings were obtained regarding cognitive trajectories and plasma biomarkers. ConclusionBreakfast skipping was linked to an increased risk of long-term cognitive decline and neurodegeneration among older adults. The link between unhealthy dietary habits and cognitive decline may be attributed to a deficiency in neurorestoration resulting from inadequate energy consumption.
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