ABSTRACT
BACKGROUND AND OBJECTIVES: As the incidence and prevalence of Alzheimer's disease increases, so does the body of epidemiological and clinical research that suggests a relationship between dietary fatty acids, in particular saturates, and cognitive decline. In this study, we investigated the association between serum apolipoprotein B48 (apoB48), saturated fatty acid intake and consumption behaviour, and cognitive performance, in healthy, older aged Australians. METHODS AND STUDY DESIGN: We retrospectively analysed fasted serum apoB48 concentrations, food frequency questionnaire, and cognitive performance data collected from 147 participants (98F|49M) over the age of 50. We used Spearman's correlations and a nested domain model to evaluate the relationship between serum apoB48, dietary behaviour and measures of cognitive performance. RESULTS: Overall, we found that higher fasted apoB48 concentrations, and/or dietary behaviours which led to increased dietary consumption of diets high in saturated fatty acids, were inversely associated with cognition. Interestingly however, dietary behaviour patterns of saturated fatty acid consumption and serum apoB48 were linked with better secondary memory and perceptual speed, respectively. CONCLUSIONS: This is the first time that fasted apoB48 has been implicated as a biomarker for cognitive decline and Alzheimer's disease risk.
Subject(s)
Apolipoprotein B-48/blood , Cognition/drug effects , Cognitive Dysfunction/blood , Diet , Dietary Fats/adverse effects , Fatty Acids/adverse effects , Feeding Behavior , Aged , Aged, 80 and over , Alzheimer Disease/blood , Alzheimer Disease/etiology , Australia , Biomarkers/blood , Cognitive Dysfunction/etiology , Dietary Fats/administration & dosage , Dietary Fats/blood , Fasting , Fatty Acids/administration & dosage , Fatty Acids/blood , Female , Humans , Male , Memory , Middle Aged , Perception , Retrospective StudiesABSTRACT
Studies suggest that migraine pain has a vascular component. The prevailing dogma is that peripheral vasoconstriction activates baroreceptors in central, large arteries. Dilatation of central vessels stimulates nociceptors and induces cortical spreading depression. Studies investigating nitric oxide (NO) donors support the indicated hypothesis that pain is amplified when acutely administered. In this review, we provide an alternate hypothesis which, if substantiated, may provide therapeutic opportunities for attenuating migraine frequency and severity. We suggest that in migraines, heightened sympathetic tone results in progressive central microvascular constriction. Suboptimal parenchymal blood flow, we suggest, activates nociceptors and triggers headache pain onset. Administration of NO donors could paradoxically promote constriction of the microvasculature as a consequence of larger upstream central artery vasodilatation. Inhibitors of NO production are reported to alleviate migraine pain. We describe how constriction of larger upstream arteries, induced by NO synthesis inhibitors, may result in a compensatory dilatory response of the microvasculature. The restoration of central capillary blood flow may be the primary mechanism for pain relief. Attenuating the propensity for central capillary constriction and promoting a more dilatory phenotype may reduce frequency and severity of migraines. Here, we propose consideration of two dietary nutraceuticals for reducing migraine risk: L-arginine and aged garlic extracts.
