Summary: | One apparent consequence of aging appears to be loss of some aspects of cognitive control. This loss is measurable as early as mid-adulthood. Since, like many aspects of cognition, there is wide variance among individuals, it is possible that behavior, such as one’s diet, could drive some of these differences. For instance, past data on older humans and non-human primates have suggested that dietary carotenoids could slow cognitive decline. In this study, we tested how early such protection might manifest by examining a sample (n = 60) of 25–45 year olds. Carotenoid status was assessed by directly measuring macular pigment optical density (MPOD) which has shown to be highly correlated with the primary carotenoid in brain, lutein. Cognitive control was measured using event-related potentials during the performance of cognitive control tasks designed to tap into different aspects of attentional (i.e., selective attention, attentional inhibition, and response inhibition) control. Our results showed that, across participants, MPOD was related to both age and the P3 component of participants’ neuroelectric profile (P3 amplitude) for attentional, but not response, inhibition. Although younger adults exhibited larger P3 amplitudes than their older adult counterparts, older subjects with higher MPOD levels displayed P3 indices similar to their younger adult counterparts in amplitude. Furthermore, hierarchical regression analyses showed that age was no longer a significant predictor of P3 amplitude when MPOD was included as a predictor in the model, suggesting that MPOD may partially contribute to the relationship between age and P3 amplitude. In addition, age and MPOD were shown to have independent associations with intraindividual variability of attentional control, such that younger individuals and individuals with higher MPOD showed less intraindividual variability. These results show a relationship between retinal carotenoids and neuroelectric indices underlying cognitive control. The protective role of carotenoids within the CNS may be evident during early and middle adulthood, decades prior to the onset of older age.
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