A double-blind, placebo-controlled study on the effects of lutein and zeaxanthin on neural processing speed and efficiency.

Emily R Bovier,Billy R Hammond,Lisa M Renzi,Kevin Mcgraw

doi:10.1371/journal.pone.0108178

Emily R Bovier, Billy R Hammond + Show 2 more

Open Access

https://doi.org/10.1371/journal.pone.0108178

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Journal: PloS one	Publication Date: Sep 24, 2014
Citations: 115	License type: CC BY 4.0

Affiliation: University of Georgia, Abbott (United States)

Abstract

Lutein and zeaxanthin are major carotenoids in the eye but are also found in post-receptoral visual pathways. It has been hypothesized that these pigments influence the processing of visual signals within and post-retina, and that increasing lutein and zeaxanthin levels within the visual system will lead to increased visual processing speeds. To test this, we measured macular pigment density (as a biomarker of lutein and zeaxanthin levels in brain), critical flicker fusion (CFF) thresholds, and visual motor reaction time in young healthy subjects (n = 92). Changes in these outcome variables were also assessed after four months of supplementation with either placebo (n = 10), zeaxanthin only (20 mg/day; n = 29) or a mixed formulation containing 26 mg/day zeaxanthin, 8 mg/day lutein, and 190 mg/day mixed omega-3 fatty acids (n = 25). Significant correlations were found between retinal lutein and zeaxanthin (macular pigment) and CFF thresholds (p<0.01) and visual motor performance (overall p<0.01). Supplementation with zeaxanthin and the mixed formulation (considered together) produced significant (p<0.01) increases in CFF thresholds (∼12%) and visual motor reaction time (∼10%) compared to placebo. In general, increasing macular pigment density through supplementation (average increase of about 0.09 log units) resulted in significant improvements in visual processing speed, even when testing young, healthy individuals who tend to be at peak efficiency.

Highlights

Even in the absence of overt neural pathology, is often accompanied by a decline in central nervous system efficiency that tends to manifest as deficits in higher-level executive functions such as short-term memory, judgment and decision-making ability, inhibition of pre-potent responses and working memory; and as deficits in more basic processing functions, such as integration of sensory and motor responses
MPOD, measured as a surrogate for L and Z levels throughout both the retinal and post-retinal visual system, has been significantly related to fixed and variable reaction time, coincidence anticipation errors, and balance ability [36]
Reduced processing speed is a central feature of cognitive decline, and current data suggest that higher MPOD is related to preservation of cognitive function [26,32,33]

Summary

Introduction

Even in the absence of overt neural pathology, is often accompanied by a decline in central nervous system efficiency that tends to manifest as deficits in higher-level executive functions such as short-term memory, judgment and decision-making ability, inhibition of pre-potent responses and working memory; and as deficits in more basic processing functions, such as integration of sensory and motor responses (e.g., reaction time). Of these deficits, a slowing of processing speed appears to be central and not as amenable to the same compensatory mechanisms available for other, less time-dependent, functions [1]. These tasks may be used to distinguish performance ability in younger and older adults alike (providing a tool for direct comparison across decades of life), and serve as methodology to assess biomarkers that could be used to characterize meaningful individual differences in brain function

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