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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #176373

Title: Effect of Dietary Lutein and Zeaxanthin Plasma Carotenoids and Their Transport in Lipoproteins in Age-Related Macular Degeneration

Author
item WANG, WEI - OREGON HLTH & SCI UNIV
item CONNOR, SONJA - OREGON HLTH & SCI UNIV
item Johnson, Elizabeth
item KLEIN, MICHAEL - OREGON HLTH & SCI UNIV
item CONNOR, WILLIAM - OREGON HLTH & SCI UNIV

Submitted to: The American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/1/2006
Publication Date: 3/1/2007
Citation: Wang, W., Connor, S.L., Johnson, E., Klein, M.L., Connor, W.E. 2007. Effect of Dietary Lutein and Zeaxanthin Plasma Carotenoids and Their Transport in Lipoproteins in Age-Related Macular Degeneration. American Journal of Clinical Nutrition. 85:762-9.

Interpretive Summary: Low levels of dietary and blood lutein (L) and zeaxanthin (Z) have been associated with a high risk of age-related macular degeneration (AMD). AMD is the major cause of visual blindness in the US. L and Z are plant pigments and are in a class of compounds called carotenoids. It is not known if the transport of L and Z in blood is different in people with and without AMD. The objective of this study was to compare the distribution of carotenoids in the blood transport vehicles (lipoproteins) of L and Z in 7 AMD and 5 control subjects. They consumed a low L+Z diet (~1.1 mg/day) for 2 weeks followed by a high L+Z diet (L+Z ~11 mg/day) for 4 weeks. HDL (the lipoprotein associated with eye and heart health) was the major transporter for L and Z, carrying about half of the total L and Z in controls and in AMDs after a low L+Z diet. Similar distribution of L and Z was observed after the high L+Z diet. The amount of L and Z in HDL was about twice that found in LDL (the lipoprotein associated with risk of AMD and heart disease). Alpha-carotene, beta-carotene, and lycopene (other major dietary carotenoids) were primarily transported by LDL in both controls and AMDs. The distribution of major carotenoids among lipoproteins was not different in controls and AMDs on either the low or high lutein+zeaxanthin diet suggesting that any abnormalities of AMD may exist beyond the blood transport step. The data further suggest that the high amounts of L and Z associated with HDL may contribute partially to the protective power of HDL in AMD and heart disease.

Technical Abstract: Low levels of dietary and plasma lutein and zeaxanthin have been associated with a high risk of age-related macular degeneration (AMD). It is not known if the transport of these carotenoids in lipoproteins is different in people with and without AMD. The objective of this study was to compare the plasma lipoprotein distribution of carotenoids in seven AMD and five control subjects. They consumed a low lutein/zeaxanthin diet (a eucaloric diet low in lutein/zeaxanthin ~1.1 mg/day) for two weeks followed by a high lutein/zeaxanthin diet (a eucaloric diet high in lutein/zeaxanthin ~11 mg/day) for four weeks. HDL was the major transporter for lutein and zeaxanthin, carrying 57.4 +/- 4.7% and 56.3 +/- 14.7% of lutein, and 47.8 +/- 5.5% and 44.3 +/- 11.1% of zeaxanthin) in controls and in AMDs respectively after a low lutein/zeaxanthin diet. Similar distribution of lutein and zeaxanthin was observed after the high lutein/zeaxanthin diet. HDL/LDL was about 2:1 for lutein and zeaxanthin. HDL was the major transporter was confirmed by single vertical spin analyses. Alpha-carotene, beta-carotene, and lycopene were primarily transported by LDL (46-65%) in both controls and AMDs. The distribution of major carotenoids among lipoproteins was not different in controls and AMDs on either the low or high lutein/zeaxanthin diet suggesting that any abnormalities of AMD may exist beyond the plasma transport step. The data further suggest that the high amounts of lutein and zeaxanthin associated with HDL may contribute partially to the protective power of HDL in coronary heart disease.