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New Xanthophyll Science

Friday, July 25, 2008


A study published in the August 2008 Journal of Lipid Research found that the xanthophyll carotenoids, lutein (LUT) and zeaxanthin (ZEA) are preferentially taken up by the retinal cells compared to beta carotene.
 
Researchers have also discovered the manner in which lutein and zeaxanthin are transported from the bloodstream to the eye, shedding further light on how these two carotenoids promote eye health.
 
Evidence has been steadily accumulating to support the role of dietary lutein and zeaxanthin in protecting against the development of age-related macular degeneration (AMD), the leading cause of vision loss in people over 55 years of age in the Western world.

Because past studies have shown that a protein called SR-B1 (scavenger receptor class B, type 1) is involved in intestinal absorption of lutein and zeaxanthin, the authors of the current study investigated whether the same protein is also involved in transporting these nutrients to the eye.

During the in vitro study, the researchers examined the uptake of lutein, zeaxanthin and beta carotene by human retinal pigment epithelial (RPE) cells. They found that the cells were more efficient at absorbing lutein and zeaxanthin compared to beta carotene and that when the protein SR-BI was active, the RPE cells absorbed the carotenoids. But when they added compounds to inhibit SR-BI, the uptake of zeaxanthin and beta-carotene were significantly decreased by between 40 and 60 percent. Inhibition of another transport protein, CD36, had no effect. This indicated that not only does SR-B1 help the intestines absorb lutein and zeaxanthin, it also helps the eyes absorb these two critical nutrients.
 
This study supports the potential of lutein and zeaxanthin to inhibit the development of age-related macular degeneration by providing a valid mechanism explaining how xanthophylls can be transported from the blood into the eyes.
 
Another study published in the June 2008 issue of Free Radical Biology Medicine suggests that lutein can decrease intracellular H(2)0(2) accumulation by scavenging superoxide and H(2)0(2) and the nuclear factor-kappaB (NF-kB) regulated inflammatory genes in lipopolysaccharide-stimulated macrophages. This suggests that lutein supplementation could be important for those at increased risk of both macular degeneration and Alzheimer's, since these diseases share many of the same genes and both diseases are suggested to have an inflammatory component.
 
It's important to note that excess body fat has also been suggested to interfere with lutein and zeaxanthin transport to the eye.
 
Ellen Troyer, MT MA
Biosyntrx Chief Research Officer

PEARL

One could assume that the only people surprised about these two study outcomes are the folks on the AREDs2 formulation design committee, since they had to be pushed so very hard to include 10 mg of lutein and and 2 mg of zeaxanthin in two of the arms of the AREDs2 study.
 
Given the fairly large number of studies that supports lutein and zeaxanthin supplementation for those at risk of, or diagnosed with AMD, doesn't it make one wonder why the National Eye Institute continues to refer to the original ARED study formulation, 500 mg vitamin C, 400 IU vitamin E, 25,000 synthetic beta carotene, 80 mg zinc oxide and 2 mg of copper, as the AMD Standard of Care?
 
Biosyntrx full-spectrum multiples, Macula Complete and Oculair, include16 mg of lutein and 4 mg of zeaxanthin, and 12 mg of lutein and 3 mg of zeaxanthin, respectively.

References

Xanthophylls are preferentially taken up compared with {beta}-carotene by retinal cells via a SRBI-dependent mechanism. During A, Doraiswamy S, Harrison EH. J Lipid Res. 2008 Aug;49(8):1715-24.[abstract]
 
The non-provitamin A carotenoid, lutein, inhibits NF-kappaB-dependent gene expression through redox-based regulation of the phosphatidylinositon 3-kinase/PTEN/Akt and NF-dappaB-incuding kinase pathways: Role of H(2)0(2) in NF-kappaB activation. Kim JH, Kim CK, et al. Free Radical Biology Medicine 2008 June 27 [abstract]