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New Eye Benefit Seen in Omega-3s
6/7/2012
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Omega-3 fatty acids from fish are proven essential to human eye health and function.
 
Scientists at the National Eye Institute (NEI) within the National Institutes of Health say there’s “consistent evidence” that omega-3s protect against damage to the blood supply and nerves of the retina (SanGiovanni JP, Chew EY 2005).
 
These benefits are tied to both of the major omega-3s in fish fat – DHA and EPA – but it’s clear that DHA plays the most important role.
 
Omega-3 DHA exerts anti-inflammatory and anti-oxidant influences on the genes in cells within the retina.
 
The body makes omega-3 EPA from DHA, and EPA suppresses inflammation as well as the overgrowth of blood vessels that causes age-related macular degeneration (AMD).
 
AMD results in loss of vision in the center of the visual field (so-called “central vision”) and is the main cause of blindness in people over 50.
 
The NEI team noted that omega-3s from fish are essential to vision: “… [omega-3] DHA insufficiency is associated with alterations in retinal function [and] visual processing deficits have been ameliorated with DHA supplementation ...” (SanGiovanni JP, Chew EY 2005).
 
For example, see “Omega-3s Linked to Eye Health… Again” and related reports in the Omega-3s & Eye Health section of our news archive.
 
And judging by the results of a mouse study from Canada’s University of Alberta, it appears we have more to learn about the importance of omega-3s – especially DHA – to eye health.
 
Their study tested the effects of omega-3 DHA on a key player in the onset of macular degeneration.
 
Lipofuscin: The blinding result of declining waste-disposal in aging eye cells
The retina is a blood- and nerve-rich layer of tissue at the back of the eye, which receives light streaming through the lens.
 
Nerve cells in the retina then transmit signals to the brain, which turns them into the miraculous phenomenon we experience as “vision”.
 
As people age, a substance called lipofuscin builds up in the eye’s retinal pigment epithelial (RPE) cells.
 
Accumulation of lipofuscin – which consists of yellow-brown pigment granules – in these retinal cells is a major risk factor for macular degeneration.
 
Lipofuscin is a byproduct of the breakdown of damaged blood cells, and is known as “the aging pigment”.
 
Buildup of lipofuscin implies declining performance by the lysosomes in retina cells. These tiny organelles serve as waste-disposal units for cells throughout the body.
 
(Lipofuscin also accumulates in the liver, kidney, heart muscle, adrenal gland, and in nerve and brain cells as we age.)
 
Damage to lysosomes probably results from earlier damage to cell membranes (where omega-3s play essential structural and functional roles) and mitochondria (energy factories).
 
Much of the retina damage associated with lipofuscin stems from accompanying buildup of a toxic component of lipofuscin called A2E, eye levels of which double as people age.
 
Canadian mouse study detects new anti-aging eye benefit from DHA
At the University of Alberta, a team of investigators led by Yves Sauve conducted an 18-month-long study in mice, to test whether supplemental omega-3 DHA would affect the buildup of lipofuscin and its A2E component in the animals’ eyes.
 
They tested DHA in both “wild-type” mice and in transgenic mice bred to develop a genetic trait found in some humans (called E4), which causes massive A2E accumulation and related retina dysfunctions.
 
No effect was seen from short-term feeding of DHA (one to three months), but when the vulnerable transgenic mice were fed DHA for six months, the function of their RPE cells was preserved.
 
And when mice were fed DHA for 12 months, this led to preservation of full retina function in the transgenic mice, which were highly vulnerable to buildup of toxic AE2.
 
After 12 to 18 months of eating DHA-fortified chow, eye levels of A2E dropped in all of the mice (wild-type and transgenic).
 
As the Canadian team concluded, “DHA supplementation was associated with: preserved retina function at mid-degenerative stages in E4 mice; prevention of age-related functional losses in WT mice; and reduced A2E levels in E4 and WT mice at the oldest age examined.”
 
“These findings imply that dietary DHA could have broad preventative therapeutic applications … on pathologic and normal age-related ocular processes” (Dornstauder B et al. 2012).
 
As Dr. Sauve noted, “… there was no increase in this toxin whatsoever. This has never been demonstrated before – that supplementing the diet with DHA could make this kind of difference. This discovery could result in a very broad therapeutic use [of DHA]” (Dornstauder B et al. 2012).
 
His team recently started another study, looking at people who have age-related macular degeneration.
 
The researchers will look for DNA markers in study participants, to determine whether people with certain genetic markers will respond better to increased intake of DHA, and if so, why.
 
Most of the funds for the study came from the Canadian Institutes of Health Research, with added support from various vision-health foundations.
 
 
Sources
  • Dornstauder B, Suh M, Kuny S, Gaillard F, Macdonald IM, Clandinin MT, Sauvé Y. Dietary Docosahexaenoic Acid Supplementation Prevents Age-Related Functional Losses and A2E Accumulation in the Retina. Invest Ophthalmol Vis Sci. 2012 Apr 24;53(4):2256-65. Print 2012.
  •  Sparrow JR, Fishkin N, Zhou J, Cai B, Jang YP, Krane S, Itagaki Y, Nakanishi K. A2E, a byproduct of the visual cycle. Vision Res. 2003 Dec;43(28):2983-90. Review.
  • Zhou J, Jang YP, Kim SR, Sparrow JR. Complement activation by photooxidation products of A2E, a lipofuscin constituent of the retinal pigment epithelium. Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16182-7. Epub 2006 Oct 23.
  • SanGiovanni JP, Chew EY. The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina. Prog Retin Eye Res. 2005 Jan;24(1):87-138. Review.
  • Wolf G. Lipofuscin and macular degeneration. Nutr Rev. 2003 Oct;61(10):342-6. Review.
  • Maurier R. Discovery may help prevent vision loss with age. May 30, 2012. Accessed at http://www.news.ualberta.ca/article.aspx?id=81EE067D2D2848E3953ABF2117E95038  
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