Retinal Support & Vitamin A
While vitamin A is generally recommended to help heal retinal conditions, there are some inherited forms of retinal deterioration where impaired utilization of vitamin A results in deposits in the photoreceptor layer of the retina.
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The condition arises through gene mutations and can cause conditions such as autosomal recessive Stargardt's, cone-rod dystrophy, fundus flavimaculatus, retinitis pigmentosa and macular degeneration. This type of gene mutation is diagnosed in 1 in 20,000 children over 6, usually identified before age 20.
ABCA4 Gene Mutation
ABCR is a large retinal protein whose code is regulated by the ABCA4 gene. That means that the gene controls the behavior of the protein which becomes unable to perform its normal function of moving energy to and from the photoreceptor (RPE) cells in the retina. The RPE layer is damaged distorting and degrading the macula and causing gradual central vision loss. These symptoms are often noticed between ages 6 to 12 and sometimes as adults.
As the effects of the mutation continue the RPE layer begins to collect oily, granular deposits, called "lipofuscin" which impinge on the healthy structure of the retina. They look like yellowish-tinted specks and form clumps called "vitamin A dimmers." Scientists at Columbia University found that they could treat mice with ABCA4 mutations with vitamin A which had been enriched with deuterium and found that the clumping effect of vitamin A was slowed considerably.1, 2
- Poor vision in dim light.
- Difficulty in close vision, such as reading, although general vision may seem fine.
- Loss of vision sharpness, poor color vision and small blind spots.
- Blurriness and distorted vision, poor light/dark adaption.
- Phantom vision or visual hallucinations.
The ABCA4 gene mutation is inherited recessively, meaning that both parents must carry the gene and a child inherits a gene from both parents. It is one of 19 known mutations of the ABCR gene producing the protein required for energy transport to and from photoreceptor cells in the retina.
Patients with this mutation do not make an enzyme that removes vitamin A waste products leading up to the buildup of lipofuscin deposits and the death of retinal cells.
Currently, there is no effective treatment for this mutation except avoiding vitamin A. Scientists continue to investigate altered forms of vitamin A.
Current research shows that UV-protective sunglasses can help, and researchers are investigating whether injection of human embryonic stem cells has some benefit.
- Nutrients without vitamin A
- Avoid vitamin A Supplemental vitamin A beyond the daily requirement is to be avoided as discussed above.
- UV protection wear UV protecting sunglasses. Researchers have reported that similarly mutated gene mice reared in dark environments have few lipofuscin deposits.
1. Deuterium Enrichment of Vitamin A at the C20 Position Slows the Formation of Detrimental Vitamin A Dimers in Wild-type Rodents,
Yardana Kaufman, et al, March 11, 2011 The Journal of Biological Chemistry, 286, 7958-7965.
2. C20-D3-vitamin A Slows Lipofuscin Accumulation and Electrophysiological Retinal Degeneration in a Mouse Model of Stargardt Disease, Li Ma, et al, March 11, 2011 The Journal of Biological Chemistry, 286, 7966-7974.