Mitochondrial Dysfunction in Eye Disease
The mitochondria are like the power plants of our cells. We have several thousand mitochondria in nearly every cell of our bodies, and they produce 90 percent of the energy our bodies need to sustain life and support organ function. When these powerhouse cells work less efficiently, a wide range of multi-systemic problems occur that can affect nearly any part of the body. Because the mitochondria perform so many different functions in different types of tissues, there are hundreds of types of mitochondrial diseases. The symptoms depend on which cells of the body are affected.
The eye and related tissues require a tremendous amount of energy, so it is no surprise that the eyes are particularly vulnerable when mitochondrial dysfunction impairs energy supply.
Mitochondria have attracted a considerable amount of attention from research scientists specializing in the pathophysiology of eye disease — particularly glaucoma. Researchers are working to understand the implications of mitochondrial dysfunction on the eyes, and the correlation between mitochondrial disorders and the optical system is becoming clearer.
Mitochondrial Dysfunction and Glaucoma
The key to understanding the relationship between mitochondrial dysfunction and glaucoma may be to recognize how mitochondrial dysfunction affects the retinal ganglion cells, or the cells that link the eye to the brain. The eye takes light and converts it to electrical signals that the brain can understand; the retinal ganglion cells are responsible for sending the electrical signals to the brain via axons. If the retinal ganglion cells die, the result is vision loss.
Mitochondrial dysfunction makes the retinal ganglion cells vulnerable to glaucoma injury because it reduces the amount of energy the cell has to repair itself; the dysfunction also makes the retinal ganglion cells more likely to die. Mitochondrial function declines naturally with age.
During the glaucomatous disease process, there is a window of opportunity to treat the optic nerve cells when they are sick so they do not die. The mitochondria die before the optic nerve cells, so intervening to normalize mitochondrial function may help the nerve cells maintain their function and fight off glaucomatous injury.
Offset Mitochondrial Dysfunction, Reverse Eye Disease
GlaucoCetin is the first medical food specifically designed to preserve the optic nerve cells by supporting and protecting the underlying mitochondrial function. By protecting the nerve cells, the highly active ingredients in GlaucoCetin help to slow the progression of glaucoma and preserve vision.
Although there is no cure for mitochondrial disease, the powerful blend of antioxidant and anti-inflammatory ingredients in the GlaucoCetin formula has been shown to reverse mitochondrial damage in glaucoma patients.
Fighting off glaucoma with nutritional treatment is a departure from conventional glaucoma therapy, which aims to reduce intraocular pressure via medicated eyedrops, laser and/or traditional incisional surgery. But there is enormous potential with the nutrition-based approach, as shown by doctors using it to treat age-related macular degeneration. The Age-Related Eye Disease Study discovered that a specific combination of antioxidants and other nutrients reduced the progression of dry macular degeneration by 25 percent.
Ultimately, the answer to treating glaucoma may include components to both reduce intraocular pressure and slow cellular degeneration.
For more information about how GlaucoCetin supports mitochondrial function and can slow the progression of glaucoma and prevent glaucoma-induced vision loss, please contact Guardion Health Sciences today.