Glaucoma is often referred to as the "silent thief" as the symptoms are typically missing until the patient one day notices a loss in peripheral vision, or until one's eye doctor sees symptoms through a thorough eye exam.
Next: Vitamins, nutrients, diet, & lifestyle tips for glaucoma.
Damage to the Optic Nerve
The development of glaucoma is brought about by damage to the optic nerve, sometimes as a result of increased pressure in the clear fluid that circulates in the inside of the eye between the cornea and the lens.
The anterior (front) chamber of the eye is bounded by the lens and iris behind and the cornea in front. The ciliary epithelium behind the upper eyelid secretes aqueous humour, a clear liquid that fills the anterior chamber, which provides oxygen and nutrients to the front of the eye. Aqueous humor is produced continuously and then exits the eyes through a mesh of tiny holes behind the lower eyelid, called the trabecular meshwork.
While it had been logical to assume that increased pressure would restrict the flow of blood to the optic nerve, causing damage, Quigley, et al found (1980) that might not be so.1 Rather, he and his collegues determined that mechanical compression of individual nerve fiber bundles was a more likely cause.
It is now known that the spongy trabecular meshwork near the lens at the front of the eye becomes clogged and does not permit correct outflow of acqueous humor into the normal body circulation, giving rise to increased intraocular pressure, which swells, sending pressure to the vitreous, and eventually starving the nerve cells of nutrients. The nerves that comprise peripheral vision fail first due to restricted blood flow and/or mechanical compression of nerve fibers.
It is further understood that damage caused by elevated eye pressure, the amount of damage, the amount of pressure and the duration of pressure are not perfectly correlated. There may be other factors involved, in part, depending on whether the head of the optic nerve, the ganglion cells and other parts of the optic nerve are damaged and to what extent.2
Glaucoma is now defined as a collection of diseases causing optic nerve damage. The diagnosis is no longer determined only on whether this pressure (Intraocular Pressure or IOL) is high.
Conventional treatment depends on the nature and severity of each case. Commonly, open angle glaucoma is treated with eye drops or oral medications. In the event this treatment does not lower the eye pressure inside the eye, laser therapy or surgery may be considered necessary.
- Oxidative Stress. Researchers are increasingly clear that damage to the trabecular meshwork which causes glaucoma is triggered by oxidative stress. Therefore the role of antioxidants in preventing and treating the condition is increasingly apparent.6, 7 Among other results, oxidative stress leads to imbalances in the biochemicals that control relaxation or constriction of blood cells through regulation of the vascular endothelium (a single layer of cells lining blood vessels).13, 14
- Inadequate blood flow due to blood vessel dysfunction at the optic disc (the point where optic nerves exit the eye) 8, or problems in regulation of blood flow to the optic disc.9 Other research finds that problems in blood circulation behind the eyeball contribute to progression of glaucoma.10, 11, 12
- Physical trauma to the eye.
- Harmful drugs. Some medications actually increase your chances of developing glaucoma. Review these harmful drugs for glaucoma.
- Computer use. Heavy computer use increases glaucoma risk. Japanese researchers have found that people who are on the computer all day are at higher risk for developing glaucoma, especially if they are myopic.
- Thyroid. Have your thyroid checked, since some causes of glaucoma have been tied to low thyroid functioning.
- Genetic Mutations. 2009 research found that simultaneous mutations of the WDR36 and STI1 gene are causal factors for glaucoma.
- Mercury, Manganese. 2015 research has identified a connection between high levels of mercury and glaucoma and between low levels and manganese and lower rates of glaucoma.
- Estrogen deficiency. Some research suggests that due to surgery to remove ovaries before menopause, subsequent estrogen deficiencies may increase the risk of developing glaucoma. Women who had the surgery (oophorectomy) before age 43 had a much higher risk of developing glaucoma, even when they were treated with estrogen.3
- Alzheimer's disease. Researchers have found a likely link between Alzheimer's and glaucoma, with Alzheimer's patients being at greater risk of developing glaucoma.4
- Retinal vein occlusion creates an increased risk of developing glaucoma.
- Smoking creates a much larger risk for the user to develop glaucoma. It is true that smoking marijuana descreases intraocular pressure slightly, but only for several hours. Learn more about smoking and glaucoma.
Types of Glaucoma
A patient deemed a "Glaucoma Suspect" is one typically with a higher than normal eye pressure (IOL), but have not as of yet developed other symptoms such as changes in the optic nerve and/or reduced peripheral vision (as compared to prior visits). Glaucoma suspects could include people with diabetes, hypertension, heart disease, heavy computer users, and people with extreme nearsightedness or farsightedness. They also include people who suffer from obesity, hyperthyroidism, and African Americans. If you are in this category you should have glaucoma testing regularly, and we recommend the nutrients above to protect your vision.
Open Angle or Chronic Glaucoma
Open Angle Glaucoma is most frequently seen. Inside the front of the eye is the trabecular meshwork, which acts as a filter for the fluid in the eye. For various reasons, this meshwork gets clogged or obstructed and does not filter the fluid efficiently, which, in turn, leads to high ocular pressure.
Even though elevated eye pressure is one of the diagnostic tests used for glaucoma, approximately 30-40 percent of patients with open angle glaucoma have normal or low eye pressure and develop optic nerve changes and progressive vision loss without having elevated eye pressure. In the case of this common type of glaucoma there are no symptoms that you will notice until the condition has progressed so that there is loss of peripheral vision. Our complementary protocol is recommended for open angle glaucoma.
Narrow (Acute) Angle Glaucoma or Angle-Closure Glaucoma
This condition is considered an ocular emergency. This results from a blockage to the aqueous fluid draining brought about by a narrow angle between the cornea and the iris that is too narrow to enable the aqueous fluid to drain as quickly as it is being produced. You might experience sudden red eye(s), with headache and visual halos, and sometimes also vomiting and nausea. If you have these symptoms go straight to emergency and call your eye doctor.
Low Tension Glaucoma
Low tension (or normal tension) glaucoma affects 15-25% of patients with glaucoma. It appears with similar problems as open angle glaucoma but the introocular pressure is in the moderate rather than high range (less than 22 mm Hg). Patients experience the same loss of peripherial vision. It can be caused by an extreme sensitivity of the nerve cells to "normal" introocular pressure or to blood circulation problems such as vasospasm. The condition is generally an indicator of poor circulation. As a result, not enough oxygen-carrying blood reaches the optic nerve and it becomes damaged.
Many conditions, including brain tumors, heart problems5, or toxic substances can cause optic nerve damage that is experienced as glaucoma. Causes include use of steriods. Other causes include eye trauma, autoimmune disease, thyroid disease, Alzheimer's, sleep apnea, and hypotension (especially in older women). Also see: optic nerve atrophy and optic neuritis.
Low tension glaucoma is more common in Japan and Korea than elsewhere in the world; it affects men more than women; and the mean age is a little older - 60 years old compared to most patients with glaucoma.
Secondary Glaucoma arises as a side result to other health conditions such as injury to the eye, inflammation of the eyes, or various drug side effects (such as steriods).
- Exfoliative glaucoma - due to lens detrioration, cell tissue flakes off and becomes clogged in the trabecular meshwork, raising IOP.
- Neovascular glaucoma - because of new blood vessels forming at the front of the eye block fluid from exiting through the trabecular meshwork, raising IOP. These abnormalities are most common in patients who have diabetes
- Pigmentary glaucoma - the iris is composed of particles of pigment. If these detach and float into the vitreous fluid inside the eye they can eventually clog the trabecular meshwork and drainage channels raising IOP.
- Traumatic glaucoma - open angle glaucoma can appear shortly after eye trauma or some time later as debris from the injury disrupts the drainage process.
- Uvetic glaucoma - if the middle layer of the eye, the uvea, becomes inflammed pressure within the eye increases.
- Ghost cell glaucoma - patients who have had vitreous hemorrhage for some time can develop rigid ghost cells which are a type of red blood cell. If these ghost cells get into the front chamber of the eye they can block the trabecular meshwork resulting in ghost cell glacuoma.
Congenital Glaucoma is that which begins within the first months after birth. It is the result of incomplete prenatal development of the eye's drainage system. It can also be inherited and can sometimes be treated surgically. Learn more about congenital glaucoma.
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1. The mechanism of optic nerve damage in experimental acute intraocular pressure elevation, Quigley, et al
2. Understanding mechanisms of pressure-induced optic nerve damage, Morrison, JD, et al, Oregon Health Sciences University, Portland, Progressive Retina Eye Research. March, 2005, 217-240.
3. The Risk of glaucoma after early bilateral oophorectomy, T.S. Vajaranant, MD., et al, Menopause, April 2014
4. Massimo Cesareo, et al, Association Between Alzheimer's Disease and Glaucoma: A Study Based on Heidelberg Retinal Tomography and Frequency Doubling Technology Perimetry, Frontiers in Neuroscience, December, 2015.
5. A. J. Lee, et al, Open-angle glaucoma and cardiovascular mortality: the Blue Mountains Eye Study, Ophthalmology, July, 2006
6. J. Zhao, et al, Oxidative stress in the trabecular meshwork, International Journal of Molecular Medicine, October 2016.
7. A.C. Gauthier, J. Liu, Neurodegeneration and Neuroprotection in Glaucoma, The Yale Journal of Biology and Medicine, March, 2016.
8. J. Flammer, S. Orgul, et al, The impact of ocular blood flow in glaucoma, Progressive Retinal Eye Research, 2002
9. F. Galassi, A. Sodi, et al, Ocular Haemodynamics and glaucoma prognosis: a colour Doppler imaging study, Archives of Opthalmology, 2003
10. M. Satilmis, S. Orgul, et al, Rate of progression of glaucoma correlates with retrobulbar circulation and intraocular pressure, American Journal of Ophthalmology, 2003
11. J.J. Zink, J.E. Grunwald, et al, Association between lower optic nerve laser Doppler blood volume measurements and glaucomatous visual field progression, British Journal of Ophthalmology, 2003
12. G. Fuchsjager-Mayrl, B. Wally, et al, Ocular blood flow and system blood pressure in patients with primary open-angle glaucoma and ocular hypertension, Investigations in Ophthalmology and Visual Science, 2004
13. M. Feletou, P.M. Vanhoutte, Endothelial dysfunction: a multifaceted disorder, American Journal of Physiology: Heart and Circulatory Physiology, 2006
14. H. Resch, G. Garhofer, et al, Endothelial dysfunction in glaucoma, Acta Ophthalmologica, June, 2008
Also see Research on glaucoma.