Glaucoma actually represents many different diseases, affecting all age groups from newborns to the elderly. It can be very painful, or can progress without any symptoms. Glaucoma is a major cause of irreversible blindness. Glaucoma is often associated with high pressure in the eyes, however a high percentage of people with glaucoma have normal or even low pressure. Ultimately, the final cause of vision loss in each type of glaucoma is an inability to get the needed nutrients to the cells of the retina and optic nerve, as well as to remove metabolic wastes and any other toxins that may be present in these tissues of the central nervous system.

Medical and surgical control of intraocular pressure are sometimes necessary and should be utilized when less invasive means of management are insufficient by themselves. Drugs and surgery appear to suppress glaucoma damage only for a limited time for each individual. Drugs and surgery do not correct or eliminate the causes of disease, which are often individual and multifactorial. Learning more about your biochemical individuality and how to be a good steward of your body are necessary in order to achieve your optimum potential for health and longevity.

As many as 15 million Americans may have glaucoma, of which 1.6 million already suffer some loss of vision, and over a quarter million are blinded by it in at least one eye. The cost is over $2.5 billion each year, mostly for medical and surgical care, including over 7 million office visits. With the aging of our population, these figures are rapidly increasing, despite the fact that 50% of glaucoma continues to go undiagnosed. Even in diagnosed cases, 70% of the vision loss occurs prior to diagnosis, despite the fact that 47% have been examined by an ophthalmologist or optometrist within one year prior to diagnosis. Loss of optic nerve fibers occurs well before any change can be detected in visual fields. With increased use of general practitioners as gate-keepers in managed care, this situation may worsen, since 78.4% of primary care practitioners falsely believe intraocular pressure (IOP) is the only diagnostic indicator of glaucoma. In truth, most people with elevated IOP, an estimated 7 million Americans, have ocular hypertension, 80% of whom never develop detectable signs of glaucoma, though they do lose 25 to 40% of the 1,200,000 nerve cells in the optic nerve. At the same time, 60% of those with glaucoma have normal or even low pressure in the eye. Glaucoma can occur at pressures as low as 12, while the optic nerve can sustain pressures as high as 24 without damage. The common category of low tension glaucoma, which can be associated with hypertension, diabetes, migraines, cold extremities and heart disease, is thought to be caused by vasoconstriction, and 30% of cases appear to show optic nerve damage from systemic causes including anemia, heart disease and hypertension. Glaucoma is actually a constellation of collagen-vascular diseases (i.e. connective tissue and blood vessel conditions related to processes like rheumatoid arthritis and atherosclerosis) which cause similar types of peripheral vision loss. The Cardiovascular Health Center at Harvard concludes that non-pharmacological approaches to cardiovascular diseases should be the first method of treatment by physicians. About 90% of glaucoma cases are of the insidious primary open angle type involving constricted blood flow and nutrition to the optic nerve with either normal (15 to 21 mm Hg) or elevated pressure (over 21 mm Hg). About 10% consist of low pressure (less than 15 mm Hg) glaucoma, which also involves decreased ocular blood flow. More rare types of glaucoma include the typically painful but periodic acute angle closure type as well as pigmentary, inflammatory and congenital glaucomas. Together, the glaucomas represent the second greatest cause of blindness in America, with 70,000 affected to the point of blindness. What these conditions have in common is not elevated intraocular pressure (IOP), but morphological changes in the collagen structure of the lamina cribrosa (the part of the sclera or white connective tissue layer of the eye through which the optic nerve passes), the papillary blood vessels (which provide nutrition to the papilla, or optic nerve head, where it passes through the lamina cribrosa), and the trabecular meshwork (the filter through which the eye fluid, or aqueous humor, passes to reach Schlemm’s canal, the drainage channel which removes fluid from the eye and delivers it back into the blood vessels). , , , Even in glaucoma cases where pressure does become elevated, causing further risk of damaging the optic nerve fibers (axons), these connective tissue changes precede the changes in IOP. In most cases of glaucoma, vision loss occurs with these micro-structural changes even without an increase in IOP. Glaucoma may be an extension of myopia (nearsightedness, involving stretching of the sclera), which occurs when the elastic limit of the sclera is exceeded by the intraocular pressure, thus causing expansion at the optic nerve (a change in shape called "cupping") with resulting loss of vascular flow and neuronal function. Both glaucoma and myopia are associated with other collagen disorders, including Ehlers-Danlos syndrome, Marfan’s syndrome, and osteogenesis imperfecta.

One study of the systemic health of glaucoma patients found that 30% had low tension glaucoma, 42% had high tension glaucoma and 28% had identifiable systemic causes including anemia, carotid obstruction, syphilis and intracranial tumor.

Large diurnal fluctuations in IOP during the day or over consecutive days, such as those associated with food sensitivities and allergies, are associated with an increased risk of for glaucoma progression over and above more traditional risk factors such as age, race and sex.

Asrani S, Zeimer R, Wilensky J, et al. Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma. 2000;9:134-42.

Diurnal pressures of normal subjects vary by only 3.7 mm Hg, while medically treated glaucoma patients still show 7.6 mm Hg variation compared to untreated patients with 11 mm Hg variation.

Drance SM. Diurnal variation of intraocular pressure in treated glaucoma: significance in patients with chronic simple glaucoma. Arch Ophth. 1963;70:302-11. Drance SM. The significance of diurnal tension variation in normal and glaucomatous eyes. Arch Ophth. 1960;64:494-501.

The Advanced Glaucoma Intervention Study found that patients whose pressure was 18 mm Hg or lower at every visit over 6 years had almost no progressive visual field loss.

The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol 2000;130(4):429-40.

In a more recent study, medical patients with a low daily IOP variance as well as low minimum and maximum IOP had the lowest probability of developing a new visual field defect over a 5-year period. Subjects treated with Travatan (PGF 2 derivative) had the lowest average IOP and the lowest variance as compared with the other treatment groups.

Nordmann JP, LePen C, Berdeaux G. Estimating the long-term visual field consequences of average daily intraocular pressure and variance. Clin Drug Invest 23(7):431-438. 2003.

Regulating intra-cellular communication via prostaglandins has demonstrated superior diurnal IOP control over all other glaucoma medications. Coleus forskohlii also regulates intra-cellular communication via c-AMP which mediates most of the effects of prostaglandin PGE 2 (see chart).

PG Endogenous Physiologic Signaling
Receptor Eicosanoid Actions Pathway

DP PGD 2 PGD 2 Increased Ca++ via PLC stimulation
EP 1 PGE 2 PGE 2 Increased Ca++ via PLC stimulation
EP 2 PGE 2 PGE 2 Increased cAMP via AC stimulation
EP 3 PGE 2 PGE 2 Decreased cAMP via AC inhibition
EP 4 PGE 2 PGE 2 Increased cAMP via AC stimulation
FP PGF 2 PGF 2 Increased Ca++ via PLC stimulation
IP PGI 2 PGI 2 Increased Ca++ via PLC stimulation
TP TxA 2 TxA 2 Increased Ca++ via PLC stimulation

Eicosanoid Precursors Analogs Local

PGD 3 Omega-3: EPA, DHA - Lower IOP without
and plant precursors inflammatory effects
PGE 2 Arachidonic acid latanoprost (Xalatan), Stimulates hyperalgesic
(high in modern diet) travoprost (Travatan), response (sensitize to pain)
bimatoprost (Lumigan) Lowers IOP
and unoprostone Promotes inflammation
isopropyl (Rescula)

PGE 3 Omega-3: EPA, DHA - Lower IOP without
and plant precursors inflammatory effects
PGF 2 - Forskolin Lower IOP
(Coleus forskohlii) Inhibits inflammation

Most anti-inflammatory drug therapies try to block pro-inflammatory physiological pathways. Prednisone, which can cause glaucoma, is used in high doses to block the liberation of arachidonic acid, the precursor of the pro-inflammatory prostaglandins. This can often be more safely acheived with supplementation of the safer steroids DHEA (or 7-Keto) or its precursor pregnenolone, as well as immune-modulating plant-analog phytosterols. Drugs that inhibit prostaglandin synthesis by blocking enzymes that convert arachidonic acid to prostaglandins include aspirin, NSAIDs and acetaminophen. In contrast, EPA provides a substrate for the anti-aggregatory, anti-inflammatory and vasodilating prostaglandin -3 series. Other effective alternatives for relief of pain and inflammation include a highly absorbable water soluble quercetin (Pain Guard forte').

Studies on omega-3 fatty acid metabolism show:

PGE3 and PGD3 lowered intraocular pressure without causing ocular inflammation in rabbit

some surveys demonstrated that in Greenland Eskimos whose marine diet is enriched with omega-3 substrate eicosapentaenoic acid, have a lower incidence of open-angle glaucoma as compared to Caucasians, whose diet is rich in arachidonic acid.

The anterior uvea synthesizes PGE3 and PGD3 in human, monkey, and rabbit and may play a role in lowering intraocular pressure.

Cyclooxygenase and lipoxygenase pathways in anterior uvea and conjunctiva.
Kulkarni PS, Srinivasan BD. Kentucky Lions Eye Research Institute School of Medicine, University of Louisville 40202. Prog Clin Biol Res 1989;312:39-52.

Lewith, G., Kenyon, J., Lewis, P. Complementary Medicine: An Integrated Approach 1996, pp. 108-9. New York: Oxford University Press.

Plant sources such as flax seed, hemp seed, chia seed, and walnut provide the precursor Omega-3 fatty acid: Alpha-linolenic acid that the human body converts, though inefficiently, to the longer chain EPA and DHA fatty acids needed for anti-inflammatory prostaglandin formation, neuro-visual development and performance (e.g. DHA for visual acuity) and other cellular needs. Soy and rape seed (Canola from Canadian Oil Company) also contain ALA but are not recommended as sources by Remission Foundation. DHA is the #1 fatty acid in the central nervous system. Fish oils contain the Omega-3 fatty acids in their physiologically active EPA and DHA forms for health benefits as immediate PG3 prostaglandin precursors, saving the time and energy of the inefficient enzymatic steps necessary to process Alpha-linolenic acid into the biologically active forms. In many health situations, these enzyme pathways limit the amount of eicosanoids the body can produce to much less than the levels requisite for optimal health and performance. Nutrients required for the anti-inflammatory EFA pathways to function include:

essential fatty acids (omega-3 and omega-6, in balance)
pyroxidine (vitamin B6) or its active form P5P
niacin (vitamin B3)
ascorbic acid (vitamin C)

Enzymes: delta-6-desaturase, delta-5-desaturase, elongase, cyclo-oxygenase and oxygenase convert alpha-linolenic acid into the beneficial, anti-inflammatory PGE3 series prostaglandins (see chart).

Omega-3 Pathway:
Substrate + Enzyme + Cofactors = Product

Omega-3: delta-6 desaturase B6, Mg, Zn Stearidonic Acid
Alpha-linolenic Acid

Stearidonic Acid elongase - Eicosatetraenoic Acid

Eicosatetraenoic Acid delta-5-desaturase B3, C, Zn Eicosapentaenoic Acid

Eicosapentaenoic Acid cyclo-oxygenase  blocked by COX PGE-3
(EPA) (COX) inhibiting drugs

Eicosapentaenoic Acid Lipoxygenase pathway promoted less inflammatory
(EPA) by COX inhibiting Leukotrienes

Omega-6 Pathway:

Substrate + Enzyme + Cofactors = Product

Linoleic Acid (LA) delta-6-desaturase B6, Mg, Zn Gamma Linolenic Acid

Gamma Linolenic Acid elongase - Dihomogamma Linolenic
(GLA) Acid (DGLA)

Dihomogamma Linolenic delta-5-desaturase B3, C, Zn preferred pathway to
Acid (DGLA) (prefers Omega-3 anti-inflammatory
oils) Series 1 Prostaglandins:
PGE1, or with Omega-3
deficiency: Arachidonic
Acid (AA)

Arachidonic Acid (AA) cyclo-oxygenase blocked by inflammatory Series 2
(COX) COX inhibiting Prostaglandins

Several investigators have demonstrated that PGE 2 and PGF 2 alpha in low doses, lower intraocular pressure in all species studied, including human, but while PGF 2 promotes inflammation that could aggravate glaucoma, PGE 2 has anti-inflammatory effects.

PGF 2 derivatives are used to medically lower IOP by affecting the FP receptor. These include latanoprost (Xalatan), travoprost (Travatan), bimatoprost (Lumigan) and unoprostone isopropyl (Rescula). Forskolin (Colforsin) works on the complementary IOP-lowering but anti-inflammatory PGE 2 pathway via the c-AMP-mediated EP 2, EP 3 and EP 4 receptors.

A rational beginning approach to glaucoma prevention therapy is to monitor IOP regularly at several times of day using the home eye pressure monitor while following a rotation diet to identify and eliminate food triggers of IOP elevation spikes and supplementing with oral Forskolin, Omega-3 fatty acids: EPA & DHA plus other IOP regulating (e.g. Melatonin at night for morning pressure spikes) and neuroprotective supplements, especially L-Carnosine, as indicated clinically and/or by resonance matching using energetic biofeedback. Drinking microwater and rebounding are also central to a balanced anti-glaucoma lifestyle. The target IOP is a daily maximum of 15 to 18 with a diurnal variability of up to 3 mm Hg.

In the same embryonic tissue layer as the connective tissue is the circulatory system. Circulation, both lymphatic and vascular, seems to be a real key to understanding and preventing glaucoma. When looking at circulatory patterns among glaucoma patients, two types of problems emerge. In one group, there is vasoconstriction, causing symptoms like cold hands. In the second distinct group, the problems relate to blood clotting, resulting in symtoms like electrocardiogram (ECG) abnormalities. The risk factors that affect glaucoma are generally those associated with vascular problems, including hypertension, hypotension, migraine, increased blood viscosity, carotid artery stenosis, heart disease, and even a familial tendency, which is true of vascular disease in general. Vascular abnormalities have been confirmed in every type of glaucoma via Doppler ultrasound. Optic disc hemorrhages are commonly seen several years before glaucoma is diagnosed, and they undoubtedly occur but go undetected in many additional cases. Dilated and tortuous retinal blood vessels are also frequently seen in the retina, and these have been linked to coronary artery disease.

Loss of optic nerve fibers is directly related to decreased pumping ability of the heart. Severe loss of visual fields are seen in 42% of glaucoma patients, but 70% of those with atrial fibrillation have severe losses. Atrial fibrillation is also twice as likely among glaucoma patients as compared to normals. Decreased blood flow to the eyes causes structural changes over time that result in increased IOP. Glaucoma patients have narrowed retinal blood vessels compared to normals. Thermography, such as used in the new field of Ophthermology, shows that 89% of glaucoma patients have cerebral vascular disease! Computed tomography (CT) has shown that 90.3% of low tension glaucoma patients have calcification of the carotid artery near the openning of the optic canal, as compared to only 20.8% of individuals the same age, but without glaucoma. Magnetic resonance imaging (MRI) shows deep white matter lesions in the brain in low tension glaucoma patients, another effect of reduced cranial blood flow. Low tension glaucoma is also associated with peripheral and central vasoconstriction (e.g. migraine) and spontaneous blood clots. Blood clot formation is more common in glaucoma patients compared to those with ocular hypertension, and low tension glaucoma patients show higher blood viscosity than those with high tension glaucoma. Blood flow measurements taken in the fingers of low tension glaucoma patients shows rates significantly below normal. 44% of low tension glaucoma patients suffer classic migraine symptoms and in elderly sufferers of low-pressure glaucoma this figure can be as high as 86%. Silent heart attacks (myocardial ischemia) is found in 3% of ‘normal’ adults, but one study found 30.8% in low tension glaucoma patients in a 24 hour period, which was double the rate found in both normal subjects and chronic open angle glaucoma. Stenosis of the carotid artery can be an underlying cause of symptoms diagnosible as glaucoma, and restoring carotid blood flow can temporarily increase and then normalize IOP. Increased blood viscosity (hematocrit above 50) is often found in glaucoma patients. This can impair blood flow when combined with elevated IOP.

Drugs and Surgery

Medical and surgical treatments are actually aimed at lowering IOP rather than improving the underlying collagen metabolism. Among individuals with ocular hypertension (elevated IOP), only those who also show cupping appear to be at risk for visual field loss. Reversal of cupping changes is sometimes seen with filtering “bleb” surgery, but has not been shown with medical treatments. According to an extensive review of the medical literature, a 30% reduction in IOP is needed to reverse cupping, and this is why the IOP reduction from most medications is not clinically significant in changing the rate of progression of vision loss in glaucoma. Beta blocker eye drops can reduce IOP somewhat (6 mm Hg, preventing further loss of peripheral vision for 3 to 6 years), but do not improve blood flow to the eyes. Medical treatment even fails to control IOP in most cases (53%) of glaucoma within just 4 years. Laser surgery fails to control IOP in 23% the first year and 70% after just 10 years. Over 50% have to take drugs treatments in addition after just 2 years. Glaucoma itself increases the risk of cataracts by 2.9 times, but when surgery is added, this jumps to 14.3 times increased risk.

Side effects of glaucoma drugs are a real problem, causing up to 62% to fail to follow the recommended treatment. Beta blocker drops commonly cause side effects including: low blood pressure, confusion, depression, dizziness, headache, impotence, hair loss, skin and nail changes, diarrhea, nausea, asthma, breathing difficulty, and increased LDL cholesterol. On average, glaucoma patients ‘forget’ to take their medication on 112 days each year. Patient surveys show that 30% experience side effects like changes in heart rhythm, congestive heart failure, and difficulty breathing. Hundreds actually die each year from respiratory problems caused by glaucoma drugs. One study also shows that 80% of glaucoma patients on beta blocker drugs experience depression, compared to only 26% of patients with serious eye problems who do not take these drugs. Beta blocker eye drops used for glaucoma have other serious implications for body chemistry. Timoptic, for example, reduces ‘good’ HDL cholesterol, while increasing ‘bad’ LDL cholesterol, enough to increase the risk of heart attack by 17%. Since heart attacks cause about half of all deaths in this country, this increased risk represents a major problem. When beta blockers fail to control IOP, treatment with other drugs with even worse side effects may be considered, such as carbonic anhydrase inhibitors (e.g. acetazolamide), which, although they can increase blood flow to the retina, cause kidney problems, fatigue, lethargy, anorexia, weight loss, depression, dementia, loss of libido, and occasionally aplastic anemia. Drug treatment decisions are often based on visual field tests which accurately show the progression of the disease only 43% of the time.

Many types of medical therapy can actually cause glaucoma. Corticosteroids in the form of eye drops, creams, pills, inhalers and injections are a common trigger, since these drugs polymerize molecules in the drainage system of the eye, while inhibiting the formation and repair of collagen and glycosaminoglycans necessary for maitaining normal structure and function of both the eye’s lamina cribrosa and the trabecular meshwork. Steroidal eye drops, for example, increase glaucoma risk seven-fold. There is no safe level of corticosteroid use and even stopping or changing medication once IOP elevation occurs does not always solve the problem, since up to a third of these cases of induced glaucoma are irreversible with standard medical/surgical treatment leaving permanent damage to the optic nerve. Even creams for eczema and inhalers (with over 8 million annual prescriptions in America alone) can cause increased IOP. Corticosteroids increase oxidative stress which impairs the phagocytic (debris clearing) ability of cells in the eye’s drainage system.

Many over-the-counter drugs can trigger acute attacks of glaucoma in susceptible individuals. Optic nerve atrophy can be caused by drugs that chelate metal ions like zinc (e.g. diodohydroxyquin, iodochlorhydroxyquin and ethambutol) and zinc supplementation has been recommended preventively for all patients on such medications. Optic nerve toxicity is also known to occur with aspirin, ibuprofen, tranquilizers, antidepressants (e.g. lithium, MAO inhibitors), antibiotics (e.g. chloramphenicol, isoniazide, ethambutol), and medications for diabetes. Visual defects caused by this kind of toxicity are usually attributed to other causes, such as glaucoma. Even the preservatives used in many eye drops, including most glaucoma medications, may trigger chronic inflammation of the eye that can worsen glaucoma. Benzalkonium chloride used to preserve Timoptic, Betoptic, Optipranolol, and Ocupress anti-glaucoma drops increases dry eye symptoms by 250%. Merck manufactures an unpreserved beta blocker eye drop called OcuDose. While unpreserved ‘artificial tear’ eye drops used for temporary eye lubrication reduce the permeability of the corneal surface of the eye by 44%, those preserved with benzalkonium chloride actually increase this leakiness by 8%, disrupting the epithelial cell membrane that protects the integrity of the eye. The concentrations used, from .4 to 1 part per thousand (equivalent to a 3X homeopathic potency) are toxic to the cornea and, through accumulation in body tissues over time, have even been documented cause such severe corneal toxicity as to require a corneal transplant. Preservatives such as benzalkonium chloride and thimerisol used in contact lens solutions can also accummulate to toxic levels within soft contact lenses themselves, thus exposing the cornea whenever wearing the lens. The chronic inflammation and allergy responses triggered by such toxic chemicals can result in the deposition of inflammatory proteins in the drainage system of the eye, thus increasing IOP and contributing to the risk for glaucoma. Inflammation in the eye area may also reduce the quality of blood and lymph drainage from the eye, which can also impair outflow of fluid from inside the eye. It also increases free radical activity, which is probably the ultimate cause of damage to nerve cells in glaucoma.

Glaucoma is not only associated with hypertension, but also with hypotension. Anti-hypertensive medications may compound this problem, often triggering low blood pressures during sleep. This may deprive the optic nerve head of needed oxygen, resulting in loss of visual fields. Cardiac events also double at diastolic pressures of 75 comparted to 85 mm Hg. At systolic pressures below 140 mm Hg, glaucoma patients show 4 times the rate of visual field deterioration. Most glaucoma patients who progressively lose vision have blood platelets that tend to clump together spontaneously.

Many drugs can also precipitate an angle closure glaucoma attack. These include motion sickness patches, and antihistamines.

Other Risk Factors

The most significant controllable risk factors according to one report are untreated hypertension and cigarette smoking. Other major risk factors include free radical damage associated with aging, reduced health, hypotension, lack of exercise, poor nutrition, diabetes and other vascular diseases, as well as allergies and digestive problems. Other toxins that damage the optic nerve may be contributing factors in the loss of vision among glaucoma sufferers. These include tobacco, aspartame, methyl alcohol, factors present in blood transfusion tea, coffee, and alcohol.

Coffee may increase cholesterol, resulting in reduced circulation to eye tissues, unless it is passed through a paper filter before consumption. While caffeine does not increase IOP, it does promote vasospasms which can contribute to glaucomatous vision loss. It can also destabilize blood sugar, which is detrimental to nerve cell health. Coffee also impairs B12 absorption and destroys beneficial bacterial flora.

While some studies have found little relationship between smoking and glaucoma, one study showed a 2.9 times increased risk! Smoking constricts the internal lumen diameter of blood vessels and blocks the ability of vessels to redilate. After smoking a cigarette, vasoconstriction causes IOP to increase by more than 5 mm Hg in 37% of glaucoma patients and 11% of normals. Tobacco by itself can cause vision loss (tobacco amblyopia) as can alcohol (alcohol amblyopia), and can also contribute to nutritional deficiencies related to vision loss, by interfering with gastric production of hydrochloric acid and therefore preventing effective digestion and assimilation of many nutrients including vitamin B12. In some cases, supplemental vitamin B12 has reversed vision loss even despite continued smoking. Nicotine reduces retinal blood flow by 9.6 to 16.4% in diabetics who are at high risk for glaucoma as well as diabetic retinopathy. It is recommended that anyone who uses alcohol or tobacco should supplement at least 1500 to 3000 micrograms of vitamin B12, glutathione precursors such as cysteine and 600 I.U. of vitamin E to counteract the toxic effects of cyanide in the optic nerve as well as 1000 micrograms of folic acid. Folic acid has also been shown to improve visual acuity in smokers with optic neuropathy, with an average increase of 5 lines of visual acuity over a 2 month period! Supplementation of 300 milligrams of vitamin B1 weekly for 3 months by intramuscular injection (together with 1,000 micrograms of B12) has also been recommended for tobacco amblyopia.

Nicotine, LDL cholesterol and free radicals block acetylcholine receptors, increasing the tendency toward vasospasm. By lowering harmful LDL cholesterol levels (e.g. with GTF chromium, garlic, vitamin C, onions, almonds, olive oil, fish oil, grape seed oil, and avocado) and taking antioxidants (including vitamin E and coenzyme Q10), vasomotor relaxation to acetylcholine has been improved, with measurable increases in coronary artery diameter. This may also improve the ability of blood vessels to dilate in response to seratonin and aggregating platelets. , Cigarette smoking is one of the major risk factors for glaucoma, along with hypertension (especially systolic), obesity and the amount of pigmentation in the iris. Blacks, having the greatest amount of pigmentation, have four times the risk of glaucoma and 8 times the risk of blindness from glaucoma compared to whites.

Familial patterns are often strong, as well, in all races, with relatives of a glaucoma victim 20 times more likely to get glaucoma themselves. This can be from hard-wired genetic patterns as well as from miasmatic inheritance which can eventually be removed through homeopathy. Environmental factors are also very important, and have been found to play a strong role in exfoliation of the lens which can cause ocular hypertension and triples the risk of glaucoma. Such environmental effects are probably mediated via free radical pathology.

Obesity affects one out of three adults, the average weight having increased by 8 pounds between 1980 and 1991 to an average of 25 (female) to 30 pounds (male) overweight. Obesity increases blood pressure and secretion of adrenal hormones. In Japan, with the highest longevity in the world, overweight is not the norm, and IOP actually tends to decrease with age, the opposite of what is seen in America. In America, 8% of people over age 40 have increased IOP, and the rate of glaucoma climbs from 0.25% at age 20 to 1% at age 40 to 7% at age 70.

Lack of oxygen to the tissues in the eye can trigger neovascularization, which in turn can cause glaucoma. Antiangioneogenesis factors present in shark and bovine cartilage may be beneficial in controlling or modulating this type of response. Oxygen therapies may also be helpful, along with antioxidants and modalities to increase ocular blood flow, such as ginkgo.

Release of histamine and other pro-inflammatory substances seems to be a significant factor especially in low-tension glaucoma. 30% of low-tension glaucoma patients have immune-related problems, compared to only 8% of those with ocular hypertension.

Laser treatments seem to be even less successful in glaucoma than are drugs. Laser may be most effective when used before any drug therapy is started, but most who have laser first still need drug treatment within 2 years. Surgery on the other hand is capable of increasing blood flow to the eye by 29%, but only in those who have not already started drug treatments. Surgery appears to have more potential benefits than conventional drug therapy in at least temporarily slowing the damage caused by glaucoma 3 to 6 times more effectively than laser or drugs, although not universally, nor without significant risks. Surgery is not effective at slowing the progression of glaucoma in the majority of cases represented by low pressure glaucoma. Also, 15% of glaucoma surgery patients report a reduced quality of life following surgery, and 40% find no perceptible improvement. Surgery also needs to be repeated in many cases. Surgery of any kind is by definition controlled damage to the body, and such an invasive approach should be reserved whenever time permits until non-invasive methods have been exhausted. This follows the physician’s oath “Primum non nocere,” to above all do no harm.

The actual damage to nerve cells in the optic nerve, resulting in loss of vision, appears to be associated with hemorrhages of the blood vessels in the optic nerve head and related loss of cellular nutrition combined with free radical activity. Similar damage to the cells of the optic nerve is now known to occur during migraine headaches, when blood vessels constrict the flow of oxygen and other nutrients to the cells. The risk of developing measurable damage to the optic nerve goes up with increased IOP levels, from 15% at 24 mm Hg to 90% at 30 mm Hg, and nearly 100% at 33 mm Hg. Patients with healthy optic nerves and no peripheral vision loss can sustain pressures of 30 for up to 20 years without losing sight. Unfortunately, approximately 50% of the nerve cells in the optic nerve are lost before glaucomatous changes in the visual fields can be detected in an eye examination. This loss of nerve cells happens 2 to 6 years before changes show up on peripheral vision tests. Intervention in the presence of ocular hypertension and other risk factors has been shown to reduce the loss of peripheral vision and optic nerve health. Prevention, and especially non-toxic preventive approaches to therapy are critically important for anyone at risk, as well as those already showing damage. At best, conventional medical and surgical interventions attempt to check the advance of this progressive degenerative condition, but in many cases, blindness still is the final result. The following complementary modalities should not be overlooked by the doctor and patient seeking the best long term outcome.

Water & Biological Terrain

In most cases, glaucoma is a chronic degenerative condition, resulting from Phase 1 conditions in the brain, eye and optic nerve area. This is also the terrain for viral conditions, and an association is seen with 28% of patients who have herpes eye infections experiencing secondary glaucoma. Phase 1 terrain is excessively oxidized, resulting in oxidation of circulating LDL cholesterol which deposits and hardens on the inner lining of the blood vessels, impairing their ability to dilate normally, thus restricting circulation. The retina of the eye has the highest oxygen demand of any tissue in the body, with local hypoxia or ischemia in the nerve fibers of the retina and optic nerve leading to further free radical activity. Lipid peroxidation can be especially destructive in the optic nerve area with its myelinated nerve fibers containing a high concentration of fatty acids which can produce a chain reaction of reactive oxygen species. It is also known that lipid peroxidation occurs in the degeneration of cells in the anterior chamber angle that drains the fluid from the eye.

Phase 1 terrain is also characterized by excessive alkalinity in the veinous blood. This is primarily due to a blocked and inefficient cellular energy metabolism, resulting in lack of acid metabolic wastes such as carbonic acid. Steroid eye drops, for example, induce a Phase 1 terrain in the eye. It has been shown that they alkalize the aqueous humor in proportion to the rise in IOP, while at the same time depleting antioxidant defences. Vitamin C levels fall by 50 to 80% throughout the eye. Thus circulation, oxygenation and cellular respiration in addition to antioxidant protection (especially the fat soluble antioxidants) are critical components to provide the physiological system if it is to mount a successful remission from this Phase 1 terrain.

Drinking alot of fluids all at once can temporarily raise IOP as much as 30%. This does not mean glaucoma patients should drink less water. Drinking 8 ounces per hour, or better yet, about 4 ounces of good water every half hour on the other hand, increases lymph flow and detoxification. Hypertension and ocular hypertension are linked, and both may be significantly related to chronic dehydration. Chronic dehydration, resulting in increased blood viscosity, can be caused by diuretics, or simply the Standard American Diet (SAD) which includes more soda than water. Increased IOP has also been associated with constipation, which is closely linked to fluid metabolism. After about 3 days of regular consumption of water, the kidneys are able to readapt and increase the efficiency of their filtration of the blood as well. The best water is that which is filtered to remove unwanted chemicals, such as heavy metals, chlorine, fluoride and pesticide residues, and then ionized. Bio-electronics of Vincent (BEV) quality filtration can be achieved by a multi-stage filter system incorporating reverse osmosis with other water purification technologies. Ionization by electrolysis imparts a negative charge which provides the most effective biocompatible anti-oxidant known. It also restructures the water, reducing the average molecular cluster size from about 16 to about 8 water molecules according to NMR studies, resulting in a 10-fold increase in penetration into the lymphatic system and even the intracellular spaces. This water, a better solvent than tap water, increases nutrient absorption and utilization, while also enhancing elimination of metabolic wastes and other toxins from tissue stores. The alkaline-reduced water that is used for drinking and cooking accelerates the body’s healing process which initially involves the re-establishment of efficient mitochondrial aerobic metabolism followed by the shift from Phase 1 to Phase 2 terrain. This water releases oxygen specifically to those tissues which are eliminating toxins, including the toxins which are released in unblocking mitochondrial electron transport chain enzymes.

(see also: Feldman RM, Steinmann WC, Spaeth GL et al: Effects of altered daily fluid intake on intraocular pressure in glaucoma patients. Glaucoma 1987;9:118-121.)

Osmotic agents like vitamin C, glycerine and salt decrease IOP by pulling fluid from the eyes. They also increase biological energy (measured in microwatts) in the blood, shifting terrain away from Phase 1 which is the low energy zone where glaucoma is most prevalent.

High body temperature, characteristic of Phase 2 terrain (e.g. associated with bacterial infection, healing crisis and spontaneous remission), is related to a temporary increase in IOP. This can, however, if not suppressed by anti-biotics or anti-pyretics like aspirin, lead to resolution of the internal causes of the problem, followed by remission from the disease. If there is damage to the myelin sheath of the optic nerve fibers, as in MS, increased body temperature from exercise or a hot bath can temporarily worsen visual fields.

Complementary medicine is used by many glaucoma patients. (Rhee DJ, Spaeth GL, Terebuh A, Myers JS, Augsburger JJ, Shatz L, Ritner JA, Katz LJ. Prevalence of the use of complementary & alternative medicine (CAM) for glaucoma. Ophthalmology 2002;109:438-443.)

Author's Bio: 

Dr. Glen was a 25 year old interning eye doctor at the world's largest outpatient vision clinic in New York City, and president of the American Optometric Student Association, representing over 4000 student doctors of optometry world-wide when he learned that he had glaucoma. Knowing that the best medical and surgical treatment would likely leave him blind before age 50, he embarked on his continuing investigation of alternative, complementary, and integrative medical approaches to the treatment, prevention and rehabilitation of glaucoma and other eye and vision conditions. 30 years later, he continues to maintain his vision without suppressive eye drops or invasive eye surgery.