Glaucoma: Underlying Factors; Part 2 of a 3-Part Series


Glaucoma: Underlying Factors; Part 2 of a 3-Part Series

In part I the failure of conventional glaucoma therapy was presented. In section II the epidemiological and etiological factors involved in glaucoma are discussed. These factors must be understood for health care practitioners to gain an understanding of how to utilize non-pharmacologic treatment to arrest vision loss caused by glaucoma.

Sir Stewart Duke-Elder made the profound statement that the etiology of chronic open-angle glaucoma would be found elsewhere than the eye, as the eye itself had been subjected to exhaustive studies.

Annals of Ophthalmology, July 1979

Types of Glaucoma

The terminology surrounding glaucoma is quite confusing. There are many types and combinations of glaucoma. Here are the most common:

Common (open-angle) glaucoma, is the prevalent garden variety of glaucoma that comprises better than 70% of all cases. In this form of glaucoma the fluid drain inside the eyes does not appear to be physically blocked yet the pressure is elevated. The entire spectrum of vascular diseases, hypertension, diabetes and heart disease, as well as smoking and excessive alcohol consumption, increase the risk of this form of glaucoma.
Angle-closure glaucoma can occur when the fluid drain becomes blocked. Sudden closure of the drain may result in pain. This can occur when the lens of the eye bulges forward from behind the iris or if it shifts forward, or when the iris pigment layer is so thick that it occludes the drain when the pupil dilates. A variety of this form of glaucoma is when the pupil becomes blocked, i.e. the iris sticks to the front of the crystalline lens impeding the flow of aqueous. Narrow-angle glaucoma is another term for this variety of glaucoma. Patients with small eyes are more prone to this type of glaucoma.
Angle-closure glaucoma is rare in most populations below age 40. Eskimos are known to have smaller eyes, thus more crowded or narrow fluid drains, and consequently exhibit a much higher incidence of angle-closure glaucoma than Caucasians. The rate of angle-closure glaucoma among Eskimos ranges from 2-8% compared to only 0.1% among Caucasians, a 20-80 times difference. Caucasians with anatomically narrow eye fluid drains incur attacks of angle-closure glaucoma at the rate of 7-10% to as high as 37%.( 1)

3. Low-pressure glaucoma: eye fluid pressure is normal or below normal but the patient experiences loss of side vision. This is now believed to be caused by vasoconstriction.
4. Ocular hypertension: eye fluid pressure is elevated but there are no other apparent signs of glaucoma (cupping of the optic disc, narrow drainage canals, loss of visual field). Ocular hypertension is estimated to affect over 7 million Americans.
5. Steroid-induced glaucoma: steroids polymerize the molecules in the drain which results in swelling of the meshwork which impedes normal drainage.
6. Pigmentary glaucoma: iris pigment flakes off the back of the iris and clogs the drain. This variety of glaucoma was first reported in 1949 and may be induced by physical exercise.( 2)
7. Pseudoexfoliative glaucoma: particles flake off the lens of the eye and are trapped in the drain, resulting in a rise in fluid pressure.
8. Allergic glaucoma: release of histamine clogs the drain.
9. Optic nerve disease secondary to toxins (tobacco, aspartame), malnutrition, pernicious anemia, malabsorption.
10. Glaucoma secondary to inflammation: inflammation can be caused as a result of viral infections or other inflammatory conditions; 28% of patients with herpes eye infections experience secondary glaucoma.( 3)

Epidemiological studies indicate black race (increased iris pigment), vascular hypertension and current cigarette smoking are the major risk factors for glaucoma.( 4) The risk of blindness resulting from glaucoma is eight times greater among blacks than whites.( 5) Family history is another factor that greatly increases the chance of developing glaucoma.

Intraocular pressure has not been found to be a predictable factor in the loss of peripheral vision due to optic nerve damage. Loss of vision has been reported with eye fluid pressure as low as 12-14 mm Hg while pressure as high as 23-24 mm Hg do not result in apparent signs of visual field loss.( 6)

The common form of glaucoma is exceptionally low among Alaskan Eskimos (0.06%) compared to a high among a black population on the Island of St. Lucia (8.8%).( 7)

Numerous studies point to obesity and systolic blood pressure as factors that influence eye fluid pressure. Obesity should be given more attention in the etiology of glaucoma since one in three American adults are overweight. The average body weight of Americans jumped by 8 pounds between 1980 and 1991. In the U.S. the typical five-foot-4-inch woman is 25 pounds overweight and the typical 5-foot-10-inch man is 30 pounds overweight.( 8)

In Europe and the United States nearly 10% of the elderly have ocular hypertension, yet in Japan the intraocular pressure decreases with advancing age. Yoshihiko Shiose of Japan, in a landmark review paper outlining the causes of glaucoma, noted that Japanese men who remain lean do not exhibit an age-related increase in eye fluid pressure as do American and European males. If a man was young, thin and hypotensive and became old, obese and hypertensive, then the odds are that his eye fluid pressure would rise. Shiose notes that the eye produces less aqueous fluid with advancing age and there should be a progressive drop in pressure, but because of obesity and hypertension, this is not seen in American and European populations.( 9) One study of Africans shows that those who remained in primitive tribal areas and ate more raw foods had lower blood pressure than their genetic-family tribesmen who had relocated to urban areas and had changed to a Western diet.( 10) Thus the common for m of glaucoma may have its origins in the diet.

Factors That Influence Eye Pressure

Eye fluid pressure that displaces 1518 mm of mercury (Hg) in a glass column is considered to be normal, while pressure of 21-22 mm Hg is generally considered to be the upper limit of normal.

There are so many factors that influence eye fluid tension that pressure readings in the doctor's office have to be seriously questioned for their validity. The normal daytime intraocular pressure may vary as much as 9 mm Hg. Here are some of the factors that influence intraocular pressure:

Time of day: pressure peaks in the morning. Unless eye exams are checked at the same time of day they are of dubious value. Daytime fluctuation of intraocular pressure varies from 5.0-6.8mm Hg.( 11) One study shows the intraocular pressure peaks shortly after waking and thus abnormally high morning pressure readings would disappear before the patient could be examined in the doctor's office.( 12) The rate of aqueous flow is 3.1 microliters per minute during the day and 1.5 microliters per minute during sleep (a 50% reduction).( 13) The common form of glaucoma has been characterized as a daytime disease. The intraocular pressure is believed to be regulated by the pineal hormone melatonin during sleep and night hours,( 14) however melatonin given as an oral supplement during the day has no effect on the rate of aqueous flow.( 15) Daytime intraocular pressure appears to be governed by the adrenal hormones. Other hormones (prostaglandin, estrogen, thyroxine) may also play a role in al tering intraocular pressure.( 16)
Fluid intake: excessive intake of fluids can increase eye fluid pressure by as much as 30%.( 17)
Gaze position: just shifting the gaze of the eyes toward the nasal or temporal view increases the intraocular pressure by about 2-3 mm Hg.( 18)
Dilatation of the pupil increases intraocular pressure.
Physical exercise decreases intraocular pressure.
A salt-loading diet decreases intraocular pressure.
High body temperature increases intraocular pressure.( 19)
Emotions are known to control fluid pressure within the eyes.
There is a seasonal variation in eye fluid pressure, being low in summer and high in winter.( 20)
Eye fluid pressure rises when the body is inverted. Fluid pressure rises in the eyes of individuals who practice yoga when they are in a body-above-head position.( 21) An inverted position causes the fluid pressure to rise above 30 mm Hg among normal individuals and even greater in glaucomatous eyes.( 22, 23)
What Is The Prevailing Cause Of Common Glaucoma?

The myriads of volumes of information concerning the causes of glaucoma, and sometimes conflicting data, can cause investigators to easily become sidetracked from identifying the major controllable factors in this disease. In order to develop new directions for the treatment of glaucoma it is important to understand where the weight of scientific evidence points in controlling, eradicating and preventing glaucoma.

In an attempt to classify the major forms of common (open-angle) glaucoma, researchers analyzed finger blood-flow measurements, blood coagulation and visual field tests. They were able to divide glaucoma sufferers into two distinct principal components. One group of patients showed a strong relationship between their visual field deficits and evidence of vasoconstriction (cold hands = shrinkage of the visual field), while the other population of glaucoma patients showed blood clotting and electrocardiogram irregularities as evidence for cardiovascular disease. This classification of glaucoma subjects defies the traditional division into high and low pressure glaucoma.( 24) Defining glaucoma by fluid pressure has sidetracked successful treatment of this disease.

The predominant feature of glaucoma is vascular disease, as evidenced by the fact that all of the primary risk factors are vascular-related: vascular hypertension and hypertension, migraines, increased blood viscosity, carotid artery stenosis and heart disease. Family history is a factor for glaucoma and all vascular diseases, for that matter. Furthermore, the fact that exercise reduces glaucoma pressure and that Doppler ultrasound confirms vascular abnormalities in all forms of glaucoma, is additional evidence for the vascular theory of this disease. D.T. Sugiyama and colleagues have stated that "glaucoma should not be viewed exclusively as a disease of the eye, rather it should be viewed as an expression of the state of health of the body in general. In the same manner that intraocular pressure is considered a risk factor, not the cause of glaucoma, vascular entities must also be considered."( 25)

Here is some of the evidence that convincingly links glaucoma with vascular disease:

Optic Disc Hemorrhages

Small, difficult to observe, hemorrhages around the optic disc often precede glaucoma by a few years. These hemorrhages are sometimes accompanied by dilated, tortuous blood vessels and are seen in a variety of ocular disorders. The existence of these abnormal blood vessels have been linked with coronary artery disease.( 26)

Glaucoma and Atrial Fibrillation

Optic nerve fiber loss observed as progressive vision loss among glaucoma subjects has been directly linked with diminished cardiac pumping activity. Severe visual field defects are more common among patients with atrial fibrillation (70%) vs. other glaucoma patients (42%). Atrial fibrillation is twice as likely to occur among glaucoma patients as healthy subjects who do not have glaucoma. Researchers at the Helsinki University Hospital believe that the intraocular pressure rise among glaucoma patients is only secondary to changes in intraocular structures as a result of diminished blood flow to the eye.( 27)

The Carotid Circulation and Glaucoma

Given the fact that vascular abnormalities have often been noted among glaucoma patients, thermography has been used to measure circulation in the ophthalmic carotid region. Thermography reveals that 32 of 39 glaucoma patients (89%) show signs of cerebral vascular disease.( 28) The role of the carotid artery in low-pressure glaucoma is now better understood. A study of 62 glaucoma patients (mean age 71.2 years) with a mean eye fluid pressure of 16.1 mm Hg reveals that 90.3% had calcifications of the carotid arteries adjacent to the opening of the optic canal whereas only 20.8% of age-matched non-glaucomatous patients exhibited the same carotid disease with computed tomography.( 29)

In 1929 Mark J. Schoenberg applied pressure to the jugular veins and measured a rise in intraocular pressure. Schoenberg noted that various factors predisposed the jugular veins (actually the carotid arteries) to "weakening and stretching," including faulty diet (abuse of strong tea, coffee, alcohol), infectious diseases, and venous congestion brought on by the strain of constipation or strenuous physical activity.( 30) Modern studies confirm Schoenberg's observations. C. B. James reports that carotid endarterectomy or bypass surgery improves ocular blood flow to an ischemic eye which temporarily raises and then normalizes intraocular pressure.( 31) A study conducted in 1987 showed that 67% of normally healthy adult male businessmen wore overly-tight neckwear that impaired their visual performance.( 32) Some patients treated for years for common (open-angle) glaucoma have been found to have stenosis of the carotid arteries.( 33) Listening for carotid bruits and screening with ultras ound should be a part of a comprehensive examination for glaucoma.

Blood Viscosity

Blood viscosity is elevated among glaucoma patients. Foulds suggests an hematocrit above 50 is the threshold for adverse clinical signs.( 34) But blood viscosity needs to be correlated with other factors such as blood pressure and intraocular pressure. When elevated blood viscosity is combined with elevated pressure upon the blood vessels supplying the optic nerve, then vasodilation is inhibited and blood flow will decrease. Blood viscosity in the higher range of normal is not usually a cause for concern but when combined with elevated intraocular pressure may impair blood flow.( 35)

Additionally, Paul Gasser has noted that mild forms of chronic dehydration can occur from taking diuretics which results in altered blood volume and increased blood viscosity.( 36) Again, blood flow to the optic nerve may be impaired. This is just another of the many subtle iatrogenic factors cited in this paper that promote glaucoma.

Disturbance Of Autoregulation

However, blood pressure is a two-edged sword. While hypertension appears to be a problem that is associated with glaucoma, so is systemic hypotension. Patients with common and low-pressure glaucoma have markedly lower systolic blood pressure.( 37) Hayreh notes that the fluid pressure within the eye is under autoregulation.( 38) Under certain conditions, such as arterial hypertension, age, or arteriosclerosis, this autoregulation is disturbed. Lack of blood supply to the optic nerve appears to be related to low systemic blood pressure. Patients with common glaucoma whose systolic blood pressure is less than 140 mm Hg. were found to have four times more tendency to visual field deterioration than those with systemic blood pressure greater than 140 mm Hg.( 39) Hayreh also notes that the rate of cardiac events below 75 mm Hg diastolic blood pressure is twice that at 85 mm Hg. Some studies show that hypertensive patients placed on medical therapy often exhibit such low blood pressure d uring sleep that the optic nerve head is deprived of adequate blood supply.( 40) This is yet another example of iatrogenic disease. Internists and family doctors, prescribing blood pressure medications may be unwittingly inducing glaucoma.

Low-Pressure Glaucoma

There are many facts which point to vascular and rheological (blood) factors in the pathogenesis of low-pressure glaucoma. Researchers, using magnetic resonance imaging, have shown that low-pressure glaucoma patients experience reduced blood flow to the cranium as evidenced by deep white-matter brain lesions.( 41) The increased frequency of migraine, abnormal peripheral circulation and the aggregation of thrombocytes is also characteristic of low-pressure glaucoma. Glaucoma patients have been shown to exhibit a greater incidence of spontaneous aggregation of blood platelets than those patients with ocular hypertension.( 42) Klaver points out that low-pressure glaucoma patients exhibit higher blood viscosity compared to individuals with common glaucoma.( 43) The blood-flow velocity in the fingertips of low-pressure glaucoma patients is significantly reduced compared to normal subjects, and this is further reduced by dipping the fingers in cold water.( 44) One study shows 44% of low-p ressure glaucoma patients also suffer common classic migraines.( 45) Among elderly sufferers of low-pressure glaucoma, migraines are found in up to 86% of patients.( 46) Another compelling piece of evidence for this type of glaucoma is the increased incidence of silent heart attacks (myocardial ischemia). The rate of silent cardiac ischemic attacks is about 3% among healthy adults. In a 24-hour period the rate of silent heart attacks in one study was 30.8% among patients with low-pressure glaucoma, twice that of patients with common (open-angle) glaucoma (14.3%) or control individuals (15%).( 47)

Vasospasm and Glaucoma

Vasospasm has been associated with a history of migraine, Raynaud's phenomenon, chronic cold hands and feet, and low-pressure glaucoma. Hayreh notes that women are more prone to vasospastic disorders than men by about five times and low-pressure glaucoma is also more prevalent among women. The vascular endothelium produces agents that either constrict (endothelin-1) or relax (nitric oxide) smooth muscle. Calcium is also known to constrict smooth muscle and the use of calcium-channel blockers has been shown to widen the visual field among those who have cold hands.( 48)

Oxygen-derived free radicals and low-density lipoproteins (LDL cholesterol) which block the normal vaso-relaxing activity of acetylcholine, combine to promote constriction of the ocular circulation while the amino acid L-arginine has an opposite effect.( 49) The use of cholesterol-lowering agents combined with antioxidants has been shown to improve vasomotor responses to acetylcholine improved coronary-artery diameters.( 50) The experimental elevation of arterial PCO( 2) levels, which is a known vasodilator, increases blood flow velocity among patients with low-pressure glaucoma.( 51)

Optic Atrophy/Pernicious Anemia

Glaucoma may masquerade as the presenting sign of pernicious anemia. This has been known since 1936 when Henry Cohen, a professor of medicine in Liverpool, reported that amblyopia was often the presenting symptom of anemia preceding any measurable blood changes. Pallor of the optic disc, often believed to be a sign of glaucoma, is a classic sign of this syndrome. Low or absent gastric acid secretion is also common. The intraocular pressure may be normal or elevated.( 52) Another classic sign of this disease is photophobia and dependence upon sunglasses.( 53) Contemporary ophthalmologists often reject a diagnosis of slowly progressive demyelinating optic neuritis. Additionally, optic nerve demyelination is almost invariable among multiple sclerosis patients and may be the presenting symptom of this disease. Visual impairment may become evident following exercise or a hot bath among MS patients.( 54) Chronic, slow-progressive atrophy of the optic nerve fits more with an etiology of d emyelination glaucoma than elevated fluid pressure. Damage to the optic nerve predates any measurable changes in peripheral vision.( 55)

Steroid-Induced Glaucoma

There is no safe dosage of steroids that will prevent the onset of glaucoma.( 5) Mild corticosteroids may produce glaucoma within months, more potent steroids within weeks. Some cases of corticosteroid-induced glaucoma, up to a third of cases, are irreversible.( 57) Stopping steroid use can normalize the intraocular pressure but damage to the optic nerve and loss of visual field appears to be permanent.( 58) The use of low-dose topical steroids to treat eczema,( 59) and the use of steroids in asthma inhalers (prescribed over 8 million times annually in the U.S.), can result in a fluid pressure rise in the eye.( 60)

Despite the cessation of steroids and the reduction of elevated intraocular pressure with the use of anti-glaucoma medications, one researcher indicates if glaucomatous cupping of the optic disc, a narrowed visual field or any loss of clarity in the lens occurs, they may be irreversible.( 61)

Exfoliative Glaucoma

Anterior layers of the capsule that surrounds the natural lens of the eye may shed, entering the flow of aqueous fluid to the narrowing angular drain within the eye. This is called exfoliation or pseudoexfoliation syndrome. In Finland 50-60% of the patients with exfoliation of the lens capsule also had glaucoma.( 62) Exfoliation increases in incidence with age. It is preceded by a subtle opaque film, like a white opalescent frosting, on the anterior lens which can be detected during an eye exam.( 63)

A study of twins reveals that exfoliation is not hereditary. It occurs more prevalently in Finland, Norway, Russia, Italy, Greece, Turkey, India, Chile and among Navajo Indians. Environmental factors are believed to play a prominent role in the etiology of pseudoexfoliative glaucoma.( 64) In a study of patients scheduled to undergo cataract surgery, glaucoma occurred three times more frequently among those with exfoliation (33.8%) than among those without exfoliation (10.8%).( 65) Exfoliation syndrome and loss of iris pigment (pigment dispersion) are believed to be a cause of ocular hypertension.( 66)

An interesting study shows that glaucoma linked with lens exfoliation was not diagnosed among adults under age 40 and the average age of patients with this form of glaucoma was 70 years. One study conducted in Japan showed that glaucoma linked with exfoliation (16.2%) occurred as frequently as common open-angle glaucoma (16.5%), and protein shed from the lens was found inside the eyes of 324 of 330 eyes with this form of glaucoma.( 67)


Glaucoma is a multifactorial disease. The optic nerve is vulnerable to fluid pressure, impaired circulation, complete lack of oxygenation to the optic nerve which leads to the neovascular form of glaucoma, lack of nutrition (anemia), vasoconstriction, demyelination of the nerve sheath which may or may not accompany other demyelinating disorders such as multiple sclerosis, and a host of factors that interfere with normal fluid drainage in the eye, including iris pigment loss, free-radical induced oxidation producing large free proteins, and allergy which releases histamine into the fluid drain. Systemic diseases may attack the vulnerable optic nerve. For example, in one study 30% of low-pressure glaucoma patients exhibited immune-related diseases compared to only 8% of patients with ocular hypertension.( 68) When physicians conducted a systemic evaluation they found only 30% had a single diagnosis of low-pressure glaucoma. Twenty-eight percent of these patients had systemic disord ers such as syphilis, intracranial tumor, anemia and carotid obstruction and another 42% had high pressure glaucoma.( 69) Other factors that may cause glaucomatous optic-nerve damage are oral, topical or periocular steroid use, blood transfusion and methyl alcohol poisoning.

More than one type of glaucoma can exist at any given time in a particular patient. Thus an anti-glaucoma regimen should include "blanket" protection from the known factors that cause the disease.

In conclusion, the primary cause of the majority of cases of glaucoma is vascular disease. Many other factors can influence intraocular pressure. Eye fluid pressure is a factor associated with, but not necessarily the cause of, glaucomatous visual field loss. Eye physicians need to go beyond being simple "pressure checkers" and gain an understanding of the underlying factors involved in glaucoma.

In part III an anti-glaucoma regimen that emphasizes non-pharmacologic remedies and lifestyle changes will be presented.

Disclaimer: The accompanying article has been written for the benefit of the readers of the Townsend Letter for Doctors and Patients. I am a medical journalist and have written an opinion regarding the treatment of glaucoma in the accompanying paper. Clinicians should seek additional information from other sources before prescribing therapeutic regimens for their patients. Only a clinician is in the unique position to obtain a patient's medical history, allergies, use of prescription drugs, diet, and other factors that are necessary prior to development of a therapeutic regimen.

Financial Disclosure: I have written a book entitled Nutrition And The Eyes (Health Spectrum Publishers), which is designed for the lay reader. I am also financially involved in Eye Communications, a California company that manufactures sun goggles and distributes nutritional supplements. No brand names or recommendations of any products are provided in this article. To my knowledge, the suggested nutritional regimen listed in this article does not currently parallel that of any commercially available product.


Bill Sardi

Health Spectrum Publishers

8851 Central Ave., G-620

Montclair, California 91763 USA

909-982-2953/Fax 909-949-3801

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Townsend Letter for Doctors & Patients.


By Bill Sardi

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