~Glaucoma, Part 2 - Causes and Treatments
CAN DRUGS CAUSE GLAUCOMA?
According to Leonard Levine, Ph.D., certain drugs can "impair the biological health of the visual system." For example, the Physicians' Desk Reference lists 94 medications that can cause glaucoma, including antihypertensives, antidepressants, and steroids, such as cortisol, which can destroy vital collagen tissue in the eye. Both herbal ephedrine and pseudoephedrine have central nervous system (CNS) stimulating properties. Ephedrine is the stronger of the two, but both are considered stronger than caffeine. The glaucomatous person should avoid these substances, particularly Ma-huang, licorice, and belladonna.
Note: Antihistamines can increase pressure within the eye. If using drugs for other conditions, always inform your doctor of an existing glaucoma condition to avoid prescribing drugs that might adversely affect the disease. Obviously, it behooves individuals relying upon prescription drugs to thoroughly acquaint themselves with the side effects.
The use of certain medications that inhibit cholinergic response has been linked to a higher incidence of glaucoma. An anticholinergic drug blocks acetylcholine receptors, resulting in the inhibition of parasympathetic nerve impulses. This action would make stronger the sympathetic nervous system, an action that could dilate the pupil and relax the iris sphincter. Dilation of the pupil could make smaller the passage between the iris and cornea, complicating the exit of the aqueous humor.
DO ALLERGIES INFLUENCE GLAUCOMA?
Individuals who suffer either food or environmental allergies appear to be at a higher risk for glaucoma. Both causative and therapeutic factors appear to link allergies and glaucoma. Persons with nonresponsive or refractory glaucoma are occasionally asked to consult an allergist, in an attempt to lessen the endogenous stress load. Greater acceptance of the allergy/glaucoma hypothesis adds another dimension to treatment.
CALCIUM--PROS AND CONS
Calcium excesses can be redistributed in the body to soft tissues, contributing to the risk of glaucoma. The more soluble forms of calcium supplementation are usually well absorbed and utilized, such as calcium citrate, calcium bis-glycinate, or microcrystalline hydroxyapatite. The problem with soft tissue damage due to calcium deposition may be more appropriately seen as a consequence of calcium shortages. When calcium levels are in short supply, the parathyroid hormone participates in a cascade that eventually asks the bones to give up a share of their calcium stores. The host loses on two fronts: (1) too many withdrawals can eventually weaken the skeletal system and (2) the release of calcium from the skeleton is not well regulated. Excesses of calcium can tie up in soft tissues, exacerbating arthritis, arteriosclerosis, kidney stones, and glaucoma. Recall that vitamin K assists in keeping calcium in the bone and not in soft tissue. Considering this, adequate amounts of dietary calcium are absolutely essential to prohibit the activity of the parathyroid gland and the subsequent calcium withdrawal from the skeletal frame.
ODDS AND ENDS
The herb bloodroot (Sanguinaria canadensis) may contribute to glaucoma. Toothpastes occasionally contain bloodroot, because the herb is a strong adjunctive component contributing to gum health. Because toothpastes and mouthwashes are not ingested, the amount of bloodroot entering the system would be minimal, but individuals concerned about glaucoma should be aware of the caveat surrounding bloodroot.
Most vitamins and minerals are nonproblematic for the individual with glaucoma, but patients should restrict their intake of niacin to not more than 200 mg daily.
LOOKING BACK AT TREATMENT
- Vitamin C
- Coleus Forskohlii
- Vitamin A
Fortunately, history provides significant therapeutics in regard to managing glaucoma. Conventional medications and interventions are the most widely used methods of treatment, but nutritional protocols have produced convincing evidence of benefit.
Vitamin C is an effective adjunct in stabilizing IOP. Some individuals respond to as little as 2 grams a day of vitamin C, although others respond to only extremely high doses, for example, 35 grams a day. Because of the variance in the amount of vitamin C required to exert a positive effect, careful monitoring by a physician is required. Intravenous administration of vitamin C results in an even greater initial reduction. The pressure-lowering action of vitamin C is long-lasting if supplementation is continued, frequently showing an average reduction of 16 mmHg. Nearly normal tension levels have been achieved in some patients using vitamin C, when acetazolamide and pilocarpine therapy failed. The beneficial mechanisms by which vitamin C lowers inner eye pressure include (1) increased blood osmolarity, a process that draws fluid from the eye and into the blood, (2) diminished production of eye fluid, and (3) improved fluid outflow.
Many of the benefits of vitamin C are likely attributable to collagen formation, an important function of this water-soluble vitamin. Collagen is the most abundant protein in the body, including the eye, giving strength and integrity to ocular tissue. Vitamin C helps preserve the collagen in the eyes' drainage tubes, the very tubes that malfunction in glaucoma. Credits directed to vitamin C appear justified when considering reduced IOP and the improved structural health of the eye.
Bioflavonoids: What Can They Accomplish?
All nutrients that support collagen metabolism, particularly at the back of the eye where the optic nerve exits and in the tissues that drain the eye, are important in glaucoma treatment. One such nutrient bioflavonoid, known as the proanthocyanidins (found in grape seeds and pine bark), cooperates with vitamin C in achieving collagen integrity. In the eye, collagen provides tensile strength and stability to the tissue. Another major function of vitamin C is the preservation of capillary integrity, a task made easier with the assistance of a bioflavonoid. The bioflavonoids work not only with vitamin C but also on behalf of vitamin C, preventing the breakdown of ascorbate. The proanthocyanidin bioflavonoids work by binding to collagen, increasing elasticity and flexibility. The proanthocyanidins are considered a powerful antioxidant, defending the collagen matrix against free-radical attack and guarding it against enzymatic breakdown through the enhanced delivery of oxygen and blood to the eye.
Rutin, a bioflavonoid from the citrus family, has demonstrated the ability to lower IOP when used in conjunction with standard drugs. Pansy (Viola) contains up to 23% rutin on a dry-weight basis. Naturopaths, for the treatment of glaucoma, often recommend sources of rutin, including pansy.
The genus Vaccinium comprises nearly 200 species of berries, all showing generous amounts of flavonoid/anthocyanidin compounds. Bilberry, Vaccinium myrtillus fructus, has historically been used in various eye conditions, including glaucoma, cataracts, macular degeneration, diabetic retinopathy, and retinitis pigmentosa. Although bilberry is not considered a curative herb in regard to glaucoma treatment, it appears to assist in halting additional damage by bringing a good flow of blood to the eyes.
When Coleus forskohlii was applied directly to the eye, it was shown, in clinical studies involving both animals and humans, to reduce IOP, making it of significant benefit in glaucoma treatment. Forskolin represents a potentially useful class of antiglaucoma agents, differing in molecular mechanism and action from previously used drugs (Caprioli et al. 1984; Hartman et al. 1988). C. forskohlii appears to have a twofold approach that delivers benefit for glaucoma by increasing intraocular circulation and decreasing aqueous humor outflow. The outflow facility remains unchanged, but the ciliary blood in the vascular tunic increases. The benefits are observable about an hour after application and reach a therapeutic peak at 2 hours. The value of C. forskohlii remains significant for at least 5 hours after application. Because C. forskohlii eye drops are not yet available, oral administration may be considered, with the hope that similar results can be obtained. C. forskohlii appears to bestow its therapeutic values without risk of major side effect.
C. forskohlii has been used to advantage in the treatment of hypothyroidism. Interestingly, subclinical hypothyroidism, so mild that it produces no symptoms, has been noted as a cofactor in some patients with glaucoma.
Hydergine has some of the same biochemical advantages as C. forskohlii. Hydergine may be capable of lowering IOP by decreasing hypoxia (reduced oxygen supply) and preventing free radical damage to critical cells.
The Value of Minerals
Magnesium has long been recognized as nature's physiological calcium blocker. Previous studies had demonstrated that calcium channel-blocking drugs offer benefits for some glaucoma patients. Armed with this revelation, researchers at the University Eye Clinic in Basel, Switzerland, evaluated the effect of supplemental magnesium on glaucoma patients. Magnesium (121.5 mg twice daily) was administered to 10 glaucoma patients for 1 month. At the conclusion of the study, results substantiated that magnesium supplementation improved the peripheral circulation, with an accompanying beneficial effect on the visual field in patients with glaucoma.
Magnesium also has the ability to turn off the sympathetic nervous system. This is a reputation that has earned magnesium credit in cardiology, acting as an antiadrenergic. An antiadrenergic drug blocks the effects of impulses transmitted by the adrenergic postganglionic fibers of the sympathetic nervous system. This act would tone and modify the sympathetic response, soothing the "fight or flight" syndrome. Recall that among the many functions controlled by the sympathetic nervous system--those normally not under conscious control--are dilation of the pupils and a general stimulatory response. Stimulation of the sympathetic nervous system would be contraindicated in glaucoma control.
Minerals are absolutely essential to longevity and quality of life. Individuals can survive longer with a vitamin deficiency than with a mineral deficiency. The importance of minerals is becoming more evident as research data amass. The trace mineral chromium has won additional credit beyond stabilization of blood glucose levels by being able to improve focusing of the eye and lower IOP. Selenium benefits ocular function, and zinc supports healthy eye structure. Selection of a good multiple will provide these vital minerals, plus additional nutrients needed for ocular health.
Less than 1 mg of melatonin has lowered pressure within the eyes of healthy people, but studies have not yet been published on the effects of melatonin on people who have glaucoma.
Many nutritionists regard vitamin A as the most important vitamin of all. Various naturopaths consider vitamin A vital to an effective glaucoma protocol. Considering ocular health, the eyes are obvious indicators of a vitamin A deficiency, often showing symptoms of dry, itchy, or inflamed eyeballs and night blindness. Vitamin A appears to counteract weak eyesight by encouraging the formation of rhodopsin or visual purple, a pigmented compound in the rods of the retina that adapts the eye to low-density light.
Vitamin A, a fat-soluble vitamin, may be accompanied by risk if it is used carelessly or if the liver is under stress. Lewith et al. (1996) reported that dosages of 25,000-50,000 IU might cause liver damage in select individuals (particularly persons with liver problems, those taking certain drugs, or heavy drinkers) if administered over a period of several months. Nonetheless, with judicious administration, such as under the supervision of a nutrition expert or physician, this underrated vitamin can perform outstanding feats.
Some individuals prefer to obtain their vitamin A by way of food sources or supplemental beta-carotene. The conversion of the provitamin beta-carotene to its active form takes place largely in the liver or during the intestinal absorption process. A healthy liver obviously makes the conversion process more of a surety, a process enhanced by the trace mineral zinc.
The National Eye Institute supported research from 1978-1984 to determine whether marijuana or any of its components could safely and effectively lower IOP. Findings substantiated that marijuana did, indeed, lower IOP when administered orally, intravenously, or by smoking. Topical application did not lower IOP. Marijuana passed the initial phase of the study, illustrating it could lower IOP, but the consensus held that the drug was not any more safe or effective than a variety of drugs already FDA-approved and easily available. The potential risk factors of increased heart rate and hypotension also negated enthusiasm associated with marijuana usage.
Research to date has not investigated whether marijuana offers any advantages over currently available glaucoma treatments or whether it could be considered useful when used in combination with standard therapies. The National Eye Institute stands ready to evaluate any well-designed study to consider the value of marijuana in glaucoma treatment.
LOOKING AHEAD TO TREATMENT
The current hypothesis regarding the causative factors of glaucoma leans toward the neurotoxicity/neuroprotection theory. Ophthalmologists refer to neurotoxicity as the "buzz word" in their profession (i.e., the focus of current glaucoma exploration). It appears to be more than a trendy, ungrounded approach to explaining the causative factors and therapeutic modalities of glaucoma. Research emanating from various prestigious universities converges when considering the neurotoxicity theory of glaucoma.
The opinions of Dr. N. N. Osborne, Nuffield Laboratory of Ophthalmology, Oxford University, echo those of many other scholars who are studying glaucoma. Dr. Osborne believes that the visual-field loss in glaucoma is due to the death of retinal ganglion cells. Reducing or slowing down the loss of ganglion cells, a concept known as neuroprotection, appears to be the "only way forward." Osborne proposes that the death of neurons (a process referred to as apoptotic cell death) in various diseases is fundamentally the same but varies in cause. Experimental data show that the death rate of neuronal populations is dependent upon the impact of the insult. Neuroprotectants are more likely to benefit a patient in which neurons die slowly, as in glaucoma. If a reliable neuroprotector can be administered in such a way that it reaches the retina in appropriate amounts and has insignificant side effects, it is likely to attenuate ganglion cell death and thus benefit the glaucoma patient. Providing a solution to neurotoxicity appears to be the therapeutic goal for future treatment.
Aminoguanidine may help preserve the vision of refractory glaucoma patients by inhibiting the build-up of nitric oxide synthase-2 (NOS-2), a substance believed to degrade neuroprotection. NOS-2 stimulates the emission of nitric oxide, a compound implicated in retinal nerve damage (Morgan et al. 1999). Reduction of nitric oxide through nitric oxide synthase inhibition provides partial but significant protection against the lethal effects of oxygen deprivation and the action of excitatory amino acids, such as glutamate and aspartate, upon retinal ganglion cells.
Interest in knowing exactly what aminoguanidine could accomplish in regard to glaucoma spurred researchers at Washington University to look at the drug more closely. Two groups of animals with glaucoma were selected for aminoguanidine research. All animals initially displayed elevated IOP, with cupping and pallor of the optic disc. One group remained untreated, and the other group was treated with aminoguanidine. At the conclusion of the 6-month study, the untreated group displayed the original benchmark symptoms, whereas the eyes of the aminoguanidine-treated group appeared normal but with continued elevations in IOP.
The Washington University study also quantified retinal ganglion cell loss in a group receiving aminoguanidine compared to a control group void of treatment. The untreated group displayed a 36% loss of retinal ganglion cells, compared to less than 10% in the treated group. To realize the importance of this latter finding, visualize the retina being composed of ten layers of various types of cells. Retinal ganglion cells are large, flask-shaped cells composing one of the ten layers. The degradation of the ganglion cells pathologically compromises the delicate nervous tissue membrane of the retina. The final consensus of the study was that aminoguanidine might prove useful as a pharmacological neuroprotector in the treatment of glaucoma, contributing to a healthier eye, with less neuronal death.
Some patients have normal (or low) tension glaucoma. Even though the eye pressure is within normal range, the optic nerve continues to be injured. Despite efficient control of IOP, retinal ganglion cell loss will continue, resulting in further visual impairment if the causative factor is not determined and treated. This revelation was considered valuable, for it exonerated IOP as being the sole antagonist in retinal degradation. Researchers at University Hospital of Wales determined that neuroprotective agents might play a role in patients with glaucoma who have progressive visual-field loss despite satisfactory control of IOP.
Continued . . .
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