Dr. Spooner Glaucoma

Submitted by Dr. Chris Spooner

Glaucoma is the second most common cause of vision loss in seniors in Canada. More than 250,000 Canadians have chronic open-angle glaucoma, the most common form of the disease.

Glaucoma involves damage to the optic nerve most often caused by high pressure inside the eye due to a build up of excess fluid. This pressure is referred to as intraocular pressure (IOP). The elevated IOP eventually leads to a condition known as glaucomatous optic neuropathy (GON) which develops slowly over time. With GON an ophthalmologist can observe a visible change in the inner surface of the eye and measurable thinning of the nerve fibre layer of the retina. This results in a gradual decrease in the visual the visual field along with a decrease in the colour and contrast of images. If glaucoma is untreated it could advance to later stages where central vision narrows to “tunnel" vision, or it may result in complete loss of vision. Early detection and treatment is essential to prevent severe vision loss or blindness.

Many East Asian groups are prone to developing angle closure glaucoma due to their shallow anterior chamber depth, with the majority of cases of glaucoma in this population consisting of some form of angle closure. Inuit are also twenty to forty times more likely than Caucasians of developing primary angle closure glaucoma. Women are three times more likely than men to develop acute angle-closure glaucoma due to their shallow anterior chambers.

Other factors can cause glaucoma, known as "secondary glaucomas," including prolonged use of steroids (steroid-induced glaucoma); conditions that severely restrict blood flow to the eye, such as severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma); ocular trauma (angle recession glaucoma); and uveitis (uveitic glaucoma).

Primary open angle glaucoma (POAG) has been found to be associated with mutations in genes. Normal tension glaucoma, which comprises one third of POAG, is associated with genetic mutations.

Glaucoma is a multifactorial disease resulting from a variety of risk factors Although elevated IOP still remains to be one of the most important risk factors, other risk factors, often referred to in the literature as 'non-IOP-dependent risk factors', have gained importance.

There is increasing evidence that ocular blood flow is involved in the development of glaucoma. Current research suggests that fluctuations in blood flow to the back of the eye are more harmful in glaucomatous optic neuropathy than steady reductions. Unstable blood pressure and dips are linked to optic nerve head damage and correlate with visual field deterioration.

Abnormalities of ocular blood flow and oxidative stress have come to be regarded as important mechanisms involved in damage of the retina. Glaucoma patients, in general, have a reduced ocular blood flow. Specifically, It is the variation in blood flow that leads to glaucomatous damage. An unstable blood flow leads to a chronic mild repeated reperfusion injury, which then leads to the production of oxygen free radicals. This results in increased oxidative stress. As a response to oxidative stress, cells produce heat-shock proteins that act to protect proteins in the eye from becoming damaged. Heat-shock proteins can also be induced naturally by the use of sauna baths.

Sauna therapy may act to increase heat shock protein Hsp90, which is induced by even modest heating of mammalian tissues. Hsp90 interacts with specific proteins that increase the availability of a compound called tetrahydrobiopterin (BH4). This in turn may lead increased levels of a compound called nitric oxide (NO) which is produced by an enzyme in the blood vessel linings called eNOS (endothelial nitric oxide synthase). NO is a key regulator of blood flow. NO availability is reduced early in vascular disease states, such as hypercholesterolemia, diabetes and hypertension, and throughout the progression of atherosclerosis. This is a result of both reduced NO production and increased NO consumption by oxygen free radical. eNOS enzymatic activity appears to be determined by the availability of its cofactor BH4 (tetrahydrobiopterin). When BH4 levels are adequate, eNOS produces NO; when BH4 levels are limiting, eNOS generates superoxide, contributing to vascular oxidative stress

and endothelial dysfunction. BH4 bioavailability is determined by a balance of enzymatic synthesis and recycling, versus oxidative degradation in damaged endothelium. Augmenting vascular BH4 levels by pharmacological supplementation, by enhancing the rate of biosynthesis or by measures to reduce BH4 oxidation have been shown in experimental studies to enhance NO bioavailability. Sauna, by stimulating the production of heat shock proteins increases the availability of BH4 through synthesis and recycling.

There are a large and rapidly increasing number of diseases that are associated with BH4 depletion and these may be candidates for sauna therapy.

Such diseases as glaucoma, hypertension, vascular endothelial dysfunction, multiple chemical sensitivity and heart failure are thought to be helped by sauna therapy. Chronic fatigue syndrome and fibromyalgia may also be helped and there are others that may be good candidates for sauna therapy.

Glaucoma is becoming recognized as a condition for which not only elevated intraocular pressure (IOP), but also non-pressure-dependent risk factors, are responsible. Better knowledge of the eye is damaged has opened up new therapeutic approaches that are often referred to as non-IOPlowering treatment.

These new avenues of treatment, some of which are still under investigation, include agents that can improve vascular regulation and blood flow to the eye and reduce oxidative stress. The use of sauna to stimulate the production of heat-shock proteins may prove to be useful adjunct to current treatments.