Technical Articles

Aren't grapes toxic to dogs?

There are a few articles in the literature about this topic, let me explain. There are two components to grapes that have nutritional benefits. The seeds of grapes are completely safe for all species evaluated so far, including dogs. The seeds of grapes contain proanthocyanidins, a group of antioxidants that benefit eyes and the rest of the body. There have been no side effects to grapeseeds known as of yet. However, there are compounds in the skins of grapes and raisins, especially darker varieties of the fruits, that cause kidney damage in dogs. Resveratrol is a potent antioxidant found in grape skins that has also been shown to potentially damage dog kidneys, at higher doses.

Tell me more about Grapeseed Extract and Proanthycyanidins!

Proanthocyanidins are naturally occurring compounds found at high concentrations in fruits, vegetables, wine, tea, nuts, seeds, flowers, bark and cacao. Proanthocyanidins have a wide range of biological activities such as antioxidant and free radical scavenging capabilities, anti-inflammatory and antimicrobial properties, inhibition of cancer cell growth, prevention of low-density lipoproteins oxidation, cardioprotection, and inhibition of viral replication.[1-4] In vitro experiments utilizing grape seed proanthocyanidin extract have shown GSE to be a more potent free radical scavenger than vitamin C or vitamin E.[3] Furthermore, GSE has been shown to prevent cataract formation in a hereditary cataractous rat model and in a diabetic rat model.[5, 6] GSE may have use as a dietary supplement to prevent and/or delay cataract formation, depending on the cataract’s etiology. GSE significantly decreases TBHP-induced intracellular ROS production and oxidant-induced cell signaling pathways associated with cataractogenesis.[7] It also lowers blood glucose levels in diabetics and improves endothelial cell function.[8] Glaucoma is also a devastating and blinding disease affected numerous purebred dogs. Oxidative stress has been shown to be an important part of this disease especially in the trabecular meshwork cells.[9, 10] Therefore, antioxidant supplementation, including polyphenols (grapeseed extract), ubiquinol and EGCG (green tea extract) may help slow the progression of the damage occurring in glaucoma.[11]

1. Oligomeric Proanthocyanidins (OPCs). Alternative Medicine Review. 2003; 8: 442-450.

2. Bagchi D, Bagchi M, Stohs SJ, Das DK, Ray SD, Kuszynski CA, Joshi SS, Preuss HG. Free radicals and grape seed proanthocyanidin extract: Importance in human health and disease prevention. Toxicology. 2000; 148: 187-197.

3. Bagchi D, Garg A, Krohn RL, Bagchi M, Tran MX, Stohs SJ. Oxygen free radical scavenging abilities of vitamins C and E, and a grape seed proanthocyanidin extract in vitro. Research Communications in Molecular Pathology and Pharmacology. 1997; 93: 179-189.

4. Bagchi D, Sen CK, Ray SD, Das DK, Bagchi M, Preuss HG, Vinson JA. Molecular mechanisms of cardioprotection by a novel grape seed proanthocyanidin extract. Mutat Res. 2003; 523-524: 87-97.

5. Yamakoshi J, Saito M, Kataoka S, Tokutake S. Procyanidin-rich extract from grape seeds prevents cataract formation in hereditary cataractous (ICR/f) rats. J Agric Food Chem. 2002; 50: 4983-4988.

6. Nguyen VC, Laki JV, Oizumi A, Ariga T, Kataoka S. Anti-cataract activity of proanthocyanidin-rich grape seed extract in streptozotosin-induced diabetic rats. The Annual Meeting of the Japan Society for Biotechnology and Agrochemistry 1999; 73: 133.

7. Barden CA, Chandler HL, Lu P, Bomser JA, Colitz CMH. The effect of grape polyphenols on oxidative stress in canine lens epithelial cells. Am J Vet Res. 2008; 69: 94-100.

8. Liu X, Wei J, Tan F, al e. Antidiabetic effect of Pycnogenol French maritime pine bark extract in patients with diabetes type II. Life Sci. 2004; 9: 449.

9. Zanon-Moreno V, Garcia-Medina JJ, Gallego-Pinazo R, Vinuesa-Silva I, Moreno-Nadal MA, Pinazo D, M.D. Antioxidant status modifications by topical administration of dorzolamide in primary open-angle glaucoma. Eur J Ophthalmol. 2009; 19: 565-571.

10. Izzotti A, Sacca SC, Longobardi M, Cartiglia C. Sensitivity of ocular anterior-chamber tissues to oxidative damage and its relevance to glaucoma pathogenesis. Invest Ophthalmol Vis Sci. 2009; Epub ahead of print.

Lutein (LUT) and zeathanthin (ZEA) are oxycarotenoids (xanthophylls) important in ocular health. They selectively accumulate in the lens and the retina, and also in the macular region in primates.3-5 There are also trace levels of lutein and zeaxanthin in the cornea and sclera; the lens and uveal structures have higher levels. The macula has 33ng and the peripheral retina has 65 ng of these carotenoids.[1] Trace levels of LUT and ZEA are found in the cornea and sclera.[2] These compounds may be particularly effective in preventing cataracts and age-related macular degeneration (ARMD) in primates. Indeed, increased dietary levels of these carotenoids are associated with significantly decreased risk of developing cataracts and AMRD. Conversely, primates fed diets lacking LUT and ZEA are significantly more susceptible to developing cataracts. LUT and ZEA appear beneficial in preventing ARMD and cataract formation, and this observation has resulted in a plethora of lutein supplements in the human health marketplace.

Unfortunately, almost all dietary supplements for human vision health contain only enough LUT/ ZEA for a mouse.

The exact importance of dietary LUT and ZEA in canine vision and cataractogenesis is unknown. Kim et al. recently reported that LUT was not detectable in the plasma of 18 month old beagles fed a standard canine dietHowever, plasma LUT increased rapidly and immune function was enhanced in response to dietary supplementation with LUT.[3] The possibility that LUT supplementation resulted in the accumulation of xanthophylls in ocular tissues was not examined. Since supplementation of humans and primates with xanthophylls induces gradual increases in retinal xanthophylls, it is feasible that LUT and ZEA will accumulate and benefit canine ocular tissues in response to supplementation.

Ocu-GLO Rx™ contains a patented pharmaceutical-grade lutein, LipoLutR, a naturally bioavailable form of carotenoids.

1. Bernstein PS. New insights into the role of the macular carotenoids in age-related macular degeneration. Resonance Raman studies. Pure Appl Chem. 2002; 74: 1419-1425.

2. Osakabe N, Yamagishi M, Natsume M, Yasuda A, Osawa T. Ingestion of proanthocyanidins derived from cacao inhibits diabetes-induced cataract formation in rats. Exp Biol Med. 2004; 229: 33-39.

Puppies fed diets high in omega-rich fish oils had improved visual performance as evidenced by increased rod response using electroretinography. They also had shorter response times, improved response to dim light and increased activation of the neural cascade. Puppies fed either flaxseed oil or only ALA (alpha linoleic acid, the precursor to EPA and subsequently DHA) had lower or minimal improvements in these parameters.[1] This is likely due to the slow and inefficient conversion of ALA to EPA, and then to DHA. Therefore, feeding preformed dietary n-3 long chain PUFAs (polyunsaturated fatty acids) is a more efficient way to enrich diets with DHA. A review of the human literature that evaluated evidence for effectiveness of omega-3 fatty acids in preventing the development or progression of retinitis pigmentosa found trends in clinical improvement. Research has also demonstrated the efficacy of omega-3 fatty acids in preventing ARMD from progressing to its advanced form.[2] Omega-3 fatty acids may protect the vascular and neural retina against inflammatory-, light-, ischemia-, oxygen-, and age-related pathology.[3] Omega-3 fatty acids have also been shown to be beneficial for the prevention of cataract in humans.[4]

1. Bauer JE. Responses of dogs to dietary omega-3 fatty acids. J Am Vet Med Assoc. 2007; 231: 1657-1661.

2. Hodge WG, Barnes D, Schachter HM, Pan YI, Lowcock EC, Zhang L, Sampson M, Morrison A, Tran K, Miguelez M, Lewin G. Evidence for the effect of omega-3 fatty acids on progression of age-related macular degeneration: a systematic review. Retina. 2007; 27: 216-221.

3. SanGiovanni JP, Chew EY. The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina. Prog Retin Eye Res. 2005; 24: 87-138.

Vitamin C is a hydrophilic molecule that scavenges free radicals. It is the strongest physiological antioxidant acting in the host’s aqueous environment.[1] It is a very safe antioxidant, with no safe upper dose limit set by the Expert Group on Vitamins and Minerals of 2003.[2] Vitamin C is found in the lens and in the aqueous humor of most species, including dogs, cats, humans, and cattle,[3] Its function relates to the redox reactions and is coupled to glutathione metabolism. One ten-year study found that Vitamin C protects against nuclear cataract formation in humans.[4] Numerous other studies found that Vitamin C supplementation and elevated blood levels of this antioxidant were associated with decreased incidence of cataract.[5] In humans, Vitamin C concentrations decrease with age and more so in patients with senile cataract.[6] A study in Cocker Spaniels found that dogs with cataracts had lower Vitamin C levels than those without cataracts,[7] suggesting that there is a decrease in antioxidant capacity in the aqueous humor of dogs with cataracts.

1. Kutlu M, Naziroglu M, Simsek H, Yilmaz T, Kukner AS. Moderate exercise combined with dietary vitamins C and E counteracts oxidative stress in the kidney and the lens of streptozotocin-induced diabetic rat. Int J Vitam Nutr Res. 2005; 75: 71-80.

2. Bartlett H, Eperjesi F. An ideal ocular nutritional supplement? Ophthal Physiol Opt. 2004; 24: 339-349.

3. Gum GG, Gelatt KN, Esson DW. Physiology of the Eye. In: Veterinary Ophthalmology. (ed. Gelatt KN). 4 ed. Blackwell Publishing Ltd, Ames, 2007; 149-182.

4. Mares-Perlman JA, Klein BEK, Klein R, Ritter LL. Relationship between lens opacities and vitamin and mineral supplement use. Ophthalmology. 1994; 101: 315-325.

5. Chiu C-J, Taylor A. Nutritional antioxidants and age-related cataract and maculopathy. Exp Eye Res. 2007; 84: 229-245.

6. Purcell EF, Lerner LH, Kinsey VE. Ascorbic acid in aqueous humor and serum of patients with and without cataract; physiologic significance of relative concentrations. AMA Arch Ophthalmol. 1954; 51: 1-6.

Vitamin E is a lipophilic antioxidant that interferes with lipid peroxidation.[1] Vitamin C works synergistically with Vitamin E; i.e. Vitamin E is oxidized to tocopheroxyl radical that is reduced back to tocopherol by Vitamin C. Numerous studies strongly suggest that consistent intake of Vitamin E and high plasma Vitamin E levels have a lower prevalence of various types of cataracts in humans. Higher blood levels of Vitamin E are also protective against ARMD in humans.[2] Vitamin E is the major antioxidant present in cell membranes; it is highly concentrated in ROS and the RPE.[2] It may also protect Vitamin A from oxidative degeneration in the retina.

1. Kutlu M, Naziroglu M, Simsek H, Yilmaz T, Kukner AS. Moderate exercise combined with dietary vitamins C and E counteracts oxidative stress in the kidney and the lens of streptozotocin-induced diabetic rat. Int J Vitam Nutr Res. 2005; 75: 71-80.

Lycopene is a major carotenoid found primarily in tomatoes. Of all known carotenoids, lycopene has been shown to have the highest physical quenching rate constant with singlet oxygen species.[1] Lycopene has been shown to protect against cataract formation in vitro and in vivo.

Zinc is an essential trace element necessary for numerous homeostatic functions. It is an antioxidant that offers protection against some, but not all, ROS-mediated injury. It competitively displaces iron from binding sites on negatively charged phospholipids and prevents its redox cycling. When combined with Vitamin E, it has synergistic protection against Fe-mediated lipid peroxidation.[1] It is also important to the health of the retina and in the function of Vitamin A.[2] Zinc deficiency reduces plasma levels of retinol-binding protein and retinol reductase, with a subsequent decrease in retinal Vitamin A levels. It has been shown to slow the progression of ARMD. Zinc is also important in protecting the lens from cataractogenesis by its antioxidant effects. Zinc deficiency in some species is associated with increased risk of cataract formation.[3]

1. Zago MP, Oteiza PI. The antioxidant properties of zinc interactions with iron and antioxidants. Free Radic Biol Med. 2001; 31: 266-274.

2. Russell RM, Cox ME, Solomons N. Zinc and the special senses. Ann Intern Med. 1983; 99: 227-239.

Both green and black teas significantly inhibit diabetic cataracts by reducing certain biochemical indicators as well as glucose;[1] it might also increase insulin activity. ECGC retards the progression of cataract in selenite-induced cataracts in rats.[2] EGCG fed to albino rats attenuated light-induced photoreceptor damage.[3] Additionally, EGCG given to rats wherein one eye had induced increase in IOP attenuated retinal neuronal death.[4] This supports evidence of EGCG’s neuroprotective capabilities, especially in glaucomatous eyes.[5]

1. Vinson JA, Zhang J. Black and green teas equally inhibit diabetic cataracts in a streptozotocin-induced rat model of diabetes. J Agric Food Chem. 2005; 53: 3710-3713.

2. Thiagarajan G, Chandan S, Sundari CS, Rao SH, Kulkarni AV, Balasubramanian D. Antioxidant properties of green and black tea, and their potential ability to retard the progression of eye lens cataract. Exp Eye Res. 2001; 73: 393-401.

3. Costa BL, Fawcett R, Li GY, Safa R, Osborne NN. Orally administered epigallocatechin gallate attenuates light-induced photoreceptor damage. Brain Res Bull. 2008; 76: 412-423.

4. Zhang B, Rusciano D, Osborne NN. Orally administered epigallocatechin gallate attenuates retinal neuronal death in vivo and light-induced apoptosis in vitro. Brain Res. 2008; 1198: 141-152.

Alpha lipoic acid is an antioxidant that potentiates Vitamin C and Vitamin E levels; it also has anti-inflammatory effects. It has traditionally been used in humans for diabetic neuropathy and in ischemia-reperfusion injury.[1] Alpha lipoic acid’s primary function is to increase the body’s production of glutathione, an important antioxidant mechanism in the crystallin lens. One study found that alpha lipoic acid protects the lens from oxidative stress.[2] Alpha lipoic acid was included in Ocu-GLO Rx™ primarily to help benefit diabetic canine patients as it promotes normal insulin sensitivity and glucose metabolism, though actual levels of insulin and glucose may not change.[3, 4] Note: It is not safe in cats at a dose higher than 30 mg/day.

1. Mandelker L, Wynn S. Cellular effects of common nutraceuticals and natural food substances. Vet Clin Small Anim. 2004; 34: 339-353.

2. Maitra I, Serbinova E, Trischler H, Packer L. Alpha-lipoic acid prevents buthionine sulfoximine-induced cataract formation in newborn rats. Free Radic Biol Med. 1995; 18: 823-829.

3. Jacob S, Henriksen EJ, Schiemann AL, Simon I, Clancy DE, Tritschler HJ, Jung WI, Augustin HJ, Dietze GJ. Enhancement of glucose disposal in patients with type 2 diabetes by alpha-lipoic acid. Arzneimittelforschung. 1995; 45: 872-874.

The B Vitamins function in a variety of essential processes and contribute to overall health of the body. Vitamin B1 (thiamine) is important in neuromuscular development and maintenance as well as carbohydrate and fat utilization for energy production and cellular metabolism. Vitamin B3 (niacin) is likewise involved in energy production but also in fat and steroid synthesis and lowers total levels of serum cholesterol, low density lipoproteins, very low density lipoproteins, and triglycerides. Vitamin B5 (pantothenic acid) is essential for breakdown of fatty acids, steroids, cholesterol and amino acids and functions as an antioxidant. It is incorporated into Coenzyme A, which is important in oxidative phosphorylation. Vitamin B6 (pyridoxine) is essential for hemoglobin formation and important for utilization for stored glucose. It is essential in the metabolism of fats, proteins, and carbohydrates. Vitamin B12 (cyanocobalamin) is an enzyme cofactor essential for normal cell growth and red blood cell development. Folic acid (aka Vitamin B9) is essential for cell growth and development and for preventing neural tube defects in the fetus. It has anticarcinogenic abilities in elderly humans and insufficient intake may result in anemia. Biotin (aka Vitamin H) is an enzyme cofactor involved in biosynthesis of fats and carbohydrates and metabolism of amino acids. Biotin has been shown to improve glucose tolerance and decrease insulin resistance. The oral administration of antioxidants in humans, including Vitamins A, B1, B2, B6 and E as well as omega-3-fatty acids, improve the quality and quantity of tears in patients with dry eye.[1]

Co-enzyme Q10 (aka CoQ10 or ubiquinol) is a lipid-soluble antioxidant that functions to protect against lipid peroxidation and therefore acts as an antioxidant. Ubiquinol mediates electron transport in the mitochondrial respiratory chain, it supports energy metabolism, and is a catalyst in ATP production.[1] CoQ10 has been measured in the human retina and it was found to decline with aging, suggesting a decrease in antioxidant capacity of the retina with age that is linked to the progression of ARMD.[2] CoQ10 also protects retinal ganglion cells from ischemia/reperfusion injury in a rat model wherein intraocular pressure was elevated to cause ischemia; synaptic glutamate became elevated and delayed the apoptosis of the retinal ganglion cells. CoQ10 with and without Vitamin E (analogue as trolox) exerts neuroprotective effects against oxidative stress in retinal ganglion cells including inhibition of apoptosis.[3] Therefore, antioxidant supplementation, including CoQ10/ubiquinol, polyphenols (grapeseed extract), and EGCG (green tea extract) may help manage the oxidative damage occurring in glaucoma.[4, 5]

1. Center SA. Metabolic, antioxidant, nutraceutical, probiotic, and herbal therapies relating to the management of hepatobiliary disorders. Vet Clin Small Anim. 2004; 34: 67-172.

2. Qu J, Kaufman Y, Washington I. Coenzyme Q10 in the human retina. Invest Ophthalmol Vis Sci. 2009; 50: 1814-1818.

3. Nakajima Y, Inokuchi Y, Nishi M, Shimazawa M, Otsubo K, Hara H. Coenzyme Q10 protects retinal cells against oxidative stress in vitro and in vivo. Brain Res. 2008; 1226: 226-233.

4. Luna C, Li G, Liton PB, Qiu J, Epstein DL, Challa P, Gonzalez P. Resveratrol prevents the expression of glaucoma markers induced by chronic oxidative stress in trabecular meshwork cells. Food Chem Toxicol. 2009; 47: 198-204.

Normal flow of aqueous humor inside the eye

Most people understand glaucoma as a high pressure inside the eye...but, there is so much more!

First, we must understand what normal intraocular pressure is, that is, pressure inside the eye.

There is a normal amount of aqueous humor made that is equal to its outflow from the eye. This production and outflow is analogous to your kitchen sink faucet turned on and the drain being open and normal; there is no build up. Aqueous humor is the fluid in the front portion of the eye and is made by special cells called ciliary body epithelial cells. These ciliary body cells are located behind the iris and next to the lens. This fluid is secreted from the ciliary body cells into the space between the iris and the lens, then through the pupil into the anterior chamber (space between the iris and cornea). From the anterior chamber, the aqueous humor exits the eye primarily through the iridocorneal angle (spaces located between the iris and cornea 360 degrees around the eye). This angle then leads out of the eye and into the general circulation. It is not possible for the ciliary body cells to make too much fluid, however in cases such as inflammation (uveitis) or normal aging in dogs, these cells can make less fluid.

Intraocular pressure=IOP

So, how does the IOP within the eye become too high?

Back to the faucet analogy, if the drain is clogged up, then the fluid will build up and rise within the sink! So, when the exit of aqueous humor is likewise backed up and cannot exit the normal way, then the fluid will build up, raising the intraocular pressure and, subsequently, causing damage to all cells of the eye, often leading to diminished vision and blindness.

Problems that cause impediment to outflow include:

1. the iridocorneal angle is too narrow or abnormally formed due to genetic factors in over 40 purebreed dogs; as the dog becomes an adult (typically between 3 and 9 years of age), these dogs can develop glaucoma because the narrow or abnormal iridocorneal angle eventually does not allow outflow of aqueous humor. This is Primary Glaucoma.

The rest of these causes are “secondary” causes of glaucoma:

2. inflammatory debris and/or cells (white and/or red blood cells) clog the outflow (like food clogging the drain in your sink);

3. tumors/neoplasia, these can grow into the outflow angle or make factors that result in the angle becoming blocked;

4. anterior lens luxation (the lens falls out of place and into the front (anterior) chamber of the eye, this can cause blockage in many ways. One way is that it blocks aqueous humor from going through the pupil from behind the iris, another way is that the weight of the lens pushes on the iris and causes the iridocorneal angle to narrow or close, or inflammation from the lens being out of place or developing cataractous changes will lead to clogging of the drainage angle;

5. retinal detachment causes VEGF (vascular endothelial growth factor) to be released, this results in formation of a membrane covering the iridocorneal angle, thus, inhibiting aqueous humor outflow from the eye.

Regardless of the cause, glaucoma is PAINFUL and will lead to blindness. Aggressive treatment and surgery can sometimes fail, still leading to blindness. It has been shown in humans and lab animal models that after the intraocular pressure has been elevated, affected cells can continue to die even if the intraocular pressure is kept in the “normal ranges.” This is a snowball effect because the cells damaged are the retinal ganglion cells as well as other retinal cells. When these cells die, they release toxins that damage nearby cells and they become unhealthy. These newly unhealthy cells can then die, doing the same to their neighbors.

Antioxidants such as coenzyme Q10 (ubiquinone), epigallocatechin gallate (green tea extract), and grapeseed extract have been shown to protect the retinal ganglion cells and other affected cells. These cells are very important to the health of the eye and sight.

Antioxidants are NOT a treatment for glaucoma, they are only supportive of the eyes’ cells. This is why it is of utmost importance that a veterinary ophthalmologist’s instructions be followed closely because this disease will cause permanent damage if the intraocular pressure in the eye remains high for more than a few hours. If the intraocular pressure is extremely elevated for more than 3 days, blindness is permanent.

How will my dog’s disease be diagnosed as glaucoma?

First, your veterinarian or veterinary ophthalmologist will determine if the “red eye” that your dog has is actually glaucoma. The way he/she will do this is by measuring the IOP (intraocular pressure) with a special instrument. The special instrument will be either a Tono-Pen (pen like instrument) or a TonoVet (instrument with a pin-head like attachment).

If the IOP in your dog’s eye is higher than it should be, then the cause is the next important step to determine. Then, the stage of glaucoma is important because it will give a prognostic indicator of your dog’s potential for vision.

Primary glaucoma is a genetic disease, this diagnosis is made based on the breed of dog, the age of the dog, and the clinical signs that your veterinary ophthalmologist sees inside the eye. This diagnosis has far-reaching implications because the dog should not be bred as he/she will pass on the defective gene(s) to its offspring. I also advise that if the siblings and parents are known, they should also be evaluated and possibly taken out of the breeding pool.

The earliest stage of primary glaucoma is early non-congestive glaucoma. Usually, there are very mild signs, if any. These signs include redness to the white part of the eye(s), tearing, pupil that does not constrict completely, changes inside the eye that your veterinarian or veterinary ophthalmologist will see with special instruments. This stage is treated with topical eyedrops and/or oral pills.

The names of the medications you may recognize include:

1. Trusopt or Azopt eyedrops

 a. Decrease the amount of aqueous humor made by the eye

2. Xalatan or Travatan eyedrops

 a. Allow the aqueous humor to exit the eye using the unconventional pathways (15% in dogs)

3. Methazolamide (pills)

 a. Similar mechanism as Trusopt or Azopt and decrease the amount of aqueous humor made by the eye

Once the IOP is managed (kept within a specific range or below a specific number in mmHg), it will be checked every 1 to 3 months. Even with perfect treatment regimens, glaucoma can become uncontrolled quickly. This is why it is imperative to take your dog to your veterinarian or veterinary ophthalmologist if you suspect that the eye does not look “right” to you.

This can be subtle and includes:

1. Affected eye is more red than the other eye

2. A bluish haze to the eye

3. Blindness, this can be difficult to assess because dogs mask this by compensating with the other eye

4. Lethargy, your dog does not appear to feel well

5. Hiding in a dark room

6. Tearing or wetness below the eye

7. The third eyelid is elevated (this can look like your dog’s eye is rolling back or like the eye is missing from its normal location)

The intermediate stage of glaucoma is next and the eye has changes that show that the IOP has been elevated in the past. The back of the eye is the most important place where these changes can be seen by your veterinary ophthalmologist. The optic nerve head is often smaller (mild to moderate changes) than the other one or than normal. The retina may have degenerative changes. The pupil may be unable to constrict completely (but medications can make the pupil smaller than normal so this is not a definitive change to look for). This stage may have unstable IOP measurements.

Treatment for the intermediate stages of glaucoma, in addition to medical management, often includes the option of different surgical procedures. These will either decrease the production of aqueous humor by the ciliary body cells or create an alternative outflow pathway for aqueous humor. These include:

1. Gonioimplants

 a. These are small tubes that are placed into the anterior chamber to give aqueous humor another way to exit the eye

 b. These have variable success because dog eyes make more inflammation than human eyes; this inflammation can plug the tube.

 c. If the inflammation can be controlled, these small tubes can work for months to years.

2. Laser surgery

 a. The most common type of laser used in veterinary ophthalmology is diode laser technology. Diode lasers target the cells in the ciliary body and destroy them. This diminishes the amount of aqueous humor being made.

 b. Diode lasers can be used in one of 2 ways:

  i. Applied to the outside of the eye over where the ciliary body resides. This method is less precise and not used as much anymore.

  ii. Endolaser technology

   a. Like an arthroscope is used to look into a joint to perform surgery, the laser is likewise put through a fiber optic tube with a camera that will allow precise laser destruction to the ciliary body cells.

3. Sometimes, this is used in conjunction with cataract surgery. Cataract surgery is concurrently performed when the lens has some cataractous changes that will preclude vision.

4. Combination approach

 a. Some veterinary ophthalmologists will perform endolaser surgery with gonioimplant placement

 b. This provides the both ways of treating glaucoma i.e. diminishing production of aqueous humor and allowing an alternative outflow for aqueous humor.

4. Medical treatment is always continued during the recovery phase. Some dogs end up on very few eyedrops once they have recovered.

5. The success rate of endolaser surgery is presently estimated to be 85 to 90%. This means that the eye is able to see and the glaucoma is controlled.

6. Like all diseases, this wonderful success rate still means that 10 to 15% of eyes will have complications. These can include:

 a. Bleeding inside the eye (usually resolves);

 b. Inflammation (all surgery has inflammation as a side effect): sometimes inflammation is very difficult to control and is case-dependent;

 c. Retinal detachment;

 d. Cataract development (can occur if the lens is not removed, but likelihood is low);

 e. Blindness: even in the most ideal of situations, glaucoma can still steal sight due to uncontrollable reasons.

What if my dog’s glaucoma cannot be controlled, the eye is painful, and the eye is blind?

Unfortunately, this occurs in some cases. There are three options that can be considered for eyes blind due to chronic glaucoma.

1. Enucleation

 a. Removal of the eye

 b. Even though this seems extreme, this is often chosen because the eye will not need eyedrops or any type of treatment anymore other than normal post-operative antibiotics and pain relief

2. Evisceration with intrascleral prosthesis

 a. This entails removing the inside structures of the eye, leaving the cornea and sclera (outside wall of the eye) and replacing them with a silicone sphere.

 b. This is a very cosmetic option

 c. This will likely still require some care and it must be watched for trauma since the eye is blind

3. Ciliary ablation

 a. This option is not for every dog.

 b. A drug named gentomicin is injected into the vitreous humor (back half) of the eye. This will destroy the cells that make aqueous humor, but also destroys the retina.

Click Here to read the article published in Clinician's Brief March 2010

In general, a true white progressing cataract cannot be stopped. It is like asking a frying egg to stop being fried and become liquid again! There are so many reactions and protein changes going on, there is no way back to clear.

Aging changes in the lens are normal in all species' eyes. This occurs because the lens grows continually throughout your life but all the cells must remain within the lens capsule. Think of an M&M candy. The candy coating remains intact and grows gradually too, but the cells must stay inside and must remain clear. Once the host (human, dog, cat, etc) become older, the cells start becoming very compressed and they start to refract light. This change, called nuclear sclerosis can cause glare in humans but typically does not affect your pet's vision. These aging changes also have protein damage and modifications and can be hastened due to environmental stressors especially the sun, smoking (second hand in our pet's case), poor diets, and environmental toxins.

The lens has antioxidant systems in the cells that are strongest while your pet and you are young, but as we all age, these systems slow down and do not keep the normal daily damage from sun, etc under control. Once this happens, the proteins and cell components that remain can become irreparably damaged, leading to cataract formation. There are numerous studies showing that people who have diets high in vitamins, antioxidants, low in carbohydrates, do not smoke, and protect themselves from the sun, have a lower incidence of this type of cataract.

Ocu-GLO Rx™ is rich in antioxidants that may slow the aging type of cataract. Once your dog has extensive changes, Ocu-GLO Rx™ will not reverse these changes.

There are also other types of cataract that occur in dogs and cause blindness. These include genetic cataracts, cataracts secondary to retinal degeneration, and diabetic cataracts.

Genetic cataracts typically occur when your dog is under 6 years of age. They are white in color and progress at varying rates. Once these are evident, it is unlikely that anything will slow them down as there are numerous cellular pathways that have been activated in response to the genetic mutation. These pathways are changing the protein folding inside the cells as well as turning on other genes that should not be on and are damaging the cells and causing opacities seen as cataracts.

Cataracts secondary to inherited retinal degeneration occur slowly and become evident once a dog has lost significant night vision. Inherited retinal degeneration occurs in dogs and, depending on the breed, can progress rapidly or slowly. Please see the article by Dr McCalla on this subject at http://www.animaleyecare.net/diseases/cataract.htm Briefly, the toxins released by the dying retinal cells are toxic to the lens cells. The lens cells can only respond by becoming opaque i.e. a cataract. Ocu-GLO Rx™ may protect the lens cells from this toxic type of damage and certainly can slow down the retinal degeneration in most cases.

Cataracts secondary to diabetes mellitus occur because there is too much glucose (sugar) in the circulation and in the fluid encircling the lens (aqueous humor). The lens cannot tolerate a high glucose level without developing cataracts. There is an enzyme called aldose reductase which is responsible for this rapidly occurring cataract. If it can be inhibited, then the diabetic cataract can be stopped or significantly slowed. Ocu-GLO Rx™ has ingredients that may inhibit this enzyme, though but we have not yet proven how well it can inhibit diabetic cataracts. Some of our clinical patients are still cataract free after over 2 years of taking Ocu-GLO Rx™, so we are very hopeful this will help our diabetic patients!

An important thing to remember is that even if Ocu-GLO Rx™ does not stop your dog's cataracts, it will make the eye cells' environments healthier so that surgery may be more successful! The most devastating problem with cataracts and the reason that the eye can develop irreparable damage is due to inflammation. Cataract cause inflammation and likewise, inflammation can cause cataracts. Some of the ingredients in Ocu-GLO Rx™ also help control inflammation so they will work with the topical and oral medications used before and after cataract surgery.

So, we dont want to risk this!