PRODUCT INFORMATION 

Animals with osteoarthritis, hip dysplasia, spondylitis and other non-specific arthritic conditions all have one thing in common; degeneration due an accumulation of free radicals in the joint. These conditions frequently have a direct effect on the pets mobility and is usually accompanied by stiffness, pain, and inflammation. 

While steroids and non-steroidal anti-inflammatory drugs (NSAID’s) are the regimen of treatment in canine and feline degenerative joint disease, long term use is known to damage chondrocytes (specialized cells which make up cartilage). Drug metabolism, cellular depletion of trace elements, Genetic control, and/or environmental factors, can increase the total body burden of free radicals (highly reactive compounds which destroy cell membranes, proteins and DNA).  

Because free radicals are toxic to cells, the body has evolved a series of defense mechanisms to prevent their accumulation to concentrations which destroy cell membranes. These defense mechanisms include a series of enzymes that convert free radicals to stable compounds before the free radical can interact with a cell membrane to produce damage to the joint. These enzymes (catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, and glutathione transferase) are commonly referred to as free radical scavenging enzymes.1 

Free radicals cause destruction to healthy cells and lead to eventual deterioration of the joint and surrounding tissue.  When an oxygen molecule loses an electron in its outer ring, it becomes a superoxide ion free radical which is highly toxic to cells. The body utilizes superoxide dismutase (SOD) to rapidly convert the superoxide ion to hydrogen peroxide which is less toxic. Hydrogen peroxide is not a free radical, but serves as a potential pool for the production of a series of highly toxic free radicals. The most toxic free radical derived from hydrogen peroxide is the hydroxyl radical. There are two known enzymatic defense systems to prevent the conversion of hydrogen peroxide to hydroxyl radicals. These enzymes and their nutrition cofactors must be provided in the diet or through nutritional supplementation.   

Catalase, (Aspergillus niger, var.), is the enzyme that converts hydrogen peroxide to water. Zinc, copper and manganese are required for its activity. Catalase is highly specific for the metabolism of hydrogen peroxide; however, it will not metabolize cellular lipid peroxides which are formed by free radicals. This is resolved with Glutathione Peroxidase (GSH-PX).  

Glutathione Peroxidase is an enzyme that also converts hydrogen peroxide to water. It can be viewed as the sweeper enzyme that metabolizes any hydrogen peroxide missed by Catalase. Even more importantly, Glutathione Peroxidase allows the repair of cell membranes back to their original status following free radical damage. Selenium is essential for the activity of Glutathione Peroxidase, and Vitamin E for converting peroxy fatty acid free radicals (PUFAO2) to non-toxic hydroxy fatty acid alcohols. Animals that are selenium deficient cannot synthesize GSH-PX and therefore lack the full protective activity of this crucial enzyme.  

Superoxide Dismutase (SOD), is the enzyme that converts the superoxide ion to the less toxic hydrogen peroxide. SOD is a “naturally occurring” enzyme that is activated with Zinc and Copper. These two minerals are required for activity in cytoplasm (the interior of the prokaryotic cell which is a watery fluid rich in dissolved salts, nutrients, enzymes and other molecules). Manganese is required for its activity in mitochondria (a small, membrane bound cellular structure responsible for converting nutrients into the energy-yielding compound; adenosine triphosphate (ATP).  Some types of zinc are known to adversely affect copper levels, and for this reason we use OptiZinc® which is a unique patented 1:1 complex of Zinc Methionine. Unlike inorganic zinc which is poorly absorbed, OptiZinc is absorbed easily and does not adversely affect the copper levels which is required for SOD activity. OptiZinc prevents free radical formation by protecting biomolecules from oxidation and limiting their production. Methionine is a sulfur containing amino acid that helps protect tissues against free radical attack. 

The body also utilizes other naturally occurring compounds to scavenge free radicals such as Vitamin A as Beta Carotene. Vitamin A protects the cells from the free radical action of rancid fats. The B-complex vitamins being water soluble, are involved in a number of enzymatic reactions including lipid, protein and carbohydrate catabolism. Vitamin C protects polyunsaturated lipids in the spinal cord from peroxidation and free radical attack. Vitamin D, Iron and Magnesium are enzyme producing agents. Choline and Inositol help to prevent lipid peroxidation. 

Glucosamine Sulfate is required for the synthesis of glycosaminoglycans (GAGS) which help to rebuild cartilage in the joint after free radical damage has extensively occurred. Glucosamine Sulfate is the preferred form of glucosamine as it is the only form backed up with over 20 double blind studies and the subject of over 300 scientific investigations. The main reason why Glucosamine Sulfate is so effective is because its small molecule size allows it to penetrate the joint cartilage and deliver it to the chondrocyte to stimulate GAG synthesis. Additionally, Glucosamine Sulfate contains the sulfur molecule, which is the essential nutrient required for joint tissue where it functions in the stabilization of connective tissue matrix of cartilage, tendons and ligaments. Both Glucosamine Hydrochloride (HCL) and N-acetyl-Glucosamine (NAG) lack the crucial sulfur molecule and it is therefore unlikely that either will show the same clinical results achieved with Glucosamine Sulfate. Condroitin Sulfate is a mixture of intact or partially hydrolized GAGS and is composed of repeating units of derivatives of Glucosamine Sulfate with attached sugar molecules. While the absorption rate of Glucosamine Sulfate is 90% to 98%, Condroitin Sulfate is estimated to be anywhere from only 0% to 13%. The major reason for the difference in absorption is largely due to the difference of the molecule size. The Chondroitin Sulfate molecule is at least 50 to 300 times larger than the Glucosamine Sulfate molecule. Condroitin Sulfate molecules are too large to be delivered to cartilage cells and provide little, if any benefit.  One group of researchers concluded that “pooled literature on condroitin sulfate biochemistry offers enough information to assert that neither intact, nor polymerized chondroitin sulfate is absorbed by mammalian gastrointestinal tract. Therefore, any direct action of orally administered chondroitin sulfate on cartilage and chondrocytes is not possible.”  

Being that Condroitin Sulfate does not have active intestinal transport, low absorption (if any), very few clinical studies, and no scientific studies, it is hardly necessary to take Glucosamine Sulfate with Condroitin Sulfate in order to achieve adequate results. It appears that taking the combination provides little, if any benefit compared to glucosamine sulfate alone...2, 3, 4.