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Glucosamine and chondroitin in mobility foods for dogs

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Abstract

Glucosamine and chondroitin in mobility foods for dogs Dog foods, snacks and nutritional supplements containing glucosamine and chondroitin make joint-health claims. Corresponding veterinary diets purport to manage osteoarthritis, a degenerative joint disease. It has not yet been studied whether dogs ingesting glucosamine and/or chondroitin maintain healthy mobility. Research in dogs with osteoarthritis indicates that the two substances do not improve the condition. Osteoarthritis is caused by progressive loss of the cartilage that protects bones where they meet. This process is associated with inflammation so that the dog's joints may become swollen and painful. Touching the joint area then elicits yelping or flinching. Dogs are reluctant to walk, run and jump, and may develop lameness and overt immobility. Joint cartilage consists of cells embedded in a gel-like matrix between the adjacent bones. A significant proportion of the matrix molecules contains glucosamine and/or chondroitin. The two compounds can be synthesized by the dog's body, but supplementation is believed to make up aging-induced low synthetic capacity. A small fraction of orally administered pure glucosamine and chondroitin is available to joint metabolism in dogs. The mere intervention of entering dogs with osteoarthritis into an experimental setting generally produces positive observations. This is caused by biased evaluation and/or course of the disease, which are taken into account by experiments with double-blind, placebo-controlled design. Data from such experiments indicate that the intake of glucosamine and/or chondroitin does not ameliorate osteoarthritis symptoms in dogs. Canine osteoarthritis Most dogs older than five years are affected by osteoarthritis in various degrees of severity. Severe cases show symptoms of chronic pain, lameness and immobility. Osteoarthritis is a degenerative and inflammatory condition in which degradation of cartilage matrix, not compensated for by synthesis, is associated with the release of pro-inflammatory cytokines. Obesity, heavy exercise and genetics are risk factors for osteoarthritis. Cartilage damage causes inflammation of the membranes lining the joint. This triggers cartilage cells to secrete enzymes (metalloproteinases) that further break down the extracellular cartilage matrix. Once osteoarthritis has arisen, it evolves into a perpetuating process with progressive loss of cartilage and increasing severity of clinical symptoms. Osteoarthritis cannot be cured. Ideally, treatment is directed towards relief of pain by inhibition of inflammatory reactions and promoting cartilage conservation. Pharmacological therapy consists of non-steroid, anti-inflammatory drugs. Various dietary supplements, including preparations containing glucosamine and chondroitin sulfate, are recommended for support of canine joint health and treatment of osteoarthritis.
Creature Companion 2015; December: 52-53.
Anton C. Beynen
Glucosamine and chondroitin in mobility foods for dogs
Dog foods, snacks and nutritional supplements containing glucosamine and chondroitin make
joint- health claims. Corresponding veterinary diets purport to manage osteoarthritis, a
degenerative joint disease. It has not yet been studied whether dogs ingesting glucosamine and/or
chondroitin maintain healthy mobility. Research in dogs with osteoarthritis indicates that the two
substances do not improve the condition.
Osteoarthritis is caused by progressive loss of the cartilage that protects bones where they meet.
This process is associated with inflammation so that the dog’s joints may become swollen and
painful. Touching the joint area then elicits yelping or flinching. Dogs are reluctant to walk, run
and jump, and may develop lameness and overt immobility.
Joint cartilage consists of cells embedded in a gel-like matrix between the adjacent bones. A
significant proportion of the matrix molecules contains glucosamine and/or chondroitin. The two
compounds can be synthesized by the dog’s body, but supplementation is believed to make up
aging-induced low synthetic capacity. A small fraction of orally administered pure glucosamine
and chondroitin is available to joint metabolism in dogs.
The mere intervention of entering dogs with osteoarthritis into an experimental setting generally
produces positive observations. This is caused by biased evaluation and/or course of the disease,
which are taken into account by experiments with double-blind, placebo-controlled design. Data
from such experiments indicate that the intake of glucosamine and/or chondroitin does not
ameliorate osteoarthritis symptoms in dogs.
Canine osteoarthritis
Most dogs older than five years are affected by osteoarthritis in various degrees of severity. Severe
cases show symptoms of chronic pain, lameness and immobility. Osteoarthritis is a degenerative and
inflammatory condition in which degradation of cartilage matrix, not compensated for by synthesis,
is associated with the release of pro-inflammatory cytokines.
Obesity, heavy exercise and genetics are risk factors for osteoarthritis. Cartilage damage causes
inflammation of the membranes lining the joint. This triggers cartilage cells to secrete enzymes
(metalloproteinases) that further break down the extracellular cartilage matrix. Once osteoarthritis
has arisen, it evolves into a perpetuating process with progressive loss of cartilage and increasing
severity of clinical symptoms.
Osteoarthritis cannot be cured. Ideally, treatment is directed towards relief of pain by inhibition of
inflammatory reactions and promoting cartilage conservation. Pharmacological therapy consists of
non-steroid, anti-inflammatory drugs. Various dietary supplements, including preparations
containing glucosamine and chondroitin sulfate, are recommended for support of canine joint health
and treatment of osteoarthritis.
Extracellular cartilage matrix
The extracellular matrix of joint cartilage is composed of collagen and proteoglycans. The large
proteoglycan molecules consist of glucosaminoglycans (GAGs) and a core protein. GAGs are
polymers of disaccharides such as hyaluronic acid, keratin sulfate and chondroitin sulfate. The first
two contain N-acetylglucosamine as one of the two monosaccharides. For chondroitin sulfate it is N-
acetylgalactosamine. The proteoglycans, which are synthesized by the cartilage cells, have high
water-holding capacity, thus providing cushioning and lubrication effectiveness.
Glucosamine and chondroitin sulfate
The dog’s body can synthesize N-acetylglucosamine and N-acetylgalactosamine from glucose. It is
hypothesized that synthesis diminishes with aging and that oral supplementation of glucosamine
and chondroitin sulfate compensates for it. Prerequisite is that two substances are usable and
available for the synthesis of GAGs. In dogs, the extent to which orally administered glucosamine
and disaccharides of chondrotin sulfate reach the general blood circulation was found to be 11 and
5% (1). Glucosamine labeled with carbon 13 made its way through the digestive tract to the joint
cartilage of dogs (2).
Glucosamine and chondroitin occur naturally in connective tissues and thus are present in dog foods
with ingredients of animal origin. In the form of GAGs, glucosamine and chondroitin may not be
nutritionally available. Glucosamine in commercial preparations is usually derived from the shells of
crab, lobster and shrimp through various steps of hydrolysis and extractions. Purified chondroitin
sulfate is manufactured from animal cartilage such as bovine tracheal rings.
Double-blind, placebo-controlled trials
For arthritic dogs subjected to control treatments in experiments, improvement is generally
reported (3-9). The improvement over time is a placebo effect as it cannot be attributed to the
investigational intervention. Double-blind, placebo-controlled trials take into account any placebo
effects. Four out of five such trials do not provide proof for efficacy of oral glucosamine and
chondroitin sulfate in dogs with osteoarthritis.
Chondroitin sulfate alone (22 mg per kg body weight per day for 12 weeks) had no effect (3).
Likewise, a mixture of glucosamine and chondroitin sulfate (25 + 30 mg per kg body weight per day
for 6 months or 46 + 37 mg for 30 days) was ineffective (7, 10). The combination (61 + 48 mg per kg
body weight per day) was slightly beneficial after 120 days in one experiment (11), but fruitless in
another study with identical design (12).
Mobility claims
There is a wide variety of commercial preparations containing glucosamine and/or chondroitin. It
cannot be excluded that some mobility foods in the marketplace are enhanced with an effective
preparation. Pet owners who wish to learn about the investigations underlying the mobility claim on
a certain petfood product should contact the manufacturer.
Literature
1. Adebowale A, Du J, Liang Z, Leslie JL, Eddington ND. The bioavailability and pharmacokinetics of
glucosamine hydrochloride and low molecular weight chondroitin sulfate after single and multiple
doses to beagle dogs. Biopharm Drug Dispos 2002; 23: 217-225.
2. Dodge GR, Regatte RR, Noyszewski EA, Hall JO, Sharma AV, Callaway DA, Reddy R. The fate of oral
glucosamine traced by 13C labeling in the dog. Cartilage 2011; 2: 279-285.
3. Dobenecker B, Beetz Y, Kienzle E. A placebo-controlled double-blind study on the effect of
nutraceuticals (chondoitin sulfate and mussel extract) in dogs with joint disease as perceived by their
owners. J Nutr 2002; 132: 1690S-1691S.
4. Gingerich DA, Strobel JD. Use of client-specific outcome measures to assess treatment effects in
geriatric, arthritic dogs: Controlled clinical evaluation of a nutraceutical. Vet Therap 203; 4: 56-66.
5. Innes JF, Fuller CJ, Grover ER, Kelly AL, Burn JF. Randomised, double-blind, placebo-controlled
parallel group study of P54FP for the treatment of dogs with osteoarthritis. Vet Rec 2003; 152: 457-
460.
6. Pollard B, Guilford WG, Ankenbauer-Perkins KL, Hedderley D. Clinical efficacy and tolerance of an
extract of green-lipped mussel (Perna canaliculus) in dogs presumptively diagnosed with
degenerative joint disease. N Z Vet J 2006; 54: 114-118.
7. Blanchard G, Dentz JJ, Paragon B-M. The placebo effect of a supplement provided to dogs with
signs of arthrosis: a double-blind clinical trial in dogs. 10th Congress of the European Society of
Veterinary and Comparative Nutrition 2006: pp 163-164.
8. Beynen AC, Van Geene HW, Grim HV, Jacobs P, Van der Vlerk T. Oral administration of gelatin
hydrolysate reduces clinical signs of canine osteoarthritis in a double-blind, placebo-controlled trial.
Am J Anim Vet Sci 2010; 5: 95-99.
9. Beynen AC, Legerstee E. Influence of dietary beta-1,3/1,6-glucans on clinical signs of canine
osteoarthritis in a double-blind, placebo-controlled trial. Am J Anim Vet Sci 2010; 5: 90-94.
10. Moreau M, Dupuis J, Bonneau NH, Desnoyers M. Clinical evaluation of a nutraceutical, carprofen
and meloxicam for the treatment of dogs with osteoarthritis. Vet Rec 2003; 152: 323-329.
11. Gupta RC, Canerdy TD, Lindley J, Konemann M, Minniear J, Carroll BA, Hendrick C, Goad TD,
Rohde K, Doss R, Bagchi M, Bagchi D. Comparative therapeutic efficacy and safety of type-II collagen
(uc-II), glucosamine and chondroitin in arthritic dogs: pain and evaluation by ground force plate. J
Anim Physiol Anim Nutr 2012: 96: 770-777.
12. D’Altilio M, Peal A, Alvey M, Simms C, Curtsinger A, Gupta RC, Canerdy TD, Goad JT. Therapeutic
efficacy and safety of undenaturated type II collagen singly or in combination with glucosamine and
chondroitin in arthritic dogs. Toxicol Mech Meth 2007; 17: 189-196.
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