The Use of Nutraceuticals and Dietary
Supplements for
Joint Support and Health in Cats and
Dogs
Presented to: Dr. Meg Smart, Small
Animal Nutrition Elective
By: Karen Choptain
Introduction
The use of
nutraceuticals and dietary supplements, either in manufactured pet foods or as
adjuncts to diet, are not necessarily new to the domestic animal world. There
have, however, been more recent use of advertisements and promotions of diets
and supplements being sold that tout the benefit of such products to aid in the
area of joint health and stabilization.
These products have become quite popular with the public, as they allow
for adjunctive therapy or alternative therapy in cats and dogs that suffer from
osteoarthritis (OA) or degenerative joint disease (DJD) (1).
What is a
nutraceutical? A nutraceutical, as
defined by the North American Veterinary Nutraceutical Council, is “a nondrug
substance that is produced in a purified or extracted form, administered orally,
to provide compounds required for normal body structure and function with the
intent of improving health and well-being” (1,2). More specifically, a
nutraceutical used in the aspect of joint support can be referred to as a
chondroprotectant. This term has been
applied to substances such as glucosamine, chondroitin sulfate, combination
products of the two, New Zealand green-lipped mussels (GLM), omega-3 fatty
acids, anti-oxidants such as Vitamin C and Vitamin E and other dietary
compounds such as P54FP, Avocado/soybean oils, Boron, Boswellia Resin, Cat’s
Claw, Creatine, and Special milk protein concentrate (3). Chondroprotectant agents base their purpose
on providing the following three primary effects: 1) to support or enhance
metabolism of chondrocytes and synoviocytes, 2) inhibit degradative enzymes
within synovial fluid and cartilage matrix, and 3) inhibit formation of thrombi
in small blood vessels supplying the joint (1).
In humans,
the use of dietary supplements is regulated under the Dietary Supplements
Health and Education Act (1). This is in order to allow consumers the
opportunity to purchase a variety of products that are marketed for joint
health and support. The products
themselves must be safe; however, they do not have to achieve pre market
approval, in contrast to pharmaceuticals or “drugs”. The aforementioned act does not apply to
dietary supplements in the veterinary market. While the Canadian Veterinary
Medical Association withholds the right to remove products from the market,
providing the product is safe and does not pose a threat to human safety it may
be sold (1). The product also may not advertise claims such as being used to
treat, cure, prevent or mitigate a disease (1).
In addition,
label claims and quality control of these products has been documented (1, 4,
5). Due to the lack of quality assurance, the consumer cannot be guaranteed
that the product itself is of the concentration listed on the label or of its
purity (1). A large variety of products
are available to consumers. Despite the
number of products, there is a drastic lack of scientific evidence that
promotes any on of these products over the other. This paper serves to provide some clarity to
the commercial foods and supplements that are available to consumers and
critically evaluate their efficacy for the use of joint support and health in
cats and dogs.
Osteoarthritis in Dogs and Cats
In order to
fully appreciate and understand the proposed use of chondroprotectants one must
first have an idea of the function of a healthy joint and how it differs from a
diseased joint. Understanding the
pathophysiology of a diseased joint can help to show areas in which
chondroprotectants may act to mitigate the disease process and alleviate the
pain, discomfort, and debilitating effects of OA.
Unlike in
the human species where OA is attributed to a normal aging process, in our
domestic species an underlying process is generally at play. OA itself is defined as being a non
inflammatory disorder of moveable joints (6, 7). In dogs and cats an underlying
pathology is suspected to be the predisposing factor for the development of OA.
Obesity causing excessive load bearing on joints, cruciate ligament tears,
fractures, and developmental disorders such as Legg-Perthes-Calves disease,
osteochondritis dessicans, osteochondral disease, hip dysplasia and patellar
luxation are all factors which can lead to the development of OA (1, 6).
The normal
diarthrodial joint is composed of a joint capsule, synovial fluid, articular
cartilage and subchondral bone (1). The
joint in question serves the purpose of providing a smooth surface that is able
to distribute the load from one bone to another. The two opposing bones are covered on the
surface by an avascular and aneural articular cartilage.
Articular Cartilage
The
articular cartilage is divided histologically into multiple zones and is
composed of chondrocytes surrounded by a matrix. This lies on top of the subchondral
bone and assists in the deliverance of load bearing forces to the underlying
bone. The chondrocytes themselves are the primary cell within the articular
cartilage. The matrix that is
surrounding these cells is composed of 70-80% water with collagen and
proteoglycans (PG) being the residual make up (6, 8). Chondrocytes produce the
PG within the Golgi apparatus (6). They also are responsible for the production
of the collagen within the matrix. These cells are essential as they possess
little mitotic ability and thusly are not readily replaced as they die (1).The
PGs make up 35% of the matrix on a dry matter basis and are composed of a core
protein with side changes of glycosaminoglycan (GAG) molecules that make up a
further 10% of the matrix (6, 9). The four primary GAGs present are
chondroitin-4-sulfate, chondroitin-6-sulfate, keratin sulfate and dermatan
sulfate (6). The GAGs are made up of
repeating disaccharide units of six unit sugars, primarily glucosamine or galactosamine
that alternate with glucuronate, iduronate or galactose (11). The PGs present
are linked by the protein hyaluronan and it is this protein that forms the
backbone of the large molecule aggrecan (6, 10). The primary collagen types
present in the cartilage are Type I and Type II with the later making up as
much as 90% of the joint, however types III-XI are also present (6, 9,
10).
A
functioning joint serves for load bearing based on the makeup of the articular
cartilage. When a load is applied to the joint, water is released from the
cartilage. This helps to lubricate the joint and disperse the load to the
underlying bone. When the force is released, the water returns to the articular
cartilage. This process also serves the function of removing waste from the
cartilage and returning nutrients to the chondrocytes.
In a
diseased joint, loss of articular cartilage occurs. This contributes to pain
and loss of function. On gross evaluation, articular loss can be seen with
fibrillation, erosion and wear lines on the surface of the articular cartilage
(11, 12). On radiographs, this can be seen as a narrowing of the joint space.
In addition, other radiographic signs can be seen in OA which include
periosteal bone proliferation, osteophyte/enthesophyte production, subchondral
bone loss and effusion of the joint. It has been proposed that initial changes
in load bearing forces leads to disruptions of the collagen cross-linkages and
subsequent PG loss (6, 14). Another cause of the cartilage loss is due to
degradation enzymes affecting the extracellular matrix leading to loss of PGs
and Type II collagen (11, 13). These enzymes include matrix metalloproteinases
(MMPs) and aggrecanses (11). These enzymes are normally present and aid in
cartilage turnover. Their control is via tissue inhibitors of
metalloproteinases (TIMPs) which unfortunately are decreased in production with
OA (11). These substances are produced from the chondrocytes when inflammatory
mediators are released from the synovial cells (6).
Joint Capsule
The joint
capsule is also several layers thick and surrounds the diarthrodial joint. The
inner vascular and neural surface is lined with synovial cells called the
synovium. The cells are broken down into Type A and Type B. Type B cells
function to provide the makeup of the fluid within the joint. They serve to
provide nourishment, remove waste products and lubricate the joint. Lubrication
of the joint is provided by the production of hyaluronic acid and lubricin (6, 9).
Conversely, Type A cells serve the
function of phagocytosis.
When loss of
the articular cartilage begins with fibrillation, the synovium serves the
purpose of phagocytosis and clearing of the cartilage fragments (6). This
occurrence leads to inflammation of the synovium and is referred to as
synovitis (6, 15, 16). This inflammation
leads to a cascade of effects within the joint. First, the inflammation leads
to an increased vascular permeability which can contribute to edema within the
joint (6, 9). Consequently, with the increased permeability, inflammatory cells
are able to enter the joint space. The synovitis also leads to a number of
cytokines released by the synovial cells. Synovial cells stimulate the
production of the previously mentioned proteases (MMPs and aggrecanase) by
chondrocytes (6, 17). The main MMPs are collagenase and stromelysin (6).
Collagenase is responsible for the breakdown of collagen and stromelysin breaks
down PGs (6, 18). In vitro studies have shown that stromelysin is also capable
of breaking down Type II collagen (11, 22).The synovial cells, as well as
chondrocytes and monocytes, are responsible for increased secretion of cytokine
IL-1, IL-6 and TNF-α (6, 18, 19, 20). While these cytokines are normally
present within the joint and help to maintain homeostasis, in OA they are
secreted in excess. IL-1 has been shown
to have inhibitory effects on TIMP and thusly contributes to the overproduction
of MMPs by the chondrocytes (6, 21). It has also been speculated that IL-1
decreases production of collagen and PG by chondrocytes and increases the
production of PGE2 (6, 19, 20). IL-6 has been shown to decrease cartilage
matrix synthesis and may stimulate TIMP (6). Increased neutrophil migration into the joint
space is detrimental, as these cell release elastase and cathepson-G which
further degrade cartilage (6). Phospholipases can act on cell membranes to
activate the COX and LOX cascade which results in production of prostaglandins
(namely PGE2) and leukotrienes (6). These substances further exacerbate
inflammation and can be attributed to the production of pain.
In vitro
studies were carried out Siminaro and colleagues (23) and they reported
increased secretion of MMP-2 and MMP-9 by arthritic chondrocytes. They found that while increased MMP within
tissue may also increase TIMP-1 secretion, the effect of NO and pro-inflammatory
cytokines was inhibitory on TIMP-1. In
addition to this, they also found the IL-1, and TNF-α that were produces by
chondrocytes, synoviocytes and macrophages leading to up-regulation of the MMP
gene expression (23).
Treatment of OA in Dogs and Cats
While the
disease processes underlying OA in dogs and cats are rather complex,
understanding the signalling cascade present within the joints provides a basis
for potential use of nutraceuticals in the aid of treatment of the
disease. A multimodal approach is
preferred in treating these patients.
Correction of an underlying congenital abnormality or traumatic injury
surgically must be considered. The use of NSAIDs, nutraceuticals, dietary
supplements, physical therapy and weight loss are all also key to alleviating
symptoms of the disease. Currently there is a large appeal to clients for using
adjunctive therapy other than prescription medications for their pets.
Nutraceuticals and dietary supplements are in the forefront of products which
are available to consumers. Oral administration provides an easy method for
people and their pets to employ. As an estimated >20% of dogs over 1 year of
age are reported to be affected by OA (3), there is certainly a need for products
that may help to decrease the pain associated with the disease.
Currently Reported
Nutraceuticals/Dietary Supplements:
1) Glucosamine
Glucosamine
is a mono amino monosaccharide that once modified to N-acetylglucosamine is a
precursor to the disaccharide units of GAGs, hyaluronan and keratin sulfate
(11). Conversion of glucosamine to galactosamine provides a component of
chondroitin sulfate and dermatan sulfate (11). In vivo, glucosamine is produced
by chondrocytes, however; in cases of OA, chondrocytes appear to have a
decreased ability to synthesize glucosamine (1, 25, 26). There are no dietary
sources of glucosamine, rather it is produced commercially from chitin; a
component of the exoskeleton of shrimp lobsters and crabs (24). The product of
glucosamine is available commercially in three forms: glucosamine sulfate,
glucosamine hydrochloride and N-acetyl-glucosamine.
Mechanism of Action
Since
glucosamine is a precursor for the formation of GAGs, it is been reported that
supplementation may increase the production of PGs. Cell culture studies have
shown the exogenous glucosamine stimulates the production of PG as well as
collagen by chondrocytes (1, 27, 28). In a rabbit model, glucosamine was shown
to significantly restore levels of GAGs within damaged cartilage (24, 29). In cultured human OA chondrocytes, it was
suggested that stimulation of messenger RNA and protein levels of aggrecan core
protein, as well as inhibition of MMPs were possible mechanisms of action of
glucosamine (24, 30). In an abstract for
a model of cartilage collage, lipoxidation was also inhibited by glucosamine
thus attributing to the claims of its use for anti-inflammatory properties (24,
31). Glucosamine has also been shown to
reduce the transcription factors involved with IL-1 (11).
Bioavailability, Recommended Doses
and Toxicity
In both dogs
and cats the oral availability of glucosamine is rather high. An intestinal
absorption rate of 87% has been documented (1, 32) with distribution to tissues
being highest in the liver, kidney and articular cartilage (1, 33, 34). When
evaluating in vitro effects and correlating the data with bioavailability, it was
determined that the effective recommended dosage of glucosamine HCL be 22mg/kg
(11, 35). Toxicity of glucosamine appears to be minimal. At doses of 5g/kg the only reported adverse
effect was mild gastrointestinal upset including flatulence.
It should be
noted that glucosamine products are not required to be monitored. In a review of 14 OTC products available, the
amount of actual glucosamine present varied from 59-138% (24).
Evidence Based Medicine with
Glucosamine
Human
efficacy:
In a review
by Neil and colleagues of a meta-analysis and quality assessment of 15
randomized double-blind placebo controlled studies, 14 out of the 15 studies
revealed beneficial effects with regards to decreasing pain and improving
mobility (11, 36). That being said, when glucosamine was compared to the use
with glucosamine and chondroitin, benefits were greater in the later.
In a 3 year
long administration of glucosamine vs. placebo, 20-25% improvement of pain and
function were reported (11, 37, 38). This may however show bias, as when a
similar short term trials were carried out, glucosamine showed no significant
improvement.
In a
randomized, controlled, double-blinded trial comparing placebo and glucosamine
on knee OA, Hughes and Carr discovered that there were significant effects on
glucosamine for lower pain and improving function (11). The trial was compared
to a similar trial that had previously been carried out with the result that
glucosamine had no significant effect.
In 2010, the Annual rheumatoid Disease journal
published the results of a 2 year study which attempted to show the clinical
efficacy of glucosamine, chondroitin sulphate, a combo of the two, celecoxib
and placebo (39). The trial was a double blinded, placebo controlled study of
583 patients followed over a 6 month period. The intent was to compare all
groups and evaluate the ability to reduce pain and improve function based on the
Western Ontario and McMaster University Osteoarthritis Index. Patients were
then followed for a further 18 months to evaluate radiographic changes to joint
space width. Those in the glucosamine
HCL group received 1500mg daily. There were no significant changes noted within
any of the groups. There were however, trends that were noted within the study.
In all groups (including that of the placebo group) improvement occurred within
the first 18 weeks of treatment with celecoxib providing the most rapid results. At the end point of the trial, glucosamine
and celecoxib groups both showed a trend for being highest at the end point.
With respect to the 2 year study, celecoxib showed the best pain and function
repair. There were also a group of
patients that at the beginning of the trial showed the most intense symptoms.
Of these patients it was shown that the combination of glucosamine and
chondroitin showed the best effects.
Again, none of these results were statistically significant.
Canine
efficacy:
There were
no studies found that evaluated the use of glucosamine as a sole agent in
dogs. Clinical trials of canine patients
all involved the administration of glucosamine in combination with
chondroitin. More information on these
studies to follow. A study of the effect of glucosamine on experimental rat
osteoarthritis was found. After OA was
surgically induced in rats, treatment groups were based on treatment with
glucosamine, without glucosamine and a sham group. The rats receiving
glucosamine were administered 1000 mg glucosamine HCL/kg/day. The elevated dose
was based on poor metabolism of the drug and poor bioavailability in the
species (46). Statistically significant reduction in degenerative changes on
the surface of articular cartilage was seen in the group treated with
glucosamine (46). In addition, biomarkers of OA were also decreased in the group
treated with glucosamine (46).
2) Chondroitin
Sulfate
Chondroitin
Sulfate is a GAG composed of glucuronic acid and sulfated N-acetylgalactosamine
(11). Chondroitin is produced in vivo by
chondrocytes of articular cartilage. Exogenous sources of cartilage can be used
as a supplement.
Mechanism of Action
Use of
chondroitin sulfate has been advocated as it has been determined it can
decrease IL-1 production, block complement, inhibit MMPs, inhibit
histamine-mediated inflammation and stimulate GAG and collagen synthesis (11,
40, 41).
Bioavailability, Recommended Dose and
Toxicity
Oral
absorption in dogs has been reported to be as high as 70% (11, 42). When evaluating
in vitro effects and correlating the data with bioavailability, it was
determined that the effective recommended dosage of 8.8mg/kg (11, 35). Plumb’s Veterinary Handbook reports a dose of
13-15mg/kg for dogs and 15-20mg/kg for cats (43, 44). Chondroitin appears to
accumulate in the serum leading to an estimated bioavailability of 200% (1, 33,
45).
The author
was unable to find any evidence based medicine including the use of chondroitin
alone. The combination of chondroitin
with glucosamine was available. This is
likely attributable to the fact that a great deal of products available have
the two compounds supplied together. A
synergistic effect can be extrapolated by an in vitro study on equine
cartilage. The use of the two components together decreased nitric oxide
production, PG degradation and inhibited MMP-9 and MMP-13 (11, 45).
Human
efficacy:
As
previously mentioned, in 2010 a 2 year human study was carried out comparing
glucosamine, chondroitin sulphate, a combination of the two, celecoxib and
placebo. While there was no scientific
significance between groups, the chondroitin and glucosamine combination showed
the most benefit in a subset of patients that had more severe signs attributed
to OA (39).
Canine
efficacy:
A randomised
double-blinded, positive-controlled trial published in 2006 by McCarthy and
colleagues showed the efficacy of glucosamine and chondroitin sulfate used in
the treatment of OA in dogs. The study
included the use of 42 dogs recruited from private practice. The dogs were in treatment groups receiving
carprofen or Synoquin SA (glucosamine/chondroitin). The dogs received the manufacturer’s
recommended doses of active ingredient. Animals were assessed prior to
initiation of treatment by both veterinarians and their owners and subsequently
on days 14, 42, 70 and 98. Dogs in the
Synoquin SA group showed significant improvement in disease score at day 70 for
pain, weight-bearing and overall condition when compared to pre-treatment score;
however lameness and joint mobility were not significantly improved (47). It should be noted that the Carprofen group
had a greater mean reduction in disease. Limitations of this research are the
lack of quantitative ground force reaction testing. The results are rather
based on subjective assessment. The data of the placebo group was also not
reported. There is no means of evaluating if a placebo effect was seen by
either the clinicians or their owners.
Based on this data, one can extrapolate that while Synoquin SA did not
provide a better means of improvement in OA over Carprofen, there were
statistically significant changes seen. This supports the recommendation of
this nutraceutical as an adjunct in the treatment of OA.
Conversely,
in a review by Budsberg and Bartges (3) contradictory results were found. In a
study by Moreau and colleagues, 71 dogs were evaluated in a prospective
double-blind study (48). Dogs were divided into groups given
glucosamine/chondroitin, carprofen and Meloxicam. The evaluation was similar to the above
study, however; ground force reaction was also measured. Changes in the ground reaction forces were
statistically significant in the dogs receiving the pharmaceuticals; however
they were not in those receiving glucosamine/chondroitin (3). Clinicians felt
that there had been an improvement with carprofen and Meloxicam, differing from
the owners’ opinions that improvement was seen only with Meloxicam (3).
In another
review by Aragon and colleges (49) a trial of 19 dogs receiving chondroitin,
glucosamine and manganese ascorbate revealed no improvement either subjectively
or objectively.
3) New Zealand Green-Lipped Mussels
New Zealand
Green-Lipped Mussels (GLM) has been known for some time as a dietary supplement
in canine diets. It was not until 1986
that dried mussel extracts were stabilized with a preservative (3). Prior to
this date no there were no published studies able to provide evidence of
beneficial effects of this substance and it has been speculated that the lack
of stabilization of the product may be a contributing factor in contradictory
results of clinical studies (3, 50).
Mechanism of Action
GLM are
published to contain GAGs, omega-3 fatty acids, amino acids, vitamin and
minerals (1, 51). Despite these varied
properties, the benefit of use of GLM in OA is thought to be from the
anti-inflammatory effects of the omega-3 fatty acid tetrenoic acid (3, 51).
Canine
efficacy:
As reviewed
by Budsberg and Bartges (3), a randomized controlled clinical study of 31 dogs
with OA was carried out with 0.3 % GLM powder added to a generic diet (52). The
dogs were evaluated with subjective arthritis score for joint swelling, pain,
crepitance and range of motion.
Statistically significant results for improvement of joint swelling and
pain were seen in the dogs that received the GLM powder. This article was also reviewed by Beale (1). In
his review, he highlighted the points that the dogs included in the study were
not officially diagnosed as having OA (1). Further to this, he also mentioned
that control dogs showed worsening of their joint pain and swelling over the 6
week study period which is uncommon of the slowly progressive disease of OA
(1). In another review by Johnston and colleagues (54), two trials conducted by
Aragon and colleagues showed that in prospective and randomized trials of GLM
showed a subjective positive effect on dogs with OA. These trials however, did not have positive
or negative controls and lacked scientific evidence (54).
In a second
study reviewed by Budsberg and Bartges (3), 71 dogs were divided into groups of
chondroitin sulfate, GLM and a placebo (53). The study included 58 dogs that
completed the 12 week trial. In this trial it was reported that none of the
groups showed any significant improvement of clinical signs (3).
4) P54FP
P54FP is an
extract of Indian and Javanese tumerics with active ingredients that include
curcuminoids and essential oils (3, 54).
Mechanism of Action
Evidence is
present supporting the capability of anti-inflammatory effects of P54FP.
Curcumin has been documented to inhibit PGE2 and cyclooxygenase-2 (3, 55, 56,
57).
Canine
efficacy:
In a
randomized, blind, placebo-controlled, parallel- group clinical trial 61 dogs
were recruited (58). The dogs were allocated to the P54FP group and a placebo
group for 8 weeks. Treatment was assessed using both clinical assessments of
lameness and joint pain by the authors as well as quantitative measurements of
affected joints, and overall response by the owners. No statistical
significance was seen in the quantitative measurement of the affected joints
(58). Interestingly, while the authors subjective assessment of improvement
showed statistical significant, the assessment of the owners did not (3).
5)
Boswellia Serrata
Resin
extracted from the tree Boswellia serrata has been shown to decrease leukocyte
infiltration, decrease antibody synthesis and inhibit the complement pathway
(59).Sharma ML, Khajuria A, 1. Kaul A, et al.
Effects of salai guggal ex-Boswellia serrata on cellular and humoral immune
responses and leukocyte migration. Agents Actions 1988;24:161-164.
Budsberg and Bartges commented on a study of this compound.
In an open, multicentric clinical trial of 29 dogs with OA 400mg per 10 kg was
administered once daily for 6 weeks (3, 60). Statistically significant
improvement was observed in 17 of the 24 dogs (3).
6) Avocado and Soybean Oils
The unsaponifiable fractions of both avocado and soybean oils
have in vitro been shown to be beneficial in OA by inhibiting IL-1 and
stimulating collagen synthesis (3, 61, 62). As reviewed by Budsberg and
Bartges, clinical trials in humans have shown both positive effects and also no
benefits for the alleviation of clinical symptoms of OA (3).
7) Boron
Boron deficiency in human diets has been suggested as a cause
of arthridities in humans. Budsberg and
Bartges referred to a double-blind placebo and boron supplementation trial in
20 patients with OA (3). A significantly positive response was seen with diets
supplemented with boron.
8) Cat’s Claw
Budsberg and Bartges refer to the plant Uncaria tomentosa. Although
studies have not been reported in dogs with OA, based on the anti-inflammatory
and antioxidant effects seen in humans with rheumatoid arthritis, they suggest
its potential for the use in domestic pet species.
9) Creatine
Creatine has been used in instances of rheumatoid arthritis
in human for the production of ATP and improvement of skeletal muscle weakness
(3). Its evidence has not been published for dogs with OA.
10) Special Milk Protein Concentrate
Anti-inflammatory properties have been attributed to
inhibition of neutrophil migration (3, 63). Components found within this
concentrate have been immunoglobulins, cytokines, enzymes, hormones and growth
factors (3). Budsberg and Bartges report that clinical trials have shown
subjective improvement in dogs with OA when administered SMPC when compared to
placebo (3).
11) Omega-3 fatty acids
Omega-3 and Omega-6 fatty acids have been considered
essential nutrients for decades. The health benefits which have been attributed
to their dietary addition have been on cardiac, renal, hepatic and
integumentary health as well as the reduced in rate and recurrence of
neoplasia. Omega-3 fatty acids have also been shown in clinical studies to aid
in the support of joint health in those affected with OA.
The parent compound of omega-6 fatty acids in linoleic acid
(18:2n-6) or LA. Primary sources of LA are vegetable oils, examples of which
being soy, corn safflower and canola oils (64). LA can be metabolized by the
body to form arachidonic acid (20:4n-6). In cats, the conversion is decreased
and thus, they must receive some AA supplementation in their diets (65). AA can
be provided with animal fats as well as the precursors to AA via black current,
borage and evening primrose oils which contain γ-linoleic acid (18:3n6) (64).
The parent compound of omega-3 fatty acids is alpha linoleic
acid (18:3n3). Dietary sources of ALA are from plants, flax and flaxseed oil
(64). Metabolites of ALA include EPA, DPA and DHA. These three metabolites can
be found in fish meal and cold water marine oils (64).
Bioavailability,
Doses and Toxicity
Ranges in the ratios of omega6:3 fatty acids have ranged
anywhere from 25:1 to 5:1 in the past. New research has shown that this ratio
has steadily been decreasing in commercial pet foods. Metabolism of LA and ALA are both via the same
enzymes. Of these, a higher affinity is present for ALA leading to the higher
recommended proportion of omega6:3. While a lower ratio has been advised,
excessive levels of DHA of more than 1.5% can lead to reduced growth, reduced
language development, behavioural changes, reduced cognitive function, and a
delay in reflexes in rodents when an adequate amount of AA is not provided (65,
69, 70, 71, 72).
In a study reviewed by Bauer (66) comparing conversion of
ALA, 84 dogs were fed with either a diet containing 3% sunflowers seed or 3%
flaxseed (67). The sunflower seed diet had 9.3% calories as LA and 0.4% as ALA
versus the flaxseed diet with 7.4% LA and 2.5% ALA (66). In the flax seed diet
accumulation of EPA began after 4 days post initiation of the feeding trial
with peak plasma levels reached at 28 days (66). DPA was also detected but did
not accumulate in the plasma as DHA.
In humans, when flax oil was compared to fish oil, flax
showed 7% efficiency in increasing plasma levels of EPA when compared to the
fish oil (65). Fish oil was also able to increase not only EPA plasma levels,
but also DPA levels. Dogs appear to be
even more less efficient than humans in the conversion of ALA to DHA (65).
Based on most research showing the inefficient conversion of
ALA to DHA, a large proportion of diets promote the use of fish oils over flax
seed oil. It has however been suggested that 1) DPA formed from ALA may be
delivered to the cells directly, which then convert it to DHA limiting an
accumulation within plasma and 2) DPA can be converted back to EPA and
contributes to the accumulation of EPA plasma levels (66).
In a study reviewed by Bauer (66), dogs were fed diets
containing ALA from flaxseed oil and EPA from fish oil, beef tallow and
safflower oil (68). While diets containing fish and flax seed oil contained
similar omega-6:3 ratios and both showed an increase in omega-3 incorporation
into neutrophilic membranes, a higher level was seen with the fish oil diets
(66).
In an unpublished study by Bauer and colleges, fish oil
supplemented diet fed to dogs with OA resulted in significant increased in both
EPA and DHA in the plasma and synovial fluid AND a decrease in AA. Reductions
in MMP-2, MMP-9 and PGE2 were also seen (66).
Mechanism of action
Upon inflammatory insult, cytokines are released from the
cell membranes. These cytokines can act as inflammatory mediators and stimulate
the production of eicosanoids which further exacerbate inflammation. PGE2,
IL-1, IL-6 and TNF-α levels all increase in plasma levels of OA patients.
EPA and DHA
have been shown to decrease these inflammatory mediators (65, 73, 74, 75). As
reviewed by Budsberg and Bartges (3), an unpublished study had 18 dogs randomly
assigned into three groups with identical diets except for the omega-6:3 ratios.
The dogs were fed the diet prior to and after surgical transaction of the
cranial cruciate ligament. The group that consumed the diet that was highest in
omega-3 (0.7:1.0) had lower serum cholesterol, triglycerides and phospholipids
(3). They also had decreased levels of PGE2 in the synovial fluid and had
stronger ground reaction forces (3).
In a
prospective, uncontrolled study of 146 dogs with OA, 88% of the dogs showed
clinical improvement in lameness after 2 months of being fed Purina JM which
contains omega-3 fatty acids from a fish oil source at a dose of 250mg/100Kcal
(65).
Antioxidants
Use of
antioxidants in the clinical situation of OA has been described primarily in
human literature. Vitamin E and vitamin
C have been reported in clinical trials; however they both have significant
contradictory results. In addition, dogs are reported to be able to synthesize
endogenous vitamin C and so its addition to diet would be redundant (3).
Commonly recommended
nutraceuticals/dietary supplements:
In March,
2012 an unpublished, collaborative survey was conducted by the author and three
other fourth year veterinary students in the small animal nutrition elective at
the Western College of Veterinary Medicine.
The survey was conducted in order to establish what kinds of supplements
and/or diets were being advised by both veterinarians and pet stores across
Saskatoon. Of the 22 veterinary hospitals only 9 responded to the survey
request. Out of the 7 pet stores, 6 responded
to the survey. The remaining store, Petsmart, refused to answer any of our
questions as they were instructed not to by the store owner. Our questions pertained to the products used
(brand name) as well as if any products were advised to be purchased at health
food stores. We also wanted to know why these particular products were advised,
and where the information about the products in question was received.
Veterinary
Dispensed/Recommended Supplements:
All of the
clinics that responded either advised or sold products containing glucosamine,
glucosamine/chondroitin and omega-3 fatty acids. The majority of these products
were sold in clinic. A small number of
clinics advised for them to be purchased at health food stores in the city. The
main reason these products were recommended were because of published
literature stating the significant effects of these products on joint
health. The table below lists the
products that we were given brand names of. The most commonly sold products
were glucosamine (56%), chondroitin (44%) and omega fatty acids (44%).
Veterinary
diets were also highly advised by the veterinary hospitals surveyed. The diets
were primarily the same for all clinics and were exclusively sold veterinary
diets. The diets were recommended based on information supplied from the
various food company representatives. The foods advised by the hospitals were
Hill’s j/d (canine), Royal Canin/Medi-cal Mobility Support (canine and feline)
and Purina JM.
The
recommendation for the diets was apparent when there was a diagnosis of OA in
patients. Omega-3 fatty acids and glucosamine/chondroitin were also recommended
as supplements for apparently healthy animals as a preventative measure by more
than 50% of the surveyed clinics.
Table 1 Brand Name Products
Recommended by Veterinary Hospitals
|
Product
|
Company
|
|
|
|
|
Dasuquin
|
Nutramax
|
|
|
Laboratories
|
|
Cosequin
|
Nutramax
|
|
|
Laboratories
|
|
Omega Pro 3
|
Pro Concepts
|
|
|
Animal Health
|
|
Ubavet Liquid
|
|
|
Plus
|
Ubavet
|
|
Flexadin
|
Vetoquinol
|
|
Zukes Hip Action
|
Zuke's
|
|
Chondro Flex
|
Champion Alstoe
|
|
|
Animal Health
|
Pet store
available supplements/diets:
7 pet stores
were also surveyed within Saskatoon. Two were larger stores and five were more
intimate/specialty pet food/supply stores.
The larger two, Petsmart and Petland, were unable to fully answer the
survey but the products available in the store were reviewed. The small
specialty stores were extremely knowledgeable about the products that they
carry. We were informed that their information regarding the products was supplied
by the manufacturers, nutritionists and own research. Local products seem to be
more popular staff were more readily available to answer any questions. In
addition, the sale of locally produced products was beneficial to the local
economy. Suppliers also had personal experience using the products that they
more readily advised to their clients.
Table 2 Brand Name Products Sold by Pet
stores
|
Product
|
Company
|
|
|
|
|
Spring Meadows
|
Spring Meadows
|
|
liquid joint care
|
|
|
|
|
|
Naturvet Hip and
|
Naturvet
|
|
Joint Formula
|
|
|
Biologic Vet
|
Biologic Vet
|
|
joint support
|
|
|
Flax Forward
|
Juka
|
|
Cetyl M
|
Response
|
|
Glucosamine +
|
21st Century Pet
|
|
Chondroitin
|
|
|
Halo hip and joint
|
Halo
|
The
specialty pet supply stores advised the use of a high quality ingredient pet
food. One store advocated the use of raw
diets, in particular the brand Spring Meadow’s. Their explanation is that they
felt it provided the best products for a balanced diet and that the company was
locally based with all ingredients being locally grown. If raw diets were not
an option a fish based diet high in omega-3 fatty acids would be preferred.
Brand names that were repeatedly brought up in all the specialty stores were
Acana, Orijen and Horizon.
A Discussion on Commercial Veterinary
Diets:
A trend
become quite apparent in the veterinary hospitals in regards to the diets that
they recommended. All of the clinics
suggested the use of a commercially available veterinary diet for the aid in
treatment of dogs and cats with OA. A comparative look at the four main canine
diets revealed that they did differ slightly in composition. All of the diets compared claimed to improve
mobility in affected dogs. They all advertised the presence of high omega-3
fatty acids. They all presented the aspect of being low in caloric density
which would be beneficial in weight reduction. Two of the diets had the
advertisement of having L-carnitine to maintain lean muscle mass. One of the
diets contained GLM as a joint support ingredient and antioxidant. All of the diets contained glucosamine and
two of the diets also contained chondroitin. Table 4 outlines a comparison of
the available information online for clients to view. Added is the amount of
glucosamine/chondroitin for Hill’s j/d and Purina JM. This data was received
from the company representatives. Table 3 displays the advertising claims of
the four diets reviewed.
Table 3 Claims Supporting Use of
Commonly Prescribed/Recommended Veterinary Diets
|
Hill’s j/d
|
Purina JM
|
Medical Mobility
Support
|
Royal Canin Weight
& Osteo
|
|
1) Improve dog’s ability to run, walk,
jump in as little as 21 days
|
1)improve mobility
|
1) improve mobility and reduce pain
with omega fa ratio
|
1) enhance joint support
|
|
2) excellent source of omega-3 fatty
acid EPA
|
2) high EPA and omega-3 fatty acids
|
2) high in omega 3 and 6 fatty acids
|
2) enriched with EPA and DHA
|
|
3) controlled calorie content
|
3) high protein/calorie ratio,
moderate fat content
|
3) reduced calorie content
|
3) restricted calorie
|
|
4) added L-carnitine to maintain
healthy weight
|
4) appropriate levels of omega 6 fatty
acids
|
4) GLMP support joints and is
anti-inflammatory
|
4) L-carnitine added
|
|
|
5) high levels of antioxidant vitamins
E and C
|
5) omega3 and 6 promote healthy skin
and coat
|
5) Vitamin E and C for antioxidant +
taurine
|
|
|
6) natural source of glucosamine
|
|
6) glucosamine added
|
|
|
7) excellent palatability
|
|
7) highly digestible protein
|
|
|
|
|
8) aids in dental health
|
|
Table 4
|
Comparison of Commonly
Prescribed/Recommended Veterinary Diets for Joint Support/Health
|
|||
|
|
|
|
|
|
|
Nutrient and Caloric
|
Hills J/D dry
|
Purina JM
|
Medi Cal Mobility
Support
|
Royal Canin Weight
& Osteo
|
|
Contents:
|
|
|
|
|
|
% dry matter
|
|
|
|
|
|
Protein
|
20.1
|
30
|
25
|
29
|
|
Fat
|
16.3
|
12
|
12
|
10
|
|
Carbohydrate
|
51.1
|
|
|
|
|
Crude Fiber
|
7.8
|
4
|
2.1
|
10.5
|
|
Calcium
|
0.71
|
|
|
0.81
|
|
Phosphorus
|
0.54
|
|
|
0.68
|
|
Potassium
|
0.79
|
|
|
0.62
|
|
Sodium
|
0.17
|
|
|
0.32
|
|
Magnesium
|
0.145
|
|
|
0.65
|
|
Carnitine
|
349 ppm
|
|
|
|
|
Vitamin C
|
203 mg/kg
|
100 mg/kg
|
|
199mg/kg
|
|
Vitamin E
|
582 IU/kg
|
800 IU/kg
|
|
597 IU/kg
|
|
EPA
|
0.493
|
|
|
0.25
|
|
ALA
|
2.73
|
|
|
|
|
LA
|
|
|
|
2.14
|
|
Omega -3 FA
total
|
3.74
|
0.85
|
0.57
|
|
|
EPA/DHA
|
0.57
|
0.36
|
||
|
GLMP
|
0.3
|
|
||
|
Glucosamine/
|
980mg/kg:674mg/kg
|
1435 mg/kg
|
1000mg/kg
|
893mg/kg:100mg/kg
|
|
chondroitin
sulfate
|
||||
|
|
|
|
|
|
|
Caloric
density
|
356 kcal/ cup
|
408 kcal/cup
|
324 kcal/cup
|
246 kcal/cup
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Ingredient List of Commonly
prescribed/recommended Veterinary Diets
|
Hills j/d:
|
whole grain corn, chicken by-product
meal, flaxseed, soybean mill run, brewers rice, soybean meal, pork fat
|
|||
|
preserved with mixed tocopherols and citric
acid), chicken liver flavour, powdered cellulose, fish oil, lactic acid
|
||||
|
potassium chloride, L-lysine, calcium
carbonate, choline chloride, iodized salt, DL-methionine,
|
||||
|
vitamin E supplement, vitamins
(L-Ascorbyl-2-polyphosphate (source of vitamin C), Vitamin E supplement,
niacin,
|
||||
|
thiamine mononitrate, vitamin A
supplement, calcium pantothenate, biotin, vitamin B12 supplement, pyridoxine
|
||||
|
hydrochloride, riboflavin, folic
acid, vitamin D3 supplement,
|
), L-threonine, taurine, soy
lecithin, glucosamine
|
|||
|
hydrochloride, minerals (ferrous
sulfate, zinc oxide, cupper sulfate, magnesium oxide, calcium iodate, sodium
|
||||
|
selenite), L-tryptophan, L-carnitine,
preserved with mixed tocopherols and citric acid
|
||||
|
Purina JM:
|
brewers rice, salmon meal, corn
gluten meal, poultry by-product meal (natural source of glucosamine), dried
|
|||
|
egg product, oat fiber, animal
digest, animal fat preserved with mixed tocopherols (form of Vitamin E)
|
||||
|
fish oil, chicken, potassium
chloride, vitamin E supplement, salt, choline chloride, taurine, zinc
sulfate,
|
||||
|
L-ascorbyl-2-polyphosphate (source of
vitamin C), ferrous sulfate, manganese sulfate, niacin, calcium carbonate,
|
||||
|
vitamin A supplement, calcium
pantothenate, thiamine mononitrate, copper sulfate, riboflavin supplement,
|
||||
|
vitamin B12 supplement, pyridoxine
hydrochloride, folic acid, vitamin D3 supplement, calcium iodate, biotin
|
||||
|
menadione sodium bisulfite complex
(source of vitamin K activity), sodium selenite
|
||||
|
Medi Cal Mobility
|
brewer's rice, chicken meal, brown
rice, corn, corn gluten meal, natural flavour, chicken fat, diet beet pulp,
|
|||
|
Support
|
fish oil, calcium carbonate, pea
fibre, potassium chloride, vegetable oil, salt, green lipped mussel powder,
|
|||
|
L-lysine, choline chloride, taurine,
glucosamine hydrochloride, vitamins (DL-alpha-tocopherol (source of
|
||||
|
vitamin E),
L-ascorbyl-2-polyphosphate (source of vitamin C), biotin, D-calcium,
pantothenate, pyridoxine
|
||||
|
hydrochloride (vitamin B6), vitamin A
acetate, niacin, thiamin mononitrate (vitamin B1), riboflavin (vitamin B12),
|
||||
|
folic acid, vitamin B12 supplement
and vitamin D3 supplement), trace minerals (zinc proteinate, manganese
|
||||
|
proteinate, zinc oxide, ferrous
sulphate, copper proteinate, copper sulphate, manganous oxide, calcium
|
||||
|
iodate, and sodium selenite),
marigold extract (source of lutein), and chondroitin sulphate. Naturally
preserved
|
||||
|
with mixed tocopherols, rosemary
extract and citric acid.
|
||||
|
Royal Canin
|
||||
|
Weight & Osteo:
|
chicken meal, brown rice, wheat
gluten, barley, powdered cellulose, rice, chicken fat, natural flavors, dried
beet
|
|||
|
pulp, fish oil, brewers dried yeast,
sodium silica aluminate, potassium chloride, dried egg product, vegetable
oil,
|
||||
|
sodium tripolyphosphate, calcium
sulfate, salt, choline chloride, DL-methionine, taurine, glucosamine
|
||||
|
hydrochloride, marigold extract,
vitamins (DL-alpha tocopherol acetate (source of vitamin E), L-Ascorbyl-2
|
||||
|
polyphosphate (source of Vitamin C),
biotin, D0calcium pantothenate, vitamin mononitrate (vitamin B1),
|
||||
|
riboflavin supplement (vitamin B2),
folic acid, vitamin B12 supplement, vitamin D3 supplement), L-carnitine,
|
||||
|
trace minerals (zinc oxide, copper
proteinate, manganese proteinate, copper sulfate, manganous oxide, copper
|
||||
|
proteinate, calcium iodate, sodium
selenite, tea (green tea extract), chondroitin sulfate, rosemary extract,
|
||||
|
preserved with natural mixed
tocopherols and citric acid.
|
||||
Addressing
the claims of these diets:
Hill’s j/d: The first claim provided by
Hill’s was based on a randomized, double-masked, practice based 6 month feeding
study (76). In this study, 131 completed the study which were representatives
from 18 different veterinary hospitals. The dogs were fed either a control food or the
prescription diet Hill’s j/d in the dry form for 6 months. Results of the study
showed a significant higher serum concentration of total omega-3 fatty acids
and EPA in dogs fed Hill’s j/d (76). In addition, these dogs also had lower
arachidonic acid (although not statistically significant) and a significant
lower serum omega-6:3 ratios. Subjectively, dogs fed Hill’s j/d had significant
improvement in their ability to rise from a resting position, running, and
playing. In comparison, while the mean subjective scores given by clinicians
improved with the Hill’s j/d diet, they were not statistically significant
(76).
Hill’s claimed to have an
excellent source of omega-3 fatty acid EPA. This report is likely true as
compared to the Royal Canin, the EPA levels were higher. This is likely
attributed to the flaxseed present in the diet. The presence of DPA was not
mentioned.
The next claim of controlled
calorie content is again questionable. This diet ranked third out of the four
compared diets with a caloric density of 365 kcal/cup.
The final claim was L-carnitine
to maintain healthy weight. In dogs, the permitted maximum amount of
L-carnitine is 750 ppm for dogs. Typically in diets it is supplied in a range
of 100-350ppm. At the level of 349 ppm, this diet has a moderate amount which
may be beneficial.
An important
note is that the diet does contain glucosamine and chondroitin sulfate. This is
not advertised as a benefit by the company. When contacted by the
representative, it was stated that there is no scientifically proven benefit of
this supplement in the diet, however; it has been placed in the food to be on
the label for clients that want this supplement in the food. Based on the feeding requirement for a large
breed dog (40lbs) if supplying dry formulation 2 1/3 cups (230 g) - 3 1/4 cups
(320 g) would need to be fed to meet the required daily intake. In this
quantity of food 225.4mg-313.6mg of glucosamine and 155.02mg-215.68mg of
chondroitin sulfate are present. Based on the advised doses of these, a dog of
this size would require 400 mg of glucosamine and 272 mg of chondroitin
sulfate. The diet thusly does not provide adequate amounts of either of these
components as a supplement if fed at the recommended feed quantity of feed.
Purina JM: Purina’s first claim is that the
diet improves mobility. This claim is based on findings of an increased force
plate gait analysis when dogs with OA were fed a diet with higher omega-3 fatty
acids. P value for this study was 0.08 (77). In a two month long clinical
feeding trial, subjective assessment of owners and clinicians felt that dogs
with OA showed a significant improvement in mobility. Clinicians were more
inclined to recommend the diet based on these observations.
The diet claims to be high in
EPA and total omega-3 fatty acids. The total EPA was not listed on their
product website, however, information provided by company representatives
stated that 8oz of diet contained 287mg of EPA and 445 mg of DHA. The total
omega-3 fatty acid content was significantly less than Hill’s j/d.
The diet touted its high
protein/calorie ratio. Oddly, when comparing the data published on the product
website to the literature provided by the company representative,
inconsistencies were present with the nutrient composition. The provided
information from the company (vs. the website) stated that the protein % was
actually 34.25 and the fat was 14.18%. While the protein content was highest of
all four diets, the caloric density was also the highest when using the
website. The literature provided from the company did state that the caloric
density was less than internet amount and was 351kcal/cup. This would then
place the diet second for highest caloric density. It may be more beneficial to
explain that the high quality meat protein would lead to a more digestible
calorie source. This was not mentioned.
The omega 6 fatty acid content
could not be discussed as these levels were not provided in the diet analysis.
The levels of vitamin C were
lower than that of Hill’s j/d, but the levels of vitamin E were double. The
internet product guide listed the vitamin E content as 800IU/kg but the
provided data sheet listed it as 1000IU/kg. The vitamin C level was not
provided but may potentially be higher as well.
Glucosamine was not listed on
the internet product guide; however literature stated it was 1435mg/kg. If we
use the body weight of a 40lb dog once again 2 ¾ cups of feed is advised. With
this volume the dog would receive approximately 360 mg of glucosamine. This is actually more than Hill’s j/d but it
still is not the adequate dose for that size of dog. The downside is that there
is no chondroitin in the diet and as previously reported, the two supplements
have been shown to act synergistically.
The final claim was that of
palatability. One can extrapolate that if dogs were fed this diet then it must
have been palatable. No reports of
gastrointestinal upset or lack of product ingestion was found. On a personal
note, this diet was fed to dogs owned by the author and it did seem to be
extremely palatable.
Medical/Royal
Canin Mobility Support:
This diet also stated that it
would improve mobility and reduce pain with the presence of omega-3 and omega-6
fatty acids. It also stated that it was high in these compounds. The
information provided failed to state the % of omega-3 fatty acids on a dry
matter basis so this statement could not be confirmed.
The diet was decreased in
caloric content when compared to the other commercial diet companies at
324kcal/cup.
The diet contained GLM powdered and
was advertised to support the joints and serve anti-inflammatory purposes. The
diet contained 0.3% on a dry matter basis. Research has shown this compound to
show a positive effect on joint health at levels of 0.3%.
Although not advertised, the
diet did contain glucosamine. A feeding
guideline of 3 2/3- 4 ¼ cups of the diet was recommended for a 40 lb dog. Based
on this, the diet also does not contain significant glucosamine unless it is
fed at the highest recommended volume (360-425mg). It does not contain chondroitin.
Royal canine
Weight & Osteo:
This diet is one that is
manufactured to be sold in pet stores. It states it has evidence of enhanced
joint support. No evidenced based medicine could be found and none was able to
be produced by the company when approached.
While it has the lowest levels
of Omega-3 fatty acids of the diets compared, it DOES have a large amount of LA
(the precursor to inflammatory eicosanoids).
It also has less EPA and DHA than the veterinary produced version of
Mobility Support.
The diet claim to be restricted
calorie is substantiated as it has the lowest caloric content of 246kcal/cup
while maintaining a high protein level. The diet itself seemed to be beneficial
for a weight loss protocol, which in turn may help to improve the load bearing
on the joints and subsequently improve clinical signs associated with OA. L-carnitine
is advertised to be added but is not listed in the nutrient profile.
Vitamin C and vitamin E levels
are consistent with the compared diets.
Glucosamine and chondroitin are
advertised components of the food. With the proposed feeding guidelines
provided, a 40lb dog would only receive 225mg glucosamine and 25.3mg of
chondroitin. Both below the recommended daily intake.
The statement of the diet being
palatable and supporting dental health could not be evaluated as there was no
literature in regards to either claim.
Horizon
Complete Senior and Weight Management:
For curiosity, the diets above
were compared to a locally produced, high ingredient grade pet food. The
following information was obtained from the bag label.
Crude Protein
(min) 24.0 % Mid
range when compared to veterinary diets
Crude Fat (min) 10.0 % lowest of all diets
Crude Fibre (max) 4.0 % lowest of all diets
Moisture (max) 10.0 %
Calcium (min) 1.1% slightly higher than other diets
Phosphorus (min) .85% slightly higher than other diets
Omega 3 (min)** 0.44 % lowest of all diets
Omega 6 (min)** 3.62 %
Glucosamine* (min) 600 mg/kg lowest of all diets
Chondroitin Sulphate* (min) 400 mg/kg highest of all diets
Crude Fat (min) 10.0 % lowest of all diets
Crude Fibre (max) 4.0 % lowest of all diets
Moisture (max) 10.0 %
Calcium (min) 1.1% slightly higher than other diets
Phosphorus (min) .85% slightly higher than other diets
Omega 3 (min)** 0.44 % lowest of all diets
Omega 6 (min)** 3.62 %
Glucosamine* (min) 600 mg/kg lowest of all diets
Chondroitin Sulphate* (min) 400 mg/kg highest of all diets
While the diet did not contain
as much omega-3 fatty acids as the veterinary diets, it is one of lower end
diets of this company. It also contained significantly higher amounts of chondroitin
sulphate.
Commercially available supplements
sold or recommended by the veterinary hospitals and pet stores in our survey:
Dasoquin
(http://www.nutramaxlabs.com/vet/Products/Dasuquin-for-dogs.aspx): Dasoquin
is a veterinary exclusive product that is manufactured by Nutramax laboratories. The product is available for both dogs and
cats. It contains not only glucosamine HCl and chondroitin sulfate, but also avocado/soy
unsaponifiables. The product for dogs is supplied in either a chewable treat or
chewable tablets. The feline product is in the form of a capsule that can be
given directly or sprinkled onto the food.
Canine chewable treats contain:
|
Ingredient
|
Large Dogs
|
Small to Medium Dogs
|
|
Glucosamine
Hydrochloride* 99%
|
900 mg
|
600 mg
|
|
Sodium
Chondroitin Sulfate*
|
350 mg†
|
250 mg†
|
|
Avocado/Soybean
Unsaponifiables* (ASU) Powder
|
90 mg‡
|
45 mg‡
|
Canine Chewable tablets: Each Chewable Tablet Contains:
|
Ingredient
|
Large Dogs
|
Small to Medium Dogs
|
|
Glucosamine
Hydrochloride* 99%
|
900 mg
|
600 mg
|
|
Sodium
Chondroitin Sulfate* (Low Molecular Weight)
|
350 mg†
|
250 mg†
|
|
Avocado/Soybean
Unsaponifiables* (ASU) Powder
|
90 mg‡
|
45 mg‡
|
Recommended
daily doses are 1-2 daily (based on body weight) for the initial 4-6 weeks and
then decreased to half daily.
Feline Capsules: Each Capsule Contains:
|
Glucosamine
Hydrochloride* 99%
|
125 mg
|
|
Sodium
Chondroitin Sulfate* (Low Molecular Weight)
|
100 mg†
|
|
Avocado/Soybean
Unsaponifiables* (ASU) Powder
|
25 mg‡
|
Cosequin DS (http://www.nutramaxlabs.com/Vet/Products): Cosequin is another joint support product that is manufactured
by Nutramax laboratories. In contrast to
Dasoquin, this product is not veterinary exclusive which make it more readily
available to consumers and also at a lower cost. In contrast to Dasoquin, this
product does not contain the unsaponifiables.
Feline Cosequin: Each Capsule Contains:
|
Glucosamine
Hydrochloride* minimum
|
125 mg
|
|
Sodium
Chondroitin Sulfate* minimum
|
100 mg†
|
|
Manganese
minimum
|
1 mg**
|
*
manganese is a cofactor for multiple enzyme functions and detoxification
of superoxide free radicals
Canine Cosequin: Each Chewable Tablet/capsule Contains:
|
Glucosamine
Hydrochloride*
|
500 mg
|
|
Sodium
Chondroitin Sulfate*
|
400 mg†
|
|
Manganese
|
5 mg**
|
Cosequin DS +
DSM Each Chewable Tablet Contains:
|
Glucosamine
Hydrochloride*
|
600 mg
|
|
Sodium
Chondroitin Sulfate*
|
300 mg†
|
|
Methylsulfonylmethane
(MSM)
|
250 mg
|
|
Manganese
|
5 mg**
|
* MSM adds
sulfur and has reported anti-inflammatory properties
Cosequin DS Each Soft Chew
Contains:
|
Glucosamine
Hydrochloride*
|
600 mg
|
|
Sodium
Chondroitin Sulfate*
|
300 mg†
|
Cosequin Regular strength Each
Capsule Contains:
|
Glucosamine
Hydrochloride*
|
250 mg
|
|
Sodium
Chondroitin Sulfate*
|
200 mg†
|
|
Manganese
|
2 mg**
|
Comparatively,
these products all contain relatively similar amounts of glucosamine and
chondroitin. The variety of products is likely to provide appeal to clients.
The differing product lines also allow for distribution of various markets.
The company
states that their production is carried out with similar standards to the
pharmaceutical industry. It also advertises that the product has been shown to
be safe, effective, and bioavailable in the labelled amounts as per peer
reviewed studies. Evidence of these studies could not be located.
Flexadin (http://www.vetuk.co.uk/joint-supplements-flexadin-for-dogs-and-cats-c-4_243/flexadin-tablets-for-dogs-and-cats): Flexadin is a veterinary exclusive
product that is manufactured by Vetoquinol. The tablet is advertised for the
use in both dogs and cats.
Each tablet contains:
|
Glucosamine
HCl
|
500mg
|
|
Chondroitin
Sulfate
|
400mg
|
|
Devil’s
Claw
|
150mg
|
|
Manganese
|
10mg
|
The
recommended dose is one tablet per 20 kg of body weight daily, with loading
dose of twice that for the first 2-4 weeks.
Chondroflex (http://www.drugs.com/vet/chondro-flex-ds-soft-chews-can.html): Is a veterinary exclusive product
that is manufactured by Champion Alstoe Animal Health. The product is advertised for the use in both
dogs and cats.
Each tablet contains:
|
Glucosamine
HCl
|
500mg
|
|
Chondroitin
Sulfate
|
400mg
|
|
Methylsulfonylmethane
|
500mg
|
|
Ascorbate (as Manganese Ascorbate)
|
66mg
|
|
Manganese (as Manganese Ascorbate)
|
10mg
|
Liquid Plus (http://www.ubavet.com/ubaeng.html): Produced by Ubavet, this product is advertised for the use in
all pets. It contains not only glucosamine, chondroitin, manganese and MSM, but
also contains GLM, bioflavinoids, as well as a number of herbs.
Each 5mL of product contains:
|
Glucosamine
HCl
|
1000mg
|
|
Chondroitin
Sulfate
|
250mg
|
|
Manganese
|
10mg
|
|
MSM
|
200mg
|
|
Ascorbic
Acid
|
70mg
|
|
GLM
|
10mg
|
|
Selenium
|
5mg
|
|
Bioflavinoids
|
10mg
|
OmegaPro-3 (http://www.drugs.com/vet/omegapro-3-liquid-can.html): OmegaPro-3 is a veterinary exclusive product produced by Pro
Concepts Animal Health. With fish oil
being the source of omega-3 fatty acids, the product it advised for the use in
dogs and cats.
Each 1mL pump (300mg) contains:
|
Vitamin
A |
200
IU
|
|
Vitamin
D |
50
IU
|
|
Vitamin
E
|
4
IU
|
|
Eicosapentaneoic
Acid
|
180
mg
|
|
Docosahexaenoic
Acid
|
120mg
|
Hip Action
(http://www.zukes.com/woof/hip-action.html): Hip Action is a chewable supplement produced by Zuke’s. The
product is advertised for the use in dogs and comes in a variety of
flavours. The chewable treats are noted
to contain 24 kcal per treat.
Each chewable contains:
|
Glucosamine
|
300mg
|
|
Chondroitin
Sulfate
|
50mg
|
Preceding
products are summarized in the following table.
Due to the number of products that were available at pet stores within
Saskatoon, the products and contents are also supplied summarized in a table.
|
Table 5 Summary of Advised
Supplements for Joint Health by Local Veterinarians
|
|
|
|
|||||
|
Product
|
Chondroflex
|
Cosequin (K9)
|
Cosequin DS
|
Dasuquin
|
Flexadin
|
Liquid Plus
|
OmegaPro-3
|
Hip Action
|
|
Manufacturer
|
Champion Alstoe Animal Health
|
Nutramax
|
Nutramax
|
Nutramax
|
Vetoquinol
|
Ubavet
|
Pro Concepts Animal Health
|
Zuke's
|
|
Country
|
Canada
|
US
|
US
|
US
|
Canada
|
Canada
|
Canada
|
US
|
|
Volume
|
1 tablet
|
1 tablet
|
1 tablet
|
1 tablet
|
1 tablet
|
5mL
|
1mL
|
1 chew
|
|
Glucosamine
|
500mg
|
250mg
|
600mg
|
600-900mg
|
500mg
|
1000mg
|
|
300mg
|
|
Chondroitin
|
300mg
|
200mg
|
300mg
|
250-350mg
|
400mg
|
250mg
|
|
50mg
|
|
Manganese
|
10mg
|
2mg
|
|
|
10mg
|
10mg
|
|
|
|
MSM
|
500mg
|
|
|
|
|
200mg
|
|
|
|
GLM
|
|
|
|
|
|
10mg
|
|
|
|
ASU powder
|
|
|
|
45-90mg
|
|
|
|
|
|
Devil's Claw
|
|
|
|
|
150mg
|
|
|
|
|
Selenium
|
|
|
|
|
|
5mg
|
|
|
|
Bioflavinoids
|
|
|
|
|
|
10mg
|
|
|
|
Ascorbic acid
|
|
|
|
|
|
70mg
|
|
|
|
Vitamin A
|
|
|
|
|
|
|
200 IU
|
|
|
Vitamin E
|
|
|
|
|
|
|
50 IU
|
|
|
EPA
|
|
|
|
|
|
|
180 mg
|
|
|
DHA
|
|
|
|
|
|
|
120 mg
|
|
|
Table 6 Summary of Products Available
of Local Pet Stores in Saskatoon, SK
|
|
|
|
|
|
||||||
|
Product
|
Manufacturer
|
MSM
|
dose
|
Gluc
|
Cetyl M
|
Garlic root
|
Bromelain
|
Ginger Root
|
Chondroitin
|
Ascorbic Acid
|
Mang.
|
|
Advanced Cetyl M
|
Response
|
|
1 tablet
|
250mg
|
250mg
|
15 mg
|
10mg
|
7.5mg
|
|
|
|
|
Biojoint*
|
Biologic Vet
|
200mg
|
5g 1scoop
|
200mg
|
|
|
144 GDU
|
|
80mg
|
|
0.5mg
|
|
Cosequin feline
|
Nutramax
|
|
1 tablet
|
125mg
|
|
|
|
|
100
mg
|
|
1mg
|
|
Cosequin DS
|
Nutramax
|
|
1 tablet
|
500mg
|
|
|
|
|
400
mg
|
|
5mg
|
|
Flax Forward+
|
Juka Organics
|
|
|
|
|
|
|
|
|
|
|
|
Glucosamine/
chondroitin**
|
21st Century
|
10mg
|
1 tablet
|
500mg
|
|
|
|
|
100
mg
|
10mg
|
5mg
|
|
Glucosamine HCL
|
Ubavet
|
|
1 tablet
|
725mg
|
|
|
|
|
375
mg
|
100mg
|
5mg
|
|
Hip+Joint Plus paw gel++
|
Nutri-Vet
|
7.5mg
|
|
|
|
|
|
|
1.5
mg
|
|
|
|
Hip+Joint Level 2 canine+++
|
Nutri-Vet
|
400mg
|
1 tablet
|
400mg
|
|
|
|
|
|
|
|
|
Hip+Joint Level 3 canine
|
Nutri-Vet
|
50mg
|
1 tablet
|
500mg
|
|
|
|
|
400
mg
|
|
|
|
Hip + Joint
|
Pet Naturals
|
200mg
|
1 tablet
|
500mg
|
|
|
|
|
200
mg
|
50mg
|
2.5mg
|
|
Joint Stress
|
Homeopet
|
contains monkshood, leopard`s bane,
pot marigold, witch hazel, st. John`s wort, chick pea and poison oak
|
|
|
|
|
|
|
|
|
|
|
Liquid Joint Care!
|
Spring Meadows
|
|
ounce
|
2ooo
mg
|
|
|
200
mg
|
|
80mg
|
|
24mg
|
|
Stride Powder
|
TRM Pet Products
|
2000mg
|
10 g
|
1080
mg
|
|
|
|
|
240
mg
|
48mg
|
76mg
|
|
Muscle & Joint!!
|
Vet`s Best
|
200mg
|
|
|
|
|
2400gdu
|
|
|
|
|
|
Vita-Glo Hip + Joint
|
Halo
|
|
|
340mg/kg
|
|
|
|
|
272
mg/kg
|
250
mg/kg
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
(*) also contains Boswellia serrata
Extract, Vitamin C, Grape Seed extract, Vitamin D3
|
|||||||||||
|
(+) contains flax oil and flax solids
(product ingredients unavailable online)
|
|||||||||||
|
(**) also contains zinc, copper,
hyaluronic acid and vitamin E
|
|||||||||||
|
(++) also contains yucca schidegera
extract, sea kelp and vitamin C
|
|||||||||||
|
(+++) all hip and joint canine
products also contain vitamin C, antioxidants, zinc, manganese and copper
|
|||||||||||
|
as well as GLM (500mg)
|
|||||||||||
|
(!) also contains yucca schidegera,
collagen, grape seed extract, citrus bioflavinoids, copper, zinc and calcium
|
|||||||||||
|
(!!) also contains Boswellia extract,
tumeric extract, yucca extract, rosemary extract, antioxidants
|
|||||||||||
Conclusion
As one can
seen, there are a large amount of choices available to consumers. While there
is scientifically significant data supporting the use of a lot of the
aforementioned supplements, there are equally confounding results that have
been published. An educated client on the causes of OA and the consequences of
it may help to make them more informed about treatment additives. It is the
opinion of the author that glucosamine/chondroitin, omega-3 fatty acids have
the most convincing evidence supporting their use as adjuncts in the treatment
of OA. If an animal is on a diet that the owner feels it does well on I do not
advocate changing the food. Instead, the addition of glucosamine at 22mg/kg,
chondroitin 15-20 mg/kg and a supplement of omega-3 fatty acids (both fish and
flax seed oils) should be considered.
Conversely, if the owner is open to diet change, the recommendation of
Purina JM can be considered. Glucosamine and chondroitin supplementation should
still be considered. More research in
the area of dietary supplements is most definitely needed. Despite the lack of scientific data
unequivocally supporting the use of supplements, the numerous subjective
reports by owners and clinicians cannot be ignored. These substances are not detrimental to the
animal. Despite the fact that they MAY not actually be contributing to the
improvement of a given animal, they are not detrimental. As there seems to be a
chance that they can contribute to joint health and the overall improvement of
animals with OA, the use of these supplements can be justified.
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