Page 940 - Adams and Stashak's Lameness in Horses, 7th Edition

906 Chapter 8

evidence of oral absorption, bioavailability, distribution, Fatty Acids
and controlled evaluation of the efficacy of oral HA Polyunsaturated fatty acids (PUFAs) are essential
VetBooks.ir blinded study using yearling Thoroughbreds that had fatty acids that are found in fish and plants. Essential
products in the horse is lacking. One controlled double‐
fatty acids are components of cell membranes, involved
arthroscopic surgery to remove osteochondritis disse-
cans (OCD) lesions from the tarsus demonstrated that in lipid transport, and serve as precursors to the eicosa-
the mean effusion score for the treated horses (100 mg noid hormone family, which regulates inflammatory
51
orally once daily) was significantly lower than for the processes. The two principle essential fatty acids are
placebo group. 11 linoleic acid and α‐linolenic acid. In the body they are
desaturated and elongated to produce analogs of arachi-
donic acid (N‐6 fatty acid) called eicosapentaenoic acid
Methylsulfonylmethane (EPA omega‐3 fatty acids) and docosahexaenoic acid
MSM is a normal oxidative metabolite product of (DHA omega‐3 fatty acids).
industrial‐grade dimethyl sulfoxide (DMSO) that is an In horses, it was reported that the source of essential
odorless and tasteless organic form of sulfur. It is natu- fatty acids affects the concentration of EPA and DHA in
110
rally found in small amounts in fruit, alfalfa, and corn serum. When horses received fish oil in the diet, there
and is very soluble in water. 122,147 It can be found as a was an increase in the concentration of EPA and DHA
product by itself or in combination with GLN and/or in their serum, compared with horses that received corn
CS. It has been used as a nutraceutical because of its oil. The anti‐inflammatory effects of fatty acids have
58
analgesic, anti‐inflammatory, and antioxidant proper- been attributed to stabilization of cell membranes, inhi-
ties. 77,114,149 There is little known about the pharmacoki- bition of the formation of inflammatory mediators, and
15,29,52
netics of MSM. Similar to DMSO, MSM has been protection against oxidation. Studies have demon-
suggested for the management of musculoskeletal pain strated that n–3 fatty acid supplementation can reduce
as well as OA. It has been suggested that MSM may or inhibit the inflammatory and matrix‐degradative
relieve muscle discomfort by decreasing the nerve response elicited by chondrocytes during OA progres-
28,29
impulses via cholinesterase inhibition and subsequently sion. An in vitro study using an LPS challenge model
reducing muscle spasm. 42 in equine synovial explants demonstrated that pretreat-
Very little is known about oral administration of MSM ment with α‐linolenic acid significantly decreased PGE
2
safety and toxicity. In a study in rats, MSM given for production induced by LPS, reducing the inflammatory
107
more than 90 days did not cause any adverse effects nor response. An in vivo study of horses examined
increase mortality. Few studies have been published to the effects of n–3 long‐chain PUFA (LCPUFA) effects
61
support the use of MSM for managing OA in horses. on LPS synovitis after 3 months of supplementation.
Horses receiving oral MSM and vitamins demonstrated Aggrecanase 1 concentrations were lower than controls,
that MSM could exert some protective effect on oxidative but there was no effect on PGE or MMP activity in the
2
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and inflammatory exercise‐induced injury related to synovial fluid compared with controls. The clinical
95
jumping. In another uncontrolled, non‐peer‐reviewed usefulness in the treatment of joint disease is still not
study, MSM was associated with improved performance entirely clear due to the uncertainty of which compo-
in Standardbred racehorses in training. 123 nents of the oils might be effective.
Cetyl myristoleate (CM) is another fatty acid that is
used in equine nutraceuticals. It is an ester, omega‐5
Avocado and Soybean Unsaponifiable Extracts fatty acid that may act by inhibiting the 5‐lipooxygenase
pathway, which is responsible for the metabolism of
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The unsaponifiable portions of avocado and soybean
oils are extracted via hydrolysis to make up fractions of leukotrienes (potent inflammatory mediators from the
one‐third avocado oil and two‐thirds soybean oil. It appears arachidonic acid cascade). One equine product demon-
that this mixture has synergistic properties; however, the strated lower lameness scores compared with placebo
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93
active ingredient is still unknown. In vitro studies have horses in a double‐blinded OA clinical trial. However,
suggested that avocado and soybean unsaponifiable (ASU) there are no published reports on safety, absorption, and
extracts may have a positive effect on both the inflamma- metabolism of CM in horses.
tory cascade and structural components of the cartilage
matrix. Studies have demonstrated that the extracts reduce
MMPs, cytokines, nitric oxide, and PGE while increasing Collagen Hydrolysate
2
growth factors and aggrecan production. 13,57,153 One con- Collagen hydrolysate (CH) is a food ingredient that
trolled study that used horses with induced OA in the mid- has been used in humans to improve joint comfort and
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dle carpal joint failed to demonstrate any significant clinical function. CH is derived from bovine or porcine skin
effects. However, the study demonstrated that ASU dis- and bones. Orally administered CH has been shown to
72
plays disease‐modifying capabilities because of a significant be absorbed intestinally and to accumulate in carti-
decrease in intimal hyperplasia and histologic cartilage dis- lage. In contrast with other nutraceuticals, no direct
164
ease score along with an increase in articular cartilage GAG analgesic and anti‐inflammatory effects have been found
synthesis in joints with OA. after using CH. The theory behind CH is that it pro-
9
ASU has been combined with GLN‐CS in some prod- vides amino acids specific to the collagen network, play-
ucts, which may help to decrease some of the sympto- ing an important role in the structure and function of
matic signs. When combined with α‐lipoic acid, an in cartilage by directly stimulating chondrocytes to synthe-
vitro study demonstrated that ASU was better able to size collagenous matrix. Several studies in humans have
inhibit PGE production from chondrocytes than either indicated that the use of CH in people with OA is safe
2
administered alone. 49 and provides improvement in some measures of joint