DOI: 10.1177/1947603514554992

Management of Osteoarthritis with Avocado/Soybean Unsaponifiables

Blaine A. Christiansen, Simrit Bhatti, Ramin Goudarzi, and Shahin Emami (2015)

Osteoarthritis (OA) is a chronic synovial joint disease, characterized by two main features: progressive damage of articular cartilage, bone remodeling, and new bone formation (osteophytes and subchondral bone sclerosis) and synovial inflammation and fibrosis of ligaments, tendons, menisci, and capsules. All joints may be affected, but the most commonly involved are knees, hands, and hips

Avocado/soybean unsaponifiables are natural vegetable extracts made from avocado and soybean oils, consisting of the leftover fraction (approximately 1%) that cannot be made into soap after saponification. ASU is composed of one third avocado and two thirds soybean unsaponifiables (A1S2U). The major components of ASU are phytosterols β-sitosterol, campesterol, and stigmasterol, which are rapidly incorporated into cells. The sterol contents of ASU preparations are the primary contributors to biological activity in articular chondrocytes

ASU possesses chondroprotective, anabolic, and anticatabolic properties. It inhibits the breakdown of cartilage and promotes cartilage repair by inhibiting a number of molecules and pathways implicated in OA
ASU stimulates the synthesis of collagen and aggrecan by inhibiting inflammatory cytokines such as IL-1, IL-6, IL-8, TNF, and PGE2 through modulation of NF-kappaB
ASU also inhibits the release and activity of collagenase (MMP2) and stromelysin 1 (MMP3) in cultured chondrocytes, increases tissue inhibitors of metalloproteinases (TIMP1), and inhibits IL1-induced ERK but not p38 or JNK in chondrocytes in vitro

In vitro studies show that ASU inhibits fibrinolysis by stimulating the expression of plasminogen activator inhibitor (PAI-1). This fibrinolytic and tissue destructive proteinase cascade may play a role in OA joint inflammation via altered expression of uPA receptors

ASUs alter growth factor levels implicated in OA pathogenesis, increasing TGF-β1 and TGF-β2 in the canine knee joint fluid,100 to repair cartilage and decreasing VEGF, which is markedly elevated in synovial fluid of patients
ASU also inhibits cholesterol absorption and endogenous cholesterol biosynthesis. Sixty percent of patients with OA exhibit high levels of oxidized low-density lipoproteins (oLDL) in serum, which mediates reactive oxygen species (ROS) activity in chondrocytes and OA pathology
At the clinical level, ASU reduces pain and stiffness while improving function in joints, resulting in decreased dependence on analgesics

ASUs may prove to be an effective treatment option for symptomatic OA, as they have been shown to possess chondroprotective, anabolic, and anticatabolic properties, as well as anti-inflammatory properties. At the clinical level, ASUs reduce pain and stiffness while improving joint function. Importantly, ASUs are a natural, slow-acting agent that do not merely address acute pain but actively prevent progression of OA symptoms

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