Management of Osteoarthritis with Avocado/Soybean Unsaponifiables

Abstract

Osteoarthritis (OA) is a painful and life-altering disease that severely limits the daily activity of millions of Americans, and is one of the most common causes of disability in the world. With obesity on the rise and the world's population living longer, the prevalence of OA is expected to increase dramatically in the coming decades, generating burdensome socioeconomic costs. This review summarizes current pharmaceutical, non-pharmaceutical, and prospective new treatments for OA, with primary focus on the dietary supplement Avocado/Soybean Unsaponifiables (ASU). ASU modulates OA pathogenesis by inhibiting a number of molecules and pathways implicated in OA. Anticatabolic properties prevent cartilage degradation by inhibiting the release and activity of matrix metalloproteinases (MMP-2,3,13) and increasing tissue inhibitors of these catabolic enzymes (TIMP-1). ASU also inhibits fibrinolysis by stimulating the expression of plasminogen activator inhibitor (PAI-1). Anabolic properties promote cartilage repair by stimulating collagen and aggrecan synthesis via inhibition of inflammatory cytokines such as IL1, IL6, IL8, TNF, ERK, and PGE2. Chondroprotective effects are mediated by correcting growth factor abnormalities, increasing TGFβ while decreasing vascular endothelial growth factor (VEGF) in synovial fluid. ASU also inhibits cholesterol absorption and endogenous cholesterol biosynthesis, which mediate reactive oxygen species pathology in chondrocytes. At the clinical level, ASU reduces pain and stiffness while improving joint function, resulting in decreased dependence on analgesics.

Keywords: Arthrocen; Osteoarthritis; avocado soybean unsaponifiables (ASU); cartilage; dietary supplements.

Figure 1.

Anteroposterior and cross-table lateral of knee osteoarthritis (OA). Symptomatic knee OA typically presents with narrowing of the joint space and bone spurs (arrows). (A and B) During the development of OA, articular cartilage breaks down over time and becomes thin. As a result, the bone surfaces rub against each other, further damaging the cartilage and bone and causing pain. (C and D) Joints with late-stage OA are often painful, warm to the touch, possibly red, swollen, have subchondral cysts, and notable loss of function.

Figure 2.

Gas chromatography–mass spectrometry analysis of major sterol components of Piascledine 300, Avocado 300 Soy Unsaponifiable with Sierra 600 mg, and Arthrocen 300. Control sample exhibited characteristic peaks corresponding to 1 = Dihydrocholesterol (5α-Cholestan-3β-ol; internal control; Sigma Aldrich), 2 = Brass (Brassicasterol), 3 = Camp (Campesterol), 4 = Stigmn (Stigmastanol), 5 = β-Sito (β-sitosterol), 6 = Stigma (Stigmasterol).