Hempseed oil as a novel source of polyunsaturated fatty acids and its effect on inflammation in sedentary horses

Chronic, low-grade inflammation is a contributing factor in diseases that impact the health and well-being of horses. Pharmaceutical treatments reduce inflammation, but their use results in negative digestive and kidney disturbances. Polyunsaturated fatty acids (PUFA) play a role in mitigating the inflammatory response and are therefore explored as a dietary approach to attenuate inflammation. γ-Linolenic acid (GLA) is a unique PUFA that when supplemented in the diet can increase the production of anti-inflammatory eicosanoids; however, it is uncommon in the dietary components normally fed to horses. Interest in industrial hemp (Cannabis sativa L.) as a novel source of PUFA stems from the presence of GLA and the potential to reduce inflammation; although, concerns over cannabinoid contamination limit its acceptance. Six Thoroughbred geldings were used in a crossover study with two 63-d periods to measure PUFA metabolism, inflammatory biomarkers, and cannabinoid accumulation in response to hempseed oil (HSO) fed to sedentary horses compared to controls (CON). Treatment diets were offered for the first 35 d of each period and then all horses resumed a uniform feeding rate from d 36 to 63. Serum and synovial fluid PUFA reflected dietary intake. GLA was greater in serum (0.465 vs. 0.046; P < 0.0001) and synovial fluid (0.270 vs. 0; P < 0.0001) in horses fed HSO compared to CON. This contributed to greater dihomo-γ-linolenic acid (DGLA) conversion in serum (0.287 vs. 0.195; P < 0.0001) and synovial fluid (0.348 vs. 0.262; P < 0.04) but not arachidonic acid (AA). Serum GLA returned to baseline concentrations by two weeks post-supplementation, but no treatment x time effect was observed for synovial fluid. HSO did not affect FA in muscle; it is likely the length or quantity of supplementation was inadequate to see changes in muscle PUFA. HSO increased serum interleukin 1β (IL1β; P = 0.01) but there was no treatment by time interaction (P = 0.62). No other inflammatory biomarkers were influenced by treatment. Stride length was not affected by HSO supplementation but was inversely correlated (P ≤ 0.01) with synovial fluid prostaglandin E2 (PGE2; r = -0.56), and positively correlated with serum tumor necrosis factor α (TNFα; r = 0.58), serum IL6 (r = 0.61), and serum IL1β (r = 0.65). Cannabinoids were measured in the HSO supplement, but no cannabinoids were detected in plasma or synovial fluid of horses fed HSO when tested to a 50-ppb limit of detection. These results demonstrate the suitability of HSO as a novel source of PUFA and, more specifically, as a source of GLA without further increasing AA, however, implications for its effect on inflammation require further evaluation.