Fish Oil Studies
Depletion of muscle and adipose tissue in cancer cachexia appears to arise not only from decreased food intake, but also from the production of catabolic factors (e.g., tumor necrosis factor and other autoimmune cytokines) secreted by certain tumors. Experiments with a cachexia-inducing tumor in mice showed that when part of the carbohydrate calories in their diet was replaced by fish oil, host body weight loss was inhibited. The catabolic-inhibiting effect occurred without an alteration of either the total calorie consumption or nitrogen intake (Tisdale 1990).
Fish oil concentrate was found to inhibit tumor-induced lipolysis directly (Beck 1991). The catabolic fat loss-preventing effect of fish oil arose from an inhibition of the elevation of cyclic AMP (adenosine monophosphate, a nucleotide involved in energy metabolism) in fat cells. The increased protein degradation in the skeletal muscle of catabolic animals was also inhibited by fish oil; this effect was due to the inhibition by fish oil of muscle prostaglandin E2 production in response to a tumor-produced proteolytic factor. Thus, reversal of cachexia by fish oil in this mouse model results from its capacity to interfere with tumor-produced catabolic factors (Tisdale 1996). Similar factors have been detected in human cancer cachexia.
Studies show that the DHA fraction of fish oil is the best documented supplement to suppress the inflammatory cytokines involved in the catabolic process such as TNF-α, IL-6, IL-1β, and prostaglandin E2 (Khalfoun 1997; De Caterina 1998, 1999; Jeyarajah 1999; Kelley 1999; James 2000; Kremer 2000; Watanabe 2000; Yano 2000; Das 2001; Tepaske 2001). Catabolic wasting patients should consider taking a combination of gamma-linolenic acid (GLA) and primarily the DHA fraction of fish oil. Both GLA and DHA significantly suppress inflammatory cytokines (Purasiri 1994; Mancuso 1997; Dirks 1998; DeLuca 1999; James 2000).