Medicine & Healthcare

Effect of a protein and energy dense n-3 fatty acid enriched oral supplement on loss of weight and lean tissue in cancer cachexia: a randomised double blind trial

Recent insights on chronic heart failure, cachexia and nutrition. Miján-de-la-Torre A.

Clinical studies have reported that oral fish oil supplementation has beneficial effects in rheumatoid arthritis and among some patients with asthma, supporting the idea that the n-3 PUFA in fish oil are anti-inflammatory. There are indications that inclusion of n-3 PUFA in enteral and parenteral formulas might be beneficial to patients in intensive care or post-surgery.

Fatty acids, the immune response, and autoimmunity: a question of n-6 essentiality and the balance between n-6 and n-3.

This study shows that by modulating the eicosanoid metabolism using a combination of n-3 fatty acids and cyclooxygenase-2 inhibitor, some of the signs and symptoms associated with a Systemic Immune-Metabolic Syndrome (SIMS) could be ameliorated.

Unlike simple starvation, where body fat is lost preferentially, cancer cachexia is associated with depletion of both fat and skeletal muscle mass. Although anorexia is frequently associated with cachexia a reduction of nutrient intake alone could not explain the progressive wasting. Instead the process appears to be mediated by circulatory tumor-produced catabolic factors acting either alone or in concert with certain cytokines. A knowledge of the mechanisms involved should lead to the development of effective pharmacological intervention. Effective therapy should not only improve the quality of life of the cancer patient, but should lead to an increase in survival. Since cachexia is so common in cancer host products may be required for tumor homeostasis. Thus further knowledge in this area may lead to the development of new agents for the treatment of cancer.

Study provides the first evidence of a direct relationship between the depression of protein synthesis in skeletal muscle by PIF and Ang II, through activation of PKR, and eIF2{alpha} phosphorylation, and the enhanced degradation of the myofibrillar protein myosin, through activation of NF-{kappa}B resulting in an increased expression and activity of the ubiquitin-proteasome proteolytic pathway. This suggests that agents that target PKR may be effective in the treatment of muscle atrophy in cancer cachexia or other wasting conditions.