But in cachexia, the issue is that patients, regardless of the adequacy of nutritional intake, have abnormally accelerated disposition of nutrients, hence a negative balance of metabolism results (Fearon and Moses, 2002). Inflammatory processes are involved in secondary PEM which are absent in primary PEM, and while primary PEM can be reversed by bolstering nutrient intake, the same benefit cannot be obtained in secondary PEM. In primary PEM there is faster loss of adipose tissue than that of lean body mass, but the loss is equally from both compartments in cachexia. Skeletal muscle loss is a feature that is peculiar to the cachexic state (Tisdale, 2003).
Previous laboratory and clinical studies have shown that omega-3 fatty acids, especially eicosapentaenoic acid (EPA) and EPA-containing supplements demonstrate molecular anti-inflammatory activity which is relevant to the attenuation of cachexia, in both humans and animal models. However, past results from multiple studies have been equivocal in their findings, and this study aims to elicit independent objective evidence in favour of or against the proposition that EPA confers significant benefit in arresting the progress of cachexia in affected patients.
Yes. There was inadequate discussion of the basis for their using the type of EPA preparations they used, as opposed to other available types. The authors could also have done a better job of reviewing the literature on the mechanistic aspects of how cachexia develops and what bearing this information will have on the approach they used for their study in terms of study design, formulations used and patient selection strategies.
These patients have undergone treatment procedures that are potentially debilitating and could contribute directly or indirectly to changes in body mass or global physical status. Such changes may confound the results of the study. It is standard practice in conducting clinical trials to exclude patients who have such conditions as could independently contribute (whether negatively or positively) to the observed end points, otherwise type 1 (false positive) or type II (false negative) errors may result during the interpretation of the results.
C-reactive protein (CRP) measurement is being used as a marker of the severity of the acute inflammatory protein response which occurs in cachexia. CRP is an acute phase protein whose synthesis is induced in cachexia by interleukin-6 and tumor necrosis factor alpha, and its level has been correlated with severity of symptoms and adverse outcomes (Tisdale, 2003).
Only half of the original population enrolled completed the 8-week course of the trial, although this was attributed to miscellaneous reasons not linked to lack of compliance or adverse effects from the EPA preparations.
For mean weight change over the 8-week period, the group