Cytokines and Anorexia General

Several proinflammatory cytokines, including interleukin-1 (IL-1), IL-2, IL-6, IL-8, tumour necrosis factor-a (TNF-a) and interferon-y (IFN-Y), reduce food intake after peripheral or central administration in laboratory animals [3, 4]. Some cytokines suppress feeding synergistically [3, 4]. The anorectic effects of cytokines are pathophysi-ologically relevant because acute antagonism of particular cytokines and/or their receptors often attenuates anorexia in various diseases or models of disease [5]. Furthermore, several immune challenges reduce food intake less in mice that are genetically deficient in a particular cytokine or cytokine receptor than in control animals (see below). Failure to establish a role for a particular cytokine in disease-related anorexia with genetic knock-out (KO) mice [5] is presumably due to the redundant and overlapping actions of cytokines, which allow for developmental compensation. Interestingly, the feeding-suppressive effect of proinflammatory cytokines appears to be enhanced by oestradiol [6], which fits the well-known modulatory effect of ovarian hormones on immune system activity and the responsiveness to cytokines in female mammals [7]. Anhedonic effects of cytokines may contribute to or enhance anorexia under certain circumstances [5, 8], but do not appear to be the major cause of their anorectic effects [5].

Breaking Bulimia

Breaking Bulimia

We have all been there: turning to the refrigerator if feeling lonely or bored or indulging in seconds or thirds if strained. But if you suffer from bulimia, the from time to time urge to overeat is more like an obsession.

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