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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e143.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Inflammation Warms Up the Metabolic Syndrome

Katherine Esposito; Miryam Ciotola; Dario Giugliano

Department of Geriatrics and Metabolic Diseases, University of Naples, Italy

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest the article by Hung et al¹ claiming that activation of interleukin 18 (IL-18) is involved in the pathogenesis of the metabolic syndrome. These data add to the mounting evidence describing association between circulating markers of vascular inflammation and features of metabolic syndrome, either alone or in combination.² The potential clinical implications of the study must be tempered by some limitations. As correctly acknowledged by the authors, an observational study cannot prove that the association between IL-18 levels and the metabolic syndrome is causal. Although they made efforts to adjust for several relevant potential confounders, they had no information about factors such drugs or mental stress, and unmeasured or unmeasurable lifestyle factors cannot be adjusted for. For instance, body mass index (BMI) showed a progressive increase in parallel with the increment in the number of the components of the metabolic syndrome; this could be a marker for a generally unhealthy lifestyle, including preference for fatty and sweet foods and sedentary lifestyle. There is evidence that IL-18 concentrations are modulated by body weight³ and macronutrients present in familiar food stuffs.⁴ Despite these limitations, most would accept that the link between inflammation and the metabolic syndrome is causal because there are several mechanisms whereby inflammation could impair insulin sensitivity.² Insulin resistance has been considered the basis of most if not all of the features of the syndrome that could be accounted for by the resistance to the actions of insulin on carbohydrate and lipid metabolism.

We . . . [Full Text of this Article]

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