{[['
']]}
']]}
We are in the midst of a worldwide epidemic of obesity and its consequences, in particular type 2 diabetes and cardiovascular disease. Clinical studies have recognized that risk factors for these conditions frequently cluster in individuals, leading to the development of the concept of the metabolic syndrome. This was soon followed by considerable controversy as to whether the syndrome is a distinct entity or not. In addition, multiple definitions and diagnostic criteria have made interpretation of data occasionally problematic. I expect that this controversy will continue, though all parties on both sides of the argument are clearly in agreement on one thing – we need action to halt the progression from risk factor development to clinical events and death. Despite the controversies on terminology, therefore, it is important to focus on the goal of effective treatment, hence the development of this book. Although our goal is to have an in-depth analysis of treatment strategies, we felt it important to first review the epidemiology and pathophysiology of the syndrome, in order to lay the groundwork for developing treatment concepts. We have also strongly emphasized the importance of lifestyle (and perhaps societal) change that is needed to halt this epidemic. Clearly, preventing and treating obesity effectively should liberate us from the syndrome. However, whether we use population strategies or individualized pharmacotherapy for obesity, the greatest impact is likely to be seen in treatments that alleviate risk factors involved in the pathogenesis of cardiovascular events such as blood pressure, lipids, inflammation
and thrombogenesis. To that end, we have focused on the impact of treatment on these factors. It is also important to recognize the impact of current treatments for individual risk factors on other components of the syndrome. This is most clearly recognizable in the effect of glucose-lowering drugs, particularly insulin sensitizers if insulin resistance is an important underlying feature of the syndrome. Some of these drugs, as well as insulin itself, paradoxically cause weight gain, yet favorably impact other features of the syndrome. Is that good or bad? The answers are currently surrounded by controversy, the essence of which we hope we have captured adequately in the text. We look forward to further clarification from ongoing clinical trials. I am most grateful to the outstanding group of authors who have contributed scholarly and up-to-date reviews in a timely fashion. Finally, I would like to dedicate this book to the city of New Orleans and to its fragile
recovery from disaster.
June 2008
