Editor's Correspondence |

Hypertension and Obesity

David M. Najman, MD; Prashant Kapoor, MD; Andres Serrano, MD; Dmitriy Tckachenko, MD
Arch Intern Med. 2003;163(9):1114-1115. doi:10.1001/archinte.163.9.1114-a.
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We read with great interest the article by Curhan et al.1 We have several questions regarding the conclusions of the study.

There has been a tremendous focus in the published literature regarding patient lifestyles, specifically physical activity and weight. This was also omnipresent in the lay media following the study by Ford et al2 demonstrating the prevalence of metabolic syndrome in the United States alone. One of the key components of metabolic syndrome is hypertension. There is overwhelming evidence that as BMI increases, so does blood pressure. We are now beginning to elucidate some of the mechanisms of this association, correlating the effects of insulin resistance up to overt diabetes on the vasculature as well as other mediating substances that are more prevalent as BMI increases. Recently, an intriguing article was published showing a clear correlation between BMI and platelet activation, with mechanisms such as inflammation (which in turn has innumerable causes) and lipid peroxidation implicated as possible causal factors.3 In a special communication regarding the primary prevention of hypertension published the week before the article by Davi et al3, the primary focus is on weight reduction.4 The data presented in this communication not only supports that a slight increase in BMI leads to an increase of blood pressure, but also that the incidence of hypertension with minimal increases in BMI exceeds the relative risks seen in the study by Curhan et al.1 Of note is that the mean fasting glucose level was normal in each of the subgroups, indicating that these changes occur early in the course of obesity, long before most patients meet any diagnostic criteria for diabetes mellitus.4

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