(Circulation. 2005;112:3030-3032.)
© 2005 American Heart Association, Inc.
Editorial |
From Stanford University School of Medicine, Stanford, Calif.
Correspondence to Gerald Reaven, MD, Division of Cardiovascular Medicine, Falk CVRC, Stanford Medical Center, 300 Pasteur Dr, Stanford, CA 94305. E-mail greaven@cvmed.stanford.edu
Key Words: Editorials insulin cardiovascular diseases
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In his 1939 Goulstonian Lectures to the Royal College of Physicians in London, Harold Himsworth addressed the "Mechanisms of Diabetes." In the course of these 3 presentations,13 he provided evidence that "diabetes mellitus is a disease in which the essential lesion is a diminished ability of the tissue to utilize glucose. The high blood sugar is a controlled and compensatory phenomenon, the object of which is to facilitate the utilization of glucose by the tissues." In addition, he challenged the conventional wisdom that "all causes of human diabetes could be explained by deficiency of insulin" and went on to utter the heretical notion that "a state of diabetes might result from inefficient action of insulin as well as from a lack of insulin." Thus, the notion of a causal role of insulin resistance in human disease was born almost 70 years ago.
Article p 3066
Despite the fact that Himsworth was among the most distinguished clinical investigators of his time and in 1949 concluded in the Oliver-Shappey Lectures to the Royal College of Physicians4 "that it appears we should accustom ourselves to the idea that primary deficiency of insulin is only one, and then not the commonest cause of the diabetes syndrome," the idea that resistance to insulin action could have adverse consequences had little resonance over the next several decades. However, this situation begin changing rapidly with the introduction of methods to quantify insulin-mediated glucose disposal,5,6 and it soon became clear7,8 that the majority of patients with type 2
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