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Letter to the Editor |
Department of Biostatistics (R.K.), University of Washington, Seattle, Washington 98115, and Kaiser Permanente of Georgia and Division of Endocrinology (J.B.), Emory University, Atlanta, Georgia 30322
Address correspondence to: Richard Kronmal, Department of Biostatistics, Building 29, Suite 310, 6200 NE 74th Street, Seattle, Washington 98115. E-mail: kronmal{at}u.washington.edu.
To the editor:
In response to the issues raised by Dr. Dandona and colleagues (1), it should be noted that we stated several times in our article (2) that the data were observational and should not be interpreted as showing a cause and effect relationship of high insulin levels with incident coronary heart disease (CHD).
We also wish to emphasize that our findings apply to a small subset of insulin-treated patients: those who are elderly, who likely already have underlying atherosclerosis, and who have extremely high insulin levels. The results cannot be extrapolated to younger populations, to those without atherosclerosis, or to those whose insulin levels are not extremely high. Indeed, there was no relationship between insulin levels and CHD events in Cardiovascular Health Study participants whose insulin levels were not extremely elevated. Even those whose insulin levels were in the second and third quartiles and much above levels considered to be normal did not have increased CHD risk. Our results, therefore, do not conflict with the elegant laboratory work that Dr. Dandona and his colleagues have done regarding the antiinflammatory effects of insulin.
Lastly, we never said that insulin was atherogenic. Rather, we stated that very high insulin levels are associated with a markedly increased risk of a coronary event, whatever the mechanism may be. At the end of the article, we enumerate several possible mechanisms.
Received August 19, 2004.
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