We thank Bell, Hardy, and Desmond (1) for their comments regarding our recent article (2), and we appreciate the opportunity to respond to the issues they have raised. Based on their analysis of two groups of patients in their practice, Bell, Hardy, and Desmond question whether there is an association between CRP and glycemic control. Several possible explanations exist for the difference in our findings. First, we used a nationally representative population-derived database that may be more diverse than the one used by them. Second, we specifically excluded people on anti-inflammatory and cholesterol-lowering medications, precisely because the use of such individuals is likely to confound the relationship between C-reactive protein (CRP) and HbA1c (insulin-sensitizing drugs were not widely available at the time of the study [1988–1994]). Another reason for the difference in our findings could be our ability to account for several other factors that might confound or mask the relationship, including age, race, sex, BMI, smoking, length of time with diabetes, and fasting insulin levels. Further supporting our findings, other researchers have found a similar association between CRP and HbA1c in nondiabetic individuals (3).
Bell, Hardy, and Desmond correctly note the limitation of fasting insulin level as a measure of insulin resistance. However, their conclusion that CRP is related to insulin resistance rather than glycemia may also be premature, since the term insulin resistance is a very general one that includes several possible underlying mechanisms. Our report did not address specific mechanisms for the association we found, but instead called for more research to further delineate the nature of the association. We agree with Bell, Hardy, and Desmond that more definitive prospective and interventional studies are needed to investigate the association between CRP and glycemia, as we urged in our article.
