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Antihypertensive Therapy and the Risk of New-Onset Diabetes

Department of Preventive Medicine, Hypertension/Clinical Research Center, Rush University Medical Center, Chicago, IL

Address correspondence to George L. Bakris, MD, Hypertension/Clinical Research Center, Department of Preventive Medicine, Rush University Medical Center, 1700 West Van Buren, Suite 470, Chicago, IL 60612. E-mail: gbakris@earthlink.net

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Numerous studies have consistently demonstrated that certain classes of antihypertensive medications have differential effects on carbohydrate and lipid metabolism in humans. In general, higher doses of thiazide diuretics (i.e., 25 mg/day hydrochlorothiazide) and ß-blockers, at any antihypertensive dose, worsen glycemic control, with ß-blockers worsening insulin sensitivity (1). Conversely, ACE inhibitors, angiotensin II receptor blockers, and calcium channel blockers (CCBs) have neutral or beneficial effects on these variables (2,3). It is noteworthy, however, that not all drugs within the same class have similar effects on insulin sensitivity. This is exemplified by the effects of vasodilating ß-blockers failing to worsen insulin resistance and consequently having neutral effects on glycemic control (4,5).

These aforementioned observations are evident in 11 randomized clinical outcome trials where development of new-onset diabetes was evaluated as a secondary end point (Table 1) (6–11). In contrast to this general trend, the STOP-2 (Swedish Trial in Old Patients with Hypertension 2) reported no difference in diabetes incidence between conventional treatment (ß-blockers or diuretics) and either ACE inhibitor–or CCB-based treatment (12). Moreover, in addition to prospective randomized trials, some long-term epidemiological studies, such as the ARIC (Atherosclerosis Research in Communities) study, have linked different classes of antihypertensive agents with development of new-onset diabetes (13).

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