Author + information
- Joshua W. Knowles, MD, PhD∗ ( and )
- Gerald Reaven, MD
- ↵∗Stanford University School of Medicine, and Cardiovascular Institute, Falk CVRC, MC 5406, 300 Pasteur Drive, Stanford, California 94305
Emdin et al. (1) indicated that increased blood pressure was a significant risk factor for developing type 2 diabetes (T2DM), and concluded that “further investigation is needed to determine whether this association is causal.” In response, we propose that there is considerable evidence that insulin resistance (IR) is the causal link between hypertension and increased risk of T2DM.
Insulin resistance is characteristic of patients with T2DM, and T2DM develops when pancreatic β-cells do not secrete enough insulin to overcome the IR (2). Normotensive, first-degree relatives of patients with hypertension are insulin resistant, prospective studies have shown that hyperinsulinemia predicts development of hypertension, and IR is increased in patients with hypertension (3,4). Given these relationships, and the importance of IR in T2DM, it is not surprising that patients with hypertension are at increased risk of incident T2DM. However, as emphasized by Emdin et al. (1), previous studies have not yielded consistent support of this relationship. One explanation is that essentially all patients with T2DM have IR, whereas only approximately 50% of patients with hypertension are insulin resistant and at enhanced risk of T2DM (5). Given this degree of variability of IR in patients with hypertension, it is not surprising that the causal link between hypertension and T2DM is not easily discerned. The huge database analyzed by Emdin et al. (1) increased the likelihood that increases in blood pressure would be shown to predict incident T2DM. We suggest that further research into the relationship between hypertension and T2DM take into account the substantial metabolic heterogeneity that exists between subpopulations subsumed under the rubric of hypertension.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2016 American College of Cardiology Foundation