Overbasalization: Addressing Hesitancy in Treatment Intensification Beyond Basal Insulin
Kevin Cowart
Abstract
The proportion of patients with type 2 diabetes achieving recommended treatment goals remains suboptimal despite advances in diabetes care (1). Only 30% of patients with type 2 diabetes who use basal insulin achieve an A1C <7%, with the probability of doing so diminishing greatly if not achieved within 1 year of insulin initiation (2–6). Factors underlying these delays are complex and may involve therapeutic inertia, which is defined as failure to intensify or deintensify therapy when appropriate (7). The clinical course of type 2 diabetes is characterized by a progressive decline in β-cell mass and function, as well as insulin resistance (8). Early in the course of the disease, the addition of basal insulin addresses decreasing β-cell function and is an efficient step in controlling fasting blood glucose but has little effect on controlling postprandial blood glucose (9). In patients with type 2 diabetes and elevated A1C, the relative contribution of fasting hyperglycemia is dominant with higher A1C, and postprandial hyperglycemia is a larger contributor when A1C is closer to 7% (10). Thus, titration of basal insulin when A1C is close to 7% will have minimal effect on postprandial hyperglycemia or on attainment of the A1C goal (11). Basal insulin is not designed to address postprandial hyperglycemia; its role is mainly to suppress hepatic glucose production, address insulin resistance, and correct fasting hyperglycemia. In theory, the ideal basal insulin dose should allow a patient with type 2 diabetes to fast for 24 hours without hypoglycemia. Once basal insulin has been initiated, appropriate titration is necessary to avoid “overbasalization,” or titration of basal insulin beyond an appropriate dose in an attempt to achieve glycemic targets. Several evidence-based titration algorithms exist (12–14); however, no particular algorithm has been shown to provide superior clinical benefit over others (15 …