Is it time to consider prediabetes and diabetes mellitus as a single entity?

Abstract

To answer the question we must consider the following evidence:

• The risk of developing T2D at 7 years of follow-up increases from high normal fasting blood glucose (FBG) values between 90 - 94 vs < 85 mg/dL HR 1.49 (CI 1.23 - 1.79) p < 0.00, between 95 – 99 vs < 85 mg/dL HR 2.33 (CI 1.95 – 2.79) p < 0.00.
• A study in Mauritius defines, using ROC curves, an initial GA of 97 mg/dL for the incidence of T2D diagnosed at 5 years using OGTT and 99 mg/dL using FBG.
• Alterations in insulin secretion begin with the decline of the first peak from 90 mg/dL of FBG, becoming clearly detectable from 100 mg/dL.
• Microvascular complications begin during prediabetes (PDT2), with evidence that there is no threshold above which retinopathy (RD), nephropathy or neuropathy increases exponentially.
• Macrovascular complications begin during PDT2, there is no threshold above which cardiovascular diseases (CVD) increase exponentially; although there are studies that guide us to think that not all those who present PDT2 increase their risk of suffering from CVD, but only those who will later progress to T2D.
• In children and adolescents with FBG ≥ 100 mg/dL, generally associated with obesity, the deterioration of insulin secretion is more accelerated than in adults and is associated with increased cardio-metabolic risk. 4 Furthermore, insulin resistance begins years before the diagnosis of T2D and even PDT2, influenced by the environment, unhealthy eating habits, sedentary lifestyle, obesity, chronic low-grade inflammation, and mitochondrial dysfunction. Hyperglycemia manifests itself when the beta cell fails to maintain normal levels, this dysfunction having a clear genetic component.

Due to the above, we should not support the diagnosis of T2D on the current cut-off points, adopted on data offered by older studies, based on the presumed threshold for increased DR, this being only one of the complications present in T2D.