Type 2 diabetes often starts as a metabolic syndrome of insulin resistance. Elevated levels of insulin promote weight gain and systemic inflammation. It makes sense that adding more insulin to the regimen of someone who is already resistant would require doses that would exacerbate the imbalance of this metabolic process.

The challenge for clinicians is that many medical systems are looking at our patients’ HbA1c levels to see if we have their diabetes under adequate control, and the most effective medicine we can use to lower HbA1c is insulin. In fact, another article in the same issue of JAMA showed this to be the case.²

So, what is one to do? If I use the most effective drug to look like I am a good doctor, I may be more likely to increase the risk for death and cancer in my diabetic patients. The best way to reverse this metabolic process and reduce the risk for death and cancer is through weight loss, good nutrition, and movement. But if the patient on metformin needs more help, I will consider a sulfonylurea; however, this can cause weight gain and hypoglycemia. Therefore, I also keep a glitazone, a glucagon-like peptide-1 receptor agonist, or a dipeptidyl pepdidase-4 inhibitor at the ready.