The bitter taste of hypoglycemia

Abstract

Hypoglycemia undoubtedly is the major obstacle to glycemic control in type 1, insulinopenic spectrum of type 2 and some other forms of diabetes, the “brittle diabetes” in particular. Strict glycemic control reduces the vascular complications of diabetes which comes at the cost of increased risk of hypoglycemia. The workgroup of the American Diabetes Association (ADA) and the Endocrine Society have defined hypoglycemia as all episodes of abnormally low plasma glucose concentration that expose the individual to potential harm [1], and the cutoff level of plasma glucose has arbitrarily been defined as 70 mg/dl. This value approximates the lower limit of plasma glucose concentration in the normal post-absorptive state. In healthy individuals, this particular level of plasma glucose is the threshold for activation of counter-regulatory mechanisms, and it is also low enough to potentially reduce the physiological defenses against subsequent hypoglycemia. More importantly perhaps, this value is higher than the plasma glucose levels required to produce symptoms of neuroglycopenia ( 15 years) in these patient subset of the UK Hypoglycaemia Study Group [2, 3]. In comparison, hypoglycemia is definitely less frequent in type 2 diabetes. However, as the patients approach towards the insulin-deficient end of the spectrum of the disease, the incidence progressively increases. For example, in the UK Hypoglycemia Study, the incidence of severe hypoglycemia in insulin treated type 2 diabetics was 10 and 70 episodes per 100 patient-years if the treatment duration was less than 2 years or more than 5 years, respectively. Hypoglycemia in diabetes is typically the outcome of relative or absolute iatrogenic hyperinsulinemia and compromised physiologic and behavioral defenses against declining plasma glucose concentrations. The well-known risk factors of hypoglycemia are wrong type or excessive or ill-timed dosing of insulin or insulin secretagogue, reduced insulin clearance (in renal failure), increased insulin sensitivity (low counter-regulatory hormones, following weight loss or exercise), decreased endogenous glucose production (liver failure), decreased exogenous glucose delivery (missed meal or fasting) and increased glucose utilization (during and shortly after exercise). Degree and duration of β-cell secretory defect, a history of severe hypoglycemia or hypoglycemia unawareness, recent antecedent hypoglycemia, prior exercise or sleep, and aggressive therapy are the indicators of compromised defenses against hypoglycemia. Other potential risk factors are some of the long-term complications of diabetes like gastroparesis, poor vision, and manual dexterity and * Subhankar Chowdhury subhankar.chowdhury@gmail.com