The hypoglycemoses include a large category of distinctly unique entities. Guidelines for a clinical, physiological approach to these disorders is presented. Within this diagnostic spectrum of hypoglycemia lies the reactive hypoglycemic disorders that are characterized by their postprandial onset, adrenergic mediated symptoms, and relatively benign causes. The spectrum of reactive hypoglycemia includes early alimentary-reactive hypoglycemia, late diabetic-reactive hypoglycemia, hormonal deficiency states, and idiopathic hypoglycemia. A new postprandial hypoglycemic disorder, fructose 1-6 diphosphatase, can be added to this list. The frequent sampling of blood-glucose values in the postprandial state will frequently lead to the finding of a biochemically low blood-glucose value of below 50 ml/100 ml, and these individuals show no hypothalamic-pituitary-adrenal stress to the low blood sugar and do not manifest adrenergic symptoms. Their low blood-glucose value simply reflects the transition in intermediary metabolism between the fed and fasting state and provides a biochemical marker of this event. We refer to this asymptomatic biochemical event as transitional low blood-glucose state. It has no clinical implication and may frequently be confused with the bona fide reactive hypoglycemic disorders. Using a symptomatic, counter-regulatory model to define hypoglycemia as a bona fide disorder, findings are presented in patients with the varying types of reactive hypoglycemia, and their results are compared to normal controls and to a weight-matched and disease patient controls. Abnormalities in insulin secretion are discussed as relating to the pathophysiology causal in the hypoglycemia. An approach to therapy is presented based upon the classification of the patient as to the type of hypoglycemia and their abnormalities in insulin secretion.