According to theory, consuming a meal should provide energy and lead to an increase in blood glucose levels in healthy individuals. However, there are instances where despite consuming a meal, such as lunch, symptoms such as shaking hands, weakness, impaired concentration, or hunger occur, which are typical indications of low blood sugar levels. Essentially, such symptoms should not occur, as the body has received an energy dose. However, it turns out that this phenomenon is relatively common and is known as reactive hypoglycemia.
Does reactive (postprandial) hypoglycemia truly originate from these processes?
Reactive hypoglycemia (alternatively referred to as postprandial hypoglycemia) is a metabolic condition characterized by a significant decline in blood glucose levels—falling below 70 mg/dl—occurring between two and five hours after consuming a meal, particularly one high in rapidly absorbable carbohydrates. While commonly associated with individuals diagnosed with diabetes, this phenomenon may also manifest in metabolically healthy persons, especially those who are overweight or obese. Additionally, it represents a frequent complication among patients who have undergone bariatric surgical procedures. The precise etiologic mechanisms underlying reactive hypoglycemia remain incompletely understood. One proposed explanation involves an aberrant insulin response following food intake: an excessive secretion of insulin triggered by a sharp rise in blood glucose, which subsequently leads to an overly pronounced reduction in glucose levels and may contribute to the development of insulin resistance. Other potential contributing factors include deficient production of glucagon—a hormone that counteracts hypoglycemia—or heightened activity of glucagon-like peptide-1 (GLP-1), which enhances the postprandial reduction of blood sugar (as evidenced in research conducted by J.E. Campbell and D.J. Drucker in 2013).
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