Understanding Reactive Hypoglycemia
Reactive hypoglycemia (RH) is a condition that is currently gaining attention in the field of Functional Medicine, though its complete understanding remains elusive.
Following a meal, glucose levels rise in response to insulin secretion and then fall back down. Reactive hypoglycemia occurs when serum glucose drops to 60mg/dL or even 50mg/dL in the hours following a meal (3). Once serum glucose levels drop to 80mg/dL, insulin secretion is halted, and counter-regulatory hormones like glucagon, epinephrine, growth hormone, and cortisol are secreted to bring glucose levels back up, with a particularly strong surge of cortisol when levels are below 60mg/dL (2). It is hypothesized that dysregulation in these hormones underlies reactive hypoglycemia.
Depending on the amount of time after eating when serum glucose falls below 70mg/dL, different types of RH are distinguished. Post-prandial RH occurs within 0.5-2 hours, idiopathic RH approximately 3 hours after eating, and late RH is observed 4-5 hours post-prandial (according to Landowska, 2022).
Reactive hypoglycemia is characterized by rapid gastric emptying, high postprandial glucose concentrations, and an excess of insulinotropic gut hormones, including glucagon-like peptide-1 (GLP-1) (1). This extremely low serum glucose level 2-5 hours after eating affects the nervous system, leading to symptoms like tachycardia, tremor, sweating, nausea, hunger, confusion, dizziness, forgetfulness, blurry vision, lethargy, and sometimes even seizures or coma (2). Notably, RH is observed in 15-20% of patients who have undergone gastric operations, suggesting a possible link to rapid gastric emptying.
The role of GLP-1 as an incretin appears to be significant, as it strongly stimulates insulin release and inhibits glucagon release, thereby influencing hepatic glucose production (1). Studies have shown that the higher the carbohydrate intake and the greater the spike in GLP-1 following a meal, the lower the serum glucose levels are 2 hours after eating (1).
Obesity seems to play a role in the severity of reactive hypoglycemia at <55mg/dL after 2 hours post-prandial. According to a study by Lv (2020), being obese increased the incidence of RH (26.1%) compared to normal body weight (5.9%) and overweight (5.4%) (p=0.05) at 3 hours post-prandial, and the incidence was 43.5% for the obese group at 4 hours compared to normal weight (14.7%) and overweight (16.2%) (p=0.02) (3). There was no difference in hypoglycemia related to BMI between 0-2 hours after eating. One hypothesis is that insulin resistance leads to a higher surge in insulin during phase 2 due to a diminished first-phase insulin response, or that insulin secretion is delayed as BMI increases (3).
References:
1. Gebhard, B., Holst, J. J., Biegelmayer, C., & Miholic, J. (2001). Postprandial GLP-1, Norepinephrine, and Reactive Hypoglycemia in Dumping Syndrome. Digestive Diseases and Sciences, 46(9), 1915–1923. https://uws.idm.oclc.org/login?url=https://search.ebscohost.com/login.aspx?direct=true&db=edssjs&AN=edssjs.42567CE1&site=eds-live&scope=site
2. Landowska, M., Zebrowska, A., Fajer, K., Adamek, P., Kruk, A., Kaluza, B., & Franek, E. (2022). Atherosclerosis Risk Factors in Patients with Reactive Hypoglycemia. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 15, 3133. https://uws.idm.oclc.org/login?url=https://search.ebscohost.com/login.aspx?direct=true&db=edsgao&AN=edsgcl.726942848&site=eds-live&scope=site
Lv, X., Fang, K., Hao, W., Han, Y., Yang, N., & Yu, Q. (2020). Identification of Reactive Hypoglycemia with Different Basic BMI and Its Causes by Prolonged Oral Glucose Tolerance Test. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 13, 4717. https://uws.idm.oclc.org/login?url=https://search.ebscohost.com/login.aspx?direct=true&db=edsgao&AN=edsgcl.649683088&site=eds-live&scope=site
