Postprandial Hypotension in Adults: Exploring Insulin Dynamics During a Mixed Meal Test

Background/Objectives: Postprandial hypotension (PPH) is an important clinical condition in patients presenting with postprandial symptoms. The aims of this study were to determine the prevalence of PPH in patients with postprandial symptoms and to investigate the relationship between PPH and insulin, particularly in healthy adults. Methods: This study was conducted with 111 adult patients who were admitted to the clinic due to postprandial symptoms. Patients underwent the mixed meal test (MMT). Blood glucose, insulin, and C-peptide levels were measured at 0, 30, 60, 90, 120, 180, 240, and 300 min along with systolic blood pressure (sBP), diastolic blood pressure (dBP), and heart rate measurements during the MMT. Results: Serum adrenocorticotropic hormone (ACTH) levels were similar (p &gt: 0.05), and cortisol levels were found to be higher in individuals without PPH compared to those with PPH before the MMT (p = 0.014). During the MMT, 23 patients (23.2%) had PPH. At the beginning of the test, serum glucose, insulin, C-peptide, and heart rate values were similar in patients with and without PPH: however sBP and dBP were significantly higher in the PPH group (p = 0.002 and p = 0.010, respectively). No correlation was found between sBP and insulin, glucose, and C-peptide at any time during the MMT except for a moderately significant positive correlation between glucose and sBP at 90 min in patients with PPH (r = 0.490, p = 0.018). A moderately negative correlation was found between the magnitude of sBP fall between 30 and 60 min and insulin and C-peptide levels in people with PPH (r = &minus:0.420, p = 0.046: r = &minus:0.564, p = 0.005: respectively). However, no significant relationships were observed between the magnitude of sBP fall at other time points and blood parameters (p &gt: 0.05). Conclusions: A significant portion of adults with postprandial symptoms might have PPH, contributing to these symptoms. The lack of a relationship between insulin and glucose suggests that other physiological mechanisms beyond insulin and glucose may play a role in the pathogenesis of PPH in healthy individuals. Therefore, further research is needed to better understand the underlying causes of PPH.