Worsening Postural Tachycardia Syndrome Is Associated With Increased Glucose-Dependent Insulinotropic Polypeptide Secretion, 2022, Nicholas C Breier

Abstract

Background: Postural tachycardia syndrome (POTS) is characterized by excessive upright tachycardia and disabling presyncopal symptoms, which are exacerbated after consuming a high-carbohydrate meal; it is unknown, however, what is the precise underlying mechanism. We seek to investigate the effect of glucose intake on orthostatic hemodynamic changes and gastrointestinal hormone secretion in POTS.

Methods: Prospective, case-control study, 12 women with POTS who reported a postprandial worsening of their POTS symptoms and 13 age-matched female controls received 75-g oral glucose and 20 mg/kg acetaminophen to assess nutrient absorption. Hemodynamic, gastrointestinal hormone and acetaminophen levels were measured for up to 120 minutes postingestion while supine and standing.

Results: Patients with POTS had significant orthostatic tachycardia, 48.7±11.2 versus 23.3±8.1 bpm, P=0.012 and elevated upright norepinephrine levels, 835.2±368.4 versus 356.9±156.7 pg/mL, P=0.004. After oral glucose, upright heart rate significantly increased in POTS, 21.2±11.9% versus 6.0±19.9%, P=0.033 with a concomitant decline in upright stroke volume, -10.3±11.90% versus 3.3±13.7%, P=0.027; total peripheral resistance, blood pressure and cardiac output remained unaltered. Acetaminophen rate of appearance was similar between groups (P=0.707), indicating comparable nutrient absorption rates. POTS had increased plasma levels of C-peptide (P=0.001), GIP (glucose-dependent insulinotropic polypeptide; P=0.001), peptide YY (P=0.016), and pancreatic polypeptide (P=0.04) following glucose consumption, but only GIP had a time-dependent association with the worsening upright tachycardia and stroke volume fall.

Conclusions: The glucose-induced worsening orthostatic tachycardia in POTS was associated with a decline in SV; these changes occurred while GIP, a splanchnic vasodilator, was maximally elevated.

https://pubmed.ncbi.nlm.nih.gov/35232225/

 

This seems significant.

 

The paywall has since been removed, presumably because the study was funded by the NIH (at least in part).

Tachycardia after eating is a major issue for me even when I lie down. I have a particularly bad time with carbs, whereas fats and protein don’t seem to cause much of a heart rate increase if at all — unfortunately, fats clash with my gastroparesis (for which carbs are instead recommended…).

The authors show that not only the hormone GIP (glucose-dependent insulinotropic polypeptide) is elevated twofold compared to controls and peaks at the same time as heart rate after a meal, but also that even with age and BMI-matched controls, the patients seemed to show some degree of reduced insulin sensitivity.

Unfortunately there currently are no approved GIP receptor antagonists, though this one seems promising - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9719863/

Perhaps metformin would help increase insulin sensitivity, but it could cause hypoglycemia too.