Did Someone Say Pyloric Valve?
I also am advocating for the preservation of the pylorus, not specifically via one surgery. Again 3 of the 4 major WLS available preserves the pylorus.
I am simply making the information available to those doing research.
Thanks to everyone for bumping my thread to help me get the word out.
Have a good evening.
~GG
Ht. 5'2 HW 234/GW 150/LW 128/CW 132 Size 18/20 to a size 4 in 9 months!
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I love your avatar! ~GG
* A few normal people get dumping symptoms very very occasionally (I personally can recall 4-5 times as an adult that I had weird symptoms after eating something that were EXACTLY what I have read is involved with dumping)
* A vanishingly few normies get RH. Most of them have pancreatic tumors.
* A few non-RNY WLS patients have such symptoms - whether caused by their WLS or not, is hard to tell, because it is not very common, and might have happened anyway, as it does to some normies.
* VERY VERY few non-RNY WLS patients get RH.
* LOTS of RNY patients get dumping.
* A significant number of RNYers get RH.
This does NOT mean that losing the function of your pyloric valve inevitably CAUSES either dumping or RH - however, it DOES mean that losing the function of your pyloric valve VASTLY increases the risk of dumping and RH.
Perhaps that RNYer needs to have her DH explain to her the logic of medical research. Just because she keeps staying the correlation isn't ABSOLUTE doesn't mean it isn't a cause.
Most people who smoke DON'T GET LUNG CANCER EITHER. Doesn't mean smoking doesn't cause lung cancer.
PS: The gastric bypass surgeons have known about this for THIRTY YEARS:
Surgery. 1982 Aug;92(2):235-40.
Altered glucose tolerance, insulin response, and insulin sensitivity after massive weight reduction subsequent to gastric bypass.
Halverson JD, Kramer J, Cave A, Permutt A, Santiago J.
Abstract
We have studied an otherwise normal group of morbidly obese subjects and compared them with patients who had experienced massive weight loss after loop gastric bypass. Compared to normal controls (NLCs), morbidly obese control patients (OBCs) had abnormal glucose tolerance curves (after glucose ingestion), elevated basal insulin levels, and increased plasma insulin concentrations, suggesting insulin insensitivity. The latter has been corroborated by the measurement of decreased insulin binding in these patients. Postoperative (PO) patients were hyperglycemic after taking oral glucose, but all PO patients had a rapid decrease in plasma glucose concentration, half reaching hypoglycemic levels. PO basal insulin levels and insulin receptor number were not statistically different from those in NLCs, indicating up-regulation of insulin receptors (and therefore, increased insulin sensitivity) postoperatively. Hyperinsulinemia seen in the PO group (greater than that in OBCs, P less than 0.001) after administration of oral glucose occurred simultaneously with a doubling of plasma concentration of gastric inhibitory polypeptide. Massive weight loss in patients after gastric bypass was accompanied by an improvement in insulin receptor number, basal hyperinsulinemia, and glucose tolerance. In addition, postoperative patients demonstrated symptomatic reactive hypoglycemia which may have resulted from the hyperinsulinemia seen subsequent to ingestion of glucose.