Hi Spirits, I'm so glad you posted this about feeling that everything is getting stuck when you eat sometimes.
Just lately, probably the past Month or 2, I'm having spells of feeling really bloated, full, my appetite seems to disappear and it feels just like everything, digestive wise, is running at a snails pace! It's not a constant thing with me, just now and then, but it's really uncomfortable, I'm going to speak to my doctor about it and see what he says, I will come back and let you know what he tells me.
there are conditions that can trigger off these problems, there are different types, it is important you get checked out,it would be a good idea if your doctor could refer you for a camera to investigate down your food pine and stomach with a camera to see what is causing it, some people suffer acid reflux, gerd,hiatus hernia and there is another condition diabetics can get where the food starts to slow down going in to the digestion point to work as it should it reduces and can stop,
the full report is here the link to it is here also hope this info helps only part is posted up here
http://journal.diabetes.org/diabetesspectrum/00v13n1/pg11.htm
Delayed gastric emptying, or gastroparesis, is a well-known problem in patients with diabetes mellitus.1-5 It is at the far end of the spectrum of motility disorders collectively referred to as diabetic gastropathy or the diabetic stomach.
Although often believed to be more common in patients with type 1 diabetes, it is actually also quite common in patients with type 2 diabetes. In one study of diabetic patients receiving oral hypoglycemic therapy, 30% were found to have delayed emptying of solids.6
A substantial proportion of patients with either type 1 or type 2 diabetes mellitus have scintigraphic evidence of delayed gastric emptying of radiolabeled solid meals, which may or may not manifest in clinical symptoms.2,6,7 Conversely, many patents may have symptoms such as nausea, vomiting, early satiety, bloating, and abdominal discomfort or pain and yet have normal gastric emptying.
Diabetic gastropathy is thought to be a manifestation of autonomic neuropathy. The underlying cause of diabetic neuropathy, as well as other complications of diabetes, is hyperglycemia.8 While the entire gastrointestinal tract may be affected by autonomic neuropathy, we have a growing awareness of the role of the diabetic stomach in particular as the locus of a vicious cycle of delayed gastric emptying, poor glycemic regulation, and ascending hyperglycemia.6,9,10
The purpose of this brief review is to focus attention on the importance of early intervention in the development of diabetic gastropathy in order to prevent the debilitating symptoms associated with it and to improve quality of life.
PATHWAYS OF DIABETIC AUTONOMIC NEUROPATHY
The pathophysiology of the neuropathic complications of diabetes follows one of at least two pathways. The first is nonenzymatic glycosylation, which occurs when a persistently elevated blood glucose level results in the excessive glycosylation of proteins such as hemoglobin, other circulating molecules, and cellular structures.8 This leads to the development of advanced glycosylation end products, impairing the normal function of tissues including collagen and basement membranes of cells and capillaries.
The second pathway is enhanced activity of the polyol pathway, in which glucose is converted to sorbitol via the enzyme aldose reductase. This results in a decrease in tissue myoinositol, with far-reaching effects throughout the nervous system. As the integrity of cellular information, including the sodium-potassium ATPase system, is disrupted, nerve conduction velocity is diminished and the anatomy of nerve fibers is altered.11
Diabetic neuropathy can impair function anywhere in the nervous system. In the gastrointestinal tract, it causes, in effect, an autovagotomy.12 In addition, hyperglycemia results in cellular anatomic disruption throughout the gastrointestinal tract, but especially in the stomach. Nerve cells may swell with the loss of myelinated fibers, and smooth muscle cells may become rounded and hyalinized. In the stomach, motility may be reduced in the antrum and proximal stomach. There may also be pylorospasm.
Hyperglycemia also has secretory effects in the stomach, including decreased secretion of hydrochloric acid.13 The net result of these changes is a reduction in effective emptying, starting first with indigestible solids, then progressing to digestible solids, and eventually to liquids.14 The myoelectric and neuroanatomic consequences of hyperglycemia may be accentuated by abnormal secretion of various hormones, including glucagon, gastrin, cholecystokinin, and gastric inhibitory peptide in patients with diabetes.3
CLINICAL IMPACT OF DIABETIC GASTROPATHY
Gastropathy may result in a variety of potentially disabling upper gastrointestinal symptoms, among them postprandial nausea with or without vomiting, early satiety, anorexia, distention, and abdominal discomfort or pain. However, some diabetic patients with impaired gastric motility are asymptomatic.4 Also, some patients may experience these symptoms without an established delay in gastric emptying. This situation may be the earliest stage of the disease process of autonomic neuropathy; the first evidence of gastroparesis may be poor glucoregulation.
Gastropathy can contribute to bezoar formation and intestinal obstruction, ulcer development, acute gastric dilatation during ketoacidosis or after endoscopy, incapacitating vomiting, respiratory aspiration, and dehydration.3 In addition to impairing quality of life and compromising nutrition, gastropathy can wreak havoc on attempts to control blood glucose through insulin administration timed to meals.
Gastropathy may further retard the entry of oral medications, including hypoglycemics and pancreatic enzymes, into the bloodstream.15 Erratic absorption of nutrients and medications may result in misleading blood glucose readings, and significant hyperglycemia may occur if blood glucose levels rise out of proportion with the expected effects of insulin.3 On the other hand, slow absorption of food may lead to hypoglycemia. The toxic effect of hyperglycemia may acutely aggravate the gastropathy,9,16,17 possibly by reducing activity of both nerve and muscle.
Gastropathy may be underrecognized in clinical practice because the symptoms, if present, are nonspecific. Furthermore, the degree of gastropathy correlates poorly with the severity of gastrointestinal symptoms or with other evidence of peripheral neuropathy.3,5 The reverse is also true: dyspeptic symptoms do not confer a diagnosis of gastropathy in every diabetic patient.
