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Originally Posted by Lisa N
Dr. Bernstein relates a story in his book (page 95 of the most recent edition if anyone cares to look it up) of a patient of his that was getting large spikes in blood sugar after her afternoon swimming workout. Her blood sugars were going from 90 pre-workout to 300+ post workout. Upon investigating, he discovered that she was in the habit of eating an entire head of lettuce prior to her workout (now that's a huge salad!). He credited the dramatic rise in blood sugar to something he terms the 'Chinese restaurant effect' in which a large but very low carb meal can cause a rise in blood sugar that cannot be accounted for by the number of carbs consumed (roughly 10 for an entire head of iceburg lettuce).
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I have read the book and this story too, and with all my respect to Dr.B, the explanation is sounds anecdotal. First, swimming burns sugar mostly, this is a near perfect workout for diabetics. So, if this women was T1 or T2 who does not make much insulin already, the spike in BGs could be more due to the liver sugar dump because of low insulin and not enough carbs eaten prior to workout, not the lettuce itself
. If I skip a meal or eat very little carbs and get a long and streneous workout, my BGs can jump up to 180, and swimming session is streneous enough!
"Chinese restaurant effect" in my book, results in Bgs spike but only y due to a large amount of hidden sugar in chinese food. Chinese food is loaded with sugar, and gives me a decent BGs spike too, unless I eat only steamed fish and vegetables.
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The explanation of this effect is that the upper small intestine secretes hormones when it is stretched as it would be in a large meal. The larger the meal, the greater the stretching and also the greater the amount of hormones released. These hormones will in turn trigger the release of insulin and also glucagon. In a diabetic, the insulin release would be small or even none at all but the glucagon would cause gluconeogenesis and glycogenolysis leading to....a large rise in blood sugars from a relatively low carb meal.
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This has nothing to do with lettice itself, all diabetics both T1 and T2 advised to either inject insulin or have a carby snack before workout to get insulin going so to speak (in those who still have a good phase 2 insulin response), which inhibits gluconeogenesis, and post-workout BGs spike. BGs spike to 300 is a sign that she was most likely T1, and did not inject enough insulin to avoid hypos on 6-12-12 plan, or T2 with a poor control.
I wonder if anyone else had BGs of 300 from eating a whole head of lettuce, which is basically freebee, and nothing else.
I am going to try it, eat enitre head of lettice alone, and check my Bgs after. See, if I can reproduce the results.
Here is some info from Medscape on Incretins, I suppose is what you refer to as intestinal hormones.
The enitre acrticle can be read at
http://www.medscape.com/viewprogram/3075_pnt
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Incretin Hormones in Diabetes and Metabolism
Introduction
The role of the gastrointestinal tract in influencing insulin secretion and glucose homeostasis has been recognized since the beginning of the 20th century.[1] Zunz and La Barre first proposed the term "incretin" in reference to an insulin-stimulatory hypoglycemic factor found in the extract of duodenum.[2] Incretin hormones have since been defined as hormones produced by the gastrointestinal tract in response to nutrient entry, which then stimulate insulin secretion. The enteroinsular axis refers to the regulation of pancreatic islet hormone secretion by such incretin hormone signals from the gastrointestinal tract.[3]
This review will focus on the current understanding of the physiologic basis of the incretin hormones and the incretin effect. Also, since it is known that patients with type 2 diabetes exhibit a significant reduction in the magnitude of meal-stimulated insulin release -- or a reduced incretin effect[4] -- this review also will focus on the therapeutic potential of incretins in type 2 diabetes.
The Incretin Effect
The concept of the incretin effect developed from the observation by Elrick and colleagues and McIntyre and colleagues that insulin responses to oral glucose exceeded those measured after intravenous administration of equivalent amounts of glucose.[5,6] They concluded that gut-derived factors, or incretins, influenced postprandial insulin release. Nutrient entry into the stomach and proximal gastrointestinal tract causes release of incretin hormones, which then stimulate insulin secretion.[7] This insulinotropism, or ability to stimulate insulin secretion, can be quantified by comparing insulin or C-peptide responses to oral vs intravenous glucose loads. In this way, it has been shown that the incretin effect is responsible for about 50% to 70% of the insulin response to oral glucose in healthy individuals.[8,9]
Although many postprandial hormones have incretin-like activity, the 2 predominant incretin hormones are glucose-dependent insulinotropic polypeptide, also known as gastric inhibitory polypeptide (GIP), and glucagon-like peptide-1 (GLP-1). The biological importance of these peptides is reviewed below.
The Incretin Hormones: GIP and GLP-1
Introduction
GIP and GLP-1 both belong to the glucagon peptide superfamily and thus share amino acid sequence homology. GIP and GLP-1 are secreted by specialized cells in the gastrointestinal tract and have receptors located on islet cells as well as other tissues. As incretins, both are secreted from the intestine in response to ingestion of nutrients, which results in enhanced insulin secretion. The insulinotropic effect of GIP and GLP-1 is dependent on elevations in ambient glucose. Both are rapidly inactivated by the ubiquitous enzyme dipeptidyl peptidase IV (DPP-IV). The characteristics of GIP and GLP-1 are summarized in the Table.
Table. Characteristics of GIP and GLP-1
GIPGLP-1Peptide42 amino acid30/31 amino acidSecreted byK cells, primarily in duodenum and proximal jejunumL cells, primarily in ileum and colonStimulated byOral ingestion of nutrientsOral ingestion of nutrientsMetabolized byDPP-IVDPP-IVEffects on insulin secretionStimulatesStimulatesEffects on gastric emptyingAccelerates?SlowsEffects on beta-cell proliferationStimulates*Stimulates*Effects on glucagon secretionNone significantSuppressesEffects on food intakeNone significantReducesEffects on insulin sensitivity?Improves?Secretion in type 2 diabetesPreservedImpairedInsulinotropic response to exogenous administration in type 2 diabetesImpairedPreserved*In cell-line studies
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Many folks have genetic defect resulting in lack of incretins, and this alone put them in diabetic cathegory. Incretins slows rate of glucose entering blood stream, inhibits gluconeogenesis, and stimulates insulin release.
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The moral of the story? If you're diabetic, stuffing yourself with even very low carb foods can cause an undesireable spike in blood sugars, so don't stuff yourself.
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Can't agree more with it more, and this is a good idea for everyone, not diabetics only