Mon, Jul-21-14, 19:51
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Senior Member
Posts: 3,199
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Plan: High protein, lower fat
Stats: 000/000/145
BF:276, 255 hi wts
Progress: 0%
Location: Michigan U.P., USA
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Quote:
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Originally Posted by JEY100
I've wondered too about his allowed legumes and other starches providing the resistant starch that others have found beneficial. I'd rather add some with real food than potato starch. Trying to keep the number of variables with this "experiment" manageable, so maybe after another week of this basic plan, I'll change up the foods too.
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Potato starch being very convenient, easy to add and calculate, is the main attraction there. There are various types of RS too and I believe it's advisable to mix them up. I read all of the RS posts on Free the Animal at one point but have fallen behind since sometime in January.
Re the legumes and other foods usually avoided by low carbers, I noted this with interest, though I thought the post ended rather abruptly just when I thought it was getting interesting!
Quote:
http://intensivedietarymanagement.c...besity-part-xx/.
One of the founding principles of the low carbohydrate approach is that insulin is the key driver of obesity. This fact seems solidly grounded in science as we have discussed before. Carbs are the major macronutrient (out of fat, protein and carbs) that cause blood sugars to go up. As blood sugar goes up, insulin is assumed to also follow. Therefore, carbohydrates are assumed to play the major role in stimulating insulin release. This is true. However, we have not considered the possibility that food may increase the insulin levels without raising blood sugars.
The breakthrough was discovered in 1997, with the publication of the insulin index. Measuring the insulin response of 1000kJ portions of food, it was no surprise that the foods that stimulated insulin the most were the carbohydrate rich foods, bakery products, and snacks and confectionary. What was astounding was the fact that protein rich foods also significantly raised insulin levels.
Where most people assumed that there was a tight correlation between glucose levels and insulin levels, it turned out that only 23% of the variability in the insulin response was due to the glucose. In other words, only 23% of the insulin response is determined by how high the blood sugars rise. The vast majority of the insulin response (77%) is not related at all. Since it is insulin, and not glucose that drives weight gain, this changes everything. This is precisely where the glycemic index diets failed. They were targeting the glucose response with the assumption that the insulin response mirrored the glucose. But this is not the case. You could lower the glucose response by diet, but you didn’t necessarily lower the insulin response. In the end, it is only the insulin response that matters.
The recent discovery of the incretin effect partially explains things. What has been recently appreciated is that the gastrointestinal tract, particularly the stomach and small intestine actively secrete hormones. There are so many neurone in the GI system that it has sometimes been called the ‘second brain’. The incretin hormones, Glucagon Like Peptide (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIP) are secreted by the fundus of the stomach in response to food. GLP-1 is known to increase insulin release by the pancreas. The main role of GIP, found in the duodenum and jejunum (small intestine) is to stimulate insulin release. Fats, amino acids and glucose all stimulate GLP-1 release and thus, increased insulin. The amino acid glutamine may be a particularly potent stimulus.
Even non nutritive sweeteners, which have no calories at all, can stimulate the insulin response. Sucralose, when studied in obese human volunteers, raises the insulin level 22% higher than water. The GI tract and the pancreas can detect sugars through taste receptors similar to those in the mouth. This may activate secretion of GLP-1 and insulin.
Furthermore, there is a well-known effect called the ‘cephalic phase’ of insulin secretion. This refers to the fact that the body starts to anticipate food as soon as you put it in your mouth and long before any nutrients hit the stomach. Studies have shown insulin release in response to sucrose and saccharine even if you swish it around your mouth and spit it out.
Insulin does not respond only to high sugars, but the incretin effect shows that fatty acids and amino acids also play a role in the stimulation of insulin. Hold on. This changes everything. The simple implication is this. If carbohydrates are not the only, or even the major stimulus to insulin secretion, then restricting carbohydrates may not have as large an effect on insulin levels as we may have believed.
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(my emphasis)
Seems like we need more studies on the insulin index, especially with more whole foods.
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