Hi,
I have heard that if you mix protein (meat) and carbs you can lower GI of meal...does this mean if you eat a piece of meat, then a piece of wholewheat bread and then maybe a piece of cake :)...does this change things ?
thanks
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Hi,
I have heard that if you mix protein (meat) and carbs you can lower GI of meal...does this mean if you eat a piece of meat, then a piece of wholewheat bread and then maybe a piece of cake :)...does this change things ?
thanks
PREFACE
The fact is that many bodybuilding, health, & fitness enthusiasts stake their entire moral judgment of carbohydrate foods based on their glycemic index (GI) without realizing that a considerable set of confounders challenges its validity. Becoming blindly enamored with something that may enhance our physiques &/or health is natural, and something we've all been guilty of. But alas, the GI data is neither perfect nor consistent, nor is it free of bugs. Consider the following facts, and re-think your obsession with GI & what you think you know about GI.
A POSSIBLE DEFINITION SHIFT
The current general definition of GI is a food's ability to raise blood sugar, which almost automatically is regarded in terms of glucose entry into the blood. However, recent eye-opening research by Schenk & colleagues clearly showed that the rate of disappearance of glucose from systemic circulation is an important determinant of GI - not just glucose's rate of entry into circulation [1]. They found that the lower GI of bran cereal was due to a quicker/sooner surge of insulin sweeping glucose out of circulation - not a slower appearance/entrance of glucose as once assumed. Although strictly speculative at this point, this phenomenon may have possible performance detriment implications (ie, rebound hypoglycemia) in sensitive individuals if meals of this nature are mistimed relative to training.
DETERMINATION VS. APPLICABILITY
GI values are determined in an overnight-fasted state using isolated foods. This is not a reflection of real life, where the digestion/absorption of previous meals, as well as the context of the carbohydrate food can drastically alter GI.
AFFECTING FACTORS
The interplay of many variables can either raise or lower GI, and are often difficult to control. Increased acidity, the presence of fiber, fat, and certain protein foods can lower glycemic response. Reduced particle size, greater ripeness, and heat in cooking can raise glycemic response.
GLYCEMIC LOAD DISPARITY
Glycemic load (GL), which is the amount of carbohydrate per serving or unit of volume, is not always directly proportional to GI. For example, watermelon has a GI of 72, which is considered high. Low-GI advocates have vilified watermelon without realizing the fact that it has a relatively low glycemic load, approximately 6g carbohydrate per 4oz serving. The same disparity of GI & GL applies to carrots, potatoes, and even sports drinks such as Gatorade.
SATIETY INDEX DISPARITY
Lower-GI foods have been associated with greater satiety, but most of this data comes from single-meal experimental designs. Longer-term studies on GI & satiety are conflicting, and not always controlled for energy intake and energy density of the test meal [2]. In the longest study to date on GI & satiety is an ad libitium 30d crossover design where Kiens & Richter observe no difference in amount of consumption [3]. In this metabolic study, a LOWER resistance to insulin was seen in the high-GI group at the end of the trial. GI does not reliably correspond with satiety index (SI). White rice, wheat bread, and potatoes all have high GIs, but rank among the top of the list for delaying the onset of hunger. In fact, Holt's team found that potatoes had by far the highest SI of all the foods tested [4].
INSULIN ISSUES
As a classic example of chaos physics, the typical rules that predict GI do not necessarily help in predicting insulin response. Unfortunately for GI-conscious people, insulin is usually what they are trying to control. Despite having a very low GI of 15-36, milk and yogurt have a high insulin index equivalent to that of the high-GI white bread [5]. Baked beans, another low-GI food, have a very high insulin index of 120. Cheese, beef, and fish have II's that are comparable to many carbohydrate foods.
Coingestion of fat with carbohydrate slows gastric emptying and thus the release of glucose into the blood, ultimately lowering GI. While this is usually true for GI, the degree of insulin response evoked by this combination is determined by the degree of the fat's saturation. For example, Collier & others observed that butter coingested with potato not only fails to lower postprandial insulinemia, it actually causes a synergistically heightened insulin response, even in healthy subjects [6,7].
Foods that should have a low GI due to their high fat content do not always have a low GI. Examples are fries, cookies, croissants, and doughnuts. Incidentally, these foods also have a high insulin index, presumably because their fat is mostly saturated. As of this writing, full-fat ice cream (low GI of appx 37) has not been tested for II, but it's safe to assume that it probably has disparate GI & II values.
Rasmussen & colleagues observed no increased insulin response with the addition of 40g or 80g olive oil, but saw a significant increase with 50g & 100g butter [8]. Joannic's team observed a coingestion of carbohydrate with fats of increasing degree of unsaturation having a corresponding decrease in insulin response [9]. A more recent study by Robertson & colleagues compared the effect of MUFA, PUFA, & SFA coingestion with carbohydrate and observed SFA's superior ability to raise postprandial insulin levels [10].
Coingestion of protein with carbohydrate is often recommended to lower GI, but it doesn't necessarily lower insulin response. Gannon & Nutall's research on type-2 diabetics showed that coingested cottage cheese & glucose raised insulin levels beyond either food separately, indicating a synergistic effect [11]. Van Loon & colleagues saw a similar phenomenon when comparing the insulin effect of various carb-protein/amino acid and carb-only solutions [12]. Those containing free leucine, phenylalanine, & arginine, and the drinks with free leucine, phenylalanine, & wheat protein hydrolysate were followed by the largest insulin response (101% and 103% greater, respectively, than with the carb-only solution).
GI & OBESITY - SLIM CHANCE FOR CORRELATION
a systematic review of human intervention studies comparing the effects of high and low-GI foods or diets arrived at the following results [13]:
---- in a total of 31 short-term studies, low-GI foods were associated with greater satiety or reduced hunger in 15 studies, whereas reduced satiety or no differences were seen in 16 other studies.
---- low-GI foods reduced ad libitum food intake in 7 studies, but not in 8 other studies. In 20 longer-term studies (<6 months), weight loss on a low-GI diet was seen in 4 and on a high-GI diet in 2, with no difference recorded in 14 studies.
---- an exhaustive assessment of these human intervention trials found no significant difference in the average weight loss between low & high GI diets. in conclusion, the current body of research evidence does not indicate that low-GI foods are superior to high-GI foods in regard to treating obesity.
SO, WHAT?!
Don't get it twisted, GI is a definitely useful tool that gives us clues to the behavior of certain foods, but that's exactly the main point of this article. Clues; mere hints are all we get from our current knowledge of GI. Successful application of GI is most consistent when we use higher GI sources to enhance the speed of postworkout glycogenesis, and lower-GI starch foods tend to be more micronutrient dense than their higher-GI counterparts, but that's really about the extent of it. Satiety, insulin response, & surrounding factors altering glucose kinetics are all much like a roll of the dice in terms of bottom-line certainty & reliability. Like all things in science - especially the deep bubbly cauldron that is applied nutritional science - it ain't all that simple. All avenues in this area are winding & complex.
References for you research nerds:
1) Schenk S, et al. Different glycemic indexes of breakfast cereals are not due to glucose entry into blood but to glucose removal by tissue. Am J Clin Nutr 2003;78(4):742-8.
2) Pi-Sunyer FX. Glycemic index and disease. Am J Clin Nutr 2002 Jul;76(1):290S-8S.
3) Kiens B, Richter EA. Types of carbohydrate in an ordinary diet affect insulin action and muscle substrates in humans. Am J Clin Nutr 1996;63:47-53.
4) Holt SH, Miller JC. A satiety index of common foods. Eur J Clin Nutr 1995 Sep;49(9):675-90.
5) Ostman EM, et al. Inconsistency between glycemic and insulinemic responses to regular and fermented milk products. Am J Clin Nutr 2001; 74(1):96-100.
6) Collier G, et al. The effect of coingestion of fat on the glucose, insulin, and gastric inhibitory polypeptide responses to carbohydrate and protein. Am J Clin Nutr 1983;37(6):941-4.
7) Collier G, et al. The acute effect of fat on insulin secretion. J Clin Endocrinol Metab 1988;66(2):323-6.
8) Rasmussen O, et al. Differential effects of saturated and monounsaturated fat on blood glucose and insulin responses in subjects with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1996 Feb;63(2):249-53.
9) Joannic JL, et al. How the degree of unsaturation of dietary fatty acids influences the glucose and insulin responses to different carbohydrates in mixed meals. Am J Clin Nutr 1997 May;65(5):1427-33.
10) Robertson MD, et al. Acute effects of meal fatty acid composition on insulin sensitivity in healthy post-menopausal women. Br J Nutr 2002;88(6):635-40.
11) Gannon MC, et al. Metabolic response to cottage cheese or egg white protein, with or without glucose, in type II diabetic subjects. Metabolism 1992;41(10):1137-45.
12) van Loon LJ, et al. Plasma insulin responses after ingestion of different amino acid or protein mixtures with carbohydrate. Am J Clin Nutr 2000;72(1):96-105.
13) Raben A. Should obese patients be counselled to follow a low-glycaemic index diet? No. Obes Rev. 2002 Nov;3(4):245-56.
per our discussion yesterday, on how high inulin levels can be raised by a carb/pro drink, this table shows that it's similar to the levels induced by the injection of the exogenous insulin
http://www.ajcn.org/cgi/content/full/72/1/96/F4
which shows spikes in natural insulin levels to exceed 82mU/ml...
here is your quote from the other post...
"This abstract deals with insulin that is infused:
Insulin was infused (0.15 mU/min per 100 ml leg) into the femoral artery to increase femoral venous insulin concentration (from 10 +/- 2 to 77 +/- 9 microU/ml) with minimal systemic perturbations.
So there is very little corelation to the other studies."
"Those containing free leucine, phenylalanine, & arginine, and the drinks with free leucine, phenylalanine, & wheat protein hydrolysate were followed by the largest insulin response (101% and 103% greater, respectively, than with the carb-only solution)."
"the subjects received a beverage volume of 3.5 mL/kg to ensure a given dose of 0.8 g carbohydrate/kg (50% as glucose and 50% as maltodextrin) and 0.4 g/kg of an amino acid and protein (hydrolysate) mixture"
good to know where doing it right, eh? not that anyone doubted...
how many people actually drink protein hydrolysate ??? I dont think any of thw wheys i have tried are hydrolysate ???
here's one i found fairly easy...i'm sure there are many products out there that do...
"MUSCLE PROVIDER is literally slammed full of high quality powerful proteins in a big way. Lab analysis revealed it consistently exceeded label claims.
MUSCLE PROVIDER consists of a very unique and exclusive multiple protein configuration. This superior blend of five top of the line protein substrates includes whey protein isolate through cross-flow micro-filtration, whey protein hydrolysate, whey protein concentrate, lactalbumin (the major component of all whey, with the biological value of 100) and egg white albumin"
i'm pretty certain it's the same thing as hydrolyzed whey...
Ha!! I just checked my ON whey protein powder - it doesnt say it has hydrolysate in the ingredients, but in the advert features on the packing it does !!! So my whey is good to go !! lol
I don't think the combination of protein and carbs can lower GI of a meal.Quote:
Originally Posted by rankin
What can lower GI of a meal is FAT and FIBER. As far as I know natural protein has no significant impact on insulin levels. That is why protein is better consumed with carbs, because carbs stimulate insulin production and as we all know, insulin transports amino acids to the muscle cells.
"Coingestion of protein with carbohydrate is often recommended to lower GI, but it doesn't necessarily lower insulin response"
Alpha thought I'd throw a few more athcha!!
Amino acids regulate skeletal muscle PHAS-I and p70 S6-kinase phosphorylation independently of insulin. Long, W., L. Saffer, L. Wei, and E. J. Barrett. Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908
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APStracts 7:0077E, 2000.
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Refeeding reverses the muscle protein loss seen with fasting. The physiological regulators and cellular control sites responsible for this reversal are incompletely defined. Phosphorylation of phosphorylated heat-acid stabled protein (PHAS-I) frees eukaryotic initiation factor 4E (eIF4E) and stimulates protein synthesis by accelerating translation initiation. Phosphorylation of p70 S6-kinase (p70S6k) is thought to be involved in the regulation of the synthesis of some ribosomsal proteins and other selected proteins with polypyrimidine clusters near the transcription start site. We examined whether phosphorylation of PHAS-I and p70S6k was increased by feeding and determined the separate effects of insulin and amino acids on PHAS-I and p70S6k phosphorylation in rat skeletal muscle in vivo. Muscle was obtained from rats fed ad libitum or fasted overnight (n = 5 each). Other fasted rats were infused with insulin (3 muU×min«minus»1×kg«minus»1, euglycemic clamp), amino acids, or the two combined. Gastrocnemius was freeze-clamped, and PHAS-I and p70S6k phosphorylation was measured by quantifying the several phosphorylated forms of these proteins seen on Western blots. We observed that feeding increased phosphorylation of both PHAS-I and p70S6k (P < 0.05). Infusion of amino acids alone reproduced the effect of feeding. Physiological hyperinsulinemia increased p70S6K (P < 0.05) but not PHAS-I phosphorylation (P = 0.98). Addition of insulin to amino acid infusion was no more effective than amino acids alone in promoting PHAS-I and p70S6k phosphorylation. We conclude that amino acid infusion alone enhances the activation of the protein synthetic pathways in vivo in rat skeletal muscle. This effect is not dependent on increases in plasma insulin and simulates the activation of protein synthesis that accompanies normal feeding.
Alpha thought I'd throw a few more athcha!!
Amino acids regulate skeletal muscle PHAS-I and p70 S6-kinase phosphorylation independently of insulin. Long, W., L. Saffer, L. Wei, and E. J. Barrett. Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908
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APStracts 7:0077E, 2000.
--------------------------------------------------------------------------------
Refeeding reverses the muscle protein loss seen with fasting. The physiological regulators and cellular control sites responsible for this reversal are incompletely defined. Phosphorylation of phosphorylated heat-acid stabled protein (PHAS-I) frees eukaryotic initiation factor 4E (eIF4E) and stimulates protein synthesis by accelerating translation initiation. Phosphorylation of p70 S6-kinase (p70S6k) is thought to be involved in the regulation of the synthesis of some ribosomsal proteins and other selected proteins with polypyrimidine clusters near the transcription start site. We examined whether phosphorylation of PHAS-I and p70S6k was increased by feeding and determined the separate effects of insulin and amino acids on PHAS-I and p70S6k phosphorylation in rat skeletal muscle in vivo. Muscle was obtained from rats fed ad libitum or fasted overnight (n = 5 each). Other fasted rats were infused with insulin (3 muU×min«minus»1×kg«minus»1, euglycemic clamp), amino acids, or the two combined. Gastrocnemius was freeze-clamped, and PHAS-I and p70S6k phosphorylation was measured by quantifying the several phosphorylated forms of these proteins seen on Western blots. We observed that feeding increased phosphorylation of both PHAS-I and p70S6k (P < 0.05). Infusion of amino acids alone reproduced the effect of feeding. Physiological hyperinsulinemia increased p70S6K (P < 0.05) but not PHAS-I phosphorylation (P = 0.98). Addition of insulin to amino acid infusion was no more effective than amino acids alone in promoting PHAS-I and p70S6k phosphorylation. We conclude that amino acid infusion alone enhances the activation of the protein synthetic pathways in vivo in rat skeletal muscle. This effect is not dependent on increases in plasma insulin and simulates the activation of protein synthesis that accompanies normal feeding.
Quote:
Originally Posted by Alpha-Male
This comes from a study on type-2 diabetes !!! It wasn't made on healthy humans. These people have an insulin problem.