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#1
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Insuln Response to HiCarb vs LoCarb?
I was under the impression that a high-fat meal would cause a lower
insulin response than a high-carb meal. If so, why does the following study seem to indicate the opposite? Meal composition affects insulin secretion in women with type 2 diabetes: a comparison with healthy controls. The Hoorn prandial study. BACKGROUND/OBJECTIVE: Early insulin secretion following a meal is representative for normal physiology and may depend on meal composition. To compare the effects of a fat-rich and a carbohydrate- rich mixed meal on insulinogenic index as a measure of early insulin secretion in normoglycemic women (NGM) and in women with type 2 diabetes mellitus (DM2), and to assess the relationship of anthropometric and metabolic factors with insulinogenic index. SUBJECTS/METHODS: Postmenopausal women, 76 with NGM and 64 with DM2, received a fat-rich meal and a carbohydrate-rich meal on separate occasions. Early insulin response was estimated as insulinogenic index ( big up tri, Deltainsulin(0-30 min)/ big up tri, Deltaglucose(0-30 min)) for each meal. Associations of fasting and postprandial triglycerides, body mass index, waist and hip circumference and alanine aminotransferase with insulinogenic indices were determined. RESULTS: Women with NGM present with higher insulinogenic index than women with DM2. The insulinogenic index following the fat-rich meal ( big up tri, DeltaI(30)/ big up tri, DeltaG(30) (fat)) was higher than the index following the carbohydrate-rich meal (big up tri, DeltaI(30)/ big up tri, DeltaG(30) (CH)) (P0.05 in women with DM2, and not significant in women with NGM). In women with DM2, homeostasis model assessment for insulin resistance was positively associated with big up tri, DeltaI(30)/ big up tri, DeltaG(30) (CH). In women with NGM, waist circumference was independently and inversely associated with big up tri, DeltaI(30)/ big up tri, DeltaG(30) (fat) and with big up tri, DeltaI(30)/ big up tri, DeltaG(30) (CH); hip circumference was positively associated with big up tri, DeltaI(30)/ big up tri, DeltaG(30) (fat). CONCLUSIONS: The insulinogenic index following the fat-rich meal was higher than following the isocaloric carbohydrate- rich meal, which might favorably affect postprandial glucose excursions, especially in women with DM2. The association between a larger waist circumference and a lower meal-induced insulinogenic index in women with NGM requires further mechanistic studies. PMID: 17987050 |
#2
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Insuln Response to HiCarb vs LoCarb?
Protein causes the strongest, long lasting insulin release after a meal..
How much protein was in the meals the study subjects ate? I don't have access to the full study, but I assume the protein in both meals were the same. This points to the fact that it's not the total amount of insulin secreted after a meal that is undesirable, it's sudden and very high secretion, apparently. *Fat does not stimulate insulin secretion. Glycemic carbs induce a sharp, sudden increase in insulin secretion. Protein induces a longer/stronger, and steady secretion. Which causes a sharper insulin response, carbs or protein? On second reading of the study, it seems it conclusions are difficult to interpret because: 1. The abstract doesn't indicate macronutrient breakdown for "fat- rich" meal. It may be mod-fat, mod-carb meal according to low-carb proponents. 2. The "Insulinogenic" index incorporate trigs and glucose levels. ------------- Below study on rabbits say cholesterol, not saturated fats, cause problems. Why does cholesterol supplementation cause major problems for rabbits. Don't rabbits have cholesterol in their blood? Is the cholesterol in this and most such experiments oxidized? Is the cholesterol in raw egg yolks oxidized? Does it become oxidized when hard boiled? Effect of High Fat Diet Without Cholesterol Supplementation on Oxidative Stress and Lipid Peroxidation in New Zealand White Rabbits. Aim: Dietary fats may affect coronary artery disease risk by influencing factors other than serum cho-lesterol. The effect of diets containing coconut oil and sunflower oil without cholesterol supplementation on oxidative stress and lipid peroxidation were studied in male New Zealand White rabbits.Methods: Animals assigned to four groups (control, cholesterol-fed, coconut oil-fed and sunflower oil-fed), given an isocaloric diet and studied for 6 months. The lipid profile, reduced glutathione, glutathione peroxidase, superoxide dismutase, vitamin C and lipid peroxidation were evaluated at the beginning of the study, at the third month and at the end of the study period. Results: Serum lipid values did not show significant variation between animals fed coconut oil and sunflower oil, but total cholesterol, triglycerides and LDL-cholesterol were significantly higher and HDL-cholesterol was reduced in cholesterol-fed animals. Lipid peroxidation was higher in cholesterol-fed and sunflower oil-fed rabbits compared to controls and coconut oil-fed rabbits. Though other parameters such as reduced glutathione, glutathione peroxidase, superoxide dismutase and ascorbate did not vary between the two oil- fed rabbit groups, cholesterol-fed rabbits showed severe oxidative stress.Conclusion: We conclude that in the absence of cholesterol supplementation, coconut oil intake up to 30% of daily energy supply did not cause hypercholesterolemia or oxidative stress in rabbits. PMID: 20032571 |
#4
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Insuln Response to HiCarb vs LoCarb?
In article ,
pamela wrote: Jarod wrote: Susan wrote: A recent meta analysis indicates that saturated fat has no causal relationship to CVD. Do you probably have a link which points me directly to this analysis? (I have full access to nearly all the public medical databases). Thanks! Here is an older one from 2000. Claims a WEAK association between fat and heart disease. Actually there was a "trend" to decreased fat being protective, but it was not statistically significant. The data opposing the classic strong link between fat and heart disease is almost 10 years old, but the contrary "expert medical opinion" has been so deeply ingrained by millions of repetitions that it will take a long time to die out. One point is how weak the supposed effect is. The statin pushers have to hide the fact that the alleged gains are miniscule for any individual. It doesn't make sense for any individual, but it's supposed to make up for it by reducing the number of cardio vascular events in large populations. Oh, and side effects are *notoriously* under reported. A little muscle weakness, a little cognitive decline etcetera (or a lot actually), may not be reported and if it is will be brushed off with "You're getting older." Sexual "side effect" are even more notoriously likely to not be reported or taken seriously. Meanwhile I have taken off like 70-80 pounds, just by carb restriction, I am not sure because I didn't want to weigh myself before the weight started coming off. -- A computer without Microsoft is like a chocolate cake without mustard. |
#5
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STATINS was Insuln Response to HiCarb vs LoCarb?
Walter Bushell wrote:
In article , pamela wrote: Jarod wrote: Susan wrote: A recent meta analysis indicates that saturated fat has no causal relationship to CVD. Do you probably have a link which points me directly to this analysis? (I have full access to nearly all the public medical databases). Thanks! Here is an older one from 2000. Claims a WEAK association between fat and heart disease. Actually there was a "trend" to decreased fat being protective, but it was not statistically significant. The data opposing the classic strong link between fat and heart disease is almost 10 years old, but the contrary "expert medical opinion" has been so deeply ingrained by millions of repetitions that it will take a long time to die out. One point is how weak the supposed effect is. The statin pushers have to hide the fact that the alleged gains are miniscule for any individual. It doesn't make sense for any individual, but it's supposed to make up for it by reducing the number of cardio vascular events in large populations. Oh, and side effects are *notoriously* under reported. A little muscle weakness, a little cognitive decline etcetera (or a lot actually), may not be reported and if it is will be brushed off with "You're getting older." Sexual "side effect" are even more notoriously likely to not be reported or taken seriously. I foolishly let myself be given statins, as a trial. There was an immediate reduction of LDL to down just below 100, but because of other "risk factors" they wanted to go even lower. Again, I foolishly went along, as a trial. Within 2 weeks, myalgia (muscle weakness) set in. I had to reduce the weights on exercise weight machines by generally 20 percent. My walking time on the inclined treadmill went down from nearly 60 minutes to about 8 minutes with fatigue and claudication. I stopped the statins immediately. Research on Pubmed.gov on the subject showed that myalgia was considered common and underreported or dismissed by the clinician as unrelated to the statin. I found one paper claiming that exercisers were especially prone to myalgia from statins, claiming that up to 20 percent of such patients would have weakness/pain problems. I found out that no one is clear on what the cause of statin induced myalgia is, and there is no clear or "official" information on what is best to do to recover from it - except stop the statins. Evidently, not all myalgia symptoms are easily eliminated, and may be permanent. Because the National Cholesterol Education Panel is heading towards getting everybody to seek ever lower levels of cholesterol, the current drugs are inadequate. One drug company reported on the existing programs to create strong statins with less tendency to induce myalgia because without such drugs, the widespread application of them will be nearly impossible. |
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