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LOW GLYCEMIC FOODS (For Weight Loss, Insulin Resistance + Diabetes) *WON'T Spike Blood Sugar!* In the morning after a Glycemic load and insulin response hour fast and during the fourth or fifth week HbAc range each inulin period, Glycemic load and insulin response participants were given qnd, lunch, and dinner that had the food and loa composition of the assigned diet period. Blood was sampled before breakfast, usually at amamamand hourly, ending at approximately pm. See eTable 3 in Supplement 2 for data on glucose and insulin area under the curve and statistical testing. A self-selected subgroup of participants were included. Carb indicates carbohydrate; GI, glycemic index. The primary outcomes were systolic blood pressure, insulin sensitivity, and levels of low-density lipoprotein LDL cholesterol, high-density lipoprotein HDL cholesterol, and triglycerides.Glycemic load and insulin response -
definitely worth testing your blood sugars before and after to see how you respond to those foods vs other foods. for example:. Excellent research and analysis. By measuring my sugar levels twice daily, I have learned what foods and their quantity I can consume to obtain my sugar levels.
This, of course, includes the effect of daily exercise and drinking lots of water. I plan to ask him about intermittent fasting. What are your thoughts on fasting? Thanks again. thanks Tony!
I have some reservations about popular fasting. you can use your blood sugar before you eat as a nice little fuel gauge to guide meal timing. Tony, it is my experience that decreasing oral type2 medications is a fairly long and complicated process. I could not have succeeded in doing that without a continuous blood glucose monitor Abbott FreeStyle Libre II You will probably have to pay for it yourself, as the monitors are generally only prescribed for type 1 diabetics at this time.
Additionally, I was also dealing with moderate non-alcoholic fatty liver. Doctors do not have a great metric for monitoring fatty liver improvement. I was also dealing with severe insulin resistance. There was no practical for getting at insulin levels. Lastly, check out these YouTube presenters.
Ken Berry and Dr. Jason Fung Based on my experience it will take 50 hours of viewing such videos to get a handle on the complicated mess of Type2 diabetes, insulin resistance, and fatty liver. I feel intermittent fasting in combo with constant blood glucose monitoring were the keys to me getting ahead of my problems.
How much does low Hemoglobin levels distort these results? Or in other words what is the correlation of Hemoglobin levels to Blood sugar levels? Do you mean your HbA1c? Your blood sugar after meals is related to what you eat while your blood sugar across the rest of the day will depend on how often and how much you eat.
Why do you make no distinction between the types of diabetes? And type 2 who have no response, no pancreatic function…with essentially a totally different disease…we react the same as well? There are multiple types of type 2… and TOTALLY different issues for type 1… they are only grouped together due to similar outcomes…similar ways they present… but differences between diabetic types are great.
Not to be swept aside by calling everyone a diabetic… not when talking about what food as an input to the system does to the body! People with T2D often produce much more insulin than everyone else, but because they are trying to hold more energy in storage than their body can comfortably handle, they see the stored energy overflow into their bloodstream.
The blood sugar response to protein for both T1D and T2D is actually quite similar, with a rise in blood sugars after eating. For both T1 and T2 it makes sense to reduce refined carbohydrates to the point that blood sugars stabilise to healthy non-diabetic levels.
Adequate dietary protein is important for both conditions but especially T2D to improve satiety and help reduce body fat until they return below their Personal Fat Threshold. I believe that your response does not give proper weight to sever insulin resistance, something that can develop over 10 years or more, even while fasting blood glucose levels are normal.
I believe in the next 10 years insulin resistance will be re named to insulin toxicity. Conversely, people with T1D can become obese and insulin resistant. And Type1 who have no response, no pancreatic function…with essentially a totally different disease…we react the same as well?
If you have a relative insulin insufficiency, you will see a similar blood sugar response, regardless of whether you are T1D or T2D. But the good news is you can reverse T2D with intelligent dietary choices. Thought provoking, again, thank you.
I am getting interested in this basal long term insulin, and also the development in insulin after 2h aka m. Late Dr. Kraft did not only measure insulin reactions, he studied them until 5 h. We know the different patterns representing unbalanced insulin reaction, which still hammeres down glucose and lipids, I presume.
junk food. Since visceral fat has more insulin reseptors fold than skin fat, sounds like packing energy into stomach even if there is no treshold difference inbetween these differerent adipose depots. In this order, speed directly proportional to reduced carbs.
Is this a question? More like deduced statement, feel anybody free to guide me to correct path… JR. Kraft is interesting. But I think wasit:height will give you a lot of the same information with a lot less hassle.
Data Driven FAsting uses premeal blood sugars to guide you to wait to ensure an energy defiit until you achieve more optimal waking blood sugars.
Hi Marty, Thank you for a prodigious effort and analysis! My query is about the graph B GC vs LF and HF meals — was the amount of protein in these diets equivalent in terms of bioavailability to ensure that protein did not influence the difference between the bsl graphs? Bioavailability may have a small impact but protein only has a negligible impact on blood glucose.
So the overall impact of protein on glucose for LC vs LF food sources will be pretty much zero. Black tea and espresso being high up the chart is a bit confusing, if you would consume kcals of those it means you drank lethal amounts right? Eager to step beyond the conventional Glycemic Index GI in managing your blood sugar levels?
What Is the Glycemic Load? Who Developed the Glycemic Index? How Is the Glycemic Index Calculated? What Is a Good Glycemic Index Score? What is the Glucose Score? Glucose Score Data How Do Carbs, Protein, Fat, and Fibre Impact Your Glucose? Net Carbohydrate vs Glycemic Index vs Glucose Score Protein vs.
Glucose Score vs. Satiety Index Low Glycemic Index Meals and Recipes Low Glucose Score Meals Glucose Response to Carbohydrates vs. Get the Optimised Food Lists. thanks for checking it out Hakan. glad you enjoyed it! For example, the GI of some everyday foods such as fruits, vegetables and cereals can be higher than foods to be eaten occasionally discretionary like biscuits and cakes.
This does not mean we should replace fruit, vegetables and cereals with discretionary choices, because the first are rich in important nutrients and antioxidants and the discretionary foods are not.
GI can be a useful concept in making good food substitution choices, such as having oats instead of cornflakes, or eating grainy bread instead of white bread. Usually, choosing the wholegrain or higher fibre option will also mean you are choosing the lower GI option.
There is room in a healthy diet for moderate to high GI foods, and many of these foods can provide important sources of nutrients. Remember, by combining a low GI food with a high GI food, you will get an intermediate GI for that meal.
The best carbohydrate food to eat varies depending on the person and situation. For example, people with type 2 diabetes or impaired glucose tolerance have become resistant to the action of insulin or cannot produce insulin rapidly enough to match the release of glucose into the blood after eating carbohydrate-containing foods.
This means their blood glucose levels may rise above the level considered optimal. Now consider 2 common breakfast foods — cornflakes and porridge made from wholegrain oats. The rate at which porridge and cornflakes are broken down to glucose is different.
Porridge is digested to simple sugars much more slowly than cornflakes, so the body has a chance to respond with production of insulin, and the rise in blood glucose levels is less.
For this reason, porridge is a better choice of breakfast cereal than cornflakes for people with type 2 diabetes. It will also provide more sustained energy for people without diabetes. On the other hand, high GI foods can be beneficial at replenishing glycogen in the muscles after strenuous exercise.
For example, eating 5 jellybeans will help to raise blood glucose levels quickly. This page has been produced in consultation with and approved by:. Learn all about alcohol - includes standard drink size, health risks and effects, how to keep track of your drinking, binge drinking, how long it takes to leave the body, tips to lower intake.
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Healthy eating. Home Healthy eating. Carbohydrates and the glycaemic index. Actions for this page Listen Print. Summary Read the full fact sheet. On this page. The measurements during the last 2 weeks were averaged and constituted the outcome variable for blood pressure, as done previously.
Plasma total and lipoprotein cholesterol, triglycerides, and apolipoproteins B, C-III, and E were measured using enzymatic kits or enzyme-linked immunosorbent assay.
Insulin sensitivity was measured by an oral glucose tolerance test, 75 g, during screening and the final 10 days of each diet period.
Blood was sampled at 0, 10, 20, 30, 60, 90, and minutes. Insulin sensitivity was calculated by the index of Matsuda and DeFronzo that uses blood glucose and serum insulin levels at 0, 30, 60, 90, and minutes.
On that day, participants were given the same diet type for that diet period for breakfast, lunch, and dinner, which had a mean , , kcal, respectively, for a typical kcal diet, the same as in the other days of the controlled diet.
Blood was sampled at fixed intervals just before eating breakfast; 30, 60, and 90 minutes after starting breakfast; and hourly thereafter through 12 hours.
This hour meal test is a process variable that determines the differences in blood glucose caused by the differences among the diets in glycemic index and amount of carbohydrate. Diets with higher glycemic index and higher amount of carbohydrate are expected to increase the hour blood glucose AUCi.
Urine collections hour were obtained once during screening and once during the last 2 weeks of each diet period. Data collection personnel were blinded to diet sequence. Information on serious adverse events was collected from participants and their medical records and reported to the institutional review board as required.
The diet contrasts pertaining to the effect of glycemic index were high glycemic index vs low glycemic index in the setting of high total carbohydrate intake and separately in the setting of low total carbohydrate intake. The trial design also allowed a test of the effects of lowering total dietary carbohydrate, separately in the setting of high—glycemic index and low—glycemic index foods.
Although this 4-period study could be analyzed as a factorial design, combining the high- and low-carbohydrate periods to test glycemic index, and combining the high— and low—glycemic index diets to test level of carbohydrate, we considered it likely that glycemic index has a stronger effect when the total carbohydrate intake is high and that carbohydrate level has a stronger effect when the glycemic index is high.
Therefore, a factorial analysis was considered inappropriate. In the protocol-specified analytical plan, the primary analysis is a comparison of the high-carbohydrate, high—glycemic index diet and the low-carbohydrate, low—glycemic index diet, representing a single integrated measure of the hypothesized maximal effect on the 5 primary outcomes of manipulating dietary carbohydrate by reducing its amount and glycemic index.
Because some participants did not provide measures on all outcomes for all diets, multiple imputation analysis was performed for the 5 primary outcomes. There was no qualitative effect of multiple imputation compared with complete case analysis.
Full details are given in the online appendix eFigure 1 in Supplement 2. The distribution of within-person differences in response variables for pairs of diets was analyzed using the t.
test function of R version 3. This provides estimates of average effect, standard error of the estimate, and limits of confidence intervals for selected confidence coefficients.
Statistical visualization and additional analyses such as multiple imputation sensitivity analysis and tests for carryover effects were also performed using R. We used standard assessments of carryover effects in crossover designs based on the comparison of distributions of sums of outcomes between groups of participants receiving treatments in different orders.
One hundred sixty-three participants completed at least 2 diets and were included in the analysis of outcomes Figure 1. For any pair of diets, there were to participants. The trial ended when at least participants completed at least 2 diets, as planned.
Participants lost an average of 1 kg of body weight from baseline to the end of each diet period, the same for each diet type. Urinary sodium and potassium excretion were similar during each diet period. At the high dietary carbohydrate content, the low— compared with the high—glycemic index level significantly reduced insulin sensitivity from 8.
At the low carbohydrate content, the low— compared with the high—glycemic index level did not affect insulin sensitivity but increased fasting blood glucose level by 2. Mean glucose and insulin levels during the oral glucose tolerance test are shown in eFigure 2 in Supplement 2.
Glycemic index level did not affect HDL cholesterol level or systolic blood pressure or diastolic blood pressure. A low compared with a high dietary carbohydrate content did not affect insulin sensitivity at either the high— or the low—glycemic index level Figure 3 and Table 3.
A low compared with a high dietary carbohydrate content significantly lowered plasma total triglycerides at both high— and the low—glycemic index levels. There was no evidence of additive effects of glycemic index level and dietary carbohydrate content on any of the outcomes.
A sensitivity analysis restricted to the participants who completed all 4 diets yielded results similar to the primary analyses eTable 5 in Supplement 2. Serious adverse events occurred in 7 participants: injuries from automobile crashes 3 participants , kidney stone 1 , acute asthma 1 , osteomyelitis 1 , and pneumonia 1.
None were judged to be related to the study procedures. There were no unintended or unanticipated effects. All 4 study diets were associated with lower systolic blood pressure by 7 to 9 mm Hg Table 3 and diastolic blood pressure by 4 to 6 mm Hg eTable 3 in Supplement 2.
Paradoxically, the low—glycemic index, high-carbohydrate diet compared with the high—glycemic index, high-carbohydrate diet decreased insulin sensitivity and increased LDL cholesterol and LDL apolipoprotein B levels while other dietary factors that affect LDL levels such as saturated fat, cholesterol, and fiber were held constant.
These findings are contrary to our hypotheses on glycemic index. As we found previously in the OmniHeart trial, 8 the beneficial effects of the DASH diet can be improved modestly by reducing its carbohydrate content. Lowering the carbohydrate content and compensating the reduced calories with unsaturated fat and protein substantially lowered triglycerides and VLDL levels and slightly lowered diastolic blood pressure, confirming previously established findings.
Thus, the new information in the present study is that composing a DASH-type diet with low—glycemic index foods compared with high—glycemic index foods does not improve CVD risk factors and may in fact reduce insulin sensitivity and increase LDL cholesterol. We found that a low compared with a high glycemic index of a high-carbohydrate diet decreased insulin sensitivity measured by an oral glucose tolerance test.
Fasting glucose level was higher on low—glycemic index than high—glycemic index dietary carbohydrate as previously reported. However, a low—glycemic index diet did not affect insulin sensitivity in other studies in which body weight either remained constant during the trial or decreased by a similar amount in the high— and low—glycemic index groups.
We chose a 5-week duration of the intervention feeding periods based on results of previous studies, which suggested that 5 weeks was sufficient to detect changes in our outcomes trial protocol in Supplement 1.
A recent meta-analysis of 14 trials that had durations of at least 6 months found no effect of lowering glycemic index on lipids or fasting glucose, although fasting insulin was reduced. This trial did not address the effect of glycemic index in a typical US diet. Rather we studied a low compared with a high glycemic index in a DASH-type diet.
However, we do not attribute the null findings on glycemic index to the healthfulness or specific content of the DASH diet. For example, in several European studies 19 , 23 , 31 , 32 and one in Brazil, 22 the researchers gave or prescribed selected foods to the participants to use in their own diets instead of providing complete diets that differed from their usual diets.
In these studies, lowering glycemic index did not increase insulin sensitivity or improve blood pressure, HDL cholesterol level, or triglyceride level; LDL cholesterol level decreased in one of these studies 19 but did not change in the others.
We showed in a subsample of the participants that the glycemic index values of individual foods computed from dietary tables, when assembled into meals, produced expected differences in blood glucose AUCi over 12 hours, a process variable, thus confirming previous results.
These results suggest that lowering glycemic index or lowering carbohydrates for breakfast, lunch, and dinner reduces blood glucose during 12 hours without any further reduction from lowering both together.
Thus, the effects of these 2 changes in dietary carbohydrate were not additive, suggesting a plateau effect, as also found in a similar study. After we started this trial, reports of trials that involved glycemic index have accumulated.
A meta-analysis of 28 trials found that lowering glycemic index did not affect HDL cholesterol or triglyceride levels and lowered LDL cholesterol level only if fiber content was also increased.
There were no increases in foods or nutrients in the low—glycemic index, high-carbohydrate diet that have known effects to raise LDL levels. In fact, the low—glycemic index, high-carbohydrate diet contained slightly less dietary cholesterol and more fiber than the other diets, but these differences would have lowered not raised LDL levels.
Low—glycemic index diets did not lower blood pressure. We also did not study the influence of glycemic index on weight loss. Lowering glycemic index may improve weight loss 6 or maintenance 40 , 41 according to a meta-analysis 6 and some more recent clinical trials, 40 , 41 although others did not find an advantage of low—glycemic index diets.
This trial oversampled black individuals because of their greater burden of type 2 diabetes and CVD that could be modifiable by dietary change. The results were similar in black and white participants.
The main dietary contrast of interest, high vs low glycemic index, included participants, exceeding the goal of However, the number of participants for each dietary contrast ranged from to Still, the precision of estimation of effects, as shown by the confidence intervals, was adequate for clinically relevant inference on the risk factors of interest.
In this 5-week controlled feeding study, diets with low glycemic index of dietary carbohydrate, compared with high glycemic index of dietary carbohydrate, did not result in improvements in insulin sensitivity, lipid levels, or systolic blood pressure.
Corresponding Author: Frank M. Sacks, MD, Department of Nutrition, Harvard School of Public Health, Huntington Ave, Boston, MA fsacks hsph. Author Contributions: Dr Sacks had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Acquisition, analysis, or interpretation of data: Sacks, Carey, Anderson, Miller, Copeland, Charleston, Harshfield, Laranjo, McCarron, Yee, Appel. Drafting of the manuscript: Sacks, Carey, Anderson, Copeland, Laranjo, Swain. Critical revision of the manuscript for important intellectual content: Sacks, Carey, Anderson, Miller, Charleston, Harshfield, McCarron, White, Yee, Appel.
Administrative, technical, or material support: Carey, Miller, Copeland, Harshfield, Laranjo, Swain, Appel. Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Sacks was an expert witness in litigation involving POM Wonderful, Hershey, Unilever, and Keebler.
No other disclosures were reported. The funding agency provided critical review of the research grant application and the protocol and monitored the progress of the study. These companies were not involved in the design, execution, analysis, interpretation, or manuscript writing or critique.
Additional Contributions: We thank David S. We also thank the Frederick Church of the Brethren, Frederick, Maryland, which provided space for distribution of food to study participants. full text icon Full Text.
Download PDF Top of Article Abstract Introduction Methods Results Discussion Conclusions Article Information References. Figure 1. Participant Screening, Enrollment, and Follow-up in the OmniCarb Study.
View Large Download. Figure 2. Effect of the Study Diets on Blood Glucose and Insulin Levels Over 12 Hours. Figure 3. Effect of Study Diets on Main Outcomes. Table 1. Nutrient Targets and Content of the 4 Study Diets a.
Table 2. Table 3. Primary Outcomes at Baseline and at the End of Feeding on Each Diet a. Audio Author Interview Glycemic Index, Cardiovascular Disease, and Insulin Sensitivity.
Video Interview. JAMA Report Video. Supplement 1. Supplement 2. eFigure 1. Multiple imputation eFigure 2. Oral glucose tolerance testing, glucose and insulin eTables 1a to 1u.
Daily menus for 7 days for the 4 study diets at , , and kcal eTable 2. Urinary nitrogen, creatinine, sodium, and potassium eTable 3. Outcomes eTable 4.
Nutrition Journal BMR and exercise 5Raspberry ketones and cholesterol levels number: 22 Cite this article. Metrics looad. Foods Glycemic load and insulin response contrasting glycemic responee when incorporated into Glycemic load and insulin response Gljcemic, are able to differentially modify gesponse and insulinemia. However, anx is known about whether this is dependent on the size of the meal. The purposes of this study were: i to determine if the differential impact on blood glucose and insulin responses induced by contrasting GI foods is similar when provided in meals of different sizes, and; ii to determine the relationship between the total meal glycemic load and the observed serum glucose and insulin responses.
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