This article on the Perils of Food Processing is based on a lecture given by Gabor Erdosi, MSc, MBA— Food News Conference, May 19, 2018 — Prague, Czech Republic.

Part 1 can be read here.

---

INTRODUCTION: In the first part of this article on the Perils of Food Processing, we considered the effect of different types of simple food processing such as grinding and cooking on the hormonal response of the incretin hormones to carbohydrate intake. While interesting, we rarely eat meals that are only made up carbohydrate, without any fat or protein. Even if we eat a slice of bread or toast and put peanut butter on top, it is now mixture of carbohydrate, fat and protein. How does a mixed meal” with fat and protein affect the body’s hormonal response to carbohydrate?  How does the presence of fiber impact this hormonal response?  Does it matter how often we eat, or how fast? This and more are covered in this article.

Response of Incretin Hormones to Meal with Fat and Carbohydrate

In the first study we’re going to look at, the researchers designed a sandwich that produced a very stable glucose response in healthy individuals.  The sandwich was made of 120 g of white bread, 20 g of butter and 10 g of dried meat. As can be seen from curve A, blood sugar rose to ~150 mg/dl (~8.3 mmol/L) and stayed relatively stable for the next 3 hours (180 minutes).

But what happened to the insulin response when these foods were eaten separately and together in a sandwich?

Looking at curve B (bottom), it can be seen when subjects ate only the dried meat, blood insulin levels didn’t rise much at first, but then rose a little bit at ~ 90 minutes and stayed relatively constant. When subjects ate only the butter, insulin levels rose a little bit more and then only increased slightly over the next several hours. But when they ate the sandwich with the white bread, butter and dried meat, you can see that blood insulin levels rose quite steeply, beginning before 30 minutes, reaching a maximum level at 60 minutes, and then decreased very slowly over the next several hours. This makes sense, because of the presence of the carbohydrate in the bread.

What is interesting is what happens to the two gut hormones, GIP (from the K-cells) and GLP-1 (from the L-cells) in response to eating these foods.

Looking at the second curve (graph on the right) it can be seen that in response to the mixed meal’ of the sandwich, GIP from the K-cells (high up in the intestine) is released rapidly and in large amounts. That is, a mixed meal results in a large stimulation of both insulin and glucagon release. Insulin moves the glucose into the cell for storage at the level of the fat cells increases lipoprotein lipase, which increases triglyceride storage. This is an anabolic process of storing nutrients for use later.

As can be seen from the first curve, when a mixed meal’ is eaten, GLP-1 is released from the L-cells lower down in the intestine responded but is much less pronounced. That is, in response to GLP-1 secretion, insulin is released to a small extent, but there is little of the signalling to decrease glucagon, which means little effect on the hunger signal and little satiety (feeling full).

Incretin Response to a Standard Western Diet Meal versus a Paleo-style Meal

In this next study, we can see the same effect in a plant-based meal, using a reference meal and a paleolithic style meal (called PAL2) that both had the same number of calories (~1600 kcals) and very similar macronutrient distributions (carbohydrate, fat, protein). The only difference between the reference diet and the Paleolithic type diet is the amount of processing.

The reference meal was made up of cooked, long grain rice, mango and boiled carrots, some fish cooked over dry heat and some olive oil.

The paleo type meal was made up of raw strawberries, raw apple, as well as the same significantly more fish cooked over dry heat, raw mushrooms, seedless raisins, zucchini (courgettes), flax seed, cinnamon and capers. While both of these meals had the same number of calories, as can be seen, there was a significant difference in the weight between these two meals — with the reference meal weighing only 248 g, uncooked and the paleo type meal weighing 718 g.

In each of these two types of meals, the response of the two gut incretin hormones, GIP from the upper intestine K-cells and GLP-1 from the lower intestinal L-cells were very different!

Looking at the bottom of the 3 graphs, it can be seen that GIP from the K-cells (high up in the intestine) was released rapidly and in large amounts in the reference meal — a meal that is quite similar to the Standard Western Diet. Recall that the GIP from the K-cells acts on the pancreas to trigger both insulin release from the beta-cells and to trigger glucagon release from the alpha cells. The insulin results in the body storing glucose from the meal and the glucagon release signals the body to release stored glucose, if the blood sugar falls too low. The rise of GIP in response to the paleo-type meal was very slow and gradual and didn’t rise very high, which means that much less insulin was triggered to be released from the pancreas’ beta-cells and much less glucogon was triggered to be released from the alpha-cells.

What happened to GLP-1 release from the L-cells in the lower intestine in response to these two different types of meals?

The Western-type meal (the reference meal) caused a very short rise in GLP-1 from the lower L-cells, which decreased back to baseline quickly.  That means that very little additional insulin was released to move additional glucose into the cells and significantly, there was very little decrease of glucagon which means that appetite was not decreased and there was little to no stimulus to increase satiety (feeling full) and little to no signal to decrease food intake.

The paleo-type meal resulted in significant release of GLP-1, which caused the pancreas to release insulin from the beta-cells and also decreases glucagon release from the alpha-cells of the pancreas — which at the level of the brain, acts to decrease appetite and increase satiety.

This is key; based on this study, a meal based on a Standard Western Diet did not trigger the signal that the body had taken in sufficient food and that appetite could now decrease.

The Effect of Food Texture even Greater than the Effect of Macronutrient Distribution

This next study is very interesting — showing that food texture has an even greater effect on obesity induced from diet than macronutrient content of the diet.

The top graph demonstrates that mice fed a ”high fat diet” — which was really high in both sugar and fat (not just high in fat) gained significantly more weight than mice fed standard mice chow.

The bottom graph shows that if you take the standard mice chow and grind it fine into a powder and feed it to the mice, they gain weight to the same degree as when fed a diet high in fat and sugar.  That is, the degree of food processing in the diet has at least as great an effect on obesity as the amount of fat and sugar in the diet itself.

There is something about grinding the food that changes the satiety/hunger signal.

Meal Size and Meal Frequency

Common advice given by nutritionists and Dietitians is that it is better to eat small, frequent meals than large meals less often, but there are some studies that support that it as far as hunger and satiety signalling are concerned, it is better to eat fewer, larger meals due to the effect of the incretin hormones.

[study on right hand side of slide]

After a low-calorie smaller meal, insulin response is proportionately higher compared to a larger meal. That is, a small meal triggers a proportionately greater insulin response that a larger meal, so if one eats small meals frequently, there is an overall greater amount of insulin released than if one eats larger meals less often.

Interestingly, it is the same for those with Type 2 Diabetes.  It is possible to modulate the beta-cell sensitivity to glucose by giving obese people and those with Type 2 Diabetes fewer large meals compared to more frequent smaller meals.

Eating Speed

If one eats more slowly the incretin hormones that trigger satiety (feeling full) are released in a more pronounced manner.  This holds true even when obese subjects eat calorically dense foods such as ice-cream. More of the satiety hormones are released when people eat slowly.

Glycemic Load as a Proxy for the Amount of Carbohydrate Processing

Glycemic Load indicates how a healthy person’s body will respond to amount of carbohydrate in one serving of a food. One usual serving of a food would be considered to have a very high Glycemic Load if it is ≥ 20, a high Glycemic Load if it is between 11-19 and a low Glycemic Load if it is ≤10.

When one compares the Glycemic Load estimated from ancient diets at the time of the Agricultural Revolution (A on the graph) compared with the Industrial Revolution (B on the graph), the Glycemic Load at the Industrial Revolution is approaching 20, and after that point, continues to go up in an almost vertical manner.  That is, Glycemic Load is a fairly accurate proxy for the degree of food processing of the diet; the more processed the diet, the higher the Glycemic Load.

Amount of Fiber as a Proxy for the Amount of Carbohydrate Processing

This next graph shows the consumption of total carbohydrate over the last century — from 1909-2000 and the amount of carbohydrate from fiber as a percentage.

As can be seen, at the beginning of the century, the total amount of carbohydrate started off high and gradually decreased until about 1954, leveled off, then began to increase again. The decrease in the fiber content in carbohydrate-based foods is also evident on this graph from ~ 1960 onward.

What happened?

Perhaps it was the introduction of supposedly “healthy” polyunsaturated vegetable oils (industrial seed oils) in the 1960s that contributed to the dramatic increase in the consumption of ultra-refined carbohydrates.

At the very same time that ultra-refined carbohydrate appeared on the scene, so were novel industrial seed oils — ultra-refined fats.  Perhaps it is the combination of the two in many processed food products which contributed to carbohydrate content of the diet climbing exponentially — and along with it, obesity and metabolic diseases.

Structure and Speed of Absorption

Recall from Part 1 of this article that there are several nutrient-sensing hormones in the small intestine, but with respect to the effect of food processing, SGLT1 is a glucose sensor and both K-cells and L-cells contain this nutrient-sensing receptor.

In the morbidly obese, intestinal glucose absorption high up in the intestine is accelerated due to SGLT-1 from the K-cells.  SGLT-1, along with GIP from the K-cells results in high insulin and high glucagon release, which results in both hyperinsulinemia and hyperglycemia.

Intact structures in grain are not accessible to the digestive enzyme amylase (which breaks down starch to glucose), so when grain is consumed intact, this delays gastric emptying and creates a barrier to starch digestion.  The degree to which grain is intact was found to be more effective in improving glucose metabolism than dietary fiber, irrespective of the type of cereal

Evidence for Why We Get Hungry 3-4 Hours After Eating Refined Carbohydrate

Recall from Part 1, the hormone ghrelin is the only hormone that can increase hunger.

Looking at the graph in the top left, we can see that when one eats carbohydrate, ghrelin decreases at first below baseline for the first two hours (120 minutes), but then begins to rise. It continues to rise, exceeding baseline at three hours (180 minutes) and continues rising until four hours; resulting in significantly increased hunger.

At the same time as ghrelin (the hunger hormone) is increasing between 3 and 4 hours after eating refined carbs, serum glucose has dipped below baseline in response to eating refined carbs (as demonstrated in Part 1 of this article) and from 3 hours to 4 hours (180 minutes – 240 minutes), so that serum glucose remains low.

That is, in response to eating refined carbohydrates alone (without combining them with protein) you end up having low blood sugar and feel hungry 3-4 hours later. Blood glucose only gradually begins to increase until it is returns to baseline again at 6 hours (360 minutes).

This next study is a comparison between normal weight and obese people.

On the right-hand side, at the top one can see that normal weight people have normal signalling. Satiety (feeling full) goes up and one can see that PYY correspondingly goes up, hunger goes down and correspondingly, ghrelin goes down.

Below that, one can see that in the morbidly obese, their signalling for hunger and satiety is dysregulated. Satiety is going down even after they’ve eaten and correspondingly, PYY shows this dysregulation in that it also goes down. While hunger goes down and the hormone ghrelin also goes down, it is to a much lesser degree that in normal subjects.

So, the obese individuals may feel slightly less hungry, but they don’t feel satiated. This holds true whether obese individuals eat carbohydrate, protein or fat but it is especially pronounced when carbohydrate is eaten. That is, signalling is largely preserved in the morbidly obese when it comes to protein and fat, but it is lost when it comes to carbohydrate.

Obese people should avoid eating diets high in refined carbohydrate because their hunger and satiety signals are dysfunctional and they don’t receive signals that they have eaten.

Here is another study showing that in obese Chinese men, a high protein meal or a high fat meal produces more satiety and better appetite hormonal response after eating than a high carbohydrate meal.

In another study, different conditions were looked at such as whether it made a difference in the hunger hormone, ghrelin, if the carbohydrate food was eaten first or last.  It turned out that it is best to eat carbs last, as ghrelin continues to decrease for 2 ½ hours (150 minutes) after eating carbohydrate.

This next illustration shows that there is positive feedback mechanism between insulin and GIP.

 

Insulin drives GIP expression but requires glucose to do it. When you eat food with carbohydrate, GIP in the upper intestines is released, resulting in insulin being released. If you keep eating carb-based foods, there is lots of glucose present, which continues to drive the release of more and more GIP, triggering more and more insulin to be released.

This next slide shows a study with two kinds of sugar, sucrose which is ordinary table sugar and isomaltulose, which is made up of the exact same molecules of fructose and glucose, just attached together in a different configuration.

As can be seen, sucrose causes a huge spike in plasma GIP secreted from the K-cells high up in the intestine compared to isomaltulose which triggers high insulin and high glucagon release and which results in both hyperinsulinemia and hyperglycemia. Sucrose also results in much lower release of GLP-1 from the L-cells, lower down in the intestine which results in some release of insulin, but a much smaller decreases glucagon so that at the level of the brain, there is less of a decrease in appetite and less of an increase satiety (feeling full).  As a result, eating foods sweetened with sucrose results in higher glucose, higher insulin, very little decrease in appetite, less feeling full and less decreased food intake, compared with isomaltulose.

As a result, sustained feeding with sucrose in mice results in insulin resistance and fatty liver.

If these sugars are eaten with a meal, instead of alone, the effect on blood glucose and insulin is removed, but GIP release is still triggered to be released to a large extent compared with isomaltulose, and fatty liver persists in the mice in the sucrose group.

The Effect of Combining Refined Carbohydrates with Fat

As can be seen from the graph on the left hand side at the bottom, when refined carbs are combined with fat, there is a huge response of GIP.

Eating boiled potato and low-fat veal didn’t result in this effect but the addition of butter to the potato dramatically changed this.

From an evolutionary perspective it makes sense, because there are no naturally occurring cases where a food has both high carbohydrates and high fat at the same time.  Our body’s have not evolved to see these two macronutrients together.

The following is from a recent overview from May 2018 which provides a summary of GIP actions in response to a high Glycemic Index meal.

When high GI carbohydrate food is eaten and passes through digestion in the stomach and then as it enters the upper small intestine, the K-cells release GIP which has several actions, including decreasing lipolysis, increasing insulin secretion in the pancreas, decreasing fat oxidation, increasing the AKT-mTOR pathway in the brain, and increasing fat storage in the liver.

How Does Bariatric Surgery / Gastric Bypass Work

Many people assume that the reason gastric bypass works is because the stomach is made smaller, so that the person cannot overeat, but this is not primarily what makes it effective.

But what occurs within a week of the Roux-en-Y gastric bypass surgery is that there is a dramatic change in the balance of the incretin hormones.

After only a week, GIP release is ½ what it was before the surgery and GLP-1 is almost doubled.

These changes in only a week are not a result of weight loss, but of the surgery’s impact on correcting the imbalance in the incretin hormones — essentially causing an opposite imbalance’ which corrects the defect cause by the Type 2 Diabetes and overeating of ultra-refined carbs.

There are other types of surgical interventions, such as the Duodenal-Jejunal bypass liner tube that impact incretin hormones, as well as numerous medications. There are selective sodium-dependent glucose transporter 1 inhibitors that block glucose absorption and impair GIP release in the same way that a roux-en-Y gastric bypass does.

There are also numerous other medications such as sodium-glucose co-transporter 2 inhibitors, Glucagon-like Peptide 1 Agonists, and Dipeptidyl Peptidase 4 Inhibitors that impact the incretin hormones to varying degrees (and even some that claim to and do nothing!).

…and there are low carbohydrate diets that significantly reduce the release of GIP from the K-cells, because there are low levels of carbohydrate consumed at any one time to trigger it’s release.  As a result, significantly less insulin is release, which is how LCHF diets followed over time lower insulin resistance.

Summary of Part 1 and Part 2 of the Perils of Food Processing

• Speed and location of intestinal nutrient absorption is crucial in determining metabolic response to a food
• The greatest effect in incretin hormone response is seen with carbohydrate rich plant processing, therefore retaining the plant or grain structure as much as possible is crucial
• Diets high in ultra-refined, quick absorbing food plausibly results in altered intestinal hormonal profile, altered hunger / satiety signalling and as a result higher food intake and increased meal frequency
• The above effect is exaggerated when ultra-processed carbohydrates are consumed in combination with significant amounts of fat (the ”doughnut effect”).
• GIP may be part of a ”thrifty mechanism” in mammals; easily digestible, high energy density foods overstimulate it (think ”honey” to hunter-gatherers).

Practical ”Takeaways”

• Processing of food that are high in fat and protein has little effect on intestinal hormone levels, so prioritize food items in terms of desired amount of macronutrients
• Plant or grain foods (carbohydrate containing) should be carefully selected based on their most dense, undisturbed structure. Processing, whether grinding, pureeing or cooking disrupts the plant / grain structure and accelerates absorption of the carbohydrate, which triggers an intestinal hormonal response which results in reduced satiety. Excluding most carbohydrate-based foods also solves this problem
• Consume carbohydrate foods at the end of the meal (after protein and fat foods)
• Have fewer, larger meals vs small, frequent ones. Avoid ”snacking” between meals
• Eat meals slowly to maximize the satiety effect and increase the release of the lower intestinal hormones.

Technical summary

1. Refined carbs trigger huge amounts of GIP, although the decreased GIP:GLP-1 ratio may be more important than the GIP AUC alone.
2. Refined carbs increase GIP response to fat and proteins, and the effect of glucose and long chain fatty acids are additive.
3. Fats and proteins both trigger large amounts of GIP, depending on the context
4. Refined carbs does not trigger GLP-1 (does it impair it?). GLP-1 secreting L cells have an hour-glass like distribution in the small and large intestine. Duodenal GLP-1 has an important role in the so-called cephalic phase of insulin response.
5. Everything triggers GLP-1, just the pattern and amount differs based on intestinal stimulation by food.
6. Quick-digesting carbs are absorbed mainly in the proximal small intestins and fail to induce gastric retention. If carbs are eaten first, a huge amount of GIP is created (i.e. balance between the incretin hormones is tilted in favour of GIP release).
7. Roughage, protein and fat delay gastric emptying and even out glucose release profile along the small intestine. That is, if carbs are eaten last, GLP-1 is slowly released to counter the effect of GIP.

 

Perhaps you wonder what all this information means for you. How should this information change the way you eat and what you eat?  What does this mean in practical terms when planning dinner, or eating dinner – especially if you have Type 2 Diabetes or insulin resistance and also if you are well now, but have a family history with many common metabolic disorders.  How can you change how you eat to stay well?

I can help.

Please send me a note using the “Contact Me” form located on the tab above to find out information about the services I offer (in-person or via Distance Consultation using telephone or Skype) and I will reply shortly.

To your good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

---

The full lecture can be watched here:

References

(continued from Part 1)

16. Carrel, G., L. Egli, C. Tran, P. Schneiter, V. Giusti, D. D’Alessio, and L. Tappy. ”Contributions of Fat and Protein to the Incretin Effect of a Mixed Meal.” American Journal of Clinical Nutrition 94, no. 4 (2011):
997—1003.

17. Bligh, H. Frances J., Ian F. Godsland, Gary Frost, Karl J. Hunter, Peter Murray, Katrina MacAulay, Della Hyliands, et al. ”Plant-Rich Mixed Meals Based on Paleolithic Diet Principles Have a Dramatic Impact on
Incretin, Peptide YY and Satiety Response, but Show Little Effect on Glucose and Insulin Homeostasis: An Acute-Effects Randomized Study.” British Journal of Nutrition 113, no. 04 (2015): 574—84.

18. Desmarchelier, Charles, Tobias Ludwig, Ronny Scheundel, Nadine Rink, Bernhard L. Bader, Martin Klingenspor, and Hannelore Daniel. ”Diet-Induced Obesity in Ad Libitum-Fed Mice: Food Texture Overrides the Effect of Macronutrient Composition.” British Journal of Nutrition 109, no. 08 (2013): 1518—27.

19. Vilsbí¸ll, T., T. Krarup, J. Sonne, S. Madsbad, A. Ví¸lund, A. G. Juul, and J. J. Holst. ”Incretin Secretion in Relation to Meal Size and Body Weight in Healthy Subjects and People with Type 1 and Type 2 Diabetes
Mellitus.” The Journal of Clinical Endocrinology & Metabolism 88, no. 6 (2003): 2706—13.

20. Alsalim, Wathik, Bilal Omar, Giovanni Pacini, Roberto Bizzotto, Andrea Mari, and Bo Ahrén. ”Incretin and Islet Hormone Responses to Meals of Increasing Size in Healthy Subjects.” The Journal of Clinical
Endocrinology & Metabolism 100, no. 2 (2015): 561—68.

21. Koopman, Karin E., Matthan W.A. Caan, Aart J. Nederveen, Anouk Pels, Mariette T. Ackermans, Eric Fliers, Susanne E. la Fleur, and Mireille J. Serlie. ”Hypercaloric Diets with Increased Meal Frequency, but Not Meal Size, Increase Intrahepatic Triglycerides: A Randomized Controlled Trial.” Hepatology 60, no. 2 (2014): 545—53.

22. Stote, Kim S., David J. Baer, Karen Spears, David R. Paul, G. Keith Harris, William V. Rumpler, Pilar Strycula, et al. ”A Controlled Trial of Reduced Meal Frequency without Caloric Restriction in Healthy, Normal-Weight, Middle-Aged Adults.” The American Journal of Clinical Nutrition 85, no. 4 (April 1, 2007): 981—88.

23. McQuaid, S. E., L. Hodson, M. J. Neville, A. L. Dennis, J. Cheeseman, S. M. Humphreys, T. Ruge, et al. ”Downregulation of Adipose Tissue Fatty Acid Trafficking in Obesity: A Driver for Ectopic Fat Deposition?” Diabetes 60, no. 1 (2010): 47—55.

24. Kokkinos, Alexander, Le Roux, Carel W, Kleopatra Alexiadou, Nicholas Tentolouris, Royce P. Vincent, Despoina Kyriaki, et al. ”Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut
Hormones, Peptide YY and Glucagon-Like Peptide-1.” The Journal of Clinical Endocrinology & Metabolism 95, no. 1 (January 1, 2010): 333—37.

25. Rigamonti, A. E., F. Agosti, E. Compri, M. Giunta, N. Marazzi, E. E. Muller, S. G. Cella, and A. Sartorio. ”Anorexigenic Postprandial Responses of PYY and GLP1 to Slow Ice Cream Consumption: Preservation in
Obese Adolescents, but Not in Obese Adults.” European Journal of Endocrinology 168, no. 3 (March 1, 2013): 429—36.

26. Llewellyn, Clare H., Van Jaarsveld, Cornelia Hm, David Boniface, Susan Carnell, and Jane Wardle. ”Eating Rate Is a Heritable Phenotype Related to Weight in Children.” The American Journal of Clinical Nutrition
88, no. 6 (December 1, 2008): 1560—66.

27. Chapter 1. in ”Sweeteners and Sugar Alternatives in Food Technology”, 2nd Edition Kay O’Donnell (Editor), Malcolm Kearsley (Editor) ISBN: 978-1-118-37397-2 Jul 2012

28. Wiley-Blackwell Gross, Lee S., Li Li, Earl S. Ford, and Simin Liu. ”Increased Consumption of Refined Carbohydrates and
the Epidemic of Type 2 Diabetes in the United States: An Ecologic Assessment.” The American Journal of Clinical Nutrition 79, no. 5 (2004): 774—779.

29. Scazzina, Francesca, Susanne Siebenhandl-Ehn, and Nicoletta Pellegrini. ”The Effect of Dietary Fibre on Reducing the Glycaemic Index of Bread.” British Journal of Nutrition 109, no. 07 (2013): 1163—74.
https://doi.org/10.1017/S0007114513000032.

30. Nguyen, Nam Q., Tamara L. Debreceni, Jenna E. Bambrick, Bridgette Chia, Judith Wishart, Adam M. Deane, Chris K. Rayner, Michael Horowitz, and Richard L. Young. ”Accelerated Intestinal Glucose Absorption in Morbidly Obese Humans: Relationship to Glucose Transporters, Incretin Hormones, and Glycemia.” The Journal of Clinical Endocrinology & Metabolism 100, no. 3 (2015): 968—76.

31. Foster-Schubert, Karen E., Joost Overduin, Catherine E. Prudom, Jianhua Liu, Holly S. Callahan, Bruce D. Gaylinn, Michael O. Thorner, and David E. Cummings. ”Acyl and Total Ghrelin Are Suppressed Strongly by Ingested Proteins, Weakly by Lipids, and Biphasically by Carbohydrates.” The Journal of Clinical Endocrinology & Metabolism 93, no. 5 (2008): 1971—79.

32. Lomenick, Jefferson P., Maria S. Melguizo, Sabrina L. Mitchell, Marshall L. Summar, and James W. Anderson. ”Effects of Meals High in Carbohydrate, Protein, and Fat on Ghrelin and Peptide YY Secretion in
Prepubertal Children.” The Journal of Clinical Endocrinology & Metabolism 94, no. 11 (2009): 4463—71.

33. Rizi, Ehsan Parvaresh, Tze Ping Loh, Sonia Baig, Vanna Chhay, Shiqi Huang, Jonathan Caleb Quek, E. Shyong Tai, Sue-Anne Toh, and Chin Meng Khoo. ”A High Carbohydrate, but Not Fat or Protein Meal Attenuates Postprandial Ghrelin, PYY and GLP-1 Responses in Chinese Men.” PLOS ONE 13, no. 1 (January 31, 2018): e0191609.

34. Shukla, Alpana P., Elizabeth Mauer, Leon I. Igel, Wanda Truong, Anthony Casper, Rekha B. Kumar, Katherine H. Saunders, and Louis J. Aronne. ”Effect of Food Order on Ghrelin Suppression.” Diabetes
Care, 2018, dc172244.

35. Hí¤gele, Franziska A, Franziska Bí¼sing, Alessa Nas, Julian Aschoff, Lena Gní¤dinger, Ralf Schweiggert, Reinhold Carle, and Anja Bosy-Westphal. ”High Orange Juice Consumption with or In-between Three
Meals a Day Differently Affects Energy Balance in Healthy Subjects.” Nutrition & Diabetes 8, no. 1 (2018).
https://doi.org/10.1038/s41387-018-0031-3.

36. Garcí­a-Martí­nez, Jose Manuel, Ana Chocarro-Calvo, Antonio De la Vieja, and Custodia Garcí­a-Jiménez. ”Insulin Drives Glucose-Dependent Insulinotropic Peptide Expression via Glucose-Dependent Regulation of
FoxO1 and LEF1/β-Catenin.” Biochimica et Biophysica Acta (BBA) – Gene Regulatory Mechanisms 1839, no. 11 (November 1, 2014): 1141—50.

37. Pfeiffer, Andreas F.H., and Farnaz Keyhani-Nejad. ”High Glycemic Index Metabolic Damage — a Pivotal
Role of GIP and GLP-1.” Trends in Endocrinology & Metabolism, 2018.

38. Collier, G., and K. O’Dea. ”The Effect of Coingestion of Fat on the Glucose, Insulin, and Gastric Inhibitory Polypeptide Responses to Carbohydrate and Protein.” The American Journal of Clinical Nutrition 37, no. 6 (June 1, 1983): 941—44.

39. McClean, P. L., N. Irwin, R. S. Cassidy, J. J. Holst, V. A. Gault, and P. R. Flatt. ”GIP Receptor Antagonism Reverses Obesity, Insulin Resistance, and Associated Metabolic Disturbances Induced in Mice by Prolonged
Consumption of High-Fat Diet.” AJP: Endocrinology and Metabolism 293, no. 6 (October 23, 2007):E1746—55.

40. Ceperuelo-Mallafré, Victí²ria, Xavier Duran, Gisela Pachón, Kelly Roche, Lourdes Garrido-Sánchez, Nuria Vilarrasa, Francisco J. Tinahones, et al. ”Disruption of GIP/GIPR Axis in Human Adipose Tissue Is Linked
to Obesity and Insulin Resistance.” The Journal of Clinical Endocrinology & Metabolism 99, no. 5 (May 2014): E908—19.

41. Gí¶gebakan, í–zlem, Martin A. Osterhoff, Rita Schí¼ler, Olga Pivovarova, Michael Kruse, Anne-Cathrin Seltmann, Alexander S. Mosig, Natalia Rudovich, Michael Nauck, and Andreas F. H. Pfeiffer. ”GIP Increases Adipose Tissue Expression and Blood Levels of MCP-1 in Humans and Links High Energy Diets to Inflammation: A Randomised Trial.” Diabetologia 58, no. 8 (August 2015): 1759—68.

42. Mohammad, S., R. T. Patel, J. Bruno, M. S. Panhwar, J. Wen, and T. E. McGraw. ”A Naturally Occurring GIP Receptor Variant Undergoes Enhanced Agonist-Induced Desensitization, Which Impairs GIP Control of
Adipose Insulin Sensitivity.” Molecular and Cellular Biology 34, no. 19 (2014): 3618—29.

43. Nie, Y., R. C. Ma, J. C. N. Chan, H. Xu, and G. Xu. ”Glucose-Dependent Insulinotropic Peptide Impairs Insulin Signaling via Inducing Adipocyte Inflammation in Glucose-Dependent Insulinotropic Peptide
Receptor-Overexpressing Adipocytes.” The FASEB Journal 26, no. 6 (2012): 2383—93.

44. Timper, K., J. Grisouard, N. S. Sauter, T. Herzog-Radimerski, K. Dembinski, R. Peterli, D. M. Frey, et al. ”Glucose-Dependent Insulinotropic Polypeptide Induces Cytokine Expression, Lipolysis, and Insulin
Resistance in Human Adipocytes.” AJP: Endocrinology and Metabolism 304, no. 1 (2012): E1—13.

45. Miyawaki, Kazumasa, Yuichiro Yamada, Nobuhiro Ban, Yu Ihara, Katsushi Tsukiyama, Heying Zhou, Shimpei Fujimoto, et al. ”Inhibition of Gastric Inhibitory Polypeptide Signaling Prevents Obesity.” Nature
Medicine 8, no. 7 (2002): 738—42.

46. Boylan, Michael O., Patricia A. Glazebrook, Milos Tatalovic, and M. Michael Wolfe. ”Gastric Inhibitory Polypeptide Immunoneutralization Attenuates Development of Obesity in Mice.” American Journal of
Physiology – Endocrinology And Metabolism 309, no. 12 (2015): E1008—18.

47. Nasteska, D., N. Harada, K. Suzuki, S. Yamane, A. Hamasaki, E. Joo, K. Iwasaki, K. Shibue, T. Harada, and N. Inagaki. ”Chronic Reduction of GIP Secretion Alleviates Obesity and Insulin Resistance Under High-Fat
Diet Conditions.” Diabetes 63, no. 7 (2014): 2332—43.

48. Althage, M. C., E. L. Ford, S. Wang, P. Tso, K. S. Polonsky, and B. M. Wice. ”Targeted Ablation of Glucose-Dependent Insulinotropic Polypeptide-Producing Cells in Transgenic Mice Reduces Obesity and
Insulin Resistance Induced by a High Fat Diet.” Journal of Biological Chemistry 283, no. 26 (2008): 18365—76.

49. Calanna, S., F. Urbano, S. Piro, R. M. Zagami, A. Di Pino, L. Spadaro, F. Purrello, and A. M. Rabuazzo. ”Elevated Plasma Glucose-Dependent Insulinotropic Polypeptide Associates with Hyperinsulinemia in
Metabolic Syndrome.” European Journal of Endocrinology 166, no. 5 (2012): 917—22.

50. Chia, Chee W., Juliana O. Odetunde, Wook Kim, Olga D. Carlson, Luigi Ferrucci, and Josephine M. Egan. ”GIP Contributes to Islet Trihormonal Abnormalities in Type 2 Diabetes.” The Journal of Clinical Endocrinology & Metabolism 99, no. 7 (July 2014): 2477—85.

51. Chen, Shu, Fumiaki Okahara, Noriko Osaki, and Akira Shimotoyodome. ”Increased GIP Signaling Induces Adipose Inflammation via a HIF-1α-Dependent Pathway and Impairs Insulin Sensitivity in Mice.” American
Journal of Physiology-Endocrinology and Metabolism 308, no. 5 (December 23, 2014): E414—25.

52. Cavin, Jean-Baptiste, André Bado, and Maude Le Gall. ”Intestinal Adaptations after Bariatric Surgery: Consequences on Glucose Homeostasis.” Trends in Endocrinology & Metabolism 28, no. 5 (May 2017):
354—64.

53. Xiong, Shao-Wei, Jing Cao, Xian-Ming Liu, Xing-Ming Deng, Zeng Liu, and Fang-Ting Zhang. ”Effect of Modified Roux-En-Y Gastric Bypass Surgery on GLP-1, GIP in Patients with Type 2 Diabetes Mellitus.”
Gastroenterology Research and Practice 2015 (2015): 1—4.

54. Falkén, Y., P. M. Hellstrí¶m, J. J. Holst, and E. Ní¤slund. ”Changes in Glucose Homeostasis after Roux-En-Y Gastric Bypass Surgery for Obesity at Day Three, Two Months, and One Year after Surgery: Role of Gut
Peptides.” The Journal of Clinical Endocrinology & Metabolism 96, no. 7 (July 1, 2011): 2227—35.

55. Salinari, S., A. Bertuzzi, S. Asnaghi, C. Guidone, M. Manco, and G. Mingrone. ”First-Phase Insulin Secretion Restoration and Differential Response to Glucose Load Depending on the Route of Administration
in Type 2 Diabetic Subjects After Bariatric Surgery.” Diabetes Care 32, no. 3 (March 1, 2009): 375—80.

56. Jirapinyo, Pichamol, Andrea V. Haas, and Christopher C. Thompson. ”Effect of the Duodenal-Jejunal Bypass Liner on Glycemic Control in Patients With Type 2 Diabetes With Obesity: A Meta-Analysis With
Secondary Analysis on Weight Loss and Hormonal Changes.” Diabetes Care 41, no. 5 (May 1, 2018):1106—15.

57. Narita, T., H. Yokoyama, R. Yamashita, T. Sato, M. Hosoba, T. Morii, H. Fujita, K. Tsukiyama, and Y. Yamada. ”Comparisons of the Effects of 12-Week Administration of Miglitol and Voglibose on the Responses of Plasma Incretins after a Mixed Meal in Japanese Type 2 Diabetic Patients.” Diabetes, Obesity and Metabolism 14, no. 3 (2012): 283—87.

58. Dobbins, Robert L., Frank L. Greenway, Lihong Chen, Yaping Liu, Sharon L. Breed, Susan M. Andrews, Jeffrey A. Wald, Ann Walker, and Chari D. Smith. ”Selective Sodium-Dependent Glucose Transporter 1
Inhibitors Block Glucose Absorption and Impair Glucose-Dependent Insulinotropic Peptide Release.” American Journal of Physiology-Gastrointestinal and Liver Physiology 308, no. 11 (2015): G946—54.

59. Zheng, Sean L., Alistair J. Roddick, Rochan Aghar-Jaffar, Matthew J. Shun-Shin, Darrel Francis, Nick Oliver, and Karim Meeran. ”Association Between Use of Sodium-Glucose Cotransporter 2 Inhibitors,
Glucagon-like Peptide 1 Agonists, and Dipeptidyl Peptidase 4 Inhibitors With All-Cause Mortality in Patients With Type 2 Diabetes.” JAMA 319, no. 15 (2018): 1580.

60. Lin, Po-Ju, and Katarina T. Borer. ”Third Exposure to a Reduced Carbohydrate Meal Lowers Evening Postprandial Insulin and GIP Responses and HOMA-IR Estimate of Insulin Resistance.” PLOS ONE 11, no.
10 (2016): e0165378.

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

This article is based on a lecture given by Gabor Erdosi, MSc, MBA— Food News Conference, May 19, 2018 — Prague, Czech Republic

Introduction — Gabor Erdosi, MSc, MBA is a Molecular Biologist from Debrecen, Hungary who is employed in the Food Industry but whose hobby is reading scientific publications and analyzing the available information. The talk that this article is based on was given at the Food News Conference, May 19, 2018 — Prague, Czech Republic  and is the condensation of approximately 4 years worth of Gabor’s studying of the literature.

Gabor founded and heads up the Lower Insulin group on Facebook which is dedicated to discussing the scientific basis of the relationship between metabolic diseases and food and lifestyle factors. At present, the group has ~5300 members.

This new series titled The Perils of Food Processing reflects Gabor’s conviction that what’s of primary importance in the interaction between food and our physiology (GI tract) is the speed and location of food absorption in the digestive system. This article is arranged according to the same principle.

The reason I am writing this series of articles is because I believe what Gabor Erdosi has come to understand about the effects of food processing on the speed and location of food absorption — especially carbohydrate, and which affects the very nature of hunger and satiety is absolutely crucial to understanding the current epidemic of metabolic diseases we now face.

This first article provides an overview of the gastrointestinal system and the so-called “incretin hormones” and how the amount a food is cooked or ground impacts how quickly it is absorbed and the energy stored.

---

When talking about Food Processing, the issue arises as to how to properly define the concept of processing’.

How do we define ‘food processing’? Humans have been processing their food in one way or another for hundreds of thousands of years — be it cutting, cooking or grinding their food in some way.  These are all forms of food processing.

In terms of the effect of Food Processing on human physiology, a few main questions that this series of articles will address, arise;

(i) are all forms of food processing created equal?

(ii) does the food processing of different macronutrients and foods have different results?

(iii) could these changes in food processing over the last few hundred years or so have anything to do with the epidemic of metabolic diseases that we now face?

1. Overview of Gastrointestinal Physiology

Before getting into the topic of the effect of different types of food processing on the speed and place of absorption, it’s necessary to provide an overview of the gastrointestinal physiology and how the digestive system works and what hormones are released in response to different nutrients.

The important concept here is that we have ”sensor cells” (K-cells, L-cells) within our gastrointestinal tract and these cells release different hormones in response to different nutrients.

K-cells release an incretin hormone called GIP and the L-cells release an incretin hormone called GLP-1, as well as GLP-2, PYY and Oxyntomodulin (OXM).

What is important to note is that the distribution of these cells is not uniform.

The K-cells are more abundant in the upper part of the small intestine and other cells, the L-cells are more abundant in the lower part of the small intestine. This uneven distribution of these incretin-hormone-releasing sensor-cells has profound implications, as will be seen later.

2. Nutrient Sensing, the Incretin Effect and Hunger-Satiety Signalling in the Gut

Nutrient-Sensing

So, what happens when we eat foods that we have evolved to see for millennia? As the food goes through the small intestine, it triggers hormonal release from these incretin-hormone-releasing sensor-cells.

If you eat meat and berries, for example, which are foods we have evolved to see for hundreds of thousands of years, they have a fairly balanced stimulatory effect on these sensor cells. These incretin hormones will be released in a more or less balanced manner.

However, as will be shown later on, when we eat food products that we have not evolved to see — relatively new food products on an evolutionary scale, these patterns are completely disrupted.

There are several nutrient-sensing hormones in the small intestine, but the one to focus on with respect to the effect of food processing is SGLT1 –  which is a glucose sensor. Both the K-cells and the L-cells contain this nutrient-sensing receptor, and most others, as well.

Keep in mind for the next articles that the distribution of these cells is uneven; with more in the K-cells higher up in the small intestine and increasing numbers further down in the L-cells.

The Incretin Effect

When we eat glucose, such as in an oral glucose tolerance test or when someone gets intravenous glucose in a hospital, the difference in the insulin response is called the ”incretin effect”.

As you can see from the diagram below, the response to an oral or intravenous glucose load is very large and can be 50-70% of the insulin response.

The majority of the insulin response is stimulated by these incretin hormones (GIP, GLP-1, etc.) secreted by the K-cells and L-cells and not directly via glucose.

The Physiological Effects of the Incretin Hormones

In addition to the insulin-stimulating effect, these incretin hormones have very different effects.

The K-cells, which are more abundant in the upper small intestine, secretes Glucose-dependent Insulinotropic Polypeptide (GIP) which acts on the pancreas — not only to result in insulin release, but also increase glucagon. At the level of the fat cells, the adipose tissue, it increases increases triglyceride storage, resulting in weight gain. In this way, GIP supports insulin’s effect on storing lipids. This is an anabolic-type of hormone and if it is very high, it can cause inflammation in adipose tissue.

The L-cells, which are more abundant in the lower small intestine, secrete Glucagon-like Peptide-1 (GLP-1) which also acts on the pancreas to increase insulin, but decreases glucagon. This GLP-1 at the level of the brain, acts to decrease appetite, increase satiety (feeling full) and decrease food intake.

1. Hunger-Satiety Signalling in the Gut

It is important to note that there is only one hormone that can increase hunger and that is ghrelin which is synthesized in the stomach.

All the other hormones, including CCK, PP, PYY, GLP-1 and OXM (Oxyntomodulin) decrease hunger. That is, all of these hormones promote satiety; the feeling of being full’. It is very important to note that four of these hormones, CCK, PYY, GLP-1 and OXM are all synthesized in the small intestine L-cells.

The above is the all the basic physiology that is needed to understand the effects of food processing on the speed and location of nutrient absorption, the nature of hunger and satiety and how the current epidemic in metabolic diseases we now face is a result of disregulation of this system.

3 a. The Effect of Cooking Foods on Body Weight

One of the most ancient forms of food processing is cooking, and there are studies which indicate that there is an association between how many raw foods people eat and their body weight.  There is a generally tendency that the more raw foods a person eats, the lower their body weight. That does not mean that eating a vegetarian diet is more desirable, it is only to point out that with more and more processing — in this case, cooking, the higher body mass tends to be.

3b. The Effect of Cooking Foods on Nutrient Availability

Carbohydrate-rich Foods

The relationship between cooking foods and body weight is particularly important with respect to carbohydrate-rich foods. For example, when grains are cooked they become much more digestible — meaning that more of the nutrients in the grain is available to be absorbed. In the case of potatoes, there is double or triple the amount of energy (calories) available to the body when they are cooked versus when they are raw. When a potato is cooked, the digestible starch increases 2-3 times, which means that these calories are now available to the body where they weren’t when they were raw.

Lipid and Protein-rich Foods

When foods that are high in lipids (fats) such as peanuts are cooked, the amount of energy the body is able to derive from the food, increases. As well, significantly more amino acids in protein-rich foods such as egg make it to the large intestine (where their nutrients are absorbed) when the protein-rich food is cooked.

3c. The Effect of Non-Thermal Food Processing on Nutrient Availability

Mechanical processing, such pounding food is also an ancient form of food processing which has an effect on how many nutrients are available to be digested. The nutrients available to the body when food is eaten raw and whole versus raw and pounded is significant, and this holds true whether the food is animal protein such as meat or a starchy vegetable such as sweet potato.

In a study with mice, one group of mice was fed meat either raw and whole or raw and pounded and then the group was crossed over to cooked and whole or cooked and pounded. The other group of mice was fed sweet potato eaten raw and whole or raw and pounded and then crossed over to cooked and whole or cooked and pounded.

When the meat or starchy vegetable (sweet potato) was eaten raw and whole, it was associated with lower body mass than the same foods eaten raw and pounded because the mice lost weight. As expected from what is known about the effect of cooking on nutrient availability (see above), when the mice ate the cooked meat or cooked sweet potatoes, they either didn’t lose as much weight (in the case of the meat) or actually gained weight (in the case of the sweet potato).

The conclusion of this study was worth noting;

”Our results indicate that human dieters who count calories and eat similar mixed diets but cook them to different extents would experience different weight gain outcomes at comparable levels of physical activity. This prediction is consistent with recent long-term data indicating that preparation-specific factors affect the relationship between caloric consumption and weight gain in humans.”

3 d. The Effect of Hydrolyzing Protein on Hormonal Response in the Small Intestine

Hydrolyzed protein, is essentially pre-digested protein and this process has an impact on which hormones are released in the small intestine when it is eaten.

In a 2010 study, comparing soy protein with soy protein hydrolysates and whey protein with whey protein hydrolysates, it was found that significantly more insulin compared to glucagon is released with the hydrolysates versus the intact protein. This means that the insulin to glucagon ratio is higher and insulin is the hormone which signals the body to store energy.  A higher insulin to glucagon ratio means that the body is storing energy rather than responding to glucagon which signals the body to use glucose and fat for energy.

4 a. The Effect of Mechanical Processing on the Blood Glucose Response of a Carbohydrate Food

Grinding / Juicing Fruit

Mechanical processing of a food doesn’t change the amount of carbohydrate that is in it. That is, when we compare 60g of whole apple with 60 g of pureed apple or 60g of juiced apple, there is the same amount of carbohydrate each. When we compare the Glycemic Index of these three, the results are very similar so this isn’t very helpful to tell us about the blood glucose response to actually eating these different foods.

When these foods are eaten, the blood glucose response 90 minutes later, is significantly  different.

Note: It’s not relevant to the outcome, but on this graph, slow and quick puree and juice as just differences in the amount of time it took for the liquid to be drunk.

As can be seen by the graph on the right, in healthy individuals blood insulin level goes very high with the juiced apple and in response, blood glucose then goes very low, below baseline.

The response that we see with the juiced apple is typical of what is seen with ultra-processed carbohydrates.

Grinding Grains

Grinding grains is another type of ancient food processing which changes the hormonal response in the small intestine.

When healthy individuals eat grain-based meals, the plasma insulin response increases the smaller the particle size of the grain.  That is, a specific amount of whole grain releases less insulin than the same amount of cracked grains, which is less than the same amount of course flour. The highest amount of insulin is released in response to eating the same amount of fine flour.

What was true for wheat in this study was true for rice as well and what was of interest, is there wasn’t a big difference between the insulin response with brown rice versus white rice.

There is no difference in the Glycemic Index or Glycemic Load of whole wheat versus ground wheat or whole rice versus ground rice, but there is a huge difference in the insulin response with difference types of mechanical processing.

It’s also important to note that the amount of  fiber that was in the grain did not make a difference in the amount of insulin released, only the amount of mechanical processing of the grain. So, eating brown rice versus white rice won’t change the amount of insulin that is released – and insulin is a hormone that signals the body to store energy (calories).

In this next study, the same response that we saw with the pureed and juiced apples (above) is also seen with finely ground wheat bread. We see plasma glucose rise rapidly and then it drops below baseline at 120 minutes (circled).

We know that the difference wasn’t due to the amount of fiber, because in this study they added back the fiber and it didn’t make a difference.

The difference had to do with the amount of disruption to the structure of the grain. So, eating whole wheat bread versus eating white bread — which is just adding the fiber that was taken out back won’t help much in terms of the insulin response.

The disruption of the structure of the grain had very adverse effects on the hormonal response; both the insulin response and GIP response, which can be seen in the next graph;

The bread made with flour resulted in a much larger insulin response and plasma GIP response than those made with whole kernel grains

Recall from the first article in this series, that GIP is released from the K-cells, which are dominant in the upper part of the small intestine. Bread made from ground flour results in a much greater and earlier hormonal response than bread made from whole grains.

The same researchers did another study a year later, this time with wheat bread, rye bread with the endosperm, traditional rye bread and high-fiber rye bread. As can be seen from these graphs (whether wheat or rye bread), it is the structural difference of the bread that explains the insulin response after a meal, not the total amount of fiber.

Note: Gabor Erdosi made a table comparing the Area Under the Curve (AUC) of the hormonal response of GIP (from the K-cells in the upper part of the small intestine) and GIP-1 (from the L-cells in the lower part of the small intestines) for the different breads which was very telling.

As can be seen from this table, there was almost double the GIP/GLP-1 ratio in the refined wheat bread (5.02) than the traditional rye bread (2.75) and this difference was largely due to significantly more GIP being released from the K-cells high up in the small intestine with the refined wheat bread than with the traditional rye bread.

It wasn’t due to fiber, because there was less GIP released with the traditional rye bread than even with the high fiber rye bread.

4 b. In-Vitro Hydrolysis of Starch Highly Correlates to Starch Digestion in the Small Intestine

This study shows a striking ability to predict how starch is hydrolyzed (broken down) in the small intestine with how it is broken down in a petri-dish in a lab using alpha-amylase. A perfect correlation would be = 1 and in this case it is 0.95.

As can be seen from these graphs, the glycemic response (blood sugar response) and the insulin response in the body can be accurately predicted using this method.

In this article we considered the effect of various kinds of food processing’ on the speed and location of food absorption of individual macronutrients (such as protein, fat and carbohydrate), but we rarely eat meals that are only carbohydrate, or only protein or only fat.

How does the presence of protein and fat-rich foods influence the hormonal response in the small intestine and how do these affect the hormonal response to carbohydrate? How does fiber content or addition of fiber affect the hormonal response, or does it? These will be the topic of the next article where we’ll look at the hormonal response of the body to mixed meals (meals with different combinations of fat, protein and carbohydrate.

Perhaps you wonder what all this information means for you.

Maybe, like many you’ve become metabolically unwell with Type 2 Diabetes or high blood pressure or high cholesterol despite eating a diet rich in whole wheat bread, whole grain rice and lots of cooked vegetables and are beginning to realize that how your food is processed is as important a factor as the nutrients it contains in it’s unprocessed form.

I can help.

Feel free to send me a note using the “Contact Me” form located on the tab above to find out information about the services I offer, both in-person in my office or via Distance Consultation (using telephone or Skype).

To your good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

Gabor’s full lecture can be watched here:

References

1. Gribble, Fiona M., and Frank Reimann. ”Enteroendocrine Cells: Chemosensors in the Intestinal Epithelium.” Annual Review of Physiology 78, no. 1 (2016): 277—99.
2. Reimann, Frank, and Fiona M Gribble. ”Mechanisms Underlying Glucose-Dependent Insulinotropic Polypeptide and Glucagon-like Peptide-1 Secretion.” Journal of Diabetes Investigation 7 (2016): 13—19.
3. Nauck, Michael A., and Juris J. Meier. ”Incretin Hormones: Their Role in Health and Disease.” Diabetes, Obesity and Metabolism 20 (2018): 5—21.
4. Perry, B., and Y. Wang. ”Appetite Regulation and Weight Control: The Role of Gut Hormones.” Nutrition & Diabetes 2, no. 1 (January 2012): e26.
5. Groopman, Emily E., Rachel N. Carmody, and Richard W. Wrangham. ”Cooking Increases Net Energy Gain from a Lipid-Rich Food.” American Journal of Physical Anthropology 156, no. 1 (2015): 11—18.
6. Evenepoel, Pieter, Dirk Claus, Benny Geypens, Martin Hiele, Karen Geboes, Paul Rutgeerts, and Yvo Ghoos. ”Amount and Fate of Egg Protein Escaping Assimilation in the Small Intestine of Humans.”
7. American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 5 (November 1999): G935—43.
8. Carmody, R. N., G. S. Weintraub, and R. W. Wrangham. ”Energetic Consequences of Thermal and Nonthermal Food Processing.” Proceedings of the National Academy of Sciences 108, no. 48 (2011):
   19199—203.
9. Morifuji, Masashi, Mihoko Ishizaka, Seigo Baba, Kumiko Fukuda, Hitoshi Matsumoto, Jinichiro Koga, Minoru Kanegae, and Mitsuru Higuchi. ”Comparison of Different Sources and Degrees of Hydrolysis of
   Dietary Protein: Effect on Plasma Amino Acids, Dipeptides, and Insulin Responses in Human Subjects.” Journal of Agricultural and Food Chemistry 58, no. 15 (August 11, 2010): 8788—97.
10. Haber, G.B., K.W. Heaton, D. Murphy, and L.F. Burroughs. ”Depletion and Disruption of Dietary Fiber” The Lancet 310, no. 8040 (1977): 679—82.
11. Heaton, K.W., S.N. Marcus, P.M. Emmett, and C.H. Bolton. ”Particle Size of Wheat, Maize, and Oat Test Meals: Effects on Plasma Glucose and Insulin Responses and on the Rate of Starch Digestion in Vitro” 47,no. 4 (1988): 675—82.
12. O’Dea, K., Nestel, P.J., and Antonoff, L. ”Physical Factors Influencing Postprandial Glucose and Insulin Responses to Starch” 33, no. 4 (April 1, 1980): 760—65.
13. Juntunen, Katri S., Leo K. Niskanen, Kirsi H. Liukkonen, Kaisa S. Poutanen, Jens J. Holst, and Hannu M. Mykkí¤nen. ”Postprandial Glucose, Insulin, and Incretin Responses to Grain Products in Healthy Subjects.”The American Journal of Clinical Nutrition 75, no. 2 (2002): 254—262.
14. Juntunen, K.S., D.E. Laaksonen, Leo K Niskanen Karin Autio Jens J Holst, Kari E Savolainen, Kirsi-Helena Liukkonen, Kaisa S Poutanen, and Mykkí¤nen, H.M. ”Structural Differences between Rye and Wheat Breadsbut Not Total Fiber Content May Explain the Lower Postprandial Insulin Response to Rye Bread” 78, no. 5(2003): 957—64.
15. Bornet, F R, A M Fontvieille, S Rizkalla, P Colonna, A Blayo, C Mercier, and G Slama. ”Insulin and Glycemic Responses in Healthy Humans to Native Starches Processed in Different Ways: Correlation with in Vitro Alpha-Amylase Hydrolysis.” The American Journal of Clinical Nutrition 50, no. 2 (1989): 315—23.

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the ”content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.