Hat-tip to Melissa McEwen for https://twitter.com/melissamcewen/status/502553259224338432
As I clicked on the video, I was thinking "I bet those instant Ramen noodles disintegrate instantly, causing a big surge of glucose into the blood".
Watch and learn. Well, did you expect that to happen? If instant Ramen noodles are a heart health risk, it's not because they digest too quickly. BPA? Something else?
Glycaemic Index etiketine sahip kayıtlar gösteriliyor. Tüm kayıtları göster
Glycaemic Index etiketine sahip kayıtlar gösteriliyor. Tüm kayıtları göster
22 Ağustos 2014 Cuma
4 Temmuz 2014 Cuma
How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.
See The Battle of the Diets: Is Anyone Winning (At Losing?) for trials where insulin resistant people get more weight loss on low-carbohydrate diets than on high-carbohydrate diets, and insulin sensitive people get more weight loss on high-carbohydrate diets than on low-carbohydrate diets.
If Gary Taubes' carbohydrate/insulin hypothesis of obesity was correct, everyone would get more weight loss on low-carbohydrate diets. This isn't the case, therefore Gary Taubes' hypothesis is not correct.
Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies"!
Change in Bodily Stores = Energy in - Energy out, where...
Energy in = Energy entering mouth - Energy exiting anus, and...
Energy out = BMR/RMR + TEF + TEA + SPA/NEAT
See The Energy Balance Equation to find out what the above terms mean.
People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.
People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. Trust me, I'm a retired Electronic Engineer. I've observed this (too) many times!
1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting massive postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Bodily stores increase. There are also accusations of sloth & gluttony!
2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Bodily stores decrease.
In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.
There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587
P.S. In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.
P.P.S. Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions.
P.P.P.S. Insulin Resistance can be fixed in the long-term. See Insulin Resistance: Solutions to problems.
Type 2 Diabetes can be fixed in the long-term. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.
Aim to fix the problem in the long-term. If a long-term fix isn't possible (due to excessive destruction of pancreatic beta cells), use a low-carbohydrate diet as an adjunct to medication.
If Gary Taubes' carbohydrate/insulin hypothesis of obesity was correct, everyone would get more weight loss on low-carbohydrate diets. This isn't the case, therefore Gary Taubes' hypothesis is not correct.
Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies"!
 |
| The Aragon Insulin Fairy |
The Energy Balance Equation
Change in Bodily Stores = Energy in - Energy out, where...
Energy in = Energy entering mouth - Energy exiting anus, and...
Energy out = BMR/RMR + TEF + TEA + SPA/NEAT
See The Energy Balance Equation to find out what the above terms mean.
People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.
People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. Trust me, I'm a retired Electronic Engineer. I've observed this (too) many times!
1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting massive postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Bodily stores increase. There are also accusations of sloth & gluttony!
2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Bodily stores decrease.
In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.
There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587
P.S. In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.
P.P.S. Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions.
P.P.P.S. Insulin Resistance can be fixed in the long-term. See Insulin Resistance: Solutions to problems.
Type 2 Diabetes can be fixed in the long-term. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.
Aim to fix the problem in the long-term. If a long-term fix isn't possible (due to excessive destruction of pancreatic beta cells), use a low-carbohydrate diet as an adjunct to medication.
12 Haziran 2014 Perşembe
Carbs, Carbs, Carbs, Carbs and Carbs.
Carbohydrates seem to get the blame for everything nowadays. "Carbohydrates made me fat". "Carbohydrates burned-out my pancreas". "Carbohydrates raised my blood glucose". "Carbohydrates raised my blood triglycerides". "Carbohydrates stole mer jerb!". O.K, I made the last one up!
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.
Also, Blue Zone populations eat a diet with a high percentage of total energy (%E) from carbohydrates. See Low serum insulin in traditional Pacific Islanders--the Kitava Study and The Kitava Study. The Kitavans eat ~70%E from carbohydrates, ~20%E from fats and ~10%E from proteins. They don't eat a significant amount of Western crap-in-a-bag/box/bottle.
Maybe it has something to do with the type of carbohydrates and with what they're eaten. In A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins , (emphasis, mine) "The very-low-fat, high-carbohydrate experimental diet was designed to supply less than 10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein." Simple carbohydrates are sugars.
The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!
1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.
2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very high glycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.
3. There are oligosachharides e.g. FOS.
4. There are polysaccharides e.g. inulin.
5. There is soluble fibre/fiber e.g. cellulose.
Although overeating sugars containing fructose & starches that rapidly hydrolyse into glucose makes the liver fatty, overeating fats also makes the liver fatty. See Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.
It's the chronic over-consumption of crap-in-a-bag/box/bottle (high in sugars and/or starches and/or fats), not just carbohydrates, that causes over-fatness and other health problems.
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.
Also, Blue Zone populations eat a diet with a high percentage of total energy (%E) from carbohydrates. See Low serum insulin in traditional Pacific Islanders--the Kitava Study and The Kitava Study. The Kitavans eat ~70%E from carbohydrates, ~20%E from fats and ~10%E from proteins. They don't eat a significant amount of Western crap-in-a-bag/box/bottle.
Maybe it has something to do with the type of carbohydrates and with what they're eaten. In A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins , (emphasis, mine) "The very-low-fat, high-carbohydrate experimental diet was designed to supply less than 10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein." Simple carbohydrates are sugars.
The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!
1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.
2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very high glycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.
3. There are oligosachharides e.g. FOS.
4. There are polysaccharides e.g. inulin.
5. There is soluble fibre/fiber e.g. cellulose.
Although overeating sugars containing fructose & starches that rapidly hydrolyse into glucose makes the liver fatty, overeating fats also makes the liver fatty. See Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.
It's the chronic over-consumption of crap-in-a-bag/box/bottle (high in sugars and/or starches and/or fats), not just carbohydrates, that causes over-fatness and other health problems.
10 Haziran 2014 Salı
Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy.
Fat storage:
Here's a plot of mean (±SEM) plasma insulin concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal. |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
100g of glucose produces a large spike in insulin concentration and 40g of fat produces no significant spike in insulin concentration. According to Gary Taubes' insulin hypothesis of obesity, in the absence of a significant spike in insulin concentration, fat cannot be stored.
Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post).
 |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
Plasma triacylglycerol concentration falls to baseline between 240min and 360min. OGTT's and OFTT's are performed with the subjects at rest for the duration of the test.
Referring to It's all in a day's work (as measured in Joules) , at rest the subject is burning ~1kcal/min with ~95% of it coming from fat, making a fat-burning rate of ~0.11g/min.
At a fat-burning rate of ~0.11g/min, it would take ~360min for plasma triacylglycerol to fall to baseline if the 40g of fat from the OFTT was only being burned and not being stored. As shown above, it only takes ~120min to fall to baseline. Therefore, fat from the OFTT that isn't burned is stored in ~120min in the absence of a significant insulin spike. Q.E.D.
A delicious analogy:
Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal (from the previous post). | ||
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
The OGTT (100g of glucose) produces a large spike in plasma glucose concentration which lasts for ~210min before returning to baseline. Higher plasma glucose concentrations glycate more than lower plasma glucose concentrations. Average plasma glucose concentration over 0 to 360min is higher with the OGTT than with the OFTT, therefore there is more glycation damage with the OGTT than with the OFTT. Don't regularly consume 100g or more of glucose!
Here's a plot of Mean (±SEM) plasma triacylglycerol concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal.
 |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
Although the plasma triacylglycerol concentration after consuming a high-carbohydrate evening meal is slightly higher than after consuming a high-fat evening meal, the two plots above are essentially flat, indicating that none of the 100g of glucose consumed was turned into fat by de novo lipogenesis (DNL) within 6 hours.
As discussed in the previous post, higher plasma triacylglycerol concentrations are more atherogenic than lower plasma triacylglycerol concentrations. Average plasma triacylglycerol concentration over 0 to 360min is higher with the OFTT than with the OGTT, therefore there is more atherogenicity with the OFTT than with the OGTT.
Don't regularly consume 40g or more of fat!
An interesting study that involved humongous fat consumption was Response of body weight to a low carbohydrate, high fat diet in normal and obese subjects , which used up to 600g of fat/day. It's possible to lose weight on an ultra-high-fat diet, but average plasma triacylglycerol concentrations would have been extremely high. Fasting TG's reduce on an ultra-high-fat diet, probably due to suppression of endogenous TG synthesis by exogenous TG intake.
Ultra-high-fat (~80%) diets: The good, the bad and the ugly.
The good:
Here's a plot of mean (±SEM) plasma glucose concentrations during an oral-glucose-tolerance test (OGTT) when preceded by either a high-fat (▪) or a high-carbohydrate (□) evening meal and during an oral-fat-tolerance test (OFTT) when also preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal. |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
An OGTT (100g of glucose dissolved in water) causes a large disturbance in blood glucose level for up to 2 hours. Ditto for insulin (see Fig. 2).
An OFTT (40g of fat as cream) doesn't cause a significant disturbance in blood glucose level. Ditto for blood insulin (see Fig. 2).
The bad:
Here's a plot of mean (±SEM) plasma triacylglycerol concentrations during an oral-fat-tolerance test (OFTT) when preceded by either a high-fat (•) or a high-carbohydrate (○) evening meal. |
| From Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism |
An OFTT (40g of fat as cream) causes a significant rise in blood triacylglycerol (a.k.a. TAG a.k.a. triglycerides a.k.a. TG's) level for up to 4 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG's is only +0.1mmol/L. Is high postprandial TG's a problem? Definitely, maybe. From Cholesterol And Coronary Heart Disease , "Cholesterol-depleted particles oxidise faster than large, cholesterol-rich ones." Chylomicrons, chylomicron remnants & VLDL-C are triglyceride-rich, cholesterol-poor, as that's the composition of the fat in the diet.
The ugly:
Here's evidence that excessive postprandial TG's significantly raise the relative risk (RR) for CHD:- See Fig. 1 in Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.Here's more evidence that postprandial saturated fatty TG's raise the RR for CHD:- See Postprandial triglyceride-rich lipoproteins promote invasion of human coronary artery smooth muscle cells in a fatty-acid manner through PI3k-Rac1-JNK signaling.
See also Postprandial triglyceride-rich lipoprotein changes in elderly and young subjects.,
Effect of a single high-fat meal on endothelial function in healthy subjects.,
Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins.,
Alimentary lipemia, postprandial triglyceride-rich lipoproteins, and common carotid intima-media thickness in healthy, middle-aged men.,
Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects.,
Association of postprandial hypertriglyceridemia and carotid intima-media thickness in patients with type 2 diabetes.,
Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress.,
High-energy diets, fatty acids and endothelial cell function: implications for atherosclerosis.,
Impact of postprandial hypertriglyceridemia on vascular responses in patients with coronary artery disease: effects of ACE inhibitors and fibrates.,
[Influence of postprandial hypertriglyceridemia on the endothelial function in elderly patients with coronary heart disease].,
Impact of postprandial variation in triglyceridemia on low-density lipoprotein particle size.,
Association between fasting and postprandial triglyceride levels and carotid intima-media thickness in type 2 diabetes patients.,
[Correlation of lipemia level after fat loading with manifestation of atherosclerosis in coronary arteries].,
Postprandial hypertriglyceridemia and carotid intima-media thickness in north Indian type 2 diabetic subjects.,
Association between postprandial remnant-like particle triglyceride (RLP-TG) levels and carotid intima-media thickness (IMT) in Japanese patients with type 2 diabetes: assessment by meal tolerance tests (MTT).,
Postprandial lipemia and remnant lipoproteins.,
Elevated levels of platelet microparticles in carotid atherosclerosis and during the postprandial state.,
Postprandial metabolic and hormonal responses of obese dyslipidemic subjects with metabolic syndrome to test meals, rich in carbohydrate, fat or protein.,
Atherosclerosis, diabetes and lipoproteins.,
Clinical relevance of non-fasting and postprandial hypertriglyceridemia and remnant cholesterol.,
Post-prandial hypertriglyceridemia in patients with type 2 diabetes mellitus with and without macrovascular disease.,
A hypertriglyceridemic state increases high sensitivity C-reactive protein of Japanese men with normal glucose tolerance.,
CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis.,
[Trends of evaluation of hypertriglyceridemia -from fasting to postprandial hypertriglyceridemia-].,
The effects of dietary fatty acids on the postprandial triglyceride-rich lipoprotein/apoB48 receptor axis in human monocyte/macrophage cells.
See also What Is the Significance of Postprandial Triglycerides Compared With Fasting Triglycerides? , Uncovering a Hidden Source of Cardiovascular Disease Risk and Postprandial Lipoproteins: The storm after the quiet!
A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG's aren't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrate, there is still glucose in the blood, thanks to the liver. Also, some carbohydrates don't spike blood glucose (or fructose) level. It's pure speculation that the subjects in the above studies had high blood glucose at the same time as high postprandial TG's. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG's, and there was no significant association between fasting TG's and the risk factor for CHD, this suggests that the subjects had no significant metabolic derangement and were not eating excessive amounts of sugar.
According to Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in Overweight Men, there's a ~50% reduction in postprandial TG's after adaptation to a very-low-carb, very-high-fat diet. However, mean energy intake was only 1,850kcals/day. The subjects were in a 500kcal/day energy deficit and the %E from fat was only 60%.
Also, some people's LDL levels go extremely high on a very-low-carb, very-high-fat diet. See Lipidaholics Anonymous Case 291 Can losing weight worsen lipids? A very high LDL level results in a high LDL particle count, even if the particles are large (Type A). A high LDL particle count is a strong risk factor for CHD. See also Fig. 1 in Some Metabolic Changes Induced by Low Carbohydrate Diets.
It's possible to get Coronary Artery Calcium (CAC) scans, to measure the amount of calcified plaque in coronary arteries. While a high CAC value means lots of plaque, a zero CAC value doesn't necessarily mean zero plaque, as young people and people with a high Vitamin K2 intake don't have significant calcification. See Stenosis Can Still Exist in Absence of Coronary Calcium.
Update 26th July 2014: See Page 10 of HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD - Nathan Pritikin. Read the text, starting with:-
"Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?"
The answer appears to be "Yes."
5 Eylül 2013 Perşembe
Boiled potatoes & Area Under the Curve (AUC): some thoughts.
Here are three "curves"... a 4 x 1 rectangle, a 2 x 2 square and a 1 x 4 rectangle.
Imagine that the three curves are for blood glucose level increase above baseline vs time.
a) "X" grams of a high-Glycaemic Index (GI) carb e.g. glucose, maltodextrin or amylopectin result in a large glucose response that goes away rapidly, as the carbs leave the gut rapidly, pass into the blood rapidly and are cleared from the blood rapidly due to the large insulin response.
b) "X" grams of a 50:50 mixture of high & low-GI carbs result in a lower but longer sustained glucose & insulin response, as some carbs leave the gut rapidly but some carbs leave the gut slowly, pass into the blood slowly and are cleared from the blood slowly due to the small insulin response.
c) "X" grams of a low-GI carb e.g. amylose or resistant starch result in an even lower glucose & insulin response that is sustained for even longer, as the carbs leave the gut very slowly, pass into the blood very slowly and are cleared from the blood very slowly due to the very small insulin response.
Will a), b) & c) produce the same satiety? I think not. I think that a) results in lower satiation than b) and b) results in lower satiation than c). Whether returning hunger is caused by a sudden drop in blood insulin level or by a sudden drop in the amount of food in the gut, I don't know.
The reason for this post is A satiety index of common foods (scanned image of full study here) and the related study An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods.
In the first study, boiled potatoes produced the highest satiety, yet in the second study, boiled potatoes produced one of the highest glucose & insulin AUCs. How can this be? Consider the preparation method for the Russet potatoes:-
"Peeled, boiled for 20 min, and stored at 4 °C overnight; reheated in a microwave oven for 2 min immediately before serving."
Potato starch when refrigerated produces resistant starch RS3, which gives it a low GI (see item 605 in International table of glycemic index and glycemic load values: 2002). Therefore, refrigerated potatoes contain a mixture of high & low-GI starches. This, I believe, is why boiled, refrigerated & reheated potatoes produced the highest satiety. The combination of water, fibre & resistant starch kept hunger pangs away the longest. I suspect that boiled potatoes that are eaten without being refrigerated won't produce quite as much satiation, as they contain no resistant starch.
EDIT: From https://en.wikipedia.org/wiki/Resistant_starch#Definition_and_categorization :-
"RS3 Resistant starch that is formed when starch-containing foods are cooked and cooled, such as pasta. Occurs due to retrogradation, which refers to the collective processes of dissolved starch becoming less soluble after being heated and dissolved in water and then cooled."
RS3 forms a gel in the stomach, which delays stomach emptying. This is most likely the reason for the increased satiation.
 |
| The AUC for all three "curves" = 4. |
a) "X" grams of a high-Glycaemic Index (GI) carb e.g. glucose, maltodextrin or amylopectin result in a large glucose response that goes away rapidly, as the carbs leave the gut rapidly, pass into the blood rapidly and are cleared from the blood rapidly due to the large insulin response.
b) "X" grams of a 50:50 mixture of high & low-GI carbs result in a lower but longer sustained glucose & insulin response, as some carbs leave the gut rapidly but some carbs leave the gut slowly, pass into the blood slowly and are cleared from the blood slowly due to the small insulin response.
c) "X" grams of a low-GI carb e.g. amylose or resistant starch result in an even lower glucose & insulin response that is sustained for even longer, as the carbs leave the gut very slowly, pass into the blood very slowly and are cleared from the blood very slowly due to the very small insulin response.
Will a), b) & c) produce the same satiety? I think not. I think that a) results in lower satiation than b) and b) results in lower satiation than c). Whether returning hunger is caused by a sudden drop in blood insulin level or by a sudden drop in the amount of food in the gut, I don't know.
The reason for this post is A satiety index of common foods (scanned image of full study here) and the related study An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods.
In the first study, boiled potatoes produced the highest satiety, yet in the second study, boiled potatoes produced one of the highest glucose & insulin AUCs. How can this be? Consider the preparation method for the Russet potatoes:-
"Peeled, boiled for 20 min, and stored at 4 °C overnight; reheated in a microwave oven for 2 min immediately before serving."
Potato starch when refrigerated produces resistant starch RS3, which gives it a low GI (see item 605 in International table of glycemic index and glycemic load values: 2002). Therefore, refrigerated potatoes contain a mixture of high & low-GI starches. This, I believe, is why boiled, refrigerated & reheated potatoes produced the highest satiety. The combination of water, fibre & resistant starch kept hunger pangs away the longest. I suspect that boiled potatoes that are eaten without being refrigerated won't produce quite as much satiation, as they contain no resistant starch.
EDIT: From https://en.wikipedia.org/wiki/Resistant_starch#Definition_and_categorization :-
"RS3 Resistant starch that is formed when starch-containing foods are cooked and cooled, such as pasta. Occurs due to retrogradation, which refers to the collective processes of dissolved starch becoming less soluble after being heated and dissolved in water and then cooled."
RS3 forms a gel in the stomach, which delays stomach emptying. This is most likely the reason for the increased satiation.
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