I never expected THAT to happen!

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?

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.

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

Average plasma triacylglycerol concentration over 0 to 360min is ~1.3mmol/L (~116mg/dL in US units).

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

Average plasma triacylglycerol concentration over 0 to 360min is ~1.0mmol/L (~89mg/dL in US units).

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."

Rigid diets & taking loadsa supplements to compensate for them.

I do not believe you want to be doing that!

This post was inspired by a recently-published study by Alan Aragon & Brad Schoenfeld, as bodybuilders are a group of people who often eat a rigid diet (some eat skinless chicken breasts, broccoli & brown rice for several meals each day).

See Nutrient timing revisited: is there a post-exercise anabolic window?
"Collectively, these data indicate an increased potential for dietary flexibility while maintaining the pursuit of optimal timing."

This post is also aimed at people who eat severely restricted diets in the (often mistaken) belief that something's making them ill.

People with type 1 diabetes who struggle to keep their blood glucose within reasonable limits (3 to 8mmol/L, or 24 to 144mg/dL) benefit from restricting their intake of high-GL carbohydrates, so this post is not aimed at them. See The problem with Diabetes.

People with type 2 diabetes who severely restrict their intake of carbohydrates must be in caloric deficit, otherwise the physiological insulin resistance caused by high serum NEFAs will mess up just about everything in their body if they are in caloric balance or caloric excess. I've read (so it could be false) that a certain non-skinny blogger who I'm in conflict with (who has type 2 diabetes and who eats a VLC diet) has heart problems and is taking medication(s) for high blood pressure. Hmmm.

People who suffer from gastrointestinal problems after eating gluten-containing foods, or mucus after eating casein-containing foods may have impaired gut integrity. See Gluten - more than just a pain in the guts?

Supplements that I consider of positive value are:-

Fish oils: If the diet is low in oily fish (tinned tuna is not an oily fish), there may be insufficient EPA & DHA (especially in men, children & post-menopausal women). Women of reproductive age can get away with taking flaxseed oil.

Magnesium: If the diet is low in veg/high in dairy, there may be too much Calcium relative to Magnesium.

Vitamin D3: If the lifestyle results in sun-avoidance, insufficiency in Vitamin D is highly likely.

Vitamin K2: If the diet is low in animal fats and/or fermented foods, insufficiency in Vitamin K2 is highly likely.

Supplements that I consider of negative value are:-

Vitamin A: If there's an insufficiency in Vitamin D, supplementing with Vitamin A/β-carotene may exacerbate it. As Vitamin D + Calcium may reduce cancer risk, supplementing with Vitamin A absent Vitamin D3 may increase cancer risk.

Vitamin E: If there's an insufficiency in γ-tocopherol, supplementing with α-tocopherol may exacerbate it. As γ-tocopherol may reduce CHD mortality risk, supplementing with α-tocopherol absent γ-tocopherol may increase CHD mortality risk. Most Vitamin E supplements contain α-tocopherol only. Some Vitamin E supplements contain mixed tocopherols and these are O.K.