I never expected THAT to happen!

Fancy some Ramen Noodles?


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 (Fig. 1).

Fig. 1 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 short-term increase in blood glucose level. Ditto for insulin (see Fig. 2 ▪ & □ below).

Fig. 2 from Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism

An OFTT (40g of fat as cream) doesn't cause a significant increase in blood glucose level (see Fig. 1 • & ○ above). Ditto for blood insulin (see Fig. 2 • & ○ above).

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 (Fig. 3).

Fig. 3 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 increase in blood triacylglycerol (a.k.a. TAG a.k.a. triglyceride a.k.a. TG) level for 3 hours. Note that the effect of a preceding high-carbohydrate meal on fasting TG is only +0.1mmol/L. Is high postprandial TG 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 high postprandial TG is atherogenic. See Fig. 1 in Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women.

People who have Insulin Resistance &/or type 2 diabetes have impaired postprandial clearance of glucose and TG, which is atherogenic. Lifestyle Intervention Leading to Moderate Weight Loss Normalizes Postprandial Triacylglycerolemia Despite Persisting Obesity.

Here's evidence that postprandial saturated fat TG is atherogenic. 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? and Uncovering a Hidden Source of Cardiovascular Disease Risk.

A counter-argument is that the subjects in the above studies were eating carbohydrate, and that postprandial TG isn't atherogenic if you're not eating much carbohydrate. Definitely, maybe. In the absence of carbohydrates, there is still glucose in the blood, thanks to the liver and kidneys. 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. As Insulin Resistance/Metabolic Syndrome and/or a high-sugar diet raise fasting TG, and there was no significant association between fasting TG 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 after adaptation to a low-carb, high-fat diet. However, mean energy intake was 1,850kcals/day, the subjects were in a 500kcal/day energy deficit and %E from fat was 60%.

Some people's LDL becomes very high on low-carbohydrate high-fat diets. See 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.

See also Page 10 of  HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD - Nathan Pritikin.
"Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?"
The answer is "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.

Diabetes: which are the safest carbohydrates?

In my previous post, I stated that people with T2DM should eat ~150g/day of carbohydrate.

Soak & cook your own beans al-dente, for slowest release carbs.

See International table of glycemic index and glycemic load values: 2002. Below is a list of carbohydrates that have a low glycaemic load, or GL (GL = glycaemic index * grams of carbohydrate in the serving).

Non-nutritive sweeteners:

It's often claimed that non-nutritive sweeteners produce a cephalic phase insulin response. The mere anticipation of eating produces a cephalic phase insulin response. See How neural mediation of anticipatory and compensatory insulin release helps us tolerate food. An insulin response suppresses serum NEFAs, so it's not all bad.

Sugars and Sugar alcohols:

Fructose is not recommended for people with T2DM, as it "barges its way" into the liver via Glu-T5 and fructokinase. People with T2DM who have a high fasting serum glucose level almost certainly already have full liver glycogen stores, so adding to them isn't advisable. Whole fruits (not juices) are fine.
Lactose has a virtually zero GL, isn't very sweet and has/hasn't a laxative effect in large quantities (lactase-dependent). Heating lactose turns it into lactulose.
Lactulose has a virtually zero GI, is sweet and has a laxative effect in large quantities.
Galactose is not recommended, as large amounts may accelerate ageing.
D-mannose has a virtually zero GI, is sweet and doesn't have a laxative effect in large quantities. It can be used to treat urinary tract infections (UTIs) caused by e.coli, due to the fact that the kidneys filter it out of the blood and pass it out in the urine. Mannose in urine reduces the adhesion of e.coli to the inside wall of the urinary tract. See Intervening with urinary tract infections using anti-adhesives based on the crystal structure of the FimH-oligomannose-3 complex.
Trehalose has a virtually zero/moderate GI, is sweet and has/hasn't a laxative effect in large quantities (trehalase-dependent).

Lactitol has a virtually zero GI and has a laxative effect in large quantities.
Sorbitol has a virtually zero GI and has a laxative effect in large quantities.
Xylitol has a virtually zero GI, minty overtones and reduces dental plaque. However, it has a laxative effect in large quantities.
Erythritol has a virtually zero GI, minty overtones and is wee'ed-out like D-mannose, so it doesn't have a laxative effect in large quantities.

Starches:

Note: Tinned starches are usually overcooked, so cook your own. Don't overcook starches, as that makes them faster-absorbing. Al dente is best.

Gram dhal a.k.a. chana dal.
Long-grain rice. Refrigerating boiled rice for 24 hours lowers the GL, by forming resistant starch. See item 275 in the table in the first link.
New potatoes. Refrigerating boiled new potatoes for 24 hours lowers the GL a lot, by forming resistant starch. See item 605 in the table in the first link. You can boil old potatoes, but they're probably not as good.
Pearl barley.
Sweet corn.
Beans.
Chickpeas.
Lentils.
Peas.
Starchy nuts e.g. peanuts , cashews and chestnuts.
Vegetables.
Root vegetables.
Raw carrots.

If even low-GL carbs spike BG too much, this indicates severe IR in liver and/or skeletal muscle. See Insulin Resistance: Solutions to problems.

The above lists also apply to people with T1DM who are having difficulty keeping their blood glucose level between 3 and 7mmol/L.

Type 2 diabetes: between a rock and a hard place.

About 85% of type 2 diabetics have excessive visceral adiposity (belly fat). This post is about them.

Which is better - the rock or the hard place?

 

1) The rock:

This is serum glucose. People with type 2 diabetes can measure their own serum glucose. Eating carbohydrates makes serum glucose increase, the rate of increase being proportional to the glycaemic index and the magnitude of the increase being proportional to the grams of carbs consumed. By limiting the intake of dietary carbohydrates, large spikes in serum glucose can be avoided. The occasional spike above 7.8mmol/L (140mg/dL) doesn't hurt. It's spending long periods of time above 7.8mmol/L that's harmful (by glycation).

A low-carb diet (~150g/day of carbohydrate) halves serum glucose fluctuations compared to a higher-carb diet (~300g/day of carbohydrate). A very-low-carb diet (~75g/day of carbohydrate) further halves serum glucose fluctuations compared to the low-carb diet. This seems like an improvement, at first glance.

2) The hard place:

This is the invisible "elephant in the room", as it's not measured by doctors and people with type 2 diabetes can't measure it themselves. It's serum Non-Esterified Fatty Acids, or NEFAs (a.k.a. Free Fatty Acids, or FFAs). Serum NEFAs are high when fasting and fall after eating foods that raise serum insulin (carbs & certain proteins). People with type 2 diabetes and excessive visceral fat (belly fat) have higher-than-normal serum NEFAs due to adipocyte insulin resistance (IR). See Insulin Resistance: Solutions to problems.

Just like with serum glucose, there's nothing wrong with serum NEFAs going up & down. It's chronically-high serum NEFAs that's harmful (except during periods of caloric restriction). See Showing posts sorted by relevance for query NEFA "type 2 diabetes" .

See Fig. 1 in Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. On a very-low-carb (less than 50g/day carbs) diet that's not calorie-restricted, serum insulin remains low all of the time. To insulin-haters, that sounds like a good thing. Unfortunately, it means that there is no insulin spike to suppress serum NEFAs by shifting the balance of NEFAs going in/coming out of fat cells. Serum NEFAs stay high all of the time, which is harmful.

Therefore, people who have type 2 diabetes and excessive visceral fat and who are permanently on a very-low-carb diet that's not calorie-restricted are harming themselves.

Low-glycaemic diet seen to reverse diastolic dysfunction of diabetes.

From http://www.medscape.com/viewarticle/802947?nlid=30763_1301&src=wnl_edit_dail (Medscape log-in required):-

"Of 32 overweight or obese diabetic patients (mean body-mass index, 34) without cardiac disease who were engaged in a "rehabilitation program in order to lose weight" that included two hours of supervised aerobic exercise per day, half followed a low-glycemic diet (25% carbohydrate, 45% fat, 30% protein) and the other half a low-fat diet (55% carbohydrate, 25% fat, and 20% protein) for three weeks. The diets provided the same amount of calories. Those on the low-fat diet then switched to the low-glycemic diet for an additional two weeks"

"....the two diets led to about the same declines in weight and waist circumference..."

The diet was 25% carbohydrate, 45% fat, 30% protein.
It was a low-carbohydrate/low-glycaemic load diet.
It was not a very-low-carb diet.

A comment, a simile and insanity.

1) The comment: I'm just about to leave the following comment on Peter (Hyperlipid)'s blog post Insulin and the Rewards of overfeeding. I thought that it was so good at summing-up, I'll post it here first!
"All,

Insulin increases the amount of glucose & FFAs entering fat cells, muscle cells & the liver.

Insulin decreases the amount of glycerol & FFAs exiting fat cells & the amount of glucose exiting the liver.

Hyperinsulinaemia (which can produce sedation) results when one or more of the following tissues loses insulin sensitivity:- fat cells, muscle cells & the liver.

So, why do people keep saying that hyperinsulinaemia locks nutrients away in fat cells only, thus robbing other cells of nutrients, thus causing lethargy?

The relative insulin sensitivity of tissues determines the relative partitioning of nutrients into those tissues.

When tissues lose sensitivity to insulin, blood glucose control becomes impaired. This results in roller-coaster blood glucose levels after eating high-glycaemic carbohydrates. A rapidly-falling blood glucose level causes ravenous hunger. I have experienced this during medically-monitored tests (OGTTs & an insulin shock test).

Low-carb/ketogenic diets don't result in a roller-coaster blood glucose level and therefore don't cause ravenous hunger. Simples!

Overeating due to ravenous hunger is NOT gluttony, just as under-moving due to sedation is NOT sloth.

THIS is gluttony."

EDIT: This didn't go in my comment but should have:- "Low-carb/ketogenic diets result in the avoidance of moreish & calorific foods such as sweets, chocolate, cake, biscuits, pizza, Pringles etc. A single bite of such foods has a negligible effect on blood glucose & insulin levels, but encourages another bite and another and another ad nauseam, due to Food Reward.


2) The simile: I use similes. I used the simile "As happy as a pig in shit" in a comment somewhere on Woos blog. Now, you may (or may not) have noticed that my user-name is Nigeepoo. We Brits are obsessed by two things - The weather and our bowel movements. I find things to do with poo and farting amusing (schoolboy humour, I know!). I used the simile "As happy as a pig in shit" because it is amusing.


3) The insanity: According to Woo in the following comment:-
"Re: the comment...Sorry, not convinced.
You are basically refusing to admit your choice of words implied moral judgement. The phrase "happier than a pig in shit" is always applied to examples of people being content in immorality/bad behavior particularly gluttony and sloth... unless it is used ironically. Only an autistic or a non-english speaker would believe this crap."

Woo, you are as mad as a March hare. IMO of course, like everything I write. Duh!

Carbohydrates: Dogs' Doodads or Spawn of Satan?

Depending on which side of the fence you're on, Carbohydrates are either the Dogs' Doodads or the Spawn of Satan. As I get older, I prefer to sit on the fence. Let's start with the basics.


What are Carbohydrates?

Carbohydrates are so named because they have the generic formula (CH2O)n. C is carbon and H2O is water hence Carbo-Hydrate. There are several different types.

1) Sugars. There are monosaccharides, the most common being Glucose (a.k.a. Dextrose), Fructose and Galactose. There are disaccharides, the most common being Sucrose, Lactose and Maltose. Disaccharides are 2 monosaccharides linked by a glycosidic bond formed by a condensation reaction (removal of a water molecule, usually by an enzyme). Disaccharides have to be hydrolysed (have a water molecule added back in, usually by an enzyme) into monosaccharides before they can be absorbed in the gut.
Sugars are simple carbohydrates.

2) Starches. These are chains of glucose molecules linked by glycosidic bonds. Starches have to be hydrolysed into glucose molecules before they can be absorbed. There are unbranched chains like amylose which is also known as resistant starch. There are branched chains like amylopectin and maltodextrin. Glycogen is a branched chain "animal starch" that is synthesised inside muscle and liver cells and which can be rapidly converted back into glucose inside cells.

3) Non-Starch Polysaccharides (NSPs). These are also known as fibre/fiber and there are 2 types: soluble (e.g. pectin, beta-glucan & cellulose) and insoluble (e.g. bran). These aren't absorbed, but gut bacteria can feed on soluble fibre/fiber. Starches and NSPs are complex carbohydrates.

For more information, see http://en.wikipedia.org/wiki/Carbohydrate

The amount of carbohydrate that someone needs varies from person to person and increases with the intensity and volume of exercise done. See Everyone is Different. What are the best carbs to eat? "Complex" ones from "wholegrain" cereals? Not necessarily.


Simple vs Complex

TV ads for breakfast cereals bang on about the wholegrain goodness of complex carbohydrates releasing energy slowly. The terms "Simple" and "Complex" actually refer purely to the chemical structure of a carbohydrate and have nothing to do with how quickly they turn into blood glucose in the body. The Glycaemic Index (GI) (or Glycemic Index if you're American) relates to how quickly carbohydrates turn into blood glucose in the body. See http://www.mendosa.com/gilists.htm for a list of 750 foods and their GI & GL (GL = Glycaemic Load = GI/100 x carb content per serving). Here are a few extracts. Note: a GI of 55 is low; a GL of 10 is low.

The last three items in the list are all simple carbohydrates. As you can see, some wholegrain complex carbohydrates turn into blood sugar faster than simple carbs. This is because the wholegrains have been ground into powder which is rapidly digested and absorbed, despite the presence of fibre/fiber.

As fructose has such a low GI, does this mean that we can eat as much of it as we like? No! When we eat fructose, it passes from the small intestine into the portal vein and goes straight to the liver. As liver cells contain an enzyme called fructokinase (which has a high affinity for fructose), all dietary fructose is absorbed by the liver where it tops-up liver glycogen. Liver glycogen is also topped-up by glucose (obtained from the digestion of starchy carbohydrates). Once liver glycogen stores are full, any further fructose is converted into fats, which are stored as ectopic liver fat and also exported as triglycerides. High serum triglycerides are heart-unhealthy. See Cholesterol And Coronary Heart Disease.

Why is GI important? When we eat carbohydrates, they raise blood glucose levels. Pancreatic beta cells secrete a hormone called insulin, which allows more glucose to pass into cells (by moving Glu-T4 transporters inside the cells). When more glucose enters cells, glucose levels in the blood fall. It's a negative feedback loop. For millions of years, we lived on a diet of natural, unrefined carbohydrates and so the secretion of insulin never had to change blood glucose levels very rapidly.

When unnatural, refined, high-GI carbs are eaten, blood glucose levels rise much faster. This results in over-secretion of insulin (hyperinsulinaemia). This shuttles too much glucose into cells and results in.......low blood glucose, followed by low blood insulin. Rapidly-falling and low blood insulin levels cause feelings of severe hunger and cravings to eat more carbs. It's a vicious circle. Hyperinsulinaemia also has other bad effects on the body. See http://www.mercola.com/2001/jul/14/insulin.htm to learn about Insulin and its Metabolic Effects.

GI has a weakness because adding fats and some proteins to high-GI foods lowers the GI but can increase the insulin response. Saturated fats, monounsaturates and omega-6 polyunsaturates raise the insulin response to carbs.

There is another index called the Insulin Index (II). See http://www.mendosa.com/insulin_index.htm.
The II contains a few surprises. Some proteins (e.g. the whey in milk & yoghurt) produce a large insulin response. Insulinogenic proteins are also glucogenic, so they don't cause low blood glucose.

On the other hand, refrigerating some foods lowers their GI & II by changing the starch in them into resistant starch, even if the food is subsequently re-heated. Rice & potatoes are two such foods.

As the terms "simple" and "complex" are meaningless in terms of carbohydrates' effects in the body, I prefer to use the terms "slow" and "fast". In a nutshell, slow carbs are good and fast carbs are bad. These terms can be applied to proteins, too. Egg is slow and whey is fast. Sticking to mostly slow foods keeps blood glucose and insulin levels stable, which results in better appetite control and better health, too.

It was soaring serum insulin levels that were sending me to sleep after carby meals years ago. Postprandial hyperinsulinaemia results in amino acids from digested foods being shuttled into cells. However, L-tryptophan isn't shuttled into cells, so the level of this amino acid in the blood rises relative to others. As L-tryptophan competes with other amino acids to cross the blood-brain barrier, now that the competition has been removed, more L-tryptophan enters the brain. It's converted into 5-hydroxytryptophan (5-HTP), then serotonin & melatonin. High melatonin levels in the brain cause sleepiness.

So remember, "Right carbs, right amounts, right times."