Lies, damned lies and statistics, part n+1. Riera-Crichton et al.

In Macronutrients and obesity: Revisiting the calories in, calories out framework, the conclusion is:-
"Our structural VAR results suggest that, on the margin, a 1% increase in carbohydrates intake yields a 1.01 point increase in obesity prevalence over 5 years while an equal percent increase in fat intake decreases obesity prevalence by 0.24 points."

So, carbohydrates are fattening but fat is slimming, eh? I declare shenanigans! Two can play at that game.

In Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating, Bray et al increased kcals by 40% by adding Fat grams. Carb grams didn't change. Protein grams changed a bit. ∴ Protein %E & Carb %E decreased by ~29%. %E means "as a percentage of total Energy".

Weight (lean body mass + body fat) increased as Fat kcals increased ± some interpersonal variation.

From Fig. 6.

_
 _Decreased P %E & C %E result in increased weight.
∴ Increased P %E & C %E result in decreased weight.

∴ Fat is fattening, but Protein & Carbohydrate is slimming! Q.E.D.

Do you see what's going on? Here's a summary:-

Diet contains A, B and C.
The amount of A increases, but the amounts of B and C remain constant.
A%E increases, but B%E and C%E decrease.  

In Riera-Crichton et al, A = Carbohydrate, B = Fat and C = Protein.
In Bray et al, A = Fat, B = Carbohydrate and C = Protein.

How low-carbohydrate diets are (incorrectly) explained to work.

Having explained how low-carbohydrate diets work, here are a few ways in which they don't work.

Uh, nope!

1. Hormonal clogs: This is a term used by Jonathan Bailor. I don't think he's referring to wooden shoes! The "clog", I'm guessing, is supposedly caused by that dastardly hormone insulin. Uh, nope!

See the following plots of RER vs exercise intensity after being on high-fat diet or low-fat diet.

RER = 0.7 ≡ 100%E from fat. RER ≥ 1.0 ≡ 100%E from carb.

The low-fat diet results in higher RER, so the body is burning a higher %E from carb and a lower %E from fat.

However, this doesn't make any difference to weight loss, as it's merely a substrate utilisation issue. In addition, when the body is burning a higher %E from carb, this depletes muscle glycogen stores faster, which lowers RER during the course of the exercise. So, it's not a problem.


2. Insulin: This is Gary Taubes' hypothesis. Insulin makes your body store carbohydrates as body fat. Uh, nope!

The only time that there's significant hepatic DNL is when there's chronic carbohydrate over-feeding. If you eat sensibly, there's no significant hepatic DNL.


3. A Calorie isn't a Calorie, where weight change is concerned: This is Richard D Feinman's hypothesis. "A calorie is a calorie" violates the second law of thermodynamics, therefore there's a metabolic advantage with low-carbohydrate diets. Uh, nope!

Where to start? Evelyn Kocur knows her Physics, so I'll start there. See The first law of thermodynamics (Part 1) and The first law of thermodynamics (Part 2).

From Second Law of Thermodynamics:-
"Living organisms are often mistakenly believed to defy the Second Law because they are able to increase their level of organization. To correct this misinterpretation, one must refer simply to the definition of systems and boundaries. A living organism is an open system, able to exchange both matter and energy with its environment."

People on ketogenic diets excrete very few kcals as ketone bodies. See STUDIES IN KETONE BODY EXCRETION. There is no significant Metabolic Advantage with low-carbohydrate diets.

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"!

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.

Some fascinating healthcare statistics: Article by Ezra Klein.

Spotted on Twitter. From Is America better at treating cancer than Europe? , by Ezra Klein.

Healthcare rankings.

I highlighted Great Britain in green.

Cancer mortality.

Saturated fats Saturated fats Saturated fats.

George Henderson left the following comment. I think that the information in it deserves a bigger audience.

Saturated fats seem to get the blame for everything nowadays. "Saturated fats clogged my arteries". "Saturated fats gave me cancer". "Saturated fats stole my job". O.K, I've done that joke before.

There are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats, there are saturated fats and there are saturated fats. Saturated fats are an ester of Glycerol (a 3-carbon alcohol) and three saturated fatty acids (SFA's). There are roughly six categories of SFA's.

1) Short chain SFA's such as Acetic acid, Propionic acid, Butyric acid (found in butter and also what soluble fibre ferments into in the colon) and Caproic acid.
2) Medium chain SFA's such as Caprylic acid, Capric acid, Lauric acid and Myristic acid.
3) Long chain SFA's such as Stearic acid.
4) SFA's behaving like Palmitic acid.
5) Odd chain SFA's such as Pentadecylic acid and Margaric acid.
6) Very long chain SFA's such as Behenic acid.

See http://en.wikipedia.org/wiki/List_of_saturated_fatty_acids

In foods, the above SFA's are associated with different things.
1) and 2) don't get associated with much polyunsaturated fatty acids (PUFA's), e.g. dairy and tropical nuts.
3) and 4) are more likely to be associated with long-chain PUFA's, e.g. meats, poultry, temperate nuts.
5) is associated with CLA and not much PUFA's, e.g. dairy from grass-fed animals.

See also Siri-Tarino et al, Forests & Trees and "Eureka!" moments and Chowdhury et al, More forests & more trees and more "Eureka!" moments with cheese.

How a B.Sc.(Hons) in Electronic Engineering is relevant to Diet & Nutrition.

The human body regulates various processes using negative feedback loops. Here's blood glucose regulation.

From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387

Here's a generic Hypothalamus-Pituitary-X Axis loop, where X may be thyroid, adrenal, gonadal etc.

From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387

Electronic Engineers understand how negative feedback systems work, such as phase-locked loops & amplifiers.

Negative feedback control systems can overshoot, especially if there's a delay in the feedback path that's longer than the rise time of the input step.

An example of this is the first-phase insulin response. Loss of the first-phase insulin response occurs in over-fat people who are hyperinsulinaemic. Without the first-phase insulin response, there's a delay between an increase in blood glucose and an increase in insulin secretion. A rapid upwards step in blood glucose (say, from eating a high-GL meal) causes a massive overshoot in insulin secretion, resulting in postprandial sleepiness, also down-regulation of insulin receptor activity in the appetite centres of the brain, causing ravenous hunger when the insulin level falls to normal.

See also Blood Glucose, Insulin & Diabetes.

People shouldn't be too quick to write-off the knowledge of an Electronic Engineer who's delving into the mysteries of the human body.

The Conflation Game.

Li-i-ife, is the name of the game, and I wanna play the game with you.....


People have been "grinding my gears" by conflating carbohydrates with sugars. All sugars are carbohydrates, but not all carbohydrates are sugars. See Carbs Carbs Carbs. to find out about the five basic different types of carbohydrates.

Krauss et al has done it again. In Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia, at the bottom of Table 1 is "carbohydrate, 50% simple and 50% complex". The carbohydrates consisted of half sugars and half starches.

The effect of such a sugary diet is as follows:-

The percentage of pattern B (small, dense) LDL particles increases significantly in proportion to the percentage of Dietary "carbohydrate". The implication of this study (also A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins ) is that high-carb, low-fat diets are atherogenic.

This is not on.

A high sugar diet is atherogenic, but carbs from new potatoes (especially if eaten cold), Basmati rice (especially if eaten cold), sweet potatoes, beans & whole fruits aren't.