Why Calories count (where weight change is concerned).

I have to add the words "where weight change is concerned", as calories have little to do with body composition or general health (unless somebody becomes morbidly obese).

From https://docs.google.com/file/d/0Bz4TDaehOqMKSXZHUUVxWnl5VTQ/edit?usp=sharing

Arguments used by Calorie Denialists include:-

1) Calories don't count because the human body isn't a Bomb Calorimeter and treats different macronutrients differently.
 
100g of liquid paraffin burns in a Bomb Calorimeter, yielding 900kcals. In a human, it passes through completely undigested. Ah-ha!, I hear you saying. This proves that the Energy Balance Equation is invalid. Uh, nope!

Calories in = Calories entering mouth - Calories exiting anus

As 100% of liquid paraffin calories entering the mouth exit the anus, Calories in = 0

This is why Sam Feltham's "Smash the Fat" "experiment" is nonsense. A high percentage of the large amount of raw almonds he ate would have exited his anus incompletely chewed, undigested & unabsorbed.

See the picture above? In the late 1800's, W.O. Atwater established Atwater Factors (3.75kcals/g for digestible Carbohydrates, 4kcals/g for Proteins, 5kcals/g for Ketones, 7kcals/g for Alcohols & 9kcals/g for Fats*) using Human Calorimeters, not Bomb Calorimeters. Atwater Factors are pretty accurate.

*Fats containing different fatty acids have slightly different kcals/g. Fats containing long-chain fatty acids are 9kcals/g. Fats containing medium-chain fatty acids e.g. coconut oil are ~8kcals/g.

For more information, see Calories ...


2) Calories don't count because Dietary Efficiency varies for different macronutrients.

Uh, nope! The Heat Power generated by the body is regulated by a NFB loop involving the Hypothalamus, Pituitary, Thyroid Axis, also Uncoupling Proteins (UCP's), also shivering, so as to maintain a body temperature of 37°C ±3°C. If this wasn't the case, different amounts & types of foods (also, changes in ambient temperature & clothing) would cause large variations in body temperature resulting in death, as the enzymes in our bodies function correctly over a limited range of temperatures.

Heat Power generated by the body (W) = Temperature difference between the body & ambient (°C) divided by Thermal resistance between the body & ambient (°C/W)

∴ Dietary Efficiency is irrelevant.

Metabolic rate, diet efficiency and thermodynamics.

From Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals

This post is based on https://www.facebook.com/richard.feinman.7/posts/667508920000715:- 
"When people say the laws of thermodynamics, they usually mean the first law, the law of conservation of energy. However, “conservation of energy” can be a sound bite, at the level of “Einstein said that everything is relative.” You have to know exactly what is being conserved. Precise definitions become very important. One of the many difficulties in understanding thermodynamics is that there are simple principles which seem obvious enough but their import is under-appreciated without a real example.

The first law says precisely that there is a parameter called the internal energy and the change (Δ) in the internal energy of a system is equal to the heat, q, added to the system minus the work, w, that the system does on the environment. (The internal energy is usually written as U so as not to confuse it with the electrical potential).

ΔU = q - w (1)

This is how thermodynamics is taught. To go to the next step you need to understand the idea of a state variable. A state variable is a variable where any change is path-independent. For example, the familiar temperature T and pressure P are state variables. It doesn’t matter whether you change the pressure quickly or slowly. The effect on the system is controlled by the difference between the pressure after the change minus the temperature before the change, that is, ΔP. The usual analogy is the as-the-crow-flies geographical distance, say, between New York and San Francisco. This is a state variable: it doesn't matter whether you fly direct or go through Memphis and Salt Lake City like the flights that I wind up on.

Now, U in equation (1) is a state variable. Any process that you carry out will have a change in U that depends only on the initial and final states. However, q and w are NOT state variables. How you design your machine will determine how much work you can get out of it and how much of the energy change will be wasted. Looking at the biological case, two metabolic changes with the same U have no theoretical reason why they should have the same relative amounts of heat and work, that is, the same efficiency (storing fat as compared to generating heat). Of course, they might but there is no theoretical barrier to difference.

In this, the first law contains the suggestion of the second law. The second law is what thermodynamics is really about.... It is the second law that embodies the special character of thermodynamics. Described by Ilya Prigogine, the Nobel-prize winning chemist and philosopher of thermodynamics, as the first revolutionary science, it is the second law that explains how one diet can be more or less efficient that the other."
Ref: Non-equilibrium thermodynamics and energy efficiency in weight loss diets.

To which I replied:-
"Uncoupling proteins (UCP's) vary ATP → ADP + heat energy, so as to maintain the human body at 37°C ±3°C, over a wide range of ambient temperatures.

Therefore, "diet efficiency" is varying over a wide range, for all diets."

Followed by:-
"Here's an example:-

To maintain a body temperature of 37°C in an ambient temperature of 20°C, the body needs to generate ~1kcal/min (~69.8W).

If Diet "A" generates 30W due to metabolic processes, UCP's generate an extra 39.8W.

If Diet "B" generates 40W due to lower "diet efficiency", UCP's generate an extra 29.8W.

According to Life and Death: Metabolic Rate, Membrane Composition, and Life Span of Animals:-
"Not all body tissues contribute equally to BMR. For example, ∼70% of the BMR of humans is contributed by internal organs that constitute only ∼7% of body mass..."

As humans must (& can) survive over a wide range of ambient temperatures while being covered with a wide range of clothing while eating a wide range of diets, UCP activity must be capable of being varied from 0 (ambient temperature ≥37°C) to a very high value (swimming in water at 0°C).

Therefore, "diet efficiency" is irrelevant, as UCP's equalise overall efficiency, to equalise the rate of heat energy generation for a given ambient temperature & clothing.

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.