Thursday, 31 July 2014

Nonequilibrium thermodynamics and energy efficiency in weight loss diets, by Richard D Feinman and Eugene J Fine.


From Nonequilibrium thermodynamics and energy efficiency in weight loss diets:-

Emphasis on kinetics and nonequilibrium thermodynamics provides a conceptual framework for understanding the effect of macronutrient composition on maintenance and change of body mass and possibly for analysis of adipocyte metabolism in general. The simple model presented is intended to be consistent with a general shift away from equilibrium thermodynamics and towards a more dynamic analysis of cellular processes."

Sounds plausible. There's only one thing wrong with Feinman et al's article - it's completely wrong!

Consider two rooms:-

Room "A" has an adjustable heater. The heater is adjusted until the room temperature is 20°C.

Room "B" has a radiator, controlled by a wall-stat set to 20°C. The radiator is on, and the room is at 20°C.

We have two rooms of the same size, at the same temperature.

If you plug in & turn on a 2kW fan heater in each room, what happens to the temperature in each room?

Room "A" gets warmer, because there is 2kW more heat power entering it.

Room "B" stays at 20°C, because the wall-stat reduces the heat power from the radiator by 2kW.

The human body stays at 37°C ±~2°C, because there's a Negative Feed-Back loop adjusting the heat power produced, via UCP's, futile cycles, thyroid hormones, shivering and heat conservation/wasting behaviours.

∴ Variable heat power generation due to variable Dietary Efficiency doesn't change Eout.

EDIT: By request, here's Figure 1 from the above study.

This suggests that fat mass & therefore weight can increase indefinitely - at maintenance energy intake, due to the effect of insulin on HSL. This, of course, is quite impossible!

From The Energy Balance Equation:-

Change in Body Stores = Ein (corr for digestion) - Eout (BMR/RMR + TEF + TEA + SPA/NEAT)
__BMR/RMR & TEA ∝ weight
weight → Eout
__If Ein = constant, Eout (Ein - Eout) → weight
weight → weight
∴ Figure 1 is wrong.

The Ketogenic Diet: Uses in Epilepsy and Other Neurologic Illnesses.

Fools claim that I am anti-ketogenic diets. Am I ****! beta-Hydroxybutyric acid has its uses...

From The Ketogenic Diet: Uses in Epilepsy and Other Neurologic Illnesses:-

"Inconsistencies in studies attempting to correlate seizure protection with levels of ketone bodies suggest that another mechanism may be involved in the diet’s beneficial effects on seizures. Several mechanisms have been proposed, including changes in ATP production making neurons more resilient in the face of metabolic demands during seizures; altered brain pH affecting neuronal excitability; direct inhibitory effects of ketone bodies or fatty acids on ion channels; and shifts in amino acid metabolism to favor the synthesis of the inhibitory neurotransmitter GABA."

GABA is an interesting neurotransmitter, as it's the chief inhibitory neurotransmitter in the mammalian central nervous system.

I know of two other substances that enhance GABA's effects - Alcohol and Benzodiazepines.

In conclusion:

I'm in favour of ketogenic diets under medical supervision, as therapy for neurologic conditions etc.

I'm not in favour of ketogenic diets under lay supervision, as a supposed aid for weight loss.

Tuesday, 29 July 2014

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base, by Richard D Feinman et al.

Another Bookmarking post.

The study in question is Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Here are my comments on the 12 points.

Point 1 is wrong. For ~85% of people who have T2DM, hyper*emia is the salient feature, where * = glucose, TG's, cholesterol, NEFAs, uric acid etc. For ~85% of people who have T2DM, it's a disease of chronic excess.

Ad lib LCHF diet↓ Blood glucose & ↓ fasting TG's, but ↑ PP TG's, ↑ LDL-C, ↑ LDL-P & ↑ NEFAs. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
↑ PP TG's is associated with ↑ RR of CHD.
↑ LDL-P is associated with ↑ RR of CHD.
↑ NEFAs are associated with ↑ RR of Sudden Cardiac Death.

Point 2: So?

Point 3 is wrong. A caloric deficit is essential, to reverse liver & pancreas ectopic fat accumulation. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Point 4 is misleading. Feinman doesn't distinguish between different types of carbohydrates. Starches, especially resistant starches (e.g. Amylose) are beneficial. See Point 11.

Point 5 is moot. Prof. Roy Taylor found that motivation determines adherence. Prof. Roy Taylor's PSMF was adhered to. See Point 3.

Point 6 is correct. Prof. Roy Taylor's PSMF is ~1g Protein/kg Bodyweight, some ω-6 & ω-3 EFAs & veggies for fibre. See Point 3.

Point 7 is misleadingSiri-Tarino et al gave a null result by including low fat studies, also a dairy fat study which had a RR < 1 for increasing intake. Chowdhury et al gave a null result, as some fats have a RR > 1 for increasing intake and some have a RR < 1 for increasing intake.

Point 8 is irrelevant. ↑ Dietary fat ↑ 2-4 hour PP TG's. See Point 1.

Point 9 is partly correct. Microvascular, yes. Macrovascular, no. See Point 8.

Point 10 is mostly irrelevant. See Point 8.

Point 11 ignores results obtained with high-starch diets, where the starch contains a high proportion of Amylose. See Walter Kempner, MD – Founder of the Rice Diet and From Table to Able: Combating Disabling Diseases with Food.

Point 12 is misleading. The low-carbohydrate part is fine. It's the high-fat part that can cause problems. See Point 8.

Saturday, 26 July 2014

Some thoughts on the essentiality of dietary carbohydrates.

I didn't know that there's a watch strap called Essentiality. I do, now.

This is a book-marking post for thoughts I had in

"The human body does not need carbohydrates from an external food source, because it is capable of very precisely and correctly assembling its own amounts of glucose that is needed in very small amounts for auxiliary and specialized functions." - Igor Butorski.

1) It's not very precise. See

2) It's not enough to fuel high-intensity exercise. See

3) Using the above argument, the human body does not need saturated fats & monounsaturated fats from an external food source, because it is capable of very precisely and correctly assembling its own amounts of saturated fats & monounsaturated fats (out of carbohydrate) that are needed in very small amounts for auxiliary and specialized functions.

If we only consumed Essential Fatty Acids, Essential Amino Acids, Vitamins, Minerals, Fibre/Fiber, Water & Anutrients, there wouldn't be much to eat. Also, there wouldn't be a source of chemical energy to generate heat energy & mechanical energy. That's what dietary carbohydrates & fats are for.

Respiratory Exchange Ratio/Respiratory Quotient (RER/RQ) varies with carbohydrate & fat intake, as the body preferentially oxidises the fuel that's most readily available.

RER/RQ varies with Exercise Intensity.
Low-intensity exercise results in mostly fats being oxidised.
High-intensity exercise results in mostly carbohydrates being oxidised.
Medium-intensity exercise results in a mixture of fats & carbohydrates being oxidised.

Friday, 25 July 2014

A *very* special dual-fuel car analogy for the human body that I just invented.

The human body is like a very special dual-fuel car.

In this very special dual-fuel car:-

Glucose is represented by Ethanol, 'cos Ethanol is a carbohydrate, according to Robert Lustig ;-)
Glucose is C6H12O6. Ethanol is C2H6O. 3(C2H6O) = C6H18O3. It's not very close, but it'll do!

Caprylic acid is represented by Octane, 'cos fatty acids are hydrocarbons, don'tcha know? ;-)
Caprylic acid is CH3(CH2)6COOH and Octane is CH3(CH2)6CH3, which is actually pretty close.

Storage depots:



For Ethanol, there's a large storage tank (≡ muscle glycogen) and a small storage tank (≡ liver glycogen). The contents of the large storage tank cannot be used to top-up the small storage tank, but the contents of the small storage tank can be used to top-up the large storage tank. The contents of the small storage tank are used to fuel a generator (≡ Hepatic Glucose Production) to keep the ECU (≡ brain) working at all times. The contents of the large storage tank are used to fuel the engine.


For Octane, there's a large storage tank (≡ subcutaneous adipose tissue) and a small storage tank (≡ visceral adipose tissue). The contents of the small storage tank are used to produce hormones etc. The contents of the large storage tank are used to fuel the engine.

Substrate Utilisation:

When the car is driven at low speed, the engine burns mostly Octane (≡ RQ=0.7).
When the car is rapidly accelerating or driven at high speed, the engine burns mostly Ethanol (≡ RQ=1).
When the car is being driven intermediately, the engine burns a mixture of Octane & Ethanol.




If the large Ethanol storage tank becomes full, excess Ethanol overspills to the small storage tank.
If the small storage tank becomes full, a gizmo kicks-in and converts excess Ethanol into Octane (≡ De-Novo Lipogenesis).
It also shifts fuel usage of the engine towards Ethanol, to deplete Ethanol as quickly as possible.
If the small storage tank becomes full, the car malfunctions (≡ fatty liver).

Conversely, if the small storage tank becomes nearly empty, it shifts fuel usage of the engine towards Octane, to conserve Ethanol.


If the large Octane storage tank becomes full, excess Octane overspills to the small storage tank.
If the small storage tank becomes full, the car malfunctions (≡ insulin resistance/metabolic syndrome/type 2 diabetes).

Monday, 21 July 2014

Ancel B. Keys' critique of "Diet and coronary thrombosis. Hypothesis and fact, by John Yudkin. The Lancet, 1957."

Ancel B. Keys has come in for a lot of flak recently over alleged "cherry-picking" of data for his 6/7 Countries studies. Here's Keys' critique:- "SUCROSE IN THE DIET AND CORONARY HEART DISEASE" of Dr. John Yudkin's "15 Countries" article.

Keys accuses Yudkin of bias, cherry-picking countries that fit his own hypothesis.

Here are some plots from Keys' 11 Countries article.
5-Year CHD cases/1,000 men vs Sucrose %E.

5-Year CHD cases/1,000 men vs Sat Fats %E.

Sucrose %E vs Sat Fats %E.

So there you have it.

Saturday, 19 July 2014

Diet and coronary thrombosis. Hypothesis and fact, by John Yudkin. The Lancet, 1957.

Twitter did it again. From
This looks like bad news for the fat-lovers.

There's good correlation between Coronary mortality and total fat intake, for countries 15 to 7. For countries 7 to 1, there's no correlation between Coronary mortality and total fat intake, suggesting that other differences (e.g. quality of health-care, social stress, antioxidant status etc) are significant factors.

This looks like bad news for the meat/fowl/fish/cheese/egg-lovers.

This looks like bad news for the sugar-lovers.

Of course, association ≠ causation.
This looks like bad news for rich people.

In conclusion, total fat intake, animal protein intake, sugar intake & annual income are all associated with increased Coronary mortality, over a certain range of values.

Thursday, 17 July 2014

Why do some people have trouble doing things in moderation?

This is related to my previous post.

Some people take low-carbing to an extreme, 'cos if reducing carbohydrate intake has benefits, reducing it to zero must be better. Oy!

We're told that eating 5 portions of fruit and vegetables a day is good for us. One patient who was admitted to St George's with malnutrition, had been eating more than 50 portions of fruit and vegetables a day, 'cos if 5 portions of fruit and vegetables a day is good for us, 50 portions of fruit and vegetables a day must be better. Oy!

People who are taking the anti-clotting medication Warfarin need to maintain an accurate balance between their warfarin dose and their Vitamin K intake to keep their INR between 2 and 3, as warfarin antagonizes vitamin K1 recycling, depleting active vitamin K1.
"Between 2003 and 2004, the UK Committee on Safety of Medicines received several reports of increased INR and risk of haemorrhage in people taking warfarin and cranberry juice. Data establishing a causal relationship is still lacking, and a 2006 review found no cases of this interaction reported to the FDA; nevertheless, several authors have recommended that both doctors and patients be made aware of its possibility. The mechanism behind the interaction is still unclear." Here's a clue...

From Possible interaction between warfarin and cranberry juice (emphasis, mine):-
"After a chest infection (treated with cefalexin), a man in his 70s had a poor appetite for two weeks and ate next to nothing, taking only cranberry juice as well as his regular drugs (digoxin, phenytoin, and Warfarin). Six weeks after starting cranberry juice he had been admitted to hospital with an INR (international normalised ratio) > 50. Before, his control of INR had been stable. He died of a gastrointestinal and pericardial haemorrhage. He had not taken any over the counter preparations or herbal medicines, and he had been taking his drugs correctly." Cranberry juice contains no Vitamin K. Oy!

"The Committee on Safety of Medicines has received seven other reports through the yellow card reporting scheme about a possible interaction between warfarin and cranberry juice leading to changes in INR or bleeding. In four cases, the increase in INR or bleeding after patients had drunk cranberry juice was less dramatic. In two cases, INR was generally unstable, and in another case INR decreased. Limited information is available about whether patients complied with their treatment in these cases.

Cranberry juice (Vaccinium macrocarpon) is popular and is also used to prevent cystitis. Interaction with warfarin is biologically plausible, because cranberry juice contains antioxidants, including flavonoids, which are known to inhibit cytochrome P450 enzymes, and warfarin is predominantly metabolised by P450 CYP2C9. The constituents of different brands of cranberry juice may vary, and this might affect their potential for interacting with drugs. Whether the constituents of cranberry juice inhibit CYP2C9 and therefore the metabolism of warfarin or interact in another way needs further investigation. Until then, patients taking warfarin would be prudent to limit their intake of this drink." Oy!

So, one man's inadvertent (his doctor should have warned him about eating next to nothing while taking warfarin) dietary extremism resulted in his own death and the restricted intake of cranberry juice for everybody else taking warfarin. Oy. :-(

P.S. It's about time an alternative to warfarin was found. It's difficult to maintain an accurate balance between warfarin dose and Vitamin K intake.

Wednesday, 16 July 2014

Jumping through hoops, and my Blog List.

I'm seeing a curious thing. The VLC "camp" seems to be "jumping through hoops" to prove a point.

From Neuron fuel and function (emphasis & formatting, mine):-
"Ketones and lactate do not drive reverse electron flow through complex I. Glucose can. Palmitate certainly can. What you want from a metabolic fuel depends on the remit of your cell types. Neurons within the brain preserve information by their continued existence.

This is best done by burning lactate or ketones. NOT glucose and, of course, not FFAs.

Anyone who claims that glucose is the preferred metabolic fuel of the brain has not though (sic) about what a neuron has to do and what an astrocyte actually does do. Or much about the electron transport chain."

Basically, glucose is bad mmm-kay. Also, anyone who claims that glucose is the preferred metabolic fuel of the brain is a dumb-ass. Damn our livers & kidneys churning out glucose! Are they trying to kill us?

∴ Carbohydrates are bad and must be avoided at all cost! This, of course, is utter nonsense.

Glucose can drive reverse electron flow through complex I. Can means that it's possible. Is it probable?

On a hypercaloric Western diet of excessive crap-in-a-bag/box/bottle, yes.

On a Kitavan diet of ~70%E from tubers, no.

On a diet of Basmati rice & beans, no.

On a diet of whole fruits, no.

See also Another crash and burn on low carb paleo and CrossFit. Enough of the 'carbs are evil' nonsense. Carbphobia is hurting a lot of people.

I have a list of blogs that I read on a regular basis. As a result of the bad science & cherry-picking displayed in various VLC blogs, I have deleted them from my Blog List.

See also Guest post: Denialism as Pseudoscientific Thinking.

Sunday, 13 July 2014

The "I'm a Celebrity... Get Me Out of Here! (losing team)" diet.

This post may be a little "tongue-in-cheek", in places.

I nearly used a certain scene from Blazing Saddles. It would have been much more entertaining.

As I said in Why you really can't outrun your fork:-
"Although I totally support the use of low-carbohydrate/calorie diets for people with insulin resistance or Type 2 diabetes, now that I'm no longer insulin resistant, I can eat natural carbohydrates without any problems.

A medium-sized (orange-fleshed) Sweet Potato takes only 4 minutes to bake in its jacket in a 700W microwave oven. The flesh is moist & sweet, unlike that of a Yam or potato.

I eat the whole thing, including the jacket. It's very filling and I'm still able to lose weight. For active and insulin sensitive people, a Kitavan-style diet is absolutely fine."

In the TV series "I'm a Celebrity... Get Me Out of Here!", there are two teams at the beginning. Members of each team compete against each other, to win food for their respective teams. The winning team gets to eat all sorts of exciting animal produce from "down-under". The losing team gets to eat rice & beans.

By the end of the series, team members (especially the over-fat celebrities) had lost a lot of body-fat. Coincidence? I think not. Combining Long-grain Rice with Beans (set Serving size: to 100g) provides all the Essential Amino Acids and is very filling. How do I know this? Guess!

I never used to like rice (it was always cooked "a l'anglaise"), but adding a squirt of Sweet Chilli Sauce to Basmati rice before cooking, makes it taste great!

Friday, 11 July 2014

Nutritional Ketosis: What is it good for?

I have a video in mind...

Having previously shown you what I look like on a diet of ~125g/day low-GL carbohydrates, here are a couple of recent pictures of Jimmy Moore, who's on a very-low-carb, very-high-fat diet (~85%E from fats), a.k.a. Nutritional Ketosis. It involves adding Kerrygold butter to just about everything, even eating sticks of it from a block. I'm not kidding.
I told you I wasn't kidding.

From Google Image Search on "Jimmy Moore" OR "Livin la Vida low carb", images in the last 7 days:-
On 6.7.14.

On 8.7.14.

The only recent footage of Fredrick Hahn, is the following video from the Low Carb Cruise...

To my eyes, Nutritional Ketosis is good for absolutely nothing. Dietary fat can be stored as body fat, in the absence of dietary carbohydrates. Gary Taubes' claim "You can basically exercise as much gluttony as you want, as long as you're eating (only) fat and protein." is pure fantasy, not supported by evidence.

The low protein intake in Nutritional Ketosis, combined with the high serum cortisol that's almost inevitable on this way of eating, results in a loss of muscle mass. I give Nutritional Ketosis a thumbs-down.


1) No Energy DeficitNo Weight Loss. There is no Metabolic Advantage to Nutritional Ketosis. See

2) Insufficient carbohydrate intake and insufficient protein intake starves the liver & kidneys of gluconeogenic pre-cursors, which raises cortisol, which converts muscle mass into gluconeogenic pre-cursors e.g. Glutamine, Alanine etc. This is standard Biochemistry. No links required.

3) While excess carbohydrates are converted into triglycerides by the liver, excess fats are converted into cholesterol by the liver, which is exported to tissues as LDL-C.

LDL-P ∝ LDL-C. High LDL-P is strongly associated with increased risk factor for CHD. See

CHD is not an inflammation-mediated phenomenon. It's an LDL-P and neovascularisation-mediated phenomenon. See

Postprandial lipaemia is atherogenic. See Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

4) Read Page 10 of, starting from "Could such a cream meal precipitate an angina attack because the oxygen-carrying capacity of the blood is lowered?" It's an actual trial on humans with clogged coronary arteries. It's not a hypothesis.

5) Chronically-raised cortisol causes aggressive behaviour (cortisol is a stress hormone) and adversely affects short-term memory storage in the Hippocampus. See

6) Eskimos, Sami, Masai, Samburu, Tokelauans etc, get ~50% of their total energy from fats. There are zero populations that get ≥80%E from fats.

Update 25th July 2014: I appear to have rustled Fredrick Hahn's Jimmies. See

I can safely state that Fredrick Hahn is a liar (I am not poking fun at anybody and I have only blocked him (not his followers) from posting here, for a flagrant breach of my Moderation Policy on his first attempt at commenting), and intellectually-dishonest (for repeatedly mis-quoting me, and using other logical fallacies). He posted the above post knowing that, as I had blocked him on Facebook, I wouldn't see it. I only learned of its existence after a friend PM'ed me on Facebook Messenger. He instructed his "followers" to leave comments here and then accuse me of lying about white-listing, back on his page, because their comments didn't appear immediately. He's a real piece of work! From ABOUT ME:-

Moderation Policy: Comments from first-time & untrusted commenters are moderated ← (click for details). Please be patient. Now that I have a Smart Phone, I can publish your comments during the day when I'm away from my lap-top, but I prefer to type replies on my lap-top. Comments from anonymous commenters, containing links in any form, are deleted.

This is a function of Disqus, as it's impossible to retrospectively white-list a commenter who's never commented here before. There appears to be a severe lack of cognitive function in these people. I really can't think why that is ;-)

Why am I being so hard on Jimmy Moore and Fredrick Hahn? I don't know these people personally.

1) These people are making money out of peddling pseudoscience.

2) These people meet all the criteria in Guest post: Science versus Pseudoscience and have created an alternative science, where sky-high LDL cholesterol, sky-high LDL-P and sky-high postprandial TG's are not risk factors for CHD, but are either harmless or beneficial.

Thursday, 10 July 2014

Only me! You don't want to be doing logical fallacies like that!

There can be only one video...

Here's only me on 9.7.14, at the Trafalgar Inn Aldershot, just before karaoke.
Only me! 9.7.14.

EDIT: And here's only me on 10.7.14, at the Lion Brewery Ash, just before the jam session.
Only me! 10.7.14.

From Here are the results after one month on my high fat, lower protein, SAME carbohydrate intake:-

Fredrick Hahn said...
"I've said this to Nigel before Tom Traynor and he insists he doesn't want muscles.

But to be fair to Nigel, he can indeed be 100% correct and at the same time be a blubbery, weak, mess of a man. You can be a great lung cancer doctor and smoke..."

Tom Traynor said...
"NK LOOKS terrible!--soft, fat and weak--and drum roll: "Doesn't want any muscle". So he is an absolute FOOL, too (loss of muscle mass predicting mortality--among MANY other facets). That's all the "science" I need."

What I actually wrote:-
Nigel Kinbrum said...
"Considering my age (59.25), I'm in pretty good condition. I'm 6' tall and weigh 198lbs. I have *no* desire to have big muscles or a 6-pack. Each to their own."

Misquoting, or quoting out of context is a Straw man fallacy. Saying that a physical characteristic invalidates knowledge is an Ad Hominem fallacy. In addition, saying that a lack of relevant qualifications invalidates knowledge is an inverse Argument from authority fallacy. Repeated use of logical fallacies is intellectual dishonesty.

Wednesday, 9 July 2014

Why you really can't outrun your fork.

Hat-tip to Yoni Freedhoff.

See Effect of school-based physical activity interventions on body mass index in children: a meta-analysis.
"Meta-analysis showed that BMI did not improve with physical activity interventions (weighted mean difference -0.05 kg/m2, 95% confidence interval -0.19 to 0.10). We found no consistent changes in other measures of body composition."

Some people believe that if going to the gym isn't making them lose weight, they're not exercising hard enough. Chronically over-exercising can chronically raise serum cortisol, which makes the kidneys retain water, causing a stall in weight-loss, as well as causing raised fasting blood glucose, irritability, poor memory and a slower metabolic rate, due to the reduced conversion of thyroxine into tri-iodothyronine.

Don't over-exercise!

A healthy body weight is made in the kitchen, not the gym. Buy produce, cook it and eat it!

Although I totally support the use of low-carbohydrate/calorie diets for people with insulin resistance or Type 2 diabetes, now that I'm no longer insulin resistant, I can eat natural carbohydrates, without any problems.

A medium-sized (orange-fleshed) Sweet Potato takes only 4 minutes to bake in its jacket in a 700W microwave oven. The flesh is moist & sweet, unlike that of a Yam or potato.

I eat the whole thing, including the jacket. It's very filling and I'm still able to lose weight. For active and insulin sensitive people, a Kitavan-style diet is absolutely fine.

Monday, 7 July 2014

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).

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.

Sunday, 6 July 2014

Metabolic rate, diet efficiency and thermodynamics.

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

This post is based on 
"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 ATPADP + 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.

Saturday, 5 July 2014

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.

Friday, 4 July 2014

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

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.