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

From http://www.caloriegate.com/the-black-box/9-pictures-that-prove-beyond-a-reasonable-doubt-that-calories-dont-count

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

"Conclusion
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 E_out.

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 = E_in (corr for digestion) - E_out (BMR/RMR + TEF + TEA + SPA/NEAT)
__BMR/RMR & TEA ∝ weight
∴ ↑ weight → ↑ E_out
__If E_in = constant, ↑ E_out → ↓ (E_in - E_out) → ↓ 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 http://www.fuelforthought.co/the-ketogenic-diet-uses-in-epilepsy-and-other-neurologic-illnesses-2/

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.

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

Another Bookmarking post.

From http://dgeneralist.blogspot.co.uk/2013/11/the-low-carb-high-fat-diet.html

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 misleading. Siri-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.

Some thoughts on the essentiality of dietary carbohydrates.

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

From https://svpply.com/item/3229602/Swatch_Skin_Collection_Silver_Essentiality

This is a book-marking post for thoughts I had in https://www.facebook.com/TheFatEmperor/posts/1442430506020812.

"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 http://nigeepoo.blogspot.co.uk/2012/04/how-eating-sugar-starch-can-lower-your.html

2) It's not enough to fuel high-intensity exercise. See http://nigeepoo.blogspot.co.uk/2011/02/funny-turns-what-they-arent-and-what.html

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.

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.

From http://www.aa1car.com/library/alternative_fuels.htm

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:

 

Carbohydrates:

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.

Fats:

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.

Overeating/Undereating:

 

Carbohydrates:

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.

Fats:

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).

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.

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

Twitter did it again. From http://www.abc.net.au/catalyst/heartofthematter/download/Yudkinssugartheory.pdf

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.