How we lose weight: Oxidation of carbohydrate & fat in the body.

1. Oxidation of Carbohydrate in the body.

Glucose is C6H12O6, or 6(CH2O)

6(CH2O)+ 6(O2) → 6(CO2) + 6(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 6 molecules of Oxygen produce 6 molecules of Carbon Dioxide, the Respiratory Exchange Ratio (RER) is 6/6 = 1

Converting molecular weights into their gram equivalents, 180g of Glucose combines with 192g of Oxygen to produce 264g of Carbon Dioxide plus 108g of water plus ~3,012kJ of energy. I'm using kJ rather than kcal, as the human body expends energy as mechanical energy (force x distance) and heat energy.

2. Oxidation of Fat in the body.

Fat is three fatty acids (Stearic Acid, say) attached to a Glycerol backbone. As ~95% of the energy released from a fat is from the three fatty acids, I'm ignoring the Glycerol backbone, to keep the maths as easy as possible.  Stearic Acid is CH3(CH2)16COOH. I'm approximating it to 18(CH2), to keep the maths as easy as possible.

54(CH2) + 81(O2) → 54(CO2) + 54(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 81 molecules of Oxygen produce 54 molecules of Carbon Dioxide, the RER is 54/81 = 0.67

Note: The RER for fats is actually 0.7, as the Glycerol backbone is converted into Glucose by the liver. As the RER for  Glucose is 1, this raises the RER of my approximated fat by ~5%.

Converting molecular weights into their gram equivalents, 756g of approximated fat combines with 2,592g of Oxygen to produce 2,376g of Carbon Dioxide plus 972g of water plus ~28,468kJ of energy.

We lose weight by breathing, weeing, pooing, sweating etc. See also Majority of weight loss occurs 'via breathing'.

This doesn't invalidate Energy Balance, as the kcal/kJ values for foods merely represents the amount of chemical energy that can be released by oxidation of the various fuels in the foods. See Why Calories count (where weight change is concerned).

We gain weight by consuming fuels & water.

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.

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.

Metabolic Inflexibility: What it really means.

Here's a picture from Metabolic Flexibility and Insulin Resistance.

The Metabolically-Inflexible (MI) & Insulin Resistance

Here's another picture.

Fig 2. ● = Metabolically-Flexible (MF). ○ = Metabolically-Inflexible (MI).

Salient points:
1) Excess serum FFA a.k.a. NEFA is bad.
2) Respiratory Quotient (RQ) a.k.a. Respiratory Exchange Ratio (RER) changes due to dietary changes are more sluggish in the MI than in the MF.
3) Under Insulin Clamp conditions, RQ/RER is lower in the MI than in the MF, due to impairment of glucose oxidation and non-oxidative glucose disposal.

I have posted this because of Danny Roddy's post Is Supplemental Magnesium A Surrogate For Thyroid Hormone? , which leads onto A Bioenergetic View of High-Fat Diets.

In the first article, Danny Roddy writes:-
"Additionally, taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient (e.g., high-fat diet, light deficiency, excessive exercise) seems pretty silly. For example, as a rule, diabetics have a reduced respiratory quotient (Simonson DC, et al. 1988), tend to have higher levels of free fatty acids or NEFA (Kahn SE, 2006), and are often deficient in magnesium (De Valk HW, 1999)."

The second sentence (diabetics have a reduced respiratory quotient...and are often deficient in magnesium) seems to contradict the first sentence (...taking magnesium while actively engaging in a diet or lifestyle that reduces the respiratory quotient seems pretty silly).

Simonson DC, et al. 1988 is Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin-dependent) diabetic patients.
"In conclusion, during the postabsorptive state and under conditions of euglycaemic hyperinsulinaemia, impairment of glucose oxidation and non-oxidative glucose disposal both contribute to the insulin resistance observed in normal weight Type 2 diabetic patients. Since lipid oxidation was normal in this group of diabetic patients, excessive non-esterified fatty acid oxidation cannot explain the defects in glucose disposal."

Impaired glucose oxidation with normal lipid oxidation lowers RQ/RER. Therefore, lower RQ/RER must be bad, right? Wrong. From the above study:-
"...euglycaemic insulin clamp studies were performed..."
Remember Salient point 3)? Simonson DC, et al. 1988 is an insulin clamp study, the results of which don't apply to free-living people (who aren't insulin clamped).

See also Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. RER/RQ increases & decreases with increases & decreases in exercise intensity. This is Metabolic Flexibility (MF). Sorry, Danny.