Monday, 28 January 2013

On burning, storing and recomposing.


I couldn't resist!

On my adventures around the interwebs, I've noticed the following:- "Humans aren't Calorimeters. Therefore calories are irrelevant to humans." While I agree with the first sentence, I don't agree with the second one.

Calorimeters burn (oxidise) foods at high temperatures with a flame using oxygen, which produces carbon dioxide, water (depending on what's being burned) & heat energy.

Humans burn (oxidise) foods at 37ºC with enzymes , charge transporters etc using oxygen, which produces carbon dioxide, water (depending on what's being burned), mechanical energy & heat energy.

As both oxygen & carbon dioxide are gases, these can be measured by a respiratory gas analyser, to establish the rate of burning and what's being burned at any instant. See It's all in a day's work (as measured in Joules). When resting, burning occurs at a rate of ~1kcal/minute and, as it's measured while fasted, ~0.11g/min of fat is burned, & ~0.01g/min of carbohydrate is burned. Also note that a lot of mechanical energy can be produced, which can increase the rate of burning by a factor of seventeen.

In conclusion, humans burn (oxidise) foods, though not with a flame, and they can produce mechanical energy in addition to heat energy. The rate of burning and what's being burned at any instant can be measured.


When we eat food, it's digested and absorbed. As a digested meal is absorbed, it appears in the blood as glucose, triglycerides & amino acids. These then disappear from the blood due to burning and storage. See Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism.

Figure 1 shows the effects of a 100g Oral Glucose load or a 40g Oral Fat load on blood glucose level over a period of 360 minutes. Note that subjects are resting during the 360 minutes. As the 100g Oral Glucose load produces a large insulin response (See Figure 2), fat-burning temporarily stops. Therefore, the ~1kcal/minute resting burning rate is derived 100% from carbohydrate. Therefore, the carbohydrate-burning rate is ~0.25g/min. At this rate, it would take ~400 minutes to burn 100g of glucose. However, it actually takes ~180 minutes for blood glucose level to fall from maximum to minimum. Therefore, some of the glucose from the Oral Glucose load is stored (mostly as glycogen in muscles and liver).

Figure 3B shows the effects of a 100g Oral Glucose load or a 40g Oral Fat load on blood triglyceride (fat) level over a period of 360 minutes. Note that subjects are resting during the 360 minutes. As the 40g Oral Fat load produces no significant insulin response (See Figure 2), fat-burning is unaffected. Therefore, the fat-burning rate is ~0.11g/min. At this rate, it would take ~364 minutes to burn 40g of fat. However, it actually takes 180 to 240 minutes for blood triglyceride (fat) level to fall from maximum to minimum. Therefore, some of the fat from the Oral Fat load is stored (as fat in adipocytes), even though there is no significant insulin response.

Therefore there are times when stuff is stored (anabolism) and there are times when stuff is withdrawn from stores (catabolism). If more stuff is stored than is withdrawn over a period of time, weight goes up, and vice-versa.


After doing intense exercise e.g. sprinting, resistance training with weights etc, muscles become very sensitive to insulin. Therefore, if intense exercise is done just before stuff is stored, amino acids & glucose are preferentially stored in muscles rather than adipocytes. This increases muscle mass relative to fat mass.

If non-intense exercise is done at times when stuff is withdrawn from stores, this maximises the amount of fat withdrawn from adipocytes and minimises the amount of amino acids withdrawn from muscles. This decreases fat mass relative to muscle mass.

It's therefore possible to increase muscle mass at certain times and decrease fat mass at other times, while keeping overall mass relatively constant i.e. it's possible to gain muscle and lose body-fat without being in an overall caloric deficit. See Body Recomposition.

Wednesday, 23 January 2013

Not exactly rocket science, is it?

If Paul (astrophysicist) Jaminet met Jack (neurosurgeon) Kruse ;-)

The paleo diet was recently ridiculed as a food fad in Natural’s Not In It. It also came last in a US News Best Diets survey.

Ways of eating such as very-low-carbohydrate, low-carbohydrate, low-reward, paleo, primal, ancestral, just eat real food etc discourage the consumption of manufactured food products and encourage the consumption of produce. If a large percentage of the population stop filling their shopping baskets with manufactured food products and start filling them with produce, who suffers? Not exactly...

This is why the food manufacturing industry tries to ensure that the population gets the best nutritional and dietetic advice that money can buy. See also New study: Big Food’s ties to Registered Dietitians.

While libertarians and anarchists moan about freedom from government interference, the food manufacturing industry has the freedom to crap all over the aforementioned diets and influence people to buy manufactured food products. Morbidity is also very profitable for healthcare and drug companies.

I think that I've now flogged this particular horse to death!

Monday, 7 January 2013

It’s the Calories, Stupid.

I thought I'd mark my return to blogging by taking the piss out of a certain Diet Doctor for his post It’s the Insulin, Stupid, who takes (and tweaks) Fig 7A from Hyperinsulinemia Drives Diet-Induced Obesity Independently of Brain Insulin Production.

At first glance, Fig 7A looks like a CIH believer's dream come true (apart from the words "High Fat Diet").

Hyperinsulinemia → Obesity.

Obesity is caused by too much insulin. Game, Set and Match to insulin.

Not so fast! Let's take a look at the rest of Fig 7.

Figure 7. Revisiting the Current Model of Obesity and Type 2 Diabetes(A) The most widely accepted model of the pathogenesis of obesity and type 2 diabetes posits that a high-fat diet leads to obesity and insulin resistance (there is debate about the relative order and causality of these). In this widely held view, insulin resistance then leads to hyperinsulinemia, which is followed by β cell exhaustion, and then type 2 diabetes. The accepted model is incompatible with our results that put the insulin hypersecretion genetically upstream of obesity.(B) Our data support a model whereby insulin levels must be kept low to maintain energy expenditure in white adipose tissue via the expression of Ucp1. Our data do not address the order of subsequent events after obesity (outside the yellow box), such as insulin resistance and/or type 2 diabetes, since they were not observed in our studies. In other words, the effects of insulin gene dosage on obesity are independent of sustained changes in glucose homeostasis or insulin resistance.

↑ Peripheral Hyperinsulinemia → ↓ Uncoupling Proteins (WAT) → ↓ Energy Expenditure → ↑ Obesity.

Obesity is caused by a reduction in energy expenditure in these mice. Game, Set and Match to The Energy Balance Equation. It’s the Calories, Stupid. In these mice, energy expenditure is strongly influenced by insulin levels. In humans, not a lot. In humans, insulin can act as a stimulant or a sedative.

I'm not an insulin denier as is obvious from my other blog posts. I'm still restricting my carbohydrate intake to ~125g/day from whole foods.

I'm not a food reward denier. I've been using food reward principles to lose even more weight.

This post will probably annoy some people. Before wasting your time writing a comment, please read my Moderation Policy.