Why you really can't outrun your fork.

Hat-tip to Yoni Freedhoff.

From https://www.blacksheepfitness.co.uk/you-cant-outrun-your-fork.html

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.

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.

Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

Serendipity strikes again!

The tipping point and the metabolic syndrome.

The picture that I used for the last post came from Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

Fascinating stuff!

Adipocyte Hyperplasia - Good or Bad?

The answer is "It depends!".

The above plot is from Fig. 4 of Cytokine-mediated modulation of leptin and adiponectin secretion during in vitro adipogenesis: Evidence that tumor necrosis factor-α- and interleukin-1β-treated human preadipocytes are potent leptin producers and shows that leptin secretion from adipocytes increases non-linearly with increasing culture period.

As adipocytes fill, there's insignificant leptin secretion up to a certain level of fullness. Above that level of fullness, leptin secretion increases non-linearly. What this means is that reducing adipocyte fullness by x% reduces leptin secretion by more than x%.

If adipocytes become full due to a chronic caloric excess, there are two possibilities.

1a: If there is continued caloric excess, no preadipocytes are converted into adipocytes. There is no additional storage capacity available for excess nutrients, so they remain in circulation. T2DM has developed = bad.

1b: If there is subsequent caloric deficit, adipocytes start to deplete, storage capacity becomes available and T2DM goes away (if beta cells haven't been destroyed). The low number of fairly full adipocytes secrete sufficient leptin, so metabolic rate is high and hunger is low = good.
EDIT: This is the principle behind the DiRECT protocol.

2a: If there is continued caloric excess, pre-adipocytes are converted into adipocytes. This is adipocyte hyperplasia. There is additional storage capacity available for excess nutrients, so T2DM doesn't develop = good.

2b: If there is subsequent caloric deficit, adipocytes start to deplete. However, there are more adipocytes than in 1b, so for a given fat mass, adipocytes are less full than in 1b. The higher number of less full adipocytes secrete less leptin than in 1b, so metabolic rate is lower and hunger is higher than in 1b = bad.

Adipocyte hyperplasia is good for preventing T2DM as fat mass increases, but bad for metabolic rate and hunger after subsequent fat mass loss. Children are growing, so have adipocyte hyperplasia. Adults aren't growing, so have less/no adipocyte hyperplasia. Therefore, adipocyte hyperplasia during childhood will result in some protection from developing T2DM, but life-long misery due to increased hunger and reduced metabolic rate after subsequent fat mass loss. This is why I believe that children need to be protected from the persuasive marketing of manufacturers of CIAB (Crap-in-a-Bag/Box/Bottle).

See Beradinelli-Seip Syndrome – stick that in your pipe and smoke it and read the comments to see why adults with insufficient adipocytes are highly likely to develop T2DM. This is why Asians who remain skinny in childhood (so have no adipocyte hyperplasia) have a high risk of developing T2DM. Sumo wrestlers are Asians who become fat in childhood (so they have a lot of adipocyte hyperplasia) so they have a lower risk of developing T2DM.

According to Adipocyte Turnover: Relevance to Human Adipose Tissue Morphology:-
"Occurrence of hyperplasia (negative morphology value) or hypertrophy (positive morphology value) was independent of sex and body weight but correlated with fasting plasma insulin levels and insulin sensitivity, independent of adipocyte volume (β-coefficient = 0.3, P < 0.0001). Total adipocyte number and morphology were negatively related (r = −0.66); i.e., the total adipocyte number was greatest in pronounced hyperplasia and smallest in pronounced hypertrophy. The absolute number of new adipocytes generated each year was 70% lower (P < 0.001) in hypertrophy than in hyperplasia, and individual values for adipocyte generation and morphology were strongly related (r = 0.7, P < 0.001). The relative death rate (∼10% per year) or mean age of adipocytes (∼10 years) was not correlated with morphology."

If you want to remain slim, high fasting serum insulin due to hepatic and/or muscular insulin resistance and/or chronic overconsumption is bad.