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Saturday, 23 November 2013

The 'CRaP' Hypothesis




What is the most important principle of weight gain?
It’s calories isn’t it? It’s what the whole weight loss industry is based around. It’s all about avoiding calories to reduce the amount of energy going in. After all it makes sense, if you reduce the amount of energy in and maintain or increase the amount of energy out then you will reduce the amount of energy stored.
In the body stored energy is largely fat, but there are other stores of energy. Your whole body is combustible fuel, your bones can be digested and so can your brain!

In this seminar I will present my argument that calorie reduction is not the most important consideration for weight/fat loss

This is one of the most basic laws of physics. As far as we know it is true and it applies to everything in the universe, even the body. I don’t disagree with this at all. I would be extremely stupid if I did.
I don’t apply Heisenburg’s uncertainty principle to my lunch when I’m aiming my cutlery, and in the same way I don’t apply the first law of thermodynamics to weight loss. 

Here’s what happens.
Crap theory doesn’t take into account any unconscious regulation. It assumes that the only way you can become overweight is either sloth and gluttony (or a combination of both). It doesn’t acknowledge hormonal influences, gut health, illness, or your resting metabolic rate

Up until recently, type 1 and type 2 diabetes were seen as distinct entities. It was understood that type 1 diabetes (or insulin-dependent diabetes) was caused by autoimmune destruction of the beta cells of the pancreas, leading to decreased insulin production, whereas type 2 diabetes was caused by insulin resistance of the liver, muscle and fat cells.
However, recent research has demonstrated that the line separating these two conditions may be much blurrier than previously thought. It is now known that type 1 diabetes, which normally begins in childhood, may slowly develop later in life. This form is referred to as latent autoimmune diabetes (LADA) or more informally as type 1.5 diabetes.

Let’s start from the top, what actually is metabolic disease
Metabolic diseases is a lifestyle disease, which is caused predominantly by the lifestyle you lead. It’s all that’s left when you take away the threat of bacteria and viruses as a cause of death. It is the final hurdle to living healthily until the end of your life, and dying a ‘natural death’.

The treatment in most cases is to reduce the calories and the fat, because it follows logically that if you want to reduce the amount of fat in your body you should reduce the amount of fat that you put in. This approach has clearly been a dismal failure.
Diabetes is not a simple maths equation do to overexposure to sugars
Diabetes can be reversed
Normal is not healthy
You can still get all metabolic diseases if you are not obese

Up until relatively recently, fat was considered an inert tissue with no biological activity. The idea was that it was just, well, there. It didn’t do much other than store excess energy.
We now know, however, that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. The metabolic activity of fat is the key to understanding its role in diabesity.

Up until relatively recently, fat was considered an inert tissue with no biological activity. The idea was that it was just, well, there. It didn’t do much other than store excess energy.
We now know, however, that fat tissue is a metabolically active endocrine organ that secretes hormones and inflammatory cytokines such as IL-6 and TNF-α. The metabolic activity of fat is the key to understanding its role in diabesity.

In healthy people, FFAs are burned in the mitochondria soon after release (lipolysis) from storage forms of fat (triglycerides and phospholipids). But in the diabese, inflammation, leptin resistance and oxidative damage impair the mitochondria’s ability to burn fats. The excess FFAs then “spill over” into non-fat tissue like the liver, pancreas and skeletal muscles. FFAs damage these metabolically active tissues because they don’t belong there. This is called lipotoxicity. Lipotoxicity has been shown in several studies to cause insulin resistance and increase the risk of T2DM.

I don’t disagree with this at all. I would be extremely stupid if I did but it requires a few assumptions to practically apply to obesity:
1.Q and W must be independent
In practice q affects w. If you eat more food then your energy expenditure will increase.
2. W must be a single form of work. In practice W is EAT and NEAT.
In practice NEAT affects EAT and vice versa. If Q stays the same and EAT increases then NEAT will decrease to adjust.
3. A calorie is a calorie: Q affects W depending on macros. Protein requires more NEAT than carbs and fat.
4. ΔU is unregulated

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