> 1: Hmm, chronically high insulin levels is caused by chronically eating too much. Beef spikes insulin just as much as table sugar (http://ajcn.nutrition.org/content/66/5/1264.full.pdf#page=1&...). So I would say the problem of "chronically high insulin levels" is a problem of eating too much food, not too much sugar.

Yes, beef does have a high insulin response, but when total consumption is taken into account, and satiety, eating beef will have a lesser effect than eating jellybeans. Look at the insulin scores in the publication you cited. Those with the highest scores, as a group, are snacks and confectionaries, foods that are commonly eaten in Western countries. Some of the worst offenders in the groups tested are: beans, potatoes, white bread, jellybeans, etc. -- carbohydrates.

> 2: This is a hugely interesting area of thinking for me. Which fat though? White or brown adipose tissue? Brown fat is darker in colour due to it's huge cellular density of mitochondria when compared to white adipose tissue. It's essential fat-buringing fat, and plays a role in regulating temperature. It basically burns fat to warm us up when we're cold. This is why Michael Phelps can eat 10 million calories a day. 6 hours a day in water requires allocating a LOT of calories to maintain core body temp. We have learned SO much about fat tissue recently, but I don't think we have all the answers yet.

In this case we're talking almost exclusively about excess visceral fat, though the role of other fats in obesity and disease is, as you said, not fully known.

>> Let’s assume two things for the sake of argument. the sugar in A’s diet causes A to become insulin resistant. And second, insulin works to put fat in fat tissue.
> I would say both assumptions are fallacious. Eating @ TDEE means 100% of the food energy is used up, and fat cannot be made from nothing.

True, but activity level must be taken into account. Fat can't be made from nothing, but the patient could reduce his overall activity level as he becomes fatter, which would make excess calories available for storage as fat. In other words, we could have causality backwards: being lazy doesn't necessarily make you fat, but becoming fat could certainly make you lazy.

> Also, the "insulin works to put fat in fat tissue" is misleading at best and completely wrong at worst, depending on how you interpret it. Insulin works to move nutrients into cells. More insulin in the blood is a signal there is food calories available, so insulin also stops fat cells from releasing their fat. This makes total sense; why dip into your savings when you just got a fist full of cash?

If insulin stops fat cells from releasing fat, then wouldn't it make sense to keep insulin levels as low possible? That means reducing carbohydrate and protein intake, and increasing dietary fat consumption to compensate: in short, a low-carb, high-fat diet.

> The point where your body transitions towards fat storage is the point where your energy intake exceed energy expenditure; again just simply eating less solves this.

Does it though? Obese people have much higher concentrations of circulating leptin than the general population, and they can become leptin resistant. What happens if we tell these people to eat less, and move more? Chances are, they're going to become very hungry. I would argue that eating less isn't enough. They need to eat less insulinogenic foods, and compensate by increasing dietary fat to satiety.

> My statements are all for average healthy people. I totally agree metabolic-syndromes like diabetes should be treated differently. But the VAST majority of people are fat because they sustain consuming more energy than they use. The micro-variables like how stressed you are (and therefor how much cortisol hormone is present) matter, but nothing gets diet-induced hormones working as they should better (in healthy people) by just eating food-energy (whatever the macros) to match your activity over the long run.

Fair enough. That's the commonly held belief at least, but I disagree. I think we have an incomplete picture. However, I believe in the scientific method, so I'd really like to see clinical trials (not epidemiological studies) to fully test the hormone theory. As I said earlier, if it's wrong, then we haven't lost anything, and we've learned more about the role hormones play in obesity. If it's correct, then the impact on nutrition and obesity will be enormous. It's worth looking into.