Originally Posted by Valtor

I'll start with a proper definition of the energy balance equation observed and tested in humans.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2764961/

Originally Posted by M Levac

Actually, I believe that the very act of eating food will make this activity monotonous. I believe the monotony is an effect, not a cause. Just like I believe overeating is an effect, not a cause. Yet at the same time, I believe that the act of eating when hungry will make this activity a most pleasurable experience. Until we are sated at least.

I believe that only food can satiate. Thus, if we eat something that does not satiate, it's not food. I also believe that there are substances that are obviously not food, like drugs for example, that cause us to overeat. Bodybuilders for example use a drug called equipoise to make them overeat like there's no tomorrow during a bulking phase. Here it's obvious that overeating is an effect yet paradoxically the same group of people believe that overeating causes obesity. In fact, that's the very reason they use this drug: The drug makes them overeat, this overeating makes them grow bigger. Not for one second did they ever consider that the drug could make them overeat by creating a caloric deficit internally.

I believe that our behavior is dictated by our cells, rather by the collectivity of all our cells. I believe that cells will open and close receptors according to food status in a negative feedback loop fashion. Like this, when there's enough food, receptors are open or the signal is present, eating stops. When there's not enough food, the receptors are closed or the signal is absent, eating continues. The point is that our behavior is an effect, not a cause.

If we can modify the behavior of this receptor or signal, then we can affect eating behavior without actually changing the amount of food. Indeed, a similar concept is the basis for drugs like sibutramine. Sibutramine is said to reduce pleasure from eating. If satiety is the reduction of pleasure from eating, then reducing pleasure from eating directly through sibutramine would simulate satiety and we should stop eating. Never mind that before we cease to obtain pleasure from our food, we obtain a boatload of pleasure in response to the hunger which drives this pleasure in the first place. It's obvious from my point of view that something in what we eat causes the receptors to fail or ultimately the signal to fail thus causes eating to continue without regard for internal food status. Some talk about leptin, others talk about ghrelin. I'm just talking about the generic concept of food, hunger and satiety.

Originally Posted by Valtor

Thank you for the clarification.

Now then, what should we make of people living their entire lives on rice and a bit of fish meat without obesity? Are they hungry all the time because they live on a high-carb diet? And they just tough it out because they have no choice?

OR

If they are not hungry all the time and fine with their diet it means that they are eating food, but then would you say it is food for them but maybe not for you?

Originally Posted by M Levac

I don't know. Maybe they're not fat because they've been starved their whole life since conception. Yet when we take this same population and switch their diet to ours, they grow just as fat just as quickly. Is it because they now eat more or is it because their previous diet was more nutritious than their new diet, as ours is now that we cut out the boatload of carbs we used to eat?

I don't know whether they are hungry all the time or not. Maybe they are, who knows. However, once they switch to our conventional diet, the same one that made us fat, they grow just as fat. Maybe they eat more, if they do, then maybe it's because they grow more hungry. Come to think of it, maybe that's why we eat more. Then when we cut out carbs, we end up eating less. Maybe we eat less because we're less hungry. Maybe we're less hungry because our diet is now more nutritious.

Originally Posted by Valtor

Now then, what should we make of people living their entire lives on rice and a bit of fish meat without obesity? Are they hungry all the time because they live on a high-carb diet? And they just tough it out because they have no choice?

Originally Posted by ubizmo

No, because many do have a choice, but still eat this way and do not become obese. There are many first-generation Asian-Americans who live here, where they can easily obtain huge amounts of rice, fish, and everything else, who still eat mostly rice and vegetables and a little fish or pork, and who do not become obese.

Even in the US, there have been plenty of carbohydrates available to everybody for much longer than the current epidemic of obesity. I just don't think a case can be made that the rise in obesity of the past 40 years is due to increased availability of carbs.

My guess is that the underlying phenomenon is hepatic insulin resistance initially caused by consumption of fructose and PUFA. Once this occurs, the ability to tolerate all carbs is severely compromised. Leptin resistance is probably also a factor, also caused by fructose overload, if Dr. Lustig is to be believed.

If fructose and PUFA cause a condition which can only be controlled by sharply restricting all carbs, it's easy to see why all carbs would be thought to be the cause in the first place.

Ubizmo

Originally Posted by Valtor

Actually, I prefer the hypothesis shown in this paper here.

http://www.ncbi.nlm.nih.gov/pubmed/20223680

In the full text it shows good evidence that an excess of any food results in insulin resistance. And then once insulin resistance sets in, you are in trouble even if you start reducing your intake of food. It then takes more than just less calories to fix the problem (if it's fixable).

Originally Posted by Mirrorball

The fructose hypothesis is getting stronger every day, and as Ubizmo says, it actually supports the conclusions in the Gluttony and sloth paper. Insulin resistance in the liver also turns the liver into a super glucose factory, which explains high blood sugar and insulin spikes better than the carbohydrate hypothesis IMO. I've just found this other article via Paleohacks:
http://www.ncbi.nlm.nih.gov/pmc/art...25/?tool=pubmed
I'm having a good time reading it.

Originally Posted by Nancy LC

Wow, that paper was really good. I'm going to start taking some Vit. C and see if it helps my IR.

Originally Posted by Valtor

Also, it is known that a ketogenic diet helps in repairing your mitochondria. But what has also been shown is that staying on a ketogenic diet for too long also has deleterious effects on metabolism.

I don't know about you, but I see a dilemma here. That is why I now take the road of moderation in all things.