How can the fat in the liver from the fructose conversion stay there when the body needs this energy?

It is my understanding that this only happens in humans when this fat is not needed (when calorie intake is higher then needed).

We've shown the problem is not overeating. So if that's not the problem, then the solution is not undereating. So the problem is not total calories. But since the problem could be fructose, it could be some calories. Yet it's not the caloric content of fructose that is the problem, it's the molecular structure of fructose that is the problem. Glucose doesn't act the same yet it contains the same amount of calories as fructose. Fat doesn't act the same as fructose yet it contains twice the calories as fructose. We can go on and on about all the caloric foods we eat. (Never mind the sub-debate about what food actually is for the moment) The point is that it's not total calories nor is it some calories. It's just not calories at all. It's the molecular structure of what we eat. Just like it's the molecular structure of the drugs we take (we also eat drugs yet we don't blame food, i.e. what we eat in this case) that is the problem, not how much calories these drugs contain (none).

That some of those problems contain calories is just incidental. Yet it seems to confuse a whole lot of people anyway.

Maybe fat is always leaving but there is so much fructose coming in constantly that fat accumulates anyway. I'm not sure.

Insulin resistance and the subsequent rise in plasma insulin and the subsequent inhibition of lipolysis from this rise in insulin. Remember James was kind enough to give us a lecture on this very point? As long as we eat fructose, we do all this which prevents the trigs in the liver from ever being released. Yet when glucose load drops in dependently but fructose intake remains the same, insulin secretion drops as well, plasma insulin drops, and the inhibition drops as well allowing a greater amount of lipolysis. Yet there's always the same pressure by fructose to produce just as much trigs in the first place. It's not the calories here either, it's the molecular structure of those foods that is to blame. Again, that these things contain calories is merely incidental.

Yeah, basically, it's the same argument about fat tissue and insulin. It's a shift toward greater fat accumulation even in the absence of greater intake. Jst substitute some calories from glucose to fructose and we create a different fuel distribution.

I'm unable to find even one paper (on humans) where this can happen without excess calorie intake.

If you guys can find one, let me know and I'll try to get the full text.

And how do you suppose this happens without excess calorie intake?

"different fuel distribution" sure, but no accumulation if it is needed.

How do you suppose it does not? Drugs and hormones don't contain calories yet they can make us fatter (or leaner as the case may be) directly without causing an increase in Ein or a drop in Eout. Drugs and hormones, like clenbuterol and growth hormone for example, act directly on fat tissue. Offhand, I don't know of a drug that acts on the liver to cause a similar effect as fructose or alcohol but the point is that the fact that fructose contains food calories has nothing to do with its action on the production of triglycerides in the liver: We could very well devise a drug that has the same effect yet contains zero calories.

Different distribution is exactly what happens when we put more fat in fat tissue to be stored than in lean tissue to be used for fuel. Shift the balance either way without an increase in Ein and we grow fatter or leaner without growing heavier. Yet we can still grow heavier as well simply because more fuel is locked in fat tissue and less is used up by lean tissue. As lean tissue has access to less fuel, it drops its fuel usage to maintain mass. As lean tissue maintains mass but fat tissue grows bigger, the entire systems grows heavier. All the while there is no increase in Ein nor a reduction in apparent activity level, i.e. they walk the same distance, climb the same amount of stairs, etc.

When lean people take the elevator, we call them opportunists. When fat people take the elevator, we call them lazy. Don't blame the elevator for the reduction in Eout. There is no reduction since a heavier system requires and spends more fuel as a matter of fact. This is all kosher with the First Law of Thermodynamics. Remember, it takes more energy to move a heavier mass. Even standing there in the elevator, the heavier man actually spends more fuel than the lighter man.

Like Taubes said, we all reach a caloric balance at some point. The trick is to figure out why some can do it on 3000 kcals while others must do it on 1500. That guy Haub, if he wants to maintain his new lower weight, he'll never be able to return to his previous caloric intake. Otherwise he'll just return to his previous weight as well. In other words, he's going to have to remain hungry for as long as he wants to maintain this new lower weight. Unless he figures out a way to reduce the hunger that invariably comes with a semi-starvation diet. It's never been done as far as I know. Maybe that's why most regain the weight.

I searched for "low-calorie high-fructose" on Google Search and haven't found anything so far. Unless we can find one, we won't know what happens when excess fructose is consumed without excess calorie intake.

New post by Chris Masterjohn: Is Insulin Resistance Really Making Us Fat?

The fat in the liver doesn't just come from fructose conversion, during the process of lipogenesis, the breakdown of fat in general decreases, and there's an increase in net storage of free fatty acids from the bloodstream as triglycerides in the liver. Fat balance in the liver doesn't have to march in step with fat balance in the body as a whole. Some foods, like alcohol and fructose, tend to be handled more by the liver, so it seems reasonable to suspect that a diet higher in these will "overfeed" the liver at a lower calorie intake than a diet that is lower in these. Not assume, just suspect.



I guess that would have to be an intervention study, it might be kind of hard to find free-living humans eating a diet high in fructose without excess calorie intake. At least large populations of them.

Do you have any studies showing a high-fructose diet in absence of excess calories is harmless to the liver?