I will add to this that I know one pathway which stores fat by boosting insulin's effect on fat cells. Which means that even at baseline insulin levels, an excess of energy could be stored. Of course, without insulin this pathway does not work. Hence why type 1 diabetics is not a good model, because non type 1 does have insulin in their blood.

So if you can get fatter without chronically high insulin levels, that pretty much disprove Taubes' carbohydrate hypothesis.

The key word here is cause and effect. The removal of insulin is the cause. The caloric deficit is the effect.

I don't understand what you mean by "there are no camps". You'll have to explain to me in detail because I don't see how it fits with all this. Is there another discussion about fat accumulation that doesn't talk about insulin, carbohydrate or calories? If so, please tell me because I'm seriously confused about that bit.

Simple. From what I can read in the comments section, you two are attributing different meanings to the same words. In other words, you are not talking the same language.

Valtor how do you understand Taubes' carbohydrate hypothesis?

I would have thought the hypothesis says insulin drives fat storage, whether or not insulin is chronically high. The crux is the hormonal milieu - whether fat is being stored or being released from storage - both of which are mediated by insulin.

The level of insulin at which fat is locked into storage is pretty low.

Now you'll really have to point out exactly which word each of us are using and what meaning we are attributing to that word. As far as I can see, he's using type 1 diabetics data to support his claims about satiety. I'm using the very same type 1 diabetics data to support my claim about fat accumulation. Indeed, even Krieger himself acknowledges everything I say about type 1 diabetics regarding emaciation and caloric deficit. Yet even then he refuses to acknowledge that this particular aspect of type 1 diabetics appear to refute his claims regarding obesity and overeating. Indeed, this is what he says about that:

If you haven't noticed yet, he himself is using one condition (type 1 diabetics and hyperphagia) and extrapolating that to a different condition (normal fat metabolism and satiety). How can he propose that it's fine if he does it but not when I do it?

Patrick, you know better than this. If you truly see a logical error or a semantic error or any kind of error, then you will point it out explicitly so we can all see what you mean and bring about the appropriate corrections. You wouldn't just claim it's there but then fail to point it out. Oh well I know it's wrong so there must a reason, but I just can't put my finger on it yet. Well you know what we call that, Patrick. Pulling at straws.

I know exactly how Krieger is wrong and I point it out repeatedly in detail.

Removal of insulin does not automatically result in a calorie deficit. The food that an uncontrolled type 1 eats may not be stored in fat cells, but these molecules (calories) are still in the body. An excess can have nefarious effects, since fat cells can't protect you anymore. The body tries to eliminate the excess the best it can. But ultimately, without insulin to help ferry proteins into your cells, you waste away.


It's not just about "insulin, carbohydrate or calories", it's about how the human body functions. So discussions about obesity must include the whole picture.

You can see how I understood it from my journal entry here.

http://forum.lowcarber.org/showpost...309&postcount=1

No here's how it works. The removal of insulin causes emaciation. There is no question about this fact. Emaciation is the result of a caloric deficit. There is no question about this fact either. Krieger himself agrees with this assessment. His own words:


The carbohydrate hypothesis is precisely about how the body works. Insulin is one of many hormones and the carbohydrate hypothesis explicitly acknowledges that there is more to it than just insulin. Indeed, the hypothesis acknowledges that there are a multitude of hormones all working in concert to regulate fat tissue, insulin merely being the primary hormone.

The opposing hypothesis says insulin is irrelevant (Krieger's own words here: Insulin is not required for fat storage), as well as every other biological mechanism we know of, and that obesity is all about calories. So when Krieger argues against insulin's own functions by using insulin's own functions (and pretty much every other biological mechanism he can think of), he unwittingly argues in favor of the carbohydrate hypothesis in spite of his claims to the contrary. Indeed, that's precisely what I've been pointing out this whole time with that bit about type 1 diabetics.

Another example of Krieger using one condition and extrapolating that to other conditions:

He's using one set of data and extrapolating it to prove a different set of data. It's fine when he does but when somebody else does it, this is what he says about it:

How many times do I have to point it out before you grok?

"The caloric deficit due to the removal of insulin is due to the massive excretion of glucose and ketones in the urine"

Martin, we are saying the same thing.

Like I said, your body will try to remove the extra molecules by other means since it can't shuttle them in fat cells. And since you can't keep energy in stores, you will end up in a deficit. If an uncontrolled type 1 could manage to eat enough food non stop to prevent a deficit, he would still not get fat but would probably die quickly from the buildup in his bloodstream that would exceed his body's capacity of removing it.


It comes down to this.
"...you are trying to take one condition (the effects of the complete absence of a hormone versus its presence), and are extrapolating that to a different condition (the effects of variation of a hormone within physiological levels). This is an erroneous extrapolation."

How do you think the following affects the carbs hypothesis? That an hormone is able, under a state of excess available energy, to boost insulin's effect on fat retention within fat cells.

EDIT: I just read your other post... #39

Look, why don't we start our own discussion. I'll start with a question. Do you believe we can grow fat by eating fat exclusively?

No, I don't.

Ah, thanks. I can see we do not agree on the basics (the thermodynamics). I think that model from physics is not a good one to use for human metabolism (the laws of thermodynamics are apply to closed systems and human metabolism isn't one of those). I am more impressed with the model outlined by John Berardi in his article "A New View of Energy Balance."

So, thanks for the clarification anyway.

Krieger told us that the removal of insulin (stop injections, no more insulin in the blood) causes hyperphagia. What he really told us is that the removal of insulin in the cells causes hyperphagia.

High insulin resistance is a feature of obesity. By causing an increase in insulin resistance, we cause a decrease in the amount of insulin that enters the cells. If the insulin production in the pancreas remains the same this will cause insulin in the blood to rise. Chronic hyperinsulinemia is also a feature of obesity.

If insulin resistance becomes so great that no insulin enters the cells, then the effect in the cells is equivalent to removing insulin in the blood. If it can't get in, it might as well not be there. If hyperphagia is a consequence of the absence of insulin in the cells, then extreme insulin resistance should also cause hyperphagia to the same degree.

Krieger says there is no linearity to insulin. Sometimes it's high but we still lose weight, sometimes it's low but we can't lose weight. The answer to this non-linearity is insulin resistance. Since the number of insulin receptors determine exactly how much insulin gets in, and since how much insulin in the cells determine what happens in the cells, then varying insulin resistance can both affect insulin in the blood and what happens in the cells. We can see how insulin in the blood can rise yet insulin in the cells can drop and this could reverse linearity such that our prediction based solely on insulin in the blood would be false.

If we want an accurate prediction model, we can't just look at insulin in the blood, we must also look at insulin resistance. Krieger only looks at insulin in the blood. Pfft, sometimes he doesn't even look at insulin in the blood like this last study he cited. The point is that Krieger is wrong because he does not have all the facts. And since he does not have all the facts, when we point out the errors he makes, he can't understand what he sees.

But don't let that deter you from believing him though.

By the way, here is how I apply thermodynamics to humans nowadays.

The Energy Balance Equation