----- "Geoffrey Purcell" <[log in to unmask]> wrote:
>
> Todd Moody is quite right re debunking most of william's notions - at the very least, William's absurd notions re Creationism are laughable at best. I only add that virtually all of the studies done on fructose are done on highly-refined fructose which makes those very studies completely meaningless when applied to raw fruits which contain UNrefined fructose.
I don't agree. I don't believe the studies are meaningless at all. Sucrose is a natural sugar that occurs in many fruits. It is 50% fructose. The only thing that refining does is to remove other substances. Fructose is fructose.
What's interesting to me about this is that, in low-carb circles, *glucose* has been the traditional villain. And so it may be, but it's also possible that it's more subtle than that. Yes, glucose goes into the blood, which triggers insulin release, in order to bring the BG back down. All that is normal and not pathological, but it becomes pathological when the BG *doesn't* go down, and inline *stays* elevated to keep trying to push it down. That's insulin resistance, and the question is: Why does it happen? The usual answer is that it's some sort of overuse syndrome. The insulin receptors become less sensitive, whatever. But more recent research suggests that at least one important mechanism of insulin resistance is non-alcoholic fatty liver disease (NAFLD), now being observed in epidemic proportions, and the main cause of NAFLD is fructose. (http://www.upi.com/Health_News/2009/03/04/Fructose-linked-to-insulin-resistance/UPI-72301236187265/) Although high-fructose corn syrup is singled out, there is no evidence that shows that HFCS is any worse than plain old sucrose, since they are almost chemically identical. If this theory is correct, it would mean that our difficulties in coping with glucose are mainly caused by the damage done by fructose.
The Eades' have a lot to say about this in their most recent book. Interestingly, one of the most potent treatments for NAFLD is...saturated fat! And polyunsaturated fat also appears to play a negative role, although not on the same scale as fructose. Moreover, Lustig points out that metabolically, the only difference between fructose and alcohol is that alcohol, but not fructose, gets into the brain. What happens in the liver is the same. I find all this quite exciting, and an interesting convergence of paleo principles and metabolic science.
> As for the palaeolithic, cooked foods, given the best evidence available, only were available in the last 10%, tail-end of the palaeolithic era, so, technically, > they could be called "palaeo", I suppose.
Indeed. And as you know, the question of when cooking started is vigorously disputed. The evidence suggests it's no later than that last 10% of the paleolithic era, but might turn out to be earlier. We just don't know. For purposes of defining "paleo" there's no good reason to say that only the first half of the paleolithic era counts, even if we had abundant information about what that would imply--which we don't have. Cooked food is paleo, and that's the end of it. It doesn't follow that one *must* eat cooked food, or that cooked food is "just as good" as uncooked food.
Another assumption that must be challenged is the assumption that any version of the paleo diet is as good as any other. There is simply no reason to believe this. Consider an analogous case. The deer in Pennsylvania are larger and more robust than the deer in Texas. They are the same species. They're all "paleo" in that they live on wild foods in their habitat. But the Pennsylvania deer thrive better than the Texas deer, because Pennsylvania is just better for deer! If discover that people following william's raw zero-carb approach to paleo are healthier than those following a variegated cooked-food diet, or a variegated raw diet, it wouldn't follow that only his way is paleo.
Todd Moody
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