Re: Glycemic Index >>> Fatty Liver

[Guest guest]

> There may be answers to all these questions. If so,

> then I will need

> to hear what they are, before I can take this

> research seriously.

Some more random thoughts on the study...

The author Ludwig is a long term fan of the Zone diet.

What I find curious is that the high GI mice ended up

with more energy stored as fat as the mice fed the low

GI diet. Now how is that possible if they consumed the

same number of calories? Only if the high GI animals

were less active and/or had a slower metabolic rate.

No one has ever shown that high GI foods promote

sedentariness in humans or animals. Well then that

leaves high GI diets slowing BMR. Again this seems

unlikely and I know of no credible data to show higher

GI foods slow the metabolic rate.

Assuming that higher GI foods do not slow the

metabolic rate or somehow depress physical activity

(both are likely true as far as I know) then how did

Ludwig's high GI rodents end up with twice as much

body fat as the low GI fed mice? The most obvious

answer is that they absorbed more calories. If correct

then we have the obvious explanation for the fatty

liver in the high GI fed mice. They consumed more

calories. Fatty liver and excess body fat stores and

insulin resistance are all largely the result of

excessive calorie intake.

Now why would the low GI diet fed mice end up with

half the body fat and yet more lean body mass? That is

a tough one. As far as I know LBM goes up with

increased calorie intake and not down. Does Ludwig

offer any explanation for this disparate finding?

When one finds something that does not fit with other

data one should at least note it and point out that

the finding is anomalous even if one has no

explanation for it. Have not seen the whole study so

perhaps Ludwig did in fact explain away some of what I

see as some data in his study that seem inconsistent

with what one would expect.

High-GI carbs after exercise lead to a more rapid

replenishment of muscle glycogen stores. Now if a

greater proportion of the CHO calories end up as

muscle glycogen on a high-GI diet than a low-GI diet

then it is hard to imagine how this could lead to

increased total body fat stores and liver fat - unless

of course, the high-GI fed mice consumed more

calories. I wonder if the low-GI starch contained

resistant starch? Resistant starch is physiologically

similar to fiber and would explain most of Ludwig's

anomalous findings.

However, how fewer calories could lead to increased

LBM (as Lugwig's data seems to indicate) is very weird

is it not?

Still wondering

Jeff