Re: Um, call me crazy, but wouldn't it be better to just eat a low carb, high protein breakfast that didn't require a protein snack first???

On Dec 21, 7:10 pm, "Ellen K." <firstinitiallastn...@xxxxxxxxxxxxxx>
wrote:
<ra...@xxxxxxx> wrote in message

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On Dec 21, 2:58 pm, "Ellen K." <firstinitiallastn...@xxxxxxxxxxxxxx>
wrote:





<ra...@xxxxxxx> wrote in message

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On Dec 21, 12:23 am, "Ellen K." <firstinitiallastn...@xxxxxxxxxxxxxx>
wrote:

<ra...@xxxxxxx> wrote in message

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What I find very interesting, but overlooked, in the discussion so far
is the following from the paper:

//
***************************************************************************­­­********************************
"The mechanism underlying the second-meal effect has
been shown to be due to suppression of plasma FFA, allowing greater
storage of glucose as muscle glycogen. They had previously
demonstrated
a strong negative correlation between the decrease of preprandial
plasma
FFA levels and the postmeal glucose increment. In the present study,
a
significant positive correlation was found between prebreakfast
plasma
FFA and the rise in postprandial plasma glucose concentration. ;
//
***************************************************************************­­­******************************

It should be noted that very low carb diets increase plasma FFAs
resulting in increased insulin resistance. There have been some recent
threads with references discussing this.

Sort of ironic that this advise is aimed for "undoing" what a very low
carb diet "does". The effect is probably only seen with very low carb
diets. It might disappear at >30% carbs.

Ofcourse,many very low carbers here maintain "decent (not great)
levels of BGs without meds, but they might handle the glucose that
comes from their liver evem better with decreased insulin resistance
that follows lower plasmas FFAs.

I believe it was Gys that was starting to worsen after years on a very
low carb diet. He discovered his FFAs were elevated, increased fiber/
carbs and turned around his condition. There's lots of data that's
easy to find on FFAs and type 2 diabetes.

Randy

Googling FFA returned Future Farmers of America, which I'm sure isn't
what
your post is referring to. Could you please post the meaning of FFA in
your
post?- Hide quoted text -

- Show quoted text -

Free Fatty Acids. Similar to TG but different (by a glycerine
molecule).

Regards
Randy.

=======================================

Thanks. :)

Is their functionality in the body also similar to triglycerides, or if
not,
how do they differ?- Hide quoted text -

- Show quoted text -

Triglycerides are fatty acids bound by a glycerine molecule (?), when
not bound together they are free fatty acids in plasma or inside the
cell (where they can be oxidized or used for cellular structural
material).

For many years FFA  have been known to increase insulin resistance in
the both muscle and liver.

Very low carb diets will increase FFAs. This is probably the mechanism
that increase insulin resistance in such diets.

Do a google scholar search on "FFA and Diabetes" and you'll have
enought enough info available till you get bored.

Here's the first link that came up.

//****************************************

Effects of Free Fatty Acids (FFA) on Glucose Metabolism: Significance
for Insulin Resistance and Type 2 Diabetes

G. Boden1
1 Division of Endocrinology/Diabetes/Metabolism and the General
Clinical Research Center, Temple University School of Medicine,
Philadelphia, PA USA

Abstract
Most obese individuals have elevated plasma levels of free fatty acids
(FFA) which are known to cause peripheral (muscle) insulin resistance.
They do this by inhibiting insulin-stimulated glucose uptake and
glycogen synthesis. The mechanism involves intramyocellular
accumulation of diacylglycerol and activation of protein kinase C.
FFAs also cause hepatic insulin resistance. They do this by inhibiting
insulin-mediated suppression of glycogenolysis. On the other hand,
FFAs support between 30 and 50 % of basal insulin secretion and
potentiate glucose-stimulated insulin secretion. The insulin
stimulatory action of FFAs is responsible for the fact that the vast
majority (∼ 80 %) of obese insulin resistant people do not develop
type 2 diabetes. They are able to compensate for their FFA mediated
insulin resistance with increased FFA mediated insulin secretion.
Individuals who are unable to do this (probably for genetic reasons)
eventually develop type 2 diabetes. FFAs have recently been shown to
activate the IκB/NFκB pathway which is involved in many inflammatory
processes. Thus, elevated plasma levels of FFAs are not only a major
cause of insulin resistance in skeletal muscle and liver but may, in
addition, play a role in the pathogenesis of coronary artery disease.

=====================

Thanks very much for the information, although I'm not sure I agree with
your conclusion in connection with the original abstract Susan posted.- Hide quoted text -

- Show quoted text -

I didn't make that conclusion, the researchers did and I agreed.

Randy

.

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