Pearls before the Choir

I had an idea this morning.

The apparent wonderful control of type II diabetes by low carb dieting might
have another new explanation. I'm pulling wild monkeys from my ass on this,
but as Alexander Graham Bell showed, the Universe reveals its secrets to
anyone, regardless of lack of credentials.

Hypothesis: The state of glycogen depletion leads to glucose control
without the mechanism of insulin.

If true, this could not only explain the normal HbA1c I get, but suggest
that a reduced total release of insulin might be achieved.

Traditional Atkins adds carbs back into the diet to find a level where
weight regulation is balanced. I believe his idea is to maintain the
highest carb level that is still low enough to have weight control. If
correct, my hypothesis would make this part of Atkins a mistake.

How do the muscles know when they can try to restore their missing glycogen
supply? One might assume that the muscles cells watch for insulin, but what
if they don't? Insulin, I believe, triggers glucose uptake by all or most
of the body's cells. In a glycogen depleted state it would be reasonable to
expect the body to have a way to restore the glycogen stores *before*
pushing glucose into the body at large.

Do the muscles cells detect blood sugar changes directly, or might there be
a new/unknown hormonal messenger that tells the muscles that the intestines
are full of carbohydrates?

This question could be addressed in a study. The total insulin release of
test subjects in identical in-hospital controlled diets could compare a two
groups. The first group begins the key part of the study with glycogen
saturated muscles. The second group begins the key part of the study with
glycogen depleted muscles. My study hypothesis is that when the two groups
are exposed to a brief dietary carbohydrate increase, that the glycogen
depleted group will have lower total insulin release and lower net glucose
levels.

In terms of glucose and insulin, I'm interested here in what is called: the
area under the curve.

Cubit

I've been thinking about my own post.

Let's assume for a moment that glycogen depletion treats diabetes, or
insulin resistance. Glycogen depletion might be achieved either through
diet, or massive exercise. Thus, if the wild ass theory were right, heavy
extensive exercise would help type II diabetes.

Hmmm.

Cubit

"Cubit" wrote in message
...
I had an idea this morning.

The apparent wonderful control of type II diabetes by low carb dieting
might have another new explanation. I'm pulling wild monkeys from my ass
on this, but as Alexander Graham Bell showed, the Universe reveals its
secrets to anyone, regardless of lack of credentials.

Hypothesis: The state of glycogen depletion leads to glucose control
without the mechanism of insulin.

If true, this could not only explain the normal HbA1c I get, but suggest
that a reduced total release of insulin might be achieved.

Traditional Atkins adds carbs back into the diet to find a level where
weight regulation is balanced. I believe his idea is to maintain the
highest carb level that is still low enough to have weight control. If
correct, my hypothesis would make this part of Atkins a mistake.

How do the muscles know when they can try to restore their missing
glycogen supply? One might assume that the muscles cells watch for
insulin, but what if they don't? Insulin, I believe, triggers glucose
uptake by all or most of the body's cells. In a glycogen depleted state
it would be reasonable to expect the body to have a way to restore the
glycogen stores *before* pushing glucose into the body at large.

Do the muscles cells detect blood sugar changes directly, or might there
be a new/unknown hormonal messenger that tells the muscles that the
intestines are full of carbohydrates?

This question could be addressed in a study. The total insulin release of
test subjects in identical in-hospital controlled diets could compare a
two groups. The first group begins the key part of the study with
glycogen saturated muscles. The second group begins the key part of the
study with glycogen depleted muscles. My study hypothesis is that when
the two groups are exposed to a brief dietary carbohydrate increase, that
the glycogen depleted group will have lower total insulin release and
lower net glucose levels.

In terms of glucose and insulin, I'm interested here in what is called:
the area under the curve.

Cubit

Cubit wrote:
I've been thinking about my own post.

Let's assume for a moment that glycogen depletion treats diabetes, or
insulin resistance. Glycogen depletion might be achieved either through
diet, or massive exercise. Thus, if the wild ass theory were right, heavy
extensive exercise would help type II diabetes.

Exercise most definetly reduces bg; a lot of diabetics use things like
taking a walk after each meal as part of their bg control strategy.

In T2s, the resultant increase in lean body mass also seems to improve
insulin resistance.

--
http://www.ornery-geeks.org/consulting/

"Cubit" wrote:

I had an idea this morning.

The apparent wonderful control of type II diabetes by low carb dieting might
have another new explanation ...

Hypothesis: The state of glycogen depletion leads to glucose control
without the mechanism of insulin.

That's the principle behind Atkins CCLL -

While in ketonuria dietary glucose is consumed by the cells and
any short term excess is buffered into glycogen, but while in
ketonuria there is no enough dietary carb to cover the total energy
budget. So we can bounce in and out of ketonuria by the hour
while under our CCLL but as long as all dietary carbs are consumed
by the end of the day there's no need to release insulin. Hence
insulin remains at its minimum output. And hence further reducing
dietary carbs no longer has any effect on insulin release so lower
isn't better for loss.

While out of ketosis (switching away from ketonuria to the harder
to determine ketosis) dietary glucose is high enough that it needs
active control to push it into cells, to push its conversion into
glycogen, to drive its conversion into stored fat. So the more
dietary carbs that are eaten the more insulin needs to be released.

The difference between ketonuria and ketosis above is why there
isn't a sharp cutover, and this range is correlated with the higher
carbs eaten during Premaint to find CCLM.

If true, this could not only explain the normal HbA1c I get, but suggest
that a reduced total release of insulin might be achieved.

Once in ketonuria further lowering dietary carbs no longer drives
insulin lower. How it might effect HbA1c isn't as clear.

Traditional Atkins adds carbs back into the diet to find a level where
weight regulation is balanced. I believe his idea is to maintain the
highest carb level that is still low enough to have weight control.

Dr A used the word loss interchangably with ketosis. Either he meant
something specific by this that he never defined or he had no idea
what he was writing about. That's why CCLL has to be about ketosis.
Add carbs back while still in ketosis (actually ketonuria, yet another
problem with his wording), understanding that his idea of loss was
month to month.

If correct, my hypothesis would make this part of Atkins a mistake.

Only if you don't read the 1972 edition to understand what he means
by the word loss. if lower were better, every single popular low carb
plan out there would drive for lower. None do that. Because glycogen
depletion does indeed lead to glucose control without the insulin
method. Nice rephrasing of the principle behind the CCLL.

How do the muscles know when they can try to restore their missing glycogen
supply? One might assume that the muscles cells watch for insulin, but what
if they don't?

Start a new exercise program and the muscle hoard glycogen for a
while. I think they know based on their most recent load compared
to their previous habitual load.

Insulin, I believe, triggers glucose uptake by all or most
of the body's cells. In a glycogen depleted state it would be reasonable to
expect the body to have a way to restore the glycogen stores *before*
pushing glucose into the body at large.

Rather like osmotic pressure - Below some point glucose is sucked
into glycogen production in the muscles. Above some point glucose
is driven into the cells by insulin.

Do the muscles cells detect blood sugar changes directly, or might there be
a new/unknown hormonal messenger that tells the muscles that the intestines
are full of carbohydrates?

There is the hormone ghrelin, but I think muscles use recent and
long term load to determine their wanted glycogen stores and they
draw the glucose from the blood based on that.

This question could be addressed in a study. The total insulin release of
test subjects in identical in-hospital controlled diets could compare a two
groups. The first group begins the key part of the study with glycogen
saturated muscles. The second group begins the key part of the study with
glycogen depleted muscles. My study hypothesis is that when the two groups
are exposed to a brief dietary carbohydrate increase, that the glycogen
depleted group will have lower total insulin release and lower net glucose
levels.

Agreed. That's what happens during a leptin reset, whose goal is
to recharge the glycogen in the muscles to its maximum. Insulin
should indeed see low release. Maybe. Except that insulin is
released in response to dietary carbs so it would be about relative
rates of reaction.

In terms of glucose and insulin, I'm interested here in what is called: the
area under the curve.

Cubit