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Pearls before the Choir

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General fitness, health and nutrition
Published
4 November 2007
Last activity
5 November 2007
Original author
Cubit
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13
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  1. 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

  2. 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" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    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

  3. 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" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    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

  4. 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" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    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

  5. 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" <[email hidden]> wrote in message
    news:[email hidden]...

    Quoted message said:

    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

  6. Cubit said:

    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/

  7. Cubit said:

    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/

  8. Cubit said:

    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/

  9. Cubit said:

    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/

  10. Cubit said:


    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

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

    Cubit

  11. Cubit said:


    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

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

    Cubit

  12. Cubit said:


    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

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

    Cubit

  13. Cubit said:


    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

    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.

    Quoted message said:

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

    Cubit

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