oatmeal

[Colt T]

In todays dlife email some diabetic woman said she cooks 1 C of dry oats
to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
makes a pretty big bowl full. She said she gets good readings, I put a
lot of cinnamon in mine.

[W. Baker]

Colt T <[email protected]> wrote:
: In todays dlife email some diabetic woman said she cooks 1 C of dry oats
: to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
: makes a pretty big bowl full. She said she gets good readings, I put a
: lot of cinnamon in mine.
Did she give her readings? One man's good is another man's spike:-)

Thas much oatmeal would send me sky high! I have learned to live withut
it, unfortunately.

Wendy

[Susan]

x-no-archive: yes

On 3/13/2012 6:29 PM, Colt T wrote:
> In todays dlife email some diabetic woman said she cooks 1 C of dry oats
> to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
> makes a pretty big bowl full. She said she gets good readings, I put a
> lot of cinnamon in mine.
>

I doubt if I'd be able to eat more than a TBS, if that.

Susan

[ray]

On Tue, 13 Mar 2012 18:29:50 -0400, Colt T wrote:

> In todays dlife email some diabetic woman said she cooks 1 C of dry oats
> to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
> makes a pretty big bowl full. She said she gets good readings, I put a
> lot of cinnamon in mine.

I can all right with some of the Irish steel cut oats from time to time -
with artificial sweetener and cream.

[Nick Cramer]

[email protected] (Colt T) wrote:
> In todays dlife email some diabetic woman said she cooks 1 C of dry oats
> to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
> makes a pretty big bowl full. She said she gets good readings, I put a
> lot of cinnamon in mine.

I use 1/4 cup of dry oats to 3/4 cup of water and nuke it for a couple of
minutes or 'til it's the consistency I like. I do corn grits the same way.
I put a lot of butter in mine!

--
Nick, KI6VAV. Support severely wounded and disabled Veterans and their
families: https://semperfifund.org https://www.woundedwarriorproject.org/
http://www.specialops.org/ http://www.helpforheroes.org.uk/ ~Semper Fi~
http://www.woundedwarriors.ca/ http://www.legacy.com.au/ ~Semper Fi~

[Chris Hogg]

On 14 Mar 2012 08:05:55 GMT, Nick Cramer <[email protected]>
wrote:

>[email protected] (Colt T) wrote:
>> In todays dlife email some diabetic woman said she cooks 1 C of dry oats
>> to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
>> makes a pretty big bowl full. She said she gets good readings, I put a
>> lot of cinnamon in mine.
>
>I use 1/4 cup of dry oats to 3/4 cup of water and nuke it for a couple of
>minutes or 'til it's the consistency I like. I do corn grits the same way.
>I put a lot of butter in mine!

My recipe is very similar: 1/4 cup oats, 1/2 cup milk, microwave for
approx. 2.5 mins until it just starts to boil, then add a teaspoonful
of coconut fat and a sprinkle of Canderel sweetener. The coconut fat
blunts and broadens the spike. I imagine the butter does the same for
you.

--

Chris

T2 DX'd 2002, D&E, HbA1c 5.7, BMI 21
Lipids:Tot 4.6 HDL 1.5 LDL 2.8 Tri 0.7

[Nick Cramer]

Chris Hogg <[email protected]> wrote:
> Nick Cramer <[email protected]> wrote:
> >[email protected] (Colt T) wrote:
> >> In todays dlife email some diabetic woman said she cooks 1 C of dry
> >> oats to make oatmeal, that would be a huge bowl full. I cook 1/2 C and
> >> that makes a pretty big bowl full. She said she gets good readings, I
> >> put a lot of cinnamon in mine.
> >
> >I use 1/4 cup of dry oats to 3/4 cup of water and nuke it for a couple
> >of minutes or 'til it's the consistency I like. I do corn grits the same
> >way. I put a lot of butter in mine!
>
> My recipe is very similar: 1/4 cup oats, 1/2 cup milk, microwave for
> approx. 2.5 mins until it just starts to boil, then add a teaspoonful
> of coconut fat and a sprinkle of Canderel sweetener. The coconut fat
> blunts and broadens the spike. I imagine the butter does the same for
> you.

I avoid milk because of the lactose. I can handle heavy cream.

--
Nick, KI6VAV. Support severely wounded and disabled Veterans and their
families: https://semperfifund.org https://www.woundedwarriorproject.org/
http://www.specialops.org/ http://www.helpforheroes.org.uk/ ~Semper Fi~
http://www.woundedwarriors.ca/ http://www.legacy.com.au/ ~Semper Fi~

[%]

Nick Cramer wrote:
> Chris Hogg <[email protected]> wrote:
>> Nick Cramer <[email protected]> wrote:
>>> [email protected] (Colt T) wrote:
>>>> In todays dlife email some diabetic woman said she cooks 1 C of dry
>>>> oats to make oatmeal, that would be a huge bowl full. I cook 1/2 C
>>>> and that makes a pretty big bowl full. She said she gets good
>>>> readings, I put a lot of cinnamon in mine.
>>>
>>> I use 1/4 cup of dry oats to 3/4 cup of water and nuke it for a
>>> couple of minutes or 'til it's the consistency I like. I do corn
>>> grits the same way. I put a lot of butter in mine!
>>
>> My recipe is very similar: 1/4 cup oats, 1/2 cup milk, microwave for
>> approx. 2.5 mins until it just starts to boil, then add a teaspoonful
>> of coconut fat and a sprinkle of Canderel sweetener. The coconut fat
>> blunts and broadens the spike. I imagine the butter does the same for
>> you.
>
> I avoid milk because of the lactose. I can handle heavy cream.


oh hold thy tongue %

[GysdeJongh]

Chris Hogg wrote:

> The coconut fat
> blunts and broadens the spike.

But ...
does that prevent damage from advanced glycation end products ????

Chemistry 101 : the amount of product formed during a chemical reaction
depends on the concentration of the reactants *and* on the reaction
*time*

Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
measure the area under the curve of blood glucose vs time and never the
maximum peak height ?

So
your long broad peak might have the same area as your thin high peak and
thus produce exactly the same damage to your arteries

except for the *extra* damage to your arteries but all the saturated fat
of course.


<http://jcem.endojournals.org/content/93/4/1143.long>

J Clin Endocrinol Metab. 2008 Apr;93(4):1143-52. Epub 2008 Jan 8.
Clinical review: The role of advanced glycation end products in progression
and complications of diabetes.
Diabetic complications appear to be multifactorial in origin, but in
particular, the biochemical process of advanced glycation, which is
accelerated in diabetes as a result of chronic hyperglycemia and increased
oxidative stress, has been postulated to play a central role in these
disorders. Advanced glycation involves the generation of a heterogenous
group of chemical moieties known as advanced glycated end products (AGEs),
this reaction occurring as a result of a nonenzymatic reaction with glucose
interacting with proteins, lipids, and nucleic acids, and involves key
intermediates such as methylglyoxal. EVIDENCE SYNTHESIS: In this review we
report on how these AGEs may exert deleterious effects in diabetes, as well
as address current strategies to interrupt the formation or action of AGEs.
First, AGEs act directly to induce cross-linking of long-lived proteins such
as collagen to promote vascular stiffness, and, thus, alter vascular
structure and function. Second, AGEs can interact with certain receptors,
such as the receptor for AGE, to induce intracellular signaling that leads
to enhanced oxidative stress and elaboration of key proinflammatory and
prosclerotic cytokines. Over the last decade, a large number of preclinical
studies have been performed, targeting the formation and degradation of
AGEs, as well as the interaction of these AGEs with receptors such as the
receptor for AGE. CONCLUSION: It is hoped that over the next few years, some
of these promising therapies will be fully evaluated in the clinical context
with the ultimate aim to reduce the major economical and medical burden of
diabetes, its vascular complications.
PMID: 18182449

[MaryL]

"Colt T" wrote in message
news:[email protected]..

In todays dlife email some diabetic woman said she cooks 1 C of dry oats
to make oatmeal, that would be a huge bowl full. I cook 1/2 C and that
makes a pretty big bowl full. She said she gets good readings, I put a
lot of cinnamon in mine.

<<<<<>>>>>
I have oatmeal almost every morning, and it has not had any adverse effect
on my readings. However, I use 1/3 cup of old fashioned oatmeal (*never*
"quick" oatmeal but sometimes steel cut) cooked in 2/3 cup of water. I
often add a small amount of cinnamon, a few walnuts, and a small handful of
fresh blueberries or strawberries. No sweetener of any kind. Barely enough
milk to moisten the oatmeal. That would be my entire breakfast--nothing
else.

MaryL

[Colt T]

Since my LDL is too low I probably shouldn't eat oats at all. Barely
flake hot cereal has twice as much soluble fiber as oats but it's likely
as hard to cook as steel cut oats.

[Susan]

x-no-archive: yes

On 3/14/2012 4:07 PM, Colt T wrote:
> Since my LDL is too low I probably shouldn't eat oats at all. Barely
> flake hot cereal has twice as much soluble fiber as oats but it's likely
> as hard to cook as steel cut oats.
>

Do you have a doctor who would agree to test your pregnenolone levels?

Here's why: http://www.cushings-help.com/downloa...id01.02.07.pdf

[Colt T]

I'll ask next time, barley flake not barely flake.

[Chris Hogg]

On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
<JonghSevenHundredElevenAtPlanet.nl> wrote:

>Chris Hogg wrote:
>
>> The coconut fat
>> blunts and broadens the spike.
>
>But ...
>does that prevent damage from advanced glycation end products ????
>
>Chemistry 101 : the amount of product formed during a chemical reaction
>depends on the concentration of the reactants *and* on the reaction
>*time*
>
>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>measure the area under the curve of blood glucose vs time and never the
>maximum peak height ?
>
>So
>your long broad peak might have the same area as your thin high peak and
>thus produce exactly the same damage to your arteries
>
Well, yes, I sort of knew that from chemistry lessons of many decades
ago! But IIRC it does depend on the reaction being first order; if
glycation is second order wrt glucose (i.e. rate proportional to the
square of the glucose conc.), then lowering the peak and broadening it
would make a big difference. But it's probably first order, although I
doubt anyone actually knows. Another complicating factor would be if
there was a threshold value below which no damage occurred.

It does raise the question as to why so much emphasis is put on peak
values here. I suppose it's because it's a quick and easy measure, and
a lot better than no measure at all.

>except for the *extra* damage to your arteries but all the saturated fat
>of course.
>
I use coconut fat deliberately. Although a hard fat, it's an medium
chain triglyceride (MCT), and AIUI is supposed to be much less
damaging.

--

Chris

T2 DX'd 2002, D&E, HbA1c 5.7, BMI 21
Lipids:Tot 4.6 HDL 1.5 LDL 2.8 Tri 0.7

[Canth]

On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:

>On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
><JonghSevenHundredElevenAtPlanet.nl> wrote:
>
>>Chris Hogg wrote:
>>
>>> The coconut fat
>>> blunts and broadens the spike.
>>
>>But ...
>>does that prevent damage from advanced glycation end products ????
>>
>>Chemistry 101 : the amount of product formed during a chemical reaction
>>depends on the concentration of the reactants *and* on the reaction
>>*time*
>>
>>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>>measure the area under the curve of blood glucose vs time and never the
>>maximum peak height ?
>>
>>So
>>your long broad peak might have the same area as your thin high peak and
>>thus produce exactly the same damage to your arteries
>>
>Well, yes, I sort of knew that from chemistry lessons of many decades
>ago! But IIRC it does depend on the reaction being first order; if
>glycation is second order wrt glucose (i.e. rate proportional to the
>square of the glucose conc.), then lowering the peak and broadening it
>would make a big difference. But it's probably first order, although I
>doubt anyone actually knows. Another complicating factor would be if
>there was a threshold value below which no damage occurred.
>

From what I understand, glycation and deglycation are competing
reactions, both moderated actively by the glucose concentration. When
glucose concentration is low, deglycation is actively promoted &
glycation is actively suppressed. When glucose levels are high,
glycation is actively promoted & deglycation is actively suppressed. A
simple area under the curve analysis therefore doesn't work. The net
amount of glycation that occurs because of high narrow peaks is
probably greater than the amount under a broader but lower peak
because the reaction catalysts are more affected by the glucose
concentrations.

>It does raise the question as to why so much emphasis is put on peak
>values here. I suppose it's because it's a quick and easy measure, and
>a lot better than no measure at all.
>
>>except for the *extra* damage to your arteries but all the saturated fat
>>of course.
>>
>I use coconut fat deliberately. Although a hard fat, it's an medium
>chain triglyceride (MCT), and AIUI is supposed to be much less
>damaging.

With peaks around 16, I don't even consider porridge in any form.

AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
I've been ignored by better people than you.

[GysdeJongh]

Canth wrote:
> On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>
>> On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>>
>>> Chris Hogg wrote:
>>>
>>>> The coconut fat
>>>> blunts and broadens the spike.
>>>
>>> But ...
>>> does that prevent damage from advanced glycation end products ????
>>>
>>> Chemistry 101 : the amount of product formed during a chemical
>>> reaction depends on the concentration of the reactants *and* on
>>> the reaction *time*
>>>
>>> Ever wondered *why* we measure HbA1c ? Ever wondered *why*
>>> experiments measure the area under the curve of blood glucose vs
>>> time and never the maximum peak height ?
>>>
>>> So
>>> your long broad peak might have the same area as your thin high
>>> peak and thus produce exactly the same damage to your arteries
>>>
>> Well, yes, I sort of knew that from chemistry lessons of many decades
>> ago! But IIRC it does depend on the reaction being first order; if
>> glycation is second order wrt glucose (i.e. rate proportional to the
>> square of the glucose conc.), then lowering the peak and broadening
>> it would make a big difference. But it's probably first order,
>> although I doubt anyone actually knows. Another complicating factor
>> would be if there was a threshold value below which no damage
>> occurred.
>>
>
> From what I understand, glycation and deglycation are competing
> reactions, both moderated actively by the glucose concentration. When
> glucose concentration is low, deglycation is actively promoted &
> glycation is actively suppressed. When glucose levels are high,
> glycation is actively promoted & deglycation is actively suppressed. A
> simple area under the curve analysis therefore doesn't work. The net
> amount of glycation that occurs because of high narrow peaks is
> probably greater than the amount under a broader but lower peak
> because the reaction catalysts are more affected by the glucose
> concentrations.




Wrong aswer, zero points.

But if you want spend your life (and money) measuring your *peak*
bloodglucose on the wrong assumptions, than I wish you lots of fun doing so.

In the mean time the non-enzymetic reaction between glucose and protein, the
Maillard reaction, is linear over a wide concentration of glucose.

In more detail the reaction proceeds via a Shiff base, followed by an
Amadori rearrangement. The initial steps are reversible. If your
bloodglucose is back within a few hours than no Advance Glycation
Endproducts are formed. That's why the dokter advice you to measure your
bloodglucose 2 hours after the start of a meal : the fast peak does not
contribute.

<http://en.wikipedia.org/wiki/Amadori_rearrangement>




>> It does raise the question as to why so much emphasis is put on peak
>> values here. I suppose it's because it's a quick and easy measure,
>> and a lot better than no measure at all.


Imo it provides an illusion of control and a reason for eating lots of fat


>>> except for the *extra* damage to your arteries but all the
>>> saturated fat of course.
>>>
>> I use coconut fat deliberately. Although a hard fat, it's an medium
>> chain triglyceride (MCT), and AIUI is supposed to be much less
>> damaging.
>
> With peaks around 16, I don't even consider porridge in any form.
>
> AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
> I've been ignored by better people than you.

[Chris Hogg]

On Thu, 15 Mar 2012 11:59:43 +1030, Canth <[email protected]>
wrote:

>On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>
>>On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>><JonghSevenHundredElevenAtPlanet.nl> wrote:
>>
>>>Chris Hogg wrote:
>>>
>>>> The coconut fat
>>>> blunts and broadens the spike.
>>>
>>>But ...
>>>does that prevent damage from advanced glycation end products ????
>>>
>>>Chemistry 101 : the amount of product formed during a chemical reaction
>>>depends on the concentration of the reactants *and* on the reaction
>>>*time*
>>>
>>>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>>>measure the area under the curve of blood glucose vs time and never the
>>>maximum peak height ?
>>>
>>>So
>>>your long broad peak might have the same area as your thin high peak and
>>>thus produce exactly the same damage to your arteries
>>>
>>Well, yes, I sort of knew that from chemistry lessons of many decades
>>ago! But IIRC it does depend on the reaction being first order; if
>>glycation is second order wrt glucose (i.e. rate proportional to the
>>square of the glucose conc.), then lowering the peak and broadening it
>>would make a big difference. But it's probably first order, although I
>>doubt anyone actually knows. Another complicating factor would be if
>>there was a threshold value below which no damage occurred.
>>
>
>From what I understand, glycation and deglycation are competing
>reactions, both moderated actively by the glucose concentration. When
>glucose concentration is low, deglycation is actively promoted &
>glycation is actively suppressed. When glucose levels are high,
>glycation is actively promoted & deglycation is actively suppressed. A
>simple area under the curve analysis therefore doesn't work. The net
>amount of glycation that occurs because of high narrow peaks is
>probably greater than the amount under a broader but lower peak
>because the reaction catalysts are more affected by the glucose
>concentrations.
>
That's interesting. All chemical reactions are, in theory, equilibria
and potentially reversible, although some are more difficult to
reverse than others. Do you have any references or citations that I
could follow up?
>
>AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
>I've been ignored by better people than you.

I've never understood your sig. I mean the line with all the +'s and
-'s. Can you enlighten me?

--

Chris

T2 DX'd 2002, D&E, HbA1c 5.7, BMI 21
Lipids:Tot 4.6 HDL 1.5 LDL 2.8 Tri 0.7

[Canth]

On Thu, 15 Mar 2012 10:25:28 +0100, "GysdeJongh"
<JonghSevenHundredElevenAtPlanet.nl> wrote:

>Canth wrote:
>> On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>>
>>> On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>>> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>>>
>>>> Chris Hogg wrote:
>>>>
>>>>> The coconut fat
>>>>> blunts and broadens the spike.
>>>>
>>>> But ...
>>>> does that prevent damage from advanced glycation end products ????
>>>>
>>>> Chemistry 101 : the amount of product formed during a chemical
>>>> reaction depends on the concentration of the reactants *and* on
>>>> the reaction *time*
>>>>
>>>> Ever wondered *why* we measure HbA1c ? Ever wondered *why*
>>>> experiments measure the area under the curve of blood glucose vs
>>>> time and never the maximum peak height ?
>>>>
>>>> So
>>>> your long broad peak might have the same area as your thin high
>>>> peak and thus produce exactly the same damage to your arteries
>>>>
>>> Well, yes, I sort of knew that from chemistry lessons of many decades
>>> ago! But IIRC it does depend on the reaction being first order; if
>>> glycation is second order wrt glucose (i.e. rate proportional to the
>>> square of the glucose conc.), then lowering the peak and broadening
>>> it would make a big difference. But it's probably first order,
>>> although I doubt anyone actually knows. Another complicating factor
>>> would be if there was a threshold value below which no damage
>>> occurred.
>>>
>>
>> From what I understand, glycation and deglycation are competing
>> reactions, both moderated actively by the glucose concentration. When
>> glucose concentration is low, deglycation is actively promoted &
>> glycation is actively suppressed. When glucose levels are high,
>> glycation is actively promoted & deglycation is actively suppressed. A
>> simple area under the curve analysis therefore doesn't work. The net
>> amount of glycation that occurs because of high narrow peaks is
>> probably greater than the amount under a broader but lower peak
>> because the reaction catalysts are more affected by the glucose
>> concentrations.
>
>
>
>
>Wrong aswer, zero points.
>
>But if you want spend your life (and money) measuring your *peak*
>bloodglucose on the wrong assumptions, than I wish you lots of fun doing so.
>
>In the mean time the non-enzymetic reaction between glucose and protein, the
>Maillard reaction, is linear over a wide concentration of glucose.
>

Always willing to learn.

Seems that there is a non-enzymatic reaction which is linear to
produce fructosamine products. Seems there are enzymes within cells
which reverses this; one is called fructosamine-3-kinase, another is
Amadoriase. These enzymes are common throughout the animal & plant
kingdoms, evidence that their function is vital.

So while the first step is linear for glycation to the Amadori
product, there is a set of competing activities acting on that Amadori
product. It can apparently further react to produce ACEs, which
cannot be reversed; it can spontaneously reverse; or it can be
enzymatically reversed. While I cannot find any articles which
indicate whether these enzymes are affected by glucose concentrations,
either in activity levels or in production, it would not surprise me
if there is a feedback mechanism making this non-linear.

>In more detail the reaction proceeds via a Shiff base, followed by an
>Amadori rearrangement. The initial steps are reversible. If your
>bloodglucose is back within a few hours than no Advance Glycation
>Endproducts are formed. That's why the dokter advice you to measure your
>bloodglucose 2 hours after the start of a meal : the fast peak does not
>contribute.
>
><http://en.wikipedia.org/wiki/Amadori_rearrangement>
>
>

Actually, I have doctors who emphasise the one hour reading, while
others the two hour reading. The joys of a rural clinic. I got so
confused I stopped reading.

>
>
>>> It does raise the question as to why so much emphasis is put on peak
>>> values here. I suppose it's because it's a quick and easy measure,
>>> and a lot better than no measure at all.
>
>
>Imo it provides an illusion of control and a reason for eating lots of fat
>
>
>>>> except for the *extra* damage to your arteries but all the
>>>> saturated fat of course.
>>>>
>>> I use coconut fat deliberately. Although a hard fat, it's an medium
>>> chain triglyceride (MCT), and AIUI is supposed to be much less
>>> damaging.
>>
>> With peaks around 16, I don't even consider porridge in any form.
>>
>> AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
>> I've been ignored by better people than you.

AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
I've been ignored by better people than you.

[Canth]

On Thu, 15 Mar 2012 09:31:45 +0000, Chris Hogg <[email protected]> wrote:

>On Thu, 15 Mar 2012 11:59:43 +1030, Canth <[email protected]>
>wrote:
>
>>On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>>
>>>On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>>><JonghSevenHundredElevenAtPlanet.nl> wrote:
>>>
>>>>Chris Hogg wrote:
>>>>
>>>>> The coconut fat
>>>>> blunts and broadens the spike.
>>>>
>>>>But ...
>>>>does that prevent damage from advanced glycation end products ????
>>>>
>>>>Chemistry 101 : the amount of product formed during a chemical reaction
>>>>depends on the concentration of the reactants *and* on the reaction
>>>>*time*
>>>>
>>>>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>>>>measure the area under the curve of blood glucose vs time and never the
>>>>maximum peak height ?
>>>>
>>>>So
>>>>your long broad peak might have the same area as your thin high peak and
>>>>thus produce exactly the same damage to your arteries
>>>>
>>>Well, yes, I sort of knew that from chemistry lessons of many decades
>>>ago! But IIRC it does depend on the reaction being first order; if
>>>glycation is second order wrt glucose (i.e. rate proportional to the
>>>square of the glucose conc.), then lowering the peak and broadening it
>>>would make a big difference. But it's probably first order, although I
>>>doubt anyone actually knows. Another complicating factor would be if
>>>there was a threshold value below which no damage occurred.
>>>
>>
>>From what I understand, glycation and deglycation are competing
>>reactions, both moderated actively by the glucose concentration. When
>>glucose concentration is low, deglycation is actively promoted &
>>glycation is actively suppressed. When glucose levels are high,
>>glycation is actively promoted & deglycation is actively suppressed. A
>>simple area under the curve analysis therefore doesn't work. The net
>>amount of glycation that occurs because of high narrow peaks is
>>probably greater than the amount under a broader but lower peak
>>because the reaction catalysts are more affected by the glucose
>>concentrations.
>>
>That's interesting. All chemical reactions are, in theory, equilibria
>and potentially reversible, although some are more difficult to
>reverse than others. Do you have any references or citations that I
>could follow up?
>>

The above was a hazy memory of the processes. Glys has pointed me to
the more precise mechanisms. The major culprit is a non-enzymatic
reaction between the carboxyl group of a sugar in its straight chain
form and any spare amine groups on proteins. This reaction is
reversible, and in isolation is linear with respect to the
concentration of glucose. Over time, in the absence of any other
reactions, the whole mess will reach equilibrium with various
products. Google Amadori reaction.

However, there are a number of factors involved as well in the body.
First, most natural sugars spend most of their time in a ring form,
which does not react as it does not have a free carboxyl group. This
reduces the sugar available for reaction. I would be interested in
knowing whether glucose is released into the blood in ring or chain
form; I cannot find anything on that.

Second, in the body there are irreversible reactions available to
further take one of the metabolite forms on towards AGEs, thereby
removing them from equilibrium. Over time, in the absence of other
factors, this will result in protein damage.

Thirdly, there are enzymes within cells which actively reverse the
initial reaction, regenerating the protein and destroying the sugar.
These will affect the curve in vivo. Unfortunately, these only
operate within the cell, and cannot affect glycation which occurs
outside of the cell, such as nerve sheaths, collagen fibres in blood
vessel walls, etc. Google fructosamine-3-kinase.

There is also a hormonal system related to childhood growth and adult
caloric restriction which affects insulin sensitivity & glucose
uptake, as well as cell division & cell clean up. This can also
affect the use of glucose and the amount available for these
reactions. Article in a recent SciAm.

>>AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
>>I've been ignored by better people than you.
>
>I've never understood your sig. I mean the line with all the +'s and
>-'s. Can you enlighten me?
Autism spectrum code. Unfortunately the interpreter has been lost;
there is someone on the Autism ng who is reverse engineering it now.
The most I can say from memory is AS! = formally diagnosed Aspergers
Syndrome. Laziness leaves it there.

AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
I've been ignored by better people than you.

[Chris Malcolm]

Chris Hogg <[email protected]> wrote:
> On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>>Chris Hogg wrote:
>>
>>> The coconut fat
>>> blunts and broadens the spike.
>>
>>But ...
>>does that prevent damage from advanced glycation end products ????
>>
>>Chemistry 101 : the amount of product formed during a chemical reaction
>>depends on the concentration of the reactants *and* on the reaction
>>*time*
>>
>>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>>measure the area under the curve of blood glucose vs time and never the
>>maximum peak height ?
>>
>>So
>>your long broad peak might have the same area as your thin high peak and
>>thus produce exactly the same damage to your arteries
>>
> Well, yes, I sort of knew that from chemistry lessons of many decades
> ago! But IIRC it does depend on the reaction being first order; if
> glycation is second order wrt glucose (i.e. rate proportional to the
> square of the glucose conc.), then lowering the peak and broadening it
> would make a big difference. But it's probably first order, although I
> doubt anyone actually knows. Another complicating factor would be if
> there was a threshold value below which no damage occurred.

> It does raise the question as to why so much emphasis is put on peak
> values here. I suppose it's because it's a quick and easy measure, and
> a lot better than no measure at all.

I checked out my post meal BG response curves and found that if I just
sat around my BG usually dropped from its peak in a curve which looked
roughly like a standard half-life decay, i.e. the rate of drop was
roughly proportional to how much higher the BG was than its flat
fasting level. If I got up and moved around it dropped faster.

With a BG response curve like that reducing the height of the post
meal peak always reduces the area under the curve. That's why I
decided it was sensible for me to follow the general advice to lower
the peaks.

--
Chris Malcolm

[Chris Malcolm]

Canth <[email protected]> wrote:
> On Thu, 15 Mar 2012 10:25:28 +0100, "GysdeJongh"
> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>>Canth wrote:
>>> On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>>>> On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>>>> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>>>>> Chris Hogg wrote:
>>>>>
>>>>>> The coconut fat
>>>>>> blunts and broadens the spike.
>>>>>
>>>>> But ...
>>>>> does that prevent damage from advanced glycation end products ????
>>>>>
>>>>> Chemistry 101 : the amount of product formed during a chemical
>>>>> reaction depends on the concentration of the reactants *and* on
>>>>> the reaction *time*
>>>>>
>>>>> Ever wondered *why* we measure HbA1c ? Ever wondered *why*
>>>>> experiments measure the area under the curve of blood glucose vs
>>>>> time and never the maximum peak height ?
>>>>>
>>>>> So
>>>>> your long broad peak might have the same area as your thin high
>>>>> peak and thus produce exactly the same damage to your arteries
>>>>>
>>>> Well, yes, I sort of knew that from chemistry lessons of many decades
>>>> ago! But IIRC it does depend on the reaction being first order; if
>>>> glycation is second order wrt glucose (i.e. rate proportional to the
>>>> square of the glucose conc.), then lowering the peak and broadening
>>>> it would make a big difference. But it's probably first order,
>>>> although I doubt anyone actually knows. Another complicating factor
>>>> would be if there was a threshold value below which no damage
>>>> occurred.
>>>>
>>>
>>> From what I understand, glycation and deglycation are competing
>>> reactions, both moderated actively by the glucose concentration. When
>>> glucose concentration is low, deglycation is actively promoted &
>>> glycation is actively suppressed. When glucose levels are high,
>>> glycation is actively promoted & deglycation is actively suppressed. A
>>> simple area under the curve analysis therefore doesn't work. The net
>>> amount of glycation that occurs because of high narrow peaks is
>>> probably greater than the amount under a broader but lower peak
>>> because the reaction catalysts are more affected by the glucose
>>> concentrations.
>>
>>Wrong aswer, zero points.
>>
>>But if you want spend your life (and money) measuring your *peak*
>>bloodglucose on the wrong assumptions, than I wish you lots of fun doing so.
>>
>>In the mean time the non-enzymetic reaction between glucose and protein, the
>>Maillard reaction, is linear over a wide concentration of glucose.

> Always willing to learn.

> Seems that there is a non-enzymatic reaction which is linear to
> produce fructosamine products. Seems there are enzymes within cells
> which reverses this; one is called fructosamine-3-kinase, another is
> Amadoriase. These enzymes are common throughout the animal & plant
> kingdoms, evidence that their function is vital.

> So while the first step is linear for glycation to the Amadori
> product, there is a set of competing activities acting on that Amadori
> product. It can apparently further react to produce ACEs, which
> cannot be reversed; it can spontaneously reverse; or it can be
> enzymatically reversed. While I cannot find any articles which
> indicate whether these enzymes are affected by glucose concentrations,
> either in activity levels or in production, it would not surprise me
> if there is a feedback mechanism making this non-linear.

>>In more detail the reaction proceeds via a Shiff base, followed by an
>>Amadori rearrangement. The initial steps are reversible. If your
>>bloodglucose is back within a few hours than no Advance Glycation
>>Endproducts are formed. That's why the dokter advice you to measure your
>>bloodglucose 2 hours after the start of a meal : the fast peak does not
>>contribute.
>>
>><http://en.wikipedia.org/wiki/Amadori_rearrangement>

> Actually, I have doctors who emphasise the one hour reading, while
> others the two hour reading. The joys of a rural clinic. I got so
> confused I stopped reading.

IMO the reason docs ask patients to test at one or two hours is
because that's what the great bulk of the research has done. So there
is plenty of scientific evidence of what results are associated with
one or two hour readings. So if you tested at say one and a half hours
your doc wouldn't be able to compare your test BGS with research
results and treatment guidelines based on them. He wouldn't know what
to say because there's "no evidence".

But there's obviously a very important difference between a diabetic
with a falling BG of 150 at one hour and one with a rising BG of 150
at one hour. That's why I decided to test not at one or two hours, but
at where my peak was most likely to be, and to test 10 or 15 mins
later to see if it was rising or falling. If it's rising I keep
testing until I see it falling.

--
Chris Malcolm

[Alice Faber]

In article <[email protected]>,
Chris Malcolm <[email protected]> wrote:

>
> IMO the reason docs ask patients to test at one or two hours is
> because that's what the great bulk of the research has done. So there
> is plenty of scientific evidence of what results are associated with
> one or two hour readings. So if you tested at say one and a half hours
> your doc wouldn't be able to compare your test BGS with research
> results and treatment guidelines based on them. He wouldn't know what
> to say because there's "no evidence".
>
> But there's obviously a very important difference between a diabetic
> with a falling BG of 150 at one hour and one with a rising BG of 150
> at one hour. That's why I decided to test not at one or two hours, but
> at where my peak was most likely to be, and to test 10 or 15 mins
> later to see if it was rising or falling. If it's rising I keep
> testing until I see it falling.

I know you know this, Chris, but it's worth restating: experienced
diabetics know that there are two kinds of BG tests, those you do for
your doctor and those you do for yourself. I'm doing well enough that my
doctor freaked out about a 109 on some recent bloodwork until I reminded
her that she'd sent me in for two specific things that didn't require
fasting, so that was after breakfast; she's happy with my A1c and a
report like "fasting is generally in the 80-95 range", which leaves me
free to test for myself. On the other hand, if she weren't happy with my
A1c, etc. (as well as the fasting number on periodic bloodwork), I'd be
testing more on her schedule.

On the third hand, she's implicitly accepted the "test your meals"
approach, by reminding me that I obviously know what to eat, and I
remind her that the fun of eating is trying new foods and new recipes .
(Which reminds me that I should have tested after the Dreamfields I had
for dinner last night, but I got wrapped up in a hockey game.)

--
"Isn't embarrassing to quote something you didn't read and then attack
what it didn't say?"--WG, where else but Usenet

[Chris Hogg]

On Fri, 16 Mar 2012 02:37:01 +1030, Canth <[email protected]>
wrote:

>On Thu, 15 Mar 2012 09:31:45 +0000, Chris Hogg <[email protected]> wrote:
>
>>On Thu, 15 Mar 2012 11:59:43 +1030, Canth <[email protected]>
>>wrote:
>>
>>>On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>>>
>>>>On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>>>><JonghSevenHundredElevenAtPlanet.nl> wrote:
>>>>
>>>>>Chris Hogg wrote:
>>>>>
>>>>>> The coconut fat
>>>>>> blunts and broadens the spike.
>>>>>
>>>>>But ...
>>>>>does that prevent damage from advanced glycation end products ????
>>>>>
>>>>>Chemistry 101 : the amount of product formed during a chemical reaction
>>>>>depends on the concentration of the reactants *and* on the reaction
>>>>>*time*
>>>>>
>>>>>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>>>>>measure the area under the curve of blood glucose vs time and never the
>>>>>maximum peak height ?
>>>>>
>>>>>So
>>>>>your long broad peak might have the same area as your thin high peak and
>>>>>thus produce exactly the same damage to your arteries
>>>>>
>>>>Well, yes, I sort of knew that from chemistry lessons of many decades
>>>>ago! But IIRC it does depend on the reaction being first order; if
>>>>glycation is second order wrt glucose (i.e. rate proportional to the
>>>>square of the glucose conc.), then lowering the peak and broadening it
>>>>would make a big difference. But it's probably first order, although I
>>>>doubt anyone actually knows. Another complicating factor would be if
>>>>there was a threshold value below which no damage occurred.
>>>>
>>>
>>>From what I understand, glycation and deglycation are competing
>>>reactions, both moderated actively by the glucose concentration. When
>>>glucose concentration is low, deglycation is actively promoted &
>>>glycation is actively suppressed. When glucose levels are high,
>>>glycation is actively promoted & deglycation is actively suppressed. A
>>>simple area under the curve analysis therefore doesn't work. The net
>>>amount of glycation that occurs because of high narrow peaks is
>>>probably greater than the amount under a broader but lower peak
>>>because the reaction catalysts are more affected by the glucose
>>>concentrations.
>>>
>>That's interesting. All chemical reactions are, in theory, equilibria
>>and potentially reversible, although some are more difficult to
>>reverse than others. Do you have any references or citations that I
>>could follow up?
>>>
>
>The above was a hazy memory of the processes. Glys has pointed me to
>the more precise mechanisms. The major culprit is a non-enzymatic
>reaction between the carboxyl group of a sugar in its straight chain
>form and any spare amine groups on proteins. This reaction is
>reversible, and in isolation is linear with respect to the
>concentration of glucose. Over time, in the absence of any other
>reactions, the whole mess will reach equilibrium with various
>products. Google Amadori reaction.
>
>However, there are a number of factors involved as well in the body.
>First, most natural sugars spend most of their time in a ring form,
>which does not react as it does not have a free carboxyl group. This
>reduces the sugar available for reaction. I would be interested in
>knowing whether glucose is released into the blood in ring or chain
>form; I cannot find anything on that.
>
> Second, in the body there are irreversible reactions available to
>further take one of the metabolite forms on towards AGEs, thereby
>removing them from equilibrium. Over time, in the absence of other
>factors, this will result in protein damage.
>
>Thirdly, there are enzymes within cells which actively reverse the
>initial reaction, regenerating the protein and destroying the sugar.
>These will affect the curve in vivo. Unfortunately, these only
>operate within the cell, and cannot affect glycation which occurs
>outside of the cell, such as nerve sheaths, collagen fibres in blood
>vessel walls, etc. Google fructosamine-3-kinase.
>
>There is also a hormonal system related to childhood growth and adult
>caloric restriction which affects insulin sensitivity & glucose
>uptake, as well as cell division & cell clean up. This can also
>affect the use of glucose and the amount available for these
>reactions. Article in a recent SciAm.
>

This exchange between yourself and Gys has been very interesting.
Thank you both. My take-away from it is that short-term peaks aren't
critically important, as long as BG comes back to normal (whatever
that may be) after two or even three hours. Obviously, the higher the
peak the longer it will take to come back down, so peaks can't be
ignored completely.

>>>AS! ds++:+++ a++ c+++ p++ t+ f-- S+ p+ e++ h++ r++ n++ i+ P+ m++ M
>>>I've been ignored by better people than you.
>>
>>I've never understood your sig. I mean the line with all the +'s and
>>-'s. Can you enlighten me?
>Autism spectrum code. Unfortunately the interpreter has been lost;
>there is someone on the Autism ng who is reverse engineering it now.
>The most I can say from memory is AS! = formally diagnosed Aspergers
>Syndrome. Laziness leaves it there.

I Googled for the code and found the alt.support.autism reference. All
is now explained. Thanks.

--

Chris

T2 DX'd 2002, D&E, HbA1c 5.7, BMI 21
Lipids:Tot 4.6 HDL 1.5 LDL 2.8 Tri 0.7

[GysdeJongh]

Chris Hogg wrote:
> On Fri, 16 Mar 2012 02:37:01 +1030, Canth <[email protected]>
> wrote:
>
>> On Thu, 15 Mar 2012 09:31:45 +0000, Chris Hogg <[email protected]>
>> wrote:
>>
>>> On Thu, 15 Mar 2012 11:59:43 +1030, Canth <[email protected]>
>>> wrote:
>>>
>>>> On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]>
>>>> wrote:
>>>>
>>>>> On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>>>>> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>>>>>
>>>>>> Chris Hogg wrote:
>>>>>>
>>>>>>> The coconut fat
>>>>>>> blunts and broadens the spike.
>>>>>>
>>>>>> But ...
>>>>>> does that prevent damage from advanced glycation end products
>>>>>> ????
>>>>>>
>>>>>> Chemistry 101 : the amount of product formed during a chemical
>>>>>> reaction depends on the concentration of the reactants *and*
>>>>>> on the reaction *time*
>>>>>>
>>>>>> Ever wondered *why* we measure HbA1c ? Ever wondered *why*
>>>>>> experiments measure the area under the curve of blood glucose vs
>>>>>> time and never the maximum peak height ?
>>>>>>
>>>>>> So
>>>>>> your long broad peak might have the same area as your thin high
>>>>>> peak and thus produce exactly the same damage to your arteries
>>>>>>
>>>>> Well, yes, I sort of knew that from chemistry lessons of many
>>>>> decades ago! But IIRC it does depend on the reaction being first
>>>>> order; if glycation is second order wrt glucose (i.e. rate
>>>>> proportional to the square of the glucose conc.), then lowering
>>>>> the peak and broadening it would make a big difference. But it's
>>>>> probably first order, although I doubt anyone actually knows.
>>>>> Another complicating factor would be if there was a threshold
>>>>> value below which no damage occurred.
>>>>>
>>>>
>>>> From what I understand, glycation and deglycation are competing
>>>> reactions, both moderated actively by the glucose concentration.
>>>> When glucose concentration is low, deglycation is actively
>>>> promoted & glycation is actively suppressed. When glucose levels
>>>> are high, glycation is actively promoted & deglycation is actively
>>>> suppressed. A simple area under the curve analysis therefore
>>>> doesn't work. The net amount of glycation that occurs because of
>>>> high narrow peaks is probably greater than the amount under a
>>>> broader but lower peak because the reaction catalysts are more
>>>> affected by the glucose concentrations.
>>>>
>>> That's interesting. All chemical reactions are, in theory,
>>> equilibria and potentially reversible, although some are more
>>> difficult to reverse than others. Do you have any references or
>>> citations that I could follow up?
>>>>
>>
>> The above was a hazy memory of the processes. Glys has pointed me to
>> the more precise mechanisms. The major culprit is a non-enzymatic
>> reaction between the carboxyl group of a sugar in its straight chain
>> form and any spare amine groups on proteins. This reaction is
>> reversible, and in isolation is linear with respect to the
>> concentration of glucose. Over time, in the absence of any other
>> reactions, the whole mess will reach equilibrium with various
>> products. Google Amadori reaction.
>>
>> However, there are a number of factors involved as well in the body.
>> First, most natural sugars spend most of their time in a ring form,
>> which does not react as it does not have a free carboxyl group. This
>> reduces the sugar available for reaction. I would be interested in
>> knowing whether glucose is released into the blood in ring or chain
>> form; I cannot find anything on that.
>>
>> Second, in the body there are irreversible reactions available to
>> further take one of the metabolite forms on towards AGEs, thereby
>> removing them from equilibrium. Over time, in the absence of other
>> factors, this will result in protein damage.
>>
>> Thirdly, there are enzymes within cells which actively reverse the
>> initial reaction, regenerating the protein and destroying the sugar.
>> These will affect the curve in vivo. Unfortunately, these only
>> operate within the cell, and cannot affect glycation which occurs
>> outside of the cell, such as nerve sheaths, collagen fibres in blood
>> vessel walls, etc. Google fructosamine-3-kinase.
>>
>> There is also a hormonal system related to childhood growth and adult
>> caloric restriction which affects insulin sensitivity & glucose
>> uptake, as well as cell division & cell clean up. This can also
>> affect the use of glucose and the amount available for these
>> reactions. Article in a recent SciAm.


> This exchange between yourself and Gys has been very interesting.
> Thank you both. My take-away from it is that short-term peaks aren't
> critically important, as long as BG comes back to normal (whatever
> that may be) after two or even three hours. Obviously, the higher the
> peak the longer it will take to come back down, so peaks can't be
> ignored completely.


Hi Chris,
you seem to be interested in the science behind this. Not as a means to
justify what you are doing already but as a means to maybe get a better
handle on this T2.

Here are a few more cents than

There is a difference between T1 and T2. Every dokter advices a T1 to check
his blood glucose 1 hour after the start of a meal. Why after the start of a
meal and not after ending a meal ? Well there is a physiological reason.
Your body notice the start of a meal by taste receptors in your mouth. There
are however also taste recpetors in your intestines and in your pancreas !!
There are an unbelieveable number of different receptors throughout your
body and brain to detect "food " No surprise because food is a strong
survival factor.

There is no equivalent physiological marker for the *end* of a meal. So
you will get the best *reproducible* blood glucose measurement if you
take the *Start* of your meal as time reference

If T1 you have no insulin production of your own and you will not only have
to inject it your self, but you must also provide the dynamic regulation.
Thus for T1 patients the dokter will advice to check your blood glucose
before and after a meal to check that you indeed injected the right amount
of insulin for this food.

There is no dokter who will advice you to measure your blood glucose before
and after a meal if you are a T2 patient. There is no point. You did not
inject insulin thus you can't modify that the next time. At this point in
time there is no evidence that self monitoring of blood glucose is
beneficial for T2.

If you look up a study on complications in *T2* the research will always
give the area under the curve for blood glucose measured by continuous blood
glucose monitoring or HbA1c as a good proxi for the total area under the
curve for the last mionth or so.

I don't know *any* article on the effect of glycemia on complications in
T2 that tries specifically to detect the peak in blood glucose and use that
to correlate the symptons with.

I agree with Chris (Malcolm) that for a T2 measuring your blood glucose 2 h
after the *start* of a meal is very usefull to find out which food should
be avoided. I did this my self for about 1 year after my diagnose. Than I
knew what foods cause an elevated blood glucose even 2 hours after the start
of a meal. That is the criterium for me : an elevated blood glucose 2 hours
after the *start* of a meal.

Everything before the 2 hour mark just has no effect because the reaction
between glucose and protein is reversible in that time frame.

So, when I go for a long ride on my bike a pauze with pancakes won't even
hit me. I'm back on my bike within two hours and my muscles greatfully
accept the glucose, even *without* *any* *insulin*.

But, when I got the flu, like today, I only eat green vegetables and maybe
some wanuts or berries. Because I don't move and don't need the energy and
like to avoid the 2h postprandial elevated blood glucose.

For me measuring my blood glucose was very beneficial during the first year
after dx. I'm not a very subborn guy. I got a pretty good idea how my body
reacts to exercise and food these days.

The take home message : measure your bg 2 h after the *start* of an
exercise or a meal if you really have no idea how it effects you.

Because the reaction between glucose and protein is reversible any value
before the 2 h mark does not contribute to the damage. You need the area
under the curve *after* the 2 h mark.

There will be people with research on the contribution of postprandial
glucose to HbA1c. I know all of them. I hope you will read the actual
articles. These are all epidemiological studies. Not randomized control
studies. So Imo here the postprandial high blood glucose is just a merker
for a very bad life style.

More cents :
The advanced glycation end products are not only formed in your body but
they can also be present already in the *food* you eat and have the same
devastating effects. Misses Vlassara H is an active researcher in this are :

Nat Rev Endocrinol. 2011 May 24;7(9):526-39. doi: 10.1038/nrendo.2011.74.
AGE restriction in diabetes mellitus: a paradigm shift.
PMID: 21610689

More cents :
Evolution decided that heated food is a survival factor. It is better
digestible and it contains less harmful microorganisms. Thus we develloped
means to get rid of the drawbacks of heated food. I agree with Canth in this
we have enzyme systems which will specifically breakdown the glycated
proteins here is an abstract :

Med Hypotheses. 2005;65(2):337-48.
Intrinsic toxicity of glucose, due to non-enzymatic glycation, is controlled
in-vivo by deglycation systems including: FN3K-mediated deglycation of
fructosamines and transglycation of aldosamines.
The deglycation hypothesis offers new paradigm for thinking about
non-enzymatic glycation and diabetic complications and offers possible
strategies for intervention in this and possibly other degenerative
conditions.
PMID: 15922110

There is another line of defense against advanced glycation end products.
The vast array of (soluble) AGE receptors. These are proteins which will
bind tightly to the Advanced Glycation End Products and make sure they are
removed from your body :

J Investig Med. 2011 Dec;59(8):1233-8.
Levels of soluble advanced glycation end product-receptors and other soluble
serum markers as indicators of diabetic neuropathy in the foot.
CONCLUSIONS: Soluble forms of the receptor for advanced glycation end
product could be an endogenous protection factor against occurrence of DF,
hence may be of therapeutic value in the treatment of DF.
PMID: 21941211

My 0.02 for T2 :
if you are not too stubborn you will know which foods will raise your blood
glucose 2h after the first bite. Further bg measurements are futile.

Your body has systems to cope with the advance glycation end products.

Changes in exercise, BMI and life style will greatly improve your T2 to the
point where futher discussions about measuring blood glucose becomes a silly
hobby

Gys

[Chris Hogg]

On Sun, 18 Mar 2012 15:36:32 +0100, "GysdeJongh"
<JonghSevenHundredElevenAtPlanet.nl> wrote:

>
>Hi Chris,
>you seem to be interested in the science behind this. Not as a means to
>justify what you are doing already but as a means to maybe get a better
>handle on this T2.
>
>Here are a few more cents than
>
>There is a difference between T1 and T2. Every dokter advices a T1 to check
>his blood glucose 1 hour after the start of a meal. Why after the start of a
>meal and not after ending a meal ? Well there is a physiological reason.
>Your body notice the start of a meal by taste receptors in your mouth. There
>are however also taste recpetors in your intestines and in your pancreas !!
>There are an unbelieveable number of different receptors throughout your
>body and brain to detect "food " No surprise because food is a strong
>survival factor.
>
>There is no equivalent physiological marker for the *end* of a meal. So
>you will get the best *reproducible* blood glucose measurement if you
>take the *Start* of your meal as time reference
>
>If T1 you have no insulin production of your own and you will not only have
>to inject it your self, but you must also provide the dynamic regulation.
>Thus for T1 patients the dokter will advice to check your blood glucose
>before and after a meal to check that you indeed injected the right amount
>of insulin for this food.
>
>There is no dokter who will advice you to measure your blood glucose before
>and after a meal if you are a T2 patient. There is no point. You did not
>inject insulin thus you can't modify that the next time. At this point in
>time there is no evidence that self monitoring of blood glucose is
>beneficial for T2.
>
>If you look up a study on complications in *T2* the research will always
>give the area under the curve for blood glucose measured by continuous blood
>glucose monitoring or HbA1c as a good proxi for the total area under the
>curve for the last mionth or so.
>
>I don't know *any* article on the effect of glycemia on complications in
>T2 that tries specifically to detect the peak in blood glucose and use that
>to correlate the symptons with.
>
>I agree with Chris (Malcolm) that for a T2 measuring your blood glucose 2 h
>after the *start* of a meal is very usefull to find out which food should
>be avoided. I did this my self for about 1 year after my diagnose. Than I
>knew what foods cause an elevated blood glucose even 2 hours after the start
>of a meal. That is the criterium for me : an elevated blood glucose 2 hours
>after the *start* of a meal.
>
>Everything before the 2 hour mark just has no effect because the reaction
>between glucose and protein is reversible in that time frame.
>
>So, when I go for a long ride on my bike a pauze with pancakes won't even
>hit me. I'm back on my bike within two hours and my muscles greatfully
>accept the glucose, even *without* *any* *insulin*.
>
>But, when I got the flu, like today, I only eat green vegetables and maybe
>some wanuts or berries. Because I don't move and don't need the energy and
>like to avoid the 2h postprandial elevated blood glucose.
>
>For me measuring my blood glucose was very beneficial during the first year
>after dx. I'm not a very subborn guy. I got a pretty good idea how my body
>reacts to exercise and food these days.
>
>The take home message : measure your bg 2 h after the *start* of an
>exercise or a meal if you really have no idea how it effects you.
>
>Because the reaction between glucose and protein is reversible any value
>before the 2 h mark does not contribute to the damage. You need the area
>under the curve *after* the 2 h mark.
>
>There will be people with research on the contribution of postprandial
>glucose to HbA1c. I know all of them. I hope you will read the actual
>articles. These are all epidemiological studies. Not randomized control
>studies. So Imo here the postprandial high blood glucose is just a merker
>for a very bad life style.
>
>More cents :
>The advanced glycation end products are not only formed in your body but
>they can also be present already in the *food* you eat and have the same
>devastating effects. Misses Vlassara H is an active researcher in this are :
>
>Nat Rev Endocrinol. 2011 May 24;7(9):526-39. doi: 10.1038/nrendo.2011.74.
>AGE restriction in diabetes mellitus: a paradigm shift.
>PMID: 21610689
>
>More cents :
>Evolution decided that heated food is a survival factor. It is better
>digestible and it contains less harmful microorganisms. Thus we develloped
>means to get rid of the drawbacks of heated food. I agree with Canth in this
>we have enzyme systems which will specifically breakdown the glycated
>proteins here is an abstract :
>
>Med Hypotheses. 2005;65(2):337-48.
>Intrinsic toxicity of glucose, due to non-enzymatic glycation, is controlled
>in-vivo by deglycation systems including: FN3K-mediated deglycation of
>fructosamines and transglycation of aldosamines.
>The deglycation hypothesis offers new paradigm for thinking about
>non-enzymatic glycation and diabetic complications and offers possible
>strategies for intervention in this and possibly other degenerative
>conditions.
>PMID: 15922110
>
>There is another line of defense against advanced glycation end products.
>The vast array of (soluble) AGE receptors. These are proteins which will
>bind tightly to the Advanced Glycation End Products and make sure they are
>removed from your body :
>
>J Investig Med. 2011 Dec;59(8):1233-8.
>Levels of soluble advanced glycation end product-receptors and other soluble
>serum markers as indicators of diabetic neuropathy in the foot.
>CONCLUSIONS: Soluble forms of the receptor for advanced glycation end
>product could be an endogenous protection factor against occurrence of DF,
>hence may be of therapeutic value in the treatment of DF.
>PMID: 21941211
>
>My 0.02 for T2 :
>if you are not too stubborn you will know which foods will raise your blood
>glucose 2h after the first bite. Further bg measurements are futile.
>
>Your body has systems to cope with the advance glycation end products.
>
>Changes in exercise, BMI and life style will greatly improve your T2 to the
>point where futher discussions about measuring blood glucose becomes a silly
>hobby
>
>Gys

Hi Gys. Thank you for all that. When I was diagnosed, ten years ago,
the nurse who gave me my meter advised me to test two hours after a
meal to make sure my BG's were back down to near 'background' levels,
but didn't seem to think it made much difference whether two hours
after the start or the end of the meal. So I reasoned that if it was a
long meal, with maybe a low carb start and a high carb finish, the
testing two hours after the start of the meal would put me right on
the glucose peak, so I opted to test 2 hours after the end of the
meal.

Ten years later, my fasting BG averages about 0.7 of a unit lower than
it was when first diagnosed (say 5.4 compared with 6.1 mmol/l). I
measure three times a day, fasting and two postprandial tests, on two
days per week. I put all the data on a spreadsheet and then do a
monthly average of the those results, graph them up and have data
going back to 2003. This is to keep an eye on long-term trends. My
HbA1C has never been above 6% (typically 5.7%) and cholesterol is also
good, so I must be doing something right.

Now I expect you'll tell me that those measurements don't really say
anything about AGE's, and that I still ought to test 2 hrs after the
start of my meals. But in reality, my meals rarely last longer than
about 15 minutes, so the difference is not great and I'm not inclined
to change!

--

Chris

T2 DX'd 2002, D&E, HbA1c 5.7, BMI 21
Lipids:Tot 4.6 HDL 1.5 LDL 2.8 Tri 0.7

[GysdeJongh]

Chris Hogg wrote:
> On Sun, 18 Mar 2012 15:36:32 +0100, "GysdeJongh"
> <JonghSevenHundredElevenAtPlanet.nl> wrote:


> Hi Gys. Thank you for all that. When I was diagnosed, ten years ago,
> the nurse who gave me my meter advised me to test two hours after a
> meal to make sure my BG's were back down to near 'background' levels,
> but didn't seem to think it made much difference whether two hours
> after the start or the end of the meal. So I reasoned that if it was a
> long meal, with maybe a low carb start and a high carb finish, the
> testing two hours after the start of the meal would put me right on
> the glucose peak, so I opted to test 2 hours after the end of the
> meal.


See, if you want to "chase peaks" it even causes a "feeling" that something
might be wrong if your meal has a high carb finish.

That is because you need the area under the curve and not the height of the
peak if you are interested in the total reaction product from the Maillard
reaction. Which will remove all ambiguities.

If you decide to lower the peak by ingesting fat with carbohydrate, then the
peak might be lower but much broader and the area under the curve, which is
now above your background value for much longer, might well be greater. So
will be the damage from advance glycation end products.

Only if you were T1 you would be interested in the dynamic regulation you
provided with your insulin shots and you would be interested in the
bloodglucose 2 h after the first bite of your meal.

I was diagnosed in 2005, on Metformin, Lyrica, Tramadol and a lot of
supplements. The dokter did not give me a bloodglucose meter and the
insurance did not pay for the meter or the strips. I bought those myself.
Since about 2 years I'm on Exercise & Diet only. My dokter says I'm nolonger
T2 but keeps me under control for 1/year instead of 4/year. My last HbA1c
was 5.4% My lipid panel is out of the danger zone. It was never better. No
more night cramps, no longer sleepy. Those were all side effects of the
med's and the supp's.
So maybe we both do something right


> Now I expect you'll tell me that those measurements don't really say
> anything about AGE's, and that I still ought to test 2 hrs after the
> start of my meals. But in reality, my meals rarely last longer than
> about 15 minutes, so the difference is not great and I'm not inclined
> to change!


Ah, there you go wrong. I will never advice you anything. I'm interested in
*why* you do *what* you do. If you show me the science behind your
personal management of T2 I might decide that it is time for me to change a
few things in your direction after I have weighted the evidence.

So for the time being I'm not going to start "chasing peaks" but avoid food
which will cause too large increase in my bloodglucose 2h after the start.

Gys

[Chris Hogg]

On Tue, 20 Mar 2012 12:32:53 +0100, "GysdeJongh"
<JonghSevenHundredElevenAtPlanet.nl> wrote:


>So for the time being I'm not going to start "chasing peaks" but avoid food
>which will cause too large increase in my bloodglucose 2h after the start.
>
Which is what I do, except it's 2h after the finish.

--

Chris

T2 DX'd 2002, D&E, HbA1c 5.7, BMI 21
Lipids:Tot 4.6 HDL 1.5 LDL 2.8 Tri 0.7

[Chris Malcolm]

Chris Hogg <[email protected]> wrote:
> On Fri, 16 Mar 2012 02:37:01 +1030, Canth <[email protected]>
> wrote:
>>On Thu, 15 Mar 2012 09:31:45 +0000, Chris Hogg <[email protected]> wrote:
>>>On Thu, 15 Mar 2012 11:59:43 +1030, Canth <[email protected]>
>>>wrote:
>>>>On Wed, 14 Mar 2012 21:26:09 +0000, Chris Hogg <[email protected]> wrote:
>>>>>On Wed, 14 Mar 2012 20:20:02 +0100, "GysdeJongh"
>>>>><JonghSevenHundredElevenAtPlanet.nl> wrote:
>>>>>>Chris Hogg wrote:
>>>>>>
>>>>>>> The coconut fat
>>>>>>> blunts and broadens the spike.
>>>>>>
>>>>>>But ...
>>>>>>does that prevent damage from advanced glycation end products ????
>>>>>>
>>>>>>Chemistry 101 : the amount of product formed during a chemical reaction
>>>>>>depends on the concentration of the reactants *and* on the reaction
>>>>>>*time*
>>>>>>
>>>>>>Ever wondered *why* we measure HbA1c ? Ever wondered *why* experiments
>>>>>>measure the area under the curve of blood glucose vs time and never the
>>>>>>maximum peak height ?
>>>>>>
>>>>>>So
>>>>>>your long broad peak might have the same area as your thin high peak and
>>>>>>thus produce exactly the same damage to your arteries
>>>>>>
>>>>>Well, yes, I sort of knew that from chemistry lessons of many decades
>>>>>ago! But IIRC it does depend on the reaction being first order; if
>>>>>glycation is second order wrt glucose (i.e. rate proportional to the
>>>>>square of the glucose conc.), then lowering the peak and broadening it
>>>>>would make a big difference. But it's probably first order, although I
>>>>>doubt anyone actually knows. Another complicating factor would be if
>>>>>there was a threshold value below which no damage occurred.
>>>>>
>>>>
>>>>From what I understand, glycation and deglycation are competing
>>>>reactions, both moderated actively by the glucose concentration. When
>>>>glucose concentration is low, deglycation is actively promoted &
>>>>glycation is actively suppressed. When glucose levels are high,
>>>>glycation is actively promoted & deglycation is actively suppressed. A
>>>>simple area under the curve analysis therefore doesn't work. The net
>>>>amount of glycation that occurs because of high narrow peaks is
>>>>probably greater than the amount under a broader but lower peak
>>>>because the reaction catalysts are more affected by the glucose
>>>>concentrations.
>>>>
>>>That's interesting. All chemical reactions are, in theory, equilibria
>>>and potentially reversible, although some are more difficult to
>>>reverse than others. Do you have any references or citations that I
>>>could follow up?
>>>>
>>
>>The above was a hazy memory of the processes. Glys has pointed me to
>>the more precise mechanisms. The major culprit is a non-enzymatic
>>reaction between the carboxyl group of a sugar in its straight chain
>>form and any spare amine groups on proteins. This reaction is
>>reversible, and in isolation is linear with respect to the
>>concentration of glucose. Over time, in the absence of any other
>>reactions, the whole mess will reach equilibrium with various
>>products. Google Amadori reaction.
>>
>>However, there are a number of factors involved as well in the body.
>>First, most natural sugars spend most of their time in a ring form,
>>which does not react as it does not have a free carboxyl group. This
>>reduces the sugar available for reaction. I would be interested in
>>knowing whether glucose is released into the blood in ring or chain
>>form; I cannot find anything on that.
>>
>> Second, in the body there are irreversible reactions available to
>>further take one of the metabolite forms on towards AGEs, thereby
>>removing them from equilibrium. Over time, in the absence of other
>>factors, this will result in protein damage.
>>
>>Thirdly, there are enzymes within cells which actively reverse the
>>initial reaction, regenerating the protein and destroying the sugar.
>>These will affect the curve in vivo. Unfortunately, these only
>>operate within the cell, and cannot affect glycation which occurs
>>outside of the cell, such as nerve sheaths, collagen fibres in blood
>>vessel walls, etc. Google fructosamine-3-kinase.
>>
>>There is also a hormonal system related to childhood growth and adult
>>caloric restriction which affects insulin sensitivity & glucose
>>uptake, as well as cell division & cell clean up. This can also
>>affect the use of glucose and the amount available for these
>>reactions. Article in a recent SciAm.

> This exchange between yourself and Gys has been very interesting.
> Thank you both. My take-away from it is that short-term peaks aren't
> critically important, as long as BG comes back to normal (whatever
> that may be) after two or even three hours. Obviously, the higher the
> peak the longer it will take to come back down, so peaks can't be
> ignored completely.

Three reasons why I take short term peaks more seriously.

1. A brief high peak sets me on a carby craving roller coaster for the
rest of the day. Seriously messes up my eating, my energy, and my
mood.

2. A brief high peak pushes up my neuropathic symptoms to a degree
that often takes days of much more careful eating to recover from. And
if another brief high peak occurs before the recovery is complete it
can take weeks to recover from it.

3. Has the above discussion covered all kinds of glycation? Is there a
possibly that in certain tissues there are less easily reversible
glycations happening? There seems some suggestive evidence in the
varying BG thresholds for various kinds of diabetic complication
damage to suggest that the glycation playing field in far from level.

--
Chris Malcolm

[Chris Malcolm]

GysdeJongh <JonghSevenHundredElevenAtPlanet.nl> wrote:

[snip]

> There is no dokter who will advice you to measure your blood glucose before
> and after a meal if you are a T2 patient.

They may be a minority, but they exist.

> There is no point. You did not
> inject insulin thus you can't modify that the next time. At this point in
> time there is no evidence that self monitoring of blood glucose is
> beneficial for T2.

Quite right. When all the study compared was those who monitored and
those who didn't. But if your monitoring doesn't cause you to change
your behaviour of course it will have no effect! There have been other
studies which compared no monitoring with people who not only
monitored but were given advice about how to use their monitoring to
adapt their eating etc. to improve their BG control. Not surprisingly
those found BGs improved in the monitoring group.

Of course there is then the question of whether that improvement in
local BGs added up to any long term benefit. AFAIK those studies
haven't been done. So there is no evidence it does any good. Which as
I'm sure you're aware is very different from saying there is evidence
that it does no good :-)

> If you look up a study on complications in *T2* the research will always
> give the area under the curve for blood glucose measured by continuous blood
> glucose monitoring or HbA1c as a good proxi for the total area under the
> curve for the last mionth or so.

> I don't know *any* article on the effect of glycemia on complications in
> T2 that tries specifically to detect the peak in blood glucose and use that
> to correlate the symptons with.

> I agree with Chris (Malcolm) that for a T2 measuring your blood glucose 2 h
> after the *start* of a meal is very usefull to find out which food should
> be avoided. I did this my self for about 1 year after my diagnose. Than I
> knew what foods cause an elevated blood glucose even 2 hours after the start
> of a meal. That is the criterium for me : an elevated blood glucose 2 hours
> after the *start* of a meal.

> Everything before the 2 hour mark just has no effect because the reaction
> between glucose and protein is reversible in that time frame.

If as I mentioned in another post the glycation damage playing field
is level. And if glycation accounts for all the damage associated with
high BGs in vivo as opposed to in vitro.

--
Chris Malcolm

[Chris Malcolm]

Chris Hogg <[email protected]> wrote:
> On Tue, 20 Mar 2012 12:32:53 +0100, "GysdeJongh"
> <JonghSevenHundredElevenAtPlanet.nl> wrote:

>>So for the time being I'm not going to start "chasing peaks" but avoid food
>>which will cause too large increase in my bloodglucose 2h after the start.

> Which is what I do, except it's 2h after the finish.

For the reasons Gys mentions the research on 2h post meal BF readings
measures two hours after the start. Which may only matter to you if
you want to compare yourself to what happens in the published studies.

--
Chris Malcolm

[Julie Bove]

"Chris Malcolm" <[email protected]> wrote in message
news:[email protected]..
> GysdeJongh <JonghSevenHundredElevenAtPlanet.nl> wrote:
>
> [snip]
>
>> There is no dokter who will advice you to measure your blood glucose
>> before
>> and after a meal if you are a T2 patient.
>
> They may be a minority, but they exist.
>
>> There is no point. You did not
>> inject insulin thus you can't modify that the next time. At this point in
>> time there is no evidence that self monitoring of blood glucose is
>> beneficial for T2.
>
> Quite right. When all the study compared was those who monitored and
> those who didn't. But if your monitoring doesn't cause you to change
> your behaviour of course it will have no effect! There have been other
> studies which compared no monitoring with people who not only
> monitored but were given advice about how to use their monitoring to
> adapt their eating etc. to improve their BG control. Not surprisingly
> those found BGs improved in the monitoring group.
>
> Of course there is then the question of whether that improvement in
> local BGs added up to any long term benefit. AFAIK those studies
> haven't been done. So there is no evidence it does any good. Which as
> I'm sure you're aware is very different from saying there is evidence
> that it does no good :-)
>
>> If you look up a study on complications in *T2* the research will
>> always
>> give the area under the curve for blood glucose measured by continuous
>> blood
>> glucose monitoring or HbA1c as a good proxi for the total area under the
>> curve for the last mionth or so.
>
>> I don't know *any* article on the effect of glycemia on complications
>> in
>> T2 that tries specifically to detect the peak in blood glucose and use
>> that
>> to correlate the symptons with.
>
>> I agree with Chris (Malcolm) that for a T2 measuring your blood glucose 2
>> h
>> after the *start* of a meal is very usefull to find out which food
>> should
>> be avoided. I did this my self for about 1 year after my diagnose. Than I
>> knew what foods cause an elevated blood glucose even 2 hours after the
>> start
>> of a meal. That is the criterium for me : an elevated blood glucose 2
>> hours
>> after the *start* of a meal.
>
>> Everything before the 2 hour mark just has no effect because the reaction
>> between glucose and protein is reversible in that time frame.
>
> If as I mentioned in another post the glycation damage playing field
> is level. And if glycation accounts for all the damage associated with
> high BGs in vivo as opposed to in vitro.
>
> --
> Chris Malcolm

I missed the OP somehow. I am type 2. Yes, I use insulin now but I didn't
always. I have always tested before eating and 2 hours after eating at
least 2 days a week per my Drs. orders. I have been to three Endos. All
wanted me to do the same thing. I also test before bed.

[Ozgirl]

"Chris Hogg" <[email protected]> wrote in message
news:[email protected]..
> On Tue, 20 Mar 2012 12:32:53 +0100, "GysdeJongh"
> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>
>
>>So for the time being I'm not going to start "chasing peaks" but
>>avoid food
>>which will cause too large increase in my bloodglucose 2h after the
>>start.
>>
> Which is what I do, except it's 2h after the finish.

In the past if I had a good reading at 2 hours post oatmeal it was
because I had a big rise early then a big drop. The first time I had a
reactive hypoglycemic episode (my RH was severe until I learned how to
control it) was half an hour after oatmeal every morning. Back then
there were no home meters (even if I had known what they were) and it
started shortly after my third child's birth. As I had 4 gestational
diabetes pregnancies after that I have to presume I may have had GD with
that pregnancy too.

I almost blamed my laundry for my symptoms, lol. It was always about
half an hour after breakfast that I trotted up the yard to my free
standing laundry to start the day's wash. My legs would buckle
underneath me and I would crawl back to the house shaking. My legs
couldn't support me at all. The next time, other than post oatmeal I was
walking up hundreds of stairs in a touristy part of Sydney, holding my 6
week old daughter while my older two kids were carrying the pram and
bags. How I didn't fall down those stairs I have no idea. Lunch not long
before had been hot dog, chips and a Coke.

So I guess what I am trying to say is that I have always chased peaks
and based my meal moderations on an early bg - sometimes even 15 -30
minutes PP

[Susan]

x-no-archive: yes

On 3/20/2012 7:47 PM, Chris Malcolm wrote:
> Chris Hogg<[email protected]> wrote:
>> On Tue, 20 Mar 2012 12:32:53 +0100, "GysdeJongh"
>> <JonghSevenHundredElevenAtPlanet.nl> wrote:
>
>>> So for the time being I'm not going to start "chasing peaks" but avoid food
>>> which will cause too large increase in my bloodglucose 2h after the start.
>
>> Which is what I do, except it's 2h after the finish.
>
> For the reasons Gys mentions the research on 2h post meal BF readings
> measures two hours after the start. Which may only matter to you if
> you want to compare yourself to what happens in the published studies.
>

Something I remembered from www.phlaunt.com/diabetes, a very well
researched site with studies about when and at what levels glucose does
damage:

Inflammation markers and metabolic characteristics of subjects with
one-hour plasma glucose levels
1. Gianluca Bardini, MD, PhD,
2. Ilaria Dicembrini, MD,
3. Barbara Cresci, MD and
4. Carlo Maria Rotella, MD ([email protected])
+Author Affiliations
1. Section of Endocrinology, Department of Clinical Pathophysiology,
University of Florence, Italy
Abstract
Objective: To assess the association of 1-h plasma glucose (1hPG) and
inflammation with normal glucose tolerance (NGT) and pre-diabetes (pre-DM).
Research Design And Methods: A cohort of 1062 subjects was enrolled.
After oral glucose load (OGTT), we compared NGT and pre-DM subjects
above and below the 1hPG cut point (155 mg/dl). Fibrinogen and
leucocytes count (WBC) for subclinical inflammation, lipid ratios,
insulin sensitivity (Matsuda Index), were determined.
Results: NGT and pre-DM patients 1hPG>155 mg/dl showed a significant
increase of inflammatory markers and lipid ratios (for all, p<0.05). In
age-sex-BMI-adjusted analysis, 1hPG is associated with a significant
higher WBC count and fibrinogen (p<0.05). Patients with elevated 1hPG
showed a highly significant lower insulin sensitivity than subjects
below 1hPG (p<0.01).


Conclusions: Elevated 1hPG in NGT and pre-DM subjects is associated to
subclinical inflammation, high lipid ratios and insulin resistance.
Therefore, 1hPG >155 mg/dl could be considered a new “marker” for
cardiovascular risk.