Post Prandial Peaks

I was challenged on the ADA forum to back up my promotion of
one-hour post-prandial blood glucose tests to review a type
2's menu.

In fact, while I do believe newbies should test at one hour
as well as two hours, my real support is for finding your
peak post-prandial (PPP) time and to use that for tests.
However, the point was made that there is no peer-reviewed
research evidence supporting my contention and that most
papers discussing post-prandial testing only refer to
two-hour tests.

I give my own logic here:
http://loraldiabetes.blogspot.com/20...-two-hour.html

I'm attempting to find any papers mentioning the use of
one-hour tests or, preferably, peak post-prandial tests, but
I doubt I'll find many. However, any references others may
have would be appreciated, even if they are oblique.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: Slovenia

"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
news:c9lp439qtraq1bitufj273j605i8i183tj@4ax.com...
>I was challenged on the ADA forum to back up my promotion of
> one-hour post-prandial blood glucose tests to review a type
> 2's menu.
>
> In fact, while I do believe newbies should test at one hour
> as well as two hours, my real support is for finding your
> peak post-prandial (PPP) time and to use that for tests.
> However, the point was made that there is no peer-reviewed
> research evidence supporting my contention and that most
> papers discussing post-prandial testing only refer to
> two-hour tests.
>
> I give my own logic here:
> http://loraldiabetes.blogspot.com/20...-two-hour.html
>
> I'm attempting to find any papers mentioning the use of
> one-hour tests or, preferably, peak post-prandial tests, but
> I doubt I'll find many. However, any references others may
> have would be appreciated, even if they are oblique.

I've said from waaay back that my peaks always come at the two hour mark.
And now I know why. I have gastroparesis, aka delayed stomach emptying.
And actually if my stomach isn't working well at all that day, I may spike
even higher than that at the 4 of 5 hour mark.

I think we're all different and we need to determine which is our peak time.

On Thu, 17 May 2007 22:33:03 GMT, Alan S
<loralgtweightandcarbs@gmail.com> wrote:

>I was challenged on the ADA forum to back up my promotion of
>one-hour post-prandial blood glucose tests to review a type
>2's menu.

I suspect the 2-hour figure is shown because that correlates with the
A1c - it's the same timescale as the irreversible glycation. So I
guess we're back to the AUC versus spike debate... there is some
literature supporting 1-hour, though.

Here's one: Figure 1 is good.
http://www.medscape.com/viewarticle/491410_1
For normal subjects:"Meal ingestion, regardless of the meal's size,
normally results in only transient increases in plasma glucose:
concentrations peak at 60 to 90 minutes, rarely exceed 160 mg/dL, and
return to preprandial values within 3 hours."[4]

For diabetics:"Both groups have impaired suppression of glucagon
secretion, reduced early insulin release, and insulin
resistance.[15,16] As a consequence, overall release of glucose is
increased after meal ingestion. Most of the excess release of glucose
occurs within the first 2 hours, is correlated with changes in
glucagon and insulin,[8] and is the result of both increased release
of endogenous glucose and glucose contained in the meal.[17] "

In other words, a diabetic's curve may be complicated by glucose
release from the liver. This certainly corresponds to my experience -
my curve normalised as my liver did.

The references may be worth following up:
4 Rizza R, Gerich J, Haymond M, et al. Control of blood sugar in
insulin-dependent diabetes: comparison of an artificial endocrine
pancreas, subcutaneous insulin infusion and intensified conventional
insulin therapy. N Engl J Med. 1980;303:1313-1318.
http://intapp.medscape.com/px/medlin...001229&cid=med

8 Woerle HJ, SzokeE, Gosmanov N, et al. Abnormal postprandial
splanchnic and peripheral glucose disposal in type 2 diabetes.
Diabetes. 2004;53(suppl 2):A374.

15 Wolfe R, Durkot M. Evaluation of the role of the sympathetic
nervous system in the response of substrate kinetics and oxidation to
burn injury. Circ Shock. 1982;9:395-406
http://intapp.medscape.com/px/medlin...811154&cid=med

16 Mitrakou A, Kelley D, Veneman T, et al. Contribution of abnormal
muscle and liver glucose metabolism in postprandial hyperglycemia in
noninsulin-dependent diabetes mellitus. Diabetes. 1990;39:1381-1390.
http://intapp.medscape.com/px/medlin...121568&cid=med

Meyer C, Woerle HJ, Dostou J, Welle S, Gerich JE. Abnormal renal,
hepatic and muscle glucose metabolism following glucose ingestion in
type 2 diabetes. Am J Physiol Endocrinol Metab. 2004 Aug 10




These guys used 1-hour figures to predict heart attack, but I can't
find a link:
Donahue RP, Abbott RD, Reed DM, Yano K: Postchallenge glucose
concentration and coronary heart disease in men of Japanese ancestry:
Honolulu Heart Program. Diabetes 36:689-692,1987

I have a vague memory of reading more Japanese studies around 1-hour
pp, but I can't find them in my link collection. I need to put a
desktop indexer on this PC...


To add a bit of anecdotal evidence; I had a large slice of fresh
pineapple as a dessert last night; main meal was a BLT on 2 slices of
3g CHO bread. The last profile I took for pineapple was months ago, so
I tested. Pre-meal was 4.8. At 15 mins I was 6.1; 30 mins, 6.7; 45
mins, 7.6; 60 mins, 5.1; 90mins, 5.0; 120 mins, 5.2. I'm still
debating with my test buds as to whether that 7.6 was acceptable. My
organic veg man brought me one large and one small pineapple this week
- the kids and I are bathing in the stuff

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.5% BMI 25

On Fri, 18 May 2007 09:01:17 +0100, Nicky
<ukc802466929@btconnect.com> wrote:

>On Thu, 17 May 2007 22:33:03 GMT, Alan S
><loralgtweightandcarbs@gmail.com> wrote:
>
>>I was challenged on the ADA forum to back up my promotion of
>>one-hour post-prandial blood glucose tests to review a type
>>2's menu.
>
>I suspect the 2-hour figure is shown because that correlates with the
>A1c - it's the same timescale as the irreversible glycation. So I
>guess we're back to the AUC versus spike debate... there is some
>literature supporting 1-hour, though.
>
>Here's one: Figure 1 is good.
>http://www.medscape.com/viewarticle/491410_1
>For normal subjects:"Meal ingestion, regardless of the meal's size,
>normally results in only transient increases in plasma glucose:
>concentrations peak at 60 to 90 minutes, rarely exceed 160 mg/dL, and
>return to preprandial values within 3 hours."[4]
>
>For diabetics:"Both groups have impaired suppression of glucagon
>secretion, reduced early insulin release, and insulin
>resistance.[15,16] As a consequence, overall release of glucose is
>increased after meal ingestion. Most of the excess release of glucose
>occurs within the first 2 hours, is correlated with changes in
>glucagon and insulin,[8] and is the result of both increased release
>of endogenous glucose and glucose contained in the meal.[17] "
>
>In other words, a diabetic's curve may be complicated by glucose
>release from the liver. This certainly corresponds to my experience -
>my curve normalised as my liver did.
>
>The references may be worth following up:
>4 Rizza R, Gerich J, Haymond M, et al. Control of blood sugar in
>insulin-dependent diabetes: comparison of an artificial endocrine
>pancreas, subcutaneous insulin infusion and intensified conventional
>insulin therapy. N Engl J Med. 1980;303:1313-1318.
>http://intapp.medscape.com/px/medlin...001229&cid=med
>
>8 Woerle HJ, SzokeE, Gosmanov N, et al. Abnormal postprandial
>splanchnic and peripheral glucose disposal in type 2 diabetes.
>Diabetes. 2004;53(suppl 2):A374.
>
>15 Wolfe R, Durkot M. Evaluation of the role of the sympathetic
>nervous system in the response of substrate kinetics and oxidation to
>burn injury. Circ Shock. 1982;9:395-406
>http://intapp.medscape.com/px/medlin...811154&cid=med
>
>16 Mitrakou A, Kelley D, Veneman T, et al. Contribution of abnormal
>muscle and liver glucose metabolism in postprandial hyperglycemia in
>noninsulin-dependent diabetes mellitus. Diabetes. 1990;39:1381-1390.
>http://intapp.medscape.com/px/medlin...121568&cid=med
>
>Meyer C, Woerle HJ, Dostou J, Welle S, Gerich JE. Abnormal renal,
>hepatic and muscle glucose metabolism following glucose ingestion in
>type 2 diabetes. Am J Physiol Endocrinol Metab. 2004 Aug 10
>
>
>
>
>These guys used 1-hour figures to predict heart attack, but I can't
>find a link:
>Donahue RP, Abbott RD, Reed DM, Yano K: Postchallenge glucose
>concentration and coronary heart disease in men of Japanese ancestry:
>Honolulu Heart Program. Diabetes 36:689-692,1987
>
>I have a vague memory of reading more Japanese studies around 1-hour
>pp, but I can't find them in my link collection. I need to put a
>desktop indexer on this PC...
>
>
>To add a bit of anecdotal evidence; I had a large slice of fresh
>pineapple as a dessert last night; main meal was a BLT on 2 slices of
>3g CHO bread. The last profile I took for pineapple was months ago, so
>I tested. Pre-meal was 4.8. At 15 mins I was 6.1; 30 mins, 6.7; 45
>mins, 7.6; 60 mins, 5.1; 90mins, 5.0; 120 mins, 5.2. I'm still
>debating with my test buds as to whether that 7.6 was acceptable. My
>organic veg man brought me one large and one small pineapple this week
>- the kids and I are bathing in the stuff
>
>Nicky.
>T2 dx 05/04 + underactive thyroid
>D&E, 100ug thyroxine
>Last A1c 5.5% BMI 25

Thanks Nicky, looks like I'll be spending the weekend
reading. More to come I hope.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: Slovenia

On Fri, 18 May 2007 09:01:17 +0100, Nicky
<ukc802466929@btconnect.com> wrote:

>These guys used 1-hour figures to predict heart attack, but I can't
>find a link:
>Donahue RP, Abbott RD, Reed DM, Yano K: Postchallenge glucose
>concentration and coronary heart disease in men of Japanese ancestry:
>Honolulu Heart Program. Diabetes 36:689-692,1987

http://tinyurl.com/2jpr2h or
http://diabetes.diabetesjournals.org...urcetype=HWCIT
and also
http://tinyurl.com/3yqsyy or
http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Citation
Only the abstract I'm afraid.

Dated 1987 - 20 years old - where is the continuing
research? The "This article has been cited by" dowsn't look
promising, but I'm wading through them.

This sounds to me like more than enough of a reason to keep
1hr PP in reasonable territory. To summarise; the higher
your BG's at one hour then the more likely you were to
suffer a fatal heart attack by significant factors:

"Postchallenge glucose concentration and coronary heart
disease in men of Japanese ancestry. Honolulu Heart Program

RP Donahue, RD Abbott, DM Reed and K Yano

Since 1965, the Honolulu Heart Program has followed 8006 men
of Japanese ancestry, aged 45-70 yr at study entry, for the
development of cardiovascular disease. To investigate the
role of glucose concentration 1 h after a 50-g challenge on
the risk of fatal coronary heart disease (CHD) and nonfatal
myocardial infarction (MI), 6394 nondiabetic men were
followed for 12 yr for the first development of CHD. The
rate of fatal CHD increased linearly with amount of glucose.
Men in the fourth quintile of postchallenge glucose (157-189
mg/dl) had twice the age-adjusted risk of fatal CHD of those
in the lowest quintile (P less than .05). Relative risk
increased to threefold among those in the top quintile and
remained statistically significant after adjustment for
other risk factors including body mass, total cholesterol,
hypertension, left ventricular hypertrophy, and hematocrit
(P less than .001). When glucose was considered as a linear
term in the proportional hazards model, a highly significant
relation was noted with fatal CHD alone and when combined
with nonfatal MI (P less than .001). We conclude that a
continuously increasing risk gradient exists between
postchallenge glucose and subsequent CHD that is independent
of other known risk factors."

Thanks again Nicky.

Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: Slovenia

There seems to me to be two trains of thought to be followed up here Alan.

1. The effect of postprandial excursions into hyperglycemia territory being
more indicative of complications (particularly of the cardio vascular
system) than the A1c. There is growing evidence backing this up including
the DCCT even though that was a type 1 study.

2. The effect of postprandial hyperglycemic episodes on the progression of
type 2 diabetes. Read the last sentence in the following:

"Both type I and type II diabetes are characterised by a progressive
decrease in beta-cell function and mass. In type I diabetes, autoimmune
destruction results in rapid loss of beta-cell function, and insulin therapy
is essential to maintain normoglycaemia. In type II diabetes, a diminished
or absent first-phase insulin release is the earliest metabolic defect,
which is accompanied by lack of prandial suppression of hepatic glucose
production, increased postprandial glucose excursions and late insulin
hypersecretion. Furthermore, chronic exposure to elevated glucose, *even to
intermittent postprandial spikes*, results in further deterioration of the
beta-cell function ('glucotoxicity')." Emphasis is mine. Good enough reason
to seriously think about spikes as being capable of causing diabetic
progression.

http://www.medscape.com/medline/abstract/15306831

"By the time type II diabetes is diagnosed, beta-cell function and mass have
declined by about 50%. With the progression of the disease and glucotoxicity
there is continuous decrease in beta-cell mass due to increased apoptosis
that results in absolute insulin deficiency. By then, patients require
insulin administration to maintain glucose control. An increasing body of
evidence demonstrates the importance of preserving endogenous beta-cell
function both in type I and type II diabetes. Early and intensive glycaemic
control, using regimens which re-create a physiological insulin profile,
controlling postprandial as well as fasting glucose levels, offers the most
promise for preserving beta-cell function, decreasing disease progression,
and reducing the chronic complications of diabetes."


"Nicky" <ukc802466929@btconnect.com> wrote in message
news:t7mq43dn8bbivt1kv3gc1lshju29or0rju@4ax.com...
> On Thu, 17 May 2007 22:33:03 GMT, Alan S
> <loralgtweightandcarbs@gmail.com> wrote:
>
> >I was challenged on the ADA forum to back up my promotion of
> >one-hour post-prandial blood glucose tests to review a type
> >2's menu.
>
> I suspect the 2-hour figure is shown because that correlates with the
> A1c - it's the same timescale as the irreversible glycation. So I
> guess we're back to the AUC versus spike debate... there is some
> literature supporting 1-hour, though.

On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
<are_we_there_yet@maccas.com> wrote:

>There seems to me to be two trains of thought to be followed up here Alan.
>
>1. The effect of postprandial excursions into hyperglycemia territory being
>more indicative of complications (particularly of the cardio vascular
>system) than the A1c. There is growing evidence backing this up including
>the DCCT even though that was a type 1 study.
>
>2. The effect of postprandial hyperglycemic episodes on the progression of
>type 2 diabetes. Read the last sentence in the following:
>
>"Both type I and type II diabetes are characterised by a progressive
>decrease in beta-cell function and mass. In type I diabetes, autoimmune
>destruction results in rapid loss of beta-cell function, and insulin therapy
>is essential to maintain normoglycaemia. In type II diabetes, a diminished
>or absent first-phase insulin release is the earliest metabolic defect,
>which is accompanied by lack of prandial suppression of hepatic glucose
>production, increased postprandial glucose excursions and late insulin
>hypersecretion. Furthermore, chronic exposure to elevated glucose, *even to
>intermittent postprandial spikes*, results in further deterioration of the
>beta-cell function ('glucotoxicity')." Emphasis is mine. Good enough reason
>to seriously think about spikes as being capable of causing diabetic
>progression.
>
>http://www.medscape.com/medline/abstract/15306831
>
>"By the time type II diabetes is diagnosed, beta-cell function and mass have
>declined by about 50%. With the progression of the disease and glucotoxicity
>there is continuous decrease in beta-cell mass due to increased apoptosis
>that results in absolute insulin deficiency. By then, patients require
>insulin administration to maintain glucose control. An increasing body of
>evidence demonstrates the importance of preserving endogenous beta-cell
>function both in type I and type II diabetes. Early and intensive glycaemic
>control, using regimens which re-create a physiological insulin profile,
>controlling postprandial as well as fasting glucose levels, offers the most
>promise for preserving beta-cell function, decreasing disease progression,
>and reducing the chronic complications of diabetes."

Bothy good points - but slightly tangential to the basic
question I was given: Why 1hr instead of 2hr? Or the way I
am interpreting that: Why peak instead of 2hr?

But I'll certainly be including those aspects.

This may take longer than the weekend; 40+ papers to wade
through so far; needle in a haystack stuff, most are only
indirectly relevant.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: Slovenia

"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
news:hgtq431bavigstf2lqva99o3gbtknp70l5@4ax.com...
> On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
> <are_we_there_yet@maccas.com> wrote:
>
> >There seems to me to be two trains of thought to be followed up here
Alan.
> >
> >1. The effect of postprandial excursions into hyperglycemia territory
being
> >more indicative of complications (particularly of the cardio vascular
> >system) than the A1c. There is growing evidence backing this up including
> >the DCCT even though that was a type 1 study.
> >
> >2. The effect of postprandial hyperglycemic episodes on the progression
of
> >type 2 diabetes. Read the last sentence in the following:
> >
> >"Both type I and type II diabetes are characterised by a progressive
> >decrease in beta-cell function and mass. In type I diabetes, autoimmune
> >destruction results in rapid loss of beta-cell function, and insulin
therapy
> >is essential to maintain normoglycaemia. In type II diabetes, a
diminished
> >or absent first-phase insulin release is the earliest metabolic defect,
> >which is accompanied by lack of prandial suppression of hepatic glucose
> >production, increased postprandial glucose excursions and late insulin
> >hypersecretion. Furthermore, chronic exposure to elevated glucose, *even
to
> >intermittent postprandial spikes*, results in further deterioration of
the
> >beta-cell function ('glucotoxicity')." Emphasis is mine. Good enough
reason
> >to seriously think about spikes as being capable of causing diabetic
> >progression.
> >
> >http://www.medscape.com/medline/abstract/15306831
> >
> >"By the time type II diabetes is diagnosed, beta-cell function and mass
have
> >declined by about 50%. With the progression of the disease and
glucotoxicity
> >there is continuous decrease in beta-cell mass due to increased apoptosis
> >that results in absolute insulin deficiency. By then, patients require
> >insulin administration to maintain glucose control. An increasing body of
> >evidence demonstrates the importance of preserving endogenous beta-cell
> >function both in type I and type II diabetes. Early and intensive
glycaemic
> >control, using regimens which re-create a physiological insulin profile,
> >controlling postprandial as well as fasting glucose levels, offers the
most
> >promise for preserving beta-cell function, decreasing disease
progression,
> >and reducing the chronic complications of diabetes."
>
> Bothy good points - but slightly tangential to the basic
> question I was given: Why 1hr instead of 2hr? Or the way I
> am interpreting that: Why peak instead of 2hr?

Important to catch the peak, especially if it's a significant spike because
of the above two trains of thought If you can't correct the spiking you
can't expect to avoid diabetic progression etc and if you don't test when
you peak then you won't know you spiked at all. Sounds logical to me

On Fri, 18 May 2007 09:00:51 GMT, Alan S
<loralgtweightandcarbs@gmail.com> wrote:

>On Fri, 18 May 2007 09:01:17 +0100, Nicky
><ukc802466929@btconnect.com> wrote:
>
>>These guys used 1-hour figures to predict heart attack, but I can't
>>find a link:
>>Donahue RP, Abbott RD, Reed DM, Yano K: Postchallenge glucose
>>concentration and coronary heart disease in men of Japanese ancestry:
>>Honolulu Heart Program. Diabetes 36:689-692,1987
>
>http://tinyurl.com/2jpr2h or
>http://diabetes.diabetesjournals.org...urcetype=HWCIT
>and also
>http://tinyurl.com/3yqsyy or
>http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Citation
>Only the abstract I'm afraid.

Cheers, Alan. I hate abstracts!!

Yano K seems to have wandered off into osteoporosis. Last thing on
Donahue I found was 2002 - still in diabetes. Abbott's into the brain
- most recent papers on Parkinsons and strokes. Reed seems to have
dropped off altogether. Wish I could find the right links - there has
been much more recent Japanese research than that, within the last
year or two.

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.5% BMI 25

On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
<are_we_there_yet@maccas.com> wrote:

>Furthermore, chronic exposure to elevated glucose, *even to
>intermittent postprandial spikes*, results in further deterioration of the
>beta-cell function

Yeah, but what's a spike? They imply that 7.5 might be, and they're
sure 15 is - but that's a lot of grey area!

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.5% BMI 25

On Fri, 18 May 2007 12:52:31 +0100, Nicky
<ukc802466929@btconnect.com> wrote:

>On Fri, 18 May 2007 09:00:51 GMT, Alan S
><loralgtweightandcarbs@gmail.com> wrote:
>
>>On Fri, 18 May 2007 09:01:17 +0100, Nicky
>><ukc802466929@btconnect.com> wrote:
>>
>>>These guys used 1-hour figures to predict heart attack, but I can't
>>>find a link:
>>>Donahue RP, Abbott RD, Reed DM, Yano K: Postchallenge glucose
>>>concentration and coronary heart disease in men of Japanese ancestry:
>>>Honolulu Heart Program. Diabetes 36:689-692,1987
>>
>>http://tinyurl.com/2jpr2h or
>>http://diabetes.diabetesjournals.org...urcetype=HWCIT
>>and also
>>http://tinyurl.com/3yqsyy or
>>http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Citation
>>Only the abstract I'm afraid.
>
>Cheers, Alan. I hate abstracts!!
>
>Yano K seems to have wandered off into osteoporosis. Last thing on
>Donahue I found was 2002 - still in diabetes. Abbott's into the brain
>- most recent papers on Parkinsons and strokes. Reed seems to have
>dropped off altogether. Wish I could find the right links - there has
>been much more recent Japanese research than that, within the last
>year or two.
>
>Nicky.

I've downloaded every available "This article has been cited
by" for reading tomorrow. There may be some interesting
stuff among those.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: Slovenia

On Fri, 18 May 2007 20:35:29 +1000, "Ozgirl"
<are_we_there_yet@maccas.com> wrote:

>
>"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
>news:hgtq431bavigstf2lqva99o3gbtknp70l5@4ax.com.. .
>> On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
>> <are_we_there_yet@maccas.com> wrote:
>>
>> >There seems to me to be two trains of thought to be followed up here
>Alan.
>> >
>> >1. The effect of postprandial excursions into hyperglycemia territory
>being
>> >more indicative of complications (particularly of the cardio vascular
>> >system) than the A1c. There is growing evidence backing this up including
>> >the DCCT even though that was a type 1 study.
>> >
>> >2. The effect of postprandial hyperglycemic episodes on the progression
>of
>> >type 2 diabetes. Read the last sentence in the following:
>> >
>> >"Both type I and type II diabetes are characterised by a progressive
>> >decrease in beta-cell function and mass. In type I diabetes, autoimmune
>> >destruction results in rapid loss of beta-cell function, and insulin
>therapy
>> >is essential to maintain normoglycaemia. In type II diabetes, a
>diminished
>> >or absent first-phase insulin release is the earliest metabolic defect,
>> >which is accompanied by lack of prandial suppression of hepatic glucose
>> >production, increased postprandial glucose excursions and late insulin
>> >hypersecretion. Furthermore, chronic exposure to elevated glucose, *even
>to
>> >intermittent postprandial spikes*, results in further deterioration of
>the
>> >beta-cell function ('glucotoxicity')." Emphasis is mine. Good enough
>reason
>> >to seriously think about spikes as being capable of causing diabetic
>> >progression.
>> >
>> >http://www.medscape.com/medline/abstract/15306831
>> >
>> >"By the time type II diabetes is diagnosed, beta-cell function and mass
>have
>> >declined by about 50%. With the progression of the disease and
>glucotoxicity
>> >there is continuous decrease in beta-cell mass due to increased apoptosis
>> >that results in absolute insulin deficiency. By then, patients require
>> >insulin administration to maintain glucose control. An increasing body of
>> >evidence demonstrates the importance of preserving endogenous beta-cell
>> >function both in type I and type II diabetes. Early and intensive
>glycaemic
>> >control, using regimens which re-create a physiological insulin profile,
>> >controlling postprandial as well as fasting glucose levels, offers the
>most
>> >promise for preserving beta-cell function, decreasing disease
>progression,
>> >and reducing the chronic complications of diabetes."
>>
>> Bothy good points - but slightly tangential to the basic
>> question I was given: Why 1hr instead of 2hr? Or the way I
>> am interpreting that: Why peak instead of 2hr?
>
>Important to catch the peak, especially if it's a significant spike because
>of the above two trains of thought If you can't correct the spiking you
>can't expect to avoid diabetic progression etc and if you don't test when
>you peak then you won't know you spiked at all. Sounds logical to me
>
Sounds totally logical to me too; but I'm not a credible
source.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: Slovenia

On May 18, 5:50 am, Alan S <loralgtweightandca...@gmail.com> wrote:
> On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
>
>
>
>
>
> <are_we_there_...@maccas.com> wrote:
> >There seems to me to be two trains of thought to be followed up here Alan.
>
> >1. The effect of postprandial excursions into hyperglycemia territory being
> >more indicative of complications (particularly of the cardio vascular
> >system) than the A1c. There is growing evidence backing this up including
> >the DCCT even though that was a type 1 study.
>
> >2. The effect of postprandial hyperglycemic episodes on the progression of
> >type 2 diabetes. Read the last sentence in the following:
>
> >"Both type I and type II diabetes are characterised by a progressive
> >decrease in beta-cell function and mass. In type I diabetes, autoimmune
> >destruction results in rapid loss of beta-cell function, and insulin therapy
> >is essential to maintain normoglycaemia. In type II diabetes, a diminished
> >or absent first-phase insulin release is the earliest metabolic defect,
> >which is accompanied by lack of prandial suppression of hepatic glucose
> >production, increased postprandial glucose excursions and late insulin
> >hypersecretion. Furthermore, chronic exposure to elevated glucose, *even to
> >intermittent postprandial spikes*, results in further deterioration of the
> >beta-cell function ('glucotoxicity')." Emphasis is mine. Good enough reason
> >to seriously think about spikes as being capable of causing diabetic
> >progression.
>
> >http://www.medscape.com/medline/abstract/15306831
>
> >"By the time type II diabetes is diagnosed, beta-cell function and mass have
> >declined by about 50%. With the progression of the disease and glucotoxicity
> >there is continuous decrease in beta-cell mass due to increased apoptosis
> >that results in absolute insulin deficiency. By then, patients require
> >insulin administration to maintain glucose control. An increasing body of
> >evidence demonstrates the importance of preserving endogenous beta-cell
> >function both in type I and type II diabetes. Early and intensive glycaemic
> >control, using regimens which re-create a physiological insulin profile,
> >controlling postprandial as well as fasting glucose levels, offers the most
> >promise for preserving beta-cell function, decreasing disease progression,
> >and reducing the chronic complications of diabetes."
>
> Bothy good points - but slightly tangential to the basic
> question I was given: Why 1hr instead of 2hr? Or the way I
> am interpreting that: Why peak instead of 2hr?

Well, if I were a medical researcher, I'd make my best guess for when
bg might be most elevated in most of the patients that are being
studied. I would even use some past research or even do a little
research first to determine when a good time-after-meal is. Then I'd
pick that time and stick to it for the duration of the study.

Looking at the CGMS graphs we were talking about here a few weeks ago,
a "non-diabetic" curve peaks up rapidly over a half hour and is on its
way back down (but not completely down) after an hour. You know how
much I liked to argue about what exactly a spike is, but I would
expect that for a typical diabetic that the curve would not go down as
rapidly as in a non-diabetic person. (In my particular case, of
course, it wouldn't go down at all if it weren't for insulin shots,
just up and up, so I cannot contribute any of my personal data
points!) You would want to measure the excess bg as compared to a non-
diabetic, and if a non-diabetic isn't really done spiking after an
hour, you'd aim for a later time when you expect the non-diabetic to
be done spiking but the diabetic to be spiking. By my eyes this would
be somewhere in the 1 to 2 hour timeframe - I would tend towards the
larger number if I wanted to not see the effect of the spikes that non-
diabetics have.

(See, I did learn something from those discussions, I'm using the word
spiking even though I pause every time after I write it and think "hey
that word doesn't apply to me!"!)

If I were a researcher wanting to compare my study's results against
other studies, to make it an apples vs apples comparison I might
choose the same time frames they used in the other studies.

So, it may be the reason that 2 hours is used in the studies, is that
some previous researchers used it.

Sometimes it is more important to just choose a standardized (if less
than optimal) measure rather and do the research, than it is to worry
and fret over how to measure something and never get any results. Look
at A1C's: horribly large variance and lab-to-lab variations, but
studies love to use them because it is a somewhat standardized
measurement. Of course the DCCT helped enormously in what
standardization it did - 25 years ago I never heard of the A1C, and
only a few years later did my doctors begin to introduce it to me as a
fancy new measurement that they were trying to work the kinks out of.

Doing continuous glucose monitoring would obviously be the richest
source of information, but getting all the test subjects to check
their bg's with fingerpricks multiple times an hour or wear one of the
new (and not totally ironed out!) CGMS sensor system might be thought
to be too burdensome. Traditionally medical studies do not tend
towards the data-rich measurements provided by continuous monitoring,
but instead work on summary measurements that they run their
statistical tools against.

I myself love rich continuous sources of data (heck, my academic
background is rich in experimental nuclear physics and math and my
current job involves a $10billion peripheral that generates
information relevant to millions of people), but sometimes I feel
overwhelmed by all my bg numbers taken in a week.

Tim.

Alan S wrote:
> I was challenged on the ADA forum to back up my promotion of
> one-hour post-prandial blood glucose tests to review a type
> 2's menu.
>
> In fact, while I do believe newbies should test at one hour
> as well as two hours, my real support is for finding your
> peak post-prandial (PPP) time and to use that for tests.
> However, the point was made that there is no peer-reviewed
> research evidence supporting my contention and that most
> papers discussing post-prandial testing only refer to
> two-hour tests.
>

Alan my strategy is different than yours, but my objective is the same.
I generally only test 2 times a day, FBG and somewhere between 8:30 PM
and bedtime. The way I see diabetes management is to do things that
change gene expression to be more like healthy nondiabetics and less
toward a pathological phenotype. Diet and exercise as well as drugs and
supplements (including moderate alcohol and caffeine consumption) fit in
with this scheme when supported by research. Two significant comments
were made in this thread the way I see it. Julie mentioned the time for
digestion which is quite variable in type 2 diabetics, so this suggest
that each person should find there own pattern. The closer one comes to
achieving more normal physiological function, then the more the pattern
should resemble that of normal glycemics. Tim mentioned the study of
normal glycemics and continuous blood glucose monitoring. The
postprandial readings were given for 30 and 60 minutes which were nearly
the same. Presumably 45 minutes would have been the peak. Also fasting
and 4 hour postprandial were in the low 80s in mg/dl (4.5 mmol/L). The
strategy for beta-cell rest in the T2 diabetic would come as close to
mirroring these numbers. Frequent small meals used by Ozgirl seems to
work for her. In my case I use low dose insulin injections to maintain a
pattern of normal blood glucose for 24 hours a day.

Most therapies used in type 2s promote more favorable gene expression,
with the exception of sulphonylureas. Therefore combination therapies
are the best route to go IMHO. I am not antimed, but rather minimal
effect dose with meds of different mechanisms.

Frank

"Nicky" <ukc802466929@btconnect.com> wrote in message
news:lt4r43t7fshrds9er2avrmf1imqcallte2@4ax.com...
> On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
> <are_we_there_yet@maccas.com> wrote:
>
> >Furthermore, chronic exposure to elevated glucose, *even to
> >intermittent postprandial spikes*, results in further deterioration of
the
> >beta-cell function
>
> Yeah, but what's a spike? They imply that 7.5 might be, and they're
> sure 15 is - but that's a lot of grey area!

Let's look at it like this. Alan's co posters on the forum need evidence to
back up his 1 hour (or peak time) test as opposed to the 2 hour. Let's say
all the co posters are happy with a 2 hour reading that is back in range.
What they aren't aware of is how high the bg spiked before coming down. So
they live blissfully unaware that spikes may be doing damage in the
meantime. For #1. of my thoughts, the spikes (out of range) can be causing
damage even though they return to "normal" by the magic 2 hour

and for #2 (IMO) any spikes (calling a spike a fast rise from say 90 to 150)
is going to put pressure on the beta cells and cause further deterioration
as per the information above.

I have never believed control and prevention of progression has been centred
around the 2 hr pp or A1c. The least thrashing the beta cells get the better
IMO, which is why I like to see little if any rise at all post prandially.

On 18 May 2007 06:53:23 -0700, Tim Shoppa <shoppa@trailing-edge.com>
wrote:

>(See, I did learn something from those discussions, I'm using the word
>spiking even though I pause every time after I write it and think "hey
>that word doesn't apply to me!"!)



>If I were a researcher wanting to compare my study's results against
>other studies, to make it an apples vs apples comparison I might
>choose the same time frames they used in the other studies.

Yeah, that would have my vote.

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.5% BMI 25

"Tim Shoppa" <shoppa@trailing-edge.com> wrote in message
news:1179496403.270231.105300@u30g2000hsc.googlegr oups.com...
> On May 18, 5:50 am, Alan S <loralgtweightandca...@gmail.com> wrote:
> > On Fri, 18 May 2007 19:06:31 +1000, "Ozgirl"
> >
> >
> >
> >
> >
> > <are_we_there_...@maccas.com> wrote:
> > >There seems to me to be two trains of thought to be followed up here
Alan.
> >
> > >1. The effect of postprandial excursions into hyperglycemia territory
being
> > >more indicative of complications (particularly of the cardio vascular
> > >system) than the A1c. There is growing evidence backing this up
including
> > >the DCCT even though that was a type 1 study.
> >
> > >2. The effect of postprandial hyperglycemic episodes on the progression
of
> > >type 2 diabetes. Read the last sentence in the following:
> >
> > >"Both type I and type II diabetes are characterised by a progressive
> > >decrease in beta-cell function and mass. In type I diabetes, autoimmune
> > >destruction results in rapid loss of beta-cell function, and insulin
therapy
> > >is essential to maintain normoglycaemia. In type II diabetes, a
diminished
> > >or absent first-phase insulin release is the earliest metabolic defect,
> > >which is accompanied by lack of prandial suppression of hepatic glucose
> > >production, increased postprandial glucose excursions and late insulin
> > >hypersecretion. Furthermore, chronic exposure to elevated glucose,
*even to
> > >intermittent postprandial spikes*, results in further deterioration of
the
> > >beta-cell function ('glucotoxicity')." Emphasis is mine. Good enough
reason
> > >to seriously think about spikes as being capable of causing diabetic
> > >progression.
> >
> > >http://www.medscape.com/medline/abstract/15306831
> >
> > >"By the time type II diabetes is diagnosed, beta-cell function and mass
have
> > >declined by about 50%. With the progression of the disease and
glucotoxicity
> > >there is continuous decrease in beta-cell mass due to increased
apoptosis
> > >that results in absolute insulin deficiency. By then, patients require
> > >insulin administration to maintain glucose control. An increasing body
of
> > >evidence demonstrates the importance of preserving endogenous beta-cell
> > >function both in type I and type II diabetes. Early and intensive
glycaemic
> > >control, using regimens which re-create a physiological insulin
profile,
> > >controlling postprandial as well as fasting glucose levels, offers the
most
> > >promise for preserving beta-cell function, decreasing disease
progression,
> > >and reducing the chronic complications of diabetes."
> >
> > Bothy good points - but slightly tangential to the basic
> > question I was given: Why 1hr instead of 2hr? Or the way I
> > am interpreting that: Why peak instead of 2hr?
>
> Well, if I were a medical researcher, I'd make my best guess for when
> bg might be most elevated in most of the patients that are being
> studied. I would even use some past research or even do a little
> research first to determine when a good time-after-meal is. Then I'd
> pick that time and stick to it for the duration of the study.
>
> Looking at the CGMS graphs we were talking about here a few weeks ago,
> a "non-diabetic" curve peaks up rapidly over a half hour and is on its
> way back down (but not completely down) after an hour. You know how
> much I liked to argue about what exactly a spike is, but I would
> expect that for a typical diabetic that the curve would not go down as
> rapidly as in a non-diabetic person. (In my particular case, of
> course, it wouldn't go down at all if it weren't for insulin shots,
> just up and up, so I cannot contribute any of my personal data
> points!) You would want to measure the excess bg as compared to a non-
> diabetic, and if a non-diabetic isn't really done spiking after an
> hour, you'd aim for a later time when you expect the non-diabetic to
> be done spiking but the diabetic to be spiking. By my eyes this would
> be somewhere in the 1 to 2 hour timeframe - I would tend towards the
> larger number if I wanted to not see the effect of the spikes that non-
> diabetics have.
>
> (See, I did learn something from those discussions, I'm using the word
> spiking even though I pause every time after I write it and think "hey
> that word doesn't apply to me!"!)
>
> If I were a researcher wanting to compare my study's results against
> other studies, to make it an apples vs apples comparison I might
> choose the same time frames they used in the other studies.
>
> So, it may be the reason that 2 hours is used in the studies, is that
> some previous researchers used it.
>
> Sometimes it is more important to just choose a standardized (if less
> than optimal) measure rather and do the research, than it is to worry
> and fret over how to measure something and never get any results. Look
> at A1C's: horribly large variance and lab-to-lab variations, but
> studies love to use them because it is a somewhat standardized
> measurement. Of course the DCCT helped enormously in what
> standardization it did - 25 years ago I never heard of the A1C, and
> only a few years later did my doctors begin to introduce it to me as a
> fancy new measurement that they were trying to work the kinks out of.
>
> Doing continuous glucose monitoring would obviously be the richest
> source of information, but getting all the test subjects to check
> their bg's with fingerpricks multiple times an hour or wear one of the
> new (and not totally ironed out!) CGMS sensor system might be thought
> to be too burdensome. Traditionally medical studies do not tend
> towards the data-rich measurements provided by continuous monitoring,
> but instead work on summary measurements that they run their
> statistical tools against.
>
> I myself love rich continuous sources of data (heck, my academic
> background is rich in experimental nuclear physics and math and my
> current job involves a $10billion peripheral that generates
> information relevant to millions of people), but sometimes I feel
> overwhelmed by all my bg numbers taken in a week.

Typically, the first phase insulin response should kick in early, (less than
ten minutes - when the first signs of rising bg's become apparent) As you
know, in type 2's that first phase is absent or faulty. By the time second
phase kicks in, for type 2's, the bg's are well on their way to being high
and once high they will remain that way unless there is medication
involvement or whatever. Let's say we have the typical type 2 on Metformin.
From a doctor's point of view, if the Metformin has brought back the bg's to
a normal range by the 2 hour mark the doc gives the type 2 a pat on the
back.

But let's say there are some more proactive diabetics who have researched
that the spikes are dangerous irrespective of the two hour reading being
back in normal range. Dangerous on 2 levels - one to cause damage,
particularly the cardiovascular system, two to promote diabetic progression
(which then involves a medley of drugs and insulin).

To me, it is logical to find a way to prevent the spiking, even if the bg
number of that spike isn't all that high. Any rise is going to put pressure
on the ailing beta cells, something (IMO) to avoid. There are now drugs that
appear to restore the first phase response, Byetta for example. Then there
is my way small, but often, meals allowing a "trickle" of carbs into the
"system". I think a little experimentation on any type 2's part will show
where the peak time is, if one eats much the same way each meal (other than
breakfast)

I can see a big rise from orange juice in 5 minutes, it doesn't stay high
but that tells me OJ is best kept for hypos. Bread will show by 20 minutes
max (for me). That one tells me to eat less or switch to low carb grain
bread. I don't think you can beat personal experimentation but I do think it
important to find when you peak. If the peak only took me up 10 points (say
90 to 100) I wouldn't change anything. If the peak showed a rise from 90 to
130 I would.

If you used a CGMS what would you, as a type 1, do with the results? I know
what I would do as a type 2 but still curious.

"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
news:c9lp439qtraq1bitufj273j605i8i183tj@4ax.com...
>I was challenged on the ADA forum to back up my promotion of
> one-hour post-prandial blood glucose tests to review a type
> 2's menu.
>
> In fact, while I do believe newbies should test at one hour
> as well as two hours, my real support is for finding your
> peak post-prandial (PPP) time and to use that for tests.
> However, the point was made that there is no peer-reviewed
> research evidence supporting my contention

That one was used for years by the tobacco company.....

>and that most
> papers discussing post-prandial testing only refer to
> two-hour tests.

Hi Alan,
I was interested in the question how fast hyperglycemia can cause damage in
diabetes : If I do it fast enough can I come away with it Well...
apparently not.....The keyword is : "Acute" .Even the ACUTE hyperglycemic
state causes oxidative stress which is responsible for all the complications
in diabetes.

So this is the logic :

1) ACUTE bg swings cause oxidative stress
2)So I want to know the total magnitude of the swing
3)So I want the total curve of bg after a glucose load (AUC)
4)If this is too cumbersome then the next best thing is the pre-prandial
value and the peak value because this difference must have the highest
correllation to the total swing.

Here is the literature I have on the ACUTE effect of hyper glycemia on the
oxidative stress :
============================================
Diabet Med. 2007 Feb;24(2):154-60.
Pancreatic B-cell function is altered by oxidative stress induced by acute
hyperglycaemia.

AIMS: Type 2 diabetes is preceded by a symptom-free period of impaired
glucose tolerance (IGT). Pancreatic B-cell function decreases as glucose
intolerance develops. In many patients with IGT, fasting blood glucose is
within normal limits and hyperglycaemia occurs only postprandially. We
examined whether pancreatic B-cell function changes during acute
hyperglycaemia induced by oral glucose loading. METHODS: We calculated the
insulinogenic index (I.I.) as an indicator of pancreatic B-cell function and
measured serum levels of thioredoxin, a marker of cellular redox state, and
8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative stress, during a
75-g oral glucose tolerance test (OGTT) in 45 subjects [24 patients with
normal glucose tolerance (NGT), 14 with IGT and seven with Type 2 diabetes].
RESULTS: Thioredoxin levels decreased after glucose loading [66.1 +/- 23.7,
*59.3 +/- 22.4, *49.3 +/- 21.2 and *37.7 +/- 18.0 ng/ml, fasting (0 min) and
at 30, 60 and 120 min, respectively; *P < 0.001 vs. fasting]. In contrast,
concentrations of 8-OHdG peaked at 30 min and then gradually decreased
(0.402 +/- 0.123, *0.440 +/- 0.120, 0.362 +/- 0.119 and 0.355 +/- 0.131
ng/ml, *P < 0.05 vs. fasting, P < 0.01 vs. 30 min). The insulinogenic index
correlated with the change in thioredoxin levels (r = 0.34, P < 0.05).
However, there was no relationship with the change in 8-OHdG levels from 0
to 30 min. CONCLUSIONS: Hyperglycaemia in response to oral glucose impairs
pancreatic B-cell function with decreasing thioredoxin levels. The augmented
oxidative stress induced by hyperglycaemia may affect the cellular redox
state. These findings strongly suggest that repeated postprandial
hyperglycaemia may play an important role in the development and progression
of diabetes mellitus.

PMID: 17257277

Quotes :

Plasma glucose levels were significantly higher in the IGT and the DM groups
than in the NGT group at 30, 60 and 120 min after glucose loading ( P <
0.01).

============================================
Diabetes Care. 2002 Mar;25(3):537-41. Related Articles, Links
Plasma F2 isoprostanes: direct evidence of increased free radical damage
during acute hyperglycemia in type 2 diabetes.

OBJECTIVES: Acute hyperglycemia in type 2 diabetes increases the generation
of plasma 8-epi-prostaglandin F2 (8-epi-PGF2alpha) isoprostane, a sensitive
direct marker of in vivo free radical oxidative damage to membrane
phospholipids. RESEARCH DESIGN AND METHODS: A total of 21 patients with type
2 diabetes underwent an oral 75-g glucose tolerance test. Plasma
8-epi-PGF2alpha isoprostane concentrations (by gas chromatography [GC]/mass
spectrometry [MS]), intralymphocyte reduced-to-oxidized glutathione ratios,
and plasma total antioxidant capacity were measured at baseline and 90 min
after glucose loading. RESULTS: Plasma 8-epi-PGF2alpha isoprostane
concentrations rose significantly (P=0. 010) from 0.241 +/- 0.1 to 0.326 +/-
0.17 ng/l after 90 min. Intracellular oxidative balance and plasma
antioxidant capacity did not change in either group. CONCLUSIONS: Plasma
concentrations of 8-epi-PGF2alpha isoprostane increase during acute
hyperglycemia in type 2 diabetes, providing direct evidence of free
radical-mediated oxidative damage and demonstrating a pathway for an
association between acute rather than fasting hyperglycemia and
macrovascular risk in type 2 diabetes.


PMID: 11874943
=====================================
JAMA. 2006 Apr 12;295(14):1681-7.

CONTEXT: Glycemic disorders, one of the main risk factors for cardiovascular
disease, are associated with activation of oxidative stress. OBJECTIVE: To
assess the respective contributions of sustained chronic hyperglycemia and
of acute glucose fluctuations to oxidative stress in type 2 diabetes.
DESIGN, SETTING, AND PARTICIPANTS: Case-control study of 21 patients with
type 2 diabetes (studied 2003-2005) compared with 21 age- and sex-matched
controls (studied in 2001) in Montpellier, France. MAIN OUTCOME MEASURES:
Oxidative stress, estimated from 24-hour urinary excretion rates of free
8-iso prostaglandin F2alpha (8-iso PGF2alpha). Assessment of glucose
fluctuations was obtained from continuous glucose monitoring system data by
calculating the mean amplitude of glycemic excursions (MAGE). Postprandial
contribution to glycemic instability was assessed by determining the
postprandial increment of glucose level above preprandial values (mean
postprandial incremental area under the curve [AUCpp]). Long-term exposure
to glucose was estimated from hemoglobin A1c, from fasting glucose levels,
and from mean glucose concentrations over a 24-hour period. RESULTS: Mean
(SD) urinary 8-iso PGF2alpha excretion rates were higher in the 21 patients
with diabetes (482 [206] pg/mg of creatinine) compared with controls (275
[85] pg/mg of creatinine). In univariate analysis, only MAGE (r = 0.86;
P<.001) and AUCpp (r = 0.55; P = .009) showed significant correlations with
urinary 8-iso PGF2alpha excretion rates. Relationships between 8-iso
PGF2alpha excretion rates and either MAGE or AUCpp remained significant
after adjustment for the other markers of diabetic control in multiple
linear regression analysis (multiple R2 = 0.72 for the model including MAGE
and multiple R2 = 0.41 for the model including AUCpp). Standardized
regression coefficients were 0.830 (P<.001) for MAGE and 0.700 (P = .003)
for AUCpp. CONCLUSIONS: Glucose fluctuations during postprandial periods
and, more generally, during glucose swings exhibited a more specific
triggering effect on oxidative stress than chronic sustained hyperglycemia.
The present data suggest that interventional trials in type 2 diabetes
should target not only hemoglobin A1c and mean glucose concentrations but
also acute glucose swings.

PMID: 16609090
========================================
Diabetes Care. 2005 Oct;28(10):2465-71.

Glycated and oxidized protein degradation products are indicators of fasting
and postprandial hyperglycemia in diabetes.
OBJECTIVE: To assess the relative importance of fasting and postprandial
hyperglycemia to vascular dysfunction in diabetes, we have measured
indicators of glycation, oxidative and nitrosative stress in subjects with
type 1 diabetes, and different postprandial glucose patterns. RESEARCH
DESIGN AND METHODS: Plasma and urinary levels of specific arginine- and
lysine-derived advanced glycation end products, as well as oxidative and
nitrosative products, were measured by liquid chromatography with triple
quadrupole mass spectrometric detection (LC-MS/MS) after 2 months of
treatment with insulin lispro or human regular insulin in 21 subjects
participating in a cross-over study. Hb-bound early glycation (Amadori)
products were also measured after each treatment period by high-performance
liquid chromatography (fructosyl-valine Hb or HbA1c [A1C]iamat) and
fructosyl-lysine Hb by LC-MS/MS (A1C:fructosyl-lysine). RESULTS: In diabetic
patients, the concentrations of protein glycation and oxidation-free adducts
increased up to 10-fold, while urinary excretion increased up to 15-fold.
Decreasing postprandial hyperglycemia with lispro gave 10-20% decreases of
the major free glycation adducts, hydroimidazolones derived from
methylglyoxal and 3-deoxyglucosone, and glyoxal-derived
Nepsilon-carboxymethyl-lysine. No differences were observed in A1Ciamat or
A1C:fructosyl-lysine with lispro or regular insulin therapy in spite of
significant decreases in postprandial glycemia with lispro. CONCLUSIONS: We
conclude that the profound increases in proteolytic products of proteins
modified by advanced glycation endproducts in diabetic patients are
responsive to changes in mean hyperglycemia and also show responses to
changes in postprandial hyperglycemia.

PMID: 16186281
==============================================
hth
Gys

"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
news:c9lp439qtraq1bitufj273j605i8i183tj@4ax.com...
>I was challenged on the ADA forum to back up my promotion of
> one-hour post-prandial blood glucose tests to review a type
> 2's menu.
>
> In fact, while I do believe newbies should test at one hour
> as well as two hours, my real support is for finding your
> peak post-prandial (PPP) time and to use that for tests.
> However, the point was made that there is no peer-reviewed
> research evidence supporting my contention and that most
> papers discussing post-prandial testing only refer to
> two-hour tests.

Oops...
Forgot this one
It's free , it's recent and it's a review with a lot of references if you
want to work your way back in time


Conclusion :

The epidemiological and intervention studies presented in the article
support the conclusion that postprandial hyperglycemia in impaired glucose
tolerance and diabetic subjects is a more powerful marker of CVD risk than
fasting hyperglycemia, then the treatment directed at specifically lowering
postprandial glucose is crucial,



Some quotes:



MECHANISMS OF POSTPRANDIAL HYPERGLYCEMIA The loss of the acute (0-10
minutes) insulin secretion, after an intravenous glucose injection, which
correlates with the first-phase insulin response during the hyperglycemic
clamp, characterizes the postprandial hyperglycemia, as well as the impaired
fasting glucose, while subjects with elevated PPG also have impaired
latephase insulin secretion, after 20 minutes of that clamp. Furthermore,
subjects with postprandial hyperglycemia have marked peripheral insulin
resistance with only mild hepatic insulin resistance. On the other hand, in
IFG there is severe hepatic insulin resistance and normal or near-normal
clamp-determined peripheral insulin sensitivity (18,19). Despite late
hyperinsulinemia, at 30 minutes after an oral glucose challenge, the
impaired glucose tolerance results primarily from reduced suppression of
hepatic glucose output due to abnormal pancreatic islet-cell function
(smaller increases in plasma insulin and smaller reductions in plasma
glucose in comparison with normal subjects, both P< 0.01) (20).
POSTPRANDIAL HYPERGLYCEMIA AND CVD Intervention studies The STOP-NIDDM trial
has shown that treatment of subjects with impaired glucose intolerance with
the aglucosidase inhibitor acarbose, which specifically reduces postprandial
hyperglycemia, was associated not only with a 36% reduction in the risk of
progression to diabetes (40), but also with a 34% risk reduc-tion in the
development of new cases of hypertension and a 49% risk reduction in
cardiovascular events (41).



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



Arq Bras Endocrinol Metabol. 2007 Mar;51(2):212-221.

Postprandial glycemia and cardiovascular disease in diabetes mellitus.

This article reviews the role of fasting and postprandial glycemia to the
overall glycemic control of patients with type 2 diabetes and glucose
intolerance, as well as their causal relationship upon micro and
macrovascular complications. Recent studies have suggested that a third
component of the glucose triad, the postprandial glucose excursions, might
have a role in the overall glycemic load and might also reflect glycemic
control. Epidemiological and intervention studies are presented in the
article, supporting the conclusion that postprandial hyperglycemia in
impaired glucose tolerance and diabetic subjects is a more powerful marker
of cardiovascular disease risk than fasting hyperglycemia, then the
treatment directed at specifically lowering postprandial glucose is crucial,
as underlined by the American Diabetes Association.



PMID: 17505628



Gys