Fasting glucose, retinopathy and diagnosis criteria

I'm going back through various subscriptions I have to
different medical reports servers.

Please excuse me if any of the reports I post have been
discussed while I was away.

A discussion on this one appeared in Endocrine Today
http://www.endocrinetoday.com/view.aspx?rid=26757

"Relation between fasting glucose and retinopathy for
diagnosis of diabetes: three population-based
cross-sectional studies."

http://tinyurl.com/3g8oo5 or
http://www.ncbi.nlm.nih.gov/pubmed/1...RVAbstractPlus

Full version (pay)
http://www.thelancet.com/journals/la...03189/fulltext

The important bits:

"However, we found inconsistent evidence of a uniform
glycaemic threshold for prevalent and incident retinopathy,
with analyses suggesting a continuous relation. The widely
used diabetes FPG cutoff of 7.0 mmol/L or higher had
sensitivity less than 40% (range 14.8-39.1) for detecting
retinopathy, with specificity between 80.8% and 95.8%."
and
"The current FPG cutoff of 7.0 mmol/L used to diagnose
diabetes did not accurately identify people with and without
retinopathy. These findings suggest that the criteria for
diagnosing diabetes could need reassessment."

7 mmol/l is 126mg/dl.

The abstract:

Centre for Eye Research Australia, University of Melbourne,
VIC, Australia. twong@unimelb.edu.au

BACKGROUND: The WHO and American Diabetes Association
criteria for diagnosing diabetes mellitus assume the
presence of a glycaemic threshold with high sensitivity for
identifying retinopathy. However, this assumption is based
on data from three previous studies that had important
limitations in detecting retinopathy. We aimed to provide
updated data for the relation between fasting plasma glucose
(FPG) and retinopathy, and to assess the diagnostic accuracy
of current FPG thresholds in identifying both prevalent and
incident retinopathy. METHODS: We examined the data from
three cross-sectional adult populations: those in the Blue
Mountains Eye Study (BMES, Australia, n=3162), the
Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
Australia, n=2182), and the Multi-Ethnic Study of
Atherosclerosis (MESA, USA, n=6079). Retinopathy was
diagnosed from multiple retinal photographs of each eye, and
graded according to the modified Airlie House Classification
system. Plasma glucose concentrations were measured from
fasting venous blood samples. FINDINGS: The overall
prevalence of retinopathy was 11.5% in BMES (95% CI
10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
(14.9-16.7). However, we found inconsistent evidence of a
uniform glycaemic threshold for prevalent and incident
retinopathy, with analyses suggesting a continuous relation.
The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
had sensitivity less than 40% (range 14.8-39.1) for
detecting retinopathy, with specificity between 80.8% and
95.8%. The area under receiver operating characteristic
curves for FPG and retinopathy was low and ranged from 0.56
to 0.61. INTERPRETATION: We saw no evidence of a clear and
consistent glycaemic threshold for the presence or incidence
of retinopathy across different populations. The current FPG
cutoff of 7.0 mmol/L used to diagnose diabetes did not
accurately identify people with and without retinopathy.
These findings suggest that the criteria for diagnosing
diabetes could need reassessment.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com
Latest:Is Testing Worthwhile?
and Cambodia
http://loraltravel.blogspot.com/2008/03/cambodia.html

On Thu, 01 May 2008 11:39:53 +1000, Alan S
<loralgtweightandcarbs@gmail.com> wrote:

>Please excuse me if any of the reports I post have been
>discussed while I was away.

G'day G'day Alan,

It wouldn't matter if they had been. There is a real need for some
things to be discussed continuously. They are so important and
relevant to what ASD is all about. Those who don't want to can use a
"ignore thread" flag.

Thank you for starting the thread. The absence of a clear cut
threshold is something many of us have suspected for many years. The
risk simply gets worse the higher the fasting blood glucose.

The other conclusion reached by many of us long ago has been that
fasting blood glucose is not the best instrument for prediction.
Lowering post prandial blood glucose made more sense to us.
What I I'm trying to say here is that it is easy when it is a matter
of guessing. That was the advantage we had. The researchers had to
find proof and I'm people are financing the type of research that
provides some of that.

Best wishes,
--
Quentin Grady ^ ^ /
New Zealand, >#,#< [
/ \ /\
"... and the blind dog was leading."

http://homepages.paradise.net.nz/quentin

Alan S wrote:
> I'm going back through various subscriptions I have to
> different medical reports servers.
>
> Please excuse me if any of the reports I post have been
> discussed while I was away.
>
> A discussion on this one appeared in Endocrine Today
> http://www.endocrinetoday.com/view.aspx?rid=26757
>
> "Relation between fasting glucose and retinopathy for
> diagnosis of diabetes: three population-based
> cross-sectional studies."
>
> http://tinyurl.com/3g8oo5 or
> http://www.ncbi.nlm.nih.gov/pubmed/1...RVAbstractPlus
>
> Full version (pay)
> http://www.thelancet.com/journals/la...03189/fulltext
>
> The important bits:
>
> "However, we found inconsistent evidence of a uniform
> glycaemic threshold for prevalent and incident retinopathy,
> with analyses suggesting a continuous relation. The widely
> used diabetes FPG cutoff of 7.0 mmol/L or higher had
> sensitivity less than 40% (range 14.8-39.1) for detecting
> retinopathy, with specificity between 80.8% and 95.8%."
> and
> "The current FPG cutoff of 7.0 mmol/L used to diagnose
> diabetes did not accurately identify people with and without
> retinopathy. These findings suggest that the criteria for
> diagnosing diabetes could need reassessment."
>
> 7 mmol/l is 126mg/dl.
>
> The abstract:
>
> Centre for Eye Research Australia, University of Melbourne,
> VIC, Australia. twong@unimelb.edu.au
>
> BACKGROUND: The WHO and American Diabetes Association
> criteria for diagnosing diabetes mellitus assume the
> presence of a glycaemic threshold with high sensitivity for
> identifying retinopathy. However, this assumption is based
> on data from three previous studies that had important
> limitations in detecting retinopathy. We aimed to provide
> updated data for the relation between fasting plasma glucose
> (FPG) and retinopathy, and to assess the diagnostic accuracy
> of current FPG thresholds in identifying both prevalent and
> incident retinopathy. METHODS: We examined the data from
> three cross-sectional adult populations: those in the Blue
> Mountains Eye Study (BMES, Australia, n=3162), the
> Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
> Australia, n=2182), and the Multi-Ethnic Study of
> Atherosclerosis (MESA, USA, n=6079). Retinopathy was
> diagnosed from multiple retinal photographs of each eye, and
> graded according to the modified Airlie House Classification
> system. Plasma glucose concentrations were measured from
> fasting venous blood samples. FINDINGS: The overall
> prevalence of retinopathy was 11.5% in BMES (95% CI
> 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
> (14.9-16.7). However, we found inconsistent evidence of a
> uniform glycaemic threshold for prevalent and incident
> retinopathy, with analyses suggesting a continuous relation.
> The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
> had sensitivity less than 40% (range 14.8-39.1) for
> detecting retinopathy, with specificity between 80.8% and
> 95.8%. The area under receiver operating characteristic
> curves for FPG and retinopathy was low and ranged from 0.56
> to 0.61. INTERPRETATION: We saw no evidence of a clear and
> consistent glycaemic threshold for the presence or incidence
> of retinopathy across different populations. The current FPG
> cutoff of 7.0 mmol/L used to diagnose diabetes did not
> accurately identify people with and without retinopathy.
> These findings suggest that the criteria for diagnosing
> diabetes could need reassessment.
>
>
> Cheers, Alan, T2, Australia.
> d&e, metformin 1500mg, ezetrol 10mg
> Everything in Moderation - Except Laughter.
> --
> http://loraldiabetes.blogspot.com
> Latest:Is Testing Worthwhile?
> and Cambodia
> http://loraltravel.blogspot.com/2008/03/cambodia.html

I thought that I had read something similar at MedScape or Diabetes in
Control: Retinopathy+diagnosis search on MedScape _
http://search.medscape.com/all-searc...hy%20diagnosis

A search of Diabetes in Control did not find anything.

Sub-basement membrane seems to be effected before more obvious symptoms.
Duration of diabetes also relates strongly to complications.

A 2004 thread in ASD - http://tinyurl.com/3unps3.

Frank

On Sat, 03 May 2008 14:28:16 -0400, Jefferson
<Jefferson@comcast.net> wrote:

<snip>
>I thought that I had read something similar at MedScape or Diabetes in
>Control: Retinopathy+diagnosis search on MedScape _
>http://search.medscape.com/all-searc...hy%20diagnosis
>
>A search of Diabetes in Control did not find anything.
>
>Sub-basement membrane seems to be effected before more obvious symptoms.
>Duration of diabetes also relates strongly to complications.
>
>A 2004 thread in ASD - http://tinyurl.com/3unps3.
>
>Frank

Thanks Frank

I found that whole thread fascinating reading, not just the
relevant posts on retinopathy. I'll post separately on one
of them.

Annette posted some wonderful info.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com
Latest:Is Testing Worthwhile?
and Cambodia
http://loraltravel.blogspot.com/2008/03/cambodia.html

Alan S <loralgtweightandcarbs@gmail.com> wrote in
news:ff7i14h4n0qkhgq2rn4rmhdijb1b5sjqf5@4ax.com:

> I'm going back through various subscriptions I have to
> different medical reports servers.
>
> Please excuse me if any of the reports I post have been
> discussed while I was away.
>
> A discussion on this one appeared in Endocrine Today
> http://www.endocrinetoday.com/view.aspx?rid=26757
>
> "Relation between fasting glucose and retinopathy for
> diagnosis of diabetes: three population-based
> cross-sectional studies."
>
> http://tinyurl.com/3g8oo5 or
> http://www.ncbi.nlm.nih.gov/pubmed/1...2?ordinalpos=1
&itool=Entrez
> System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_ DiscoveryPanel.Pub
m
> ed_RVAbstractPlus
>
> Full version (pay)
> http://www.thelancet.com/journals/la...14067360860318
9
> /fulltext
>
> The important bits:
>
> "However, we found inconsistent evidence of a uniform
> glycaemic threshold for prevalent and incident retinopathy,
> with analyses suggesting a continuous relation. The widely
> used diabetes FPG cutoff of 7.0 mmol/L or higher had
> sensitivity less than 40% (range 14.8-39.1) for detecting
> retinopathy, with specificity between 80.8% and 95.8%."
> and
> "The current FPG cutoff of 7.0 mmol/L used to diagnose
> diabetes did not accurately identify people with and without
> retinopathy. These findings suggest that the criteria for
> diagnosing diabetes could need reassessment."
>
> 7 mmol/l is 126mg/dl.
>
> The abstract:
>
> Centre for Eye Research Australia, University of Melbourne,
> VIC, Australia. twong@unimelb.edu.au
>
> BACKGROUND: The WHO and American Diabetes Association
> criteria for diagnosing diabetes mellitus assume the
> presence of a glycaemic threshold with high sensitivity for
> identifying retinopathy. However, this assumption is based
> on data from three previous studies that had important
> limitations in detecting retinopathy. We aimed to provide
> updated data for the relation between fasting plasma glucose
> (FPG) and retinopathy, and to assess the diagnostic accuracy
> of current FPG thresholds in identifying both prevalent and
> incident retinopathy. METHODS: We examined the data from
> three cross-sectional adult populations: those in the Blue
> Mountains Eye Study (BMES, Australia, n=3162), the
> Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
> Australia, n=2182), and the Multi-Ethnic Study of
> Atherosclerosis (MESA, USA, n=6079). Retinopathy was
> diagnosed from multiple retinal photographs of each eye, and
> graded according to the modified Airlie House Classification
> system. Plasma glucose concentrations were measured from
> fasting venous blood samples. FINDINGS: The overall
> prevalence of retinopathy was 11.5% in BMES (95% CI
> 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
> (14.9-16.7). However, we found inconsistent evidence of a
> uniform glycaemic threshold for prevalent and incident
> retinopathy, with analyses suggesting a continuous relation.
> The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
> had sensitivity less than 40% (range 14.8-39.1) for
> detecting retinopathy, with specificity between 80.8% and
> 95.8%. The area under receiver operating characteristic
> curves for FPG and retinopathy was low and ranged from 0.56
> to 0.61. INTERPRETATION: We saw no evidence of a clear and
> consistent glycaemic threshold for the presence or incidence
> of retinopathy across different populations. The current FPG
> cutoff of 7.0 mmol/L used to diagnose diabetes did not
> accurately identify people with and without retinopathy.
> These findings suggest that the criteria for diagnosing
> diabetes could need reassessment.
>
>
> Cheers, Alan, T2, Australia.
> d&e, metformin 1500mg, ezetrol 10mg
> Everything in Moderation - Except Laughter.
> --
> http://loraldiabetes.blogspot.com
> Latest:Is Testing Worthwhile?
> and Cambodia
> http://loraltravel.blogspot.com/2008/03/cambodia.html
>

For some time it has been becoming clearer and clearer that
prediabetes is, in fact, frank diabetes and the high end of normal is
probably also diabetes. I just finished a quick read through of the
article and it is one more result lending credence to that conclusion.

One criticism I would make is that they looked only at FPG which is
reflected in the prediabetes state as Impaired Fasting Glucose, IFG.
The alternate presentation of diabetes through a Oral Glucose
Tolerance Test, OGTT, is reflected in the prediabetic state as
Impaired Glucose Tolerance, IGT. Some research has made a case that
IFC and IGT are really two distinct flavors of (pre)diabetes. This,
of course, complicates things but that is just par for the course in
diabetes.

Their conclusion that there is no "evidence of a clear and consistent
glycemic threshold for the presence or incidence of retinopathy"
matches the DCCT conclusion that there is no magic A1c below which a
diabetic is "safe" from complications.

--
-------
Charly Coughran
ccoughran@DELETE-TO-RESPOND-UCSD.EDU

On Tue, 6 May 2008 23:40:43 +0000 (UTC), Charly Coughran
<ccoughran@REMOVE-TO-DELETE-UCSD.EDU> wrote:
<snipped but read>
>Their conclusion that there is no "evidence of a clear and consistent
>glycemic threshold for the presence or incidence of retinopathy"
>matches the DCCT conclusion that there is no magic A1c below which a
>diabetic is "safe" from complications.

Thanks Charly

Yet another reason to keep all the indicator numbers (A1c,
FBG, PPBG's, trigs) as close to normal as we are prepared to
go when assessing the balance between the difficulty of
doing that, hypo dangers, and lifestyle costs.


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com
Latest:What to Eat Until You Get Your Meter.
and Cambodia
http://loraltravel.blogspot.com/2008/03/cambodia.html

On May 6, 7:40*pm, Charly Coughran <ccough...@REMOVE-TO-DELETE-
UCSD.EDU> wrote:
> Their conclusion that there is no "evidence of a clear and consistent
> glycemic threshold for the presence or incidence of retinopathy"
> matches the DCCT conclusion that there is no magic A1c below which a
> diabetic is "safe" from complications.

Is that an actual DCCT conclusion? I certainly came to that conclusion
for myself when I looked at the DCCT graphs for the various
complications vs A1C, but despite that there are many docs, medical
organizations, usenet posters, etc. who tout a particular A1C as being
the point where everyone should be under with either an implied or
sometimes an explicit guarantee that it's a good number to be at.

It certainly is more productive to have a goal than it is to say that
no goal is good enough.

Tim.

Tim Shoppa <shoppa@trailing-edge.com> wrote in
news:38516a0c-3725-44de-9f4d-031f64da3b40@8g2000hse.googlegroups.com:

> On May 6, 7:40*pm, Charly Coughran <ccough...@REMOVE-TO-DELETE-
> UCSD.EDU> wrote:
>> Their conclusion that there is no "evidence of a clear and
>> consistent glycemic threshold for the presence or incidence of
>> retinopathy" matches the DCCT conclusion that there is no magic A1c
>> below which a diabetic is "safe" from complications.
>
> Is that an actual DCCT conclusion? I certainly came to that
> conclusion for myself when I looked at the DCCT graphs for the
> various complications vs A1C, but despite that there are many docs,
> medical organizations, usenet posters, etc. who tout a particular
> A1C as being the point where everyone should be under with either an
> implied or sometimes an explicit guarantee that it's a good number
> to be at.
>
> It certainly is more productive to have a goal than it is to say
> that no goal is good enough.
>
> Tim.
>

As you point out, it is certainly a conclusion that jumps out at
anyone looking at the DCCT results. It was presented as quite a
suprise to the investigators by the one that gave a local talk on the
results just after the big results paper was published. They fully
expected to see a knee in the risk vs. A1c curve.

I don't think there is a conflict between saying that risk is linear
with A1c down to the limit of our knowledge and providing a specific
goal for patients. The most commonly published goal of 7% is, after
all, based on the DCCT (and the UKPDS). 7% was the mean of the
intensively treated DCCT patients. It was not picked because it was
magic, but rather because it represents an "achievable" goal without
increasing the risk of severe hypoglycemia to an unacceptable level.
You can argue, and I do, about whether 7% really achieves that
balance, but that is what was decided.

Rather than think of it as, "no goal is good enough", I prefer
"improvement independent of your current level is good". This, of
course, ignores potential hypoglycemia problems which rise sharply as
you near the high end of normal A1c.

--
-------
Charly Coughran
ccoughran@DELETE-TO-RESPOND-UCSD.EDU

On Tue, 6 May 2008 23:40:43 +0000 (UTC), Charly Coughran
<ccoughran@REMOVE-TO-DELETE-UCSD.EDU> wrote:

>
>For some time it has been becoming clearer and clearer that
>prediabetes is, in fact, frank diabetes and the high end of normal is
>probably also diabetes. I just finished a quick read through of the
>article and it is one more result lending credence to that conclusion.
>
>One criticism I would make is that they looked only at FPG which is
>reflected in the prediabetes state as Impaired Fasting Glucose, IFG.
>The alternate presentation of diabetes through a Oral Glucose
>Tolerance Test, OGTT, is reflected in the prediabetic state as
>Impaired Glucose Tolerance, IGT. Some research has made a case that
>IFC and IGT are really two distinct flavors of (pre)diabetes. This,
>of course, complicates things but that is just par for the course in
>diabetes.
>
>Their conclusion that there is no "evidence of a clear and consistent
>glycemic threshold for the presence or incidence of retinopathy"
>matches the DCCT conclusion that there is no magic A1c below which a
>diabetic is "safe" from complications.

I can't disagree with any of that.

I have just been looking back through my collection of downloaded
papers and I suspect these guys wouldn;t disagree either

http://www.medscape.com/viewprogram/4685_pnt

On Tue, 6 May 2008 23:40:43 +0000 (UTC), Charly Coughran
<ccoughran@REMOVE-TO-DELETE-UCSD.EDU> wrote:

>For some time it has been becoming clearer and clearer that
>prediabetes is, in fact, frank diabetes and the high end of normal is
>probably also diabetes. I just finished a quick read through of the
>article and it is one more result lending credence to that conclusion.

IMHO it doesn't matter much whether something is called prediabetes or
diabetes. What matters is that it recognised that the person is at
risk of complications then. When it comes to the complications
commonly associated with diabetes it is important to recognize that
they begin before an official diagnosis of T2 diabetes is made.

>One criticism I would make is that they looked only at FPG which is
>reflected in the prediabetes state as Impaired Fasting Glucose, IFG.
>The alternate presentation of diabetes through a Oral Glucose
>Tolerance Test, OGTT, is reflected in the prediabetic state as
>Impaired Glucose Tolerance, IGT. Some research has made a case that
>IFC and IGT are really two distinct flavors of (pre)diabetes. This,
>of course, complicates things but that is just par for the course in
>diabetes.

Good point.

BTW, it is something Jenny Ruhl goes into in her book, Sugar 101 in
some detail. It's one of the reasons I like her book very much. She
doesn't run from complications yet she comes up with startlingly
simple conclusions.

>Their conclusion that there is no "evidence of a clear and consistent
>glycemic threshold for the presence or incidence of retinopathy"
>matches the DCCT conclusion that there is no magic A1c below which a
>diabetic is "safe" from complications.

Absolutely. A1c isn't as magically as some people have thought.
Having a low A1c isn't a pass card for avoiding complications. Two
hour or peak post prandial glucose levels are much better indicators.

>Charly Coughran

Thank Charly, Hope you get to read my reply.
I confine my posts to ASD and don't cross post replies.

Best wishes,
--
Quentin Grady ^ ^ /
New Zealand, >#,#< [
/ \ /\
"... and the blind dog was leading."

http://homepages.paradise.net.nz/quentin

In alt.support.diabetes Charly Coughran <ccoughran@remove-to-delete-ucsd.edu> wrote:
> Alan S <loralgtweightandcarbs@gmail.com> wrote in
> news:ff7i14h4n0qkhgq2rn4rmhdijb1b5sjqf5@4ax.com:

>> A discussion on this one appeared in Endocrine Today
>> http://www.endocrinetoday.com/view.aspx?rid=26757
>>
>> "Relation between fasting glucose and retinopathy for
>> diagnosis of diabetes: three population-based
>> cross-sectional studies."
>>
>> http://tinyurl.com/3g8oo5 or
>> http://www.ncbi.nlm.nih.gov/pubmed/1...2?ordinalpos=1
> &itool=Entrez
>> System2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_ DiscoveryPanel.Pub
> m
>> ed_RVAbstractPlus
>>
>> Full version (pay)
>> http://www.thelancet.com/journals/la...14067360860318
> 9
>> /fulltext
>>
>> The important bits:
>>
>> "However, we found inconsistent evidence of a uniform
>> glycaemic threshold for prevalent and incident retinopathy,
>> with analyses suggesting a continuous relation. The widely
>> used diabetes FPG cutoff of 7.0 mmol/L or higher had
>> sensitivity less than 40% (range 14.8-39.1) for detecting
>> retinopathy, with specificity between 80.8% and 95.8%."
>> and
>> "The current FPG cutoff of 7.0 mmol/L used to diagnose
>> diabetes did not accurately identify people with and without
>> retinopathy. These findings suggest that the criteria for
>> diagnosing diabetes could need reassessment."
>>
>> 7 mmol/l is 126mg/dl.
>>
>> The abstract:
>>
>> Centre for Eye Research Australia, University of Melbourne,
>> VIC, Australia. twong@unimelb.edu.au
>>
>> BACKGROUND: The WHO and American Diabetes Association
>> criteria for diagnosing diabetes mellitus assume the
>> presence of a glycaemic threshold with high sensitivity for
>> identifying retinopathy. However, this assumption is based
>> on data from three previous studies that had important
>> limitations in detecting retinopathy. We aimed to provide
>> updated data for the relation between fasting plasma glucose
>> (FPG) and retinopathy, and to assess the diagnostic accuracy
>> of current FPG thresholds in identifying both prevalent and
>> incident retinopathy. METHODS: We examined the data from
>> three cross-sectional adult populations: those in the Blue
>> Mountains Eye Study (BMES, Australia, n=3162), the
>> Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
>> Australia, n=2182), and the Multi-Ethnic Study of
>> Atherosclerosis (MESA, USA, n=6079). Retinopathy was
>> diagnosed from multiple retinal photographs of each eye, and
>> graded according to the modified Airlie House Classification
>> system. Plasma glucose concentrations were measured from
>> fasting venous blood samples. FINDINGS: The overall
>> prevalence of retinopathy was 11.5% in BMES (95% CI
>> 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
>> (14.9-16.7). However, we found inconsistent evidence of a
>> uniform glycaemic threshold for prevalent and incident
>> retinopathy, with analyses suggesting a continuous relation.
>> The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
>> had sensitivity less than 40% (range 14.8-39.1) for
>> detecting retinopathy, with specificity between 80.8% and
>> 95.8%. The area under receiver operating characteristic
>> curves for FPG and retinopathy was low and ranged from 0.56
>> to 0.61. INTERPRETATION: We saw no evidence of a clear and
>> consistent glycaemic threshold for the presence or incidence
>> of retinopathy across different populations. The current FPG
>> cutoff of 7.0 mmol/L used to diagnose diabetes did not
>> accurately identify people with and without retinopathy.
>> These findings suggest that the criteria for diagnosing
>> diabetes could need reassessment.

> For some time it has been becoming clearer and clearer that
> prediabetes is, in fact, frank diabetes and the high end of normal is
> probably also diabetes. I just finished a quick read through of the
> article and it is one more result lending credence to that conclusion.

They are starting from a position of accepting that there is merit in
the current diagnostic thresholds, and therefore, as good scientists,
they require good reasons for changing their minds. But where did the
current diagnostic thresholds come from?

I haven't made a comprehensive study, but the impression I get is that
there was never a good scientific reason for adopting those thresholds
in the first place. They simply happened, in the absence of anything
better at the time, to be therapeutically convenient and it was
possible in the state of medical knowledge at the time to cook up a
plausible rationale for the guess.

I quite agree that a scientist needs good evidence to overturn a
previously established and well accepted scientific view. But IMHO
it's just a waste of everyone's time and money trying to establish a
good scientific case for overturning an ossified plausible guess which
never had a good scientific foundation in the first place. And pegging
the diagnostic thresholds at a point where the progression of the
disorder has caused enough damage that is it no longer curable seems
an extremely questionable medical practice.

I can't understand why so much cautious fuss is being made about
overturning such a questionable idea.

--
Chris Malcolm cam@infirmatics.ed.ac.uk DoD #205
IPAB, Informatics, JCMB, King's Buildings, Edinburgh, EH9 3JZ, UK
[http://www.dai.ed.ac.uk/homes/cam/]

Charly Coughran wrote:
> convicted neighbor Alan S <loralgtweightandcarbs@gmail.com> wrote:
>
http://groups.google.com/group/sci.m...85732b737675e?
>
> > I'm going back through various subscriptions I have to
> > different medical reports servers.
> >
> > Please excuse me if any of the reports I post have been
> > discussed while I was away.
> >
> > A discussion on this one appeared in Endocrine Today
> > http://www.endocrinetoday.com/view.aspx?rid=26757
> >
> > "Relation between fasting glucose and retinopathy for
> > diagnosis of diabetes: three population-based
> > cross-sectional studies."
> >
> > http://tinyurl.com/3g8oo5
> >
> > Full version (pay)
> > http://www.thelancet.com/journals/la...03189/fulltext
> >
> > The important bits:
> >
> > "However, we found inconsistent evidence of a uniform
> > glycaemic threshold for prevalent and incident retinopathy,
> > with analyses suggesting a continuous relation. The widely
> > used diabetes FPG cutoff of 7.0 mmol/L or higher had
> > sensitivity less than 40% (range 14.8-39.1) for detecting
> > retinopathy, with specificity between 80.8% and 95.8%."
> > and
> > "The current FPG cutoff of 7.0 mmol/L used to diagnose
> > diabetes did not accurately identify people with and without
> > retinopathy. These findings suggest that the criteria for
> > diagnosing diabetes could need reassessment."
> >
> > 7 mmol/l is 126mg/dl.
> >
> > The abstract:
> >
> > Centre for Eye Research Australia, University of Melbourne,
> > VIC, Australia. twong@unimelb.edu.au
> >
> > BACKGROUND: The WHO and American Diabetes Association
> > criteria for diagnosing diabetes mellitus assume the
> > presence of a glycaemic threshold with high sensitivity for
> > identifying retinopathy. However, this assumption is based
> > on data from three previous studies that had important
> > limitations in detecting retinopathy. We aimed to provide
> > updated data for the relation between fasting plasma glucose
> > (FPG) and retinopathy, and to assess the diagnostic accuracy
> > of current FPG thresholds in identifying both prevalent and
> > incident retinopathy. METHODS: We examined the data from
> > three cross-sectional adult populations: those in the Blue
> > Mountains Eye Study (BMES, Australia, n=3162), the
> > Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
> > Australia, n=2182), and the Multi-Ethnic Study of
> > Atherosclerosis (MESA, USA, n=6079). Retinopathy was
> > diagnosed from multiple retinal photographs of each eye, and
> > graded according to the modified Airlie House Classification
> > system. Plasma glucose concentrations were measured from
> > fasting venous blood samples. FINDINGS: The overall
> > prevalence of retinopathy was 11.5% in BMES (95% CI
> > 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
> > (14.9-16.7). However, we found inconsistent evidence of a
> > uniform glycaemic threshold for prevalent and incident
> > retinopathy, with analyses suggesting a continuous relation.
> > The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
> > had sensitivity less than 40% (range 14.8-39.1) for
> > detecting retinopathy, with specificity between 80.8% and
> > 95.8%. The area under receiver operating characteristic
> > curves for FPG and retinopathy was low and ranged from 0.56
> > to 0.61. INTERPRETATION: We saw no evidence of a clear and
> > consistent glycaemic threshold for the presence or incidence
> > of retinopathy across different populations. The current FPG
> > cutoff of 7.0 mmol/L used to diagnose diabetes did not
> > accurately identify people with and without retinopathy.
> > These findings suggest that the criteria for diagnosing
> > diabetes could need reassessment.
>
> For some time it has been becoming clearer and clearer that
> prediabetes is, in fact, frank diabetes and the high end of normal is
> probably also diabetes.

Incorrect.

Instead, the correct diagnosis would be metabolic syndrome (MetS).

It is our collective clinical experience that the PIACs from VAT are
the cause of the inflammation-associated conditions such as
retinopathy, neuropathy, myopathy, and vasculopathy for folks with
MetS instead of their hyperglycemia, which can even be absent for
those blessed with a strong pancreas.

Frank type-2 diabetes is simply a more extreme form of MetS.

Be hungry... be healthy... be hungrier... be euglycemic...

Prayerfully in the awesome name of LORD Jesus Christ,

Andrew <><
--
http://groups.google.com/group/sci.m...918679e6b3d6f?

Chris Malcolm wrote:
> In alt.support.diabetes Charly Coughran <ccoughran@remove-to-delete-ucsd.edu> wrote:

>>For some time it has been becoming clearer and clearer that
>>prediabetes is, in fact, frank diabetes and the high end of normal is
>>probably also diabetes. I just finished a quick read through of the
>>article and it is one more result lending credence to that conclusion.
>
>
> They are starting from a position of accepting that there is merit in
> the current diagnostic thresholds, and therefore, as good scientists,
> they require good reasons for changing their minds. But where did the
> current diagnostic thresholds come from?
>
> I haven't made a comprehensive study, but the impression I get is that
> there was never a good scientific reason for adopting those thresholds
> in the first place. They simply happened, in the absence of anything
> better at the time, to be therapeutically convenient and it was
> possible in the state of medical knowledge at the time to cook up a
> plausible rationale for the guess.
>
> I quite agree that a scientist needs good evidence to overturn a
> previously established and well accepted scientific view. But IMHO
> it's just a waste of everyone's time and money trying to establish a
> good scientific case for overturning an ossified plausible guess which
> never had a good scientific foundation in the first place. And pegging
> the diagnostic thresholds at a point where the progression of the
> disorder has caused enough damage that is it no longer curable seems
> an extremely questionable medical practice.
>
> I can't understand why so much cautious fuss is being made about
> overturning such a questionable idea.
>

The criteria for using cutoffs often involves the economics of
evaluating a general population. Arbitrary cutoffs in this sense become
starting points for further evaluation. Sure there is a continuum of
risks for various micro or macro vascular complications related to
diabetes. Economics basically relates to the allocation of scare
resources.

Note that the pubmed source listed of related articles including the
following 1994 article: Comparison of tests for glycated haemoglobin and
fasting and two hour plasma glucose concentrations as diagnostic methods
for diabetes - http://www.bmj.com/cgi/content/full/308/6940/1323. The
pubmed takes another step backwards to 1993: Diabetologia. 1993
May;36(5):428-32. Glycated haemoglobin, plasma glucose and diabetic
retinopathy: cross-sectional and prospective analyses.
Liu QZ, Pettitt DJ, Hanson RL, Charles MA, Klein R, Bennett PH, Knowler WC.
Among Pima Indians with Type 2 (non-insulin-dependent) diabetes
mellitus the relationships between glycated haemoglobin (HbA1), fasting
or 2-h post-load plasma glucose and diabetic retinopathy were examined
by cross-sectional and prospective analyses, and the strengths of the
associations were directly compared by receiver operating characteristic
analysis. In the cross-sectional analysis, HbA1, fasting and 2-h plasma
glucose were each significantly related to retinopathy among 789
diabetic subjects by separate logistic models. In a stepwise multiple
logistic model in which HbA1, fasting and 2-h plasma glucose were
included, HbA1 was selected as having the strongest association with
retinopathy and neither fasting nor 2-h plasma glucose contributed
significantly to the model once HbA1 was entered. Similarly, in the
prospective analysis, HbA1, fasting and 2-h plasma glucose all predicted
retinopathy in 227 diabetic subjects by separate proportional-hazards
models. In a stepwise proportional-hazards model with HbA1, fasting and
2-h plasma glucose available to the model, HbA1 was again selected as
having the strongest association with the incidence of retinopathy, and
neither fasting nor 2-h plasma glucose significantly added to the
prediction of retinopathy. A receiver operating characteristic analysis
was used to determine if HbA1 was statistically significantly better
than fasting or 2-h plasma glucose in assessing the risk for
retinopathy. In neither the cross-sectional nor the prospective data did
the area under the receiver operating characteristic curve for HbA1
differ significantly from that for fasting or 2-h plasma glucose (p >
0.05 for each).(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 8314447 [PubMed - indexed for MEDLINE]

A Medspace search shows 37 articles for retinopathy Pima indians -
http://tinyurl.com/53gqz4, but I like the graphic (slide 21) for a more
general population - http://www.medscape.com/viewarticle/412864_8 that
shows a rectangle where the incidence of retinopathy increases at an
increasing rate with A1c of 6%, FBG of 109 mg/dl, and 2 hr. PP of 154
mg/dl. The incidence below these levels does show the notion of a
continuum, but approximately at 3 to 5 percent for various glucose
measurements. The Pima graphic (slide 22) shows a similar but a
retinopathy pattern at higher levels. The idea of 5% A1c, 90 mg/dl FBG,
and 2hh PP of 110-116 mg/dl as being safe or normal cutoff levels isn't
too far off. Obviously these would be very tight goals for a diabetic.

Frank

On Sat, 17 May 2008 12:32:28 -0400, Jefferson <Jefferson@comcast.net>
wrote:

>Chris Malcolm wrote:
>> In alt.support.diabetes Charly Coughran <ccoughran@remove-to-delete-ucsd.edu> wrote:
>
>>>For some time it has been becoming clearer and clearer that
>>>prediabetes is, in fact, frank diabetes and the high end of normal is
>>>probably also diabetes. I just finished a quick read through of the
>>>article and it is one more result lending credence to that conclusion.
>>
>>
>> They are starting from a position of accepting that there is merit in
>> the current diagnostic thresholds, and therefore, as good scientists,
>> they require good reasons for changing their minds. But where did the
>> current diagnostic thresholds come from?
>>
>> I haven't made a comprehensive study, but the impression I get is that
>> there was never a good scientific reason for adopting those thresholds
>> in the first place. They simply happened, in the absence of anything
>> better at the time, to be therapeutically convenient and it was
>> possible in the state of medical knowledge at the time to cook up a
>> plausible rationale for the guess.
>>
>> I quite agree that a scientist needs good evidence to overturn a
>> previously established and well accepted scientific view. But IMHO
>> it's just a waste of everyone's time and money trying to establish a
>> good scientific case for overturning an ossified plausible guess which
>> never had a good scientific foundation in the first place. And pegging
>> the diagnostic thresholds at a point where the progression of the
>> disorder has caused enough damage that is it no longer curable seems
>> an extremely questionable medical practice.
>>
>> I can't understand why so much cautious fuss is being made about
>> overturning such a questionable idea.
>>
>
>The criteria for using cutoffs often involves the economics of
>evaluating a general population. Arbitrary cutoffs in this sense become
>starting points for further evaluation. Sure there is a continuum of
>risks for various micro or macro vascular complications related to
>diabetes. Economics basically relates to the allocation of scare
>resources.

This is true - assuming the only treatment you apply is medication.
I've just been re-reading a whole bunch of papers I downloaded,
including Medscape CMEs, and there's a lot of useful information in
there to be sure, especially the recent emphasis on postprandial
numbers BUT the emphasis has only come about due to Byetta coming on
the market - this can trim the postprandial numbers neatly by having
more action at higher numbers and less action when approaching goal
unlike pancreas stimulators such as the Sulphs.

However the changes many of us have achieved through dietary changes
alone seem to have slipped right past the medics - and what resources
are required? Test strips . . . and clueful information . . .

On Apr 30, 9:39*pm, Alan S <loralgtweightandca...@gmail.com> wrote:
> I'm going back through various subscriptions I have to
> different medical reports servers.
>
> Please excuse me if any of the reports I post have been
> discussed while I was away.
>
> A discussion on this one appeared in Endocrine Todayhttp://www.endocrinetoday.com/view.aspx?rid=26757
>
> "Relation between fasting glucose and retinopathy for
> diagnosis of diabetes: three population-based
> cross-sectional studies."
>
> http://tinyurl.com/3g8oo5orhttp://ww...1&itool=Entrez...
>
> Full version (pay)http://www.thelancet.com/journals/la...40673608603189...
>
> The important bits:
>
> "However, we found inconsistent evidence of a uniform
> glycaemic threshold for prevalent and incident retinopathy,
> with analyses suggesting a continuous relation. The widely
> used diabetes FPG cutoff of 7.0 mmol/L or higher had
> sensitivity less than 40% (range 14.8-39.1) for detecting
> retinopathy, with specificity between 80.8% and 95.8%."
> and
> "The current FPG cutoff of 7.0 mmol/L used to diagnose
> diabetes did not accurately identify people with and without
> retinopathy. These findings suggest that the criteria for
> diagnosing diabetes could need reassessment."
>
> 7 mmol/l is 126mg/dl.
>
> The abstract:
>
> Centre for Eye Research Australia, University of Melbourne,
> VIC, Australia. tw...@unimelb.edu.au
>
> BACKGROUND: The WHO and American Diabetes Association
> criteria for diagnosing diabetes mellitus assume the
> presence of a glycaemic threshold with high sensitivity for
> identifying retinopathy. However, this assumption is based
> on data from three previous studies that had important
> limitations in detecting retinopathy. We aimed to provide
> updated data for the relation between fasting plasma glucose
> (FPG) and retinopathy, and to assess the diagnostic accuracy
> of current FPG thresholds in identifying both prevalent and
> incident retinopathy. METHODS: We examined the data from
> three cross-sectional adult populations: those in the Blue
> Mountains Eye Study (BMES, Australia, n=3162), the
> Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
> Australia, n=2182), and the Multi-Ethnic Study of
> Atherosclerosis (MESA, USA, n=6079). Retinopathy was
> diagnosed from multiple retinal photographs of each eye, and
> graded according to the modified Airlie House Classification
> system. Plasma glucose concentrations were measured from
> fasting venous blood samples. FINDINGS: The overall
> prevalence of retinopathy was 11.5% in BMES (95% CI
> 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
> (14.9-16.7). However, we found inconsistent evidence of a
> uniform glycaemic threshold for prevalent and incident
> retinopathy, with analyses suggesting a continuous relation.
> The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
> had sensitivity less than 40% (range 14.8-39.1) for
> detecting retinopathy, with specificity between 80.8% and
> 95.8%. The area under receiver operating characteristic
> curves for FPG and retinopathy was low and ranged from 0.56
> to 0.61. INTERPRETATION: We saw no evidence of a clear and
> consistent glycaemic threshold for the presence or incidence
> of retinopathy across different populations. The current FPG
> cutoff of 7.0 mmol/L used to diagnose diabetes did not
> accurately identify people with and without retinopathy.
> These findings suggest that the criteria for diagnosing
> diabetes could need reassessment.
>
> Cheers, Alan, T2, Australia.
> d&e, metformin 1500mg, ezetrol 10mg
> Everything in Moderation - Except Laughter.
> --http://loraldiabetes.blogspot.com
> Latest:Is Testing Worthwhile?
> and Cambodiahttp://loraltravel.blogspot.com/2008/03/cambodia.html

Exactly what is it that causes retinopathy? Is it high blood sugar
alone? Or high insulin, or high blood pressure, or occlusion of the
veins arteries? A combination? Pritikin reported that people in
parts of the world on a high carb low fat diet who do have diabetes
seem to have fewer complications. I have no way of checking this
out. Is it possible to get your numbers really low, yet be eating in
a way that will occlude arteries and thus promote retinopathy.

I want to mention that someone on another group came across a study
which showed that in a diet high in potassium, higher blood pressures
did not make people more susceptible to stroke despite the higher
pressure. Potassium in the diet (from fruits and vegetables) seems to
have some protective effect. So is it possible that you might not get
a linear relationship between retinopathy and blood sugar because of
differences in the micro and macronutrients in various diets?

Dolores

I go to my ophthalmologist who is a retina specialist twice a year.
I hope everyone on this group is diligent in having his retinas
checked.

On May 21, 4:57 pm, dorsy1943 <dtm...@usadatanet.net> wrote:
> On Apr 30, 9:39 pm, Alan S <loralgtweightandca...@gmail.com> wrote:
>
>
>
> > I'm going back through various subscriptions I have to
> > different medical reports servers.
>
> > Please excuse me if any of the reports I post have been
> > discussed while I was away.
>
> > A discussion on this one appeared in Endocrine Todayhttp://www.endocrinetoday.com/view.aspx?rid=26757
>
> > "Relation between fasting glucose and retinopathy for
> > diagnosis of diabetes: three population-based
> > cross-sectional studies."
>
> >http://tinyurl.com/3g8oo5orhttp://ww...pubmed/1831350......
>
> > Full version (pay)http://www.thelancet.com/journals/la...40673608603189...
>
> > The important bits:
>
> > "However, we found inconsistent evidence of a uniform
> > glycaemic threshold for prevalent and incident retinopathy,
> > with analyses suggesting a continuous relation. The widely
> > used diabetes FPG cutoff of 7.0 mmol/L or higher had
> > sensitivity less than 40% (range 14.8-39.1) for detecting
> > retinopathy, with specificity between 80.8% and 95.8%."
> > and
> > "The current FPG cutoff of 7.0 mmol/L used to diagnose
> > diabetes did not accurately identify people with and without
> > retinopathy. These findings suggest that the criteria for
> > diagnosing diabetes could need reassessment."
>
> > 7 mmol/l is 126mg/dl.
>
> > The abstract:
>
> > Centre for Eye Research Australia, University of Melbourne,
> > VIC, Australia. tw...@unimelb.edu.au
>
> > BACKGROUND: The WHO and American Diabetes Association
> > criteria for diagnosing diabetes mellitus assume the
> > presence of a glycaemic threshold with high sensitivity for
> > identifying retinopathy. However, this assumption is based
> > on data from three previous studies that had important
> > limitations in detecting retinopathy. We aimed to provide
> > updated data for the relation between fasting plasma glucose
> > (FPG) and retinopathy, and to assess the diagnostic accuracy
> > of current FPG thresholds in identifying both prevalent and
> > incident retinopathy. METHODS: We examined the data from
> > three cross-sectional adult populations: those in the Blue
> > Mountains Eye Study (BMES, Australia, n=3162), the
> > Australian Diabetes, Obesity and Lifestyle Study (AusDiab,
> > Australia, n=2182), and the Multi-Ethnic Study of
> > Atherosclerosis (MESA, USA, n=6079). Retinopathy was
> > diagnosed from multiple retinal photographs of each eye, and
> > graded according to the modified Airlie House Classification
> > system. Plasma glucose concentrations were measured from
> > fasting venous blood samples. FINDINGS: The overall
> > prevalence of retinopathy was 11.5% in BMES (95% CI
> > 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA
> > (14.9-16.7). However, we found inconsistent evidence of a
> > uniform glycaemic threshold for prevalent and incident
> > retinopathy, with analyses suggesting a continuous relation.
> > The widely used diabetes FPG cutoff of 7.0 mmol/L or higher
> > had sensitivity less than 40% (range 14.8-39.1) for
> > detecting retinopathy, with specificity between 80.8% and
> > 95.8%. The area under receiver operating characteristic
> > curves for FPG and retinopathy was low and ranged from 0.56
> > to 0.61. INTERPRETATION: We saw no evidence of a clear and
> > consistent glycaemic threshold for the presence or incidence
> > of retinopathy across different populations. The current FPG
> > cutoff of 7.0 mmol/L used to diagnose diabetes did not
> > accurately identify people with and without retinopathy.
> > These findings suggest that the criteria for diagnosing
> > diabetes could need reassessment.
>
> > Cheers, Alan, T2, Australia.
> > d&e, metformin 1500mg, ezetrol 10mg
> > Everything in Moderation - Except Laughter.
> > --http://loraldiabetes.blogspot.com
> > Latest:Is Testing Worthwhile?
> > and Cambodiahttp://loraltravel.blogspot.com/2008/03/cambodia.html
>
> Exactly what is it that causes retinopathy? Is it high blood sugar
> alone? Or high insulin, or high blood pressure, or occlusion of the
> veins arteries? A combination? Pritikin reported that people in
> parts of the world on a high carb low fat diet who do have diabetes
> seem to have fewer complications. I have no way of checking this
> out. Is it possible to get your numbers really low, yet be eating in
> a way that will occlude arteries and thus promote retinopathy.
>
> I want to mention that someone on another group came across a study
> which showed that in a diet high in potassium, higher blood pressures
> did not make people more susceptible to stroke despite the higher
> pressure. Potassium in the diet (from fruits and vegetables) seems to
> have some protective effect. So is it possible that you might not get
> a linear relationship between retinopathy and blood sugar because of
> differences in the micro and macronutrients in various diets?
>
> Dolores
>
> I go to my ophthalmologist who is a retina specialist twice a year.
> I hope everyone on this group is diligent in having his retinas
> checked.

Diabetics Retinopathy is one of the diabetes long term complications
caused by high blood glucose levels which effects the blood supplying
to the retina.

In order to control the diabetes retinopathy , first of all diabetes
levels should be controlled. Every diabetic should have his complete
checkups including eyes twice a year as this will prevent from
developing major complications.

Eating foods high in potassium helps in insulin resistance and can be
beneficial(banana, apricot, tomato)

For more on diabetic neuropathy visit
http://www.reddiabetes.com/Eye_Diseases.html

I hope that every diabetic will find it helpful.

"Tehmina" <tehminasmazher@gmail.com> wrote in message
news:4a4bc24f-1090-4597-b45e-adec93e6806c@x35g2000hsb.googlegroups.com...
[snip]
> Eating foods high in potassium helps in insulin resistance and can be
> beneficial(banana, apricot, tomato)
>
The high level of carbohydrates in bananas isn't beneficial for type 2
diabetics (that is, most diabetics). I'll let diabetics of other types tell
you whether it's OK for those types.

On Wed, 21 May 2008 04:57:27 -0700 (PDT), dorsy1943
<dtms69@usadatanet.net> wrote:

>Exactly what is it that causes retinopathy? Is it high blood sugar
>alone? Or high insulin, or high blood pressure, or occlusion of the
>veins arteries? A combination?

I'd bet on a combo. My favourite post on the subject is Quentin's, on
quercetin, sorbitol and lutein - try a google for it?

My understanding of the mechanism is that something causes a blood
vessel in your eye to become weak. I don't like the sound of sorbitol
and the eye taking up glucose with ease, myself... anyway, you have
this break. The normal repair mechanisms rush to sort it out - but
something stops the repairs ending; you get a preliferation of little
bleeds from wildly growing veins, and it's that which makes the holes
in your vision.

>So is it possible that you might not get
>a linear relationship between retinopathy and blood sugar because of
>differences in the micro and macronutrients in various diets?

For sure. Eat your spinach...

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.6% BMI 25

On Wed, 21 May 2008 04:57:27 -0700 (PDT), dorsy1943
<dtms69@usadatanet.net> wrote:

>Exactly what is it that causes retinopathy? Is it high blood sugar
>alone? Or high insulin, or high blood pressure, or occlusion of the
>veins arteries? A combination?

Yes.

There are several pathways to the peripheral damage, one is from the
excessive glucose per se, which in the eye leads to a buildup of
sorbitol (ping Quentin! repost required!) , increased levels of AGEs
as tissues get glycated, increased levels of cytokines etc. etc.

Buggerit, I've been reading some Medscape stuff and can't find it when
I need it, here

http://www.medscape.com/resource/mic...microvascular1

probably more than you wanted to know, go dig through that lot and
report back <G>

>Pritikin reported that people in
>parts of the world on a high carb low fat diet who do have diabetes
>seem to have fewer complications. I have no way of checking this
>out. Is it possible to get your numbers really low, yet be eating in
>a way that will occlude arteries and thus promote retinopathy.
>
>I want to mention that someone on another group came across a study
>which showed that in a diet high in potassium, higher blood pressures
>did not make people more susceptible to stroke despite the higher
>pressure. Potassium in the diet (from fruits and vegetables) seems to
>have some protective effect. So is it possible that you might not get
>a linear relationship between retinopathy and blood sugar because of
>differences in the micro and macronutrients in various diets?

Also you don't get a linear relationship because of a gazillion and a
half genetic factors and others.

At the end of the day probably the best you can do is to keep your BG
down and ensure you have plenty of bioflavinoids and other
micronutrients in your diet

http://www.macular-degeneration-vitamins.com/index.htm

You don't have to buy the stuff these guys sell, make sure you get
them from dietary sources.

>I go to my ophthalmologist who is a retina specialist twice a year.
>I hope everyone on this group is diligent in having his retinas
>checked.

Damn right! To join the Eye Police see Wendy for details

In alt.support.diabetes Nicky <ukc802466929@btconnect.com> wrote:
: On Wed, 21 May 2008 04:57:27 -0700 (PDT), dorsy1943
: <dtms69@usadatanet.net> wrote:

: >Exactly what is it that causes retinopathy? Is it high blood sugar
: >alone? Or high insulin, or high blood pressure, or occlusion of the
: >veins arteries? A combination?

: I'd bet on a combo. My favourite post on the subject is Quentin's, on
: quercetin, sorbitol and lutein - try a google for it?

: My understanding of the mechanism is that something causes a blood
: vessel in your eye to become weak. I don't like the sound of sorbitol
: and the eye taking up glucose with ease, myself... anyway, you have
: this break. The normal repair mechanisms rush to sort it out - but
: something stops the repairs ending; you get a preliferation of little
: bleeds from wildly growing veins, and it's that which makes the holes
: in your vision.

: >So is it possible that you might not get
: >a linear relationship between retinopathy and blood sugar because of
: >differences in the micro and macronutrients in various diets?

: For sure. Eat your spinach...

: Nicky.

IIRC there is growth of new blood vessels in the retina which are weaker
than the old ones adn can easily leak, leading, ultimately, to blindness
if there is enough bleeding. The lasering tries to catch a weak spot
before it bleeds and cauterizes it, leaving a tiny scar to which your eye
adjusts. Generally, if you get control of the bgs this wild growth in the
retina wil stop and further treatment will not be necessary. this I
learned some 12 years ago, so my memory may well be a bit hazy.
non-proliferative reetinopathy is the earlier stage when some changes
occur in the retina and may well not progress, particularly if good
control is gained. Proliferative retinopaty is a more advanced stage
when the growth(proliferation) of new blood vessels is occurring. This is
when laser or steriod treatments become useful or necessary.

I hope ths helps a bit.

Wendy-in "eye police" mode

dorsy1943 <dtms69@usadatanet.net> wrote in
news:0f6fe35b-7a1e-41de-8fac-53bbfe853b77@g16g2000pri.googlegroups.com:

>
> Exactly what is it that causes retinopathy? Is it high blood sugar
> alone? Or high insulin, or high blood pressure, or occlusion of the
> veins arteries? A combination?
>
> Dolores
>
> I go to my ophthalmologist who is a retina specialist twice a year.
> I hope everyone on this group is diligent in having his retinas
> checked.

The state of understanding the cause of retinopathy is probably best
described by saying there are a number of candidate causes and the
consensus is that no single cause provides the full explanation.

Hypertension is probably better called an exacerbate condition rather
than a cause. If you have microaneurysms (weak and leaky bulges) in the
capillaries in the eye which is often the first symptom of retinopathy,
having higher than normal blood pressure is certainly going to make
things worse. If I recollect correctly in the DCCT there was almost a
40% reduction in some of the clinical endpoints which evaluated
retinopathy with aggressive treatment of hypertension. This is not to
claim, however, that there are no mechanisms proposed for a causal role
of hypertension in diabetic retinopathy.

Hyperglycemia is the driver for most of the causal mechanisms I have
encountered. In no particular order:

SORBITOL PATHWAY - Glucose can be converted into sorbitol by the enzyme
aldose reductase. The sorbitol can be metabolized into fructose by
sorbitol dehydrogenase. The second reaction, however, goes much more
slowly. Since sorbitol doesn't generally diffuse across cell membranes,
it can accumulate rapidly in the presence of excessive glucose. One of
several mechan