Hi Alan,

well.....

There is more actually if you want to accept a some what indirect line of
evidence .There is becoming ever more literature which proves that the
progression of Diabetes Type II is highly dependent on

1) the bloodglucose itself

2) but also on the HbA1c

3) also on the fasting bloodglucose

4) most stongly on the post prandial bloodglucose

There is evidence that the progression of diabetes Type II depends on the
level of anti oxidants in fruits ,wine ,nuts ; or healthy diets.There is now
a theory which connects all the steps from high bloodglucose to protein
glycation to Diabetes Type II

Conclusion : the best thing for preventing progression of diabetes type II
is controlling your bloodglucose.

Roger clearly found one way of doing that 25 years !!!!!!!! :

Re: The Diabetes Conundrum: What Physicians are Teaching You may be Killing
You (Mercola)

Let's see: 48-23=25!

No complications and living LC.  No meds & plenty of exercise.

I guess it will be 26 years in a couple of months or so....roughly, anyhow.

IMO, complications can definitely be put off, if you get things under

control in time, that is, and if you keep them under control.

And I personally think he is right . Here is a recent  article where it was
found that the post prandial bloodglucose is an important parameter , or
"eat to your meter"  :)   But don't forget to keep an eye on other things on
your diet.....Please notice the words "acute" in "acute hyperglycemia" and
"oral glucose loading" of course.It means that the beta cells die also from
a high bloodglucose during a short period after eating things !!!! And not
only from a prolonged too high bloodglucose !!!!

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, dagger0.362 +/- 0.119 and dagger0.355
+/- 0.131 ng/ml, *P < 0.05 vs. fasting, daggerP < 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. Diabet. Med. 24, 154 -160 (2007).

PMID: 17257277

Here is another one on the progression process :

Diabetes Care. 2007 Feb;30(2):263-9.

The loss of postprandial glycemic control precedes stepwise deterioration of
fasting with worsening diabetes.

OBJECTIVE: The aim of the study was to determine whether the loss of fasting
and postprandial glycemic control occurs in parallel or sequentially in the
evolution of type 2 diabetes. RESEARCH DESIGN AND METHODS: In 130 type 2
diabetic patients, 24-h glucose profiles were obtained using a continuous
glucose monitoring system. The individuals with type 2 diabetes were divided
into five groups according to A1C levels: 1 (<6.5%, n = 30), 2 (6.5-6.9%, n
= 17), 3 (7-7.9%, n = 32), 4 (8-8.9%, n = 25), and 5 (>/=9%, n = 26). The
glucose profiles between the groups were compared. The overall glucose
concentrations for the diurnal, nocturnal, and morning periods, which
represent the postprandial, fasting, and the dawn phenomenon states,
respectively, were also compared. RESULTS: Glucose concentrations increased
steadily from group 1 to 5 in a stepwise manner. The initial differences in
mean glucose concentrations reaching statistical significance occurred 1)
between groups 1 and 2 (6.4 vs. 7.7 mmol/l, P = 0.0004) for daytime
postprandial periods, followed by differences; 2) between groups 2 and 3
(7.5 vs. 9.3 mmol/l, P = 0.0003) for the morning periods (dawn phenomenon);
and finally 3) between groups 3 and 4 (6.3 vs. 8.4 mmol/l, P < 0.0001) for
nocturnal fasting periods. CONCLUSIONS: The deterioration of glucose
homeostasis in individuals with type 2 diabetes progressed from postprandial
to fasting hyperglycemia following a three-step process. The first step
related to the three diurnal postmeal periods considered as a whole, the
second step occurred during the morning period, and the third and final step
corresponded to sustained hyperglycemia over the nocturnal fasting periods.
Such a description of the key stages in the evolution of type 2 diabetes may
be of interest for implementing antidiabetes treatment.

PMID: 17259492

Gys