Question

A question for those of you experienced with this diabetes stuff.

I had a bood test that showed a blood sugar level of 123 and a urine
protein of 300. I've not been previously diagnosed with diabetes but
it seems pretty evident to me. Would this be a normal indicator of
diabetes?

"Bill" <bill@nospam.null> wrote in message
news:6ks1l257l4h56lntkqb5cssv3vq09hbvr8@4ax.com...
:A question for those of you experienced with this diabetes stuff.
:
: I had a bood test that showed a blood sugar level of 123 and a urine
: protein of 300. I've not been previously diagnosed with diabetes but
: it seems pretty evident to me. Would this be a normal indicator of
: diabetes?

Really depends. Was that glucose level fasting or mid day? If mid day
how long after you'd eaten? and what did you eat? None of us are
doctors here and one can have protein in their urine without being
diabetic. One normally will NOT have glucose in their urine without
being diabetic.

I'd get a ref to a kidney doctor and get it checked out.. High levels of
protein in urine means your kidneys aren't working properly.

Good luck.



--
Reisa, T1, Animas IR1250 Pumper
DX-5/00 ASD-7/00
A1C: 6.2% (8/24/06)
Daily CHO: 150-200gm
TDD: 34-38u

x-no-archive: yes

Bill wrote:
> A question for those of you experienced with this diabetes stuff.
>
> I had a bood test that showed a blood sugar level of 123 and a urine
> protein of 300. I've not been previously diagnosed with diabetes but
> it seems pretty evident to me. Would this be a normal indicator of
> diabetes?

Bill, if that was a fasting number, you should know that post meal
numbers are usually well into the diabetic range long before fasting
glucose is. A fasting of 100 or above is associated with loss of
pancreatic insulin producing cells.

In people who are otherwise previously healthy without major disease,
diabetic damage to kidneys is the most common/likely cause of protein in
the urine.

It could be worth getting your hands on a blood glucose meter and
testing your blood glucose at one and two hours after meals to see if
you're running above 140, the threshold for cellular damage.

Susan

On Tue, 07 Nov 2006 16:33:41 -0500, Susan <nevermind@nomail.com>
wrote:

>It could be worth getting your hands on a blood glucose meter and
>testing your blood glucose at one and two hours after meals to see if
>you're running above 140, the threshold for cellular damage.


Thanks, Susan.

Bill wrote:
> A question for those of you experienced with this diabetes
stuff.
>
> I had a bood test that showed a blood sugar level of 123
and a urine
> protein of 300. I've not been previously diagnosed with
diabetes but
> it seems pretty evident to me. Would this be a normal
indicator of
> diabetes?

What did the doctor say when he/she gave you the results?
Did they let you walk away with a high protein level with no
follow up? Was your blood pressure checked?

On Tue, 07 Nov 2006 22:55:38 GMT, "Ozgirl"
<are_we_there_yet@maccas.com> wrote:

>What did the doctor say when he/she gave you the results?
>Did they let you walk away with a high protein level with no
>follow up? Was your blood pressure checked?


She was assigning me follow-up with a kidney specialist. As for my
blood pressure, it's always remarkably well when checked.

On Tue, 07 Nov 2006 14:56:53 -0600, Bill <bill@nospam.null>
wrote:

>A question for those of you experienced with this diabetes stuff.
>
>I had a bood test that showed a blood sugar level of 123 and a urine
>protein of 300. I've not been previously diagnosed with diabetes but
>it seems pretty evident to me. Would this be a normal indicator of
>diabetes?

In addition to the comments from the others - what did your
doctor say?

Cheers, Alan, T2, Australia.
d&e, metformin 1000mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: The Vatican

Bill wrote:
> On Tue, 07 Nov 2006 22:55:38 GMT, "Ozgirl"
> <are_we_there_yet@maccas.com> wrote:
>
>>What did the doctor say when he/she gave you the results?
>>Did they let you walk away with a high protein level with
no
>>follow up? Was your blood pressure checked?
>
>
> She was assigning me follow-up with a kidney specialist.
As for my
> blood pressure, it's always remarkably well when checked.

Good news. For both. Let us know how it pans out.

rk wrote:
> "Bill" <bill@nospam.null> wrote in message
> news:6ks1l257l4h56lntkqb5cssv3vq09hbvr8@4ax.com...
> :A question for those of you experienced with this diabetes stuff.
> :
> : I had a bood test that showed a blood sugar level of 123 and a urine
> : protein of 300. I've not been previously diagnosed with diabetes but
> : it seems pretty evident to me. Would this be a normal indicator of
> : diabetes?
>
> Really depends. Was that glucose level fasting or mid day? If mid day
> how long after you'd eaten? and what did you eat? None of us are
> doctors here and one can have protein in their urine without being
> diabetic. One normally will NOT have glucose in their urine without
> being diabetic.
>
> I'd get a ref to a kidney doctor and get it checked out.. High levels of
> protein in urine means your kidneys aren't working properly.
>
> Good luck.

Bill, I was about to type the same thing and then read a few of the
posts and RK's comes very close to what I was going to say. I also
read that you are going to see a kidney specialist as a referral from
your doctor. That's a good thing. You might also ask if your doctor
will refer you to an Endocrinologist to run some more tests regarding
your concern about having diabetes.

Best,
Kurt

"Susan" <nevermind@nomail.com> wrote in message
news:4rccdlFqfhvaU1@mid.individual.net...
> x-no-archive: yes
>
> Bill wrote:
>> A question for those of you experienced with this diabetes stuff.
>>
>> I had a bood test that showed a blood sugar level of 123 and a urine
>> protein of 300. I've not been previously diagnosed with diabetes but
>> it seems pretty evident to me. Would this be a normal indicator of
>> diabetes?
>
> Bill, if that was a fasting number, you should know that post meal numbers
> are usually well into the diabetic range long before fasting glucose is.
> A fasting of 100 or above is associated with loss of pancreatic insulin
> producing cells.
>
> In people who are otherwise previously healthy without major disease,
> diabetic damage to kidneys is the most common/likely cause of protein in
> the urine.

I would also add that hypertension can cause kidney damage. Any idea how
your BP is running, Bill?
--
Michelle, T2
diet & exercise


>
> It could be worth getting your hands on a blood glucose meter and testing
> your blood glucose at one and two hours after meals to see if you're
> running above 140, the threshold for cellular damage.
>
> Susan

On Wed, 8 Nov 2006 11:17:57 -0800, "Michelle" <bookbug2005@gmail.com>
wrote:

>I would also add that hypertension can cause kidney damage. Any idea how
>your BP is running, Bill?


Well, I do have a high a very stress job. However, on the infrequent
times that I have had it checked, which is during Doc visits, it seems
to be ok. However, I am always very calm and at ease during those
times too.

"Michelle" <bookbug2005@gmail.com> wrote in message
news:15n924-esr.ln1@news.air-internet.com...
:
: "Susan" <nevermind@nomail.com> wrote in message
: news:4rccdlFqfhvaU1@mid.individual.net...

: > A fasting of 100 or above is associated with loss of pancreatic insulin
: > producing cells.

This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.

--
Reisa, T1, Animas IR1250 Pumper
DX-5/00 ASD-7/00
A1C: 6.2% (8/24/06)
Daily CHO: 150-200gm
TDD: 34-38u

On Wed, 08 Nov 2006 21:43:51 GMT, "rk"
<p_haha_medium@gmail.com> wrote:

>"Michelle" <bookbug2005@gmail.com> wrote in message
>news:15n924-esr.ln1@news.air-internet.com...
>:
>: "Susan" <nevermind@nomail.com> wrote in message
>: news:4rccdlFqfhvaU1@mid.individual.net...
>
>: > A fasting of 100 or above is associated with loss of pancreatic insulin
>: > producing cells.
>
>This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
>having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.

No need for that last comment.

He didn't say a lack of insulin; he said "loss of pancreatic
insulin producing cells". While insulin resistance is
commonly a major factor in the various variants of type 2,
so is the loss of beta cells, and that, in part, may be due
IMO to the stress of over-production of insulin attempting
to counter that IR; eventually that over-production may fail
as beta cell loss progresses.

I use "may" a lot because "does" and "will" cannot often be
applied to the wide spectrum of variables in type 2. One of
the reasons we use YMMV a lot. Or we should.

Cheers, Alan, T2, Australia.
d&e, metformin 1000mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: The Vatican

x-no-archive: yes

rk wrote:

> This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
> having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.
>

I know you can't help it becase, as you adamantly and repeatedly
asserted, your brain is a muscle.

Type 2 begins with hyperinsulinemia, which is overproduction of insulin
as a result of insensitivity by insulin receptors. Eventually, the
exhausted pancreas runs low on insulin producing capacity, and IR
progresses to DM type2, which is characterized by insufficient insulin.

Beta cells begin to die off in the "normal" fasting range of 100. It has
been well demonstrated that DM is usually well advanced before type 2
fbg starts rising into diagnostic ranges.


http://www.springerlink.com/content/mv0l2yk570h8gmkg/


"Conclusion/interpretation When the plasma insulin response to oral
glucose is related to the glycaemic stimulus and severity of insulin
resistance, there is a progressive decline in beta-cell function that
begins in "normal" glucose tolerant individuals."


Susan

> On Wed, 08 Nov 2006 21:43:51 GMT, "rk"
>>
>>This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
>>having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.



> "Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
> No need for that last comment.
>
> He didn't say a lack of insulin; he said "loss of pancreatic
> insulin producing cells". While insulin resistance is
> commonly a major factor in the various variants of type 2,
> so is the loss of beta cells, and that, in part, may be due
> IMO

Soon as i get to your "IMO".. i now know i can spend
my time better else where.
however it does add more credability to RK's saying
"more incrrect BS"
Not that I am saying you are wrong. but if i want to find the truth
and make my own opinion i have learned its best to find out for myself.

Tom

"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
news:t6k4l296oghdpkgegb21a778f8oe5jfcdh@4ax.com...
: On Wed, 08 Nov 2006 21:43:51 GMT, "rk"
: <p_haha_medium@gmail.com> wrote:
:
: >"Michelle" <bookbug2005@gmail.com> wrote in message
: >news:15n924-esr.ln1@news.air-internet.com...
: >:
: >: "Susan" <nevermind@nomail.com> wrote in message
: >: news:4rccdlFqfhvaU1@mid.individual.net...
: >
: >: > A fasting of 100 or above is associated with loss of pancreatic
insulin
: >: > producing cells.
: >
: >This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
: >having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.
:
: No need for that last comment.
:
: He didn't say a lack of insulin; he said "loss of pancreatic
: insulin producing cells". While insulin resistance is
: commonly a major factor in the various variants of type 2,
: so is the loss of beta cells, and that, in part, may be due
: IMO to the stress of over-production of insulin attempting
: to counter that IR; eventually that over-production may fail
: as beta cell loss progresses.
:
: I use "may" a lot because "does" and "will" cannot often be
: applied to the wide spectrum of variables in type 2. One of
: the reasons we use YMMV a lot. Or we should.
:
: Cheers, Alan, T2, Australia.
: d&e, metformin 1000mg, ezetrol 10mg
: Everything in Moderation - Except Laughter.
: --
: http://loraldiabetes.blogspot.com/
: http://loraltravel.blogspot.com/
: latest: The Vatican

"what does... "loss of pancreatic insulin producing cells" mean?".
Is exactly what I asked my endo a few ago when I emailed her and
her reply was exactly as I said.. which means when one loses cells
they no longer produce insulin.. HELLO? which part of that did ya
miss in Biology? IR has NOTHING to do with loss of cells. It's the cells
inability too allow insulin in to transport carbs properly.

I'm SO done


--
Reisa, T1, Animas IR1250 Pumper
DX-5/00 ASD-7/00
A1C: 6.2% (8/24/06)
Daily CHO: 150-200gm
TDD: 34-38u

x-no-archive: yes

rk wrote:

> "what does... "loss of pancreatic insulin producing cells" mean?".

It means that type 2 DM is characterized by insufficient insulin,
exactly the opposite of your assertion.

> Is exactly what I asked my endo a few ago when I emailed her and
> her reply was exactly as I said.. which means when one loses cells
> they no longer produce insulin.. HELLO? which part of that did ya
> miss in Biology? IR has NOTHING to do with loss of cells. It's the cells
> inability too allow insulin in to transport carbs properly.
>
> I'm SO done
>
>

You were done the moment you began.

ROFL.

Susan

On Wed, 08 Nov 2006 22:13:01 GMT, "rk"
<p_haha_medium@gmail.com> wrote:

>"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
>news:t6k4l296oghdpkgegb21a778f8oe5jfcdh@4ax.com.. .
>: On Wed, 08 Nov 2006 21:43:51 GMT, "rk"
>: <p_haha_medium@gmail.com> wrote:
>:
>: >"Michelle" <bookbug2005@gmail.com> wrote in message
>: >news:15n924-esr.ln1@news.air-internet.com...
>: >:
>: >: "Susan" <nevermind@nomail.com> wrote in message
>: >: news:4rccdlFqfhvaU1@mid.individual.net...
>: >
>: >: > A fasting of 100 or above is associated with loss of pancreatic
>insulin
>: >: > producing cells.
>: >
>: >This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
>: >having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.
>:
>: No need for that last comment.
>:
>: He didn't say a lack of insulin; he said "loss of pancreatic
>: insulin producing cells". While insulin resistance is
>: commonly a major factor in the various variants of type 2,
>: so is the loss of beta cells, and that, in part, may be due
>: IMO to the stress of over-production of insulin attempting
>: to counter that IR; eventually that over-production may fail
>: as beta cell loss progresses.
>:
>: I use "may" a lot because "does" and "will" cannot often be
>: applied to the wide spectrum of variables in type 2. One of
>: the reasons we use YMMV a lot. Or we should.
>:
>: Cheers, Alan, T2, Australia.
>: d&e, metformin 1000mg, ezetrol 10mg
>: Everything in Moderation - Except Laughter.
>: --
>: http://loraldiabetes.blogspot.com/
>: http://loraltravel.blogspot.com/
>: latest: The Vatican
>
>"what does... "loss of pancreatic insulin producing cells" mean?".
>Is exactly what I asked my endo a few ago when I emailed her and
>her reply was exactly as I said.. which means when one loses cells
>they no longer produce insulin.. HELLO? which part of that did ya
>miss in Biology? IR has NOTHING to do with loss of cells. It's the cells
>inability too allow insulin in to transport carbs properly.
>
>I'm SO done

"loss of pancreatic insulin producing cells" means exactly
what it says. That doesn't mean that the remaining cells
can't overproduce - while they still remain.
Cheers, Alan, T2, Australia.
d&e, metformin 1000mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: The Vatican

rk wrote:
> "Alan S" <loralgtweightandcarbs@gmail.com> wrote in
message
> news:t6k4l296oghdpkgegb21a778f8oe5jfcdh@4ax.com...
>: On Wed, 08 Nov 2006 21:43:51 GMT, "rk"
>: <p_haha_medium@gmail.com> wrote:
>:
>: >"Michelle" <bookbug2005@gmail.com> wrote in message
>: >news:15n924-esr.ln1@news.air-internet.com...
>: >:
>: >: "Susan" <nevermind@nomail.com> wrote in message
>: >: news:4rccdlFqfhvaU1@mid.individual.net...
>: >
>: >: > A fasting of 100 or above is associated with loss of
pancreatic
>: >: > insulin producing cells.
>: >
>: >This isn't true with Type 2 DM. Type 2 is mainly
Insulin
>: >Resistance and having too MUCH insulin, not a lack, that
is Type 1.
>: >More incorrect BS.
>:
>: No need for that last comment.
>:
>: He didn't say a lack of insulin; he said "loss of
pancreatic
>: insulin producing cells". While insulin resistance is
>: commonly a major factor in the various variants of type
2,
>: so is the loss of beta cells, and that, in part, may be
due
>: IMO to the stress of over-production of insulin
attempting
>: to counter that IR; eventually that over-production may
fail
>: as beta cell loss progresses.
>:
>: I use "may" a lot because "does" and "will" cannot often
be
>: applied to the wide spectrum of variables in type 2. One
of
>: the reasons we use YMMV a lot. Or we should.
>:
>: Cheers, Alan, T2, Australia.
>: d&e, metformin 1000mg, ezetrol 10mg
>: Everything in Moderation - Except Laughter.
>: --
>: http://loraldiabetes.blogspot.com/
>: http://loraltravel.blogspot.com/
>: latest: The Vatican
>
> "what does... "loss of pancreatic insulin producing cells"
mean?".
> Is exactly what I asked my endo a few ago when I emailed
her and
> her reply was exactly as I said.. which means when one
loses cells
> they no longer produce insulin.. HELLO? which part of that
did ya
> miss in Biology? IR has NOTHING to do with loss of cells.
It's the
> cells inability too allow insulin in to transport carbs
properly.
>
> I'm SO done

Reisa, here is a link to help you better understand the
mechanics behind type 2. I am very surprised at your endo's
answer, this has been known for a very long time and
universally accepted. Type 2's have the unfortunate
situation of having insulin resistance AND some degree of
beta cell loss. Eventually some type 2's will lose all beta
cell function and be entirely dependant on insulin for
survival. There are many ways to arrive at a dead pancreas.

http://www.mgh.harvard.edu/diabetes/...tory_type2.htm

"The primary cause of Type 2 diabetes is insulin resistance,
the loss of the ability to respond normally to insulin,
followed by the gradual destruction of the insulin secreting
beta cells. Predisposition to diabetes is inherited and it
is much more likely to occur in those who are obese but
there is much more to be learned about this disease."

Once a person actually tips over into diabetes there is
further loss of beta cells from high glucose, this may go on
for years before a person is diagnosed. By diagnosis there
is a significant percentage of beta cell loss. Taking the
stress off the pancreas by means of diet, exercise and
medication helps control but there is then still the IR to
consider as well. A person with a lot of IR and a
significant loss of beta cells will find controlling
extremely difficult. There are a few who pass through here
that have been in that category.

Early intervention IMO (long before the bg's get to the
diagnostic level) would prevent a lot of pre-diabetics
losing a lot of beta cell function.

This is why we often hear in here that even if weight is
lost and IR is reduced, we type 2's are still not cured,
just controlled. If there were no loss of beta cells that
may be a totally different ball-game, unfortunately that's
not the scenario.

rk <p_haha_medium@gmail.com> wrote:
> "Michelle" <bookbug2005@gmail.com> wrote in message
> news:15n924-esr.ln1@news.air-internet.com...
> :
> : "Susan" <nevermind@nomail.com> wrote in message
> : news:4rccdlFqfhvaU1@mid.individual.net...

> : > A fasting of 100 or above is associated with loss of pancreatic insulin
> : > producing cells.

> This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
> having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.


--
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/]

rk <p_haha_medium@gmail.com> wrote:
> "Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
> news:t6k4l296oghdpkgegb21a778f8oe5jfcdh@4ax.com...
> : On Wed, 08 Nov 2006 21:43:51 GMT, "rk"
> : <p_haha_medium@gmail.com> wrote:
> :
> : >"Michelle" <bookbug2005@gmail.com> wrote in message
> : >news:15n924-esr.ln1@news.air-internet.com...
> : >:
> : >: "Susan" <nevermind@nomail.com> wrote in message
> : >: news:4rccdlFqfhvaU1@mid.individual.net...
> : >
> : >: > A fasting of 100 or above is associated with loss of pancreatic
> insulin
> : >: > producing cells.
> : >
> : >This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
> : >having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.
> :
> : No need for that last comment.
> :
> : He didn't say a lack of insulin; he said "loss of pancreatic
> : insulin producing cells". While insulin resistance is
> : commonly a major factor in the various variants of type 2,
> : so is the loss of beta cells, and that, in part, may be due
> : IMO to the stress of over-production of insulin attempting
> : to counter that IR; eventually that over-production may fail
> : as beta cell loss progresses.
> :
> : I use "may" a lot because "does" and "will" cannot often be
> : applied to the wide spectrum of variables in type 2. One of
> : the reasons we use YMMV a lot. Or we should.
> :
> : Cheers, Alan, T2, Australia.
> : d&e, metformin 1000mg, ezetrol 10mg
> : Everything in Moderation - Except Laughter.
> : --
> : http://loraldiabetes.blogspot.com/
> : http://loraltravel.blogspot.com/
> : latest: The Vatican

> "what does... "loss of pancreatic insulin producing cells" mean?".
> Is exactly what I asked my endo a few ago when I emailed her and
> her reply was exactly as I said.. which means when one loses cells
> they no longer produce insulin.. HELLO? which part of that did ya
> miss in Biology? IR has NOTHING to do with loss of cells. It's the cells
> inability too allow insulin in to transport carbs properly.

> I'm SO done

Sorry to hear it. Let me explain. Type 2s at diagnosis typically have
already lost 50% of their beta cells, and thus have lost 50% of their
insulin producing capacity. But since the average non-diabetic has
about four times the insulin producing capacity they usually need this
poses no problem in actual production for T2s. In fact because they
usually have IR, they need to produce more than normal, which because
they still have enough production capacity, they do. The problem is
that if they're producing more than normal with less than normal
amount of beta cells then their beta cells are working much harder,
possibly flat out, whereas the normal non-diabetic is ticking over at
1/4 maximum revs.

In sum, the typical early T2 is producing more insulin with
less beta cells. This exhausts the beta cells and they
continue to die off, hence the progression of the disorder.

You can find all this in the T2 pages on the ADA web site. It's been
known for ages and there's nothing controversial about it.

I see that your endo apparently didn't know any of that. Time to get a
new endo?

--
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/]

Susan <nevermind@nomail.com> wrote:
: x-no-archive: yes

: rk wrote:

: > This isn't true with Type 2 DM. Type 2 is mainly Insulin Resistance and
: > having too MUCH insulin, not a lack, that is Type 1. More incorrect BS.
: >

: I know you can't help it becase, as you adamantly and repeatedly
: asserted, your brain is a muscle.

: Type 2 begins with hyperinsulinemia, which is overproduction of insulin
: as a result of insensitivity by insulin receptors. Eventually, the
: exhausted pancreas runs low on insulin producing capacity, and IR
: progresses to DM type2, which is characterized by insufficient insulin.

: Beta cells begin to die off in the "normal" fasting range of 100. It has
: been well demonstrated that DM is usually well advanced before type 2
: fbg starts rising into diagnostic ranges.


: http://www.springerlink.com/content/mv0l2yk570h8gmkg/


: "Conclusion/interpretation When the plasma insulin response to oral
: glucose is related to the glycaemic stimulus and severity of insulin
: resistance, there is a progressive decline in beta-cell function that
: begins in "normal" glucose tolerant individuals."


: Susan

The simple way I learned it some 20 years ago is that because of insulin
resistance, the betacells have to over-prodce insulin. after a whle
(yers) they wear out and no longer over-produce to cover the resistance,
so bgs go up because there is not enough insulin to deal with the
resistance. That is usually when diabeetes is diagnosed and named. Sulfs
serve to push or force the remaining beta cells to continue to
over-produce, so the bg's are reduced. In fact, if they over-produce too
much they can result in a hypo, with too much inuslin running around in
the system.

Many of us don't like using the sulfs because we believe tht they will
led to more beta cell death. In addition, it an b e lkehaving too much
basal, so insulin is there all the time, causing increased appetite or
hpos between meals. Some of the newer beta cell pushere, like Prandin and
Starlix, only work for a short period so you take them with or just a bit
before a meal and they deal with the need for insulin after eatng carby
foods. These put less pressure on the beta cells. These meds can be used
to help cover a more carby meal, but will only do so much, unlike insulin
for a type 1 where the dose can be increased to deal with the number of
carbs eaten. It seems to be much less precise and more limitedfor the
beta cell pushers.

Newer meds work to deal with the resistance. Actos and Avandia do this,
asdoes metformin, by reducing the relese of sugar products from the liver,
theu reducing the need for additional insulin.

Insulin resistance is the reason that type 2's who loose all there beta
cell function(or most of it) do not turn into type 1s and why they need to
use very large amounts of insulin to keep their bgs in order. they have
to take enoughnot only to cover their fod, but, also thier insulin
resistance. That is why they often continue t take oral meds like
metformin.

I hope this makes some sense to you, RK. It is just a whole different
issue.

Wendy

"Ozgirl" <are_we_there_yet@maccas.com> wrote in message
news:hcu4h.61522$rP1.8411@news-server.bigpond.net.au...
> This is why we often hear in here that even if weight is
> lost and IR is reduced, we type 2's are still not cured,
> just controlled. If there were no loss of beta cells that
> may be a totally different ball-game, unfortunately that's
> not the scenario.
>

There's also the fact that T2s' beta cells don't replace themselves like
everyone else's on the planet because of cell aptosis. Something (not the
autoimmune thing that T1s have, that's something different) kills them off
before they can start producing insulin; and no-one seems to know what,
other than some vague references to plaque, or if anything can be done about
it.

That's why some of the early Byetta results look so interesting, because it
looked like there was some beta cell regrowth. Not so easy to prove in the
human model, though - anyone want to stand still long enough for the
autopsy? : )

Nicky.

--
A1c 10.5/5.5/<6 T2 DX 05/2004
100ug Thyroxine
95/72/72Kg

On Thu, 9 Nov 2006 12:38:38 -0000, "Nicky"
<ukc802466929@btconnect.com> wrote:

>There's also the fact that T2s' beta cells don't replace themselves like
>everyone else's on the planet because of cell aptosis. Something (not the
>autoimmune thing that T1s have, that's something different) kills them off
>before they can start producing insulin; and no-one seems to know what,
>other than some vague references to plaque, or if anything can be done about
>it.
>
>That's why some of the early Byetta results look so interesting, because it
>looked like there was some beta cell regrowth. Not so easy to prove in the
>human model, though - anyone want to stand still long enough for the
>autopsy? : )
>
>Nicky.

Were you volunteering as the vivisectee?

Cheers, Alan, T2, Australia.
d&e, metformin 1000mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: The Vatican

"Alan S" <loralgtweightandcarbs@gmail.com> wrote in message
news:4v86l2p4u2lhq474burfr47s6fhedccrn5@4ax.com...
> On Thu, 9 Nov 2006 12:38:38 -0000, "Nicky"
> <ukc802466929@btconnect.com> wrote:
>
>>There's also the fact that T2s' beta cells don't replace themselves like
>>everyone else's on the planet because of cell aptosis. Something (not the
>>autoimmune thing that T1s have, that's something different) kills them off
>>before they can start producing insulin; and no-one seems to know what,
>>other than some vague references to plaque, or if anything can be done
>>about
>>it.
>>
>>That's why some of the early Byetta results look so interesting, because
>>it
>>looked like there was some beta cell regrowth. Not so easy to prove in the
>>human model, though - anyone want to stand still long enough for the
>>autopsy? : )
>>
>>Nicky.
>
> Were you volunteering as the vivisectee?

I have a nice, sharp set of scalpels Unfortunately, I don't think anyone
on Byetta is in my kill-file : )

Nicky.

--
A1c 10.5/5.5/<6 T2 DX 05/2004
100ug Thyroxine
95/72/72Kg

In article <eiu1rl$oth$1@reader2.panix.com>,
"W. Baker" <wbaker@panix.com> wrote:

> Insulin resistance is the reason that type 2's who loose all there beta
> cell function(or most of it) do not turn into type 1s and why they need to
> use very large amounts of insulin to keep their bgs in order.

Uh, I'm not sure what you mean by "turn into type 1s." A type 2 can
develop type 1 as well if they develop the autoimmune problem. Both
type 1s and type 2s can be dependent upon exogenous insulin.

Priscilla

In article <4rglriFrbho6U1@mid.individual.net>,
"Nicky" <ukc802466929@btconnect.com> wrote:

> That's why some of the early Byetta results look so interesting, because it
> looked like there was some beta cell regrowth. Not so easy to prove in the
> human model, though - anyone want to stand still long enough for the
> autopsy? : )

Gee, I'd have thought they'd want us to be lying down for that. ;-)

Priscilla

Priscilla H. Ballou <vze23t8n@verizon.net> wrote:
: In article <eiu1rl$oth$1@reader2.panix.com>,
: "W. Baker" <wbaker@panix.com> wrote:

: > Insulin resistance is the reason that type 2's who loose all there beta
: > cell function(or most of it) do not turn into type 1s and why they need to
: > use very large amounts of insulin to keep their bgs in order.

: Uh, I'm not sure what you mean by "turn into type 1s." A type 2 can
: develop type 1 as well if they develop the autoimmune problem. Both
: type 1s and type 2s can be dependent upon exogenous insulin.

: Priscilla

Most type 2s on insulin have not developed the autoimmune type 1, they
have just pretty much exhaused their beta cells. They can still benfit
form oral mds that reduce their IR, which wouldnot help type 1s in
general, unless they also develop IR later in life so really become
ty1+2's, much the same as a type 2 who develops teh autoimmune, type 1
later in life, a fairly rare, but not unheard of situation.

If a type 2 has practically no or no beta cells producing , theywill, of
course need insulin, and in very large doses.

Wendy

Doc contacted me today. Apparently, I am type 2 and will be taking 500
mg of Glucopagh <sp?> every day.

On Thu, 09 Nov 2006 17:08:27 -0600, Bill <bill@nospam.null>
wrote:

>Doc contacted me today. Apparently, I am type 2 and will be taking 500
>mg of Glucopagh <sp?> every day.

Hi Bill

Well, you knew it was coming - but I'll offer a belated
welcome to the club you didn't really want to join.

By now you have probably read this:
http://www.alt-support-diabetes.org/NewlyDiagnosed.htm

If not - do it now. Print it out, and start acting on it. If
you don't already have your meter, get one. Yhat is the most
important weapon in your armoury in your battle with the
beast.

Others will be along, so I'll leave it there. Good luck;

Cheers, Alan, T2, Australia.
d&e, metformin 1000mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com/
http://loraltravel.blogspot.com/
latest: The Vatican

Nicky <ukc802466929@btconnect.com> wrote:

> "Ozgirl" <are_we_there_yet@maccas.com> wrote in message
> news:hcu4h.61522$rP1.8411@news-server.bigpond.net.au...
>> This is why we often hear in here that even if weight is
>> lost and IR is reduced, we type 2's are still not cured,
>> just controlled. If there were no loss of beta cells that
>> may be a totally different ball-game, unfortunately that's
>> not the scenario.

> There's also the fact that T2s' beta cells don't replace themselves like
> everyone else's on the planet because of cell aptosis. Something (not the
> autoimmune thing that T1s have, that's something different) kills them off
> before they can start producing insulin; and no-one seems to know what,
> other than some vague references to plaque, or if anything can be done about
> it.

> That's why some of the early Byetta results look so interesting, because it
> looked like there was some beta cell regrowth. Not so easy to prove in the
> human model, though - anyone want to stand still long enough for the
> autopsy? : )

I suspect it's not so much that there's normally no beta cell
regeneration in the average T2 as that the rate of cell death exceeds
the rate of birth. That means that if the cell killer call be reined
in a bit, the cell regrowth that still exists will start repopulating
the pancreas. I can't recall where, but I've seen some clues in some
reports that suggest that's what's happening. It's also the more usual
general case in biology. Complete absence of regeneration is very much
rarer than it being overwhelmed by the death rate, and in recent years
some of those rare exceptions, such as in the brain, have turned out
to be errors.

--
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/]

Chris Malcolm wrote:
> Nicky <ukc802466929@btconnect.com> wrote:
>
>> "Ozgirl" <are_we_there_yet@maccas.com> wrote in message
>> news:hcu4h.61522$rP1.8411@news-server.bigpond.net.au...
>>> This is why we often hear in here that even if weight is
>>> lost and IR is reduced, we type 2's are still not cured,
>>> just controlled. If there were no loss of beta cells
that
>>> may be a totally different ball-game, unfortunately
that's
>>> not the scenario.
>
>> There's also the fact that T2s' beta cells don't replace
themselves
>> like everyone else's on the planet because of cell
aptosis.
>> Something (not the autoimmune thing that T1s have, that's
something
>> different) kills them off before they can start producing
insulin;
>> and no-one seems to know what, other than some vague
references to
>> plaque, or if anything can be done about it.
>
>> That's why some of the early Byetta results look so
interesting,
>> because it looked like there was some beta cell regrowth.
Not so
>> easy to prove in the human model, though - anyone want to
stand
>> still long enough for the autopsy? : )
>
> I suspect it's not so much that there's normally no beta
cell
> regeneration in the average T2 as that the rate of cell
death exceeds
> the rate of birth.

That is true, when the cell regeneration can't keep up with
the rate of destruction then it is usually the time when a
person tips into type 2.

That means that if the cell killer call be reined
> in a bit, the cell regrowth that still exists will start
repopulating
> the pancreas. I can't recall where, but I've seen some
clues in some
> reports that suggest that's what's happening.

IR is a big contender. Improve the IR with whatever means it
takes. Unfortunately it is going to be a very long time, if
ever, before the medical fraternity decide to treat the so
called "pre-diabetes" sooner rather than later. There is
plenty of diabetes prevention literature available here,
including advertising from time to time, about how to
prevent diabetes (lose weight, eat better, exercise, change
lifestyle etc). But that is only part of the answer.
Recognising IR before it causes too much damage will go a
long way in preventing the real deal type 2. But the powers
that be seem very reluctant to pay for prevention, they much
prefer coughing up for the after diagnosis treatment.

Ozgirl <are_we_there_yet@maccas.com> wrote:
> Chris Malcolm wrote:

>> I suspect it's not so much that there's normally no beta
> cell
>> regeneration in the average T2 as that the rate of cell
> death exceeds
>> the rate of birth.

> That is true, when the cell regeneration can't keep up with
> the rate of destruction then it is usually the time when a
> person tips into type 2.

> That means that if the cell killer call be reined
>> in a bit, the cell regrowth that still exists will start
> repopulating
>> the pancreas. I can't recall where, but I've seen some
> clues in some
>> reports that suggest that's what's happening.

> IR is a big contender. Improve the IR with whatever means it
> takes. Unfortunately it is going to be a very long time, if
> ever, before the medical fraternity decide to treat the so
> called "pre-diabetes" sooner rather than later. There is
> plenty of diabetes prevention literature available here,
> including advertising from time to time, about how to
> prevent diabetes (lose weight, eat better, exercise, change
> lifestyle etc). But that is only part of the answer.
> Recognising IR before it causes too much damage will go a
> long way in preventing the real deal type 2. But the powers
> that be seem very reluctant to pay for prevention, they much
> prefer coughing up for the after diagnosis treatment.

I wish I didn't keep wondering whether the profits to be made from
people who're going to take medication for the rest of their lives has
something to do with the apparent reluctance to spend any money
helping people to avoid becoming lifelong medication users.

--
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/]