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04-14-2008, 03:45 AM
| | Member
I am a: Pre-Diabetic | | Join Date: Mar 2006 Location: Dover, NJ
Posts: 483
| | Your Path to Type 1.5 diagnosis Hi Everyone:
I'm curious about your path to the diagnosis of Type-1.5. Why? As a diagnosed Pre-Diabetic with a normal, albeit low-normal, C-Peptide reading of 1.3 I have the feeling that, over time I'm going to be chaning my Type heading.
I'm interested in your story of how the medical professionals finally figured out you aren't a Type-2. Was there a particular test done, a change of MD, some pivotal act in the journey that sealed the diagnosis?
Many of you already know me from other posts so I won't bother with my usual self-introduction when I first post on a new sub-forum.
__________________
Be well, do good work, and keep in touch [Garison Keilor]
Ronin (a.k.a, George N. Wells, CPIM)
Tandemist/Lay Theologian
Enjoying Life and Learning about myself everyday.
Pre-D -- Not on Insulin  (yet)
For Cholesterol though:
2500 mg Niacin
5 mg Zocor
2008 cycling miles: 2654 (03 Jul)
Fasting C-Peptide 1.3 HbA1c's:
01 Jan 2008 -- 5.3%
01 Feb 2008 -- 5.0%
01 Mar 2008 -- 5.4%
01 Apr 2008 -- 5.3%
01 May 2008 -- 5.1%
01 June 2008 -- 5.1% | 
04-14-2008, 04:10 AM
|  | Senior Member
I am a: Type 1 | | Join Date: Oct 2006
Posts: 912
| | | I'm not 1.5, but along with a low C-pep, a 1.5 would most likely be postive for GAD antibodies, I think. I realize there seems to be some fuzziness on the matter, but the general rule for division between the 1/1.5 set and type 2 set is the GAD antibodies which are present due to the autoimmune attack on the beta cells. | 
04-14-2008, 05:11 AM
|  | Senior Member
I am a: Type 1.5 | | Join Date: Feb 2006 Location: France
Posts: 674
| | | Not the antibody test, that was done but inconclusive.Only 70-80% of type 1s do test positive for GAD.To add to the complication there is a division between type 1a(autoimmune ) and type 1b (idiopathic) My Doctor(only last week) suggested that I could be either.
I think that the C peptide showed that I still was producing some insulin.
The main reason for a diagnosis of type 1.5 rather than type 2 with beta cell exhaustion was my history.I presented with high fasting BG and ketones but only needing relatively small amounts of insulin to lower it and get rid of the ketones. History of initial weight loss, three years off and on with diabetes symtoms followed by further rapid weight loss.
I've just gone on a pump 3 years after diagnosis, so I've had diabetes for at least 6 years. Its early days but at the moment my basal/bolus ratio is 40%:60% which according to John Walsh may be because I still have some insulin of my own at least 6 years after the first symptoms.
If you can get the antibody tests do so. They may confirm 1.5 but if negative it doesn't mean that type 1(1.5) of some sort is out of the question. | 
04-14-2008, 06:08 AM
| | Junior Member
I am a: Type 1 | | Join Date: Dec 2006 Location: SW Wisconsin
Posts: 86
| | | The difference between T1/1.5 and T2 is the cause... an autoimmune attack for the T1/T1.5, and Insulin Resistance for the T2. The T2 also produces more than ample amounts of insulin which will generally cause weight gain.
Both Scratch and Helen are correct that a positive GAD65 antibody test will show definitively that you are T1 if your pancreas are still producing some insulin. Your C-peptide fasting test result of 1.3 is low but not definitive. Your high A1c at diagnosis, weight loss and no sign of either high blood pressure, cholesterol issues nor obesity are good indications that you may have the slow progressing autoimmune T1/T1.5, more accurately called LADA (Latent Autoimmune Diabetes in Adults) which can take months or even years to develop fully into T1 with no insulin production.
Adding exogenous insulin is a good way to preserve your beta cells although it is harder to control BGs in a consistent manner because your pancreas still make some although its release may be erratic.
__________________
NoraWI
LADA (T1)
Lantus, Novolog, levothyroxine
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04-14-2008, 06:32 AM
| | Junior Member
I am a: Type 1.5 | | Join Date: Apr 2006 Location: Massachusetts
Posts: 86
| | | I pretty much had to figure out my diagnosis myself, as my doctors assumed I was a classic Type 2 and when I started hypoing on what should have been small doses of insulin and tested for normal C-peptide and very high post-prandial blood sugars they had no idea what was happening.
I was lucky to find out about MODY by reading the site provided by Dr. Hattersley and then I corresponded with Dr. Hattersley who confirmed that my history was suggestive of MODY.
When I managed to hypo on 1/8 of 1mg of Amaryl, that seemed to confirm it, though I haven't had the gene testing due to expense. I was in a study that ruled out a form of MODY I knew I didn't have, but though the recruiter for the study told me he'd test for other genes, they didn't.
Whatever the diagnosis, the really important thing is that you get access to whatever tools you need to normalize your blood sugar. It's high blood sugars that cause the complications, not the underlying defect. So if you control the sugars your prospects are good, long term.
__________________
A1c 5.7% 10 years after diagnosis.
| 
04-15-2008, 03:50 AM
| | Member
I am a: Pre-Diabetic | | Join Date: Mar 2006 Location: Dover, NJ
Posts: 483
| | | Everyone:
My take on this thread is that the only difinitive test is the test for the GAD antibody. Now all I need to do is convince my primary care that the test is worth doing.
I am also interested in what constitutes a "low" C-Peptide level. The scale used by the VA laboratory says "normal" is between 1 and 5, and therefore, my 1.3 is "low-normal." I've already convinced my primary care that this should be checked annually to monitor if it is dropping or holding.
What I do realize about the low C-Peptide is that I process glucose a bit slower (ah, the "impaired glucose response") due to having less than average insulin production. From that I wonder at the wisdom of pancreatic stimulation drugs that are often prescribed as I would think that all they would do is hasten the demise of already overworked Beta-Cells. Wouldn't small doses of suplamental insulin be the better course of treatment?
__________________
Be well, do good work, and keep in touch [Garison Keilor]
Ronin (a.k.a, George N. Wells, CPIM)
Tandemist/Lay Theologian
Enjoying Life and Learning about myself everyday.
Pre-D -- Not on Insulin  (yet)
For Cholesterol though:
2500 mg Niacin
5 mg Zocor
2008 cycling miles: 2654 (03 Jul)
Fasting C-Peptide 1.3 HbA1c's:
01 Jan 2008 -- 5.3%
01 Feb 2008 -- 5.0%
01 Mar 2008 -- 5.4%
01 Apr 2008 -- 5.3%
01 May 2008 -- 5.1%
01 June 2008 -- 5.1% | 
04-15-2008, 05:10 AM
| | Junior Member
I am a: Type 1 | | Join Date: Feb 2008 Location: Florida
Posts: 71
| | Quote:
Originally Posted by Ronin From that I wonder at the wisdom of pancreatic stimulation drugs that are often prescribed as I would think that all they would do is hasten the demise of already overworked Beta-Cells. Wouldn't small doses of suplamental insulin be the better course of treatment? |
That is my understanding, though I am not the expert at all.
my c-peptide was .6 so even lower, but my endo and I talked about how what you state is the method that makes the most sense. No point in stressing the body out, of course the honeymoon (stupid term) sometimes makes me want to hasten the demise. 
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