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How do doctors differentiate between types.

Most Type 1's are children who suffer from an autoimmune disease and lose all function of the pancreas. An adult suddenly getting type 1 would presumably go straight to hospital on a stretcher.

Type 2's are invariably adults with progressive failing of the pancreas. I suppose if you are walking about and arguing with your doctor then you are probably a Type 2.
 
age comes into it I believe and family history. Also if ketones are present in blood or urine as well as how high bg are.

I was 2.5 with blood sugar off the scale and had lost considerable weight. I was also in a diabetic coma so it was a blues and twos job.
 
There are a couple of tests which can help. A GAD antibody test can tell if you have the auto-immune type of diabetes. Also, a C-Peptide test can indicate how much insulin you are naturally producing. These tests are not cheap and some docs routinely do them whilst others do not. There are also many docs that don't even use T1 and T2 any more. They refer to patients as insulin dependant or non insulin dependant.
 
Sorry Squire, I don't agree. There are many Late onset T1s who are initially mis-diagnosed as T2 (I'm one of those) because many GPs guess like mine did and don't use or don't know about the two tests Mo mentions. Overweight T2s suffer insulin resistance and the pancreas only starts failing after a long period of time if ever. Any diabetic who presents with diabetic symptoms, but not necessarily ketones, but is slim and has possibly lost weight recently is likely to have failing islet cells not insulin resistance and is probably a late onset T1. Late onset T1 (LADA) can come on at widely varying rates.
 
My GP will not pay for GAD or c-peptide tests. I was treated as T2 for seven years although GP stated at the time that I had probably been T2 for 30 years. Went to hell in a handcart Oct 2013 and "re-classified" as late onset T1 (LADA). They need to get some form of standardisation in place,as I was so ill for many, many months before they commenced treatment.




Late onset T1, several auto immune issues.
Humalogmix25 twice a day, Methotrexate 25mg once per week, FolicAcid 5mg once per week, prednisolone 5mg daily, Allopurinol 300mg, Calcichew-D3 800iu, Levothyroxine 50mcg, Atenolol 50mg, Losarten 100mg, Aspirin 75mg, Nicorandil 20mg, Nitrolingual GTN spray, Metformin 2000mg, Allimemazine 10mg, Lanzoprazole 30mg, Atorvastatin 20mg, Co Codamol 8/500mg, Depo Medrone (Methylprednisolone) or double Prednisolone for 7 days in case of RA flare.
 
When I was diagnosed I asked my nurse how she knows I am Type 2. She said because if you were Type 1 you would be very ill with a lot of unpleasant symptoms. She was very careful not to say because you are 66 and overweight!
 
(Here's my story which shows that you can develop T1 quite gradually as an adult and how they decided that I had it. I was in France and had what I think was excellent care; once I told anyone I had a problem.

I had had the first symptoms over 2 years before, (these were 'classic' urination, weight loss etc). I confirmed to myself I had D with urine tests. I thought I had T2, as every source seemed to say that only children got T1 and didn't really know how serious T2 was, I decided to 'treat' myself and adopted a low GI diet. This must have successfully kept glucose levels down for some time.(stupid I know but was in a new country and didn't speak the language well)

Further down the line, the symptoms returned, my daughter was very worried about my weight but I kept putting off seeing a doc. Eventually, I had had to abort a bike ride through difficulties in breathing. I went to an unknown doc and told him that I thought I had diabetes and had had it for some time.(he looked bemused!)

Had fasting tests next day , GP was faxed blood test results with very high fasting glucose plus opalescent serum (an indicator of the breakdown of fat). He was then extremely proactive,. He spoke to the consultant on the phone whilst I was there (couldn't understand the French though!)
I was sent straight to the hospital, it was only a quarter of a mile , I went under my own steam and was still standing when I got there. At the time I really didn't realise why he was so concerned.( still thought I had T2, and didn't believe it to be serious).
At hospital was kept in and put onto insulin.
I had tests for antibodies (positive) and c peptide (negligible) . My HbA1c was also 'only' around 7% ie glucose levels hadn't averaged 20+ for the last 2 months but my fasting glucose was in the middle 20s.. That's when I was told they thought I had T1 . When I said I thought that only happened in children, and happened quickly, he told me about LADA.
(then I had every test and scan they could think of, I think to eliminate other possibilities and because I hadn't seen a doctor for so long.

On the whole children develop the condition more quickly than Adults but even then many are diagnosed before they are critical, when alert parents and sensible doctors investigate the normal symptoms (weight loss, frequent urination, thirst and tiredness) rather than needing to be on a stretcher.
 
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The way that doctors should perform a differential diagnosis between Type 1 and Type 2 (ignoring subtypes such as LADA and MODY) is with GAD antibody tests and C-peptide tests for insulin secretion / beta-cell function.

However in practice they rarely bother, and just generalise based on the age and weight of the patient at presentation. If a presumed T2 later keels over they revise their opinion and say he or she is a T1 LADA.
 
Spiker said:
The way that doctors should perform a differential diagnosis between Type 1 and Type 2 (ignoring subtypes such as LADA and MODY) is with GAD antibody tests and C-peptide tests for insulin secretion / beta-cell function.

However in practice they rarely bother, and just generalise based on the age and weight of the patient at presentation. If a presumed T2 later keels over they revise their opinion and say he or she is a T1 LADA.
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GAD antibodies are often considered to define LADA (though occasionally other antibodies are present) I agree that is what seems to happen in the UK. It doesn't seem to be the case here and interestingly when I mentioned LADA in the forum for the COUSERA diabetes course a medic from Greece said that they would do antibody tests on a slim person diagnosed with diabetes symptoms but not on an overweight one which he said sometimes led to misdiagnosis.
 
@phoenix: What was happening to your pancreas in the time before you were properly diagnosed?

Does your insulin producIng ability shut down slowly (I imagine that if it didn't you'd be dead)?

Do T1s maintain any insulin producing ability at all (albeit at a very low level), or are some of you unable to produce any at all?
 
have said full story before but briefly, was 33, been losing considerable weight for a while, but was getting out of breath very quickly. Went to docs a few times over the years about similar symptoms (and more) , when, eventually other symptoms indicated diabetes (thirst, toilet, extreme weight loss) and gp arranged nurse to take blood and test immediately. At the time on the spot test showed 9, was told by nurse probably got diabetes will take blood to run further tests, go home phone back for results.next week. 3 days later felt very sick so phoned gp to explain, at which time tests had come back showing very high ketones, off to a and e, where they ran tests and said was type 1, let out after a few days on sliding scale, and fixed doses.
So, probably been lada a lot longer, left untreated, and slowly proceeded to type 1, which, when.it did happened rapidly.
nurse did make a comment that probably type 2, purely, I think because of my age. Had it not been for having ketones and going to a and e when I did I think I would of probably ben mis diagnosed, if at all.


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Borofergie
Presumably pancreas was gradually losing beta cell function. As as long as I kept insulin resistance/weight/ endogenous insulin production in balance then my glucose levels were OK . I've also seen thesuggestion that the loss of function in LADA is not a straight line but there is some loss, followed by new cells but not quite as many as before and then further loss and regain. Eventually there are too few functioning cells for survival without injected insulin.
In retrospect even during quiescent periods, I think that my BG rose sharply when I occasionally ate very high GI carb because I felt very uncomfortable This was often followed by thrush ,( the worst culprits were croissants which we only had when we had visitors, but then had every morning and are definitely not low GI .. I think I've only eaten a couple since diagnosis).
The last three months before diagnosis I also became very sedentary; that bike ride was an attempt to get myself going. (I knitted three jumpers in that time, I hadn't knitted a jumper before or since!)

It does seem that beta cell loss is much slower than previously thought and some people who have had T1 for over 50 years have some residual insulin function. One thing that has altered perception is the development of assays that can detect lower C peptide levels.
Heres a graph of loss from Denise Faustmann
beta cell loss.PNG
edit: for grammar (original post very rushed as dinner was ready!)
 
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borofergie said:
Do T1s maintain any insulin producing ability at all (albeit at a very low level), or are some of you unable to produce any at all?
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Yes. New techniques can now detect levels of insulin production that were previously undetectable. These demonstrate that secretion continues, though at a minute level.

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Interesting comments. I wonder whether a more standardised protocol will ever come into place. I was told in a&e that I had a borderline case, yet neither a c-peptide or GAD antibody test was performed. I had been feeling unwell for 3 years previously, but my GP was reluctant to investigate as he said I was just stressed. I have also been told by a DN that GAD is not particularly conclusive as a number of non-diabetic people also test positive.... Oh what a minefield!! Hurry up with a **** cure already!!


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Wish there was a cure for us all, meanwhile we will continue the support we all need it at time to time x
 
Becki84 said:
Interesting comments. I wonder whether a more standardised protocol will ever come into place. I was told in a&e that I had a borderline case, yet neither a c-peptide or GAD antibody test was performed. I had been feeling unwell for 3 years previously, but my GP was reluctant to investigate as he said I was just stressed. I have also been told by a DN that GAD is not particularly conclusive as a number of non-diabetic people also test positive.... Oh what a minefield!! Hurry up with a **** cure already!!


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Click to expand...

Hi. I feel the c-peptide test is a reasonable measure although not infallible. If low it implies you are not producing insulin and have depleted islet cells i.e you are T1'ish. If high you are swimming in insulin but insulin resistant i.e. a T2. My GAD was negative but my c-peptide proved I had very little insulin which told me I needed insulin. The problem with GAD is that the anti-bodies are not the only cause of islet cell failure.
 
Age 51, I suspected diabetes for a while as I had chronic weight loss, thirst and excessive peeing over 6 months.This did noticeably start with a particularly bad weekend after flying for 13 hours after a fluish headcold... but I put off a doctor's visit as I had a lot more back to back international travel and didn't want to disrupt my life! Although my GP at first thought I was classic metabolic syndrome /Type 2 she asked for early endocrinologist opinion. He asked me to start on insulin initially to allow pancreas to "recover", then a month later tested for GAD anitbodies and C-peptide. Perhaps to both our surprise, I had antibodies through the roof and non existant insulin production - so handed the Type 1 label. With hindsight, I was progressively LADA? I must of had a little insulin production for awhile - unfortunately now missing insulin makes me extremely unwell and quickly goes to critical DKA status. While no one diagnostic test is 100% confirmatory, I think it is a shame that at least the c-peptide test isn't offered more frequently to help immediately define whether insulin lack or insulin resistance is the major clinical challenge for diabetic patients.
 
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