Can type 2 diabetes become type 1 diabetes?

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Amity Island said:
You're very chatty today MikeyB.:D

No is true, but what we do often see is a type 2 diagnoses turning into a type 1 diagnosis.
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I think misdiagnosis is rife because c-peptide/insulin testing is rarely used for diagnosis in the UK.
 
Amity Island said:
You're very chatty today MikeyB.:D

No is true, but what we do often see is a type 2 diagnoses turning into a type 1 diagnosis.
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The usual story for that is that this is misdiagnosis. Type 1 can look a lot like Type 2 initially, particularly in a adults, and NICE recommendation is against universal testing (Type 2 is much more common, after all, so usually Type 2 will be the right diagnosis).

That seems plausible enough to me.
 
Bruce Stephens said:
The usual story for that is that this is misdiagnosis. Type 1 can look a lot like Type 2 initially, particularly in a adults, and NICE recommendation is against universal testing (Type 2 is much more common, after all, so usually Type 2 will be the right diagnosis).

That seems plausible enough to me.
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Please could you point us to that nice recommendation? Thanks
 
Amity Island said:
Thanks for the link. So what exactly is the recommendation on using c-peptide tests?
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I'm not sure there is any precise recommendation. It's more to "consider using"...

Probably because they consider the evidence on diagnosing to be relatively poor, see the interpretation (page 31) in https://www.nice.org.uk/guidance/ng17/evidence/c-diagnosis-of-diabetes-pdf-11013435183

Linked from https://www.nice.org.uk/researchrec...e-test-in-distinguishing-subtypes-of-diabetes

Guidance for children and young people is different to that in adults, but again it seems mostly to see if type 2 is more likely when type 1 has been assumed: https://www.nice.org.uk/guidance/ng18/chapter/Recommendations#diagnosis
 
Bruce Stephens said:
I'm not sure there is any precise recommendation. It's more to "consider using"...

Probably because they consider the evidence on diagnosing to be relatively poor, see the interpretation (page 31) in https://www.nice.org.uk/guidance/ng17/evidence/c-diagnosis-of-diabetes-pdf-11013435183

Linked from https://www.nice.org.uk/researchrec...e-test-in-distinguishing-subtypes-of-diabetes

Guidance for children and young people is different to that in adults, but again it seems mostly to see if type 2 is more likely when type 1 has been assumed: https://www.nice.org.uk/guidance/ng18/chapter/Recommendations#diagnosis
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Interesting......They seem to be saying (below) there isn't any particular way to determine which type it is. Interestingly they say it safer to to put people on insulin and to find out they are type 2 at a later date.

The most common misdiagnosis is type 1 diabetes being misdiagnosed as type 2, which could lead to the person not receiving insulin treatment and a subsequent risk of diabetic ketoacidosis.

It is less harmful to be diagnosed with type 1 diabetes when the person actually has type 2 diabetes. However, there are still harms, including:
  • the long-term effects and costs of unnecessary insulin therapy
  • the missed opportunity for oral diabetes therapies
  • the psychological impact of misdiagnosis.

There was no new definitive evidence on clinical features for identifying diabetes type, so recommendation 1.1.1 remains unchanged from the 2015 guideline. Because of this lack of new evidence, the committee made a recommendation for research on identifying diabetes type.

The evidence showed that no single clinical feature had a sufficient predictive value to make a diagnosis by itself. The committee were particularly concerned that age and body mass index (BMI) might be used in isolation. They noted that the average BMI in people with type 1 diabetes is increasing, and the age at which people are diagnosed with type 2 diabetes is decreasing. This means these clinical features are becoming less useful on their own to differentiate between the subtypes. Despite this, the committee agreed that these characteristics are still useful for making an initial working diagnosis of diabetes subtype in many people. However, further testing is increasingly needed, as previously 'atypical' features of type 1 and 'uncertain' classifications become more common.
 
Amity Island said:
The evidence showed that no single clinical feature had a sufficient predictive value to make a diagnosis by itself
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This is what I find completely baffling..

If you are hyperinsulinemic you are highly likely to be T2 with high blood sugars and insulin resistance.

If you are hypoinsulinemic T1 or one of the variants of T1 (LADA, 1.5 etc).

Yet when i asked at a PHC conference if doctors tested fasting insulin not one had ever done in on the NHS.
Ony 3 people in the room had ever had the test (2 attendees and one doctor) and we had all had it done privately.

When I asked at my surgery they hadn't really heard of it.
 
bulkbiker said:
This is what I find completely baffling..

If you are hyperinsulinemic you are highly likely to be T2 with high blood sugars and insulin resistance.

If you are hypoinsulinemic T1 or one of the variants of T1 (LADA, 1.5 etc).

Yet when i asked at a PHC conference if doctors tested fasting insulin not one had ever done in on the NHS.
Ony 3 people in the room had ever had the test (2 attendees and one doctor) and we had all had it done privately.

When I asked at my surgery they hadn't really heard of it.
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Hi @bulkbiker

I understand what you are saying and it makes sense. I'm not sure about type 2, I did find this info at webmd. What do you make of it?

Hyperinsulinemia (hi-pur-in-suh-lih-NEE-me-uh) means the amount of insulin in the blood is higher than what's considered healthy. On its own, hyperinsulinemia isn't diabetes. But hyperinsulinemia often is associated with type 2 diabetes.


Insulin is a hormone that the pancreas makes. It helps control blood sugar. Hyperinsulinemia is connected to insulin resistance — a condition in which the body doesn't respond as it should to the effects of insulin. In that situation, the pancreas makes more insulin in order to overcome the resistance, leading to higher levels of insulin in the blood. Type 2 diabetes develops when the pancreas can no longer make the large amounts of insulin needed to keep blood sugar at a healthy level.


Hyperinsulinemia usually doesn't cause symptoms in people with insulin resistance. In people who have insulinomas, hyperinsulinemia may lead to low blood sugar, a condition called hypoglycemia.
 
Results from cPeptide and GAD aren’t as cut and dried as we might hope unfortunately. That’s why they aren’t advised to be used routinely. The trial data for the 2015 update wasn’t very positive for the use of the tests as they lacked the specifity and sensitivity to be used as part of routine diagnosis.

The more different antibodies you check for the lower the chances of a false positive, but you can get a false negative a while after a person has had T1, because they may already have got rid of their beta cells, and no longer be making the antibodies.

The best way of discerning likely type is more often than not by clinical factors by a specialist.

It’s interesting that the forum has a pretty good nose for oddities in presentation which might benefit from further investigation, and that many of those ‘red flags’ that are spotted do end up meaning someone is mis-classified

But no, T2 doesn’t turn into T1. If it was mis-classification it was always T1.

It’s perfectly possible to get both, of course. You can have T1 and develop T2, or have T2 and develop T1.

But the two are completely different.
 
I'm sure I came across some guidelines somewhere that used metabolic syndrome (i.e the stuff linked to IR) as an indicator of potential T2 and to start treatment with tablets - if this wasn't present, and the patient was thin, but hyperglycaemic, then the route to go down was testing for T1. Can't remember if this was part of NICE, but it was in a pdf with flowcharts aimed at doctors.

However, it's all bit blurred, as you can be thin, without IR and still be T2 (I know one).
 
everydayupsanddowns said:
Results from cPeptide and GAD aren’t as cut and dried as we might hope unfortunately. That’s why they aren’t advised to be used routinely. The trial data for the 2015 update wasn’t very positive for the use of the tests as they lacked the specifity and sensitivity to be used as part of routine diagnosis.

The more different antibodies you check for the lower the chances of a false positive, but you can get a false negative a while after a person has had T1, because they may already have got rid of their beta cells, and no longer be making the antibodies.

The best way of discerning likely type is more often than not by clinical factors by a specialist.

It’s interesting that the forum has a pretty good nose for oddities in presentation which might benefit from further investigation, and that many of those ‘red flags’ that are spotted do end up meaning someone is mis-classified

But no, T2 doesn’t turn into T1. If it was mis-classification it was always T1.

It’s perfectly possible to get both, of course. You can have T1 and develop T2, or have T2 and develop T1.

But the two are completely different.
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If you overproduce insulin you are T2.
If you underproduce insulin you are a T1 or variant ofT1.
The c-peptide or fasting insulin could probably sort that out in one test yet its rarely is ever done as a diagnostic.
Instead GP's use HbA1c which is a poor proxy as everyone here knows..
 
bulkbiker said:
If you overproduce insulin you are T2.
If you underproduce insulin you are a T1 or variant ofT1.
The c-peptide or fasting insulin could probably sort that out in one test yet its rarely is ever done as a diagnostic.
Instead GP's use HbA1c which is a poor proxy as everyone here knows..
Click to expand...

You can also under produce insulin as a T2 (if you’ve burnt out your beta cells and lost beta cell mass).

And you can be GAD negative and classically T1.

It all depends on the case, and the timing of the checks after diabetes onset.

At least that’s what the clinical trial data shows. Which is why the 2015 T1 update could not recommend routine use of GAD etc as a diagnostic tool.

Of course (as many members here will testify) diagnosis on clinical factors can give rise to false positives / false negatives too. But arguably that depends more on the expertise and experience of the clinician involved.

But the trial data simply don’t currently support routine use of GAD / cPep
 
bulkbiker said:
If you overproduce insulin you are T2.
If you underproduce insulin you are a T1 or variant ofT1.
The c-peptide or fasting insulin could probably sort that out in one test yet its rarely is ever done as a diagnostic.
Instead GP's use HbA1c which is a poor proxy as everyone here knows..
Click to expand...

That’s not right. Some Type 2s underproduce insulin as their beta cells have burnt out. The GAD tests are sometimes borderline. It’s a combination of factors that lead to the correct diagnosis.
 
Inka said:
Some Type 2s underproduce insulin as their beta cells have burnt out.
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Then they aren't T2...just misdiagnosed?
 
bulkbiker said:
Then they aren't T2...just misdiagnosed?
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Ultimately T2 is not ONLY insulin resistance / high insulin production. There are other forms and stages.

Beta cell loss in T1 is autoimmune, and different.
 
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bulkbiker said:
Then they aren't T2...just misdiagnosed?
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No - T1 is caused by an autoimmune reaction in the body, when the pancreas was previously completely normal and then the beta cells are suddenly killed off. Which is completely different from the cells wearing out due to overproduction of insulin when the pancreas is frantically trying to get blood sugars down in T2.
 
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