type 1 or 1.5

[GlitterSparkles]

Hi i was diagonsed as type 1 but we are now looking into the fact i could have a rare type like 1.5 and not type 1 i would like it if you could comment the differnces

Thank you

 

[pjayem1964]

Hi Glittersparkles, I think that Type 1.5 is the same as LADA diabetes but I’m sure someone will come along soon and explain the difference. LADA is usually found in older people and a slower onset of diabetes.

Hope this helps a little

Paula

 

[LooperCat]

From what I understand, T1 comes on very quickly - in my case a viral gastric flu sent my immune system into overdrive and it just killed my pancreas pretty much overnight. With LADA, I believe the beta cells pack up much more slowly, hence the slow onset of the symptoms, and why a lot of people are initially diagnosed type 2. But eventually the beta cells stop producing insulin, and then it’s treated just the same as T1, with insulin. It seems to be the speed at which the pancreas stops producing insulin, as far as I understand it.

 

[michita]

Hi i was diagonsed as type 1 but we are now looking into the fact i could have a rare type like 1.5 and not type 1 i would like it if you could comment the differnces

Thank you

1.5 or Lada is a subset of type 1 meaning type 1.5 is always type 1. It just means late on set and have a longer honeymoon period.

 

[DCUKMod]

Unless my memory is worse than I thought, @GlitterSparkles is one of our younger members, and certainly still of school age. I just thought I'd add that to the mix.

 

[KK123]

Hi glitter, I think you're 11 or 12 aren't you?, can you tell us why they think possibly 1.5/lada? x

 

[Robinredbreast]

Hi i was diagonsed as type 1 but we are now looking into the fact i could have a rare type like 1.5 and not type 1 i would like it if you could comment the differnces

Thank you[/QUO

A couple of helpful links.

Diabetes LADA
LADA stands for Latent Autoimmune Diabetes of Adulthood. LADA is a form of type 1 diabetes that develops later into adulthood.

LADA tends to develop more slowly than type 1 diabetes in childhood and, because LADA can sometimes appear similar to type 2 diabetes, doctors may mistakenly diagnose LADA as type 2 diabetes.

The definition provided by Prof. David Leslie, Principle Investigator of Action LADA, is that in Europe:

LADA is defined as initially non-insulin requiring diabetes diagnosed in people aged 30-50 years with antibodies to GAD - glutamic acid decarboxylase.

How does LADA compare with other diabetes types?
LADA is sometimes referred to as type 1.5 diabetes. This is not an official term but it does illustrate the fact that LADA is a form of type 1 diabetes that shares some characteristics with type 2 diabetes.





How is LADA diagnosed?
Often LADA will be initially diagnosed as diabetes by way of the usual diagnosis procedures.

Following a diagnosis of diabetes, your doctor or you may have reason to suspect that the type of diabetes present is LADA.

Determining the presence of LADA is achieved by examining the presence of elevated levels of pancreatic autoantibodies amongst patients who have recently been diagnosed with diabetes but do not require
PubMed
US National Library of MedicineNational Institutes of Health



J Pediatr Endocrinol Metab. 2004 Nov;17(11):1565-9.
Latent autoimmune diabetes mellitus in children (LADC) with autoimmune thyroiditis and Celiac disease.
Aycan Z1, Berberoglu M, Adiyaman P, Ergür AT, Ensari A, Evliyaoglu O, Siklar Z, Ocal G.
Author information

Abstract
Latent autoimmune diabetes mellitus in adults (LADA) is characterized by clinical presentation as type 2 diabetes mellitus after 25 years of age, initial control achieved with oral hypoglycemic agents for at least 6 months, presence of autoantibodies and some immunogenetic features of type 1 diabetes mellitus. An 8.3 year-old girl was referred to our pediatric endocrinology department because of incidental glucosuria. She did not complain of polyuria, polydipsia, or weight loss. Her body mass index (BMI) was at the 80th percentile. Fasting glucose was 126 mg/dl, and OGTT glucose level at 120 min was 307 mg/dl. Although C-peptide levels were normal, her first phase insulin response (FIR) was lower than the 1st percentile. Anti-insulin antibody (AIA), islet cell antibody (ICA), and anti-glutamic acid decarboxylase (antiGAD) were negative. According to the clinical and laboratory findings, she was diagnosed as having type 2 diabetes mellitus. She was started with oral anti-diabetic treatment for a period of 1 year. Insulin had to be initiated for worsening of HbA1c levels. In the fourth year of follow-up, she was admitted to our hospital with diabetic ketoacidosis although she was on an intensive insulin regimen. At this time, C-peptide levels were low, antiGAD and AIA were positive with HLA DR3/DQ2 haplotype. In addition, her thyroid peroxidase antibody and endomysium antibody were found to be high at follow-up. Small intestinal biopsy revealed celiac disease. This patient may represent the first case of latent autoimmune diabetes mellitus in children (LADC) with autoimmune thyroiditis and celiac disease.

• NCBI
• Skip to main content
• Skip to navigation
• Resources
• How To
• About NCBI Accesskeys

PubMed
US National Library of MedicineNational Institutes of Health
Search database
Search term

• Advanced
• Help

Result Filters

• Format: Abstract

Send to



J Pediatr Endocrinol Metab. 2004 Nov;17(11):1565-9.
Latent autoimmune diabetes mellitus in children (LADC) with autoimmune thyroiditis and Celiac disease.
Aycan Z1, Berberoglu M, Adiyaman P, Ergür AT, Ensari A, Evliyaoglu O, Siklar Z, Ocal G.
Author information

Abstract
Latent autoimmune diabetes mellitus in adults (LADA) is characterized by clinical presentation as type 2 diabetes mellitus after 25 years of age, initial control achieved with oral hypoglycemic agents for at least 6 months, presence of autoantibodies and some immunogenetic features of type 1 diabetes mellitus. An 8.3 year-old girl was referred to our pediatric endocrinology department because of incidental glucosuria. She did not complain of polyuria, polydipsia, or weight loss. Her body mass index (BMI) was at the 80th percentile. Fasting glucose was 126 mg/dl, and OGTT glucose level at 120 min was 307 mg/dl. Although C-peptide levels were normal, her first phase insulin response (FIR) was lower than the 1st percentile. Anti-insulin antibody (AIA), islet cell antibody (ICA), and anti-glutamic acid decarboxylase (antiGAD) were negative. According to the clinical and laboratory findings, she was diagnosed as having type 2 diabetes mellitus. She was started with oral anti-diabetic treatment for a period of 1 year. Insulin had to be initiated for worsening of HbA1c levels. In the fourth year of follow-up, she was admitted to our hospital with diabetic ketoacidosis although she was on an intensive insulin regimen. At this time, C-peptide levels were low, antiGAD and AIA were positive with HLA DR3/DQ2 haplotype. In addition, her thyroid peroxidase antibody and endomysium antibody were found to be high at follow-up. Small intestinal biopsy revealed celiac disease. This patient may represent the first case of latent autoimmune diabetes mellitus in children (LADC) with autoimmune thyroiditis and celiac disease.

 

[Daibell]

Yes, Type 1.5 (aka LADA) is just T1 but coming on more slowly later in life. Both represent failing or failed beta cells.

 

[MangosteenElbow]

At a high level it is useful to say type 1.5 is a kind of type 1. The numbers do not mean anything. Using those numbers has been clumsy over many years but better than jargon for any high level use.

The statement that type 1.5 shares features with type 2 is very outdated. It relied on poor understanding of both. This poor understanding was highly prevalent at the level of primary health care provider (e.g . doctor) who dispensed care by the numbers not by any knowledge. That's how so many of us around the world got wrongly diagnosed.

Even at the level of specialist health care providers (e.g. endocrinologist) they did not know the pathologies of what was lumped in as type 1.5. In the absence of a functionally useful body of clinical knowledge about something that looked close to type 1 but had differences (e.g. late onset; honeymoon period, higher microsecretions of insulin) common medical approaches included: not treating it differently from type 1 since there would be less liability in the absence of medical guild or national government endorsed guidelines and position statements on care; deliberately less advice on interventionist approaches*; and medication for type 2 which had the effect of masking the outcome of the pathologies of type 1.5 but not actually treating the pathologies (e.g. metformin).

Only in the last 18 months or so have there been published decent, science based papers on the various pathologies that could be grouped as type 1.5.
The 2004 etc papers were brave but in a very early phase of clinically relevant knowledge. That stage is reflected by asking the question: "what are types 1 and 1.5?".
Since "type 1.5" was an abstract notion of just being somehat different from type 1 but not type 2, it became apparent that it was the wrong question.

Skipping over a few years and ideas, the better question (for now!) is: what are the pathologies that matter that we can find out in a reaonably practical way for patients?

That's the question that I think matters most, especially for the younger patient (with "type 1.5").

Answering that gives the best info on what actually is happening inside the patient (not just seeing an almost total loss of insulin making capacity).

The anti-autoimmunity bodies are both biomarkers of deficiencies and responses to deficiencies - I don't think it is correct to assume an assay of test results reflects a simple map of pathologies of type 1.5.
That could be the same kind of logical and scientific errors as assuming that a high serum level of LDLs is a marker of CVD (or, worse, of absolute risk of CVD).

On a similar point, some are pushing for redefining diabetes categories into numerous groups. The explanations are very disappointing: almost nothing on pathologies and mostly on a statistical basis of grouping for the sake of safe treatment by doctors. It virtually locks in assumptions of appropriate treatment for pre-chosen groupings.
This approach would be a triumph of stats based bueacratic risk mitigation for health care providers over personalised and optimised treatment and without regard to science based knowledge of pathologies.

So, instead of asking " am I type 1.5?", the question should be: "what am I?"

This begs the question: what should I be looking for that matters?
("looking for" means affordable biomarker tests)
The 2004 papers are way behind current knowledge and hypthotheses. Doctors and endos are also miles from current advanced insight.

I am reluctant to cite the several papers that I found to be most helpful. They have a standard of evidence less than appropriate for clinical care (and were never intended for that).
They expect to be superceded.

*Anyway, apart from a better understanding of the pathologies and biomarkers of "not quite fully the same as type 1" there is diddly squat in the thousands (and I absolutely mean thousands) of published papers on interventionist treatments.
By this I mean the things that can be done to improve the body's overall system for managing what it has to deal with, not just respond to the obvious shortcomings.

This is a huge topic and with lots of speculation.
That's risky for assuming relevance to an individual.
Just for helping illustrate this:
Doctor / endo #A: I have decided you are type 1.5. This means you will have a honeymoon period but end up totally insulin dependent (wrong!). Take metformin and ... for now. It will help. When on insulin, start to learn to carb count. Tough. (Non interventionist).

Doctor / endocrinologist #B: hmmm. We'd class you as type 1.5 but that does not tell you what's going on and what you can do to help everything going on.
I'm going to tell you of your options but I appreciate that not everything is possible in daily life or suits you. Better that you know of you options than just take pills.
Frankly, we don't know much about what's going on so we don't really know what's best.
It should be trial and error for you. Don't be afraid to make mistakes (just not deadly overnight hypos!). There's no fixed menu of successful interventions and we are far from having sufficient evidence for clinical application that have been endorsed by our protectioniat guilds but they can still work for you so I feel bound to tell you of them.

So, here goes... [I'll work on this list for another post ... this already far too long].

 

[Diakat]

I seem to remember the diagnostic criteria for LADA includes being over 30.

 

[Daibell]

My simplistic view has always been that the start point in classifications should be whether the pancreas is over or underproducing insulin as the causes and treatment are very different. The use of 'T2' as a dumping ground for anyone who isn't GAD positive either thru testing or lack of any testing is remarkably stupid and certainly caused me to have the wrong medication for a few years. One day the 'experts' will wake up to this but thankfully NICE appears to be getting it.

 

[DCUKMod]

My simplistic view has always been that the start point in classifications should be whether the pancreas is over or underproducing insulin as the causes and treatment are very different. The use of 'T2' as a dumping ground for anyone who isn't GAD positive either thru testing or lack of any testing is remarkably stupid and certainly caused me to have the wrong medication for a few years. One day the 'experts' will wake up to this but thankfully NICE appears to be getting it.

Diabell, at the risk of derailing this thread, which I obviously don't want to do, I would comment that there seems to be, in my observation, a lot of diagnosis on the basis of best guessing going on - particularly in a sliding scale set of conditions, like Diabetes and to an extent other endocrine issues.