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Diabetes is actually five separate diseases, research suggests

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Northerner

Northerner

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Type 1
Scientists say diabetes is five separate diseases, and treatment could be tailored to each form.

Diabetes - or uncontrolled blood sugar levels - is normally split into type 1 and type 2.

But researchers in Sweden and Finland think the more complicated picture they have uncovered will usher in an era of personalised medicine for diabetes.

Experts said the study was a herald of the future of diabetes care but changes to treatment would not be immediate.

Diabetes affects about one in 11 adults worldwide and increases the risk of heart attack, stroke, blindness, kidney failure and limb amputation.

http://www.bbc.co.uk/news/health-43246261

They've surely missed Cluster 6 - those who were older and like Cluster 1. We don't seem to get a look in 🙄 Not to mention Type 3, or weirdos like me who only need bolus insulin. I doubt Joe Public will get his head around more than two types, let alone 500 subtypes! 😱 🙄
 
Aye, I read this story and thought it was guff. And you’re right - folks like us who developed T1 later in life, or the pancreatic diabetes owners don’t get a mention. They’re on their own with this idea, it’ll never catch on. For the simple reason that there aren’t that many different treatments.
 
Unfortunately the article is paywalled. Maybe LADA are actually Cluster 2 on a later onset and in this article isn't clear


Found on Reddit

http://www.mdmag.com/medical-news/a-study-proposes-five-new-distinct-types-of-adultonset-diabetes
Group 1, SAID (severe autoimmune diabetes): LADA + type 1. Low age, poor metabolic control. Loss of insulin production and GADA-antibodies

Group 2, SIDD (severe insulin-deficient diabetes): Patient without antibodies, with high HbA1C, poor insulin production and mediocer insuline resistence. High prevalence of retinopathy

Group 3, SIRD (severe insulin-resistant diabetes): Obese, severese insuline resistence. High prevalens of kidney damage. Group 4, MOD (mild obesity-related diabetes, MOD): severly overweight patients in relative young age

Group 5, MARD (mild age-related diabetes, MARD): Largest group (40%). Includes the oldest patients.
Click to expand...
 
Aye, Robin, this new classification is more trouble then it’s worth. It’ll confuse NICE, anyway, as to who and who doesn’t get access to insulin pumps.
 
It's also missing the various MODY types. But those are defined as single genetic defects so I guess they are reasonably well defined.
 
Some people have enough trouble now getting a correct diagnosis of which type they have, or a round brick being shoved into a square hole . I can just imagine what it will belike if they bring this in. And they seem to have ignored people who develope T1 when older as well as type 3
Don’t get me wrong I am all for personalised medicalised care. I think the money spent on this research could have been spent far better on other things to do with Diabetes.
 
Ljc said:
Some people have enough trouble now getting a correct diagnosis of which type they have, or a round brick being shoved into a square hole . I can just imagine what it will belike if they bring this in. And they seem to have ignored people who develope T1 when older as well as type 3
Don’t get me wrong I am all for personalised medicalised care. I think the money spent on this research could have been spent far better on other things to do with Diabetes.
Click to expand...
At the moment care is around treating the symptoms more then what caused it. This sort of study is useful because it starts to consider the underlying reasons. You could take it further and ask what is common about those in Cluster 2 for instance and then possible look at genetics to see if there are any common patterns.

The issue here is because it is a statistical analysis, any outlying data points (which might be rarer forms) would probably of been discarded. It also is limited to the genetics of Norway. UK and EU generally have a somewhat different mix.
 
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Some interesting points from this. Assuming Clusters 1 and 2 are T1 then what causes Cluster 2 if it's not autoimmune? This could have implications for a possible cure.
 
Matt Cycle said:
Some interesting points from this. Assuming Clusters 1 and 2 are T1 then what causes Cluster 2 if it's not autoimmune? This could have implications for a possible cure.
Click to expand...
I've often wondered where I fall. My pancreas still obviously has quite a few functioning beta cells, and appeared to increase their number in the first 4 years after diagnosis as illustrated by the fact that my lantus dose steadily declined to zero over that time period, from 20 units down to zero. I have no signs of insulin resistance, weight doesn't play any part, it just seems that the virus I caught around diagnosis time caused most of my beta cells to die off and then they've been replaced over time.
 
Matt Cycle said:
Some interesting points from this. Assuming Clusters 1 and 2 are T1 then what causes Cluster 2 if it's not autoimmune? This could have implications for a possible cure.
Click to expand...
Reading the actual paper, it looks like they only looked for GAD antibodies to determine if the person was autoimmune. I'm aware that there is at least another 2 test's you can do and my consultant told me that there were other autoimmune causes for which there was no test currently.

I seem to fit quite well within the Cluster 2 cohort.
 
I read this article this morning and for the life of me couldn't decide which "cluster" i am in. I totally subscribe to @Ljc 's comments to be frank
 
What does a personalised treatment mean?

I need insulin to live and I have a pump/meter/cgm to try and control my blood sugar as best I can. There isn't anything else around to make it more useful to me as far as I know.
I personalise my own treatment in that I tweak my own insulin doses according to the results I get.

It is interesting that they are researching a broader spectrum of types of diabetes. It's a leap forward from when I was diagnosed when the options were juvenile onset or maturity onset diabetes.
 
Northerner said:
I've often wondered where I fall. My pancreas still obviously has quite a few functioning beta cells, and appeared to increase their number in the first 4 years after diagnosis as illustrated by the fact that my lantus dose steadily declined to zero over that time period, from 20 units down to zero. I have no signs of insulin resistance, weight doesn't play any part, it just seems that the virus I caught around diagnosis time caused most of my beta cells to die off and then they've been replaced over time.
Click to expand...

Mine points to 'classic' T1 or whatever cluster they want to put it in. I don't think I have any functioning beta cells left. I've just got back from the pump clinic and last year in spite of having T1 for over 30 years I had to have a C-peptide as part of the pump application to the CCG. I saw this report before I left this morning and asked the consultant what my test showed and he said it came back as C-peptide - not detectable! He hadn't seen the report but mentioned they do get people who who present with very high blood glucose, are put on insulin but then this is reduced to nothing, then put on tablets (metformin etc) so not really a T1 honeymoon, then over a number of years go back on insulin. Not sure what cluster that would be.
 
Flower said:
What does a personalised treatment mean?

I need insulin to live and I have a pump/meter/cgm to try and control my blood sugar as best I can. There isn't anything else around to make it more useful to me as far as I know.
I personalise my own treatment in that I tweak my own insulin doses according to the results I get.

It is interesting that they are researching a broader spectrum of types of diabetes. It's a leap forward from when I was diagnosed when the options were juvenile onset or maturity onset diabetes.
Click to expand...
I think this one of the latest medical buzz words , as I have seen it in relation to research and cancer treatments.
 
I suspect for T1's it makes very little difference, since other then injecting insulin not much can be done.

For T2's it could make a difference. Right now according to NICE we are generally treated the same regardless, it's only when you find a good surgery that you might get somewhat personalised treatment.
 
Matt Cycle said:
Mine points to 'classic' T1 or whatever cluster they want to put it in. I don't think I have any functioning beta cells left. I've just got back from the pump clinic and last year in spite of having T1 for over 30 years I had to have a C-peptide as part of the pump application to the CCG. I saw this report before I left this morning and asked the consultant what my test showed and he said it came back as C-peptide - not detectable! He hadn't seen the report but mentioned they do get people who who present with very high blood glucose, are put on insulin but then this is reduced to nothing, then put on tablets (metformin etc) so not really a T1 honeymoon, then over a number of years go back on insulin. Not sure what cluster that would be.
Click to expand...
What appears to happen with me is that I actually 'cover' my basal needs with novorapid during the day and my liver goes to sleep at night, doesn't release much glucose, then kicks in big time in the morning when I 'need' around 8 units novorapid for a slice of Burgen toast. There have been a handful of members here over the years with a similar presentation. These researchers ought to read the forums if they want to know how many different types of diabetes there are 🙂
 
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