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LADA diagnosis

Thanks SB2015. It's helpful to hear from other people who have gone through this awkward bit of diagnosis to treatment
 
it really should be treated like type 1.

Your endocrinologist disagrees with that.

There is some research that suggests introducing insulin earlier can help retain functioning beta cells longer

You have a link to that research?

The official proof Interventions for latent autoimmune diabetes (LADA) in adults, which supposively showed "preserved beta-cell function as evidenced by a maintained stimulated C-peptide response" really says: "FCP levels decreased in the insulin‐alone group (from 368 to 179 pmol/L, P = 0.006)".

Other than that I can only find studies comparing insulin to SU's but not to for example lifestyle changes, which according to the article you just posted can be enough to control LADA without any medications.


That's an interesting overview:

"Patients with LADA have a relatively slow autoimmune process and more residual islet β-cell function at onset, allowing a time window to protect residual islet β cells and delay or inhibit disease progression".

I wish I could share more on that topic so others could benefit from it.
 

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You have a link to that research?
You could follow the links in the article that @everydayupsanddowns has linked to in post #10. Section 4.1 admits the possibility of immediate insulin therapy having a beta cell preserving effect, and references three studies in the footnotes 93-95.
I haven’t got time to read them, I can only say that when I was treated, my hospital's pragmatic view was that they would use whatever therapy they needed to, to lower the patients blood glucose. This included insulin straight way in my case, because I had been under my GPs care for 6 months, and being treated as Type 2, with all the glucose lowering drugs available at the time and a very low carb diet, which may have prevented a rapid descent into DKA, but only led to an improved HbA1c of 12%, from the 16% at diagnosis, and a steady progression downwards in my glucose control from that point. I will never know whether I have laid myself open to long term complications by being on ineffective treatments for so long.
 
You could follow the links in the article that @everydayupsanddowns has linked to in post #10. Section 4.1 admits the possibility of immediate insulin therapy having a beta cell preserving effect, and references three studies in the footnotes 93-95.

Thanks @Robin

The summary description in that paper is here (my emphasis):

4.1 Insulin

Certain studies have reported that insulin therapy is rational and essential for intervention in progressive β-cell deterioration in LADA patients, especially in patients with the early onset and more preserved β-cell function (9395). The possible reason for protecting β-cell function using insulin in LADA patients may be due to a decrease in antigen expression and autoimmune attack on β cells as a result of exogenous insulin inhibition of β-cell activity (94). Furthermore, exogenous insulin may lead to immune tolerance and inhibit subsequent immune pathways, thereby protecting residual β cells (94). Additionally, exogenous insulin prevents the accumulation of amylin-positive amyloid in β cells, which is considered one of the most important pathogenic mechanisms of β-cell failure (94). One study reported that therapy with intensive insulin in newly diagnosed type 2 diabetic patients has a great significance for the recovery and maintenance of β-cell function (96). We speculate that intensive insulin therapy can protect islet β-cell function in LADA patients.

One of the most significant challenges when discussing LADA is that no one really agrees what it is. This from earlier in the paper…

There is no universal agreement on LADA classification, diagnosis, and management. It is called slowly evolving immune-mediated diabetes and is classified as a type of hybrid forms of diabetes in the Classification of Diabetes Mellitus 2019 of the World Health Organization (7). However, it is also classified as a subtype of type 1 diabetes because of its autoimmune destruction of islet β cells according to the Diagnosis and Classification of Diabetes Mellitus of the American Diabetes Association in 2022 (8). Currently, the exact underlying mechanisms of LADA are poorly understood, and specific etiological treatment of LADA remains an issue.

Loss of islet β-cell function due to autoimmunity is the key factor in LADA occurrence and progression, and individuals with LADA have more residual islet β cells at onset compared with classic type 1 diabetes (9, 10). After diagnosis, the ability to retain residual β-cell function is heterogeneous, being influenced by the age of onset, genetics, and immune mechanisms.


And the heterogeneity (lots of different things being called the same thing) makes understanding LADA very difficult - because different Drs can assign the label to very different conditions - one which might be a slightly odd version of T2, and another which is more or less classic T1, but diagnosed not in childhood.
 
Following from a diabetic check up I was told I'm LADA (like that rust bucket car from the Soviet Union which is accurate enough given how I feel sometimes...) but without any explanation other than it's between one and two and the meds (metformin and lantus) are doing well enough so they'll keep everything as it is. I did a bit of research and there was really nothing worrying or that required any change to the advice I had been previously given.
 
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