Yeah I sometimes wonder if the progression with LADA is so slow that folks who require insulin may for a very long time still have some islet cell function, enough to provide a degree of buffering to aid control, even if not enough to be an obvious honeymoon state. I also wonder if there are other effects on body systems from such a long course of the disease that affect how diabetes functions in childhood-onset diabetes vs adult, and/or if the nature of the immune damage might be different in ways beyond what it does to insulin production capabilities.
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This is an old discussion so perhaps this isn’t needed: I was diagnosed LADA last November. Previous to that I had been misdiagnosed T2 eight years back. LADA, though conjectured 10+ years ago, is often misdiagnosed as T2. LADA is an auto immune disease that relatively slowly produces antibodies that attack the beta cells in the pancreas that produce insulin, etc. At first, the body overcomes it by making the pancreas work harder until it finally gives up. It can take years (I’m living proof); there are tests for the antibodies but you have to have a doc that knows what to look for and request. There is still discussion today whether LADA is a separate type (1.5) or exists on a continuum between T1 and T2. Either way, those of us with it end up very similar to/the same as T1s requiring insulin. Those accurately diagnosed early in the onset, even if put on insulin, will eventually be dependent on it. Example: I was on Metformin for eight years, it quit “working” last summer. Glyburide was added 2+ years ago and it also stopped working. Even with insulin, it’s just a matter of time until the antibodies kill all the beta cells. I’m sure there is much more a Doc could add…
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Thanks for the explanation
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@TomH , we exist here for discussions, you had a great addition to the thread, don’t feel shy about resurrecting old threads, although it might be even better if you start new ones! New threads is what brings us up in the search engines and leads to more members.
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