Immune-mediated diabetes (Type 1A). This form of diabetes results from a cellular-mediated autoimmune destruction of the beta cells of the pancreas. Markers of the immune destruction of the beta cell include islet cell autoantibodies and other antibodies. One and usually more of these autoantibodies are present in 85 - 90% of individuals when fasting hyperglycemia is initially detected. Also, the disease has strong HLA associations.
Idiopathic diabetes (Type 1B). Some forms of Type 1 diabetes have no known etiologies. Some of these patients have permanent insulin deficiency and are prone to ketoacidosis but have no evidence of autoimmunity. Although only a minority of patients with Type 1 diabetes fall into this category, of those who do, most are of African, Hispanic, or Asian origin. Individuals with this form of diabetes suffer from episodic ketoacidosis and exhibit varying degrees of insulin deficiency between episodes. This form of diabetes is strongly inherited, lacks immunological evidence for beta cell autoimmunity, and is not HLA associated. An absolute requirement for insulin replacement therapy in affected patients may come and go.
I'm getting my GAD antibodies tested (tells whether you are predisposed for autoimmune diabetes) and also my C-peptide levels tested (tells whether you are still producing any insulin or not) in February so I may find out soon! I'm thinking I have type 1A since I was diagnosed shortly after having a viral infection.
Based on the limited research I have previously done on idiopathic diabetes, I assume I have immune-mediated diabetes. On some of the research articles, the two things repeatedly mentioned are its inheritance and constant ketoacidosis. When diagnosed, I didn't even have ketoacidosis, and to this day, I only get starvation ketoacidosis when I get VERY sick. As for inheritance, ummm, I think I'm the only one with type 1.... although perhaps one of my mom's cousins may have had it, but I'm not quite sure.
Not to strap a monkey to your wrench but since you are giving insulin and in pretty good control, wouldn't you expect the C-peptide levels to be very low regardless?
If not, please help educate me here - the little I have read seemed to indicate that giving insulin would supress producing insulin even if you were able to do so...
I am 80% sure I have the immune-mediated - my dx came 1 year after an appendecitis that was leaking when they removed it - large immune response yada, yada, yada - you all know the rest of the song... ;)
ooohhh, I wanted to comment on the C-peptides too! NOTE TO A-D, I am not answering your question since I have no idea... sorry!
From my understanding, I think that the levelsof c-peptides are lower if you have T1B, but I thought that this was during early diagnosis or at max two years??? I'm confused :) <--- and yes, a smiley face b/c I really want to hear what you have to say.
Seriously, the things you learn on Juvenation are amazing!
The reason I'm looking forward to it myself, is... I require about 0 basal insulin. I didn't use my pump for the last few days; I was giving my favorite sites some time to recover. Even on only fast-acting shots during meal-time, I was able to achieve perfect control. So, I figure I must be producing some basal insulin... or else I'm just really good at calculating my circulating insulin from my shots.
I know it will be low... but I'm anxious to see if it's higher than most.
So, based on that last post. This would be something that would convince me that I may have type 1B. "An absolute requirement for insulin replacement therapy in affected patients may come and go" is mentioned under type 1B. I haven't heard of many other type 1's who require such low (almost 0) basal insulin like I do.
This diabetes thing... It just doesn't want to fit neatly inside a well-defined box like other disease states.
It's the two types of diabetes that the ADA puts under the umbrella of "type 1 diabetes". Both have almost exactly the same presentations, symptoms, and treatments... but a lot of people are interested in type 1B as it relates to finding a cure, among other things. If some of your insulin-producing cells are still working and a stem cell cure is developed, it is supposed that type 1B's will have greater success since they still have some functioning insulin-producing cells left.
It never ends..... :-{O I'm going to have to make a chart to keep track of this all for crying out loud!
'No, sir, I don't have diabetes: I have type 1 diabetes, category A, subcadagory III, sub-subcategory ABCDF backwards, on my mother's side and three times removed.'
HAHAHAHA. I couldn't agree more. I had to write a report on vitamin D's relationship to Type 1 Diabetes, and I'll show you a little blurb of the scientific jargon I had to search through...
"The frequency of carriers of the BB genotype in type 1 diabetic patients was significantly higher than that in controls (p < 0.01, odds ratio 3.65). Moreover, IFN-gamma production upon anti-CD3 stimulation in the BB genotype group was significantly higher than that in the Bb and bb genotype groups (p < 0.05), suggesting that the polyclonal T cell response in BB genotype patients is Th1 dominant."
Shimada A, Kanazawa Y, Motohashi Y, Yamada S, Maruyama T, Ikegami H, et al. Evidence for association between vitamin D receptor BsmI polymorphism and type 1 diabetes in Japanese. Journal of Autoimmunity 2008;30(4):207-11.
So, what you meant to say Alyssa is: 'No, sir, I don't have diabetes: I have type 1 diabetes, cadagory A, subcadagory III, sub-subcadagory ABCDF backwards, on my mother's side and three times removed becuse I have the polyclonal T cell response found in BB genotype patients that is Th1 dominant.'
Oh, and 'cadagory' is actually spelled category. I kinda like the looks of 'cadagory' though, maybe we can change it.
Sorry, should have done a spell check. Running a bit high right now... 2 am, 340 mg/dL a little bit ago, down 100 points now... sort of out of it :) Thanks for catching it, though
It seems I have not gotten around to thanking you often enough, so I want to take a sec and do it in the middle of this thread.You bring a lot of good information to light and do a great deal to help me keep learning, keep thinking and keep current.I am quite grateful for your input and responses!
And, I assure you that this is definitely not the last bit of research I'm going to bring up. I'm a complete science nerd, through and through. I can spend hours surfing around PubMed (a scientific journal archive online), so I guess by wanting to eventually become a doctor I am choosing the right career.
Even with Type IB functioning dwindles/burns out. So insulin production stops after the honeymoon period. It is a similar theory as with Type 2 DM. Eventually, type 2 diabetics stop producing insulin because their beta cells burn out from overuse secondary to the oral anti-glycemic agents and resistance. So that leaves them as insulin dependant DM2. They do require significantly more insulin due to the fact that they are still insulin resistant as well as not producing insulin. I will do some more research on differences in insulin requirements between 1A and 1B but cannot logically see a physiological explanation. 1A or 1B, each diabetic is so different that it would require a significant study population to support a generalizable theory on insulin requirement. Especially since only 10% of all Type 1 is genetic, finding those numbers (as seen in Trial Net study) is very difficult.