I just want to know if a type2 diabetic can become a type1 diabetic, or if it is even possible. I know this is out in left field but I am curious.
Type 1 and Type 2 diabetes are two completely different diseases. Type 1 diabetes is the autoimmune destruction of insulin-producing cells. Type 2 is a combination of insulin resistance and/or the insulin-producing cells not producing enough insulin, but there is no autoimmune attack.
Type 2 diabetics can sometimes become completely insulin dependent like a Type 1, but this is due to their insulin-producing cells “burning out” over many years, and so is still a different cause and the treatment may possibly be different (using oral medications in addition to insulin).
Hope this helps.
Theoretically yes. A person who already has Type 2 can suffer an autoimmune attack on the remaining beta cells, and then be considered a Type 1 with insulin resistance, or a “double diabetic”. That’s because the genetics of Type 1 and Type 2 are different, and there is no reason they can’t occur in the same person. The onset of the autoimmune attack in Type 1 requires some unknown trigger, and some people don’t encounter that trigger until later in life. It’s far more frequent for someone with Type 1 to develop insulin resistance and become a double diabetic than the other way around, but it’s not impossible.
I do not think so, they are different, but Type 2 can progress to needing insulin, like Type 1 but that type 2 produces some insulin, but either insufficient to deal with glucose in the blood or of poor quality.
I do not know but if you are talking about yourself…you were only dxd. about 7 years ago. Perhaps you have Type 1.5 (LADA). They are okay on oral meds, diet and exercise for a certain amount of years but then they need Insuin full time. You may have been misdiagnosed as many Type 2’s have been.
There is evidence now that some type 2 is an autoimmune disease so I guess when enough of your pancreas dies you become a type 1.
Even today many diabetics with T1 are misdiagnosed as T2. Antibody tests like the GAD can report a false negative and this is true for other test too. Furthermore there are still doctors in the field not familiar with late onset T1 diabetes - also called LADA or T1.5. Thus they assume just from age and physical appearance the patient must be T2 diabetic. All diabetics even T1 will react to T2 medication. It just depends on the remaining capability to produce insulin. This positive reaction to T2 medication might be convincing that the diagnosis was correct. But 1 to 2 years later these misdiagnosed patients will face a serious and possibly life threatening ketosis.
There is also a subgroup called ketosis prone T2 diabetics. Just from the fact that these diabetics experience a ketosis the diagnosis of T1 was concluded. In the past these patients were always put on insulin. Later some medications for T2 and changes in lifestyle can put these patients off insulin - even off medication. Halle Berry is a good and bad example. She has not been cured from T1 diabetes - she never had it because she was misdiagnosed. She is very likely the ketosis prone T2 type. With her physical fitness and dietary changes she can control her T2 for now. She did not transform from T1 to T2 and she is certainly not cured from T2.
Another important point is that most T2 patients are diagnosed very late. At the time of their diagnosis their beta cells had to produce massive amounts of insulin to overcome the insulin resistance. High production levels over longer periods of time are very harmful for the insulin producing beta cells. Thus many of these patients have only 30% of their production capability left when they are properly diagnosed. Very likely this will degrade further. We know that these remaining cells are very important for being complication free over longer periods of time. The Joslin studies with long term T1 diabetics show that there is a positive correlation between being complication free and having some residual beta cells. So we have T1 patients with 1% to 5% remaining beta cells and T2 patients with 30% remaining beta cells. The 25% difference will make life easier for the T2 using insulin. But at the end this depends on the level of control that is achieved. If you are one of those T2 needing insulin combined with a nervous liver and dawn phenomen you will have a hard time too. At this stage it is not easy to differentiate between the types anymore - at least from the perspective of treatment.
I was a type 2 diabetic and now I am a type 1 because pancreas, I have had alot of attacks and now it doesn’t work anymore so they retyped me.
You can have both conditions…however, under “normal” circumstances, type 2 does not become type 1…as they are two different entities. The fact that a type 2 may require insulin does not make him/her a type 1.
Holger, remember that Type 2 is being diagnosed earlier and earlier these days, even among children. Also, the theory that having beta cell function results in fewer complications is flawed, because so many Type 2’s who DO have remaining beta cells nevertheless develop complications, often even before they’re diagnosed!
Well, the question was how the diagnosis can change from T2 to T1. Here the misdiagnosis is the most important problem newly diagnosed diabetics are facing.
Many studies fail in identifying clusters of diabetics with comparable quality of control. Homogenous clusters are fundamental to find the factors to successfully avoid/prevent complications. For me it is clear that decent control like an A1c of 7% is not enough to avoid complications over long periods of time. It needs good control and with good I mean an A1c below 6.3% (or even better below 6%) combined with less glucose variability. With uncontrolled diabetes the remaining beta cells will of course not help to prevent complications. But if you have remaining beta cells they will give you that little extra to have less glucose spikes. Over decades this will make a big difference in the development rates of complications. Likely other genetical factors are involved too that will protect people from the negative effects of high blood glucose. But this is just a subgroup that has less complications despite their uncontrolled diabetes. For me the real focus should be good control for all diabetics. For that the finding of Joslin that T1 with less complications will likely have residual beta cells is really remarkable. This finding also points into the direction that the variability of glucose within short periods of time is something to control too. Other studies are pointing in the same direction. Also this does not mean that diabetics without beta cells can not avoid complications. But it means that they need to invest much more in controlling their diabetes: more awareness, more persistence, more strictness, more abstinence, more thoughtfulness and the effective utilization of available technology and medication.
No, rare situations aside, the short answer is that Type 2 does not “turn into” Type 1. Two things can happen. A Type 1 (usually LADA/type 1) can be misdiagnosed as Type 2 due to age and rate of onset; later they are correctly diagnosed as type 1. Or Type 2’s after a number of years can no longer produce sufficient insulin and need to be put on exogenous insulin. They haven’t become type 1’s, they are just insulin dependent type 2’s. They are two different conditions.
Type 1 is an autoimmune disorder
Type 2 is a metabolic disorder
They both suck
Though I read recently that type 2 is now considered to be autoimmune as well!! I’ll try to find the info.
Here is the article on T-cell autoimmunity in Type 2. It doesn’t apply to all Type 2’s, just some of them. Which begs the question of whether they are really Type 1’s in disguise.
Natalie, that was new to me. What a remarkable study. Maybe they should look for this type of autoimmunity in LADAs too.
Well, what it proves is that diabetes is a very complex disease, and there are no simple answers to what SHOULD be simple answers! My own experience leads me to believe (with no particular evidence other than observation) that it is really a spectrum – more antibodies, younger age, less insulin resistance, quicker onset = Classic Type 1. Fewer antibodies (or none), older age, more insulin resistance, slower onset = Classic Type 2. But there seems to be a range of people in the middle, not squarely fitting into either box. LADA’s are one subset, thin Type 2’s are another subset.
For me, it was only hints, because I was diagnosed before testing for antibodies became available. But there are some arguments for Type 1, and some for Type 2: neither parent had diabetes, I was not obese at diagnosis, although I was about 10 - 15 lb. overweight, I tried Glucotrol (a sulfonylurea) for 5 months and it did nothing, I had proven Hashimoto’s Thyroiditis, which is auto-immune, and I responded readily to insulin. But on the other hand, I have metabolic syndrome, which may be a coincidence, because I inherited high cholesterol from my father, who was not diabetic, and the tendency to belly fat from my mother who was not diabetic, and hypertension, which may be because I have Inappropriate Sinus Tachycardia, and not true hypertension. In any case, those conditions were easily treated, and now I am within normal weight ranges, but the diabetes has not only not gone away, but actually needs more insulin than it did years ago. I have had 2 CDEs independently tell me I’m Type 1, but it’s NOT classic, and I really think I’m somewhere in the middle, but I tell docs and medical personnel I’m Type 1, because I do need Type 1 protocols in the hospital.
Oh, and one other thing I forgot to mention in my earlier post. I KNOW one person who started out as an obese Type 2, and had bariatric surgery. Then she lost weight, and the diabetes went away. After a couple of years, she became symptomatic, and started to lose too much weight, and they did antibody tests on her, and lo and behold, she was a Type 1. So, in spite of the naysayers, I KNOW it can happen, and this is not hearsay.
People with LADA have one or more autoantibodies indicative of Type 1 diabetes (GAD, ICA, IA-2).
But there is also a problem with killer T-cells, which attack beta cells. The three antibodies you mention are not the whole story in Type 1, since something like 10% or 15% of people presenting in ketoacidosis, with low C-peptide, nevertheless do not show those antibodies.
Hi Natalie: Completely true, I am just pointing out that LADA is defined as antibody positive. What’s interesting about that Diabetes Care article is that 7 of the 36 subjects are antibody positive (GAD, ICA, and/or IA-2) so would be classified as Type 1. Then there are the subjects who are positive for islet reactive T-cells (as tested by cellular immunoblotting). All I can say is, it is incredibly complex!