If you are diagnosed with Type I as an adult are you automatically considered LADA? Or, can you be the faster onset Type I? I think I read somewhere on TuDiabetes that you have to have all of the Antibodies to be a full Type I and LADA has only GAD65. Is that correct?
Does 1.5 suggest that you have both Type I and Type 2???
Ok, first question first. LADA is a different form of Type 1 than “Adult Onset Type 1”. LADA also comes on in adulthood, sometimes even very late adulthood (I was diagnosed at age 58!), but it also comes on very slowly which is why so many of us were misdiagnosed as Type 2. For me, for example I was managed on oral meds with good numbers for 15 months (and very little diet changes!). Then my numbers started to rise and I rediagnosed myself. Adult Onset Type 1 has the same sudden presentation as any other Type 1, often with DKA. That is the main distinction between LADA and Adult Onset Type 1. (Yes, LADAs often only have GAD65, but, at least to me, the more important differential is the time of onset.
“Type 1.5” is just another name for LADA. And it is not one I personally like or would use. The reason is because everyone then assumes what you said “you have both type 1 and type 2” or that you are “halfway between Type 1 and Type 2.”. LADA is Type 1; it’s an autoimmune disorder and its chief characteristic is insulin deficiency, though this happens slower than regular type 1’s. Type 2 is NOT an autoimmune disorder and its chief characteristic (at least initially) is insulin resistance.
I wish they would get read of the designation “Type 1.5” as it’s misleading and sounds like software. What I REALLY wish they would get rid of is the term Juvenile Diabetes. More Type 1’s are diagnosed as adults than as children, and I know many Type 1’s who were diagnosed as children or teens and are now in their 30s to 80s. I don’t think any of them would like being called Juvenile!
LADA is Type 1. The term 1.5 just generated to distinguish it from juvenile onset. But it’s the same disease. Speed is really not relevant to type. The reason sometimes people say it has elements of Type 2 is because many times it is diagnosed while there is still some insulin production. So it it often looks like Type 2 at first (and may respond to type 2 drugs for a short time) and is often misdiagnosed. The antibodies are the same as Type 1. The usual test is for GAD65 and 1a-2. I have both. I self identify as LADA simply because I think it’s important for people to know that Type 1 can hit as an adult. If more people are aware of this than maybe fewer LADAs will be misdiagnosed as Type 2. Type 1.5 and LADA are not clinical terms - clinically they are Type 1. As Zoe says, the term juvenile diabetes is a part of the problem.
I have LADA and was negative for GAD65. I have islet cell antibodies. I wonder if one of the differences is that LADA, because of its slow progression, is often diagnosed early, so the honeymoon phase can be prolonged. I think once you have lost all your insulin production there is no difference between LADA and any other Type 1.
So, if you are diagnosed as an adult, do you usually have all the antibodies that you get when you are diagnosed as a child? Do they ususally test children for all antibodies or just Gad65?
There is an article on Diabetes 101 which shows the differences between LADA, Type 1 and Type 2. It’s very informative.
http://www.phlaunt.com/diabetes/18382053.php
I also read somewhere that LADAs often have the genes for Type 2 as well as Type 1, but I don’t remember where I read it. It might be in one of the articles cited in the above URL.
This has been very informative. I was diagnosed at age 47 and went through what seems to be the usual course - treated as a Type 2 until the meds stopped working and rediagnosed as Type 1. To be frank, my endo told me that’s what was going to happen.
Anyway, I tell people I’m Type 1. I only call myself LADA or Type 1.5 with other diabetics because I view it as code for “I was diagnosed later in life.” Besides, it confuses non-diabetics.
Terry
Yes, they are the same antibodies. I do not know what the protocol is for testing children. Typically not all of the beta cells have been destroyed by the autoimmune system at time of diagnosis. There will be remnant beta cells that will ultimately be destroyed. In some – particularly infants and children, the beta cells are destroyed very quickly. In others - particularly adults, the process is slower. That slower process that often occurs in adults is often confusingly referred to as the initial honeymoon period or the Type 2 period. It really is neither – it is just the timing of the onset of the Type 1. But it will vary among adults. That period for me was quite short – about 2 months (if that). Others have much longer periods. All of these extra terms lead to confusion in the public about what LADA really is. It truly is Type 1. It is neither a hybrid of T1 and T2 nor a different disease. The LADA distinction just really tells you that a person was older when they got it. It is not a clinical term. To add to the confusion is this the mistaken belief that anyone who is insulin dependent is Type 1. Indeed, all Type 1s are insulin dependent. But T2s can reach the point in the disease where they need insulin too. And some use it in combination with other drugs to assist insulin production in the pancreas. But a T2 that goes on insulin does not become a T1. They are still T2. Type 1 is caused by an autoimmune problem. Type 2 is not.
My endo calls my dx LADA. I have both antibodies. I was dx one year ago on April 1st with a A1C of 10.7 and had previously had it done the September earlier (b/c I was having numbness and tingling) and it was 6.1. So, I believe this onset was very rapid. When I was dx’d in April I had lost 15-20 pounds in 2 weeks and had blurred vision among other sx. She started me on oral meds and I had absolutely no response. She stopped them about 3 weeks later and started me on MDI.
So, does this make me a LADA diabetic or a late onset Adult Type 1?
Yes. Your endo must have tested for the antibodies. You are Type 1 but you can use the term LADA, Type 1.4 or late onset adult Type 1 - -all are true. Like Terry, I call myself LADA just because it is short hand for “I got Type 1 when I was an adult.”
My endo calls me a “possible early caught type 1” and was more interested in my c-pep than the high GAD. I had that tested last year myself when I saw that even with great weight loss my a1c kept slowly going up since I was first dx’d a prediabetic in 2004. My highest a1c was 5.8 I think, in 2009. I started low carbing almost 2 years ago and with that I can stay under the radar without a diagnosis of D. My a1c about a month ago was 5.3. If I started eating just a little bit more carbs, especially grains of any kind, all bets would be off. My fbg then quickly goes into the diabetic range. My fasting c-pep is very low normal, but it went up a bit in my recent lab work. And my GADs were down a little bit. Well, 20%. C-pep was up 20%.
My question is…I wonder if I was on the way to type 2 when I got the autoimmune attack? Or have the GADs been intermittent and that slow…when I gave up grains and kept my carbs low, the weight just peeled off so I don’t think my insulin resistance was that bad. I’m sure I have some though.
No other signs of metabolic syndrome, just the impaired glucose tolerance.
My doc seems to think I may not ever get any worse as long as I don’t gain weight. She doesn’t comment on my diet and the grains issue. I also have Hashimoto’s, which is autoimmune, for 15 years now.
I take no meds except for thyroid hormone, and I’m 61 y o.
Comments? My doc only recognizes types 1 and 2.
I had rapid onset Type 1 with very low C Peptide and a GAD of >250. There was no LADA from my endo. It was “you are Type 1” . Came out of nowhere and hit me like a bulldozer.
If you search through papers for LADA over the last decade or two, you’ll find a very confusing mess. Like Zoe, I don’t like the term 1.5. It seems that that was originally applied because most patients present somewhere in between T1-like and T2-like. But it’s now clear that while the progression is slower than ‘classic’ T1 (if there is such a thing), it progresses toward the same end – just more completely in some than in others. While older age of onset usually means slower progression, there are only correlations and no actual rules that it follows.
That does not mean that you can’t also develop T2/insulin resistance. But the T1 will mask any official diagnosis of T2. And, I think Zoe posted elsewhere – and I believe that there is some evidence for it – T2 genes may influence the development of LADA. Stressed out beta cells may be one of the events that precipitates the autoimmune reaction. But right now, this is just very interesting speculation.
To me, the importance of the term LADA mostly has to do with awareness. Since T1 (formerly juvenile D and IDDM) is often thought of as a childhood disease, I think it helps to highlight the fact that many T1s are diagnosed in adulthood (even to medical personel). It may have greater weight in the future as (hopefully) new treatments and preventative or curative therapies are developed because LADA’s are more likely to retain a higher functional beta cell mass for longer. But there’s no line there either, because even among T1s diagnosed in childhood there is wide variation in preserved endogenous insulin/c-peptide production.
I guess the point of that ramble was that, LADA is a sub-category of T1. Whether you want to make the distinction is entirely up to you. Like Terry, I just don’t see the need. D is such an individual disease that there are probably as many differences between 2 LADAs as there are between a childhood T1 and a LADA.
I was diagnosed as an adult and LADA was never really mentioned. Mine was caught “early” and before I was in DKA, and I still had some insulin production, which caused some confusion with getting a correct diagnosis (and I have in fact been diagnosed with every type of diabetes, first GD since I happened to be pregnant, then T2 because of being labeled with GD, then T1, but I never actually had GD or T2), but I fault the doctor I was seeing at the time more than anything else - once I saw a real endo and not an internist on a power trip things were straightened out very quickly. I never showed any insulin resistance, or excessive insulin production (I did have “normal” c-peptide levels for a little while, but they were at the bottom of the lab range) or any other signs that I “should” have been diagnosed with GD or T2. I never responded to oral meds at all… which was ultimately why I changed doctors. My internist wouldn’t even let me use insulin, and berated me for self-medicating highs over 300, telling me I had to give those medications “time to work”. My perspective on that is a bit different than hers was, obviously.
LADA is simply slower onset T1, I don’t personally think that it’s really as different as a lot of people seem to want to make it. I actually find it comical that so many LADAs seem to think they can prolong the inevitable and be the exception that doesn’t eventually need insulin… if your pancreas quits working you have to make up for it somehow.
I suppose by definition, given that I was diagnosed in October of 2000 with GD, immediately put on insulin, told to stop it when my #'s returned to normal in the hospital after delivery (January 2001), then I was diagnosed with T2 in March of 2001, and I was officially re-diagnosed in June of 2001 when my antibody tests came back confirming T1, and there was some time during that when I was off insulin completely (for maybe 6-7 weeks… it was the time following my pregnancy before my GTT) I might fit the LADA model, but it just wasn’t really discussed. From the point i decided to fire my internist I started taking NPH in addition to using regular. I walked out of my first endo appointment with scripts for Lantus and Humalog.
I’ve always considered myself a T1, my diagnosis was just a bit complicated and not typical of a T1, but even back when I was first diagnosed with GD I suspected that it was incorrect (not because I was in denial, more because I’d never heard of anyone else with GD being diagnosed with a BG over 500).
The signs (GAD, low c-peptide, Hashimoto’s) are that you are on the path to T1. Many LADAs are able to initially treat with low-carb diets – it basically allows remaining beta cell mass to function more easily. But, as more beta cells are destroyed and the balance tips, your glucose tolerance can deterioriate. The rate of progression is different for everyone, so keep a close eye on it. I will cross my fingers that it takes the next 61 years of your life to progress, but I think perhaps your doctor is too optimistic.
Keep an eye out for yourself (keep testing, and any signs of unexpected weight loss, thirst, frequent urination, etc get to the doctor or emergency clinic immediately). There are too many stories on here of doctors unwilling to see what’s in front of their eyes. Unfortunately, you may have to advocate strongly for yourself, and even consider changing doctors if he seems to reluctant to consider this. I wish you luck!
You do not have to have ALL antibodies + - just 1.
Thanks for your response, Tom. Better than my doctor’s, actually. She has not
encouraged me to test and even forgets to order an a1c regularly. Maybe she thinks I’m already keeping a close enough eye on things She does test my thyroid pretty well though.
She’s an endo but has some peculiar ideas that I haven’t heard anyone else express…for
example she told me to try and get in a clinical trial and maybe I can get turned
from a type 1 to a type 2…??! Now I have heard that some are saying lines are blurred
between the two as more studies are done so ok maybe she believes that…but I don’t even have a diagnosis, which is required for a clinical trial, and I’m older than they want. 45 years is the cutoff… she should know these things.
Whatever happens in my future, well I’d like to be prepared to deal with effectively, so thanks for the information you’ve kindly provided. I will keep a close eye on myself. I do have a sister with type 2 and one that has been told she was probably always a type 1 and was just misdiagnosed. She has been on insulin since the early 1980’s after only a couple of years on oral meds. We all have Hashi’s, but neither of my parents had thyroid or blood sugar problems. Strange.
I like your spirit! You’re welcome. Some doctors are just too reluctant to issue a T1 diagnosis when there is still X amount of c-peptide. It’s as if they are afraid to mistake a T2 for a T1, but not the other way around. It’s unfortunate, but as long as you’re keeping your eye on it then you’ll know when to push for insulin and a new diagnosis. You can teach her something!
My family is similar – it’s just me and my brother with T1. A perfect storm of bad genes from both mom and dad!
I think they don’t want to diagnose a Type 2 mistakenly as a Type 1, because Type 1’s have to use insulin, and they think everyone’s afraid of needles. When I was on Glucotrol, in the beginning, and it was doing exactly nothing for me, my doc was content to let it ride, but I pointed out that peaking at 250 - 300 after meals was not acceptable, and I wanted insulin, so he started me on it, but again, using a Type 2 protocol, which was one shot of NPH at bedtime. Which didn’t fix the peaking problem. Then it was 70/30 twice a day, which gave me horrendous lows both at night and during the day. Then I finally got him to let me use N and R, and take shots before meals – horrors, MDI!! Now I have a pump, a CGM and a new doc!
I have not been tested for any other than the GAD 65. I have noticed this in my case though…my bgs are very predictable…compared to everything I’ve read re T2’s experiences and T1’s. I don’t get unexplainable liver dumps, don’t have a huge dawn phen effect. I get about a 2 pt. jump in bgs for every carb I eat most of the time. Fat slows that down some, but it actually takes a lot of fat to do that. Evenings are my best time for keeping a good bg, mornings worst.
I’m assuming that I have this predictable scenario because I DO have some significant pancreatic action left and I have less of the insulin resistance and liver signaling problems that plague a T2. Controlling my carbs also controls my weight amazingly. If I had known that would be the case for me I would have been eating low carb decades ago. Weight was always a big struggle for me, and I tried everything to lose it. I finally have stability and my weight is in the normal range.
I’m not too afraid of needles and when the time comes I will push for insulin as opposed to anything else. Oh, also it seems most T2’s have trouble with cholesterol, bp, etc. I don’t have that either, never have.
In my case LADA looks like a very slow T1. It does seem like every case is different and we have to figure out an awful lot for ourselves. And things can change anytime…autoimmune troubles run in my family.