Well ... here I AM.

[foxl]

GAD > 30.

I KNEW IT!!! Why oh why did I have to ask 3 times.

So ... off to the Endo.

[Tomax]

Good luck, foxl!

[foxl]

Thanks! It's kind of a relief ... very mixed feelings, too of course. I know it can be a roller coaster, but perhaps as long as I am vigilant ... insulin will be easier for me.

It's a relief just knowing what happened. It's a relief that I can try to afford some protection for my beta cells. It's a relief that I won't have someone telling me to "try harder" on diet and exercise when I earnestly already AM trying my best.

I still want to exercise and low carb, obviously!

[zoelula]

Welcome to our special little club, Linda. I know there are some people who were diagnosed LADA from the start, but most of us were misdiagnosed as Type 2 and have had to figure things out ourselves and then convince doctors, not people known for their openness that we knew what we were talking about! In February I was puzzled why my oral meds had stopped working in just a year, seeing numbers in the 300s, then on way too high a dose of long acting insulin only so I was experiencing both lows and post prandial peaks. Now I'm on the right basal/bolus regimen and learning what foods do and don't work and actually getting better control all the time as a Type 1.5. For me it has been a relief.

[BlueSky]

Congratulations on getting to the bottom of it ;) . Discovering the truth and being able to use the right tools to deal with it is very empowering.

[Ategeler]

Congrats on your dx. Perserverance pays off in the end! Good luck to you!

[soso]

Hi Linda
I am just coming up to 5 yrs and still have some beta cells working.. I put this down to doing low carb from the start and getting on insulin as soon as I could not keep my spikes below 7 and fbg under 5.7..I started with bolus and added basal a year later.. I may be wrong and I am just lucky, but I do think my strategy has worked in my favour... knowledge is power.. my best wishes and good luck to you...

[sumi]

Big news Linda! I guess you are going to have even more interesting work to do. Don't forget those of us who knew you when you were a lowly type 2.

[mortis505]

Well now you gone and done it. The 3 time thing will get you every time.

Congrats on the proper diagnosis. Get a proper basal/bolus regimen going and everything will fall into place.

[rak1978]

Welcome to the 1.5 club!
:)

[SoCal]

So, I've been "type 2" for a little over 8 years. Been on metformin which worked just fine until about 18 months ago when my A1C started creeping up from the 6's to 7's to 8's to about 9.1 when my PCP started me on Glipizide. Had been increasing the dosage on the met to no avail.

I had been 5'11'' and 185 when originally diagnosed and dropped 40 pounds initially and have stayed in the low 140's ever since (nothing really changes my weight regardless of calories consumed, etc.) No history of diabetes in my family and no other risk factors.

I was talking with a friend whose husband and daughter are both type 1's and she asked if I had heard of 1.5 because she thought it sounded like me from what she had been reading. So at my last Dr. visit (after having done a bit of research myself on LADA) I asked him about it - and of course he had never heard of it. (By the way, my A1C had dropped back below 7 after starting on the Glipizide so pancreas is still working to some extent.) After the visit, I emailed some info to the doc and requested that we run a cpep test. He, thankfully, agreed and when the results came back with low cpep in the presence of elevated random BG's he consulted an Endo who ordered GAD65 and ICA tests. Guess what? Positive on the GAD and negative ICA - thus I am now officially type 1.5.

Started on Lantus (the Endo wrote the scrip for the solostar pen and itsy bitsy needles so the injections are easy) at 10 units at bedtime. Stopped the Metformin and Glipizide and will add back in the Glip as I establish some basis for how I am doing.

First morning after the Lantus I woke up low - 62 with sweats and shaking - not a pleasant experience, but since then have been consistently below 120 and mostly under 110 in the morning. My post-prandials have been pretty good as well - rarely spiking over 150 (although today post-lunch was in the low 200's after being at 101 pre-lunch so I'm going to have to do some tweaking with that).

Anyway, nice to have a real diagnosis and treatment plan that makes sense given my situation and background. I'd always been a bit perplexed with why I was type 2 before.

I'd like to get stabilized on the Lantus and put off bolusing as long as possible - which given my long "honeymoon" should be a reasonable expectation.

[Subby]

Well done. Hopefully it means less confusion, more clarity, and an improvement in your life. I'm not referring to the possible med change as such, but more that whatever you do, it might make more sense and yuo can make better decisions (you know this already, eh). Did you get a C-pep result?

[foxl]

Well done. Hopefully it means less confusion, more clarity, and an improvement in your life. I'm not referring to the possible med change as such, but more that whatever you do, it might make more sense and yuo can make better decisions (you know this already, eh). Did you get a C-pep result?

Thanks, all, and I gotta say, it feels better to be here, rather than trying to consider both possiblities at once, and barking up the wrong tree (and I am barking HARD, LOL!).

Subby, my C-peptisw was 1.3, that was the first thing my MD told me. Not bad, lower limits of normal for that lab, but still, certainly not Type 2-like. I knew in my gut from before I even SAW my MD (I tested at home first) that it had to be autoimmune. And I am good at these hunches -- I told my husband 6 months before diagnosis that I had hypothyroidism, too!

Yes, even if I do not start on insulin immediately, I now know what part of the metabolic cascade I am dealing with. I do hope to continue low-carbing and exercising, though I may indeed try to do more consistent daily workouts instead of the emphasis on sprints (though I LIKE them, may try to do one set a week at least!), to keep the glycogen stores lower ...

And I probably do have some insulin resistance as well ... I think we all do, right? But I now know that what precipitated my diagnosis was not only resistance, and treating only resistance is not an effective longterm strategy!

[foxl]

Got Endo appt. ... Aug 24, so that is ... 8 weeks. Ack. I am sure I will survive till then ... plenty of time to research and take notes!

Was expecting to go to an Edno my co-worker sees (not a great personality reputedly) but got another one, female (which is neither here nor there, of course), instead. Now I gotta go research her.

[Grunch]

I don't believe this 1.5 thing. How can there be a new type of disease if they are not even capable of determining objective parameters to define the disease?

Congratz on finding the truth. If you could choose though, what type would you rather be? Don't sit on the fence, cmon.

[foxl]

I don't believe this 1.5 thing. How can there be a new type of disease if they are not even capable of determining objective parameters to define the disease?

Congratz on finding the truth. If you could choose though, what type would you rather be? Don't sit on the fence, cmon.


The well-REGULATED type!!!

And Grunch, Type 1.5 is also called LADA, or slow-onset autoimmune diabetes of adults. 1.5 is merely a nickname.

[Grunch]

Argh, you sat on the fence, I knew it!

I know it's called LADA, what I'm saying is there is no objective difference between LADA and type 1. Saying the onset is slow doesn't define it because you'd have to determine exactly how slow it is. As far as we know the speed of onset could follow a normal distribution, and arbitrarely defining a cutoff speed that separates type 1 from 1.5 is silly.

[Subby]

Why would you ask someone to choose to be one or the other? Things are just the way they are... and experience can vary so widely between and within types, and change, too.

And as Linda says, you just gotta do the best with the hand you are played.

[Subby]

Argh, you sat on the fence, I knew it!

I know it's called LADA, what I'm saying is there is no objective difference between LADA and type 1. Saying the onset is slow doesn't define it because you'd have to determine exactly how slow it is. As far as we know the speed of onset could follow a normal distribution, and arbitrarely defining a cutoff speed that separates type 1 from 1.5 is silly.

A LADA may have significantly different experience of treatment for many years compared to a classic type 1. That's the important thing - how to be approaching it. A difference in onset IS an objective difference. Variability in that attribute does not negate it.

[foxl]

But Grunch, ya you got a point and there is nothing "incorrect" about calling it Type 1.

But the thing is, Type 1 VERSUS Type 2 is indeed simplistic. Type 1's can have insulin resistance, and Type 2's eventually lose beta cell function.

And we all can benefit from each others' experience and wisdom.

[rak1978]

All of this makes me wonder....
Do type LADA'ers eventually loose ALL beta cell function?
Do type 1's have ANY beta cell function?
If LADA'ers do loose all function, but at a slower progression, at what point do they/we just become type 1? The lines are getting blurred to me.
As time goes on with this, I'm having a hard time seeing the difference between types. My dr. just tells me that I'm essentially a type 1 with some aspects of type 2 (mainly insulin resistance), but the way he explains it, or really doesn't explain, to me is all very confusing.
The internet does not provide that much info on lada or type 1.5. All sites that I've seen pretty much give the same schpeel and do not go into depth.

So confused.

[foxl]

Yeah you get better info from books for sure.

Yes, many type 2's end up losing all beta cell function. As do LADAs. As do type 1's who have residual activity.

The difference is the cause of the disease, although some Type 1's are not autoimmune; they can have surgical or medical destruction of beta cells. But Type 2 is primarily insulin resistance: the insulin is produced, even overproduced, but not usable by the body.

[lorilei]

congrats...u can play left field...

[warrenav]

It is not clear if *all* LADA folks will lose all beta function. My endo has indicated that I may be very much as I am today in 10 years time. I was just diagnosed recently (after 11 years as an atypical "type 2") as really LADA with a GAD positive (but only a little over the normal limit) and low C-peptide (but only a little under the normal limit). Still not using insulin and no near-term plans to change even with the new knowledge.

Warren.

[foxl]

It is not clear if *all* LADA folks will lose all beta function. My endo has indicated that I may be very much as I am today in 10 years time. I was just diagnosed recently (after 11 years as an atypical "type 2") as really LADA with a GAD positive (but only a little over the normal limit) and low C-peptide (but only a little under the normal limit). Still not using insulin and no near-term plans to change even with the new knowledge.

Warren.

Very true. Looking through your other posts, you appear to be nearer the Type 2's on the spectrum between 2's and 1's. Interesting that you have a low GAD titer, and higher C-peptide than I have, measured only 5 months after first diabetes diagnosis. How come they even checked GAD and C-peptide on you? Just curious -- did you have symptoms that led to it?

[warrenav]

Very true. Looking through your other posts, you appear to be nearer the Type 2's on the spectrum between 2's and 1's. Interesting that you have a low GAD titer, and higher C-peptide than I have, measured only 5 months after first diabetes diagnosis. How come they even checked GAD and C-peptide on you? Just curious -- did you have symptoms that led to it?

Changed to a new endo, who thought my story (and other measures, like lipids) matched closer to type 1 than type 2. I was skeptical, based on (relative) success of metformin and exercise, and recollection that (probably c-peptide) tests 11 years ago showed insulin production. But the test results, although grey (type 1.75? :-)) have provided some additional information to help explain things and motivate a change to a lower carb diet. After my next A1c I'll probably try cutting back some on the metformin to try to recalibrate the effect of it.

Warren.

[foxl]

Changed to a new endo, who thought my story (and other measures, like lipids) matched closer to type 1 than type 2. I was skeptical, based on (relative) success of metformin and exercise, and recollection that (probably c-peptide) tests 11 years ago showed insulin production. But the test results, although grey (type 1.75? :-)) have provided some additional information to help explain things and motivate a change to a lower carb diet. After my next A1c I'll probably try cutting back some on the metformin to try to recalibrate the effect of it.

Warren.

Cool! I really think I want to stay on met (but NOT actos!) and add insulin to save my betas -- but I am more like 1.5 than 1.75. I like what met does for my appetite and am pretty sure I have got SOME insulin resistance (I envision two lines crossing to culminate in DKA, on my graph), so am happy to find someone else who thinks in grays about this.

I am kind of looking forward to learning to use insulin ... at the same thinking that that is a bit weird. But I also know I will feel better, knowing I am resting my betas!

My lipid profile was not quite classic metabolic syndrome, either -- low HDL, high LDL, but my trigs have always been FINE. And my BP while not so hot recently, has been pretty normal, too. One reason I questioned striaght Type2 as a dx.

[Scratch]

The difference is the cause of the disease, although some Type 1's are not autoimmune; they can have surgical or medical destruction of beta cells. But Type 2 is primarily insulin resistance: the insulin is produced, even overproduced, but not usable by the body.

That's not accurate. The medical definition of type 1 is a disease of autoimmunity, where the immune system destroys the insulin producing beta cells. If the beta cells are lost for reasons other than that, it is a form of diabetes but not type 1.

[foxl]

That's not accurate. The medical definition of type 1 is a disease of autoimmunity, where the immune system destroys the insulin producing beta cells. If the beta cells are lost for reasons other than that, it is a form of diabetes but not type 1.

You are right, calling people with aninulinemia from other causes Type 1 is incurate, but it is common practice since people do not get it.

A friend whose husband had Type 2 for 20 yrs just asked me the difference between Type 1 and Type 2. Whaddya do??

[Scratch]

All of this makes me wonder....
Do type LADA'ers eventually loose ALL beta cell function?
Do type 1's have ANY beta cell function?


Even in long term type 1 diabetics, there is still evidence of small amounts of beta cell function. It generally seems that the later in life one develops autoimmunity, the more beta cell function that is retained. That is, type 1 diabetics who develop it near infancy will have the lowest levels of c-peptide and those who develop type 1 in their late teens will have greater amounts.

Since the autoimmune attack tends to be less strenuous in type 1.5s, generally there'll be even greater retention of residual beta cell function.

Some of this is due simply to the body attempting to regenerate its beta cell mass. It is that fact which gives hope that if a way is found to thwart the autoimmune attack, the person should likely be able to see a return of the beta cell function over time.

[lorilei]

wonderful...now if only the pancreas's would listen to these definitions...geesh!

[foxl]

wonderful...now if only the pancreas's would listen to these definitions...geesh!

You said it. I just want my MDs to know WHAT is happening, even if they diagree on what to call it, frankly. I did find a reference to surgically-induced type 1 in an Endo textbook, BTW, scratch. So not much point quibbling if the experts do not agree.
Just so we know whose definition we are operating under ...

[CountYourselfIn]

congrats...u can play left 4 dead...

Sweet as*.

Great game. ;)

[CountYourselfIn]

You must be in the weirdest headspace ever.

But then again, you're getitng to see what life is like for all diabetics, playing each of these lil roles. That's kinda neat, is it not?

If anyone challenges you, you can just slam that card down, and it'll be the end-all.

Congrats on getting to the bottom of it. It's not a big win, really, but knowing is exceptionally empowering, and you totally deserve that.

:o

[Scratch]

You said it. I just want my MDs to know WHAT is happening, even if they diagree on what to call it, frankly. I did find a reference to surgically-induced type 1 in an Endo textbook, BTW, scratch. So not much point quibbling if the experts do not agree.
Just so we know whose definition we are operating under ...
No problem. I know there'll always be some differences between how people define things. I suppose I just find that the autoimmunity feature of type 1 and 1.5 to be the most critical feature, from how it arises and to how it presents for diagnosis and how type 1 and 1.5s are both at greater risk of other autoimmune dysfunction. The cure for a disease of autoimmune origin will likely be much different from that of a cure for something that was surgically created.

[foxl]

No problem. I know there'll always be some differences between how people define things. I suppose I just find that the autoimmunity feature of type 1 and 1.5 to be the most critical feature, from how it arises and to how it presents for diagnosis and how type 1 and 1.5s are both at greater risk of other autoimmune dysfunction. The cure for a disease of autoimmune origin will likely be much different from that of a cure for something that was surgically created.


Cures, yes. Management in the meantime, pretty similar.

I do think approaching the disease from a pathophysiologic standpoint would be more constructive ... ;) (HAH -- take that, Endo consult!)