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Does pre-LADA exist?

Glink

Well-Known Member
Were any of you diagnosed with prediabetes that eventually was diagnosed as LADA?

I'm a thin, fit, prediabetic with no family history of diabetes, but some family history of autoimmune stuff and possibly other autoimmune stuff going on myself. My doctors won't do GAD testing at this "pre" level because they feel it would not affect treatment.

When I was diagnosed I immediately dropped to a very low carb diet, which worked wonders at first and then slowly got less effective. After about 6 mos I was put on metformin, and then a higher dose of metformin. It seems to be helping (in conjunction with LCHF diet) for the past few months, bit I'm not really able to relax about my sugars because I'm worried things will continue to deteriorate.

If anyone has any advice on this, I'd love to hear it. My understanding is that if LADA is an option, metformin is really the only oral I should take, and that if it's LADA it will eventually deteriorate to cross into full diabetes. But, if it's just atypical pre-T2 then I could take other orals if things get worse--not sure how I would know which type it was, though, without GAD testing.

Thanks for any insight you can offer! I'd love to be less concerned about this.
 
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Glink said:
But, if it's just atypical pre-T2 then I could take other orals if things get worse--not sure how I would know, though, without testing.
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Well my first thought on this statement is get a meter and start testing. You can get a meter from home-health-uk.com; the complete kit is about £12 and the strips are about £7/50 strips

I am surprised if you are pre-diabetic that the doctor has prescribed metformin. I didn't think it was licensed for pre-D (wonder if the license has changed)

Have you considered paying for your own GAD test if the doctor will not do it? Not sure of the cost but can't believe it is that costly.

Oh and BTW Steve Redgrave was slim fit and became T2! T2 seems to be a bucket categorisation for "well sugars are high but we do not have a clue and can't be bothered to investigate further to work out the cause"
 
I was diagnosed as Type 2... Almost 12 years before being confirmed as LADA/ type 1. I've been 'honeymooning' this whole time.

Plenty of times, I have dipped into pre diabetic or even non diabetic status. My last A1C was 5.6 and that was before any insulin, just Metformin and diet and exercise controlled.

For me LADA is the weirdest possible type of diabetes, just because my circumstances. I can't make any sense of it.
 
Don't know about pre-d. I had gestational d, for the all clear after delivery, told to have annual check in case of type 2 once I hit 40. Again showing all clear. Then at 43 suddenly type 1. Mid way through a test cycle so sugars normal 6 months before then suddenly hbac1 of 79.
 
Sorry- I've edited my original post to indicate that I do have a metre and have been testing some (although I think if I want to keep this up I may need to pay for strips out of pocket soon). I tested a lot at first, then stopped for a while because there seemed to be nothing I could do about bad #s so it was just stressing me out. I go back to the doctor in a month, so I tested again yesterday and today to see how the increased metformin was working...still prediabetes, it seems.

I'm not sure if my metformin prescription is off label or not. They gave it to me as my #s were slowly creeping up even though I have literally zero risk factors (in my 30s, no history of gestational diabetes, etc.), was already biking and weight lifting (no reasonable way to increase exercise), and went from regular-thin to quite thin on a very strict low carb (but not low calorie) diet. Since nothing else was working and I was starting to have diabetic-level fasting #s on my home test, and my A1C was creeping up too, my GP said we'd try some medication. I think it has helped, especially with the fasting #s, which I just could not budge any other way. But nothing has been able to "reverse" things, and I have a lingering concern that this is not the full story. FWIW, I had tons of classic diabetes symptoms when diagnosed (ploydipsia, polyuria, swelling feet and hands, blurred vision, moods), which return if my sugars get high, and I've had some diabetes associated conditions (frozen shoulder, foot numbness) in the past year as well.

Guess I'm just not sure what, if anything, I should be doing/monitoring differently given that LADA has been raised as a definite possibility for what's going on with me.
 
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@Glink
polydipsia, polyuria, swelling feet and hands, blurred vision, moods), which return if my sugars get high, and I've had some diabetes associated conditions (frozen shoulder, foot numbness)
I had all these symptoms before diagnosis and I have all the type 1 diabetic antibodies. You should definetely have a bloodtest for all type one antibodies done
 
Hi @Glink .

You should press for the GAD and C-peptide tests. If you are LADA, you should be put on insulin rather than Metformin. In the meantime, low-carbing can help.
 
Well, I will bring up GAD testing again. However, my GP says he won't (can't?) order the GAD test and my endo sent me back to my GP until my #s get worse, so I'm not super optimistic. I did have a c-peptide last fall and the lab report said the results were normal (619 pmol/L, fasting 11 hr, with glucose at 5.9 mmol/L).

It's just kind of discouraging. I am eating quite strict low carb and still getting symptoms no one can explain. But, the strict diet is keeping the #s low enough that no one is terribly worried--except me, since I'm concerned the other shoe will be dropping at some point. I'm due for my 1-year review in a month, so I suppose I will see updated #s then. Hopefully the metformin will be helping, as if it's not I think my GP will want to add in other oral meds and I understand they are contraindicated if it does turn out to be lada. I just wish I had a clear diagnosis and plan of action...feels like I'm just flailing around out here in prediabetes land where none of the usual prediabetes advice actually makes a difference to my sugars and quality of life. :/
 
I lost a lot of weight initially--maybe 30-35 lbs, which on me is a lot--but that seems to have slowed this spring. Most of that was suddenly and bizarrely gained out of nowhere over a few short months right before it disappeared again and took some extra with it. For me--someone who has been the same (thin) size since age 13--this was all quite startling. I'm now thinner than I have been in years (since I was sick with something else about 10 yrs ago). I have had to be stricter and stricter on carbs to keep BS good, yes, and fasting never got better, just a little worse, until the metformin which I think has helped fasting #s. Also things like the thirst, blurry vision, waking to urinate, fatigue, come back when my sugars are higher (but to be clear, they're never super high, like over 11). I've also had a mysterious foot numbness the past couple months out of the blue. I'm sure I'm still making insulin now or I'd be much sicker, but things just aren't adding up and the usual prediabetes control measures aren't fixing things. I'd like to be more proactive somehow, but I'm not sure how and my doctor is not that much help.
 
I too would insist on a GAD. LADA is slow onset type 1. Loosing weight, backing down meals , lowering carbs and bs not getting better are all signs. Type 2 meds won't help. You need to see where your antibodies are at. Not just a c peptide.

Funny you mention it getting worse since being sick 10 years ago. I think mine accelerated after a nasty virus. Took about 6 years to be full blown type 1.
 
The virus thing is interesting. I first started feeling bad in the way that I now understand to be high blood sugar after I got mono a couple years ago. But my endocrinologist dismissed this connection as coincidental when I mentioned it. I also started to get other odd vaguely autoimmune seeming things like recurrent low fevers with joint swelling and hair loss after the mono--but nothing ever came of pursuing that and it seems to happen less frequently now.
(The thing 10 yrs ago that caused me to get skinny turned out to be an adult-onset horrific multiple-allergy situation, which really did a number on my lungs among other things.)
 

There are a few people with LADA that oral medication can help. if you're someone that doesn't produce enough insulin and is insulin resistant - well then you've hit the genetic jackpot.
 
The possibilities include LADA and one of the "MODY's". Don't expect doctors to know a lot about either of these categories. MODY 3 and MODY 1 can be dormant until middle age, and they can lead to the usual diabetic complications. It is common for people with MODY's to be misclassified as Type 1. One of the key differences between them and Type 1 is that with them, significant insulin producing capacity persists, even if it's not enough. That is what MODY's and LADA (at least early LADA) have in common.

As for GADA testing, there are 4 more autoantibodies relevant to LADA.

In three studies on LADA published since 2011 (Venn diagrams included), people were tested for multiple beta cell autoAb's. Most people with one or more Ab's have just one. Based on the studies, you probably should request to be tested for the trio of GADA, ZnT8A, and IA-2A. (The final A's stand for 'autoantibody'.) GADA is by far the most prevalent, but in the Argentine study, GADA prevalence was under 60%, and ZnT8A was almost as frequent as GADA. ZnT8 was discovered less than 10 years ago.

Older research always cited 'ICA', "islet cell autoantibodies" (always in the plural). The research is usually vague as to what these are, and they may just be "Ab's other than GADA".

As for MODY's, see diabetesgenes.org and diapedia.org. Almost everyone with a MODY has MODY 3 (HNF1A gene) or MODY 1 (HNF4A gene). (MODY 2 doesn't lead to diabetes.)
 

This is strange to hear, although I don't know it to be incorrect. The one thing metformin does not do for diabetes is to stimulate insulin secretion or production. It has an impressively long list of beneficial effects, but most of them are mild, and essentially, it is appropriate for insulin resistance (Type 2) diabetes.

The progression and severity of LADA depends partly on how many autoantibodies the patient is positive for.

It's relatively easy to tell if you have T2. T2 is in theory a matter of progressing insulin resistance. Evidence for IR is its complications and having high fasting insulin. T2 is a progressive condition, from normal to prediab to diab. You would want to keep taking measurements of these four things to establish that the progression is happening. The common complications are higher blood pressure, higher triglycerides, and lower HDL.
 

There's too many unknowns about how Metformin works exactly to make a blanket statement like that. I've been reading a lot of research that it doesn't actually help IR, but more controls the dumping effects of the liver, which is thought to be increased in T2 diabetics. So there's a lot of different view points on it.

I've been on Metformin for a year now, and I thought it was due to insulin resistance. I finally asked at my last appt why I was on it, and I come to find out that my endo puts a lot of her LADA patients on it, because she feels whatver insulin we (honeymooners) are producing our bodies become just that much more sensitive to it. 'Making the most' of whatver is left.
 
sud5nala said:
This is strange to hear, although I don't know it to be incorrect. The one thing metformin does not do for diabetes is to stimulate insulin secretion or production.
Click to expand...

I think the reason for @Glink 's statement that a LADA shouldn't be taking other oral diabetic medications (other than metformin)'is because those that do stimulate insulin production are thought to more quickly exhaust residual beta cell function and end the honeymoon which many LADAs/1.5s are trying to extend.
 
Thanks, catapillar, for that explanation.

Speaking of the response to the insulin secretagogue medications, I am aware of the news that they are known to "burn out" the beta cells in the long run. Among monogenic diabeteses, the most frequent variety by far is the one involving the HNF1A gene. This syndrome is known as "MODY 3". I learned that one of its key features is "hypersensitivity" (meaning hyperresponsiveness) to the sulphonylureas (SU), the best known category of secretagogues. Does the hyperresponsiveness mean that those patients could avoid the burnout phenomenon; or does it mean that at least they could remain not insulin dependent for a long time? There has probably been no research on these questions as the study of the MODY's is in its infancy.

There are two bigger objections to raise to the concern over beta cell burnout. First, a key feature of both MODY 3 and MODY 1 is that the beta cells can still produce insulin, they just can't deliver it. Maybe the beta cells of these patients are not in danger of burning out from medication. Second, we have available two non-SU secretagogues, whose category name is 'meglitinide'. Are MODY 3 patients also hyperresponsive to the meglitinides?

The biggest clinical impact of testing positive for MODY 3 or MODY 1 is that you can give up insulin. People who were found to have MODY after living for years with the T1 diagnosis have written of their joy in being rid of daily injecting.

In one published study of people diagnosed with either T1 or T2, half of the supposed T1's, and 1/11 of the supposed T2's, turned out to have the HNF1A mutation, which means they had been misdiagnosed with the T1 or the T2. If -- if -- the study population is not too statistically unrepresentative of all people with a diabetes diagnosis, then MODY 3 is more frequent than T1, and at least 10 times more frequent than currently supposed .
 
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