Oral medication v injections for LADA?

[CliffH]

I am amazed that you can be eating such a high carbohydrate diet and yet needing so little insulin. It doesn't sound as if you are counting your carbs to adjust your insulin dose. I wonder if you are actually diabetic at all.
Some others may have more idea though.

Lol: perhaps I've got 'phantom diabetes'! I do count my carbs to an extent - although tbh after eight years I've got a pretty good idea of how much insulin I need for any given meal. Crucially, though, the amount of cycling that I do has a very direct and significant impact on the amount of insulin I need - regardless of what I eat. I haven't been cycling since last Friday and this evening for dinner I had steak pie with boiled potatoes and vegetables. I took 8 units of NovaRapid before dinner. It was clearly a slight underestimate of what I needed though: my blood sugar was 5.3 before dinner and I've gone up to 8.1 now. I'm not worried though: I know that it will come down by itself overnight to just over 5 by the morning.

 

[CliffH]

No, I am not on insulin, according to UKPDS two out of three older patients with a diagnosis of LADA will not need insulin within 6 years.

Metformin increases GLP-1 secretion (which means it is effective in LADA), but unfortunately it also does this:

View attachment 31502

Unfortunately it's many years since I studied Maths 'A' Level and so I'll need to ask if you can interpret those data for me! Thanks very much.

 

[Inka]

Going up to 8.1 sounds fine @CliffH and not an underestimate 🙂 Have you never taken basal insulin?

 

[CliffH]

Going up to 8.1 sounds fine @CliffH and not an underestimate 🙂 Have you never taken basal insulin?

I meant that usually I can gauge it so that I wouldn't go up to more than 6 or 7 post-dinner. However, lately I'm being more conservative than I used to be with my insulin, as I've been dipping below 4 more often. I used to take Lantus every day but I hardly ever take it now: my Consultant advised me to stick to NovaRapid given how much of a pain it usually is keeping myself above a blood sugar level of 4 if I take Lantus - unless I've been doing no cycling for a few weeks and have been eating out a lot!

 

[CliffH]

Going up to 8.1 sounds fine @CliffH and not an underestimate 🙂 Have you never taken basal insulin?

False alarm: I'm back down to 6.1 already 🙄

 

[Robin]

@Robin - you had somehow grabbed a ‘post’ link. For the start of the thread you would need to grab the thread web address from your browser, and then remove the numbers after the # (which is an ‘anchor’ directing the browser to a specific post on the page). I accept this is probably gibberish to most people

Oh, that’s how you do it! Thanks, Mike, I’ve tidied up my post.

 

[Inka]

I think I know what you meant @CliffH 🙂 I was just saying that being at 8.1 after a meal is good. The aim is to be back in range by the next meal, ie between 4 and 7. As you say, aiming too low can just lead to nuisance hypos, which are never great but particularly annoying in the evening and night, I find.

To my mind, I’d consider your ‘base’ as what you need when you’re not cycling. I remember I did a hike, suffered a pump incident and ended up only taking a tiny amount of insulin that day, presumably helped by my hours of strenuous activity, but I don’t consider that as my baseline. Apart from normal walking about, shopping and so on, I see exercise as a separate thing that affects my diabetes and if someone asked me my doses, I’d ignore exercise, illness, etc and give my normal doses without any ‘add-ons’ from things that affect it.

That sounded very long-winded and clumsy but I hope it made some sense!

You’re back to 6.1? Do you know roughly how many carbs were in your meal?

 

[CliffH]

Well currently I'm building my cycling back up, now that I'm semi-retired. Annoyingly, given my age, I have to have complete days off the bike too, as 'recovery' days. So, it's difficult to know exactly what my current 'base' is, as it's changing. I do know that I need significantly less insulin than when I was diagnosed - even when I'm not cycling.

I'd guess that there were more carbs in my dinner this evening than the human mind can possibly imagine. Three-quarters of a steak pie and lots of boiled potatoes 😱. However, I find that I need less insulin for potatoes (and pastry) than for pasta, interestingly.

 

[Inka]

My mind can imagine lots of carbs @CliffH ! Especially of the cake, chocolate and cheesecake variety! I was just wondering as I wondered how many carbs your 8 units was covering and whether it was a little too much insulin for the carbs maybe.

I took less insulin than when I was diagnosed for a long time (honeymoon period, as they call it). Then that gradually increased a bit and now seems to have gone down again, which I presume is hormone related - or just diabetes being its usual tricky self!

 

[CliffH]

When I was first diagnosed I had the 'Carbs and cals' book and app but I stopped referring to them once I learnt how much insulin I needed for most meals - and I don't remember how to calculate it now. Luckily I don't have a particularly sweet tooth: just like Boris Johnson, though, cheese is my danger food

 

[Inka]

Lots of carbs are on the packaging of stuff like sliced bread, cereal, pasta, pies, yoghurts, biscuits, etc. I’ve had Type 1 30 years so know lots of non-packaged foods from memory. Potatoes I do by eye if I’m having little boiled ones like I did tonight. At diagnosis I was told that 10g carbs of potato was a potato (or bits of potato) the size of an egg, so I peer at my little potatoes and count the ‘eggs’.

I have some meals where I do like you - have the same things and same amounts and just know how much insulin works, but carb counting is useful if you eat something different from your usual fare as you can then have a pretty good stab at the carb amount and inject the appropriate amount of insulin.

 

[CliffH]

Yes, I find eating out a minefield. Last Friday I went to an Italian restaurant and had lasagne, as I usually do. I don't usually bother with dessert but my mother was having the home-made tiramisu and so I had to have it too, to avoid her being the only person having dessert

 

[Bubbleblower]

I can’t find a reference to a majority of people with LADA in UKPDS coming off insulin.

Who talks about that reference, you change my words.

Here is the reference I was talking about:

"The UKPDS, it will be remembered, randomised patients to insulin or sulfonylurea at diagnosis, and in so doing set up the conditions for a controlled trial of early therapy for LADA. The study confirmed that patients with a diagnosis of LADA are more likely to progress to insulin, but it also showed that after 10 years, or indeed at any point in between, those initially randomised to diet or sulfonylurea therapy did not differ in any respect from those initially randomised to insulin [21]. On present evidence, therefore, two out of three older patients with a diagnosis of LADA will not need insulin within 6 years"

And I got plenty more studies finding the same, for example
High GADA titer increases the risk of insulin requirement in LADA patients: a 7-year follow-up (NIRAD study 7)
(NIRAD = non insulin dependant autoimmune disease)

"Results: During the follow-up, the drop out was 4% in both groups. A total of 119 (56.1%) out of 212 LADA patients required insulin during the 7 years of follow-up."

In other words after 7 years 44% of LADA patients did not need insulin yet. Both results are from large studies.

ALSO THERE IS ZERO PROOF INSULIN THERAPY PRESERVES BETA CELLS, (on the contrary)
I challenge you to come up with any real evidence it does.

 

[everydayupsanddowns]

Here is the reference I was talking about:

Thanks. I was able to get the link (2005) from the text you posted, I think.

Latent autoimmune diabetes in adults: a guide for the perplexed - Diabetologia

link.springer.com

Unfortunately the other link you posted seems to have a security glitch, and my browser advised against following it.

ALSO THERE IS ZERO PROOF INSULIN THERAPY PRESERVES BETA CELLS,

Yes, that was also in the study I found. Although as I understand it UKPDS showed that starting insulin early did not slow down autoimmune destruction of beta cells in LADA vs oral meds, but the progression to insulin in LADA is generally faster than classic T2.

I found this very interesting from the editorial/commentary you posted

Does LADA exist?​

Is LADA a distinct disease entity or one end of a spectrum of immune-mediated diabetes? Given that it is logically impossible to distinguish between two conditions when one (LADA) is defined solely by the characteristics it shares with the other (type 1 diabetes), this easily becomes an exercise in semantics. There is currently no reason to assume that the underlying aetiology is any different. A simple example may help. Jack Spratt is a lean middle-aged jogger and Humphrey Dumpty is his indolent overweight neighbour. Both suffer from progressive beta cell failure and have high levels of GAD antibodies. Jack Spratt is lean and insulin-sensitive, so his blood glucose does not begin to rise until he approaches end-stage beta cell failure. He needs insulin straight away. Humphrey Dumpty, in contrast, is relatively insulin-resistant. He can still make useful amounts of insulin when diabetes is detected. He goes on a diet, enrols at a gym, and starts treatment with an insulin secretagogue, an insulin sensitiser, or both. This corrects the short-term imbalance between insulin secretion and sensitivity and a year or more will pass before he too requires insulin. Jack is considered to have late-onset type 1 diabetes, whereas Humphrey will be said to have LADA, but they differ only in sensitivity to insulin, and the underlying process of beta cell failure is exactly the same. At our present level of understanding, it makes more sense to regard autoimmune diabetes as a continuum, and to devote less time and energy to drawing artificial distinctions between its various manifestations.​

And the summary

In summary, the grounds for designating LADA as a distinct aetiological entity are insubstantial, its epidemiology is plagued by methodological problems, and the clinical value of diagnosing it has not been demonstrated.​

Which backs up the general feedback from members that many Drs in the period since this was written have moved away from using the term LADA, and no longer find it helpful.

I guess the sharp end, at least in the UK, is really that a diagnosis with T1 (of which LADA when used is generally seen to be a subset) gives you access to various course, and types of therapy like insulin pump, that you can’t get access to if you have T2.