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Lada and Gliclazide

NCC1701

NCC1701

Member
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14
Hi, I've recently been diagnosed with Lada after a c peptide test. Originally diagnosed TE 28 years ago. Currently being treated with Metformin and Gliclazide.

Hba1c mid 40s. 40mg Gliclazide breakfast and dinner. Lost 4kg in 4 months. Levels go above 10 mmol/L for an hour or two. Sometimes up to over 12 mmol/L but i can usually do 10mins running to bring it down to under 10.

Early morning levels are about 6.0 and steadily climb. 'Dawn Effect'? I take 2 Metformin and 1 x 40mg Gliclazide. Little exercise but usually 15-18 g carbs with protein. Such as porridge with tbsp peanut butter. Lunch and dinner usually 6 or 7 pre prandial but it crashes to 4 sometimes 3.8 if I don't 'top-up' with an oatcake or two.

I try to have 40-60g carbs 9-10pm to beat a sharp down turn that always happens that time of night.

I now think this is the wrong thing to do and is causing overcompensation by the Gliclazide causing 'reactive hypoglycemia' ?

This means I need jelly babies to bring me back from 3.6mmol/l to 4.5 and then I can sleep through the night safely. Again waking to 5.9 mmol/l.

Tonight, I'll try having a 15g carb snack 8pm and a small carb supper 10pm before bed to see if helps stop the Gliclazide forcing my pancreas to make an exhausting effort to counteract the dinner carbs of 40-60g.

I take around 140-160 carbs a day.

Trying to up the protein to min 60g daily to also help smooth out any spikes and crashes.

My question is: should I even be on Gliclazide at all as it appears to be forcing my pancreas to work harder.

Healthcare team at hospital have said I'll need to go on insulin at some point but not said right you need to start it now.

They seem to be leaving it to me to mentally psych myself up to say I want to start it.

I've read early insulin therapy is good for LADA as gives the remaining beta cells a rest and so they may live longer.

Do you think:

I should ask to come off Gliclazide and see how I do with a SGLT 2 inhibitor like Dapagliflozin

I should bite the bullet and ask to start early insulin therapy before by beta cells are all gone.

Many thanks for reading.
 
Hey @NCC1701 my brother has LADA. He was diagnosed after losing a lot of weight, high ketones, very low C-Peptides, and positive auto antibodies. He was put on insulin immediately. I believe the current medical opinion aligns with starting insulin therapy early to help extend beta cells life, they will of course succumb, but preserving pancreas function for as long as possible.
 
There's another thing which they can perhaps do to delay things a little their is fairly strict criteria however may well be worth while asking about Teplizumab effects immune system which could help delay unsure exactly what current qualifying is.. I can tell if wish what the criteria was last year I believe it has changed slightly.. you would need weigh up risk Vs reward if it were offered after best wishes
 
Melgar said:
Hey @NCC1701 my brother has LADA. He was diagnosed after losing a lot of weight, high ketones, very low C-Peptides, and positive auto antibodies. He was put on insulin immediately. I believe the current medical opinion aligns with starting insulin therapy early to help extend beta cells life, they will of course succumb, but preserving pancreas function for as long as possible.
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Thanks Melgar. Appreciate this
 
For my own understanding.
Can you be LADA when you are still producing enough insulin from your pancreas to require a significant amount of carbohydrates?
My next step in medication is likely to be Gliclazide but I have had no suggestion (so far) of LADA.
 
That's what diabetic doctor told me is I have LADA. Not seen dietician yet but I've read stuff on university hospital Sussex web site and 150g is enough apparently. Unfortunately I panicked and went to under 100g and caused hypo with gluclazide. I'm now up to 150g cho daily and upping the protein and cals from low carb foods as I'm very honey and gaunt. Still awaiting dietician and to be told when to go on insulin. Hospital can see my libre2 results.
 
LittleGreyCat said:
For my own understanding.
Can you be LADA when you are still producing enough insulin from your pancreas to require a significant amount of carbohydrates?
Click to expand...
I don't understand your question.
Non diabetics produce insulin to match their needs, they do not need carbs because they are producing insulin.

Going hypo unmedicated can happen in early lada (but also in early T2) but is pretty uncommon as far as I know.
 
I was put on gliclazide and it wasn't quite working so was put on dapagliflozin. I was on it for about 4 months and got progressively thinner, dizzier and sicker. Was producing ketones and felt like death. They took me off it and put me on a very small dose of insulin. That was a year ago and I feel so much healthier. I'm still on very low doses but I personally had a horrendous experience on dapagliflozin.
 
Antje77 said:
I don't understand your question.
Non diabetics produce insulin to match their needs, they do not need carbs because they are producing insulin.

Going hypo unmedicated can happen in early lada (but also in early T2) but is pretty uncommon as far as I know.
Click to expand...
As I understand it LADA is (more or less) delayed onset T1.
Although checking on line now there is still a lot of confusion.
Is the main diagnostic of LADA the presence of antibodies, indicating that the immune system is in the process of destroying Beta cells?

My confusion is over the level of insulin production.
If Gliclazide can stimulate the pancreas to over produce insulin, such that hypos are a major risk, how badly damaged is the pancreas?

From my ongoing T2 I suspect that the control mechanisms are shot.
For example, I can produce enough insulin to bring levels down to (or below) normal but that doesn't always seem to kick in.

I am also wondering at what point someone with a T2 diagnosis should be tested for LADA.
Or is the view that the treatment is the same, so why test?
 
It’s primarily the presence of auto antibodies @LittleGreyCat . Yes, low C-Peptides is a strong indicator, but the presence of the known T1 antibodies is a core requirement. I believe it is the same with most if not all autoimmune disorders, unless the person is seronegative. Seronegative is recognized by the medical community but only if there are obvious signs of T1, like extremely low C-Peptides < 100 pmols.

The immune distruction will continue until there are no beta cells left - no insulin is produced. Once this happens then the body will not produce autoantibodies.
 
Melgar said:
Have you done a non-fasting C-Peptide test @LittleGreyCat ?
Click to expand...
I did a private HOMAR-IR test a good few years back which showed some insulin resistance.
Insulin level lower part of normal, but BG still elevated.
Therefore some insulin resistance.

I have never had any antibody tests.
 
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