Stubborn and inquisitive

[Bubbleblower]

Hello, I am 57 years young from Amsterdam.

I was diagnosed June last year, first with T2D and later after an antibodies test with LADA.
All my live I used to be very active and in 1997 my HbA1c was 5.4%.
But then unfortunately I found out I was good at poker, which also means sitting for many hours straight without breaks. One day I suddenly had to walk a distance and discovered I couldn't anymore because of claudication. When I saw the doctor for that she also had my blood checked and my HbA1c turned out to be 14.3%.

In a way I am lucky, because at least I know what caused my diabetes. Recently diagnosed I am still in the optimistic stage; I am convinced diabetes is a certain genetic expression, in my case triggered most of all by a lack of exercise as well as a SAD diet. My bloodsugar goes through the roof every morning and I suspect former betacells are now producing glucagon. I need to switch that off and switch another expression on so they produce insulin again.

Doctors, who have to follow guidelines pretty much determined by the pharmaceutical- and food industry, say I will inevitably need insulin, while scientists who aren't paid by these industries showed they can halt the progression of new-onset type 1 diabetes. I read tons of research papers and experiment a lot to figure out how exactly and also look for advice on this excellent forum, I have a million questions.

 

[LittleGreyCat]

I suspect former beta cells are now producing glucagon

I would be interested in any research papers which describe this.
My understanding of T1 was that your own immune system destroyed your Beta cells, and your ability to produce insulin.

https://www.diabetes.co.uk/body/glucagon.html
This describes glucagon as being produced by the Alpha cells, not the Beta cells (repurposed or otherwise).

I did hear a very interesting talk at a diabetes conference a couple of years back where researches had discovered Beta cells in T1s which seemed to be masquerading as Alpha cells to avoid the immune system and then reverting to Beta cells. Described as guerrilla Beta cells. I wonder if you are thinking of this?

 

[VashtiB]

Hello and welcome,

I don't really know anything about LADA but there are people here that do. It is always great when someone is willing to spend some time researching things. It is one (of many) of the strengths of this site. I have certainly benefited from other people's research. So you are very welcome.

 

[EllieM]

In a way I am lucky, because at least I know what caused my diabetes. Recently diagnosed I am still in the optimistic stage; I am convinced diabetes is a certain genetic expression, in my case triggered most of all by a lack of exercise as well as a SAD diet. My bloodsugar goes through the roof every morning and I suspect former betacells are now producing glucagon. I need to switch that off and switch another expression on so they produce insulin again.

Welcome to the forums.

I've heard of some LADA folk who manage to preserve their dwindling beta cells for a decade (or more) with a low carb diet, but my understanding has always been that T2 is the genetic diabetes, while T1, though some genetics can play a part, is more of a mystery in that it's caused by an autoimmune reaction which kills off your beta cells and no one really knows what triggers that reaction (I was told it could be a virus, a sudden shock or accident, ie they really don't know).

As for your morning spike in blood sugar, it's pretty normal to need a bit more insulin then, as the dawn phenomena happens to both T1 and T2 diabetics. If your body isn't able to produce that insulin then your bg goes up.

But I wouldn't be afraid of insulin. A small amount might be able to smooth over any spikes and keep your beta cells working for longer (supposedly they don't like high blood sugars). Insulin is an incredible life saver for T1s. 100 years ago, T1 was a death sentence.

But anyway, I will be very interested if you decide to share your research on these forums. Good luck.

ps Tagging @Daibell @Antje77 and @searley who are frequent posters who know more about LADA than me.

 

[Antje77]

ps Tagging @Daibell @Antje77 and @searley who are frequent posters who know more about LADA than me.

I tend to follow science, which so far says LADA is Latent Autoimmune Diabetes in Adults.
Latent because it can take a while, sometimes a long while before needing insulin, Autoimmune because the aito-immune system attacks beta cells, Diabetes and Adults speak for themselves.
This means I'm convinced LADA is not triggered by lack of exercise or a SAD diet, instead I'm convinced we do not know at the moment what cause or causes there are.
My blood sugars rise in the morning as well (for which I take insulin) but I'm more mainstream in thinking this is my helpful liver dumping glucose to get me going for the day, not former betacells going rogue.

So thanks for the tag, @EllieM , but for now I think my thinking and the OP's are so far apart I can't bring anything useful to this thread. We do share our birth city though, which is cool!
Wish you all the best, @Bubbleblower , and I hope you'll find what you're looking for!

 

[searley]

I tend to follow science, which so far says LADA is Latent Autoimmune Diabetes in Adults.
Latent because it can take a while, sometimes a long while before needing insulin, Autoimmune because the aito-immune system attacks beta cells, Diabetes and Adults speak for themselves.
This means I'm convinced LADA is not triggered by lack of exercise or a SAD diet, instead I'm convinced we do not know at the moment what cause or causes there are.
My blood sugars rise in the morning as well (for which I take insulin) but I'm more mainstream in thinking this is my helpful liver dumping glucose to get me going for the day, not former betacells going rogue.

So thanks for the tag, @EllieM , but for now I think my thinking and the OP's are so far apart I can't bring anything useful to this thread. We do share our birth city though, which is cool!
Wish you all the best, @Bubbleblower , and I hope you'll find what you're looking for!

I pretty much mirror this post on my beliefs..

Yes I get I rise in the morning I’ve always considered it my body getting ready for my day.. what cements this feeling is I used to get up 0730 every day so my rise would start at 0645 ish

I now get up 0345 every day and my bg starts to rise about 0300.

To be fair though I won’t dispute anything said as little is know about LADA it’s a fairly recent and rarer classification.

And there may still be other unknown types.. and everyone is different etc etc..

But mine certainly wasn’t poor diet. Overweight or poor lifestyle

I do however have a strong family history of T1

 

[Bubbleblower]

I would be interested in any research papers which describe this.

My understanding of T1 was that your own immune system destroyed your Beta cells, and your ability to produce insulin.

(I can't link yet)

This describes glucagon as being produced by the Alpha cells, not the Beta cells (repurposed or otherwise).

Look for "β-cell dedifferentiation", you'll find a lot of papers.
From what I understand beta cells can turn back into progenitor cells and then into alpha cells.

Hello and welcome,

I don't really know anything about LADA but there are people here that do. It is always great when someone is willing to spend some time researching things. It is one (of many) of the strengths of this site. I have certainly benefited from other people's research. So you are very welcome.

Thanks

I've heard of some LADA folk who manage to preserve their dwindling beta cells for a decade (or more) with a low carb diet, but my understanding has always been that T2 is the genetic diabetes, while T1, though some genetics can play a part, is more of a mystery in that it's caused by an autoimmune reaction which kills off your beta cells and no one really knows what triggers that reaction (I was told it could be a virus, a sudden shock or accident, ie they really don't know).

The more I read about it the less clear the differences are to me, diabetes seems an umbrella term for many diseases we don't understand. It's hopefull there is a lot of research and anecdotal evidence on preserving and regenerating beta cells in both T1 and T2 diabetics.

I tend to follow science, which so far says LADA is Latent Autoimmune Diabetes in Adults.

Latent because it can take a while, sometimes a long while before needing insulin, Autoimmune because the aito-immune system attacks beta cells, Diabetes and Adults speak for themselves.

This means I'm convinced LADA is not triggered by lack of exercise or a SAD diet, instead I'm convinced we do not know at the moment what cause or causes there are.

Ok, but at least we know lack of exercise can cause diabetes, I just assumed so does a SAD diet.
Come to think of it; if it did I should have diabetes much earlier, so you are right it didn't.

And there may still be other unknown types.. and everyone is different etc etc..

Exactly.

 

[VashtiB]

You say we know lack of exercise cause diabetes. Do you have any references for that? In my case I exercise most days for a least an hour and have done so before I had diabetes so I am interested in that.

 

[LittleGreyCat]

Look for "β-cell dedifferentiation", you'll find a lot of papers

Thanks - interesting.

Only read one paper so far but it seems to describe the Beta cells changing to avoid immunosuppression.
Which may be aligned with the "guerrilla Beta cells" I heard described.
I haven't found anything yet (will work through some more) which suggests that they become active Alpha cells secreting Glucagon.

Noting that if the control mechanisms are working, extra Alpha cells should not result in more Glucagon and raised BG.
Also noting that damaged control mechanisms seem to cover a lot of the metabolic pathways associated with BG regulation.

 

[Bubbleblower]

You say we know lack of exercise cause diabetes. Do you have any references for that? In my case I exercise most days for a least an hour and have done so before I had diabetes so I am interested in that.

Same here, I found my bloodsugar goes back up if I exercise any less. Here are two studies that specifically looked at the effect of not exercising (I can't link them yet).

"Effects of exercise and lack of exercise on glucose tolerance and insulin sensitivity", which says:

"The blunted insulinresponse to a glucose load is lost rapidly, before significant changes in TO, max and body fat content occur, when physically trained individuals stop exercising. There is a concomitant decline in insulin binding to monocytes and a decrease in sensitivity to insulin, which was reflected in our subjects by higher glucose levels despite much higher plasma insulin concentrations following a glucose load"*.

And:

“Effects of exercise and lack of exercise on insulin sensitivity and responsiveness”, which says:

* "The plasma insulin response to an oral glucose load was more than twofold higher after 10 days without exercise than when the subjects were exercising regularly".

I haven't found anything yet (will work through some more) which suggests that they become active Alpha cells secreting Glucagon.


Noting that if the control mechanisms are working, extra Alpha cells should not result in more Glucagon and raised BG.

Also noting that damaged control mechanisms seem to cover a lot of the metabolic pathways associated with BG regulation.

In many or may be all cases the control mechanisms aren't working properly. You'll find this study interesting:

"Role of transcription factors in the transdifferentiation of pancreatic islet cells":

“β-to-α as well as α-to-β transdifferentiation can take place under certain experimental circumstances”.

“While diabetes is traditionally cast as a disease of relative (type 2) or absolute (type 1) insufficiency in β cell mass, it is less appreciated that hyperglucagonemia secondary to the loss of the normal inhibitory tone on α cells from β cells contributes to the etiology of diabetes by aggravating hyperglycemia“.

This one is less interesting:

"Iterations in Beta Cell Identity in Type 1 and Type 2 Diabetes", but it says:

“altered identity of mature β cells in diabetes also involves transdifferentiation of β cells into other islet hormone producing cells. For example, overexpression of α cell specific transcription factor Arx or ablation of Pdx1 resulted in an increase of α cell numbers and a decrease in β cell numbers in rodents”.

I have a ton of research on both these topics, but unfortunately not that well organised, so it could take me forever to find a specific study.

LADA is Latent Autoimmune Diabetes in Adults. .

I still have one question if you dont mind; how do you (or does one) know you have LADA?


Edited to fix the layout and to insert the links.

 

[Antje77]

I still have one question if you dont mind; how do you (or does one) know you have LADA?

Antibodies show your diabetes is an autoimmune condition and thus type 1 (or LADA, which falls under the T1 umbrella), although antibodies are not always found in people who are clearly T1 or LADA, a C-peptide test can show you how much, if any, insulin you are still producing.
High insulin production = T2, low insulin production = T1 (or possibly very long standing T2), normal = inconclusive.
Of course this is a simplification leaving out things like gestational diabetes, the various faces of MODY, type 3C and steroid induced diabetes, MIDD, and the recent influx of diabetics after covid of which it isn't clear if they fit in the existing types or if they have a new type altogether.

Edit: and also how do I get control over the lay-out?

Not a clue, I'm close to a complete idiot when it comes to IT.

 

[LittleGreyCat]

(I can't link them yet)

Nothing to stop you typing in the link longhand.
This will not provide a clickable link but will allow others to see the URL and to copy/paste if they wish.

 

[KK123]

Same here, I found my bloodsugar goes back up if I exercise any less. Here are two studies that specifically looked at the effect of not exercising (I can't link them yet).

"Effects of exercise and lack of exercise on glucose tolerance and insulin sensitivity", which says:

"The blunted insulinresponse to a glucose load is lost rapidly, before significant changes in TO, max and body fat content occur, when physically trained individuals stop exercising. There is a concomitant decline in insulin binding to monocytes and a decrease in sensitivity to insulin, which was reflected in our subjects by higher glucose levels despite much higher plasma insulin concentrations following a glucose load"*.

And:

“Effects of exercise and lack of exercise on insulin sensitivity and responsiveness”, which says:

* "The plasma insulin response to an oral glucose load was more than twofold higher after 10 days without exercise than when the subjects were exercising regularly".



In many or may be all cases the control mechanisms aren't working properly. You'll find this study interesting:

"Role of transcription factors in the transdifferentiation of pancreatic islet cells":

“β-to-α as well as α-to-β transdifferentiation can take place under certain experimental circumstances”.

“While diabetes is traditionally cast as a disease of relative (type 2) or absolute (type 1) insufficiency in β cell mass, it is less appreciated that hyperglucagonemia secondary to the loss of the normal inhibitory tone on α cells from β cells contributes to the etiology of diabetes by aggravating hyperglycemia“.

This one is less interesting:

"Iterations in Beta Cell Identity in Type 1 and Type 2 Diabetes", but it says:

“altered identity of mature β cells in diabetes also involves transdifferentiation of β cells into other islet hormone producing cells. For example, overexpression of α cell specific transcription factor Arx or ablation of Pdx1 resulted in an increase of α cell numbers and a decrease in β cell numbers in rodents”.

I have a ton of research on both these topics, but unfortunately not that well organised, so it could take me forever to find a specific study.



I still have one question if you dont mind; how do you (or does one) know you have LADA?


Edited to fix the layout.

I think we all know exercise (or a lack of it) can affect glucose levels but that still does not mean that it's CAUSING it.

 

[NicoleC1971]

I would be interested in any research papers which describe this.
My understanding of T1 was that your own immune system destroyed your Beta cells, and your ability to produce insulin.

https://www.diabetes.co.uk/body/glucagon.html
This describes glucagon as being produced by the Alpha cells, not the Beta cells (repurposed or otherwise).

I did hear a very interesting talk at a diabetes conference a couple of years back where researches had discovered Beta cells in T1s which seemed to be masquerading as Alpha cells to avoid the immune system and then reverting to Beta cells. Described as guerrilla Beta cells. I wonder if you are thinking of this?

Not sure what the OP was thinking of but fundamentally with a high hba1c this is surely caused by glucagon doing it's normal thing (stimulating the liver to produce glucose to keep the brain supplied) versus ever decreasing functional beta cells given the very high hba1c they are experiencing? I think those guerillas have forgotten which side they are on.

 

[Bubbleblower]

Of course this is a simplification leaving out things like gestational diabetes,

That is the only thing you can leave out in my case.
It seems they want to put us in boxes that we don't necessarily fit in.

Nothing to stop you typing in the link longhand.
This will not provide a clickable link but will allow others to see the URL and to copy/paste if they wish.

Ok, I think the hypothesis in this study describes the guerilla beta cells:
Mechanisms of β-cell dedifferentiation in diabetes: recent findings and future research directions
I tried to put the URL here but still got the spam like message.
“β-cell dedifferentiation could be an adaptive mechanism to escape cell death under chronic hyperglycemia at the price of altered identity and function”.

I think we all know exercise (or a lack of it) can affect glucose levels but that still does not mean that it's CAUSING it.

I don't understand that, doesn't anything that raises bloodsugars significantly cause diabetes?

Not sure what the OP was thinking

I have that too sometimes.

Edited to insert link.

 

[Antje77]

It seems they want to put us in boxes that we don't necessarily fit in.

If you have diabetes and you've tested positive for antibodies, like you have, the box is a very clear T1. Diabetes caused by an auto-immune response, or you wouldn't have the antibodies.