Gallbladder issues affect my blood sugar levels

[scaramouche]

I have been type 2 for around 8 years. I have been taking 30mg pioglitazone and 320mg gliclazide daily, which controls my BS levels to between 12 and 20, for the last year or so. My last HIB1NC (or whatever it is!) was 92. At the beginning of March 2019, I developed severe chest pains which an MRI scan showed as being an enlarged and infected gallbladder. A drain was put in to remove the goo, and I am awaiting a gallbladder removal operation next month. Whilst in hospital, my blood sugar levels plummeted, to such an extent that the hospital stopped ALL my medication and put me on sugary drinks etc (but low fat of course), and my levels ranged 2.7 to 5.8 at the highest. I was for sure eating less, but as time progressed and my appetite improved, the levels remained very low. I am still on just the 30mg pioglitazone, and BS levels have gradually increased to 9.8 to 11.5 with a normal (low sugar, low fat) diet. I do get regular hypos (around 2.5 to 3.5 when I feel them). My diabetes nurse admits to having no idea why the gallbladder issue should have had such an immediate and dramatic effect on the BS levels, but the doctor said there "might be some connection". My question is if other T2 sufferers have experienced similar issues? Followed by: Should I be pleased at the current level with the low meds and be happy with that? And put up with the regular hypos? What may happen when my gallbladder is removed next month? And please accept my apologies if this has all been aired before, I couldn't locate much in searching the forums.

 

[mikeyB]

The connection is physical. The legendary Sphincter of Oddi. The outflow from the tubing from the gall bladder passes through the head of the pancreas, sharing the output of bile acids with exocrine enzymes from the pancreas through the Sphincter of Oddi.

If the whole GB is inflamed, the tubing gets inflamed and reduces the output of both organs in digesting food. That’s why your BG went down. Now things are settled, the pancreas can work normally, and your BGs are returning to normal.

My advice to you is to go buy a lottery ticket, because if that sphincter had completely blocked, you would have developed acute pancreatitis, which you definitely don’t want - it carries a 25% mortality rate. Bet nobody told you that.

Keep up with the low meds, your digestive system is probably running in second gear at the moment. It’s as much the meds as the digestion that’s causing the hypos.

It’s all down to plumbing. Bad design, if you ask me.

 

[scaramouche]

I have been type 2 for around 8 years. I have been taking 30mg pioglitazone and 320mg gliclazide daily, which controls my BS levels to between 12 and 20, for the last year or so. My last HIB1NC (or whatever it is!) was 92. At the beginning of March 2019, I developed severe chest pains which an MRI scan showed as being an enlarged and infected gallbladder. A drain was put in to remove the goo, and I am awaiting a gallbladder removal operation next month. Whilst in hospital, my blood sugar levels plummeted, to such an extent that the hospital stopped ALL my medication and put me on sugary drinks etc (but low fat of course), and my levels ranged 2.7 to 5.8 at the highest. I was for sure eating less, but as time progressed and my appetite improved, the levels remained very low. I am still on just the 30mg pioglitazone, and BS levels have gradually increased to 9.8 to 11.5 with a normal (low sugar, low fat) diet. I do get regular hypos (around 2.5 to 3.5 when I feel them). My diabetes nurse admits to having no idea why the gallbladder issue should have had such an immediate and dramatic effect on the BS levels, but the doctor said there "might be some connection". My question is if other T2 sufferers have experienced similar issues? Followed by: Should I be pleased at the current level with the low meds and be happy with that? And put up with the regular hypos? What may happen when my gallbladder is removed next month? And please accept my apologies if this has all been aired before, I couldn't locate much in searching the forums.

The connection is physical. The legendary Sphincter of Oddi. The outflow from the tubing from the gall bladder passes through the head of the pancreas, sharing the output of bile acids with exocrine enzymes from the pancreas through the Sphincter of Oddi.

If the whole GB is inflamed, the tubing gets inflamed and reduces the output of both organs in digesting food. That’s why your BG went down. Now things are settled, the pancreas can work normally, and your BGs are returning to normal.

My advice to you is to go buy a lottery ticket, because if that sphincter had completely blocked, you would have developed acute pancreatitis, which you definitely don’t want - it carries a 25% mortality rate. Bet nobody told you that.

Keep up with the low meds, your digestive system is probably running in second gear at the moment. It’s as much the meds as the digestion that’s causing the hypos.

It’s all down to plumbing. Bad design, if you ask me.

The connection is physical. The legendary Sphincter of Oddi. The outflow from the tubing from the gall bladder passes through the head of the pancreas, sharing the output of bile acids with exocrine enzymes from the pancreas through the Sphincter of Oddi.

If the whole GB is inflamed, the tubing gets inflamed and reduces the output of both organs in digesting food. That’s why your BG went down. Now things are settled, the pancreas can work normally, and your BGs are returning to normal.

My advice to you is to go buy a lottery ticket, because if that sphincter had completely blocked, you would have developed acute pancreatitis, which you definitely don’t want - it carries a 25% mortality rate. Bet nobody told you that.

Keep up with the low meds, your digestive system is probably running in second gear at the moment. It’s as much the meds as the digestion that’s causing the hypos.

It’s all down to plumbing. Bad design, if you ask me.

 

[scaramouche]

Many thanks Mike for your response. I have to admit to being somewhat confused though. If the output from the pancreas (insulin) is reduced, why do the BG levels go down and not up? Or is it that the reduction in bile from the gallbladder reduces the food digestion which stops the BG in its tracks? Anyway, I have never heard of the "Sphincter of Oddi" and had anyone mentioned it, I would probably have thought it was a joke! If the pancreas is now beginning to work normally, it seems to be doing so by reducing the output of insulin, not increasing it, thus my BG is returning to normal (i.e. elevated) from the lower levels I would have liked to maintain. I am probably completely missing the point here, as I have never been able to understand why my BG levels fluctuate in the way that they do. I certainly have no real idea what my "normal" BG levels are anyway. And nobody has mentioned that little gem about pancreatitus - I think probably I was better off being ignorant of it!

 

[mikeyB]

The production of insulin is an endocrine function of the pancreas. That would proceed normally with the gall bladder problem. An endocrine function is one that is released directly into the bloodstream, so it wouldn’t get blocked or reduced.

The exocrine function of the pancreas is to release digestive enzymes into the gut, and that is controlled by the Sphincter of Oddi, the release valve for bile acids and pancreatic enzymes.

In the situation I described (not clearly enough, I admit) the insulin churns out into the bloodstream, while the digestive enzymes are partially blocked from swilling into the gut. In simple terms, the insulin is fired up by the amount of food you eat, but the pancreas can’t get sufficient enzymes into the gut to digest the food, particularly starches that allow the bacteria in your gut to shovel glucose into your bloodstream lower down in the gut.

There is therefore a mismatch between the insulin in the blood and the expected glucose load, hence the low BGs. The insulin is in the blood, waiting for the glucose, meanwhile there aren’t enough digestive enzymes in the gut to allow production of glucose to match it.

When the pancreatic enzymes can get past the partial blockage, food gets digested properly, starch gets converted to glucose and your BG gets back to normal, as balance is restored.

That is a grossly simplified explanation of why it happens, basically because I’ve missed out all the control systems, but that would take pages of text.

I hope that has clarified things for you.

By the way, Sphincter of Oddi dysfunction is the only condition that describes its effects. The name is shortened to SOD, which is what it is.

 

[scaramouche]

Many thanks for the clarification Mike. I was obviously looking at things much too simply. It does lead me to wonder what will happen when my gallbladder is removed next month, but I am assuming that in fact both endocrine and exocrine functions of the pancreas will be allowed to perform normally again, and my somewhat limited control of BG will therefore be restored. Possibly I should expect to see the BG increase to the levels I was recording before the gb infection affected things with the pancreas. Not overly keen on that possibility but I sure hate the hypos. Having looked at SOD on the net, it seems to me that hopefully it was purely the gallbladder infection affecting the sphincter, and not a condition of the sphincter itself. Intriguingly, one site declared SOD appears to affect women who have had their gallbladder removed! I hope that doesn't read across to me! At least the BG changes seem to be due to the gb issue and not some weird diabetes effects. Thanks again for your help.

 

[mikeyB]

It’s an uncommon side effect of gall bladder removal. GB removal used to be as common as muck, but I’ve never seen SOD in clinical practice, hospital or GP. Won’t have any effect on your BG readings either, except immediately post op as the body reacts to the bodily damage of surgery itself. Always happens, so don’t worry too much. They may well do it laparoscopically, meaning less surgical trauma, and you get chucked out of hospital quicker.🙂