I wonder if it is just that? I wonder if there is also something to do with the RH body thinking that it has released glucagon and then releasing insulin to cover that, much like you see with whey protein and insulin in T1s.Increasing insulin isn't the problem, it's the way our body converts our food into glucose initially that is the key.
I wonder if it is just that? I wonder if there is also something to do with the RH body thinking that it has released glucagon and then releasing insulin to cover that, much like you see with whey protein and insulin in T1s.
Looks like the reason that @nosher8355 was put on Sitagliptin (a DPP-4 inhibitor) is the same as the reason you have been put on Bydureon (a GLP-1 inhibitor). Aside from all the other aspects of the drug, it seems to enhance insulin release at time of eating. It has been put forward (as @Brunneria said) that it is the immediate insulin response to meals that is missing/faulty in RH, and both these drugs enhance that insulin release.Ok thanks just googled it interesting will it stop pancreas producing too much insulin? Or is that why its a trial?
Looks like the reason that @nosher8355 was put on Sitagliptin (a DPP-4 inhibitor) is the same as the reason you have been put on Bydureon (a GLP-1 inhibitor). Aside from all the other aspects of the drug, it seems to enhance insulin release at time of eating. It has been put forward (as @Brunneria said) that it is the immediate insulin response to meals that is missing/faulty in RH, and both these drugs enhance that insulin release.
And I quote;Another one for you @nosher8355 - https://link.springer.com/article/10.1186/1750-1172-7-26 - looking at metabolic diseases that cause hypoglycaemia. One of the things it notes (and I can't find anything via google that gives the opposite view) is that RH is rarely linked to Hereditary Fructose Intolerance, rather than it being particularly commonly linked.
Unfortunately my consultant is reluctant to prescribe Sitagliptin for me because of potential further weight loss. I'm slowly gaining some weight now after losing loads and nearly becoming underweight.Kat, the idea is not to have hypos at all if possible, and the T2 shouldn't give her the hypos, unless she is on insulin, which is very unlikely!
I would give the metformin a wide berth honestly, if it was me.
The old lady, does she know her trigger?
I know my meds have helped, but I haven't had a hypo in over two years now, except for the glucose test in hospital.
If any meds you would probably benefit from, I would suggest the sitagliptin.
Hi Kaz,Unfortunately my consultant is reluctant to prescribe Sitagliptin for me because of potential further weight loss. I'm slowly gaining some weight now after losing loads and nearly becoming underweight.
One of the the points that regularly comes up is sensitivity to epinephrine (adrenalin) causing the symptoms to be worse, which would make sense in your case if you lack it naturally. Add to that a lack of epinephrine and as you say, you don't have a good feedback response mechanism to counter regular insulin, let alone excess insulin.If I throw in my other problem which is adrenal failure (like addisons disease) does that help or hinder the glycogen discussion. My problem is that sometimes I cannot rescue myself when going hypo as no cortisol to mobilise liver to release glycogen ( I take a replacement) so once it goes down it just keeps on going hence the sever hypos.
The answer to this is always "It depends". One or two readings between 3.5 and 4 per day seems normal. Does that qualify as hypo? Typically for me, anything below 3.5 is what I consider hypo, and that's about twice a month, usually exercise or carb count failure related. I'm not sure what the average is.Tim does the average type 1 get a lot of hypos? Do many of you 'over there' (other thread!) try the low carb options? Perhaps we need to share a bit more with the other types?