Metformin

[Nicola M]

Hi All,

My consultant has recommended I try metformin as I’m quite insulin resistant and it should help. I know I’m Type 1 so it’s probably not used as much for us but I’m wondering if anyone has any advice for limiting possible side effects, how they’ve found it etc. I’ll be starting on once a day to move up to twice a day after 2-3 weeks.

Thanks

 

[AndBreathe]

Hi All,

My consultant has recommended I try metformin as I’m quite insulin resistant and it should help. I know I’m Type 1 so it’s probably not used as much for us but I’m wondering if anyone has any advice for limiting possible side effects, how they’ve found it etc. I’ll be starting on once a day to move up to twice a day after 2-3 weeks.

Thanks

Full disclosure: I have never been prescribed Metformin, but from lots of reading, here and elsewhere it does help to take it with food.

 

[Resurgam]

Hi All,

My consultant has recommended I try metformin as I’m quite insulin resistant and it should help. I know I’m Type 1 so it’s probably not used as much for us but I’m wondering if anyone has any advice for limiting possible side effects, how they’ve found it etc. I’ll be starting on once a day to move up to twice a day after 2-3 weeks.

Thanks

I never found anything which reduced the effects of Metformin - I'd advise staying at home until you find out if you are one of the lucky ones who can take it without problems.
My encounter with the tablets left me with a professional quality carpet cleaner and a determination not to take tablets if Humanly possible.

 

[Rachox]

I took Metformin for six years from diagnosis, I took one dose with breakfast, then increased to two doses so took the other dose with dinner. I tolerated it well after the first week. Had no side effects from then on. I did however come off it in favour of a GLP1 med in 2023. After a year due to the GLP1 becoming unavailable I went back on Metformin which on that occasion disagreed with my tummy, so stopped it and went on another GLP1.
There’s always the option of the slow release version of Metformin if the standard version don’t work for you.

Edit for typo.

 

[Melgar]

Hi All,

My consultant has recommended I try metformin as I’m quite insulin resistant and it should help. I know I’m Type 1 so it’s probably not used as much for us but I’m wondering if anyone has any advice for limiting possible side effects, how they’ve found it etc. I’ll be starting on once a day to move up to twice a day after 2-3 weeks.

Thanks

@Nicola M , my brother, who is T1 takes Metformin 500mg slow release, but he should be on 1000 mg. He says he can only tolerate 500 mg else he suffers digestive issues. He takes it before food. So his way of dealing with it is not to take the full dose, which is obviously his decision. He has an insulin resistant liver so the Metformin increases liver insulin sensitivity.

 

[Antje77]

I've tried metformin for about 8 months to see if it would help with my fluctuating insulin needs or reduce my overall insulin needs.
As for side effects, I did some experimenting and I definitely need to take it with food. I couldn't go over 1000 mg a day either but 1000 went ok, as long as I took it with food.

It didn't do much for me though so after 8 months I decided the experiment was over.

@Nicola M , my brother, who is T1 takes Metformin 500mg slow release, but he should be on 1000 mg. He says he can only tolerate 500 mg else he suffers digestive issues. He takes it before food. So his way of dealing with it is not to take the full dose, which is obviously his decision. He has an insulin resistant liver so the Metformin increases liver insulin sensitivity.

What is an insulin resistant liver?
I have no idea what (if any) type of insulin resistance I have, but my endo wasn't worried when I needed about 150 units of insulin a day, it worked for me.
Why should he be on a higher dose if this would keep him glued to the loo and having nighttime accidents? This would make me very unhappy, and there are other ways to deal with T1 and insulin resistance if a medication doesn't sit well with you.

 

[Melgar]

@Antje77 I’ll try. An insulin resistant liver means the cells in the liver (hepatocytes) do not effectively respond to insulin. What does that mean? In short insulin signaling is disrupted. In a healthy liver insulin usually regulates blood sugar levels by suppressing glucose production (gluconeogenesis) and promotes the storage of glucose. When your liver is resistant to insulin this process is disrupted.

In short, insulin signalling is effected due to insulin resistance. The liver continues to produce glucose despite high blood sugars making hyperglycaemia worse. It also leads to the over productions of lipids, such as Triglycerides. Insulin resistance in the Liver is one of the main drivers of metabolic syndrome. It can have major consequences, one of the major consequences of a resistant liver is Non-Alcoholic Fatty Liver Disease (NAFLD). This is a condition that affects both T1 and T2. Hopefully that makes sense. @Chris24Main would likely explain it better.


Edited to provide links

Insulin resistance in the liver: Deficiency or excess of insulin? - PMC

In insulin-resistant states (obesity, pre-diabetes, and type 2 diabetes), hepatic production of glucose and lipid synthesis are heightened in concert, implying that insulin deficiency and insulin excess coexists in this setting. The fact that ...

pmc.ncbi.nlm.nih.gov

Resolving the Paradox of Hepatic Insulin Resistance - PMC

Insulin resistance is associated with numerous metabolic disorders, such as obesity and type II diabetes, that currently plague our society. Although insulin normally promotes anabolic metabolism in the liver by increasing glucose consumption and ...

pmc.ncbi.nlm.nih.gov

 

[Melgar]

Sorry @Antje77 I placed the links in your reply to me, instead of in my reply to you.

 

[Antje77]

In short, insulin signalling is effected due to insulin resistance. The liver continues to produce glucose despite high blood sugars making hyperglycaemia worse. It also leads to the over productions of lipids, such as Triglycerides. Insulin resistance in the Liver is one of the main drivers of metabolic syndrome.

May I ask how your brother was diagnosed with this? I'm sometimes frustrated with what I think is insulin resistance (but not sure about that).
The liver produces glucose all day anyway, regardless of BG, that's why we need basal insulin.
As for lipids, mine were all out of whack upon diagnosis, but they settled nicely in the green when my BG normalised.
Is there a particular reason why your brother can'tget his BG down with insulin? For most, metformin doesn't make that much of a difference although it does for some. And I think anyone with serious side effects from a medication should be looking at other possibilities than upping the meds, pooping your pants in public simply isn't fun. And there are lots of medications to try.

 

[Antje77]

Sorry @Antje77 I placed the links in your reply to me, instead of in my reply to you.

What links?

 

[Melgar]

What links?

I accidentally put my links in your reply to me, so I deleted them and put them in my post as they are source of my information about liver resistance.

 

[Melgar]

May I ask how your brother was diagnosed with this? I'm sometimes frustrated with what I think is insulin resistance (but not sure about that).
The liver produces glucose all day anyway, regardless of BG, that's why we need basal insulin.
As for lipids, mine were all out of whack upon diagnosis, but they settled nicely in the green when my BG normalised.
Is there a particular reason why your brother can'tget his BG down with insulin? For most, metformin doesn't make that much of a difference although it does for some. And I think anyone with serious side effects from a medication should be looking at other possibilities than upping the meds, pooping your pants in public simply isn't fun. And there are lots of medications to try.

@Antje77 I believe his liver stats were raised when they did a panel.

As for your question about insulin resistance and fatty liver disease in T1’s it’s easier if I quote directly from the research paper. Here is the abstract:

“Autoimmune destruction of pancreatic β-cells results in the permanent loss of insulin production in type 1 diabetes (T1D). The daily necessity to inject exogenous insulin to treat hyperglycemia leads to a relative portal vein insulin deficiency and potentiates hypoglycemia which can induce weight gain, while daily fluctuations of blood sugar levels affect the hepatic glycogen storage and overall metabolic control. These, among others, fundamental characteristics of T1D are associated with the development of two distinct, but in part clinically similar hepatopathies, namely non-alcoholic fatty liver disease (NAFLD) and glycogen hepatopathy (GlyH). Recent studies suggest that NAFLD may be increasingly common in T1D because more people with T1D present with overweight and/or obesity, linked to the metabolic syndrome. GlyH is a rare but underdiagnosed complication hallmarked by extremely brittle metabolic control in, often young, individuals with T1D. Both hepatopathies share clinical similarities, troubling both diagnosis and differentiation. Since NAFLD is increasingly associated with cardiovascular and chronic kidney disease, whereas GlyH is considered self-limiting, awareness and differentiation between both condition is important in clinical care. The exact pathogenesis of both hepatopathies remains obscure, hence licensed pharmaceutical therapy is lacking and general awareness amongst physicians is low. This article aims to review the factors potentially contributing to fatty liver disease or glycogen storage disruption in T1D. It ends with a proposal for clinicians to approach patients with T1D and potential hepatopathy.” Quoted from ‘Hepatopathy Associated With Type 1 Diabetes: Distinguishing Non-alcoholic Fatty Liver Disease From Glycogenic Hepatopathy’. I have provide the link here to read in more detail.

Hepatopathy Associated With Type 1 Diabetes: Distinguishing Non-alcoholic Fatty Liver Disease From Glycogenic Hepatopathy - PMC

Autoimmune destruction of pancreatic β-cells results in the permanent loss of insulin production in type 1 diabetes (T1D). The daily necessity to inject exogenous insulin to treat hyperglycemia leads to a relative portal vein insulin deficiency and ...

pmc.ncbi.nlm.nih.gov

 

[ViktoriaM]

I used to take Metformin and tolerated it very well for a couple of years. Then there was a change in the brand I got prescribed and then I had side effects. So sometimes it‘s worth it to try different brands if you have the option. As in its effectiveness it worjed great to reduce my bolus Insulin and a little bit on my basal needs.

 

[Chris24Main]

@Antje77 - I say this only from my kind of dual-state of having been a Type 1 and also Type 2 - but the view of what insulin is and does tends to be a polar opposite - because it is - type 1; not enough and type 2; too much.

The role of reducing blood glucose is life-saving for Type one, but is far from being the most important role that it plays - more than 100 different effects, and critically on every cell in your body. Different effects on different cells.

If you think about the "classic" presentation of diabetics 150 year ago before synthetic insulin, the most crucial aspect was that they were physically wasting away; the body could not hold on to any energy. Blood (and of course urine) glucose was secondary to losing weight rapidly, running out of energy and quickly dying was the primary condition.

insulin is all about energy regulation.

In the most obvious case of chronically elevated insulin, different cells will develop a "too much of a good thing, need more to have the same result" building up of insulin resistance, but because of the hugely complex and interacting nature of insulin, where it can be both cause and effect, you can become insulin resistant for lots of reasons that have nothing to do with food - like getting pregnant (the most striking example).

For the vast majority of T1 - you usually are never in a state of chronic high insulin, you are in total control of what you inject, and the active life of that insulin is finite - you are not generating any from non-food stimulus like Cortisol.

But - the other way to think about it is that with perfect control of your dosing, you can only be close to what the functioning pancreas would deliver - ie, just like everyone else; and depending on the food you eat, your level of needed insulin may be high enough chronically to develop insulin resistance. Just like everyone else.

To address the insulin resistant liver question - that's easy (indeed that is right in my wheelhouse) - because what is foie gras? - it's a goose with a very insulin resistant liver. A goose with a very fat liver, too; but not a fat goose. How do you achieve this? - by feeding that goose with lots of high fructose corn syrup in the last weeks of it's life. Why ? because the liver must metabolise fructose. The liver turns that fructose into fat, which it must store itself. When that happens, the liver cells swell up, causing internal inflammation, and resistance to the insulin (which is causing that fat to be stored in the first place). Thus - insulin resistant liver.

All of that can happen without ever seeing a change in blood glucose, because glucose is never involved... This is the particularly insidious thing about fructose.

 

[Chris24Main]

@Nicola M - I've really gone deep on what Metformin is and what it does - there is no question at all that it's the med with the least side effects, but it does many, many things - to the point that we just don't know all the things and in some cases, why they have the effect they do.

There are trials going on right now looking at metformin as a longevity enhancing med, and they are talked of as having cancer risk reduction effects as well as some other things. When I had the choice, I decided not to take mine, but that was mainly because I would have had to take them on an empty stomach, and as others have said -that isn't a good idea - they are far too powerful to leave them alone in your stomach.

But - (and I've had this argument directly with my GP) - the primary reason they work is that they reduce the livers ability to produce glucose, leading to a reduction in blood glucose - which is interpreted as reducing insulin resistance - the argument for them actually - directly increasing insulin sensitivity is much weaker, secondary effect which I could spend all day trying to explain.

For me, I decided that the better route was to reduce the amount of glucose in my whole body - not just stop it from being released via the liver. That's very much a type 2 pathway though.

See how it goes - many people have good experience, as you can see from the replies - just be aware that generally the diabetic team will be focussed on blood glucose - not the level of insulin itself. The most powerful effect on circulating blood insulin (thus directly affecting insulin resistance) will always be about not having to inject as much, because you lower the need by lowering carbs - this goes back to the very first person to start measuring blood glucose - Richard Bernstein.

Please understand that I offer this only as biology - there is a link to Bernstein and his work in this forum, it's not controversial or my opinion - but I do not offer it as advice to do anything.

 

[choggii]

Hi All,

My consultant has recommended I try metformin as I’m quite insulin resistant and it should help. I know I’m Type 1 so it’s probably not used as much for us but I’m wondering if anyone has any advice for limiting possible side effects, how they’ve found it etc. I’ll be starting on once a day to move up to twice a day after 2-3 weeks.

Thanks

Ask for the slow release metformin it's much kinder on the gut.

 

[Cumbrianjudith]

I’m a type 3c diabetic apparently now, 10+ years after post septic shock/ acute pancreatitis, no longer producing any insulin. But early in my diabetic journey was put on metformin 2x1000 mg and gliclazide, then long-lasting insulin was added, and then replaced with Toujeo and Fiasp when though gliclazide was removed the metformin continued. I remember the diabetic nurse encouraging me to stay on it as it was becoming to be regarded as remarkable drug beyond its diabetic role as Chris24Main has indicated. What I don’t remember is ever being told what metformin was supposed to do, how to take it (news to me it should be with food, even though diabetic nurses know for last 2 years I have been intermittent fasting 14-16 hours a day), nor side effects… yes ok perhaps I should have read the metformin leaflet but I thought very specialist staff would be better informed than GPs etc. I now know this not to be true, certainly when it comes to type 3c diabetes. I have had ‘odd’ guts but thought this was due to the lack of pancreatitic sufficiency, not even considered metformin to be a cause. What Chris24 Main has said about the non alcoholic fatty liver disease/ metabolic syndrome etc is most interesting, as at one point a gastroenterologist threatened me with it ( till this day I cannot work out whether he was saying I was likely to get it or had signs of it), but nothing was ever suggested to improve it. Perhaps loosing 3+ stone in weight, without trying, post post acute pancreatitis/ septic shock solved the problem, at least then. At that time my GP was one who when she saw any blood work that was 1 unit above or below the range she insisted I saw a specialist consultant; now I don’t get tested or out of range has to be very obviously so. It was interesting to read the ‘what is best: low BG due to low carb diet, or high insulin to keep BG in range’…I have queried this myself with three diabetic nurses who seem to be in the ‘now you can eat cake and adjust insulin jab’ camp. This is rather contrary to my wishes; about 3 months ago I was put on a hypertensive drug, indapamide, which I have proof raises my insulin needs by 40+%…I don’t want this but DNs and Gp not bothered … is their a paper that might suggest that low insulin is the more healthy route? Sorry seem to have got away from metformin…but I suspect it goes to show everyone is different how they react, and many staff wouldn’t be able to answer what seems to be a extremely complex query! Incidentally I have had Long Covid with cardiovascular problems for nearly last 5 years which has rather shifted my health concerns in differing directions….however metformin is being prescribed to many of them ‘off label’!

 

[Ian4]

Hi All,

My consultant has recommended I try metformin as I’m quite insulin resistant and it should help. I know I’m Type 1 so it’s probably not used as much for us but I’m wondering if anyone has any advice for limiting possible side effects, how they’ve found it etc. I’ll be starting on once a day to move up to twice a day after 2-3 weeks.

Thanks

all i would say is try eating a little bit of food then have the tablet with water and then continue eating the rest for f your food in the meal. lowers risk of side affects. plus keep hydrated.

 

[RichardHawkings]

all i would say is try eating a little bit of food then have the tablet with water and then continue eating the rest for f your food in the meal. lowers risk of side affects. plus keep hydrated.

I'll second that, I went from none to 2g daily over a few weeks, lots of water & little food each time, no issues

 

[Binky21]

Hiya

I have been on Metformin for Type 2 for 19 years, I am obese so very insulin resistant. I have had 19 years of running to the toilet and although was on 1000mg twice a day, I am now down to 1250mg daily because as I get older and older the gastric/bowel issues worsen. I find 500mgs twice a day fairly tolerable. I keep taking it because for me as a Type 2, it really makes a difference no matter what else I take. Its also as others will attest, good for all sorts of other things. Take with food as it can also cause reflux if you are prone to this. I find it best tolerated in the evening.

Hope this helps.