Insulin Sensitivity

[lindisfel]

Does being a Reactive hypoglycemic mean we have better insulin sensitivity than most T2D's?


For us, carbohydrate restriction seems to be the only solution to our problem and I have not found another believable strategy. I know what spikes my insulin.

Of course the above doesn't mean we don't have a measure of insulin resistance but I assume this is related to an excess of second stage insulin over the long term.
regards
Derek

 

[kitedoc]

It sounds to me more like a mistiming of and disproportionate insulin secretion.

 

[Brunneria]

@lindisfel

I have lots of insulin resistance. I am obese, am fairly sedentary, have a prolactinoma (pituitary gland tumour), polycystic ovary syndrome and am on meds which have 'may cause insulin resistance' written on the patient info leaflet. My Freestyle Libre clearly shows that sustained brisk exercise lowers my insulin resistance, which kind of proves that it is present the rest of the time. Unfortunately, the amount of brisk exercise needed to do that is unsustainable for me with my current lifestyle and joint problems.

All of which means that I haven't a clue whether my RH is a factor in IR - and if it is, whether the effect is to raise or lower that IR. It is all a big unknown.

I do know that when/if I eat carbs, my IR increases temporarily and then subsides again. But without a means to test it and get comparable figures, I can only guess how that compares to other people with RH and other T2s.

 

[lindisfel]

It sounds to me more like a mistiming of and disproportionate insulin secretion.

Hi kitedoc,
Please, do type 1's need the same amount of insulin to cover carbs? How much does it vary?
Do they have both insulin sensitivity and insulin resistance at the same time?

 

[lindisfel]

Sorry to be pedantic Brunneria, but doesn't exercise improve insulin sensitivity? One assumes it doesn't lessen or increase the amount of insulin produced at the point of stepping out after a meal.

Or am I confusing insulin sensitivity and insulin resistance?
regards
Derek

@lindisfel

I have lots of insulin resistance. I am obese, am fairly sedentary, have a prolactinoma (pituitary gland tumour), polycystic ovary syndrome and am on meds which have 'may cause insulin resistance' written on the patient info leaflet. My Freestyle Libre clearly shows that sustained brisk exercise lowers my insulin resistance, which kind of proves that it is present the rest of the time. Unfortunately, the amount of brisk exercise needed to do that is unsustainable for me with my current lifestyle and joint problems.

All of which means that I haven't a clue whether my RH is a factor in IR - and if it is, whether the effect is to raise or lower that IR. It is all a big unknown.

I do know that when/if I eat carbs, my IR increases temporarily and then subsides again. But without a means to test it and get comparable figures, I can only guess how that compares to other people with RH and other T2s.

 

[Brunneria]

Yes, exercise definitely improves insulin resistance (lowers IR).
And, for me, eating carbs makes it worse (raises IR).

But i don’t know of a way to assess what impact RH has on either of those things, in comparison with a T2 or a person with ‘normal’ glucose regulation.

 

[Lamont D]

Does being a Reactive hypoglycemic mean we have better insulin sensitivity than most T2D's?


For us, carbohydrate restriction seems to be the only solution to our problem and I have not found another believable strategy. I know what spikes my insulin.

Of course the above doesn't mean we don't have a measure of insulin resistance but I assume this is related to an excess of second stage insulin over the long term.
regards
Derek

Hi Derek,
Hope to find you in good health.

I don't think that insulin sensitivity is the correct way to describe the action of how sensitive we are to carbs, glucose or insulin itself.
I think that our second insulin response can be dependent on what our triggers response is to how much glucose is in our blood at the time of the pancreas produces the response. It is, if it turns itself off, I believe that mine has not got a way to stop production, until the liver decides to kick in whilst being hypoglycaemic, during Glucogenesis, my production still exists but is not enough to stave off the glucagon/glucose/glycagon response of my liver, so the blood glucose levels rise and of course we get into the phase of hyper, hypo, hyper, hypo, fluctuating bloods. The rebound effect we try to avoid.
We have to recognise that our first insulin response is weak, hence the second supplements the first, and doesn't behave itself.
Insulin resistance is a long term effect of having too much circulating insulin in your blood, this effect can cause the high blood glucose levels we can get if we don't get control, it also is the reason why it is necessary to fast for as long as possible before an eOGTT, so before diagnosis your blood levels can be as low if not in normal levels as possible. That was why my second eOGTT was repeated because my glucose levels were too high even though I had fasted. Diagnosis is dependent on having normal levels pre test.

I know of no other strategy or treatment, except that I use sitagliptin as an insurance against spikes, despite being in ketosis.

Best wishes mate.

 

[lindisfel]

Hi Lamont,
Thanks for your response.
As always if it is not measured we are guessing.
I hope you are ok I am fine but find it hard to believe I am 79 next week.

If I am still here is twenty years time I'll know LCHF works!

I was just really trying to tease out the subtle difference that Ivor Cummings referred to in one video between insulin sensitivity and insulin resistance.
Re: using the evidence from RH.

Basically I think they are two sides of the same coin.
However with RH, actually we have even more variables than 'normal' diabetics.

best wishes
Derek

Hi Derek,
Hope to find you in good health.

I don't think that insulin sensitivity is the correct way to describe the action of how sensitive we are to carbs, glucose or insulin itself.
I think that our second insulin response can be dependent on what our triggers response is to how much glucose is in our blood at the time of the pancreas produces the response. It is, if it turns itself off, I believe that mine has not got a way to stop production, until the liver decides to kick in whilst being hypoglycaemic, during Glucogenesis, my production still exists but is not enough to stave off the glucagon/glucose/glycagon response of my liver, so the blood glucose levels rise and of course we get into the phase of hyper, hypo, hyper, hypo, fluctuating bloods. The rebound effect we try to avoid.
We have to recognise that our first insulin response is weak, hence the second supplements the first, and doesn't behave itself.
Insulin resistance is a long term effect of having too much circulating insulin in your blood, this effect can cause the high blood glucose levels we can get if we don't get control, it also is the reason why it is necessary to fast for as long as possible before an eOGTT, so before diagnosis your blood levels can be as low if not in normal levels as possible. That was why my second eOGTT was repeated because my glucose levels were too high even though I had fasted. Diagnosis is dependent on having normal levels pre test.

I know of no other strategy or treatment, except that I use sitagliptin as an insurance against spikes, despite being in ketosis.

Best wishes mate.

 

[lindisfel]

It sounds to me more like a mistiming of and disproportionate insulin secretion.

You could be right.
I often wondered if a small shot of insulin immediately after we had carbs would head off the later roller coaster? But if it didn't we would feel pretty groggy!
D.

 

[Lamont D]

You could be right.
I often wondered if a small shot of insulin immediately after we had carbs would head off the later roller coaster? But if it didn't we would feel pretty groggy!
D.

Hi Lamont,
Thanks for your response.
As always if it is not measured we are guessing.
I hope you are ok I am fine but find it hard to believe I am 79 next week.

If I am still here is twenty years time I'll know LCHF works!

I was just really trying to tease out the subtle difference that Ivor Cummings referred to in one video between insulin sensitivity and insulin resistance.
Re: using the evidence from RH.

Basically I think they are two sides of the same coin.
However with RH, actually we have even more variables than 'normal' diabetics.

best wishes
Derek

This is the role that sitagliptin plays.
The drug changes the first insulin response, so lowers the glucose levels derived from the meal because it urges the pancreas to produce more insulin. That change alters the level of the spike. The problem is, even though we don't get the high spikes, there is still enough to produce a secondary response of insulin to give you the overshoot.
This why, I still eat very low carb.
During my last eOGTT, my spike was in the 8s, rather than in the teens. But I still went hypo! My endocrinologist was really pleased with the results. Not the hypo though!

Yes I'm getting near to pension age myself, another three years!
I hop that I can keep as healthy as I am now, it's really good to know that you are good, with those added years on mine.
I'm convinced that it's all down to what I eat and with a bit of luck, we will still be as active as we are now!

Best wishes mate

 

[Mimi's]

@lindisfel

I have lots of insulin resistance. I am obese, am fairly sedentary, have a prolactinoma (pituitary gland tumour), polycystic ovary syndrome and am on meds which have 'may cause insulin resistance' written on the patient info leaflet. My Freestyle Libre clearly shows that sustained brisk exercise lowers my insulin resistance, which kind of proves that it is present the rest of the time. Unfortunately, the amount of brisk exercise needed to do that is unsustainable for me with my current lifestyle and joint problems.

All of which means that I haven't a clue whether my RH is a factor in IR - and if it is, whether the effect is to raise or lower that IR. It is all a big unknown.

I do know that when/if I eat carbs, my IR increases temporarily and then subsides again. But without a means to test it and get comparable figures, I can only guess how that compares to other people with RH and other T2s.

 

[Mimi's]

Hi! What all medications do you have now?
Do you feel tired/ dizzy and unwell most of the time? How to know if it's hyper or hypo?

 

[Lamont D]

Hi! What all medications do you have now?
Do you feel tired/ dizzy and unwell most of the time? How to know if it's hyper or hypo?

I know Brun will answer your question

No, I feel really good, because I'm in ketosis and have been for four years.
If I get a sense that my levels are going hyper, the symptoms are I get sweaty, my eyesight blurs, I go lightheaded, a bit dizzy, and my headache starts behind my eyes.
My anxiety increases, I reach for my glucometer and test, depending on the results, I sometimes test twice.
What it shows is that my blood glucose levels have risen higher than I want them to be, this is what RH ers really need to avoid.

However, in some patients, hypers and hypos have the same symptoms and until you actually test, you just don't know. Some have similar symptoms but more pronounced, some have different symptoms for each.

Do you have dietary issues and what advice regarding carbs, fats and proteins have you had?

 

[Brunneria]

I’m not on any medication for RH.

The best way to check whether you are hyper or hypo is to check your blood glucose using a meter and test strips. Without those you are working blind, and ‘false hypos’ are surprisingly common - along with all sorts of other conditions that have similar symptoms.

I don’t get many symptoms when I am hyper. Just a little jittery hyperactivity and lack of mental focus.
Hypos on the other hand... muscle weakness and wobbly knees, lost words, inability to make decisions, follow instructions or understand. Numb cheekbones. Vicious rage sometimes... they vary a lot. Usually followed by black depression, body aches and apathy. Now I have things under control they are now VERY rare, I am delighted to say.

 

[kokhongw]

Depending on when you discover it. Before or after T2D diagnosis.

But basically it means there is already a significant loss in 1st phase insulin response. So the second phase insulin response is disproportionately larger than necessary and tends to overshoot. If this carries on meal after meal, the insulin resistance will worsen.

The critical question is whether it is possible to restore 1st phase insulin response and therefore remove the huge secondary response thru dietary changes...

Thus far, only the Newcastle diet has some reported success with restoring 1st phase insulin response...

 

[Brunneria]

Thus far, only the Newcastle diet has some reported success with restoring 1st phase insulin response...

I think I disagree.
The Newcastle Diet (intended for T2s with fatty livers) was intended to see if replacing bariatric surgery with a dietary intervention would replicate the blood glucose 'reversal' that happens with some T2s after the surgery.

So bariatric surgery restores 1st phase insulin response in some people.

Also, there have been numerous examples of members posting on this forum who have 'reversed' their T2 using weight loss (mainly LCHF, but other dietary choices such as low cal as well), without using a very low calorie diet option such as the ND.

Basically I suppose that I am saying if your 1st phase insulin response is compromised due to a fatty liver, then any weight loss option that reduces the fatty liver will work. The Newcastle Diet is documented as achieving this, in some people. But it isn't the only way. I can recall people posting to a number of studies showing that low carbing achieves just as good (or better) weight loss than low calorie, and other studies showing that low carbing is effective in reducing a fatty liver. I will see if I can find some links to the studies. I know one of them was by the DCUK Newsbot, several months ago.

Edited to add the following links:
https://www.diabetes.co.uk/news/201...-in-people-with-type-2-diabetes-94851578.html
and
https://www.dietdoctor.com/new-study-can-low-carb-help-reverse-fatty-liver
and
https://www.liverdoctor.com/research-proves-fatty-liver-is-best-cured-with-a-low-carb-diet/

Actually, I would be very interested to know if any RHer has improved their RH by weight loss alone, while being on a carby diet. That would be fascinating data. I know lots of us lose weight, but is that a benefit to RH, or a very nice side effect?

All of which is only relevant if the failure of 1st phase insulin response is caused by a fatty liver.
I have always been suspicious of that theory in my case.
My RH started as a slim 4 year old child, on a very 'sensible' diet in a family which has never eaten excessive carbs or a fatty-liver-inducing diet. My mother has never served a processed food in her life. Everything cooked fresh. None of my blood tests in the last 47 years have ever indicated any liver issues or prompted investigation, and my RH has been just as present no matter whether I have been slim, fat, or obese.

 

[Lamont D]

Just to put my experience of my fatty liver, which everyone thought was due to alcohol excess, it was definitely insulin resistance and circulating insulin levels.
As I lost a lot of weight initially, it just helped with symptoms and a clarity because my insulin resistance and levels became normal (ish).
As my health problems receded, the less I needed my secondary insulin response.
I do believe that without losing weight or dietary intervention, your liver will still be suspect to problems with a fatty liver. One cannot happen without the other.

As for eating a modicum of carbs and not having symptoms and hypers and hypos, I don't believe that is possible, without having to just to live with it, I mean the symptoms and such.
Before diagnosis, I didn't have a clue, despite being on calorie diets, I still put on weight. Maybe ignorance is bliss.
However, I knew it was something other than the misdiagnosis I got!

 

[Kailee56]

Hi kitedoc,
Please, do type 1's need the same amount of insulin to cover carbs? How much does it vary?
Do they have both insulin sensitivity and insulin resistance at the same time?

Type 1’s use personalized amounts of insulin to cover the same amount of carbs. Large adults will need more than small children. While insulin production is insufficient, some people may still have a few cells working which would lower their insulin injection needs. Some people take a mixture of long and short acting insulin, so any supplement would be different than someone who uses a basal + bonus for food schedule. What the carbs are, what fats/proteins/fiber are included in the meal, and how fast are they digested may also impact insulin requirements. From what I’ve read the amount can vary by a lot, but has a degree of consistency for the person.

While my reflex answer would be that type 1’s are insulin sensitive, I also worked with a man who was huge with terrible self management. He would take massive amounts of insulin and then eat massive amounts of food and then go in the break room and be practically unresponsive or stumble around the unit dripping sweat. His sugars had to be all over the place. Very scary to work with him. The point, however, is that insulin resistance develops when there are consistently elevated insulin levels. I would not be surprised if this man had a level of resistance just by over dosing and going hyper/hypo all the time.

As for insulin resistance with reactive hypoglycemia, I’m the opposite of Brunneria. I’m very insulin sensitive, but have poor first phase response and overshoot my second phase. Then again, I just found out I am a very early LADA which explains my odd initial labs. It also explains my new interest in insulin, since it will be in my future.

 

[Lamont D]

The imbalance of insulin has a very detrimental effect on people's health and hyperinsulinaemia along with insulin resistance and high circulating insulin levels can be one of the major causes of prediabetes and T2.
And if tested early, the onset of diabetes can be drastically reduced.
Yet, it is rarely tested.

Mind boggling!

 

[Lamont D]

Type 1’s use personalized amounts of insulin to cover the same amount of carbs. Large adults will need more than small children. While insulin production is insufficient, some people may still have a few cells working which would lower their insulin injection needs. Some people take a mixture of long and short acting insulin, so any supplement would be different than someone who uses a basal + bonus for food schedule. What the carbs are, what fats/proteins/fiber are included in the meal, and how fast are they digested may also impact insulin requirements. From what I’ve read the amount can vary by a lot, but has a degree of consistency for the person.

While my reflex answer would be that type 1’s are insulin sensitive, I also worked with a man who was huge with terrible self management. He would take massive amounts of insulin and then eat massive amounts of food and then go in the break room and be practically unresponsive or stumble around the unit dripping sweat. His sugars had to be all over the place. Very scary to work with him. The point, however, is that insulin resistance develops when there are consistently elevated insulin levels. I would not be surprised if this man had a level of resistance just by over dosing and going hyper/hypo all the time.

As for insulin resistance with reactive hypoglycemia, I’m the opposite of Brunneria. I’m very insulin sensitive, but have poor first phase response and overshoot my second phase. Then again, I just found out I am a very early LADA which explains my odd initial labs. It also explains my new interest in insulin, since it will be in my future.

Hi,
I have never heard of RH turning to LADA.
How can you need insulin with LADA, yet avoid insulin overshoot if you hyper then hypo?
And I thought I was weird!

Could you have been misdiagnosed T2, like I was?