Confused About Insulin Resistance

[Miss_Dior]

Types 1 and 2 diabetes mean that your cells do not get insulin because your body doesn't manufacture insulin (for different reasons, not important to my question).

Insulin resistance means that your pancreas produces adequate insulin, but the cells don't respond properly. The two conditions are totally different...but they are ALWAYS linked, in the literature I have read.

Why? What is the relationship between the two?

 

[Heathenlass]

Not quite true.
No, or very little insulin is produced by the pancreas in type 1 diabetes, whereas in Type 2 insulin is still being produced, but the mechanism of the blood chemistry is unable to allow insulin access to the cells. I rather like the lock and key analogy- in Type 1 no key ( insulin) exists to unlock and allow glucose to be used by the body's cells. In type two, the key exists, but the lock won't allow the insulin in to do its job, therefore a Type 2 is insulin resistant from the outset.

In a Type 1, you can become insulin resistant , or be insulin resistant to a degree from the outset, therefore higher and higher doses of insulin are needed to overcome this, or else the addition of a drug such as metformin to the regime. The reasons for this are many and complex , but doesn't always happen in Type 1, whereas it is always present in Type 2 and has been since the outset.

Signy

 

[Miss_Dior]

Thanks for reply, but the differences between T2 and T1 aren't my concern.I understand the differences between the two. What I am confused about is why curing the plugged up pancreas problem would solve matters if the cells are resistant to insulin.

Here's my understanding, based entirely on the findings of Prof. Taylor of Newcastle - and so far, I've not read anything to contradict Prof. Taylor's findings. We all have a personal fat threshold (PFT for short); some people can have a normal BMI and still their pancreas is plugged with fat. When that happens, you get T2 diabetes. The Newcastle diet (or any very low calorie diet) will reduce that fat and "unplug" the pancreas, thus allowing proper B-cell function, thus enabling the insulin to flow to the cells.

My confusion is: what good is allowing insulin to flow, if the cells are insulin resistant? Then what?

 

[Squire Fulwood]

Your question about insulin resistance is one I have asked my DN about in the past and she says that nobody really knows the answer but I am not happy with that.

I did some reading and I like the explanation given by Dr. Kendrick. It basically says that when your sugar stores are full then the insulin is out of a job, doesn't seem to be working and puts the glucose in the fat cells and keeps it there until the insulin goes away.

http://drmalcolmkendrick.org/2013/08/09/the-most-unutterable-balls/

I then thought that if you restrict carb intake to a level that is low enough that the cells can take the glucose produced on board then the blood glucose will get lower, insulin will not be produced in such quantities, fat will be released and a miracle cure announced.

Probably all wrong but I am not content with being given phrases like insulin resistance without trying to get a better understanding.

Phd (Calcutta failed).

 

[Miss_Dior]

Your question about insulin resistance is one I have asked my DN about in the past and she says that nobody really knows the answer but I am not happy with that.
....
Probably all wrong but I am not content with being given phrases like insulin resistance without trying to get a better understanding.

Phd (Calcutta failed).

Hi & thanks! It is good to know I'm not the only one who is confused. So I'll go further - IR and diabetes (of whatever kind, doesn't matter) are two totally different metabolic states and we are right to be puzzled at their constant conflation.

Now, I'll go and read Dr. K's words and see if I can understand them.

 

[Lamont D]

My metabolism is different again.

I flush insulin and this caused weight problems, as well as the many symptoms that occur with Hypoglycaemia.
All my over producing insulin goes to visceral fat, therefore, the more insulin, the worse I was getting.
I needed to control my intake and lower my carb and sugars and also eat more slow acting meats and veg.

I now take a gliptin which reduces the spike after eating, and it also regulates the glucose and glucagon levels in my blood.

All the science is to be found on Wikipedia if you understand it.

 

[Miss_Dior]

Have a look at this:

Especially the stuff about T2:

"Type 2 diabetes is caused by insulin resistance, in which the body does not properly use insulin. Generally, diabetes type 2 is thought to result from a combination of genetic factors along with lifestyle factors such as obesity, high alcohol intake, and being sedentary."

Well, that may not be true.

"Adhering to the strict 600 calorie-a-day diet causes fat levels in the pancreas to plummet, restoring normal function, found Prof Roy Taylor of Newcastle University.

The discovery, a "radical change" in understanding of the condition, holds out the possibility that sufferers could cure themselves - if they have the willpower.

Prof Taylor explained that too much fat "clogged up" the operation of the pancreas at a cellular level, preventing normal secretion of insulin which regulates blood sugar.

When this fat was removed - by way of the diet - normal function resumed.

He said: "This is a radical change in understanding Type 2 diabetes. It will change how we can explain it to people newly diagnosed with the condition."

Now, I realize that these results have to be checked and re-checked to see if the people who were "cured" have kept up, but my issue is, this seems to disprove the "IR causes T2" theory, doesn't it? Newcastle proved that T2 is simply lack of insulin.

And that's what confuses me. When these people's beta cells functioned properly, were they then also cured of IR?

 

[Squire Fulwood]

Hi & thanks! It is good to know I'm not the only one who is confused. So I'll go further - IR and diabetes (of whatever kind, doesn't matter) are two totally different metabolic states and we are right to be puzzled at their constant conflation.

Now, I'll go and read Dr. K's words and see if I can understand them.

I shall probably get deleted for heresy in a minute .......so what's new?

Correlation or causation are key words at the moment. To my mind there is a correlation with obesity (insulin makes you fat) and diabetes ......that is unless you don't have a propensity for fatness in which case you can still get type 2 and be thin. My personal opinion is that high blood sugar causes damage and if it damages the pancreas then you have the start of a cascade effect leading to diabetes.

Getting rid of some of the fat can slow down further damage and possibly improve matters but once the damage is done you can't cure it.

 

[Miss_Dior]

I shall probably get deleted for heresy in a minute .......so what's new?

Correlation or causation are key words at the moment. To my mind there is a correlation with obesity (insulin makes you fat) and diabetes ......that is unless you don't have a propensity for fatness in which case you can still get type 2 and be thin. My personal opinion is that high blood sugar causes damage and if it damages the pancreas then you have the start of a cascade effect leading to diabetes.

Getting rid of some of the fat can slow down further damage and possibly improve matters but once the damage is done you can't cure it.

I enjoy heresy & heretics. Have you read about the Newcastle study? If not, read up. Yes, you can get T2 and be "thin" because of the personal fat threshold issue. Prof. Taylor appears to have cleared up the correlation/causation issue. First you clog up pancreas with fat, then you get T2.

Beta cells can apparently repair, it's not irreversible.

The critical issue is the difference between subcutaneous fat and visceral fat. It's not the fat on your butt. It's the fat clogging your organs. There's a lot of stuff in PUBMED about this. I am thinking of one study in particular but I can't find it now. Later. Got to exercise.

 

[Lamont D]

I shall probably get deleted for heresy in a minute .......so what's new?

Correlation or causation are key words at the moment. To my mind there is a correlation with obesity (insulin makes you fat) and diabetes ......that is unless you don't have a propensity for fatness in which case you can still get type 2 and be thin. My personal opinion is that high blood sugar causes damage and if it damages the pancreas then you have the start of a cascade effect leading to diabetes.

Getting rid of some of the fat can slow down further damage and possibly improve matters but once the damage is done you can't cure it.

This would explain the reason why I was misdiagnosed as T2 and prediabetic before that.
The high uncontrolled spikes and weight gain.
As more insulin turned to fat the more my pancreas reacted to the loaded carbs and sugar, I also had liver function, kidney function, fatty liver and my blood pressure was high.
Now that I've lost the weight, everything other than my over producing insulin has returned to normal and healthy.

 

[Miss_Dior]

This would explain the reason why I was misdiagnosed as T2 and prediabetic before that.
The high uncontrolled spikes and weight gain.
As more insulin turned to fat the more my pancreas reacted to the loaded carbs and sugar, I also had liver function, kidney function, fatty liver and my blood pressure was high.
Now that I've lost the weight, everything other than my over producing insulin has returned to normal and healthy.

Are you insulin resistant?
Do they test for this?

 

[Lamont D]

No I have a condition called Late Reactive Hypoglycaemia.

I flush insulin, the more carbs and sugars I digest, the more insulin I produce.

Are you insulin resistant?
Do they test for this?

And yes I have been tested for insulin resistance.
If you want to read more got to the forum ' Ask a Question' and read about Reactive Hypoglycaemia.
Or read my first blog about my long struggle to get diagnosed. I called 'A Reactionary' use the search function in the blog forum at the top of the page.

And yes I have had many, many tests, simply because it is a rare blood, metabolic condition.

 

[Daibell]

Hi. It is avery complex set of interactions and no one, I repeat no one, fully understand all the possibilities. Porf Taylor is entitled to talk about the pancreas being stuffed with fat even if you may be thin but I suspect he nas no 'proof' of that and I would like to see the scientific research behind it. The Newcastle studies focus around fat intake and calories whereas others focus around carbs and carb intake. I go along with the view that many of the thin 'T2s' are LADA and not T2 with a fatty pancreas. I was one of those and there is no reason to believe I had a fatty pancreas. There are of course no absolutes in all of this. To address the OP, the two conditions of T1 and T2 are in fact a continuum and they all tend to result in insulin not reaching the muscle cells etc. In this sense they become linked.

 

[Indy51]

My understanding is that Prof Taylor's study was accompanied by extensive MRIs of visceral fat and they developed a way of quantifying the amount of pancreatic etc fat so that changes could be measured. I'm assuming that's the proof he is using to justify his theory.

 

[AndBreathe]

Types 1 and 2 diabetes mean that your cells do not get insulin because your body doesn't manufacture insulin (for different reasons, not important to my question).

Insulin resistance means that your pancreas produces adequate insulin, but the cells don't respond properly. The two conditions are totally different...but they are ALWAYS linked, in the literature I have read.

Why? What is the relationship between the two?

Hello there.

I can appreciate from this thread that you are doing lots of reading, following your diagnosis of prediabetes, but what is the underlying issue? Understanding a mechanism is all very well, but what are you going to do with that information?

- Are you looking for a way you may be able to knock yourself back out of prediabeyes?
- I can't ascertain from either your profile, or image, if you may be carrying any relevant poundage that could be helped by attempting to de-fat your liver

Depending on your objective you may receive replies that help in that context.

Good luck with it.

 

[Daibell]

My understanding is that Prof Taylor's study was accompanied by extensive MRIs of visceral fat and they developed a way of quantifying the amount of pancreatic etc fat so that changes could be measured. I'm assuming that's the proof he is using to justify his theory.

Visceral fat is known to be a problem but to extrapolate that to include pancreatic fat may be a step too far? If you are a slim 'T2' then although you may have some visceral fat equally you may not. I think Prof Taylor may be looking for tests and people who fit his hypothesis rather than broadening it's scope.

 

[Indy51]

Visceral fat is known to be a problem but to extrapolate that to include pancreatic fat may be a step too far? If you are a slim 'T2' then although you may have some visceral fat equally you may not. I think Prof Taylor may be looking for tests and people who fit his hypothesis rather than broadening it's scope.

Why a "step too far"? Since the pancreas is so pivotal to diabetes, I can't see it being a huge leap of logic. I find it a bit odd that you're accusing a respected academic of cherry-picking data without any proof offered to back that assertion up. Do you have any proof that he screened people and chose only those with fatty pancreases to include in the study?

Maybe I find the assertion more convincing as I had an abdominal ultrasound around the time of diagnosis and the report specified fatty pancreas as well as fatty liver. Maybe fatty pancreas and fatty liver go in hand? Unless there is a mass image screening of every diagnosed Type 2 we're fairly unlikely to prove that one way or the other. And how likely is that kind of mass screening given the general lack of funds towards treatment of Type 2?

 

[Miss_Dior]

Why a "step too far"? Since the pancreas is so pivotal to diabetes, I can't see it being a huge leap of logic. I find it a bit odd that you're accusing a respected academic of cherry-picking data without any proof offered to back that assertion up. Do you have any proof that he screened people and chose only those with fatty pancreases to include in the study?

Maybe I find the assertion more convincing as I had an abdominal ultrasound around the time of diagnosis and the report specified fatty pancreas as well as fatty liver. Maybe fatty pancreas and fatty liver go in hand? Unless there is a mass image screening of every diagnosed Type 2 we're fairly unlikely to prove that one way or the other. And how likely is that kind of mass screening given the general lack of funds towards treatment of Type 2?

I am amazed that you had an abdominal ultrasound. I don't believe that diabetics in the US have this. I mentioned the Newcastle results to my DOCTORS and none of them had heard of it. I was disgusted. And yes, you have the right idea - the study was very precise, the fat levels in the liver & pancreas were exhaustively measured with nuclear MRI, and that was what they found: that fat in the pancreas & liver interfered with proper insulin b-cell function. They also reversed insulin resistance.

As to what I am doing about all this, I reduced my caloric intake drastically and my BGs have responded, almost miraculously. But of course it goes day by day. If I return to my former eating habits, I'll get my former blood glucose results.

 

[Indy51]

@Miss_Dior - sorry if I was confusing, but I wasn't given the ultrasound because of the diabetes diagnosis. It was given as part of various ongoing tests to try and discover whether I had gallstones (I do) because of digestive issues I was having at the time. Was shortly after that I was diagnosed with Type 2.

Glad to hear you're doing well with your BG control

 

[Miss_Dior]

@Miss_Dior - sorry if I was confusing, but I wasn't given the ultrasound because of the diabetes diagnosis. It was given as part of various ongoing tests to try and discover whether I had gallstones (I do) because of digestive issues I was having at the time. Was shortly after that I was diagnosed with Type 2.

Glad to hear you're doing well with your BG control

Thanks for encouraging words. I'm not giving up until I look like your avatar.

And thanks as well for clearing up the confusion, but, isn't this yet another piece of evidence that Prof. Taylor is on the right track?

I've been doing a lot of reading about insulin resistance. I'm not a scientist so it's hard going but I'm getting the gist. I think that IR underlies a lot of the weight issues in our society. (Our society being the sedentary, 24/7 eating west. I realize that most here are not from the US, which I find refreshing. BTW I am from a part of the US which is supposedly not very obese - NYC - and believe me, obesity is very prevalent here.)