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Insulin Resistance and Insulin Production

Jim Lahey said:
Indeed, to my knowledge you can return normal liver function tests whilst having significant fat content in the liver. This misunderstanding is probably why many with insulin resistance claim that they do not have fatty liver.
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Thank you for agreeing with me. I have no idea if I have or had a fatty liver. My liver function tests have always been ideal, but I did have a large spare tyre in that area before I lost my weight. (All gone now!)
 
Bluetit1802 said:
Thank you for agreeing with me. I have no idea if I have or had a fatty liver. My liver function tests have always been ideal, but I did have a large spare tyre in that area before I lost my weight. (All gone now!)
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Well since insulin resistance essentially begins in the liver when its capacity to convert glucose into fat is diminished, I wouldn’t mind betting that almost every T2 has or has had some level of fat deposition in and around the organs. I guess they will always be a few outliers but I imagine it’s rare.

EDIT: the onset is probably more prolific in TOFI who don’t have the subcutaneous tissue in which the liver can transport the lipids to.
 
Jim Lahey said:
Indeed, to my knowledge you can return normal liver function tests whilst having significant fat content in the liver. This misunderstanding is probably why many with insulin resistance claim that they do not have fatty liver.
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Perhaps we should note that people aren't usually tested for insulin resistance either.
I paid for a private test because I had no idea what was going on; did I have IR or just poor insulin production?
Bit of both, it turns out.

The NHS site I read to check how fatty liver is diagnosed suggested that there was no really reliable way of testing apart from some kind of scan.
 

Yeah I think a scan is the only reliable diagnosis, but hepatic insulin resistance and excessive dawn phenomenon is the single best practical marker we have as patients. I wouldn’t expect the average doctor to be versed in these details if I’m honest.
 

Yes, I have just been reading up on NAFLD and it appears that scans of one sort or another are necessary to determine if fatty liver exists or not. Liver function tests may raise a warning, but are not used for diagnosis.
 
I've started a separate thread on scans,
 
I’m uncomfortable with the assumption that all T2s have a fatty liver. Beta cells fail for various reasons, and T2 is an umbrella term for various factors which result in high blood glucose. It a generalisation to say that to reverse T2 is simply a matter of combining fasting and weight loss to achieve a reduction in visceral fat to make everything OK.

I have never seen evidence that ALL T2’s raised blood glucose is due to fatty livers, have you?
The participants of the Newcastle Diet were carefully screened for suitability for the study.
There are a lot of other T2s out there who wouldn’t fit the study criteria.

Because of this, i would hate people to be reading this and assuming that it is simply process of losing visceral fat to achieve reversal.

Just because it happens for some type 2s (the lucky ones) doesn’t mean it will happen for them all.

Those for whom it has happened, and who have found it ‘simple’ or ‘easy’ seem to be implying that ‘if I can do it, anyone can’.
And we know that is never true.
 

I recall Jason Fung saying that something like 88% of his T2 patients have a fatty liver. Respectfully, T2DM is not an umbrella term for raised glucose. That is why other types are defined. T2DM is a symptom of excessive insulin circulation causing resistance. The resistance begins in the liver. Other types are other types.

Also, any implications that it is “easy” to fix, might be considered as optimistic encouragement.
 
I understand that but I felt your post was coming over as being critical of a newbie who may just have been reiterating what his GP has told him, just as I have done. We don't all know about extra tests. I certainly didn't when I had been here for only a month. I feel that the ALT test is a good enough indicator for me, it's what my doctor uses after all.
 
Bluetit1802 said:
Fatty liver - the various hormones (not just insulin) that trigger the liver to stop dumping can't access the liver, so it continues to dump?
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Or as in my case Prednisolone desensitising the liver to indigenous insulin produced by the pancreas causing the same effect.
 
In the past I have seen many articles saying that in 'T2s' the muscle cells have fat deposited making it difficult for the insulin to work. I have always assumed this was a common cause of high BS if you are overweight and not specifically the liver. Prof Taylor of ND fame always seems to talk about a fatty pancreas as well
 
I believe Sarah Hallberg has said in a recent talk that people who have Type2 that are slightly overweight when diagnosed but not obese are one of the most difficult groups to fix especially when it comes to fasting glucose and insulin resistance. I fit into this category. I was just overweight when diagnosed and have been on a strict keto diet for the last 3.5 years and fasting 16/8. My fasting insulin has been tested 3 times and is between 3 and 5 but my fasting glucose is always in the 6s. I have managed to get my HbA1c down to 39 but it takes seriously hard work to maintain this. I now weigh about 58kgs and have no fat on me but still have severe insulin resistance. There is obviously something else going on that is not just to do with fat accumulating round the organs. Wish I knew the answer
 

Nope, not being critical. I was just interested.
 

Same here. I was TOFI and fixing my insulin resistance was not a walk in the park. It took me two years of dedication and quite extreme measures. It’s thought to be markedly easier in those who are more able to store unused glucose as subcutaneous fat, thus making it easier to free up more capacity for their liver to work with. TOFI basically have their glycogen stores and little else before the fat starts backing up in the organs and once again increases resistance.
 
Jim Lahey said:
Respectfully, T2DM is not an umbrella term for raised glucose.
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You say that 88% of Jason Fung’s patients have a fatty liver.
Therefore 11% do not.
Therefore not all T2s have a fatty liver.
Nor does Jason Fung have test results for all T2s.

And

We see numerous mis-diagnoses of T2 mentioned on the forum every week.
All it takes to be diagnosed T2 in most countries is an HbA1c above the local cut off, confirmed with a second test.
So yes, T2s are regularly diagnosed on the basis of raised blood glucose levels.

That catches a lot of non insulin resistants under the umbrella - haemochromatosis is a good example, and frequently goes undiagnosed until the irreversible symptoms are so bad it is recognised. Also those with LADA, other genetic contributory factors, those with other (non fatty) liver and pancreas issues, even beta cells packing up through age. We don’t automatically get a fatty liver through age. Many reactive hypoglycaemics are also misdiagnosed as T2. Although RHers may or may not have insulin resistance.

Not all of the above are ever re-diagnosed to the appropriate category, and it would be unfortunate if they fell into the assumption that all it takes is a bit of weight loss and their problems will all be sorted. Of course, the ideal would be systematic and comprehensive diagnosis of every T2 eliminating all the other possibilities, but until that happens (never) those people will go through their lives identifying as T2 because a healthcare professional gave them an official diagnosis.

Again, I would like to point out that all I am doing it speaking out against sweeping generalisations - because sound bites and easy answers are usually too easy and can be quite harmful when applied to one of the (speculative) 11%.
 
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I agree that could well be the case but short of starving myself or getting a scan to see exactly what's going on it is very difficult. I also think that menopausal women who are TOFI struggle with hormone balance issues and this can have a very negative effect on insulin resistance ..... sadly! However, I take my hat off to you @Jim Lahey for all your hard work at gaining such fantastic control.
 

All true, but since no one is asserting that everything applies to everyone, then I don’t really see a reason for complaint. All anyone can do is explain things as they see them and offer opinions based on their own experiences and research. We are all adults and have the ability to sift through opinion and decide which pieces we would like to investigate further. In fact I believe I had already stated before your complaint that “almost” everyone with T2DM has or “has had” fatty liver. To the best of my knowledge this is accurate. I am not discussing LADA or any other type of diabetes. Others can do so if they wish, and their opinions will also be as valid as anyone else’s.

I feel that your protestations are misplaced, but then again you’re also free to voice your opinion, so hey ho
 

The trouble is Jim, that unless someone points out, in detail, why these sweeping generalisations are unhelpful, then more and more people just assume that they are true and eventually people start quoting them as fact. They become an urban (or forum) myth.

In the past have seen members leap straight on the diet and fasting band wagon (LCHF or Newcastle Diet) because they have fallen for the reversal hype, only to be crushed because they didn’t get the results they thought would be automatic. Not everyone loses weight. Not everyone can maintain the loss. Not everyone’s insulin resistance drops to non diabetic levels. Not everyone can stop the medications. Not everyone’s insulin resistance is easily rectified by diet, since medication and hormones play a huge part for some. This can be utterly crushing for them.

In the case of @LittleGreyCat (goodness, you knew that eventually I would address the thread topic, didn’t you ) I simply do not think it is appropriate be making declarations or assumptions based on the test results in the OP.
Not enough detail. Not enough medical history. And of course we are not medically qualified.

Suggesting that just losing more weight will solve his insulin resistance is, in my opinion, just making too many unverified assumptions.
 
I'm with @Brunneria here.
The sweeping statements from @Jim Lahey that "almost all" T2s have or have had a fatty liver implies that all T2s are tested for a fatty liver.
To the best of my knowledge very few T2s are tested for a fatty liver.
If I am correct, then the above is speculation and not scientific fact.

I haven't read anywhere so far that definitively says that T2 is defined by insulin resistance caused by a fatty liver (which Jim seems to be implying) and anything else isn't T2. As far as I am aware T2 is used as a global catch all for impaired glucose management where there isn't a more specific diagnosis.

When I was diagnosed over 11 years ago I was told that there were two main causes of T2 - insulin resistance or a failing pancreas.
I was also told that nobody tested for this because regardless of the cause the treatment was the same.

Now I don't really agree with this, because I would have found it much more helpful to know what was going on, but at the time I took the GP's word for it. This was a very diabetes aware GP practice, as well.

I had the opportunity to chat to Prof Roy Taylor at a conference a year or so ago and he said that the longer you had T2 the less chance you had to reverse T2 by dramatic weight loss, but a good target was to have the same weight and waist measurement as when you were late teens/early twenties. If it doesn't cure you it certainly won't do you any harm. Still not quite there.

At the Diabetes UK conference this year there was much excitement about recent research which suggested that T1 Beta cells might be able to regenerate. However it seems that nobody had really joined the dots up and wondered why the T2 beta cells were not regenerating. I was asked if I wanted to donate my pancreas to them for research, but declined as I was still using it.

So there are still more unknowns than knowns about diabetes and blanket statements can at times be misleading.

Edit: forgot to say that the statistic used to be that 80% of T2s on diagnosis were overweight or obese. That is a reasonable starting point to assume that many or most of them are likely to have a fatty liver. However there is that minority of 20% to consider. Also, correlation/causation and stuff.
 
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