Joseph Kraft and hidden diabetes

[SunnyExpat]

The question is really "what is the cause of the insulin resistance?" as the CVD is a by product of the excess insulin.

I suspect it's a couple of things. Poor diet and sedentary lifestyle.

All the Kraft observational data shows (and it isn't really research) is that an awful lot of people over 30 years had unexpectedly elevated insulin levels, that they also had CVD in various stages and that by putting them on a low carb diet, the insulin levels could be reduced back to reasonably normal, ergo, whatever insulin resistance was there had been reduced. Very similar, in fact, to the Newcastle diet.

The difficulty with the data is that there is a lot missing from it. There is no information about lifestyle changes. The sample is around 14,000 people over 30 years. There is no control.

While I believe that what he has observed is correct (and based on the observations of a lot of other people corroborated) it's not really the type of evidence that many MDs like.

The question for T2s is what have you found better. Exercise, diet or changing both?

Both.
I find not eating carbs, and living off fat akin to putting a plaster on the problem.
Everything may seem good, but simply because I don't need to deal with carbs doesn't mean I'm no longer insulin resistant, it just means I don't see high figures any more.
Exercise does seem to change my insulin resistance though.
It has to be anaerobic exercise then I see a marked improvement in my insulin resistance, and a marked improvement in response to carbs.
Which I believe is actually dealing with the problem.
But, this suits me, and it's something I am able to do, I know others aren't as fortunate, but then again, I didn't, and indeed couldn't do much exercise when I was diagnosed.

 

[FatEmperor]

It needs repeating that fat does not 'fix' diabetes. And exercise DOES 'fix' part of diabetes - the insulin resistance. And without insulin resistance, the body (of a Type 2, we're now leaving aside Type 1s at Lucy's request) does not go into hyperinsulemia. So, it excels LCHF as a means of treatment.

So the fat eating 'fix' becomes superfluous or optional - but none of these people whose work you advocate so vigorously deals with that part of the data. It's called "selective observation" or "confirmatory bias."

The argument that "exercise is not a factor because it's good for everyone" is rather weak, to put it mildly. As is, "well, people won't do it, they'd rather just eat fat and avoid carbs." In the first case, exercise is especially important for those with a tendency (whether inherited or environmental) to insulin resistance. In the second, that's exactly the reason doctors push meds onto Type 2s without insisting on life-style changes. And I've lost count of the number of times I've heard LCHFers on here pouring contempt on doctors and nurses for doing that.

Oh, and the 'source' of the problem is not carbs. It's insulin resistance. And gluconeogenesis from protein also requires insulin, so not eating carbs is not a "cure"

Ooops Ruth - a veritable blizzard of straw-man misrepresentations there - ouch! If you read again:

(a) I didn't claim fat 'fixed' diabetes - you did. I said it helps massively if carb is held low & protein moderate (otherwise no deal)
(b) I didn't say "exercise is not a factor because it's good for everyone" - you did. I said exercise is a difficult fix to deploy, because with the best of intentions, millions just won't do it in spite of the obvious IS & other benefits.
(c) I didn't "pour contempt on doctors" for prescribing before lifestyle, but it's a fair point...
(d) the primary source of hyperinsulinemia leading to the IR state is excessive digestible carb (not fibrous veggies) - excessive protein follows.as secondary in most cases. That's pretty much a law of nature, fundamental biochemistry, but by all means deny it if you will.

 

[FatEmperor]

Both.
I find not eating carbs, and living off fat akin to putting a plaster on the problem.
Everything may seem good, but simply because I don't need to deal with carbs doesn't mean I'm no longer insulin resistant, it just means I don't see high figures any more.
Exercise does seem to change my insulin resistance though.
It has to be anaerobic exercise then I see a marked improvement in my insulin resistance, and a marked improvement in response to carbs.
Which I believe is actually dealing with the problem.
But, this suits me, and it's something I am able to do, I know others aren't as fortunate, but then again, I didn't, and indeed couldn't do much exercise when I was diagnosed.

"everything may seem good" - because biochemically and pathologically - it is. And Kraft proved what Dr. Jason Fung and myriad others are now - that lowering carbohydrate can resolve hyperinsulinemia and hence switch off the Pattern 2,3,and 4 T2 Diabetes in Situ response. I might add a quote from the great doctor:

""Hyperinsulinemia Is Insulin Resistance. They Are Not Combatants. They Are One And The Same."

Each actually drives the other, in a beautiful but malign self-reinforcing feedback loop. I prefer to say:

"They are Not Combatants. They are Brothers in Arms" because there is an exception to the Hyperinsulinemia = IR rule. That is a healthy low-carb person, who has a natural, 'physiological IR' state (glucose-sparing mode) while being simultaneously hypoinsulinemic (Pattern 5). This is a great state to aim for btw....it is the precise opposite of the diabetic state.

 

[FatEmperor]

We all know that lots of people don't like low carb. If anyone's really enjoying the fight Exercise versus Low Carb, by all means get to it, but please, somewhere else. The Kraft research and the question of what it means for insulin and disease process, specifically cardiovascular disease, is really interesting.

Agreed Lucy - a fight between two good things as to which is better is less than productive. Do both ideally - they can be synergistic then.

 

[FatEmperor]

What if it's the sugar that causes the inflammation. If it were the insulin, we would be better just running round and leaving our blood sugars high. less insulin, fewer problems.

But that isn't the evidence, is it? The research done by others shows that its high glycation, not high insulin that correlates with the damage.

Both are pathological; as Dr. Jason Fung nicely put it: there is glucotoxicity and Insulin Toxicity - both must be addressed. The sad thing is that I suspect they are synergistic also, so being high in both is worse than the sum of their damages to your vascular system. For a high level view of Insulin pathological mechanisms, this is a good start: https://www.dropbox.com/s/xvtbzl6zz...atheroma. 20-yr perspectivestout1990.pdf?dl=0

 

[FatEmperor]

For sure high blood glucose causes damage. The question is what damage does elevated plasma insulin cause, if any? Good question, especially with lots more people having elevated insulin than elevated blood glucose.

Again, this is just a taster of what's out there - but the concept is VERY unpopular, as billions in food and pharma revenue depend on the population staying hyperinsulinemic, and sick... https://www.dropbox.com/s/xvtbzl6zz...atheroma. 20-yr perspectivestout1990.pdf?dl=0

 

[FatEmperor]

For sure high blood glucose causes damage. The question is what damage does elevated plasma insulin cause, if any? Good question, especially with lots more people having elevated insulin than elevated blood glucose.

here's another taster - and illustrates the methodological flaws in much of the published literature - not too shocking that they missed the big picture:

http://www.thefatemperor.com/blog/2...-opportunity-of-the-helsinki-policemans-study

 

[tim2000s]

Whilst I don't deny that mechanics of what we are discussing are very real, we should also be aware that in the paper that @LucySW linked, this statement is made: "It should be noted that the random population studied was heavily weighted with patients suspect of diabetes referred specifically for identification"

This leads to a question as to the prevalence of the patterns identified. Whilst 73% of the subjects had abnormal insulin profiles, many of them were already suspected to be diabetic. I'd suggest this skews that paper's view somewhat.

 

[SunnyExpat]

"everything may seem good" - because biochemically and pathologically - it is. And Kraft proved what Dr. Jason Fung and myriad others are now - that lowering carbohydrate can resolve hyperinsulinemia and hence switch off the Pattern 2,3,and 4 T2 Diabetes in Situ response. I might add a quote from the great doctor:

""Hyperinsulinemia Is Insulin Resistance. They Are Not Combatants. They Are One And The Same."

Each actually drives the other, in a beautiful but malign self-reinforcing feedback loop. I prefer to say:

"They are Not Combatants. They are Brothers in Arms" because there is an exception to the Hyperinsulinemia = IR rule. That is a healthy low-carb person, who has a natural, 'physiological IR' state (glucose-sparing mode) while being simultaneously hypoinsulinemic (Pattern 5). This is a great state to aim for btw....it is the precise opposite of the diabetic state.

I might expect more quotes.
Which is the problem of making your mind up first, then trawling the internet for evidence to prove your view is correct.
Ultimately, if you only selectively link and quote to those views that prove you are correct, every other view can be easily ignored, as there is no doubt left.

The downside of that is the people you are trying to convince can trawl the internet themselves, them make up their own minds.
(Which is probably a more balanced way round as well). Having done that, it's then very easy to spot those quoting very selective evidence where presented.

 

[FatEmperor]

Whilst I don't deny that mechanics of what we are discussing are very real, we should also be aware that in the paper that @LucySW linked, this statement is made: "It should be noted that the random population studied was heavily weighted with patients suspect of diabetes referred specifically for identification"

This leads to a question as to the prevalence of the patterns identified. Whilst 73% of the subjects had abnormal insulin profiles, many of them were already suspected to be diabetic. I'd suggest this skews that paper's view somewhat.

Tim

The key point of Kraft's work is not to estimate the population level of diabetes - for that you would need to do his test on a random population sample for sure. The point of the work is that it compares the glucose-based diagnostic power against the insulin-response based diagnostic power.

If this was an engineering study and I wanted to characterise the diagnostic value of two different test suites for a problem in produced units , I would actually use a population of 'affected' units (similar to the majority of Kraft's people). I would take a large sample of units that had varying extents of the problem being experienced - then assess the different tests using these. You also include 'non-affected units' to validate the analysis, and ensure that you don't get false negatives or positives (Kraft had many walk-in patients also which fulfilled this aspect).

So, putting the population prevalence question aside, and returning to the diagnostic power of the test - it blows away fasting glucose, and easily beats OGTT. Kraft's point is that we SHOULD be using this test widely, in order to properly identify the afflicted at the earliest possible stage, so that they can take action. In this he is entirely correct I would say....

Note 1: you can switch a pattern 2,3 or 4 to pattern 1 (euinsulinemia) or pattern 5 (hypoinsulinemia) with dietary strategy - many of my MD friends are doing this all the time. However, you need a proper test to verify what you are doing - just like in high-volume manufacture of engineered units

Note 2: If the pancreas is shot, obviously there is less chance of recovery - but the same dietary strategies will apply for optimisation of the situation....

 

[tim2000s]

@FatEmperor, no issue with that. Just wanted to be clear what this is really getting at.

 

[FatEmperor]

@FatEmperor, no issue with that. Just wanted to be clear what this is really getting at.

Thx Tim - here's a bauble for you - lots of references !

http://highsteaks.com/science-diabetes-vs-low-carb-keto-diets/

 

[FatEmperor]

I might expect more quotes.
Which is the problem of making your mind up first, then trawling the internet for evidence to prove your view is correct.
Ultimately, if you only selectively link and quote to those views that prove you are correct, every other view can be easily ignored, as there is no doubt left.

The downside of that is the people you are trying to convince can trawl the internet themselves, them make up their own minds.
(Which is probably a more balanced way round as well). Having done that, it's then very easy to spot those quoting very selective evidence where presented.

I'll wrap up our chat with a reference-based pressie


http://highsteaks.com/science-diabetes-vs-low-carb-keto-diets/

 

[SunnyExpat]

I'll wrap up our chat with a reference-based pressie


http://highsteaks.com/science-diabetes-vs-low-carb-keto-diets/

Well, it certainly proves if you spend long enough looking, you can carefully select a lot of quotes you like the sound of.
Which is what I said.

 

[FatEmperor]

Well, it certainly proves if you spend long enough looking, you can carefully select a lot of quotes you like the sound of.
Which is what I said.

I thought you'd be more interested in the references - they're down at the bottom of the quote list....!

 

[phoenix]

I just found a discussion of this 1990 paper, which seems to be saying that radioimmunoassays of plasma insulin overstate insulin levels because they include proinsulin, which is a precursor to fully formed insulin but isn't biologically active, and which is also over-produced in relation to insulin by both T1Ds and T2Ds. That article is behind a paywall so one can't see if it discussed Kraft. One of the authors was John Yudkin, he of Pure, White and Deadly, so far ahead of his time. OTOH if it isn't discussing Kraft, it may be that it's discussing a different radioimmunoassay technology. One of Kraft's gripes was that procedures were not standardised and therefore were not comparable, so somewhat meaningless.

I don't pretend to make claims about what the detail of this means.

Edit: From the title of this 2007 article,'''Insulin immunoassays: fast approaching 50 years of existence and still calling for standardization,' enough said.

This is still quite old but it discusses the problems c.1999 shedding some light on insulin assays and their interpretation http://www.em-consulte.com/en/article/79835

 

[martykendall]

Hey guys. Sorry I didn't see this earlier. Thanks Indy for bringing it to my attention.

Seems Kraft's worth highlights the need to adopt a lower insulin load diet sooner rather than later.

My recent data analysis seems to suggest that a lower net carb moderate to high protein diet is also the most nutritious.

Although there are lots of things that seem to contribute to insulin resistance, it seems a diet high in empty carb calories the drives up insulin also compounds insulin resistance.

 

[LucySW]

No you are just shouting not discussing .

You yourself appealed to the authority of these three men, and if I remember felt it necessary in your first post to quote your own qualifications, why was that? Personally I think you are appealing to 2 celebrity doctors and cherry picking a third so it's slightly ironic that you accuse me (very rudely ) of appealing to authority.

You acknowledge Dr Unger's work on Glucagon but somehow ignore the rest of his work on insulin which is very relevant to this discussion.
Why is that? Do you really think that peer review somehow works for his paper on insulin but not for the rest of his work? How do you decide?
He has worked on islet cell, insulin. glucagon and how the pancreas loses function in Type 2 and the consequences of the lack of function in T1 for 50 years . So yes I would consider him far more of an authority than you ( someone who arrives claiming that Type 1s could develop T2 [happens sometimes but not that often ] and Type 2 becomes T1 , no it doesn't)

You certainly haven't addressed at the mechanisms of the development of insulin resistance mentioned in either the paper or my earlier post. You suggest that digestible carbs alone increase obesity, this increases insulin production and release and this is followed by insulin resistance.
Why then does weight loss by whatever means even very high carbohydrate diets reduce insulin resistance ? Certainly, as Hall has recently demonstrated, lowering insulin is not essential for fat loss.I'm sure you've seen Carston Chows recent piece, but others may not(and yes I think that he and Kevin Hall are more of an authority than either you or I) https://sciencehouse.wordpress.com/2015/09/09/the-world-of-gary-taubes/

Neither have you addressed whether indeed 'too much' exogenous insulin maybe a problem in T1. This was one of the original points of the thread Interestingly Unger has addressed this fairly recently. And indeed, levels needed for tight control may be contributing to risk although.. perhaps not Unger is a little ambiguous ( From my own point of view, there are no long term outcomes in this study and the main findings are from animals . We do know that people who keep their levels below around 7% have much better long term outcomes. We also know that people who omit insulin are at much higher risk of all types of complications so to me this places the emphasis on hyperglycemia )

http://www.jdcjournal.com/article/S1056-8727(12)00269-3/fulltext#back-bb0050

Here's the working link below to the Unger et al. article on whether iatrogenic hyperinsulinemia is bad for T1s.

Totally agree with you, @tim2000s, that there's not much point worrying about it.

http://www.jdcjournal.com/article/S1056-8727(12)00269-3/pdf

Or this one: http://www.jdcjournal.com/article/S1056-8727(12)00269-3/abstract

 

[Oedett]

I have read Dr Kraft's book and watched his interview with the Fat emperor on his blog site. Dr Kraft was a pathologist as well as researching diabetes he did over 14,300 5 hour fasting glucose tolerance tests with insulin assays patients age between age 3 and 90 plus. His findings were that over 75% had raised insulin levels while some patients had normal blood sugars, weight and cholesterol levels.
He states that it is the insulin that is causing the inflammation in the blood vessels
This is what is causing the pathology leading to the damage heart eyes kidneys and the rest.Dr Kraft did over three thousand post-mortem's and saw the damaging pathology. His conclusion is that
Random blood sugars,fasting bloods, and standard 2 hour glucose tolerance test our poor diagnostic tools and only pick up type 2 diabetics in the late stage of the process,the damage is caused by the high level of insulin so do we need to re look at diagnosis of gestation diabetics, insulin resistance, and the obese not forgetting that you can be thin too and these diabetics can be treated treat with diet and fasting.
Changes to reverse the type 2 diabetic early in the disease process thus preventing the damage that can be caused years before the patient know they are diabetic. The savings to the patient relatives and the public purse are vast.

 

[phoenix]

One of the first links https://www.dropbox.com/s/xvtbzl6zz...atheroma. 20-yr perspectivestout1990.pdf?dl=0 interested me because I think it is a subject worth looking at.
However on my first scan I read thirty rats were fed a standard diet and injected daily with 20U /kg of lente insulin and then didn't develop standard markers of cardiac risk but did develop lesions and a thickened arterial wall . I haven't read the paper in detail because I have to wonder what that has to do with us. If I took 20U per kilo of insulin I would be taking 1280 units of insulin a day. Certainly excess insulin and it would kill me rather faster than my arterial walls would thicken. (why didn't it kill the rats?)For the most part people that take that sort of insulin are those that have very few fat cells; they have lipoatrophic diabetes. They never get DKA, they are very thin, they do have lots of ectopic fat around their organs and that amount of insulin saves their lives (and leptin helps) but it has s** all to do with the rest of us, (I did look a bit further and found that most was about NIDDM so not relevant again to those who are insulin dependent)
Doubt though that I will get a sensible reply from the person who decided to save ourselves from ourselves

Ivor Cummins ‏@FatEmperor Sep 12

Help #diabetes sufferers by signing up here and explaining #LCHF to the uninitiated: http://www.diabetes.co.uk/forum/threads/joseph-kraft-and-hidden-diabetes.83741/page-5…

Sorry @LucySW but this patronising tweet, made me unusually angry, probably maybe fuelled by the stormy weather. The weather though meant I had to go off line; maybe just as well.
Pity because it is an important subject to discuss.(I shall retire now )