Joseph Kraft and hidden diabetes

LucySW

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This is a long post. Sorry – it’s worth it. I do not know what to think and would realIy welcome input. @Spiker, @tim2000s, @phoenix, @martykendall, @Brunneria, @Indy.

I’m feeling a bit gobsmacked, having read the Joseph R. Kraft book, Diabetes Epidemic & You. He published it in 2008 after, presumably, frustration at his numerous papers in the 1970s and 1980s not getting anywhere. It’s available on Kindle. Here is a PDF of one of his papers giving a summary of his work.

Anyway, the point is that at the University of Illinois medical school in Chicago, Kraft and others were using a technique that never took off anywhere else to measure blood insulin levels during the OGTT test. And what they found – what he documents – was that most of the patients who passed the OGTT with normal blood sugar levels were not actually normal. 78% of the normal glucose tolerance group had massively raised blood insulin levels, which were keeping their blood sugars normal. In other words, 78% of the ‘normal’ blood sugar patients who passed the OGTT test were already launched on the diabetes disease process, but it was invisible because it hadn’t shown up in the blood sugar yet.

There are a number of questions this raises, but first here’s a sketch of what Kraft did.

He was a Chicago MD and clinical pathologist who in the 1950s (he's 95 ! but still alive) worked at the Oak Ridge Institute of Nuclear Studies in Tennessee. He was trained there, with some other clinical pathologists, to use radioisotope technology for laboratory examinations. This was because existing lab test techniques were considered unacceptably inaccurate.

Then he went to teach at the Pathology Dept in the University of Illinois medical school in Chicago. Some others in that department had a research interest in measuring plasma insulin. This had been done a bit in the 1950s but was difficult. So when a new insulin testing substance was released in 1970, the department started to run radioisotope insulin assays as a part of the OGTT tests they ran on patients referred to them. This procedure began in 1972 and continued till 1998. (Kraft retired then.) It seems it was a particular research interest of the Illinois U. medical school, and it doesn’t seem to have been done anywhere else. (There are other tests for insulin plasma levels, but Kraft says they are much less informative, and that it’s useless to test fasting insulin levels, because they’re low in everybody including full-blown T2Ds.)

So he conducted the OGTT together with a radioisotope insulin assay on 14,000 patients between 1972 and 1988. He says, “The 14,384 subjects were healthy persons submitted by their physicians for oral glucose tolerance with insulin assays, 100-g glucose load. This was for the purpose of excluding or identifying diabetes mellitus. The age span was from the very young (less than 14 years of age) to the elderly (greater than 80 years of age). “

He developed three types of insulin profile:

1. A normal profile: insulin peaks at half to one hour, then falls quickly (with the sum of the 2hr and 3hr levels <= x2 the normal fasting range) and is back to fasting levels by 4hr.

2. Three profiles indicating very highly increased insulin levels: insulin peaks later at 1-2 hrs and at much higher levels, back to fasting levels only at 5 hrs.

3. A level indicating very inadequate insulin production, predicting T1D.

The OGTT test classified the subjects as having Normal Glucose Tolerance, Impaired Glucose Tolerance, or DM (Diabetes) Glucose Tolerance. But of the Normal Glucose Tolerant group, 22% showed what he defined as a normal insulin response; 74% showed abnormal insulin profiles; and 4% showed the T1D-predicting lowered insulin profile.

Kraft sees the abnormal insulin profiles as indicating the early stages of the T2D disease process, what he called the ‘occult’ stage (because hidden, because blood sugars were still in the normal range). The blood sugars were kept normal at the cost of vastly escalated insulin production, because of insulin resistance.

These 15,000-odd included 117 children aged 3–13. 45% of these had normal glucose profiles but had hyperinsulinemic profiles. And 651 teenagers aged 14–20, of whom 67% had normal glucose tolerance but hyperinsulemic profiles. And on and on – more in the older age groups, of course. As he says, diabetes is an age-related risk.

The patients were not tracked over time, but Kraft says it is beyond doubt that the hyperinsulinemia was the very early stages of the diseased metabolism that leads eventually to full-blown T2D after some years. High BG levels would only show at the end of this process.

He makes a couple of points:

1. That monitoring BG levels catches only a very late stage of the disease process. So if we tested in a different way, the process could be caught earlier, while we can still reverse it with dietary change, etc.

2. That within the bodies of these apparently healthy people, including the 117 children and the 651 teenagers, the pathology of diabetes was already unfolding, causing atherosclerosis aka heart disease and complications throughout the body. He says, “The pathology of diabetes mellitus is vascular. This includes all major arteries, all minor arteries, and all capillaries.”

3. He is actually saying - on the basis of his autopsies, he was a real autopsy fiend, at least 3,000 - that the cause of atherosclerosis and heart disease is diabetes. Not LDL cholesterol, but diabetes. He argues that insulin causes inflammation in the endothelium, and there you are.

Edit Sept. 2016: Others would say that rather than diabetes (and it was never tracked which patients went on to develop diabetes), it is hyperinsulinemia, raised insulin circulating in the blood, that should be seen as having these effects.

Back to original post:

My questions are different. What does it mean that there were so many diseased insulin profiles among these patients and among the children too? Does it mean the children inherited these faulty metabolisms from diabetic parents? Could the American diet of the 1970s/1980s really explain this crazy dysfunctionality? Or does it mean that actually we have to regard insulin dysfunction as a physical deterioration that’s part of the ageing process, something that was always there and we didn’t know about it? (But then if this pattern had always existed, the lifestyle diseases associated with insulin resistance – diabetes, high blood pressure, atherosclerosis, some cancers – shouldn’t have peaked in the twentieth century.)

Jason Fung refers to this work recently. I've linked a PDF summarising Kraft's work at the top. Otherwise, the book is available on Kindle for £5 and there are a few posts by Ivor Cummins (The Fat Emperor) about it including an interview. Otherwise, nothing.

As I said, gobsmacked.

Lucy, and thanks to @Indy for flagging this.

Oops, perhaps this should be in Discussions.

Edit: If you watch the video of Ivor Cummins interviewing Kraft, you get to see Kraft talking about his colleague's love affair with the kidneys ...
 
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tim2000s

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The issue with this is that there was no follow up undertaken to determine whether the "diseased" profiles did result in T2D.

In this fairly large screening of 14,000 or so people, only 25% have ended up with "normal" insulin metabolism. If diseased profiles were the only precursor to T2D, surely a larger percentage of the elderly population would now be T2?
 
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Brunneria

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This is fascinating. Thank you @LucySW

- it certainly opens the debate on 'what is normal bg' even wider!

In response to your questions, I am afraid I am going to fall back on my old standby that we, the human race, are simply not intended to eat the modern diet. And if a bad diet is fed to a population (whether they are rats, cats or humans) for enough generations, then that population will deteriorate in health.

What Kraft saw developing in blood tests, has now progressed to 'the diabetes epidemic', as we are now a generation further on...

But I am sorry, Lucy, those are glib pre-judgements. I really need to read the book and then see if I still feel the same.
 
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Brunneria

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@Indy51 brilliant - I have been trying to remember the name of the study - and it was Pottinger's.

It has been years since I saw that. And sadly, I am 3rd generation. At least.
Each of the 2 preceding generations in my family took great care of their health - in later life.
They did nothing to look after themselves and their diet until after they had produced the next generation => me.
 
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reidpj

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Maybe the whole population (yeah, I know it's not going to happen) should be given a OGTT with their c-peptide tested at the same time (pro insulin is cleaved into one molecule of insulin and one of c-peptide). Anyone with raised insulin levels (indicated by raised c-peptide) could then be advised accordingly.
 
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NoCrbs4Me

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I read this book as well - it's quite enlightening. That's when I decided that "eating to your meter" is not quite the panacea for type 2 self treatment that seems to be generally believed here, although it is infinitely better than eating to the NHS healthy plate and not self-testing.

Yes, you can lower the grams of carbohydrate per meal to the point where your BG only rises a small amount, but you have absolutely no idea how much insulin you are producing to achieve that. I changed my approach to consuming as little carbohydrate as possible. I agree with Brunneria that we are not meant to eat lots of refined carbs or starchy plants constantly, day after day.
 
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Lamont D

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As someone who has a regular glucose test. And flushes insulin!
I'm going to consume this before replying.
I knew that excessive insulin causes problems and my high range of glucose levels when I was ill, could have done irreparable damage.
Only too glad to have found you lot to put me straight!

I might need help with the scientific bits tho!
 
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Gravity-Carb

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I read this book as well - it's quite enlightening. That's when I decided that "eating to your meter" is not quite the panacea for type 2 self treatment that seems to be generally believed here, although it is infinitely better than eating to the NHS healthy plate and not self-testing.

Yes, you can lower the grams of carbohydrate per meal to the point where your BG only rises a small amount, but you have absolutely no idea how much insulin you are producing to achieve that. I changed my approach to consuming as little carbohydrate as possible. I agree with Brunneria that we are not meant to eat lots of refined carbs or starchy plants constantly, day after day.

@NoCrbs4Me with your theory, which I agree with (in theory!), it would explain why some people might lose a little weight when embarking on a LCHF diet although their meter readings are good for them, if they are still producing epic amounts of insulin in response to foods consumed then the fat will stay. Following that train of thought, T2 can't really say they have their beast in remission if they don't know if they've got hyperinsulinema(sp?) or not.....interesting.

So some money is to be had if someone came up with an accruate insulin meter... wonder if dragon's den would cover it.

@LucySW thank you for the research....
 
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andcol

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What I take from it is that he is identifying the large percentage of the population that has ice age genes and we should be eating fat and not carbs. I don't think they are diabetic in situ as he states. I would prefer generically unsuitable for today's hclf diets and society will kill them. The sooner we are all tested in our early years and told the better instead of waiting until it is too **** late.
 
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LucySW

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This is fascinating. Thank you @LucySW

- it certainly opens the debate on 'what is normal bg' even wider!

In response to your questions, I am afraid I am going to fall back on my old standby that we, the human race, are simply not intended to eat the modern diet. And if a bad diet is fed to a population (whether they are rats, cats or humans) for enough generations, then that population will deteriorate in health.

What Kraft saw developing in blood tests, has now progressed to 'the diabetes epidemic', as we are now a generation further on...

But I am sorry, Lucy, those are glib pre-judgements. I really need to read the book and then see if I still feel the same.
Or watch the video. It's got a better explanation. Plus you get to see his sweet little knees
 
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phoenix

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We don't know without a follow up study if these 75% did go onto develop diabetes or not, numbers suggest not since diabetes rates don't approach that sort of figure (and seem to have peaked in the West) . Perhaps his definition of what is normal is not correct; it certainly wasn't the norm.
I realise that he suggested fasting insulin wasn't a good test but nevertheless fasting insulin does show differences between groups. Kitavan Islanders have been shown to have very much lower fasting insulin levels than a randomly selected group of Swedes. Waist circumference levels also predicted fasting insulin in both Kitavans and Swedes. As a group Kitavans have a very low (miniscule) incidence of heart disease.
(and of course as you can probably guess they eat very few processed foods but they eat a very high carbohydrate diet ;) http://wholehealthsource.blogspot.fr/2010/12/interview-with-kitavan.html)
Have the Kitavans got a different genetic makeup to us? I suspect not that different, just as our genes aren't that different to our ancestors who didn't develop T2
( caveat on genes: epigenetics; ie the way some genes are expressed and others not can be altered in the womb so that would be a possible cause of rapid inherited change ) http://learn.genetics.utah.edu/content/epigenetics/inheritance/
 
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LucySW

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We don't know without a follow up study if these 75% did go onto develop diabetes or not, numbers suggest not since diabetes rates don't approach that sort of figure (and seem to have peaked in the West) . Perhaps his definition of what is normal is not correct; it certainly wasn't the norm.
]

We don't know enough about the testees. They were all referred for OGTT testing - it wasn't a trial - so altho he says they were normal and healthy, they must have been selected for something.

So yes, of course more detail needed. But even so - what do these hyperinsulinemia patterns tell us? They do require explaining.
 

NoCrbs4Me

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This is kind of interesting regarding hyperinsulinemia with respect to western diets and pre-western contact diets:

http://wholehealthsource.blogspot.ca/2008/08/cardiovascular-risk-factors-on-kitava_17.html

"We can guess that total fat, saturated fat and carbohydrate do not cause hyperinsulinemia, based on data from the Inuit, the Masai and the Kitavans, respectively. We can also guess that there's not some specific food that protects these populations, since they eat completely different things. Exercise also can not completely account for these findings. What does that leave us with? Western food habits. In my opinion, the trail of metabolic destruction that has followed Westerners throughout the world is probably due in large part to industrial foods, including refined wheat flour, sugar and seed oils."
 
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Brunneria

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Just watched the interview video.

Huge food for thought.

I am actually less interested in whether the abnormal insulin producers (the majority) developed diabetes than in whether they developed the capillary damage to kidneys and heart.

The test showed insulin resistance. That was clear. The data on organ damage pre diabetic diagnosis is something we see on this forum all the time.

Unfortunately, that data won't ever be collated.

And what a lovely man.

I'm tagging @Winnie53 because I am sure she will find this fascinating too.

Once again, thank you @LucySW
 
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LucySW

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That's what primarily interests me too, B. The prospect of hidden vascular damage.

I don't think there's any question about his assay test either. I think the findings are impregnable. It's a question of what they mean.

And this is *so* important: the question of what dysinsulinemia (? can we call it that?) can do to us. And the suggestion, along with Gary Taubes, that it's too-high insulin that does the damage.

Lucy
 
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Gravity-Carb

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That's what primarily interests me too, B. The prospect of hidden vascular damage.

I don't think there's any question about his assay test either. I think the findings are impregnable. It's a question of what they mean.

And this is *so* important: the question of what dysinsulinemia (? can we call it that?) can do to us. And the suggestion, along with Gary Taubes, that it's too-high insulin that does the damage.

Lucy

Not high blood glucose? Sorry not watched the video yet as still collating receipts for accountant, but I thought it was the high BG that was "powdered glass, in blood causing inflammation where ever blood goes" or summut like that....
 

NoCrbs4Me

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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.
 
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