Joseph Kraft and hidden diabetes

[SunnyExpat]

They all have a lifetime of clinical experience and research, and your comment is thus scandalous, but I see many like it sadly. So please don't do the 'appeal to official authority' stuff - research is not limited to the peer-reviewed system which is acknowledged to be severely compromised. These are particularly mild and restrained discussions - some very eminent medical leaders have been far harsher: http://michaelnielsen.org/blog/three-myths-about-scientific-peer-review/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420798/

That said the answer to your question is becoming obvious - primary root cause is excessive digestible carbohydrate with the accelerant factor donated by fructose via the liver mechanisms. When you have true root cause it can be easily demonstrated. Removing the mentioned factors massively reduces Met Syn, T2D, Obesity and all associated inflammatory markers. Without heavy calorific reduction. Without major exercise. QED. Thank you for listening

Not really.
Simply ignoring exercise as part of the study is simply leaving out data as you've decided on what the conclusion is, and only including the information that with fit into that outcome.
Good 'engineering' takes all of it into account,

When you listen to that, you'll have a sensible argument.

 

[FatEmperor]

Not really.
Simply ignoring exercise as part of the study is simply leaving out data as you've decided on what the conclusion is, and only including the information that with fit into that outcome.
Good 'engineering' takes all of it into account,

When you listen to that, you'll have a sensible argument.

exercise is a given, universal benefit and is not under debate in itself. The main 'engineering' problem with this exercise factor, is the impracticality of getting everyone to do it. The most universally 'addressable' factor is the key focus - the only thing holding back this is misunderstanding of the science. Fix the latter, and the people can have a delicious, nutritious method to help manage their diabetes. The current unscientific fear of fat, and lack of realization that it is only problematic in the presence of excessive carbohydrate, needs to be fixed to stem the epidemic. And of course they hopefully will exercise too, as everyone knows this helps hugely...

People may find this primer helpful; read it and weep - at our current strategy for Type 2 Diabetes:

http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext

Best
Ivor

 

[FatEmperor]

exercise is a given, universal benefit and is not under debate in itself. The main 'engineering' problem with this exercise factor, is the impracticality of getting everyone to do it. The most universally 'addressable' factor is the key focus - the only thing holding back this is misunderstanding of the science. Fix the latter, and the people can have a delicious, nutritious method to help manage their diabetes. The current unscientific fear of fat, and lack of realization that it is only problematic in the presence of excessive carbohydrate, needs to be fixed to stem the epidemic. And of course they hopefully will exercise too, as everyone knows this helps hugely...

People may find this primer helpful; read it and weep - at our current strategy for Type 2 Diabetes:

http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext

Best
Ivor

Actually, someone pointed out that my manner is high-handed and unhelpful - apologies for this. I just find it intensely frustrating that science is being subverted all around us, for the benefit of the lucrative status quo as it applies to food and pharma companies. Perhaps read through the last paper above, which will help explain my frustration having studied this area for some time. The more you learn about the genuine data around this, the more the arguments take on surreal nature...

http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext

 

[SunnyExpat]

exercise is a given, universal benefit and is not under debate in itself. The main 'engineering' problem with this exercise factor, is the impracticality of getting everyone to do it. The most universally 'addressable' factor is the key focus - the only thing holding back this is misunderstanding of the science. Fix the latter, and the people can have a delicious, nutritious method to help manage their diabetes. The current unscientific fear of fat, and lack of realization that it is only problematic in the presence of excessive carbohydrate, needs to be fixed to stem the epidemic. And of course they hopefully will exercise too, as everyone knows this helps hugely...

People may find this primer helpful; read it and weep - at our current strategy for Type 2 Diabetes:

http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext

Best
Ivor

No thanks, I prefer exercise to sitting around reading mindless studies on the internet all day, that are carefully selected by people that have decided their lifestyle is the only one that works.

Fix that, and you'll see improvements.
I think maybe switching the internet off for 2 days out of 7 would be more beneficial for the human race then spending it trying to convince them high fat is the only way to eat.

 

[tim2000s]

Just a play for optimum health, productivity and longevity - I guess it's a personal choice. Hyperinsulinemia and hyperglycemia are both problems - there is an over-focus on the glucose, and an under-appreciation of insulin toxicity (for example see ACCORD study - higher treatment, much lower blood glucose metrics achieved....and higher mortality - this confuses them, though it shouldn't). Besides its sub-optimum nature, modern treatment disposes towards wide fluctuations in blood glucose (due to using exogenous insulin which is not nearly as effective as pancreatic release - shotgun rather than sniper rifle). So you have all the sinusoidal fluctuations in toxicity and indeed wellness. Anyway, I'm kinda busy so moving on - it's been good to connect.

For someone engaging in debate on a forum, you are very brusque, and certainly demonstrate an "I'm always right" attitude that can be slightly annoying, however, I can't say I disagree with the comment relating to modern diabetes treatment methods.

This particular post appears to portray a misunderstanding of the management of T1 and some of the additional medical issues unrelated to insulin levels that affect T1s, which are not limited to auto-immune conditions and bone structure issues. Whilst I am not advocating that T1s should eat what they want and dose huge amounts of insulin, the only area that you can truly control Glucose levels is via food intake and there are multiple ways of doing this. Bernstein's is one.

Unfortunately there are many other factors that can cause hyperglycaemia (where we regard it to be more than the "normal" levels) and these require insulin to control. Even with reduced insulin resistance in general, it is still required and still effectively is an induced form of hyperinsulinemia as a result of hyperglycaemia over which a T1 has no control, save for sitting in a sterile box, and doing absolutely nothing. As most of us don't fancy that kind of life, many of us make a fist of getting on with it. As exogenous insulin induces Hyperinsulinemia under any circumstances and there is essentially no research into what might be considered a "safe" level of insulin, there seems little point in worrying, as a T1, whether we have it.

It's a bit like death. All T1s know they are mortal. We do stuff to stay alive. Many of us do stuff to stay alive with as few of the rapid onset nasties that hyperglycaemia can induce as possible. Excess insulin is a fact of life for a T1. The question is simply to what degree. As there are many other things out there trying to kill us, it is basically a risk assessment, and to try and enjoy life. As we are inherently at greater risk of all the side effects of hyperinsulinemia, than anyone else, including T2s and non-diabetics, even with a low carb diet, there seems little point in over focussing on it.

 

[Celeriac]

The University of Sydney's Sydney eScholarship Repository link to Kirstine Bell's postgraduate thesis ' Clinical Application of the Food Insulin Index to Diabetes Mellitus ' http://hdl.handle.net/2123/11945

Somewhere in that, I seem to remember that in one experiment, they gave people without diabetes and T2s the same food and measured their insulin response and the T2s put out up to 142% more insulin.

Presently, I am working out the FII for food that I buy, because I want to lower insulinogenic proteins as well as carbs.

My ophthalmologist says that it's likely that my eyes have improved because of the food that I eat.

I take the view that my body is firing on fewer cylinders, as it were, so I try to give it really nutritious food to give it the tools to do as well as it can despite diabetes. My ophthalmologist agrees that if you give your body as much help as you can, it will help you back.

I am not bugged at all by people sharing studies, I think that's helpful. I think even some stuff from Ayurvedic medicine, naturopathy etc can be helpful. (I don't believe in homeopathy though). Poster's personal experiences can be useful too.

What bugs me, is that so many posters act all smug about getting good numbers when eating toast. Toast is like soo nutritious, I don't think. Ditto Paleo mug cakes with weirdo flours and a tonne of artificial sweeteners. It's rubbish, nutritionally.

Dr Gillian McKeith was found not to be a doctor, but the title of her book, 'You Are What You Eat' still holds true.

Dr Jason Fung says that diabetes is a symptom of insulin resistance, that the medical profession wouldn't treat a fever and not treat the underlying infection, yet by treating high blood glucose not insulin resistance, that's what it's doing.

I look at it as why eat stuff that doesn't keep you healthy, and take any risk that the insulin resistance, which isn't being treated, is getting worse. Because we know that while low carb diets lower blood glucose, high fat can cause insulin resistance.

 

[FatEmperor]

The University of Sydney's Sydney eScholarship Repository link to Kirstine Bell's postgraduate thesis ' Clinical Application of the Food Insulin Index to Diabetes Mellitus ' http://hdl.handle.net/2123/11945

Somewhere in that, I seem to remember that in one experiment, they gave people without diabetes and T2s the same.e food and measured their insulin response and the T2s put out up to 142%more insulin.

Presently, I am working out the FII for food that I buy, because I want to lower insulinogenic proteins as well as carbs.

Bravo Celeriac - and you reminded me of a crucial document penned by an engineering friend of mine - his wife is a Type 1 diabetic so he studied the arena intensively, and produced this masterpiece:

http://www.thefatemperor.com/blog/2...imate-guide-to-insulin-carb-and-protein-count

Best of luck!

 

[FatEmperor]

No thanks, I prefer exercise to sitting around reading mindless studies on the internet all day, that are carefully selected by people that have decided their lifestyle is the only one that works.

Fix that, and you'll see improvements.
I think maybe switching the internet off for 2 days out of 7 would be more beneficial for the human race then spending it trying to convince them high fat is the only way to eat.

Fair enough SunnyExpat - as a final gift: http://www.thefatemperor.com/blog/2...imate-guide-to-insulin-carb-and-protein-count

 

[tim2000s]

Bravo Celeriac - and you reminded me of a crucial document penned by an engineering friend of mine - his wife is a Type 1 diabetic so he studied the arena intensively, and produced this masterpiece:

http://www.thefatemperor.com/blog/2...imate-guide-to-insulin-carb-and-protein-count

Best of luck!

You should read the topic posted on this very paper about six months ago. There was a significant amount of debate and further refinement provided by many of us, including myself. There have been many interactions with Marty on this as well as topics discussing the best way to administer insulin to respond to protein and fat in the diet. Such a small world!

 

[LucySW]

Bravo Celeriac - and you reminded me of a crucial document penned by an engineering friend of mine - his wife is a Type 1 diabetic so he studied the arena intensively, and produced this masterpiece:

http://www.thefatemperor.com/blog/2...imate-guide-to-insulin-carb-and-protein-count

Best of luck!

Indeed - I tagged @martykendall at the off. I wish he'd come in.

Can we please take questions of how T1Ds can manage their insulin to a new thread, and return this one to discussing what Kraft's findings might mean for insulin metabolism.

Lucy

 

[Celeriac]

Fat Emperor and tim2000s yes I have read lots of Marty's stuff, still got a lot to read. I'm working out the FII values for all my food thanks to Dr Ted Naiman's calculator so I can prioritise low FII where poss.

Dr Jason Fung has said that T2 diabetes is a dietary disease so that's how it should be treated.

In the UK we're left to the NHS Eat Well plate. The majority of dieticians and doctors daren't deviate from NHS policy so apart from the few brave ones e.g. Dr Aseem Malhotra, and those in private practice eg Dr John Briffa, Dr Charles Clarke, we have to rely on American doctors or celebrity nutritional therapists like Amelia Freer or Ella Woodward. I just don't think there's enough good British nutrition advice and I feel lucky to live in the Internet Age !

I low carbed using conventional food, cooking from scratch from 2010 - 2012 and lost weight, but the real health marker improvements and retinopathy improvement came since I switched to organic in 2012.

 

[RuthW]

exercise is a given, universal benefit and is not under debate in itself. The main 'engineering' problem with this exercise factor, is the impracticality of getting everyone to do it. The most universally 'addressable' factor is the key focus - the only thing holding back this is misunderstanding of the science. Fix the latter, and the people can have a delicious, nutritious method to help manage their diabetes. The current unscientific fear of fat, and lack of realization that it is only problematic in the presence of excessive carbohydrate, needs to be fixed to stem the epidemic. And of course they hopefully will exercise too, as everyone knows this helps hugely...

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"

 

[LucySW]

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.

 

[Celeriac]

I'm buying an exercise bike so that I can pedal away while listening to music and surfing the net, without getting run over by a bus.

 

[tim2000s]

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.

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?

 

[zand]

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

Diet definitely. But then maybe I haven't found the right exercise?

 

[NoCrbs4Me]

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"

Not eating carbs while eating lots of fat cured me, without much exercise. Just saying...

 

[phoenix]

They all have a lifetime of clinical experience and research, and your comment is thus scandalous, but I see many like it sadly. So please don't do the 'appeal to official authority' stuff - research is not limited to the peer-reviewed system which is acknowledged to be severely compromised. These are particularly mild and restrained discussions - some very eminent medical leaders have been far harsher: http://michaelnielsen.org/blog/three-myths-about-scientific-peer-review/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1420798/

That said the answer to your question is becoming obvious - primary root cause is excessive digestible carbohydrate with the accelerant factor donated by fructose via the liver mechanisms. When you have true root cause it can be easily demonstrated. Removing the mentioned factors massively reduces Met Syn, T2D, Obesity and all associated inflammatory markers. Without heavy calorific reduction. Without major exercise. QED. Thank you for listening

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 )

The fact that the endogenous hyperinsulinemia of T2D has been implicated in the increased incidence of atherogenic complications raises the possibility of differences in the lipogenic and cholesterologenic activities of exogenous and endogenous hyperinsulinemia. While this could simply reflect a greater hepatic uptake of insulin delivered via the portal vein, despite normal insulin levels far below those of hyperinsulinemic TID mice, nondiabetic mice expressed the CAD risk markers at the same levels as most hyperinsulinemic T1D mice. This fact supports earlier observations(1958Madison, L.L. and Unger, R.H. The physiologic significance of the secretion of endogenous insulin into the portal circulation. )However, the purpose of this study was to determine if “tight control” in patients with T1DM carries an increased risk of macrovascular disease. Our results suggest that intensive glycemic control in type 1 diabetes can contribute to an increased risk for CAD via inflammation independent of hepatic cholesterol metabolism

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

 

[RuthW]

He argues that insulin causes inflammation in the endothelium, and there you are.

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.

 

[LucySW]

Phoenix, can you improve that link? It doesn't work.