Joseph Kraft and hidden diabetes

[RuthW]

Type 1 people are exposed to the ravages of insulin / insulin resistance if they don't minimize their physiological needs via low carb living - a very long life is possible via this route, exploiting pure biochemical reality.
.

Er, no actually, thanks for the entirely unnecessary and wholly incorrect advice. The single way to reduce insulin resistance is extraordinarily simple: exercise. The harder, the better. Anything else is just tinkering round the edges.

I realize that pouring fatty foods down my neck is much more attractive to my lazier side, but in the long-term, for me, exercise is the way to go.

If you take a look at Diabetic Athlete's Handbook, for example, I think you will find that every athlete whose case history is found in there eats more carbs in an hour than some of our most enthusiastic LCHF people eat in a day. And they repeat that hour over and over again. And they are far healthier and less insulin resistant.

So, even if you don't want to be a top athlete, there is another very effective way to reduce insulin resistance. I prefer it.

 

[RuthW]

A virus? for Type 2 Diabetes? Oh lord, this goes against pretty much ALL science and engineering on the topic. I give up. (As for Kraft missing the point - you will have to give a cogent argument as to why that could possibly be true - the stuff you said above is rather risible...)

http://www.webmd.com/diabetes/news/20110203/cold-virus-may-trigger-type-1-diabetes

You know what "trigger" means, right? I suggested a "trigger" mechanism, which is pretty widely accepted for both Type 1 and schizophrenia. And I posted the link between schizophrenia and Type 2. But you may be right. It may be a different environmental trigger for Type 2. Or maybe it is different for SOME Type 2s. Maybe for some the environmental factor is just old-fashioned gluttony. Have it your own way. But I know it can't be for everybody because some Type 2s (my dad, my aunt, my grandfather, my great uncle) are skinny., both before and after diagnosis.

But laugh away. I'm sure it's all risible unless it agrees with your point of view.

 

[FatEmperor]

Er, no actually, thanks for the entirely unnecessary and wholly incorrect advice. The single way to reduce insulin resistance is extraordinarily simple: exercise. The harder, the better. Anything else is just tinkering round the edges.

I realize that pouring fatty foods down my neck is much more attractive to my lazier side, but in the long-term, for me, exercise is the way to go.

If you take a look at Diabetic Athlete's Handbook, for example, I think you will find that every athlete whose case history is found in there eats more carbs in an hour than some of our most enthusiastic LCHF people eat in a day. And they repeat that hour over and over again. And they are far healthier and less insulin resistant.

So, even if you don't want to be a top athlete, there is another very effective way to reduce insulin resistance. I prefer it.

Exercise is great for insulin sensitivity, but it can't fully counteract hyperinsulinemia:

http://www.diabetes.co.uk/celebrities/steve-redgrave.html

http://www.thenoakesfoundation.org/

There are many more athletes who succumbed , and legions who died of hyperinsulinemia induced heart disease...

"Those with cardiovascular disease not identified with diabetes....are simply undiagnosed". Joseph R. Kraft MD, MS, FCAP

Kraft was a captain in the US Army Medical Corps during WWII, and spent the rest of his career decoding this mess. The smartest medical and engineering minds out there are circling in on his profound learnings - it's only a matter of time, in spite of the massive industry funding to subvert science and keep the profit pools brimming over. Sad but w'e're gaining ground on correct science - and the people are waking up...

 

[FatEmperor]

http://www.webmd.com/diabetes/news/20110203/cold-virus-may-trigger-type-1-diabetes

You know what "trigger" means, right? I suggested a "trigger" mechanism, which is pretty widely accepted for both Type 1 and schizophrenia. And I posted the link between schizophrenia and Type 2. But you may be right. It may be a different environmental trigger for Type 2. Or maybe it is different for SOME Type 2s. Maybe for some the environmental factor is just old-fashioned gluttony. Have it your own way. But I know it can't be for everybody because some Type 2s (my dad, my aunt, my grandfather, my great uncle) are skinny., both before and after diagnosis.

But laugh away. I'm sure it's all risible unless it agrees with your point of view.

Sorry about the 'risible' - it was a tad gratuitous. Triggers are fine, but engineers mine for broad, demonstrable root cause. Our art depends on it. The science is already there, it just (like many complex engineering problems) requires some integration and communication. We are getting there. And we will succeed. The health of future generations depends on us doing so.

 

[RuthW]

You can't get "hyperinsulemia" as a Type 1 who exercises properly. Obviously you don't produce any insulin and you cut what you inject. And that's my point. Exercise gives far more control over dosage than LCHF does. And it increases muscle:fat ratio, which further reduces your need for insulin.

I wish the people who rave about LCHF on here were even a quarter as keen on exercise.

 

[TooMuchGlucose]

You can't get "hyperinsulemia" as a Type 1 who exercises properly. Obviously you don't produce any insulin and you cut what you inject. And that's my point. Exercise gives far more control over dosage than LCHF does. And it increases muscle:fat ratio, which further reduces your need for insulin.

I wish the people who rave about LCHF on here were even a quarter as keen on exercise.

You seem to be missing a bit of your own point here, yes exercise increases insulin sensitivity but clearly the lower amount of carbs you inject will mean the lower amount of insulin you inject which would also in turn increase insulin sensitivity to some degree.

 

[FatEmperor]

You can't get "hyperinsulemia" as a Type 1 who exercises properly. Obviously you don't produce any insulin and you cut what you inject. And that's my point. Exercise gives far more control over dosage than LCHF does. And it increases muscle:fat ratio, which further reduces your need for insulin.

I wish the people who rave about LCHF on here were even a quarter as keen on exercise.

Can cut by exercise yes, but crucially by preventing the technical source of the insulin requirement itself. How about you do both - now that would be an engineering solution for sure - removing primary root cause, and enhancing margin by deploying other mitigating parameters. Nice.

 

[RuthW]

You seem to be missing a bit of your own point here, yes exercise increases insulin sensitivity but clearly the lower amount of carbs you inject will mean the lower amount of insulin you inject which would also in turn increase insulin sensitivity to some degree.

No, that's a fallacy. Simply reducing the amount of carbs you eat does NOT increase insulin sensitivity at all. It might spare your beta cells if you have any for a while, but that's not insulin sensitivity. You take less insulin, sure. But that's not insulin sensitivity either. It's just a lower dose matched to slower requirement.

But it is not actually improving your health in any positive way. Exercise actually improves insulin sensitivity - your basal rate goes down, and your insulin to carb ratio goes down, while your calorie and carb intake can both go up without any detrimental effect on HbA1c. In fact, with an accompanying improvement in HbA1c. It's harder to manage at first than LCHF. But LCHF is merely avoiding further damage. It is not actually improving your physiology.

Exercise improves just about everything.

 

[phoenix]

@FatEmperor

Type 1 become Type 2 when over-requiring injected insulin, and Type 2 become Type 1 when they finally exhaust their pancreatic beta cells. The tragedy is that both can prevent progression of disease by removing the root causal factor - excessive carbohydrate. Please help others understand this fundamental reality. I'd suggest you google Dr. Jason Fung also - an insightful nephrologist who has rather cracked the case open....

Type ones do not normally become type 2, and type 2s do not normally become type 1, it is an entirely different process. (one an autoimmune condition with a genetic predisposition, Type 2 probably not just one condition but a conglomerate of conditions with different aetiologies so probably in need of differing treatments (see Gale http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(12)62207-7/abstract)
Tell me, what do you suggest a high insulin dose is for someone who produces negligible insulin of their own ?
The 50 year medallists in the Joslin study took on average 0.46 ± 0.20.units per kg per day. These people were of the era when in the early years fine control was difficult. (and their average HbA1c was in the 7s)
I weigh 64kg so on that I would be taking about 29units per day so I'm a bit under that average. I eat what I think is perfectly normal moderate carbohydrate diet as recommended by my dietitian (I'm in France so less incentive to eat highly processed foods) I use between 22 and 25 units a day and when I exercise more I take less (I'm 63 so mostly walk, I gave up marathons three years ago) My last HbA1c was 5.8%
Tell me why I should turn to a diet that has fewer micronutrients yet requires insulin for non carbohydrate insulinogenic foods (http://care.diabetesjournals.org/content/34/10/2146.abstract) or a high fat diet with even fewer micronutrients than produces what hyperlipid calls physiological insulin resistance and therefore requires more basal insulin to deal with it ? (see Wolever many studies)

 

[RuthW]

Can cut by exercise yes, but crucially by preventing the technical source of the insulin requirement itself. How about you do both - now that would be an engineering solution for sure - removing primary root cause, and enhancing margin by deploying other mitigating parameters. Nice.

Right, again, I am Type 1, not Type 2, so I cannot "prevent the technical source of the insulin requirement itself." My beta cells bid me farewell nearly fifty years ago. I'm still here with no significant complications because of exercise. And I mean that. Because I pre-date blood sugar meters, MDI, human insulin, fast-acting insulin, pumps, the works.

Exercise also is anti-inflammatory, so damage caused by high blood sugars is at least partially repaired by it.

 

[tim2000s]

And herein we come to some interesting questions.

1. What would be considered hyperinsulinemia in a T1. T1 by its very definition is Hyperinsulinemia. Non-T1s don't produce anything like the levels a T1 injects. Is this why T1s suffer higher than normal occurrence of all the associated conditions?

2. Glucagon action, outside of carbs is the key driver of increased glucose levels. Amylin iseems to be the main suppressant of Glucagon although, based on the Afrezza results, circulatory insulin also limits glucagon action on the liver, without necessarily suppressing the glucagon. Based on the mice studies, if you were to exercise regularly, suppress glucagon and eat low carb, would the body be able to manage what glucose was around and also use amino acids with an absence of insulin?

3. Is there any data in Kraft's work pertaining to the diets of those 14000 people?

4. Exercise can be inflammatory. I have experienced this and the associated insulin resistance that follows. Should diabetics therefore have a specific set of guidelines as to what not to do in order to include exercise in their regime?

 

[FatEmperor]

No, that's a fallacy. Simply reducing the amount of carbs you eat does NOT increase insulin sensitivity at all. It might spare your beta cells if you have any for a while, but that's not insulin sensitivity. You take less insulin, sure. But that's not insulin sensitivity either. It's just a lower dose matched to slower requirement.

But it is not actually improving your health in any positive way. Exercise actually improves insulin sensitivity - your basal rate goes down, and your insulin to carb ratio goes down, while your calorie and carb intake can both go up without any detrimental effect on HbA1c. In fact, with an accompanying improvement in HbA1c. It's harder to manage at first than LCHF. But LCHF is merely avoiding further damage. It is not actually improving your physiology.

Exercise improves just about everything.

Exercise is great, and if you need practically no insulin via that route alone then you are doing very well. Countless millions will never achieve this. They need full engineering solutions.

 

[FatEmperor]

Right, again, I am Type 1, not Type 2, so I cannot "prevent the technical source of the insulin requirement itself." My beta cells bid me farewell nearly fifty years ago. I'm still here with no significant complications because of exercise. And I mean that. Because I pre-date blood sugar meters, MDI, human insulin, fast-acting insulin, pumps, the works.

Exercise also is anti-inflammatory, so damage caused by high blood sugars is at least partially repaired by it.

Type 1's can 'prevent (or minimise) the technical source of the insulin requirement itself' - the source of the requirement for insulin is the ingestion of carbohydrate foods (and to an extent protein). Remove this insulin-requiring source in as much as possible. And do your exercise too of course - it is a very healthy pursuit for sure.

 

[FatEmperor]

Kraft switched off the hyperinsulinemic response of T2D with low carb - demonstrated, as it's being demonstrated all over the world currently - snippit near bottom of this post:

http://www.thefatemperor.com/blog/2015/9/7/kraft-summary-re-post-for-those-who-missed-it

Guys on this website should watch ALL of Dr. Bernstein's lecture series (he's an engineer, doctor and T1 for life - and he's cracked it all):

https://www.youtube.com/watch?t=98&v=Z80-c0CXYqc

 

[RuthW]

And herein we come to some interesting questions.

1. What would be considered hyperinsulinemia in a T1. T1 by its very definition is Hyperinsulinemia. Non-T1s don't produce anything like the levels a T1 injects. Is this why T1s suffer higher than normal occurrence of all the associated conditions?

2. Glucagon action, outside of carbs is the key driver of increased glucose levels. Amylin iseems to be the main suppressant of Glucagon although, based on the Afrezza results, circulatory insulin also limits glucagon action on the liver, without necessarily suppressing the glucagon. Based on the mice studies, if you were to exercise regularly, suppress glucagon and eat low carb, would the body be able to manage what glucose was around and also use amino acids with an absence of insulin?

3. Is there any data in Kraft's work pertaining to the diets of those 14000 people?

4. Exercise can be inflammatory. I have experienced this and the associated insulin resistance that follows. Should diabetics therefore have a specific set of guidelines as to what not to do in order to include exercise in their regime?

Those are all good points. On the first one, yes but what we inject is not identical to what non-diabetics produce.

On the last one, yes, it is first inflammatory - we are, so to speak, deliberately causing inflammation in our muscles, in order to cause them to develop - and one of the beneficial side effects of that is that our body then produces healing/anti-inflammatory substances. The process is beautifully limited, unlike the pathological inflammation we may get from, say, a flu infection. It's second beautiful feature is that as the anti-inflammatory substances course around our bodies, they have a lovely effect on other bits too!

So yes, weight lifting or anaerobic exercise produces a certain amount of insulin resistance, for a limited time, but it has a useful function in the body. And it occurs in non-diabetics too. Which is another reason why I was not over-impressed with Kraft's observations and definitions of "normal" as presented here. If non-diabetics also have insulin resistance maybe that doesn't mean they have "hidden diabetes", maybe it means insulin resistance has a useful biological function in the body. And it is therefore frequent.

 

[FatEmperor]

Those are all good points. On the first one, yes but what we inject is not identical to what non-diabetics produce.

On the last one, yes, it is first inflammatory - we are, so to speak, deliberately causing inflammation in our muscles, in order to cause them to develop - and one of the beneficial side effects of that is that our body then produces healing/anti-inflammatory substances. The process is beautifully limited, unlike the pathological inflammation we may get from, say, a flu infection. It's second beautiful feature is that as the anti-inflammatory substances course around our bodies, they have a lovely effect on other bits too!

So yes, weight lifting or anaerobic exercise produces a certain amount of insulin resistance, for a limited time, but it has a useful function in the body. And it occurs in non-diabetics too. Which is another reason why I was not over-impressed with Kraft's observations and definitions of "normal" as presented here. If non-diabetics also have insulin resistance maybe that doesn't mean they have "hidden diabetes", maybe it means insulin resistance has a useful biological function in the body. And it is therefore frequent.

Unfortunately you guys are fixated by Insulin Resistance. Wider focus needed. Outside of one exception:

"Hyperinsulinemia Is Insulin Resistance. They Are Not Combatants. They Are One And The Same." Joseph R. Kraft MD, MS, FCAP

The obsession with Insulin Resistance is in some ways distracting - focus on the hyperinsulinemia. The exception to Kraft's insightful quote above is that healthy Low-Carb people have what is called 'physiological Insulin resistance'. The body spares glucose for non-muscle tissues as an elegant efficiency measure. There is no hyperinsulinemia per se present.

The pathological hyperinsulinemia response that most Americans have can be switched off after a period on low carbohydrate. This makes perfect sense under the three pillars of engineering root cause proof: 1. KT or correlational 2. Mechanistic 3. Experimental.

Busy now with more pressing matters - learn from Dr. Kraft, Dr. Bernstein and Dr. Unger - three pillars of medicine, all in their eighties. And honorary engineers, every one.

 

[NoCrbs4Me]

And it occurs in non-diabetics too. Which is another reason why I was not over-impressed with Kraft's observations and definitions of "normal" as presented here. If non-diabetics also have insulin resistance maybe that doesn't mean they have "hidden diabetes", maybe it means insulin resistance has a useful biological function in the body. And it is therefore frequent.

Insulin resistance is likely not normal, except in the context that it is a normal response to too much refined carbohydrate in the diet. However, a diet high in refined carbohydrates is not the normal diet for humans up until very recently in our evolutionary path. I doubt very much that elevated insulin levels are healthy, but they are probably healthier than massively high blood glucose levels.

 

[SunnyExpat]

Er, no actually, thanks for the entirely unnecessary and wholly incorrect advice. The single way to reduce insulin resistance is extraordinarily simple: exercise. The harder, the better. Anything else is just tinkering round the edges.

I realize that pouring fatty foods down my neck is much more attractive to my lazier side, but in the long-term, for me, exercise is the way to go.

If you take a look at Diabetic Athlete's Handbook, for example, I think you will find that every athlete whose case history is found in there eats more carbs in an hour than some of our most enthusiastic LCHF people eat in a day. And they repeat that hour over and over again. And they are far healthier and less insulin resistant.

So, even if you don't want to be a top athlete, there is another very effective way to reduce insulin resistance. I prefer it.

Right on the mark.
Exercise is the best way to overcome insulin resistance.
Regular gym sessions, (or my case today, knocking down an old out building), and my BG is much better than LCHF alone.
For days afterwards as well.
I'm not knocking those that can't do exercise, as obviously then LCHF is the main attack they have.

 

[SunnyExpat]

Insulin resistance is likely not normal, except in the context that it is a normal response to too much refined carbohydrate in the diet. However, a diet high in refined carbohydrates is not the normal diet for humans up until very recently in our evolutionary path. I doubt very much that elevated insulin levels are healthy, but they are probably healthier than massively high blood glucose levels.

Well, that cheery nod to Darwinism means we're the dead end of the evolutionary tree.
If we can't take the modern diet, evolution will weed us out.

 

[phoenix]

@FatEmperor
So what does Unger, the only one of your three who has really done any real scientific research (rather than anecdote) suggest is the route to the metabolic syndrome? Not any one macronutrient but a fifty year experiment in overexposure to too much food (both fat and carbohydrates) an:
" unremitting caloric surplus complicated by failure of adipocytes to maintain protection against lipotoxicity"
http://www.ncbi.nlm.nih.gov/pubmed/20223680
Which is I think what I suggested in my first post.