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Joseph Kraft and hidden diabetes

phoenix said:
One of the first links https://www.dropbox.com/s/xvtbzl6zz...atheroma. 20-yr perspectivestout1990.pdf?dl=0 says' 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. 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,
Doubt though that I will get a sensible reply from the person who decided to save ourselves from ourselves

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 )
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I thought it was quite funny, if you mean the one where he quoted me as well on page 5?
I always find people who have no acceptance of any other viewpoint, and simply patronise those who do seek to discuss other options quite amusing.
I said on another thread, I don't normally bother looking at links that agree with my diet, I prefer to read those that disagree with me.
Other's obviously don't have the same view.
 
phoenix said:
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
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Ah Phoenix, I am not appealing to their authority, merely their data to date - I found Unger's data on glucagon particularly fascinating is all, so I shared it. The Hall study you mention was tragically misinterpreted - it set out to isolate insulin, but the calorie restriction dropped the insulin levels similarly in both arms - oops; sorry - need read right down for the insulin bit, also attached snippit though:

http://metabolismandmedicine.blogspot.ie/2015/08/did-low-fat-oust-low-carb-for-fat-loss.html

Six days allowed no time for metabolic adaptation, and their extrapolation to long term was thus one of the most absurd flights of fancy I have nearly ever seen. There are many analyses of the study far less restrained than the one I've linked to above.

The ACCORD study showed worse outcomes on average for intensive insulin treatment, even though they got great glucose-lowering - so a reduction in glycotoxicity and an increase in insulin toxicity - not an ideal scenario. Surely best to lower the glucose AND insulin through lowering what produces a demand for insulin, that's all I would suggest. And of course exercise is a given - again no-one is questioning the value of that vector.

I'm more focused on the Type 2 Diabetes epidemic to be honest, and the technical stratgegy to stem it. I guess Bernstein is best resource for Type 1's all told.

I see more strident replies later in this thread, so forgive me if I get back a little to my many other pressing work - thanks for listening just the same.

best
ivor
 

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phoenix said:
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

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 )
Click to expand...

I'll leave you to re-read, and yes it was focussed on NIDDM in fairness; I didn't realise this was a very T1-centric thread (95% of diabetes sufferers are T2, and it's the one with epidemic status, so that's where I tend to gravitate). Recent work has identified that SMC's are far more involved in negative vascular activity than previously thought - this is where the proliferation mechanisms of insulin will need re-assessing, but we'll see:

https://www.fightaging.org/archives/2015/07/reassessing-smooth-muscle-cells-in-atherosclerosis.php

Stout covered many studies in that summary, and in a very balanced way - he did note that the rat experiment was in a species notoriously resistant to atherosclerosis, which may have explained the high doses used to look for effect. He also had many other results where physiologic and pathophysiologic doses were used to gain learnings. My prediction is that we will eventually prove a synergy between hyperinsulinemia and hyperglycemia/hyperlipidemia - but that achieving very low fasting and post-prandial insulin will act as a controlling variable in the milieu...

Anyway, it's been interesting - I'll leave people to continue on their journey of discovery.

Very best of luck
Ivor
 
FatEmperor said:
I'll leave you to re-read, and yes it was focussed on NIDDM in fairness; I didn't realise this was a very T1-centric thread (95% of diabetes sufferers are T2, and it's the one with epidemic status, so that's where I tend to gravitate). Recent work has identified that SMC's are far more involved in negative vascular activity than previously thought - this is where the proliferation mechanisms of insulin will need re-assessing, but we'll see:

https://www.fightaging.org/archives/2015/07/reassessing-smooth-muscle-cells-in-atherosclerosis.php

Stout covered many studies in that summary, and in a very balanced way - he did note that the rat experiment was in a species notoriously resistant to atherosclerosis, which may have explained the high doses used to look for effect. He also had many other results where physiologic and pathophysiologic doses were used to gain learnings. My prediction is that we will eventually prove a synergy between hyperinsulinemia and hyperglycemia/hyperlipidemia - but that achieving very low fasting and post-prandial insulin will act as a controlling variable in the milieu...

Anyway, it's been interesting - I'll leave people to continue on their journey of discovery.

Very best of luck
Ivor
Click to expand...

Final reference - I think this group have done a great job summarising the data around low carb strategy for T2D management - covering the glycaemic improvement aspects, whatever about my technical beliefs around insulin...perhaps it's best for people to just ponder this collection of data.

http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext
 
I j
FatEmperor said:
The ACCORD study showed worse outcomes on average for intensive insulin treatment, even though they got great glucose-lowering - so a reduction in glycotoxicity and an increase in insulin toxicity - not an ideal scenario.
Click to expand...

When I looked at the graphs for ACCORD I was immediately struck by the number of hypos which those on intensive tight glycemic control suffered. My ophthalmologist says that it's the spikes and drops which damage eyes. Therefore I wonder whether the unstable rollercoaster of blood glucose has more of an effect than we realise.
 
Hmm, that's three final posts on this page alone.
I think there may be several months reading ahead, to get through the reading list for the 'homework'.
Maybe later.
(Is it just me, or does anyone else feel they have had a 'Sheldon' moment?)
 
I am reading his book now it is really incredible! In an interview on youtube he said he sometimes failed his own diabetes test, and he figured it fitted in with his shifting weight. If you see the interview with him on youtube, you notice he got a little pouch on his stomach! And yeah he is over 90.

The most interesting is how some people with normal fasting bloodsugar can get diabetes like responses on an oral glucose tolerance test.
 
SunnyExpat said:
Hmm, that's three final posts on this page alone.
I think there may be several months reading ahead, to get through the reading list for the 'homework'.
Maybe later.
(Is it just me, or does anyone else feel they have had a 'Sheldon' moment?)
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Don't leave all your homework 'til late on Sunday night now Sunny !

No replies on Sheldon, so I guess it's just you... :-)
 
Roytaylorjasonfunglover said:
I am reading his book now it is really incredible! In an interview on youtube he said he sometimes failed his own diabetes test, and he figured it fitted in with his shifting weight. If you see the interview with him on youtube, you notice he got a little pouch on his stomach! And yeah he is over 90.

The most interesting is how some people with normal fasting bloodsugar can get diabetes like responses on an oral glucose tolerance test.
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Thanks Roy - also, any lover of the insightful Jason Fung is a friend of mine :-)

 
I guess the peace is shattered again, but at least you can get a sixth final post in if you're fast. ;)

( You're slipping though, you made a post on this page without a random link in)
 
SunnyExpat said:
I guess the peace is shattered again, but at least you can get a sixth final post in if you're fast. ;)

( You're slipping though, you made a post on this page without a random link in)
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Wow Sunny you're fast on the draw - you're obviously not too busy - get and do your homework now, there's a good gal ;)
 
Obviously not, but it's interesting to see you're rattled, two without links now, is that a record.
Looking forward to another final post ;)
 
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So, the bottom line is that most of us Type 2s have had elevated insulin levels for years with associated inflammatory damage to all our organs. Because the damage occurs years before the diagnosis. So we need to change the test.
And heart disease is always a consequence of diagnosed or undiagnosed diabetes.
And the only solution is Bernstein's joyless, pudding-less extreme diet.
 
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tuatara said:
So, the bottom line is that most of us Type 2s have had elevated insulin levels for years with associated inflammatory damage to all our organs. Because the damage occurs years before the diagnosis. So we need to change the test.
And heart disease is always a consequence of diagnosed or undiagnosed diabetes.
And the only solution is Bernstein's joyless, pudding-less extreme diet.
Click to expand...

Ah now Tuatura - I gorge on delicious fatty lamb and vegetables, juicy ribeye steaks, fine cheeses, olives, nuts and pate. I I even enjoy dark chocolate with whipped double-fat cream. Of course I guzzle plenty of strong red wine - I'm practically a gourmand in a sense. But I minimize that trashy, empty-calorie carbohydrate. And being on a high-fat diet, I am perfectly fat adapted - so I can fast intermittently with ease. Crucially, I keep my insulin secretion on the goddamn floor throughout. So I can feast safely with minimal inflammatory response, while really spoiling myself... :-)
 
FatEmperor said:
Ah now Tuatura - I gorge on delicious fatty lamb and vegetables, juicy ribeye steaks, fine cheeses, olives, nuts and pate. I I even enjoy dark chocolate with whipped double-fat cream. Of course I guzzle plenty of strong red wine - I'm practically a gourmand in a sense. But I minimize that trashy, empty-calorie carbohydrate. And being on a high-fat diet, I am perfectly fat adapted - so I can fast intermittently with ease. Crucially, I keep my insulin secretion on the goddamn floor throughout. So I can feast safely with minimal inflammatory response, while really spoiling myself... :)
Click to expand...


Well I agree the diet is fine, but the thought that it's too late and my heart is already damaged and just waiting to murder me is pretty depressing. All the cheese in the world isn't going to cheer me up about that...
 
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