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.
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
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
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.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.
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.
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.
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!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.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!
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...
The question is really "what is the cause of the insulin resistance?" as the CVD is a by product of the excess insulin.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 for T2s is what have you found better. Exercise, diet or changing both?
Not eating carbs while eating lots of fat cured me, without much exercise. Just saying...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"
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
http://www.jdcjournal.com/article/S1056-8727(12)00269-3/fulltext#back-bb0050The 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
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.He argues that insulin causes inflammation in the endothelium, and there you are.
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