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Insulin load index / most ketogenic foods

Steady on there. You need to be much more careful with how you define 'health' in that first statement. And you really need to explain how you get the second statement as a conclusion from the first.

ACCORD purports to show (among many other things) that aggressive blood sugar targets are counterproductive beyond a certain point. There is nothing in that the generalises to non diabetics and it's a weak argument from that to say that low insulin is better than high insulin.

I would actually agree that we should be keeping insulin levels low, but not from the ACCORD data. I think Gary Taubes makes this 'case against high insulin' pretty well.
 
martykendall said:
I see lots of people on the TYPEONEGRIT group use the small doses to combat GNG. A nice luxury for those on a CGM (they're prohibitively expensive in Australia).
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If you mean a succession of small doses using a CGM, this is sometimes called "sugar surfing". Not ideal as you are always clearing glucose from the blood after it has risen, rather than preventing it from ever rising. But a useful technique that CGMs enable. I do use it.
The TAGers will split their carb and protein doses with the protein dose being given as a square wave over a number of hours. This overcomes the issue with the insulin acting before the protein has time to digest.
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I do this, though I am not a TAGer. I use an immediate bolus for carbs and an extended 2 hr, non delayed bolus for protein.
No, I don't think you want to be relying on the fact that insulin is slow. It isn't. It's fast enough to give us severe hypos when we get the carb dose wrong. It's easily fast enough to outstrip GNG. That Leucine boost at the beginning that @tim2000s has identified is probably a lifesaver.
 
I don't think you are seeing the problem quite from a T1 point of view. T1s have no endogenous insulin, so it does not matter to us so much whether a food is quick or slow to deliver glucose into the blood: the total BG rise will be the same, regardless (unlike a T2, a non diabetic, or a honeymooning T1/LADA with some insulin response remaining).
 
martykendall said:
Rather than using insulin load to calculate insulin doses I think the primary power is to use it to select for low insulin load foods and then the margin for error is lower (whether you elect to allow for 0 or 80% for protein).
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That doesn't work if the person simply selects foods with low ILI. Because they might end up eating more total food in terms of total insulin load. It only works if people select a lower total ILI. In effect this means 'counting' ILI of all the quantities of all the food consumed. Just like carb counting and protein counting. Otherwise there is no 'law of small numbers' benefit as you describe.
 
martykendall said:
the liver act as a reservoir for glucose that that reservoir can be filled by GNG from ingested protein. If you get to a point where the liver is full then the excess spills over into the blood.
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I don't think there is any basis for this second statement. It's just as likely that glycogen deposition is inhibited when the liver is 'full'. I don't know, but this kind of statement needs to be researched rather than guessed.

Generally what happens is that glycogen release is downregulated by insulin and it is upregulated by glucagon. I don't know what regulates glycogen deposition. In T1s, glycogen 'spills' constantly because of inadequate insulin regulation. This is the main reason for taking basal insulin, to inhibit this constant spilling.
 
The other factor to account for in this is that once glycogen stores are maximized, insulin causes adipose tissues to take additional glucose out of the bloodstream and convert it to triglycerides, which eventually end up as fat.

Essentially, if you have enough or excess insulin in the body it removes glucose from the blood. It works alongside glut4 receptors to provide an energy source to muscles, It replenishes glycogen as a second action, but there is a limited amount of capacity here and finally stores it off as fats.

Any excess glucose from gng will therefore be turned into fats, given enough insulin of the right sort.

The other aspect of this equation is that diabetics seem to be predisposed to greater amount of gng than non-diabetics. This will therefore also have an impact on the rise in bg levels seen as a result of gng.
 
For what it's worth, arginine is the amino acid reputed to stimulate the highest production of both insulin and glucagon.
 
As a further input to the study, prior to bed tonight, my bg level has been running on the verging on low level at 4 mmol/l. To counter this I've drunk a protein shake containing 48g protein and 4g carbs. As it is a complete shake, rather than pure whey, and consists of egg white and milk protein alongside 40% whey, I expect an initial lift of 3-5 mmol then a slower increase over the next four hours. I'll post the graph in here tomorrow morning.
 
martykendall said:
My understanding is that in Australia and the US fibre is not subtracted while in the UK and some other European countries fibre is already removed, so it's a null argument. The nutrition guidelines have already decided it is irrelevant.
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Strange, I'm in Australia and have always thought the opposite - our fibre is listed separately to carbohydrates and is already deducted from the total carbs? The Australian Calorie King website I use to track my intake definitely seems to work that way. Their entry for avocado would seem to show net carbs and not carbs including fibre:

http://www.calorieking.com.au/foods...0MDEyNTU5JnBvcz0xJnBhcj0ma2V5PWF2b2NhZG8.html
 
PhilT said:
For what it's worth, arginine is the amino acid reputed to stimulate the highest production of both insulin and glucagon.
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Yes arginine is used experimentally to max out insulin response from beta cells. I didn't realise it was an amino acid though.
 
I think if the liver is 'full' the liver turns excess into fat, insulin resistance comes into it too.
 
Protein effect on bg levels - a graphical response.



But what's actually going on? To put this in context, I had eaten no carbs from about 6pm yesterday evening., as shown in this image.



Basal insulin was taken at 9.30 as usual and the protein shake was ingested at around 9.30pm-9.45pm. After about 10 mins, I see an ifg level climb from 4 to 9 that takes about an hour (ignore the lows showing on the libre scan prior to this, I wasn't in the red according to bg tests). This corresponds to my normal increase due to roughly 18g of carbs and the rate of increase is similar to that seen with brown rice. This continues till roughly 11pm-11.30pm. This shows a rate of increase of ~2.5mmol/l per hour.

The curve then flattens off, in as much as the rate of increase drops to around a quarter, but there is a clear rise from 9 to 13 between roughly 11.30 and 5am that I attribute to gng. The rate of change here is (again approximately) 0.7mmol/l/hour in this period.

For full disclosure, the nutritional information relating to the protein shake, which was made with a mix of coconut milk and water, is as follows:

Shake:
CHO: 1.8g
Protein: 46.6g
Fat: 2.6g

Coconut Milk:
CHO: 3.8g
Protein: 0.2g
Fat: 2g

Total carb content 5.6g.

Protein Content: Whey Protein Concentrate (Milk, Soya), Milk Protein Concentrate,Egg White Powder
Additional Amino Acids: Glutamine in the form Glutamine Peptides

These are just my observations but I think it clearly shows what I regularly see.
 
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As Indy says in Australia and New Zealand , as in the UK and Europe, fibre is already deducted from the carb content and listed separately on labels.
Above that, what is contained in the fibre fraction and what is contained in the digestible starch fraction differs between countries. It's all down to the changing definitions of what digestible fibre is and the methods of analysis.

There is a push to harmonise methods and definitions on an International basis .(CODEX alimentarius )
Australia and NZ have changed. The US is going to change but hasn't yet. The EU has accepted the definition but guidance (not law) about methods leaves it up to countries to make sure that methods produce results that comply
http://www.megazyme.com/resources/dietary-fiber/dietary-fiber-regulations
http://www.nutritionj.com/content/13/1/34

In the UK fibre has been defined in a specific way for many years (Non starch polysaccharide) and it's method of analysis was different to that used in the US, All the figures used in British reference lists and surveys and currently used for the recommendations for fibre intake were based on this
The method used means some types of fibre including resistant starch, resistant malto dextrins and oligosaccharides aren't included in the fibre content. ( these latter seem to be things like inulin found in veggies like endive ,leeks, onions, Jerusalem artichokes)
I assume, but don't know , that this results in these starches being included in the dietary carb fraction rather than the fibre fraction )

Labels on some products may use NSP for fibre eg packers of veggies may use a list to label. . There is a FSA guideline (not law) recommending that manufacturers change to the AOAC method especially if they want to make any claims for fibre

.

 

Jason Fung makes the clearest case I've seen regarding insulin toxicity.

 
martykendall said:
Jason Fung makes the clearest case I've seen regarding insulin toxicity.
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Then I suggest citing Fung rather than a vague statement invoking ACCORD. If Fung quotes ACCORD then quote what he says. Your manifesto will be stronger for it.

Fung is a very good guy.

Like I said, I don't dispute insulin toxicity, I believe in it. But to reach those who don't believe, you will need robust, clear, evidenced claims.
 
martykendall said:
Jason Fung makes the clearest case I've seen regarding insulin toxicity.
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Dr Fung is the new Dr Bernstein. Which is a great relief because the old Dr Bernstein ain't going to be around for much longer.

Dr Fung should be voted on to the advisory board of DUK and every other national diabetes charity, if not the governing board, and should be put in charge of diabetes by the NHS.
 
martykendall said:
Jason Fung makes the clearest case I've seen regarding insulin toxicity.

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This Jason Fung video is AWESOME.
+100 Likes for this post. Every diabetic and every HCP should watch this video. I will be taking the references to my next consultant appointment. Maybe he will finally give me some d**m metformin.
 
I've been reading some criticism of Fung's work lately and the author has a point about Fung basing a lot of his argument on the (flawed) ACCORD study which Jenny Ruhl and others have done a pretty good demolition job on. If you haven't read Steve Cooksey's articles, they are here:

http://www.diabetes-warrior.net/2015/04/20/fung-us-among-us/
http://www.diabetes-warrior.net/2015/04/24/what-the-fung/

Jenny Ruhl's various articles about ACCORD:
http://phlaunt.com/diabetes/SearchR...aunt.com/diabetes/index.php&ref=&ss=85j7225j2
 
I'm not sure he is. Dr B pushes insulin for t2s to release pressure on beta cells. Fung says insulin drives insulin resistance and therefore shouldn't be administered. Seems like completely opposite end of the spectrum.

Or maybe that Dr B is looking from a slightly different perspective.
 
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