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Insulin load index / most ketogenic foods


Thanks @Spiker.

There is a "Bernstein template" in there too at https://optimisingnutrition.wordpress.com/2015/03/22/best_diet/

Bernstein's approach does pretty well overall, but if you wanted to get even better blood sugars and reduce your insulin load I would suggest 15 or 20% protein (depending on activity level) with 7% carbs (from nutrient dense non-starchy veggies) would give you an even better outcome.

You could probably get away with even fewer carbs if you were eating a significant amount of organ meats but I don't see that becoming a "thing" in a hurry.
 

@tim2000s I'm trying to get my head around the things that influence GNG. It seems that a bunch of things mediate the release of glucose into the blood stream from the storage in the liver, but when you stand back you can only release into the blood stream what you put into the system.

There just has to be a high level link between the quantity of glucogenic materials you give the body and the insulin required to matabolise it.

If you decrease the total glucose (i.e. carbs plus excess glucogenic amino acids plus any aminos from the muscle on the body during calorie restriction) then there is only so much glucose that can be released into the blood stream.

The liver may be a buffer that moderates the timing of release, but if you only give the body so much glucose as inputs there is a limit to what can be released into the blood and used for fuel if you stand back and look at it on a month to month basis rather than a meal to meal basis.

I'm still trying to come to grips with this stuff. Any reflections / guidance would be appreciated. I've got a post at https://optimisingnutrition.wordpre...e-insulin-reaction-to-protein-dose-dependent/ with a bunch comments that will show you where my head is at coming to grips with this issue.

I think it's important. Just protein doesn't raise the blood sugar in healthy non-diabetic people doesn't mean that the energy from the protein magically disappears. In the end calories count and the conservation of energy still applies does it not?
 
It remains controversial whether any glucose can be derived from metabolising fat.

As you say, T1 diabetics with CGMs are an ideal lab rat. Or "experimental model", as we lab rats prefer to be called. ;-)

At the moment my feeling is that TAG may be right, but for the wrong reasons. I believe that fat does not yield any net glucose in lipolysis. But, more dramatic than the supposed 10% glucose yield from fat, is the decreased insulin sensitivity caused by fat. This increases the insulin requirements for any carbs and protein eaten around the same time. So actually TAG is right to add extra insulin when eating fat.

The critical test would be a pure fat bolus (free of possible allergens or stimulants) in a T1 with known nil insulin production and known stable basal dose.

Even then you might see a small blood sugar rise but it would be ambiguous whether the rise was caused by fat lipolysis creating net glucose, or by transient insulin resistance causing the basal insulin concentration to be temporarily insufficient to suppress and /or clear the glycogen drip from the liver.
 
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It's a good point. Let me qualify that and say "glucogenic" inputs. Potentially including fat as well as protein and of course carbs IF it turns out to be the case that fat lipolysis does yield some net glucose.

And it's good to view the liver as a glucose buffer because it's exactly that. In fact it's part of a glucose homeostat system, in which the pancreas is the "thermostat" and the liver is the "climate control". The "thermostat" senses and signals the changes in "heat", and the liver actually makes the "heat" rise or (to an extent) fall.

The liver raises blood sugar when low, by increasing the glycogen dumping in response to the glucagon signal. But if blood sugar is high it helps to lower blood sugar by sequestering glucose as triglycerides for storage in adipose cells or hepatic fat, in response to the insulin signal.
 
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martykendall said:
In the end calories count and the conservation of energy still applies does it not?
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Yes and no. This is where the simplistic "calories in, calories out" orthodoxy falls down. People invoke thermodynamics (conservation of energy) but they ignore too much detail. Calories only "count if the fuel is fully burned in a perfectly efficient reaction (and thermodynamics tells us there is no such thing).

The body is great but it's not a bomb calorimeter, it doesn't fully oxidise everything and it's not perfect. Very good, but not perfect. The body has a limited number of metabolic pathways available and while some are very good, others are compromises. So for example there are significant energy losses in GNG. More to the point sometimes nutrients are just excreted unused.
 
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Spiker said:
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.
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Yes, but it is all about Type 2. So what do Type 1s take away from this, other than the basic preference some of us already had for keeping insulin doses as low as possible, possibly by adding Metformin (which our doctors probably won't let us do), and by keeping carbs/protein low and fat high? Intermittent fasting sounds wonderful, but is it safe for us to do it? We adjust basal a bit downwards, or what? Even if that's safe, in what sense can we be increasing insulin sensitivity if we're fasting in the presence of injected basal insulin?

I don't see where to go from here. When I eat, I have to inject (and much, much less than others). It's simple. So how do T-1s lower their insulin resistance, other than by lowering carb/protein intake? Especially if they don't want to lose any more weight.

If this is your whole point Spiker and I've missed it, sorry, more explanation needed
 
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Also, I thought the Accord findings about increased mortality had been misinterpreted/misstated, as Jenny Ruhl was saying. OTOH he has stacks of studies, not just Accord.
 
No, sorry Lucy, you're right. I was really just reacting on behalf of T2s. From a T1 perspective there are few takeaways.
 
I think T1s could try intermittent fasting, similar benefits to strength exercising, in improved insulin sensitivity. I think in a steady state the improved insulin sensitivity would be stable rather than variable (if I understand Fung correctly). So your good point about the basal rate would even out after an initial adaption. Maybe.

For me the article was worth it just as an argument for Metformin for T1s and I will be taking the references to my next consultant appointment. Not just to get him to prescribe for me, but to try to persuade his whole department to consider it for all T1s.
 
LucySW said:
Also, I thought the Accord findings about increased mortality had been misinterpreted/misstated, as Jenny Ruhl was saying. OTOH he has stacks of studies, not just Accord.
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I think he is out of order on this point actually. I found some statements attributed to him, on another site, which if he did say them are totally unacceptable. Basically saying 'blood sugar control clearly does not prevent complications' and "we have known that since 1998". Completely misrepresenting ACCORD.
 

Agreed. It's interesting to note that protein has a higher thermic effect than carbs, some of the aminos are ketogenic rather than glucogenic, some of it may be excreted.

But at the end after all those loses I think there is likely a glucogenic effect that is worth considering. Maybe I'm making a bigger deal of this than necessary, but I think it's worth trying to quantify, particularly for those on a low carb, higher protein approach.
 

Hi Spiker, great post! I need to decode and then apply to myself, as currently I am going through a weight plateau for 2 months. Yes, as you said in another post, each moment is a learning something new.
 
LucySW said:
Intermittent fasting sounds wonderful, but is it safe for us to do it? We adjust basal a bit downwards, or what? Even if that's safe, in what sense can we be increasing insulin sensitivity if we're fasting in the presence of injected basal insulin?
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I wouldn't see any issue with IF for type 1s as long as you've got your basal set correctly.

It should improve insulin sensitivity and fatty liver just like for the rest of the population.

Type 1s aren't that special and unique. They just don't have a working pancreas. The rest of the metabolism is still the same.
 
They are injecting additional insulin. They have to. So how can they hone insulin resistance.
 
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Yes of course there's a glucogenic effect. And it's reasonably quantifiable - with some uncertainties. But that's not the point re "calories in, calories out". The rebuttal to "calories in, calories out" is, that some calories behave differently from others, in different contexts.
 
@LucySW Insulin resistance isn't a function of where the insulin comes from, rather the reaction of the bold to it. In an exogenous form, we are injecting typically 50-100% more insulin than we would need from the pancreas, so there's nothing stopping insulin resistance from occurring.

I noticed that as I did more exercise, lost weight and ate a much less carb intense diet, my insulin sensitivity increased. I wasn't taking enormous amounts of exogenous insulin, but clearly the three prior actions have decreased my insulin resistance. So I think it depends on the side of the coin you are looking at.

IDDs carrying excess fat tend to require more insulin than those who don't. I don't know if any studies have been done, but I wouldn't be surprised to see the mount they needed drop as body fat percentage reduced.
 
And you would expect them to given the different processes the body uses to break them down and use them as energy. As you've said previously, the body is not 100% efficient and some processes (glucose metabolism for example) seem more efficient than others (protein and fat metabolisms).
 
martykendall said:
I wouldn't see any issue with IF for type 1s as long as you've got your basal set correctly.

It should improve insulin sensitivity and fatty liver just like for the rest of the population.
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I think you're missing Lucy's point. If insulin sensitivity were to vary in response to intermittent fasting that would throw of our basal demand and lead to hypos or require adjustment of basal rates, which is a fairly tricky (though necessary) process.

Type 1s aren't that special and unique. They just don't have a working pancreas. The rest of the metabolism is still the same.
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Not really. The consequences of losing control of insulin, glucagon and amylin regulation are severe and far reaching, and complex. The entire metabolism is affected. It's dangerous to generalise any metabolic effect from non diabetics or T2s to T1s. Or vice versa. Our metabolisms really are quite different with those elements missing.
 
Fair point. I am. I've tried intermittent fasting in the past and it didn't affect basal appreciably. The two things that have really helped that were body fat reduction via low carb and increased exercise leading to increased muscle mass..

I agree with your point on metabolism. We've only known about amylin loss since 1987. We still have little idea of the impact of beta cell loss and how it breaks the closed feedback loops that the body relies on. This thread alone has highlighted that certain amino acid or protein combinations typically invoke an insulin and glucagon response due to receptors somewhere trying to trigger alpha and beta cells, and the body not knowing it has no beta cells in T1s. We therefore have little idea what else may be missing or its effects.
 
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