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  #1   ^
Old Tue, Jul-03-18, 22:03
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Pashta Pashta is offline
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Default The Carbohydrate-Insulin Model of Obesity Beyond “Calories In, Calories Out”

This is a great read and good news! July 2nd, 2018

The Carbohydrate-Insulin Model of Obesity
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  #2   ^
Old Wed, Jul-04-18, 02:37
Grav Grav is online now
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Now that's a URL I plan on keeping handy. Great read, thanks for the link.
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  #3   ^
Old Wed, Jul-04-18, 04:14
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JEY100 JEY100 is offline
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As you can see at the end of this, Dr Ludwig has heavy hitter funding and support to complete this long study. You can imagine this article already has had push-back on Twitter, not really the place to discuss good science or government policy.
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  #4   ^
Old Wed, Jul-04-18, 06:14
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teaser teaser is offline
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Quote:
On a conventional high-carbohydrate diet, the brain is critically dependent on glucose, requiring more than 100 g/d. With severe carbohydrate restriction, the body must initially break down protein from lean tissue for conversion into glucose. However, this catabolic response is only temporary because, over time, the concentration of ketones (produced in the liver from fatty acids) increases markedly, replacing glucose as the primary fuel for the brain. For this reason, the hallmark of a very-low-carbohydrate diet (and prolonged fasting) is development of nutritional ketosis—giving rise to the term “ketogenic diet.”


This part is interesting in the context of the ongoing discussion in the "stakez is chocolate cakez" should we worry about protein becoming glucose? area. The idea that gluconeogenesis is demand-driven rather than substrate--bothers me, because "demand" sounds like a word that requires agency, who is doing the demanding? Anyways, if we insist on using the word--what Ludwig is saying seems to imply that with increased ketosis, demand for glucose goes down. If you accept this, and accept that protein has some antiketogenic effect, then when ketones are high enough to be a factor, increased protein by decreasing ketones might increase that "demand" for glucose--so that at certain levels of ketosis, gluconeogenesis might be substrate driven, if indirectly, if the substrate increases the demand for glucose by decreasing ketosis...

I actually disagree a bit, though, anyways. Early adaptation to a low carb diet doesn't necessarily mean producing more ketones, as muscle adapts to more fat oxidation and less glucose, this could spare glucose for the brain and actually result in lower ketosis--and thus spare protein as well. Free fatty acids do most of the work and get little of the glory. Alternately, if eating the same ketogenic diet two weeks in really does result in an increased ketosis--are the ketones sparing the protein? Or is reduced total body protein degradation basically releasing less anti-ketogenic amino acids, and this increasing ketosis?

Also the bits about there being less energy available due to fuel partitioning and insulin--this can set us up for some contention. The impression that high insulin means there's not enough fuel "available" in the blood gets people like CarbSane excited, because lots of overweight people have plenty of fuel in the blood, if anything too much. But fuel availability goes beyond it being "there," muscle cells with full glycogen are going to be more reliant on glucose vs. fat.
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  #5   ^
Old Wed, Jul-04-18, 06:59
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BillyHW BillyHW is offline
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I really appreciate Dr. Ludwig's emphasis on hunger.
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  #6   ^
Old Wed, Jul-04-18, 09:08
whynot18 whynot18 is offline
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From the study: "On a conventional high-carbohydrate diet, the brain is critically dependent on glucose, requiring more than 100 g/d. With severe carbohydrate restriction, the body must initially break down protein from lean tissue for conversion into glucose. However, this catabolic response is only temporary because, over time, the concentration of ketones (produced in the liver from fatty acids) increases markedly, replacing glucose as the primary fuel for the brain. For this reason, the hallmark of a very-low-carbohydrate diet (and prolonged fasting) is development of nutritional ketosis—giving rise to the term “ketogenic diet.”

What happens, then, if you do low carb for several days, then have a higher carb day? (I know some people (Timothy Ferris comes to mind) have said they do this.) Does that mess up the body's progression into using ketones and mean that your body keeps pulling energy stores from muscle? If so, that doesn't seem like that would be good for your muscle mass.
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  #7   ^
Old Wed, Jul-04-18, 09:23
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teaser teaser is offline
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Quote:
Originally Posted by whynot18

What happens, then, if you do low carb for several days, then have a higher carb day? (I know some people (Timothy Ferris comes to mind) have said they do this.) Does that mess up the body's progression into using ketones and mean that your body keeps pulling energy stores from muscle? If so, that doesn't seem like that would be good for your muscle mass.


There have been at least one study looking at this by Jacob Wilson, they had people work out with either a cyclic ketogenic diet, or on keto full-time. At the end they did a carb-up. There was a greater increase in lean mass on keto full time than with cyclic keto, they theorized that what you suggest here happens, there's greater wasting with the people being out of ketosis, Wilson said after a weekend carb-up they'd not be at a significant level of ketosis until thursday.

I'm suspicious about this, though. In earlier studies, high carb seemed to do better than low carb, but it turned out that they weren't making proper allowance for glycogen stores. If you fast somebody, or put them on a ketogenic diet, and then carb up, you get an overshoot of glycogen stores--so it's possible that the steady state keto dieters got more of this overshoot than the cyclic ketogenic dieters.

Do ketones spare amino acids? Well, yes. So does glucose. I don't know that this is an advantage of a ketogenic diet, so much as not a disadvantage.
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  #8   ^
Old Wed, Jul-04-18, 13:46
M Levac M Levac is offline
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Quote:
Thus, the carbohydrate-insulin model of obesity (CIM) proposes that a high-carbohydrate diet — including large amounts of refined starchy foods and sugar, as commonly consumed in the low-fat diet era — produces postprandial hyperinsulinemia, promotes deposition of calories in fat cells instead of oxidation in lean tissues, and thereby predisposes to weight gain through increased hunger, slowing metabolic rate, or both.

So, carbs and insulin used to confirm CICO.
Quote:
Like the conventional model, the CIM obeys the First Law of Thermodynamics specifying conservation of energy. However, the CIM considers overeating a consequence of increasing adiposity, not the primary cause. That is, the causal pathway relating energy balance to fat storage flows opposite to the conventional direction (Figure, B). From this perspective, calorie restriction can be viewed as symptomatic treatment, destined to fail for most people in the modern food environment. Low-calorie, low-fat diets may actually exacerbate the underlying metabolic problem by further restricting energy available in the blood — triggering the starvation response comprised of rising hunger, falling metabolic rate, and elevated stress hormone levels.

Euh, that's not what the first part of the paragraph said. If causality is indeed reversed, it should say instead: "predisposes to weight gain through fat deposition in fat cells, and in turn this promotes increased hunger and slower metabolic rate, or both".

That's all fine and dandy, but it's still incomplete. Fat gain and loss occurs not during a meal, but in-between meals. It may be caused by the meal content, but that's not when the subsequent gain and loss occurs. Here, we're dealing with fasting insulin. We're no longer dealing with insulin stimulus from the meal. Instead, we're dealing with insulin degradation at the liver. I can't use Ludwig's explanation for that, just doesn't cut it. To explain that, we need my paradigm (link).

In short, ketones activate insulin receptors. Insulin inhibits ketogenesis. Too much insulin (from a high-carb meal) results in little or no ketones that would otherwise activate insulin receptors in the liver, where a sequence of steps occurs, ending with degradation of insulin. Failure to perform this last step allows insulin in the blood to remain higher than otherwise.

I skimmed the rest. Good start, but Ludwig is out of his element on some mechanistic and logic stuff.
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  #9   ^
Old Wed, Jul-04-18, 14:01
M Levac M Levac is offline
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Quote:
Originally Posted by teaser
Do ketones spare amino acids? Well, yes. So does glucose. I don't know that this is an advantage of a ketogenic diet, so much as not a disadvantage.

Ketones stimulate chaperone-mediated autophagy, the recycling of glycated protein, thereby sparing protein elsewhere which would otherwise be used to compensate the glycation. Glucose doesn't do any of that. Instead, it glycates protein, decreasing available protein, the protein elsewhere must be dismantled to compensate. However, dietary carbs stimulate insulin, which in turn stimulates protein synthesis so there's some counter-compensation with that. However again, the glycated protein creates a net loss overall, because even though there's more protein being made by the extra insulin, the pool of protein from which to draw is smaller by virtue of glycation. To compensate for that, eat more protein, but then that's just as good with a ketogenic diet.
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  #10   ^
Old Thu, Jul-05-18, 15:52
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mike_d mike_d is offline
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Quote:
With severe carbohydrate restriction, the body must initially break down protein from lean tissue for conversion into glucose.
I take issue with this statement. Due to an increase in HGH and enough dietary protein and fat available muscle will be spared, glycogen stores utilized and as ketosis ramps up less glucose will be required so lower blood glucose is well tolerated. There is no evidence of a catabolic response, even while fasting for several days, most likely quite the opposite occurs.

Last edited by mike_d : Thu, Jul-05-18 at 16:07.
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  #11   ^
Old Thu, Jul-05-18, 16:06
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teaser teaser is offline
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It's more accurate to say that the body does, rather than that it must. It's not that it must do this so much as that adaptations that reduce this take some time. There is a catabolic response early on in fasting, it's been measured in terms of nitrogen balance. I don't consider the loss of protein that occurs in the first 24 hours of fasting a big deal, you get it back with refeeding, but it does happen.
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  #12   ^
Old Thu, Jul-05-18, 16:12
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mike_d mike_d is offline
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Quote:
There is a catabolic response early on in fasting, it's been measured in terms of nitrogen balance.
The urea nitrogen can come from protein in the diet, autophagy or from muscle.

Last edited by mike_d : Thu, Jul-05-18 at 16:12. Reason: tag
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  #13   ^
Old Thu, Jul-05-18, 16:23
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teaser teaser is offline
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Okay, maybe we're losing from a non-protein amino acid pool, or maybe the protein we're losing sucked. Catabolism is still catabolism.
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  #14   ^
Old Thu, Jul-05-18, 20:36
M Levac M Levac is offline
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Quote:
Originally Posted by mike_d
I take issue with this statement. Due to an increase in HGH and enough dietary protein and fat available muscle will be spared, glycogen stores utilized and as ketosis ramps up less glucose will be required so lower blood glucose is well tolerated. There is no evidence of a catabolic response, even while fasting for several days, most likely quite the opposite occurs.

Yeah, I agree, I got a problem with Ludwig's statement too. I think your explanation is right on, with just the order I might see differently. The first thing that happens when we cut carbs is excess insulin drops, then excess glycogen is released, then the rest like you said. The rate of either is mutually regulated. I mean, insulin can't just drop like a stone and let all the glycogen go in one big bolus, right?

The thing about insulin is that it inhibits proteolysis, so as long as it's still too high, no protein will be wasted like that. Ima say it would take about a week before insulin gets low enough to allow proteolysis to some degree, but then there's all those other things you said, so pfft. The fear of losing lean tissue comes from long-ish-term fasting experiments, I think. Well, Ludwig's statement ain't about any kind of fasting, it's about low-carb. Even better, if we're really dumb about it, we're just gonna eat tons of very lean meat for induction, cuz you know, fear of fat and stuff. The A-TO-Z experiment showed something like 35% protein for Atkins induction.
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  #15   ^
Old Thu, Jul-05-18, 20:44
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BillyHW BillyHW is offline
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Is the fear of losing lean tissue while fasting overblown? Wouldn't this lean tissue just return on its own after refeeding?

Apart from weight training, wouldn't the body have a natural "lean-tissue" set point that it will enforce once you're eating again?
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