High-Fructose-High-Coconut-Oil Diet Disregulates Leptin, Stearoyl-CoA Desaturase, And Spatial Memory

Kartoffel

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Substantially lower fasting glucose and insulin in the soybean oil/fructose group compared to the CO/fructose group.

And what does that tell you about CHO oxidation rates?
 

Kartoffel

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That's clearly insulin resistance, which in itself is a symptom of impaired glucose oxidation.

I doubt it very much. Your argument might be valid in the context of a diet containing a lot of glucose, but since there was no glucose in their diet I don't think that the fasting insulin and glucose levels tell you anything about CHO oxidation rates. Many studies demonstrate that PUFA stimulate lipolysis to a much greater extent, and inhibit CHO oxidation much more than SFA. I don't see why that would be different here.
 
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grenade

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I doubt it very much. Your argument might be valid in the context of a diet containing a lot of glucose, but since there was no glucose in their diet I don't think that the fasting insulin and glucose levels tell you anything about CHO oxidation rates. Many studies demonstrate that PUFA stimulate lipolysis to a much greater extent, and inhibit CHO oxidation much more than SFA. I don't see why that would be different here.

In the case of a fructose only diet, what *would* tell us something about CHO oxidation rates?
 

Kartoffel

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In the case of a fructose only diet, what *would* tell us something about CHO oxidation rates?

Well, measuring it ;)
Compared to glucose, fructose greatly increases CHO oxidation. It upregulates all the enzymes involved in the oxidation of glucose, such as pyruvate dehydrogenase. Since most fructose is metabolized in the liver, it's capacity is quickly reached so that the liver starts producing glycogen and de novo lipogenesis. That's why you normally see an increase in triglycerides, and sometimes FFA, in high-fructose diets. But this doesn't mean that it reduces CHO oxidation.
 

Peater Piper

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I doubt it very much. Your argument might be valid in the context of a diet containing a lot of glucose, but since there was no glucose in their diet I don't think that the fasting insulin and glucose levels tell you anything about CHO oxidation rates. Many studies demonstrate that PUFA stimulate lipolysis to a much greater extent, and inhibit CHO oxidation much more than SFA. I don't see why that would be different here.
Then fasting glucose shouldn't have trouble entering the cells, and insulin shouldn't be up. It's insulin resistance, probably due to the massive increase in triglycerides, indicating the liver is getting hammered. Also, the majority of that fructose will be burned as glucose in the end, it just becomes a more convoluted process. Denise Minger showed some evidence, in humans, that saturated fat in a very carbocentric diet can pose health risks, and tyw wrote extensively about the electron transport chain. Neither SFA, nor fructose are bad, but shouldn't necessarily be combined. Admittedly CO is a bit of a different scenario since we're now talking more about medium chain fatty acids.
 

Kartoffel

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Then fasting glucose shouldn't have trouble entering the cells, and insulin shouldn't be up. It's insulin resistance, probably due to the massive increase in triglycerides, indicating the liver is getting hammered. Also, the majority of that fructose will be burned as glucose in the end, it just becomes a more convoluted process. Denise Minger showed some evidence, in humans, that saturated fat in a very carbocentric diet can pose health risks, and tyw wrote extensively about the electron transport chain. Neither SFA, nor fructose are bad, but shouldn't necessarily be combined. Admittedly CO is a bit of a different scenario since we're now talking more about medium chain fatty acids.

Ok, can you briefly explain the process in which saturated fat would cause insulin resistance in combination with fructose, and PUFA would not? Just because saturated fat increased fasting glucose and insulin in this context doesn't mean that the animals had become "resistant" to insulin relative to their physiological requirements. It's a normal physiological adaptation to an extreme diet. If the animals were "resistant" to insulin and had disturbed glucose uptake, then why were they leaner than the soybean animals, and leaner even than the controls?
 
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Ok, can you briefly explain the process in which saturated fat would cause insulin resistance in combination with fructose, and PUFA would not? Just because saturated fat increased fasting glucose and insulin in this context doesn't mean that the animals had become "resistant" to insulin relative to their physiological requirements. It's a normal physiological adaptation to an extreme diet. If the animals were "resistant" to insulin and had disturbed glucose uptake, then why were they leaner than the soybean animals, and leaner even than the controls?
Absolutely.
Dr. Peat has explained this numerous times. Postprandial glucose and insulin isn't the full story. The time span spent allow to create a full picture. A1c plus those measurements gets one closer but as I believe haidut even showed recently, these measurements are acute snapshots in time. Dr peat has said this effect could happen but does not in any way mean resistance or pathology. It's a temporary adaptation. In the long run, one can see over time how animals exposed to pufa exhibit degenerative disease and metabolic issues. Who cares what short term measurements show.
 

Peater Piper

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Ok, can you briefly explain the process in which saturated fat would cause insulin resistance in combination with fructose, and PUFA would not? Just because saturated fat increased fasting glucose and insulin in this context doesn't mean that the animals had become "resistant" to insulin relative to their physiological requirements. It's a normal physiological adaptation to an extreme diet. If the animals were "resistant" to insulin and had disturbed glucose uptake, then why were they leaner than the soybean animals, and leaner even than the controls?
They were lighter and fatter. Failure to thrive. Look at a long term diabetic without enough insulin to get glucose into the cells. They start wasting. Elevated triglycerides + elevated glucose + elevated insulin = excess energy in the blood stream failing to get utilized or stored. Not good. The highly elevated HDL is also not a good sign.

I recommend reading tyw's posts in the following thread if you're interested in the specific mechanics of how various lipids and carbohydrates are utilized, and their effect on insulin resistance:

https://raypeatforum.com/community/threads/how-the-sugar-industry-shifted-blame-to-fat.15368/
 

Kartoffel

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They were lighter and fatter.

How would you know that? There is nothing in that paper saying that the coconut oil animals had higher total body fat, and the data that they do show strongly indicates that total body fat was much lower.
 

Jon

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Not surprised at this studies findings at all. @grenade

Studies have shown time and time again humans only have so much affinity to digest so much fructose at a time. Most of the time a higher glucose to fructose ratio is optimal as these sugars work SYNERGISTICALLY to premote optimal metabolism.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

Normal Roles for Dietary Fructose in Carbohydrate Metabolism

Fructose Malabsorption and Intolerance: Effects of Fructose with and without Simultaneous Glucose Ingestion

The Ability of the Normal Human Small Intestine to Absorb Fructose: Evaluation by Breath Testing

I understand the top study has its weaknesses but I still find it to be validated by the other studies and by my own experiences. People often forget that starch is important for butyric acid (and other healthful acids) production:

https://www.tandfonline.com/doi/pdf/10.3402/fnr.v45i0.1801
 
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Peater Piper

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How would you know that? There is nothing in that paper saying that the coconut oil animals had higher total body fat, and the data that they do show strongly indicates that total body fat was much lower.
Look at where they measured the fat, then think of the guy with a huge beer belly and NAFLD. Accumulation of fat in the epididymal pads is associated with metabolic disease in rats. Chris Masterjohn has written about the phenomenon in humans, where some people remain thin subcutaneously, because they can't export all of the lipids from their livers. The ability to get fat under energy excess is sometimes the better of two evils. Then there's the high fasting numbers, and the high cholesterol, and high triglycerides, and elevated fructosamine. Everything is pointing to metabolic disturbance. I feel like you're pissing into the wind here, especially over a mostly meaningless study. I doubt anyone's going to go buy a tub of soybean oil over it.
 

Jon

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Absolutely.
Dr. Peat has explained this numerous times. Postprandial glucose and insulin isn't the full story. The time span spent allow to create a full picture. A1c plus those measurements gets one closer but as I believe haidut even showed recently, these measurements are acute snapshots in time. Dr peat has said this effect could happen but does not in any way mean resistance or pathology. It's a temporary adaptation. In the long run, one can see over time how animals exposed to pufa exhibit degenerative disease and metabolic issues. Who cares what short term measurements show.

I just posted a study showing this trend in humans. It's not an infallible study but I think you'd find it validating.
 

Kartoffel

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Look at where they measured the fat, then think of the guy with a huge beer belly and NAFLD. Accumulation of fat in the epididymal pads is associated with metabolic disease in rats. Chris Masterjohn has written about the phenomenon in humans, where some people remain thin subcutaneously, because they can't export all of the lipids from their livers. The ability to get fat under energy excess is sometimes the better of two evils. Then there's the high fasting numbers, and the high cholesterol, and high triglycerides, and elevated fructosamine. Everything is pointing to metabolic disturbance. I feel like you're pissing into the wind here, especially over a mostly meaningless study. I doubt anyone's going to go buy a tub of soybean oil over it.

I'm not pissing into the wind, I am just disagreeing with simplistic interpretations of the results, and false statements such as yours. Fructosamine was elevated in both high-fat groups. Their adiposity index only accounts for 6%/8% of body fat, which is only a small fraction of total body fat since even lean mice have 13-14% body fat. I think it is reasonable to assume that the mice in this experiment had >20% body fat. Since the coconut oil group weighed 60g less you can easily guess how we get the lower percentage for the CO mice. Saying that the CO mice had less lean tissue is just a lame assumption that isn't based on any data in that paper. Since they used non-hydrogenated CO there should have been enough "EFA" to prevent a defiency and any growth retardation. I also would think they would have reported an important factor like growth retardation/ significantly lower lean tissue mass.

Btw I have read tyw's theory that seems to be based mostly on the H2O2 theory of insulin sensitivity made up by that low-carb guy. I read his article and I can't see any evidence backing up his claims and it doesn't take long to find multiple papers immediately discarding the idea.
 

Peater Piper

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I'm not pissing into the wind, I am just disagreeing with simplistic interpretations of the results, and false statements such as yours. Fructosamine was elevated in both high-fat groups. Their adiposity index only accounts for 6%/8% of body fat, which is only a small fraction of total body fat since even lean mice have 13-14% body fat. I think it is reasonable to assume that the mice in this experiment had >20% body fat. Since the coconut oil group weighed 60g less you can easily guess how we get the lower percentage for the CO mice. Saying that the CO mice had less lean tissue is just a lame assumption that isn't based on any data in that paper. Since they used non-hydrogenated CO there should have been enough "EFA" to prevent a defiency and any growth retardation. I also would think they would have reported an important factor like growth retardation/ significantly lower lean tissue mass.

Btw I have read tyw's theory that seems to be based mostly on the H2O2 theory of insulin sensitivity made up by that low-carb guy. I read his article and I can't see any evidence backing up his claims and it doesn't take long to find multiple papers immediately discarding the idea.
Fructosamine was higher in the CO group, even though it was elevated in the soybean group as well. Both were much higher than controls. The area where fat accumulated in the CO group is associated with metabolic disturbance and insulin resistance in rats. We have the other numbers also pointing to the same thing. I don't really see why we're debating this. If the results were reversed, would you be defending the soybean oil group because they're slightly lighter, despite all the other numbers?

You can disprove the mechanics of the theory, or you can find evidence that saturated fat doesn't increase insulin resistance? If it's the latter, then I've probably already read it, plus plenty of studies showing otherwise.
 

Jon

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Fructosamine was higher in the CO group, even though it was elevated in the soybean group as well. Both were much higher than controls. The area where fat accumulated in the CO group is associated with metabolic disturbance and insulin resistance in rats. We have the other numbers also pointing to the same thing. I don't really see why we're debating this. If the results were reversed, would you be defending the soybean oil group because they're slightly lighter, despite all the other numbers?

You can disprove the mechanics of the theory, or you can find evidence that saturated fat doesn't increase insulin resistance? If it's the latter, then I've probably already read it, plus plenty of studies showing otherwise.

Wouldn't it make sense that the saturated fat group had more visceral fat because medium chain triglycerides and fructose both require metabolism via the liver and so an abundance of both bottle necked it leading to hepatic build up and subsequent metabolic syndromes?
 

Kartoffel

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I don't really see why we're debating this. If the results were reversed, would you be defending the soybean oil group because they're slightly lighter, despite all the other numbers?

Well, mostly I was debating your statement that the CO rats were fatter. In the absence of significant growth retardation this statement is simply not true.

You can disprove the mechanics of the theory

Can you tell me in your own words what these mechanics are? I find the theory that cellular insulin response is controlled by superoxide produced at complex I unconvincing and don't see much evidence for it. The theory can't even explain why omega-3 would behave very differently from o-6.
 

Jon

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I just posted a study showing this trend in humans. It's not an infallible study but I think you'd find it validating.

Here ya go, it was up the page a ways:

Not surprised at this studies findings at all. @grenade

Studies have shown time and time again humans only have so much affinity to digest so much fructose at a time. Most of the time a higher glucose to fructose ratio is optimal as these sugars work SYNERGISTICALLY to premote optimal metabolism.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

Normal Roles for Dietary Fructose in Carbohydrate Metabolism

Fructose Malabsorption and Intolerance: Effects of Fructose with and without Simultaneous Glucose Ingestion

The Ability of the Normal Human Small Intestine to Absorb Fructose: Evaluation by Breath Testing

I understand the top study has its weaknesses but I still find it to be validated by the other studies and by my own experiences. People often forget that starch is important for butyric acid (and other healthful acids) production:

https://www.tandfonline.com/doi/pdf/10.3402/fnr.v45i0.1801
 

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