Fructose series part 1: fructose depletes ATP?

[salvio]

Green tea has the same effects on glucose.

Green tea catechins ameliorate adipose insulin resistance by improving oxidative stress - PubMed

Epidemiological data have suggested that drinking green tea is negatively associated with diabetes, and adipose oxidative stress may have a central role in causing insulin resistance, according to recent findings. The aim of this work is to elucidate a new mechanism for green tea's anti-insulin...

pubmed.ncbi.nlm.nih.gov

 

[schultz]

Glycation is about a sugar that bonds to a protein, PUFA isn't pertinent in sugars and proteins AGEs.

Oh silly me

Although a monosaccharide is not needed for glycation to occur, which was sort of my point. PUFA produce AGEs significantly more than monosaccharides. But not only that, fats produce less carbon dioxide than sugars do and I mentioned that carbon dioxide protects against the formation of AGEs via formation of carbamino groups. Theoretically, fructose could be even more protective than glucose because it increases carbon dioxide more than glucose does.

Glyoxal can be used for glycation. --> Glyoxal derived from triglyceride participating in diet-derived Nε-carboxymethyllysine formation

In this study glucose produced insignificant amounts of CML, whereas glyoxal did --> Investigating the Glycating Effects of Glucose, Glyoxal and Methylglyoxal on Human Sperm

And the MX Fu study I cited earlier (here) which says...

"We now report that CML is also formed during metal-catalyzed oxidation of polyunsaturated fatty acids in the presence of protein... These results suggest that lipid peroxidation, as well as glycoxidation, may be an important source of CML in tissue proteins in vivo and that CML may be a general marker of oxidative stress and long term damage to protein in aging, atherosclerosis, and diabetes."

And here we're talking on fructose and glucose not PUFA.

I thought we were talking about advanced glycation end-products? I'm trying to make the point that glucose and especially fructose are unlikely to be significant sources of AGEs in the organism (see my argument for CO2, and PUFA derived AGEs). Hyperglycemia is often blamed for increased amounts of AGEs, however during such times it is likely FFAs are also elevated and thus there is an increase in glyoxal and methylglyoxal. I happen to think it is these things that are the main problem, not the hyperglycemia.

An in vivo study in rats showed that fructose feeding massively lowers mortality caused by endotoxin

And there is research showing increased triglycerides in the liver (made from fructose, so likely palmitic acid?) are protective against endotoxin.

 

[salvio]

Oh silly me

Although a monosaccharide is not needed for glycation to occur, which was sort of my point. PUFA produce AGEs significantly more than monosaccharides. But not only that, fats produce less carbon dioxide than sugars do and I mentioned that carbon dioxide protects against the formation of AGEs via formation of carbamino groups. Theoretically, fructose could be even more protective than glucose because it increases carbon dioxide more than glucose does.

Glyoxal can be used for glycation. --> Glyoxal derived from triglyceride participating in diet-derived Nε-carboxymethyllysine formation

In this study glucose produced insignificant amounts of CML, whereas glyoxal did --> Investigating the Glycating Effects of Glucose, Glyoxal and Methylglyoxal on Human Sperm

And the MX Fu study I cited earlier (here) which says...

"We now report that CML is also formed during metal-catalyzed oxidation of polyunsaturated fatty acids in the presence of protein... These results suggest that lipid peroxidation, as well as glycoxidation, may be an important source of CML in tissue proteins in vivo and that CML may be a general marker of oxidative stress and long term damage to protein in aging, atherosclerosis, and diabetes."




I thought we were talking about advanced glycation end-products? I'm trying to make the point that glucose and especially fructose are unlikely to be significant sources of AGEs in the organism (see my argument for CO2, and PUFA derived AGEs). Hyperglycemia is often blamed for increased amounts of AGEs, however during such times it is likely FFAs are also elevated and thus there is an increase in glyoxal and methylglyoxal. I happen to think it is these things that are the main problem, not the hyperglycemia.



And there is research showing increased triglycerides in the liver (made from fructose, so likely palmitic acid?) are protective against endotoxin.

Are we talking on PUFA or Fructose in this post?

 

[salvio]

Anyway it looks that green Tea, if the problem are PUFAs can block the effects on the body.

 

[schultz]

Are we talking on PUFA or Fructose in this post?

I was talking about both of them.

 

[CLASH]

Anyway it looks that green Tea, if the problem are PUFAs can block the effects on the body.

Not entirely. When the PUFA is incorporated to the membranes, particularly the mitochondrial membrane, the risk for peroxidation is increased compared to the MUFA or SAFA.

 

[Tarmander]

I would be curious to hear what you guys think about these podcasts from Peter Attia.


View: https://youtu.be/LbSic4Oo8ME



View: https://youtu.be/V02z9mqTWzg


I am paraphrasing, and this isn't my specialty so I may be getting it wrong. But the argument isn't that fructokinase lowers ATP (I think most sugars when metabolized consume ATP), but that when it lowers ATP to begin metabolizing fructose, it does so in an uninhibited manner...so if large amounts of fructose are consumed, ATP can be lowered by such a large amount at first that a certain threshold is triggered where cells get the signal to LOWER metabolism and store fat.

Where as glucose and other sugars, if ATP gets lowered too much, metabolism of those sugars is slowed/stopped so these "store fat, prepare for winter" signals are not generated.

In other words it's the dose that may make fructose store fat, lower metabolism, and cause metabolic syndrome. Just a little bit of sugar, that is slower to absorb, like in fruit, is no problem. But drinking down a large bolus of HFCS in like a soda can lower ATP in cells so much as to cause these distressing signals.

Anyways would be interested to hear some takes on these podcasts. Some of the things mentioned in them really lines up with my experience of fructose.

 

[Sefton10]

I would be curious to hear what you guys think about these podcasts from Peter Attia.


View: https://youtu.be/LbSic4Oo8ME



View: https://youtu.be/V02z9mqTWzg


I am paraphrasing, and this isn't my specialty so I may be getting it wrong. But the argument isn't that fructokinase lowers ATP (I think most sugars when metabolized consume ATP), but that when it lowers ATP to begin metabolizing fructose, it does so in an uninhibited manner...so if large amounts of fructose are consumed, ATP can be lowered by such a large amount at first that a certain threshold is triggered where cells get the signal to LOWER metabolism and store fat.

Where as glucose and other sugars, if ATP gets lowered too much, metabolism of those sugars is slowed/stopped so these "store fat, prepare for winter" signals are not generated.

In other words it's the dose that may make fructose store fat, lower metabolism, and cause metabolic syndrome. Just a little bit of sugar, that is slower to absorb, like in fruit, is no problem. But drinking down a large bolus of HFCS in like a soda can lower ATP in cells so much as to cause these distressing signals.

Anyways would be interested to hear some takes on these podcasts. Some of the things mentioned in them really lines up with my experience of fructose.

It lines up with my experience. I've tried the no starch approach a couple of times, and it ultimately fails. I get a distinct sense that it is anti-metabolic in that I don't 'feel' a boost in metabolism from a heavy sugar diet. If anything, it feels the opposite, especially when I go heavy on honey. A combination of starch from sprouted oats and lentils, some sugars from fruit and a little juice, and lactose from a bit of milk feels much more balancing to me when it comes to carbohydrates.

 

[Vanset]

generally the starch based vegans, mcdougal style tend to look MUCH better than fruitarians and it's not even comparable. many fruitarians have that taut and thin skin and terrible teeth. now whetver it's the fructose or something like protein (starch based vegans tend to get much more from grains, potatoes etc.) it's debatable. this is just an observation i have made.

 

[aliml]

Fructose Metabolism from a Functional Perspective: Implications for Athletes

Fructose Metabolism from a Functional Perspective: Implications for Athletes

www.gssiweb.org

Replacing glucose with fructose as a dietary energy source during exercise has some consequences on muscle energy efficiency (Tappy et al., 2013) (Fig. 1). Glucose is taken up by contacting skeletal muscles and results in the total synthesis of 29.5 ATP. Overall, the oxidation of 1 molecule of plasma glucose uses 6 molecules of oxygen (O2) and 2 ATP and produces 6 molecules of carbon dioxide (CO2) and 29.5 ATP, corresponding to 27.5 ATP gained in working muscle, i.e., 4.58 ATP/O2 molecule.

In comparison, ATP, O2 and CO2 fluxes slightly vary when fructose is first metabolized in the liver to be secondarily oxidized in muscle (Tappy et al., 2013). When fructose is converted into glucose in the liver it consumes 2 ATP. When this newly synthesized glucose is subsequently oxidized in skeletal muscle, the overall metabolic pathway uses 6 O2 and 4 ATP and produces 6 CO2 and 29.5 ATP for each fructose molecule, representing a net gain of 25.5 ATP, or 4.25 ATP/O2. Interestingly, the energy yield in skeletal muscle is identical to that of glucose, but there is additional energy expended in the liver.

When fructose is converted into lactate, which is subsequently oxidized in contracting muscle, the overall metabolic process uses 6 O2 and 2 ATP and produces 6 CO2 and 29.5 ATP as with direct oxidation. In the liver, however, fructolysis consumes 2 ATP and conversion to pyruvate produces 4 ATP, resulting in 2 ATP gained. In contrast, in skeletal muscle, 2 lactates are transported into the cells through facilitated diffusion, and their complete mitochondrial oxidation requires 6 O2 and produces 25.5 ATP, corresponding to 4.25 ATP/O2.

In summary, the energy efficiency for fructose oxidation in muscle is somewhat lower than for dietary glucose or starch oxidation. However, hepatic fructolysis into lactate may provide a substantial energy supply to the working muscle when the glycolysis rate is limiting.

 

[Hans]

I would be curious to hear what you guys think about these podcasts from Peter Attia.


View: https://youtu.be/LbSic4Oo8ME



View: https://youtu.be/V02z9mqTWzg


I am paraphrasing, and this isn't my specialty so I may be getting it wrong. But the argument isn't that fructokinase lowers ATP (I think most sugars when metabolized consume ATP), but that when it lowers ATP to begin metabolizing fructose, it does so in an uninhibited manner...so if large amounts of fructose are consumed, ATP can be lowered by such a large amount at first that a certain threshold is triggered where cells get the signal to LOWER metabolism and store fat.

Where as glucose and other sugars, if ATP gets lowered too much, metabolism of those sugars is slowed/stopped so these "store fat, prepare for winter" signals are not generated.

In other words it's the dose that may make fructose store fat, lower metabolism, and cause metabolic syndrome. Just a little bit of sugar, that is slower to absorb, like in fruit, is no problem. But drinking down a large bolus of HFCS in like a soda can lower ATP in cells so much as to cause these distressing signals.

Anyways would be interested to hear some takes on these podcasts. Some of the things mentioned in them really lines up with my experience of fructose.

I don't think we should pay much attention to it.

View: https://youtu.be/5AZD5wcl6v0


And also, read this study: Misconceptions about fructose-containing sugars and their role in the obesity epidemic

 

[Sefton10]

I don't think we should pay much attention to it.

View: https://youtu.be/5AZD5wcl6v0


And also, read this study: Misconceptions about fructose-containing sugars and their role in the obesity epidemic

Hans, am I right in thinking you're pretty low carb these days? I think I heard you say in one of your recent vids that you were around 100g a day in order to lean out a little?

 

[Hans]

Hans, am I right in thinking you're pretty low carb these days? I think I heard you say in one of your recent vids that you were around 100g a day in order to lean out a little?

I'm at 273g daily now. I was trying alternative day deficits and in those deficit days, my carbs were a bit lower. I stopped though. I don't like dieting lol. But I have to continue to cut, so I'll probably end up around 200g daily.

 

[Tarmander]

I don't think we should pay much attention to it.

View: https://youtu.be/5AZD5wcl6v0


And also, read this study: Misconceptions about fructose-containing sugars and their role in the obesity epidemic

I watched the video and read most of the study but I don't think the point I outlined above was tackled. Did you listen to the podcasts? They were long so understandable if you didn't.

I really do not care for the sugar is poison vs sugar is good debate...and the studies are so conflicting that I have a hard time telling who is telling the truth. For every study saying sugar is good there is its mirror.

The point above from the podcast was that fructose metabolism does not have the ATP lowering rate limiter in the same way that glucose and other sugars do. Because fructose can temporarily lower ATP so much, this sends the cells into a fat storing, metabolic slowing, insulin resistant state. So 50g of fructose sipped on all day may not trigger this, but chugged down in 5 minutes may. Now I guess you could say most fructose is converted into glucose, so it isn't an issue, in which case they would say the body converts glucose into fructose as well. Back and forth it goes.

Anyways, you may not have an answer but for anyone curious about some of what the other side is saying, the above podcasts are good

 

[SamYo123]

I watched the video and read most of the study but I don't think the point I outlined above was tackled. Did you listen to the podcasts? They were long so understandable if you didn't.

I really do not care for the sugar is poison vs sugar is good debate...and the studies are so conflicting that I have a hard time telling who is telling the truth. For every study saying sugar is good there is its mirror.

The point above from the podcast was that fructose metabolism does not have the ATP lowering rate limiter in the same way that glucose and other sugars do. Because fructose can temporarily lower ATP so much, this sends the cells into a fat storing, metabolic slowing, insulin resistant state. So 50g of fructose sipped on all day may not trigger this, but chugged down in 5 minutes may. Now I guess you could say most fructose is converted into glucose, so it isn't an issue, in which case they would say the body converts glucose into fructose as well. Back and forth it goes.

Anyways, you may not have an answer but for anyone curious about some of what the other side is saying, the above podcasts are good

durianrider aint fat

 

[Hans]

I watched the video and read most of the study but I don't think the point I outlined above was tackled. Did you listen to the podcasts? They were long so understandable if you didn't.

I really do not care for the sugar is poison vs sugar is good debate...and the studies are so conflicting that I have a hard time telling who is telling the truth. For every study saying sugar is good there is its mirror.

The point above from the podcast was that fructose metabolism does not have the ATP lowering rate limiter in the same way that glucose and other sugars do. Because fructose can temporarily lower ATP so much, this sends the cells into a fat storing, metabolic slowing, insulin resistant state. So 50g of fructose sipped on all day may not trigger this, but chugged down in 5 minutes may. Now I guess you could say most fructose is converted into glucose, so it isn't an issue, in which case they would say the body converts glucose into fructose as well. Back and forth it goes.

Anyways, you may not have an answer but for anyone curious about some of what the other side is saying, the above podcasts are good

I didn't listen yet, but might. These people love AMPK as well. What happens when ATP drops? AMP and ADP go up which activates AMPK. AMPK improves insulin sensitivity and enhances glucose and fat uptake and oxidation. Plus, the rest of glycolysis, which fructolysis feeds into, regenerates more ATP that was lost. So I don't see it as a net loss or detriment.

 

[Tarmander]

I didn't listen yet, but might. These people love AMPK as well. What happens when ATP drops? AMP and ADP go up which activates AMPK. AMPK improves insulin sensitivity and enhances glucose and fat uptake and oxidation. Plus, the rest of glycolysis, which fructolysis feeds into, regenerates more ATP that was lost. So I don't see it as a net loss or detriment.

Well if you want some decent content, those videos have a hundred thousand views together and the podcast probably even more. I bet a rebuttal of their points would be a decent video

 

[Hans]

Well if you want some decent content, those videos have a hundred thousand views together and the podcast probably even more. I bet a rebuttal of their points would be a decent video

Good point, I'll see what I can do.

 

[Motorneuron]

What does Ray think about ATP and fructose?

 

[zoan]

@Hans Hi, is there any reason you ve removed the article on Fructose, and articles on sugar as well, i saved the pages few month ago but the links are not working anymore ?
Kind regards