Fructose series part 1: fructose depletes ATP?

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Hans

Hans

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Liver can handle at max 100 grams of fructose converting into glycogen
Per minute, hour or day?
Fructose gets oxidized as fuel if it's not stored as glycogen.

People that eat too much tend to get fatty liver regardless if it's from fructose or not. High GI high PUFA foods are a major cause.
 

salvio

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Per minute, hour or day?
Fructose gets oxidized as fuel if it's not stored as glycogen.

People that eat too much tend to get fatty liver regardless if it's from fructose or not. High GI high PUFA foods are a major cause.
It's oxidixed if you need to burn it to produce energy, but usually animals use fats when they're fasting.

Your question is not well done, cause you have a store of more or less 100 grams, now if you're a sedentary person it's really really easy to have all 100 grams there and eating more can cause conversion in fats creating NAFLD. If you eat few carbs and move your storage at unit of time increase cause your storage becomes empty faster.

About this you're right maybe the problem isn't the fructose in sè or SFA but eating a lot, but the question is, how much is a lot? How much is High PUFA?
 
OP
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It's oxidixed if you need to burn it to produce energy, but usually animals use fats when they're fasting.

Your question is not well done, cause you have a store of more or less 100 grams, now if you're a sedentary person it's really really easy to have all 100 grams there and eating more can cause conversion in fats creating NAFLD. If you eat few carbs and move your storage at unit of time increase cause your storage becomes empty faster.

About this you're right maybe the problem isn't the fructose in sè or SFA but eating a lot, but the question is, how much is a lot? How much is High PUFA?
The body can burn glucose/fructose with no problem at all.
I recommend you listen to this vid and read these articles:

Myth: Fructose is bad for you. Busted!

Does fruit juice increase triglycerides?

Why the side effects of sugar are based on flawed research and how to make sugar work for you instead of against you

Why sugar doesn’t make you fat – the ultimate guide on lipogenesis

 

Jerkboy

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Fructose/fruit sugars make me strong as ****. Nothing compares.
 

salvio

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These are self-referential articles, please post studies.

The can burn fructose if it needs to be burned otherwise it will be accumulated.

Don't be upset but I don't trust on the first I meet on a forum, post evidences please.
 

salvio

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@Hans


This prove that if you eat carbs and fats using intermittent fasting you can have the maximum of metabolic flexibility burning one or another fuel.

So you can burn fructose as fat if you eat a lot but you don't have to eat lots of fats cause in this case liver is overwhelmed by the excess of fructose.

The same for starch and glucose with a net difference: liver can handle fructose and glucose, muscle handle only glucose unless someone doesn't eat few fats and glucose in that case can handle glucose.

I didn't say fructose is bad at all amount, used at night with fats can be very very helpful cause can reefed liver and can be released as glucose to burn with fats all the night, but I think that is impossible not to saturate liver if eat more than 50 grams per day without caloric restriction and/or physical activity. Anyway I read on a book that better adsorption is when ratio glucose/fructose si nearly 1.

I thing that fructose, SFAs, fiber and proteins are very very good when the meal is low in carbs, rich in fats and after you won't eat for hours, otherwise it's difficult to balance the amount to avoid some problems.

Obviously the gut microbiome can help in this if there's no dysbiosis to regulate the amount of energy that the body has to adsorb, but if there si unbalanced microbiome this can be very very dangerous especially about LPS traslocation in the blood.
 
OP
Hans

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These are self-referential articles, please post studies.

The can burn fructose if it needs to be burned otherwise it will be accumulated.

Don't be upset but I don't trust on the first I meet on a forum, post evidences please.
Those articles contain all the references. I quote many of the studies as well.
 

salvio

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Abstract​

Fructose is associated with the biochemical alterations that promote the development of metabolic syndrome (MetS), nonalcoholic fatty liver disease, and type 2 diabetes. Its consumption has increased in parallel with MetS. It is metabolized by the liver, where it stimulates de novo lipogenesis. The triglycerides synthesized lead to hepatic insulin resistance and dyslipidemia. Fructose-derived advanced glycation end products (AGEs) may be involved via the Maillard reaction. Fructose has not been a main focus of glycation research because of the difficulty in measuring its adducts, and, more importantly, because although it is 10 times more reactive than glucose, its plasma concentration is only 1% of that of glucose. In this focused review, I summarize exogenous and endogenous fructose metabolism, fructose glycation, and in vitro, animal, and human data. Fructose is elevated in several tissues of diabetic patients where the polyol pathway is active, reaching the same order of magnitude as glucose. It is plausible that the high reactivity of fructose, directly or via its metabolites, may contribute to the formation of intracellular AGEs and to vascular complications. The evidence, however, is still unconvincing. Two areas that have been overlooked so far and should be actively explored include the following: 1) enteral formation of fructose AGEs, generating an inflammatory response to the receptor for AGEs (which may explain the strong association between fructose consumption and asthma, chronic bronchitis, and arthritis); and 2) inactivation of hepatic AMP-activated protein kinase by a fructose-mediated increase in methylglyoxal flux (perpetuating lipogenesis, fatty liver, and insulin resistance). If proven correct, these mechanisms would put the fructose-mediated Maillard reaction in the limelight again as a contributing factor in chronic inflammatory diseases and MetS.


And:

A Dual Sugar Challenge Test for Lipogenic Sensitivity to Dietary Fructose​


Context:
Increased hepatic de novo lipogenesis (DNL) in response to dietary sugar is implicated in dyslipidemia, fatty liver, and insulin resistance.

Objective:
The aim of the study was to develop a simple outpatient tolerance test for lipogenic sensitivity to dietary sugar.
Design and Setting:
In inpatients given repeated doses of fructose, protocol 1 compared the acute increase in DNL determined from the percentage of palmitate (“new palmitate”) and the percentage of isotopically labeled palmitate (“%DNL”) in very low-density lipoprotein triglyceride (TG). Protocol 2 compared the increase in new palmitate in outpatients given three different sugar beverages in a randomized crossover design.

Participants:
There were 15 lean and overweight volunteers in protocol 1 and 15 overweight volunteers in protocol 2.

Interventions:
In protocol 1, subjects received 1.4 g/kg fructose in divided oral doses over 6 h; in protocol 2, subjects received 0.5 g/kg fructose, 0.5 g/kg fructose plus 0.5g/kg glucose, or 1 g/kg fructose plus 1g/kg glucose each as a single oral bolus.
Main Outcome Measures:
We measured the increase in DNL by two methods.

Results:
After repeated doses of fructose, new palmitate was significantly correlated with the increase in %DNL (Δ, r = 0.814; P < 0.001) and with fasting insulin levels (area under the curve, r = 0.754; P = 0.001). After a single sugar dose, new palmitate showed a dose effect and was greater after fructose plus glucose. Very low-density lipoprotein TG and total TG significantly increased in both protocols.

Conclusions:
A single oral bolus of fructose and glucose rapidly increases serum TG and TG palmitate in overweight subjects. A dual sugar challenge test could prove useful to identify individuals at risk for carbohydrate-induced dyslipidemia and other adverse effects of increased DNL.

 
OP
Hans

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Abstract​

Fructose is associated with the biochemical alterations that promote the development of metabolic syndrome (MetS), nonalcoholic fatty liver disease, and type 2 diabetes. Its consumption has increased in parallel with MetS. It is metabolized by the liver, where it stimulates de novo lipogenesis. The triglycerides synthesized lead to hepatic insulin resistance and dyslipidemia. Fructose-derived advanced glycation end products (AGEs) may be involved via the Maillard reaction. Fructose has not been a main focus of glycation research because of the difficulty in measuring its adducts, and, more importantly, because although it is 10 times more reactive than glucose, its plasma concentration is only 1% of that of glucose. In this focused review, I summarize exogenous and endogenous fructose metabolism, fructose glycation, and in vitro, animal, and human data. Fructose is elevated in several tissues of diabetic patients where the polyol pathway is active, reaching the same order of magnitude as glucose. It is plausible that the high reactivity of fructose, directly or via its metabolites, may contribute to the formation of intracellular AGEs and to vascular complications. The evidence, however, is still unconvincing. Two areas that have been overlooked so far and should be actively explored include the following: 1) enteral formation of fructose AGEs, generating an inflammatory response to the receptor for AGEs (which may explain the strong association between fructose consumption and asthma, chronic bronchitis, and arthritis); and 2) inactivation of hepatic AMP-activated protein kinase by a fructose-mediated increase in methylglyoxal flux (perpetuating lipogenesis, fatty liver, and insulin resistance). If proven correct, these mechanisms would put the fructose-mediated Maillard reaction in the limelight again as a contributing factor in chronic inflammatory diseases and MetS.


And:

A Dual Sugar Challenge Test for Lipogenic Sensitivity to Dietary Fructose​


Context:
Increased hepatic de novo lipogenesis (DNL) in response to dietary sugar is implicated in dyslipidemia, fatty liver, and insulin resistance.

Objective:
The aim of the study was to develop a simple outpatient tolerance test for lipogenic sensitivity to dietary sugar.
Design and Setting:
In inpatients given repeated doses of fructose, protocol 1 compared the acute increase in DNL determined from the percentage of palmitate (“new palmitate”) and the percentage of isotopically labeled palmitate (“%DNL”) in very low-density lipoprotein triglyceride (TG). Protocol 2 compared the increase in new palmitate in outpatients given three different sugar beverages in a randomized crossover design.

Participants:
There were 15 lean and overweight volunteers in protocol 1 and 15 overweight volunteers in protocol 2.

Interventions:
In protocol 1, subjects received 1.4 g/kg fructose in divided oral doses over 6 h; in protocol 2, subjects received 0.5 g/kg fructose, 0.5 g/kg fructose plus 0.5g/kg glucose, or 1 g/kg fructose plus 1g/kg glucose each as a single oral bolus.
Main Outcome Measures:
We measured the increase in DNL by two methods.

Results:
After repeated doses of fructose, new palmitate was significantly correlated with the increase in %DNL (Δ, r = 0.814; P < 0.001) and with fasting insulin levels (area under the curve, r = 0.754; P = 0.001). After a single sugar dose, new palmitate showed a dose effect and was greater after fructose plus glucose. Very low-density lipoprotein TG and total TG significantly increased in both protocols.

Conclusions:
A single oral bolus of fructose and glucose rapidly increases serum TG and TG palmitate in overweight subjects. A dual sugar challenge test could prove useful to identify individuals at risk for carbohydrate-induced dyslipidemia and other adverse effects of increased DNL.

Hyperinsulinemia and inflammation drive DNL, so lowering those will solve a lot of problems. Cortisol and serotonin are also heavily involved in fatty liver. When they don't overfeed patients, then DNL becomes insignificant.
 

salvio

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Hyperinsulinemia and inflammation drive DNL, so lowering those will solve a lot of problems. Cortisol and serotonin are also heavily involved in fatty liver. When they don't overfeed patients, then DNL becomes insignificant.
And how do you solve the problem of ages? You didn't ask me only saying the things again and again.
 
OP
Hans

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And how do you solve the problem of ages? You didn't ask me only saying the things again and again.
Solve what problem and ask you what?
 

salvio

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Sorry the problem of AGEs (Advanced Glycation End Products).

Fructose tends to create them with proteins seven fold than glucose.
 

schultz

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And how do you solve the problem of ages?

Don't eat PUFA I suppose.


Ray provides some interesting things to consider in some of his newsletters. In one of his articles he mentions that...

"lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do"

He cites Fu, et al., 1996, which I have admittedly not read.

Ray has also mentioned that when carbon dioxide is abundant, AGE's are not formed. Fructose happens to increase CO2 to a greater degree than glucose (Brundin, et al. 1993)

From Ray Peat's Newsletter entitled: "Fats, functions & malfunctions"
"An adequate amount of sugar maintains both a high rate of metabolism, and a high respiratory quotient, i.e., high production of carbon dioxide. Mole rats, bats, and queen bees, with an unusually great longevity, are chronically exposed to high levels of carbon dioxide. Carbon dioxide forms carbamino bonds with the amino groups of proteins, inhibiting their reaction with the reactive "glycating" fragments of PUFA."
 

salvio

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Don't eat PUFA I suppose.


Ray provides some interesting things to consider in some of his newsletters. In one of his articles he mentions that...

"lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do"

He cites Fu, et al., 1996, which I have admittedly not read.

Ray has also mentioned that when carbon dioxide is abundant, AGE's are not formed. Fructose happens to increase CO2 to a greater degree than glucose (Brundin, et al. 1993)

From Ray Peat's Newsletter entitled: "Fats, functions & malfunctions"
"An adequate amount of sugar maintains both a high rate of metabolism, and a high respiratory quotient, i.e., high production of carbon dioxide. Mole rats, bats, and queen bees, with an unusually great longevity, are chronically exposed to high levels of carbon dioxide. Carbon dioxide forms carbamino bonds with the amino groups of proteins, inhibiting their reaction with the reactive "glycating" fragments of PUFA."
Glycation is about a sugar that bonds to a protein, PUFA isn't pertinent in sugars and proteins AGEs.

And here we're talking on fructose and glucose not PUFA.
 
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So fructose, as well as galactose, kept cells from using too much glycolysis, because they are so pro- metabolic. Even during a LPS challenge, the oxygen comsumption was still much higher compared to glucose. Lactate was much lower in the fructose group, as expected from a substance that increases PDH and lowers PDH kinase. More evidence that that one isotope study about fructose where it produced a lot of lactate was badly designed. It seems to lower lactate instead of increasing it.

A strong, transient elevation in inflammatory markers can be useful to get rid of the problem. Nitric oxide, when elevated strategically during infection, can be extremely useful. But regardless, having more oxidative phosphorilation is the best path in pretty much any situation, if the goal is to create or maintain organismic complexity. If fructose has the same effect in cancer cells, it would be anti- cancer, since the Warburg Effect, that is, excess lactate production( defective oxidative metabolism), is actually a cause of cancer. And in the study in the OP, fructose didn't lower the viability of the cells, it was the same as in the glucose group.

An in vivo study in rats showed that fructose feeding massively lowers mortality caused by endotoxin: Diet-induced protection against lipopolysaccharide includes increased hepatic NO production - PubMed

The study below shows that fructose or orange juice doesn't cause any inflmmation or oxidative stress, but pure glucose does.
 

salvio

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So fructose, as well as galactose, kept cells from using too much glycolysis, because they are so pro- metabolic. Even during a LPS challenge, the oxygen comsumption was still much higher compared to glucose. Lactate was much lower in the fructose group, as expected from a substance that increases PDH and lowers PDH kinase. More evidence that that one isotope study about fructose where it produced a lot of lactate was badly designed. It seems to lower lactate instead of increasing it.

A strong, transient elevation in inflammatory markers can be useful to get rid of the problem. Nitric oxide, when elevated strategically during infection, can be extremely useful. But regardless, having more oxidative phosphorilation is the best path in pretty much any situation, if the goal is to create or maintain organismic complexity. If fructose has the same effect in cancer cells, it would be anti- cancer, since the Warburg Effect, that is, excess lactate production( defective oxidative metabolism), is actually a cause of cancer. And in the study in the OP, fructose didn't lower the viability of the cells, it was the same as in the glucose group.

An in vivo study in rats showed that fructose feeding massively lowers mortality caused by endotoxin: Diet-induced protection against lipopolysaccharide includes increased hepatic NO production - PubMed

The study below shows that fructose or orange juice doesn't cause any inflmmation or oxidative stress, but pure glucose does.
Good finally we talk about fact. I want to read the researches you posted before answering you, ok?

Anyway I suppose it's impossible eating fructose without glucose.
 
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salvio

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Anyway it's possible that Vitamin C in orange fruit can reduce ROS. I'd like to read the entire researches even that one before where thay demonstrated that glucose creates lots of ROS.
 

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