Fructose series part 1: fructose depletes ATP?

[Hans]

Every heard that fructose might deplete ATP? That's one silly argument that I debunk here.

Fructose series part 1: fructose depletes ATP? » MENELITE

Fructose is the most evil monosaccharide there is according to most nutritionists out there. One of the main reasons why is because it’s thought to deplete ATP. Glucose is thought … Continue reading Fructose series part 1: fructose depletes ATP?

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[Hans]

Forgot to add the following related articles (and references) to the bottom of the article.

• Insulin: the wrongly accused hormone
• Myth: Fructose is bad for you. Busted!
• Why the side effects of sugar are based on flawed research and how to make sugar work for you instead of against you
• Does fruit juice increase triglycerides?
• Why sugar doesn’t make you fat – the ultimate guide on lipogenesis

 

[MeatOrchid]

BRAVO HANS!

 

[David90]

Great Aricle @Hans

Thankfully it's getting Debunked. Upping Fructose in the Last Few Years was (for me) one of the Best Things ever.

It does not only raise ATP but it also increases Metabolism and Thyroid Function and Improves Insulin Sensitivity and fills also Liver Glycogen. So It should be a No-Brainer to consume more Fructose.

 

[Hans]

So It should be a No-Brainer to consume more Fructose.

Lol for sure. If people would just look at the evidence.

 

[Amazoniac]

Since ATP here is donating a phosphate group, dextructokinase and levilokinase cancel out. At one stage, both processes yield dihydroxyacetorn phosphate and glyceraldehyde as products of aldolases. In dextructolysis, glyceraldehyde had the phosphate added in advance, whereas in levilolysis it occurs after the action of aldolase. Again, canceling out. Their representation was an environmental toxin, they could've put those last leviloses on the same.. level and chosen 'Y' instead of 'V' arrows to not give the impression that it's either one or the other when the toxin is split.

Spoiler

On depletion, I haven't looked at it. If it occurs, extreme conditions are probably needed, but I wouldn't jump to the conclusion that such thing is impossible just because there is a return later on, a fair assessment would require considering reaction rates, enzyme capacities and sites of metabolism. For example, there can be too much of it concentrating in liver at once, a mismatch of enzyme activity and transient reduction of ATP.

 

[Hans]

a fair assessment would require considering reaction rates, enzyme capacities and sites of metabolism.

Definitely.

For example, there can be too much of it concentrating in liver at once, a mismatch of enzyme activity and transient reduction of ATP.

Yes, but still highly unlikely. GLUT5 can most likely be saturated at a certain concentration and can still limit entry. Evidence is needed if one of the enzymes in glycolysis and fructolysis are rate-limited and what determines where the fructose goes. I'd imagine in a reduced state, G-3-P will be slow as well as PDH, thus more will go through the PPP perhaps as well as towards lactate and glycerol.

 

[Amazoniac]

Definitely.

Yes, but still highly unlikely. GLUT5 can most likely be saturated at a certain concentration and can still limit entry. Evidence is needed if one of the enzymes in glycolysis and fructolysis are rate-limited and what determines where the fructose goes. I'd imagine in a reduced state, G-3-P will be slow as well as PDH, thus more will go through the PPP perhaps as well as towards lactate and glycerol.

Yeah, excess levilose on its own is barely absorbed, it would require synergistic intoxication. Digestion would likely slow down and it can be peed as emergency, but if this doesn't occur and it doesn't show up in blood (as it happens with dextructose after a meal), it's taken up by cells, mostly liver. The concerning part that I haven't looked at is the limitations and differences in processing between each step prior to the formation of the metabolites that you mentioned, their claim is that the initial processing is poorly-regulated and won't adjust well to match the activity of the next events.

 

[Amazoniac]

Saving for later, but it's not impossible. I wonder how pure dextructose fares in comparison.
- Higher Dietary Fructose Is Associated with Impaired Hepatic ATP Homeostasis in Obese Individuals with Type 2 Diabetes
- Investigating the effects of an oral fructose challenge on hepatic ATP reserves in healthy volunteers: A 31P MRS study
- Investigating Alterations in Hepatic ATP Levels Following Fructose and Fructose+Glucose Ingestion: A Simple Non-Invasive Technique to Assess Liver Function Using 31P MRS
- Health Outcomes Of A High Fructose Intake: The Importance Of Physical Activity

 

[gaze]

so would fructose be considered a weak adaptogen like caffeine or is that an incorrect way to view it?

 

[CLASH]

Saving for later, but it's not impossible. I wonder how pure dextructose fares in comparison.
- Higher Dietary Fructose Is Associated with Impaired Hepatic ATP Homeostasis in Obese Individuals with Type 2 Diabetes
- Investigating the effects of an oral fructose challenge on hepatic ATP reserves in healthy volunteers: A 31P MRS study
- Investigating Alterations in Hepatic ATP Levels Following Fructose and Fructose+Glucose Ingestion: A Simple Non-Invasive Technique to Assess Liver Function Using 31P MRS
- Health Outcomes Of A High Fructose Intake: The Importance Of Physical Activity

In the first study fructose was injected somewhere around 10g (250mg/kg) over the course of a minute. I think this may adjust the actual effects on fructose metabolism so it makes it hard to draw conclusions.

In the second study a 75g oral dose of fructose was given, considering fructose malabsorption and endotoxemia its hard to parse out an effect from endotoxin vs. fructose.

The third study is better, it compared a 75g oral dose of fructose with a 75g dose of glucose and fructose divided equally between the two. The lone 75g dose of fructose has the same issue as study number 2, but the glucose and fructose mixture tells us a little more. It would be best to compare a 75g dose of glucose, with a 75g dose of fructose + glucose.

The last study links to your post on the benefits of urate produced by fructose in apple juice as an antioxidant. Pretty interesting, what did you want us to get from this, specifically?

 

[Amazoniac]

In the first study fructose was injected somewhere around 10g (250mg/kg) over the course of a minute. I think this may adjust the actual effects on fructose metabolism so it makes it hard to draw conclusions.

In the second study a 75g oral dose of fructose was given, considering fructose malabsorption and endotoxemia its hard to parse out an effect from endotoxin vs. fructose.

The third study is better, it compared a 75g oral dose of fructose with a 75g dose of glucose and fructose divided equally between the two. The lone 75g dose of fructose has the same issue as study number 2, but the glucose and fructose mixture tells us a little more. It would be best to compare a 75g dose of glucose, with a 75g dose of fructose + glucose.

The last study links to your post on the benefits of urate produced by fructose in apple juice as an antioxidant. Pretty interesting, what did you want us to get from this, specifically?

I thought of that as well, but once you have injected and ingested, you already rule out the influence of endotoxins. Such amount administered surpasses a comfortable rate of oxidation and avoids intestinal metabolism, but it's not absurd (as I was expecting to find).

Soon enough there will be members trying to screen the experiments for PUFA to discredit it, which is alright, but if you search for 'fructose atp depletion' or related terms, there's an overwhelming volume of articles on it, it's not something obscure. It took me a few minutes to locate those and it's surprising how it didn't raise doubt in anyone about the validity of the phenomenon. Other than having to compare with dextructose, it would be great to contrast the effect of purified sugars with a nutritious food, not sure if apples produce the cut.

The claim is that ATP isn't being regenerated fast enough, peerate would be a product of its degradation. But there's this..
- Misconceptions about fructose-containing sugars and their role in the obesity epidemic

 

[Hans]

Fructose is absorbed at a certain rate in the intestine, which can help to prevent system overload. There are also enzymes in the intestine that convert some of the fructose to glucose before absorption. In some unhealthy individuals, there can be fructose malabsorption which feeds bacteria to produce endotoxin and excess acetate, which can inhibit energy production and lead to excess synthesis of fat.

A big isolate bolus of sugar might cause issues for some people, but (refined) sugar in solid food is a different issue. There there's the difference between refined and natural sources.

 

[Amazoniac]

I skimmed through those articles and the doses used seem reasonable. Although the largest fructose load on its own is excessive, the body rejects a good portion of it, so it's in effect similar to consuming less.

Endotoxin can be suspected, but in one of the experiments above, a fructose-only group had greater ATP availability than fructose with glucose, which would be in line with glucose promoting its uptake and perhaps increasing the rate of oxidation as well.
- Fructose metabolism in humans – what isotopic tracer studies tell us

With higher doses, I thought that vaginate (C3H5O3−) stemming from the intestine (Mito, 2018) could play a role in lowering ATP if it happens to overwhelm its metabolizing capacity, however it's the same case as before, once there are experiments showing similar effects when it avoids the gut, something else has to explain. Injecting 20 g or so could represent an amount that escapes intestine metabolism and reaches the liver. In case it's generated in there, it's supposed to relieve the strain, not tax it further.

There's a rate of glucose injection that keeps blood stable, I suppose that it's lower for fructose. Apparently, the phosphorylation is what traps these toxins in cells in preventing their interaction with CP, the Contamination Portals (Glutton1, 2..). Since the liver is a major expression site for fructokinase, that's where fructose stays.

Franklin mentions the ability of this trash to lower nephrosate, must be related.

- Calcium and Fructose Intake in Relation to Risk of Prostate Cancer

"Dietary fructose can reduce plasma phosphate levels by 30 to 50% for more than 3 h due to the rapid shift of phosphate from the extracellular to intracellular compartment (18, 19). This hypophosphatemia occurs because fructose is very rapidly phosphorylated in the liver, catalyzed by fructokinase (20), which by-passes the phosphofructokinase regulatory step in glycolysis (21)."​

The person would probably feel when something is off, those decreases are too great to pass unnoticed, or innoticed as I say. The victims not being used to the punishment should have a negative influence. Perhaps crematine is of help in speeding up ATP repletion.

 

[LOL]

I saw another thread here and started thinking about acquired fructose malabsorption, not the rare genetic variant, but that the body actively rejects fructose by suppressing transporter enzymes. Some points I put up after skimming the web:
- It's interesting to note that fructose malabsorption has a very high occurence in northern populations. Maybe it has to do with low vit D or related
- Calcium and fructose might have some kind of regulatory interaction because of fructose effect on phosphate
- This article investigated effect of high fructose on calcium absorption in growing rats: DOI: 10.1152/ajpendo.00582.2012 High fructose lowered vitamin D3 levels and inhibited calcium absorption, when rats were supplied vitamin D3 in their food the expression of calcium transporters was restored.

 

[David90]

Lol for sure. If people would just look at the evidence.

Right. Also i make sure to not go over 40g of Fructose per Day (Risk of getting NAFLD? ..... Despite having Choline in the Diet?) but their are only Pro's to eating more Fructose.

 

[Hans]

Right. Also i make sure to not go over 40g of Fructose per Day (Risk of getting NAFLD? ..... Despite having Choline in the Diet?) but their are only Pro's to eating more Fructose.

If the fructose comes from fruit or other natural sources (e.g. honey, maple syrup, etc.), then someone can easily consume 200g or more of fructose daily without the risk of getting fatty liver.

 

[David90]

If the fructose comes from fruit or other natural sources (e.g. honey, maple syrup, etc.), then someone can easily consume 200g or more of fructose daily without the risk of getting fatty liver.

Ok. Good to know. Thanks for the Info

 

[salvio]

It seems that when there is an intestinal barrier compromising the only thing to avoid endotoxemia is eating a very low cal diet.

Effect of caloric restriction on gut permeability, inflammation markers, and fecal microbiota in obese women - Scientific Reports

Recent findings suggest an association between obesity, loss of gut barrier function and changes in microbiota profiles. Our primary objective was to examine the effect of caloric restriction and subsequent weight reduction on gut permeability in obese women. The impact on inflammatory markers...

www.nature.com

Problem is that we should see in lean women.

 

[salvio]

If the fructose comes from fruit or other natural sources (e.g. honey, maple syrup, etc.), then someone can easily consume 200g or more of fructose daily without the risk of getting fatty liver.

Liver can handle at max 100 grams of fructose converting into glycogen. Now if someone spends more there's no problem but otherwise the risk of NAFLD is high, surely if someone eats a little of fats, he uses these fats to create energy.

The problem seems always the energy expenditure between two meals.