Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial

rei

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This is a very alarming study that seems to indicate sucrose and fructose as very problematic. I did not find any glaring errors in the methodology, so i am curious to see what you think. Seems like Lustig has a new case of ammo for his assault...
 
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ReSTART

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This study bears some limitations. Inherent problems of this type of study remain i) little control for compliance to the protocol of individual subjects and ii) unknown intestinal capacities (fructose tolerability) of the subjects to take up fructose. Accordingly, intersubject variability may reflect individual compliance and differences in the intestinal fructose uptake. Though a valuable tool for tracing in vivo kinetics of human metabolism, tracer based methodology provides only estimations of kinetics as it is based on various assumptions and possibly simplifications and mathematical models. Thus, in the present study the use of 13C-acetate as tracer and MIDA may have led to an underestimation of de novo fatty acid synthesis. We measured the synthesis and secretion of VLDL-TAG formed from plasma glycerol which represents a fraction of total VLDL-TAG. The contribution of VLDL-TAG with glycerol originating from the glyceroneogenic or glycolytic pathway has not been assessed in the study.
 
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rei

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Please provide your analysis of what that means instead of just quoting it.

To me it seems to mean "the p-value might not be entirely accurate" and "due to methological uncertainty the effect might be larger" which makes it even more troublesome from a peaty perspective as the measured effect is so clear it is unlikely to be due to things like compliance.
 

AndrogenicJB

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This is a very alarming study that seems to indicate fructose as very problematic. I did not find any glaring errors in the methodology, so i am curious to see what you think. Seems like Lustig has a new case of ammo for his assault...
bump
 
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rei

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Pretty early for bumping, no?

My take at this point: if this is not accurate, there must be some serious methodological error in the study, some assumption that does not hold true, or outright fraud. My guess would be that the body can differentiate between 13c and 12c containing molecules and tries to (or ends up to) primarily process the unnatural ones.
 

AndrogenicJB

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Pretty early for bumping, no?

My take at this point: if this is not accurate, there must be some serious methodological error in the study, some assumption that does not hold true, or outright fraud. My guess would be that the body can differentiate between 13c and 12c containing molecules and tries to primarily process the unnatural ones.
All I know is that I feel great on fructose, I have over 100 grams of it a day and can get very lean. All I need to do is supplement with choline bitartrate for the liver health
 

Hans

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Fructose and sugar are less insulinogenic than glucose so it doesn't shut lipolysis down as effectively as glucose, so FFAs stay elevated giving the impressions that fructose stimulates lipogenesis.
The SSB groups, especially the sugar and fructose group had less protein in their diet which is known to promote fat gain during overfeeding. But if you look at the stats, only the glucose group gained a significant amount of fat and actually lost muscle compared to the fructose and sucrose groups.

The sucrose group boosted RQ to 1.2 which does indicate stimulation of lipogenesis, but despite consuming sugar for 7 weeks, it never accumulated in the liver or was actually a problem.
Also, lipogenesis can crease anti-inflammatory insulin sensitizing branch chain fatty acids so it's not like lipogenesis are all bad. Elongation and unsaturation is how Mead acid is created.
When total fat content in the diet drops, lipogenesis goes up. That's not a bad thing.

So according to this 7 weeks study, despite the fact that sugar stimulates lipogenesis, it didn't cause fatty liver or insulin resistance.

"Neither fasting plasma TAG, glucose and insulin concentrations nor overall insulin (HOMA-IR) and adipose tissue insulin sensitivity (Adipo-IR) changed throughout the study. Furthermore, glucose tolerance assessed by an oral glucose tolerance test (75g glucose) was not changed by the dietary interventions."
 

MitchMitchell

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Fructose consumption correlates with low nutrient density, high energy diets. Excess energy is toxic. Fructose tends to accumulate in the liver more than glucose. Don’t drink gallons of sugar each week. Case closed
 

Jon2547

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Fructose consumption correlates with low nutrient density, high energy diets. Excess energy is toxic. Fructose tends to accumulate in the liver more than glucose. Don’t drink gallons of sugar each week. Case closed
That seems pretty straightforward, and I agree.
 

schultz

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Fructose consumption correlates with low nutrient density, high energy diets. Excess energy is toxic. Fructose tends to accumulate in the liver more than glucose. Don’t drink gallons of sugar each week. Case closed

A gallon of sugar is like 12,000 calories. Multiples of that would be insane!
 
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Blaze

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This is a very alarming study that seems to indicate sucrose and fructose as very problematic. I did not find any glaring errors in the methodology, so i am curious to see what you think. Seems like Lustig has a new case of ammo for his assault...
I guess anything in excess has specific detrimental effects. I think the science is sound that Fructose can cause liver issues in excessive amounts in some individuals since it is processed differently than the other sugars. Storing sugar as fat in the liver is much worse than storing it in the other fat storage tissues. But, fruit is a good thing. Damage or benefit would be dose dependent. Only in excess do you see these issues. How much qualifies as an excessive amount?

That probably varies greatly from person to person based on their ability to metabolize, store it or use it.
 
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Mito

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Only in exceHow much qualifies as an excessive amount?

That probably varies greatly from person to person based on their ability to metabolize, store it or use it.
“High doses of fructose (≥1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota. Intestinal fructose clearance is augmented both by prior exposure to fructose and by feeding. We propose that the small intestine shields the liver from otherwise toxic fructose exposure.”


“Essentially this data suggests that if you were to feed me (85kg male) 255 grams of straight glucose, 255 grams of straight fructose, or 340 grams of straight fructose per day and not really exercise that I would see decreases in insulin sensitivity and have some liver fat accumulation, but it would not occur if you fed me 127.5 grams of fructose. Keep this data in your mind to refer to in our discussion below (8)."

"Now for the most controversial one. When consumed, some fructose is indeed converted into VLDL triglycerides. By nature, this metabolic process presents limitations in methodology so only two studies have been done with isotopic tracers that allow us to get a good picture of what is going on. In one study, the authors showed that lipogenic potential of fructose seems to be small, since only 0.05% and 0.15% of fructose were converted to de novo fatty acids and TG-glycerol at 4 hour, respectively (7). Fructose actually appears to alter current lipid metabolism by favoring esterfication but does not itself contribute to fatty acid synthesis to any meaningful extent. I.e. the conversion of fructose to any lipid is almost meaningless at normal to slightly high intakes (0.75 g/kg)
 

lampofred

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I think Dr. Peat thinks lipogenesis from sugar is a good thing. It's only the lipogenesis driven by too much iron that's bad.
 

Nathan777

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Curious if anyone has additional thoughts on this study now that it's been out a bit? Just came across it and found it a little alarming.
 
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