I have watched a video which summarized the findings in examining the sugar addiction in rats. The presenter talked about how they conditioned the rats to binge on sugar. One slide, however, reported GLUCOSE consumption patterns at 13:25 minute of the video:
So the principle of attractive sweetness of fructose, which Dr Lustig has repeatedly highlighted, could not be applied here. In fact, rodents such as mice and rats naturally crave starches or sugars such as grains and fruits they find in nature, not the cheese as the cartoons notoriously portray them. Scroll down to point 3 in this article to find out yourself.
Further in the video you will see how both groups of rats: 1. having short availability of large amounts of sugar and 2. having sugar available over 24-hours have increased their sugar consumption, but the first group had overall much higher sugar intake than those in the second group. Bingeing rats therefore compensated for the periods of no sugar availability and consumed overall more sugar. Interesting to see. But this was not to contrast with humans, it was just an interesting input from the curiosity.
What I found appealing was the slide (22:24) and the presenter mentioned it as well, was that high-fructose corn syrup (HFCS) had different metabolic effect from sucrose.
That it is different from glucose is obvious. But from sucrose? I wonder where they got this information when my research and also Dr Lustig consistently report that there is no significant difference between the absorption and metabolism of HFCS and sucrose. This was not discussed in the video.
The two possible explanations would be that some people do not have sucrase - an enzyme cleaving sucrose into free glucose and fructose, which the HFCS actually is and in these people/animals the sucrose is not absorbed. But this is unlikely the case here. More probable explanation is the different content of fructose in HFCS than is in sugar. Especially the beverages contain HFCS-55, which has 5% more fructose than sugar, but solid foods tend to contain HFCS-42, which has 8% LESS fructose than sugar. And as such, in the first case there might be less insulin produced than in the second case, due to the proportionally different content of glucose. But is it that much? Again, the experts have reached the consensus that there is no significant difference in metabolism between HFCS and sugar.
Moreover, going back to another point of the slide above: HFCS releases triglycerides (like a fat), if you have read my previous articles about fructose metabolism, you now might be aware that fructose contributes only little to the formation of new fats. Most of the increased triglycerides in the blood stream were the re-esterified free fatty acids that were already present in the blood stream - as their concentration always decreased after fructose intake challenge. Did they measure the free fatty acids concentration in the rats, or were they only happy to see the triglycerides rise and make the conclusion above? This was not said and I do not see any legible details of the study itself to check these details.
The further slide suggest possible addiction-like properties of HFCS, but you could see that the rats behaved the same when receiving sucrose or even glucose.
These results correspond with the previous slide above - adverse metabolic effect of HFCS. But it also informs us about increased body weight after feeding rats with HFCS. The amount of HFCS was 8% supplementation of the standard chow diet:
However, nothing was said whether these 8% of extra HFCS were within or on top of the balanced energy intake. By balanced energy intake I mean the amount of calories needed to maintain stable body weight. When doing my research the studies on humans also varied in this: some were in isocaloric settings, when fructose or sugar replaced some other calories, others were in hypercaloric setting, providing calories on top of the balanced state. Any wonder why people gained weight?
But, to be on the neutral side, I should also refer to this:
The slide and information presented by the speaker suggests that rats which were bingeing on sugar did not increase their body weight, because although they consumed more sugar than any other group of rats, they compensated for the excess energy intake by consuming less of their normal chow.
HOWEVER:
1. this latter case was the observation for only 27 days, not 6 months.
2. the whole study design is different between these two cases: the HFCS study was not binge eating, the rats had normal feeding pattern, just consumed probably excess 8% of calories in a form of HFCS.
It is therefore not wise to compare these two studies as it was a single trial comparing the effect of sugar and HFCS in one.
Moreover, from the following slide you can see that all rats gained weight, whether having ad libitum access to HFCS over 12 hours (top curve), bingeing on HFCS when having it available for only 12 hours (middle black curve), and also when consuming a normal chow (bottom curve). Only the two former cases led to a higher weight gain and of these two the first led to even higher than the second one. But the same was reported for SUGAR, do you remember? Check again the third paragraph of this article above.
What does that actually say?
Note the title of this slide: it mentions 5 weeks, but the whole x-axis covers 24 weeks. That is fine, but when you look above the point of 5 weeks, the difference in gained weight between the three designs is not that big, is it?
From the physiology point of view: deprivation of favorite substance (HFCS or sugar) causes an individual to overeat on it when it is available, especially after a fasting period. And that is typical for humans and rats. That also means that higher bulk of this substance is consumed in a shorter period of time - leading to increased insulin level and enhanced fat storage. So not only more calories are consumed at once when bingeing, but the physiological response to the excess of glucose mediates fat storage via insulin. Moreover, the excessive amount of fructose leads to increased fat synthesis, especially in rodents which are more effective in de-novo lipogenesis than humans are, do you remember? So these results cannot be directly applied to humans.
I would like to finally explain the difference between just supplementation of diet with HFCS and bingeing on a substance, separately from consuming the usual and rather boring rat chow. The Summary slide I posted here did not specify, how the HFCS was supplemented: whether it was in a sweetened drink or mixed with the chow. Since rats like sweet taste, if their chow was sweetened, they were likely to consume more of it and finally gain weight, especially if those 8% were on top of their energy needs. In contrast, having sugar to binge on and then consuming the chow which did not taste as appealing in comparison to sugar, might have been a factor in a self-limiting intake of calories, leading to a stable body weight over time in those rats. The Summary slide also did not inform us about bingeing, so the rats probably only had their diet spiked with 8% of HFCS. This amount of sugar would represent extra 200 kcal, if consumed on top of the energy needs in a person requiring 2500 kcal per day. Overeating 200 kcal on daily basis for 6 months would definitely lead to increased body weight and also perhaps altered biochemistry in the body. One tin of sugary soft drink contains about 150 kcal, just for the comparison.
And the persisting discrepancy between the body weight on sugar and HFCS bingeing rats over 5 weeks? This would require a closer look into the actual designs of the studies. But maybe rats really have different absorption or metabolism of sucrose from HFCS than humans. It would be interesting to find out what was behind these different results. For now I can tell you, if you have not watched the video to the very end, Dr Lustig was in the audience and questioned this discrepancy as well. But the speedy answer of Ms Avene, the presenter, did not sound convincing to me and I can only guess that Dr Lustig was not completely happy with her reasoning either.
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