High-Fructose Corn Syrup - the Controversy

Well, that's fructose, though, not HFCS which is only 55% fructose.Recall that fructose, or "fruit sugar", is the primary sugar in fruits so shouldn't fruits make you fat?Have you ever heard of someone getting fat from fruit? Getting diabetic from fruit? Me neither.That's the mystery, I guess; according to the food scare crowd, fructose (fruit) is ok, and fructose+glucose (sucrose) is ok, and glucose is ok, but 55% fructose/43% glucose gives you instant diabetes.

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Recall that fructose, or "fruit sugar", is the primary sugar in fruits so shouldn't fruits make you fat?

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Have you ever heard of someone getting fat from fruit? Getting diabetic from fruit? Me neither.

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That's the mystery, I guess; according to the food scare crowd, fructose (fruit) is ok, and fructose+glucose (sucrose) is ok, and glucose is ok, but 55% fructose/43% glucose gives you instant diabetes.

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Taq covered that in Message 13. Fructose MetabolismThe article goes on to explain that a piece of fruit contains only 5-8 grams of fructose. We don't tend to accumulate the same volume of fructose by just eating whole fruits as we do when we consume sodas, fruit juices, and foods containing fructose. No webpage found at provided URL: Fructose - Sweet But DangeriousSo the volume is more the issue. Imagine eating enough whole fruit to equal 62 grams of fructose and then eat a meal with it.

Interesting research. However, I was unable to find a comparison between the effects of fructose and those of other sugars. Based on the information in the study, fructose consumption leads to increased food intake and weight. But nothing is said of how other sugars may affect these behaviors and functions. It may still be possible that replacing HFCS with other sugars in a diet will lead to the same negative health consequences, as the consequences may be from the consumption of sugar in general and not from any one sugar in particular. The study does not answer this fundamental question.Jon

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"Can we say the chair on the cat, for example? Or the basket in the person? No, we can't..." - Harriet J. Ottenheimer

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"Dim bulbs save on energy..." - jar

But not worse than sucrose.Right?

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But not worse than sucrose.

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Right?

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Not if we're just talking about fructose it seems. If we get specially into HFCS as the experiment you noted in the OP, there does seem to be a difference when consuming HFCS and sucrose. I haven't found anything on just fructose (not HFCS) vs sucrose.Concerning HFCS, I found this article and I'm not a chemist so I can't really comment on anything from that standpoint. Looking at the results something is different between those two specific sugars. A sweet problem: Princeton researchers find that high-fructose corn syrup prompts considerably more weight gainSo I guess the question is does the imbalanced ratio make a difference to our bodies?
How are the higher saccharides metabolized by our bodies?
Does the "extra step" fructose has to endure when ingested as sucrose make a difference in how the body responds to it?
Is it the combination of all the above that causes our bodies to react differently to HFCS than sucrose when it comes to weight gain?From the tests there does seem to be a difference whether we understand it totally or not. I haven't been able to find anything on the larger sugar molecules called higher saccharides. At least nothing I can understand anyway.The rats tested reacted differently. They still seem to be searching for the why.

Fructose vs. Glucose
There are major differences in the human body breakdown of fructose and the more common simple sugar, glucose. Furctose must be converted by the liver into energy, fat, or glucose before it can be used by other organs. Conversely, Glucose is directally usable by virtually all tissues and organs and is the preffered energy source for the brain. Glucose and fructose breakdown in the liver both result in energy and fat production among other products. However, the glucose breakdown pathway is turned off when there is an accumulation of energy and fat, thereby preventing excess production. Fructose breakdown does not have this feedback mechanism, so energy and fat production depends solely on the presence of fructose. Therefore, a massive ingestion of fructose would result in an overwhelming production of energy and fat.
Source:
fructose.biz - contact with domain owner | Epik.com

As you can see fructose and glucose share the majority of the Embden-Meyerhoff-Parnas pathway. Doesn't that strike you as evolutionarily untenable, that human beings would completely lack any kind of regulation of our fructose intake given the near-universality of fructose as a natural sugar in fruits? I mean, we're apes. The ape diet contains a ton of fruit.And it's all very well and good to say that fructose isn't subject to feedback satiety, but fructose is almost never eaten in isolation - in sugar, in corn-based sweeteners, and in honey, fructose comes with a nearly-equal amount of glucose.And it seems highly contradictory to posit that "fructose doesn't elicit an insulin response, hence you keep eating it" (even though you're not just eating fructose ever; you're consuming it either with equal parts glucose, or with starches, fibers, protein, and fats, which do elicit satiety) on one hand, and then posit "fructose causes Type 2 diabetes by creating the persistent high insulin levels that lead to T2 insulin insensitivity."I mean, which is it? I'm not accusing you of making both, or either, arguments, but both of those arguments are made by fructose's opponents, frequently simultaneously. I don't see how it can be both.And, look, fructose is regulated by fructose-6-phosphate inhibition, just like glucose.

Here are the negative things I've heard about High-Fructose Corn Syrup. You can tell me if you think they're true or not:1) Fructose must be processed by the liver. Small amounts of fructose are fine, but too much can toxify the liver, cause insulin levels to be elevated for longer after intake which leads to weight gain, and increase risk of diabetes.2) It is highly processed which presents opportunities for industrial or biological contaminants to get into it. Studies found that half of HFCS products tested contained traces of mercury.3) The corn from which it originates was likely GMO and sprayed with pesticides and industrial fertilizers.

Guys, look - if the only thing you know about human metabolism of HFCS is that "the liver processes fructose differently", thanks for contributing, honestly, but you're not exactly who I want to talk to on this subject. And we covered the liver's metabolism of fructose already. We know that the liver "processes fructose differently." But HFCS and sucrose have almost the same amount of fructose and glucose.I'd like to try to square what I've studied as an undergraduate biochemistry major with a semester of metabolism with the claims of the anti-HFCS crowd, if possible. But if you don't know what "Embden-Meyerhof-Parnas pathway" means, for instance, then again - thank you very much for your interest but I'm looking for contributions from a greater level of expertise. No offense.

An aside: that italicised portion is very likely true. The problem is, it's probably also true of half the organically-grown apples and jungle-picked papayas, and likely 90% of the fish you'll ever eat. Mercury (and lead and cadmium and......) is a normal part of our environment and so shows up in many places in our environment. It can do that with no help at all from us polluting humans, and we can detect it at insanely low levels. Don't you imagine that pesticides and fertilizers are used on sugarbeets and sugarcane? And what genetic modifications are going to sneak into syrup from GM corn, exactly?And no, I don't know enough about HFCS to have a real opinion on whether it's any worse than sucrose. I feel, without proof, that the high intake of sugars in general is a big reason for lots of poor health outcomes, and maybe even a contributor to my fat belly. But Crash is almost surely correct: HFCS is getting demonized when it is not very different from sucrose.It's pretty hard to believe that the beet/cane lobby can even stay in the game against the corn lobby, too. Maybe the corn boys have been spending all their time on the big scam of corn ethanol for fuel.

The issue for me at least is the fact that the BT toxin has been found in streams some distance from the GM crops. It appears that the organic detritus left after harvesting is decomposing in runoff waters. Hoocoodanode?Iirc they are lookiong into doing some research into what effects the BT toxin has on insect populations in these streams and other riparian ecosystems. I think the problem is that HFCS, like that found in soft drinks, is in such a large amount (the fructose found in fruits is at small enough amounts that the liver is able to matabolize it) that the liver starts storing fats that accumulate in the liver and inhibit proper insulin production and increase LDL in the blood.Because sucrose is made up of both glucose and fructose less overall must be processed by the liver.

The Bt "toxin" is just a protein, and it's harmful only to lepidopterans and beetle larva, and only in the basic pH of their foregut. Cry1Bb isn't a bioaccumulating compound, it's just a protein. Proteins out in the natural world hydrolyze rapidly, or are scavenged by microflora. The safety and low ecological impact of Bt toxin is why it's one of the pesticides that organic farmers can spray.That's right - organic farmers spray Bt "toxin" all over their crops. But you think the major source of Bt in runoff and streams is GMO corn. Once again, the conventional farmer is slammed for consequences that organic farming exacerbates. Hoocoodanode indeed? But HFCS is also made up of both glucose and fructose, at almost the exact same proportion as in sucrose. So why would there be a difference? Did you see what I said before? One of you is telling me that high fructose in the diet causes insulin upregulation and therefore diabetes, due to acquired insulin sensitivity. (So-called "metabolic syndrome" or sometimes "pre-diabetes.") Now you're telling me that high fructose in the diet suppresses insulin, causing... something. Fats, I guess.I continue to believe that the food-scare hysteria surrounding fructose and HFCS is founded on no sound science, and it's for this reason - if there were some sound science counterindicating HFCS, food-scare proponents would be able to agree on what was bad about it.

It is the fact that fructose is ONLY processed in the liver. Once Fructose is used to replenish the glycogen stores the rest is used to produce triglycerides which are released into the blood stream. File:Fructose-triglyceride.jpg - WikipediaTriglycerides are a great source of energy for the heart since it mainly uses fatty acid oxidation as its source of energy. However, excess triglycerides are take up by adipocytes and stored as fat, hence fructose caused obesity.Evolutionarily, humans seem primed for fat storage due to our history of a feast-famine lifestyle. Only recently have our extended life spans and sedentary lifestyle become a problem for a metabolism set up for very active and relatively short lived (ca. 45 years) humans.

I don't think that's true. Fructose in muscle and kidney tissues can enter glycolysis by phosphorylation by hexokinase. It has a slightly different pathway in the liver (utilizing fructokinase instead) but Lehninger's Principles of Biochemistry is pretty clear that fructose metabolism occurs in muscles. It's a fact that the glycolytic pathway has a lot of feed-ins, because the critical intermediate - phosphorylated fructose - can be formed from a wide variety of hexoses by easily-reversible isomerizing reactions.Is it as prominent as traditional glycolysis? No idea. But, again, we're not talking about pure fructose - we're talking about blends of nearly equal glucose and fructose. (I'm wondering why I have to constantly push back the efforts to conflate HFCS and pure fructose.) For the seventh time, or so: I grant the connection between sugar and obesity. Any hexose digestible by the body is going to wind up as pyruvate and acetyl-CoA, once glycogen is "full." What's the connection between HFCS-55 specifically (55% fructose, 43% glucose) and obesity that isn't present for sucrose (50% fructose, 50% glucose)?I didn't think that I was unclear on the OP, or that I phrased the question in an unclear way. Taq, can you help me understand the difficulty you're having with the parameters of the topic?

From further reading it is not true that fructose is ONLY metabolized in the liver. However, it is preferrentially metabolized in the liver. The liver actively takes up fructose, and being that the fructose rich blood from the intestines must first pass through the liver it stands to reason that the liver is an important factor here. Also, from here:

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In normal subjects infusion of fructose (1 g/kg/hr) for 4 hrs resulted in an increase in the glycogen content of the m. quadriceps femoris of 3.3 g/kg wet muscle (muscle samples obtained by needle biopsy). This was equal to the amount of glycogen formed after a glucose infusion of the same magnitude. In muscle depleted of glycogen by exercise, infusion of glucose resulted in twice as much glycogen formed, as did a fructose infusion. Formation of liver glycogen was much higher after fructose than after glucose infusion (liver samples obtained by Menghini biopsy). Studies by hepatic vein catheterization indicated that glucose formation by the liver was insufficient to account for the synthesis of muscle glycogen, which presumably occurred directly from fructose taken up by the muscle.
Just a moment...

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So we see a big boost in glycogen production in the liver with fructose compared to glucose which means that the liver is preferrentially taking up fructose and then feeding into the triglyceride pathway. The question is whether this increase in fructose over an even balance like that with pure sucrose is enough to increase TG levels and subsequent obesity. I understood it just fine. Perhaps you are misunderstanding my posts? The question is how an increase in overall fructose consumption can lead to higher rates of obesity and other health problems.In the OP you linked to a mouse or rat study where they found higher weight gain in the HCFS group compared to the non-HCFS group. The possible mechanism for this is the increased triglycerides produced by the liver in response to increased fructose compared to the control group. Obesity can also lead to increased insulin tolerance which is the cause of type 2 diabetes. I'm not saying that I agree with this conclusion, but it does seem to be the hypothesis that is being put forth.