Opening Comments

Welcome back for part 2 of the great HFCS debate. Before I begin, I’d like to briefly recap last week’s arguments (for those who may have missed it) by simply copying and pasting my concluding remarks:

In summary, energy from added sugars, namely HFCS, is higher now than it was in 1970, but it increased at a slower rate than that of other macronutrients in proportion to our total caloric intake. Also, availability of HFCS has also been on the decline since 1999 yet obesity prevalence still continued to rise. Finally, total energy has not been driven up disproportionally by HFCS, but rather the diet as a whole. Simply stated; we’re eating more of EVERYTHING. 

So, now that we’re all caught up, we can all agree that increased consumption of HFCS doesn’t prove a thing and we can now move on to today’s focus, which I’m just going to jump right into. Basically there needs to be a compelling and convincing argument that HFCS is indeed different from sucrose (which we’ve already seen really isn’t the case, at least not compositionally) and is uniquely obesogenic, meaning that it causes you to gain weight more so than sucrose could. In lieu of this theory there has been a surge of studies within the past couple of decades on fructose and HFCS. These studies help to provide a biological rationale (mechanism) for why our increased consumption is potentially causing obesity. Much of these studies, however, are based on rodent data and/or studies which involve HUGE doses of fructose (some without accompanying glucose) that are irrelevant to normal human consumption patterns. Although these types of studies provide insight to certain, albeit rarely used, biochemical pathways, and in doing so show us the harms of massive quantities of fructose, my retort is that what nutrient in massive excess WON’T cause adverse effects? Abuse anything well enough and of course you’re going to see detrimental outcomes. That being said, let us begin.

Fructose Metabolism

A common argument when talking about HFCS and obesity is that fructose metabolism is markedly different from that of glucose, and fructose strongly favors fat synthesis, otherwise known as de novo lipogenesis (DNL), a topic I covered in depth a couple of weeks ago. Although the metabolism of fructose is indeed different than that of glucose metabolism, this argument holds PLENTY of water.

First off, upon fructose consumption (which I will say right now, almost NEVER happens devoid of glucose consumption) most of it (~50%) is either oxidized in the liver [1] or is converted to glucose and is then oxidized by other tissues in the body [2]. Either way you look at it, almost half of what you consume is immediately oxidized to CO2 (i.e. not stored as fat). The rest of the fructose is either; 1) converted and stored as liver glycogen (~17%) [3]; 2) converted and released as lactate (~25%) [4-6]; or 3) converted into fatty acids by way of DNL (~8%). However, as you can see, DNL is not a major pathway, as shown by various studies [7-9], and most likely does not contribute to any appreciable gain in body fat (see previous article on DNL).

This, however, is not to say that studies don’t exist where appreciable levels of plasma triglycerides (fat floating around in the blood stream) were made from fructose. There are two that I know of: one was in a hamster study, which is irrelevant because the pathway that was seen in hamsters hasn’t been found in humans yet, and the other was done in humans about 12 years ago. Here a group of researchers saw that a group of healthy males who were fed diets containing fructose increased their plasma triglycerides by 32% [10]. The diet, however, contained 17% of total calories as fructose. Even looking at estimated fructose intake from 1999, when fructose and HFCS consumption were THE HIGHEST THEY HAD EVER BEEN, fructose only accounted for ~8% of total kcals. And it can easily be assumed that this number is lower today due to reduced consumption since that time (see previous HFCS article). Therefore this study is irrelevant to what normal people usually eat. And just to stress the point, if you do the calculations, 17% of today’s kcal intake (which is ~2,700kcals) is about 460kcals. That equates to ~115g of fructose alone. You would have to consume nearly 2 liters of soda a day in order to get that much fructose. Which brings me to the point I will continue to stress within everything I write on this site; and that is context.

Context!!!

Without context, research means nothing. The fact of the matter is that we’re talking about the effects of HFCS within NORMAL consumption patterns. No one in their right mind consumes almost a fifth of their calories as fructose (be it from HFCS or any other sources). And sure, maybe you do know someone who drinks a 2-liter bottle of Coke a day, but my guess is that they’ve probably got a whole host of other things going on rather than JUST fructose consumption (i.e. sedentary behavior, other poor dietary habits, poor sleep/wake cycle, etc.). Moving on.

Fructose and its Effects on Insulin, Leptin and Subsequent Food Intake

The next huge argument surrounding HFCS and obesity is fructose’s effects (or lack thereof) on insulin and subsequently, leptin. Insulin, as many of you may know, is a storage hormone released by the pancreas in response to a rise in glucose concentration in the bloodstream. As I suspect, most of you don’t know what leptin is, so long story short, leptin is a hormone, stimulated by insulin, which tells the brain to stop eating and increase metabolism (double awesome!). Based on this principle, many researchers believe that, because fructose has such a minimal effect on insulin release, there is no leptin response and therefore no satiety signals on which the brain can act. Simply put; fructose may have no effect on appetite suppression.

No insulin = no leptin = keep on eating. But is this true?

Well, indeed the glycemic index, and therefore the insulin response, of fructose is much (about fivefold) less than that of glucose [11], but this isn’t to say that fructose doesn’t have any insulin response when consumed. If you remember, I mentioned earlier that fructose is converted into glucose in the body. This conversion requires the use of insulin in order to take up the newly formed glucose. So, in fact, there is a small amount of insulin released in response to actual fructose consumption.

But when do you EVER eat fructose by itself? Probably never. It’s nearly impossible to do unless you go to a health food store and buy a bag of fructose powder… and then only eat that. So yea, probably not likely. And let’s not forget, we’re talking about HFCS and not just fructose. If you remember the nice little table I provided last week, you should know that HFCS is nearly HALF glucose! Glucose DOES stimulate insulin, glucose DOES affect leptin. How easily we forget. So the better question would be; is HFCS any different from sucrose at stimulating insulin and leptin?

It just so happens that there is a couple of studies which show just that. A number of then show that not only do sucrose and HFCS BOTH elicit a leptin response, but they also have appetite suppressing effects [12-16]. Let me say that again. They were shown to actually SUPRESS participant’s appetites. How’s that for throwing a wrench into the gears?

And, if we want to take the original argument and pin fructose against glucose, it was shown that when looking at fructose solutions and glucose solutions given before a meal, studies show either NO DIFFERENCE in caloric intake between the two solutions, or a LESSER intake for people who consumed pure fructose before eating a meal [17-21]. There is one study which does show a greater consumption of food after consuming a fructose solution, however, this study had participants consume roughly 30% of their calories as pure fructose [5]. Now remember, just above we talked about how much 17% of total kcals is… now double that! These people were drinking almost 4-liters worth of soda a day. Now I ask you again, how relevant is that to NORMAL human consumption?

Fructose and Thermogenesis

Just to drive the point home, there happen to be a handful of human studies that saw higher levels of thermogenesis (energy expenditure, not fat storage) in men and women, as well as in obese women, after a mixed meal with 75g of carbs coming SOLELY from a fructose solution compared to another meal with 75g of glucose. In other words, there was higher carbohydrate OXIDATION (burning) and higher thermic effect of food (TEF) when fructose is given as the only carbohydrate source [1, 22-25]. This again shows that even high amounts of fructose might not get deposited as triglyceride, at least not in the short term.

Conclusions

Now I know I sound like a soda company’s wet dream right now, but it is my firm belief that, as a future dietitian and advocate for nutrition, we must not succumb to misinformation. We must learn how to accurately and effectively discern the relevant from the irrelevant. My goal over the past two weeks has been to show you all that certain views persist even in the face of solid research saying the exact opposite. HFCS doesn’t make people fat, food does, along with physical inactivity and a whole host of other factors. Trying to use HFCS as a scapegoat isn’t justified as far as I’m concerned. So with that being said, I will leave you all with some key points, taken directly from a paper written by metabolic researcher Dr. Geoffrey Livesey [26], who in my mind is the voice of reason needed within a world of fructose (mainly HFCS) hysteria. If you have never heard of him, I suggest you look him up; he is a world renowned metabolism expert. A few of his Key Points from said paper (not in any particular order) are as follows:

1. Moderate doses of fructose have neutral or diametrically opposite effects to those expected for very high or excessive fructose intakes and show evidence of improved glycemic control.
2. There is reason to believe that modest fructose ingestion could be beneficial for public health, whereas excess intake would be a risk to health. Practical application will depend on future research.
3. Epidemiological studies are difficult to interpret. The roles of [glycemic load] and other factors collinear with fructose intake need to be examined.
4. Intervention studies using humans use fructose at doses that are excessive compared with amounts generally eaten by adults; such are not interpretable for purposed of public health policy in adult nutrition.
5. Animal studies often use doses of fructose in excess of what humans would normally consume and so have a high potential to mislead about the public health aspects of fructose.

References

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