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August 12, 2013 | By:  Luke De
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HFCS Kills Baby Giraffes; Myths about sugar, fructose, and your health.



My last blog post was about fat and its affect on the brain. I was surprised when one of my students asked a follow up question. Why do people say that HFCS is so bad for you? This meant two things. 1. Somebody actually read my blog and 2. I was going to have to write another one about nutrition. Like the Godfather, "just when I thought I was out, they pull me back in."

On this subject in particular, there is a lot of fake science out there. I would fail my ninth graders and their future first born children if they conducted some of the “MD and Ph.D." endorsed experiments I found.[i] However, I came upon two particularly interesting studies that were not in this category.

The studies were done in parallel at different places. They compared the level of obesity caused by HFCS vs sucrose when administered as part of a diet. Both studies were published at about the same time (2009-2010), compared the effects of fructose to other sugars, and were conducted by reputable scientists. Here I look at a paper written by Bocarsly (2010) in the Hoebel lab down at Princeton. You can look at the second, by Stanhope. It is in the references.

The Experiment

In the first experiment there were four groups of male rats: 1. Free access to food 2. Free access to food + HFCS 3. Free access to food, but HFCS half the day 4. Free access to food but sucrose half the day. The experiment lasted 8 weeks. Group 3 showed the greatest significant weight gain, implying that the HFCS was responsible for the additional gain in weight. There are some other really interesting trends you can see here. For example, the animals consumed a similar number of calories despite the difference in diet. Interestingly, the HFCS groups consumed more calories from food than the sucrose group. This means that calorically the HFCS group consumed less sugar than the sucrose group. There are other interesting trends, but not ones that I saw much follow up data for. (Link to data)

The second experiment went 3 times longer, 6 months. Four groups were examined 1. Free access to HFCS and food 2. 12hr access to HFCS and food. 3. 12 hour sucrose and food. 4. Free access to food. Males consuming HFCS gained more weight than those that ate only food. Much of this weight was gained in fat. The groups consuming HFCS had larger fat pads than the controls, and more of that fat was gained in the abdomen. (The sucrose group was excluded in males) Females consuming HFCS gained more weight than the other two groups, 3 and 4. I didn’t see caloric data for the second experiment. (Link to data) The female HFCS groups began weighing more than the males at 5 weeks, and the difference became significant at 25 weeks. I was a little surprised by the inclusion of females in this experiment. Because of shifting hormones, it can be difficult to attribute weight gain to the variable.

They concluded that HFCS contributed more to obesity than sucrose or food, a mix of molecules. 1 2 Fat is stored in sacs, and it is very interesting that the abdominal sac, beer gut, grew the most in the fructose fed rats. Accumulation of abdominal fat is actually worse than accumulation of other kinds of fat. Stanhope found similar evidence but he compared glucose to fructose. In this case fructose contributed more to visceral fat. From these two studies one could conclude that high fructose diets would generate a larger beer gut than diets high in other sugars. . . right? Unfortunately, it is not that simple.

Here is the problem:

As interesting as it is, you can’t draw conclusions from one study. There are many studies concerning sucrose, fructose, and obesity. Unfortunately many of these seem to refute the Stanhope and Bocarsly papers. 3 At the top of those reasons is the evidence that sugars don’t effect obesity at 25%, a direct contradiction.[ii] 3 4

BMI, the method many researchers use to study obesity, is not an adequate indicator of belly fat vs. subcutaneous fat. Basically if your BMI increases it could be a result of visceral fat, subcutaneous fat, or even just muscle. More importantly BMI provides little understanding as to the mechanism of what sugar is doing. So studies that may have provided more information about the subject don’t help to answer our particular question because the majority of the data was BMI.

Here is what I am drawing from all the evidence I looked at, again after I excluded the ones with horrible, ugly experimental designsn.

1, I did not see any epidemics that arose from diets low in sugar.

2. There is mounting evidence that sugar AT A CERTAIN LEVEL raises the level of triglycerides in the blood, increases obesity, and leads to insulin resistance. 6 7 8

3. Nobody is quite sure where that level is. 3

4. I have seen evidence for long term effects of high sugar consumption by pregnant women on their children. (Let’s be clear, this is from a single study) 9

5. Sometimes you really just want to draw false conclusions from data to make writing your blog easier, more interesting, and certainly more sensational.

Here is the discussion. In large amounts HFCS, a mixture of fructose and sucrose, might be worse for you than sucrose alone. The data does not seem to be strong enough to make a definitive statement. The following is more concrete. There is more simple sugar in commercially available foods than there should be. In a 2000 calorie diet, with 25% of calories coming from pure sugar or 500 calories, you could drink 2, 20 oz bottles of Sprite, and nothing else containing sugar.

The World Health Organization said, in 2003, that no more than 10% of your calories should be from sugar. Many others have shown the beginning of metabolic syndrome at levels around 25%. I need to cut down on sugar.

I was really hoping to dispel some myths when I started this article, but there is just too much contradictory evidence out there. I couldn’t really make definitive statements.

But here is something that I can address:

Is raw sugar better for your health than refined sugar? The brown in raw sugar is just a tinge of color from the small percentage of molasses left in the sugar. The brown does not make it healthy. There are also some minerals in raw sugar. None of that will matter if 30% of your calories are coming from sugar. There is a good chance that you will increase your fat content, increase the levels of fat in your blood, and possibly start yourself down the path to insulin resistance. The same goes for agave nectar, sugar cane, and any other source of sugar. There is no heart healthy sugar.

Some people make the argument for raw sugar claiming that it is “natural[iii]” and is therefore better for you. Opium, marijuana, crocodiles, bacon, Rush Limbaugh and the most powerful neurotoxins in the world are all natural. Eating them is not good for you. NATURAL DOES NOT MEAN HEALTHY. It can be argued that like fruit Raw sugar is natural, but unlike fruit raw sugar does not have the added benefits of fiber, which will manage the absorption of sugar, and vitamins.

Fruits have fructose in them. Does this mean that fruits are bad for you? Absolutely. If you snort them, bludgeon someone with one, or eat fruits in excess, bad things will happen. I have no doubt that excess fruit consumption will lead to increases in metabolic syndrome. More importantly, fruits come with other things, specifically fiber, which will slow the absorption of sugar in to the blood. They also contain vitamins, minerals, and other nutrients. So don’t stop eating fruits, but you can certainly eat too much fruit/sugar. Mom and Dad, what you may want to do is remove fruits from the snack bowl, and replace them with vegetables. Make fruits a regular controlled part of your meals.

In the end, and I hate to say this, more data are necessary. BMI needs to be taken with additional data including blood triglyceride levels, glucose/insulin challenges, and fat depot accumulation. If you are a researcher, get crazy, go ahead and stick that mouse in the MRI machine. Get more accurate numbers on lean mass and fat mass. If you are doing a "sac" weigh the amdominal fat pads seperately. If you are a doctor, take the time to evaluate a patient on more than just height and weight. Do some actual diagnostic work. Experiments need to be run with proper controls and designs. We just aren’t going to get a good answer until we do those things.

Thank you to Cara Solina and Kalil Cassimally.

This seemingly innocuous but oddly disturbing image is once again the work of Cara Solina, who has nothing better to do with her time and is available to create disturbing images for your blog as well. (Contact her through me)

Thanks to Khalil, as always, for editing.

Next time:

In light of Cory Monteith’s overdose, we will be looking at heroin, but not the fun part. Rather we will look at the creative way it destroys your peace of mind, or what George Koob calls "The Dark Side of Addiction."

Citations

1.

Stanhope, K. et al., Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. Journal of Clinical Investigation 119 (5), 1322-34 (2009).

2.

Bocarsly, M., Powell, E., Avena, N. & Hoebel, B., High-fructose corn syrup causes characteristics of obesity in rats: increased body weight, body fat and triglyceride levels. Pharmacol Biochem Behav. 97 (1), 101-106 (2010).

3.

Klurfeld, D., Foreyt, J., Angelopoulos, T. & Rippe, J., Lack of evidence for high fructose corn syrup as the cause of the obesity epidemic. International Journal of Obesity (2012).

4.

Empie, M. & Sun, S., Fructose metabolism in humans - what isotopic tracer studies tell us. Nature Metabolism, 89 (2012).

5.

Feinman RD, F. E., Fructose in Perspective. Nutrition and Metabolism (2013), http://www.ncbi.nlm.nih.gov/pubmed/23815799.

6.

Stanhope, K. L., Role of Fructose-Containing Sugars in the Epidemics of Obesity and Metabolic Syndrome Annual Review of Medicine. Annual Reviews 63, 329-343 (2012).

7.

Hoffman, S. & Tschop, M., Dietary sugars: a fat difference. Journal of Clinical Investigation 119 (1089-192) (2009).

8.

Ha, V. et al., Fructose-Containing Sugars, Blood Pressure, and Cardiometabolic Risk: A Critical Review. Current Hypetension Reports (2013) (http://www.ncbi.nlm.nih.gov/pubmed/23793849).

9.

Sferruzzi-Perri, A. et al., An obesogenic diet during mouse pregnancy modifies maternal nutrient partitioning and the fetal growth trajectory.. FASEB (2013).

10.

Du, L. & Heaney, A., Regulation of adipose differentiation by fructose and GluT5. Molecular Endocrinology 10, 1773-82 (2012).

11.

Tappy L, M. B., Fructose toxicity: is the science ready for public health actions? Current Opinions in Clinical Nutrition Metabolism Care, 357-361 (2012).

12.

Cox, C. et al., Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans. Nutrition & Metabolism (2012).

13.

Lowndes, J. et al., The effects of four hypocaloric diets containing different levels of sucrose or high fructose corn syrup on weight loss and related parameters. Nutrition Journal (2012).

14.

Malik, V., Schulze, M. & Hu, F., Intake of sugar-sweetened beverages and weight gain: a systematic review. Am. J. Clin. Nutr. 84, 274-288 (2006).

15.

Duffey, K., Gordon-Larsen, P., Steffen, L., Jacobs, D. & Popkin, B., Drinking caloric beverages increases the risk of adverse cardiometabolic outcomes in the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am. J. Clin. Nutr. 92, 954-959 (2010).

16.

Welsh, J. et al., Caloric sweetener consumption and dyslipidemia among US adults.. Journal of the American Medical Association 303, 1490-97 (2010).

End Notes


[i] Misinformation: If you come upon a study described by a source on the web, consider it false until you check the legitimacy of the lab it was done in and see if other scientists have reviewed it.

1. You should be able to find the original data in pubmed. Type the name of the person conducting the research and the year in to the search field at http://www.pubmed.gov If the article you read doesn’t include the name of the person conducting the research, disregard it and move on.

2. Once you find the original article, look to the right of the pubmed screen. If the article isn’t brand new and has been cited by many people, it’s a good sign.

3. Google the name of the journal and the word impact factor. For example “Nature Impact Factor” This will tell you the perceived level of trust people have for articles published in the journal.

[ii] Some argue that the companies that refine sugars paid a great deal of money to generate these contradicting studies, I can’t speak to that.

[iii] Heroin is also natural, that does NOT mean it is good for you.

9 Comments
Comments
October 12, 2013 | 12:25 AM
Posted By:  Myranda D
I enjoyed reading about this study, but you are correct about more data being needed. Regardless of how much data is collected, something will always change or new evidence will come along. That's the hard part about science, it's always changing. I have read many articles about HFCS, and there is always just as much evidence on both sides. I of course have my own opinion, but it does not change the fact that it can not be 100% confirmed. I would like to see this study done on more than rats.
August 10, 2013 | 05:39 AM
Posted By:  Deanna Russell

The point is, HFCS, is a combination of the same two monosaccharides that make up sucrose. Fruits contain both fructose and glucose, honey contains both fructose and glucose even agave nectar contains both glucose and fructose and but all of them have different ratios. Agave nectar is over 60% fructose which is why it tastes sweeter than sucrose which is only 50% fructose.
August 10, 2013 | 05:38 AM
Posted By:  Deanna Russell
@Luke
Sucrose is a dissacharide composed of one monosaccharide of glucose and one monosaccharide of fructose which are weakly linked by a glycosidic bond.

The sucrose is broken down by sucrase in the duodenum before entering the small intestine where the receptors for fructose reside. That is the gut fructose sensing mechanism of which I was speaking. Sucrose is never absorbed as a disaccharide. Only glucose and fructose monosaccharides are taken up by cells.

HFCS-55 is the most common used form used in foods, but yes HFCS can have varying ratios but are less often used in food manufacturing.
Fructose, glucose and galactose do act very differently on uptake, metabolism and endocrine function. For example, fructose alone does not stimulate insulin secretion, but glucose does. Too much fructose, just like alcohol, can cause fatty liver disease.
August 10, 2013 | 05:05 AM
Posted By:  Luke De
I don't think that sucrose is really half glucose and half fructose. It can be broken down in to those components. So a sucrose sensing mechanism would not be a fructose sensing mechanism.
High fructose corn syrup is actually composed of the two sugars. And there are many types of high fructose corn syrup, that contain different ratios of fructose and sucrose.

Glucose, fructose, and sucrose differ in the way they are brought in to the cell, and the way that they are metabolized. Fructose entry is not insulin mediated. If you look at source 4, it really cleared up some of the differences between the sugars.

August 10, 2013 | 02:51 AM
Posted By:  Deanna Russell
@Luke
"I do believe that people are going to see a difference in fructose and other sugars..."

Yes! Scientifically, the differences between fructose and glucose are very interesting. You should read up on nutrient sensing in gut, they have found the same fructose receptors in the gut as are found in the tongue. So, our gut "tastes" the sweet which starts a signal cascade that increase glucose uptake and alters insulin levels. So cool!
August 10, 2013 | 02:41 AM
Posted By:  Deanna Russell
Bottom line, I have not seen any compelling evidence to suggest a difference between HFCS and sucrose on human health. HFCS-55 is 55% fructose and 42% glucose while sucrose, aka table sugar, is 50% fructose and 50% glucose. Given their compositional similarity, it follows that they would have the same metabolic and endocrine responses (evidence to date). Like the author, I am inclined to believe that the problem with HFCS is its all-encompassing presence in our food. And I believe the reason it is so prevalent is due, at least in part, to corn subsidies which keeps HFCS cheaper than sugar.

If all the HFCS would suddenly disappear, food wouldn't necessarily get healthier, it would just cost more because manufacturers would have to use the more expensive sugar or honey, or etc. to sweeten it. Or we would all need to pull our sweet tooth!
August 10, 2013 | 02:02 AM
Posted By:  Luke De
Thank you as always, Deanna, for catching my slip up with glucose, sucrose, and fructose in the Stanhope article.
August 10, 2013 | 02:01 AM
Posted By:  Luke De
I think that there was a guy who ate one or two big macs a day in the movie supersize me. It is that fat activation of reward pathway stuff!

Thanks for the datum/data correction. I fixed it.

I do believe that people are going to see a difference in fructose and other sugars, and I have a prediction, but I don't think it was appropriate for this.
-Luke (The author guy)
August 09, 2013 | 08:48 PM
Posted By:  Ilona Miko
Thanks for breaking down the more trustworthy studies.And some nice tips are included here on misinformation.

More data *are* necessary!

LOVE the sugar image.

As for long term effects of long term exposure to HFCS, wasn't there a news report recently about a woman who drank only cola (no other liquid) for something like 20 years? anyone? This wasn't a controlled study, just a medical news anecdote. But it's a human data point about excess. Needless to say, she was very jacked up.
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