When you publish a website, you often leave yourself open to public scrutiny, which often leads to “Fan Mail“, as I like to call it. Most of the time I ignore it, but sometimes I feel compelled to reply. This is one of those occasions. Now, the topic is High Fructose Corn Syrup, again, but it has become a kind of crusade for me to bring logic into this odd, enduring, little topic. I basically stated my case, and left it for people to take it or leave it. Basically, an “opinion”, on a blog no less! But, it seems people still like to chastise me for it, so here is my scientifically accurate response.
First, lets take a look at some of the “;motivating” comments made by Lee. His/her first comment looked kind of like a “;conspiracy theorist” account of how HFCS were introduced on a “;mass scale” in the 1980’s and “;it isn’t a coincidence that Americans became obese”. My response was “;Your comment is garbage”, and then followed with an explanation. Probably not the best way to respond, but if you are going to argue with me, quote me real research, not coincidences.
Of course Lee responded, and my statement seemed to irk him (it could be a her, I’m not sure). The response is as follows:
Your lame method of personal attacks is garbage Darcy.
And I think If you’re going to lecture the public about nutrition and counter the arguments of those that actually study this field, and incidentally have a level of education higher than an technologist degree, you should offer some quantitative facts and reference a peer reviewed paper or empirically based study. This obviously isn’t your area of expertise so therefore your myopic and general opinions do not carry much weight on their own. There’s a lot more to this issue than just “caloric intake”.
Lee is very sensitive it seems, and gets really testy when challenged. I didn’t attack “;Lee” I challenged the “;comment” and assumptions about HFCS. When someone can’t see the difference, this automatically puts up a red flag of credibility. Lee has request “;quantitative facts”, and I will provide them. I’ve read this stuff, but never realized a “;blog” was suppose to be fully referenced. Five points though for using the word “;myopic”.
FYI Carrots, corn, sweet peas, and potatoes all contain comparable amounts of sucrose to many fruits. Some fruits conversely contain low amounts of sugar. As they exist in nature these foods do not lead one to obesity or diabetes because the body is able to process them
efficiently. When you turn fruit into “juice”, or process HFCS however this changes. The body simply does not process sugars well in these unnatural forms. With HFCS in the diet the situation is worse because only the liver is capable [sic] of metabolizing fructose and the body tends to store this as fat.
Another red flag is the “;unnatural forms” of sugar comment or the idea that juicing makes things “;unnatural”.
HFCS is simply a mixture of glucose and fructose, both are very real, and very natural sugars. The liver does need to convert fructose, into glucose, but it isn’t an issue in normal consumption quantities. It becomes a problem when you suck back a 72oz Big Gulp on a daily basis. The liver is a really tough organ and there are things far more toxic to it than fructose.
Also the process for converting cornstarch into HFCS uses a series of natural enzymes. I’ve read some people who are scared of the word “;Alpha-amylase” which is one of the enzymes. People fear what they don’t know, and the reality is that you pretty much always have that stuff in your mouth 24/7, it is one of the key enzymes in saliva. Another enzyme, glucoamylase, used to process cornstarch, is found in our small intestine. Without these we couldn’t digest starchy food. No more McDonald french fries for you!
Saying HFCS is “;dangerous” is a pretty big over reaction considering what we put into our bodies. Ethanol and smoking are far more serious “;poisons” than HFCS. Even the caramel colouring in colas and charring on a steak, is more of a health hazard.
There’s also the effect of HFCS on appetite. Studies have shown that the body produces less leptin which curbs appetite. This is precisely why HFCS is so dangerous and there is loads of historical data to back this up.
The appetite and leptin statement are also not acurate. Research, in 2007 / 2008 (listed below) concluded that “;Sucrose and HFCS do not have substantially different endocrine/metabolic effects.” The leptin statement comes from older research (2004) and from a less “;strenuously” peer reviewed journal. The study had an extremely small sample size, 12 people, which in scientific terms is pretty light. Basically, limited research is quoted as definitive. This research paper has been a pain in the ass ever since.
Simple as caloric intake PERIOD? please. I’d have to be wearing leg warmers and playing Olivia Newton John to believe that bunk. It’s a little more complicated than that Mr know it all.
Really, weight gain is a matter of intake versus output. You can’t magically gain weight if you don’t eat. Also, if your daily output (physical activity, biological functions) burn more calories than you intake, then you will lose weight. The real problem is that people have lost sight of what a “;portion size” is. In most restaurants the average meal size is designed to satisfy a 200 pound man. Average daily caloric maintenance levels are in the range of 1800 to 26oo calories.
Health care system? Yeah, let’s blame them after the fact for our bad diet. As if anyone
that was morbidly obese ever became healthy because they had access to a physician anyway. please. It’s a ridiculous notion. That’s the least realistic arguement [sic] I’ve ever heard in my life.
When discussing obesity, and HFCS, we need to factor in access to healthcare. In Canada, we have a public system, which means everybody gets to go to a doctor. Politics aside, this has been statistically shown to help improve quality of life and lower obesity. Doctors don’t sit passively by as your blood pressure, cholesterol, blood sugar and BMI rise, they will actually try to help. Obviously people still have free will and not all take their physicians advice, but many do and it makes improvements. The point is that Canada uses HFCS in many products, and has relatively the same diet as the US, but we have lower total obesity than the US.
As far as implying that I get my info from the “internet” isn’t this a blog I am reading Mr big shot? Again, what’s your expertise on nutrition? If you are any authority on this issue then why aren’t you writing for a peer reviewed journal? Save me the “real research, not
just highly publicized research” BS and your bar stool mixology.
My Internet comment has to do with what people have access too. For those who are new, or don’t know me, I write about cocktails and drinks, bartend on and off, but I also work part-time in a research lab at the University of Western Ontario. I have full access to PubMed, JStore, Medline and many other journal sites, but very few people have full access. Most people will use Google to search for info, which can be misleading. Here is what you find in the top 10 Google results for “;high fructose corn syrup”:
2. The Murky World of High Fructose Corn Syrup
3. Video Results: Conspiracy for Fat America and High Fructose…
4. High Fructose Corn Syrup: Why is it so bad for me?
5. The Science of Creative Quarterly Our Sweet Ending
6. High Fructose Corn Syrup | Sprol (how it causes health problems)
7. How to avoid High Fructose Corn Syrup
8. High Fructose Corn Syrup (HFCS) Part 1 (Art of Drink)
9. Fructose Sets Table for Weight Gain without warning
10. Is High Fructose Corn Syrup Really Good for You?
Aside from the Wikipedia article, and my article, is there anything in that list that doesn’t sound scary? This is what most people read, and base their opinions on. Of all those articles only two make mention of any scientific research, and almost all of them base their commentary on a single, small sample size (12 people) study, that I mentioned before.
7. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity (2004)
There is never mention of the peer reviewed, follow up research, that challenges the conclusions of this earlier study. For example:
1. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. American Journal of Clinical Nutrition 2008: Sucrose and HFCS do not have substantially different short-term endocrine/metabolic effects. In male subjects, short-term consumption of sucrose and HFCS resulted in postprandial TG responses comparable to those induced by fructose. (Sample Size: 34 people)
2. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads. American Journal of Nutrition 2008: Energy balance consequences of HFCS-sweetened soft drinks are not different from those of other isoenergetic drinks, eg, a sucrose-drink or milk. (Sample Size: 70 people)
3. Sugars and satiety: does the type of sweetener make a difference? American Journal of Nutrition 2007: There was no evidence that commercial cola beverages sweetened with either sucrose or HFCS have significantly different effects on hunger, satiety, or short-term energy intakes. (Sample size 37 people)
4. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. Nutrition 2007: These short-term results suggest that, when fructose is consumed in the form of HFCS, the measured metabolic responses do not differ from Sucrose in lean women. (Sample Size: 30 women)
5. Appetite hormones and energy intake in obese men after consumption of fructose, glucose and whey protein beverages. International Journal of Obesity 2007: In obese men, fructose- and glucose-based beverages had similar effects on appetite and associated regulatory hormones, independent of the differing glycaemic and insulinaemic responses. (Sample Size: 28 Obese men)
There are many more research papers that come to similar conclusions, but I think you get the point.
I’m not writing this for Lee’s sake, it’s obvious that his / her opinion is so firmly entrenched that I doubt even clinical research will convince him / her otherwise. Fear of the unknown is a powerful motivator.
For my regular readers, always take a look at the facts and be willing to change your opinion. There is nothing diabolical about HFCS that I can see, except for the fact that the North American diet includes too much of them, plus other sugars, and not enough exercise. It is a matter of over consumption, not twisted evil scientists, managed by the Rand Corporation, in cooperation with the Corn People, under the supervision of the Reverse Vampires, that have it out for people. Yes, I regularly quote “;The Simpson’s”.
In a concession from my first discussions on HFCS, I will say that American Coke definitely has a corn syrup like quality compared to Canadian Coke, but that is a flavour issue, not a health issue.
1. Twenty-four-hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals.[American Journal of Clinical Nutrition May 2008] Stanhope KL, Griffen SC, Bair BR, Swarbrick MM, Keim NL, Havel PJ.
2. No differences in satiety or energy intake after high-fructose corn syrup, sucrose, or milk preloads. .[American Journal of Clinical Nutrition December 2007] Soenen S, Westerterp-Plantenga MS
3. Sugars and satiety: does the type of sweetener make a difference? [American Journal of Clinical Nutrition July 2007] Monsivais P, Perrigue MM, Drewnowski A.
4. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. [Nutrition February 2007] Melanson KJ, Zukley L, Lowndes J, Nguyen V, Angelopoulos TJ, Rippe JM.
5. A critical examination of the evidence relating high fructose corn syrup and weight gain. 
6. Intake of sugar-sweetened beverages and weight gain: a systematic review.
7. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. [Am. J. Clin. Nutr. 2004] Bray GA, Nielsen SJ, Popkin BM.