Here we go again with high fructose corn syrup (HFCS), one of the food substances that, along with GMO and MSG, forms the evil tripartite of food substances in the minds of some. And like the overhyped, and subsequently thoroughly debunked, article that tried to link GMO crops to cancers in rats, there is a new a paper
But first, what is high fructose corn syrup? I wrote about HFCS a few weeks ago, debunking some of the myths about HFCS with real science.
Basically, HFCS consists of 24% water, and the rest fructose and glucose. There are two main types of HFCS, HFCS 55 (used mostly in soft drinks) which is approximately 55% fructose and 42% glucose; and HFCS 42 (used in other types of beverages and processed foods), which is approximately 42% fructose, and 53% glucose. There is another type, HFCS-90, approximately 90% fructose and 10% glucose, which is used in small quantities for specialty applications (interestingly, low calorie drinks, because, for the same sweetness about 33% less calories are added), but it is primarily blended with HFCS 42 to make HFCS 55.
Well before the advent of HFCS, in the 1950′s, candy and soft drink manufacturers utilized “invert sugar” by exposing sucrose (a disaccharide of fructose and glucose) to a weak acid solution, then recrystallizing which dissociated the covalent bond between the glucose and fructose, and exposing the fructose molecule, which, of course, is so sweet, that it made the overall effect to be much more sweet with the same amount of sucrose. This allowed the manufacturers of the candy and sodas to get more sweetness with less sugar, saving a lot of money. So, “high fructose” has been around since the 1950′s, exploiting the greater sweetness of fructose even before HFCS was available.
So, why was HFCS developed?
First, corn syrup is much cheaper than sucrose (table sugar), but it’s not as sweet because it has a higher glucose to fructose ratio than sucrose (and as we mentioned, fructose is very sweet). Second, it retained moisture better than sucrose (twice as many molecules). Third, it was available in a liquid form and didn’t caramelize as readily as sucrose (this last one could be an advantage or a disadvantage, depending on the use).
But here’s the most important point: HFCS allowed soda manufacturers to use less sugar — and thus fewer calories — in their products without reducing its sweetness. Using sucrose, sugar from cane or beets, would require 20% more sugar (along with 20% more sugar calories) than using HFCS 55.
But as I discussed in my previous article about HFCS, it is demonized for all sorts of ills, even though it is a “natural” sugar syrup, made up of fructose and glucose. Those molecules are the same if you find them in corn, apples, honey, or in a chemistry lab.
Just this week, Goran et al. published an article in a journal called Global Public Health that concluded that the “results suggest that countries with higher availability of HFCS have a higher prevalence of Type 2 diabetes independent of obesity.” They came to this conclusion by stating that Americans consumed the most high fructose corn syrup compared to those from 41 other countries.
Goran et al. based their conclusion on “diabetes prevalence was 20% higher in countries with higher availability of HFCS compared to countries with low availability, and these differences were retained or strengthened after adjusting for country-level estimates of body mass index (BMI), population and gross domestic product.” According to the authors, an average American ate about 55 pounds of high fructose corn syrup each year. Other countries that consumed large amounts of high fructose corn syrup were Hungary, Canada, Slovakia, Bulgaria, Belgium, Argentina, Korea, Japan and Mexico.
But is this a useful study? Does it tell actually tell us that HFCS is the cause of type 2 diabetes? Of course, many news sites are “promoting” this study as “proof” that HFCS is dangerous. Here are a few:
- More Corn Syrup, More Diabetes–dailyRx.
- High Fructose Corn Syrup Consumption Linked With Type 2 Diabetes Prevalence–Huffington Post.
- Study finds link between high fructose corn syrup, Type 2 diabetes – latimes.com.
This latest article by Dr. Goran is severely flawed, misleading and risks setting off unfounded alarm about a safe and proven food and beverage ingredient. There is broad scientific consensus that table sugar and high fructose corn syrup are nutritionally and metabolically equivalent. It is, therefore, highly dubious of Dr. Goran – without any human studies demonstrating a meaningful nutritional difference between high fructose corn syrup and sugar – to point an accusatory finger at one and not the other.
Despite the rather harsh indictment of Dr. Goran, the Corn Refiners Association points out a couple of concerns that mirror my own issues with this study (and many like it). Before we start, The article was published in Global Public Health, a relatively new journal with a very low (less than 1.00) impact factor, which means that every article published in the journal is, on average, cited less than 1 time by other journals. That’s abysmal. This alone makes me want to dismiss Goran’s research, but let’s go on to other points.
First, the difference between sucrose (table sugar) and HFCS is nonexistent from both a nutritional and metabolic perspective. This is science. Sucrose is simply glucose and fructose. HCFS is glucose and fructose. HCFS does not contain some weirdly different chemical structure for its glucose and fructose. Glucose and fructose, as I’ve stated, are the same no matter how or where it’s produced.
Second, Goran’s article is a complete violation of the Post hoc ergo propter hoc fallacy, where you prove a correlation, and but do not show causation. In fact, in the case of HFCS, it’s not the corn syrup itself that may lead to Type 2 diabetes, but it’s probably the excessive consumption of all sugars. The article’s conclusion didn’t upset me as much as reading that the average American consumes 55 lbs (24.9 kg) of HFCS. Add in other types of sugars from milk, fruits, cereals, breads (I could go on forever), and Americans consume, on average, over 100 lbs (45.4 kg) of sugar per year. Without discussing the excessive sugar consumption, Goran wants us to accept that HFCS is the cause of the Type 2 diabetes epidemic.
Third, Goran ignores all of the confounding factors that may lead to Type 2 diabetes. Exercise, diet, genes, and other factors are known causes of Type 2 diabetes.
Fourth, and probably the most important issue, Goran is looking at this data from a global perspective. There are much better studies, that accumulate data on an individual level from which you can draw better conclusions. For example, a review of fructose consumption, concluded that “a moderate dose (≤ 50g/day) of added fructose has no deleterious effect on fasting and postprandial triglycerides, glucose control and insulin resistance. There is no existing evidence for a relation between moderate fructose consumption and hypertension. Fructose may induce hyperuricaemia, but mainly in patients with gout.” In other words, eating moderate amounts of fructose have no ill-effects. The issue remains that if you eat too much fructose (and any other sugar), there are deleterious metabolic effects, and that should be the major issue.
Goran’s study could be considered a good analysis of sugar consumption vs. Type 2 diabetes prevalence at a country-level. But to conclude that HFCS is the only, or even primary, cause of diabetes is ridiculous. Worse yet, we shouldn’t cherry-pick one study to support HFCS as the only cause of diabetes; there are plenty of others peer-reviewed studies that actually show it’s all sugars in total that are responsible.
The troubling fact remains that an average American eats 100 pounds of sugar. That is a dietary issue in America that’s infinitely more important than the unscientific canards about HFCS.
- Goran MI, Ulijaszek SJ, Ventura EE. High fructose corn syrup and diabetes prevalence: A global perspective. Glob Public Health. 2012 Nov 27. [Epub ahead of print] PubMed PMID: 23181629.
- Rizkalla SW. Health implications of fructose consumption: A review of recent data. Nutr Metab (Lond). 2010 Nov 4;7:82. PubMed PMID: 21050460; PubMed Central PMCID: PMC2991323.
- Séralini GE, Clair E, Mesnage R, Gress S, Defarge N, Malatesta M, Hennequin D, de Vendômois JS. Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food Chem Toxicol. 2012 Nov;50(11):4221-31. doi: 10.1016/j.fct.2012.08.005. Epub 2012 Sep 19. PubMed PMID: 22999595.
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