People demonize food additives all the time. Just see monosodium glutamate, as just one example. And there’s high fructose corn syrup, a sugar that is blamed for everything from cancer to diabetes to climate change. OK, maybe not climate change.
High fructose corn syrup is just sugar, but because it has a complicated name, it must be bad. It’s part of the “chemophobia,” the fear of anything that sounds like a chemical.
The so-called Food Babe has made a lot of money endorsing a belief that all chemicals are evil. Of course, such claims ignore the simple fact that all life, the air, and water are made of chemicals.
They want us to believe that man-made chemicals are more dangerous than “natural” chemicals, but that betrays several things about science:
- Many “natural” chemicals are dangerous.
- Those “natural” chemicals didn’t evolve for the benefit of humans, so they are not inherently better for humans.
- Nature isn’t always better.
And high fructose corn syrup (HFCS) is considered one of the evil “chemicals” that are destroying humanity. But is it? Let’s answer that question.
What is a “sugar”?
A lot of people think that they know the answer to this question. But the actual answer is a lot of heavy science. We’re going to head down the path of heavy science because we need to describe exactly what is high fructose corn syrup.
Before we can discuss HFCS, we really need to answer the question – what exactly is sugar? For most people, it’s the white stuff on the table, and according to everything we hear today, it should be avoided. However, like most things, sugar is much more complicated than that.
There are around twenty individual, naturally-found sugars, called monosaccharides. Of all of those sugars, only four play any significant role in human nutrition – glucose, fructose, galactose, and ribose (which has a very minor nutritional role, though a major one as the backbone of DNA and RNA).
Got that? Humans can only use four sugars, specifically those monosaccharides, in all of the biochemical mechanisms in every cell.
There are other monosaccharides found in nature that can be consumed, but they either just feed the gut flora or are enzymatically converted into one of the four basic sugars in the gut.
But here it gets a bit more complicated. Many monosaccharide sugars form disaccharides which are sugars made of two covalently bound monosaccharides.
Table sugar, the white stuff we put in our coffee, is called sucrose – it is a disaccharide made of one molecule of glucose covalently bound to one molecule of fructose. Sucrose is also the main sugar in most other commercially purchased sugars that you find including brown sugar, molasses, beet sugar, and maple sugar.
There are two other examples of disaccharides that are consumed by humans (and other organisms):
- Much of the sugar in milk is lactose, which is glucose bonded to galactose. The reason some people are “lactose intolerant” is that they lack the enzyme lactase, which breaks down lactose into glucose and galactose. Since lactose cannot be absorbed in the human gut, it is used by gut flora which produces a lot of gas making it very uncomfortable for those individuals.
- Maltose, or malt sugar, is two glucose molecules.
Each monosaccharide and disaccharide have a slightly different taste, and some rare ones provide unique tastes to certain fruits and vegetables. But when these disaccharides enter the intestinal tract, they are quickly disassociated by water or acids plus enzymes into simple monosaccharides.
So when you put sucrose in your coffee and consume it, it will be broken down into two sugars that actually can be used by the body – glucose and fructose.
But we need to provide you with even more science (it’s not bad, I promise) about sugars.
Starches, sometimes called carbohydrates, are also sugars. They are just long chains, or polysaccharides, of individuals sugars, almost always glucose. Cellulose, which is a major component of paper, wood, natural plant fibers, and many other items, are glucose polymers. So are insect shells.
Generally, these long-chain polysaccharides cannot be broken down by humans, though our intestinal flora can use them for food. In addition, bulk fiber, an important part of your diet for intestinal motility, is generally a long polysaccharide chain.
Remember, humans can only absorb monosaccharides like glucose, fructose, galactose, and ribose. In other words, all of those disaccharides and polysaccharides must be broken down into the constituent monosaccharides before it has any usefulness for a human.
The gut has a variety of different enzymes that break down these starches and disaccharides – so sucrose cannot be absorbed, but it is broken down by sucrase into glucose and fructose, then absorbed.
By the way, any disaccharide or polysaccharide that isn’t broken down remains in the gut, providing food for our gut bacteria, thereby maintaining a “healthy” digestive system. No, I’m not advocating colon cleansing.
There is one more crucial point to note about these sugars, which will be important as we move along with this story. Each sugar has a different sugar taste to humans.
For example, fructose tastes 1.73 times sweeter than sucrose despite having the same exact caloric content. So technically, you could use about 58% less fructose than sucrose to get the same sweetness. You’re probably seeing where this is going, but stay tuned.
All individual sugars are the same across the planet. Glucose, fructose, galactose or ribose, whether produced by a plant, an animal, a bacteria, or a manufacturing plant in Iowa, are exactly the same molecule.
The constituent elements in all sugars are carbon, hydrogen, and oxygen, and they don’t differ if they’re used by a plant, animal, fungi, bacteria, or that high fructose corn syrup manufacturing plant in Iowa.
Fructose is fructose, sucrose is sucrose, glucose is glucose, no matter the source.
This is one of the major misconceptions of the pseudoscience of the natural food world, that somehow a sugar from a living organism is magically different from sugar produced in a manufacturing plant.
What is high fructose corn syrup?
HFCS consists of 24% water, and the rest fructose and glucose – the water just makes the fructose and glucose into a syrup. That’s it, nothing more than fructose, glucose and water, no different than all of the other fructose, glucose and water molecules made into a syrup.
There is simply no difference between the fructose and glucose in HFCS, and the fructose and glucose in sucrose, the disaccharide derived from cane sugar. The chemical formulas are exactly the same. It’s the exact same carbons, the exact same hydrogens, and the exact same oxygens. No difference.
More science below, you can skip unless you’re just like me, obsessed with information:
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% fewer 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 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 sugar.
This allowed the manufacturers of 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–candy manufacturers exploited the greater sweetness of fructose even before HFCS was available.
So, high fructose corn syrup is not only just sugar, it’s badly named. HFCS doesn’t mean it’s 99% fructose, it means it has slightly more fructose than glucose in solution. Human physiology is not going to notice much (or any) difference between HFCS and sucrose.
I cannot repeat this enough, so I will. The components of sucrose from sugar beets or sugar cane are chemically and scientifically identical. Neither is more or less “natural” than the other.
No organism’s physiology could distinguish between the fructose and glucose in HFCS from the fructose and glucose in cane sugar. All organisms, including humans, biologically metabolizes each fructose and glucose in relatively the same way. We should not endow HFCS with some special properties that it simply does not have.
So, why was HFCS developed?
First, high fructose corn syrup is much cheaper than sucrose (table sugar), but it’s sweeter because it has lower 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.
But aren’t natural sugars better?
So how does HFCS compare to natural sugar products that we believe are better for you? Remember, the fructose and glucose in HFCS are exactly the same as the fructose and glucose in all other sugars.
So, unless you buy into that naturalistic fallacy, which claims that natural is better somehow, most naturally sweet products are very similar to HFCS in fructose content:
- Honey: about 17% water, with almost all the remainder being sugars. The main sugars are fructose 38%, glucose 31%, maltose 7%, sucrose 1.3%, other sugars 1.5%. In other words, honey could be considered a “high fructose” type of sweetener, but we know that HFCS was misnamed, so it doesn’t really matter.
- Maple syrup – about 60% sugar, with that sugar being 95% sucrose, 4% glucose and 1% fructose.
- Apples: over 10% sugar, 57% fructose, 23% glucose, and 20% sucrose. Very high fructose.
- Peaches: 8.4% sugar, 57% sucrose, 23% glucose, and 18% fructose.
- Pears: 9.8% sugar, 64% fructose, 28% glucose, and 8% sucrose.
- Grapes: 15% sugar, with the sugars being 53% fructose and 47% glucose.
In other words, some of these “natural” foods have as high or even higher levels of fructose than HFCS. And since we’ve established that fructose is fructose, no matter the source, consuming these foods will provide you more fructose than an equivalent amount of HFCS.
But is fructose bad for you?
Now the answer gets much more complicated, and frankly, we’ve got to go to some more esoteric science. Remember, because the food manufacturers are using less HFCS to get the same sweetness as sucrose, the amount of fructose consumed between a drink that contains just sucrose and one that contains just HFCS (and has the same sweetness level) is almost the same.
In other words, you’re getting the same amount of taste (because of the fructose), but consuming fewer calories, and the same amount of fructose as you would from sucrose. So your worries shouldn’t be about the fructose.
Moreover, strong scientific meta-reviews of clinical research have established that there is little evidence of links between increased fructose intake and any deleterious health effects:
- Health implications of fructose consumption: A review of recent data – “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 hyperuricemia, but mainly in patients with gout.” In other words, eating moderate amounts of fructose has no ill-effects. The issue remains that if you eat too much fructose (or any other sugar), there are deleterious metabolic effects, and that should be the major issue.
- Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal-weight individuals – “The results of the analysis indicate that fructose does not cause biologically relevant changes in TG (triglycerides) or bodyweight when consumed at levels approaching 95th percentile estimates of intake.”
- Metabolic effects of fructose and the worldwide increase in obesity – “There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related to adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than the consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.”
So, let’s review. Fructose is just a monosaccharide that is metabolized by the body. It is sweeter than other mono- and disaccharides, so less is needed, a lot less. HFCS is just natural corn syrup with slightly higher fructose to glucose ratio to make it taste sweeter, so less is needed for the same sweetness.
Most naturally sweet products also have high fructose contents, hence their high sweet tastes. And from scientific reviews, there is no evidence that fructose has any effect on obesity or metabolic disease beyond what is expected from the overconsumption of any other sugar.
Does HFCS cause diabetes?
Fructose does enter a different metabolic pathway than glucose, sometimes called fructolysis. I know I’m repeating myself, almost every sugar-containing food has fructose, sometimes at higher levels than in HFCS.
The reasons that scientists speculate about the link between HFCS and diabetes are a result of how galactose, fructose, and glucose are treated by metabolically.
Glucose passes through the liver unchanged and can be used by all cells for energy. The level of glucose is controlled by insulin, which causes it to be stored if the blood levels get high, and glucagon, another hormone which causes the release of glucose from storage.
This control system is highly complicated, and in non-diabetics, it is a finely tuned system.
Fructose and galactose don’t signal insulin but are captured by the liver, eventually processed into a couple of different biochemicals, one of which is glucose itself.
So, because fructose is treated in a different manner by the body, speculation has been that fructose might be implicated in type 2 diabetes mellitus (T2DM). How the body controls blood sugar levels, and how fructose and galactose are involved in that control, is incredibly complex and would take at least a year of graduate-level classwork to even begin to understand the physiology.
To be fair, there are some issues with this speculation about fructose and T2DM. For example, fructose has a very low glycemic index of 19 ± 2, compared with 100 for glucose and 68 ± 5 for sucrose. Because fructose is 1.73X sweeter than sucrose, diabetics can consume significantly less fructose (than other forms of sugars) for an equivalent level of sweetness.
Studies show that fructose consumed before a meal may even lessen the glycemic response of the meal. In other words, specifically because of the sweetness and lower insulin reactivity, fructose may actually be preferred for those who are attempting a low glycemic index diet.
There are a few very poorly done studies (one that relied strictly on a simple questionnaire) which seems to claim that high fructose in the diet may lead to more hunger (possibly because it doesn’t trigger the feedback loops for hunger that glucose does).
These studies barely meet the minimum standards of quality in scientific research. But these studies completely ignore the fact that fructose is rarely consumed alone, it’s usually associated with glucose, which will trigger the hunger-fullness feedback loops.
However, I admit to vastly oversimplifying how these sugars interact in the complex blood sugar regulation system. There is just not any convincing and plausible evidence that shows fructose, as opposed to all other monosaccharides, has some specific and unique effect on human metabolism.
More about fructose and Type 2 diabetes
A lot of the current “mania” about HFCS and type 2 diabetes mellitus (T2DM) results from a recent article in an open-source journal, Global Public Health (with a very low impact factor of 0.92), by Goran et al. The authors tried to establish a correlation between availability of HFCS foods and the incidence of Type 2 diabetes.
This type of study is at the population level, which may seem like it would give you great numbers. Unfortunately, it doesn’t.
The problem is that it allowed so many confounding factors to be included (dietary patterns, quality and quantity of food, smoking, drinking, anything), while it ignored all sorts of other data that might provide us with a clear indication of causality. In other words, it is simply not a way to establish correlation, let alone causation.
Specifically, the problems with this study were:
- They assume that the availability of HFCS foods is the major cause of obesity. It simply isn’t. They ignore the possibility that individuals who consumed a lot of HFCS-containing soft drinks also consumed a lot of Big Macs and fries at the same time. We simply don’t know.
- Obesity itself is not the single causal factor in T2DM, it is one of a number of causes of the disease – obesity, diet, sedentary lifestyle, and genetics are all implicated in T2DM.
- Even though the researchers attempted to control for other factors, there are just too many factors that may skew the results at a country level. The best type of epidemiological study would a prospective study, which would allow for controlling different factors along with getting more detailed data about each patient. A prospective study takes time, is expensive, but gives some of the best results upon which to confirm or refute a hypothesis about HFCS being causal to T2DM.
- The authors of this study took the easiest and simplest route to write a paper: they obtained country-level data for T2DM, Gross domestic product, HFCS production in foodstuffs, and calories consumed. This type of work takes a few days and would require you just to leave the computer for sustenance. I could look up the sales of Xbox and Playstations in each country and compare it to T2DM, get it published in a bad journal, and make a name for myself that video gaming is correlated to Type 2 diabetes. And even if I could show some correlation between video gaming and diabetes, it wouldn’t be worth anything, though I’d make a big name for myself.
- Nutritional studies are incredibly difficult to interpret or to use as evidence-based medicine. It relies upon memories and diaries to determine quantities of food consumed, which are often highly inaccurate.
In a review article examining the health implications of HFCS, the author, James Rippe, MD, states that “most of the studies being cited to support the proposed linkages between fructose consumption and obesity and other metabolic conditions employ epidemiologic data that establishes associations rather than cause and effect.”
The study by Goran et al. above is a perfect example of the type of study dismissed by Dr. Rippe, who concluded that:
While the fructose hypothesis is an interesting one, it poses the danger of distracting us from further exploration and amelioration of the known causes of obesity and related metabolic conditions. It is important to remember that many of the metabolic abnormalities currently being postulated as attributable to fructose consumption may also be ascribed to obesity itself.
The epidemiologic evidence being cited to support metabolic abnormalities related to fructose consumption leaves many questions unanswered. There are compelling data to support excessive caloric consumption as the major dietary driver of obesity. The fructose hypothesis is based largely on epidemiologic data that do not establish cause and effect.
All too often, we have been led astray by confusing associations with cause and effect. With the fructose argument, we are in danger of repeating mistakes frequently made in the past by basing judgments on insufficient evidence.
High-quality meta-reviews of the research about the correlation between HFCS and T2DM and other metabolic conditions have consistently provided data that does not show any causality between fructose and metabolic disease.
We could cherry-pick a few poorly designed epidemiological studies or force-feeding rats to induce diabetes studies, but neither of those types of studies provides us with solid or even intriguing evidence that HFCS has some responsibility for T2DM.
However, until we have two pieces of information – one, a high powered prospective epidemiological study, and two, a definitive explanation of how fructose could disrupt the metabolism leading to T2DM, we completely lack any reliable evidence to think that HFCS itself causes T2DM rather than simply any sugar. Because the hypothesis that is well understood, and well supported by evidence, is the one that says any sugar can lead to obesity, thus leading to a higher risk of T2DM.
If I were raising children, and frankly, I have, I would keep them from HFCS. And sucrose. And honey. And fruit juices. And cotton candy. And chocolate bars. And fatty foods. And potato chips. There is absolutely no reasonable and plausible evidence that HFCS is any more problematic than over-eating any food, playing too many video games, or whatever else is today’s cause of type 2 diabetes.
Therefore, you shouldn’t be eating sugars and sticking with whole-grain foods to prevent type 2 diabetes. Oh wait, there’s little evidence that whole-grain foods do anything special for human health.
Sugar and the environment
There is a “movement” to push real (read cane) sugar back into many of our foods. So-called real sugar sodas that use cane sugar instead of HFCS are popular and more expensive.
The problem with cane sugar is that it’s bad for the environment. Producing cane sugar results in deforestation, pollution, wildlife habitat destruction, and industrial waste. Large portions of the Florida Everglades, the largest tropical wetland in the USA, have been drained for sugar cane plantations.
The fertilizers used, along with high concentrations of nitrogen and phosphorus that are the byproduct of decayed soil necessary for sugarcane production, were pumped into WCAs south of the EAA. The introduction of large amounts of these chemicals provided opportunities for exotic plants to take hold in the Everglades.
One can argue that corn farming has some of the same issues, but HFCS is a tiny portion of corn farming. Getting table sugar is almost the only reason to grow cane sugar.
Nevertheless, if we switched more to HFCS and other sugar sources, this can reduce the push for more cane sugar fields, which will have a major impact on the health of the planet, especially in tropical areas.
Summary, the TL;DR version
It’s clear that there are individuals want to “prove” that high fructose corn syrup is unsafe and causes all sorts of problems to humans. But HFCS is sugar syrup, close to honey in the ratio of fructose to glucose. Just because it has this scary chemical name, high fructose corn syrup, people must think that it’s made up of some evil fructose chemical. But all fructose molecules are exactly the same, whether it’s in honey, a fruit, maple syrup, cane sugar, or HFCS.
In case you skipped all that boring science above, here’s the basic information.
- High fructose corn syrup is just two simple sugars connected together in a solution.
- All of its components are the same carbons, hydrogens, and oxygen atoms that are found everywhere in nature.
- The fructose and glucose components of HFCS are exactly the same as all other fructose and glucose in nature.
- Despite poorly designed research studies, there is no substantive evidence that HFCS causes excessive weight gain.
- HFCS probably has no effect on metabolic diseases, such as Type 2 diabetes, no more than any other sugar or foods.
- Dolan LC, Potter SM, Burdock GA. Evidence-based review on the effect of normal dietary consumption of fructose on development of hyperlipidemia and obesity in healthy, normal weight individuals. Crit Rev Food Sci Nutr. 2010 Jan;50(1):53-84. Review. PubMed PMID: 20047139.
- Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ. Fructose, weight gain, and the insulin resistance syndrome.Am J Clin Nutr. 2002 Nov;76(5):911-22. Review. PubMed PMID: 12399260.
- Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002.Am J Clin Nutr. 2002 Jul;76(1):5-56. PubMed PMID: 12081815.
- Goran MI, Ulijaszek SJ, Ventura EE. High fructose corn syrup and diabetes prevalence: a global perspective. Glob Public Health. 2013;8(1):55-64. doi: 10.1080/17441692.2012.736257. Epub 2012 Nov 27. PubMed PMID: 23181629. Impact factor=0.920.
- Heacock PM, Hertzler SR, Wolf BW. Fructose prefeeding reduces the glycemic response to a high-glycemic index, starchy food in humans. J Nutr. 2002 Sep;132(9):2601-4. PubMed PMID: 12221216.
- Rippe JM. The health implications of sucrose, high-fructose corn syrup, and fructose: what do we really know? J Diabetes Sci Technol. 2010 Jul 1;4(4):1008-11. PubMed PMID: 20663468; PubMed Central PMCID: PMC2909536.
- 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.
- Sievenpiper JL, de Souza RJ, Mirrahimi A, Yu ME, Carleton AJ, Beyene J, Chiavaroli L, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, Jenkins DJ. /span>Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis. Ann Intern Med. 2012 Feb 21;156(4):291-304. doi: 10.7326/0003-4819-156-4-201202210-00007. Review. PubMed PMID: 22351714.
- Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23-46. Review. PubMed PMID: 20086073.
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