Is High-Fructose Corn Syrup more harmful to your health than Sucrose?

[icon name=”user” class=”” unprefixed_class=””]  Gary Franke, Ph.D.


Given the current obesity epidemics in the U.S. and around the world, the role of various nutrients on our health is increasingly important yet controversial. In general, there are vast amounts of scientific data and information available. At the same time, many researchers and medical doctors have conflicts of interests or biases. As a result, it can be hard for the average person, or even scientists, to arrive at unbiased, accurate conclusions on the effects of specific nutrients to our health.

The role of sugar on obesity and related disorders, such as type II diabetes, is an urgent public health issue and the subject of intense research and debate. The rapid rise in obesity rates has coincided with increased sugar consumption in many places. Many doctors now regard sugar as harmful or even toxic at the high amounts commonly consumed. But does it matter the form of sugar we consume? In other words, is there any difference in consuming table sugar (sucrose), high-fructose corn syrup (HFCS), or less processed forms such as honey or sugar from fruits or vegetables? Many people believe that less processed forms of food must be better for our health. As a result, organic and “all natural” foods are very popular. In terms of sugar, many products now boast about lacking high-fructose corn syrup. For example, soda lacking high-fructose corn syrup (HFCS) and containing cane sugar (sucrose) instead is increasingly popular. Many consumers in the U.S., for example, buy Mexican soda which contains cane sugar instead of HFCS. On the other hand, companies and organizations that use or make large amounts of HFCS, such as soda companies and the Corn Refiners Association, claim that HFCS is a useful and harmless sweetener, no different than sucrose. What does the evidence say on this issue?

What exactly is HFCS?

Because of the hype and various opinions concerning HFCS, it is useful to understand exactly what it is and something about how it is made and why it is used. HFCS is a syrup that contains two types of sugars: glucose and fructose. Glucose and fructose are both simple sugars (monosaccharide) that are chemically similar yet have different effects on our bodies. They are the same sugars found in fruits, vegetables and honey. In contrast, sucrose is a disaccharide, meaning it contains two sugar units linked together. The two sugars present in sucrose are also glucose and fructose. The sucrose we consume comes mainly from sugar cane or beets.

The name high-fructose corn syrup can be misleading because there is not really a large amount of fructose in it compared to other forms of sugar, as its name suggests. A better name might be glucose/fructose syrup, which HFCS is sometimes called. The proportion of fructose in HFCS can vary. The most common forms contain either 55% fructose (HFCS-55 – used in soda and other beverages) or 42% fructose (HFCS-42 – used in baked goods). These proportions are roughly similar to the proportion of fructose in fruits, honey and sucrose. Although glucose and fructose are metabolized differently, it is important to keep in mind that these two sugars always occur together in nature and are almost never consumed alone by people. Therefore, sucrose and HFCS contain the same sugars in similar proportions.

How is HFCS made and why is it used?

For most of history, people consumed only small amounts of sugar, mostly from fruits and honey. During the 18th century, large-scale trade resulted in the import of large amounts of sugar cane into Europe. For the first time, large amounts of refined sugar were available. Initially, this sugar was used to sweeten coffee and tea. Later, it was used in baked goods and candy. Sugar consumption soared in Europe. In England, for example, sugar consumption increased 1,500% between the 18th and 19th centuries.

Until the 1960’s, sucrose (from sugar cane or beets) was the almost exclusive sweetener in use. During the 1960’s, however, an alternative to sucrose was developed, called HFCS. As its name suggests, corn is the raw material used to make this sweetener. To make HFCS, starch is first extracted from corn. This starch contains long chains of glucose molecules. Enzymes are added to first break the large glucose chains into shorter chains, and the shorter chains into glucose (forming corn syrup). Finally, an enzyme is added to convert a portion of the glucose in corn syrup to fructose, resulting in a syrup containing glucose and fructose (HFCS).

The main motivation for developing HFCS in the U.S. was to have a sweetener that was a cheap and reliable alternative to sucrose. Food scientists wanted to develop a sweetener that was not dependent on trade with potentially volatile countries. As an abundant crop suitable for temperate climates, corn was the perfect raw material for such a sweetener. HFCS became extremely popular for many reasons, including its low cost, ability to provide food with a long shelf life and moisture for baked products. For these reasons, by the year 2000, HFCS made up over 40% of all sugar consumed in the U.S. (according to the U.S.D.A. Economic Research Service). HFCS is consumed mainly in the U.S., although Japan and South Korea also consume significant amounts. In most other countries, sucrose is the major sweetener and only small amounts, or no, HFCS is used (The World Health Organization).

Absorption of HFCS and sucrose

Sucrose and HFCS contain approximately equal amounts of glucose and fructose. Sucrose is 50% glucose and 50% fructose. The two most common forms of HFCS are HFCS-55 and HFCS-42, containing 55% and 42% fructose respectively. Most of the remaining syrup is glucose with small amounts of water and other sugars.

Given that HFCS and sucrose contain roughly equal amounts of glucose and fructose, does it matter that, in sucrose, the glucose and fructose are chemically linked while in HFCS they are not? The answer depends on how sugars are absorbed and digested in the small intestines. Disaccharides (such as sucrose) are fragmented into monosaccharides by brush border enzymes in the intestinal microvilli. For example, the enzyme sucrase splits the bond linking glucose to fructose in a molecule of sucrose. Since there is an excess of the enzyme sucrase, glucose and fructose are released from the sucrose consumed. Therefore, both sugars are eventually transported into the liver, whether the original source of the sugars was sucrose or HFCS. In the liver, glucose and fructose are either stored as glycogen (long chains of glucose) or broken down to carbon dioxide to release energy for the body. Therefore, since the enzyme sucrase splits sucrose into glucose and fructose, there is essentially no difference between the absorption of sucrose and HFCS in the body.

Differences between glucose and fructose metabolism

Despite their similar chemical structures, there are some significant differences between the metabolism of glucose and fructose and their effects on the body. These differences have led some scientists to speculate that fructose may be more harmful to our health than glucose. In order to understand why, it is helpful to understand how consuming carbohydrates and sugars affect the release of key hormones involved in metabolism and appetite.

After a meal, sugars such as glucose and fructose are converted to glycogen and stored in the liver. Between meals, as the body needs energy, glycogen is first broken down into glucose. The glucose can then be broken down, ultimately, to carbon dioxide, releasing energy in the process. Insulin and glucagon are key hormones that regulate these processes. Insulin promotes the absorption of glucose and synthesis of glycogen in the liver. Insulin also promotes the secretion of the hormone leptin, which is secreted from fat cells and results in a sensation of fullness after a meal. Glucagon, on the other hand, stimulates the breakdown of glycogen and release of glucose from the liver, as needed by the body. In this way, the concentration of blood glucose is tightly controlled between about 70 and 110 mg/dL. Because glucose and fructose are processed differently by the body, their consumption ultimately results in different levels of the hormones insulin and leptin. Since leptin controls appetite, these sugars also potentially have different effects on appetite and feeding.

The first difference between glucose and fructose is that the rate fructose is absorbed by the liver is greater than for glucose. Fructose absorption is not under the control of insulin as glucose is. Once fructose enters the liver, it can by-pass the regulation and controls that glucose is subject to. The breakdown of glucose (glycolysis) is tightly controlled yet fructose metabolism is not. Excess fructose is therefore uncontrollably broken down and metabolized to produce unlimited amounts of glucose, glycogen, lactate and pyruvate. These by-products can then be converted into raw material (such as two carbon acyl units) for fat synthesis.

Fructose is sometimes called lipogenic (meaning it promotes fat synthesis). One reason for this is that uncontrolled metabolism of excess fructose can provide the raw materials (such as acyl groups) for fat synthesis. Fructose also turns on genes involved in fat synthesis, such as Fatty Acid Synthase (FAS). As a result, excess fructose consumption leads to increased levels of fats such as triglycerides and cholesterol, visceral adiposity (stomach fat) and insulin resistance. Possible mechanisms of fructose induced insulin resistance include a reduced number of insulin receptors, or reduced activity of these receptors in the liver and skeletal muscle.

Whatever the mechanism, consuming fructose results in different levels of the hormones insulin and leptin compared to consuming glucose. A study published in The Journal of Clinical Endocrinology and Metabolism in 2004, for example, examined the effects of consuming glucose or fructose on hormone levels and appetite in women. In this study, the subjects consumed either a beverage containing glucose or fructose, at 30% of total calories consumed. The results were that both insulin and leptin levels were lower in the subjects consuming the fructose compared to subjects consuming glucose. Consistent with fructose promoting fat synthesis, triglyceride levels were also higher in subjects consuming fructose compared to glucose. Interestingly, despite lower leptin levels for subjects consuming fructose, appetite levels were not significantly different between subjects consuming glucose or fructose.

In conclusion, glucose and fructose have significant differences in their metabolism and on the release of key hormones that regulate metabolism.

Comparison of HFCS and sucrose on hormone levels and appetite

The differences between pure glucose and fructose on metabolism are scientifically interesting. However, since pure glucose and fructose are never normally consumed, it has little practical relevance. Instead, glucose and fructose are consumed together, whether in the form of sucrose, HFCS, honey or fruits and vegetables. By far, the largest sources of sugar in the U.S. are sucrose and HFCS. Therefore, there is great relevance in directly comparing the effects of sucrose and HFCS on human metabolism. As already described, the compositions of sucrose and HFCS are very similar, with the same sugars in similar proportions. The two common forms of HFCS have either slightly more (HFCS-55) or less (HFCS-42) fructose compared to sucrose. Are there any differences between sucrose and HFCS on the release of the key hormones insulin and leptin, or on appetite?

A study published in 2007 in the journal Nutrition was one of the first to directly compare the effects of sucrose and HFCS on the levels of key hormones and appetite. Specifically, the levels of the hormones insulin and leptin as well as plasma glucose and appetite were compared in subjects consuming either sucrose or HFCS-55 sweetened beverages. Previously, most studies compared the effects of pure glucose to fructose on metabolism. For this study, only lean, healthy women were used as subjects. The study also only examined short term responses to sucrose or HFCS (one day). Because of this, the results of this study cannot be extended to either men or the overweight and obese. The subjects were fed a standardized diet in which 30% of calories were from either sucrose or HFCS-55 sweetened beverages. The results from this study indicate that consuming sucrose or HFCS resulted in essentially the same levels of glucose, insulin, leptin and appetite.

A subsequent study, published in 2008 in the journal American Journal of Clinical Nutrition, confirmed and extended the results of the first study. This study also examined only short-term responses to sugar intake. However, men and women, as well as the overweight and obese were used as subjects. Like the first study, the effects of sucrose and HFCS-55 sweetened beverages on hormone levels and appetite were compared. In addition, the effects of pure glucose and fructose were examined, and the levels of triglycerides and free fatty acids (FFAs) were measured. Instead of 30%, sugar accounted for 25% of calories consumed in this study. Otherwise, the design of this study was similar to the first. The results were also similar. There was no difference between sucrose and HFCS on the levels of glucose or leptin. Sucrose consumption, however, resulted in slightly higher levels of insulin. This makes sense because sucrose has 10% more glucose compared to HFCS-55.

Overall, scientists are now largely in agreement that there is no metabolic or endocrine difference between sucrose and HFCS. In fact, the American Medical Association and Academy of Nutrition and Dietetics have made statements that there is no difference between sucrose and HFCS in the likelihood of causing obesity.

Relationship between HFCS consumption and obesity rates in the U.S.

Many people prefer foods and beverages that are perceived as more natural, and HFCS is more highly processed than sucrose. With this background, a commentary published in 2004 in the journal American Journal of Clinical Nutrition fueled the debate on the potential role of HFCS on increasing obesity rates and metabolic disorders such as type II diabetes. In this commentary, Bray et al. note a correlation between the rise in HFCS consumption and obesity rates in the U.S. between 1960 and 2000. The authors hypothesize that HFCS may be a unique factor that is contributing to obesity. The paper notes that the U.S. is the primary user of HFCS, which accounted for over 40% of sweetener use by the year 2000. In Figure 1 of the paper, a graph shows the rise of both obesity rates and HFCS consumption between 1960 and 2000 in the U.S. But what is the exact relationship between HFCS consumption and the obesity rate in the U.S.?

It is important to note that many variables other than HFCS consumption contribute to obesity and metabolic disorders. Additionally, a correlation between obesity rates and HFCS consumption does not mean that HFCS is actually causing obesity. Nonetheless, it is interesting to examine how changes in HFCS consumption relate to changes in the obesity rate. A closer inspection of the data from the Bray et al. 2004 paper, as well as other sources, reveals that there is not a precise relationship between HFCS consumption and obesity rates in the U.S., although both increased greatly between 1960 and 2000.

First, HFCS consumption rose dramatically during the 1970’s and early 1980’s, and then at a much slower pace during the late 1980’s and 1990’s. More specifically, HFCS accounted for just 0.4% of sugar consumption in 1970, but increased to 35.1% in 1985. In the next 15 years, HFCS consumption rose much more modestly, to account for 42.0% of sugar consumption in 2000. According to data from the U.S.D.A. Economic Research Service, HFCS consumption peaked in 1999, at 63.3 pounds per person per year. By 2012, per capita consumption of HFCS declined to 46.2 pounds, a decline of 37%. In fact, by 2012, HFCS accounted for only 35.7% of sugar consumption in the U.S., down from 43.9% at its peak in 1999.

The pattern of increase in the obesity rate in the U.S. during this time was different. According to data from the National Health and Nutrition Examination Survey (published in a JAMA 2002 article), the obesity rate in the U.S. increased by only about 0.1% per year during the 1960’s and 1970’s. For example, during 1960-1962, the obesity rate was 13.4%, which increased slightly to 15.0% during 1976-1980. During the 1980’s, the increase in the obesity rate accelerated to 0.64% per year (from 15.0% in 1976-1980 to 23.3% in 1988-1994). During the 1990’s, the increase in obesity accelerated again, to 0.89% per year (to 30.9% in 1999-2000). Overall, the obesity rate more than doubled from the late 1970’s to 2000, from 15.0% to 30.9%. After 2000, the increase in obesity in the U.S. slowed down, to a rate of about 0.33% per year (to 34.9% in 2011-2012).

Therefore, during most of the time HFCS consumption rose most rapidly (such as the 1970’s), the obesity rate in the U.S. was rising slowly. Conversely, during most of the time HFCS consumption was rising slowly, or even decreasing, the obesity rate was rising rapidly (during the 1990’s). Even with steadily declining use of HFCS since 2000, the obesity rate continued to rise, although at a slower pace than in the 1980’s and 1990’s. Although high sugar consumption, including HFCS, may contribute to obesity, it does not seem that HFCS consumption is uniquely driving obesity in the U.S.

The relationship between HFCS consumption and obesity worldwide

What is the relationship between HFCS consumption and obesity rates worldwide? First, it is important to note that HFCS is not commonly used outside of the U.S. According to data from the World Health Organization (taken from the European Union Starch Organization website), HFCS accounts for only 8% of sweetener use worldwide compared to over one third is the U.S. In Japan and South Korea, HFCS accounts for about a quarter of sweetener use. In most other countries, very little or no HFCS is used.

If HFCS is a unique factor contributing to obesity world-wide, then a relationship between HFCS consumption and obesity would be expected, with high consumption of HFCS correlated to high obesity rates. In the U.S., HFCS consumption and the obesity rate are, in fact, both high. However, in other countries there appears to be no association. For example, there are obesity epidemics in countries throughout the world, despite the fact that very little HFCS is used in most countries. South Korea and Japan, for example, consume relatively large amounts of HFCS (about 25%), yet both also have very low obesity rates (5% or less). Conversely, Mexico consumes very little HFCS (less than 5% of sweeteners) yet has obesity rates that are approaching those of the U.S. (45% for women and 30% for men) according to data from the World Health Organization. Therefore, based on these data, it does not appear that HFCS has a unique role in promoting obesity.


In conclusion, there is a lack of evidence that HFCS is more harmful to human health than sucrose. Both have similar chemical compositions and result in the absorption of glucose and fructose by the liver. Both forms of sugar also have similar effects on the release of key metabolic hormones such as insulin and leptin, as well as appetite. Obesity rates in the U.S. continue to rise despite reduced consumption of HFCS. World-wide, there is no association between obesity and HFCS consumption as obesity now plagues much of the world, yet HFCS is not consumed in most countries. Therefore, although replacing HFCS with sucrose may be popular, it is unlikely to have any health benefits.


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