Guest article

Analyst Insight: The battle between fructose and glucose

Manufacturers should not look at replacing fructose with glucose, but rather reduce its reliance on sugar and HFCS, says Mintel expert Laura Jones.

Manufacturers should look to reduce overall use and reliance on sugar and not focus on replacing fructose with glucose, while concerns over HFCS should start to disperse as newer research invalidates current thinking, says Laura Jones of Mintel.

Sugar continues to be a hot topic when it comes to nutrition, with its excessive consumption being blamed for the steep rise in the level of overweight and obese individuals globally and the resulting health complications.

However, manufacturers’ focus should not be on reducing or replacing fructose sugars with glucose sugars, rather focus on reducing overall use and reliance on sugar. While health concerns connected to high fructose corn syrup (HFCS) should start to disperse as newer research invalidates adverse effects of fructose on health compared to glucose

Fructose targeted

Although not proven, fructose and fructose-containing sugars; in particular HFCS has been accused of being more detrimental to an individual’s health than glucose and glucose-containing sugars.

Fructose is a naturally occurring monosaccharide sugar, found in fruits, some vegetables and honey. Being the sweetest natural sugar, it is only present in very small amounts naturally. Much of the concerns around HFCS are linked to the increasing amounts consumed in modern western diets.

With HFCS now a common ingredient in processed foods, we no longer just eat small quantities found in natural sources.

HFCS free

In response advertising the fact that products are free from HFCS has become more common over the past five years, although launches of “HFCS free” products dipped slightly in 2013.

The use of “HFCS free” claims appeals to those consumers actively trying to avoid HFCS. This includes more than one third of US respondents who consider no HFCS claims important when purchasing non-alcoholic drinks and almost three in 10 US respondents who use low-/no-calorie sugar substitutes to avoid HFCS.

Metabolic differences?

HFCS’s bad reputation stems from biochemical differences between glucose and fructose. Despite fructose and glucose holding the same calorific values, the two sugars are processed differently in the body, causing different responses on ingestion.

Consequently HFCS has been linked to fuelling the obesity epidemic, with its rising usage in processed foods since the 1980s tracking the upward trajectory of obesity.

Fructose is poorly absorbed from the gastrointestinal tract and is almost entirely metabolised by the liver. Whereas glucose, the body’s preferred source of energy, is metabolised within the gastrointestinal tract, entering the bloodstream almost immediately causing blood sugars to rise and in response the body releases insulin to help normalise blood sugar levels.

Glucose molecules bind to the insulin and are transported to cells that need extra energy, any unused glucose is deposited in fat cells, stored as fat. In comparison fructose does not stimulate the release of insulin, as it is processed in the liver. When too much fructose enters the liver, the liver cannot always process it fast enough for the body to use it as sugar, so instead it is converted into glycerol, a key component of triglycerides.

This has been suggested as inadvertently raising the level of free triglycerides in the blood, a key risk factor for heart disease.

It has also been suggested that the different metabolic process fructose follows means it evades the normal appetite signalling system, by not stimulating the release of insulin and other key appetite regulating hormones like leptin.

Despite the somewhat negative image of HFCS, it is still used extensively in the food industry to reduce or replace sugar, and typically offers a cost saving and extended shelf life. This is reflected by its increasing use in food and drink launches globally in recent years.

Replacing fructose with glucose sugars is not the answer

However, evidence supporting the proposition that the metabolic differences between glucose and fructose means fructose is more detrimental to one’s health than glucose is so far inconclusive.

A recent study published in the Current Opinion in Lipidology journal looked further into the metabolic differences between fructose and glucose by assessing the effect isocaloric replacement of glucose with fructose has on cardiometabolic risk factors.

The study found that consuming fructose in place of glucose can in fact increase total cholesterol and postprandial triglycerides in some cases, but on the other hand fructose did not affect insulin production, other fat levels in the blood stream or makers of fatty liver disease any more than glucose did. It also reported that fructose may actually hold some advantages over glucose including being better at promoting healthy body weight, blood pressure and glycaemic control.

However, the research admits that there are some limitations in the data and to address some of the remaining uncertainties, larger, longer and high quality ‘real world’ trials are required.

The real focus should not be on replacing fructose in the diet with glucose, rather shifting attention to limiting and reducing the consumption of all highly refined carbohydrates.


Based in the London office, Laura Jones joined Mintel as a Global Food Science Analyst in 2012. Laura holds a Bachelor of Science, with a major in Food Science and Nutrition, along with a Post Graduate Diploma in Bioscience Enterprise. Prior to her role at Mintel, she worked in the refrigeration and cooking division of a New Product Development Team for an appliance company in New Zealand.

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Comments (1)

Ken - 07 Jul 2014 | 10:33

Persistent myths

The "potential" HFCS-obesity hypothesis of 2004 was based on flawed suppositions that have not withstood the rigours of scientific inquiry. For a start, the dry weight ratios of 41% glucose to 55% fructose in HFCS-55, the most commonly consumed form of the sweetener, are not considerably greater than that of table sugar at 50% glucose and 50% fructose when digested. The proposed hypothesis was that the consumption of HFCS may have been responsible for the obesity epidemic in the U.S. in the years from 1970 to 2004. According to data from the USDA Economic Service, however, no substantive increase in the consumption of fructose has occurring in the U.S. since 1920; the ratio of glucose to fructose intakes from all dietary sources for the period of 1970 to 2010 was greater than 5 to 1; and no correlation was shown between fructose intake and the increased rate of obesity. The data also shows that over the 20 years since the introduction of HFCS in the 1960s, the sweetener replaced only close to 50% of the market for table sugar. After its use peaked in 1999, the use of HFCS in 2010 was close to levels found approximately 20 years earlier in 1989. Whereas the estimated mean intake of fructose in 1978 accounted for 8.1% of energy compared to 9.1% in 2004, in the same span of time, Americans increased their intake of calories from all foods by 18%. For the period of 1970 to 2005, for which the HFCS-obesity hypothesis was proposed, per capita consumption of calories increased in the U.S. by 24%. In 2009, a detailed analysis of the period by researchers at the World Health Organization Collaborating Centre for Obesity Prevention concluded that the increase would be more than enough to account for the U.S. obesity epidemic. A further analysis of the data of the USDA in 2013 revealed that, after adjustments for losses, including spoilage and plate waste, the per capita increase in calories for the period of 1970 to 2010 was 449 per day. When the respective food categories contributing to the increased energy intake were examined, more than 90% was from added fats and oils and products made from refined grains. Caloric sweeteners comprised less than 8% of the increase in calories or 34 per day. In 2008, an estimate of the daily amounts of fructose consumed in the U.S. was obtained from the National Health and Nutrition Examination Survey (NHANES) for the period of 1988–1994. As the authors of the analysis pointed out, the NHANES is “the only nationally representative survey in the past 20 years to have included fructose content as a reported variable.” The data showed that the estimated mean consumption of fructose in the U.S. was 54.7 g/day. The following year, an examination of the dietary intake data of the NHANES for 1999–2004 showed that the mean total intake of fructose across all age groups for the period had decreased from the previous 54.7 g/day to 49 g/day and supplied a mean energy intake of 9.1% of calories. The range of mean total intakes was 32–75 g/day. The only segment of the population consuming fructose at or above 70 g/day were males, aged 15–22 years, for whom mean intakes were 75 g/day. Since the average age in the U.S. is 37.1 years, they would hardly be representative of “average” Americans. Far from the norm, at the 95th percentile or increment of intake representing ~5% of the population, the mean consumption of fructose was 87 g/day. Extremely high daily intakes of ≥100 g were only found among males, aged 15–50 years, and females, aged 19–22 years, and then only at the 90th or 95th percentile, or ~5–10% of the population. The highest level of fructose consumption at the 95th percentile was found among males in the age group of 19–22 years who consumed 121–134 g/day, mostly (65.6%) from sugar-sweetened beverages. Only at that percentile of intake and only among males and females of that age group was the intake so high that it reached 18% of kcal from fructose, or nearly twice the mean daily intake of 9.1% of calories and 49 g/day. Another myth perpetrated on the gullible is that because the molecules of fructose and glucose in HFCS are in “free” form, one absorbs them in far greater amounts than if they were in their natural state of being joined, as in the disaccharide sucrose (regular or table sugar). Fruit and vegetables contain less simple sugars (fructose and glucose) per gram than either table sugar or HFCS, but they also contain them in free form as well as in the bound form as sucrose. The concept that the absorption of fructose is much different when ingested in bound form was apparently predicated on speculation. The absorption of HFCS and regular sugar are essentially no different. After enzymes in the gastrointestinal tract hydrolyze the bond responsible for its disaccharide form as sucrose, glucose and fructose are individually absorbed as monosaccharides in free form. One of the most widely held misconceptions is that all the fructose we consume is entirely processed in the liver and that it all turns to fat as triglycerides. Apart from the fact that the American Heart Association does not accept that triglycerides are by themselves a risk factor for cardiovascular disease, in terms of the amount of dietary glucose processed by the liver, an early and outdated estimation of 20% was from short-term studies in humans and animals. Whereas the same studies suggest that fructose is largely though not exclusively metabolized in the liver, following its absorption by the liver, 50% of dietary fructose rapidly converts to glucose. The ratio of glucose to fructose in the “whole body” then becomes closer to 11:1, which is higher than the ratio of glucose to fructose of >5:1 when the sugar is first supplied by the diet. Although the difference is not widely appreciated, instead of 1:1, the ratio of glucose to fructose in the liver becomes 3:1. In its most recent (2011) official scientific statement on cardiovascular disease and triglycerides, the American Heart Association (AHA) recommends that individuals with already elevated (>200 mg/dL) or borderline-high triglyceride levels (150–199 mg/dL) limit their intake of fructose. Noting that triglyceride levels have in the past been recognized as an independent risk factor for cardiovascular disease (CVD), but not as being directly atherogenic, the AHA states: “Taken together, the independence of triglyceride level as a causal factor in promoting CVD remains debatable. Rather, triglyceride levels appear to provide unique information as a biomarker of risk, especially when combined with low HDL-C and elevated LDL-C [low-density-lipoprotein-cholesterol].” The AHA cited the most extensive analysis to date on lipid levels and risk of coronary heart disease (CHD). Using data from over 300,000 individuals, the authors of the analysis concluded that, “in contrast with previous findings based on much less data, triglyceride concentration was not independently related with CHD risk after controlling for HDL-C, non–HDL-C, and other standard risk factors, including findings in women and under nonfasting conditions.” In making their recommendation, the AHA referred to a meta-analysis of over 60 human trials of fructose.52/51 The analysis showed that in place of the same amount of calories from other carbohydrates (ie glucose, sucrose or starch), a significant dose-dependent elevation of fasting triglyceride levels was not found from doses of up to 100 g/day. (Fasting levels refers to those measured when subjects were in a fasted state; the manner in which triglyceride levels are routinely quantified.) Postprandial (non-fasting or ‘after-meal’) triglyceride levels were not dose-dependently raised unless the amount was over 50 g/day. Less fructose would be required to elevate triglyceride levels when measured after meals because common dietary fats and carbohydrates contribute to the production of triglycerides on their own. Based on the results of the meta-analysis, the AHA stated that “those with triglycerides outside the normal range should limit fructose consumption to 50 to 100 grams per day.” The first systematic evidence-based reviews on fructose and triglyceride levels were published 2 years after the meta-analysis. The conclusions of the authors were partly predicated on the use of criteria recommended by the FDA for the grading of studies in evaluations of health claims with respect to adverse effects. For healthy individuals of normal weight, the reviewers found no evidence suggesting that the consumption of fructose, when “not consumed in caloric excess”, causes a biologically significant or “clinically relevant” (outside of normal values) increase in fasting plasma triglycerides at intakes of ≤136 g/day in men and ≤133 g/day in women. With respect to fasting triglyceride levels in obese or overweight men and women, the amount of evaluable data from studies utilizing fructose at over 100 g/day was more limited; however, no effect was indicted from intakes of up to 100 g/day. Human clinical studies have shown that in subjects given beverages sweetened with sucrose compared to HFCS, levels of the target “appetite” hormones (ghrelin, insulin, and leptin) and food consumption were not significantly different. In a review of the studies in 2008 by Melanson et al., the authors concluded as follows: “ . . . insufficient scientific evidence currently exists to indicate that HFCS disrupts short-term energy balance signals or increases short-term appetite and energy intake more than do other tested sweeteners. The metabolic and endocrine responses that have been measured to date are similar between HFCS and sucrose”. Apart from those comparing HFCS and sucrose, the reviewers noted 2 studies showing that subjects preloaded with glucose had less hunger and food intake compared to those preloaded with fructose; 5 showing that fructose pre-loads resulted in less hunger and food intake compared to glucose; and 5 in which the effects of glucose were no different compared to fructose. Evidence for the effects of fructose on feelings of fullness or “satiety” in humans was the subject of a critical review published in 2009. The author, Timothy H. Moran of Johns Hopkins University School of Medicine, is an expert on the subject of appetite. His conclusion was that “the case for a lower satiating efficacy of fructose as a contributor to the current obesity epidemic is simply not compelling.” He added that, collectively, the results of the studies are remarkably inconsistent, as are the designs of the experiments. Given their inconsistencies, the “questionable relevance” of using doses at levels higher than those normally consumed, and the uncertainties of applying the results of individual studies to the general population, he concluded that overall, the evidence for fructose producing less satiety than glucose or that for sucrose being more satiating than HFCS is lacking. The following year, similar conclusions were made by the authors of a review including studies on the effects of fructose on satiety in obese and overweight individuals: compared to glucose at doses of 40 g to 75 g, 2–4 hours before meals, the majority of studies showed no indication that fructose at the same doses had any greater effect on satiety, food consumption, or total energy intake. One study that did report a difference was randomized but not blinded, so it scarcely represents the best evidence. Normal-weight (NW) men and women (n = 8) and over-weight (OW) women (n = 6), aged 22–50 years, were randomly assigned to ingest one of the following in test beverages: 50 g of fructose; 50 g of glucose; 250 mg of aspartame; or the unsweetened base beverage. Each beverage was consumed 38 minutes before a buffet lunch. Although food intake was higher in the OW women versus the NW subjects no matter what beverage they ingested beforehand, compared to those who drank the beverages containing glucose, aspartame, or no sweetener, significantly less fat and overall calories (P<0.03 and P<0.06, respectively) were consumed by the NW and OW subjects who ingested the fructose-sweetened beverage. Regardless of the results and the fact that fructose would rarely be consumed to the complete exclusion of glucose, the collective evidence from human studies is not sufficient to conclude that consuming fructose increases or decreases satiety or food intake compared to glucose.

07-Jul-2014 at 22:33 GMT

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