Claims that there is a link between fructose and obesity are based on unproven hypotheses and statistical correlation, not scientific data. There is no evidence to support a unique role for fructose in the global epidemic of obesity. In fact, data has shown that Americans‟ intake of calories from sugar has stayed the same or gone down in the past decade, while the intake of calories from fat has gone up (USDA, 2012; White, 2013).
Numerous studies and systematic reviews have found that consumption of fructose does not lead to overweight and obesity (Rippe, 2013; Sievenpiper, 2012; Carden & Carr, 2013; Dolan, 2010; Rizkalla, 2010). A review by Rippe (2013) found that randomized controlled trials, the gold standard for scientific studies, do not support a causal link between weight change and fructose consumption.
Another systematic review by Sievenpiper et al. (2012) found that fructose did not cause weight gain when it substituted for other carbohydrates in the diet. The authors concluded that it was likely not the excess fructose intake that lead to weight gain, but rather the intake of excess calories (Sievenpiper et al., 2012). Likewise, a review by Carden & Carr (2013) assessed intake data from the US Department of Agriculture‟s (USDA) food availability data system and found that excess energy intake was likely a significant contributor to the increase in obesity rates in the US. Further, the authors noted that consumption of fructose has decreased over the past decade while the rate of obesity has continued to increase, suggesting other factors are responsible for the obesity epidemic (Carden & Carr, 2013). A systematic review by Dolan et al. (2010) found no evidence to suggest that fructose ingestion leads to significant changes in body weight. This held true for those consuming fructose at levels up to the 95th percentile estimates of intake (Dolan et al., 2010). Similarly, a systematic review by Rizkalla (2010) found that moderate to high consumption of fructose (50-≤100g/day) did not influence body weight.
Because fructose is a carbohydrate that provides energy (calories), consumption of it will decrease hunger and help to signal satiety.
A comprehensive review by Dolan et al. in 2010 found that fructose consumption did not increase overall food intake. It is unclear if fructose affects hunger and satiety to the same extent as other carbohydrates. In a Moyer and Rodin (1993) study that investigated the potential role of fructose as a hunger suppressant, the investigators found that fructose may be more satiating than other carbohydrates (Moyer & Rodin, 1993). A 2009 review study by Moran found that the results of studies comparing the effect of fructose on satiety to that of other sugars were mixed, with some studies showing differences while others did not.
Robust scientific data has shown that consumption of fructose does not lead to an increase in blood pressure.
A systematic review by Ha et al. (2012) found that isocaloric intake of fructose did not lead to increased blood pressure, and that hypercaloric intake of fructose did not significantly affect mean arterial blood pressure. Likewise, a systematic review of large cohort studies by Forman et al. (2009) found no association between fructose intake and hypertension. A review by Rippe (2013) also concluded that the hypothesized association between fructose consumption and increased blood pressure is not supported by other meta-analyses or randomized controlled trials.
Research shows that consumption of fructose does not cause dyslipidemia.
A systematic review by Sievenpiper et al. (2009) found that isocaloric substitution of fructose for other carbohydrates did not lead to increased circulation of blood lipids. Likewise, a systematic review by Dolan et al. (2010) showed no evidence that the consumption of fructose at normal levels of intake caused biologically relevant changes in triglycerides in overweight or obese individuals. In another review, Dolan et al. (2010) found that fructose consumption at levels approaching 95th percentile estimates of intake did not cause changes in triglyceride levels in healthy weight people. Another systematic review by Wang et al. (2013) found that, when fructose replaced other carbohydrates, it did not lead to a rise in postprandial triglycerides. The authors noted that overall energy intake appeared to be the dominant factor for a possible association between postprandial triglyceride levels and hypercaloric intake of fructose (Wang et al., 2013). A review article by Rippe (2013) also concluded that overall caloric intake might be more to blame than merely fructose when it comes to increased triglyceride levels.
When consumed in typical amounts, there is no scientific evidence that fructose causes obesity or metabolic syndrome.
The incidence of metabolic syndrome has risen over the past few decades while Americans‟ intake of calories from sugar has stayed the same or gone down in the past ten years (Rippe, 2013; USDA, 2012; Mozumdar, 2011). There is no evidence to support a unique role for fructose in development of metabolic syndrome. Rather, there is evidence to show that fructose is not implicated in the cause of metabolic syndrome. It is more likely that an increase in caloric consumption and added sugars rather than fructose alone that is associated with an increased risk of metabolic syndrome and related outcomes, such as diabetes and cardiovascular disease (Tappy et al., 2010). Systematic reviews by Sievenpiper et al. have shown that fructose in isocaloric substitution for other carbohydrates does not increase body weight, serum lipids, blood pressure, or insulin levels, all of which are components of metabolic syndrome (Sievenpiper, 2012).
The consumption of any sugar, including fructose, does not cause diabetes as diabetes is a complex disease brought on by the convergence of many factors. In fact, fructose may be beneficial for those trying to control their blood sugar levels. Fructose has a low glycemic index and results in moderate release of insulin to the bloodstream relative to glucose and sucrose.
A review article by Bantle et al. (2009) noted that studies in people both with and without diabetes have demonstrated that fructose produces a smaller postprandial rise in plasma glucose and serum insulin than other common carbohydrates. Similarly, a systematic review, by Cozma et al. (2012) found that fructose consumption did not significantly affect fasting insulin or glucose among diabetics. A meta-analysis by Sievenpiper et al. (2012) found that „catalytic‟ doses of fructose significantly reduced glycosylated hemoglobin (HbA1c) (a measure of blood sugar control over a period of several months) and fasting glucose levels without adversely effecting body weight, triglycerides, or insulin levels. A review conducted by Rippe (2013) found that most studies do not support an association between sugar consumption and increased risk of diabetes. Further, stronger studies, including randomized controlled trials and cohort studies, suggest that there is no link (Rippe, 2013).
While it has been postulated that fructose consumption could lead to non-alcoholic fatty liver disease, this is not supported by the totality of the scientific research.
Proponents of this theory argue that because fructose may be metabolized by de novo lipogenesis, that fructose could adversely affect the liver. However, de novo lipogenesis is a minor pathway in the overall human energy economy (Rippe & Etherton, 2012; Tappy & Le, 2010). Portion size and overall caloric consumption are more likely causes of non-alcoholic fatty liver disease. A double blind trial by Johnston et al. (2013), found that a high fructose diet did not cause any of the features of non-alcoholic fatty liver disease in participants. They concluded that, “…any advice on low fructose diets in NAFLD remains unjustified.” A ten week, randomized, prospective, partially blinded, parallel investigation by Bravo et al. (2013) showed that when fructose was consumed as part of the usual diet, there was no promotion of fat storage in the liver.
There is no consistent evidence to show that fructose consumption can lead to elevated serum uric acid levels. While some studies have speculated about a potential association between fructose consumption and elevated serum uric acid levels, those experiments have used extreme diets that do not resemble real world human exposures; and, thus, have limited relevance.
Systematic reviews and meta-analyses on the subject have found that controlled feeding of fructose does not lead to increased uric acid production. A systematic review by Wang et al. (2012) found that, in an isocaloric setting, “there was no effect of fructose substitution for other carbohydrates on uric acid concentrations.” A review of US National Health and Nutrition Examination Survey (NHANES) results by Sun et al. (2010) found that increased dietary fructose intake was not associated with increased risk of elevated uric acid production. Further, the authors found that those in the highest fructose intake group were more likely to have lower levels of uric acid production (Sun et al., 2010).
There is no evidence that consuming fructose has an unfavorable effect on cognitive abilities.
In fact, a study by Miller et al. (2013) found that consuming fructose resulted in comparable cognitive abilities as glucose without raising blood sugar levels as much as glucose. They also found that consumption of fructose produced similar executive functioning as consumption of glucose with a comparable number of anagrams being solved by both groups. The authors concluded that, “fructose (a sugar that has little effect on blood glucose levels, does not have reinforcing value post-ingestion, and inhibits cortical responding) can enhance executive control to the same degree as glucose” (Miller et al., 2013).
Fructose is also found in sucrose (table sugar), honey, agave nectar, fruit juices, fruit juice concentrates, pure crystalline fructose and high fructose corn syrup (HFCS).
The only proven health risk of nutritive sweeteners at typical consumption levels is dental caries (also known as tooth decay). When compared to all other sugars, fructose is among the least likely to cause tooth decay.
Fructose is not responsible for the obesity epidemic or any other health issues the U.S. is facing. Obesity is a multi-faceted condition brought on by several factors, not just one. Allegations that fructose causes increased fat production or increased appetite are based on poorly constructed experiments which often test unrealistically high levels of fructose, much higher than the levels found in a typical human diet. These studies are also often carried out in animals that are poor models for human fructose metabolism. Consequently, the findings from these studies are extreme, and not applicable to real-life situations.
Limiting fructose or HFCS in the diet would not have an impact on global obesity. Food formulators would simply reformulate products by substituting alternate sweeteners, many of which contain fructose as one of their components. Further, obesity is a global phenomenon while HFCS is primarily used in the United States. Obesity rates in Europe and South America are high whereas these areas do not use HFCS as a sweetening agent for food and beverages.
Fructose is absorbed from the small intestines by well-characterized mechanisms. Rarely, some individuals experience difficulty absorbing fructose, usually because of a hereditary deficiency in the transport mechanism. Most people absorb fructose quickly and easily.
Yes. Fructose has a low glycemic index and does not lead to the same spikes in blood sugar or insulin that result from glucose consumption. In addition, the excellent sweetness of fructose means that less of it is required to sweeten foods or beverages and this can translate to fewer calories consumed.
For one simple reason: fructose is a high quality ingredient with many useful physical and functional properties. In addition to sweetness, fructose provides flavor enhancement, mixes well with other sweeteners and starches, extends the shelf life of acidic beverages, improves humectancy and protects fruit textures in frozen foods.
The metabolism of fructose has been studied for decades and is well documented in the scientific literature. Fructose is metabolized primarily by the liver. Fructose is not toxic to the liver, as has been suggested. Regardless of the fructose source (e.g., fruits, vegetables, honey, HFCS, crystalline fructose or table sugar) it is metabolized using the same pathways.
Because pure crystalline fructose is sweeter than sugar, less of it is used in products to achieve the same level of sweetness. Thus, pure crystalline fructose can be used in making lower-sugar and lower-calorie foods. Consumer research from the Calorie Control Council shows that 187 million adult Americans are incorporating low-calorie and sugar-free foods and beverages into their diet as part of a healthy lifestyle. People will continue to demand a greater variety of low calorie products as they strive to make healthier food choices.
Fructose has been used in whole new categories of food and beverage products, such as shelf-stable nutrition bars, soft moist cookies, pourable frozen juice concentrates and energy-reduced products.
It has also been suggested that fructose be used for individuals with special dietary or nutritional needs, like endurance athletes.
Primary applications for crystalline fructose include dry mix beverages, low calorie products, enhanced or flavored water, still and carbonated beverages, sports and energy drinks, chocolate milk, breakfast cereals, baked goods, yogurt, fruit packs and confections.
Fructose makes up about 9% of calories in the typical diet.
Pure crystalline fructose has had a negligible effect on the amount of total dietary fructose consumed because of the small volume of this sugar produced relative to all other naturally occurring and added starches, syrups and sweeteners. Because pure crystalline fructose is sweeter than sugar, less of it is used in products to achieve the same level of sweetness, which also contributes to its negligible effect on total fructose intake.
Fructose is found in many places. People often think of high fructose corn syrup (HFCS) when they think of fructose, however HFCS is more like sucrose (sugar) than fructose. A lesser known source of fructose is crystalline fructose. Pure crystalline fructose consists of only fructose, while sucrose and HFCS contain almost equal amounts of fructose and glucose. The ratio of glucose to fructose in HFCS varies, but is typically around 55% fructose and 45% glucose — about the same percentages found in sucrose or table sugar.
Yes, fructose is a natural sugar. It is found throughout nature as a component of many of the foods we eat.
Sucrose and HFCS have long been considered Generally Recognized As Safe (GRAS). As a significant component of these two sweeteners, the safety of fructose has been thoroughly documented in several scientific reviews performed by the Food and Drug Administration (FDA) and other expert panels. The FDA concluded, “High fructose corn syrup is as safe for use in food as sucrose, corn syrup and invert sugar.”
An International Life Sciences Institute (ILSI) Expert Panel concluded, “Fructose is a valuable, traditional source of food energy, and there is no basis for recommending increases or decreases in its use in the general food supply or in special dietary use products.”
A Joint Consultation of the World Health Organization and the United Nations Food and Agriculture Organization found that consumption of sugars is not a causative factor in any disease, including obesity.