The effects of added sugars on various chronic conditions are highly controversial. Some investigators have argued that added sugars increase the risk of obesity, diabetes and cardiovascular disease. However, few randomized controlled trials are available to support these assertions. The literature is further complicated by animal studies, as well as studies which compare pure fructose to pure glucose (neither of which is consumed to any appreciable degree in the human diet) and studies where large doses of added sugars beyond normal levels of human consumption have been administered. Various scientific and public health organizations have offered disparate recommendations for upper limits of added sugar. In this article, we will review recent randomized controlled trials and prospective cohort studies. We conclude that the normal added sugars in the human diet (for example, sucrose, high-fructose corn syrup and isoglucose) when consumed within the normal range of normal human consumption or substituted isoenergetically for other carbohydrates, do not appear to cause a unique risk of obesity, diabetes or cardiovascular disease.
Few topics in nutrition are as controversial as added sugars.1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17 It has been argued that added sugars may be associated with increased risk of obesity,4, 8 diabetes18, 19 and cardiovascular disease (CVD),20, 21 and a variety of other adverse health consequences. These assertions are largely based on epidemiologic studies or animal data. The issue is further clouded by published literature comparing the effects of pure fructose to pure glucose, despite the fact that neither is consumed to any appreciable degree in the human diet.22, 23, 24, 25 The major sources of added sugars in the human diet are sucrose (50% fructose and 50% glucose), high-fructose corn syrup (HFCS; either HFCS-55, which is 55% fructose and 45% glucose or glucose polymers; or HFCS-42, which is 42% fructose and 58% glucose or glucose polymers).13, 14 HFCS is also called isoglucose in Europe. Thus, the major sources of added sugars in the human diet contain roughly 50% fructose and 50% glucose, which is also the way that they are found in nature in many fruits, vegetables and nuts.
Concern over the potential adverse consequences of added sugar has caused the American Heart Association,26 the Scientific Advisory Committee on Nutrition in England,27 the World Health Organization28 and the Dietary Guidelines Advisory Committee 2015 (ref. 21) to recommend restricting added energy from sugar to no more than 10% of energy intake. In contrast, the Institute of Medicine Carbohydrate report,29 on which the 2010 Dietary Guidelines for Americans30 was based, suggests an upper limit of no more than 25% of energy intake.
Sugars may be classified as ‘naturally occurring’ or ‘added’. Added sugars are defined as sugars or syrups added to foods during processing or preparation including those sugars and syrups added at the table.31 In this review, we will focus largely on added sugars with a particular emphasis on sucrose and HFCS, which are the most common sources of added sugars in the human diet.
The purpose of the current review is to present data from recent randomized controlled trials (RCTs) and other high-level evidence such as systematic reviews and meta analyses of prospective cohorts, on added sugars and their potential effect on obesity, diabetes and CVD. Although it has been argued that these three metabolically based conditions are so closely allied that we ought to consider them all as one entity that some investigators have called ‘cardiodiaobesity’, for the purposes of this review, we will separate the three into separate entities. We also intend to offer comments on our view for the appropriate upper limit of added sugars in the human diet.
Many of the theoretical arguments concerning fructose-containing sugars are based on the well-known differences in metabolism between fructose and glucose.32 Fructose metabolism differs from glucose in two major ways:
Nearly complete hepatic extraction of fructose.
Different enzymatic reactions in the initial steps of fructose versus glucose metabolism.
Although the pathways of metabolism are different in the liver, it must be emphasized that they are interactive. Indeed, multiple studies have shown that approximately 50% of fructose metabolized by the liver is converted into glucose in hepatic cells, approximately 15–18% of the glucose is converted into glycogen and 25% to lactate, while several percent is immediately oxidized to CO2.32, 33 A small portion of either fructose or glucose may be converted in the process of de novo lipogenesis into fatty acids that may be stored as triglycerides in hepatocytes or released in the systemic circulation in the very low-density lipoprotein particle. In human beings, de novo lipogenesis is a minor pathway consisting of no more than 1–5% of fructose converted into fatty acids or triglycerides.32, 33, 34
Moreover, as fructose and glucose are rarely, if ever, consumed in isolation in the human diet, the consumption of fructose and glucose together may further alter the metabolism of both these sugars. It has also been argued that minor differences in HFCS and sucrose may alter metabolism. In particular, it has been argued that the covalent bond between glucose and fructose in sucrose is different as compared with the fructose and glucose found separately in HFCS. As a practical matter, however, the enzyme sucrase, in the small intestine, immediately cleaves virtually all the bonds between glucose and fructose in sucrose. Thus, both HFCS and sucrose enter the blood stream as pure fructose and pure glucose.21 Numerous studies have shown that there are no physiologic or metabolic differences between HFCS and sucrose.17 Furthermore, it should also be pointed out that many of the covalent bonds between fructose and glucose in sucrose are likely to have been broken before even ingesting sucrose-containing products through the process of inversion.14 In fact, in a 3-month study, all the sucrose consumed was ultimately found to be inverted into its components of fructose and glucose before consumption.
Many misconceptions about the consumption of added sugars have resulted in the focus on reducing these nutrients as a strategy for lowering the risk of obesity and other public health concerns. Perhaps the most prevalent misconception is that sugar consumption has risen dramatically over the past 4 years.14 Figure 1 compares the trends in consumption of sugar, HFCS, fructose and added sugars. This figure is derived from USDA-ERS per capita availability data that are adjusted for loss.35 It provides a reasonable estimate for consumption figures based on production figures after corrections for amounts wasted (uneaten), which occur between manufacturing and ingestion.
A number of points are apparent from studying this figure. First, from 1970 to 1989, the amount of HFCS in the American diet increased substantially. However, the amount of sucrose consumed declined in an almost mirror image manner. Thus, the total amount of sugars consumed remained relatively constant. Furthermore, total sugar intake in the United States peaked in 1999 and has been in a substantial decline since that time, whereas obesity rates have continued to rise, or remain stable, in most population groups. These data are consistent with those reported by Welsh et al.36 based on an analysis of NHANES data, which estimated a 15% decrease in added sugar consumption in the United States from 2000 to 2012.
Added sugars, obesity and body composition
Initial interest in the United States in a potential linkage between sugar consumption and obesity can be traced back as early as 1950 with the publication of a book by John Yudkin entitled ‘Pure, White and Deadly’.37 Interest in this topic, however, was minimal compared with the role of fats in the diet through the publication of Ancel Keys’ classic Seven Countries Study.38
The issue of a potential role for sugars in obesity resurfaced in 2004, when George Bray and Barry Popkin argued that increasing use of HFCS in the United States was temporally associated with a rapid increase in obesity prevalence.4 These authors based their argument on the differences in metabolism of fructose compared with glucose, which they argued could lead to over-consumption of energy. Subsequent research trials, however, have failed to support the hypothesized unique linkage between HFCS and obesity and have demonstrated that HFCS and sucrose are virtually identical with regard to energy, sweetness and absorption.39, 40, 41, 42, 43 As a result of this expanding research literature, emphasis has shifted to a consideration whether or not fructose-containing sugars, in general (for example, sucrose, HFCS and concentrated fruit juices and so on), might be causally linked to obesity.
There have been three recent systematic reviews and meta analyses of RCTs of sugar consumption or sugar-sweetened beverage consumption and body weight.44, 45, 46 These meta analyses of RCTs demonstrate that when sugar is replaced with energy-equivalent macronutrients, no increase in body weight occurs. These meta analyses provided some evidence to suggest that if energy consumption is increased by adding sugar to an already isoenergetic diet in adults, this may lead to modest weight gain. The weight gain, however, appeared to be a function of increased energy consumption rather than sugars per se. Prospective cohort trials have yielded similar results.
The problem with many published studies results from failure to adjust for total energy intake. Once this adjustment has been made, results have typically shown no relation between sugar consumption and body weight. Several recent summary articles have reached the same result concluding that there is a lack of high quality evidence linking sugars uniquely to obesity.3, 44, 47 RCTs performed in our research laboratory have shown that consumption of average amounts of fructose-containing sugars do not yield increased body weight in either a 10-week free-living study39 or a 24-week study (unpublished data). Thus, a variety of sources of high quality evidence do not support the contention that sugars per se make a unique contribution to obesity.
Further evidence counter to a unique role for sugars stimulating obesity comes from the observation that obesity rates have continued to rise not only in the United States48 and Great Britain,49 but also in Australia,50 while sugar-sweetened beverage consumption has declined. This has become known as the ‘Australian Paradox’ and adds further suggestive evidence that there is no unique relationship between sugars and obesity.
Finally, it should be emphasized that in a condition as complicated as obesity, it is highly unlikely that a single nutrient would uniquely cause this condition. This view is consistent with a recent scientific statement from the American Society of Nutrition, which cautioned against isolating one component of the diet as a primary driver of weight gain and obesity and emphasized the complexity of energy regulation.51 Americans and individuals in many other countries around the world are becoming more obese largely because they are eating more of everything, not just sugars. In fact, in the United States, it has been reported that the average energy intake increased by 454 kcal per day between 1970 and 2010, while only 39 of these kcal came from all added sugars combined (9% of the increase).35
Sugar and diabetes
Diabetes has emerged as a major and rapidly growing worldwide health concern in the twenty-first century. The prevalence of diabetes is predicted by the International Diabetes Federation to double by 2035.52 This dramatic increase in diabetes has paralleled the worldwide increase in obesity and has prompted further investigation of potential nutritional links to diabetes. One of the factors that has been suggested as a unique link to diabetes is the consumption of fructose-containing sugars.
Several recent ecological studies have suggested that as sugar consumption has increased in countries so has the prevalence of diabetes.18, 19 However, these analyses are considered a very weak form of scientific evidence and have been criticized on multiple levels, particularly for utilizing production data and confusing it with consumption data.47 Furthermore, other ecologic studies from the United States, England and Australia have all suggested that obesity rates continue to rise, despite decreasing sugar consumption.48, 49, 50
The central question about whether sugar is the unique cause of diabetes has not been specifically addressed in any RCT. Thus, most of the data related to this issue come from studies looking at risk factors for diabetes rather than diabetes per se.
Prospective cohort studies provide mixed evidence concerning sugar consumption and diabetes.53, 54 Some studies have suggested an effect of sugar-sweetened beverages on the incidence of diabetes.53, 54 However, many did not adjust findings for energy intake and body weight. Other prospective cohort studies have not found a significant association between sugar intake and diabetes.55, 56
Several recent RCTs conducted in our laboratory have not demonstrated an increase in risk factors for diabetes in response to multiple levels of added sugar consumption between 8% and 30% of energy.57, 58, 59 In one study where individuals consumed 18% of total energy from either sucrose or HFCS or 9% of energy from fructose and glucose, no increase in fasting glucose, insulin or insulin resistance via the homeostatic model assessment occurred.59 In another study with 267 individuals who consumed either 8%, 18% or 30% of total energy from added sugars, no increases in glucose, insulin or insulin resistance were found.57 Furthermore, a previous study in our research laboratory involving 68 individuals consuming either HFCS or sucrose at up to 30% of total energy did not show any increase in ectopic fat in muscle or liver, both of which have been implicated in increased insulin resistance.60
Just as with obesity, the etiology of type 2 diabetes is certainly complicated and not entirely resolved. However, the most likely primary pathologic event is excess energy intake leading to overweight and obesity. Taken together, the current available evidence does not suggest that sugar consumption per se uniquely increases the risk of diabetes.
Sugars and cardiovascular disease
There have been no RCTs to explore the relationship between sugars and cardiovascular disease per se. Thus, most of these scientific studies have focused on the relationship between sugars and risk factors for CVD.
Diets that are high in simple sugars (>20% of total energy) may result in elevated fasting triglycerides, an established risk factor for CVD.61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74 For this reason, the American Heart Association Scientific Statement on triglycerides lists avoiding fructose as one mechanism for preventing hypertriglyceridemia.75 Elevated triglycerides may result from increased hepatic triglyceride synthesis as well as reduced peripheral clearance of triglycerides, both of which have been attributed to increased fructose metabolism. In our research laboratory, an isoenergetic trial involving 65 individuals, where no weight gain occurred, did not result in increased triglycerides.76 However, a much larger study involving 355 men and women between the ages of 20–60 years, who were randomly assigned to consume either 8, 18 or 30% of total energy as sucrose or HFCS resulted in a 10% increase in triglycerides.57 However, in this latter trial, individuals consumed an average of over 200 kcals per day more by the end of the study, compared with baseline, and gained an average of over two pounds (1 kg). Thus, it is not clear that the increased triglycerides were a function of weight gain and increased energy intake or sugars per se. Several recent systematic reviews and meta analyses have reported that hypercaloric feeding of fructose results in increased triglycerides, but studies where fructose is substituted isoenergetically for other carbohydrate sources have not resulted in increased triglycerides.77, 78
Diets high in simple sugars have been reported to also result in decreased HDL cholesterol.79, 80 However, diets that are high in complex carbohydrates, such as the DASH diet, which substitute fat with complex carbohydrates and low-fat dairy products, fruits and vegetables and whole grains have not been reported to increase triglycerides, although they may result in a modest decrease in HDL cholesterol.
The effects of sugar on total cholesterol and LDL cholesterol have been variable. Some investigators have found increases in LDL cholesterol,65, 69, 70, 74 while others have not demonstrated such increases.81 Many of the studies that have shown increases in LDL have given either large doses of sugars well above the physiologic normal range69, 70 or have given very large doses of either pure fructose or pure glucose.82 Trials in our laboratory at levels of sugar consumption between the 25th and 95th population consumption level have not demonstrated changes in LDL following 10 weeks of a free-living environment compared with baseline.57
Thus, it would appear that there is a marker for increased triglycerides when levels of >20% of total energy are consumed as sugars, particularly in hypercaloric settings. However, the effects of fructose-containing sugars on LDL cholesterol remain in dispute, particularly in isoenergetic trials.
Johnson et al.83 have proposed a model where increased consumption of fructose may be linked to increases in blood pressure. According to this model, rapid metabolism of fructose in the liver may deplete adenosine triphosphate, which is degraded into adenosine monophosphate and ultimately metabolized to uric acid. Uric acid, in turn, in this model is thought to lead to endothelial dysfunction, which increases the risk of high blood pressure.
Clinical trials, however, on blood pressure and sugar consumption have reported variable results.84, 85, 86, 87 Studies from our research laboratory and others have shown neither increases in blood pressure, nor uric acid levels resulting from 10 weeks of sugar consumption at up to 30% of total energy, which represents the 95% percentile population consumption level of fructose.17 Systematic reviews and meta analyses have also reported conflicting results with regard to added sugar and blood pressure. Ha et al.85 reported a systematic review and meta analysis of 18 studies (n=355) and showed slight decreases in both diastolic and mean blood pressure when fructose was substituted either isoenergetically (13 trials) for other carbohydrates or in hypercaloric trials (two trials). Te Morenga et al.20 reported 12 trials (n=324) with no significant effects of higher sugar intake on systolic blood pressure overall (mean difference: 1.1 mm Hg; P=0.32). Higher sugar intake was, however, associated with greater diastolic blood pressure of 1.1 mm Hg (P=0.02). Many of the trials reported in this systematic review, however, used levels of added sugar consumption above the 90th percentile population consumption level.
Thus, the effects of simple sugars on blood pressure at normal population levels remain in dispute, with most of the high quality evidence from trials within the normal range of human consumption reporting no unique linkage.
What are the appropriate upper limits of added sugar consumption?
As already indicated, numerous scientific bodies have offered recommendations for upper limits of sugar consumption. The American Heart Association recommends no more than 150 kcals per day in added sugars for the average adult male and no more than 100 kcals per day for the average adult female.26 The World Health Organization has recommended no more than 10% of calories from added sugars with an ultimate goal of reducing this to 5%.28 The Scientific Advisory Committee on Nutrition has issued similar recommendations to the World Health Organization.27 The recently released Dietary Guidelines Advisory Committee 2015 also recommended an upper limit of sugars of no more than 10% of energy.21 The Institute of Medicine Carbohydrate Report, however, sets the recommended upper limit at no more than 25% of energy,29 and this recommended upper limit was also used in the Dietary Guidelines for Americans 2010.30
A number of research studies in our laboratory, as well as systematic reviews and meta analyses by a number of other investigators, have suggested that even at levels up to 30% of energy from added sugars there is no increased risk of obesity, CVD or diabetes, provided that the sugars are substituted isocalorically for other carbohydrates. With this as background, it would appear that the recommendation of restricting energy at the level recommended by the American Heart Association, World Health Organization, Scientific Advisory Committee on Nutrition and the Dietary Guidelines Advisory Committee 2015 may be unduly conservative. We do believe, however, that consumption of 20% of energy or more from added sugar, particularly in a hypercaloric setting, may increase triglycerides. We believe that this represents a reasonable level of recommendation for an upper limit of consumption of sugars.
The worldwide pandemic of obesity and the dramatic increases in diabetes, coupled with the fact that heart disease remains the leading cause of mortality around the world, has appropriately led to the exploration of factors which might be amenable to change to help reduce the public health burden of these three widespread conditions. Although we believe that it is prudent to avoid excessive consumption of fructose-containing sugars, levels within the normal range of human consumption when substituted isoenergetically in diets for other carbohydrates do not appear to cause any unique risk. It is our judgment that attention should be focused more on reducing established risk factors for obesity, diabetes and heart disease as recommended by numerous public health organizations rather than focusing undue attention on sugars.
Rippe JM, Angelopoulos TJ . Sucrose, high-fructose corn syrup, and fructose, their metabolism and potential health effects: what do we really know? Adv Nutr 2013; 4: 236–245.
Rippe J . The metabolic and endocrine response and health implications of consuming sweetened beverages: findings from recent, randomized, controlled trials. Adv Nutr 2013; 4: 677–686.
Kahn R, Sievenpiper JL . Dietary sugar and body weight: have we reached a crisis in the epidemic of obesity and diabetes? We have, but the pox on sugar is overwrought and overworked. Diabetes Care 2014; 37: 957–962.
Bray GA, Popkin BM . Dietary sugar and body weight: have we reached a crisis in the epidemic of obesity and diabetes? Health Be Damned! Pour on the Sugar. Diabetes Care 2014; 37: 950–956.
Klurfeld DM, Foreyt J, Angelopoulos TJ, Rippe JM . Lack of evidence for high fructose corn syrup as the cause of the obesity epidemic. Int J Obes (Lond) 2012; 27: 771–773.
Bray GA, Nielsen SJ, Popkin BM . Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004; 79: 537–543.
Lustig RH . Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc 2010; 110: 1307–1321.
Lustig RH, Schmidt LA, Brindis CD . Public health: the toxic truth about sugar. Nature 2012; 482: 27–29.
Bray G . Fructose: pure, white, and deadly? Fructose, by any other name, is a health hazard. J Diabetes Sci Technol 2010; 4: 1003–1007.
Rippe JM . The health implications of sucrose, high-fructose corn syrup, and fructose: what do we really know? J Diabetes Sci Technol 4: 1008–1011 2010.
Sievenpiper JL, de Souza RJ, Kendall CW, Jenkins DJ . Is fructose a story of mice but not men? J Am Diet Assoc 2011; 111: 219–220, author reply 220–212.
van Buul V, Tappy L, Brouns F . Misconceptions about fructose-containing sugars and their role in the obesity epidemic. Nutr Res Rev 2014; 27: 199–130.
White J . Straight talk about high-fructose corn syrup. What it is and what it ain't. Am J Clin Nutr 2008; 88: 1716S–1721S.
White JS . Challenging the fructose hypothesis: new perspectives on fructose consumption and metabolism. Adv Nutr 2013; 4: 246–256.
Rippe JM, Angelopoulos TJ . Sugars and Health Controversies. What does the Science Say? Adv Nutr 2015; 6 (Suppl): 493S–503S.
Ha V, Cozma AI, Choo VLW, Mejia SB, de Souza RJ, Sievenpiper JL . Do fructose-containing sugars lead to adverse health consequences? Results of recent systematic reviews and meta-analyses. Adv Nutri 2015; 6: 504S–511S.
Angelopoulos TJ, Lowndes J, Sinnett S, Rippe JM . Fructose containing sugars do not raise blood pressure or uric acid at normal levels of human consumption. J Clin Hypertens 2014; 17: 87–94.
Basu S, Yoffe P, Hills N, Lustig RH . The relationship of sugar to population-level diabetes prevalence: an econometric analysis of repeated cross-sectional data. PLoS One 2013; 8: e57873.
Goran MI, Ulijaszek SJ, Ventura EE . High fructose corn syrup and diabetes prevalence: a global perspective. Glob Public Health 2013; 8: 55–64.
Te Morenga LA, Howatson AJ, Jones RM, Mann J . Dietary sugars and cardiometabolic risk: Systematic review and meta-analyses of randomized controlled trials of the effects on blood pressure and lipids. Am J Clinic Nutr 2014; 100: 65–79.
Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2015. US Department of Agriculture, Center for Nutrition Policy and Promotion, Washington, DC, USA.
Stanhope K, Havel P . Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose or high-fructose corn syrup. Am J Clin Nutr 2008; 88: 1733S–1737S.
Teff KL, Grudziak J, Townsend RR, Dunn TN, Grant RW, Adams SH . Endocrine and metabolic effects of consuming fructose- and glucose-sweetened beverages with meals in obese men and women: influence of insulin resistance on plasma triglyceride responses. J Clin Endocrinol Metab 2009; 94: 1562–1559.
Stanhope K, Griffen S, Keim N, Ai M, Otokozawa S, Nakajimak SE et al. Consumption of fructose-, but not glucose sweetened beverages produces an atherogenic lipid profile in overweight/obese men and women. Diabetes 2007; 56 (Suppl 1): A16.
Havel P . Dietary fructose: implications for dysregulation of energy homeostasis and lipid/carbohydrate metabolism. Nutr Rev 2005; 63: 133–157.
Johnson RK, Appel LJ, Brands M, Howard BV, Lefevre M, Lustig RH et al. Dietary sugars intake and cardiovascular health, a scientific statement from the American Heart Association. Circulation 2009; 120: 1011–1020.
Scientific Advisory Committee on Nutrition. Draft Carbohydrates and Health Report, 2014. Available from http://www.sacn.gov.uk/.
World Health Organization The Global Burden of Disease: 2004 Update. World Health Organization: Geneva, Switzerland, 2008.
Institute of Medicine Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids. Institute of Medicine of the National Academies. National Academies Press: Washington, DC, USA, 2005.
Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010. US Department of Agriculture, Center for Nutrition Policy and Promotion, Washington, DC, USA.
White JS . Sucrose, HFCS, and fructose: history, manufacture, composition, applications, and production. In: Rippe JM (ed). Fructose, High Fructose Corn Syrup, Sucrose and Health. Springer Publishing: New York, NY, USA, 2014.
Tappy L, Le KA . Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev 2010; 90: 23–46.
Sun SZ, Empie MW . Fructose metabolism in humans: what isotopic tracer studies tell us. Nutr Metab 2012; 9: 89.
Hellerstein MK, Schwarz JM, Neese RA . Regulation of hepatic de novo lipogenesis in humans. Annu Rev Nutr 1996; 16: 523–557.
USDA-ERS. Food Availability (Per capita) Data System: Loss-adjusted food availability [Internet]. Sugar and sweeteners (added), sugar.xls, updated 4 December 2014 [cited 10 March 2015]. Available from http://www.ers.usda.gov/data-products/food-availability-(per-capita)-data-system/.aspx.
Welsh JA, Sharma AJ, Grellinger L, Vos MB . Consumption of added sugars is decreasing in the United States. Am J Clin Nutr 2011; 94: 726–734.
Yudkin J . Pure, White and Deadly. Penguin Books: New York, NY, USA, 1972.
Keys A . Seven Countries. A Multivariate Analysis of Death and Coronary Heart Disease. Harvard University Press: Cambridge, MA, USA, 1980; 1–381.
Melanson KJ, Summers A, Nguyen V, Brosnahan J, Lowndes J, Angelopoulos TJ et al. Body composition, dietary composition, and components of metabolic syndrome in overweight and obese adults after a 12-week trial on dietary treatments focused on portion control, energy density, or glycemic index. Nutr J 2012; 11: 57.
Melanson K, Zuckley L, Lowndes J, Nguyen V, Angelopoulos T, Rippe J . Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. Nutrition 2007; 23: 103–112.
Yu Z, Lowndes J, Rippe J . High-fructose corn syrup and sucrose have equivalent effects on energy-regulating hormones at normal human consumption levels. Nutr Res 2013; 33: 1043–1052.
Soenen S, Westerterp-Plantenga MS . No differences in satiety or energy intake after high fructose corn syrup, sucrose, or milk preloads. Am J Clin Nutr 2007; 86: 1586–1594.
Lowndes J, Sinnett S, Pardo S, Nguyen V, Melanson K, Yu Z et al. The effect of normally consumed amounts of sucrose or high fructose corn syrup on body composition and related parameters in overweight/obese subjects. Nutrients 2014; 6: 1128–114.
Kaiser KA, Shikany JM, Keating KD, Allison DB . Will reducing sugar-sweetened beverage consumption reduce obesity? Evidence supporting conjecture is strong, but evidence when testing effect is weak. Obes Rev 2013; 14: 620–633.
Te Morenga L, Mallard S, Mann J . Dietary sugars and body weight: systematic review and meta-analysis of randomized controlled trials and cohort studies. BMJ 2013; 346: e7492.
Malik VS, Pan A, Willett WC, Hu FB . Sugar-sweetened beverages and weight gain in children and adults: a systematic review and meta-analysis. Am J Clin Nutri 2013; 98: 1084–1102.
Tappy L, Lê K-A . Health effects of fructose and fructose-containing caloric sweeteners: where do we stand 10 years after the initial whistle blowings? Curr Diab Rep 2015; 15: 1–12.
Flegal KM, Carroll MD, Ogden CL, Curtin LR . Prevalence and trends in obesity among US adults, 1999-2008. JAMA 2010; 303: 235–241.
Cozma A, Ha V, de Souza RJ, Sievenpiper J . Sweeteners and diabetes. In: Rippe J (ed). Fructose, High Fructose Corn Syrup, Sucrose and Health. Springer Publishing: New York, NY, USA, 2014.
Barclay AW, Brand-Miller J . The Australian Paradox: a substantial decline in sugars intake over the same timeframe that overweight and obesity have increased [published erratum appears in Nutrients 2014; 6: 663–664]. Nutrients 2011; 3: 491–504.
Hall KD, Heymsfield SB, Kemnitz JW, Klein S, Schoeller D, Speakman J . Energy balance and its components: implications for body weight regulation. Am J Clin Nutri 2012; 95: 989–994.
International Diabetes Federation, IDF Diabetes Atlas. Epidemiology and Morbidity, 2015. International Diabetes Federation Available from www.idf.org.
Malik VS, Popkin BM, Bray GA, Despres JP, Willett WC, Hu FB . Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis. Diabetes Care 2010; 33: 2477–2483.
Janket SJ, Manson JE, Sesso H, Buring JE, Liu S . A prospective study of sugar intake and risk of type 2 diabetes in women. Diabetes Care 2003; 26: 1008–1015.
Hodge AM, English DR, O'Dea K, Giles DD . Glycemic index and dietary fiber and the risk of type 2 diabetes. Diabetes Care 2004; 27: 2701–2706.
Colditz GA, Manson JE, Stampfer MJ, Rosner B, Willett WC, Speizer FE . Diet and risk of clinical diabetes in women. Am J Clin Nutri 1992; 55: 1018–1023.
Lowndes J, Sinnett S, Fullerton Z, Angelopoulos T, Rippe J . The effects of fructose containing sugars on weight, body composition and cardiometabolic risk factors when consumed at up to the 90th percentile population consumption level for fructose. Nutrients 2014; 6: 3153–3168.
Lowndes J, Rippe JM, Sinnett S . No change in oral glucose tolerance tests as a result of ten weeks of consumption of various fructose containing sugars or glucose. Diabetes: Clinical Physiology and Treatment SUN-1018-SUN-1018. The Endocrine Society 2014. Available from https://endo.confex.com/endo/2014endo/webprogram/Paper12047.html.
Lowndes J, Sinnett S, Rippe JM . No effect of added sugar consumed at median american intake level on glucose tolerance or insulin resistance. Nutrients 2015; 7: 8830–8845.
Bravo S, Lowndes J, Sinnett S, Yu Z, Rippe J . Consumption of sucrose and high-fructose corn syrup does not increase liver fat or ectopic fat deposition in muscles. Appl Physiol Nutr Metab 2013; 38: 681–688.
Rippe JM, Angelopoulos TJ . Fructose containing sugars and cardiovascular disease. Adv Nutr 2015; 6: 430–439.
Aeberli I, Gerber PA, Hochuli M, Kohler S, Haile SR, Gouni-Berthold I et al. Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial. Am J Clin Nutr 2011; 94: 479–485.
Antar MA, Little JA, Lucas C, Buckley GC, Csima A . Interrelationship between the kinds of dietary carbohydrate and fat in hyperlipoproteinemic patients. 3. Synergistic effect of sucrose and animal fat on serum lipids. Atherosclerosis 1970; 11: 191–201.
Bantle JP, Swanson JE, Thomas W, Laine DC . Metabolic effects of dietary sucrose in type 2 diabetic subjects. Diabetes Care 1993; 16: 1301–1305.
Black RN, Spence M, McMahon RO, Cuskelly GJ, Ennis CN, McCance DR et al. Effect of eucaloric high- and low-sucrose diets with identical macronutrient profile on insulin resistance and vascular risk: a randomized controlled trial. Diabetes 2006; 55: 3566–3572.
Cooper PL, Wahlqvist ML, Simpson RW . Sucrose versus saccharin as an added sweetener in non-insulin-dependent diabetes: short- and medium-term metabolic effects. Diabet Med 1988; 5: 676–680.
Groen JJ, Balogh M, Yaron E, Cohen AM . Effect of interchanging bread and sucrose as main source of carbohydrate in a low fat diet on the serum cholesterol levels of healthy volunteer subjects. Am J Clin Nutr 1966; 19: 46–58.
Lowndes J, Kawiecki D, Pardo S, Nguyen V, Melanson KJ, Yu Z et al. The effects of four hypocaloric diets containing different levels of sucrose or high fructose corn syrup on weight loss and related parameters. Nutr J 2012; 11: 55.
Maersk M, Belza A, Stodkilde-Jorgensen H, Ringgaard S, Chabanova E, Thomsen H et al. Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. Am J Clin Nutr 2012; 95: 283–289.
Marckmann P, Raben A, Astrup A . Ad libitum intake of low-fat diets rich in either starchy foods or sucrose: effects on blood lipids, factor vii coagulant activity, and fibrinogen. Metabolism 2000; 49: 731–735.
Raben A, Vasilaras T, Møller A, Astrup A . Sucrose compared with artificial sweeteners: different effects on ad libitum food intake and body weight after 10 wk of supplementation in overweight subjects. Am J Clin Nutr 2002; 76: 721–729.
Sorensen LB, Raben A, Stender S, Astrup A . Effect of sucrose on inflammatory markers in overweight humans. Am J Clin Nutr 2005; 82: 421–427.
Stanhope K, Griffen S, Bair B, Swarbrick M, Kelm N, Havel P . Twenty four hour endocrine and metabolic profiles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucose-sweetened beverages with meals. Am J Clin Nutr 2008; 87: 1194–1203.
Stanhope KL, Bremer AA, Medici V, Nakajima K, Ito Y, Nakano T et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-b in young men and women. J Clin Endocrinol Metab 2011; 96: E1596–E1605.
Miller M, Stone N, Ballantyne C, Bittner V, Criqui M, Ginsberg H et al. Triglycerides and cardiovascular disease: a scientific statement from the American Heart Association. Circulation 2011; 123: 2292–2333.
Lowndes J, Sinnett S, Pardo S, Nguyen V, Melanson K, Yu Z et al. The effect of normally consumed amounts of sucrose or high fructose corn syrup on body composition and related parameters in overweight/obese subjects. Nutrients 2014; 6: 1128–1144.
Chiavaroli L, Mirrahimi A, De Souza RJ, Cozma AI, Ha V, Wang DD et al. Does fructose consumption elicit a dose-response effect on fasting triglycerides? A systematic review and meta-regression of controlled feeding trials. Can J Diabetes 2012; 36: S37.
Wang D, Sievenpiper JL, de Souza RJ, Cozma AI, Chiavaroli L, Ha V et al. Effect of fructose on postprandial triglycerides: A systematic review and meta-analysis of controlled feeding trials. Atherosclerosis 2014; 232: 125–133.
Obarzanek E, Sacks F, Vollmer W, Bray G, Miller E III, Lin P et alDASH Research Group. Effects on blood lipids of a blood pressure-lowering diet: the Dietary Approaches to Stop Hypertension (DASH) Trial. Am J Clin Nutr 2001; 74: 80–89.
Howard B, Van Horn L, Hsia J, Manson J, Stefanick M, Wassertheil-Smoller S et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA 2006; 295: 655–666.
Stanhope KL, Havel PJ . Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. Curr Opin Lipidol 2008; 19: 16–24.
Marckmann P . Dietary treatment of thrombogenic disorders related to the metabolic syndrome. Br J Nutr 2000; 83 (Suppl 1): S121–S126.
Johnson R, Segal M, Sautin Y, Nakagawa T, Feig D, Kang D et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr 2007; 86: 899–906.
Feig D, Soletsky B, Johnson R . Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. JAMA 2008; 300: 924–932.
Ha V, Sievenpiper J, de Souza R, Chiavaroli L, Wang D, Cozma A et al. Effect of fructose on blood pressure: a systematic review and meta-analysis of controlled feeding trials. Hypertension 2012; 59: 787–795.
Nguyen S, Choi H, Lustig R, Hsu C . Sugar-sweetened beverages, serum uric acid, and blood pressure in adolescents. J Pediatr 2009; 154: 807–813.
Bremer A, Auinger P, Byrd R . Relationship between insulin resistance-associated metabolic parameters and anthropometric measurements with sugar-sweetened beverage intake and physical activity levels in US adolescents: findings from the 1999–2004 National Health and Nutrition Examination Survey. Arch Pediatr Adolesc Med 2009; 163: 328–335.
This article is based on a symposium entitled ‘Sweeteners and Health: Findings from Recent Research and their Impact on Obesity and Related Metabolic Conditions’ presented at the 22nd European Congress on Obesity, Prague, on 7 May 2015 with sponsorship from Rippe Lifestyle Institute.
JMR and Rippe's research laboratory have received unrestricted grants and JMR has received consulting fees from ConAgra Foods, Kraft Foods, Florida, Department of Citrus, PepsiCo International, The Coca Cola Company, Dr. Pepper/Snapple Group, Corn Refiners Association, Weight Watchers International as well as royalties and editorial office support from CRC Press, Sage Publishing and Springer Publishers. The remaining author (TJA) declares no conflict of interest.
This article is based on a presentation at a symposium entitled ‘Sweeteners and Health: Findings from Recent Research and their Impact on Obesity and Related Metabolic Conditions’ held at the European Congress on Obesity (ECO) on 7 May 2015. This symposium was supported, in part, by an educational grant from Rippe Lifestyle Institute.
About this article
Cite this article
Rippe, J., Angelopoulos, T. Added sugars and risk factors for obesity, diabetes and heart disease. Int J Obes 40, S22–S27 (2016). https://doi.org/10.1038/ijo.2016.10
Eating and Weight Disorders - Studies on Anorexia, Bulimia and Obesity (2021)
International Journal of Obesity Supplements (2020)