doi: 10.1161/01.CIR.0000019552.77778.04
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(Circulation. 2002;106:523.)
© 2002 American Heart Association, Inc.
AHA Scientific Statement |
Sugar and Cardiovascular Disease
A Statement for Healthcare Professionals From the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association
Key Words: AHA Scientific Statements • diet • nutrition • sugar
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Introduction |
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Top
Introduction
DefinitionsThe purpose of this report is to review the effects of dietary sugar on health, with an emphasis on cardiovascular disease (CVD) and its risk factors. Although there are no dietary trials linking sugar consumption and CVD, there are several reasons why sugar consumption should be limited.
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Definitions |
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There are many, sometimes confusing, terms used in the literature. Simple carbohydrate (sugar) refers to mono- and disaccharides; complex carbohydrate refers to polysaccharides such as starch. Common disaccharides are sucrose (glucose+fructose), found in sugar cane, sugar beets, honey, and corn syrup; lactose (glucose+galactose), found in milk products; and maltose (glucose+glucose), from malt. The most common naturally occurring monosaccharide is fructose (found in fruits and vegetables). The term dextrose is used to refer to glucose. Intrinsic or naturally occurring sugar refers to the sugar that is an integral constituent of whole fruit, vegetable, and milk products; extrinsic or added sugar refers to sucrose or other refined sugars in soft drinks and incorporated into food, fruit drinks, and other beverages.
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Sugar Consumption in the United States |
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Added sugar was not a significant component of the human diet until the advent of modern food-processing methods. Since then, the intake of sugar has risen steadily. The average US sugar utilization per capita on the basis of food disappearance data was 55 kg (120 lb) per year in 1970, and it reached 68 kg (150 lb) per year in 1995 (almost 0.5 lb per day).1 Sugar (simple carbohydrate) intake averages 25% of total energy intake. Data from the 1989 to 1991 Continuing Survey of Food Intake by Individuals indicate that soft drinks and sugars added at the table (eg, sugar/syrups and jams) are 2 of the top 4 carbohydrate sources for US adults.2
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Sugar and Coronary Heart Disease |
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Yudkin and colleagues in the 1960s3 and 1970s4 found that a higher intake of sugar was associated with increased CVD in both within-country and cross-country comparisons. A few recent studies have examined the link between sugar consumption and coronary heart disease (CHD). The Iowa Women’s Health Study5 showed no relation between the intake of sweets or desserts and risk of ischemic heart disease in 34 492 women monitored for 9 years. However, some major sources of sugar such as soft drinks were not considered. The Scottish Heart Health Study6 of 10 359 men and women found that neither extrinsic nor intrinsic sugars were significant independent correlates of prevalent CHD after adjustment for other major risk factors, but the data were not adjusted for other dietary variables. A recent report from the Nurses’ Health Study showed that women who consumed diets with a high glycemic load* (increased blood glucose excursions associated with intake of sweets or highly processed starches and sweets) had an increased CHD risk, with those in the highest quintile having a >2-fold risk during 10 years of follow-up.7 Simple carbohydrate alone was also predictive but did not reach statistical significance. This analysis controlled for total energy intake and other major dietary and nondietary risk factors.
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Dietary Sugar and Plasma Lipoproteins |
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A number of studies link dietary sugar with adverse changes in lipoproteins. Several studies have shown an inverse association between dietary sucrose and high-density lipoprotein (HDL) cholesterol.8,9 Data from the Coronary Artery Risk Development In young Adults (CARDIA) study show a consistent inverse association between increased dietary sucrose intake and HDL cholesterol concentrations, in both cross-sectional and longitudinal analyses in blacks and whites, in both men and women, and after adjustment for other covariates.10
A diet high in sucrose (ie, >20% of energy) is associated with an elevation of plasma triglyceride concentrations.11,12 This increase is due to both increased hepatic secretion and impaired clearance of very-low-density lipoprotein. Triglyceride response to dietary sugar may vary, however, according to the amount of sugar and the presence of other nutrients.12
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Dietary Sugar, Insulin Resistance, and Diabetes |
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Few epidemiological studies have directly examined the relationship between sugar intake and diabetes incidence. In general, prospective data show no association, and in fact, several dietary studies show an inverse association between total carbohydrate intake and diabetes incidence.13–15 This observation, however, is confounded because diets lower in carbohydrate are higher in fat (high fat intake predicts diabetes risk because of increased obesity).16 On the other hand, two recent prospective cohort studies have reported food frequency consumption data that showed that a history of consumption of foods with a high glycemic load predicts the development of type 2 diabetes in women17 and men.18
No epidemiological study has examined the effects of dietary sugar on insulin resistance. Several clinical studies have shown that altering the proportion of carbohydrates in the diet for up to 4 months in humans does not influence insulin resistance,19 but the effects of varying sugar content per se were not examined.
It is widely believed that individuals with diabetes should avoid sugar to maintain glycemic control. However, there is considerable debate about whether high-sugar diets have adverse effects on glucose control in diabetic individuals. A number of studies that assessed the effects of single meals containing 12% to 25% of calories as sucrose found no adverse effects of sucrose on average glycemia.20,21 Some long-term studies up to several months in duration showed that providing as much as 38% of calories as sucrose had no effect on average glucose control.22–24 Diabetic individuals, however, may experience fluctuations in blood glucose levels with a habitual diet that is high in concentrated sweets, especially if they make errors with regard to the amount of carbohydrates they consume.
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Diet and Advanced Glycation End Products |
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Advanced glycation end products (AGEs) form when sugar is nonenzymatically linked to proteins, inducing cross-linking of the glycated proteins. AGEs form at room temperature, but heating speeds up their formation; therefore, all cooked foods contain AGEs (formerly referred to as Maillard browning pigments). Dietary AGEs react with tissue proteins to form substances that reduce tissue elasticity and impede cellular function. AGEs have been identified as a pathogenic mechanism in diabetic nephropathy25 and vascular complications.26 Approximately 10% of ingested AGEs enter the circulation, but only one third are excreted within 3 days of ingestion.25 Diabetes is associated with impairment in AGE excretion. In one study, urinary clearance of diet-derived AGE was 5% in diabetic individuals compared with 30% in the control group.27 Thus, caution is warranted with regard to the potential effects of a high sugar intake on AGE formation and increased risk of nephropathy.27 Additional research is needed to determine whether limiting intake of sugar in protein- and fat-containing foods reduces circulating AGE levels and risk of nephropathy.
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Dietary Sugar and Overweight/Obesity |
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Because obesity has emerged as a major health problem in the United States28 and as a definite cause of cardiovascular morbidity and mortality,29 it is important to consider the potential impact of dietary sugar on weight gain. In human metabolic ward studies, the substitution of sucrose or other dietary carbohydrate for fat or protein in isocaloric diets shows no effect on weight or changes in energy expenditure.30 Some studies show that body mass index is correlated inversely with sugar consumption31; however, this observation is confounded because dietary fat is correlated with obesity,32 and high-fat diets are lower in total and simple carbohydrate. Diets low in sugar have been associated with weight loss in some ad lib dietary studies,33 perhaps as a result of lower total calorie consumption. Another relationship between sugar and obesity comes from studies of food preferences, which report that foods high in sugar are common choices of obese individuals.34 To lose weight, obese persons need to limit calorie intake; thus, limiting consumption of foods that are high in sugar (most of which have high energy density) can be a strategy for weight reduction.
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Sugar and Other Health Problems |
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There have been a number of studies that link sugar consumption to hypertension in animals.35 In humans, there is one report that high dietary sugar intake enhances the risk of CHD in diabetic individuals who use diuretics.36
Sugar intake can increase carbohydrate fuel reserves and physical performance.30 However, this enhancement occurs only at exercise intensities and levels of physical activity associated with endurance performance of at least 30 minutes in duration. Blood glucose and liver and muscle glycogen provide the predominant fuels for muscle contraction. When these substances reach critically low amounts, fatigue may occur and consumption of sugar may rapidly return blood glucose levels to normal. For most low- to moderate-intensity activities like walking or housework, sugar consumption does not influence performance.
Another major area of interest has been the relationship between dietary sugar and behavior and cognitive function. The belief in a relationship between sugar and hyperactivity was based on two hypotheses. The first was a possible allergic response; the second was that hyperactive children might experience functional reactive hypoglycemia. Neither of these hypotheses has been proved, and a meta-analysis of 16 randomized trials in hyperactive children showed that decreasing the sugar content of the diet resulted in no improvement in degree of hyperactivity.37
On the other hand, sugar is a well-established risk factor for dental caries.38–40 This observation is based on short-term cohort studies and comparisons of rates of dental caries across countries with wide variations in sugar consumption,38 although there is a lack of research findings regarding sugar consumption and periodontal disease.41
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High-Sugar Diets and Nutritional Adequacy |
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Diets high in sugar may adversely affect nutritional adequacy. Foods high in extrinsic sugar include soft drinks, candy, pastry, and cereals with high sugar content (Table 1). Fat-free manufactured foods are often high in calories because of inclusion of high amounts of sugar. American Heart Association dietary guidelines stress consumption of fruits, vegetables, grains, and complex carbohydrates so that nutritional requirements for vitamins and minerals may be met by whole foods rather than by foods that are supplemented with vitamins. High-sugar foods displace whole foods (eg, soft drinks displace milk and juice consumption in children) and contribute to nutritional deficiencies, adding empty calories that few Americans need42 (Table 2). Some studies that have assessed the nutritional adequacy of high-sugar diets do not necessarily show differences in vitamin and mineral intake1 because of the supplementation of these foods with vitamins and minerals instead of the preferred intake of these elements through the diet. Among children in the Bogalusa Heart Study,43 a linear decrease in the intake of many essential nutrients was associated with increasing total sugar intake.
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The Role of Dietary Fructose, Sorbitol, and Mannitol |
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Sugars such as fructose (monosaccharide), sorbitol, and mannitol (sugar alcohols) are used to replace sucrose in food products and may lower the postprandial rise in glucose. In the 1970s, high-fructose syrup manufactured from starch began to be used as a replacement for sucrose in beverages and baked goods.44 Sorbitol and mannitol are used in a variety of "sugar-free" food products because they have fewer calories per gram than do either sucrose or fructose; in the liver they are readily converted to fructose.45 Fructose bypasses the phosphofructokinase regulatory step of glycolysis, in which glucose can be converted to glycogen rather than entering the glycolytic pathway. As a result, fructose increases hepatic pyruvate and lactic acid production, activates pyruvate dehydrogenase, and shifts the balance from oxidation to esterification of fatty acids, which can increase very-low-density lipoprotein synthesis. In feeding studies, fructose has had inconsistent effects on plasma triglyceride levels, which may be related to factors such as the amount of fructose consumed; energy balance; and baseline triglyceride, insulin, and glucose levels.46 The postprandial rise in triglyceride levels after fat intake may be augmented with the addition of fructose to a test meal.47 However, a study in individuals with type 2 diabetes showed a lack of significant variation in glucose, lipid, and insulin responses to three 28-day isocaloric feeding periods when 20% of calories were either fructose, sucrose, or starch.48 For most individuals, consuming fructose either free or in the form of sucrose has neither beneficial nor adverse effects.
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Summary and Conclusion |
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As with most other dietary constituents, long-term trial data relating sugar consumption to the development of CVD events are unavailable. Longitudinal cohort studies relating sugar consumption to CVD are equivocal because of the many potential confounders that cannot be adequately controlled in the analyses. Shorter-term studies show consistent adverse effects of sugar consumption on HDL and triglyceride levels, which could accelerate atherosclerosis. High sugar consumption may worsen diabetes control, and the combination of sugar with protein and fats promotes formation of dietary AGEs, which may be especially detrimental to those with diabetes. Although increasing the amount of sugar in an isocaloric diet does not directly lead to changes in energy expenditure or weight gain in controlled feeding studies, high-sugar foods, which are sweet and calorie dense, may increase calorie consumption and lead to weight gain. Furthermore, replacement of whole foods with high-sugar foods compromises attainment of adequate dietary vitamin and mineral intake from whole food sources.
In the absence of definitive evidence, recommendations must rely on professional judgment. No data suggest that sugar intake per se is advantageous, and some data suggest it may be detrimental. The studies above, taken in total, indicate that high sugar intake should be avoided. Sugar has no nutritional value other than to provide calories. To improve the overall nutrient density of the diet and to help reduce the intake of excess calories, individuals should be sure foods high in added sugar are not displacing foods with essential nutrients or increasing calorie intake.
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Footnotes |
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The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.
This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on October 19, 2001. A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Ask for reprint No. 71-0230. To purchase additional reprints: up to 999 copies, call 800-611-6083 (US only) or fax 413-665-2671; 1000 or more copies, call 410-528-4426, fax 410-528-4264, or e-mail kbradle@lww.com. To make photocopies for personal or educational use, call the Copyright Clearance Center, 978-750-8400.
*Glycemic load refers to a diet with many foods that have a high glycemic index. Glycemic index is a measure of the rise in glucose induced by ingestion of a carbohydrate. Foods that contain refined sugars make a major contribution to glycemic load; other contributors include refined starches, such as white bread and rice. It should be noted that glycemic index is determined by feeding individual foods. 
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References |
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1. Putnam JJ, Allshouse JE. Food consumption, prices, and expenditures, 1970–97. Economic Research Service, US Department of Agriculture; April 1999. Statistical Bulletin No. 965. Available at: http://ers.usda.gov/publications/sb965. Accessed June 12, 2002.
2. Subar AF, Krebs-Smith SM, Cook A, et al. Dietary sources of nutrients among US adults, 1989 to 1991. J Am Diet Assoc. 1998; 98: 537–547.[CrossRef][Medline] [Order article via Infotrieve]
3. Yudkin J. Sugar and ischaemic heart disease. Practitioner. 1967; 198: 680–683.[Medline] [Order article via Infotrieve]
4. Yudkin J. Dietary factors in atherosclerosis: sucrose. Lipids. 1978; 13: 370–372.[Medline] [Order article via Infotrieve]
5. Jacobs DR Jr, Meyer KA, Kushi LH, et al. Whole-grain intake may reduce the risk of ischemic heart disease death in postmenopausal women: the Iowa Women’s Health Study. Am J Clin Nutr. 1998; 68: 248–257.[Abstract]
6. Bolton-Smith C, Woodward M. Coronary heart disease: prevalence and dietary sugars in Scotland. J Epidemiol Community Health. 1994; 48: 119–122.
7. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr. 2000; 71: 1455–1461.
8. Ernst N, Fisher M, Smith W, et al. The association of plasma high-density lipoprotein cholesterol with dietary intake and alcohol consumption. The Lipid Research Clinics Prevalence Study. Circulation. 1980; 62: 41–52.
9. Nutrient intake and its association with high-density lipoprotein and low-density lipoprotein cholesterol in selected US and USSR subpopulations. The US-USSR Steering Committee for Problem Area I: the pathogenesis of atherosclerosis. Am J Clin Nutr. 1984; 39: 942–952.
10. Archer SL, Liu K, Dyer AR, et al. Relationship between changes in dietary sucrose and high density lipoprotein cholesterol: the CARDIA Study. Coronary Artery Risk Development in Young Adults. Ann Epidemiol. 1998; 8: 433–438.[CrossRef][Medline] [Order article via Infotrieve]
11. Parks EJ, Hellerstein MK. Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms. Am J Clin Nutr. 2000; 71: 412–433.
12. Frayn KN, Kingman SM. Dietary sugars and lipid metabolism in humans. Am J Clin Nutr. 1995; 62 (suppl): 250S-261S.[Medline] [Order article via Infotrieve]
13. Feskens EJ, Kromhout D. Habitual dietary intake and glucose tolerance in euglycemic men: the Zutphen Study. Int J Epidemiol. 1990; 19: 953–959.
14. Marshall JA, Hoag S, Shetterly S, et al. Dietary fat predicts conversion from impaired glucose tolerance to NIDDM: the San Luis Valley Diabetes Study. Diabetes Care. 1994; 17: 50–56.[Abstract]
15. Fujimoto WY, Bergstrom RW, Boyko EJ, et al. Diabetes and diabetes risk factors in second- and third-generation Japanese Americans in Seattle, Washington. Diabetes Res Clin Pract. 1994; 24 (suppl): S43–S52.[Medline] [Order article via Infotrieve]
16. Howard BV. Dietary fatty acids, insulin resistance, and diabetes. Ann N Y Acad Sci. 1997; 827: 215–220.[Medline] [Order article via Infotrieve]
17. Salmeron J, Manson JE, Stampfer MJ, et al. Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA. 1997; 277: 472–477.
18. Salmeron J, Ascherio A, Rimm EB, et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care. 1997; 20: 545–550.[Abstract]
19. Howard BV. Diet, insulin resistance, and atherosclerosis. Proceedings of the 15th International Diabetes Federation Congress, Kobe, 6–11 November 1994. Excerpta Medica International Congress Series 1100, Diabetes 1994,Eds. Baba S, Kaneko T 446–450, 1995.
20. Bornet F, Haardt MJ, Costagliola D, et al. Sucrose or honey at breakfast have no additional acute hyperglycaemic effect over an isoglucidic amount of bread in type II diabetic patients. Diabetologia. 1985; 28: 213–217.[Medline] [Order article via Infotrieve]
21. Forlani G, Galuppi V, Santacroce G, et al. Hyperglycemic effect of sucrose ingestion in IDDM patients controlled by artificial pancreas. Diabetes Care. 1989; 12: 296–298.[Abstract]
22. Bantle JP, Swanson JE, Thomas W, et al. Metabolic effects of dietary sucrose in type II diabetic subjects. Diabetes Care. 1993; 16: 1301–1305.[Abstract]
23. Bantle JP, Laine DC, Thomas JW. Metabolic effects of dietary fructose and sucrose in types I and II diabetic subjects. JAMA. 1986; 256: 3241–3246.
24. Wise JE, Keim KS, Huisinga JL, et al. Effect of sucrose-containing snacks on blood glucose control. Diabetes Care. 1989; 12: 423–426.[Abstract]
25. He C, Sabol J, Mitsuhashi T, et al. Dietary glycotoxins: inhibition of reactive products by aminoguanidine facilitates renal clearance and reduces tissue sequestration. Diabetes. 1999; 48: 1308–1315.[Abstract]
26. Stitt AW, He C, Vlassara H. Characterization of the advanced glycation end-product receptor complex in human vascular endothelial cells. Biochem Biophys Res Commun. 1999; 256: 549–556.[CrossRef][Medline] [Order article via Infotrieve]
27. Koschinsky T, He CJ, Mitsuhashi T, et al. Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Proc Natl Acad Sci U S A. 1997; 94: 6474–6479.
28. Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the evidence report. National Institutes of Health. Obes Res. 1998; 6 (suppl 2): 51S–209S.[Medline] [Order article via Infotrieve]
29. Eckel RH, Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. AHA Nutrition Committee. Circulation. 1998; 97: 2099–2100.
30. Hill JO, Prentice AM. Sugar and body weight regulation. Am J Clin Nutr. 1995; 62 (suppl 1): 264S-273S.[Medline] [Order article via Infotrieve]
31. Ruxton CH, Garceau FJ, Cottrell RC. Guidelines for sugar consumption in Europe: Is a quantitative approach justified? Eur J Clin Nutr. 1999; 53: 503–513.[CrossRef][Medline] [Order article via Infotrieve]
32. Klesges RC, Klesges LM, Haddock CK, et al. A longitudinal analysis of the impact of dietary intake and physical activity on weight change in adults. Am J Clin Nutr. 1992; 55: 818–822.
33. Colditz GA, Willett WC, Stampfer MJ, et al. Patterns of weight change and their relation to diet in a cohort of healthy women. Am J Clin Nutr. 1990; 51: 1100–1105.
34. Drewnowski A, Kurth CL, Rahaim JE. Taste preferences in human obesity: environmental and familial factors. Am J Clin Nutr. 1991; 54: 635–641.
35. Preuss HG, Zein M, MacArthy P, et al. Sugar-induced blood pressure elevations over the lifespan of three substrains of Wistar rats. J Am Coll Nutr. 1998; 17: 36–47.
36. Sherman WM. Metabolism of sugars and physical performance. Am J Clin Nutr. 1995; 62 (suppl): 228S-241S.[Medline] [Order article via Infotrieve]
37. Wolraich ML, Wilson DB, White JW. The effect of sugar on behavior or cognition in children: a meta-analysis. JAMA. 1995; 274: 1617–1621.
38. Rugg-Gunn AJ, Murray JJ. The role of sugar in the aetiology of dental caries: 2. The epidemiological evidence. J Dent. 1983; 11: 190–199.[CrossRef][Medline] [Order article via Infotrieve]
39. Sreebny LM. Sugar availability, sugar consumption and dental caries. Community Dent Oral Epidemiol. 1982; 10: 1–7.[CrossRef][Medline] [Order article via Infotrieve]
40. Sreebny LM. Sugar and human dental caries. World Rev Nutr Diet. 1982; 40: 19–65.[Medline] [Order article via Infotrieve]
41. Makinen KK, Isokangas P. Relationship between carbohydrate sweeteners and oral diseases. Prog Food Nutr Sci. 1988; 12: 73–109.[Medline] [Order article via Infotrieve]
42. Krebs-Smith SM, Cleveland LE, Ballard-Barbash R, et al. Characterizing food intake patterns of American adults. Am J Clin Nutr. 1997; 65 (suppl 4): 1264S–1268S.[Medline] [Order article via Infotrieve]
43. Farris RP, Nicklas TA, Myers L, et al. Nutrient intake and food group consumption of 10-year-olds by sugar intake level: the Bogalusa Heart Study. J Am Coll Nutr. 1998; 17: 579–585.
44. Park YK, Yetley EA. Intakes and food sources of fructose in the United States. Am J Clin Nutr. 1993; 58 (suppl): 737S–747S.[Medline] [Order article via Infotrieve]
45. Mayes PA. Intermediary metabolism of fructose. Am J Clin Nutr. 1993; 58 (suppl): 754S–765S.[Medline] [Order article via Infotrieve]
46. Hollenbeck CB. Dietary fructose effects on lipoprotein metabolism and risk of coronary artery disease. Am J Clin Nutr. 1993; 58 (suppl): 800S–809S.[Medline] [Order article via Infotrieve]
47. Jeppesen J, Chen YI, Zhou MY, et al. Postprandial triglyceride and retinyl ester responses to oral fat: effects of fructose. Am J Clin Nutr. 1995; 61: 787–791.
48. Malerbi DA, Paiva ES, Duarte AL, et al. Metabolic effects of dietary sucrose and fructose in type II diabetic subjects. Diabetes Care. 1996; 19: 1249–1256.[Abstract]
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C. W. Baker, J. Wylie-Rosett, and B. V. Howard Sugars and Cardiovascular Disease * Response Circulation, February 25, 2003; 107 (7): e48 - e48. [Full Text] [PDF]
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