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11 Macronutrients and Healthful Diets SUMMARY Acceptable Macronutrient Distribution Ranges (AMDRs) for indi- viduals have been set for carbohydrate, fat, n-6 and n-3 poly- unsaturated fatty acids, and protein based on evidence from interventional trials, with support of epidemiological evidence that suggests a role in the prevention or increased risk of chronic dis- eases, and based on ensuring sufficient intakes of essential nutrients. The AMDR for fat and carbohydrate is estimated to be 20 to 35 and 45 to 65 percent of energy for adults, respectively. These AMDRs are estimated based on evidence indicating a risk for coro- nary heart disease (CHD) at low intakes of fat and high intakes of carbohydrate and on evidence for increased risk for obesity and its complications (including CHD) at high intakes of fat. Because the evidence is less clear on whether low or high fat intakes during childhood can lead to increased risk of chronic diseases later in life, the estimated AMDRs for fat for children are primarily based on a transition from the high fat intakes that occur during infancy to the lower adult AMDR. The AMDR for fat is 30 to 40 percent of energy for children 1 to 3 years of age and 25 to 35 percent of energy for children 4 to 18 years of age. The AMDR for carbo- hydrate for children is the same as that for adults—45 to 65 percent of energy. The AMDR for protein is 10 to 35 percent of energy for adults and 5 to 20 percent and 10 to 30 percent for children 1 to 3 years of age and 4 to 18 years of age, respectively. 769

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770 DIETARY REFERENCE INTAKES Based on usual median intakes of energy, it is estimated that a lower boundary level of 5 percent of energy will meet the Adequate Intake (AI) for linoleic acid (Chapter 8). An upper boundary for linoleic acid is set at 10 percent of energy for three reasons: (1) individual dietary intakes in the North American population rarely exceed 10 percent of energy, (2) epidemiological evidence for the safety of intakes greater than 10 percent of energy are generally lacking, and (3) high intakes of linoleic acid create a pro-oxidant state that may predispose to several chronic diseases, such as CHD and cancer. Therefore, an AMDR of 5 to 10 percent of energy is estimated for n-6 polyunsaturated fatty acids (linoleic acid). An AMDR for α-linolenic acid is estimated to be 0.6 to 1.2 percent of energy. The lower boundary of the range meets the AI for α-linolenic acid (Chapter 8). The upper boundary corresponds to the highest α-linolenic acid intakes from foods consumed by indi- viduals in the United States and Canada. A growing body of litera- ture suggests that higher intakes of α-linolenic acid, eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) may afford some degree of protection against CHD. Because the physiological potency of EPA and DHA is much greater than that for α-linolenic acid, it is not possible to estimate one AMDR for all n-3 fatty acids. Approximately 10 percent of the AMDR can be consumed as EPA and/or DHA. No more than 25 percent of energy should be consumed as added sugars. This maximal intake level is based on ensuring sufficient intakes of certain essential micronutrients that are not present in foods and beverages that contain added sugars. A daily intake of added sugars that individuals should aim for to achieve a healthy diet was not set. A Tolerable Upper Intake Level (UL) was not set for saturated fatty acids, trans fatty acids, or cholesterol (see Chapters 8 and 9). This chapter provides some guidance in ways of minimizing the intakes of these three nutrients while consuming a nutritionally adequate diet. INTRODUCTION Unlike micronutrients, macronutrients (fat, carbohydrate, and pro- tein) are sources of body fuel that can be used somewhat interchangeably. Thus, for a certain level of energy intake, increasing the proportion of one macronutrient necessitates decreasing the proportion of one or both of the other macronutrients. The majority of energy is consumed as carbo-

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771 M ACRONUTRIENTS AND HEALTHFUL DIETS hydrate (approximately 35 to 70 percent, primarily as starch and sugars), and fat (approximately 20 to 45 percent), while the contribution of protein to energy intake is smaller and less varied (10 to 23 percent) (Appendix Tables E-3, E-6, and E-17). Therefore, a high fat diet (high percent of energy from fat) is usually low in carbohydrate and vice versa. In addition to these macronutrients, alcohol can provide on average up to 3 percent of energy of the adult diet (Appendix Table E-18). A small amount of carbohydrate and as n-6 (linoleic acid) and n-3 (α-linolenic acid) polyunsaturated fatty acids and a number of amino acids that are essential for metabolic and physiological processes, are needed by the brain. The amounts needed, however, each constitute only a small percentage of total energy requirements. Food sources vary in their con- tent of particular macro- and micronutrients. While some nutrients are present in both animal- and plant-derived foods, others are only present or are more abundant in either animal or plant foods. For example, animal-derived foods contain significant amounts of protein, saturated fatty acids, long-chain n-3 polyunsaturated fatty acids, and the micronutrients iron, zinc, and vitamin B12, while plant-derived foods provide greater amounts of carbohydrate, Dietary Fiber, linoleic and α-linolenic acids, and micronutrients such as vitamin C and the B vitamins. It may be difficult to achieve sufficient intakes of certain micronutrients when consuming foods that contain very low amounts of a particular macronutrient. Alternatively, if intake of certain macronutrients from nutrient-poor sources is too high, it may also be difficult to consume sufficient micronutrients and still remain in energy balance. Therefore, a diet containing a variety of foods is considered the best approach to ensure sufficient intakes of all nutrients. This concept is not new and has been part of nutrition education pro- grams since the early 1900s. For example, the first U.S. food guide was developed by the U.S. Department of Agriculture in 1916 and suggested consumption of a combination of five different food groups (Guthrie and Derby, 1998). This food guide has evolved to become known as the Food Guide Pyramid (USDA, 1996). Similarly, Canada has developed Canada’s Food Guide to Healthy Eating (Health Canada, 1997). A growing body of evidence indicates that an imbalance in macro- nutrients (e.g., low or high percent of energy), particularly with certain fatty acids and relative amounts of fat and carbohydrate, can increase risk of several chronic diseases. Much of this evidence is based on epidemio- logical studies of clinical endpoints such as coronary heart disease (CHD), diabetes, cancer, and obesity. However, these studies demonstrate associa- tions; they do not necessarily infer causality, such as would be derived from controlled clinical trials. Robust clinical trials with specified clinical endpoints are generally lacking for macronutrients. Of importance, fac- tors other than diet contribute to chronic disease, and multifactorial cau-

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772 DIETARY REFERENCE INTAKES sality of chronic disease can confound the long-term adverse effects of a given macronutrient distribution. It is not possible to determine a defined level of intake at which chronic disease may be prevented or may develop. For example, high fat diets may predispose to obesity, but at what percent of energy intake does this occur? The answer depends on whether energy intake exceeds energy expenditure or is balanced with physical activity. This chapter reviews the scientific evidence on the role of macro- nutrients in the development of chronic disease. In addition, the nutrient limitations that can occur with the consumption of too little or too much of a particular macronutrient are discussed. In consideration of the inter- relatedness of macronutrients, their role in chronic disease, and their association with other essential nutrients in the diet, Acceptable Macro- nutrient Distribution Ranges (AMDRs) are estimated and represented as percent of energy intake. These ranges represent (1) intakes that are asso- ciated with reduced risk of chronic disease, (2) intakes at which essential dietary nutrients can be consumed at sufficient levels, and (3) intakes based on adequate energy intake and physical activity to maintain energy balance. When intakes of macronutrients fall above or below the AMDR, the risk for development of chronic disease (e.g., diabetes, CHD, cancer) appears to increase. DIETARY FAT AND CARBOHYDRATE There are a number of adverse health effects that may result from consuming a diet that is too low or high in fat or carbohydrate (starch and sugars). Furthermore, chronic consumption of a low fat, high carbohydrate or high fat, low carbohydrate diet may result in the inadequate intake of certain essential nutrients. Low Fat, High Carbohydrate Diets of Adults The chronic diseases of greatest concern with respect to relative intakes of macronutrients are CHD, diabetes, and cancer. In this section, the rela- tionship between total fat and total carbohydrate intakes are considered. Comparisons are made in terms of percentage of total energy intake. For example, a low fat diet signifies a lower percentage of fat relative to total energy. It does not imply that total energy intake is reduced because of consumption of a low amount of fat. The distinction between hypocaloric diets and isocaloric diets is important, particularly with respect to impact on body weight. Low and high fat diets can still be isocaloric. The failure to identify this distinction has led to considerable confusion in terms of the role of dietary fat in chronic disease.

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773 M ACRONUTRIENTS AND HEALTHFUL DIETS In the past few decades, the prevalence of overweight and obesity has increased at an alarming rate in many populations, particularly in the United States. Overweight and obesity contribute significantly to various chronic diseases. Consequently, there are two issues to consider for the distribution of fat and carbohydrate intakes in high-risk populations: the distributions that predispose to the development of overweight and obesity, and the distributions that worsen the metabolic consequences in popula- tions that are already overweight or obese. These issues will be considered in the following sections. Maintenance of Body Weight A first issue is whether a certain macronutrient distribution interferes with sufficient intake of total energy, that is, sufficient energy to maintain a healthy weight. Sonko and coworkers (1994) concluded that an intake of 15 percent fat was too low to maintain body weight in women, whereas an intake of 18 percent fat was shown to be adequate even with a high level of physical activity (Jéquier, 1999). Moreover, some populations, such as those in Asia, have habitual very low fat intakes (about 10 percent of total energy) and apparently maintain adequate health (Weisburger, 1988). Whether these low fat intakes and consequent low energy consumptions have con- tributed to a historically small stature in these populations is uncertain. An issue of more importance for well-nourished but sedentary popula- tions, such as that of the United States, is whether the distribution between intakes of total fat and total carbohydrate influences the risk for weight gain (i.e., for development of overweight or obesity). It has been shown that when men and women were fed isocaloric diets containing 20, 40, or 60 percent fat, there was no difference in total daily energy expenditure (Hill et al., 1991). Similar observations were reported for individuals who consumed diets containing 10, 40, or 70 percent fat, where no change in body weight was observed (Leibel et al., 1992), and for men fed diets containing 9 to 79 percent fat (Shetty et al., 1994). Horvath and colleagues (2000) reported no change in body weight after runners consumed a diet containing 16 percent fat for 4 weeks. These studies contain two important findings: fat and carbohydrate provide similar amounts of metabolic energy predicted from their true energy content, and isocaloric diets provide similar metabolic energy expenditure, regardless of their fat–carbohydrate distribution. In other words, at isocaloric intakes, low fat diets do not produce weight loss. A number of short- and long-term intervention studies have been con- ducted on normal-weight or moderately obese individuals to ascertain the effects of altering the fat and energy density content of the diet on body weight (Table 11-1). In general, significant reductions in the percent of

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TABLE 11-1 Decreased Fat Intake and Body Weight Change in Normal-Weight or Moderately Obese 774 Individuals Dietary Fat Weight Change Reference Study Design (% of energy) (kg) Comments Short-term studies (< 1 year) Boyar et al., 19 women –5.1 Decreased fat intake 34 → 21% 1988 6-mo intervention associated with Ad libitum diet decreased energy intake Buzzard et al., 29 postmenopausal –2.8 Decreased fat intake 38 → 23% 1990 women –1.3 associated with 39 → 35% 3-mo parallel decreased energy intake Ad libitum diet Bloemberg 80 men –0.94 39 → 34% et al., 1991 26-wk parallel +0.06 38 → 37% Ad libitum diet Kendall et al., 13 women 20–25% –2.54 Decreased fat intake 1991 11-wk crossover 35–40% –1.26 associated with Controlled diet decreased energy intake Low fat diet, hypocaloric Leibel et al., 13 men and women 0, 40, or 70% No significant Isocaloric diets 1992 15- to 56-d intervention changes in body Controlled diet weight Westerterp 217 men and women +0.3 35 → 33% et al., 1996 6-mo parallel +1.1 36 → 41% Ad libitum diet

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Raben et al., 11 women –0.7 Decreased fat intake 46 → 28% 1997 14-d crossover associated with Ad libitum decreased energy intake Gerhard et al., 22 women 20% –1.1 Low fat diet, hypocaloric 2000 4-wk crossover 40% –0.3 Controlled diet Saris et al., 398 men and women –0.9 Decreased fat intake 36 → 26% 2000 6-mo parallel –1.8 associated with 36 → 28% Ad libitum diet +0.8 decreased energy intake 36 → 37% Long-term studies (≥ 1 year) 6 mo 12 mo Decreased fat intake Lee-Han et al., 57 women 1988 1-y parallel –1.16 –0.93 associated with 36 → 23 → 26% Ad libitum diet +0.07 +0.62 decreased energy intake 36 → 34 → 36% Boyd et al., 206 women –1.0 37 → 21% 1990 1-y parallel 0 37 → 35% Ad libitum diet Sheppard et al., 276 women 0 to 1 y Decreased fat intake 1991 1- and 2-y parallel –3.0 associated with 39 → 22% Ad libitum diet –0.4 decreased energy intake 39 → 37% 1 y to 2 y +1.1 22 → 23% continued 775

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TABLE 11-1 Continued 776 Dietary Fat Weight Change Reference Study Design (% of energy) (kg) Comments Baer, 1993 70 men –5.0 Decreased fat intake 38 → 31% 1-y parallel +1.0 associated with 37 → 36% Ad libitum diet decreased energy intake Kasim et al., 72 women –3.4 Decreased fat intake 36 → 18% 1993 1-y parallel –0.8 associated with 36 → 34 % Ad libitum diet decreased energy intake Black et al., 76 men and women –2.0 40 → 21% 1994 2-y parallel –1.0 39 → 39% Ad libitum diet Knopp et al., 137 men –2.9 36 → 27% 1997 1-y parallel –2.9 35 → 22% Ad libitum diet Women Men Women Men Decreased fat intake Stefanick 177 postmenopausal et al., 1998 women and 190 men 23% 22% –2.7 –2.8 associated with 1-y parallel 28% 30% +0.8 +0.5 decreased energy intake Ad libitum diet Kasim-Karakas 54 postmenopausal 4 mo 12 mo et al., 2000 women –1.3 –5.9 34 → 14 → 12% 1-y intervention Controlled diet 4 mo Ad libitum diet 8 mo

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777 M ACRONUTRIENTS AND HEALTHFUL DIETS energy consumed as fat (greater than 4 percent) resulted in small losses in body weight. The only study that provided isocaloric diets showed no dif- ferences in weight gain or loss, despite a wide range in the percent of energy from fat (Leibel et al., 1992). Four meta-analyses of long-term intervention studies associating a low fat diet with body weight concluded that lower fat diets lead to modest weight loss or prevention of weight gain (Astrup et al., 2000; Bray and Popkin, 1998; Hill et al., 2000; Yu-Poth et al., 1999). These studies thus suggest that low fat diets (low percentage of fat) tend to be slightly hypocaloric compared to higher fat diets when com- pared in outpatient intervention trials. The finding that higher fat diets are moderately hypercaloric when compared with reduced fat intakes under ad libitum conditions provides a rationale for setting an upper boundary for percentage of fat intake in a population that already has a high prevalence of overweight and obesity. However, a second issue must also be addressed: whether the distribution of fat and carbohydrate modifies the metabolic consequences of over- weight and obesity. Two of the more important consequences of obesity are dyslipidemic changes in serum lipoproteins (which predispose to CHD) and changes in glucose and insulin metabolism that accentuate an under- lying insulin resistance (which may predispose to both CHD and diabetes). These consequences are discussed in the following sections. Risk of CHD Low fat, high carbohydrate diets, compared to higher fat intakes, can induce a lipoprotein pattern called the atherogenic lipoprotein pheno- type (Krauss, 2001) or atherogenic dyslipidemia (National Cholesterol Education Program, 2001). In populations where people are routinely physically active and lean, the atherogenic lipoprotein phenotype is mini- mally expressed. In sedentary populations that tend to be overweight or obese, very low fat, high carbohydrate diets clearly promote the develop- ment of this phenotype. Whether this phenotype promotes development of coronary atherosclerosis when it is specifically induced by low fat diets is uncertain, but it is a pattern that is associated with increased risk for CHD when expressed in the general American population. The atherogenic lipoprotein phenotype is characterized by higher triacylglycerol and decreased high density lipoprotein (HDL) cholesterol concentrations and small low density lipoprotein (LDL) particles. A predominance of small LDL particles is associated with a greater risk of CHD (Austin et al., 1990), but it is not known if this association is independent of increased triacylglycerol and decreased HDL cholesterol concentrations. Table 11-2 and Figures 11-1 and 11-2 show that with decreasing fat and increasing carbohydrate intake, plasma triacylglycerol concentrations

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778 DIETARY REFERENCE INTAKES TABLE 11-2 Fat and Carbohydrate Intake and Blood Lipid Concentrations in Healthy Individuals Total Fat/ Carbohydrate Intake Study Designa Reference (% of energy) Coulston et al., 11 men and women 1983 10-d crossover 21 P/S = 1.2–1.3 41 Bowman et al., 19 men 29/60 1988 10-wk parallel 33/58 P/S = 0.4 45/42 46/42 Borkman et al., 8 men and women 20/55 P/S = 0.46 1991 3-wk crossover 50/31 P/S = 0.22 Kasim et al., 72 women 18 1993 1-y parallel 34 P/S = 0.68–0.75 Leclerc et al., 7 men and women 11/64 1993 7-d crossover 30/45 40/45 Krauss and 105 men 24/60 Dreon, 1995 6-wk crossover 46/39 P/S = 0.69–0.74 O’Hanesian 10 men and women 17/63 P/S = 0.25 et al., 1996 10-d crossover 28/57 P/S = 2.2 42/39 P/S = 1.7 Jeppesen et al., 10 postmenopausal 25/60 1997 women 45/40 3-wk crossover P/S = 1.0 Kasim-Karakas 14 postmenopausal 14 P/S = 1.2 et al., 1997 women 23 P/S = 1.0 4-mo intervention 31 P/S = 0.9 Yost et al., 25 men and women 25/55 1998 15-d crossover 50/30 P/S = 0.3 Straznicky 14 men 25/54 P/S = 1.3 et al., 1999 2-wk crossover 47/36 P/S = 0.1 Kasim-Karakas 54 postmenopausal 12/71 et al., 2000 women 14/69 4- to 12-mo 34/50 crossover P/S = 0.64

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779 M ACRONUTRIENTS AND HEALTHFUL DIETS Postintervention Blood Lipid Concentration (mmol/L)b Triacylglycerol HDL-C LDL-C 1.51c 0.98c 1.02d 1.16d 0.91c 1.42c 2.35c 1.11c 1.22c 2.17c 0.84c 1.53c 2.59c 1.01c 1.50c 2.40c 0.82c (+49%) 0.84c (–24%) 2.88c (–20%) 0.55c 1.10d 3.60d 1.35c 1.44c (–8%) 2.79c (–10%) 1.25d 1.56d 3.09d 1.11c 1.03c 2.29c 1.29c 1.15d 2.47c 0.87d 1.32e 3.05d 1.59c 1.09c 3.26c 1.13d 1.27d 3.69d 0.8 1.1 2.4 0.8 1.2 2.5 0.8 1.3 3.0 1.97c 1.38c 2.74c 1.29d 1.49d 2.81c 2.47c 1.24c 2.61c 2.10d 1.32d 2.93d 1.85e 1.34d 2.89d 1.14c 1.22c 0.88d 1.30d 0.8c 1.05c 2.6c 0.8c 1.28d 3.5d 1.49c 1.40c 3.49c 2.00c 1.29c 3.18c 1.57c 1.53d 3.57c continued

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869 M ACRONUTRIENTS AND HEALTHFUL DIETS Pearce ML, Dayton S. 1971. Incidence of cancer in men on a diet high in poly- unsaturated fat. Lancet 1:464–467. Peiris AN, Struve MF, Mueller RA, Lee MB, Kissebah AH. 1988. Glucose metabo- lism in obesity: Influence of body fat distribution. J Clin Endocrinol Metab 67:760–767. Pelkman CL, Coval SM, Mauger DT, Zhao G, Kris-Etherton PM. 2001. A meta- analysis of low-fat versus high-MUFA diets. FASEB J 15:394. Pelletier DL, Frongillo EA, Schroeder DG, Habicht J-P. 1995. The effects of mal- nutrition on child mortality in developing countries. Bull World Health Organ 73:443–448. Perez-Jimenez F, Espino A, Lopez-Segura F, Blanco J, Ruiz-Gutierrez V, Prada JL, Lopez-Miranda J, Jimenez-Pereperez J, Ordovas JM. 1995. Lipoprotein con- centrations in normolipidemic males consuming oleic acid-rich diets from two different sources: Olive oil and oleic acid-rich sunflower oil. Am J Clin Nutr 62:769–775. Perez-Jimenez F, Catrso P, Lopez-Miranda J, Paz-Rojas E, Blanco A, Lopez-Segura F, Velasco F, Marin C, Fuentes F, Ordovas JM. 1999. Circulating levels of endothelial function are modulated by dietary monounsaturated fat. Athero- sclerosis 145:351–358. Perez-Jimenez F, Lopez-Miranda J, Pinillos MD, Gomez P, Pas-Rojas E, Montilla P, Marin C, Velasco MJ, Blanco-Molina A, Jimenez Pereperez JA, Ordovas JM. 2001. A Mediterranean and a high-carbohydrate diet improves glucose metabolism in healthy young persons. Diabetologica 44:2038–2043. Peterson S, Sigman-Grant M. 1997. Impact of adopting lower-fat food choices on nutrient intake of American children. Pediatrics 100:E4. Pfeuffer M, Ahrens F, Hagemeister H, Barth CA. 1988. Influence of casein versus soy protein isolate on lipid metabolism of minipigs. Ann Nutr Metab 32:83–89. Phillips RL. 1975. Role of life-style and dietary habits in risk of cancer among Seventh-Day Adventists. Cancer Res 35:3513–3522. Pietinen P, Ascherio A, Korhonen P, Hartman AM, Willett WC, Albanes D, Virtamo J. 1997. Intake of fatty acids and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Epidemiol 145:876–887. Poppitt SD, Swann DL. 1998. Dietary manipulation and energy compensation: Does the intermittent use of low-fat items in the diet reduce total energy intake in free-feeding lean men? Int J Obes Relat Metab Disord 22:1024–1031. Poppitt SD, Swann DL, Murgatroyd PR, Elia M, McDevitt RM, Prentice AM. 1998. Effect of dietary manipulation on substrate flux and energy balance in obese women taking the appetite suppressant dexfenfluramine. A m J Clin Nutr 68:1012–1021. Popp-Snijders C, Schouten JA, Heine RJ, van der Meer J, van der Veen EA. 1987. Dietary supplementation of omega-3 polyunsaturated fatty acids improves insulin sensitivity in non-insulin-dependent diabetes. Diabetes Res 4:141–147. Porrini M, Crovetti R, Riso P, Santangelo A, Testolin G. 1995. Effects of physical and chemical characteristics of food on specific and general satiety. Physiol Behav 57:461–468. Prentice AM. 2001. Overeating: The health risks. Obes Res 9:234S–238S. Price JM, Grinker J. 1973. Effects of degree of obesity, food deprivation, and palatability on eating behavior of humans. J Comp Physiol Psychol 85:265–271.

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870 DIETARY REFERENCE INTAKES Promislow JHE, Goodman-Gruen D, Slymen DJ, Barrett-Conner E. 2002. Protein consumption and bone mineral density in the elderly. The Rancho Bernardo Study. Am J Epidemiol 155:636–644. Proserpi C, Sparti A, Schutz Y, Di Vetta V, Milon H, Jéquier E. 1997. Ad libitum intake of a high-carbohydrate or high-fat diet in young men: Effects on nutri- ent balances. Am J Clin Nutr 66:539–545. Raben A, Macdonald I, Astrup A. 1997. Replacement of dietary fat by sucrose or starch: Effects on 14 d ad libitum energy intake, energy expenditure and body weight in formerly obese and never-obese subjects. Int J Obes Relat Metab Disord 21:846–859. Ramon JM, Bou R, Romea S, Alkiza ME, Jacas M, Ribes J, Oromi J. 2000. Dietary fat intake and prostate cancer risk: A case-control study in Spain. Cancer Causes Control 11:679–685. Rath R, Masek J, Kujalová V, Slabochová Z. 1974. Effect of a high sugar intake on s some metabolic and regulatory indicators in young men. Nahrung 18:343–353. Reaven GM. 1988. Banting lecture 1988. Role of insulin resistance in human dis- ease. Diabetes 37:1595–1607. Reaven GM. 1995. Pathophysiology of insulin resistance in human disease. Physiol Rev 75:473–486. Reaven GM. 2001. Insulin resistance, compensatory hyperinsulinemia, and coro- nary heart disease: Syndrome X revisited. In: Jefferson LS, Cherrington AD, Goodman HM, eds. Handbook of Physiology. Section 7: The Endocrine System. Vol- ume II: The Endocrine Pancreas and Regulation of Metabolism. Oxford: Oxford University Press. Pp. 1169–1197. Reaven P, Parthasarathy S, Grasse BJ, Miller E, Almazan F, Mattson FH, Khoo JC, Steinberg D, Witztum JL. 1991. Feasibility of using an oleate-rich diet to reduce the susceptibility of low-density lipoprotein to oxidative modification in humans. Am J Clin Nutr 54:701–706. Reaven P, Parthasarathy S, Grasse BJ, Miller E, Steinberg D, Witztum JL. 1993. Effects of oleate-rich and linoleate-rich diets on the susceptibility of low density lipoprotein to oxidative modification in mildly hypercholesterolemic subjects. J Clin Invest 91:668–676. Reaven PD, Grasse BJ, Tribble DL. 1994. Effects of linoleate-enriched and oleate- enriched diets in combination with alpha-tocopherol on the susceptibility of LDL and LDL subfractions to oxidative modification in humans. Arterioscler Thromb 14:557–566. Reddy BS. 1992. Dietary fat and colon cancer: Animal model studies. L ipids 27:807–813. Reddy BS, Burill C, Rigotty J. 1991. Effect of diets high in ω-3 and ω -6 fatty acids on initiation and postinitiation stages of colon carcinogenesis. Cancer Res 51:487–491. Reiser S, Handler HB, Gardner LB, Hallfrisch JG, Michaelis OE, Prather ES. 1979. Isocaloric exchange of dietary starch and sucrose in humans. II. Effect on fasting blood insulin, glucose, and glucagon and on insulin and glucose response to a sucrose load. Am J Clin Nutr 32:2206–2216. Rémésy C, Behr SR, Levrat M-A, Demigné C. 1992. Fiber fermentability in the rat cecum and its physiological consequences. Nutr Res 12:1235–1244. Renaud S, de Lorgeril M, Delaye J, Guidollet J, Jacquard F, Mamelle N, Martin JL, Monjaud I, Salen P, Toubol P. 1995. Creten Mediterranean diet for preven- tion of coronary heart disease. Am J Clin Nutr 61:1360S–1367S.

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