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11
Macronutrients and Healthful Diets
SUMMARY
Acceptable Macronutrient Distribution Ranges (AMDRs) for individuals have been set for carbohydrate, fat, n-6 and n-3 polyunsaturated 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 diseases, 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 coronary 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 carbohydrate 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.
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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 individuals in the United States and Canada. A growing body of literature 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 protein) 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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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 content 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 programs 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 macronutrients (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 epidemiological studies of clinical endpoints such as coronary heart disease (CHD), diabetes, cancer, and obesity. However, these studies demonstrate associations; 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, factors other than diet contribute to chronic disease, and multifactorial cau-
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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 macronutrients 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 Macronutrient Distribution Ranges (AMDRs) are estimated and represented as percent of energy intake. These ranges represent (1) intakes that are associated 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 relationship 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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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 populations 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 contributed to a historically small stature in these populations is uncertain.
An issue of more importance for well-nourished but sedentary populations, 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 conducted 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 Individuals
Reference
Study Design
Dietary Fat (% of energy)
Weight Change (kg)
Comments
Short-term studies (< 1 year)
Boyar et al., 1988
19 women
6-mo intervention
Ad libitum diet
34 → 21%
−5.1
Decreased fat intake associated with decreased energy intake
Buzzard et al., 1990
29 postmenopausal women
3-mo parallel
Ad libitum diet
38 → 23%
39 → 35%
−2.8
−1.3
Decreased fat intake associated with decreased energy intake
Bloemberg et al., 1991
80 men
26-wk parallel
Ad libitum diet
39 → 34%
38 → 37%
−0.94
+0.06
Kendall et al., 1991
13 women
11-wk crossover
20–25%
35–40%
−2.54
−1.26
Decreased fat intake associated with Controlled diet decreased energy intake
Low fat diet, hypocaloric
Leibel et al., 1992
13 men and women
15- to 56-d intervention
Controlled diet
0, 40, or 70%
No significant changes in body weight
Isocaloric diets
Westerterp et al., 1996
217 men and women
6-mo parallel
Ad libitum diet
35 → 33%
36 → 41%
+0.3
+1.1
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Raben et al., 1997
11 women
14-d crossover
Ad libitum
46 → 28%
−0.7
Decreased fat intake associated with decreased energy intake
Gerhard et al., 2000
22 women
4-wk crossover
Controlled diet
20%
40%
−1.1
−0.3
Low fat diet, hypocaloric
Saris et al., 2000
398 men and women
6-mo parallel
Ad libitum diet
36 → 26%
36 → 28%
36 → 37%
−0.9
−1.8
+0.8
Decreased fat intake associated with decreased energy intake
Long-term studies (≥ 1 year)
Lee-Han et al., 1988
57 women
1-y parallel
Ad libitum diet
36 → 23 → 26%
36 → 34 → 36%
6 mo
−1.16
−0.93
12 mo
+0.07
+0.62
Decreased fat intake associated with decreased energy intake
Boyd et al., 1990
206 women
1-y parallel
Ad libitum diet
37 → 21%
37 → 35%
−1.0
0
Sheppard et al., 1991
276 women
1- and 2-y parallel
Ad libitum diet
0 to 1 y
39 → 22%
39 → 37%
−3.0
−0.4
Decreased fat intake associated with decreased energy intake
1 y to 2 y
22 → 23%
+1.1
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Reference
Study Design
Dietary Fat (% of energy)
Weight Change (kg)
Comments
Baer, 1993
70 men
1-y parallel
Ad libitum diet
38 → 31%
37 → 36%
−5.0
+1.0
Decreased fat intake associated with decreased energy intake
Kasim et al., 1993
72 women
1-y parallel
Ad libitum diet
36 → 18%
36 → 34 %
−3.4
−0.8
Decreased fat intake associated with decreased energy intake
Black et al., 1994
76 men and women
2-y parallel
Ad libitum diet
40 → 21%
39 → 39%
−2.0
−1.0
Knopp et al., 1997
137 men
1-y parallel
Ad libitum diet
36 → 27%
35 → 22%
−2.9
−2.9
Stefanick et al., 1998
177 postmenopausal women and 190 men
1-y parallel
Ad libitum diet
Women
23%
28%
Men
22%
30%
Women
−2.7
+0.8
Men
−2.8
+0.5
Decreased fat intake associated with decreased energy intake
Kasim-Karakas et al., 2000
54 postmenopausal women
1-y intervention
Controlled diet 4 mo
Ad libitum diet 8 mo
34 → 14 → 12%
4 mo
−1.3
12 mo
−5.9
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energy consumed as fat (greater than 4 percent) resulted in small losses in body weight. The only study that provided isocaloric diets showed no differences 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 compared 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 overweight 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 underlying 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 phenotype (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 minimally expressed. In sedentary populations that tend to be overweight or obese, very low fat, high carbohydrate diets clearly promote the development 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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TABLE 11-2 Fat and Carbohydrate Intake and Blood Lipid Concentrations in Healthy Individuals
Reference
Study Designa
Total Fat/Carbohydrate Intake (% of energy)
Coulston et al., 1983
11 men and women
10-d crossover
P/S = 1.2–1.3
21
41
Bowman et al., 1988
19 men
10-wk parallel
P/S = 0.4
29/60
33/58
45/42
46/42
Borkman et al., 1991
8 men and women
3-wk crossover
20/55 P/S = 0.46
50/31 P/S = 0.22
Kasim et al., 1993
72 women
1-y parallel
P/S = 0.68–0.75
18
34
Leclerc et al., 1993
7 men and women
7-d crossover
11/64
30/45
40/45
Krauss and Dreon, 1995
105 men
6-wk crossover
P/S = 0.69–0.74
24/60
46/39
O’Hanesian et al., 1996
10 men and women
10-d crossover
17/63 P/S = 0.25
28/57 P/S = 2.2
42/39 P/S = 1.7
Jeppesen et al., 1997
10 postmenopausal women
3-wk crossover
P/S = 1.0
25/60
45/40
Kasim-Karakas et al., 1997
14 postmenopausal women
4-mo intervention
14 P/S = 1.2
23 P/S = 1.0
31 P/S = 0.9
Yost et al., 1998
25 men and women
15-d crossover
P/S = 0.3
25/55
50/30
Straznicky et al., 1999
14 men
2-wk crossover
25/54 P/S = 1.3
47/36 P/S = 0.1
Kasim-Karakas et al., 2000
54 postmenopausal women
4- to 12-mo crossover
P/S = 0.64
12/71
14/69
34/50
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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
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Representative terms from entire chapter:
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