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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.
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-
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.
MACRONUTRIENTS AND HEALTHFUL DIETS 773
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
775
Raben et al.,
11 women
Decreased fat intake
14-d crossover
associated with
Ad libitum
decreased energy intake
Gerhard et al.,
22 women
Low fat diet, hypocaloric
4-wk crossover
Controlled diet
Saris et al.,
398 men and women
Decreased fat intake
6-mo parallel
associated with
Ad libitum diet
decreased energy intake
Long-term studies (
1 year)
Lee-Han et al.,
57 women
6 mo
12 mo
Decreased fat intake
1-y parallel
associated with
Ad libitum diet
decreased energy intake
Boyd et al.,
206 women
1-y parallel
Ad libitum diet
Sheppard et al.,
276 women
0 to 1 y
Decreased fat intake
1- and 2-y parallel
associated with
Ad libitum diet
decreased energy intake
1 y to 2 y 22
continued
776
Baer, 1993
70 men
Decreased fat intake
1-y parallel
associated with
Ad libitum diet
decreased energy intake
Kasim et al.,
72 women
Decreased fat intake
1-y parallel
associated with
Ad libitum diet
decreased energy intake
Black et al.,
76 men and women
2-y parallel
Ad libitum diet
Knopp et al.,
137 men
1-y parallel
Ad libitum diet
Stefanick
177 postmenopausal
Women
Men
Women
Men
Decreased fat intake
et al., 1998
women and 190 men
associated with
1-y parallel
decreased energy intake
Ad libitum diet
Kasim-Karakas
54 postmenopausal
4 mo
12 mo
et al., 2000
women
1-y interventionControlled diet 4 moAd libitum diet 8 mo
TABLE 11-
Continued
Dietary Fat
Weight Change
Reference
Study Design
(% of energy)
(kg)
Comments
778 DIETARY REFERENCE INTAKES
TABLE 11-2 Fat and Carbohydrate Intake and Blood Lipid Concentrations in Healthy Individuals Total Fat/ Carbohydrate Intake Reference Study Design a^ (% of energy)
- 1983 10-d crossover Coulston et al., 11 men and women
- Bowman et al., 19 men 29/
- Borkman et al., 8 men and women 20/55 P/S = 0.
- 1991 3-wk crossover 50/31 P/S = 0.
- Kasim et al., 72 women
- Leclerc et al., 7 men and women 11/
- 1993 7-d crossover 30/ - 40/
- Krauss and 105 men 24/
- Dreon, 1995 6-wk crossover 46/
- O’Hanesian 10 men and women 17/63 P/S = 0.
- et al., 1996 10-d crossover 28/57 P/S = 2. - 42/39 P/S = 1.
- Jeppesen et al., 10 postmenopausal 25/
- Kasim-Karakas 14 postmenopausal 14 P/S = 1.
- et al., 1997 women 23 P/S = 1.
- 4-mo intervention 31 P/S = 0.
- Yost et al., 25 men and women 25/
- Straznicky 14 men 25/54 P/S = 1.
- et al., 1999 2-wk crossover 47/36 P/S = 0.
- Kasim-Karakas 54 postmenopausal 12/
- et al., 2000 women 14/
- 4- to 12-mo 34/
- P/S = 0. crossover
MACRONUTRIENTS AND HEALTHFUL DIETS 779
continued
Postintervention Blood Lipid Concentration (mmol/L) b
Triacylglycerol HDL-C LDL-C
1.51 c^ 0.98 c 1.02 d^ 1.16 d
0.91 c^ 1.42 c^ 2.35 c 1.11 c^ 1.22 c^ 2.17 c 0.84 c^ 1.53 c^ 2.59 c 1.01 c^ 1.50 c^ 2.40 c
0.82 c^ (+49%) 0.84 c^ (–24%) 2.88 c^ (–20%) 0.55 c^ 1.10 d^ 3.60 d
1.35 c^ 1.44 c^ (–8%) 2.79 c^ (–10%) 1.25 d^ 1.56 d^ 3.09 d
1.11 c^ 1.03 c^ 2.29 c 1.29 c^ 1.15 d^ 2.47 c 0.87 d^ 1.32 e^ 3.05 d
1.59 c^ 1.09 c^ 3.26 c 1.13 d^ 1.27 d^ 3.69 d
1.97 c^ 1.38 c^ 2.74 c 1.29 d^ 1.49 d^ 2.81 c
2.47 c^ 1.24 c^ 2.61 c 2.10 d^ 1.32 d^ 2.93 d 1.85 e^ 1.34 d^ 2.89 d
1.14 c^ 1.22 c 0.88 d^ 1.30 d
0.8 c^ 1.05 c^ 2.6 c 0.8 c^ 1.28 d^ 3.5 d
1.49 c^ 1.40 c^ 3.49 c 2.00 c^ 1.29 c^ 3.18 c 1.57 c^ 1.53 d^ 3.57 c
MACRONUTRIENTS AND HEALTHFUL DIETS 781
c,d,e (^) Within each study, LDL-C, HDL-C, or Lp(a) concentrations that are significantly
different between treatment groups have a different superscript.
Proportion of Energy Derived from Carbohydrates (%)
Serum HDL CholesterolConcentration (mmol/L)
mg/dL
FIGURE 11-2 Relationship between proportion of energy from carbohydrates and serum high density lipoprotein (HDL) cholesterol concentration. • = Mean values for approximately 120 boys from five countries, o = individuals values for boys from the Philippines, FI= Finland, NE = Netherlands, GH = Ghana, IT = Italy, PH = Philippines. SOURCE: Knuiman et al. (1987).
Postintervention Blood Lipid Concentration (mmol/L) b
Triacylglycerol HDL-C LDL-C
0.81 c^ 1.34 c^ 2.43 c 0.70 d^ 1.56 d^ 2.71 d
+0.4 –0.09 –0. –0.09 –0.005 –0.
782 DIETARY REFERENCE INTAKES
increase and plasma HDL cholesterol concentrations decrease. The reduc-
tion in HDL cholesterol concentration with low fat intake results in a rise
in the total:HDL cholesterol concentration ratio (Figure 11-3). The total:HDL
cholesterol ratio has been shown to be an important risk factor for CHD
(Castelli et al., 1992; Kannel, 2000). Whether diet-induced changes in the
total:HDL cholesterol ratio predispose to CHD remains unclear (Brussard
et al., 1982; Jeppesen et al., 1997; Krauss and Dreon, 1995; West et al.,
1990; Yost et al., 1998).
In support of the interventional studies, carbohydrate intake is nega-
tively associated with HDL cholesterol concentrations (Table 11-3). None-
theless, the association between atherogenic lipoprotein phenotype (higher
y = 0.578x + 14.
R
2 = 0.
0
5
10
15
20
25
(^10 15 20 25 30 35 40 45 50 )
Dietary Total Fat (% energy)
Percent Changes in TC:HDL-C Ratios
FIGURE 11-3 Relationship between total fat intake and change in total cholester- ol (TC):high density lipoprotein (HDL) cholesterol ratio. Weighted least-squares regression analyses were performed using the mixed procedure to test for differ- ences in lipid concentrations (SAS Statistical package, version 8.00, SAS Institute, Inc., 1999). DATA SOURCES: Berry et al. (1992); Curb et al. (2000); Garg et al. (1988, 1992a, 1994); Ginsberg et al. (1990); Grundy (1986); Grundy et al. (1988); Jansen et al. (1998); Kris-Etherton et al. (1999); Lefevre et al., unpublished; Lopez-Segura et al. (1996); Mensink and Katan (1987); Nelson et al. (1995); Parillo et al. (1992); Pelkman et al. (2001); Perez-Jimenez et al. (1995, 1999, 2001).
784 DIETARY REFERENCE INTAKES
total:HDL cholesterol ratios) and CHD risk provides one rationale for
establishing a lower boundary for the Acceptable Macronutrient Distribu-
tion Range (AMDR) for high-risk populations.
Risk of Hyperinsulinemia, Glucose Intolerance, and Type 2 Diabetes
Other potential abnormalities accompanying changes in distribution
of fat and carbohydrate intakes include increased postprandial responses
in plasma glucose and insulin concentrations. These abnormalities are
more likely to occur with low fat, high carbohydrate diets. They potentially
could be related to the development of both type 2 diabetes and CHD. In
particular, repeated daily elevations in postprandial glucose and insulin
concentrations could “exhaust” pancreatic β-cells of insulin supply, which
could hasten the onset of type 2 diabetes. Some investigators have further
suggested these repeated elevations could worsen baseline insulin sensitivity,
which could cause susceptible persons to be at increased risk for type 2
diabetes. This form of diabetes, defined by an elevation of fasting serum
glucose concentration, is characterized by two defects in glucose metabolism:
insulin resistance, a defect in insulin-mediated uptake of glucose by cells,
particularly skeletal muscle cells, and a decline in insulin secretory capacity
by pancreatic β-cells (Turner and Clapham, 1998). Insulin resistance typi-
cally precedes the development of type 2 diabetes by many years. It is
known to be the result of obesity, physical inactivity, and genetic factors
(Turner and Clapham, 1998). Before the onset of diabetic hyperglycemia,
the pancreatic β-cells are able to respond to insulin resistance with an
increased insulin secretion, enough to maintain normoglycemia. However,
in some persons who are insulin resistant, insulin secretory capacity declines
and hyperglycemia ensues (Reaven, 1988, 1995).
The mechanisms for the decline in insulin secretion are not well
understood, but one theory is that continuous overstimulation of insulin
secretion by the presence of insulin resistance leads to “insulin exhaustion”
and hence to decreased insulin secretory capacity (Turner and Clapham,
1998). Whether insulin exhaustion is secondary to a metabolic dysfunction
of cellular production of insulin or to a loss of β-cells is uncertain. The
accumulation of pancreatic islet-cell amyloidosis may be one mechanism
for loss of insulin-secretory capacity (Höppener et al., 2000).
High carbohydrate diets frequently causes greater insulin and plasma
glucose responses than do low carbohydrate diets (Chen et al., 1988;
Coulston et al., 1987). These excessive responses theoretically could pre-
dispose individuals to the development of type 2 diabetes because of pro-
longed overstimulation of insulin secretion (Grill and Björklund, 2001).
The reasoning is similar to that for insulin resistance, namely, excessive
stimulation of insulin secretion over a period of many years could result in
MACRONUTRIENTS AND HEALTHFUL DIETS 785
insulin exhaustion, and hence to hyperglycemia (Turner and Clapham,
1998). This mechanism, although plausible, remains hypothetical. None-
theless, in the mind of some investigators, it deserves serious consideration.
Other consequences of hyperglycemic responses to high carbohydrate
diets might be considered. For example, higher postprandial glucose
responses might lead to other changes such as “desensitization” of β-cells
for insulin secretion and production of glycated products or advanced
glycation end-products, which could either promote atherogenesis or the
“aging” process (Lopes-Virella and Virella, 1996). Again, these are hypo-
thetical consequences that need further examination.
Epidemiological Evidence. A number of noninterventional, epidemio-
logical studies have shown no relationship between carbohydrate intake
and risk of diabetes (Colditz et al., 1992; Lundgren et al., 1989; Marshall et
al., 1991; Meyer et al., 2000; Salmerón et al., 1997), whereas other studies
have shown a positive association (Bennett et al., 1984; Feskens et al.,
1991a).
Interventional Evidence. Interventional studies in healthy individuals on
the influence of high carbohydrate diets on biomarker precursors for type
2 diabetes are lacking and the available data are mixed (Table 11-4) (Beck-
Nielsen et al., 1980; Chen et al., 1988; Dunnigan et al., 1970; Fukagawa et
al., 1990; Rath et al., 1974; Reiser et al., 1979). Factors such as carbo-
hydrate quality, body weight, exercise, and genetics make the interpretation
of such findings difficult. Nonetheless, in overweight and sedentary groups
(which carry a heavy burden of insulin resistance and are common in
North America), the accentuation of postprandial glucose and insulin
concentrations that accompany high carbohydrate diets are factors to con-
sider when setting an upper boundary for AMDRs for dietary carbohydrate
(and a lower boundary for dietary fat).
Risk of Nutrient Inadequacy or Excess
Diets Low in Fats. For usual diets that are low in total fat, the intake of
essential fatty acids, such as n -6 polyunsaturated fatty acids, will be low
(Appendix K). In general, with increasing intakes of carbohydrate and
decreasing intakes of fat, the intake of n -6 polyunsaturated fatty acids
decreases. Furthermore, low intakes of fat are associated with low intakes
of zinc and certain B vitamins.
The digestion and absorption of fat-soluble vitamins and provitamin A
carotenoids are associated with fat absorption. Jayarajan and coworkers
(1980) reported that the addition of 5 or 10 g of fat to a low fat (5 g) diet
MACRONUTRIENTS AND HEALTHFUL DIETS 787
Results
No diet effect on glucose tolerance and plasma insulin
Serum insulin (μg/mL) Serum glucose (mg/dL) 5.4 a^ 87.0 a 11.8 b^ 81.1 b
Serum insulin (μmunits/mL) Serum glucose (mg/dL) 9.8 a^ 92.5 a 11.9 b^ 94.5 a
No significant difference in insulin concentrations The high fructose diet was accompanied by a significant reduction in insulin binding and insulin sensitivity
Glucose disappearance Insulin sensitivity index (%/min) 5.6 a^ 2.2 a 6.1 b^ 2.3 b 3.9 a,c^ 1.6 a,c
5.6 a^ 2.2 a 6.1 b^ 2.3 b 3.9 a,c^ 1.6 a,c
Carbohydrate intake of women who developed diabetes (212 g/d) was not significantly different than women who did not develop diabetes (228 g/d)
Glucose disposal Serum insulin (pmol/L) (μmol/kg/min) 67.4 a^ 21.2 a 50.2 b^ 27.8 b
788 DIETARY REFERENCE INTAKES
significantly improved serum vitamin A concentrations. However, the addi-
tion of 10 g compared to 5 g did not provide any further benefit. The level
of dietary fat has also been shown to improve vitamin K 2 bioavailability
(Uematsu et al., 1996). Dose–response data are limited on the amount of
dietary fat needed to achieve the optimal absorption of fat-soluble vitamins,
but it appears that the level is quite low.
Diets High in Fiber. Most diets that are high in fiber are also high in
carbohydrate. High fiber diets have the potential for reduced energy
density, reduced energy intake, and poor growth. However, poor growth is
unlikely in the United States where most children consume adequate
energy and fiber intake is relatively low (Williams and Bollella, 1995). Miles
(1992) tested the effects of daily ingestion of 64 g or 34 g of Dietary Fiber for
10 weeks in healthy adult males. The ingestion of 64 g/d of Dietary Fiber
resulted in a reduction in protein utilization from 89.4 to 83.7 percent and
in fat utilization from 95.5 to 92.5 percent. Total energy utilization
decreased from 94.3 to 91.4 percent. Because most individuals consuming
high amounts of fiber would also be consuming high amounts of energy,
the slight depression in energy utilization is not significant (Miles, 1992).
In other studies, ingestion of high amounts of fruit, vegetable, and cereal
fiber (48.3 to 85.6 g/d) also resulted in decreases in apparent digestibilities
of energy, crude protein, and fat (Göranzon et al., 1983; Wisker et al.,
1988). Again, however, the Dietary Fiber intakes were very high, and because
the recommendation for Total Fiber intake is related to energy intake, the
high fiber consumers would also be high energy consumers.
Diets High in Added Sugars. Increased consumption of added sugars
can result in decreased intakes of certain micronutrients (Table 11-5).
This can occur because of the abundance of added sugars in energy-dense,
nutrient-poor foods, whereas naturally occurring sugars are primarily
found in fruits, milk, and dairy products that also contain essential micro-
nutrients. Because some micronutrients (e.g., vitamin B 6 , vitamin C, and
folate), dietary fiber, and phytochemicals were not examined, the association
between these nutrients and added sugars intakes is not known. Bowman
(1999) used data from Continuing Survey of Food Intakes of Individuals
(CSFII) (1994–1996) to assess the relationship between added sugars and
intakes of essential nutrients in Americans’ diets. The sample ( n = 14,704)
was divided into three groups based on the percentage of energy consumed
from added sugars: (1) less than 10 percent of total energy ( n = 5,058),
(2) 10 to 18 percent of total energy ( n = 4,488), and (3) greater than
18 percent of total energy ( n = 5,158). Group 3, with a mean of 26.7 percent
of energy from added sugars, had the lowest absolute mean intakes of all
