Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 769
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
OCR for page 770
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-
OCR for page 771
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-
OCR for page 772
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.
OCR for page 773
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
OCR for page 774
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
OCR for page 775
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
OCR for page 776
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
OCR for page 777
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
OCR for page 778
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
OCR for page 779
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
OCR for page 869
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.
OCR for page 870
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.
OCR for page 871
871
M ACRONUTRIENTS AND HEALTHFUL DIETS
Ricketts CD. 1997. Fat preferences, dietary fat intake and body composition in
children. Eur J Clin Nutr 51:778–781.
Rissanen AM, Heliövaara M, Knekt P, Reunanen A, Aromaa A. 1991. Determinants
of weight gain and overweight in adult Finns. Eur J Clin Nutr 45:419–430.
Robertson WG, Peacock M. 1982. The pattern of urinary stone disease in Leeds
and in the United Kingdom in relation to animal protein intake during the
period 1960–1980. Urol Int 37:394–399.
Robertson WG, Heyburn PJ, Peacock M, Hanes FA, Swaminathan R. 1979. The
effect of high animal protein intake on the risk of calcium stone-formation in
the urinary tract. Clin Sci 57:285–288.
Roche HM, Zampelas A, Jackson KG, Williams CM, Gibney MJ. 1998. The effect of
test meal monounsaturated fatty acid:saturated fatty acid ratio on postprandial
lipid metabolism. Br J Nutr 79:419–424.
Rodier M, Colette C, Crastes de Paulet P, Crastes de Paulet A, Monnier L. 1993.
Relationships between serum lipids, platelet membrane fatty acid composition
and platelet aggregation in type 2 diabetes mellitus. Diabete Metab 19:560–565.
Rolland-Cachera MF, Deheeger M, Akrout M, Bellisle F. 1995. Influence of macro-
nutrients on adiposity development: A follow up study of nutrition and growth
from 10 months to 8 years of age. Int J Obes Relat Metab Disord 19:573–578.
Rolls BJ, Hetherington M, Burley VJ. 1988. The specificity of satiety: The influence
of foods of different macronutrient content on the development of satiety.
Physiol Behav 43:145–153.
Rolls BJ, Laster LJ, Summerfelt A. 1989. Hunger and food intake following con-
sumption of low-calorie foods. Appetite 13:115–127.
Rolls BJ, Kim-Harris S, Fischman MW, Foltin RW, Moran TH, Stoner SA. 1994.
Satiety after preloads with different amounts of fat and carbohydrate: Implica-
tions for obesity. Am J Clin Nutr 60:476–487.
Romieu I, Willett WC, Stampfer MJ, Colditz GA, Sampson L, Rosner B, Hennekens
CH, Speizer FE. 1988. Energy intake and other determinants of relative weight.
Am J Clin Nutr 47:406–412.
Rose DP, Connolly JM. 2000. Regulation of tumor angiogenesis by dietary fatty
acids and eicosanoids. Nutr Cancer 37:119–127.
Rugg-Gunn AJ, Hackett AF, Jenkins GN, Appleton DR. 1991. Empty calories?
Nutrient intake in relation to sugar intake in English adolescents. J Hum Nutr
Diet 4:101–111.
Rush D, Stein Z, Susser M. 1980. A randomized controlled trial of prenatal nutri-
tion supplementation in New York City. Pediatrics 65:683–697.
Rustan AC, Hustvedt B-E, Drevon CA. 1993. Dietary supplementation of very long-
chain n-3 fatty acids decreases whole body lipid utilization in the rat. J Lipid Res
34:1299–1309.
Salmerón J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC. 1997.
Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes
mellitus in women. J Am Med Assoc 277:472–477.
Salmerón J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB, Willett WC.
2001. Dietary fat intake and risk of type 2 diabetes in women. Am J Clin Nutr
73:1019–1026.
Salomon O, Steinberg DM, Zivelin A, Gitel S, Dardik R, Rosenberg N, Berliner S,
Inbal A, Many A, Lubetsky A, Varon D, Martinowitz U, Seligsohn U. 1999.
Single and combined prothrombic factors in patients with idiopathic venous
thromboembolism. Prevalence and risk assessment. Arterioscler Thromb Vasc Biol
19:511–518.
OCR for page 872
872 DIETARY REFERENCE INTAKES
Saltzman E, Dallal GE, Roberts SB. 1997. Effect of high-fat and low-fat diets on
voluntary energy intake and substrate oxidation: Studies in identical twins
consuming diets matched for energy density, fiber, and palatability. Am J Clin
Nutr 66:1332–1339.
Samaras K, Kelly PJ, Chiano MN, Arden N, Spector TD, Campbell LV. 1998. Genes
versus environment. The relationship between dietary fat and total and central
abdominal fat. Diabetes Care 21:2069–2076.
Sanders TAB, Hinds A. 1992. The influence of a fish oil high in docosahexaenoic
acid on plasma lipoprotein and vitamin E concentrations and haemostatic
function in healthy male volunteers. Br J Nutr 68:163–173.
Sanders TAB, Oakley FR, Miller GJ, Mitropoulos KA, Crook D, Oliver MF. 1997.
Influence of n-6 versus n-3 polyunsaturated fatty acids in diets low in saturated
fatty acids on plasma lipoproteins and hemostatic factors. Arterioscler Thromb
Vasc Biol 17:3449–3460.
Saris WHM, Astrup A, Prentice AM, Zunft HJF, Formiguera X, Verboeket-van de
Venne WPHG, Raben A, Poppitt SD, Seppelt B, Johnston S, Vasilaras TH, Keogh
GF. 2000. Randomized controlled trial of changes in dietary carbohydrate/fat
ratio and simple vs complex carbohydrates on body weight and blood lipids:
The CARMEN study. Int J Obes Relat Metab Disord 24:1310–1318.
Sasaki S, Horacsek M, Kesteloot H. 1993. An ecological study of the relationship
between dietary fat intake and breast cancer mortality. Prev Med 22:187–202.
Sawaya AL, Fuss PJ, Dallal GE, Tsay R, McCrory MA, Young V, Roberts SB. 2001.
Meal palatability, substrate oxidation and blood glucose in young and older
men. Physiol Behav 72:5–12.
Saynor R, Gillott T. 1992. Changes in blood lipids and fibrinogen with a note on
safety in a long term study on the effects of n-3 fatty acids in subjects receiving
fish oil supplements and followed for seven years. Lipids 27:533–538.
Schmidt EB, Lervang H-H, Varming K, Madsen P, Dyerberg J. 1992. Long-term
supplementation with n-3 fatty acids. I: Effect on blood lipids, haemostasis and
blood pressure. Scand J Clin Lab Invest 52:221–228.
Schønberg S, Krokan HE. 1995. The inhibitory effect of conjugated dienoic
derivates (CLA) of linoleic acid on the growth of human tumor cell lines is in
part due to increased lipid peroxidation. Anticancer Res 15:1241–1246.
Schuurman AG, van den Brandt PA, Dorant E, Brants HAM, Goldbohm RA. 1999.
Association of energy and fat intake with prostate carcinoma risk. Results from
the Netherlands Cohort Study. Cancer 86:1019–1027.
Seagle HM, Davy BM, Grunwald G, Hill JO. 1997. Energy density of self-reported
food intake: Variation and relationship to other food components. Obes Res
5:78S.
Serdula MK, Ivery D, Coates RJ, Freedman DS, Williamson DF, Byers TE. 1993. Do
obese children become obese adults? A review of the literature. Prev Med
22:167–177.
Severson RK, Nomura AMY, Grove JS, Stemmermann GN. 1989. A prospective
study of demographics, diet, and prostate cancer among men of Japanese
ancestry in Hawaii. Cancer Res 49:1857–1860.
Shannon BM, Tershakovec AM, Martel JK, Achterberg CL, Cortner JA, Smiciklas-
Wright HS, Stallings VA, Stolley PD. 1994. Reduction of elevated LDL-
cholesterol levels of 4- to 10-year-old children through home-based dietary
education. Pediatrics 94:923–927.
OCR for page 873
873
M ACRONUTRIENTS AND HEALTHFUL DIETS
Shea S, Basch CE, Stein AD, Contento IR, Irigoyen M, Zybert P. 1993. Is there a
relationship between dietary fat and stature or growth in children three to five
years of age? Pediatrics 92:579–586.
Sheppard L, Kristal AR, Kushi LH. 1991. Weight loss in women participating in a
randomized trial of low-fat diets. Am J Clin Nutr 54:821–828.
Shetty PS, Prentice AM, Goldberg GR, Murgatroyd PR, McKenna APM, Stubbs RJ,
Volschenk PA. 1994. Alterations in fuel selection and voluntary food intake in
response to isoenergetic manipulation of glycogen stores in humans. Am J Clin
Nutr 60:534–543.
Shide DJ, Rolls BJ. 1995. Information about the fat content of preloads influences
energy intake in healthy women. J Am Diet Assoc 95:993–998.
Shu XO, Zheng W, Potischman N, Brinton LA, Hatch MC, Gao YT, Fraumeni JF.
1993. A population-based case-control study of dietary factors and endometrial
cancer in Shanghai, People’s Republic of China. Am J Epidemiol 137:155–165.
Shultz TD, Leklem JE. 1983. Dietary status of Seventh-day Adventists and non-
vegetarians. J Am Diet Assoc 83:27–33.
Shultz TD, Chew BP, Seaman WR, Luedecke LO. 1992. Inhibitory effect of conju-
gated dienoic derivates of linoleic acid and β-carotene on the in vitro growth
of human cancer cells. Cancer Lett 63:125–133.
Sierakowski R, Finlayson B, Landes RR, Finlayson CD, Sierakowski N. 1978. The
frequency of urolithiasis in hospital discharge diagnoses in the United States.
Invest Urol 15:438–441.
Simell O, Niinikoski H, Rönnemaa T, Lapinleimu H, Routi T, Lagström H, Salo P,
Jokinen E, Viikari J. 2000. Special Turku Coronary Risk Factor Intervention
Project for Babies (STRIP). Am J Clin Nutr 72:1316S–1331S.
Singh RB, Rastogi SS, Verma R, Laxmi B, Singh R, Ghosh S, Niaz MA. 1992.
Randomised controlled trial of cardioprotective diet in patients with recent acute
myocardial infarction: Results of one year follow up. Br Med J 304:1015–1019.
Singh RB, Ghosh S, Niaz AM, Gupta S, Bishnoi I, Sharma JP, Agarwal P, Rastogi SS,
Beegum R, Chibo H. 1995. Epidemiologic study of diet and coronary risk
factors in relation to central obesity and insulin levels in rural and urban
populations of north India. Int J Cardiol 47:245–255.
Singh RB, Niaz MA, Sharma JP, Kumar R, Rastogi V, Moshiri M. 1997. Random-
ized, double-blind, placebo-controlled trial of fish oil and mustard oil in
patients with suspected acute myocardial infarction: The Indian Experiment
of Infarct Survival—4. Cardiovasc Drugs Ther 11:485–491.
Siscovick DS, Raghunathan TE, King I, Weinmann S, Wicklund KG, Albright J,
Bovbjerg V, Arbogast P, Smith H, Kushi LH, Cobb LA, Copass MK, Psaty BM,
Lemaitre R, Retzlaff B, Childs M, Knopp RH. 1995. Dietary intake and cell
membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of
primary cardiac arrest. J Am Med Assoc 274:1363–1367.
Skinner JD, Carruth BR, Moran J, Houck K, Coletta F. 1999. Fruit juice intake is
not related to children’s growth. Pediatrics 103:58–64.
Skov AR, Toubro S, Ronn B, Holm L, Astrup A. 1999. Randomized trial on protein
vs carbohydrate in ad libitum fat reduced diet for the treatment of obesity. Int
J Obes Relat Metab Disord 23:528–536.
Slattery ML, Potter JD, Sorenson AW. 1994. Age and risk factors for colon cancer
(United States and Australia): Are there implications for understanding dif-
ferences in case-control and cohort studies? Cancer Causes Control 5:557–563.
Slattery ML, Caan BJ, Potter JD, Berry TD, Coates A, Duncan D, Edwards SL. 1997.
Dietary energy sources and colon cancer risk. Am J Epidemiol 145:199–210.
OCR for page 874
874 DIETARY REFERENCE INTAKES
Sonko BJ, Prentice AM, Poppitt SD, Prentice A, Jequier E, Whitehead RG. 1994.
Could dietary fat intake be an important determinant of seasonal weight
changes in a rural subsistence farming community in The Gambia? In: Nestlé
Foundation for the Study of the Problems of Nutrition in the World. Annual Report
1994. Lausanne, Switzerland: Nestlé Foundation. Pp. 74–87.
Sonnenberg LM, Quatromoni PA, Gagnon DR, Cupples LA, Franz MM, Ordovas
JM, Wilson PWF, Schaefer EJ, Millen BE. 1996. Diet and plasma lipids in
women. II. Macronutrients and plasma triglycerides, high-density lipoprotein,
and the ratio of total to high-density lipoprotein cholesterol in women: The
Framingham Nutrition Studies. J Clin Epidemiol 49:665–672.
Stamler J. 1979. Population studies. In: Levy R, Rifkind B, Dennis B, Ernst N, eds.
Nutrition, Lipids, and Coronary Heart Disease. New York: Raven Press. Pp. 25–88.
Stangl GI. 2000. Conjugated linoleic acids exhibit a strong fat-to-lean partitioning
effect, reduce serum VLDL lipids and redistribute tissue lipids in food-
restricted rats. J Nutr 130:1140–1146.
Stary HC. 1989. Evolution and progression of atherosclerotic lesions in coronary
arteries of children and young adults. Arteriosclerosis 9:I19–I32.
Stefanick ML, Mackey S, Sheehan M, Ellsworth N, Haskell WL, Wood PD. 1998.
Effects of diet and exercise in men and postmenopausal women with low
levels of HDL cholesterol and high levels of LDL cholesterol. N Engl J Med
339:12–20.
Steinberg D, Parthawarathy S, Carew TE, Khoo JC, Witztum JL. 1989. Beyond choles-
terol. Modifications of low-density lipoprotein that increase its atherogenicity. N
Engl J Med 320:915–924.
Storlien LH, Kraegen EW, Chisholm DJ, Ford GL, Bruce DG, Pascoe WS. 1987.
Fish oil prevents insulin resistance induced by high-fat feeding. S cience
237:885–888.
Storlien LH, Jenkins AB, Chisholm DJ, Pascoe WS, Khouri S, Kraegen EW. 1991.
Influence of dietary fat composition on development of insulin resistance in
rats. Relationship to muscle triglyceride and ω-3 fatty acids in muscle phospho-
lipid. Diabetes 40:280–289.
Straznicky NE, O’Callaghan CJ, Barrington VE, Louis WJ. 1999. Hypotensive effect
of low-fat, high-carbohydrate diet can be independent of changes in plasma
insulin concentrations. Hypertension 34:580–585.
Strong JP, Malcom GT, Newman WP, Oalmann MC. 1992. Early lesions of athero-
sclerosis in childhood and youth: Natural history and risk factors. J Am Coll
Nutr 11:51S–54S.
Stubbs RJ, Harbron CG, Murgatroyd PR, Prentice AM. 1995a. Covert manipulation
of dietary fat and energy density: Effect on substrate flux and food intake in
men eating ad libitum. Am J Clin Nutr 62:316–329.
Stubbs RJ, Ritz P, Coward WA, Prentice AM. 1995b. Covert manipulation of the
ratio of dietary fat to carbohydrate and energy density: Effect on food intake and
energy balance in free-living men eating ad libitum. Am J Clin Nutr 62:330–337.
Stubbs RJ, Harbron CG, Prentice AM. 1996. Covert manipulation of the dietary fat
to carbohydrate ratio of isoenergetically dense diets: Effect on food intake in
feeding men ad libitum. Int J Obes Relat Metab Disord 20:651–660.
Sugano M, Tsujita A, Yamasaki M, Noguchi M, Yamada K. 1998. Conjugated linoleic
acid modulates tissue levels of chemical mediators and immunoglobulins in
rats. Lipids 33:521–527.
OCR for page 875
875
M ACRONUTRIENTS AND HEALTHFUL DIETS
Swinburn BA, Boyce VL, Bergman RN, Howard BV, Bogardus C. 1991. Deteriora-
tion in carbohydrate metabolism and lipoprotein changes induced by modern,
high fat diet in Pima Indians and Caucasians. J Clin Endocrinol Metab 73:156–165.
Swinburn BA, Metcalf PA, Ley SJ. 2001. Long-term (5-year) effects of a reduced-fat
diet intervention in individuals with glucose intolerance. D iabetes Care
24:619–624.
Takahashi M, Przetakiewicz M, Ong A, Borek C, Lowenstein JM. 1992. Effect of
omega 3 and omega 6 fatty acids on transformation of cultured cells by irra-
diation and transfection. Cancer Res 52:154–162.
Talamini R, Franceschi S, La Vecchia C, Serraino D, Barra S, Negri E. 1992. Diet
and prostatic cancer: A case-control study in Northern Italy. N utr Cancer
18:277–286.
Tao SC, Huang ZD, Wu XG, Zhou BF, Xiao ZK, Hao JS, Li YH, Cen RC, Rao XX.
1989. CHD and its risk factors in the People’s Republic of China. Int J Epidemiol
18:S159–S163.
Tate G, Mandell BF, Laposata M, Ohliger D, Baker DG, Schumacher HR, Zurier
RB. 1989. Suppression of acute and chronic inflammation by dietary gamma
linolenic acid. J Rheumatol 16:729–733.
Teixeira SR, Potter SM, Weigel R, Hannum S, Erdman JW, Hasler CM. 2000. Effects
of feeding 4 levels of soy protein for 3 and 6 wk on blood lipids and
apolipoproteins in moderately hypercholesterolemic men. A m J Clin Nutr
71:1077–1084.
Terpstra AHM, Holmes JC, Nicolosi RJ. 1991. The hypocholesterolemic effect of
dietary soybean protein vs. casein in hamsters fed cholesterol-free or cholesterol-
enriched semipurified diets. J Nutr 121:944–947.
Thomas CD, Peters JC, Reed GW, Abumrad NN, Sun M, Hill JO. 1992. Nutrient
balance and energy expenditure during ad libitum feeding of high-fat and
high-carbohydrate diets in humans. Am J Clin Nutr 55:934–942.
Thomsen C, Rasmussen O, Christiansen C, Pedersen E, Vesterlund M, Storm H,
Ingerslev J, Hermansen K. 1999. Comparison of the effects of a monounsaturated
fat diet and a high carbohydrate diet on cardiovascular risk factors in first
degree relatives to type-2 diabetic subjects. Eur J Clin Nutr 52:818–823.
Tillotson JL, Grandits GA, Bartsch GE, Stamler J. 1997. Relation of dietary carbo-
hydrates to blood lipids in the special intervention and usual care groups in
the Multiple Risk Factor Intervention Trial. Am J Clin Nutr 65:314S–326S.
Tobin J, Spector D. 1986. Dietary protein has no effect on future creatinine clear-
ance (Ccr). Gerontologist 26:59A.
Toft I, Bønaa KH, Ingebretsen OC, Nordøy A, Jenssen T. 1995. Effects of n-3
polyunsaturated fatty acids on glucose homeostasis and blood pressure in
essential hypertension. A randomized, controlled trial. A nn Intern Med
123:911–918.
Toniolo P, Riboli E, Shore RE, Pasternack BS. 1994. Consumption of meat, animal
products, protein, and fat and risk of breast cancer: A prospective cohort
study in New York. Epidemiology 5:391–397.
Tonstad S, Sivertsen M. 1997. Relation between dietary fat and energy and micro-
nutrient intakes. Arch Dis Child 76:416–420.
Torun B, Chew F. 1999. Protein-energy malnutrition. In: Shils ME, Olson JA, Shike
M, Ross AC, eds. Modern Nutrition in Health and Disease, 9th ed. Baltimore, MD:
Williams and Wilkins. Pp. 963–988.
Tremblay A, Plourde G, Despres J-P, Bouchard C. 1989. Impact of dietary fat con-
tent and fat oxidation on energy intake in humans. Am J Clin Nutr 49:799–805.
OCR for page 876
876 DIETARY REFERENCE INTAKES
Tremblay A, Lavallee N, Almeras N, Allard L, Despres J-P, Bouchard C. 1991.
Nutritional determinants of the increase in energy intake associated with a
high-fat diet. Am J Clin Nutr 53:1134–1137.
Tremblay MS, Willms JD. 2000. Secular trends in the body mass index of Canadian
children. Can Med Assoc J 163:1429–1433.
Tremoli E, Maderna P, Marangoni F, Colli S, Eligini S, Catalano I, Angeli MT,
Pazzucconi F, Gainfranceschi G, Davi G, Stragliotto E, Sirtori CR, Galli C.
1995. Prolonged inhibition of platelet aggregation after n-3 fatty acid ethyl
ester ingestion by healthy volunteers. Am J Clin Nutr 61:607–613.
Trevisan M, Krogh V, Freudenheim J, Blake A, Muti P, Panico S, Farinaro E,
Mancini M, Menotti A, Ricci G. 1990. Consumption of olive oil, butter, and
vegetable oils and coronary heart disease risk factors. The Research Group
ATS-RF2 of the Italian National Research Council. J Am Med Assoc 263:688–692.
Trichopoulou A, Katsouyanni K, Stuver S, Tzala L, Gnardellis C, Rimm E,
Trichopoulos D. 1995. Consumption of olive oil and specific food groups in
relation to breast cancer risk in Greece. J Natl Cancer Inst 87:110–116.
Trinidad TP, Wolever TMS, Thompson LU. 1993. Interactive effects of Ca and
SCFA on absorption in the distal colon of men. Nutr Res 13:417–425.
Trinidad TP, Wolever TMS, Thompson LU. 1996. Effect of acetate and propionate
on calcium absorption from the rectum and distal colon of humans. Am J Clin
Nutr 63:574–578.
Troiano RP, Flegal KM, Kuczmarski RJ, Campbell SM, Johnson CL. 1995. Over-
weight prevalence and trend for children and adolescents: The National
Health and Nutrition Examination Surveys, 1963 to 1991. Arch Pediatr Adolesc
Med 149:1085–1091.
Tsuboyama-Kasaoka N, Takahashi M, Tanemura K, Kim H-J, Tange T, Okuyama H,
Kasai M, Ikemoto S, Ezaki O. 2000. Conjugated linoleic acid supplementation
reduces adipose tissue by apoptosis and develops lipodystrophy in mice.
Diabetes 49:1534–1542.
Tucker LA, Kano MJ. 1992. Dietary fat and body fat: A multivariate study of 205
adult females. Am J Clin Nutr 56:616–622.
Tuomilehto J, Lindström J, Eriksson JG, Valle TT, Hämäläinen H, Ilanne-Parikka
P, Keinänen-Kiukaanniemi S, Laakso M, Louheranta A, Rastas M, Salminen V,
Uusitupa M. 2001. Prevention of type 2 diabetes mellitus by changes in lifestyle
among subjects with impaired glucose tolerance. N Eng J Med 344:1343–1350.
Turini ME, Powell WS, Behr SR, Holub BJ. 1994. Effects of a fish-oil and vegetable-
oil formula on aggregation and ethanolamine-containing lysophospholipid
generation in activated human platelets and on leukotriene production in
stimulated neutrophils. Am J Clin Nutr 60:717–724.
Turner NC, Clapham JC. 1998. Insulin resistance, impaired glucose tolerance and
non-insulin-dependent diabetes, pathologic mechanisms and treatment:
Current status and therapeutic possibilities. Prog Drug Res 51:33–94.
Uauy R, Mize CE, Castillo-Duran C. 2000. Fat intake during childhood: Metabolic
responses and effects on growth. Am J Clin Nutr 72:1354S–1360S.
Uematsu T, Nagashima S, Niwa M, Kohno K, Sassa T, Ishii M, Tomono Y, Yamato
C, Kanamaru M. 1996. Effect of dietary fat content on oral bioavailability of
menatetrenone in humans. J Pharm Sci 85:1012–1016.
USDA (U.S. Department of Agriculture). 1996. The Food Guide Pyramid. Home and
Garden Bulletin No. 252. Washington, DC: U.S. Government Printing Office.
OCR for page 877
877
M ACRONUTRIENTS AND HEALTHFUL DIETS
Uusitupa M, Schwab U, Mäkimattila S, Karhapää P, Sarkkinen E, Maliranta H,
Ågren J, Penttilä I. 1994. Effects of two high-fat diets with different fatty acid
compositions on glucose and lipid metabolism in healthy young women. Am J
Clin Nutr 59:1310–1316.
van Amelsvoort JM, van Stratum P, Kraal JH, Lussenburg RN, Houtsmuller UMT.
1989. Effects of varying the carbohydrate:fat ratio in a hot lunch on post-
prandial variables in male volunteers. Br J Nutr 61:267–283.
van Amelsvoort JM, van Stratum P, Dubbelman GP, Lussenburg RN. 1990. Effects
of meal size reduction on postprandial variables in male volunteers. Ann Nutr
Metab 34:163–174.
van den Berg JJM, Cook NE, Tribble DL. 1995. Reinvestigation of the antioxidant
properties of conjugated linoleic acid. Lipids 30:599–605.
van den Brandt PA, van’t Veer P, Goldbohm RA, Dorant E, Volovics A, Hermus
RJJ, Sturmans F. 1993. A prospective cohort study on dietary fat and the risk of
postmenopausal breast cancer. Cancer Res 53:75–82.
Van Dokkum W, Wesstra A, Schippers FA. 1982. Physiological effects of fibre-rich
types of bread. 1. The effect of dietary fibre from bread on the mineral balance
of young men. Br J Nutr 47:451–460.
van Stratum P, Lussenburg RN, van Wezel LA, Vergroesen AJ, Cremer HD. 1978.
The effect of dietary carbohydrate:fat ratio on energy intake by adult women.
Am J Clin Nutr 31:206–212.
van’t Veer P, Kok FJ, Brants HAM, Ockhuizen T, Sturmans F, Hermus RJJ. 1990.
Dietary fat and the risk of breast cancer. Int J Epidemiol 19:12–18.
Vartiainen E, Puska P, Pietinen P, Nissinen A, Leino U, Uusitalo U. 1986. Effects of
dietary fat modifications on serum lipids and blood pressure in children. Acta
Paediatr Scand 75:396–401.
Veierød MB, Laake P, Thelle DS. 1997a. Dietary fat intake and risk of lung cancer:
A prospective study of 51,452 Norwegian men and women. Eur J Cancer Prev
6:540–549.
Veierød MB, Laake P, Thelle DS. 1997b. Dietary fat intake and risk of prostate
cancer: A prospective study of 25,708 Norwegian men. Int J Cancer 73:634–638.
Velie E, Kulldorff M, Schairer C, Block G, Albanes D, Schatzkin A. 2000. Dietary
fat, fat subtypes, and breast cancer in postmenopausal women: A prospective
cohort study. J Natl Cancer Inst 92:833–839.
Vessby B. 2000. Dietary fat and insulin action in humans. Br J Nutr 83:S91–S96.
Vessby B, Uusitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, Nälsén
C, Berglund L, Louheranta A, Rasmussen BM, Calvert GD, Maffetone A,
Pedersen E, Gustafsson I-B, Storlien LH. 2001. Substituting dietary saturated
for monounsaturated fat impairs insulin sensitivity in healthy men and women:
The KANWU study. Diabetologia 44:312–319.
Visonneau S, Cesano A, Tepper SA, Scimeca JA, Santoli D, Kritchevsky D. 1997.
Conjugated linoleic acid suppresses the growth of human breast adeno-
carcinoma cells in SCID mice. Anticancer Res 17:969–974.
Vobecky JS, Vobecky J, Normand L. 1995. Risk and benefit of low fat intake in
childhood. Ann Nutr Metab 39:124–133.
von Schacky C, Angerer P, Kothny W, Theisen K, Mudra H. 1999. The effect of
dietary ω-3 fatty acids on coronary atherosclerosis. A randomized, double-
blind, placebo-controlled trial. Ann Intern Med 130:554–562.
Walker AR, Walker BF. 1978. High high-density-lipoprotein cholesterol in African
children and adults in a population free of coronary heart disease. Br Med J
2:1336–1337.
OCR for page 878
878 DIETARY REFERENCE INTAKES
Walser M. 1992. The relationship of dietary protein to kidney disease. In: Liepa
GU, Beitz DC, Beynen AC, Gorman MA, eds. Dietary Proteins: How They Alleviate
Disease and Promote Better Health. Champaign, IL: American Oil Chemists’
Society. Pp. 168–178.
Ward MH, Zahm SH, Weisenburger DD, Gridley G, Cantor KP, Saal RC, Blair A.
1994. Dietary factors and non-Hodgkin’s lymphoma in Nebraska (United
States). Cancer Causes Control 5:422–432.
Waterlow JC. 1976. Classification and definition of protein-energy malnutrition.
Monogr Ser World Health Organ 62:530–555.
Weisburger JH. 1988. Comparison of nutrition as customary in the Western World,
the Orient, and northern populations (Eskimos) in relation to specific disease
risk. Arctic Med Res 47:110–120.
West CE, Sullivan DR, Katan MB, Halferkamps IL, van der Torre HW. 1990. Boys
from populations with high-carbohydrate intake have higher fasting triglyceride
levels than boys from populations with high-fat intake. A m J Epidemiol
131:271–282.
West KM, Kalbfleisch JM. 1971. Influence of nutritional factors on prevalence of
diabetes. Diabetes 20:99–108.
Westerterp KR, Verboeket-van de Venne WPHG, Westerterp-Plantenga MS,
Velthuis-te Wierik EJM, de Graaf C, Weststrate JA. 1996. Dietary fat and body
fat: An intervention study. Int J Obes Relat Metab Disord 20:1022–1026.
Whigham LD, Cook ME, Atkinson RL. 2000. Conjugated linoleic acid: Implica-
tions for human health. Pharmacol Res 42:503–510.
Whiting SJ, Anderson DJ, Weeks SJ. 1997. Calciuric effects of protein and potassium
bicarbonate but not of sodium chloride or phosphate can be detected acutely
in adult women and men. Am J Clin Nutr 65:1465–1472.
Willett WC. 1997. Specific fatty acids and risks of breast and prostate cancer: Dietary
intake. Am J Clin Nutr 66:1557S–1563S.
Willett WC. 1998. Is dietary fat a major determinant of body fat? Am J Clin Nutr
67:556S–562S.
Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Hennekens CH, Speizer FE.
1987. Dietary fat and the risk of breast cancer. N Engl J Med 316:22–28.
Willett WC, Stampfer MJ, Colditz GA, Rosner BA, Speizer FE. 1990. Relation of
meat, fat, and fiber intake to the risk of colon cancer in a prospective study
among women. N Engl J Med 323:1664–1672.
Willett WC, Hunter DJ, Stampfer MJ, Colditz G, Manson JE, Spiegelman D, Rosner
B, Hennekens CH, Speizer FE. 1992. Dietary fat and fiber in relation to risk of
breast cancer. An 8-year follow-up. J Am Med Assoc 268:2037–2044.
Williams CL, Bollella M. 1995. Is a high-fiber diet safe for children? Pediatrics
96:1014–1019.
Wisen O, Hellstrom PM, Johansson C. 1993. Meal energy density as a determinant
of postprandial gastrointestinal adaptation in man. S cand J Gastroenterol
28:737–743.
Wisker E, Maltz A, Feldheim W. 1988. Metabolizable energy of diets low or high in
dietary fiber from cereals when eaten by humans. J Nutr 118:945–952.
Wolfe BMJ, Piché LA. 1999. Replacement of carbohydrate by protein in a
conventional-fat diet reduced cholesterol and triglyceride concentrations in
healthy normolipidemic subjects. Clin Invest Med 22:140–148.
Wolk A, Bergström R, Hunter D, Willett W, Ljung H, Holmberg L, Bergkvist L,
Bruce Å, Adami H-O. 1998. A prospective study of association of mono-
unsaturated fat and other types of fat with risk of breast cancer. Arch Intern
Med 158:41–45.
OCR for page 879
879
M ACRONUTRIENTS AND HEALTHFUL DIETS
Wooley SC. 1972. Physiologic versus cognitive factors in short term food regulation
in the obese and nonobese. Psychosom Med 34:62–68.
Wu Y, Zheng W, Sellars TA, Kushi LH, Bostick RM, Potter JD. 1994. Dietary choles-
terol, fat, and lung cancer incidence among older women: The Iowa Women’s
Health Study (United States). Cancer Causes Control 5:395–400.
Yao M, Roberts SB. 2001. Dietary energy density and weight regulation. Nutr Rev
59:247–258.
Yeomans MR, Gray RW, Mitchell CJ, True S. 1997. Independent effects of palatability
and within-meal pauses on intake and appetite ratings in human volunteers.
Appetite 29:61–76.
Yost TJ, Jensen DR, Haugen BR, Eckel RH. 1998. Effect of dietary macronutrient
composition on tissue-specific lipoprotein lipase activity and insulin action in
normal-weight subjects. Am J Clin Nutr 68:296–302.
Yu-Poth S, Zhao G, Etherton T, Naglak M, Jonnalagadda S, Kris-Etherton PM.
1999. Effects of the National Cholesterol Education Program’s Step I and Step
II dietary intervention programs on cardiovascular disease risk factors: A meta-
analysis. Am J Clin Nutr 69:632–646.
Zambell KL, Keim NL, Van Loan MD, Gale B, Benito P, Kelley DS, Nelson GJ.
2000. Conjugated linoleic acid supplementation in humans: Effects of body
composition and energy expenditure. Lipids 35:777–782.
Zhang J, Sasaki S, Amano K, Kesteloot H. 1999. Fish consumption and mortality
from all causes, ischemic heart disease, and stroke: An ecological study. Prev
Med 28:520–529.
Ziboh VA, Fletcher MP. 1992. Dose-response effects of dietary γ-linolenic acid-
enriched oils on human polymorphonuclear-neutrophil biosynthesis of
leukotriene B4. Am J Clin Nutr 55:39–45.
Zock PL, Katan MB. 1992. Hydrogenation alternatives: Effects of trans fatty acids
and stearic acid versus linoleic acid on serum lipids and lipoproteins in
humans. J Lipid Res 33:399–410.
Zock PL, Katan MB. 1998. Linoleic acid intake and cancer risk: A review and meta-
analysis. Am J Clin Nutr 68:142–153.
Zurier RB, Rossetti RG, Jacobson EW, DeMarco DM, Liu NY, Temming JE, White
BM, Laposata M. 1996. Gamma-linolenic acid treatment of rheumatoid arthri-
tis. A randomized, placebo-controlled trial. Arthritis Rheum 39:1808–1817.
Representative terms from entire chapter:
clin nutr
