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Department of Food Science and Human Nutrition, Washington State University, Pullman, WA 99164-6376;
*
Program in Statistics, Washington State University, Pullman, WA 99164-3144; and
Department of Animal and Veterinary Sciences, University of Idaho, Moscow, ID 83844-2330
3To whom correspondence should be addressed. E-mail: smcguire{at}wsu.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • conjugated linoleic acid • CLA • rumenic acid • diet • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). The
c9,t11-octadecadienoic acid, also referred to as
rumenic acid (RA) (Kramer et al. 1998
), is the
predominant form found naturally in foods such as dairy and beef
(Chin et al. 1992
). Conjugated linoleic acid has been
proven unequivocally to inhibit carcinogenesis in animal models
(National Research Council 1996
) as well as in in vitro
cell cultures (Schonberg and Krokan 1995
, Shultz et al. 1992
). In addition, CLA appears to be involved in growth
modulation (Ostrowska et al. 1999
, Park et al. 1999a
); control and CLA-supplemented animals in these
studies exhibited similar body weights, but body fat percentages were
reduced in CLA-supplemented animals. Intake of CLA may also
influence diabetes (Houseknecht et al. 1998
), bone
health (Li et al. 1999
) and the immune system
(Hayek et al. 1999
, Turek et al. 1998
).
It is thought that the major source of CLA in human tissues is the diet
(Kamlage et al. 1999
). Typical human consumption of CLA
estimated from 3-d written dietary record (DR) and semiquantitative
food-frequency questionnaire (FFQ) methodologies (Herbel et al. 1998
, Park et al. 1999b
) ranges from 20 to
290 mg/d. Because these methods of estimating dietary intake may be
somewhat inaccurate (Lee and Nieman 1996
), validation
against more direct methodologies (e.g., 3-d food duplicates; FD)
seemed prudent. Thus, the major objective of this study was to estimate
current and chronic CLA intakes in a representative sample of men and
women, aged 18–60 y. In addition, recent work by Wolk et al. (1998)
and Smedman et al. (1999)
suggests that
the content of pentadecanoic (C15:0) and heptadecanoic fatty acids
(C17:0) present in subcutaneous adipose tissue as well as serum C15:0
are useful markers of dietary milk fat intake. Both fatty acids are
synthesized by ruminant bacterial flora and not by humans; they have
been suggested to be potential markers for dairy and beef intake and
thus, perhaps, dietary CLA intake in humans. Consequently, we also
investigated the relationship between intakes of CLA or RA and C15:0 or
C17:0. Further, to our knowledge, no data investigating the
relationship between CLA intake and body composition in humans have
been published. Therefore, another objective of this study was to
examine the relationship between CLA or RA intake and body composition
in humans.
In summary, rigorous documentation of CLA intake in any human population has not been reported. Further, the relationship between CLA intake and body composition in humans has not been investigated. Therefore, this study was designed to test the following general hypotheses: 1) Chronic and current CLA and RA intakes in the U.S. population do not exceed 500 mg/d. 2) A positive relationship exists between CLA or RA intake estimated by 3-d DR and FD methodologies. 3) There is no relationship between CLA or RA intake and body composition in humans.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Men (n = 51) and women (n = 51) were recruited from the communities of Pullman, WA and Moscow, ID. To be eligible for inclusion, subjects had to be between the ages of 18 and 60 y, healthy (self-reported) and not suffering from eating disorders. All data were collected within a 1-y period (April 1997–March 1998). Physical activity levels of subjects were assessed using defined categories (sedentary or slightly, moderately, very and extremely active). The Human Subjects Institutional Review Board of Washington State University and the Human Assurances Committee at the University of Idaho approved all procedures used, and written informed consent was obtained.
Dietary assessment.
Chronic total CLA and RA intakes were estimated using a FFQ that we
developed (Park et al. 1999b
); the FFQ assessed
long-term intakes of 70 foods containing CLA. Collection of current
dietary intake data occurred during a period that included two weekdays
and one weekend day (Lee and Nieman 1996
). Data
collected by DR and FFQ were evaluated using a computerized nutrient
database (Food Processor, Version 7.02; ESHA Research, Salem, OR),
which we modified to contain quantities of total CLA and RA (mg/g fat)
in 
190 foods (Chin et al. 1992
, Fritsche and Steinhart 1998
, Ha et al. 1989
, Hanson and McGuire 1998
, Lin et al. 1995
, Dr. Michael
Pariza (University of Wisconsin, Madison; personal communication),
Shantha et al. 1992, 1994 and 1995
, Werner et al. 1992
). When individual CLA isomers were not reported for foods,
the published CLA content was classified as "total CLA." However,
for most food items, two categories were created, i.e., RA and total
CLA. It is noteworthy that very few published manuscripts reported
which CLA isomers were included in the estimate of total CLA. When
possible, ingredients of complex food items were entered individually
to ensure inclusion of total CLA and RA concentrations and a more
complete fatty acid profile. Composite FD were collected simultaneously
to the recording of DR during the study. All food collected was kept
refrigerated by the subjects until the food was weighed by study
personnel, homogenized and frozen at -20°C for later fatty acid
analysis. We also created two categories related to CLA intake as
estimated by FD, i.e., RA and total CLA, which was a sum of the RA and
t10,c12–18:2 isomers. These were the
only CLA isomers that were detectable in our analyses.
Anthropometric assessment.
Anthropometric measurements were made in the morning after the last day
of food collection and dietary assessment between 0600 and 0900 h
while the subjects were fasting. All anthropometric measurements were
made on the right side of the body by a single investigator while
subjects were dressed in light clothing. Skinfold measurements were
obtained in duplicate using a Lange skinfold caliper (Cambridge
Scientific Industries, Cambridge, MD) for the estimation of body
density (BD) and ultimately the percentage of body fat (BF). Standard
procedures were used to measure the following 7 skinfold sites:
pectoral, umbilicus, thigh, triceps, suprailiac, axilla and subscapular
(Jackson and Pollock 1985
). Body density was estimated
using previously published equations (Jackson and Pollock 1985
). The conversion of BD to BF was derived from the equation
developed by Siri (1961)
. Weight (± 0.1 kg) was
measured using an electronic scale (Seca Alpha, Model 770, Hamburg,
Germany), and height (± 0.1 cm) was measured using a wooden height
board (Seca Measure-All). Body mass index (BMI) was calculated as
weight (kg) divided by height squared (m2).
Lipid and fatty acid analyses.
Methanol, chloroform, hexane (all HPLC grade) and diethyl ether (reagent grade) were obtained from Fisher Scientific (Santa Clara, CA). Sodium methoxide was purchased from Fluka (Milwaukee, WI); methyl acetate and oxalic acid were purchased from Sigma-Aldrich Chemical (St. Louis, MO), and the anhydrous milk fat reference standard was obtained from the Commission of the European Communities (CRM 164; European Community Bureau of Reference, Brussels, Belgium). Conjugated octadecadienoic acid (99% c9,t11–18:2) and a complex fatty acid methyl esters (FAME) mixture (C8:0-C22:1, KEL-FIM-FAME-5) were obtained from Matreya (Bellefonte, PA) to determine retention times for individual fatty acids.
Lipids of FD composites were extracted in triplicate using a modified
Folch procedure (Clark et al. 1982
). Each homogenized
food composite (2 g) was diluted with 38 mL of a 2:1
chloroform/methanol mixture, sonicated 40 s, centrifuged (400
x g) for 10 min and filtered into tubes containing
0.58 g/L saline. After a second centrifugation, the upper phase was
removed and the lower phase was dried under nitrogen. Samples were
diluted with hexane to contain 0.25 g lipid/L; triplicates were
combined and stored at -20°C for analysis of FAME.
Samples were methylated using a methanolic sodium methoxide solution
(Christie 1982
). The methylation reagent, containing 400
mL sodium methoxide (5.4 mol/L) and 1.75 mL methanol, was prepared
daily, and 40 µL was added after 40
µL methyl acetate. The reaction proceeded for 10 min
at room temperature and was terminated by the addition of 60
µL of a mixture containing 1 g oxalic acid in 30
mL diethyl ether. After centrifugation for 2 min (400 x g), a clear liquid supernatant was transferred into
tubes containing 2 g anhydrous calcium chloride and allowed to
equilibrate for 60 min. The remaining liquid was transferred to
injection vials, flushed with N2 and capped.
Quantification of FAME was performed on a gas chromatograph
(Hewlett-Packard 6890, Hewlett-Packard, Wilmington, DE) fitted with
a flame ionization detector. Fatty acid profiles were determined by
split injection (13.4:1; 2-µL sample) onto a
CP-Sil 88 fused silica capillary column (100 m x 0.25 mm
x 0.25 µm, Chrompack, Raritan, NJ) using a
previously described temperature gradient (Griinari et al. 1998
). The hydrogen carrier gas pressure was held constant (210
kPa), and the injector and detector temperatures were 255°C. Fatty
acid concentrations were determined as percentages of total fatty
acids. Correction factors for individual fatty acids were determined
through use of the previously mentioned anhydrous milk fat reference
standard with certified values.
Statistical analyses.
Statistical analyses were conducted using MINITAB Statistical Software
(Release 12.0; State College, PA). 
2 tests were used to
analyze the effect of gender on total CLA and RA food distribution.
Pearson correlation coefficients (r) were calculated to
determine the relationships between lipid and fatty acid intakes as
estimated by DR and FD, and CLA/RA intakes as estimated by DR or FFQ
and FD. Two-way, paired t tests were used to test
for differences between means obtained using different dietary intake
methodologies. Multiple regression analyses were performed to determine
independent and interactive relationships between and among gender and
lipid intakes estimated by DR or FFQ on total lipid and fatty acid
intakes as estimated by FD. Fatty acid intake data obtained by FD were
log transformed to meet the assumption of equal variance. In addition,
data for CLA and RA intakes, age, energy intake (kJ) and activity level
were centered to reduce the inflation of variance of the regression
coefficients that resulted from multicollinearity (Myers 1990
). A second series of multiple regression analyses was
conducted to explore possible effects of gender, age, energy and CLA or
RA intake (as estimated by FD), physical activity, and the interactions
between the following: 1) CLA or RA intake and age;
2) CLA or RA intake and gender; 3) CLA or
RA intake and activity; and 4) CLA or RA intake and
energy intake on body composition (BF or BMI). The final regression
model was determined by best subset regression (Ott 1993
). For t test and regression equations,
individual and main effects were considered significant at
P 
0.05. Interaction terms in the multiple
regression analyses were considered significant at P
0.10.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Data from 9 subjects were excluded from the analyses: 4 subjects (2
men, 2 women) withdrew for personal reasons, 1 subject (male) became
ill during the study and 4 subjects (2 men, 2 women) were excluded due
to incomplete data collection. Thus, the majority of data reported
represent those of 46 men and 47 women. In addition, data from two
women were excluded from the body composition analyses due to either
inappropriate application of the body composition equation (lactating
subject), or because the percentage of BF was outside the range of the
method employed (extremely obese subject). Furthermore, in 4 subjects
(2 men, 2 women), activity level was not documented. Descriptive
statistics of our study population are shown in Table 1
.
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Chronic total CLA intake as estimated by FFQ was 197 ± 19 and 93
± 11 mg/d and for RA 151 ± 15 and 72 ± 9 mg/d for men
and women, respectively (Fig. 1
). Information concerning dietary intake estimated by DR is presented in
Table 2
and Figure 1
. Using DR, total CLA intakes were 176 and 104 mg/d and RA
intakes 133 and 79 mg/d for men and women, respectively. Dietary
intakes of total lipid and fatty acids as estimated by DR and FD
methodologies are summarized in Table 3
. Using FD, total CLA intakes were 212 and 151 mg/d and RA intakes 193
and 140 mg/d for men and women, respectively. In men, estimates of all
fatty acid intakes except C18:3 were affected (P < 0.05) by the methodology used (i.e., DR vs. FD). Total lipid and C14:0,
C16:0, C18:0 and C18:1 intakes were higher when estimated by DR; the
opposite was found for C12:0, C18:2, RA and total CLA. In women, only
intakes of C14:0, C16:0, C18:2, RA and total CLA differed between DR
and FD methodologies and followed the same patterns as those seen in
men. When expressed as proportion (%) of total lipid, only intakes of
C18:1 in women and C18:3 in both genders were affected (P
< 0.05) by the methodology used (data not shown).
|
|
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. In men, the relationship between mean
total CLA intakes estimated by DR or FFQ and FD was weak (r
= 0.38 and 0.22, respectively), and the correlation was
significant only for the relationship between DR and FD (P
= 0.05). The relationship between RA intakes estimated by DR or
FFQ and FD was weak but significant (r = 0.42 and 0.43,
respectively, P < 0.005; Fig. 2
). In women, relationships between total CLA intake estimated by DR or
FFQ and FD were slightly stronger (r = 0.56 and 0.44,
respectively) and significant (P = 0.002); similar
results were found for RA (Fig. 2)
. Together, these data suggest a
systematic underestimation of total CLA and RA intakes by DR and FFQ
methodologies in both genders.
|
Dietary intakes of C15:0 from FD were 174.3 ± 19.5 and 91.0 ± 16.2 mg/d for men and women, respectively. Dietary intakes of C17:0 were 89.4 ± 16.4 and 116.9 ± 28.0 mg/d for men and women, respectively. A weak but significant correlation was found between C15:0 and total CLA intake estimated by FD for both men and women (r = 0.37 and 0.36, respectively; P < 0.05) and for RA intake (r = 0.30 and 0.36, respectively; P < 0.05). No correlation was apparent between intake of C17:0 and total CLA or RA.
Dietary sources of CLA and RA.
The distribution of foods that provided dietary total CLA and RA was
determined using data collected by DR (Fig. 3
). Because both total CLA and RA distributions of food sources were
similar between genders, data were combined for purposes of
presentation. Dairy products contributed the majority of CLA and RA
followed by beef. Among dairy products, cheese was the primary source,
contributing 30 and 33% of total CLA and RA intakes, respectively.
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After elimination of nonsignificant interactions, the final regression model predicting BF from total CLA intake (adjusted R2 = 0.41) was as follows: BF = 11.1 + 7.59 (gender) - 0.18 (CLA by FD) + 1.97 (age) + 0.75 (energy intake) - 2.34 (activity level). The final model using RA intake was as follows: (adjusted R2 = 0.38): BF = 14.0 + 7.13 (gender) - 0.07 (RA by FD) + 1.88 (age) + 0.7 (energy intake) - 1.24 (activity level). As expected, gender, age and activity level were significantly (P < 0.05) related to BF, suggesting that older, female and less active individuals tend to have a higher percentage of BF. Statistical analysis suggested no significant relationship between total CLA or RA intake and BF. When BMI was used instead of BF as an indicator of body composition, similar results were obtained for total CLA: BMI = 24.3 - 1.85 (gender) - 0.40 (CLA by FD) + 0.79 (age) + 0.79 (energy intake) - 0.66 (activity level) + 0.91 (age · CLA by FD) and RA: BMI = 25.0 - 2.01 (gender) - 0.15 (RA by FD) + 0.86 (age) + 0.82 (energy intake) - 0.45 (activity level) + 0.56 (age · RA by FD). Gender and age were again significant (P = 0.01 and 0.004, respectively; adjusted R2 = 0.30) in the model using RA, whereas only age was significant when using total CLA in the model (P = 0.01; adjusted R2 = 0.23). However, total CLA and RA intake were not significantly related to BMI.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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), with the exception of stearic acid
intake in men as estimated by FD, which was only 50% of the mean CSFII
estimate. Thus, we conclude that the mean total CLA and RA intakes (as
estimated by FD) in this study may be representative of the average
U.S. population intake. Results confirm our first hypothesis that total
CLA and RA intake is < 500 mg/d. Furthermore, intakes of all
commonly consumed fatty acids studied here were significantly
correlated when DR and FD methodologies were compared, suggesting that
these methodologies were properly utilized.
Results from Herbel et al. (1998)
who reported a mean
dietary CLA intake of 139 mg/d in young men and women, and Park et al. (1999b)
who estimated mean CLA intake in lactating women
during periods of low and high dairy consumption (20 and 290 mg/d,
respectively) support our data concerning CLA intake. The FFQ used in
this study was developed initially and used previously by Park et al. (1999b)
who reported a mean chronic CLA intake in
lactating women of 227 ± 180 mg/d; this value is higher than the
mean chronic CLA intake in the men (150 ± 15 mg/d) but more than
threefold that of the women (72 ± 9 mg/d) studied here. The lower
dietary lipid intake in our study compared with that of the lactating
women studied by Park et al. (1999b)
may explain in part
the lower chronic CLA intake in the women reported in this study.
Additional data suggest that dietary CLA intakes in other countries are
somewhat comparable to that of the U.S. population. Among older Swedish
men, mean CLA intake was 160 mg/d (Jiang et al. 1999
) as
estimated by 7-d weighed DR and 24-h recalls. Further, Fritsche and Steinhart (1998)
using a national consumption survey
estimated that German men and women consume 430 and 350 mg RA/d,
respectively. These estimates are approximately twice those estimated
for the U.S. population. However, Germans consume 10% more energy
from fat than do Americans (Adolf et al. 1994
).
A number of factors may have potentially influenced the accuracy of the
data collected in this study. For example, the incompleteness of
individual fatty acid quantities in the nutrient database may have
resulted in an underestimation of the calculated data obtained from DR
and FFQ. This concern may be especially pertinent for the total CLA and
RA data. It is important for future investigators to report individual
CLA isomers when documenting the CLA content of foods. Moreover, the
use of a variety of oils and fats by food manufacturers introduces
additional variation (Worley 1994
). Furthermore,
although the FD methodology may provide a more accurate measurement of
actual dietary nutrient intake compared with calculations based on food
composition tables, the additional time and effort invested by the
subjects associated with this method may result in underestimation of
usual nutrient intake (Lee and Nieman 1996
).
Nonetheless, because our FD methodology resulted in total CLA and RA
intake values that were greater than those obtained by DR or
FFQ, we believe that these values probably do not appreciably
underrepresent true intakes.
Results also confirm our second hypothesis, i.e., that a positive
relationship exists between total CLA or RA intake estimated by 3-d DR
and FD methodologies. Although the correlations between total CLA or RA
intakes as estimated by DR or FFQ and those estimated by FD were strong
in both genders, mean total CLA and RA intakes estimated by these
methods were quite different and suggested a systematic underestimation
of total CLA and RA intake by FFQ and DR. The weak correlation between
total CLA or RA intake estimated by DR and FD methodologies suggests
that high natural variation in the CLA concentration of similar food
products may result in major difficulties in constructing an adequate
database of CLA contents in food. Natural variation in food CLA is
likely to occur by differences in, for example, diet, season, maturity
and breed of animal (Bauman et al. 2000
). Therefore,
food CLA concentrations used for computation of dietary intake
represent mere estimates. Nonetheless, we believe that the data
presented here, especially those collected by FD methodology, quite
accurately reflect CLA intake in the population investigated. In
conclusion, DR and FFQ methodologies underestimate the mean group
intake of total CLA and RA, and researchers should use them with
caution when estimating CLA intakes of individuals.
Animal data have suggested that consumption of a diet containing as
little as 0.1 g CLA/100 g dry diet is sufficient to significantly
reduce tumors (Ip et al. 1994
) and may be useful as a
reference for dietary intake recommendations in humans. Recently,
Ip et al. (1999)
demonstrated that RA is the
biologically active anticarcinogenic CLA isomer. Noteworthy is the fact
that this suggestion is based on an animal model that involves the
administration of massive doses of a chemical carcinogen. Because
humans are typically exposed to much lower concentrations of
carcinogens, the effective RA dose for human cancer protection is
likely to be less than what animal models suggest. Nonetheless, when
calculated on a dry weight basis, both men and women in our study
consumed diets containing approximately 0.03 g/100 g RA. Further, our
data suggest that RA intake must be 620 and 441 mg/d for men and women,
respectively, to exhibit a cancer protective effect (i.e., 0.1 g/100 g
diet). Due to the lack of experimental human data, extrapolation from
animals to humans provides the only means of dietary intake estimates.
However, these represent very rough estimates and should be interpreted
cautiously.
Increasing dietary CLA consumption to these levels could be
accomplished by altering the consumption of CLA-containing foods.
However, an increase in CLA consumption should be promoted with caution
because a diet rich in CLA is also often high in fat. Alternatively,
food products rich in CLA can be substituted for similar foods
containing lower amounts of CLA (e.g., butter vs. margarine). An
alternative approach to increasing dietary CLA intake is to naturally
enhance CLA concentrations in food. For example, administration of
sunflower oil to the lactating cow increases CLA concentrations
approximately fivefold (Kelly et al. 1998
). An increase
of this magnitude would raise daily dietary RA intake in the present
study to 551 and 491 mg/d in men and women, respectively.
A secondary objective of this study focused on the putative growth
modulating characteristics of CLA and RA (Ostrowska et al. 1999
, Park et al. 1997 and 1999a
, Sisk et al. 1998
). Results of the present study suggest, however, that
total CLA and RA intakes were not related to the percentage of BF or
BMI. This finding supports our initial hypothesis.
Finally, to investigate the relationship between total CLA or RA and C15:0 or C17:0, we determined intakes of both fatty acids from FD. Results indicate that there was a weak correlation between C15:0 and total CLA or RA, and an even weaker relationship between C17:0 and total CLA or RA. Thus, C15:0 or C17:0 intakes are not reliably related to either total CLA or RA intakes.
In summary, our data suggest that chronic as well as current total CLA and RA intakes in men and women do not exceed 500 mg/d. Dairy products were the primary source of total CLA and RA, followed by beef. A positive relationship existed between individual total CLA and RA intakes estimated by DR and FD. However, both DR and FFQ methodologies underestimated mean total CLA and RA intakes. In both genders, neither FFQ nor DR methodology can be used to predict individual CLA or RA intake, but may be used as indicators of relative CLA or RA intake among groups of people. In the future, more accurate and reliable methods to estimate individual total CLA as well as CLA isomer intake must be investigated when the use of FD methodology is not appropriate or possible. For example, the relationship between CLA isomer concentrations in blood or adipose stores and dietary CLA isomer intake may be considered. Finally, we found no relationship between body composition and CLA or RA intake, suggesting that dietary CLA has little effect on body composition in humans.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Supported in part by a grant from the National Cattlemen’s Beef Association, Chicago, IL.
4 Abbreviations used: BD, body density; BF, percentage of body fat; BMI, body mass index; CLA, conjugated linoleic
acid; CSFII, Continuing Survey of Food Intakes by Individuals; DR, 3-d written dietary record; FAME, fatty acid methyl esters; FD, 3-d food duplicates; FFQ, semiquantitative food-frequency questionnaire; RA, rumenic acid.
Manuscript received August 29, 2000. Initial review completed October 12, 2000. Revision accepted January 23, 2001.
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REFERENCES |
|---|
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Adolf T., Eberhardt W., Heseker H., Hartmann S., Herwig A., Matiaske B., Moch K. J., Schneider R., Kuebler W. Lebensmittel und Naehrstoffaufnahme in der Bundesrepublic Deutschland. Kueble W. Anders H. J. Heeschen W. eds. VERA Schriftenreihe 1994;XII Wissenschaftlicher Fachverlag Fleck Niderkleen.
2. Bauman, D. E., Baumgard, L. H., Corl, B. A. & Griinari, J. M. (2000) Biosynthesis of conjugated linoleic acid in ruminants. Proc. Am. Soc. Anim. Sci., 1999. Available at: http://www.asas.org/jas/sympsia/proceedings/0937.pdf. Accessed {06/10/2000}.
3. Chin S. F., Liu W., Storkson J. M., Ha Y. L., Pariza M. W. Dietary sources of conjugated dienoic isomers of linoleic acid, a newly recognized class of anticarcinogens. J. Food Comp. Anal. 1992;5:185-197
4. Christie W. W. A simple procedure for rapid transmethylation of glycerolipids and cholesteryl esters. J. Lipid Res. 1982;23:1072-1075[Abstract]
5. Clark R. M., Ferris A. M., Fey M., Brown P. B., Hundrieser K. E., Jensen R. G. Changes in the lipids of human milk from 2 to 16 weeks postpartum. J. Pediatr. Gastroenterol. Nutr 1982;1:311-315[Medline]
6. Fritsche J., Steinhart H. Amounts of conjugated linoleic acid (CLA) in German foods and evaluation of daily intake. Z. Lebensm.-Unters.-Forsch. A 1998;2065:77-82
7. Griinari J. M., Dwyer D. A., McGuire M. A., Bauman D. E., Palmquist D. L., Nurmela K.V.V. Trans-octadecenoic acids and milk fat depression in lactating dairy cows. J. Dairy Sci. 1998;81:1251-1261[Abstract]
8. Ha Y. L., Grimm N. K., Pariza M. W. Newly recognized anticarciongenic fatty acids: identification and quantification in natural and processed cheeses. J. Agric. Food Chem. 1989;3:75-81
9. Hanson T. W., McGuire M. A. Evaluation of conjugated linoleic acid content in the meat of wildlife from the Pacific Northwest. Proceedings of the Second Comparative Nutrition Society Symposium 1998:68-73 Banff Alberta, Canada.
10.
Hayek M. G., Han S. N., Wu D., Watkins B. A., Meydani M., Dorsey J. L., Smith D. E., Meydani S. N. Dietary conjugated linoleic acid influences the immune response of young and old C57BL/6NCrlBR mice. J. Nutr. 1999;129:32-38
11. Herbel B. K., McGuire M. K., McGuire M. A., Shultz T. D. Safflower oil consumption does not increase plasma conjugated linoleic acid concentrations in humans. Am. J. Clin. Nutr. 1998;67:332-337[Abstract]
12. Houseknecht K. L., Vanden Heuvel J. P., Moya-Camarena S. Y., Portocarrero C. P., Peck L. W., Nickel K. P., Belury M. A. Dietary conjugated linoleic acid normalizes impaired glucose tolerance in the Zucker diabetic fatty fa/fa rat. Biochem. Biophys. Res. Commun. 1998;244:678-682[Medline]
13.
Ip C., Banni S., Angioni E., Carta G., McGinley J., Thompson H. J., Barbano D., Bauman D. Conjugated linoleic acid-enriched butter fat alters mammary gland morphogenesis and reduces cancer risk in rats. J. Nutr. 1999;129:2135-2142
14.
Ip C., Singh M., Thompson H. J., Scimeca J. A. Conjugated linoleic acid suppresses mammary carcinogenesis and proliferative activity of the mammary gland in the rat. Cancer Res 1994;54:1212-1215
15. Jackson A. S., Pollock M. L. Practical assessment of body composition. Physician Sportsmed 1985;13:76-90
16.
Jiang J., Wolk A., Vessby B. Relation between the intake of milk fat and the occurrence of conjugated linoleic acid in human adipose tissue. Am. J. Clin. Nutr. 1999;70:21-27
17.
Kamlage B., Hartmann L., Gruhl B., Blaut M. Intestinal microorganisms do not supply associated gnotobiotic rats with conjugated linoleic acid. J. Nutr. 1999;129:2212-2217
18.
Kelly M. L., Berry J. R., Dwyer D. A., Griinari J. M., Chouinard P. Y., Van Amburgh M. E., Bauman D. E. Dietary fatty acid sources affect conjugated linoleic acid concentrations in milk from lactating cows. J. Nutr. 1998;128:881-885
19. Kramer J.K.G., Parodi P. W., Jensen R. G., Mossoba M. M., Yurawecz M. P., Adlof R. O. Rumenic acid: a proposed common name for the major conjugated linoleic acid isomer found in natural products. Lipids 1998;33:835[Medline]
20. Lavillonniere F., Martin J. C., Bougnoux P., Sebedio J. L. Analysis of conjugated linoleic acid isomers and content in French cheeses. J. Am. Oil. Chem. Soc 1998;75:343-352
21. Lee R. D., Nieman D. C. Nutritional Assessment 2nd ed. 1996 Mosby Chicago, IL.
22. Li Y., Seifert M. F., Ney D. M., Grahn M., Grant A. L., Allen K. G., Watkins B. A. Dietary conjugated linoleic acids alter serum IGF-I and IGF binding protein concentrations and reduce bone formation in rats fed (n-6) or (n-3) fatty acids. J. Bone Miner. Res. 1999;14:1153-1162[Medline]
23. Lin H., Boylston T. D., Chang M. J., Luedecke L. O., Shultz T. D. Survey of the conjugated linoleic acid content of dairy products. J. Dairy Sci. 1995;78:2358-2365[Abstract]
24. National Research Council Carcinogens and Anticarcinogens in the Human Diet: A Comparison of Naturally Occurring and Synthetic Substances 1996 National Academy Press Washington, DC.
25. Myers R. H. Detecting and combating multicollinearity. Classical and Modern Regression 2nd ed. 1990:384-385 Duxbury Press Belmont, CA.
26.
Ostrowska E., Muralitharan M., Cross R. F., Bauman D. E., Dunshea F. R. Dietary conjugated linoleic acids increase lean tissue and decrease fat deposition in growing pigs. J. Nutr. 1999;129:2037-2042
27. Ott R. L. More on multiple regression. An Introduction to Statistical Methods and Data Analysis 4th ed. 1993:647-766 Duxbury Press Belmont, CA.
28. Park Y., Albright K. J., Liu W., Storkson J. M., Cook M. E., Pariza M. W. Effect of conjugated linoleic acid on body composition in mice. Lipids 1997;32:853-858[Medline]
29. Park Y., Albright K. J., Storkson J. M., Liu W., Cook M. E., Pariza M. W. Changes in body composition in mice during feeding and withdrawal of conjugated linoleic acid. Lipids 1999a;34:243-248[Medline]
30.
Park Y., McGuire M. K., Behr R., McGuire M. A., Evans M. A., Shultz T. D. High fat dairy product consumption increases 
9c,11t-18:2 (rumenic acid) and total lipid concentrations of human milk. Lipids 1999b;34:543-549[Medline]
31. Schonberg S., Krokan H. E. The inhibitory effect of conjugated dienoic derivatives (CLA) of linoleic acid on the growth of human tumor cells lines is in part due to increased lipid peroxidation. Anticancer Res 1995;15:1241-1246[Medline]
32. Shantha N. C., Crum A. D., Decker E. A. Evaluation of conjugated linoleic acid concentrations in cooked beef. J. Agric. Food Chem. 1994;42:1757-1760
33. Shantha N. C., Decker E. A., Ustunol Z. Conjugated linoleic acid concentration in processed cheese. J. Am. Oil Chem. Soc. 1992;69:425-428
34. Shantha N. C., Ram L. N., O’Leary J., Hicks L. C., Decker E. A. Conjugated linoleic acid concentrations in dairy products as affected by processing and storage. J. Food Sci. 1995;60:695-697
35. Shultz T. D., Chew B. P., Seaman W. R., Luedecke L. O. Inhibitory effect of conjugated dienoic derivatives of linoleic acid and ß-carotene on the in vitro growth of human cancer cells. Cancer Lett 1992;63:125-133[Medline]
36. Siri W. E. Body composition from fluid spaces and density: analysis of methods. Techniques for Measuring Body Composition 1961:223-244 National Academy of Sciences National Research Council, Washington, DC.
37. Sisk M., Azain M. J., Hausman D. B. Effect of conjugated linoleic acid on fat pad weights and cellularity in Sprague-Dawley and Zucker rats. FASEB J 1998;12:A536(abs.)
38.
Smedman A. E., Gustafsson I. B., Berglund L. G., Vessby B. O. Pentadecanoic acid in serum as a marker for intake of milk fat: relations between intake of milk fat and metabolic risk factors. Am. J. Clin. Nutr. 1999;69:22-29
39. Turek J. J., Li Y., Schoenlein I. A., Allen K.G.D., Watkins B. A. Modulation of macrophage cytokine production by conjugated linoleic acids is influenced by the dietary n-6:n-3 fatty acid ratio. J. Nutr. Biochem. 1998;9:258-266
40. U.S. Department of Agriculture/Agriculture Research Service (1997) Data tables: intakes of 19 individual fatty acids: results from 1994–96 continuing survey of food intakes by individuals, [Online]. AGR Food Surveys Research Group. Available at: http://www.barc.usda.gov/bhnrc/foodsurvey/home.htm. Accessed {11/04/98}.
41. Werner S. A., Luedecke L. O., Shultz T. D. Determination of conjugated linoleic acid content and isomer distribution in three cheddar-type cheeses: effects of cheese cultures, processing, and aging. J. Agric. Food Chem. 1992;40:1817-1821
42. Wolk A., Vessby B., Ljung H., Barrefors P. Evaluation of a biological marker of dairy fat intake. Am. J. Clin. Nutr. 1998;68:291-295[Abstract]
43. Worley A. E. Labeling of foods in relation to fat and fatty acid and cholesterol content. Code of Federal Regulation; Food and Drug. 21 CFR 101.25 1994 U.S. Government Printing Office Washington, DC.
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