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*
Department of Medical Epidemiology, Karolinska Institutet, Box 281, SE-171 77 Stockholm, Sweden and
Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden
2To whom correspondence should be addressed. E-mail: Alicja.Wolk{at}mep.ki.se
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • biological markers • adipose tissue • serum • fatty acids • milk fat • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Because serum samples are usually more often available
in different epidemiological studies than adipose tissue, the
usefulness of fatty acid composition of cholesterol esters and
phospholipids in serum as marker for intake of milk fat is also of
interest. Two saturated fatty acids with an odd number of carbon atoms
[i.e., pentadecanoic acid (15:0) and heptadecanoic acid (17:0)] are
characteristic of dairy fat. They are synthesized by the bacterial
flora in the rumen of ruminants (Barrefors et al. 1995
,
Wu and Palmquist 1991
). Because these fatty acids
contain an uneven number of carbon atoms, they cannot be synthesized in
the human body and are virtually specific for milk fat, but they are
also present in the fat from ruminants, i.e., beef and lamb meat.
Although they are present in low concentrations, it is possible to
quantify the proportions of 15:0 and 17:0 in human adipose tissue and
serum lipids. Because these fatty acids are not produced endogenously,
they possess the characteristics required for a biological marker. In the present study, we investigated whether the content of 15:0 and 17:0 in serum lipids can be used as an alternative biological marker to the content of these fatty acids in adipose tissue when evaluating long-term dairy fat consumption from milk and milk products. Furthermore, we investigated whether another saturated fatty acid that is mainly present in milk fat [myristic acid (14:0)] can have a similar value as a biomarker for milk fat consumption. This fatty acid is easier to measure than 15:0 and 17:0 due to its higher content in adipose tissue and serum. It is also easier to calculate its intake, because 14:0 content in different foods is available in most food tables.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The study was approved by the ethical committees of the Uppsala University Hospital and the Karolinska Institutet. The 790 men, who were 40–76 y old, were randomly selected within age strata 40–49, 50–59, 60–69 and 70–76 from the total population register of Uppsala (city) and Knutby (countryside) in central Sweden. The men were invited to participate in a validation study of a food frequency questionnaire, and 469 of them filled in the form. We used 14 x 24-h diet recall interviews and 2 x 7-d dietary records (DR)3 as reference methods. Because of the high degree of cooperation required in such a study, only 308 men participated in repeated 24-h recall interviews, and among them, 158 participated in two 7-d DR. At the conclusion of the study, a subcutaneous fat biopsy and blood samples were obtained from 124 consecutive men. Among them, 123 participated in 24-h recall interviews and 114 in food DR. We decided to use in our main analyses the group of 114 men with both the 2 x 7-d food DR and the repeated 24-h diet recall interviews. Among this group, we had serum available from 104 subjects.
Analysis of fatty acid composition in serum lipids and in adipose tissue triacylglycerols.
Venous blood samples were drawn from an antecubital vein after a 12-h overnight fast. After coagulation at 2 h at room temperature, serum was separated by low speed centrifugation (2000 x g) and stored at -70°C until analysis.
Subcutaneous fat aspirate samples were taken from the upper outer
quadrant of a buttock with a needle attached to a vacuum tube. The
samples (
10–30 mg) were left in the connector, stored frozen at
-70°C, protected from light and analyzed within a few weeks
(Beynen and Katan 1985
).
The adipose tissue biopsies were weighed, dissolved in 1 mL hexane and
homogenized in a tissue grinder twice for 15 min. The hexane was
pipetted off, and the solvent was evaporated completely after
separation of the fatty acids in serum lipid esters by thin layer
chromatography. The fatty acids in the serum cholesterol esters and
phospholipids and in adipose tissue triacylglycerols were separated by
gas-liquid chromatography after transmethylation as described
earlier (Boberg et al. 1985
). The fatty acid methyl
esters from the serum lipids were separated on a 25-m-wall coated, open
tubular, glass capillary column coated with SLP OV-351 (Quadrex, New
Haven, CT) and from the adipose tissue triacylglycerols on a 50-m fused
silica capillary column coated with CP-SIL 88 (Chrompack,
Middlebuy, The Netherlands), with helium as a
carrier gas. A Hewlett-Packard system (Avondale, PA) consisting of
model GLC 5890, integrator 3392A and autosampler 7671A was used. The
temperature was programmed to 100–210°C. The fatty acids were
identified by comparing retention times with those of NuCheck Prep
(Elysian, MN) fatty acid methyl esters standards and polyunsaturated
fatty acid (PUFA) mix no. 2 (Supelco, Bellefonte, PA).
The amounts of the fatty acids were given as the relative percentage of the sum of the fatty acids analyzed. The within-analyses CV of 15:0 was 13.4% in cholesterol esters and 9.1% in phospholipids. The CVs for all other fatty acids analyzed in the serum lipids were <1–5.5% except for 18:0 in cholesterol esters (9.9%) and 17:0 (6.3%) and 18:3(n-3) (8.2%) in phospholipids. When determining the proportions of fatty acids in adipose tissue, the CV was 1.6% for 14:0, 5.3% for 15:0 and 9.1% for 17:0. For comparison, CV for 18:2(n-6) was 0.7%.
DR.
An experienced dietitian provided detailed instructions to small groups
of participants or individually about weighing and recording all foods
consumed. The DR were kept for two 1-wk periods, 6 mo apart. Each
study participant was provided with an electronic scale, a set of
plastic standard household measures of volume [100 mL, 50 mL, 15 mL
(=1 tablespoon), 5 mL (=1 teaspoon) and 1 mL] and a food diary
(including detailed written instructions). Participants were encouraged
to use mainly the electronic scale. After the return of each 1-wk DR,
the dietitian reviewed the diary and, if needed, telephoned the
participants to resolve ambiguities. The DR were entered using a
personal computer nutrient software package MATS (Nordin 1992
). For nutrient calculations, we used the Swedish Food
Administration Food Database PC version 1992, which includes 1593 foods
and dishes (Bergström 1992
). For reported dishes
not included in this database, the dietitian obtained recipes from the
participants and entered appropriate amounts of the component foods.
The PC 1992 database provides information on total fat and 14 specific
fatty acids, including 14:0. However, this database does not include
the two specific fatty acids of our main interest: 15:0 and 17:0. We
estimated the total milk fat intake directly by summarizing the amount
of fat from all dairy products (milk, sour milk, yogurt, cheese, cream,
butter) and from dishes that include these products (taking into
account the amount of a specific milk product in the recipe). Then we
estimated the amounts of 15:0 and 17:0 specifically, using the
assumption based on empirical data that they represent 1.05 and 0.61
g/100 g, respectively, of total milk fat. These percentages are based
on analyses of 73 milk samples obtained from 10 commercial dairy herds
from the two different study regions in Sweden. The samples were
collected at afternoon milkings, immediately frozen to -20°C and
transported to the laboratory (Wolk et al. 1998
).
Furthermore, we estimated the total fat intake from ruminant meat
(beef, lamb). We estimated the amounts of 15:0 and 17:0 from this
source by using the assumption that they represent 0.43 and 0.83 g/100
g, respectively, of ruminant fat (Wolk et al. 1998
).
Repeated 24-h diet recall interviews.
Starting 1 mo after the first week of food DR, the dietitian
telephoned once every month to each participant in the study to
interview him about diet. She used a 24-h diet recall technique
completed with probing questions. With the help of a special
administrative program to choose days for consecutive interviews for
each individual, the dietitian obtained dietary information covering
all weekdays as well as weekends. Portion sizes were described in
household measures. All foods and dishes were computerized in exactly
the same way as the food DR.
Statistical analyses.
The analyses of dietary fat intake and adipose tissue composition were based on 114 subjects for whom adipose tissue as well as two dietary measurements (DR and 24-h recalls) were available. Serum analyses were based on a subsample of 104 subjects. The mean ± SD values are presented for total dairy and ruminant fat intake and for specific fatty acids. Natural logarithmic transformations were used to improve normality when necessary. To evaluate the association between intake of 14:0, 15:0 and 17:0 in the diet and their relative contents in triacylglycerols in adipose tissue as well as in cholesterol esters and phospholipids in serum, we used Pearson’s product-moment correlations and Spearman’s rank correlations. Spearman’s correlation coefficients were similar to Pearson’s correlation coefficients; therefore, we present only Pearson’s correlations in the tables. We also performed correlation analyses of adipose tissue composition in a subgroup of 104 subjects with available serum values to compare correlation coefficients for triacylglycerols, cholesterol esters and phospholipids among the same subjects. The SAS program was used for analyses (SAS Institute, Cary, NC). Values in the text are given and means ± SD.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. Absolute estimates of milk fat, fat from ruminant meat and 14:0, 15:0
and 17:0 intake based on the DR and repeated 24-h diet recalls were
very similar. The same estimates expressed as proportions of total fat
intake were also similar. Dairy fat was a source of 72% of 14:0 intake
[Pearson’s correlation, r, between total dairy fat intake
and 14:0 intake was 0.94 (DR)].
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Ratios between 15:0 and 17:0 in triacylglycerols in adipose tissue and
according to dietary intake estimates by DR and by 24-h recalls were
similar, namely 1.5. Interestingly, this ratio was 2 in
cholesterol esters in serum and 0.5 in phospholipids in serum,
indicating a differentiated incorporation of these fatty acids into
different lipid esters. Ratios between 14:0 and 15:0 were also
different: 20 according to daily intake (DR and 24-h recall), 10 in
adipose tissue, 5 in cholesterol esters and 2 in phospholipids
(r = 0.70 between 15:0 in adipose tissue
triacylglycerols and in serum cholesterol esters, r = 0.66 between 15:0 in adipose tissue triacylglycerols and in serum
phospholipids and r = 0.72 between 15:0 in serum
cholesterol esters and in serum phospholipids).
The correlations between the estimated intakes of dairy and ruminant
fat and the intakes of 14:0, 15:0 and 17:0 based on DR and fatty acid
composition of adipose tissue, serum cholesterol esters and
phospholipids are presented in Table 2
. The highest Pearson’s correlation was observed between total dairy
fat and 15:0 in triacylglycerols in adipose tissue (r = 0.71). However, even 14:0 in triacylglycerols was a good indicator of
total dairy fat intake (r = 0.64). Corresponding
Pearson’s correlation coefficients in a subgroup of 104 subjects (with
available serum) were the same. Generally, all correlations between
dairy fat intake and 14:0 and 15:0 fatty acid composition of
cholesterol esters and phospholipids in serum were lower than for
triacylglycerols but were higher for 17:0.
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. Pearson’s correlation between total dairy fat and 15:0 in adipose
tissue was similar to that for food DR (r = 0.74) and
the same as that for 14:0 (r = 0.64). Correlations in
the subgroup of 104 subjects were almost identical to those in the
whole group.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). The present findings are extended to an observation
of relatively high correlations between dairy fat intake and proportion
of 15:0 and 17:0 in serum cholesterol esters and phospholipids.
Furthermore, the findings are extended to show that the correlation of
total dairy fat intake with 14:0 in adipose tissue was similar to that
with 15:0. However, this correlation was weaker for phospholipids and
cholesterol esters. We also observed that dietary intake of 14:0 (of
which the content in foods is available in most of the food tables, and
therefore the intake of 14:0 is much easier to calculate than the
intake of total dairy fat or of 15:0 or 17:0) was relatively highly
correlated with the proportion of 15:0 and 15:0 plus 17:0 in adipose
tissue as well as in cholesterol esters and phospholipids.
The association observed in the present study between estimated total
dairy fat intake and the proportion of 15:0 in adipose tissue in men is
even slightly stronger (r = 0.74) than we reported
previously for women (r = 0.63) (Wolk et al. 1998
), indicating again that a relative content of this fatty
acid in adipose tissue is a valid biomarker for total dairy fat intake.
The relative content of 15:0 in serum cholesterol esters and
phospholipids, although it seems to be a poorer indicator of dairy fat
intake (r = 0.47–0.53) than triacylglycerols in
adipose tissue, might still be used as a biomarker in situations where
adipose tissue is not available. Laboratories that have difficulty in
analyzing 15:0 and 17:0 may instead consider analyses of 14:0 in
adipose tissue as an equivalent choice. However, 14:0 content in serum
cholesterol esters and phospholipids is probably not a sufficient
biomarker (r = 0.29–0.34) for dairy fat intake.
A slightly higher correlation of adipose tissue fat composition with 24-h recalls than with food DR has been expected, because 14 independent 24-h dietary recalls distributed over 1 y probably better reflect the true variation in long-term intake than do two 7-(consecutive) d food DR performed 6 mo apart. It has also been suspected that the process of keeping a DR may change an individual’s normal diet, thus decreasing the correlation of the records with the "truth."
The observed correlations in the present study may also be influenced
by biological variability and laboratory measurement error. Both of
these factors may contribute to within-person variation in measured
fatty acid levels in adipose tissue and serum cholesterol esters and
phospholipids. In our study, we only have information about the
variation of laboratory assays for 14:0, 15:0 and 17:0 in adipose
tissue and serum. We have not collected repeated samples (after, for
example, 1 y), so we do not have information about biological
variability of these fatty acids in adipose tissue and/or serum. To our
knowledge, there are no reports published on the kinetics of the
incorporation of these fatty acids into serum lipids and adipose
tissue. However, by comparison with kinetics of other fatty acids, it
may be assumed that the biological within-subject variability of
the composition of these fatty acids may be higher in the (fasting)
serum lipid esters than in the adipose tissue (probable half-lives
days/weeks versus years) (Katan et al. 1997
). These two
types of variation (laboratory and biological) influencing our measure
of fatty acid levels are reflected in the correlations. The observed
correlation coefficients are indeed lower for serum analyses of fatty
acids than for adipose tissue, due to higher variation in laboratory
analyses (CV for 15:0 = 13.4% in serum cholesterol esters and
9.1% in phospholipids versus 5.3% in adipose tissue) and possibly
also higher biological variation in serum. Our results are not likely
to be influenced by selection bias, because age distributions were
similar in this subgroup of 114 men (representing 124 first consecutive
men) and in the main validation study of a food frequency
questionnaire.
The strength of relation in our study between the estimated intake of
total dairy fat and the proportion of 15:0 in adipose tissue is of a
similar order (Tjønneland et al. 1993, van
Staveren et al. 1986, Wolk et al. 1998a) or
stronger (Hunter et al. 1992
) than those described
earlier between the intake of PUFA and adipose tissue fatty acids.
Tjønneland et al. (1993
) reported a correlation
coefficient of 0.74 between two 7-d DR and fat aspirate measures of
PUFA for Danish men. In our study of women, we found a correlation of
0.72 between PUFA content in adipose tissue and dietary intake
estimates from four 7-d weighed food DR (Wolk et al. 1998a
). In a Dutch study of women, a correlation of 0.68 was
observed compared with 19 different 24-h recalls (van Staveren
et al. 1986). Hunter et al. (1992) reported a
correlation coefficient of 0.49 between two 7-d DR and fat aspirate
measures of PUFA for men.
Recently it was reported that the proportion of 15:0 in serum
cholesterol esters and phospholipids can be used as a marker for intake
of total milk fat, with correlations of 0.46 and 0.34, respectively
(Smedman et al. 1999
). Our results support this finding
and indicate that 15:0 content in serum phospholipids or cholesterol
esters might be considered as a valid biological marker of dairy fat
intake, although 15:0 content in adipose tissue significantly better
reflects long-term intake of dairy fat.
Milk fat is of special interest in the development of artery disease
because of its atherogenic and thrombogenic properties; 67% of milk
fat consists of saturated fatty acids (Ulbright and Southgate, 1991
). In ecological studies, per capita consumption
of milk and milk products is significantly correlated with increased
coronary artery disease mortality rates (Artaud-Wild et al. 1993
). However, many prospective cohort studies do not confirm
the expected positive association of saturated fat with this chronic
disease (Willett 1998
). These discrepancies may in part
result from poor validity of dietary assessment of the consumption of
dairy products based on subjective self-administered
questionnaires. Therefore, identifying a valid, objective biological
marker of dairy fat intake might be of considerable importance for
epidemiological nutritional studies. However, the high correlation
between 15:0 in adipose tissue and total dairy fat intake estimated
from repeated 24-h recalls suggests that we do not really know whether
the biomarker or intake estimates are superior: our study indicates
that both are informative. In practice, it means that they are
equivalent choices in epidemiological studies.
In our study population, milk fat represented 29.9% and meat fat from ruminants represented 5.2% of the total fat intake. The small percentage from ruminant fat explains why adding information about the intake of 15:0 and 17:0 from ruminant fat did not increase correlations. However, it should be noted that these relations between total dietary intake of 15:0 and 17:0 and adipose tissue composition might be different in populations with a high intake of ruminant fat (beef and lamb) and a low intake of milk fat. The value of 14:0 content in adipose tissue as a biomarker for dairy fat intake might also differ among populations. In our study population, 72% of this fatty acid was from dairy fat; in populations with different dietary habits, this proportion might be lower and therefore the validity of 14:0 as a biomarker for dairy fat intake might be also lower.
In conclusion, 15:0 or 14:0 content in adipose tissue is a valid biomarker for dairy fat intake. In a case where adipose tissue is not available, 15:0 content in serum cholesterol esters or phospholipids might be used. However, it should be noted that intake data based on repeated 24-h recalls is equally informative and may be an equivalent choice in nutritional studies.
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FOOTNOTES |
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3 Abbreviations used: DR, dietary record; PUFA,
polyunsaturated fatty acid.
Manuscript received July 24, 2000. Initial review completed September 21, 2000. Revision accepted November 29, 2000.
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