Nutrient Intakes and Adenocarcinoma of the
Esophagus and Distal Stomach
Honglei Chen, Katherine L. Tucker, Barry I. Graubard,
Ellen F. Heineman, Rodney S. Markin, Nancy A. Potischman,
Robert M. Russell, Dennis D. Weisenburger, and Mary H. Ward
Abstract: We studied the relationship between nutrient in-
takes and adenocarcinoma of the esophagus and distal stom-
stomach cancer cases, and 449 controls in a population-
based case-control study in eastern Nebraska. The residual
method was used to adjust nutrient intake quartiles or tertiles
for energy intake. We observed significant inverse associa-
tions with risk of esophageal adenocarcinoma for dietary
intakes of total vitamin A [highest vs. lowest quartile, multi-
variate odds ratio (OR) = 0.5, P for trend = 0.05], ?-crypto-
folate (OR = 0.5, P = 0.03), zinc (OR = 0.5, P = 0.05), dietary
fiber (OR = 0.5, P = 0.05), protein (OR = 0.5, P = 0.02), and
carbohydrate (OR = 0.4, P = 0.02). For distal stomach can-
cer, only vitamin C (OR = 0.6, P = 0.04), dietary fiber (OR =
inversely associated with risk. Our analyses showed signifi-
cant interaction between dietary fat intake, but not intakes of
other nutrients, and respondent type for both cancer sites.
Subgroup analyses among self-respondents revealed positive
associations between saturated fat intake and risk of esopha-
geal adenocarcinoma (OR = 1.0, 4.1, and 4.6 for intake
tertiles, P for trend = 0.02) and risk of distal stomach cancer
(OR = 1.0, 1.2, and 3.6, P = 0.03). However, no such associa-
tions were found among proxy respondents. Our data suggest
that greater intake of dietary fiber, certain carotenoids, and
vitamins may decrease the risk of esophageal adenocarci-
noma, whereas greater intake of saturated fat may increase
the risk of esophageal adenocarcinoma and distal stomach
The incidence and mortality of esophageal adenocarci-
noma have been increasing for >20 yr in the United States. A
3.5-fold increase in incidence was observed among white
men from 1974 to 1994, and a 2-fold increase was seen
among black men from 1980 to 1994 (1). In contrast, during
the same period, esophageal squamous cell cancer rates were
relatively stable. Rates for stomach cancer have been decreas-
stomach cancer still ranks second in cancer incidence and
mortality rates worldwide, just behind lung cancer (4).
The underlying reasons for the increase in esophageal
adenocarcinoma are not well understood, and risk factors for
this cancer have been the focus of recent investigations.
Studies suggest that obesity (5–9), gastroesophageal reflux
diseases, and Barrett’s esophagus (10–12) are strongly asso-
ciated with risk for esophageal adenocarcinoma, whereas
smoking (13,14) and low socioeconomic status (15) are as-
sociated with moderately increased risk.
Diet plays an important role in the pathogenesis of stom-
ach cancer, and the decline of this cancer over the past sev-
eral decades may be partially attributable to the increased
availability of fresh fruit and vegetables (2,4). Numerous ep-
idemiological studies have suggested that higher intake of
fruit and vegetables, vitamin C, and β-carotene may de-
crease risk of stomach cancer and higher intake of salt may
increase the risk (4). Fewer studies have examined the asso-
ciations between diet and esophageal adenocarcinoma.
Lower risk has been observed with higher intake of fruit and
vegetables (5,16–18), dietary fiber (5,13,16,17), vitamin C
(5,16), β-carotene (19), vitamin A (16), and lutein, niacin,
vitamin B-6, and zinc (17), whereas greater risk has been ob-
served for higher intake of red meat, processed meat, and
gravy (20), as well as dietary fat (13,17) and vitamin A from
animal sources (13). Therefore, we hypothesized that nutri-
ents from fruits and vegetables are inversely associated with
risk of esophageal adenocarcinoma and distal stomach can-
cer and that dietary fat is positively associated with the risk
of esophageal adenocarcinoma.
NUTRITION AND CANCER, 42(1), 33–40
H. Chen, K. L. Tucker, and R. M. Russell are affiliated with the Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111. H.
Chen, B. I. Graubard, E. F. Heineman, and M. H. Ward are affiliated with the Division of Cancer Epidemiology and Genetics and N. A. Potischman with the
Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD 20892. R. S. Markin and D. D. Weisenburger are affiliated with
the Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198.
Materials and Methods
We conducted a population-based case-control study in
the 66 counties of eastern Nebraska to evaluate potential
roles of occupational and dietary risk factors in esopha-
geal adenocarcinoma, stomach cancer, and adult glioma. A
detailed description of the methods has been published else-
where (20). Briefly, incident cases of esophageal and stom-
ach adenocarcinomas were identified from the Nebraska
Cancer Registry (1 July 1988–1990) or by a review of dis-
charge diagnoses and pathology records at the 14 participat-
ing hospitals in Omaha, Lincoln, and Grand Island, NE
(1991–30 June 1993), covering >90% of the population of
these 66 counties in eastern Nebraska. Eligible cases were
white male or female residents of these counties, ≥21 yr old.
Cases were limited to whites, because the controls were
sampled from a previous study (as described below) that in-
cluded only whites because of the expected small numbers
of other ethnic groups. Concurrently, a separate group of
adult glioma patients with the same selection criteria was
also identified. Only cases confirmed as adenocarcinoma
of the esophagus and stomach were retained in the analyses.
A gastrointestinal pathologist (RM) reviewed all initial
diagnoses of stomach cancer, except lymphomas, leiomyo-
sarcomas, and reticulosarcomas, and all diagnoses of esoph-
ageal cancer, except those located in the upper and cervical
esophagus (ICD-O codes 150.0 and 150.3), which are al-
most exclusively squamous cell carcinomas.
For efficiency and to reduce the cost of the study, con-
trols were randomly selected from the population-based
controls of a previous case-control study of hematopoietic
cancers conducted in 1986–1987 in the same counties (21).
Details of control selection in that study have been published
previously (21,22). Controls in the present study were fre-
quency matched to the overall distribution of the esopha-
geal, stomach, and glioma cases by age, gender, and vital
status (20). We selected deceased controls so that the reli-
ability of the interview information would be more com-
parable to that for deceased cases. Living controls were
oversampled to allow for more study power in subgroup
analyses by respondent type.
Telephone interviews with cases and controls or their
proxies were performed during 1992–1994 by trained inter-
viewers. Cases and controls were asked to report their di-
etary intakes, history of smoking, alcohol intake, usual adult
weight and height, occupational history, and other factors
before 1985. To aid their memory of this time frame, the in-
terviewers reminded respondents about local and national
events in 1985 and asked them to recall any major event in
their life around that time. A total of 137 eligible esophageal
adenocarcinoma cases, 170 stomach cancer cases, and 502
controls or their proxy respondents completed interviews
with overall response rates of 88%, 79%, and 83%, respec-
tively. The response rate of controls in the previous study,
which took into account the refusals at Stage 1 of the ran-
dom-digit-dialing screening, was 87%. Therefore, the ad-
justed rate was 72% for reinterviewed controls in the present
study. Because of the poor prognoses of these cancers, inter-
views were conducted with the next-of-kin for 76% of
esophageal adenocarcinoma cases and 80% of stomach can-
cer cases. A total of 61% of control interviews involved
proxy respondents. Among all proxy respondents, 45.4%
were spouses of the participants, 36.2% were their children,
10% were their parents, and the rest were other relatives or
A modified version of the short Health Habits and His-
tory Questionnaire (23) was used to collect dietary informa-
tion. Nutrient intakes calculated from the short version of the
Health Habits and History Questionnaire are strongly corre-
lated with intakes calculated from the full questionnaire
(23,24). Age- and gender-specific portion sizes and most nu-
trient values came from the DIETSYS database (25) with
nutrient values appropriate for the food supply in the 1980s.
Values for total provitamin A carotenoids and five specific
carotenoids (α-carotene, β-carotene, β-cryptoxanthin, lyco-
pene, and lutein + zeaxanthin) were from a database devel-
oped by Block (25–27). Because carotenoid databases have
changed over time, problems with an older database would
introduce error in properly classifying and ranking individu-
als, making it more difficult to find associations. However,
carotenoid values derived from this database have been
shown to correlate well with values derived from the later
US Department of Agriculture-National Cancer Institute da-
tabase (27) and are reasonably correlated with serum param-
Subjects with unknown intakes for ≥20% of the food
questions were excluded from analyses. This left 124 (91%)
esophageal adenocarcinoma cases, 154 (91%) stomach can-
cer cases, and 449 (89%) controls in the dietary analysis. A
total of 124 stomach cancer cases arose in the distal part of
the stomach and 30 in the stomach cardia. Because of the
small number of cardia cases and because cardia cancer is
hypothesized to have different risk factors from distal stom-
ach cancers, we excluded cardia cases from our analyses.
Odds ratios (ORs) and their 95% confidence intervals (CIs)
were calculated by unconditional logistic regression. All sig-
nificance tests were two-sided (α = 0.05).
The importance of adjusting for energy intake in dietary
research has been discussed (28). In this study, nutrient in-
take was categorized into quartiles after adjustment for en-
ergy intake using the residual method (28). Tertiles, rather
than quartiles, were used in the subgroup analyses by re-
spondent type because of the small sample size. We tested
for linear trend by including the median of each quartile or
tertile as a continuous variable in the model and testing for
the significance of the slope. The ORs were adjusted in the
analyses for age, gender, alcohol use (never, past, and cur-
rent drinkers), tobacco use (nonsmokers, <30/day, ≥30/day),
education level (college graduates: yes/no), family history of
respective cancers (yes/no), and vitamin supplement use
(yes/no). Body mass index (BMI, kg/m2), a known risk fac-
tor for esophageal adenocarcinoma, and age squared were
also adjusted for esophageal adenocarcinoma. We tested for
34Nutrition and Cancer 2002
interactions between nutrient intakes and respondent type on
a multiplicative scale. The results are reported separately
when there were significant interactions or the results were
meaningfully different across respondent type; otherwise,
we adjusted for respondent type in all analyses.
Table 1 shows characteristics of the study population in
the dietary analyses by case-control status. Esophageal ade-
nocarcinoma cases were predominantly men. Cases were
more likely than controls to be past drinkers and smokers
and to have a higher average BMI. In a separate analysis, we
found a strong positive association between BMI and risk
for esophageal adenocarcinoma [multivariate ORs for BMI
<20, 20–24.9, 25–29.9, and ≥30 kg/m2were 1.0 (reference),
2.2, 3.8, and 6.1, respectively, P for trend = 0.001]. Esopha-
geal adenocarcinoma cases also reported higher energy in-
take than controls. Stomach cancer cases were older and less
likely than controls to be past smokers or drinkers. Also the
percentage of college graduates and vitamin supplement us-
ers was lower among stomach cancer cases. Cases were also
more likely than controls to report a positive family history
of respective cancers.
The mean values for nutrient intakes for cases and con-
trols are reported in the Appendix. Multivariate adjusted
associations between selected nutrient intakes and adeno-
carcinoma of the esophagus and distal stomach are described
in Tables 2 and 3. The results were not meaningfully differ-
ent by respondent type for these nutrients. For esophageal
adenocarcinoma, the highest intake quartiles of total vitamin
A, β-cryptoxanthin, riboflavin, folate, zinc, dietary fiber,
protein, and carbohydrate were each associated with an
~40–50% decrease in risk compared with the lowest quar-
tiles, and significant inverse trends were observed for these
nutrients. Inverse associations with the risk of distal stomach
cancer were observed for intakes of vitamin C, dietary fiber,
and carbohydrate. Subjects in the highest intake quartile of
β-cryptoxanthin also had a 40% lower risk than those in the
lowest quartile; however, the associations did not reach sta-
tistical significance. Sodium intake was not associated with
either cancer, and we did not find any association with the
frequency of adding salt to foods (seldom or never, some-
times, often, or always). However, in a separate analysis of
salty preference categories (very salty, somewhat salty, not
very salty, and not salty at all), we found nonsignificantly el-
evated risk for distal stomach cancer with a preference for
“very salty” food vs. “not salty at all” (multivariate OR =
1.8, 95% CI = 0.6–5.3).
We found significant interactions between dietary fat in-
takes and respondent type for both cancer sites; therefore,
data are presented separately by respondent type. We pre-
sent results for esophageal cancer adjusted for age, age
squared, gender, and BMI and results for stomach cancer ad-
justed for only age and gender; there was no adjustment for
other factors because of the small sample sizes. Saturated fat
was positively associated with risk for both cancer sites
among self-respondents (Table 4). There was no association
between fat intake and cancer risk among those with proxy
respondents. Among proxies, the multivariate adjusted ORs
associated with tertiles of saturated fat intakes were 1.0 (ref-
Vol. 42, No. 135
Table 1. Characteristics of the Study Population by Case-Control Statusa,b
(n = 449)
(n = 124)
Distal stomach cancer
(n = 124)
Energy intake, MJ
Alcohol use, %
Tobacco use, %
College education, %
Family history, %
Ever took vitamin supplement, %
59.8 ± 17.6
25.0 ± 4.4
8.5 ± 3.5
62.3 ± 12.4
26.4 ± 3.6†
9.2 ± 3.8*
70.3 ± 11.4†
25.3 ± 3.7
9.0 ± 3.7
a: Means ± SD are presented for continuous variables and compared by Student’s t-test; proportions are presented for categorical variables and compared by
Mantel-Haenszel χ2test. BMI, body mass index.
b: Statistical significance is as follows: *, P < 0.05; †, P < 0.01 vs. control.
36Nutrition and Cancer 2002
Table 2. ORs and 95% CIs for Esophageal Adenocarcinoma by Quartiles of Nutrient Intake Residualsa,b
Intake Residual Quartiles
P for Trend
Total vitamin A
Provitamin A carotenoids
Lutein + zeaxanthin
a: Compared with lowest quartile [Q1: odds ratio (OR) = 1.0], with adjustment for age, age squared, gender, respondent type, BMI, alcohol use, tobacco use,
education level, family history of respective cancers, and vitamin supplement use. CIs, confidence intervals.
b: Statistical significance is as follows: *, P < 0.05 vs. Q1.
Table 3. ORs and 95% CIs for Distal Stomach Cancer by Quartiles of Nutrient Intake Residualsa,b
Intake Residual Quartiles
Nutrient Q1Q2 Q3 Q4
P for Trend
Total vitamin A
Provitamin A carotenoids
Lutein + zeaxanthin
a: Compared with lowest quartile (Q1: OR = 1.0), with adjustment for age, gender, respondent type, alcohol use, tobacco use, education level, family history
of respective cancers, and vitamin supplement use.
b: Statistical significance is as follows: *, P < 0.05; †, P < 0.01 vs. Q1.
erence), 1.4, and 0.7 for esophageal adenocarcinoma (P for
trend = 0.3) and 1.0, 1.7, and 1.2 for distal stomach cancer (P
Approximately 39% of controls took some type of vita-
min supplement before 1985, with most (86%) reporting the
use of multiple vitamins. Individual vitamin supplement use
was less common (vitamin A, 3%; vitamin C, 15%; vitamin
E, 7%; cod liver oil, 9%). There was no association between
any vitamin supplement use and risk of esophageal adeno-
carcinoma. However, those who had used any vitamin sup-
plements had a significantly lower risk of distal stomach
cancer than nonusers (OR = 0.6, 95% CI = 0.3–1.0). Results
for individual vitamin supplement use and risk of distal
stomach cancer were unstable because of small sample sizes
(data not shown).
Our results show that higher intakes of total vitamin A, β-
cryptoxanthin, riboflavin, folate, zinc, dietary fiber, protein,
and carbohydrate were associated with lower risk of esopha-
geal adenocarcinoma and that higher intakes of vitamin C,
dietary fiber, and carbohydrate were associated with lower
risk of distal stomach cancer. Greater intake of saturated fat
was related to higher risk at both cancer sites. The overall as-
sociations tended to be stronger for esophageal adenocar-
Several studies have investigated the role of diet in
esophageal adenocarcinoma, and inverse associations have
been reported with dietary fiber (5,13,16,17), dietary antiox-
idants (5,16,19), and fruit and vegetables (5,16–18). Our re-
sults support these findings. In our study, dietary fiber was
associated with a reduced risk in esophageal adenocarci-
noma and distal stomach cancer. A potential role of dietary
fiber in cancer etiology, particularly in colorectal cancer, has
been brought into question by recent prospective studies
(29–31). Nevertheless, the present evidence suggests inverse
associations between dietary fiber intake and risk of esopha-
geal adenocarcinoma (5,13,16,17) and stomach cancer (32,
33). Burkitt et al. (34,35) found that higher intake of dietary
fiber was associated with lower risk of hiatus hernia, which
has been implicated as a risk factor for esophageal adeno-
Carotenoids are thought to play important roles in cancer
prevention due to a variety of mechanisms (36,37). Some ca-
rotenoids have been inversely associated with risk of esoph-
ageal adenocarcinoma and stomach cancers in previous
studies (19,38). We observed an inverse association with
risk of esophageal adenocarcinoma for β-cryptoxanthin, but
not for other carotenoids. Folate and riboflavin are important
cofactors in DNA metabolism, and substantial epidemiolog-
ical evidence suggests that lower folate intake is associated
with higher risk for other epithelial tumors (39,40). Several
mechanisms have been proposed, which primarily involve
prevention of DNA hypomethylation and maintenance of
the integrity of the DNA repair system (41). Vitamin C is an
important antioxidant and inhibitor for endogenous synthe-
sis of N-nitroso compounds (42,43), which are strong carcin-
ogens to the esophagus and stomach in animal models (44).
Some epidemiological studies suggest that greater salt in-
take is associated with a higher risk of stomach cancer (4).
Salt per se is not a carcinogen (45); rather, it is thought to act
as an irritant to the stomach mucosa protective layer and
may enhance carcinogenesis induced by other carcinogens
(4,46). Despite the high reported intake of sodium (mean
3,603 mg/day, range 743–10,962 mg/day), we found no evi-
dence that sodium intake from foods or adding salt to foods
was positively associated with risk for either cancer site.
However, a preference for very salty foods was associated
with a nonsignificant elevated risk at both cancer sites.
Previous studies have found a nonsignificant inverse as-
sociation between protein intake and risk of esophageal
adenocarcinoma, with ORs of 0.4–0.8 between extreme in-
take categories (5,16,17). A similar OR was observed in this
study with a significant trend. Greater carbohydrate intake
Vol. 42, No. 1 37
Table 4. ORs and 95% CIs for Adenocarcinomas of the Esophagus and Distal Stomach by Tertiles of Dietary Fat Intake
Residuals Among Self-Respondentsa,b
Esophageal AdenocarcinomaDistal Stomach Cancer
ControlCase OR (95% CI) ControlCase OR (95% CI)
P for trend
P for trend
a: Compared with lowest tertile (T1: OR = 1.0), with adjustment for age and gender for both cancers and age squared and BMI for esophageal
b: Statistical significance is as follows: *, P < 0.05 vs. T1.
has been positively associated with higher risks of esopha-
geal squamous carcinoma (47–49) and stomach cancer
(49,50). In contrast with these previous studies, we found
that carbohydrate intake was inversely associated with risks
for esophageal adenocarcinoma and distal stomach cancer in
this population. Carbohydrate intake only accounted for an
average of 38% of total energy intake among controls and
was negatively correlated with fat intake (partial correlation
coefficient = −0.54 among self-respondent controls). There-
fore, a higher intake of carbohydrate in this population may
just represent a lower fat intake and a more balanced diet,
which may partially explain its inverse associations with
both cancer sites.
Positive associations with risk of stomach cancer have
been reported for dietary intakes of total fat or saturated fat
(32,33,51,52), although the results are not entirely consistent
(53,54). Epidemiological studies of fat intake and esopha-
geal adenocarcinoma are limited, and the findings have been
inconsistent (5,13,16,17). Two studies (13,17) reported an
approximately two- to threefold higher risk of esophageal
adenocarcinoma for those in the highest quartile of total fat
intake than for those in the lowest, whereas Brown et al. (5)
found no association with total dietary fat and only a slight
and nonsignificant increase in risk with greater saturated fat
In our study, the average energy contribution from di-
etary fat among eligible controls was 41% (range 15–57%).
Thus the high upper intake level and wide range of fat intake
afforded us a good opportunity to evaluate the intake of fat
as a risk factor for these cancers. Our data suggest potential
positive associations between saturated fat intake and risks
at both cancer sites. The association tends to be stronger for
esophageal adenocarcinoma than for distal stomach cancer.
However, because of the small sample sizes in our dietary
fat analyses and the lack of an association among proxy re-
spondents, our results need to be confirmed in other large
Our study had several limitations. The major limitation
was that, because of the poor survival rates for these cancers,
the majority of the cases had died before we were able to in-
terview them, and we obtained information from their next-
of-kin. We interviewed next-of-kin of deceased controls to
make the quality information between cases and controls
comparable. The use of deceased controls could introduce
selection bias, because they might differ from the base popu-
lation in terms of exposure and potential confounder distri-
butions (55,56). However, except for dietary fats, nutrient
intakes among controls were similar by respondent type af-
ter adjustment for age, gender, and total energy intake. Re-
called diet has been found to be more closely associated with
past than with present diet (57); however, recall over many
years contains error due to memory (58). Furthermore,
cancer symptoms, particularly the gastric reflux that is asso-
ciated with esophageal adenocarcinoma, could result in di-
etary changes that may have affected the cases’ reporting of
their usual adult diet. However, our results are consistent
with results from other case-control studies, and possible re-
porting bias could only be excluded in prospective studies.
Finally, we did not collect the amount of supplement use in
this study; therefore, results of micronutrients should be
considered as from food sources.
Testing associations for many nutrients within the same
study is subject to the criticism of multiple comparisons. We
did not use adjustment for multiple comparisons in this
study; therefore, any individual comparison must be judged
with caution. However, the overall pattern of our results is
internally consistent and is also consistent with available lit-
In summary, our study suggests that higher intake of cer-
tain nutrients from plant sources, including dietary fiber,
certain carotenoids, and vitamins, is associated with lower
risks for adenocarcinoma of the esophagus and distal stom-
ach, whereas higher intake of saturated fat may increase risk
for both cancers.
Acknowledgments and Notes
The authors acknowledge Shannon Merkle and Jane Curtin (Informa-
tion Management Services) for programming support. The authors thank
Carol Russell, Bob Saal (Westat), and Casey Boudreau (Survey Research
Associates) for their contribution to data collection and management;
Monica Seeland and the Nebraska Cancer Registry for providing data; in-
terviewers and support staff for their diligent work; the many physicians,
hospital staff, and study participants who cooperated in the study; and Dr.
Wong-Ho Chow for valuable comments. Address correspondence to
M. H. Ward, Occupational Epidemiology Branch, National Cancer Insti-
tute, 6120 Executive Blvd., EPS-8104, MSC-7420, Bethesda, MD 20892-
7420. E-mail: firstname.lastname@example.org.
Submitted 17 July 2001; accepted in final form 29 November 2001.
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40Nutrition and Cancer 2002
Nutrient Intakes Across Case-Control Statusa,b
(n = 449)
(n = 124)
Distal stomach cancer
(n = 124)
Total vitamin A, IU
Provitamin A carotenoids, µg
Lutein + zeaxanthin
Vitamin B-6, mg
Vitamin C, mg
Vitamin E, mg α-TE
Dietary fiber, g
Protein, % of energy
Carbohydrate, % of energy
Dietary fat, % of energy
Saturated fat, % of energy
8,799 ± 5,172
2,861 ± 1,844
410 ± 362
2,360 ± 1,493
71 ± 50
1,074 ± 845
1,509 ± 1,229
1,025 ± 718
2.4 ± 1.1
1.9 ± 0.8
334 ± 147
23 ± 9.2
126 ± 69
8.5 ± 4.1
14 ± 6.4
14 ± 5.8
1,002 ± 524
3,603 ± 1,618
11 ± 4.6
18 ± 3.2
38 ± 6.7
41 ± 6.6
16 ± 3.1
8,098 ± 4,306
2,745 ± 1,817
360 ± 293
2,249 ± 1,415
59 ± 52*
1,029 ± 874
1,465 ± 1,293
962 ± 592
2.2 ± 0.9
1.9 ± 0.7
314 ± 132
24 ± 8.5
111 ± 60*
8.7 ± 4.0
14 ± 5.1
15 ± 5.3
904 ± 468
3,831 ± 1,529
11 ± 4.8
17 ± 3.3*
36 ± 6.8†
41 ± 7.4
16 ± 3.2
8,798 ± 4,777
2,851 ± 1,829
389 ± 332
2,370 ± 1,477
64 ± 46
1,069 ± 936
1,424 ± 969
1,047 ± 635
2.5 ± 1.1
2.0 ± 0.9
326 ± 148
23 ± 9.5
116 ± 64
8.7 ± 4.4
14 ± 6.0
15 ± 5.4
1,035 ± 554
3,731 ± 1,454
11 ± 4.5
18 ± 3.3
36 ± 6.2†
42 ± 6.2*
17 ± 3.0†
a: Values (means ± SD) are presented for continuous variables and compared by Student’s t-test. α-TE, α-tocopherol equivalents.
b: Statistical significance is as follows: *, P < 0.05; †, P < 0.01 vs. control.
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