Professional Documents
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INTRODUCTION
202
populations with different cultural backgrounds (412). However, not all studies are consistent (13), and, because these studies
focused on patterns of food group intake rather than on intakes of
single food groups, conclusions about whether fruit and vegetables per se slow down weight gain cannot be inferred directly
from these findings.
Cross-sectional studies that specifically addressed the relation of fruit and vegetable intake with body weight often yielded
null results (14). However, the temporality of this relation
cannot be addressed in cross-sectional studies because it is
possible that persons who have gained weight change their food
consumption patterns. In prospective studies, high intakes of
fruit (15, 16), vegetables (17), or both combined (8, 18, 19) were
related to smaller weight gains. However, some prospective studies
reported that fruit and vegetable intake was not associated with
change in body weight (20, 21) or waist circumference (22),
1
From the German Institute of Human Nutrition (DIfE) Potsdam-Rehbrucke, Department of Epidemiology, Nuthetal, Germany (BB, MBS, and
HB); the Division of Human Nutrition, Wageningen University, Wageningen, Netherlands (EJMF); the Department of Public Health Nutrition, Technical University Munich, Munich, Germany (MBS); the Medical Research
Council Epidemiology Unit, Elsie Widdowson Laboratories, Cambridge,
United Kingdom (NGF, NJW, and SS); the CSPO-Scientific Institute of
Tuscany, Molecular and Nutritional Epidemiology Unit, Florence, Italy
(DP and GT); the Danish Cancer Society, Institute of Cancer Epidemiology,
Copenhagen, Denmark (JH and AT); the Departments of Clinical Epidemiology (MUJ and KO) and of Cardiology (KO), Aarhus University Hospital,
Aalborg, Denmark; the National Institute for Public Health and the Environment, Bilthoven, Netherlands (HD and DLvdA); and the Institute of Preventive Medicine, Copenhagen University Hospital, Centre for Health and
Society, Copenhagen, Denmark (TIAS).
2
None of the sponsors of DiOGenes (Diet, Obesity, and Genes) had a role
in the study design, data collection, analysis, or interpretation of the data in
the written report or in the decision to submit for publication. This integrated
program was set up to target the issue of the obesity problem from a dietary
perspective, seeking new insights and new routes to prevention.
3
Supported by the European Committee, contract number FP6-513946.
The parties of the project are listed on the website of the project (http://www.
diogenes-eu.org/).
4
Address correspondence to B Buijsse, German Institute of Human Nutrition Potsdam-Rehbrucke, Department of Epidemiology Arthur-ScheunertAllee 114-116, 14558 Nuthetal, Germany. E-mail: brian.buijsse@dife.de.
Received December 19, 2008. Accepted for publication April 7, 2009.
First published online May 20, 2009; doi: 10.3945/ajcn.2008.27394.
Am J Clin Nutr 2009;90:2029. Printed in USA. 2009 American Society for Nutrition
ABSTRACT
Background: High fruit and vegetable intakes may limit weight
gain, particularly in susceptible persons, such as those who stop
smoking.
Objective: The objective was to assess the association of fruit and
vegetable intake with subsequent weight change in a large-scale
prospective study.
Design: The data used were from 89,432 men and women from 5
countries participating in the European Prospective Investigation
into Cancer and Nutrition (EPIC). The association between fruit
and vegetable intake and weight change after a mean follow-up of
6.5 y was assessed by linear regression. Polytomous logistic regression was used to evaluate whether fruit and vegetable intake relates
to weight gain, weight loss, or both.
Results: Per 100-g intake of fruit and vegetables, weight change
was 214 g/y (95% CI: 219, 29 g/y). In those who stopped smoking
during follow-up, this value was 237 g/y (95% CI: 258, 215 g/y;
P for interaction , 0.0001). When weight gain and loss were analyzed separately per 100-g intake of fruit and vegetables in a combined model, the odds ratios (95% CIs) were 0.97 (0.95, 0.98) for
weight gain 0.5 and ,1 kg/y, 0.94 (0.92, 0.96) for weight gain 1
kg/y, and 0.97 (0.95, 0.99) for weight loss 0.5 kg/y. In those who
stopped smoking during follow-up, the odds ratios (95% CIs) were
0.93 (0.88, 0.99), 0.87 (0.81, 0.92), and 0.97 (0.88, 1.07), respectively (P for interaction , 0.0001).
Conclusions: Fruit and vegetable intake relates significantly, albeit
weakly inversely, to weight change. For persons who stop smoking,
high fruit and vegetable intakes may be recommended to reduce the
risk of weight gain.
Am J Clin Nutr 2009;90:2029.
which makes the overall view of the role of fruit and vegetable in
the prevention of weight gain less consistent.
In the present study, we assessed whether fruit and vegetable
intake is associated with subsequent changes in body weight
within a multicenter European prospective cohort study. Because
of our large sample size, we were able to evaluate whether the
relation between fruit and vegetable consumption and weight
change was stronger in situations in which persons are susceptible
to weight gain, with smoking cessation the most well-known
factor (2325).
SUBJECTS AND METHODS
Study population
203
204
BUIJSSE ET AL
Statistical analysis
We first evaluated the shape of the association of fruit and
vegetable intake with weight change by using spline regression
with knots placed at quartiles of the distribution (37). After
confirming a linear relation, we chose to analyze fruit and vegetable intake as a continuous variable.
The association of fruit and vegetable intake with weight change
was first assessed by linear regression methods. The difference
in weight change and corresponding 95% CI by intake of fruit
and vegetables was estimated with annual weight change as the
dependent variable. In polytomous logistic regression models
(PROC CATMOD; SAS Institute Inc, Cary, NC), annual weight
change was classified as minor weight gain (0.5 to ,1 kg/y),
major weight gain (1 kg/y), weight loss (0.5 kg/y), or weight
stable ( 20.5 to ,0.5 kg/y weight change). Odds ratios and
their 95% CIs of weight gain and weight loss were calculated
per 100-g intake of fruit and vegetables per day.
All analyses were adjusted for age (continuous), sex, cohort (5
dummy variables with DK-CopAa as the reference), duration of
follow-up (years), and baseline weight (continuous). In multivariable-adjusted models, we also included level of education
(dummy variables for none/primary school, secondary school,
technical/professional school, missing values; university degree =
reference), height at baseline (continuous), smoking behavior
(dummy variables for stable smokers, starters, quitters, and unknown smoking status; nonsmokers = reference), physical activity (inactive, moderately active, active, missing; moderately
inactive = reference), alcohol intake (dummy variables for 0,
.1830, .3060, and .60 g/d; because of higher intakes in
men, intakes .60 g/d in this group was split as .6096 and
.96 g/d; .018 g/d = reference), and, in women, postmenopausal status and postmenopausal hormone use (both yes
or no). In additional models we also adjusted for total energy
intake (continuous).
Stratified analyses were conducted by sex, cohort, age, smoking
behavior, and follow-up duration (DiOGenes-wide median split
at 5.5 y). Effect modification was statistically tested by entering
cross-product [fruit and vegetable intake times sex, cohort in
categories, age in 2 categories, BMI in 2 categories, follow-up
duration in 2 categories (median split), and smoking in categories] terms along with main effects in the multivariable model
(model C). We observed effect modification by cohort in the
linear regression analysis (P , 0.0001), but not in the polytomous logistic regression analysis (P = 0.25). The effect modification was due to a positive association in the UK-Nor cohort
[25 g/y weight change per-100 g fruit and vegetable (95% CI: 3
47 g/y) in adjusted analyses], whereas nonsignificant or inverse
associations were observed in the other cohorts. After the UKNor data were omitted from the linear regression analysis, the
effect modification by cohort was no longer evident (P = 0.12).
Because we could not explain why the relation in UK-Nor deviated from that of other cohorts, the interaction of this cohort
was taken into account in the linear regression analyses by entering a cross-product term between UK-Nor (dummy variable
with value 1 indicating UK-Nor, value 0 if not) and fruit and
vegetable intake (continuous) along with main effects.
Finally, we assessed the effect of excluding participants with
incident cardiovascular diseases, diabetes, or cancer during followup as well as those with missing data on covariates. All analyses
were conducted by using SAS software (version 9.1; SAS Institute Inc).
RESULTS
activity was classified as sedentary occupation, standing occupation, manual work, heavy manual work, unemployed, or missing.
Type and duration of different leisure-time physical activities
were ascertained at baseline, and reported activities included
walking, cycling, gardening, sports, household work, home repair, stair climbing, and vigorous recreational activity. Each type
of activity was converted into metabolic equivalent-hours (MET-h)
(36). A variable of total physical activity was created in which
participants were cross-classified on the basis of sex-specific quartiles of leisure-time activity and on categories of occupational work.
This variable was coded as inactive, moderately inactive, moderately active, and active. Missing values were assigned to 3319
participants (3.7%).
Information on smoking habits was collected by questionnaire
at baseline and follow-up. Smoking behavior was defined in 4
categories: nonsmokers (never smokers and those who stopped
smoking before baseline), stable smokers (those who reported
smoking at baseline and follow-up), stopped smokers (those who
stopped smoking during follow-up), and started smokers (those
who started smoking during follow-up). Smoking status was
unknown for 1440 participants (1.6%).
Information on highest achieved education [missing values
were assigned for 1579 participants (1.8%)], alcohol consumption, and, in women, postmenopausal status and postmenopausal
hormone use was provided by questionnaire at baseline. Similarly, the prevalence and incidence of diabetes, cardiovascular
disease, and cancer were assessed by questionnaire, interview,
and/or hospital discharge information.
205
Women
(n = 52,307)
Q1
Q3
Q5
Q1
Q3
Q5
Q1
Q3
Q5
17,886
147
(60, 265)
52.6 6 9.13
17,886
307
(176, 460)
53.5 6 8.7
17,886
510
(331, 731)
53.1 6 7.7
7425
115
(43, 229)
53.9 6 7.9
7425
284
(155, 448)
53.6 6 8.5
7425
466
(282, 662)
53.8 6 7.7
10,461
168
(76, 290)
51.3 6 9.8
10,461
332
(200, 500)
53.5 6 8.9
10,461
535
(356, 770)
52.9 6 7.7
28.9
23.5
31.4
32.7
21.6
26.8
26.5
25.2
32.9
38.8
37.9
27.0
35.3
32.8
23.4
44.2
41.2
28.7
12.3
18.5
20 (11, 37)
10.9
25.1
14 (7, 24)
17.3
23.6
10 (4, 19)
9.1
21.1
27 (17; 47)
9.9
33.7
23 (15, 37)
13.9
34.6
21 (12, 32)
16.1
12.1
12 (7, 20)
12.1
18.5
10 (5, 17)
18.2
19.7
8 (3, 14)
56.5
31.4
8.9
2.2
76.0
14.8
5.6
1.6
77.4
13.2
6.3
1.6
54.1
33.9
9.1
2.2
71.3
18.0
7.0
2.1
77.1
13.3
6.0
1.8
59.5
29.3
8.2
1.8
77.8
13.7
4.8
1.5
77.7
13.0
6.5
1.4
25.3
26.9
31.2
10.9
53.9
21.4
28.3
35.7
10.6
58.9
19.1
26.6
42.7
10.8
58.7
26.8
26.4
31.8
11.1
NA
26.6
27.2
29.8
11.6
NA
28.1
29.2
30.8
10.1
NA
22.1
28.5
31.8
10.6
53.9
18.0
28.5
39.7
10.4
58.9
14.5
24.9
48.7
11.3
58.7
22.8
67.2 6 11.5
163.5 6 6.3
25.1 6 4.1
80.4 6 10.5
18.5
66.8 6 11.5
162.7 6 6.4
25.2 6 4.1
79.1 6 10.4
21.3
22.8
75.9 6 13.3 72.9 6 13.4
171.1 6 8.9 168.5 6 9.1
25.9 6 3.8 25.6 6 3.8
89.8 6 12.0 85.9 6 12.1
2273
36.3
15.0
40.2
6
6
6
6
18.5
NA
71.1 6 13.3 80.6 6 11.8
166.5 6 8.8 175.6 6 6.6
25.6 6 3.9
26.1 6 3.4
83.4 6 12.1 94.7 6 9.8
20 6 5
22 6 5
26 6 5
2538
36.6
14.6
38.8
6
6
6
6
NA
81.5 6 11.4
176.5 6 6.7
26.1 6 3.2
94.2 6 9.4
NA
21.3
81.6 6 11.5 67.8 6 11.5
175.7 6 6.8 163.6 6 6.5
26.4 6 3.3
25.4 6 4.3
93.8 6 9.6
81.7 6 10.9
21 6 4
25 6 5
29 6 5
1835
35.6
15.4
42.3
6
6
6
6
18 6 4
21 6 4
1929
34.1
15.6
46.8
6
6
6
6
234
2.8
1.6
3.0
24 6 4.8
NA, not applicable; HRT, hormone replacement therapy. P values for differences in characteristics across quintiles of fruit and vegetable intake were
based on chi-square tests for discrete variables or, for continuous variables, on modeling median values as one continuous variable in linear regression
analyses; because of the large sample size, all P values were significant (P , 0.05), with the exception of age in the total study population.
2
Median unadjusted values (25th percentile, 75th percentile) based on 24-h dietary recalls in a subsample of n = 6790.
3
Mean 6 SD (all such values).
4
Percentages do not add up to 100 because of missing values.
5
Median values (25th percentile; 75th percentile) based on calibrated intake values.
(Figure 1). Although the spline indicated a weaker relation toward higher intakes of fruits and vegetables, the nonlinearity
was not statistically significant (P = 0.72) and led us to conclude
that the assumption of a linear effect of fruit and vegetable intake is acceptable.
Fruit and vegetable intake was weakly inversely associated
with weight change (Table 2). Additional adjustment for baseline body weight compared with the adjusted model with age,
sex, cohort, and years of follow-up attenuated the association
particularly for studying vegetable intake. Because the mean
No. of subjects
Fruit and vegetable
intake (g/d)2
Age (y)
Education (%)4
No school degree or
primary school
Technical or
professional school
Secondary school
University degree
Alcohol intake (g/d)5
Smoking behavior (%)4
Nonsmokers
Stable smokers
Stopped smokers
Started smokers
Total physical
activity (%)4
Inactive
Moderately inactive
Moderately active
Active
Postmenopausal
(% women)
HRT (% women)
Weight (kg)
Height (cm)
BMI (kg/m2)
Waist circumference
(cm)
Daily dietary intake
Total energy (kcal)
Fat (% of energy)
Protein (% of energy)
Carbohydrates (%
of energy)
Fiber (g)
Men
(n = 37,125)
206
BUIJSSE ET AL
TABLE 2
Association between fruit and vegetable intake, combined and separately,
and subsequent weight change in linear regression analyses1
Weight change (95% CI)
Model A2
Model B3
Model C4
Fruit
Vegetables
g/y
217 (223, 211)
214 (220, 28)
216 (222, 210)
1
Values are coefficients for the linear regression of weight change (g/y)
on fruit and vegetable intake (per 100-g/d increase in intake) in the total
study population (n = 89,432).
2
Adjusted for age, sex, cohort, product term UK-Nor (United Kingdom, Norfolk cohort) fruit/vegetable intake (for details see text), and years
of follow-up (continuous).
3
As for model A, with additional adjustment for baseline weight (continuous).
4
As for model B, with additional adjustment for baseline height (continuous), change in smoking status (dummy variables), baseline total physical activity (dummy variables), education (dummy variables), alcohol intake
(dummy variables), and, in women, postmenopausal status (yes or no) and
postmenopausal hormone use (yes or no).
DISCUSSION
207
Weight change
(95% CI)3
P for
interaction
g/y
g/y
358
333
27 (215, 1)
212 (218, 25)
0.02
346
354
0.05
329
368
0.01
351
345
,0.0001
387
288
306
356
213
25
237
24
,0.0001
(219, 27)
(217, 6)
(258, 215)
(243, 35)
Values are coefficients of the linear regression of weight change (g/y) on fruit and vegetable intake (per 100-g/
d increase in intake) stratified by sex, baseline age, follow-up duration, baseline BMI, and smoking behavior.
2
Mean fruit and vegetable intakes based on 24-h dietary recalls in a subsample of n = 6790, adjusted for cohort and
(mutually for) age, sex, follow-up duration, BMI, and smoking.
3
Adjusted for age, sex, cohort, product term UK-Nor (United Kingdom, Norfolk cohort) fruit/vegetable intake (for
details see text), years of follow-up (continuous), baseline weight (continuous), baseline height (continuous), change in
smoking status (where applicable dummy variables), baseline total physical activity (dummy variables), education (dummy
variables), alcohol intake (dummy variables), and, in women, postmenopausal status (yes or no) and postmenopausal
hormone use (yes or no).
predictors for short-term weight gain are prior weight loss and
prior weight cycling, whereas prior weight gain was not predictive (38). Third, we only relied on baseline fruit and vegetable consumption and therefore assume a stable consumption
over time. Finally, we cannot exclude the possibility that the
association between fruit and vegetable intake and weight change
is partly explained by confounding factors that were incompletely
accounted for.
TABLE 4
Multivariable-adjusted odds ratios (95% CIs) for gaining and losing weight per 100-g increase in fruit and vegetable intake in polytomous logistic regression
analysis according to smoking status1
Odds ratio (95% CI)
All (n = 89,432)3
Smoking behavior
Nonsmokers (n = 63,675)
Stable smokers (n = 16,837)
Stopped smokers (n = 5916)
Started smokers (n = 1564)
Weight stable
20.5 to ,0.5 kg/y
Weight gain
0.5 to ,1.0 kg/y
Weight gain
1.0 kg/y
Weight loss
0.5 kg/y
1
1
1
1
0.97
0.96
0.93
1.07
0.97
0.95
0.87
1.15
0.99
0.95
0.97
1.13
(0.95,
(0.93,
(0.88,
(0.94,
0.99)
1.00)
0.99)
1.22)
(0.95,
(0.90,
(0.81,
(0.99,
1.00)
1.00)
0.92)
1.34)
(0.97,
(0.91,
(0.88,
(1.02,
1.02)
0.99)
1.07)
1.26)
P for interaction2
,0.0001
Adjusted for age, sex, cohort, product term UK-Nor (United Kingdom, Norfolk cohort) fruit/vegetable intake (for details, see text), years of follow-up
(continuous), baseline weight (continuous), baseline height (continuous), change in smoking status (where applicable dummy variables), baseline total
physical activity (dummy variables), education (dummy variables), alcohol intake (dummy variables), and, in women, postmenopausal status (yes or no)
and postmenopausal hormone use (yes or no).
2
P for interaction based on modeling smoking behavior as a categorical variable fruit and vegetable intake in participants with known information on
smoking (n = 87,992).
3
Includes also 1440 participants with an unknown smoking status.
1
Sex
Men (n = 37,125)
Women (n = 52,307)
Baseline age
,60 y (n = 69,353)
60 y (n = 20,079)
Follow-up duration
,5.5 y (n = 43,235)
5.5 y (n = 46,197)
Baseline BMI
,25 kg/m2 (n = 42,819)
25 kg/m2 (n = 46,613)
Smoking behavior
Nonsmokers (n = 63,675)
Stable smokers (n = 16,837)
Stopped smokers n = 5916)
Started smokers (n = 1564)
208
BUIJSSE ET AL
was designed to study the effects of a diet low in fat and high in
fruit, vegetables, and whole grain on cancer, and the PPT was
designed to test the effects of a high-fiber, high-fruit-and-vegetable, low-fat diet on adenomatous polyp recurrence. In the WHI,
women in the intervention group did not gain weight over
a period of 7.5 y compared with controls (40), whereas the intervention group in the PPT had, on average, a 0.7-kg lower body
weight after 4 y compared with a 0.3-kg weight gain in controls
(41). In summary, these findings suggest a weak effect of an
increased fruit and vegetable intake on weight control.
Our findings suggest that persons who quit smoking are likely
to benefit the most from an increased intake of fruit and vegetables. No other prospective studies have reported a similar result
(8, 1521). Also, a biological plausible explanation why stopped
smokers would specifically benefit from an increased fruit and
vegetable intake is lacking; it might be that other groups at increased risk of weight gain also benefit more from higher fruit and
vegetable intakes. However, if our finding is confirmed, it may
have important implications because smoking cessation is accompanied by weight gain (2325), which may prevent smokers
from quitting. Increasing the intake of fruit and vegetables is one
strategy for limiting weight gain in those who stop smoking.
In conclusion, although fruit and vegetable intake was weakly
related with weight change in the present study, the findings have
public health relevance and support initiatives to increase the
intake of fruit and vegetables. Our findings are also of relevance
to the massive smoking cessation initiatives in Europe, which
suggest that adding a fruit and vegetable component to programs
directed at stopping cigarette smoking may help to limit weight
gain in those who stop smoking.
The authors responsibilities were as followsBB: performed the data
analysis and wrote the manuscript; MBS, HB, EJMF, and TIAS: contributed
to the conception and design of the study; HB: helped with the interpretation
and contributed to the writing of the manuscript; SS: provided statistical expertise and gave critical comments on the manuscript; EJMF, MBS, NGF,
NJW, SS, DP, GT, JH, AT, MUJ, KO, DLvdA, HD, and TIAS: helped with
the interpretation of the results and gave critical comments on the manuscript;
and EJMF, DP, NJW, AT, KO, TIAS, and HB: contributed to providing funding. TIAS has industrial collaborations as listed at http://www.ipm.regionh.
dk/person/tias/Disclosures.html. None of the other authors declared a conflict
of interest.
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