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The American Journal of GASTROENTEROLOGY VOLUME 108
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INTRODUCTION
Nonalcoholic fatty liver disease (NAFLD) is pathogenically asso-
ciated with obesity and insulin resistance and has been identi-
fed as a predictor of cardiovascular disease and type 2 diabetes
mellitus in adults and children ( 1 ). As the prevalence of obes-
ity and diabetes has increased worldwide over the past two
decades, NAFLD is now the leading cause of liver injury ( 1 ).
NAFLD may progress to cirrhosis, risking complications of
hepatocellular carcinoma and liver failure, and is becoming an
increasingly common indication for liver transplant ( 2 ). Te
pediatric and adolescent age group has not been immune to the
global overweight and obesity epidemic, with the prevalence of
NAFLD ranging between 3 and 13 % in these populations ( 1,3 ),
and NAFLD afects up to 52 % of overweight and obese children
( 4 ). Tese children are potentially at a life-long risk of developing
NAFLD-related complications.
The Western Dietary Pattern Is Prospectively Associated
With Nonalcoholic Fatty Liver Disease in Adolescence
Wendy H. Oddy , BAppSci, MPH, PhD
1
, Carly E. Herbison , BSc (Hons)
1
, Peter Jacoby , BA, MSc
1
, Gina L. Ambrosini , BAppSci, MPH, PhD
2
,
Therese A. O Sullivan , BHlthSci, BAppSci, PhD
1

,

3
, Oyekoya T. Ayonrinde , MBBS, FRACP
4



6
, John K. Olynyk , MBBS, FRACP, MD
4



7
,
Lucinda J. Black , BSc, PhD
1
, Lawrence J. Beilin , MBBS, FRCP, FRACP, FCSANZ, MD
4
, Trevor A. Mori , BSc (Hons), MRACI CChem,
PhD (Distinction)
4
, Beth P. Hands , BEd, BSocWk, MEd, PhD
8
and Leon A. Adams , MBBS, FRACP, PhD
4

OBJECTIVES: Poor dietary habits have been implicated in the development of nonalcoholic fatty liver disease
(NAFLD); however, little is known about the role of specic dietary patterns in the development
of NAFLD. We examined prospective associations between dietary patterns and NAFLD in a
population-based cohort of adolescents.
METHODS: Participants in the Western Australian Pregnancy Cohort (Raine) Study completed a food frequency
questionnaire at 14 years and had liver ultrasound at 17 years ( n = 995). Healthy and Western dietary
patterns were identied using factor analysis and all participants received a z -score for these
patterns. Prospective associations between the dietary pattern scores and risk of NAFLD were
analyzed using multiple logistic regression.
RESULTS: NAFLD was present in 15.2 % of adolescents. A higher Western dietary pattern score at 14 years was
associated with a greater risk of NAFLD at 17 years (odds ratio (OR) 1.59; 95 % condence interval
(CI) 1.17 2.14; P < 0.005), although these associations were no longer signicant after adjusting
for body mass index at 14 years. However, a healthy dietary pattern at 14 years appeared protective
against NAFLD at 17 years in centrally obese adolescents (OR 0.63; 95 % CI 0.41 0.96; P = 0.033),
whereas a Western dietary pattern was associated with an increased risk of NAFLD.
CONCLUSIONS: A Western dietary pattern at 14 years in a general population sample was associated with an
increased risk of NAFLD at 17 years, particularly in obese adolescents. In centrally obese
adolescents with NAFLD, a healthy dietary pattern may be protective, whereas a Western dietary
pattern may increase the risk.
SUPPLEMENTARY MATERIAL is linked to the online version of the paper at http://www.nature.com/ajg
Am J Gastroenterol 2013; 108:778785; doi: 10.1038/ajg.2013.95; published online 2 April 2013

1
Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia , Perth , Western Australia , Australia ;
2
Medical
Research Council Human Nutrition Research , Cambridge , UK ;
3
School of Exercise and Health Sciences, Edith Cowan University , Joondalup , Western Australia ,
Australia ;
4
School of Medicine and Pharmacology, The University of Western Australia , Perth , Western Australia , Australia ;
5
Department of Gastroenterology,
Fremantle Hospital , Fremantle , Western Australia , Australia ;
6
Curtin Health Innovation Research Institute, Curtin University of Technology , Perth , Western
Australia , Australia ;
7
Institute for Immunology and Infectious Diseases, Murdoch University , Perth , Western Australia , Australia ;
8
School of Health Sciences,
University of Notre Dame , Fremantle , Western Australia , Australia . Correspondence: Wendy H. Oddy, BAppSci, MPH, PhD , Telethon Institute for Child Health
Research , PO Box 855 West Perth , WA 6872 , Australia . E-mail: wendyo@ichr.uwa.edu.au
Received 19 October 2012; accepted 10 March 2013
2013 by the American College of Gastroenterology The American Journal of GASTROENTEROLOGY
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The Western Dietary Pattern and Fatty Liver Disease
Te pathogenesis of NAFLD and obesity is traditionally thought
to be due to excess caloric intake in association with reduced energy
expenditure ( 5 ); however, there is a paucity of evidence examining
specifc dietary habits and the development of NAFLD. Although
excess adiposity is a major risk factor for NAFLD, it is not known
whether specifc dietary patterns predispose to NAFLD independ-
ently of excessive adiposity. Conversely, as not all overweight indi-
viduals will develop NAFLD, it is unknown whether specifc dietary
patterns may protect against the development of NAFLD in normal
or overweight groups. Diet consists of complex combinations of
foods and nutrients ingested together that may act independently
or interact in a complimentary, synergistic, or antagonistic man-
ner. Dietary pattern analysis examines the overall efect of diet ( 6 ),
allowing quantifcation of the cumulative efect of multiple foods
and nutrients and avoids issues of confounding and colinearity.
Tere are a number of studies reporting a prospective associa-
tion between dietary patterns, adiposity, and the metabolic syn-
drome in children ( 7 10 ); however, the evidence relating dietary
patterns to NAFLD is limited. To our knowledge, an association
between dietary patterns and NAFLD has not been reported,
although a higher intake of sof drinks and meat the main com-
ponents of a Western dietary pattern has previously been associ-
ated with NAFLD in adults ( 11 ). We investigated the prospective
relationship between dietary patterns at age 14 years with NAFLD
at 17 years in adolescents participating in the Western Australian
Pregnancy Cohort (Raine) Study.
METHODS
Study population
Te Western Australian Pregnancy Cohort (Raine) Study is a
prospective longitudinal study, the details of which have been
published previously ( 12 ). In brief, 2,900 pregnant women were
recruited through the public antenatal clinic and local private
clinics in Perth, Western Australia between 1989 and 1991. A total
of 2,804 women (97 % ) had 2,868 live births, and these children
have undergone serial assessment at birth and at ages 1, 2, 3, 5,
8, 10, 14, and 17 years. All data collection for the Raine Study
occurred in accordance with the Australian National Health
and Medical Research Council Guidelines for Ethical Conduct
in Human Research and was approved by the ethics commit-
tees of King Edward Memorial Hospital for Women and Princess
Margaret Hospital for Children, Perth, Western Australia.
Informed consent was obtained in writing from the adolescent
and their primary caregiver.
Dietary patterns assessment at age 14 years
Identifcation of the Western and healthy dietary patterns in this
cohort at age 14 years has previously been described ( 13 ) and
evaluated ( 14 ). An evaluated semiquantitative food frequency
questionnaire (FFQ) ( 15 ) was mailed to the primary caregivers of
the study adolescents to complete with the adolescent. Te FFQ
provided usual frequency of consumption and serving size infor-
mation on 212 foods or dishes, which were collapsed into 38 food
groups that were defned a priori ( 13 ). Foods with a factor loading
greater than an absolute value of 0.30 were considered important
components of each pattern.
Te healthy and Western dietary patterns difered predomi-
nantly in fat and sugar intakes and explained 84 % of the total
variance in food intakes ( 13 ). Te healthy pattern was positively
correlated with whole grains, fruit, vegetables, legumes, fsh, fber,
folic acid, and most micronutrients, and was inversely correlated
with energy from total fat, saturated fat, and refned sugar ( 13 ). Te
Western pattern was characterized by high intakes of take-away
foods, red meats, processed meats, full-fat dairy products, fried
potatoes ( hot chips or French fries ), refned cereals, cakes and
biscuits, confectionery, sof drinks, crisps, sauces, and dressings.
Tis pattern was positively correlated with most micronutrients
except vitamin C and folic acid. Each subject received a z -score for
each pattern, indicating how closely their reported dietary intake
corresponded with the two patterns.
Dietary misreporting is a common source of measurement error
that can obscure diet disease relationships ( 16 ). Dietary misre-
porting was estimated using the Goldberg method ( 17 ), which
estimates the cutof levels for plausible reporting based on energy
intake relative to basal metabolic rate and is an established method
to identify the level of misreporting from dietary surveys ( 18,19 ).
Tese cutofs were used to classify respondents as likely underre-
porters, plausible reporters, or overreporters. As dietary under-
reporting is strongly associated with the risk of overweight ( 20 ),
excluding underreporters would have removed those participants
at greatest risk. Terefore, a categorical variable for misreporting
was included as a covariate in the logistic regression models.
Liver ultrasonography at age 17 years
Liver ultrasonography was conducted at the 17-year follow-up.
Trained ultrasonographers performed liver ultrasound using a
Siemens Antares ultrasound machine, with a CH 6-2 curved array
probe (Sequoia, Siemens Medical Solutions, Mountain View, CA)
according to the protocol described by Hamaguchi et al. ( 21 ) that
provides 92 % sensitivity and 100 % specifcity for the histological
diagnosis of fatty liver. A single specialist radiologist, blinded to
the clinical and laboratory characteristics of the subjects, inter-
preted the ultrasound images. Scores of 0 3, 0 2, and 0 1 were
determined from captured images for liver echotexture (bright
liver and hepatorenal echo contrast), deep attenuation (dia-
phragm visibility), and vessel blurring (intrahepatic vessel visibil-
ity), respectively. Te diagnosis of FLD required a total score of at
least 2, including echotexture score of at least 1.
Information on alcohol intake over the past 12 months was
obtained from the FFQ and lifestyle questionnaire. Adolescents
with sonographic fatty liver and a self-reported weekly alcohol
intake of < 210 and 140 g for males and females, respectively, were
classifed as having NAFLD ( 22 ). Medications and a comprehen-
sive medical history were documented to exclude secondary causes
of NAFLD and concomitant liver disease.
Biochemistry at age 17 years
Venous blood samples were taken afer an overnight fast. Results
from nonfasting samples were excluded from this analysis. Serum
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insulin, glucose, triglycerides, high-density lipoprotein cholesterol,
alanine transaminase, -glutamyltransferase, and high-sensitivity
C-reactive protein were measured as previously described ( 23 ).
Homeostasis model assessment for insulin resistance (HOMA-IR),
as a measure of insulin resistance, was calculated by insulin ((mU /
l) glucose (mmol / l) / 22.5) ( 24 ).
Anthropometry
Height, weight, and waist circumference were measured by
trained assessors using standardized methods at 14 and 17 years.
Body mass index (BMI: weight (kg) / height (m)
2
) was calculated
and subjects were grouped into underweight, normal weight,
overweight, and obese categories using International Obesity Task
Force (IOTF) criteria at 14 years ( 25,26 ). Waist circumference was
measured as the mid-point between the iliac crest and the lower
costal margin by horizontally positioning a tape measure across
the belly button and at the smallest girth at the back, taking the
average of two measurements. Central obesity was defned as
waist circumference 80 cm in females and 94 cm in males, consist-
ent with International Diabetes Federation (IDF) criteria ( 27 ).
Family income
Primary caregivers were asked to report their gross family income
per year at the 14-year follow-up (2003 2006). Eleven categories
of income (in Australian dollars) were collapsed into four catego-
ries ( $ 30,000 p.a., $ 30,001 $ 50,000 p.a., $ 50,001 $ 78,000 p.a., and
> $ 78,000 p.a.).
Physical activity and sedentary behavior
At the 14-year follow-up, hours of physical activity per week and
time spent watching television were assessed using a self-reported
written questionnaire. Participants detailed the time spent exer-
cising vigorously during physical education at school, and how
ofen and for how long they got out of breath or perspired while
exercising outside school hours.
Statistical methods
Te
2
tests were used to compare the characteristics of study par-
ticipants at 14 years, including sex, family income, BMI status,
dietary misreporting, physical activity per week, and sedentary
behavior (television viewing) according to NAFLD status at
17 years. Independent samples t -tests were used to compare
mean values for biochemistry and central adiposity according to
NAFLD status at 17 years. Te odds of NAFLD were analyzed in
relation to z -scores for both dietary patterns using logistic regres-
sion. Furthermore, dietary pattern scores were analyzed in quar-
tiles based on the total sample distribution. Associations between
the dietary pattern as a continuous score and in quartiles are pre-
sented for three diferent models. Te frst model included scores
for both healthy and Western dietary patterns, sex, and dietary
misreporting. A second model additionally adjusted for family
income, frequency, and intensity of physical activity and sedentary
behavior at 14 years. Te third model adjusted for adolescent BMI
at 14 years. A subgroup of adolescents with central obesity
was examined in logistical regression models, adjusting for
dietary patterns, sex, dietary misreporting, physical activity, and
television viewing.
To further explore any associations between the dietary patterns
and NAFLD, intakes of key food groups in each pattern, i.e., those
having a factor loading of 0.30 ( 13 ), were examined in relation to
NAFLD risk. Tese were converted into quartiles and entered into
separate logistic models adjusting for covariates, as per the models
described above. In addition, the healthy and Western dietary pat-
tern scores were retained in the models to test if food group asso-
ciations were independent of the overall dietary patterns.
Initial exploratory analyses in the continuous models also tested
the importance of aerobic ftness (watts) and alcohol intake at
14 years of age as confounders. However, these did not improve
the model or alter the associations between dietary patterns and
NAFLD risk and were, therefore, not retained in fnal models. All
data analyses were conducted using IBM SPSS Statistics Release
Version 19.0.0.1 (IBM SPSS, 2010, Chicago, IL).
RESULTS
Study participant characteristics
At the 14-year follow-up, there were 2,337 adolescents eligible
(alive and not withdrawn from the study) and at 17 years, 2,168
adolescents were eligible to participate. A total of 1,857 (79.5 % of
traced) adolescents responded to the 14-year follow-up, of whom
1,613 had complete plausible data from the FFQ (because of highly
implausible energy intakes ( < 3,000 kJ / day or >20,000 kJ / day) 18
respondents were excluded from analysis). At age 17 years 1,170
adolescents underwent hepatic ultrasound. Complete data were
available for 995 adolescents who provided dietary information
and had ultrasound assessment for NAFLD. Of the 995 study par-
ticipants with complete data, NAFLD was present in 151 (15.2 % )
at age 17 years ( Table 1 ). Of those with NAFLD at age 17 years,
54.1 % were overweight or obese at age 14 years.
Biochemistry and anthropometry prole at 17 years
Te serum biochemistry and anthropometry profles of study par-
ticipants at 17 years are shown in order to characterize NAFLD
in the cohort ( Table 2 ). Subjects with NAFLD had higher insu-
lin resistance (HOMA-IR), raised triglycerides and reduced
high-density lipoprotein cholesterol, elevated alanine transami-
nase, -glutamyltransferase, and high-sensitivity C-reactive pro-
tein, as well as greater adiposity (BMI, waist circumference, and
waist-to-hip ratio).
Dietary patterns and NAFLD
Associations between the dietary pattern scores at 14 years and
NAFLD at 17 years are shown in Table 3 . In the total population,
the healthy dietary pattern did not show any associations with
the odds of NAFLD, either as a continuous outcome (model 2:
odds ratio (OR) 1.15; 95 % confdence interval (CI) 0.92 1.44;
P = 0.212) or as quartiles. However, a higher score for the Western
dietary pattern was positively associated with the odds of NAFLD
at 17 years (model 2: OR 1.59; 95 % CI 1.17 2.14; P = 0.003).
Tere was a signifcant association between increasing quartiles
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The Western Dietary Pattern and Fatty Liver Disease
of Western dietary pattern scores and the odds of NAFLD ( P for
trend = 0.030). Tose in the highest quartile for the Western die-
tary pattern had a 2.6 times greater odds of NAFLD (OR 2.64;
95 % CI 1.34 5.18; P = 0.005) compared with those in the lowest
quartile (model 2). However, afer adjustment for BMI at age 14
years (model 3), these associations were attenuated and no longer
statistically signifcant, indicating that the association between the
Western dietary pattern and NAFLD is likely acting through an
obesity pathway. Tese associations did not change if waist cir-
cumference or abdominal skinfold was applied instead of BMI.
Te same result was found when BMI at 17 years was included
in the model (data not shown). Figure 1 shows the association
between Western dietary pattern and the risk of NAFLD strati-
fed by sex. Tere was a signifcant interaction between sex and
the Western dietary pattern scores ( P = 0.008) but not for the
healthy dietary pattern, nor when BMI was included in the model
( P = 0.079).
In a subgroup of adolescents with central obesity at age 17 years
( n = 191), a healthy dietary pattern was signifcantly associated
with a reduced risk of NAFLD (OR 0.63; 95 % CI 0.41 0.96;
P = 0.033). Tere was a strong trend toward the Western dietary
pattern increasing the risk of NAFLD in this subgroup (OR 1.53;
95 % CI 0.94 2.50; P = 0.090).
Components of the Western dietary pattern
As the Western dietary pattern was signifcantly associated with
the risk of NAFLD following adjustment for covariates, Table 4
illustrates the Western dietary pattern and main food components
that make up the pattern, including the mean and median intakes
in grams per day as well as the interquartile range of intake of
Table 1 . Characteristics of participants at 14 years and nonalcoholic fatty liver disease (NAFLD) at 17 years
NAFLD, n (row % )
P value
a
Total, n No Yes
995 844 (84.8) 151 (15.2)
Characteristics at 14 years
Sex n (column % ) < 0.001
Female 496 400 (47.4) 96 (63.6)
Male 499 444 (52.6) 55 (36.4)
Family income 979 0.092
$ 30,000 per year 131 (15.8) 34 (22.8)
$ 30,001 $ 50,000 per year 164 (19.8) 34 (22.8)
$ 50,001 $ 78,000 per year 235 (28.3) 34 (22.8)
> $ 78,000 per year 300 (36.1) 47 (31.5)
Misreporting 963 < 0.001
Underreporting 307 (37.6) 88 (60.3)
Plausible reporting 450 (55.1) 53 (36.3)
Overreporting 60 (7.3) 5 (3.4)
Physical activity 958 0.020
4 + times per week 288 (35.4 ) 35 (24.1)
1 3 times per week 447 (54.9) 97 (66.9)
1 time per month or less 79 (9.7) 13 (9.0)
TV viewing per day 958 0.026
< 2 h per day 430 (52.9) 59 (40.7)
2 4 h per day 277 (34.1) 62 (42.8)
> 4 h per day 106 (13.0) 24 (16.6)
Body mass index 961 < 0.001
Underweight 55 (6.7) 5 (3.4)
Healthy weight 610 (74.8) 62 (42.5)
Overweight 123 (15.1) 48 (32.9)
Obese 27 (3.3) 31 (21.2)

a
The
2
test.
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these components. Adolescents in the top quartile for sof drink
and sauces / dressings consumption had twice the odds of NAFLD.
Te sex-specifc results of Table 4 are provided in Supplementary
Tables S1 and S2 online .
In multilinear models, the Western dietary pattern was a signif-
cant risk for BMI at 14 years ( 1.41; 95 % CI 1.12 1.82; P < 0.0005),
abdominal skinfold at 17 years ( 2.14; 95 % CI 1.26 3.03;
P < 0.0005), and being in the top 25 % of BMI categories at 17 years
(OR: 2.17; 95 % CI 1.65 2.85; P < 0.0005).
DISCUSSION
A Western dietary pattern characterized by a high intake of takea-
way foods, confectionary, red meat, refned grains, processed
meats, chips, sauces, full-fat dairy products, and sof drinks was
prospectively associated with NAFLD independent of sex, dietary
misreporting, family income, frequency of physical activity, and
sedentary behavior. In particular, high intakes of sof drinks,
sauces, and dressings were associated with an increased risk of
NAFLD. Te association between the Western dietary pattern and
NAFLD was not independent of BMI, suggesting that this die-
tary pattern acts predominantly on NAFLD via obesity. Indeed,
other studies have linked similar dietary patterns with obesity
in adolescents ( 28,29 ). Although we did not observe any protec-
tive relationship between the healthy dietary pattern and NAFLD
in the total cohort, in those females and males who had waist
circumferences >80 and 94 cm, respectively, the healthy dietary
Table 2 . Biochemistry and adiposity prole at age 17 years
NAFLD
No Yes
Mean (s.d.) P value
a

Biochemistry ( n =827)
b

HOMA-IR 1.8 (1.6) 3.1 (5.4) < 0.001
Triglycerides (mmol / l) 1.0 (0.5) 1.2 (0.6) 0.003
Cholesterol (mmol / l) 4.1 (0.7) 4.2 (0.9) 0.248
LDL-C (mmol / l) 2.3 (0.6) 2.4 (0.8) 0.095
HDL-C (mmol / l) 1.3 (0.3) 1.2 (0.3) < 0.001
ALT (U / l) 20.3 (10.4) 27.4 (21.4) < 0.001
GGT (U / l) 14.2 (7.4) 17.3 (11.6) < 0.001
hsCRP (mg / l) 1.5 (5.2) 2.8 (4.6) 0.010
Adiposity ( n =994)
Body mass index 22.0 (3.2) 27.7 (6.1) < 0.001
Waist circumference (cm) 77.3 (8.7) 90.4 (15.8) < 0.001
Waist / hip ratio 0.81 (0.06) 0.85 (0.08) < 0.001
ALT, alanine transaminase; GGT, -glutamyltransferase; HDL-C, high-density
lipoprotein cholesterol; HOMA-IR, homeostasis model assessment for insulin
resistance; hsCRP, high-sensitivity C-reactive protein; LDL-C, low-density
lipoprotein cholesterol; NAFLD, nonalcoholic fatty liver disease.

a
Independent samples t -test.

b
Fasting blood samples.
Table 3 . Adjusted multiple logistic regression models of dietary patterns and risk of NAFLD
Risk of NAFLD
Model 1
a
( n = 965) Model 2
b
( n = 942) Model 3
c
( n = 940)
OR (95 % CI) P value OR (95 % CI) P value OR (95 % CI) P value
Continuous measure
Healthy dietary pattern 1.14 (0.91 1.42) 0.240 1.15 (0.92 1.44) 0.212 1.05 (0.83 1.35) 0.674
Western dietary pattern 1.67 (1.26 2.23) < 0.001 1.59 (1.17 2.14) 0.003 1.12 (0.81 1.55) 0.513
Quartiles
Healthy dietary pattern
Q1 (ref.) 1.00 0.38 1.00 0.441 1.00 0.657
Q2 1.29 (0.78 2.15) 0.318 1.39 (0.83 2.33) 0.83 1.29 (0.74 2.27) 0.371
Q3 1.01 (0.59 1.73) 0.967 1.04 (0.60 1.81) 0.888 0.92 (0.51 1.67) 0.781
Q4 1.36 (0.80 2.30) 0.261 1.41 (0.82 2.45) 0.219 1.10 (0.61 1.98) 0.744
Western dietary pattern
Q1 (ref.) 1.00 0.005 1.00 0.030 1.00 0.858
Q2 1.30 (0.80 2.14) 0.293 1.25 (0.76 2.08) 0.380 1.02 (0.60 1.75) 0.931
Q3 2.11 (1.20 3.72) 0.010 1.97 (1.09 3.55) 0.024 1.22 (0.65 2.30) 0.529
Q4 3.12 (1.63 5.97) 0.001 2.64 (1.34 5.18) 0.005 1.32 (0.64 2.72) 0.447
CI, condence interval; NAFLD, nonalcoholic fatty liver disease; OR, odds ratio; Q, quartile.

a
Adjusted for healthy and western dietary patterns, sex, and misreporting at 14 years.

b
Adjusted as for model 1 plus family income, TV use (sedentary behavior), and frequency of physical activity at 14 years.

c
Adjusted as for model 2 plus body mass index (BMI) at 14 years.
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The Western Dietary Pattern and Fatty Liver Disease
pattern reduced the risk of subsequent NAFLD, whereas the West-
ern dietary pattern was associated with the risk of NAFLD at age
17 years. As dietary habits are formed during childhood and
retained into adulthood, the Western dietary pattern has a potential
infuence on the perpetuation of NAFLD risk. Tese results sup-
port our previous fnding in the Raine Study linking the Western
dietary pattern with greater cardiometabolic risk ( 30 ). Although
relationships with the dietary patterns were diferent for males
and females, both were positively related to NAFLD.
Few studies have looked at the association of dietary patterns
and NAFLD. One previous cross-sectional study of Israeli adults
aged 24 to 70 years ( n = 375) found an increased risk of NAFLD in
those with a higher intake of sof drinks, whereas a higher intake
of omega-3-rich foods reduced the risk ( 11 ).
A Western diet high in processed sugars and fat has been shown
to cause deleterious efects in nonobese rats, with such a diet lead-
ing to the development of hepatic steatosis ( 31 ). We showed that
a higher consumption of sof drink was associated with a greater
risk of NAFLD, and the mechanism behind this may be through
provision of excess kilojoules and large amounts of sugars such
as fructose ( 29,32 ). Te consumption of fructose has been linked
to NAFLD, as well as various aspects of the metabolic syndrome,
including dyslipidemia, visceral adiposity, insulin resistance, and
high blood pressure ( 33 ). Sof drinks may contain large amounts
of high-fructose corn syrup (55 % fructose; 45 % glucose), the
consumption of which has increased substantially in the past
30 years ( 34 ).
Foods common in the Western dietary pattern including
refned grains, white bread, and confectionary cause a rapid
increase in postprandial plasma glucose and insulin levels and are
associated with obesity, insulin resistance, and diabetes ( 36 ). Such
high glycemic index foods cause increased hepatic fat storage in
animal studies ( 37 ), with a similar association seen in humans,
where high dietary glycemic index was associated with increased
hepatic steatosis, particularly in insulin-resistant subjects ( 38 ). It is
0
2
4
6
8
10
12
4 3 2 1
Western dietary pattern quartile
O
R

(
9
5
%

C
I
)
Males
Females
Figure 1 . Adjusted * model of Western dietary pattern (in quartiles) and
risk of nonalcoholic fatty liver disease, stratied by sex. * Adjusted for
healthy dietary pattern, misreporting, family income, frequency of physical
activity, and TV viewing. CI, condence interval; OR, odds ratio.
Table 4 . Quartiles of the western dietary pattern and components of the pattern (g / day) at 14 years and risk of NAFLD at 17 years
( n =940)
a

Risk of NAFLD, OR (95 % CI)
Total Mean g / day Median g / day
Interquartile
range g / day Q1 Q2 Q3 Q4
P value
for trend
Western pattern 1.00 1.25 (0.76 2.08) 1.97 (1.09 3.55)
b
2.64 (1.34 5.18)
b
0.030
Soft drinks 266.7 197.2 65.7 370.0 1.00 1.41 (0.82 2.43) 1.64 (0.94 2.86) 1.93 (1.04 3.56)
b
0.188
Full-fat dairy 298.5 158.5 57.1 456.5 1.00 0.90 (0.55 1.47) 0.74 (0.44 1.23) 0.61 (0.33 1.14) 0.398
Rened grains 184.4 168.5 119.3 232.3 1.00 0.79 (0.48 1.31) 0.58 (0.33 1.01) 0.96 (0.52 1.76) 0.195
Red meat 62.1 57.4 37.7 80.4 1.00 0.98 (0.60 1.61) 0.76 (0.44 1.31) 0.94 (0.51 1.75) 0.760
Takeaway foods 58.9 49.2 29.3 78.8 1.00 0.85 (0.51 1.42) 0.72 (0.40 1.27) 0.96 (0.51 1.82) 0.635
Potato, not fried 50.3 44.6 26.8 64.5 1.00 1.43 (0.85 2.40) 0.87 (0.49 1.54) 1.28 (0.73 2.25) 0.242
Confectionary 43.4 30.6 15.0 54.3 1.00 0.86 (0.51 1.45) 1.14 (0.67 1.96) 1.12 (0.61 2.05) 0.745
Processed meats 34.1 29.3 15.7 47.3 1.00 0.88 (0.52 1.48) 1.21 (0.71 2.05) 1.27 (0.71 2.28) 0.556
Cakes, biscuits 31.1 25.8 12.3 43.8 1.00 0.79 (0.47 1.32) 1.05 (0.63 1.76) 1.05 (0.58 1.90) 0.686
Potato, fried chips 14.7 13.6 6.3 20.4 1.00 1.17 (0.67 2.04) 0.83 (0.49 1.42) 0.78 (0.42 1.48) 0.560
Sauces, dressings 11.0 8.6 2.9 14.3 1.00 1.65 (0.97 2.80) 0.78 (0.43 1.40) 1.95 (1.12 3.41)
b
0.003
Crisps 8.7 4.3 2.0 12.9 1.00 0.81 (0.45 1.46) 0.68 (0.40 1.15) 1.03 (0.54 1.99) 0.307
CI, condence interval; NAFLD, nonalcoholic fatty liver disease; OR, odds ratio; Q, quartile.

a
Adjusted for western dietary pattern, healthy dietary pattern, sex, misreporting, TV viewing, frequency of physical activity, and family income.

b
Individual quartile compared with reference quartile, P < 0.05.
The American Journal of GASTROENTEROLOGY VOLUME 108
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Oddy et al.
CONFLICT OF INTEREST
Guarantor of the article : Wendy H. Oddy, BAppSci, MPH, PhD.
Specifc author contributions : W.H.O. was responsible for the
collection of nutrition data, coordinated the data analysis,
interpreted the data, and wrote the manuscript; C.H. conducted the
statistical analyses and contributed to the interpretation of results
and manuscript preparation; P.J. advised on the statistical analysis;
G.L.A. derived the dietary patterns and contributed to manuscript
preparation; T.A.O S. contributed to interpretation of results and
manuscript preparation; L.A.A., O.T.A., J.K.O., L.J.B., B.H., and
T.A.M. contributed to study design, data collection and analysis,
interpretation of results, and manuscript preparation.
Financial support : Te Raine Study is funded by the University of
Western Australia (UWA), the Raine Medical Research Foundation,
the National Health and Medical Research Council of Australia
(NHMRC), the Telethon Institute for Child Health Research, the
UWA Faculty of Medicine, Dentistry and Health Sciences, Women s
and Infants Research Foundation, and Curtin University.
Specifcally, the study was supported by NHMRC grant IDs 353514,
403981, and 634445, the Commonwealth Scientifc and Industrial
Research Organisation, and the Australian Heart Foundation /
Beyond Blue Strategic Research Initiative (ID G08P4036). John
K. Olynyk is the recipient of a NHMRC Practitioner Fellowship
(1042370), Wendy H. Oddy is the recipient of an NHMRC Popula-
tion Health Fellowship, and Trevor A. Mori is the recipient of an
NHMRC Senior Research Fellowship. Gina Ambrosini is supported
by an MRC program grant (U105960389 Nutrition and Health).
Potential competing interests : None.
Study Highlights
WHAT IS CURRENT KNOWLEDGE
3 Nonalcoholic fatty liver disease (NAFLD) is linked to
obesity but many patients have a normal body mass index
(BMI).
3 Particular dietary components increasing risk are poorly
documented.
WHAT IS NEW HERE
3 A Western style diet increased the risk of NAFLD in a
population cohort of adolescents.
3 In adolescents with central obesity, a healthy dietary
pattern reduced the risk of NAFLD, whereas a Western
dietary pattern increased the risk of NAFLD.
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consumed in large serving sizes may cause rapidly increased
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ACKNOWLEDGMENTS
We thank the Raine Study participants, their families, and the
Raine Study executive and staf. We would specifcally acknowledge
the NHMRC grants ID 353514, 403981, and 634445, the Common-
wealth Scientifc and Industrial Research Organisation and the
Australian Heart Foundation / Beyond Blue Strategic Research
Initiative for supporting this research (ID G08P4036).
2013 by the American College of Gastroenterology The American Journal of GASTROENTEROLOGY
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The Western Dietary Pattern and Fatty Liver Disease
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