Original Article | doi: 10.1111/j.1365-2796.2010.02290.
Effects of a healthy Nordic diet on cardiovascular risk factors
in hypercholesterolaemic subjects: a randomized controlled
trial (NORDIET)
V. Adamsson1, A. Reumark2, I.-B. Fredriksson3, E. Hammarström3, B. Vessby1, G. Johansson4 & U. Risérus1
From the 1Department of Public Health and Caring Sciences ⁄ Clinical Nutrition and Metabolism, Uppsala University, Uppsala; 2Lantmännen R&D,
Stockholm; 3Bollnäs Heart Clinic, Mitt Hjärta, Bollnäs; and 4School of Social and Health Sciences, Halmstad University, Halmstad, Sweden
Abstract. Adamsson V, Reumark A, Fredriksson I-B,
Hammarström E, Vessby B, Johansson G, Risérus U
(Uppsala University, Uppsala; Lantmännen R&D,
Stockholm; Bollnäs Heart Clinic, Mitt Hjärta, Bol-
lnäs; Halmstad University, Halmstad, Sweden).
Effects of a healthy Nordic diet on cardiovascular risk
factors in hypercholesterolaemic subjects: a ran-
domized controlled trial (NORDIET). J Intern Med
2011; 269: 150–159.
Objective. The aim of this study was to investigate the ef-
fects of a healthy Nordic diet (ND) on cardiovascular
risk factors.
Design and subjects. In a randomized controlled trial
(NORDIET) conducted in Sweden, 88 mildly hyper-
cholesterolaemic subjects were randomly assigned to
an ad libitum ND or control diet (subjects’ usual Wes-
tern diet) for 6 weeks. Participants in the ND group
were provided with all meals and foods. Primary out-
come measurements were low-density lipoprotein
(LDL) cholesterol, and secondary outcomes were
blood pressure (BP) and insulin sensitivity (fasting
insulin and homeostatic model assessment-insulin
resistance). The ND was rich in high-fibre plant foods,
fruits, berries, vegetables, whole grains, rapeseed oil,
nuts, fish and low-fat milk products, but low in salt,
added sugars and saturated fats.
Introduction
Cardiovascular disease (CVD) is a major cause of pre-
mature death in the Western world. Increased plasma
low-density lipoprotein cholesterol (LDL-C) is one of
the most established risk factors of CVD [1, 2]. Con-
trolled trials show plaque regression and decreased
cardiovascular mortality with LDL-C-lowering drugs
[3]. However, other effects also contribute to the pre-
vention of CVD, for example by decreasing blood
pressure (BP), inflammation and insulin resistance
150 ª 2010 The Association for the Publication of the Journal of Internal Medicine
Results. The ND contained 27%, 52%, 19% and 2% of
energy from fat, carbohydrate, protein and alcohol,
respectively. In total, 86 of 88 subjects randomly as-
signed to diet completed the study. Compared with
controls, there was a decrease in plasma cholesterol
()16%, P < 0.001), LDL cholesterol ()21%,
P < 0.001), high-density lipoprotein (HDL) choles-
terol ()5%, P < 0.01), LDL ⁄ HDL ()14%, P < 0.01)
and apolipoprotein (apo)B ⁄ apoA1 ()1%, P < 0.05) in
the ND group. The ND reduced insulin ()9%,
P = 0.01) and systolic BP by )6.6 ± 13.2 mmHg
()5%, P < 0.05) compared with the control diet. De-
spite the ad libitum nature of the ND, body weight de-
creased after 6 weeks in the ND compared with the
control group ()4%, P < 0.001). After adjustment for
weight change, the significant differences between
groups remained for blood lipids, but not for insulin
sensitivity or BP. There were no significant differ-
ences in diastolic BP or triglyceride or glucose con-
centrations.
Conclusions. A healthy ND improves blood lipid profile
and insulin sensitivity and lowers blood pressure at
clinically relevant levels in hypercholesterolaemic
subjects.
Keywords: cardiovascular risk factors, cholesterol,
diet, Nordic foods, nutrition.
[4]. In addition to lipid-lowering drugs that reduce
LDL-C in long-term trials ()30%) [5], several dietary
factors can also reduce LDL-C. In contrast to drugs,
dietary modifications reduce LDL-C without the risk
of side effects. Two dietary options are available:
either substituting single nutrients ⁄ foods or chang-
ing the whole diet to achieve advantages by combin-
ing several dietary components. Substituting unsat-
urated vegetable fats for saturated fats has well-
known LDL-C-lowering effects [6–8]. Similar effects
may also be achieved by increasing dietary fibre from
 V. Adamsson et al.
| Diet and cardiovascular risk factors
oats and barley [9]. The plasma LDL-C-reducing ef-
fect of plant sterols, soy protein, almonds, psyllium
and ß-glucan from oats and barley varies between 5%
and 14% [9–12]. Several studies have demonstrated
that a vegetarian-based Portfolio diet including a
combination of foods with cholesterol-lowering effi-
cacy can reduce plasma LDL-C [13] to similar levels
to those achieved by first-generation statins [5]. Fur-
thermore, adherence to a Mediterranean diet con-
taining plenty of legumes, cereals, fruit, vegetables
and olive oil but low in meat and milk products is
associated with improved cardiovascular risk [14].
The National Cholesterol Education Program (NCEP)
(I, II, III), a diet designed to reduce dietary saturated
fats, also has an LDL-C-reducing effect [6]. The Die-
tary Approaches to Stop Hypertension (DASH) diet,
which is rich in fruits, vegetables and low-fat dairy
products, can substantially lower elevated BP [15].
All these diets are similar in their food and macronu-
trient composition and represent diets tested both in
American and in European populations. However, no
randomized controlled dietary interventional studies
have investigated the effects of a diet with traditional
foods originating from Nordic countries. We hypothe-
sized that a healthy Nordic diet (ND) may reduce cho-
lesterol concentrations and improve overall cardio-
vascular risk profile. The aim of this study was to
investigate the effects of a healthy ND, eaten ad libi-
tum, on cardiovascular risk factors in mildly hyper-
cholesterolaemic subjects.
Methods
Ethics statement
Written informed consent was given by all subjects,
and the study was approved by the regional ethical
committee in Uppsala. The trial was registered in the
Current Controlled Trials database (http://
www.controlled-trials.com); International Standard
Randomized Controlled Trial Number (ISRCTN):
77759305. The protocol for this trial and supporting
CONSORT checklist are available as supporting
information; see Checklist and Protocol.
Subjects
Subjects living in the Swedish city Bollnäs were re-
cruited by advertisements in the local newspaper
during December 2007. The intervention was final-
ized in May 2008. After screening 212 subjects, 88
were eligible for the study (Fig. 1). Inclusion criteria
were healthy (as assessed by a physician) men and
women between 25 and 65 years of age, plasma LDL-
ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159
C ‡ 3.5 mmol L)1, body mass index ‡20 and £31
kg m)2 and haemoglobin concentration ‡120 g L)1
for women and ‡130 g L)1 for men. Exclusion criteria
were use of lipid-lowering drugs from 2 months prior
to screening and throughout the study, BP
>145 ⁄ 85 mmHg, plasma triglyceride (TG) concen-
trations >4.5 mmol L)1, use of products or supple-
ments fortified with plant sterols, omega-3, omega-6
or omega-9 fatty acids within 3 weeks prior to base-
line visit, allergy to certain foods, weight-loss diets or
drugs, special diets (e.g. vegan and gluten free), preg-
nancy or lactation.
All subjects were informed that the present study was
not a weight-loss study and were advised to maintain
their usual lifestyle habits throughout the study,
without changing their physical activity level, alcohol
consumption or any other part of their lifestyle be-
sides adhering to their prescribed diet during the
study.
Outcome measures
The primary outcome measure was change in the le-
vel of plasma LDL-C and other blood lipids after
6 weeks. Secondary outcomes were changes in BP
and insulin sensitivity [fasting insulin and homeo-
static model assessment-insulin resistance (HOMA-
IR)].
Study design
The trial was conducted between February and May
2008 and was a randomized, controlled, parallel-
group, nonblinded study including 88 voluntary
subjects (Fig. 1). At baseline, the subjects were ran-
domly assigned to one of two groups: ND or a control
diet (CD). A study nurse enrolled and assigned par-
ticipants into the study in accordance with the ran-
domization procedure. The randomization list was
generated by a biostatistician at the Uppsala Clini-
cal Research Centre. The random allocation se-
quence was carried out in blocks of two using sas
version 9.1. Clinical and laboratory assessments
were performed at baseline and after 6 weeks of fol-
low-up.
In the ND group, the first 11 randomly assigned sub-
jects entering the trial were offered the opportunity to
continue the ND for an additional 4 weeks; that is, an
extended intervention of 10 weeks was conducted in
this subgroup (Fig. 1). Not all subjects were included
in the extended intervention because of logistical rea-
son and study budget limitations.
151
 V. Adamsson et al.
| Diet and cardiovascular risk factors

Fig. 1 Flow diagram of the

phases of the randomized trial
(NORDIET). After the end of the
intervention, a subgroup of 11
subjects in the intervention group
received the Nordic diet for an
additional 4 weeks.

age). For every item consumed, subjects ticked the

Intervention
All foods were prepared and supplied throughout the
study to participants randomly assigned to the ND.
In the ND, all main meals were cooked, weighed and
packed in meal boxes and labelled. Beverages were,
however, not provided to the intervention group; only
advice was given (Table S1 in Supplemental Mate-
rial). The subjects were provided with a 21-day rotat-
ing menu plan, including breakfast, lunch and din-
ner, and two snacks per day. Subjects collected
cooler bags twice per week. The cooler contained up
to eight food boxes (lunch and dinner). Staple foods
for breakfast and snacks such as cereals, bread,
nuts, jam, margarine, biscuits and snacks were pro-
vided to subjects at the baseline visit. All subjects re-
ceived instructions on how to prepare their break-
fast. In addition, subjects received daily study
checklists (DSCs) including menus for up to 4 days
to monitor dietary compliance. The DSC described
the main meals for each day (i.e. which breakfast
should be eaten, amount and type of snack, amount
and type of bread and fruit and a suggested bever-
DSC. Subjects were also asked to comment and de-
scribe any deviation from the menu. Uneaten food
was not returned.
Nordic diet
The nutrient profile of the ND (Table S2 in Supple-
mental Material) was based on Nordic nutrition rec-
ommendations 2004 [16] and inspired by the Medi-
terranean, Portfolio and DASH diets and the NCEP.
The ND was based on typical foods consumed in Nor-
dic countries including fruits (e.g. apples and pears)
and berries (e.g. lingonberries and blueberry jam),
vegetables, legumes, low-fat dairy products and fatty
fish (e.g. salmon, herring and mackerel). The ND also
included LDL-C-lowering foods (e.g. oats, barley, soy
protein, almonds and psyllium seeds) [9–12]. The dai-
ly menu (Table S1 in Supplemental Material) was
based on eating habits in Sweden. Except for rusks,
all foods included in the menu were available at local
markets. For one meal per week, the participants
could eat foods outside the ND menu, provided they

152 ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159
 V. Adamsson et al.
| Diet and cardiovascular risk factors
registered that meal ⁄ snack in the DSC. The ND was
provided ad libitum and was thus neither energy re-
stricted nor isocaloric on an individual level. To facili-
tate the distribution of diets to participants and esti-
mate the approximate amount of food ⁄ meals to be
delivered, the ND was calculated on an isocaloric ba-
sis (on a group level) using validated formulas [16].
Control diet
Subjects in the control group were advised to follow
their habitual diet, also eaten ad libitum, and main-
tain their usual physical activity. Thus, the CD in-
cluded ordinary foods chosen by the participants. In
contrast to the intervention group, the control group
was not provided with any foods or meals. To increase
motivation and compliance in the CD group, all sub-
jects were offered the ND for 6 weeks after study com-
pletion (i.e. after 6 weeks of the CD). Subjects ran-
domly assigned to CD were, however, requested to
avoid dietary supplements fortified with plant sterols
or omega-3, omega-6 or omega-9 fatty acids through-
out the study.
Dietary assessments and compliance
All subjects who met the inclusion criteria completed
a dietary history interview [17] performed by trained
dieticians. The first dietary history interview (DH1)
preceded the ND and CD baseline visits; the second
dietary history interview (DH2) was assessed after
6 weeks to detect any possible changes from DH1 in
the CD. Each subject was asked about their habitual
food intake during 1- to 2-h interview. The aim was to
assess the habitual dietary intake for the preceding
month. Subjects described average portion sizes of
food items in terms of household measures, standard
weights of food items and validated food portion pho-
tographs of known weights. The DSC, which was
filled in by the ND group during the study, was analy-
sed at 6 weeks to estimate actual food and nutrient
intake to assess compliance to the interventional diet.
Dietist XP version 3.0, a computer program based on
the Swedish National Food Administration database
2005-02-01, was used to calculate the ND and die-
tary assessments.
Clinical assessment
Subjects visited the clinic in the morning after a 12-h
fast. Body weight was measured (kg) on a digital scale
in light clothing without shoes. Height (cm) was mea-
sured without shoes. BP was measured manually by
cuff and stethoscope in a sitting position on the right
ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159
arm after a 5-min rest. Two measurements were per-
formed with a 2-min interval, and the average value
was calculated. A case report form was completed for
each subject with medication information recorded
by a nurse.
Biochemical analysis
Blood samples were drawn from an antecubital vein
using Vacutainer tubes. The samples were collected
and handled according to hospital routines. TG, total
cholesterol and high-density lipoprotein (HDL)-C
plasma concentrations were measured by enzymatic
peroxidase reaction, using a Roche Diagnostics Ltd
Cobas 6000 (c501module). Plasma LDL-C was cal-
culated by Friedewalds formula [18], and apolipopro-
tein (apo)A1 and apoB were measured by an immuno-
turbidometric method [19] at the Centre for
Laboratory Medicine at Uppsala University Hospital.
Glucose was measured by UV test, an enzymatic
hexokinase reference method, developed by Roche
Diagnostics using the Cobas 6000 analyzer. Plasma
insulin was measured by an enzyme-linked immuno-
assay kit (Mercodia AB, Uppsala, Sweden). Homeo-
stasis model assessment-insulin resistance (HOMA-
IR) was calculated as plasma insulin · glucose ⁄ 22.5
[20]. Plasma high-sensitivity C-reactive protein (CRP)
was measured by an immunological particle en-
hanced reaction, developed by Roche Diagnostics,
using the Cobas 6000 analyzer.
Statistical methods
Data are presented as mean ± SD. Per protocol analy-
sis was used to assess effects on outcome measures.
Variables not normally distributed were logarithmi-
cally transformed. Paired t-test was used to assess
change within groups and unpaired t-tests to com-
pare mean changes between groups. It was estimated
that 92 subjects were required for 80% power with a
type I error of 5% to detect a difference of
0.25 mmol L)1 in plasma LDL-C levels with an SD of
±0.56 mmol L)1. In secondary analyses, we also
tested within-group changes and between-group dif-
ferences during follow-up using ancova, with base-
line values and weight change as covariates; t-tests
were two-tailed, and P < 0.05 was regarded as signifi-
cant. spss version 16.0 for Windows was used for sta-
tistical analysis.
Results
Of 88 subjects randomly assigned to the two diets (34
men and 54 women), only two subjects (one subject
153
 V. Adamsson et al.
| Diet and cardiovascular risk factors

in each dietary group) were lost to follow-up, provid- Effects on cardiovascular risk factors
ing 86 subjects for analysis (Fig. 1). There were no
The ND caused a significant lowering of plasma levels
significant differences between the ND and CD
of cholesterol, LDL-C, HDL-C, apoA1 and apoB com-
groups in baseline clinical characteristics after ran-
pared with the CD (Table 3). ApoB ⁄ apoA1 and
domization (Table 1). Likewise, the two groups were
LDL ⁄ HDL ratios were significantly decreased after
similar at baseline with regard to nutrient intake
the ND compared with the CD. Compared to the CD
(Table 2).
group, there was also a significant decrease in insulin
concentrations and HOMA-IR, as well as systolic BP
Dietary changes (SBP) in the ND group (Table 3). Reduction in diastolic
BP (DBP) after 6 weeks of the ND was not statistically
After 6 weeks, the nutrient content of the ND (Table 2)
significant. Body weight decreased by 3 kg after the
agreed with that of the planned diet (Table S2 in Sup-
ND compared to the CD (Table 3). There were no sig-
plemental Material). Except for alcohol (P < 0.19), the
nificant effects of either diet on plasma glucose, TG or
change in nutrient intake between baseline and week
CRP concentrations (Table 3). No adverse events were
6 within the ND group was significant for all nutrients
reported in either group. Results were similar if the
(P < 0.001), indicating high compliance. Compliance
baseline value of each outcome measure was added
was also high according to the completed DSC. When
as a covariate (data not shown).
expressed as percentage of prescribed calories con-
sumed during 6 weeks, compliance was 93% in the
ND group. All participants reported that they were Adjustments for weight loss
eating as much food as they were capable of. No sig-
The difference in LDL-C and apoB levels between
nificant dietary changes were observed in the CD
groups remained after adjusting for weight change
group.

Table 1 Baseline characteristics

Characteristics Control diet Nordic diet Pa after randomization to diets
Subjects, n 42 44
Age (year) 53.4 ± 8.1 52.6 ± 7.8 0.63
Men ⁄ women 15 ⁄ 27 17 ⁄ 27 0.83
Body weight (kg) 78.0 ± 13.3 76.0 ± 10.5 0.44
Body mass index (kg m)2) 26.5 ± 3.3 26.3 ± 3.2 0.79
Systolic blood pressure (mmHg) 129.8 ± 13.6 127.9 ± 12.4 0.50
Diastolic blood pressure (mmHg) 83.4 ± 9.3 80.8 ± 7.5 0.16
Plasma glucose (mmol L)1) 4.9 ± 0.6 4.9 ± 0.5 0.54
Plasma insulin (mU L)1) 6.1 ± 2.8 5.8 ± 3.0 0.57
Insulin resistance (HOMA-IR) 1.3 ± 0.6 1.2 ± 0.6 0.47
Plasma triglycerides (mmol L)1) 1.4 ± 0.8 1.6 ± 0.8 0.32
Plasma cholesterol (mmol L)1) 6.4 ± 0.7 6.2 ± 0.8 0.36
Plasma LDL cholesterol (mmol L)1) 4.2 ± 1.0 4.0 ± 0.6 0.33
Plasma HDL cholesterol (mmol L)1) 1.6 ± 0.5 1.5 ± 0.4 0.28
LDL ⁄ HDL ratio 2.8 ± 0.9 2.9 ± 0.8 0.80
Plasma apolipoprotein A1 (g L)1) 1.5 ± 0.3 1.5 ± 0.3 0.76
Plasma apolipoprotein B (g L)1) 1.1 ± 0.2 1.1 ± 0.2 0.85
ApoB ⁄ A1 ratio 0.8 ± 0.2 0.8 ± 0.2 0.77
)1 b
C-reactive protein (mg L ) 1.5 ± 1.4 1.6 ± 1.7 0.78

CRP, C-reactive protein; HDL, high-density lipoprotein; HOMA-IR, homeostasis model

assessment-insulin resistance; LDL, low-density lipoprotein.
a
Differences between groups using unpaired two-tailed t-test. bn=40; subjects with baseline
CRP >10 mg L)1 were excluded.

154 ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159
 V. Adamsson et al.
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Table 2 Nutrient intake at baseline and at 6 weeks in the Nordic diet and control groups

Control diet Nordic diet

Baselinea 6 weeksa Pb Baselinea 6 weeksc Pb
Subjects, n 42 42 44 44
Energy (kcal day)1) 2450 ± 646 2457 ± 642 0.31 2509 ± 671 1989 ± 275 <0.001
Protein (E%d) 17 ± 2.6 17 ± 2.6 0.76 17 ± 2.2 19 ± 0.8 <0.001
Alcohol (E%) 2.1 ± 3.1 2.0 ± 2.8 0.17 1.7 ± 1.6 2.1 ± 2.0 0.19
Carbohydrates (E%) 46 ± 5.9 46 ± 5.6 0.49 47 ± 6.1 52 ± 1.8 <0.001
Dietary fibre (g day)1) 31 ± 11 31 ± 11 0.17 30 ± 9.5 54 ± 7.4 <0.001
Beta-glucan (g day)1) 0.4 ± 0.7 0.4 ± 0.7 e
0.3 ± 0.4 4.9 ± 1.0 <0.001
Fat (E%) 34 ± 4.9 34 ± 5.0 0.20 34 ± 5.0 27 ± 0.9 <0.001
Saturated fat (E%) 13 ± 3.0 13 ± 3.0 0.40 14 ± 3.1 5.2 ± 0.4 <0.001
Mono-unsaturated fat (E%) 12 ± 2.3 12 ± 2.3 0.32 12 ± 2.1 11 ± 0.5 <0.001
Polyunsaturated fat (E%) 5.6 ± 1.7 5.6 ± 1.7 0.07 4.9 ± 1.1 6.3 ± 0.3 <0.001
Dietary cholesterol (mg day)1) 355 ± 135 356 ± 135 0.28 349 ± 125 131 ± 17 <0.001
)1
Sodium (mg day ) 3518 ± 968 3517 ± 969 0.97 3727 ± 1214 1545 ± 305 <0.001

a
Assessed by dietary history interview. bDifference within the group using paired sample t-test. cAssessed by daily study check-
list. dPercentage of daily energy intake. eCould not be computed because the standard error of the difference is zero.

(P < 0.001 for both), as well as for total cholesterol,
HDL-C, apoA1, LDL ⁄ HDL and apoB ⁄ apoA (all
P < 0.05). However, the differences did not remain
statistically significant for plasma insulin and BP.
Extended intervention and subgroup analysis
All subjects in the extended subgroup (n = 11) com-
pleted the additional 4-week intervention. This sub-
group thus followed the ND for a total period of
10 weeks. In line with the total intervention group,
the risk factors were significantly reduced after
6 weeks in the subgroup (n = 11) and continued to
decrease over the 10 weeks. Data are shown for LDL-
C, total cholesterol, LDL ⁄ HDL ratio, insulin, SBP and
body weight (Fig. 2). All values except for apoB ⁄ apoA1
(P = 0.09) were significantly different (P < 0.05) from
baseline to 10 weeks: LDL-C ()31%), total cholesterol
()24%), LDL ⁄ HDL ()25%), apoB ⁄ apoA1 ()10%),
insulin ()28%), SBP ()9%) and body weight ()6%)
(Fig. 2).
Discussion
To our knowledge, this is the first study to investigate
the clinical effects of a diet based on foods mainly orig-
inating from Nordic countries. This randomized,
strictly controlled study shows that an ad libitum ND
improves cardiovascular risk factors in mildly hyper-
cholesterolaemic subjects. The ND caused a clinically
relevant improvement in blood lipid profile and also
lowered SBP and insulin resistance compared with a
habitual CD. There was a moderate but significant
decrease in body weight compared with the CD. The
pronounced effects suggest that a ND may be a prom-
ising treatment for hypercholesterolaemia and possi-
bly also for the prevention of obesity, hypertension,
insulin resistance and CVD.
Consistent with prior studies investigating the effects
of ad libitum diets on blood lipids [6, 13–15], the ND
caused a significant decrease in plasma cholesterol
and LDL-C levels. In addition, the improved insulin
sensitivity accords with previous studies of similar
diets [21, 22]. The reduction in SBP is comparable to
the decrease observed in hypertensive subjects on
DASH diets [15, 23]. The low sodium content of the
ND probably contributed to the BP-lowering effect.
The LDL-C-lowering effect was, however, more pro-
nounced with the ND when compared with the DASH
diet [24]. This may be partly because of the significant
weight loss that occured after the ND, but not after
the DASH diet, which is isocaloric.
The ND is a plant-based diet similar to the Portfolio
diet including legumes, whole grain cereals and die-
tary fibre from oats and barley [25]. However, in con-
trast to the Portfolio diet, which is a vegetarian diet
including plant sterol-enriched margarines, the ND
does include some poultry, red meat, fish and low-fat

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 V. Adamsson et al.
| Diet and cardiovascular risk factors

Table 3 Absolute and relative

Characteristics Control diet Nordic diet Pb change in cardiovascular risk
Subjects, n 42 44 factors from baseline to week 6
Body weight (kg) 0.03 ± 1.47 (0.04) )3.00 ± 1.86 ()4) <0.001 of control and Nordic dietsa
Body mass index (kg m)2) )0.01 ± 0.51 ()0.04) )1.04 ± 0.60 ()4.0) <0.001
Systolic blood pressure (mmHg) 0.60 ± 11.25 (0.5) )6.55 ± 13.18 ()5.0) 0.008
Diastolic blood pressure (mmHg) 0.48 ± 9.46 (0.6) )2.99 ± 8.90 ()4) 0.08
Plasma glucose (mmol L)1) 0.05 ± 0.34 (1) 0.00 ± 0.41 (0) 0.52
Plasma insulin (mU L)1) 0.90 ± 2.88 (15) )0.51 ± 2.25 ()9) 0.01
Insulin resistance (HOMA-IR) 0.22 ± 0.64(17) )0.11 ± 0.51()9) 0.01
Plasma triglycerides (mmol L)1) )0.03 ± 0.40 ()2) 0.11 ± 0.58 (7) 0.46
)1
Plasma cholesterol (mmol L ) 0.23 ± 0.55 (4) )0.98 ± 0.75 ()16) <0.0001
Plasma LDL-C(mmol L)1) 0.10 ± 0.53 (2) )0.83 ± 0.67 ()21) <0.001
Plasma HDL-C (mmol L)1) 0.11 ± 0.19 (7) )0.08 ± 0.23 ()5) 0.001
LDL ⁄ HDL ratio )0.11 ± )0.35 ()4) )0.42 ± )0.57 ()14) 0.003
Plasma apolipoprotein A1 (g L)1) 0.11 ± 0.14 (7) )0.11 ± 0.20 ()7) <0.001
Plasma Apo B (g L)1) 0.16 ± 0.12 (14) )0.09 ± 0.15 ()8) <0.001
Apo B ⁄ A1 ratio 0.05 ± 0.10 (7) )0.01 ± 0.13 ()1) 0.02
C-reactive protein (mg L)1) 0.33 ± 1.87 (20) 0.10 ± 1.91 (6) 0.40

HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment-insulin resis-

tance; LDL, low-density lipoprotein.
a
Data are means ± SD (percentages from baseline). bDifferences between groups using un-
paired t-test.

milk products, but no foods enriched with plant ster-
ols. Thus, the LDL-C-lowering effect of the ND is not
because of added plant sterols. Even though there are
differences between the diets, the ND lowers plasma
LDL-C concentration to a similar extent to the Portfo-
lio diet [13] but the ND causes a greater reduction in
SBP [13]. Compared with a similar plant-based diet
[26], the ND causes a greater reduction (21% versus
9%) in LDL-C.
The diet-induced change in risk factors may be
achieved by a combined effect of various nutrients
and foods. It is well known that replacing saturated
fat with polyunsaturated fat reduces LDL-C [7]. In
addition to the reduced saturated fat, the decreased
dietary cholesterol may also have contributed to the
lowering of LDL-C. It has also been suggested that
replacing saturated fat with polyunsaturated or
monounsaturated fat improves insulin sensitivity
[27]. After the ND, vegetable fats from polyunsatu-
rated (both n-6 and n-3) but not monounsaturated
fat intake increased. Increased intake of fatty fish also
contributed to the increase in polyunsaturated fat.
Furthermore, the increase in dietary fibre from whole
grains, legumes, fruit and vegetables may contribute
to the favourable effects.
It is interesting that there was a moderate reduction
(4%) in mean body weight after the ND despite the fact
that the diet was given ad libitum. This potential ‘anti-
obesity effect’ also seemed to be sustained ()4.4 kg,
)6%) for at least 10 weeks according to the subgroup
analyses of the extended follow-up. According to sub-
jects’ reports, the ND was associated with high satia-
tion, possibly partly because of the large amount of fi-
bre-rich foods. The substantial average increase in
dietary fibre from an already relatively high intake of
30 g day)1 at baseline to 54 g day)1 is noteworthy.
As a consequence, energy balance could not be main-
tained during the ND period despite ad libitum condi-
tions. The ND was not an energy-restricted diet, and
subjects were advised to eat until they felt satiated.
Participants were allowed to leave foods or ask for
more food boxes. Indeed, the calculated energy intake
from the DSC shows a decrease in mean energy in-
take of 522 kcal day)1 from baseline to 6 weeks,
which corresponds well to the weight loss of 3 kg after
6 weeks of the ND. The effects on cholesterol and apo-
lipoproteins were independent of weight change but
effects on insulin sensitivity and BP were not. It is,
however, unclear how much of the insulin sensitivity
and BP changes were mediated by moderate weight
change.

156 ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159
 V. Adamsson et al.
| Diet and cardiovascular risk factors

Fig. 2 Change in cardiovascular risk factors from baseline to 6 weeks in the Nordic diet group and from baseline to 10 weeks in
the subgroup allocated to extended intervention. Change in cardiovascular risk factors from baseline to 6 weeks in the Nordic
diet group (ND; n = 44) including the extended intervention subgroup (n = 11) from week 6 to week 10 showing results from base-
line to 10 weeks. For the extended intervention subgroup, P-values show difference from baseline to 10 weeks. All P-values are
within-group comparisons.

Notably, virtually all ND foods are widely available in
supermarkets and the diet is high in unprocessed
food including fruits, legumes and vegetables. This
improves reproducibility of this study and facilitates
the use of this diet amongst the general population.
The LDL-C-lowering effect ()21%) caused by the ND
is impressive and comparable to first-generation sta-
tins [5], and after 10 weeks, the effect was even more
notable ()31%) as observed in the extended interven-
tion subgroup. There was a significant decrease in
HDL-C after the ND, probably because of the re-
stricted fat intake. However, improved LDL ⁄ HDL and
apoB ⁄ apoA1 ratios suggest this effect alone is not of
clinical relevance. Indeed, the overall risk factor pro-
file was improved. Of importance, the large reduction
in SBP by nearly 7 mmHg after the ND is clinically
noteworthy. At a population level, this effect may cor-
respond to an approximately 18% reduced risk of
CVD mortality [28]. In addition, SBP decreased by
9.5 mmHg from baseline in the 4-week extended
intervention subgroup.
Of interest, the apparent satiating effect of the ND
could be useful for managing overweight individuals
and preventing obesity. It is also noteworthy that the
combined improvement in lipid and glucose metabo-
lism as well as BP may be clinically more important
than improving single risk factors.
There are limitations to this study. This was a con-
trolled 6-week trial in which participants assigned to
the ND were provided with all foods. This trial was not
a long-term study, but we did also follow a subgroup
for 10 weeks and showed a clear continuation of the
favourable effects. This suggests that the risk factor
improvement may have been underestimated as a
steady state was not reached in the extended inter-
vention, even after 10 weeks on the ND. Finally, we

ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159 157
 V. Adamsson et al.
| Diet and cardiovascular risk factors
did not monitor physical activity to assess differences
between the groups. However, both groups were
encouraged to maintain their habitual lifestyle,
including physical activity level, during the study.
The strengths of this study include the randomized
controlled design, and the fact that all food was pro-
vided for the ND group. The latter allowed us to moni-
tor dietary compliance directly using a DSC recording
of any uneaten foods; compliance in the ND group
was high. In this study, we used the dietary history
for food registration. An advantage of the dietary his-
tory method is that relatively long time-periods can
be studied and thereby intake on an individual level
can be obtained. Also, by good communication, the
interviewer can help to minimize the drop-out rate.
The dietary history interview may also provide more
valid data on intake as it has been shown to record
average energy intake closer to the energy expendi-
ture, compared with other methods [29]. Further-
more, repeated food records may result in increased
under-reporting of energy intake.
This study was conducted in middle-aged healthy
Caucasians with mild hypercholesterolaemia; the ef-
fects in other populations are unknown. An impor-
tant practical finding was the surprisingly low drop-
out rate indicating good acceptance of the ND.
Conclusion
This is the first study to investigate the health effects
of a ND. These clinically relevant results suggest that
a diet based on foods originating from Nordic coun-
tries may be an option for treating hypercholesterola-
emia as well as lowering BP and insulin resistance.
The two latter effects were partly mediated by a mod-
erate weight loss. In fact, the ND was surprisingly
effective in lowering body weight despite being pro-
vided ad libitum. The favourable effects of the ND sup-
port current dietary guidelines in Europe, including
the Nordic countries, as well as recommendations
from the American Heart Association [16, 30, 31]. The
results of the ND are also in agreement with those of
similar diets in other populations, such as the DASH
and Mediterranean diets [15, 23, 26, 28, 30]. Further
studies are needed to verify the present promising re-
sults in a more uncontrolled setting.
Acknowledgements
For assistance during the intervention, we thank the
teachers (Håkan Höglund and Marina Tillman) and
students at the Hotel and Restaurant program at
158 ª 2010 The Association for the Publication of the Journal of Internal Medicine Journal of Internal Medicine 269; 150–159
Torsbergs Senior High School in Bollnäs. We also
thank the following: the study nurses Kurt Trosell,
Britt-Marie Persson and Marie Eriksson; computer
programmer Claes Wallentinsson; registered dieti-
cians Maria Allard, Helena Jonsson and Karin Wi-
berg; Pär Hommerberg from the Swedish Heart and
Lung Association; Lars-Erik Nilsson, Linda Adams-
son and Lena Larsson, at Segersta Central, who
helped with recruitment; and the diploma student
Therese Hedlund.
Funding
The present study was financed by a research grant
from the Cerealia Foundation. UR was funded by a
grant from NordForsk (SYSDIET, Centre of Excel-
lence in Food, Nutrition and Health) and received a re-
search grant from The Swedish Diabetes Association
(Diabetesfonden).
Conflict of interest statement
VA is a PhD student at Uppsala University, and also
employed by Lantmännen R&D which is a research
and development department within the Lantmän-
nen group. Lantmännen group is owned by Swedish
farmers and operates within the food, energy and
agricultural industries. The corresponding author
(UR) had full access to all data and was responsible
for all data interpretation. UR is fully employed as a
researcher by Uppsala University.
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Correspondence: Dr Ulf Risérus, Department of Public Health and
Caring Sciences ⁄ Clinical Nutrition and Metabolism, Uppsala Uni-
versity, Uppsala Science Park, 751 85 Uppsala, Sweden.
(fax: +46186117976; e-mail: ulf.riserus@pubcare.uu.se).
Supporting Information
Additional Supporting Information may be found in
the online version of this article:
Table S1. Representative daily menu for the Nordic
diet.
Table S2. Nutritional profile of planned Nordic diet.
Please note: Wiley-Blackwell are not responsible for
the content or functionality of any supporting materi-
als supplied by the authors. Any queries (other than
missing material) should be directed to the corre-
sponding author for the article.
159