SEARCH

SEARCH BY CITATION

Keywords:

  • cardiovascular risk factors;
  • cholesterol;
  • diet;
  • Nordic foods;
  • nutrition

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

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, Bollnäs; Halmstad University, Halmstad, Sweden). Effects of a healthy Nordic diet on cardiovascular risk factors in hypercholesterolaemic subjects: a randomized controlled trial (NORDIET). J Intern Med 2011; 269: 150–159.

Objective.  The aim of this study was to investigate the effects of a healthy Nordic diet (ND) on cardiovascular risk factors.

Design and subjects.  In a randomized controlled trial (NORDIET) conducted in Sweden, 88 mildly hypercholesterolaemic subjects were randomly assigned to an ad libitum ND or control diet (subjects’ usual Western diet) for 6 weeks. Participants in the ND group were provided with all meals and foods. Primary outcome 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.

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 assigned to diet completed the study. Compared with controls, there was a decrease in plasma cholesterol (−16%, < 0.001), LDL cholesterol (−21%, < 0.001), high-density lipoprotein (HDL) cholesterol (−5%, < 0.01), LDL/HDL (−14%, < 0.01) and apolipoprotein (apo)B/apoA1 (−1%, < 0.05) in the ND group. The ND reduced insulin (−9%, = 0.01) and systolic BP by −6.6 ± 13.2 mmHg (−5%, < 0.05) compared with the control diet. Despite the ad libitum nature of the ND, body weight decreased 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 differences in diastolic BP or triglyceride or glucose concentrations.

Conclusions.  A healthy ND improves blood lipid profile and insulin sensitivity and lowers blood pressure at clinically relevant levels in hypercholesterolaemic subjects.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

Cardiovascular disease (CVD) is a major cause of premature 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]. Controlled trials show plaque regression and decreased cardiovascular mortality with LDL-C-lowering drugs [3]. However, other effects also contribute to the prevention of CVD, for example by decreasing blood pressure (BP), inflammation and insulin resistance [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 changing the whole diet to achieve advantages by combining several dietary components. Substituting unsaturated 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 oats and barley [9]. The plasma LDL-C-reducing effect 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 efficacy can reduce plasma LDL-C [13] to similar levels to those achieved by first-generation statins [5]. Furthermore, adherence to a Mediterranean diet containing 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 Dietary 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 macronutrient 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 hypothesized that a healthy Nordic diet (ND) may reduce cholesterol concentrations and improve overall cardiovascular risk profile. The aim of this study was to investigate the effects of a healthy ND, eaten ad libitum, on cardiovascular risk factors in mildly hypercholesterolaemic subjects.

Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

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

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

Subjects living in the Swedish city Bollnäs were recruited by advertisements in the local newspaper during December 2007. The intervention was finalized 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-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) concentrations >4.5 mmol L−1, use of products or supplements fortified with plant sterols, omega-3, omega-6 or omega-9 fatty acids within 3 weeks prior to baseline visit, allergy to certain foods, weight-loss diets or drugs, special diets (e.g. vegan and gluten free), pregnancy or lactation.

image

Figure 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.

Download figure to PowerPoint

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 besides adhering to their prescribed diet during the study.

Outcome measures

The primary outcome measure was change in the level of plasma LDL-C and other blood lipids after 6 weeks. Secondary outcomes were changes in BP and insulin sensitivity [fasting insulin and homeostatic 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 randomly assigned to one of two groups: ND or a control diet (CD). A study nurse enrolled and assigned participants into the study in accordance with the randomization procedure. The randomization list was generated by a biostatistician at the Uppsala Clinical Research Centre. The random allocation sequence 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 follow-up.

In the ND group, the first 11 randomly assigned subjects 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 reason and study budget limitations.

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 Material). The subjects were provided with a 21-day rotating menu plan, including breakfast, lunch and dinner, 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 provided to subjects at the baseline visit. All subjects received instructions on how to prepare their breakfast. 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 beverage). For every item consumed, subjects ticked the DSC. Subjects were also asked to comment and describe any deviation from the menu. Uneaten food was not returned.

Nordic diet

The nutrient profile of the ND (Table S2 in Supplemental Material) was based on Nordic nutrition recommendations 2004 [16] and inspired by the Mediterranean, Portfolio and DASH diets and the NCEP. The ND was based on typical foods consumed in Nordic 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 daily 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 registered that meal/snack in the DSC. The ND was provided ad libitum and was thus neither energy restricted nor isocaloric on an individual level. To facilitate the distribution of diets to participants and estimate the approximate amount of food/meals to be delivered, the ND was calculated on an isocaloric basis (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 maintain their usual physical activity. Thus, the CD included 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 subjects were offered the ND for 6 weeks after study completion (i.e. after 6 weeks of the CD). Subjects randomly assigned to CD were, however, requested to avoid dietary supplements fortified with plant sterols or omega-3, omega-6 or omega-9 fatty acids throughout 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 photographs of known weights. The DSC, which was filled in by the ND group during the study, was analysed 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 dietary 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 measured without shoes. BP was measured manually by cuff and stethoscope in a sitting position on the right arm after a 5-min rest. Two measurements were performed 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 calculated by Friedewalds formula [18], and apolipoprotein (apo)A1 and apoB were measured by an immunoturbidometric 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 immunoassay kit (Mercodia AB, Uppsala, Sweden). Homeostasis 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 enhanced reaction, developed by Roche Diagnostics, using the Cobas® 6000 analyzer.

Statistical methods

Data are presented as mean ± SD. Per protocol analysis was used to assess effects on outcome measures. Variables not normally distributed were logarithmically transformed. Paired t-test was used to assess change within groups and unpaired t-tests to compare 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 differences during follow-up using ancova, with baseline values and weight change as covariates; t-tests were two-tailed, and < 0.05 was regarded as significant. spss version 16.0 for Windows was used for statistical analysis.

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

Of 88 subjects randomly assigned to the two diets (34 men and 54 women), only two subjects (one subject in each dietary group) were lost to follow-up, providing 86 subjects for analysis (Fig. 1). There were no significant differences between the ND and CD groups in baseline clinical characteristics after randomization (Table 1). Likewise, the two groups were similar at baseline with regard to nutrient intake (Table 2).

Table 1. Baseline characteristics after randomization to diets
CharacteristicsControl dietNordic dietPa
  1. CRP, C-reactive protein; HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment-insulin resistance; LDL, low-density lipoprotein.

  2. aDifferences between groups using unpaired two-tailed t-test. bn=40; subjects with baseline CRP >10 mg L−1 were excluded.

Subjects, n4244 
Age (year)53.4 ± 8.152.6 ± 7.80.63
Men/women15/2717/270.83
Body weight (kg)78.0 ± 13.376.0 ± 10.50.44
Body mass index (kg m−2)26.5 ± 3.326.3 ± 3.20.79
Systolic blood pressure (mmHg)129.8 ± 13.6127.9 ± 12.40.50
Diastolic blood pressure (mmHg)83.4 ± 9.380.8 ± 7.50.16
Plasma glucose (mmol L−1)4.9 ± 0.64.9 ± 0.50.54
Plasma insulin (mU L−1)6.1 ± 2.85.8 ± 3.00.57
Insulin resistance (HOMA-IR)1.3 ± 0.61.2 ± 0.60.47
Plasma triglycerides (mmol L−1)1.4 ± 0.81.6 ± 0.80.32
Plasma cholesterol (mmol L−1)6.4 ± 0.76.2 ± 0.80.36
Plasma LDL cholesterol (mmol L−1)4.2 ± 1.04.0 ± 0.60.33
Plasma HDL cholesterol (mmol L−1)1.6 ± 0.51.5 ± 0.40.28
LDL/HDL ratio2.8 ± 0.92.9 ± 0.80.80
Plasma apolipoprotein A1 (g L−1)1.5 ± 0.31.5 ± 0.30.76
Plasma apolipoprotein B (g L−1)1.1 ± 0.21.1 ± 0.20.85
ApoB/A1 ratio0.8 ± 0.20.8 ± 0.20.77
C-reactive protein (mg L−1)1.5 ± 1.4b1.6 ± 1.70.78
Table 2. Nutrient intake at baseline and at 6 weeks in the Nordic diet and control groups
 Control dietNordic diet
Baselinea6 weeksaPbBaselinea6 weekscPb
  1. aAssessed by dietary history interview. bDifference within the group using paired sample t-test. cAssessed by daily study checklist. dPercentage of daily energy intake. eCould not be computed because the standard error of the difference is zero.

Subjects, n4242 4444 
Energy (kcal day−1)2450 ± 6462457 ± 6420.312509 ± 6711989 ± 275<0.001
Protein (E%d)17 ± 2.617 ± 2.60.7617 ± 2.219 ± 0.8<0.001
Alcohol (E%)2.1 ± 3.12.0 ± 2.80.171.7 ± 1.62.1 ± 2.00.19
Carbohydrates (E%)46 ± 5.946 ± 5.60.4947 ± 6.152 ± 1.8<0.001
Dietary fibre (g day−1)31 ± 1131 ± 110.1730 ± 9.554 ± 7.4<0.001
Beta-glucan (g day−1)0.4 ± 0.70.4 ± 0.7e0.3 ± 0.44.9 ± 1.0<0.001
Fat (E%)34 ± 4.934 ± 5.00.2034 ± 5.027 ± 0.9<0.001
Saturated fat (E%)13 ± 3.013 ± 3.00.4014 ± 3.15.2 ± 0.4<0.001
Mono-unsaturated fat (E%)12 ± 2.312 ± 2.30.3212 ± 2.111 ± 0.5<0.001
Polyunsaturated fat (E%)5.6 ± 1.75.6 ± 1.70.074.9 ± 1.16.3 ± 0.3<0.001
Dietary cholesterol (mg day−1)355 ± 135356 ± 1350.28349 ± 125131 ± 17<0.001
Sodium (mg day−1)3518 ± 9683517 ± 9690.973727 ± 12141545 ± 305<0.001

Dietary changes

After 6 weeks, the nutrient content of the ND (Table 2) agreed with that of the planned diet (Table S2 in Supplemental Material). Except for alcohol (< 0.19), the change in nutrient intake between baseline and week 6 within the ND group was significant for all nutrients (< 0.001), indicating high compliance. Compliance was also high according to the completed DSC. When expressed as percentage of prescribed calories consumed during 6 weeks, compliance was 93% in the ND group. All participants reported that they were eating as much food as they were capable of. No significant dietary changes were observed in the CD group.

Effects on cardiovascular risk factors

The ND caused a significant lowering of plasma levels of cholesterol, LDL-C, HDL-C, apoA1 and apoB compared with the CD (Table 3). ApoB/apoA1 and LDL/HDL ratios were significantly decreased after the ND compared with the CD. Compared to the CD group, there was also a significant decrease in insulin concentrations and HOMA-IR, as well as systolic BP (SBP) in the ND group (Table 3). Reduction in diastolic BP (DBP) after 6 weeks of the ND was not statistically significant. Body weight decreased by 3 kg after the ND compared to the CD (Table 3). There were no significant effects of either diet on plasma glucose, TG or CRP concentrations (Table 3). No adverse events were reported in either group. Results were similar if the baseline value of each outcome measure was added as a covariate (data not shown).

Table 3. Absolute and relative change in cardiovascular risk factors from baseline to week 6 of control and Nordic dietsa
CharacteristicsControl dietNordic dietPb
  1. HDL, high-density lipoprotein; HOMA-IR, homeostasis model assessment-insulin resistance; LDL, low-density lipoprotein.

  2. aData are means ± SD (percentages from baseline). bDifferences between groups using unpaired t-test.

Subjects, n4244 
Body weight (kg)0.03 ± 1.47 (0.04)−3.00 ± 1.86 (−4)<0.001
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
Plasma cholesterol (mmol L−1)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 ratio0.05 ± 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

Adjustments for weight loss

The difference in LDL-C and apoB levels between groups remained after adjusting for weight change (< 0.001 for both), as well as for total cholesterol, HDL-C, apoA1, LDL/HDL and apoB/apoA (all < 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) completed the additional 4-week intervention. This subgroup 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 (= 0.09) were significantly different (< 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).

image

Figure 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 baseline to 10 weeks. For the extended intervention subgroup, P-values show difference from baseline to 10 weeks. All P-values are within-group comparisons.

Download figure to PowerPoint

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

To our knowledge, this is the first study to investigate the clinical effects of a diet based on foods mainly originating from Nordic countries. This randomized, strictly controlled study shows that an ad libitum ND improves cardiovascular risk factors in mildly hypercholesterolaemic 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 promising treatment for hypercholesterolaemia and possibly 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 pronounced 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 dietary fibre from oats and barley [25]. However, in contrast 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 milk products, but no foods enriched with plant sterols. 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 Portfolio 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 polyunsaturated (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 subjects’ reports, the ND was associated with high satiation, possibly partly because of the large amount of fibre-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 maintained during the ND period despite ad libitum conditions. 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 intake 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 apolipoproteins 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.

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 statins [5], and after 10 weeks, the effect was even more notable (−31%) as observed in the extended intervention subgroup. There was a significant decrease in HDL-C after the ND, probably because of the restricted fat intake. However, improved LDL/HDL and apoB/apoA1 ratios suggest this effect alone is not of clinical relevance. Indeed, the overall risk factor profile 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 correspond 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 metabolism as well as BP may be clinically more important than improving single risk factors.

There are limitations to this study. This was a controlled 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 intervention, even after 10 weeks on the ND. Finally, we 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 provided for the ND group. The latter allowed us to monitor 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 history 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 expenditure, compared with other methods [29]. Furthermore, 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 effects in other populations are unknown. An important practical finding was the surprisingly low drop-out rate indicating good acceptance of the ND.

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

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 countries may be an option for treating hypercholesterolaemia as well as lowering BP and insulin resistance. The two latter effects were partly mediated by a moderate weight loss. In fact, the ND was surprisingly effective in lowering body weight despite being provided ad libitum. The favourable effects of the ND support 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 results in a more uncontrolled setting.

Acknowledgements

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

For assistance during the intervention, we thank the teachers (Håkan Höglund and Marina Tillman) and students at the Hotel and Restaurant program at 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 dieticians Maria Allard, Helena Jonsson and Karin Wiberg; Pär Hommerberg from the Swedish Heart and Lung Association; Lars-Erik Nilsson, Linda Adamsson and Lena Larsson, at Segersta Central, who helped with recruitment; and the diploma student Therese Hedlund.

Funding

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

The present study was financed by a research grant from the Cerealia Foundation. UR was funded by a grant from NordForsk (SYSDIET, Centre of Excellence in Food, Nutrition and Health) and received a research grant from The Swedish Diabetes Association (Diabetesfonden).

Conflict of interest statement

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

VA is a PhD student at Uppsala University, and also employed by Lantmännen R&D which is a research and development department within the Lantmännen 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.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information
  • 1
    Shepherd J, Cobbe SM, Ford I et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995; 333: 13017.
  • 2
    Ballantyne CM, Herd JA, Dunn JK, Jones PH, Farmer JA, Gotto Jr AM. Effects of lipid lowering therapy on progression of coronary and carotid artery disease. Curr Opin Lipidol 1997; 8: 35461.
  • 3
    Baigent C, Keech A, Kearney PM et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005; 366: 126778.
  • 4
    Van Horn L, McCoin M, Kris-Etherton PM et al. The evidence for dietary prevention and treatment of cardiovascular disease. J Am Diet Assoc 2008; 108: 287331.
  • 5
    The Scandinavian Simvastatin Survival Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 13839.
  • 6
    National Cholesterol Education Program. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106: 3143421.
  • 7
    Erkkilä A, de Mello VDF, Risérus U, Laaksonen DE. Dietary fatty acids and cardiovascular disease: an epidemiological approach. Prog Lipid Res 2008; 47: 17287.
  • 8
    Mensink RP, Katan MB. Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler Thromb 1992; 12: 9119.
  • 9
    Theuwissen E, Mensink RP. Water-soluble dietary fibers and cardiovascular disease. Physiol Behav 2008; 94: 28592.
  • 10
    Plat J, Mensink RP. Plant stanol and sterol esters in the control of blood cholesterol levels: mechanism and safety aspects. Am J Cardiol 2005; 96: 15D22D.
  • 11
    Anderson JW, Johnstone BM, Cook-Newell ME. Meta-analysis of the effects of soy protein intake on serum lipids. N Engl J Med 1995; 333: 27682.
  • 12
    Phung OJ, Makanji SS, White CM, Coleman CI. Almonds have a neutral effect on serum lipid profiles: a meta-analysis of randomized trials. J Am Diet Assoc 2009; 109: 86573.
  • 13
    Jenkins DJ, Kendall CW, Faulkner D et al. A dietary portfolio approach to cholesterol reduction: combined effects of plant sterols, vegetable proteins, and viscous fibers in hypercholesterolemia. Metabolism 2002; 51: 1596604.
  • 14
    Sofi F, Cesari F, Abbate R, Gensini GF, Casini A. Adherence to Mediterranean diet and health status: meta-analysis. BMJ 2008; 337: a1344.
  • 15
    Appel LJ, Moore TJ, Obarzanek E et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997; 336: 111724.
  • 16
    Becker W, Lyhne N, Pedersen A, Aro A, Fogelholm M, Thórsdottír I. Nordic Nutrition Recommendations 2004. Integrating nutrition and physical activity. Copenhagen: Nordic Council of Ministers, 2004.
  • 17
    Nelson M, Bingham SA. Assessment of food consumption and nutrient intake. In: MargettsBM, NelsonM, eds Design Concepts in Nutritional Epidemiology. New York: Oxford University Press Inc, 2000; 12369.
  • 18
    Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972; 18: 499502.
  • 19
    Dreon DM, Fernstrom HA, Williams PT, Krauss RM. Reduced LDL particle size in children consuming a very-low-fat diet is related to parental LDL-subclass patterns. Am J Clin Nutr 2000; 71: 16116.
  • 20
    Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985; 28: 4129.
  • 21
    Jula A, Marniemi J, Huupponen R, Virtanen A, Rastas M, Ronnemaa T. Effects of diet and simvastatin on serum lipids, insulin, and antioxidants in hypercholesterolemic men: a randomized controlled trial. JAMA 2002; 287: 598605.
  • 22
    Estruch R, Martinez-Gonzalez MA, Corella D et al. Effects of a Mediterranean-style diet on cardiovascular risk factors: a randomized trial. Ann Intern Med 2006; 145: 111.
  • 23
    Sacks FM, Svetkey LP, Vollmer WM et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med 2001; 344: 310.
  • 24
    Obarzanek E, Sacks FM, Vollmer WM et al. Effects on blood lipids of a blood pressure-lowering diet: the Dietary Approaches to Stop Hypertension (DASH) Trial. Am J Clin Nutr 2001; 74: 809.
  • 25
    Jenkins DJ, Josse AR, Wong JM, Nguyen TH, Kendall CW. The portfolio diet for cardiovascular risk reduction. Curr Atheroscler Rep 2007; 9: 5017.
  • 26
    Gardner CD, Coulston A, Chatterjee L, Rigby A, Spiller G, Farquhar JW. The effect of a plant-based diet on plasma lipids in hypercholesterolemic adults: a randomized trial. Ann Intern Med 2005; 142: 72533.
  • 27
    Riserus U, Willett WC, Hu FB. Dietary fats and prevention of type 2 diabetes. Prog Lipid Res 2009; 48: 4451.
  • 28
    Whelton PK, He J, Appel LJ et al. Primary prevention of hypertension: clinical and public health advisory from The National High Blood Pressure Education Program. JAMA 2002; 288: 18828.
  • 29
    Black AE, Goldberg GR, Jebb SA, Livingstone MB, Cole TJ, Prentice AM. Critical evaluation of energy intake data using fundamental principles of energy physiology: 2. Evaluating the results of published surveys. Eur J Clin Nutr 1991; 45: 58399.
  • 30
    WHO. Diet, nutrition and the prevention of chronic diseases. World Health Organ Tech Rep Ser 2003; 916: i-viii, 1149, backcover.
  • 31
    Lichtenstein AH, Appel LJ, Brands M et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation 2006; 114: 8296.

Supporting Information

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Subjects
  6. Results
  7. Discussion
  8. Conclusion
  9. Acknowledgements
  10. Funding
  11. Conflict of interest statement
  12. References
  13. Supporting Information

Table S1. Representative daily menu for the Nordic diet.

Table S2. Nutritional profile of planned Nordic diet.

FilenameFormatSizeDescription
JOIM_2290_sm_TableS1.doc36KSupporting info item
JOIM_2290_sm_TableS2.doc31KSupporting info item

Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.