Stine Marie Ulven

Prof. Stine Marie Ulven

Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, Blindern, 0317 Oslo, Norway

Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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16 November 2018 in Nutrients
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Journal Article
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VTVibeke Telle-Hansen
Vibeke Telle-Hansen
KHKirsten B. Holven
Kirsten B. Holven
Stine Marie UlvenStine Marie Ulven
Stine Marie Ulven
Gut microbiota have recently been suggested to play a part in low-grade systemic inflammation, which is considered a key risk factor for cardiometabolic disorders. Diet is known to affect gut microbiota; however, the effects of diet and dietary components on gut microbiota and inflammation are not fully understood. In the present review, we summarize recent research on human dietary intervention studies, investigating the effects of healthy diets or dietary components on gut microbiota and systemic inflammation. We included 18 studies that reported how different dietary components altered gut microbiota composition, short-chain fatty acid levels, and/or inflammatory markers. However, the heterogeneity among the intervention studies makes it difficult to conclude whether diets or dietary components affect gut microbiota homeostasis and inflammation. More appropriately designed studies are needed to better understand the effects of diet on the gut microbiota, systemic inflammation, and risk of cardiometabolic disorders.

29 September 2020 in Nutrients
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Journal Article
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JNJosefine Nelson
Josefine Nelson
HSHelen Sjöblom
Helen Sjöblom
IGInger Gjertsson
Inger Gjertsson
Stine Marie UlvenStine Marie Ulven
Stine Marie Ulven
HLHelen Maria Lindqvist
Helen Maria Lindqvist
LBLinnea Bärebring
Linnea Bärebring
The aim was to compile the evidence from Randomized Controlled Trials (RCTs) of diet or dietary supplements used to reduce disease activity in adults with Rheumatoid Arthritis (RA). Searches were performed in the databases PubMed, Scopus and Cochrane. Only RCT studies of diets, foods or dietary supplements, looking at effects on the Disease Activity Score in 28 joints (DAS28) among adults with RA, published in peer-reviewed journals, were included. A total of 27 articles were included—three of whole diets (Mediterranean diet, raw food and anti-inflammatory diet), five of food items, five of n-3 fatty acids, five of single micronutrient supplements, four of single antioxidant supplements and five of pre-, pro- or synbiotics. Studies that showed moderate strength evidence for positive effects on disease activity in RA included interventions with a Mediterranean diet, spices (ginger powder, cinnamon powder, saffron), antioxidants (quercetin and ubiquinone), and probiotics containing Lactobacillus Casei. Other diets or supplements had either no effects or low to very low strength of evidence. In conclusion, RCT studies on diet or dietary supplements are limited in patients with RA, but based on the results in this review there is evidence that some interventions might have positive effects on DAS28.

7 September 2022 in BMJ
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SBSonja H Brunvoll
Sonja H Brunvoll
ANAnders B Nygaard
Anders B Nygaard
MEMerete Ellingjord-Dale
Merete Ellingjord-Dale
PHPetter Holland
Petter Holland
MIMette Stausland Istre
Mette Stausland Istre
ASArne Søraas
Arne Søraas
Objective To determine if daily supplementation with cod liver oil, a low dose vitamin D supplement, in winter, prevents SARS-CoV-2 infection, serious covid-19, or other acute respiratory infections in adults in Norway. Design Quadruple blinded, randomised placebo controlled trial. Setting Norway, 10 November 2020 to 2 June 2021. Participants 34 601 adults (aged 18-75 years), not taking daily vitamin D supplements. Intervention 5 mL/day of cod liver oil (10 µg of vitamin D, n=17 278) or placebo (n=17 323) for up to six months. Main outcome measures Four co-primary endpoints were predefined: the first was a positive SARS-CoV-2 test result determined by reverse transcriptase-quantitative polymerase chain reaction and the second was serious covid-19, defined as self-reported dyspnoea, admission to hospital, or death. Other acute respiratory infections were indicated by the third and fourth co-primary endpoints: a negative SARS-CoV-2 test result and self-reported symptoms. Side effects related to the supplementation were self-reported. The fallback method was used to handle multiple comparisons. Results Supplementation with cod liver oil was not associated with a reduced risk of any of the co-primary endpoints. Participants took the supplement (cod liver oil or placebo) for a median of 164 days, and 227 (1.31%) participants in the cod liver oil group and 228 (1.32%) participants in the placebo group had a positive SARS-CoV-2 test result (relative risk 1.00, multiple comparison adjusted confidence interval 0.82 to 1.22). Serious covid-19 was identified in 121 (0.70%) participants in the cod liver oil group and in 101 (0.58%) participants in the placebo group (1.20, 0.87 to 1.65). 8546 (49.46%) and 8565 (49.44%) participants in the cod liver oil and placebo groups, respectively, had ≥1 negative SARS-CoV-2 test results (1.00, 0.97 to 1.04). 3964 (22.94%) and 3834 (22.13%) participants in the cod liver oil and placebo groups, respectively, reported ≥1 acute respiratory infections (1.04, 0.97 to 1.11). Only low grade side effects were reported in the cod liver oil and placebo groups. Conclusion Supplementation with cod liver oil in the winter did not reduce the incidence of SARS-CoV-2 infection, serious covid-19, or other acute respiratory infections compared with placebo. Trial registration ClinicalTrials.gov NCT04609423.

13 February 2019 in The Journal of Nutrition
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PHPatrik Hansson
Patrik Hansson
KHKirsten B. Holven
Kirsten B. Holven
LØLinn K L Øyri
Linn K L Øyri
HBHilde K Brekke
Hilde K Brekke
ABAnne S Biong
Anne S Biong
Stine Marie UlvenStine Marie Ulven
Stine Marie Ulven
Postprandial lipemia is a risk factor for cardiovascular disease. Dairy products differ in nutrient content and food matrix, and little is known about how different dairy products affect postprandial triglyceride (TG) concentrations. We investigated the effect of meals with similar amounts of fat from different dairy products on postprandial TG concentrations over 6 h in healthy adults. A randomized controlled cross-over study was performed on 47 subjects (30% men), with median (25th–75th percentile) age of 32 (25–46) y and body mass index of 23.6 (21.0–25.8) kg/m2. Meals included 1 of butter, cheese, whipped cream, or sour cream, corresponding to 45 g of fat (approximately 60 energy%). Serum concentrations of TGs (primary outcome), and total cholesterol (TC), low density lipoprotein cholesterol (LDL cholesterol), high density lipoprotein cholesterol (HDL cholesterol), insulin, glucose, non-esterified fatty acids, and plasma glucose-dependent insulinotropic polypeptide (secondary outcomes) were measured before the meal and 2, 4, and 6 h postprandially. Incremental AUC (iAUC) was calculated for the responses, and data were analyzed using a linear mixed model. Sour cream induced a 61% larger TG-iAUC0–6 h compared to whipped cream (P < 0.001), a 53% larger TG-iAUC0–6 h compared to butter (P < 0.001), and a 23% larger TG-iAUC0–6 h compared to cheese (P = 0.05). No differences in TG-iAUC0–6 h between the other meals were observed. Intake of sour cream induced a larger HDL cholesterol-iAUC0–6 h compared to cheese (P = 0.01). Intake of cheese induced a 124% larger insulin iAUC0–6 h compared to butter (P = 0.006). No other meal effects were observed. High-fat meals containing similar amount of fat from different dairy products induce different postprandial effects on serum TGs, HDL cholesterol, and insulin in healthy adults. The potential mechanisms and clinical impact of our findings remain to be further elucidated. The study was registered at www.clinicaltrials.gov as NCT02836106.

14 October 2016 in British Journal of Nutrition
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Journal Article
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Stine Marie UlvenStine Marie Ulven
Stine Marie Ulven
LLLena Leder
Lena Leder
EEElisabeth Elind
Elisabeth Elind
IOInger Ottestad
Inger Ottestad
JCJacob J. Christensen
Jacob J. Christensen
KHKirsten B. Holven
Kirsten B. Holven
The healthy Nordic diet has been previously shown to have health beneficial effects among subjects at risk of CVD. However, the extent of food changes needed to achieve these effects is less explored. The aim of the present study was to investigate the effects of exchanging a few commercially available, regularly consumed key food items (e.g. spread on bread, fat for cooking, cheese, bread and cereals) with improved fat quality on total cholesterol, LDL-cholesterol and inflammatory markers in a double-blind randomised, controlled trial. In total, 115 moderately hypercholesterolaemic, non-statin-treated adults (25–70 years) were randomly assigned to an experimental diet group (Ex-diet group) or control diet group (C-diet group) for 8 weeks with commercially available food items with different fatty acid composition (replacing SFA with mostly n-6 PUFA). In the Ex-diet group, serum total cholesterol (P<0·001) and LDL-cholesterol (P<0·001) were reduced after 8 weeks, compared with the C-diet group. The difference in change between the two groups at the end of the study was −9 and −11 % in total cholesterol and LDL-cholesterol, respectively. No difference in change in plasma levels of inflammatory markers (high-sensitive C-reactive protein, IL-6, soluble TNF receptor 1 and interferon-γ) was observed between the groups. In conclusion, exchanging a few regularly consumed food items with improved fat quality reduces total cholesterol, with no negative effect on levels of inflammatory markers. This shows that an exchange of a few commercially available food items was easy and manageable and led to clinically relevant cholesterol reduction, potentially affecting future CVD risk.

26 April 2019 in The American Journal of Clinical Nutrition
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Journal Article
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Stine Marie UlvenStine Marie Ulven
Stine Marie Ulven
JCJacob J Christensen
Jacob J Christensen
ONOttar Nygård
Ottar Nygård
ASAsbjørn Svardal
Asbjørn Svardal
LLLena Leder
Lena Leder
KHKirsten B. Holven
Kirsten B. Holven
Replacing dietary saturated fatty acids (SFAs) with polyunsaturated fatty acids (PUFA) reduces the plasma low-density lipoprotein (LDL) cholesterol and subsequently the risk of cardiovascular disease. However, beyond changes in LDL cholesterol, we lack a complete understanding of the physiologic alterations that occur when improving dietary fat quality. The aim of this study was to gain knowledge of metabolic alterations paralleling improvements in the fat quality of the diet. We recently conducted an 8-wk, double-blind, randomized controlled trial replacing SFAs with PUFAs in healthy subjects with moderate hypercholesterolemia (n = 99). In the present substudy, we performed comprehensive metabolic profiling with multiple platforms (both nuclear magnetic resonance- and mass spectrometry-based technology) (n = 99), and analyzed peripheral blood mononuclear cell gene expression (n = 95) by quantitative real-time polymerase chain reaction. A large number of lipoprotein subclasses, myristoylcarnitine and palmitoylcarnitine, and kynurenine were reduced when SFAs were replaced with PUFAs. In contrast, bile acids, proprotein convertase subtilisin/kexin type 9, acetate, and acetoacetate were increased by the intervention. Some amino acids were also altered by the intervention. The mRNA levels of LXRA and LDLR were increased, in addition to several liver X receptor α target genes and genes involved in inflammation, whereas the mRNA levels of UCP2 and PPARD were decreased in peripheral blood mononuclear cells after replacing SFAs with PUFAs. Partial least squares-discriminant analysis showed that the 30 most important variables that contributed to class separation spanned all classes of biomarkers, and was in accordance with the univariate analysis. Applying metabolomics in randomized controlled dietary intervention trials has the potential to extend our knowledge of the biological and molecular effects of dietary fat quality. This study was registered at clinicaltrials.gov as NCT 01679496.