Jacob J. Christensen
University of Oslo
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Publication
Featured researches published by Jacob J. Christensen.
British Journal of Nutrition | 2016
Stine M. Ulven; Lena Leder; Elisabeth Elind; Inger Ottestad; Jacob J. Christensen; Vibeke H. Telle-Hansen; Anne Juul Skjetne; Ellen Raael; Navida A. Sheikh; M. Holck; Kristin Torvik; Amandine Lamglait; Kari Thyholt; Marte Gjeitung Byfuglien; Linda Granlund; Lene Frost Andersen; 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.
Atherosclerosis | 2015
Ingunn Narverud; Jeanine Roeters van Lennep; Jacob J. Christensen; Jorie Versmissen; Jon Michael Gran; Per Ole Iversen; Pål Aukrust; Bente Halvorsen; Thor Ueland; Stine M. Ulven; Leiv Ose; Marit B. Veierød; Eric J.G. Sijbrands; Kjetil Retterstøl; Kirsten B. Holven
BACKGROUND AND AIMS Pregnancy exerts metabolic changes with increasing levels of total cholesterol and triglycerides as prominent features. Maternal hypercholesterolemia may thus contribute to an unfavorable in utero environment potentially influencing the susceptibility of adult cardiovascular disease in the offspring. We investigated the impact of maternal familial hypercholesterolemia (FH) on pre-treatment plasma lipids and C-reactive protein (CRP) levels in non-statin treated FH children. METHODS Children with FH (n = 1063) aged between 0 and 19 years were included. Of these, 500 had inherited FH maternally, 563 paternally and 97.6% had a verified FH mutation. Information about inheritance, mutation type and pretreatment levels of blood lipids and CRP was retrieved from the medical records. RESULTS There were no significant differences in the plasma levels of lipids and C-reactive protein (CRP) in children with maternal FH compared with children with paternal FH, (0.12 ≤ P ≤ 0.90). Independent of which parent transmitted FH, children with LDL receptor negative mutations had significantly higher levels of total and LDL cholesterol and Apolipoprotein (Apo) B, and lower levels of HDL cholesterol and ApoA1, compared with children with other LDL receptor mutations (P < 0.001). CONCLUSION Maternal inheritance of FH was not associated with detectable long-term effects in the offsprings phenotype measured by adverse lipid profiles and increased CRP levels, whereas a LDL receptor negative mutation was associated with an unfavorably phenotype in FH offspring. Our findings do not support the fetal origin of adulthood disease hypothesis, while at the same time not excluding the hypothesis since other pathways leading to atherosclerosis may be involved.
Genes and Nutrition | 2017
Vibeke H. Telle-Hansen; Jacob J. Christensen; Stine M. Ulven; Kirsten B. Holven
BackgroundObesity, a major cause of death and disability, is increasing worldwide. Obesity is characterized by a chronic, low-grade inflammatory state which is suggested to play a critical role in the development of obesity-related diseases like cardiovascular diseases and type 2 diabetes. In fact, in the hours following consumption of a meal, a transient increase in inflammatory markers occurs, a response that is exaggerated in obese subjects. Dietary composition, including content of dietary fatty acids, may affect this inflammatory response both acutely and chronically, and thereby be predictive of progression of disease. The aim of the review was to summarize the literature from 2010 to 2016 regarding the effects of dietary fat intake on levels of inflammatory markers in overweight and obesity in human randomized controlled trials.Methods and resultsWe performed a literature search in MEDLINE, EMBASE, and PubMed databases. The literature search included human randomized controlled trials, both postprandial and long-term interventions, from January 2010 to September 2016. In total, 37 articles were included. Interventions with dairy products, vegetable oils, or nuts showed minor effects on inflammatory markers. The most consistent inflammatory-mediating effects were found in intervention with whole diets, which suggests that many components of the diet reduce inflammation synergistically. Furthermore, interventions with weight reduction and different fatty acids did not clearly show beneficial effects on inflammatory markers.ConclusionMost interventions showed either no or minor effects of dietary fat intake on inflammatory markers in overweight and obese subjects. To progress our understanding on how diet and dietary components affect our health, mechanistic studies are required. Hence, future studies should include whole diets and characterization of obese phenotypes at a molecular level, including omics data and gut microbiota.
Data in Brief | 2017
Jacob J. Christensen; Liv T. Osnes; Bente Halvorsen; Kjetil Retterstøl; Martin P. Bogsrud; Cecilie Wium; Arne Svilaas; Ingunn Narverud; Stine M. Ulven; Pål Aukrust; Kirsten B. Holven
The data in this relies on a previous publication: “Altered leukocyte distribution under hypercholesterolemia: a cross-sectional study in children with familial hypercholesterolemia” (Christensen et al. 2016) [1]. In the present paper, whole blood leukocyte distribution and plasma inflammatory proteins were measured for association with cholesterol concentration and CRP in children with familial hypercholesterolemia (FH) and healthy children.
Atherosclerosis | 2017
Jacob J. Christensen; Liv T. Osnes; Bente Halvorsen; Kjetil Retterstøl; Martin P. Bogsrud; Cecilie Wium; Arne Svilaas; Ingunn Narverud; Stine M. Ulven; Pål Aukrust; Kirsten B. Holven
Atherosclerosis | 2017
Jacob J. Christensen; Stine M. Ulven; Kjetil Retterstøl; Ingunn Narverud; Martin P. Bogsrud; Tore Henriksen; Jens Bollerslev; Bente Halvorsen; Pål Aukrust; Kirsten B. Holven
Journal of Clinical Lipidology | 2016
Jacob J. Christensen; Kjetil Retterstøl; Kristin Godang; Marie Cecilie Paasche Roland; Elisabeth Qvigstad; Jens Bollerslev; Thor Ueland; Tore Henriksen; Kirsten B. Holven
Genes and Nutrition | 2017
Håvard Hamarsland; Truls Raastad; Inger Ottestad; Jacob J. Christensen; Kristin Eckardt; Christian A. Drevon; Anne Sofie Biong; Stine M. Ulven; Kirsten B. Holven
Tidsskrift for Den Norske Laegeforening | 2017
Ingunn Narverud; Jacob J. Christensen; Inger Ottestad; Stine M. Ulven; Kirsten B. Holven
Atherosclerosis | 2015
Stine M. Ulven; Lena Leder; Elisabeth Elind; Inger Ottestad; Jacob J. Christensen; Vibeke H. Telle-Hansen; Anne Juul Skjetne; Kristin Torvik; Ellen Raael; Navida A. Sheikh; M. Holck; Kari Thyholt; Marte Gjeitung Byfuglien; Linda Granlund; Lene Frost Andersen; Kirsten B. Holven
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Oslo and Akershus University College of Applied Sciences
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