Hide metadata

dc.date.accessioned2020-01-20T15:26:43Z
dc.date.available2020-01-20T15:26:43Z
dc.date.issued2020
dc.identifier.urihttp://hdl.handle.net/10852/72312
dc.description.abstractVitamin A is an essential fat-soluble nutrient with important functions in growth, development and the visual process. The major bioactive form of vitamin A, retinoic acid, can stimulate expression of genes involved in the regulation of many important metabolic processes and can influence risk factors of cardiovascular disease (CVD) such as apolipoproteins and the amino acid homocysteine. We investigated whether circulating vitamin A can modify risk of myocardial infarction associated with blood concentrations of apolipoproteins B and A1, and homocysteine in a large cohort consisting of more than 4000 patients with established CVD. In the first two studies, we observed an increased risk of myocardial infarction in patients with higher concentrations of apolipoprotein B and homocysteine ​​and low concentrations of apolipoprotein A1. The risk was highest in patients who also had higher blood concentrations of vitamin A. In the most recent work, we observed that markers of impaired renal function (creatinine), the amino acid cysteine and the inflammatory marker uric acid were positively associated with vitamin A concentrations in the blood. Although vitamin A is a nutrient, there was little evidence indicating that intake of specific food groups or nutrients were associated with vitamin A concentrations in the blood. Taken together, we can conclude that vitamin A can modify the risk of acute myocardial infarction associated with traditional risk factors such as apolipoproteins and homocysteine. In addition, renal function but also amino acids and inflammatory markers are associated with vitamin A concentrations in blood, while diet appears to play a minor role, suggesting that vitamin A concentrations are under homeostatic control. The clinical relevance of the work is unknown, and replication is essential.en_US
dc.language.isoenen_US
dc.relation.haspartPAPER I: Olsen T, Vinknes KJ, Svingen GFT, Pedersen ER, Tell GS, Blomhoff R, Drevon CA, Ueland PM, Midttun O, Refsum H, Nygard OK (2017) Cardiovascular disease risk associated with serum apolipoprotein B is modified by serum vitamin A. Atherosclerosis. doi:10.1016/j.atherosclerosis.2017.07.020. The article is included in the thesis. Also available at: https://doi.org/10.1016/j.atherosclerosis.2017.07.020
dc.relation.haspartPAPER II: Olsen T, Vinknes KJ, Svingen GFT, Pedersen ER, Dhar I, Tell GS, Blomhoff R, Ueland PM, Midttun O, Refsum H, Nygard OK (2018) The risk association of plasma total homocysteine with acute myocardial infarction is modified by serum vitamin A. Eur J Prev Cardiol 25 (15):1612-1620. doi:10.1177/2047487318788587. The article is included in the thesis. Also available at: https://doi.org/10.1177/2047487318788587
dc.relation.haspartPAPER III: Olsen T, Vinknes KJ, Blomhoff R, Lysne V, Midttun Ø, Ueland PM, Svingen GFT, Pedersen EKR, Drevon CA, Refsum H, Nygård OK (2019) Amino acids of homocysteine metabolism, inflammatory markers and creatinine are associated with serum retinol in patients with cardiovascular disease. Published as: Creatinine, total cysteine and uric acid are associated with serum retinol in patients with cardiovascular disease. Eur J Nutr (2019), doi: 10.1007/s00394-019-02086-2. The paper is included in the thesis. The published version is available at: https://doi.org/10.1007/s00394-019-02086-2
dc.relation.urihttps://doi.org/10.1016/j.atherosclerosis.2017.07.020
dc.relation.urihttps://doi.org/10.1177/2047487318788587
dc.relation.urihttps://doi.org/10.1007/s00394-019-02086-2
dc.titleLipids, Homocysteine and Vitamin A: Perspectives and new hypotheses from patients with cardiovascular diseaseen_US
dc.typeDoctoral thesisen_US
dc.creator.authorOlsen, Thomas
dc.identifier.urnURN:NBN:no-75444
dc.type.documentDoktoravhandlingen_US
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/72312/3/PhD-Olsen-2020.pdf


Files in this item

Appears in the following Collection

Hide metadata