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Latest Paper:

Proc R Soc Med. 1938 Apr ;31 (6):557-558 19991463 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1931 Jun ;24 (8):1029-1030 19988183 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1931 Feb ;24 (4):429-434 19987955 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1929 Dec ;23 (2):130-134 19987243 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1928 Dec ;22 (2):152-153 19986742 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1928 May ;21 (7):1162-1164 19986487 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1928 Jan ;21 (3):444-445 19986263 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1928 Jan ;21 (3):441-443 19986262 (P,S,G,E,B)
D Evan Bedford
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Proc R Soc Med. 1927 Feb ;20 (4):328-330 19985533 (P,S,G,E,B)
D Evan Bedford
Keywords:
Atherosclerosis. 2009 Aug 21;: 19748619 (P,S,G,E,B,D)
Hugh Sinclair Unit of Nutrition, School of Chemistry, Food Biosciences and Pharmacy, University of Reading, Reading RG6 6AP, UK.
OBJECTIVES: To investigate the impact of apolipoprotein E (apoE) genotype on the response of the plasma lipoprotein profile to eicosapentaenoic acid (EPA) versus docosahexaenoic acid (DHA) intervention in humans. METHODS AND RESULTS: 38 healthy normolipidaemic males, prospectively recruited on the basis of apoE genotype (n=20 E3/E3 and n=18 E3/E4), completed a double-blind placebo-controlled cross-over trial, consisting of 3x4 week intervention arms of either control oil, EPA-rich oil (ERO, 3.3g EPA/day) or DHA-rich oil (DRO, 3.7g DHA/day) in random order, separated by 10 week wash-out periods. A significant genotype-independent 28% and 19% reduction in plasma triglycerides in response to ERO and DRO was observed. For total cholesterol (TC), no significant treatment effects were evident; however a significant genotype by treatment interaction emerged (P=0.045), with a differential response to ERO and DRO in E4 carriers. Although the genotypextreatment interaction for LDL-cholesterol (P=0.089) did not reach significance, within DRO treatment analysis indicated a 10% increase in LDL (P=0.029) in E4 carriers with a non-significant 4% reduction in E3/E3 individuals. A genotype-independent increase in LDL mass was observed following DRO intervention (P=0.018). Competitive uptake studies in HepG2 cells using plasma very low density lipoproteins (VLDL) from the human trial, indicated that following DRO treatment, VLDL(2) fractions obtained from E3/E4 individuals resulted in a significant 32%(P=0.002) reduction in LDL uptake relative to the control. CONCLUSIONS: High dose DHA supplementation is associated with increases in total cholesterol in E4 carriers, which appears to be due to an increase in LDL-C and may in part negate the cardioprotective action of DHA in this population subgroup.
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