Combined fish oil and high oleic sunflower oil supplements neutralize their individual effects on the lipid profile of healthy men

Both n-3 and n-9 fatty acids share a common metabolic pathway and can potentially and individually improve cardiovascular disease risk factors. Dietary n-6 is known to weaken the efficacy of n-3 fatty acids due to competition for the same enzymes. Still unclear is whether a similar competition exists between n-3 and n-9 fatty acids. Thus, a 12-week intervention study was conducted to investigate the effect of different combinations of fish oil and high-oleic sunflower oil (OSO) on healthy subjects. Included were five groups (98 subjects): three groups received a fixed amount of n-9 (8 g-day) with varying amounts of n-3 (1, 2 or 4 g-day), one group was given n-3 fatty acids only (2 g-day) and another was given n-9 only (8 g-day). We found that fish oil supplement (2 g-day) was able to decrease TAG by about 13 percent, this effect was diminished with the co-ingestion of n-9 (OSO). Intake of OSO (8 g-day) reduced both total and LDL cholesterol by about 10 percent, this effect was reduced by the addition of fish oil. Both fish oil and OSO failed to have any significant effect on both glycemic and blood pressure parameters. In conclusion; the impact of oleic acid (n-9) on total and LDL cholesterol was altered by the addition fish oil (n-3). These effects may have been the result of enzymatic competition between the two types of fatty acids. © 2013 AOCS.

Balk EM, 2006, ATHEROSCLEROSIS, V189, P19, DOI 10.1016-j.atherosclerosis.2006.02.012; BENNER KG, 1990, LIPIDS, V25, P534, DOI 10.1007-BF02537160; Berbert AA, 2005, NUTRITION, V21, P131, DOI 10.1016-j.nut.2004.03.023; Brenna JT, 2002, CURR OPIN CLIN NUTR, V5, P127, DOI 10.1097-00075197-200203000-00002; Damsgaard CT, 2008, J NUTR, V138, P1061; Fedor D, 2009, CURR OPIN CLIN NUTR, V12, P138, DOI 10.1097-MCO.0b013e3283218299; FESKENS EJM, 1991, DIABETES CARE, V14, P935, DOI 10.2337-diacare.14.11.935; Food and Drug Administration, QUAL HLTH CLAIMS; FRIEDEWA.WT, 1972, CLIN CHEM, V18, P499; Geleijnse JM, 2002, J HYPERTENS, V20, P1493, DOI 10.1097-00004872-200208000-00010; Gibson RS, 2005, PRINCIPLES NUTR ASSE; Harris WS, 1997, AM J CLIN NUTR, V65, P1645; Kaushik M, 2009, AM J CLIN NUTR, V90, P613, DOI 10.3945-ajcn.2008.27424; Kris-Etherton PM, 1999, CIRCULATION, V100, P1253; Lauritzen L, 2001, PROG LIPID RES, V40, P1, DOI 10.1016-S0163-7827(00)00017-5; Le HD, 2009, PROSTAG LEUKOTR ESS, V81, P165, DOI 10.1016-j.plefa.2009.05.020; Lovejoy JC, 2002, AM J CLIN NUTR, V76, P1000; Marckmann P, 1997, ARTERIOSCL THROM VAS, V17, P3384; MENSINK RP, 1989, NEW ENGL J MED, V321, P436, DOI 10.1056-NEJM198908173210705; Mente A, 2009, ARCH INTERN MED, V169, P659, DOI 10.1001-archinternmed.2009.38; Nasreddine L, 2006, PUBLIC HEALTH NUTR, V9, P194, DOI 10.1079-PHN2005855; NOSSEN JO, 1986, BIOCHIM BIOPHYS ACTA, V879, P56, DOI 10.1016-0005-2760(86)90266-3; Olano-Martin E, 2010, ATHEROSCLEROSIS, V209, P104, DOI 10.1016-j.atherosclerosis.2009.08.024; Perez-Jimenez F, 2007, MOL NUTR FOOD RES, V51, P1199, DOI 10.1002-mnfr.200600273; PHILLIPSON BE, 1985, NEW ENGL J MED, V312, P1210, DOI 10.1056-NEJM198505093121902; Rivellese AA, 2003, ATHEROSCLEROSIS, V167, P149, DOI 10.1016-S0021-9150(02)00424-0; Ruiz-Gutierrez V, 1998, J NUTR, V128, P570; RuizGutierrez V, 1996, J HYPERTENS, V14, P1483, DOI 10.1097-00004872-199612000-00016; Salmeron J, 2001, AM J CLIN NUTR, V73, P1019; St-Denis C, 2012, LIPIDS, V47, P1073, DOI 10.1007-s11745-012-3718-6; STORLIEN LH, 1991, DIABETES, V40, P280, DOI 10.2337-diabetes.40.2.280; Tholstrup T, 2011, AM J CLIN NUTR, V94, P1426, DOI 10.3945-ajcn.111.018846; Truswell AS, 1998, EUR J CLIN NUTR, V52, P312, DOI 10.1038-sj.ejcn.1600566; Vessby B, 2001, DIABETOLOGIA, V44, P312, DOI 10.1007-s001250051620; Zhou YP, 2012, BRIT J NUTR, V108, P408, DOI 10.1017-S0007114512002036

0

0