Combining 21 trials evaluating lipid outcomes , fish oil consumption result ed in a summary net change in triglycerides of -27 ( 95 % CI -33 , -20)mg/dL , in HDL cholesterol of + 1.6 ( 95 % CI + 0.8 , + 2.3)mg/dL , and in LDL cholesterol of + 6 ( 95 % CI + 3 , + 8)mg/dL. There was no effect of fish oil on total cholesterol .
Across studies , higher fish oil dose and higher baseline levels were associated with greater reductions in serum triglycerides .
The evidence supports a dose-dependent beneficial effect of fish oil on serum triglycerides , particularly among people with more elevated levels .
Fish oil consumption also modestly improves HDL cholesterol , increases LDL cholesterol levels , but does not appear to adversely affect glucose homeostasis .
The evidence regarding the effects of omega-3 fatty acids on hs-CRP is inconclusive , as are data on ALA
Greater fish oil consumption has been associated with reduced CVD risk , although the mechanisms are unclear .
Plant- source oil omega-3 fatty acids ( ALA ) have also been studied regarding their cardiovascular effect .
Supplementation with omega3 polyunsaturated fatty acids and all-rac alpha-tocopherol alone and in combination failed to exert an anti-inflammatory effect in human volunteers.
There is growing evidence supporting the importance of inflammation in all stages of atherosclerosis . While both omega-3 polyunsaturated fatty acids ( n3PUFA ) and the lipid-soluble antioxidant alpha-tocopherol ( AT ) have been shown to independently have significant anti-inflammatory effects , there is paucity of data examining the effect of n3PUFA alone and in combination with AT on markers of inflammation and monocyte function . Therefore , we tested the effect of n3PUFA alone , all-rac ( synthetic ) AT alone , and the combination on markers of inflammation and monocyte function . Healthy nonsmoking volunteers were r and omly assigned to 1 of 4 groups ( n = 20 per group ) : 1.5 g/d n3PUFA , 800 IU/d AT , 1.5 g n3PUFA + 800 IU/d AT , or placebo in a parallel double-blinded study . Compared to baseline , 12 weeks of supplementation result ed in no changes in plasma lipids regardless of treatment . Plasma AT was significantly increased only in those groups that received AT ( P < .0001 ) . Similarly , groups receiving n3PUFA showed a significant increase in plasma docosahexaenoic acid ( P < .0001 ) . No significant within- or between-group differences were found for plasma levels of high-sensitivity C-reactive protein ( hsCRP ) . Furthermore , there were no differences in monocyte proinflammatory cytokine release ( interleukin [IL]-1beta , tumor necrosis factor [TNF]-alpha and IL-6 ) after activation with monocyte chemotactic protein-1 ( MCP-1 ) . In conclusion , supplementation with n3PUFA and all-rac AT at these doses is not anti-inflammatory
Combining 21 trials evaluating lipid outcomes , fish oil consumption result ed in a summary net change in triglycerides of -27 ( 95 % CI -33 , -20)mg/dL , in HDL cholesterol of + 1.6 ( 95 % CI + 0.8 , + 2.3)mg/dL , and in LDL cholesterol of + 6 ( 95 % CI + 3 , + 8)mg/dL. There was no effect of fish oil on total cholesterol .
Across studies , higher fish oil dose and higher baseline levels were associated with greater reductions in serum triglycerides .
The evidence supports a dose-dependent beneficial effect of fish oil on serum triglycerides , particularly among people with more elevated levels .
Fish oil consumption also modestly improves HDL cholesterol , increases LDL cholesterol levels , but does not appear to adversely affect glucose homeostasis .
The evidence regarding the effects of omega-3 fatty acids on hs-CRP is inconclusive , as are data on ALA
Greater fish oil consumption has been associated with reduced CVD risk , although the mechanisms are unclear .
Plant- source oil omega-3 fatty acids ( ALA ) have also been studied regarding their cardiovascular effect .