human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: High doses of n-3 PUFA found in fish oils can reduce the circulating concentration of triacylglycerol ( TG ) , which may contribute to the positive impact of these fatty acids on the risk of CVD . The present study aim ed to establish the differential impact of EPA and docosahexaenoic ( DHA ) on plasma lipids and apo in adults . Forty-two normolipidaemic adult subjects completed a double-blind placebo controlled parallel study , receiving an EPA-rich oil ( 4.8 g EPA/d ) , DHA-rich oil ( 4.9 g DHA/d ) or olive oil as control , for a period of 4 weeks . No effects of treatment on total cholesterol , LDL-cholesterol or HDL-cholesterol were evident . There was a significant 22 % reduction in TG level relative to the control value following the DHA treatment ( P=0.032 ) , with the 15 % decrease in the EPA group failing to reach significance ( P=0.258 ) . There were no significant inter-group differences in response to treatment for plasma apoA1 , -C3 or -E levels , although a significant 15 % within-group increase in apoE was evident in the EPA ( P=0.006 ) and DHA ( P=0.003 ) groups . In addition , a within-group decrease in the apoA1:HDL-cholesterol ratio was observed in the DHA group , suggesting a positive impact of DHA on HDL particle size . The DHA intervention result ed in a significant increase in the proportion of EPA P=0.000 and DHA P=0.000 in plasma phospholipids , whilst significant increases in EPA P=0.000 and docosapentaenoic acid P=0.002 , but not DHA P=0.193 , were evident following EPA supplementation ( P<0.05 ) . Our present results indicate that DHA may be more efficacious than EPA in improving the plasma lipid profile Animal studies suggest that the 2 major omega3 fatty acids found in fish , eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) , may have differential effects on blood pressure ( BP ) and heart rate ( HR ) . The aim of this study was to determine whether there were significant differences in the effects of purified EPA or DHA on ambulatory BP and HR in humans . In a double-blind , placebo-controlled trial of parallel design , 59 overweight , mildly hyperlipidemic men were r and omized to 4 g/d of purified EPA , DHA , or olive oil ( placebo ) capsules and continued their usual diets for 6 weeks . Fifty-six subjects completed the study . Only DHA reduced 24-hour and daytime ( awake ) ambulatory BP ( P<0.05 ) . Relative to the placebo group , 24-hour BP fell 5.8/3.3 ( systolic/diastolic ) mm Hg and daytime BP fell 3.5/2.0 mm Hg with DHA . DHA also significantly reduced 24-hour , daytime , and nighttime ( asleep ) ambulatory HRs ( P=0 . 001 ) . Relative to the placebo group , DHA reduced 24-hour HR by 3 . 5+/-0.8 bpm , daytime HR by 3.7+/-1.2 bpm , and nighttime HR by 2 . 8+/-1.2 . EPA had no significant effect on ambulatory BP or HR . Supplementation with EPA increased plasma phospholipid EPA from 1 . 66+/-0.07 % to 9.83+/-0.06 % ( P<0.0001 ) but did not change DHA levels . Purified DHA capsules increased plasma phospholipid DHA levels from 4.00+/-0.27 % to 10.93+/-0.62 % ( P<0.0001 ) and led to a small , nonsignificant increase in EPA ( 1.52+/-0.12 % to 2.26+/-0.16 % ) . Purified DHA but not EPA reduced ambulatory BP and HR in mildly hyperlipidemic men . The results of this study suggest that DHA is the principal omega3 fatty acid in fish and fish oils that is responsible for their BP- and HR-lowering effects in humans . These results have important implication s for human nutrition and the food industry 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 , prospect ively 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 3 x 4 week intervention arms of either control oil , EPA-rich oil ( ERO , 3.3 g EPA/day ) or DHA-rich oil ( DRO , 3.7 g DHA/day ) in r and om 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 genotype x treatment 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 result ed 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 BACKGROUND Recent studies suggest that eicosapentaenoic ( EPA ) and docosahexaenoic ( DHA ) acids have distinct effects on cardiometabolic risk factors . The Omega-3 Index ( O3I ) , which is calculated as the proportion of EPA and DHA in red blood cell ( RBC ) membranes , has been inversely associated with the risk of coronary heart diseases and coronary mortality . The objective of this study was to compare the effects of EPA and DHA supplementation on the O3I in men and women with abdominal obesity and sub clinical inflammation . METHODS In a double-blind controlled crossover study , 48 men and 106 women with abdominal obesity and sub clinical inflammation were r and omized to a sequence of three treatment phases : 1 - 2.7g/d of EPA , 2 - 2.7g/d of DHA , and 3 - 3g/d of corn oil ( 0 g of EPA+DHA ) . All supplements were provided as 3 × 1 g capsules for a total of 3g/d . The 10-week treatment phases were separated by nine-week washouts . RBC membrane fatty acid composition and O3I were assessed at baseline and the end of each phase . Differences in O3I between treatments were assessed using mixed models for repeated measures . RESULTS The increase in the O3I after supplementation with DHA ( + 5.6 % compared with control , P<0.0001 ) was significantly greater than after EPA ( + 3.3 % compared with control , P<0.0001 ; DHA vs. EPA , P<0.0001 ) . Compared to  control , DHA supplementation decreased ( -0.8 % , P<0.0001 ) while EPA increased ( + 2.5 % , P<0.0001 ) proportion of docosapentaenoic acid ( DPA ) in RBCs ( DHA vs. EPA , P<0.0001 ) . The baseline O3I was higher in women than in men ( 6.3 % vs. 5.8 % , P=0.011 ) . The difference between DHA and EPA in increasing the O3I tended to be higher in men than in women ( + 2.6 % vs. + 2.2 % respectively , P for the treatment by sex interaction=0.0537 ) . CONCLUSIONS The increase in the O3I is greater with high dose DHA supplementation than with high dose EPA , which is consistent with the greater potency of DHA to modulate cardiometabolic risk factors . The extent to which such differences between EPA and DHA in increasing the O3I relates to long-term cardiovascular risk needs to be investigated in the future Fish oils containing both EPA and DHA have been shown to have beneficial cardiovascular effects , but less is known about the independent effects of DHA . This study was design ed to examine the effects of DHA on plasma lipid and lipoprotein concentrations and other biomarkers of cardiovascular risk in the absence of weight loss . In this r and omized , controlled , double-blind trial , 36 overweight or obese adults were treated with 2 g/d of algal DHA or placebo for 4.5 mo . Markers of cardiovascular risk were assessed before and after treatment . In the DHA-supplemented group , the decrease in mean VLDL particle size ( P ≤ 0.001 ) and increases in mean LDL ( P ≤ 0.001 ) and HDL ( P ≤ 0.001 ) particle sizes were significantly greater than changes in the placebo group . DHA supplementation also increased the concentrations of large LDL ( P ≤ 0.001 ) and large HDL particles ( P = 0.001 ) and decreased the concentrations of small LDL ( P = 0.009 ) and medium HDL particles ( P = 0.001 ) . As calculated using NMR-derived data , DHA supplementation reduced VLDL TG ( P = 0.009 ) and total TG concentrations ( P = 0.006 ) . Plasma IL-10 increased with DHA supplementation to a greater extent than placebo ( P = 0.021 ) , but no other significant changes were observed in glucose metabolism , insulin sensitivity , blood pressure , or markers of inflammation with DHA . In summary , DHA supplementation result ed in potentially beneficial changes in some markers of cardiometabolic risk , whereas other markers were unchanged The aim of this study was to determine whether eicosapentaenoic acid ( EPA ) or docosahexaenoic acid ( DHA ) , or both , were responsible for the triglyceride (TG)-lowering effects of fish oil . EPA ( 91 % pure ) and DHA ( 83 % pure ) , a fish oil concentrate ( FOC ; 41 % EPA and 23 % DHA ) and an olive oil ( OO ) placebo ( all ethyl esters ) were tested . A total of 49 normolipidemic subjects participated . Each subject was given placebo for 2–3 wk and one of the n-3 supplements for 3 wk in r and omized , blinded trials . The target n-3 fatty acid ( FA ) intake was 3 g/day in all studies . Blood sample s were drawn twice at the end of each supplementation phase and analyzed for lipids , lipoproteins , and phospholipid FA composition . In all groups , the phospholipid FA composition changed to reflect the n-3 FA given . On DHA supplementation , EPA levels increased to a small but significant extent , suggesting that some retroconversion may have occurred . EPA supplementation did not raise DHA levels , however , FOC and EPA produced significant decreases in both TG and very low density lipoprotein ( VLDL ) cholesterol ( C ) levels ( P<0.01 ) and increases in low density lipoprotein ( LDL ) cholesterol levels ( P<0.05 ) . DHA supplementation did not affect cholesterol , triglyceride , VLDL , LDL , or high density lipoprotein ( HDL ) levels , but it did cause a significant increase in the HDL2/HDL3 cholesterol ratio . We conclude that EPA appears to be primarily responsible for TG-lowering ( and LDL-C raising ) effects of fish oil Fourteen healthy volunteers were r and omly allocated to receive 4 g highly purified ethyl esters of eicosapentaenoic acid ( EPA ) ( 95 % pure , n=7 ) or docosahexaenoic acid ( DHA ) ( 90 % pure , n=7 ) daily for 5 wk in supplement to their ordinary diet . The n−3 fatty acids were given with a st and ard high-fat meal at the beginning and the end of the supplementation period . EPA and DHA induced a similar incorporation into chylomicrons which peaked 6 h after the meal . The relative uptake of EPA and DHA from the meal was > 90 % compared with the uptake of oleic acid . During absorption , there was no significant elongation or retroconversion of EPA or DHA in total chylomicron fatty acids . The concentration of EPA decreased by 13 % and DHA by 62 % ( P<0.001 ) between  
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: High doses of n-3 PUFA found in fish oils can reduce the circulating concentration of triacylglycerol ( TG ) , which may contribute to the positive impact of these fatty acids on the risk of CVD . The present study aim ed to establish the differential impact of EPA and docosahexaenoic ( DHA ) on plasma lipids and apo in adults . Forty-two normolipidaemic adult subjects completed a double-blind placebo controlled parallel study , receiving an EPA-rich oil ( 4.8 g EPA/d ) , DHA-rich oil ( 4.9 g DHA/d ) or olive oil as control , for a period of 4 weeks . No effects of treatment on total cholesterol , LDL-cholesterol or HDL-cholesterol were evident . There was a significant 22 % reduction in TG level relative to the control value following the DHA treatment ( P=0.032 ) , with the 15 % decrease in the EPA group failing to reach significance ( P=0.258 ) . There were no significant inter-group differences in response to treatment for plasma apoA1 , -C3 or -E levels , although a significant 15 % within-group increase in apoE was evident in the EPA ( P=0.006 ) and DHA ( P=0.003 ) groups . In addition , a within-group decrease in the apoA1:HDL-cholesterol ratio was observed in the DHA group , suggesting a positive impact of DHA on HDL particle size . The DHA intervention result ed in a significant increase in the proportion of EPA P=0.000 and DHA P=0.000 in plasma phospholipids , whilst significant increases in EPA P=0.000 and docosapentaenoic acid P=0.002 , but not DHA P=0.193 , were evident following EPA supplementation ( P<0.05 ) . Our present results indicate that DHA may be more efficacious than EPA in improving the plasma lipid profile Animal studies suggest that the 2 major omega3 fatty acids found in fish , eicosapentaenoic acid ( EPA ) and docosahexaenoic acid ( DHA ) , may have differential effects on blood pressure ( BP ) and heart rate ( HR ) . The aim of this study was to determine whether there were significant differences in the effects of purified EPA or DHA on ambulatory BP and HR in humans . In a double-blind , placebo-controlled trial of parallel design , 59 overweight , mildly hyperlipidemic men were r and omized to 4 g/d of purified EPA , DHA , or olive oil ( placebo ) capsules and continued their usual diets for 6 weeks . Fifty-six subjects completed the study . Only DHA reduced 24-hour and daytime ( awake ) ambulatory BP ( P<0.05 ) . Relative to the placebo group , 24-hour BP fell 5.8/3.3 ( systolic/diastolic ) mm Hg and daytime BP fell 3.5/2.0 mm Hg with DHA . DHA also significantly reduced 24-hour , daytime , and nighttime ( asleep ) ambulatory HRs ( P=0 . 001 ) . Relative to the placebo group , DHA reduced 24-hour HR by 3 . 5+/-0.8 bpm , daytime HR by 3.7+/-1.2 bpm , and nighttime HR by 2 . 8+/-1.2 . EPA had no significant effect on ambulatory BP or HR . Supplementation with EPA increased plasma phospholipid EPA from 1 . 66+/-0.07 % to 9.83+/-0.06 % ( P<0.0001 ) but did not change DHA levels . Purified DHA capsules increased plasma phospholipid DHA levels from 4.00+/-0.27 % to 10.93+/-0.62 % ( P<0.0001 ) and led to a small , nonsignificant increase in EPA ( 1.52+/-0.12 % to 2.26+/-0.16 % ) . Purified DHA but not EPA reduced ambulatory BP and HR in mildly hyperlipidemic men . The results of this study suggest that DHA is the principal omega3 fatty acid in fish and fish oils that is responsible for their BP- and HR-lowering effects in humans . These results have important implication s for human nutrition and the food industry 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 , prospect ively 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 3 x 4 week intervention arms of either control oil , EPA-rich oil ( ERO , 3.3 g EPA/day ) or DHA-rich oil ( DRO , 3.7 g DHA/day ) in r and om 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 genotype x treatment 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 result ed 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 BACKGROUND Recent studies suggest that eicosapentaenoic ( EPA ) and docosahexaenoic ( DHA ) acids have distinct effects on cardiometabolic risk factors . The Omega-3 Index ( O3I ) , which is calculated as the proportion of EPA and DHA in red blood cell ( RBC ) membranes , has been inversely associated with the risk of coronary heart diseases and coronary mortality . The objective of this study was to compare the effects of EPA and DHA supplementation on the O3I in men and women with abdominal obesity and sub clinical inflammation . METHODS In a double-blind controlled crossover study , 48 men and 106 women with abdominal obesity and sub clinical inflammation were r and omized to a sequence of three treatment phases : 1 - 2.7g/d of EPA , 2 - 2.7g/d of DHA , and 3 - 3g/d of corn oil ( 0 g of EPA+DHA ) . All supplements were provided as 3 × 1 g capsules for a total of 3g/d . The 10-week treatment phases were separated by nine-week washouts . RBC membrane fatty acid composition and O3I were assessed at baseline and the end of each phase . Differences in O3I between treatments were assessed using mixed models for repeated measures . RESULTS The increase in the O3I after supplementation with DHA ( + 5.6 % compared with control , P<0.0001 ) was significantly greater than after EPA ( + 3.3 % compared with control , P<0.0001 ; DHA vs. EPA , P<0.0001 ) . Compared to  control , DHA supplementation decreased ( -0.8 % , P<0.0001 ) while EPA increased ( + 2.5 % , P<0.0001 ) proportion of docosapentaenoic acid ( DPA ) in RBCs ( DHA vs. EPA , P<0.0001 ) . The baseline O3I was higher in women than in men ( 6.3 % vs. 5.8 % , P=0.011 ) . The difference between DHA and EPA in increasing the O3I tended to be higher in men than in women ( + 2.6 % vs. + 2.2 % respectively , P for the treatment by sex interaction=0.0537 ) . CONCLUSIONS The increase in the O3I is greater with high dose DHA supplementation than with high dose EPA , which is consistent with the greater potency of DHA to modulate cardiometabolic risk factors . The extent to which such differences between EPA and DHA in increasing the O3I relates to long-term cardiovascular risk needs to be investigated in the future Fish oils containing both EPA and DHA have been shown to have beneficial cardiovascular effects , but less is known about the independent effects of DHA . This study was design ed to examine the effects of DHA on plasma lipid and lipoprotein concentrations and other biomarkers of cardiovascular risk in the absence of weight loss . In this r and omized , controlled , double-blind trial , 36 overweight or obese adults were treated with 2 g/d of algal DHA or placebo for 4.5 mo . Markers of cardiovascular risk were assessed before and after treatment . In the DHA-supplemented group , the decrease in mean VLDL particle size ( P ≤ 0.001 ) and increases in mean LDL ( P ≤ 0.001 ) and HDL ( P ≤ 0.001 ) particle sizes were significantly greater than changes in the placebo group . DHA supplementation also increased the concentrations of large LDL ( P ≤ 0.001 ) and large HDL particles ( P = 0.001 ) and decreased the concentrations of small LDL ( P = 0.009 ) and medium HDL particles ( P = 0.001 ) . As calculated using NMR-derived data , DHA supplementation reduced VLDL TG ( P = 0.009 ) and total TG concentrations ( P = 0.006 ) . Plasma IL-10 increased with DHA supplementation to a greater extent than placebo ( P = 0.021 ) , but no other significant changes were observed in glucose metabolism , insulin sensitivity , blood pressure , or markers of inflammation with DHA . In summary , DHA supplementation result ed in potentially beneficial changes in some markers of cardiometabolic risk , whereas other markers were unchanged The aim of this study was to determine whether eicosapentaenoic acid ( EPA ) or docosahexaenoic acid ( DHA ) , or both , were responsible for the triglyceride (TG)-lowering effects of fish oil . EPA ( 91 % pure ) and DHA ( 83 % pure ) , a fish oil concentrate ( FOC ; 41 % EPA and 23 % DHA ) and an olive oil ( OO ) placebo ( all ethyl esters ) were tested . A total of 49 normolipidemic subjects participated . Each subject was given placebo for 2–3 wk and one of the n-3 supplements for 3 wk in r and omized , blinded trials . The target n-3 fatty acid ( FA ) intake was 3 g/day in all studies . Blood sample s were drawn twice at the end of each supplementation phase and analyzed for lipids , lipoproteins , and phospholipid FA composition . In all groups , the phospholipid FA composition changed to reflect the n-3 FA given . On DHA supplementation , EPA levels increased to a small but significant extent , suggesting that some retroconversion may have occurred . EPA supplementation did not raise DHA levels , however , FOC and EPA produced significant decreases in both TG and very low density lipoprotein ( VLDL ) cholesterol ( C ) levels ( P<0.01 ) and increases in low density lipoprotein ( LDL ) cholesterol levels ( P<0.05 ) . DHA supplementation did not affect cholesterol , triglyceride , VLDL , LDL , or high density lipoprotein ( HDL ) levels , but it did cause a significant increase in the HDL2/HDL3 cholesterol ratio . We conclude that EPA appears to be primarily responsible for TG-lowering ( and LDL-C raising ) effects of fish oil Fourteen healthy volunteers were r and omly allocated to receive 4 g highly purified ethyl esters of eicosapentaenoic acid ( EPA ) ( 95 % pure , n=7 ) or docosahexaenoic acid ( DHA ) ( 90 % pure , n=7 ) daily for 5 wk in supplement to their ordinary diet . The n−3 fatty acids were given with a st and ard high-fat meal at the beginning and the end of the supplementation period . EPA and DHA induced a similar incorporation into chylomicrons which peaked 6 h after the meal . The relative uptake of EPA and DHA from the meal was > 90 % compared with the uptake of oleic acid . During absorption , there was no significant elongation or retroconversion of EPA or DHA in total chylomicron fatty acids . The concentration of EPA decreased by 13 % and DHA by 62 % ( P<0.001 ) between  
    Output:
    