Lipids, Apolipoproteins, and Their Ratios in Relation to Cardiovascular Events With Statin Treatment Should both HDL-C and LDL-C be targets for lipid therapy? A review of current evidence. Correlation of non-high-density lipoprotein cholesterol with apolipoprotein B: effect of 5 hydroxymethylglutaryl coenzyme A reductase inhibitors on non-high-density lipoprotein cholesterol levels. PREVENTION OF ATHEROSCLEROSIS WITH LDL-C LOWERING - LIPOPROTEIN CHANGES AND INTERACTIONS: THE SANDS STUDY. Is Hypertriglyceridemia a Risk Factor for Atherosclerotic Cardiovascular Disease? A Simple Question with a Complicated Answer Epidemiologic Evidence on Serum Adiponectin Level and Lipid Profile Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation Achieving LDL cholesterol, non-HDL cholesterol, and apolipoprotein B target levels in high-risk patients: Measuring Effective Reductions in Cholesterol Using Rosuvastatin therapY (MERCURY) II. Canadian Cardiovascular Society position statement--recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease. Lipid, lipoprotein, and apolipoprotein profiles in active and sedentary men with tetraplegia. Lipid-modifying efficacy and tolerability of extended-release niacin/laropiprant in patients with primary hypercholesterolaemia or mixed dyslipidaemia. Beyond low-density lipoprotein cholesterol: respective contributions of non-high-density lipoprotein cholesterol levels, triglycerides, and the total cholesterol/high-density lipoprotein cholesterol ratio to coronary heart disease risk in apparently healthy men and women. Fasting insulin and apolipoprotein B levels and low-density lipoprotein particle size as risk factors for ischemic heart disease. Lipoprotein Particle Profiles by Nuclear Magnetic Resonance Compared With Standard Lipids and Apolipoproteins in Predicting Incident Cardiovascular Disease in Women LDL‐C/HDL‐C ratio in subjects with cardiovascular disease and a low HDL‐C: results of the RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) study Effects of infliximab treatment on lipoprotein profile in patients with rheumatoid arthritis and ankylosing spondylitis. Effect of a new HMG-CoA reductase inhibitor, atorvastatin, on lipids, apolipoproteins and lipoprotein particles in patients with elevated serum cholesterol and triglyceride levels. Corn oil intake favorably impacts lipoprotein cholesterol, apolipoprotein and lipoprotein particle levels compared with extra-virgin olive oil Effects of tamoxifen therapy on lipid and lipoprotein levels in postmenopausal patients with node-negative breast cancer. Consistency of Extended-Release Niacin/Laropiprant Effects on Lp(a), ApoB, non-HDL-C, Apo A1, and ApoB/ApoA1 Ratio Across Patient Subgroups Non-HDL cholesterol, apolipoproteins A-I and B100, standard lipid measures, lipid ratios, and CRP as risk factors for cardiovascular disease in women. Rationale and design of the Department of Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial (HIT) for secondary prevention of coronary artery disease in men with low high-density lipoprotein cholesterol and desirable low-density lipoprotein cholesterol. Low fat-monounsaturated rich diets containing high-oleic peanuts improve serum lipoprotein profiles
Background — Low-density lipoprotein ( LDL ) cholesterol is the principal target of lipid-lowering therapy , but recent evidence has suggested more appropriate targets . We compared the relationships of on-treatment levels of LDL cholesterol , non – high-density lipoprotein ( HDL ) cholesterol , and apolipoprotein B , as well as ratios of total/HDL cholesterol , LDL/HDL cholesterol , and apolipoprotein B/A-I , with the occurrence of cardiovascular events in patients receiving statin therapy .  Methods and Results — A post hoc analysis was performed that combined data from 2 prospect i ve , r and omized clinical trials in which 10 001 ( “ Treating to New Targets ” ) and 8888 ( “ Incremental Decrease in End Points through Aggressive Lipid Lowering ” ) patients with established coronary heart disease were assigned to usual-dose or high-dose statin treatment . In models with LDL cholesterol , non-HDL cholesterol and apolipoprotein B were positively associated with cardiovascular outcome , whereas a positive relationship with LDL cholesterol was lost . In a model that contained non-HDL cholesterol and apolipoprotein B , neither was significant owing to collinearity . Total/HDL cholesterol ratio and the apolipoprotein B/A-I ratio in particular were each more closely associated with outcome than any of the individual proatherogenic lipoprotein parameters . Conclusions — In patients receiving statin therapy  , on-treatment levels of non-HDL cholesterol and apolipoprotein B were more closely associated with cardiovascular outcome than levels of LDL cholesterol . Inclusion of measurements of the antiatherogenic lipoprotein fraction further strengthened the relationships . These data support the use of non-HDL cholesterol or apolipoprotein B as novel treatment targets for statin therapy . Given the absence of interventions that have been proven to consistently reduce cardiovascular disease risk through raising plasma levels of HDL cholesterol or apolipoprotein A-I , it seems premature to consider the ratio variables as clinical ly useful The current guidelines for treatment of high-risk of lipid disorders do not specify a therapeutic target level of high-density lipoprotein cholesterol ( HDL-C ) for prevention of vascular disease in high-risk population s. However , there is a substantial body of evidence from basic science and epidemiologic studies and from clinical trials , providing the strong , consistent message that raising HDL-C by therapeutic means will effectively and independently reduce cardiovascular risk . This review summarizes epidemiologic evidence and the results of a meta- analysis of 23 published , prospect i ve , r and omized , placebo-controlled clinical trials . It focuses on the effects of lipid therapies on coronary stenosis progression , as measured by quantitative arteriography and /or , on clinical cardiovascular endpoints . Among the seven drug/treatment classes into which individual study results were categorized and averaged , reduction in stenosis progression and reduction in clinical events are both very highly correlated with the composite lipid variable ( % ΔHDL-C - % Δ low-density lipoprotein cholesterol [ LDL-C ] ; where % Δ is percent change relative to the placebo group response ) . This holds true for all lipid drug classes or combinations of lipid drug therapy , with the exception of the unexpectedly anomalous effects of the torcetrapib-atorvastatin combination . There is a strong and consistent body of evidence that therapeutic HDL-C-raising is at least as effective as comparable percentages of LDL-C-lowering for reduction of atherosclerosis progression or clinical cardiovascular events over a broad range of risk levels . Adoption of this strategy into guidelines probably awaits results of at least one large controlled HDL-C-raising clinical trial , of which two are ongoing and one other is planned Apolipoprotein B has been shown to be a better predictor of coronary heart disease than low-density lipoprotein ( LDL ) cholesterol , and non-high-density lipoprotein ( non-HDL ) cholesterol may also be a better parameter for coronary heart disease risk assessment and as a target for therapy . Data from the Atorvastatin Comparative Cholesterol Efficacy and Safety Study ( ACCESS ) were used to assess the correlation between lipid and apolipoprotein B levels before and after lipid-lowering therapy and to examine the effects of 5 hydroxymethylglutaryl coenzyme A reductase inhibitors on lipids and apolipoprotein B. The 54-week study r and omized 3,916 hypercholesterolemic patients to atorvastatin , fluvastatin , lovastatin , pravastatin , or simvastatin , initiated at recommended starting doses with titrations as needed at weeks 6 , 12 , and 18 to achieve National Cholesterol Education Program LDL targets . Compared with LDL cholesterol , non-HDL cholesterol correlated better with apolipoprotein B levels at baseline ( r = 0.914 , p < 0.0001 ) and at week 54 ( r = 0.938 , p < 0.0001 ) , and the correlation was strong across all baseline triglyceride strata . At starting doses , atorvastatin ( 10 mg ) lowered non-HDL cholesterol by 33.3 % compared with 26.6 % with simvastatin ( 10 mg ) , 24.1 % with lovastatin ( 20 mg ) , 17.2 % with fluvastatin ( 20 mg ) , and 17.0 % with pravastatin ( 10 mg ) . Atorvastatin also provided greater reductions in non-HDL cholesterol after dose titration , and a greater percentage of patients taking atorvastatin achieved non-HDL cholesterol targets . Baseline triglyceride did not affect non-HDL cholesterol reductions with any of the 5 hydroxymethylglutaryl coenzyme A reductase inhibitors . Fewer patients achieved non-HDL cholesterol targets than LDL cholesterol targets , particularly among high-risk patients , implying that if non-HDL cholesterol was used as a target for treatment , more patients would need to be treated more aggressively than National Cholesterol Education Program guidelines require BACKGROUND : Lowering low-density lipoprotein cholesterol ( LDL-C ) with statins reduces atherosclerosis . LDL and high-density lipoprotein ( HDL ) are commonly measured by their cholesterol content , but non-HDL cholesterol , LDL particle number ( LDL-P ) , or total apolipoprotein B ( apoB ) may better predict cardiovascular risk . Few studies have examined relations among lipoprotein levels and composition before and after interventions to lower LDL-C and non-HDL-C. OBJECTIVE : To measure changes in carotid artery intimal media thickness ( CIMT ) and lipid concentration and composition during 36 months of statin therapy . METHODS : Analyses were conducted on 418 diabetic individuals , with complete data and no prior cardiovascular events , who were r and omized to aggressive ( AG ) versus st and ard ( STD ) treatment for LDL-C , non-HDL-C , and systolic blood pressure ( SBP ) as part of the Stop Atherosclerosis in Native Diabetics Study ( S AND S ) . RESULTS : The AG group achieved average LDL-C and non-HDL-C of 71mg/dL and 100mg/dL and a decrease in CIMT . No significant interactions were observed between treatment effect and initial levels of LDL-C , non-HDL-C , HDL-C , triglycerides , apoB , or LDL-P. Decreases in LDL-C ( p<.005 ) and non-HDL-C ( p<.001 ) were independently correlated with CIMT regression in the AG group . Changes in apoB and LDL-P showed borderline correlations with CIMT regression ( p=.07 and p=.09 ) . CONCLUSIONS : In diabetic adults with no prior cardiovascular events , treatment to current targets for lipids and SBP reduces atherosclerosis progression and when more aggressive targets are met , atherosclerosis regresses . The aggressive targets for LDL-C and non-HDL-C appeared to be the main determinants of CIMT regression and were more predictive of this outcome than changes in LDL-P or The role of hypertriglyceridemia in the pathogenesis of atherosclerotic cardiovascular disease has been controversial for many years [ 1 , 2 ] . It remains so despite extensive investigation by basic scientists , clinicians , and epidemiologists . The lack of resolution of this issue derives mainly from the complexity inherent in the lipoprotein transport system [ 3 ] . Although it is not possible to either unravel all of this complexity or resolve the controversy here , I attempt to provide a balanced review of the relevant literature , concluding with a suggested approach to the evaluation and treatment of the many patients who have elevated plasma triglyceride levels . I focus on the lipid aspects of this issue , but it should not be forgotten that elevated triglyceride levels have been associated with several abnormalities of the clotting-fibrinolytic systems [ 4 ] . Triglyceride does not accumulate in the vessel wall . Its atherogenicity must be based , therefore , on the association , within lipoproteins , between triglyceride and cholesterol , the lipid that does accumulate in atherosclerotic plaque . Thus , proponents of an association between hypertriglyceridemia and atherosclerotic cardiovascular disease must postulate that disordered metabolism of the triglyceride-rich lipoproteins-very low density lipoprotein ( VLDL ) or chylomicron or both-is proatherogenic . This concept is not extreme : Even the well-accepted link between cholesterol and atherosclerotic cardiovascular disease relies on the accumulation of low-density lipoprotein ( LDL ) cholesterol , not simply plasma cholesterol , in lesions . The concept that several lipoprotein species can contribute cholesterol to lesion formation is not , therefore , unreasonable . Indeed , ample studies have shown that chylomicron remnants ( the lipoprotein formed from chylomicrons after removal of much , but not all , of the chylomicron triglyceride ) and VLDL ( or its remnants ) enter the subendothelial space of the vessel wall [ 5 , 6 ] . These lipoproteins can also be internalized by monocyte macrophages , result ing in formation of foam cells . Recent studies in transgenic mice dramatically demonstrated the atherogenic potential of VLDL and chylomicron remnants , even when the mice were consuming normal chow diets [ 7 ] . If the delivery of cholesterol to the vessel wall by triglyceride-rich lipoproteins is , in fact , involved in the pathophysiology of atherosclerotic cardiovascular disease , epidemiologic data should show links between hypertriglyceridemia and this disease . When examining the role of triglyceride by univariate analyses , most prospect i ve cohort studies have shown a positive relation between triglyceride levels and risk [ 2 ] . In multivariate analyses , however , triglyceride has often been shown to no longer be significantly associated with risk . Important exceptions may be seen in women with hypertriglyceridemia and patients with diabetes . I focus here only on three potential confounders of this statistical approach : the inverse relation between plasma levels of triglyceride and high-density lipoprotein ( HDL ) cholesterol , the potential atherogenicity of postpr and ial hypertriglyceridemia , and the biochemical and physical heterogeneity of triglyceride-rich lipoproteins . High-density lipoprotein cholesterol is widely accepted as being protective against atherosclerotic cardiovascular disease [ 8 ] . The evidence has primarily been derived from prospect i ve cohort studies and from secondary analyses of intervention trials in which lowering LDL cholesterol levels was the primary goal . The leading theory invokes a role for HDL in the reverse cholesterol transport pathway , whereby cellular cholesterol can associate with HDL ; in turn , the latter delivers cellular cholesterol to the liver for excretion . In most population s , triglyceride and HDL cholesterol levels are inversely related . Thus , analyses of triglyceride as a risk factor that use HDL cholesterol as a covariate will be confounded by the lack of independence of the two variables ; both of these variables affect risk for atherosclerotic cardiovascular disease , but in opposite directions . Although recent studies in gene-knockout and transgenic mice support direct antiatherogenic roles for HDL [ 9 , 10 ] , the physiologic basis for the inverse relation between plasma levels of triglyceride and HDL cholesterol suggests that low HDL cholesterol levels may simply reflect proatherogenic disorders of triglyceride-rich lipoproteins . Increased levels of VLDL and chylomicrons stimulate the exchange of their triglyceride for cholesterol in HDL . Although this exchange , which is mediated in plasma by cholesteryl ester transfer protein [ 11 ] , may be an alternate pathway for reverse cholesterol transport ( with delivery of the cholesterol to the liver by VLDL and chylomicron remnants ) , movement of HDL cholesterol into triglyceride-rich lipoproteins could also result in the delivery of some cholesterol back to peripheral cells . Over time , such short-circuiting of the reverse cholesterol transport system could result in accumulation of cholesterol in tissues , including the arterial wall . Essentially all of the epidemiologic data linking lipids and lipoproteins to risk for atherosclerotic cardiovascular disease are based on fasting levels [ 2 ] . Plasma levels of triglycerides vary widely throughout the day , however , because we absorb many grams of dietary fat after each meal . In the past decade , evidence for the atherogenicity of postpr and ial triglyceride-rich lipoproteins has increased . Several recent studies have indicated that postpr and ial levels of triglyceride and chylomicron remnants are predictive of the presence of atherosclerotic cardiovascular disease even when other risk factors , including HDL cholesterol , are considered [ 12 , 13 ] . The role of triglyceride in atherogenesis might have been more readily demonstrated if epidemiologic studies had used nonfasting blood levels . Another important reason for the difficulty in linking triglyceride levels to risk for atherosclerotic cardiovascular disease is the physical and biochemical heterogeneity of VLDL and chylomicrons . In particular , the size , number , and cholesterol content of these lipoproteins can vary greatly among individual persons . Size is important because very large particles can not easily pass into the subendothelial space , the site of initiation of the atherogenic process . The number of triglyceride-rich particles in the bloodstream is also crucial , in part because the presence of more particles increases the probability that they will enter and be retained in the vessel wall , and in part because for any triglyceride level , more particles mean smaller , more atherogenic particles . Finally , the cholesterol content of the triglyceride-rich lipoproteins can vary significantly , and persons with more cholesterol-enriched particles will be at greater risk . Because of differences in the size , number , and cholesterol content of triglyceride-rich particles , patients with similar levels of plasma triglyceride may have very different risks for atherosclerotic cardiovascular disease . So what is the clinician to do with the not uncommon , middle-aged patient who has hypertriglyceridemia ? The National Cholesterol Education Program ( NCEP ) has not developed precise guidelines on which to base therapy [ 14 ] . Moreover , neither of the reports of two intervention trials gives a clearcut answer . The Helsinki Heart Study subgroup analysis [ 15 ] indicated that patients who had pure hypertriglyceridemia and were receiving  gemfibrozil had a risk reduction similar to that of patients with either pure hypercholesterolemia or combined hyperlipidemia ; however , the size of the subgroup was small . In the Stockholm Ischemic Heart Disease Study [ 16 ] , the reductions in the rate of coronary events seen in patients treated with clofibrate and niacin correlated with reductions in triglyceride levels , but neither HDL nor LDL cholesterol levels were measured . In the face of these suggestive but incomplete data , one approach would be to use the NCEP guidelines , particularly focusing on the presence of other risk factors commonly associated with hypertriglyceridemia ( hypertension , diabetes , low HDL cholesterol levels ) to guide the intensity of therapy focused on LDL cholesterol . Thus , if the patient is a man older than 45 years of age or a postmenopausal woman , it is likely that he or she will have two or more of the risk factors listed in the NCEP guidelines [ 14 ] and will require an LDL cholesterol level less than 130 mg/dL. If the patient has clinical atherosclerotic cardiovascular disease , an LDL cholesterol level less than 100 mg/dL would be the goal . When a patient with hypertriglyceridemia but not clinical atherosclerotic cardiovascular disease has an LDL cholesterol  less than 130 mg/dL , however , the NCEP guidelines do not provide clear direction for therapy , regardless of the number of additional risk factors . Here , the LDL : HDL ratio might be helpful ; both the Helsinki Study [ 17 ] and the Procam Study [ 18 ] indicated that patients with ratios exceeding 5.0 and triglyceride levels exceeding 200 mg/dL had markedly increased risk . It must be understood , however , that no data support the value of further lowering LDL cholesterol levels that are already less than 130 mg/dL in patients without clinical atherosclerotic cardiovascular disease . Measurement of apoprotein B levels ( when st and ardization programs are widely available ) might be of particular benefit in these patients [ 19 ] . Because of the multiple links between elevated triglyceride levels and risk for atherosclerotic cardiovascular disease , it seems prudent to screen for the presence of hypertriglyceridemia when determining a patient 's risk for atherosclerotic cardiovascular disease . A therapeutic program for hypertriglyceridemia should obviously include diet , exercise , and weight loss programs : These are even more important in patients with hypertriglyceridemia than in persons with The concentration of adiponectin , a hormone which is secreted from adipose tissue , is inversely correlated with body fat mass . This hormone has anti inflammatory and anti atherogenic properties . Its concentration reduces in metabolic syndrome and cardiovascular diseases . This study review s the evidence on the relationship between serum  adiponectin concentration and lipid profile .  In this study former clinical trials , cross sectional and prospect i ve studies have been review ed . The PubMed search engine has been used to find related research for the topic by considering dyslipidemia , total cholesterol ( TC ) , high and low density protein ( HDL and LDL ) , triglyceride ( TG ) , lipid profile ( LP ) and adiponectin as the key words . Finally , 25 articles were recruited to review in the present article . Serum adiponectin level was positively correlated with plasma HDL cholestrol concentrations . There was a significant inverse relationship between plasma triglyceride and serum adiponectin . An inverse correlation between very low density lipoprotein ( VLDL ) and LDL levels and adiponectin was reported from the studies . So , Adiponectin has an important role in the metabolism of lipid profile including HDLc Background Recent studies have demonstrated a relationship between fructose consumption and risk of developing metabolic syndrome . Mechanisms by which dietary fructose mediates metabolic changes are poorly understood . This study compared the effects of fructose , glucose and sucrose consumption on post-postpr and ial lipemia and low grade inflammation measured as hs-CRP . Methods This was a r and omized , single blinded , cross-over trial involving healthy subjects ( n = 14 ) . After an overnight fast , participants were given one of 3 different isocaloric drinks , containing 50 g of either fructose or glucose or sucrose dissolved in water .  Blood sample s were collected at baseline , 30 , 60 and 120 minutes post intervention for the analysis of blood lipids , glucose , insulin and high sensitivity C-reactive protein ( hs-CRP ) . Results Glucose and sucrose supplementation initially result ed in a significant increase in glucose and insulin levels compared to fructose supplementation and returned to near baseline values within 2 hours . Change in plasma cholesterol , LDL and HDL-cholesterol ( measured as area under curve , AUC ) was significantly higher when participants consumed fructose compared with glucose or sucrose ( P < 0.05 ) . AUC for plasma triglyceride levels however remained unchanged regardless of the dietary intervention . Change in AUC for hs-CRP was also significantly higher in subjects consuming fructose compared with those consuming glucose ( P < 0.05 ) , but not sucrose ( P = 0.07 ) . Conclusion This study demonstrates that fructose as a sole source of energy modulates plasma lipids and hsCRP levels in healthy individuals . The significance of increase in HDL-cholesterol with a concurrent increase in LDL-cholesterol and elevated hs-CRP levels remains to be delineated when considering health effects of feeding fructose-rich diets . Registration number for clinical BACKGROUND National Cholesterol Education Program Adult Treatment Panel III guidelines for patients at a high risk of coronary heart disease set a low-density lipoprotein cholesterol ( LDL-C ) target of < 100 mg/dL. This target can be difficult to attain with diet and current therapy . METHODS In a 16-week multinational trial , 1993 high-risk patients were r and omized to rosuvastatin 20 mg , atorvastatin 10 mg , atorvastatin 20 mg , simvastatin 20 mg , or simvastatin 40 mg for 8 weeks . Patients either remained on starting treatment or switched to lower or milligram-equivalent doses of rosuvastatin for 8 more weeks . RESULTS At 16 weeks , more patients achieved their LDL-C target by switching to rosuvastatin 10 mg than staying on atorvastatin 10 mg ( 66 % vs 42 % , P < .001 ) or simvastatin 20 mg ( 73 % vs 32 % , P < .001 ) . Changing to rosuvastatin 20 mg brought more patients to their LDL-C target than staying on atorvastatin 20 mg ( 79 % vs 64 % , P < .001 ) or simvastatin 40 mg ( 84 % vs 56 % , P < .001 ) . More very high risk patients achieved an LDL-C target of < 70 mg/dL when changed to rosuvastatin from atorvastatin or simvastatin ( within-arm comparisons P < .01 ) . More hypertriglyceridemic patients ( triglycerides > or = 200 mg/dL ) met LDL-C , non-high-density lipoprotein cholesterol ( non-HDL-C ) , and apolipoprotein B targets by changing to rosuvastatin . Switching to rosuvastatin produced greater reductions in LDL-C , total cholesterol , non-HDL-C , apolipoprotein B , and lipid ratios . All treatments were well tolerated , with no differences among treatment groups in skeletal muscle , hepatic , or renal toxicity . CONCLUSION Rosuvastatin 10 or 20 mg is an effective and safe therapeutic option for high-risk patients to achieve their lipid and apolipoprotein targets Since the last publication of the recommendations for the management and treatment of dyslipidemia , new clinical trial data have emerged that support a more vigorous approach to lipid lowering in specific patient groups . The decision was made to up date the lipid guidelines in collaboration with the Canadian Cardiovascular Society . A systematic electronic search of medical literature for original research consisting of blinded , r and omized controlled trials was performed . Meta-analyses of studies of the efficacy and safety of lipid-lowering therapies , and of the predictive value of established and emerging risk factors were also review ed . All recommendations are evidence -based , and have been review ed in detail by primary and secondary review panels . Major changes include a lower low-density lipoprotein cholesterol ( LDL-C ) treatment target ( lower than 2.0 mmol/L ) for high-risk patients , a slightly higher intervention point for the initiation of drug therapy in most low-risk individuals ( LDL-C of 5.0 mmol/L or a total cholesterol to high-density lipoprotein cholesterol ratio of 6.0 ) and recommendations regarding additional investigations of potential use in the further evaluation of coronary artery disease risk in subjects in the moderate-risk category OBJECTIVE To investigate whether the risk profile of coronary heart disease ( CHD ) is more favorable in physically active men with tetraplegia compared with sedentary men with tetraplegia . DESIGN Using a cross-sectional design , the lipid and (apo)lipoprotein concentrations of 11 active and 13 sedentary men with tetraplegia were compared . Regression analysis was applied to investigate the influence of subject characteristics and behavioral factors on the risk profile of CHD . MAIN OUTCOME MEASURES Total plasma cholesterol ( TC ) , high-density lipoprotein cholesterol ( HDL-C ) , triglycerides , apolipoprotein-A1 ( ApoA1 ) , and apolipoprotein-B ( ApoB ) concentrations were determined . Low-density lipoprotein cholesterol ( LDL-C ) and the ratios TC/HDL-C , LDL-C/HDL-C , ApoA1/ApoB , and HDL-C/ApoA1 were calculated . RESULTS A significantly higher HDL-C and ApoA1/ApoB and lower TC/HDL-C were found in the active group . Age and body mass index were important determinants of the lipids and (apo)lipoproteins .  Sport activity was the only significant determinant of HDL-C. CONCLUSIONS Results suggest a positive influence of sport activity on HDL-C in men with tetraplegia , which may reduce the risk of CHD BACKGROUND Improving lipids beyond low-density lipoprotein cholesterol ( LDL-C ) lowering with statin monotherapy may further reduce cardiovascular risk . Niacin has complementary lipid-modifying efficacy to statins and cardiovascular benefit , but is underutilised because of flushing , mediated primarily by prostagl and in D(2 ) ( PGD(2 ) ) . Laropiprant ( LRPT ) , a PGD(2 ) receptor ( DP1 ) antagonist that reduces niacin-induced flushing has been combined with extended-release niacin ( ERN ) into a fixed-dose tablet . METHODS AND RESULTS Dyslipidaemic patients were r and omised to ERN/LRPT 1 g ( n = 800 ) , ERN 1 g ( n = 543 ) or placebo ( n = 270 ) for 4 weeks . Doses were doubled ( 2 tablets/day ; i.e. 2 g for active treatments ) for 20 weeks . ERN/LRPT 2 g produced significant changes vs. placebo in LDL-C ( -18.4 % ) , high-density lipoprotein cholesterol ( HDL-C ; 20.0 % ) , LDL-C : HDL-C ( -31.2 % ) , non-HDL-C ( -19.8 % ) , triglycerides ( TG ; -25.8 % ) , apolipoprotein ( Apo ) B ( -18.8 % ) , Apo A-I ( 6.9 % ) , total cholesterol ( TC ; -8.5 % ) , TC : HDL-C ( -23.1 % ) and lipoprotein(a ) ( -20.8 % ) across weeks 12 - 24 . ERN/LRPT produced significantly less flushing than ERN during initiation ( week 1 ) and maintenance ( weeks 2 - 24 ) for all prespecified flushing end-points ( incidence , intensity and discontinuation because of flushing ) . Except for flushing , ERN/LRPT had a safety/tolerability profile comparable with ERN . CONCLUSION Extended-release niacin/LRPT 2 g produced significant , durable improvements in multiple lipid/lipoprotein parameters . The improved tolerability of ERN/LRPT supports a simplified 1 g-->2 g dosing regimen of niacin , a therapy proven to reduce cardiovascular risk OBJECTIVES This study was design ed to test the hypothesis that at any low-density lipoprotein cholesterol ( LDL-C ) level , other lipid parameters such as non-high-density lipoprotein cholesterol ( HDL-C ) levels , triglyceride ( TG ) levels , and the total cholesterol (TC)/HDL-C are still associated with an increased coronary heart disease ( CHD ) risk . BACKGROUND Although LDL-C is considered to be the primary target of lipid-lowering therapy , other parameters of the lipoprotein-lipid profile may more closely associated with CHD risk . METHODS In the EPIC ( European Prospect i ve Investigation Into Cancer and Nutrition)-Norfolk prospect i ve population study , 21,448 participants without diabetes or CHD between age 45 and 79 years were followed for 11.0 years . A total of 2,086 participants developed CHD during follow-up . RESULTS Among individuals with low LDL-C levels ( < 100 mg/dl ) , after adjustment for age , sex , smoking , systolic blood pressure , waist circumference , physical activity , and hormone replacement therapy ( in women ) , those with non-HDL-C > 130 mg/dl had a hazard ratio ( HR ) for future CHD of 1.84 ( 95 % confidence interval [ CI ] : 1.12 to 3.04 ) when compared with those with non-HDL-C levels < 130 mg/dl . In a similar model , individuals with TG levels > 150 mg/dl had an HR of 1.63 ( 95 % CI : 1.02 to 2.59 ) when compared with those with TG levels < 150 mg/dl , and individuals with a TC/HDL-C ratio > 5 had an HR of 2.19 ( 95 % CI : 1.22 to 3.93 ) when compared with those with a TC/HDL-C ratio < 5 . CONCLUSIONS In this prospect i ve study , independently of their plasma LDL-C levels , participants with high non-HDL-C levels , high TG levels , or with an elevated TC/HDL-C ratio were at increased CHD risk . CHD risk assessment algorithms as well as lipid targets of lipid-lowering trials may also need to consider other easily available parameters such as CONTEXT Epidemiological studies have established a relationship between cholesterol and low-density lipoprotein cholesterol ( LDL-C ) concentrations and the risk of ischemic heart disease ( IHD ) , but up to half of patients with IHD may have cholesterol levels in the normal range . OBJECTIVE To assess the ability to predict the risk of IHD using a cluster of nontraditional metabolic risk factors that includes elevated fasting insulin and apolipoprotein B levels as well as small , dense LDL particles . DESIGN Nested case-control study . SETTING Cases and controls were identified from the population -based cohort of the Quebec Cardiovascular Study , a prospect i ve study conducted in men free of IHD in 1985 and followed up for 5 years . PARTICIPANTS Incident IHD cases were matched with controls selected from among the sample of men who remained IHD free during follow-up . Matching variables were age , smoking habits , body mass index , and alcohol consumption . The sample included 85 complete pairs of nondiabetic IHD cases and controls . MAIN OUTCOME MEASURES Ability of fasting insulin level , apolipoprotein B level , and LDL particle diameter to predict IHD events , defined as angina , coronary insufficiency , nonfatal myocardial infa rct ion , and coronary death . RESULTS The risk of IHD was significantly increased in men who had elevated fasting plasma insulin and apolipoprotein B levels and small , dense LDL particles , compared with men who had normal levels for 2 of these 3 risk factors ( odds ratio [ OR ] , 5.9 ; 95 % confidence interval [ CI ] , 2.3 - 15.4 ) . Multivariate adjustment for LDL-C , triglycerides , and high-density lipoprotein cholesterol ( HDL-C ) did not attenuate the relationship between the cluster of nontraditional risk factors and IHD ( OR , 5.2 ; 95 % CI , 1.7 - 15.7 ) . On the other h and , the risk of IHD in men having a combination of elevated LDL-C and triglyceride levels and reduced HDL-C levels was no longer significant ( OR , 1.4 ; 95 % CI , 0.5 - 3.5 ) after multivariate adjustment for fasting plasma insulin level , apolipoprotein B level , and LDL particle size . CONCLUSION Results from this prospect i ve study suggest that the measurement of fasting plasma insulin level , apolipoprotein B level , and LDL particle size may provide further information on the risk of IHD compared with the information provided by conventional lipid variables Background — Nuclear magnetic resonance ( NMR ) spectroscopy measures the number and size of lipoprotein particles instead of their cholesterol or triglyceride content , but its clinical utility is uncertain . Methods and Results — Baseline lipoproteins were measured by NMR in 27 673 initially healthy women followed up for incident cardiovascular disease ( n=1015 ) over an 11-year period . After adjustment for nonlipid risk factors , hazard ratios and 95 % confidence intervals for the top versus the bottom quintile of NMR-measured lipoprotein particle concentration ( measured in particles per liter ) were 2.51 ( 1.91 to 3.30 ) for low-density lipoprotein ( LDLNMR ) , 0.91 ( 0.75 to 1.12 ) for high-density lipoprotein ( HDLNMR ) , 1.71 ( 1.38 to 2.12 ) for very low – density lipoprotein ( VLDLNMR ) , and 2.25 ( 1.80 to 2.81 ) for the LDLNMR/HDLNMR ratio . Similarly adjusted results for NMR-measured lipoprotein particle size ( measured in nanometers ) were 0.64 ( 0.52 to 0.79 ) for LDLNMR size , 0.65 ( 0.51 to 0.81 ) for HDLNMR size , and 1.37 ( 1.10 to 1.70 ) for VLDLNMR size . Hazard ratios for NMR measures were comparable but not superior to st and ard lipids ( total cholesterol 2.08 [ 1.63 to 2.67 ] , LDL cholesterol 1.74 [ 1.40 to 2.16 ] , HDL cholesterol 0.52 [ 0.42 to 0.64 ] , triglycerides 2.58 [ 1.95 to 3.41 ] , non-HDL cholesterol 2.52 [ 1.95 to 3.25 ] , total/HDL cholesterol ratio 2.82 [ 2.23 to 3.58 ] ) and apolipoproteins ( B100 2.57 [ 1.98 to 3.33 ] , A-1 0.63 [ 0.52 to 0.77 ] , and B100/A-1 ratio 2.79 [ 2.21 to 3.54 ] ) . Essentially no reclassification improvement was found with the addition of the LDLNMR particle concentration or apolipoprotein B100 to a model that already included the total/HDL cholesterol ratio and nonlipid risk factors ( net reclassification index 0 % and 1.9 % , respectively ) , nor did the addition of either variable result in a statistically significant improvement in the c-index . Conclusions — In this prospect i ve study of healthy women , cardiovascular disease risk prediction associated with lipoprotein profiles evaluated by NMR was comparable but not superior to that of st and ard lipids or apolipoproteins ABSTRACT Background : The ratio of low-density lipoprotein cholesterol and high-density lipoprotein cholesterol ( LDL‐C/HDL‐C ) is a reliable predictor of cardiovascular risk . Low HDL‐C levels in patients with coronary artery disease are associated with a high risk for cardiovascular events . Objectives : This study compared the effects of rosuvastatin and atorvastatin on the LDL‐C/HDL‐C ratio in patients with cardiovascular disease and low HDL‐C. Methods : Patients aged 40–80 years with established cardiovascular disease and HDL‐C < 1.0 mmol/L ( < 40 mg/dL ) entered a 6‐week dietary run-in period , before r and omisation to open-label treatment with rosuvastatin 10 mg ( n = 230 ) or atorvastatin 20 mg ( n = 231 ) for 6 weeks . Doses were increased after 6 weeks to rosuvastatin 20 mg or atorvastatin 40 mg , and after 12 weeks to rosuvastatin 40 mg or atorvastatin 80 mg . Serum lipid parameters were measured at baseline and 6 , 12 and 18 weeks . Results : After 6 weeks of treatment , mean percentage change from baseline in LDL‐C/HDL‐C ratio was –47.0 % in the rosuvastatin group and –41.9 % in the atorvastatin group ( p < 0.05 for between-group comparison ) . After 12 and 18 weeks of treatment , change from baseline was –53.0 % and –57.3 % , respectively , for rosuvastatin , compared with –47.9 % and –49.6 % , respectively , for atorvastatin ( p < 0.01 and p < 0.001 , respectively , for between-group comparison ) . Rosuvastatin also reduced LDL‐C , total cholesterol and non-HDL‐C significantly more than atorvastatin at all three time points , and significantly improved total cholesterol/HDL‐C and apolipoprotein B/A‐I ratios . Conclusions : Rosuvastatin 10 , 20 and 40 mg is significantly more effective than atorvastatin 20 , 40 and 80 mg , respectively , in improving the LDL‐C/HDL‐C ratio in patients with cardiovascular disease and low HDL‐C. Further studies are required to clarify the benefits of rosuvastatin for reduction of cardiovascular risk OBJECTIVE To investigate the longterm effects of the anti-tumor necrosis factor ( TNF ) therapy infliximab , a drug known to reduce disease activity in patients with rheumatoid arthritis ( RA ) and ankylosing spondylitis ( AS ) . METHODS Eighty-two patients ( 50 with RA , 32 with AS ) aged 17 - 77 years were enrolled . All patients were treated with intravenous infliximab .  Lipid profile was assessed at baseline and after 6 months of treatment . RESULTS Disease activity significantly decreased in patients with RA and AS at the end of infliximab therapy . Infliximab treatment significantly increased total cholesterol from 206 to 216 mg/dl ( p < 0.05 ) and triglycerides from 109 to 122 mg/dl ( p < 0.05 ) . The low density lipoprotein ( LDL ) and high density lipoprotein ( HDL ) cholesterol did not change during treatment . Furthermore , the total cholesterol/HDL cholesterol and triglycerides/HDL cholesterol ratios did not change significantly . CONCLUSION The influence of infliximab treatment on lipid profile seems to be neutral , since neither LDL cholesterol levels nor total cholesterol/HDL cholesterol and triglycerides/HDL cholesterol ratios changed significantly during the 6-month therapy . Our findings suggest that the favorable effect of infliximab treatment on cardiovascular comorbidity may not be mainly mediated by the effects on the lipid profile , but further investigations are needed in order to confirm this hypothesis The effects of atorvastatin ( lipitor ) on cholesterol-rich and triglyceride-rich lipoproteins were evaluated in this multicenter trial . Following a 6-week baseline period , 47 patients with elevated cholesterol and triglyceride levels were treated with atorvastatin 10 mg once daily ( QD ) for the initial 12 weeks ( Period 1 ) increasing to 20 mg QD for the following 12 weeks ( Period 2 ) . At both the 10 and 20 mg doses , atorvastatin treatment result ed in significant reductions compared to pretreatment levels in low-density lipoprotein cholesterol ( LDL-C ) , total cholesterol ( TC ) , very low-density lipoprotein cholesterol ( VLDL-C ) , apolipoprotein ( apo ) B , apoB in LDL ( LDL-apo B ) , apo B in VLDL ( VLDL-apo B ) , lipoprotein (Lp)B , lipoprotein B-complex ( LpBc ) , triglycerides ( TG ) , low-density lipoprotein triglycerides ( LDL-TG ) , very low-density lipoprotein triglyceride ( VLDL-TG ) , high-density lipoprotein triglycerides ( HDL-TG ) , and apo C-III .  Atorvastatin 10 and 20 mg QD also result ed in significant increases in high-density lipoprotein cholesterol ( HDL-C ) , apo AI , and LpAII : B : C : D : E. Due to its unique ability to normalize both cholesterol-rich and triglyceride-rich particles , atorvastatin is a promising c and i date for monotherapy in a broad range of patients including those with varying degrees of hypercholesterolemia and hypertriglyceridemia Background : Corn oil ( CO ) and extra-virgin olive oil ( EVOO ) are rich sources of unsaturated fatty acids ( UFA ) , but UFA profiles differ among oils , which may affect lipoprotein levels . Objectives : The objective of this study was to assess the effects of CO versus EVOO intake on fasting lipoprotein and subfraction cholesterol levels , apolipoprotein ( apo ) A1 , apo B , and low-density lipoprotein particle concentrations in men and women . Subjects/ Methods : As part of a weight maintenance diet , men and women were provided with food items prepared with 54 g per day of CO or EVOO ( 21-day treatment , 21-day washout ) in a r and omized , double-blind , controlled-feeding , crossover trial . Fasting lipoprotein cholesterol and related variables were determined with density gradient ultracentrifugation . Results : Among the 54 completers , CO reduced total cholesterol , low-density lipoprotein cholesterol ( LDL-C ) , very low-density lipoprotein cholesterol ( VLDL-C ) , non-high-density lipoprotein cholesterol ( non-HDL-C ) , apo B and LDL particle concentration to a greater extent compared with EVOO intake . Changes in LDL-C and VLDL-C contributed to the larger reduction in non-HDL-C with CO compared with EVOO intake ( −0.39 mmol/l vs −0.04 mmol/l ; P<0.001 ) . The larger reduction in LDL-C by CO intake was attributable to changes ( P<0.05 ) caused by CO vs EVOO in large LDL1 + 2-C ( −0.22 mmol/l ) and intermediate-density lipoprotein cholesterol ( −0.12 mmol/l ) . HDL-C responses did not differ between treatments , but apo A1 increased more with EVOO compared with CO intake ( 4.6 versus 0.7 mg/dl , respectively , P=0.016 ) . Conclusions : CO intake reduced atherogenic lipoprotein cholesterol and particle concentrations to a larger extent than did EVOO , which may have implication s for cardiovascular disease risk We conducted a 2-year , r and omized , double-blind , placebo-controlled toxicity trial of therapy with tamoxifen ( 10 mg twice a day ) in 140 postmenopausal women with a history of breast cancer and histologically negative axillary lymph nodes . These women had been treated with surgery with or without radiotherapy .  At a 3-month evaluation , tamoxifen-treated women showed a significant decrease in fasting plasma levels of total cholesterol and low-density lipoprotein ( LDL ) cholesterol , which persisted at 6- and 12-month evaluations . During the first 12 months , plasma triglyceride levels increased ; small but significant decreases in high-density lipoprotein cholesterol ( HDL ) were observed in tamoxifen-treated women , but ratios of total cholesterol to HDL cholesterol and of LDL to HDL cholesterol changed favorably . While data relating lipid/lipoprotein profiles and cardiovascular disease are limited in women , current evidence suggests that total cholesterol and possibly low-density lipoprotein cholesterol are risk factors . We conclude that during the first 12 months of treatment , tamoxifen exerts a favorable effect on the lipid profile in postmenopausal women with early stage breast cancer Background According to prior analyses , extended-release niacin/laropiprant ( ERN/LRPT ) consistently reduces low-density lipoprotein cholesterol ( LDL-C ) and triglycerides ( TG ) and increases high-density lipoprotein cholesterol ( HDL-C ) levels across a wide range of dyslipidemic patient subgroups . Objectives This analysis examined ERN/LRPT ’s consistency across four phase III , r and omized , double-blind trials in improving other lipid/lipoprotein parameters associated with cardiovascular risk , across several key dyslipidemic patient subgroups . Methods In three of the studies , the r and omized population included patients with primary hypercholesterolemia or mixed hyperlipidemia ; in the remaining study , the population included patients with type 2 diabetes mellitus . The lipid-altering consistency of ERN/LRPT ’s efficacy was evaluated versus the predefined comparator ( placebo or active control ) among key subgroups of sex , race ( White , non-White ) , region ( US , ex-US ) , baseline age ( < 65 years , ≥65 years ) , use of statin therapy ( yes , no ) , coronary heart disease ( yes , no ) , risk status ( low , multiple , high ) , and type of hyperlipidemia ( primary hypercholesterolemia , mixed dyslipidemia ) , as well as across baseline LDL-C , HDL-C , and TG levels . The consistency of the treatment effects on lipoprotein(a ) [ Lp(a ) ] , apolipoprotein B ( ApoB ) , non-HDL-C , ApoA1 , and ApoB/ApoA1 ratio was evaluated by examining treatment difference estimates of the percentage change from baseline with 95 % confidence intervals . Results Treatment with ERN/LRPT produced significantly greater improvements in Lp(a ) , ApoB , non-HDL-C , ApoA1 , and ApoB/ApoA1 ratio compared with placebo/active comparator in each study . These effects were generally consistent across key subgroups within each study . Conclusion ERN/LRPT  produced lipid-altering efficacy on the parameters evaluated in four controlled studies ; these effects were generally consistent across all examined subgroups . ERN/LRPT represents an effective and reliable therapeutic option for the treatment of dyslipidemia in a wide range of patient types . Clinical Trial Registration Registered as Clinical trials.gov NCT00269204 , NCT00269217 , NCT00479388 , and NCT00485758 CONTEXT Current guidelines for cardiovascular risk detection are controversial with regard to the clinical utility of different lipid measures , non-high-density lipoprotein cholesterol ( non-HDL-C ) , lipid ratios , apolipoproteins , and C-reactive protein ( CRP ) . OBJECTIVE To directly compare the clinical utility of total cholesterol , low-density lipoprotein cholesterol ( LDL-C ) , HDL-C , non-HDL-C , apolipoproteins A-I and B(100 ) , high-sensitivity CRP , and the ratios of total cholesterol to HDL-C , LDL-C to HDL-C , apolipoprotein B(100 ) to apolipoprotein A-I , and apolipoprotein B(100 ) to HDL-C as predictors of future cardiovascular events in women . DESIGN , SETTING , AND PARTICIPANTS Prospect i ve cohort study of 15,632 initially healthy US women aged 45 years or older ( interquartile range , 48 - 59 years ) who were enrolled between November 1992 and July 1995 . All participants were followed up over a 10-year period for the occurrence of future cardiovascular events . MAIN OUTCOME MEASURE Hazard ratios ( HRs ) and 95 % confidence intervals ( CIs ) for first-ever major cardiovascular events ( N = 464 ) according to baseline levels of each biomarker . RESULTS After adjustment for age , smoking status , blood pressure , diabetes , and body mass index , the HRs for future cardiovascular events for those in the extreme quintiles were 1.62 ( 95 % CI , 1.17 - 2.25 ) for LDL-C , 1.75 ( 95 % CI , 1.30 - 2.38 ) for apolipoprotein A-I , 2.08 ( 95 % CI , 1.45 - 2.97 ) for total cholesterol , 2.32 ( 95 % CI , 1.64 - 3.33 ) for HDL-C , 2.50 ( 95 % CI , 1.68 - 3.72 ) for apolipoprotein B(100 ) , 2.51 ( 95 % CI , 1.69 - 3.72 ) for non-HDL-C , and 2.98 ( 95 % CI , 1.90 - 4.67 ) for high-sensitivity CRP ( P<.001 for trend across all quintiles ) . The HRs for the lipid ratios were 3.01 ( 95 % CI , 2.01 - 4.50 ) for apolipoprotein B(100 ) to apolipoprotein A-I , 3.18 ( 95 % CI , 2.12 - 4.75 ) for LDL-C to HDL-C , 3.56 ( 95 % CI , 2.31 - 5.47 ) for apolipoprotein B(100 ) to HDL-C , and 3.81 ( 95 % CI , 2.47 - 5.86 ) for the total cholesterol to HDL-C ( P<.001 for trend across all quintiles ) . The correlation coefficients between high-sensitivity CRP and the lipid parameters ranged from -0.33 to 0.15 , and the clinical cut points for CRP of less than 1 , 1 to 3 , and higher than 3 mg/L provided prognostic information on risk across increasing levels of each lipid measure and lipid ratio . CONCLUSIONS Non-HDL-C and the ratio of total cholesterol to HDL-C were as good as or better than apolipoprotein fractions in the prediction of future cardiovascular events . After adjustment for age , blood pressure , smoking , diabetes , and obesity , high-sensitivity CRP added prognostic information beyond that conveyed by all lipid measures Although a large body of epidemiologic evidence suggests that low levels of high-density lipoprotein ( HDL ) cholesterol are strongly associated with an increased risk of coronary artery disease ( CAD ) , no large-scale clinical trials focusing on this association have been reported . This report describes the rationale and design of the Department of Veterans Affairs HDL Intervention Trial ( HIT ) , a multicenter , r and omized , controlled clinical trial design ed to determine whether lipid therapy reduces the combined incidence of CAD death and nonfatal myocardial infa rct ion in men with established CAD who have low levels of HDL cholesterol with " desirable " levels of low-density lipoprotein ( LDL ) cholesterol . Twenty-five hundred men with CAD and HDL cholesterol < or = 40 mg/dl , LDL cholesterol < or = 140 mg/dl , and triglycerides < or = 300 mg/dl are being recruited at 20 Department of Veterans Affairs medical centers , r and omized to either gemfibrozil or placebo  , and followed in a double-blind manner for an average of 6 years . In this population , gemfibrozil is expected to increase HDL cholesterol by 10 to 15 % , have a negligible effect on LDL cholesterol , and lower triglycerides by 30 to 40 % . Because an estimated 20 to 30 % of patients with CAD have a low HDL cholesterol as their primary lipid abnormality , the results of this trial are expected to have far-reaching clinical implication Postmenopausal hypercholesterolemic women are at risk for cardiovascular disease and are encouraged to follow low-fat ( LF ) ( ≤30 % energy ) diets . However , these diets may have undesirable effects on high density lipoprotein cholesterol ( HDL-C ) , apolipoprotein A-I ( apo A-I ) and triglycerides , whereas diets high in monounsaturated fats do not . Twenty postmenopausal hypercholesterolemic women previously consuming high-fat diets ( 34 % energy ) were placed on a low fat-monounsaturated rich diet ( LFMR : 26 % , 14 % energy , respectively ) for 6 mon . Sixteen women already eating LF diets  ( 24 % energy ) were also followed to monitor variations in serum lipids due to seasonal variations . Twenty-five women successfully completed the study ( LFMR=12 , LF=13 ) . Serum cholesterol decreased 10 % ( 264 to 238 mg/dL , P≤0.01 ) and low density lipoprotein cholesterol ( LDL-C ) decreased 12 % ( 182 to 161 mg/dL , P≤0.01 ) in the LFMR group , but did not change in the LF group . The reduction in serum cholesterol in the LFMR group was greater than estimated by predictive formulas . Serum triglycerides and apo A-I did not change in the LFMR group . A modest decrease in HDL-C , HDL3-C , and apolipoprotein B ( apo B ) occurred in both groups , but only the LFMR group showed a trend toward beneficial changes in LDL-C/HDL-C and apo A-I/apo B ratios . Overall , the LFMR diet was well tolerated and result ed in an improved serum lipid and apolipoprotein profile
Fructose had no effect on LDL-C , non-HDL-C , apolipoprotein B , triglycerides , or HDL-C in isocaloric trials .
Conclusions Pooled analyses showed that fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories ( + 21 % to 35 % energy ) .
When isocalorically exchanged for other carbohydrates , fructose had no adverse effects on blood lipids .
Background Debate over the role of fructose in mediating  cardiovascular  risk remains active .
To up date the evidence on the effect of fructose on established therapeutic lipid targets for cardiovascular disease ( low-density lipoprotein cholesterol [LDL]-C , apolipoprotein B , non-high-density lipoprotein cholesterol [ HDL-C ] ) , and metabolic syndrome ( triglycerides and HDL-C ) , we conducted a systematic review and meta- analysis of controlled feeding trials .