***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: CONTEXT High levels of lipoprotein(a ) are associated with increased risk of myocardial infa rct ion ( MI ) . OBJECTIVE To assess whether genetic data are consistent with this association being causal . DESIGN , SETTING , AND PARTICIPANTS Three studies of white individuals from Copenhagen , Denmark , were used : the Copenhagen City Heart Study ( CCHS ) , a prospect i ve general population study with 16 years of follow-up ( 1991 - 2007 , n = 8637 , 599 MI events ) ; the Copenhagen General Population Study ( CGPS ) , a cross-sectional general population study ( 2003 - 2006 , n = 29 388 , 994 MI events ) ; and the Copenhagen Ischemic Heart Disease Study ( CIHDS ) , a case-control study ( 1991 - 2004 , n = 2461 , 1231 MI events ) . MAIN OUTCOME MEASURES Plasma lipoprotein(a ) levels , lipoprotein(a ) kringle IV type 2 ( KIV-2 ) size polymorphism genotype , and MIs recorded from 1976 through July 2007 for all participants . RESULTS In the CCHS , multivariable-adjusted hazard ratios ( HRs ) for MI for elevated lipoprotein(a ) levels were 1.2 ( 95 % confidence interval [ CI ] , 0.9 - 1.6 ; events/10,000 person-years , 59 ) for levels between the 22nd and 66th percentile , 1.6 ( 95 % CI , 1.1 - 2.2 ; events/10,000 person-years , 75 ) for the 67th to 89th percentile , 1.9 ( 95 % CI , 1.2 - 3.0 ; events/10,000 person-years , 84 ) for the 90th to 95th percentile , and 2.6 ( 95 % CI , 1.6 - 4.1 ; events/10,000 person-years , 108 ) for levels greater than the 95th percentile , respectively , vs levels less than the 22nd percentile ( events/10,000 person-years , 55 ) ( trend P < .001 ) . Numbers of KIV-2 repeats ( sum of repeats on both alleles ) ranged from 6 to 99 and on analysis of variance explained 21 % and 27 % of all variation in plasma lipoprotein(a ) levels in the CCHS and CGPS , respectively . Mean lipoprotein(a ) levels were 56 , 31 , 20 , and 15 mg/dL for the first , second , third , and fourth quartiles of KIV-2 repeats in the CCHS , respectively ( trend P < .001 ) ; corresponding values in the CGPS were 60 , 34 , 22 , and 19 mg/dL ( trend P < .001 ) . In the CCHS , multivariable-adjusted HRs for MI were 1.5 ( 95 % CI , 1.2 - 1.9 ; events/10,000 person-years , 75 ) , 1.3 ( 95 % CI , 1.0 - 1.6 ; events/10,000 person-years , 66 ) , and 1.1 ( 95 % CI , 0.9 - 1.4 ; events/10,000 person-years , 57 ) for individuals in the first , second , and third quartiles , respectively , as compared with individuals in the fourth quartile of KIV-2 repeats ( events/10,000 person-years , 51 ) ( trend P < .001 ) . Corresponding odds ratios were 1.3 ( 95 % CI , 1.1 - 1.5 ) , 1.1 ( 95 % CI , 0.9 - 1.3 ) , and 0.9 ( 95 % CI , 0.8 - 1.1 ) in the CGPS ( trend P = .005 ) , and 1.4 ( 95 % CI , 1.1 - 1.7 ) , 1.2 ( 95 % CI , 1.0 - 1.6 ) , and 1.3 ( 95 % CI , 1.0 - 1.6 ) in the CIHDS ( trend P = .01 ) . Genetically elevated lipoprotein(a ) was associated with an HR of 1.22 ( 95 % CI , 1.09 - 1.37 ) per doubling of lipoprotein(a ) level on instrumental variable analysis , while the corresponding value for plasma lipoprotein(a ) levels on Cox regression was 1.08 ( 95 % CI , 1.03 - 1.12 ) . CONCLUSION These data are consistent with a causal association between elevated lipoprotein(a ) levels and increased risk of MI In a r and omized double-blind parallel study in 36 subjects the effect on serum cholesterol of a daily dose of 2 g lipid extracted from green Arabica and Robusta coffee beans was studied . Arabica oil elevated serum total cholesterol by 1.1 mmol/L ( 95 % CI for the difference from placebo : 0.41 , 1.73 mmol/L ) ; the effect of robusta oil ( + 0.5 mmol/L ) was not statistically significant ( 95 % CI : -0.01 , 0.92 mmol/L ) . Arabica oil also raised plasma triglycerides by 0.8 mmol/L ( 95 % CI : 0.26 , 1.25 mmol/L ) . The effect of  robusta oil on triglycerides was + 0.14 mmol/L and not significant ( 95 % CI : -0.26 , 0.42 mmol/L ) . In the 12 subjects taking arabica oil an average serum alanine amino-transferase elevation of 18 U/L ( 95 % CI : 9.4 , 28.4 U/L ) was observed . Because only arabica oil contains kahweol and arabica coffee contains more cafestol than does robusta oil , this is further evidence for the role of diterpenes in the rise of serum cholesterol and alanine aminotransferase after consumption of boiled coffee OBJECTIVE The aim of this study was to compare the effects of medium light roast ( MLR ) and medium roast ( MR ) paper-filtered coffee on  cardiovascular risk factors in healthy volunteers . METHODS This r and omized crossover trial compared the effects of consuming three or four cups ( 150 mL ) of MLR or MR coffee per day for 4 wk in 20 healthy volunteers .  Plasma lipids , lipoprotein(a ) ( Lp[a ] ) , total homocysteine , and endothelial dysfunction-related inflammation biomarkers , serum glycemic biomarkers , and blood pressure were measured at baseline and after each intervention . RESULTS Both roasts increased plasma total cholesterol , low-density lipoprotein-cholesterol , and soluble vascular cell adhesion molecule-1 ( sVCAM-1 ) concentrations ( 10 % , 12 % , and 18 % for MLR ; 12 % , 14 % , and 14 % for MR , respectively ) ( P < 0.05 ) . MR also increased high-density lipoportein-cholesterol concentration by 7 % ( P = 0.003 ) . Plasma fibrinogen concentration increased 8 % after MR intake ( P = 0.01 ) , and soluble E-selectin increased 12 % after MLR intake ( P = 0.02 ) . No changes were observed for Lp(a ) , total homocysteine , glycemic biomarkers , and blood pressure . CONCLUSION Moderate paper-filtered coffee consumption may have an undesirable effect on plasma cholesterol and inflammation biomarkers in healthy individuals regardless of its antioxidant content Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more Objective : Earlier studies and trials have shown a serum cholesterol raising effect of unfiltered coffee , which is reduced by about 80 % in filtered coffee . Recent cross-sectional studies and trials , however , have indicated that filtered coffee may have a more pronounced serum cholesterol raising effect than previously anticipated . The objective of this controlled study was to assess the effects of the intake and abstention of filtered brewed coffee on blood lipids . Design : A prospect i ve , controlled study with four consecutive trial periods . The first and third periods were 3 weeks of total coffee abstention . The second and fourth periods consisted of 4 weeks with the subjects consuming 600 ml filter brewed coffee/day . Setting : Free-living population . Volunteers . Subjects : A total of 121 healthy , nonsmoking men and women aged 29–65 y. Interventions : Not applicable . Main outcome measures : Serum total cholesterol , serum HDL cholesterol , serum triglycerides , serum lipoprotein ( a ) ( Lp(a ) ) , blood pressure and heart rate . Results : The two coffee abstention periods were associated with a decline in serum cholesterol of 0.22 mmol/l ( 95 % CI −0.31 , −0.13 ) and 0.36 mmol/l ( 95 % CI −0.46 , −0.26 ) , respectively . Filtered coffee/day 600 ml increased serum cholesterol by 0.25 mmol/l ( 95 % CI 0.15 , 0.36 ) and 0.15 mmol/l ( 95 % CI 0.04 , 0.26 ) during the two coffee drinking periods . Conclusions : Coffee abstention for 3 weeks decreased total serum cholesterol by 0.22–0.36 mmol/l . A volume of 600 ml ( about four cups ) of filtered coffee/day during 4 weeks raised total serum cholesterol by 0.15–0.25 mmol/l . Sponsorship : None Objective : Unfiltered coffee raises serum LDL cholesterol  in humans , owing to the presence of the diterpenes cafestol and kahweol . Norwegians with a chronic high intake of unfiltered coffee  also had elevated serum levels of lipoprotein(a ) , an LDL-like particle which is insensitive toward dietary interventions . We now experimentally studied the influence of coffee diterpenes on lipoprotein(a ) levels . Design : Four r and omised controlled trials . Subjects : Healthy , normolipidemic volunteers . Interventions : Coffee , coffee oil , and pure diterpenes for 4–24 weeks . Main outcome measures : The circulating level of lipoprotein(a ) . Results : In 22 subjects drinking five to six strong cups of  cafetiere coffee  per day , the median fall in lipoprotein(a ) was 1.5 mg/dL after two months ( P=0.03 ) , and 0.5 mg/dL after half a year ( P>0.05 ) , relative to 24 filter coffee drinkers . Coffee oil doses equivalent to 10–20 cups of unfiltered coffee  reduced lipoprotein(a ) levels by up to 5.5 mg/dL ( P<0.05 ) in two separate trials ( n=12–16 per group ) . A purified mixture of cafestol and kahweol , as well as cafestol alone , were also effective in reducing Lp(a ) levels ( n=10 ) . Averaged over the four trials , each 10 mg/d of cafestol ( plus kahweol)—the amount present in two to three cups of cafetiere coffee — decreased Lp(a ) levels by 0.5 mg/dL or 4 % from baseline values after four weeks ( n=63 ) . Conclusions : Coffee diterpenes are among the few dietary exceptions shown to influence serum lipoprotein(a ) levels . However , the Lp(a)-reducing potency of coffee diterpenes may subside in the long run , and their adverse side effects preclude their use as lipoprotein(a)-reducing agents . Sponsorship : Supported by the Netherl and s Heart Foundation through grant No. 900 - 562 - 091 of the Netherl and s Organization of Scientific Research ( NWO ) , plus supplemental funding by the Institute for Scientific Information on Coffee Boiled coffee contains an unidentified lipid that raises serum cholesterol . We studied the effects of the ingestion of coffee oil fractions of increasing purity in volunteers in order to identify the cholesterol-raising factor . In 15 volunteers who ingested 0.75 g/d of a non-triglyceride-fraction from coffee oil for 4 weeks , mean cholesterol increased by 48 mg/dl ( 1.2 mmol/l ) relative to placebo . In contrast , a coffee oil stripped of the non-triglyceride lipids cafestol and kahweol had no effect . In three volunteers , purified cafestol ( 73 mg/d ) plus kahweol ( 58 mg/d ) increased cholesterol by 66 m 
    Output:
    
The effect of coffee on Lp(a ) is complex and may follow a biphasic time-course .
The type of coffee and the method of preparation appear to be important to determining the effect on Lp(a )