***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: The effect on serum high density lipoprotein subfractions of a low fat diet with a high ratio of polyunsaturated-to-saturated fatty acids was studied in 38 middle-aged volunteers ( 19 men and 19 women ) in North Karelia , Finl and . The mean serum HDL2 cholesterol decreased from 32 + /- 2 mg/dl ( mean + /- SE ) to 28 + /- 2 mg/dl ( p less than 0.001 ) during the experimental diet and returned to 33 + /- 2 mg/dl ( p less than 0.001 ) after a return to the original diet . No changes were observed in the concentration of HDL3 cholesterol . A highly significant decrease was observed in serum apoprotein A-I concentration , but not in apoprotein A-II concentration during the experimental diet . It is concluded that a low-fat , high-P/S ratio diet lowers LDL and HDL2 cholesterol in healthy volunteers , but does not influence the level of HDL3 subfraction The Minnesota Coronary Survey was a 4.5-year , open enrollment , single end-time , double-blind , r and omized clinical trial that was conducted In six Minnesota state mental hospitals and one nursing home . It Involved 4393 Institutionalized men and 4664 Institutionalized women . The trial compared the effects of a 39 % fat control diet ( 18 % saturated fat , 5 % polyunsaturated fat , 16 % monounsaturated fat , 446 mg dietary cholesterol per day ) with a 38 % fat treatment diet ( 9 % saturated fat , 15 % polyunsaturated fat , 14 % monounsaturated fat , 166 mg dietary cholesterol per day ) on serum cholesterol levels and the Incidence of myocardlal Infa rct ions , sudden deaths , and all-cause mortality . The mean duration of time on the diets was 384 days , with 1568 subjects consuming the diet for over 2 years . The mean serum cholesterol level In the pre-admission period was 207 mg/dl , falling to 175 mg/dl in the treatment group and 203 mg/dl In the control group . For the entire study population , no differences between the treatment and control groups were observed for cardiovascular events , cardiovascular deaths , or total mortality . A favorable trend for all these end-points occurred In some younger age groups It has been suggested that alpha-tocopherol , a safe and effective antioxidant , be used in clinical trials to evaluate the ability of antioxidant therapy to inhibit atherosclerosis . Recent reports , however , have raised the possibility that there may be greater enrichment of plasma low density lipoprotein ( LDL ) in alpha-tocopherol result ing from the use of the naturally occurring RRR-alpha-tocopherol isomer compared with the other isomers present in the synthetic racemic form of alpha-tocopherol . Therefore , we fed equal dosages ( 1,600 mg/day ) of the two forms of vitamin E to 16 men and women for 8 weeks and compared the effects of this supplementation on the susceptibility of isolated lipoproteins to oxidation . Neither form of vitamin E had appreciable effects on lipid or lipoprotein levels . alpha-Tocopherol levels in LDL increased at a similar rate in both groups and were nearly twofold higher than baseline levels by the end of the study . The susceptibility of LDL to oxidation was measured by formation of conjugated dienes , lipid peroxides , and thiobarbituric acid-reactive substances , as well as by macrophage degradation of LDL exposed to oxidizing conditions in vitro . The susceptibility of LDL to oxidation was decreased in both vitamin E groups compared with the baseline value , and this reduction occurred to a similar extent in both vitamin E-supplemented groups . alpha-Tocopherol levels in LDL also strongly correlated with all measures of LDL oxidation . This study demonstrates that , at this dosage , supplementation with either the natural or synthetic form of alpha-tocopherol provided equal antioxidant protection to LDL The effects of high oleic acid rapeseed oil compared with polyunsaturated fats on serum lipoprotein levels are largely unknown . Therefore , we fed 30 women and 29 men a baseline diet rich in saturated fat , which was followed by a diet rich in high oleic and low erucic acid rapeseed oil ( total energy content of fat , 38 % ; saturates , 12.4 % ; monounsaturates , 16 % ; n-6 polyunsaturates , 6 % ; and n-3 polyunsaturates , 2 % ) and one rich in sunflower oil ( total energy content of fat , 38 % ; saturates , 12.7 % ; monounsaturates , 10 % ; n-6 polyunsaturates , 13 % ; and n-3 polyunsaturates , 0 % ) . The oils were incorporated into mixed natural diets that were dispensed in a r and om order for 3.5 weeks each in a blinded crossover design . The diet composition was confirmed by analysis of duplicate diets . Both test diets reduced serum total cholesterol ( TC ) and low density lipoprotein ( LDL ) cholesterol levels from baseline , the monounsaturated rapeseed oil diet more than the polyunsaturated sunflower oil diet ( TC : -15 % versus -12 % , p less than 0.01 ; LDL cholesterol : -23 % versus -17 % , p less than 0.01 ) . Very low density lipoprotein ( VLDL ) cholesterol and total , VLDL , and LDL triglyceride levels were lower during the sunflower oil diet compared with the rapeseed oil diet .  Total high density lipoprotein ( HDL ) cholesterol levels remained unchanged by both diets . The consumption of rapeseed oil result ed in a more favorable HDL2 to LDL cholesterol ratio ( 0.43 + /- 0.19 versus 0.39 + /- 0.18 , p less than 0.01 ) and an apolipoprotein A-I to B ratio ( 3.0 + /- 1.4 versus 2.4 + /- 1.6 , p less than 0.001 ) than did the sunflower oil . ( ABSTRACT TRUNCATED AT 250 WORDS This report describes the effects of feeding linoleate- or oleate-enriched diets to subjects who were concurrently taking 1200 mg/d of alpha-tocopherol on the susceptibility of low-density lipoprotein ( LDL ) and buoyant and dense LDL subfractions to oxidation . LDL isolated from subjects who consumed linoleate-enriched diets  was more susceptible to copper-mediated oxidation , as measured by formation of conjugated dienes and lipid peroxides and loss of unsaturated fatty acids , compared with LDL isolated from subjects who consumed their usual or oleate-enriched diets . In all subjects , buoyant LDL had a higher content of alpha-tocopherol per particle and a lower 18:2 to 18:1 ratio and was considerably more resistant to oxidation than dense LDL . Although dense LDL from all groups had comparable alpha-tocopherol levels , dense LDL from the linoleate group was most susceptible to oxidation , followed by that from the st and ard diet , whereas dense LDL isolated from the oleate diet group was most resistant . In summary , high dosages of alpha-tocopherol did not prevent enhanced susceptibility to oxidation of LDL isolated from subjects fed linoleate-enriched diets . Furthermore , dense LDL was more susceptible to oxidation than was buoyant LDL , and this effect was greatly exaggerated in the dense LDL isolated from subjects fed linoleate-enriched diets . Conversely , dense LDL isolated from subjects fed oleate-enriched diets was the most protected . If oxidation of LDL is important in the pathogenesis of atherosclerosis , then these data suggest that in people with increased amounts of small , dense LDL , dietary enrichment in oleic acid may decrease the susceptibility of their LDL to oxidation Effects of small amounts of sitosterol , sitostanol and sitostanol esters ( < 1 g/day of free sterols ) dissolved in rapeseed oil ( RSO ) were studied on serum lipids and cholesterol metabolism in patients with primary hypercholesterolemia and different apolipoprotein E phenotypes on an RSO diet . One of the four groups was an RSO-fed control .  Serum total and LDL cholesterol reductions were small in different plant sterol-fed groups , tended to be highest in the sitostanol ester group ( -7 % ) , but were significantly reduced by about 5 % in the combined plant sterol groups . The reductions were -8 % in the subjects with epsilon 4 allele and insignificant in those with apo E3/3 phenotype . Cholesterol precursor sterols in serum , markers of cholesterol synthesis , were increased only in the subjects with epsilon 4 allele . Cholesterol absorption was reduced by 7 % , being 31 % in the subjects with epsilon 4 allele , and fecal elimination of cholesterol was increased , a finding also indicating increased cholesterol synthesis . The changes in cholesterol absorption were related to those in fecal plant sterols ( change in dietary intake ) and serum total and LDL cholesterol ( P = 0.04 , 0.01 and 0.05 , respectively ) . Thus , small amounts of dietary plant sterols ( < 1 g/day ) , especially sitostanol esters dissolved in dietary fats , decrease serum total and LDL cholesterol by a proportional decrease in cholesterol absorption which , in turn , is associated with a compensatory increase in cholesterol synthesis . The effects are most consistent in subjects with epsilon 4 allele , but for effective hypocholesterolemic treatment dietary amount of sitostanol ester should exceed 1 g/day Background Do the benefits of intensive lipid-lowering therapy seen in symptomatic patients extend to high-risk subjects who have never had symptoms ? Methods and ResulsOf 120 men completing the FATS trial , 91 were symptomatic and 29 asymptomatic . All had apolipoprotein B 2125 mg/dL , a positive family history , and coronary atherosclerosis . All were counseled in diet and r and omized to intensive therapy : colestipol 10 g TID plus either niacin 1 g QID or lovastatin 20 mg BID or to conventional therapy : placebos , or colestipol if low-density lipoprotein cholesterol was elevated . End points included quantitative arteriographic disease change and clinical events over a 2.5-year interval . At baseline , symptomatic and asymptomatic patients had comparable risk profiles , but proximal stenosis severity averaged 36 % for symptomatic and 23 % for asymptomatic patients ( P<.001 ) . Among the 91 symptomatic patients , those in the intensive group experienced definite ( .101%S ) proximal lesion progression less frequently than conventional ( 24 % of intensive versus 48 % of conventional ) and definite regression more frequently ( 36 % of intensive versus 15 % of conventional ) ( P=.009 ) . Similarly , among the 29 asymptomatic patients , 19 % of intensive versus 38 % of conventional had progression and 31 % of intensive versus 0%1 of conventional , regression ( P=.04 ) . Ischemia on baseline exercise tolerance testing was associated with significantly greater proximal disease progression among the asymptomatic patients . Clinical cardiovascular events ( death , infa rct ion , or revascularization ) occurred in 10 of 38 symptomatic patients originally assigned to conventional therapy , compared with 5 of 76 symptomatic patients assigned to intensive ( P<.01 ) ; no asymptomatic patient had an event . ConcluionsAsymptomatic subjects with this high-risk profile have less coronary disease at baseline than comparable symptomatic patients , and they have an excellent short-term clinical prognosis . However , asymptomatic subjects are indistinguishable from symptomatic patients in terms of their arterial disease progression with conventional therapy and their regression with intensive . These findings may justify an active treatment strategy in such subjects , particularly those with provokable ischemia The primary aim of this study was to estimate the relation between cholesterol reduction and total mortality and coronary heart disease ( CHD ) incidence . Secondarily , the clinical issues of whether the efficacy of cholesterol lowering is dependent on the treatment modality , presence of CHD at baseline , or the simultaneous introduction of other interventions was explored . All r and omized clinical intervention trials of cholesterol reduction were used in an overview analysis of total mortality rate and CHD incidence ; analysis was performed with weighted linear regression . The trials include those that used primary and secondary intervention , diet and drugs , and single or multifactor design .  Nineteen trials were analyzed for total mortality , and of the 19 , 16 were analyzed for CHD incidence rate .  Net difference in cholesterol change between study groups was used as the independent variable , and the three previously mentioned dichotomous design characteristics were used as additional independent variables . For every 1 % reduction in cholesterol , an estimated 2.5 % reduction in CHD incidence is indicated ( 95 % CL : 1.1 , 3.9 ) . With regard to CHD drug trials tended toward better efficiency in cholesterol lowering than did dietary trials . 
    Output:
    
No significant difference was noted for the majority of secondary outcomes for any of the planned comparisons .