***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 
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    Input: BACKGROUND Previous observational studies of self-reported dairy product consumption and stroke risk have reported mixed findings . Few studies have used circulating biomarkers that provide objective measures of dairy fat intake . OBJECTIVES We tested the hypothesis that the circulating biomarkers of dairy fat , pentadecanoic acid ( 15:0 ) , heptadecanoic acid ( 17:0 ) , and trans palmitoleate ( trans 16:1n-7 ) , were associated with lower incidence of stroke , especially ischemic stroke . Secondarily , we evaluated 14:0 , which is obtained from dairy products and beef , and also endogenously synthesized . DESIGN In participants from 2 large US cohorts ( the Health Professionals Follow-Up Study : 51,529 men ; the Nurses ' Health Study : 121,700 women ) with stored blood sample s in 1993 - 1994 ( n = 18,225 ) and 1989 - 1990 ( n = 32,826 ) , respectively , we prospect ively identified 594 incident stroke cases ( median follow-up : 8.3 y ) and matched them 1:1 to risk-set- sample d control subjects by age , sex , race , and smoking . Total plasma and red blood cell ( RBC ) fatty acids were measured by using gas-liquid chromatography . Covariates were assessed by using vali date d question naires . Stroke events and subtypes were adjudicated by using medical records or other supporting documentation . We used conditional logistic regression to estimate associations of fatty acids with incident stroke , and cohort-specific findings were combined by inverse-variance weights . RESULTS After adjustment for demographic characteristics , lifestyle , cardiovascular disease risk factors , diet , and other circulating fatty acids , no significant associations with total stroke were seen for plasma 15:0 ( pooled HR for highest compared with lowest quartiles : 0.85 ; 95 % CI : 0.54 , 1.33 ) , 17:0 ( 0.99 ; 0.67 , 1.49 ) , trans 16:1 n-7 ( 0.89 ; 0.55 , 1.45 ) , or 14:0 ( 1.05 ; 0.62 , 1.78 ) . Results were similar for ischemic and hemorrhagic stroke subtypes , for RBC fatty acids , and in several different sensitivity analyses . CONCLUSION In 2 large prospect i ve cohorts , circulating biomarkers of dairy fat were not significantly associated with stroke Background It may be useful to examine associations of fat intakes with total mortality as a basis for dietary recommendations . We aim ed to eluci date associations between dietary fat and total mortality among Japanese population s with low fat intake . Methods We conducted a prospect i ve study consisting of 58,672 men and women aged 40 to 79 years .  Fat intakes were estimated using a food frequency question naire .  Multivariate-adjusted hazard ratios ( HRs ) for mortality by sex were computed according to quintiles of energy-adjusted fat intakes . Results During the follow-up period ( median duration , 19.3 years ) , 11,656 deaths were recorded . In men , we found no clear association between total fat and total mortality . HRs across quintiles of total fat intake were 1.00 , 1.03 ( 95 % confidence interval [ CI ] , 0.95–1.12 ) , 1.02 ( 0.94–1.10 ) , 0.98 ( 0.90–1.07 ) , and 1.07 ( 0.98–1.17 ) . No significant association was detected in regard to types of fat . In women , HR was lowest in the fourth quintile of total fat intake followed by the top quintile ; HRs across quintiles were 1.00 , 1.03 ( 0.94–1.11 ) , 1.00 ( 0.92–1.09 ) , 0.88 ( 0.81–0.96 ) , and 0.94 ( 0.86–1.03 ) . Regarding types of fat in women , total mortality was inversely associated with intakes of saturated fatty acids ( SFA ) , monounsaturated fatty acids ( MUFA ) , and polyunsaturated fatty acids ( PUFA ) ; the lowest HR was in the top quintile of intake for SFA , MUFA , and PUFA : 0.91 ( 95 % CI , 0.83–1.00 ) , 0.91 ( 0.83–0.99 ) and 0.88 ( 0.80 - 0.97 ) , respectively ( trend P across quintiles , 0.020 , 0.012 , and 0.029 , respectively ) . Causes of death other than cancer and cardiovascular disease contributed most to decreases in HRs for total and types of fat . In women , analysis with finer categories revealed that the lowest risk for total mortality appeared at total fat intake of 28 % of energy . Conclusions Our findings from a large cohort study among population s with relatively low fat intake provide evidence regarding optimal levels of fat intakes Recently , there has been interest in whether intakes of specific types of fat are associated with breast cancer risk independently of other types of fat , but results have been inconsistent . We identified 8 prospect i ve studies that met predefined criteria and analyzed their primary data using a st and ardized approach . Holding total energy intake constant , we calculated relative risks for increments of 5 % of energy for each type of fat compared with an equivalent amount of energy from carbohydrates or from other types of fat . We combined study -specific relative risks using a r and om effects model . In the pooled data base , 7,329 incident invasive breast cancer cases occurred among 351,821 women . The pooled relative risks ( 95 % confidence intervals [ CI ] ) for an increment of 5 % of energy were 1.09 ( 1.00 - 1.19 ) for saturated , 0.93 ( 0.84 - 1.03 ) for monounsaturated and 1.05 ( 0.96 - 1.16 ) for polyunsaturated fat compared with equivalent energy intake from carbohydrates . For a 5 % of energy increment , the relative risks were 1.18 ( 95 % CI 0.99 - 1.42 ) for substituting saturated for monounsaturated fat , 0.98 ( 95 % CI 0.85 - 1.12 ) for substituting saturated for polyunsaturated fat and 0.87 ( 95 % CI 0.73 - 1.02 ) for substituting monounsaturated for polyunsaturated fat . No associations were observed for animal or vegetable fat intakes . These associations were not modified by menopausal status . These data are suggestive of only a weak positive association with substitution of saturated fat for carbohydrate consumption ; none of the other types of fat examined was significantly associated with breast cancer risk relative to an equivalent reduction in carbohydrate consumption Aims /hypothesis . The amount and quality of fat in the diet could be of importance for development of insulin resistance and related metabolic disorders . Our aim was to determine whether a change in dietary fat quality alone could alter insulin action in humans . Methods . The KANWU study included 162 healthy subjects chosen at r and om to receive a controlled , isoenergetic diet for 3 months containing either a high proportion of saturated ( SAFA diet ) or monounsaturated ( MUFA diet ) fatty acids . Within each group there was a second assignment at r and om to supplements with fish oil ( 3.6 g n-3 fatty acids/d ) or placebo . Results . Insulin sensitivity was significantly impaired on the saturated fatty acid diet ( -10 % , p = 0.03 ) but did not change on the monounsaturated fatty acid diet ( + 2 % , NS ) ( p = 0.05 for difference between diets ) . Insulin secretion was not affected . The addition of n-3 fatty acids influenced neither insulin sensitivity nor insulin secretion . The favourable effects of substituting a monounsaturated fatty acid diet for a saturated fatty acid diet on insulin sensitivity were only seen at a total fat intake below median ( 37E % ) . Here , insulin sensitivity was 12.5 % lower and 8.8 % higher on the saturated fatty acid diet and monounsaturated fatty acid diet respectively ( p = 0.03 ) . Low density lipoprotein cholesterol ( LDL ) increased on the saturated fatty acid diet ( + 4.1 % , p < 0.01 ) but decreased on the monounsaturated fatty acid diet ( MUFA ) ( –5.2 , p < 0.001 ) , whereas lipoprotein ( a ) [ Lp(a ) ] increased on a monounsaturated fatty acid diet by 12 % ( p < 0.001 ) . Conclusions /interpretation . A change of the proportions of dietary fatty acids , decreasing saturated fatty acid and increasing monounsaturated fatty acid , improves insulin sensitivity but has no effect on insulin secretion . A beneficial impact of the fat quality on insulin sensitivity is not seen in individuals with a high fat intake ( > 37E % ) . [ Diabetologia ( 2001 ) 44 : 312–319 Objectives To investigate the association between long term intake of individual saturated fatty acids ( SFAs ) and the  risk of coronary heart disease  , in two large cohort studies . Design Prospect i ve , longitudinal cohort study . Setting Health professionals in the United States . Participants 73 147 women in the Nurses ’ Health Study ( 1984 - 2012 ) and 42 635 men in the Health Professionals Follow-up Study ( 1986 - 2010 ) , who were free of major chronic diseases at baseline . Main outcome measure Incidence of coronary heart disease ( n=7035 ) was self-reported , and related deaths were identified by search ing National Death Index or through report of next of kin or postal authority . Cases were confirmed by medical records review . Results Mean intake of SFAs  accounted for 9.0 - 11.3 % energy intake over time , and was mainly composed of lauric acid ( 12:0 ) , myristic acid ( 14:0 ) , palmitic acid ( 16:0 ) , and stearic acid ( 18:0 ; 8.8 - 10.7 % energy ) . Intake of 12:0 , 14:0 , 16:0 and 18:0 were highly correlated , with Spearman correlation coefficients between 0.38 and 0.93 ( all P<0.001 ) . Comparing the highest to the lowest groups of individual SFA intakes , hazard ratios of coronary heart disease were 1.07 ( 95 % confidence interval 0.99 to 1.15 ; Ptrend=0.05 ) for 12:0 , 1.13 ( 1.05 to 1.22 ; Ptrend<0.001 ) for 14:0 , 1.18 ( 1.09 to 1.27 ; Ptrend<0.001 ) for 16:0 , 1.18 ( 1.09 to 1.28 ; Ptrend<0.001 ) for 18:0 , and 1.18 ( 1.09 to 1.28 ; Ptrend<0.001 ) for all four SFAs combined ( 12:0 - 18:0 ) , after multivariate adjustment of lifestyle factors and total energy intake . Hazard ratios of coronary heart disease for isocaloric replacement of 1 % energy from 12:0 - 18:0 were 0.92 ( 95 % confidence interval 0.89 to 0.96 ; P<0.001 ) for polyunsaturated fat , 0.95 ( 0.90 to 1.01 ; P=0.08 ) for monounsaturated fat , 0.94 ( 0.91 to 0.97 ; P<0.001 ) for whole grain carbohydrates , and 0.93 ( 0.89 to 0.97 ; P=0.001 ) for plant proteins . For individual SFAs , the lowest risk of coronary heart disease was observed when the most abundant SFA , 16:0 , was replaced . Hazard ratios of coronary heart disease for replacing 1 % energy from 16:0 were 0.88 ( 95 % confidence interval 0.81 to 0.96 ; P=0.002 ) for polyunsaturated fat , 0.92 ( 0.83 to 1.02 ; P=0.10 ) for monounsaturated fat , 0.90 ( 0.83 to 0.97 ; P=0.01 ) for whole grain carbohydrates , and 0.89 ( 0.82 to 0.97 ; P=0.01 ) for plant proteins . Conclusions Higher dietary intakes of major SFAs are associated with an increased risk of coronary heart disease . Owing to similar associations and high correlations among individual SFAs , dietary recommendations for the prevention of coronary heart disease should continue to focus on replacing total saturated fat with more healthy sources of energy BACKGROUND Substitution of dietary polyunsaturated for 
    Output:
    
Trans fats are associated with all cause mortality , total CHD , and CHD mortality , probably because of higher levels of intake of industrial trans fats than ruminant trans fats .