***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: In 1998 , the American Heart Association convened Prevention Conference V to examine strategies for the identification of high-risk patients who need primary prevention . Among the strategies discussed was the measurement of markers of inflammation.1  The Conference concluded that “ many of these markers ( including inflammatory markers ) are not yet considered applicable for routine risk assessment because of : ( 1 ) lack of measurement st and ardization , ( 2 ) lack of consistency in epidemiological findings from prospect i ve studies with endpoints , and ( 3 ) lack of evidence that the novel marker adds to risk prediction over and above that already achievable through the use of established risk factors . ” The National Cholesterol Education Program Adult Treatment Panel III Guidelines identified these markers as emerging risk factors,1a which could be used as an optional risk factor measurement to adjust estimates of absolute risk obtained using st and ard risk factors . Since these publications , a large number of peer- review ed scientific reports have been published relating inflammatory markers to cardiovascular disease ( CVD ) . Several commercial assays for inflammatory markers have become available . As a consequence of the exp and ing research base and availability of assays , the number of inflammatory marker tests ordered by clinicians for CVD risk prediction has grown rapidly . Despite this , there has been no consensus from professional societies or governmental agencies as to how these assays of markers of inflammation should be used in clinical practice . On March 14 and 15 , 2002 , a workshop titled “ CDC/AHA Workshop on Inflammatory Markers and Cardiovascular Disease : Applications to Clinical and Public Health Practice ” was convened in Atlanta , Ga , to address these issues . The goals of this workshop were to determine which of the currently available tests should be used ; what results should be used to define high risk ; which patients should be tested ; and the indications for which the tests would be most useful . These Background Diet is known to play a key role in atherogenesis and in the development of cardiovascular events . Dietary factors may mediate these processes acting as potential modulators of inflammation . Potential Links between inflammatory properties of diet and the occurrence of cardiovascular events have not been tested previously . Objective We aim ed to assess the association between the dietary inflammatory index ( DII ) , a method to assess the inflammatory potential of the diet , and incident cardiovascular disease . Methods In the prospect i ve , dynamic SUN cohort , 18,794 middle-aged , Spanish university graduates were followed up for 8.9 years ( median ) . A vali date d 136-item food-frequency question naire was used to calculate the DII . The DII is based on scientific evidence about the relationship between diet and inflammatory biomarkers ( C-reactive protein , IL-1β , IL-4 , IL-6 , IL-10 and TNF-α ) . Cox proportional hazard models were used to estimate hazard ratios ( HR ) and 95 % confidence intervals ( CI ) for the association between the DII and incident cardiovascular disease ( myocardial infa rct ion , stroke or cardiovascular death ) . Results The risk for cardiovascular events progressively increased with each increasing quartile of DII ( ptrend = 0.017 ) . The multivariable-adjusted HR for participants in the highest ( most pro-inflammatory ) vs. the lowest quartile of the DII was 2.03 ( 95 % CI 1.06–3.88 ) . Conclusions A pro-inflammatory diet was associated with a significantly higher risk for developing cardiovascular events Inflammation plays a central role in pancreatic cancer etiology and can be modulated by diet . We aim ed to examine the association between the inflammatory potential of diet , assessed with the  Dietary Inflammatory Index  ( DII ® ) , and pancreatic cancer risk in the Prostate , Lung , Colorectal and Ovarian Cancer Screening Trial prospect i ve cohort . Our study included 101,449 participants aged 52 - 78 years at baseline who completed both baseline question naire and a diet history question naire .  Energy-adjusted DII ( E-DII ) scores were computed based on food and supplement intake . Cox proportional hazards models and time dependent Cox models were used to estimate hazard ratios ( HRs ) and 95 % confidence intervals ( CIs ) with participants in the lowest E-DII quintile ( most anti-inflammatory scores ) as referent . After a median 8.5 years of follow-up , 328 pancreatic cancer cases were identified  . E-DII scores were not associated with pancreatic cancer risk in the multivariable model ( HRQ5vsQ1 = 0.94 ; 95 % CI = 0.66 - 1.35 ; p-trend = 0.43 ) . Time significantly modified the association ( p-interaction = 0.01 ) . During follow up < 4 years , there was suggestive evidence of an inverse association between E-DII and pancreatic cancer ( HRQ5vsQ1 = 0.60 ; 95 % CI = 0.35 - 1.02 ; p-trend = 0.20 ) while there was a significant positive trend in the follow up ≥4 years ( HRQ5vsQ1 = 1.31 ; 95 % CI = 0.83 - 2.08 ; p-trend = 0.03 ) . Similar results were observed for E-DII from food only . Our study does not support an association between inflammatory potential of diet and pancreatic cancer risk ; however , heterogeneous results were obtained with different follow-up times . These divergent associations may result from the influences of undetected disease in the short-term Previous studies have reported an association between a more pro-inflammatory diet profile and various chronic metabolic diseases . The Dietary Inflammatory Index ( DII ) was used to assess the inflammatory potential of nutrients and foods in the context of a dietary pattern . We prospect ively examined the association between the DII and the incidence of cardiovascular disease ( CVD : myocardial infa rct ion , stroke or cardiovascular death ) in the PREDIMED ( Prevención con Dieta Mediterránea ) study including 7216 high-risk participants . The DII was computed based on a vali date d 137-item food frequency question naire . Multivariate-adjusted hazard ratios ( HR ) and 95 % confidence intervals of CVD risk were computed across quartiles of the DII where the lowest ( most anti-inflammatory ) quartile is the referent . Risk increased across the quartiles ( i.e. , with increasing inflammatory potential ) : HRquartile2 = 1.42 ( 95%CI = 0.97–2.09 ) ; HRquartile3 = 1.85 ( 1.27–2.71 ) ; and HRquartile4 = 1.73 ( 1.15–2.60 ) . When fit as continuous the multiple-adjusted hazard ratio for each additional st and ard deviation of the DII was 1.22 ( 1.06–1.40 ) . Our results provide direct prospect i ve evidence that a pro-inflammatory diet is associated with a higher risk of cardiovascular clinical events The possible relationship between diet-related inflammation and the risk of prediabetes  requires further investigation , especially in non-Western population s. We examined the ability of the dietary inflammatory index ( DII )  to predict the risk of prediabetes in a case-control study conducted at specialized centers in Esfahan , Iran . A total of 214 incident cases of prediabetes were selected with the nonr and om sampling procedure , and the 200 controls r and omly selected from the same clinics were frequency-matched on age ( ±5 years ) and sex . DII scores were computed based on  dietary intake assessed using a vali date d and reproducible 168-item food-frequency question naire . Linear and logistic regression models were used to estimate multivariable beta estimates and odds ratios ( ORs ) . Subjects in tertile 3 versus tertile 1 ( T3VS1 ) of DII had significantly higher fasting plasma glucose ( DIIT3VS1 : b = 4.49 ; 95 % CI 1.89 , 7.09 ) , oral glucose tolerance ( DIIT3VS1 : b = 8.76 ; 95 % CI 1.78 , 15.73 ) , HbA1c ( DIIT3VS1 : b = 0.30 ; 95 % CI 0.17 , 0.42 ) , low-density lipoprotein ( DIIT3VS1 : b = 16.37 ; 95 % CI 11.04 , 21.69 ) , triglyceride ( DIIT3VS1 : b = 21.01 ; 95 % CI 8.61 , 33.42 ) and body fat ( DIIT3VS1 : b = 2.41 ; 95 % CI 0.56 , 4.26 ) and lower high-density lipoprotein ( DIIT3VS1 : b = -3.39 ; 95 % CI -5.94 , -0.84 ) and lean body mass ( DIIT3VS1 : b = -3.11 ; 95 % CI -4.83 , -1.39 ) . After multivariate adjustment , subjects in the most pro-inflammatory DII group had 19 times higher odds of developing prediabetes compared with subjects in tertile 1 ( DIIT3VS1 : OR = 18.88 ; 95 % CI 7.02 , 50.82 ) . Similar results were observed when DII was used as a continuous variable , ( DIIcontinuous : OR = 3.62 ; 95 % CI 2.50 , 5.22 ) . Subjects who consumed a more pro-inflammatory  diet were at increased risk of prediabetes compared with those who consumed a more anti-inflammatory diet SCOPE Low- grade chronic inflammation is associated with several chronic conditions , and diet is known to play a role in chronic inflammation . We aim ed to evaluate the association between the inflammatory potential of the diet and mortality in the Spanish population from the European Prospect i ve Investigation into Cancer and Nutrition ( EPIC-Spain ) . METHODS AND RESULTS The study included 41 199 participants ( 62 % female ) aged 29 - 69 years from five Spanish regions . During 18 years of follow-up 3316 deaths were identified . The dietary inflammatory potential was assessed by means of an inflammatory score of the diet ( ISD ) , calculated using 30 dietetic components and their corresponding inflammatory scores ( weights ) . The association between the ISD and mortality was analyzed by multivariate Cox regression models . There was a significant association between ISD and mortality : subjects classified in the fifth quintile of the ISD ( more proinflammatory diets ) had a hazard ratio of 1.42 ( 95%-confidence interval 1.25 - 1.60 ) as compared with those in the first quintile ; the corresponding figures were 1.89 ( 1.48 - 2.40 ) for cardiovascular diseases mortality and 1.44 ( 1.22 - 1.69 ) for death by cancer . CONCLUSION Consuming more proinflammatory diets , expressed by means of the ISD , is associated with higher mortality ; this effect seems to be stronger for deaths by cardiovascular diseases BACKGROUND Inflammation is known to be related to the leading causes of death including cardiovascular disease , several types of cancer , obesity , type 2 diabetes , depression-suicide and other chronic diseases . In the context of whole dietary patterns , the  Dietary Inflammatory Index  ( DII ® ) was developed to appraise the inflammatory potential of the diet . OBJECTIVE We prospect ively assessed the association between DII scores and all-cause mortality in two large Spanish cohorts and valuated the consistency of findings across these two cohorts and results published based on other cohorts . DESIGN We assessed 18,566 participants in the " Seguimiento Universidad de Navarra " ( SUN ) cohort followed-up during 188,891 person-years and 6790 participants in the " PREvencion con DIeta MEDiterránea " ( PREDIMED ) r and omized trial representing 30,233 person-years of follow-up .  DII scores were calculated in both cohorts from vali date d FFQs . Higher DII scores corresponded to more proinflammatory diets . A total of 230 and 302 deaths occurred in SUN and PREDIMED , respectively . In a r and om-effect meta- analysis we included 12 prospect i ve studies ( SUN , PREDIMED and 10 additional studies ) that assessed the association between DII scores and all-cause mortality . RESULTS After adjusting for a wide array of potential confounders , the comparison between extreme quartiles of the DII showed a positive and significant association with all-cause mortality in both the SUN ( hazard ratio [ HR ] = 1.85 ; 95 % CI : 1.15 , 2.98 ; P-trend = 0.004 ) and the PREDIMED cohort ( HR = 1.42 ; 95 % CI : 1.00 , 2.02 ; P-trend = 0.009 ) . In the meta- analysis of 12 cohorts , the DII was significantly associated with an increase of 23 % in all-cause mortality ( 95 % CI : 16%- 
    Output:
    
Conclusion : The findings proposed that adherence to diets with high DII ® scores was associated with increased WC .