***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: Background : Failure to adhere to medication regimes is a significant problem in clinical and research setting s yet reliable , consistent identification of key psychosocial predictors remains elusive . Studies of mood and personality related to adherence show mixed results —compliance and objective ly measured cognitive function are intuitively related but empirical support is lacking . Purpose : This study is a secondary analysis to examine the relations between adherence with a medication regime for lowering serum cholesterol and several domains of psychological and cognitive functioning . Methods : Participants in the initial study completed a measure of personality and a battery of neuropsychological measures  at baseline ; anxiety and depression  were measured at baseline and at 4-week intervals .  Medication adherence was tracked with electronic cap monitors for 24 weeks . Results : Only 23 % of the sample was fully adherent to medication regimes at least 80 % of the time over the 6-month study period . Conscientiousness , according to the Five Factor Theory of Personality , and estimated IQ remained robust predictors of adherence in hierarchical regression analyses . Depression and anxiety , mental flexibility , and visuospatial-constructional ability were less robust but statistically significant ( p < .05 ) correlates of adherence . Conclusions : Although results of this analysis explain only a portion of the variance in adherence , they demonstrate the importance of trait psychological and cognitive factors in adherence research Previous findings on the association of statins , plasma lipids , and  Parkinson 's disease ( PD ) are confounded by the fact that statins also affect lipid profiles . We prospect ively examined plasma lipids and  statin  use in relation to PD in the Atherosclerosis Risk in Communities ( ARIC ) Study .  Statin use and plasma lipids were assessed at baseline ( visit 1 , 1987 - 89 ) and at three triennial visits thereafter ( visits 2 - 4 ) until 1998 . Potential PD cases were identified from multiple sources and vali date d where possible . The primary analysis was limited to incident PD cases diagnosed between 1998 and 2008 . Odds ratios and 95 % confidence intervals were derived from multivariate logistic regression models .  Statin use was rare at baseline ( 0.57 % ) but increased to 11.2 % at visit 4 . During this time frame , total-cholesterol levels decreased , particularly among statin users . Fifty-six PD cases were identified after 1998 . Statin use before 1998 was associated with significantly higher PD risk after 1998 ( odds ratio = 2.39 , 95 % confidence interval 1.11 - 5.13 ) after adjusting for total cholesterol and other confounders . Conversely , higher total cholesterol was associated with lower risk for PD after adjustment for statin usage and confounders . Compared with the lowest tertile of average total cholesterol , the odds ratios for PD were 0.56 ( 0.30 - 1.04 ) for the second and 0.43 ( 0.22 - 0.87 ) for the third tertile ( P(trend ) = 0.02 ) . Statin use may be associated with a higher PD risk , whereas higher total cholesterol may be associated with lower risk . These data are inconsistent with the hypothesis that statins are protective against PD OBJECTIVE To prospect ively examine whether use of statins is associated with altered risk of Parkinson disease ( PD ) .  DESIGN , SETTING , AND PARTICIPANTS A prospect i ve study including 38 192 men and 90 874 women participating in 2 ongoing US cohorts , the Health Professional Follow-up Study and the Nurses ' Health Study , was conducted . Information on regular cholesterol-lowering drug use ( ≥2 times/wk ) was collected in 1994 in both cohorts via question naire . Relative risks ( RRs ) and 95 % CIs were computed using Cox proportional hazards models adjusting for age , smoking , caffeine intake , duration of hypercholesterolemia , and other covariates . MAIN OUTCOME MEASURE Incident PD . RESULTS During 12 years of follow-up ( 1994 - 2006 ) , we documented 644 incident PD cases ( 338 women and 306 men ) . The risk of PD was lower among current statin users ( adjusted pooled RR = 0.74 ; 95 % CI , 0.54 - 1.00 ; P = .049 ) relative to nonusers . A significant association was observed in participants younger than 60 years at baseline ( adjusted pooled RR = 0.31 ; 95 % CI , 0.11 - 0.86 ; P = .02 ) but not among those who were older ( adjusted pooled RR = 0.83 ; 95 % CI , 0.60 - 1.14 ; P = .25 ) ( P for interaction = .03 ) . CONCLUSIONS We found that regular use of statins was associated with a modest reduction in PD risk . The possibility that some statins may reduce PD risk deserves further consideration Objective To quantify the unintended effects of statins according to type , dose , and duration of use . Design Prospect i ve open cohort study using routinely collected data . Setting 368 general practice s in Engl and and Wales supplying data to the Q Research data base . Participants 2 004 692 patients aged 30 - 84 years of whom 225 922 ( 10.7 % ) were new users of statins : 159 790 ( 70.7 % ) were prescribed simvastatin  , 50 328 ( 22.3 % ) atorvastatin , 8103 ( 3.6 % ) pravastatin , 4497 ( 1.9 % ) rosuvastatin , and 3204 ( 1.4 % ) fluvastatin . Methods Cox proportional hazards models were used to estimate effects of statin type , dose , and duration of use . The number needed to treat ( NNT ) or number needed to harm ( NNH ) was calculated and numbers of additional or fewer cases estimated for 10 000 treated patients . Main outcome measure First recorded occurrence of cardiovascular disease , moderate or serious myopathic events , moderate or serious liver dysfunction , acute renal failure , venous thromboembolism , Parkinson ’s disease , dementia , rheumatoid arthritis , cataract , osteoporotic fracture , gastric cancer , oesophageal cancer , colon cancer , lung cancer , melanoma , renal cancer , breast cancer , or prostate cancer . Results Individual statins were not significantly associated with risk of Parkinson ’s disease , rheumatoid arthritis , venous thromboembolism , dementia , osteoporotic fracture , gastric cancer , colon cancer , lung cancer , melanoma , renal cancer , breast cancer , or prostate cancer . Statin use was associated with decreased risks of oesophageal cancer but increased risks of moderate or serious liver dysfunction , acute renal failure , moderate or serious myopathy , and cataract . Adverse effects were similar across statin types for each outcome except liver dysfunction where risks were highest for fluvastatin . A dose-response effect was apparent for acute renal failure and liver dysfunction . All increased risks persisted during treatment and were highest in the first year . After stopping treatment the risk of cataract returned to normal within a year in men and women . Risk of oesophageal cancer returned to normal within a year in women and within 1 - 3 years in men . Risk of acute renal failure returned to normal within 1 - 3 years in men and women , and liver dysfunction within 1 - 3 years in women and from three years in men . Based on the 20 % threshold for cardiovascular risk , for women the NNT with any statin to prevent one case of cardiovascular disease over five years was 37 ( 95 % confidence interval 27 to 64 ) and for oesophageal cancer was 1266 ( 850 to 3460 ) and for men the respective values were 33 ( 24 to 57 ) and 1082 ( 711 to 2807 ) . In women the NNH for an additional case of acute renal failure over five years was 434 ( 284 to 783 ) , of moderate or severe myopathy was 259 ( 186 to 375 ) , of moderate or severe liver dysfunction was 136 ( 109 to 175 ) , and of cataract was 33 ( 28 to 38 ) . Overall , the NNHs and NNTs for men were similar to those for women , except for myopathy where the NNH was 91 ( 74 to 112 ) . Conclusions Cl aims of unintended benefits of statins , except for oesophageal cancer , remain unsubstantiated , although potential adverse effects at population level were confirmed and quantified . Further studies are needed to develop utilities to individualise the risks so that patients at highest risk of adverse events can be monitored closely Several recent findings suggest a role of lipid and cholesterol metabolism in the pathogenesis of Parkinson 's disease . Therefore , the authors examined the association between serum levels of cholesterol  and the  risk of Parkinson 's disease in the prospect i ve , population -based Rotterdam Study among 6,465 subjects aged 55 or more years with repeated in-person examination and on average 9.4 years of follow-up ( 1990 - 2004 ) . Higher serum levels of total cholesterol were associated with a significantly decreased risk of Parkinson 's disease ( age- and sex-adjusted hazard ratio per mmol/liter increase in cholesterol = 0.77 , 95 % confidence interval : 0.64 , 0.94 ) , with evidence for a dose-effect relation . The association was restricted to women and remained unchanged after adjustment for multiple potential confounders . These findings may indicate a role of lipids in the pathogenesis of Parkinson 's disease . Alternatively , they could reflect the strong correlation-especially in women-between levels of serum cholesterol and the antioxidant coenzyme Q10 .  If confirmed , this would provide further support for an important role of oxidative stress in the pathogenesis of Parkinson 's disease Objective : To determine whether history of hypertension , hypercholesterolemia , or diabetes is associated with risk of Parkinson disease ( PD ) . Methods : Prospect i ve study among participants in two large cohorts : the Nurses ’ Health Study ( 121,046 women ) and the Health Professionals Follow-up Study ( 50,833 men ) . Mean duration of follow-up was 22.9 years in women , aged 30 to 55 years at baseline , and 12.6 years in men , aged 40 to 75 years at baseline . Relative risks ( RRs ) of PD were estimated from a Cox proportional hazards model adjusting for potential confounders . Results : We identified a total of 530 incident cases of PD during the follow-up .  Risk of PD was not associated with self-reported history of hypertension ( RR = 0.96 , 95 % CI = 0.80 to 1.15 ) , high cholesterol ( RR = 0.98 , 95 % CI = 0.82 to 1.19 ) , or diabetes ( RR = 1.04 , 95 % CI = 0.74 to 1.46 ) , after adjusting for age and smoking in pack-years . Risk of PD decreased modestly with increasing levels of self-reported total cholesterol  ( RR for a 50-mg/dL increase in total cholesterol = 0.86 , 95 % CI = 0.78 to 0.95 , p for trend = 0.02 ) , but use of cholesterol-lowering drugs was not associated with PD risk ( RR comparing users with nonusers = 0.85 , 95 % CI = 0.59 to 1.23 ) . Among individuals with PD , systolic blood pressure was similar to noncases up to the time of diagnosis but declined afterward . Conclusions : Results of this large prospect i ve study suggest that Parkinson disease risk is not significantly related to history of hypertension , hypercholesterolemia , or diabetes but may modestly decline with increasing blood cholesterol levels . GLOSSARY : ACE = angiotensin-converting enzyme ; BMI = body mass index ; DBP = diastolic blood pressure ; HPFS = Health Professionals Follow-up Study ; METS = metabolic equivalent tasks ; NHS = Nurses ’ Health Study ; NSAID = nonsteroidal anti-inflammatory drug ; PD = Parkinson disease ; RR = relative risk ; SBP = systolic blood pressure Low-density  lipoprotein cholesterol ( LDL-C )  levels are suggested to be associated inversely with Parkinson 's disease ( PD ) . To test the hypothesis that LDL-C levels may increase PD risk , we studied a prospect i ve cohort of 3,233 men ( Honolulu-Asia Aging Study ) for whom the LDL-C from fasting lipid profiles was obtained during 1991 to 1993 . The cohort was followed longitudinally until 2001 for incident Parkinson 's cases . During follow-up , 41 men developed PD ( 18.4/10,000 person-years ) . Although the incidence of PD increased with decreasing LDL-C in a dose-dependent manner , the association 
    Output:
    
The apparent protective effect of statins on risk of PD is at least partially explained by confounding by statin indication .