Caffeine consumption and risk of dyskinesia in CALM-PD.
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ABSTRACT:
SUBMITTER: Wills AM
PROVIDER: S-EPMC3608707 | biostudies-literature | 2013 Mar
REPOSITORIES: biostudies-literature
Publications
Caffeine consumption and risk of dyskinesia in CALM-PD.
Wills Anne-Marie A AM Eberly Shirley S Tennis Marsha M Lang Anthony E AE Messing Susan S Togasaki Daniel D Tanner Caroline M CM Kamp Cornelia C Chen Jiang-Fan JF Oakes David D McDermott Michael P MP Schwarzschild Michael A MA
Movement disorders : official journal of the Movement Disorder Society 20130121 3
<h4>Background</h4>Adenosine A2A receptor antagonists reduce or prevent the development of dyskinesia in animal models of levodopa-induced dyskinesia.<h4>Methods</h4>We examined the association between self-reported intake of the A2A receptor antagonist caffeine and time to dyskinesia in the Comparison of the Agonist Pramipexole with Levodopa on Motor Complications of Parkinson's Disease (CALM-PD) and CALM Cohort extension studies, using a Cox proportional hazards model adjusting for age, baseli ...[more]
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Project description:BACKGROUND:Caffeine has been shown to prevent ultraviolet radiation-induced carcinogenesis and to inhibit growth of melanoma cells in experimental studies. We evaluated the association among caffeine intake, coffee consumption, and melanoma risk among three large cohort studies. METHODS:The analysis used data from 89,220 women in the Nurses' Health Study II (1991-2009), 74,666 women in the Nurses' Health Study (1980-2008), and 39,424 men in the Health Professionals Follow-up Study (1986-2008). We used Cox proportional hazards models to estimate the hazard ratios (HR) with 95% confidence intervals (CIs) of melanoma associated with dietary intakes. RESULTS:We documented 2,254 melanoma cases over 4 million person-years of follow-up. After adjustment for other risk factors, higher total caffeine intake was associated with a lower risk of melanoma (?393 mg/day vs. <60 mg/day: HR = 0.78, 95% CI = 0.64, 0.96; Ptrend = 0.048). The association was more apparent in women (?393 mg/day vs. <60 mg/day: HR = 0.70, 95% CI = 0.58, 0.85; Ptrend = 0.001) than in men (HR = 0.94, 95% CI = 0.75, 1.2; Ptrend = 0.81), and more apparent for melanomas occurring on body sites with higher continuous sun exposure (head, neck, and extremities; ?393 mg/day vs. <60 mg/day: HR = 0.71, 95% CI = 0.59, 0.86; Ptrend = 0.001) than for melanomas occurring on body sites with lower continuous sun exposure (trunk including shoulder, back, hip, abdomen, and chest; HR = 0.90, 95% CI = 0.70, 1.2; Ptrend = 0.60). This pattern of association was similar to that for caffeinated coffee consumption, whereas no association was found for decaffeinated coffee consumption and melanoma risk. CONCLUSIONS:Increasing caffeine intake and caffeinated coffee consumption is associated with decreased risk of cutaneous malignant melanomas.
| S-EPMC4600068 | biostudies-literature
Project description:Study questionIs caffeine and caffeinated beverage consumption associated with the risk of spontaneous abortion (SAB)?Summary answerWhile preconceptional caffeine consumption was not materially associated with an increased risk of SAB, consumption during early pregnancy was associated with a small increased risk of SAB, although the relation was not linear.What is known alreadyCaffeine has been hypothesized as a risk factor for SAB since the 1980s; however, results from previous studies have been conflicting.Study design, size, durationThis prospective cohort study included 5132 Danish women planning pregnancy and enrolled from 2007 to 2010.Participants/materials, setting, methodsParticipants were women who conceived after entry into the Snart-Gravid cohort and who were aged 18-40, in a stable relationship with a male partner, and did not use fertility treatments to conceive. Women reported their daily caffeine and caffeinated beverage consumption on questionnaires before conception and during early pregnancy. All exposure measurements were prospective with respect to outcome ascertainment. We estimated hazard ratios (HRs) of SAB for categories of caffeine consumption in milligrams (mg) per day and the corresponding 95% confidence intervals (CIs) using Cox proportional hazards regression models with gestational weeks as the time scale.Main results and the role of chanceThere were 732 women (14.3%) who were identified as having a SAB. In the preconceptional period, caffeine consumption was not materially associated with SAB risk (HR comparing ≥300 with <100 mg/day: 1.09; 95% CI: 0.89, 1.33). In early pregnancy, the HRs for 100-199, 200-299 and ≥300 mg/day of caffeine consumption were 1.62 (95% CI: 1.19, 2.22), 1.48 (95% CI: 1.03, 2.13) and 1.23 (95% CI: 0.61, 2.46), respectively, compared with that for <100 mg/day.Limitations, reasons for cautionThe observed results may be affected by non-differential exposure misclassification, reverse causation and residual confounding.Wider implications of the findingsThis is the largest study to date of prospectively measured, preconception caffeine consumption and risk of SAB. We were able to reduce the likelihood of differential left truncation bias and recall bias present in other analyses.Study funding/competing interestsSnart-Gravid was funded by the NICHD (R21-050264). Dr. Hahn's work was funded in part by the BU Reproductive, Perinatal, and Pediatric Epidemiology Training Grant NIH #T32HD052458. There are no competing interests.
| S-EPMC4400202 | biostudies-literature
Project description:Caffeine is widely consumed in foods and beverages and is also used for a variety of medical purposes. Despite its widespread use, relatively little is understood regarding how genetics affects consumption, acute response, or the long-term effects of caffeine.This paper reviews the literature on the genetics of caffeine from the following: (1) twin studies comparing heritability of consumption and of caffeine-related traits, including withdrawal symptoms, caffeine-induced insomnia, and anxiety, (2) association studies linking genetic polymorphisms of metabolic enzymes and target receptors to variations in caffeine response, and (3) case-control and prospective studies examining relationship between polymorphisms associated with variations in caffeine response to risks of Parkinson's and cardiovascular diseases in habitual caffeine consumers.Twin studies find the heritability of caffeine-related traits to range between 0.36 and 0.58. Analysis of polysubstance use shows that predisposition to caffeine use is highly specific to caffeine itself and shares little common disposition to use of other substances. Genome association studies link variations in adenosine and dopamine receptors to caffeine-induced anxiety and sleep disturbances. Polymorphism in the metabolic enzyme cytochrome P-450 is associated with risk of myocardial infarction in caffeine users.Modeling based on twin studies reveals that genetics plays a role in individual variability in caffeine consumption and in the direct effects of caffeine. Both pharmacodynamic and pharmacokinetic polymorphisms have been linked to variation in response to caffeine. These studies may help guide future research in the role of genetics in modulating the acute and chronic effects of caffeine.
| S-EPMC4242593 | biostudies-literature
Project description:BackgroundThe effect of caffeine intake during pregnancy on the risk of preterm delivery has been studied for the past 3 decades with inconsistent results.ObjectiveWe performed a meta-analysis examining the association between caffeine consumption during pregnancy and risk of preterm birth.DesignWe searched MEDLINE and EMBASE articles published between 1966 and July 2010, cross-referenced reference lists of the retrieved articles, and identified 15 cohort and 7 case-control studies that met inclusion criteria for this meta-analysis.ResultsThe combined odds ratios (ORs) obtained by using fixed-effects models for cohort studies were 1.11 (95% CI: 0.96, 1.28), 1.10 (95% CI: 1.01, 1.19), and 1.08 (95% CI: 0.93, 1.27) for risk of preterm birth comparing the highest with the lowest level of caffeine intake (or no intake) (mg/d) during the first, second, and third trimesters, respectively. Results for the case-control studies yielded no associations for the first (OR: 1.07; 95% CI: 0.84, 1.37), second (OR: 1.17; 95% CI: 0.94, 1.45), or third (OR: 0.94; 95% CI: 0.79, 1.12) trimesters. No overall heterogeneity was found by region, publication decade, exposure and outcome assessment, caffeine sources, or adjustment for confounding, which was largely driven by individual studies.ConclusionIn this meta-analysis, we observed no important association between caffeine intake during pregnancy and the risk of preterm birth for cohort and case-control studies.
| S-EPMC2954446 | biostudies-literature
Project description:The ergogenic effects of caffeine are well documented, yet despite the potential benefits of supplementation, there is a lack of understanding of caffeine habits and supplementation within fencing. British fencers (n = 136) completed a Web-based questionnaire, exploring self-reported caffeine consumption, reasons for use and education. Fencers (94.1%) habitually consumed caffeine, primarily due to the taste of the products (93.8%). Respondents ingested 183.4 ± 137.5 mg of caffeine daily, with a significant difference between age groups (p < 0.05). Many respondents (30.1%) consumed caffeine 60 mins prior/during fencing training and/or competition with the main reason highlighted as cognitive performance enhancement. Respondents ingested 140.8 ± 104.6 mg of caffeine during training/competition, mainly as energy drinks, bars, and powders. Education on caffeine supplementation was low (25.7%), with significant associations between age groups (p < 0.05). Evidence implies caffeine toxicity has been experienced by 35% of fencers, highlighting the need for education on caffeine consumption. To conclude there is evidence of caffeine supplementation in fencing, primarily to magnify cognitive performance. However, there is a requirement for targeted education on caffeine supplementation to fencers, so that negative side effects and potential anti-doping infringements can be avoided.
| S-EPMC9691662 | biostudies-literature
Project description:BackgroundThe association between coffee and caffeine consumption and the risk of renal cell carcinoma was inconsistent among observational studies, and whether these observed associations were causal remained unclear. Therefore, we performed two-sample Mendelian randomization (MR) study to assess the causal nature of the association.Materials and methodsIn this study, 12 and two independent single nucleotide polymorphisms (SNPs) related to coffee and caffeine consumption at a genome-wide significance level of p < 5 × 10-8 were used as instrumental variables (IVs), respectively. Summary-level data for renal cell carcinoma were taken from the FinnGen consortium with up to 174,977 individuals, and the International Agency for Research on Cancer (IARC) with 13,230 individuals. We used inverse-variance weighted (IVW) as the main method, followed by the weighted median method, the MR-Egger regression method, and the MR robust adjusted profile score method. Outlier and pleiotropic variants were assessed by the MR Pleiotropy RESidual Sum and Outlier test and MR-Egger regression. We used meta-analysis methods in fixed-effects to combine the estimates from the two sources.ResultsThe genetically predicted coffee consumption was not associated with the risk of renal cell carcinoma in the FinnGen consortium, and the relationship was consistent in the IARC consortium. The pooled odds ratio (OR) per 50% increase of coffee consumption was 0.752 [95% confidence interval (CI), 0.512-1.105; p = 0.147]. In addition, complementary analyses that separated the coffee-related SNPs according to their relationship with blood levels of caffeine metabolites (higher, lower, or unrelated) found no relationship with renal cell carcinoma. The results were consistent after excluding eight SNPs due to potential risk factors at genome-wide significance (p < 5 × 10-8). Moreover, genetically predicted per 80-mg increase in caffeine consumption was not associated with the risk of renal cell carcinoma (pooled OR = 0.872, 95% CI: 0.676-1.125, p = 0.292).ConclusionOur MR study provided no convincing evidence for a causal effect between coffee and caffeine consumption and the risk of renal cell carcinoma. The associations for renal cell carcinoma need to be verified in well-powered studies.
| S-EPMC9441794 | biostudies-literature
Project description:ImportanceCaffeine is known to decrease vasodilation and have immunosuppressant effects, which may potentially decrease the risk of rosacea. However, the heat from coffee may be a trigger for rosacea flares. The relationship between the risk of rosacea and caffeine intake, including coffee consumption, is poorly understood.ObjectiveTo determine the association between the risk of incident rosacea and caffeine intake, including coffee consumption.Design, setting, and participantsThis cohort study included 82 737 women in the Nurses' Health Study II (NHS II), a prospective cohort established in 1989, with follow-up conducted biennially between 1991 and 2005. All analysis took place between June 2017 and June 2018.ExposuresData on coffee, tea, soda, and chocolate consumption were collected every 4 years during follow-up.Main outcomes and measuresInformation on history of clinician-diagnosed rosacea and year of diagnosis was collected in 2005.ResultsA total of 82 737 women responded to the question regarding a diagnosis of rosacea in 2005 in NHS II and were included in the final analysis (mean [SD] age at study entry, 50.5 [4.6] years). During 1 120 051 person-years of follow-up, we identified 4945 incident cases of rosacea. After adjustment for other risk factors, we found an inverse association between increased caffeine intake and risk of rosacea (hazard ratio for the highest quintile of caffeine intake vs the lowest, 0.76; 95% CI, 0.69-0.84; P < .001 for trend). A significant inverse association with risk of rosacea was also observed for caffeinated coffee consumption (HR, 0.77 for those who consumed ≥4 servings/d vs those who consumed <1/mo; 95% CI, 0.69-0.87; P < .001 for trend), but not for decaffeinated coffee (HR, 0.80; 95% CI, 0.56-1.14; P = .39 for trend). Further analyses found that increased caffeine intake from foods other than coffee (tea, soda, and chocolate) was not significantly associated with decreased risk of rosacea.Conclusions and relevanceIncreased caffeine intake from coffee was inversely associated with the risk of incident rosacea. Our findings do not support limiting caffeine intake as a means to prevent rosacea. Further studies are required to explain the mechanisms of action of these associations, to replicate our findings in other populations, and to explore the relationship of caffeine with different rosacea subtypes.
| S-EPMC6583325 | biostudies-literature
Project description:Caffeine is the most commonly used psychoactive substance, and consumption by adolescents has risen markedly in recent years. We identified the effects of adolescent caffeine consumption on cocaine sensitivity and determined neurobiological changes within the nucleus accumbens (NAc) that may underlie caffeine-induced hypersensitivity to cocaine. Male Sprague-Dawley rats consumed caffeine (0.3?g/l) or water for 28 days during adolescence (postnatal day 28-55; P28-P55) or adulthood (P67-P94). Testing occurred in the absence of caffeine during adulthood (P62-82 or P101-121). Cocaine-induced and quinpirole (D2 receptor agonist)-induced locomotion was enhanced in rats that consumed caffeine during adolescence. Adolescent consumption of caffeine also enhanced the development of a conditioned place preference at a sub-threshold dose of cocaine (7.5?mg/kg, i.p.). These behavioral changes were not observed in adults consuming caffeine for an equivalent period of time. Sucrose preferences were not altered in rats that consumed caffeine during adolescence, suggesting there are no differences in natural reward. Caffeine consumption during adolescence reduced basal dopamine levels and augmented dopamine release in the NAc in response to cocaine (5?mg/kg, i.p.). Caffeine consumption during adolescence also increased the expression of the dopamine D2 receptor, dopamine transporter, and adenosine A1 receptor and decreased adenosine A2A receptor expression in the NAc. Consumption of caffeine during adulthood increased adenosine A1 receptor expression in the NAc, but no other protein expression changes were observed. Together these findings suggest that caffeine consumption during adolescence produced changes in the NAc that are evident in adulthood and may contribute to increases in cocaine-mediated behaviors.
| S-EPMC4330515 | biostudies-literature
Project description:BackgroundCaffeine is the most commonly consumed psycho-stimulant in the world. The effects of caffeine on the body have been extensively studied; however, its effect on the structure of the brain has not been investigated to date.ResultsIn the present study we found that the long-term consumption of caffeine can induce ventriculomegaly; this was observed in 40% of the study rats. In the caffeine-treated rats with ventriculomegaly, there was increased production of CSF, associated with the increased expression of Na(+), K(+)-ATPase and increased cerebral blood flow (CBF). In contrast to the chronic effects, acute treatment with caffeine decreased the production of CSF, suggesting 'effect inversion' associated with caffeine, which was mediated by increased expression of the A1 adenosine receptor, in the choroid plexus of rats chronically treated with caffeine. The involvement of the A1 adenosine receptor in the effect inversion of caffeine was further supported by the induction of ventriculomegaly and Na+, K+-ATPase, in A1 agonist-treated rats.ConclusionThe results of this study show that long-term consumption of caffeine can induce ventriculomegaly, which is mediated in part by increased production of CSF. Moreover, we also showed that adenosine receptor signaling can regulate the production of CSF by controlling the expression of Na(+), K(+)-ATPase and CBF.
| S-EPMC2744679 | biostudies-literature
Project description:BackgroundIt is somewhat controversial whether caffeine consumption is associated with an increased risk of developing atrial fibrillation (AF).ObjectiveWe prospectively assessed the relation between caffeine intake and incident AF.DesignA total of 33,638 initially healthy women who participated in the Women's Health Study and who were gt 45 y of age and free of cardiovascular disease and AF at baseline were prospectively followed for incident AF from 1993 to 2 March 2009. All women provided information on caffeine intake via food-frequency questionnaires at baseline and in 2004.ResultsDuring a median follow-up of 14.4 y (interquartile range: 13.8-14.8 y), 945 AF events occurred. Median caffeine intakes across increasing quintiles of caffeine intake were 22, 135, 285, 402, and 656 mg/d, respectively. Age-adjusted incidence rates of AF across increasing quintiles of caffeine intake were 2.15, 1.89, 2.01, 2.24, and 2.04 events, respectively, per 1000 person-years of follow-up. In Cox proportional hazards models updated in 2004 by using time-varying covariates, the corresponding multivariable-adjusted hazard ratios (95% CI) were 1.0, 0.88 (0.72, 1.06), 0.78 (0.64, 0.95), 0.96 (0.79, 1.16), and 0.89 (0.73, 1.09) (P for linear trend: 0.45). None of the individual components of caffeine intake (coffee, tea, cola, and chocolate) were significantly associated with incident AF.ConclusionsIn this large cohort of initially healthy women, elevated caffeine consumption was not associated with an increased risk of incident AF. Therefore, our data suggest that elevated caffeine consumption does not contribute to the increasing burden of AF in the population. This trial was registered at clinicaltrials.gov as NCT00000479.
| S-EPMC2921535 | biostudies-literature