scholarly journals Coffee Consumption and Risk of Dementia and Alzheimer’s Disease: A Dose-Response Meta-Analysis of Prospective Studies

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1501 ◽  
Author(s):  
Susanna Larsson ◽  
Nicola Orsini

Coffee consumption is associated with a reduced risk of several diseases but uncertainty remains about the influence of coffee consumption on the risk of dementia. We performed a dose-response meta-analysis to summarize the prospective data on coffee consumption and associated risk of dementia and Alzheimer’s disease. We identified studies by searching PubMed (from January 1966) and Web of Science (from January 1945) through 4 October 2018 and by scrutinizing the reference lists of pertinent publications. Two researchers independently reviewed the literature. Results were combined using a restricted cubic spline random-effects dose-response meta-analysis based on a one-stage approach. Eight relevant prospective studies were identified. These studies included 7486 dementia cases diagnosed among 328,885 individuals during an average follow-up of 4.9–25 years. Meta-analysis of all eight studies indicated no statistically significant association between coffee consumption and the risk of dementia and no deviations from a linear trend (p = 0.08). The relative risk of dementia per 1 cup/day increment of coffee consumption was 1.01 (95% confidence interval (CI) 0.98–1.05; p = 0.37). Meta-analysis of five studies that focused on Alzheimer’s disease revealed no association between coffee consumption and Alzheimer’s disease and no deviations from a linear trend (p = 0.79). The relative risk of Alzheimer’s disease per 1 cup/day increment of coffee consumption was 1.01 (95% confidence interval 0.95–1.07; p = 0.80). These results do not support an association between coffee consumption and an increased risk of overall dementia or Alzheimer’s disease specifically, but further research on the association of coffee consumption with dementia risk is needed.

Author(s):  
Ahmet Turan Isik ◽  
Neziha Erken ◽  
Idil Yavuz ◽  
Derya Kaya ◽  
Mehmet Selman Ontan ◽  
...  

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S641-S641
Author(s):  
Shanna L Burke

Abstract Little is known about how resting heart rate moderates the relationship between neuropsychiatric symptoms and cognitive status. This study examined the relative risk of NPS on increasingly severe cognitive statuses and examined the extent to which resting heart rate moderates this relationship. A secondary analysis of the National Alzheimer’s Coordinating Center Uniform Data Set was undertaken, using observations from participants with normal cognition at baseline (13,470). The relative risk of diagnosis with a more severe cognitive status at a future visit was examined using log-binomial regression for each neuropsychiatric symptom. The moderating effect of resting heart rate among those who are later diagnosed with mild cognitive impairment (MCI) or Alzheimer’s disease (AD) was assessed. Delusions, hallucinations, agitation, depression, anxiety, elation, apathy, disinhibition, irritability, motor disturbance, nighttime behaviors, and appetite disturbance were all significantly associated (p<.001) with an increased risk of AD, and a reduced risk of MCI. Resting heart rate increased the risk of AD but reduced the relative risk of MCI. Depression significantly interacted with resting heart rate to increase the relative risk of MCI (RR: 1.07 (95% CI: 1.00-1.01), p<.001), but not AD. Neuropsychiatric symptoms increase the relative risk of AD but not MCI, which may mean that the deleterious effect of NPS is delayed until later and more severe stages of the disease course. Resting heart rate increases the relative risk of MCI among those with depression. Practitioners considering early intervention in neuropsychiatric symptomology may consider the downstream benefits of treatment considering the long-term effects of NPS.


2021 ◽  
Author(s):  
Dongqing Gu ◽  
Shan Ou ◽  
Guodong Liu

Introduction: Previous studies have investigated the potential role of traumatic brain injury (TBI) in subsequent development of dementia and Alzheimer’s disease (AD) but reported inconsistent results. We aim to determine the association between TBI and subsequent occurrence of dementia and AD. Methods: We performed a systematic search in PubMed and Web of Science for studies that quantitatively investigated the association between TBI and risk of dementia and AD and were published on or before September 21, 2021. A random-effect model was used to combine the estimates. Results: Twenty-five eligible articles were included in this meta-analysis. The results suggested that TBI was associated with an increased risk of dementia (pooled odds ratio [OR] = 1.81, 95% confidence interval [CI] = 1.53 - 2.14). However, no association was observed between TBI and Alzheimer’s disease (pooled OR = 1.02, 95% CI = 0.91 - 1.15). In the subgroup analysis, TBI with loss of consciousness was not associated with risk of dementia (pooled OR = 0.96, 95% CI = 0.84 - 1.09). Besides, Asian ethnicity, male gender, and mean age of the participants less than 65 were associated with a higher risk of dementia. Conclusion: Our study suggests an increased risk of dementia among individuals with TBI, highlighting the need for more intensive medical monitoring and health education in individuals with TBI. Biological mechanisms linking TBI and the development of dementia are needed in future studies.


Author(s):  
Lars-Gunnar Gunnarsson ◽  
Lennart Bodin

Objectives: To carry out an integrated and stratified meta-analysis on occupational exposure to electromagnetic fields (EMFs), metals and pesticides and its effects on amyotrophic lateral sclerosis (ALS) and Parkinson’s and Alzheimer’s disease, and investigate the possibility of publication bias. Methods: In the current study, we updated our recently published meta-analyses on occupational exposures in relation to ALS, Alzheimer’s and Parkinson’s disease. Based on 66 original publications of good scientific epidemiological standard, according to the Meta-analysis of Observational Studies in Epidemiology (MOOSE) and the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) guidelines, we analysed subgroups by carrying out stratified meta-analyses on publication year, statistical precision of the relative risk (RR) estimates, inspection of the funnel plots and test of bias. Results: Based on 19 studies the weighted RR for occupational exposure to EMFs was 1.26 (95% confidence interval (CI) 1.07–1.50) for ALS, 1.33 (95% CI 1.07–1.64) for Alzheimer’s disease and 1.02 (95% CI 0.83–1.26) for Parkinson’s disease. Thirty-one studies concerned occupational exposure to pesticides and the weighted RR was 1.35 (95% CI 1.02–1.79) for ALS, 1.50 (95% CI 0.98–2.29) for Alzheimer’s disease and 1.66 (95% CI 1.42–1.94) for Parkinson’s disease. Finally, 14 studies concerned occupational exposure to metals and only exposure to lead (five studies) involved an elevated risk for ALS or Parkinson’s disease and the weighted RR was 1.57 (95% CI 1.11–2.20). The weighted RR for all the non-lead exposures was 0.97 (95% CI 0.88–1.06). Conclusions: Exposure to pesticides increased the risk of getting the mentioned neurodegenerative diseases by at least 50%. Exposure to lead was only studied for ALS and Parkinson’s disease and involved 50% increased risk. Occupational exposure to EMFs seemed to involve some 10% increase in risk for ALS and Alzheimer’s disease only.


2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Chris B. Guure ◽  
Noor A. Ibrahim ◽  
Mohd B. Adam ◽  
Salmiah Md Said

The association of physical activity with dementia and its subtypes has remained controversial in the literature and has continued to be a subject of debate among researchers. A systematic review and meta-analysis of longitudinal studies on the relationship between physical activity and the risk of cognitive decline, all-cause dementia, Alzheimer’s disease, and vascular dementia among nondemented subjects are considered. A comprehensive literature search in all available databases was conducted up until April 2016. Well-defined inclusion and exclusion criteria were developed with focus on prospective studies ≥ 12 months. The overall sample from all studies is 117410 with the highest follow-up of 28 years. The analyses are performed with both Bayesian parametric and nonparametric models. Our analysis reveals a protective effect for high physical activity on all-cause dementia, odds ratio of 0.79, 95% CI (0.69, 0.88), a higher and better protective effect for Alzheimer’s disease, odds ratio of 0.62, 95% CI (0.49, 0.75), cognitive decline odds ratio of 0.67, 95% CI (0.55, 0.78), and a nonprotective effect for vascular dementia of 0.92, 95% CI (0.62, 1.30). Our findings suggest that physical activity is more protective against Alzheimer’s disease than it is for all-cause dementia, vascular dementia, and cognitive decline.


2014 ◽  
Vol 112 (5) ◽  
pp. 725-734 ◽  
Author(s):  
D. C. Greenwood ◽  
D. E. Threapleton ◽  
C. E. L. Evans ◽  
C. L. Cleghorn ◽  
C. Nykjaer ◽  
...  

The intake of sugar-sweetened soft drinks has been reported to be associated with an increased risk of type 2 diabetes, but it is unclear whether this is because of the sugar content or related lifestyle factors, whether similar associations hold for artificially sweetened soft drinks, and how these associations are related to BMI. We aimed to conduct a systematic literature review and dose–response meta-analysis of evidence from prospective cohorts to explore these issues. We searched multiple sources for prospective studies on sugar-sweetened and artificially sweetened soft drinks in relation to the risk of type 2 diabetes. Data were extracted from eleven publications on nine cohorts. Consumption values were converted to ml/d, permitting the exploration of linear and non-linear dose–response trends. Summary relative risks (RR) were estimated using a random-effects meta-analysis. The summary RR for sugar-sweetened and artificially sweetened soft drinks were 1·20/330 ml per d (95 % CI 1·12, 1·29,P< 0·001) and 1·13/330 ml per d (95 % CI 1·02, 1·25,P= 0·02), respectively. The association with sugar-sweetened soft drinks was slightly lower in studies adjusting for BMI, consistent with BMI being involved in the causal pathway. There was no evidence of effect modification, though both these comparisons lacked power. Overall between-study heterogeneity was high. The included studies were observational, so their results should be interpreted cautiously, but findings indicate a positive association between sugar-sweetened soft drink intake and type 2 diabetes risk, attenuated by adjustment for BMI. The trend was less consistent for artificially sweetened soft drinks. This may indicate an alternative explanation, such as lifestyle factors or reverse causality. Future research should focus on the temporal nature of the association and whether BMI modifies or mediates the association.


2019 ◽  
Vol 104 (11) ◽  
pp. 5349-5359 ◽  
Author(s):  
Asma Salari-Moghaddam ◽  
Alireza Milajerdi ◽  
Pamela J Surkan ◽  
Bagher Larijani ◽  
Ahmad Esmaillzadeh

Abstract Context Prospective studies on caffeine and different types of coffee intake in relation to the risk of ovarian cancer have shown conflicting results. Objective The aim of the present study was to perform a dose–response meta-analysis of cohort studies on the association between dietary caffeine intake, different types of coffee consumption, and the risk of ovarian cancer. Data sources PubMed/Medline, ISI Web of Science, Scopus, and EMBASE were searched to identify relevant studies reported until October 2018. Study selection Prospective cohort studies that had considered caffeine or different types of coffee as the exposure variable and ovarian cancer as the main outcome variable or as one of the outcome variables were included in our systematic review and meta-analysis. Two of us independently screened 9344 publications. A total of 14 cohort studies were included in the meta-analysis. Data extraction Two of us independently extracted the data. Any disagreements were resolved in consultation with the principal investigator. Results Combining 13 effect sizes, we found no substantial association between coffee consumption and risk of ovarian cancer [risk ratio (RR), 1.08; 95% CI, 0.89 to 1.33]. Also, one additional cup daily of coffee consumption was marginally associated with an increased risk of ovarian cancer (RR, 1.02; 95% CI, 0.99 to 1.05; P = 0.21; I2 = 0.0%; Pheterogeneity = 0.68). No statistically significant association was observed between caffeine intake or caffeinated or decaffeinated coffee consumption and the risk of ovarian cancer. Conclusions We found no statistically significant association between caffeine intake or different types of coffee and the risk of ovarian cancer.


2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Zhi-Wei Dai ◽  
Ke-Dan Cai ◽  
Fu-Rong Li ◽  
Xian-Bo Wu ◽  
Guo-Chong Chen

Abstract Background Current evidence remains equivocal as to whether and how consumption of coffee may be associated with risk of bladder cancer, and potential influence of confounding by smoking on this association is yet to be elucidated. We conducted an updated meta-analysis of prospective studies to address these issues. Methods Relevant studies were identified by searching PubMed and EMBASE databases from inception to April 2019. A random-effects model was used to estimate summary relative risk (RR) with corresponding 95% confidence interval (CI) of bladder cancer associated with coffee consumption. Results The final analysis included 16 prospective studies comprising 2,122,816 participants and 11,848 bladder cancer cases. Overall, coffee consumption was not associated with risk of bladder cancer (RR high-vs-low = 1.07, 95% CI: 0.96–1.20). The lack of association persisted in the strata defined by sex or participants’ smoking status. Meta-regression analyses identified the number cases (Pdifference = 0.06) and the degree of adjustment for smoking (Pdifference = 0.04) as potential sources of heterogeneity. There was an increased risk of bladder cancer related to higher coffee consumption among studies with fewer cases (RR high-vs-low = 1.38, 95% CI: 1.05–1.81) and among those with poorer adjustment for smoking (RR high-vs-low = 1.48, 95% CI: 1.14–1.93). Results were similar in the dose-response analyses (RR 1 cup/d = 1.01, 95% CI: 0.98–1.03). Conclusion Best evidence available to date does not support an independent association between coffee consumption and bladder cancer risk. Some direct associations observed in individual studies may be a result of residual confounding by smoking.


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