Alzheimer’s disease (AD) and vascular dementia are the 2 most common types of dementia. Gout, a form of inflammatory arthritis, has recently emerged as a topic of interest in the context of dementia. Understanding the relationship between gout and dementia could provide valuable insights into potential preventive and therapeutic strategies for these conditions.
A recent meta-analysis in Frontiers of Aging Neuroscience sought to investigate the association between gout and the risk of all-cause dementia, AD, and vascular dementia. “Because of the importance of the issue, the limitations of the previous review, and the availability of new evidence, we conducted a systematic review and meta-analysis to evaluate the association between gout alone and the risk of all-cause dementia,” the authors wrote.
The data included 6 cohort studies involving 2,349,605 individuals, which were collected from multiple sources, including PubMed, Embase, the Cochrane Library, and the reference lists of the studies included. Cohort studies were selected to examine the association between gout and the risk of all-cause dementia, AD, and vascular dementia. The risk of bias in the included studies was evaluated using the Newcastle-Ottawa Quality Assessment Scale. The overall certainty of evidence was assessed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) system. Risk ratios (RRs) and 95% CI were calculated using a random-effects model to pool the data, and publication bias was assessed through funnel plots and Egger’s test.
Regarding the results of the analysis, the authors of the study wrote, “Our meta-analysis involving 2,349,605 individuals found a reduced risk of all-cause dementia in patients with gout, particularly in those with a history of medication therapy. Meanwhile, gout seems to be a protective factor for AD and vascular dementia, although the quality of evidence is low or very low.”
Gout patients showed a decreased risk of all-cause dementia compared with individuals without gout. The RR was 0.67 (95% CI, 0.51-0.89), indicating a significant association. However, the quality of evidence supporting this finding was deemed very low by the authors.
The risk of AD was also reduced in gout patients, with an RR of 0.70 (95% CI, 0.63-0.79). This result suggests a potentially protective effect of gout against AD. However, the quality of evidence supporting this association was again classified as very low.
Gout patients exhibited a decreased risk of vascular dementia compared with those without gout, with an RR of 0.68 (95% CI, 0.49-0.95). This finding suggests a potential protective role of gout against vascular dementia. Similar to the other associations, the quality of evidence supporting this link was classified as very low.
“The main advantage of our meta-analysis is the application of the GRADE system for grading the quality of evidence, which seems to be relatively rare in previous meta-analyses based on observational studies,” the authors noted, although they addressed several limitations of the study.
Importantly, the analysis indicated substantial heterogeneity among the included studies. Nevertheless, sensitivity analysis suggested that the results were robust, and there was limited evidence of publication bias. Firstly, there is clinical heterogeneity among the gout patients included in the analysis. Variations in the severity, disease status, and duration of gout among the patients may introduce inconsistencies in the results. Secondly, the meta-analysis exhibits a notable degree of statistical heterogeneity, as indicated by the larger I2 value. Although sensitivity analysis was performed to assess the robustness of the results, the presence of heterogeneity decreases the overall reliability of the findings.
In conclusion, the authors said, “The risk of all-cause dementia, AD, and vascular dementia is decreased in gout patients, but the quality of evidence is generally low. More studies are still needed to validate and explore the mechanisms of this association.”
Source: Frontiers in Aging Neuroscience