PubMed · 8367341
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
L Sarna. 1993. Reader comments on recent article.. https://pubmed.ncbi.nlm.nih.gov/8367341/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Observational studies suggest an association between glioblastoma (GBM) and cardiovascular diseases (CVDs), but a causal relationship remains unestablished. This study aimed to investigate the causal link between multiple CVDs and GBM risk. The inverse variance weighted method indicated that all 18 CVDs had significant causal associations with GBM (P < .05). Genetically predicted CVDs were uniformly associated with a lower risk of GBM (odds ratio < 1), identifying them as potential protective factors. Sensitivity analyses confirmed the absence of significant heterogeneity or horizontal pleiotropy, and the MR-Steiger test validated the correct causal direction. This Mendelian randomization (MR) study provides evidence that a range of CVDs are causally associated with a decreased risk of developing GBM. These findings suggest shared biological pathways and offer new insights for understanding GBM etiology. We conducted a 2-sample MR analysis using publicly available genome-wide association study data. GBM was the outcome, and 18 cardiovascular-related traits (including coronary artery disease, myocardial infarction, and venous thromboembolism) were exposures. Instrumental variables were single-nucleotide polymorphisms significantly associated with exposures (P < 5 × 10-8). The primary analysis used the inverse variance weighted method, supplemented with MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses, including Cochran Q test, MR-Egger intercept test, leave-one-out analysis, and MR-Steiger directionality test, were performed to ensure robustness.
OBJECTIVE: To assess whether causal criteria can be used to find out whether there is support in published research for maintaining that menopause causes depression. DESIGN: Ninety four articles from 30 years of research examining the relation of natural menopause to depression were traced by using Medline and systematic follow up of reference lists. Specified exclusion and inclusion criteria were applied, and the resulting 43 epidemiological primary research articles were classified and tabulated according to sample and measures used and the researchers' own conclusion as to whether or not an association had been established. This material was qualitatively evaluated with Hill's nine criteria for causality. RESULT: There is insufficient evidence at present to maintain that menopause causes depression. In addition to methodological and statistical problems, a temporal problem in the menopause concept hinders research in this area. CONCLUSION: Causal criteria can usefully be used to structure a literature review. Further theoretical work is required to integrate standard clinical epidemiological concepts.
Symptoms witnessed by a bed partner are probably the strongest clue. Polysomnography confirms the diagnosis. Lifestyle changes, continuous positive airway pressure, or oral/dental devices are often effective.