scholarly journals Blood lipids and prostate cancer: a Mendelian randomization analysis

2016 ◽  
Vol 5 (6) ◽  
pp. 1125-1136 ◽  
Author(s):  
Caroline J. Bull ◽  
Carolina Bonilla ◽  
Jeff M. P. Holly ◽  
Claire M. Perks ◽  
Neil Davies ◽  
...  

2018 ◽  
Vol 110 (9) ◽  
pp. 1035-1038 ◽  
Author(s):  
James Yarmolinsky ◽  
Carolina Bonilla ◽  
Philip C Haycock ◽  
Ryan J Q Langdon ◽  
Luca A Lotta ◽  
...  


2017 ◽  
Author(s):  
Tracy M. Layne ◽  
Shakira M. Nelson ◽  
Stephanie J. Weinstein ◽  
Eric Karlins ◽  
Stephen J. Chanock ◽  
...  


2021 ◽  
Author(s):  
Liangliang Ren ◽  
Chenhao Yu ◽  
Zhenwei Zhou ◽  
Gonghui Li

Abstract Background: Previous observational studies showed a conflict with the correlation between circulating adiponectin levels and prostate cancer. Methods: In this study, we employed Mendelian randomization analysis to identify the causal effects between them. 14 single nucleotide polymorphisms were screened from the largest-scale genome-wide association study meta-analysis of adiponectin in a multi-ethnic population. The SNP outcome effects were obtained from Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome and Japanese Encyclopedia of Genetic Associations by Riken. Inverse variance weighted model with random-effects was the main effect estimation in our study, alongside weighted median, MR-Egger, and weighted mode models.Results: The results showed no significant causal estimate but a potential protective effect of adiponectin on prostate cancer. In addition, two other research of adiponectin repeated the analysis to avoid the bias of human species showing the similar results. Conclusion: Our study did not provide significant evidence to support the causal effects of circulating adiponectin levels on prostate cancer, but most of our results showed a potential protective effect requiring larger-scale MR analysis to confirm.



2017 ◽  
Author(s):  
James Yarmolinsky ◽  
Carolina Bonilla ◽  
Philip C Haycock ◽  
Ryan JQ Langdon ◽  
Luca A Lotta ◽  
...  

AbstractIn the Selenium and Vitamin E Cancer Prevention Trial (SELECT), selenium supplementation (causing a median 114 μg/L increase in circulating selenium) did not lower overall prostate cancer risk, but increased risk of high-grade prostate cancer and type 2 diabetes. Mendelian randomization analysis uses genetic variants to proxy modifiable risk factors and can strengthen causal inference in observational studies. We constructed a genetic risk score comprising eleven single-nucleotide polymorphisms robustly (P<5x10−8) associated with circulating selenium in genome-wide association studies. In a Mendelian randomization analysis of 72,729 men in the PRACTICAL Consortium (44,825 cases, 27,904 controls), 114 μg/L higher genetically-elevated circulating selenium was not associated with prostate cancer (OR: 1.01; 95% CI: 0.89-1.13). Concordant with findings from SELECT, selenium was weakly associated with advanced (including high-grade) prostate cancer (OR: 1.21; 95% CI: 0.98-1.49) and type 2 diabetes (OR: 1.18; 95% CI: 0.97-1.43; in a type 2 diabetes GWAS meta-analysis with up to 49,266 cases, 249,906 controls). Mendelian randomization mirrored the outcome of selenium supplementation in SELECT and may offer an approach for the prioritization of interventions for follow-up in large-scale randomized controlled trials.



2016 ◽  
Vol 140 (2) ◽  
pp. 322-328 ◽  
Author(s):  
Amy E. Taylor ◽  
Richard M. Martin ◽  
Milan S. Geybels ◽  
Janet L. Stanford ◽  
Irene Shui ◽  
...  




2021 ◽  
Author(s):  
Abdolhalim Rajabi ◽  
Azadeh Shojaei ◽  
Leila Janani ◽  
Mojtaba Farjam ◽  
Hamid Reza Baradaran ◽  
...  


Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 409
Author(s):  
Dhruba Tara Maharjan ◽  
Ali Alamdar Shah Syed ◽  
Guan Ning Lin ◽  
Weihai Ying

Testosterone’s role in female depression is not well understood, with studies reporting conflicting results. Here, we use meta-analytical and Mendelian randomization techniques to determine whether serum testosterone levels differ between depressed and healthy women and whether such a relationship is casual. Our meta-analysis shows a significant association between absolute serum testosterone levels and female depression, which remains true for the premenopausal group while achieving borderline significance in the postmenopausal group. The results from our Mendelian randomization analysis failed to show any causal relationship between testosterone and depression. Our results show that women with depression do indeed display significantly different serum levels of testosterone. However, the directions of the effect of this relationship are conflicting and may be due to menopausal status. Since our Mendelian randomization analysis was insignificant, the difference in testosterone levels between healthy and depressed women is most likely a manifestation of the disease itself. Further studies could be carried out to leverage this newfound insight into better diagnostic capabilities culminating in early intervention in female depression.



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