Title: Causal effects of genetically determined metabolites and metabolite ratios on esophageal
diseases: A two-sample Mendelian randomization study
Version: 0 Date: 19 Jun 2024
Reviewer's report:
In this study, the authors explored the causality of genetically determined metabolites (GDMs)
on ED through Mendelian Randomization (MR) study, uncovering several key metabolic
features in ED pathogenesis. These findings have potential as novel biomarkers for ED and
provide insights into the disease's etiology and progression. This study remains several issues
that should be addressed.
1. It would be helpful to mark line numbers in the text.
2. In Table 1, summary GWAS data for some of Eds were from UK Biobank (UKB) and others
were from FinnGen consortium R9 release data. How to choose these two datasets? Was there
any criterion?
3. In METHODS, SNPs associated with each metabolite at genome-wide significance (P <
 1E-05) was first screened as an IV. How was the P-value threshold determined and was there
a reference available?
4. In the first paragraph of DISCUSSION, the authors tried to discuss in detail the causal
associations they identified. It would be better to divide paragraphs according to diseases or
metabolite types, which makes it more clearer.
Title: Causal effects of genetically determined metabolites and metabolite ratios on esophageal
diseases: A two-sample Mendelian randomization study
Version: 0 Date: 19 Jun 2024
Reviewer's report:
In this study, the authors explored the causality of genetically determined metabolites (GDMs)
on ED through Mendelian Randomization (MR) study, uncovering several key metabolic
features in ED pathogenesis. These findings have potential as novel biomarkers for ED and
provide insights into the disease's etiology and progression. This study remains several issues
that should be addressed.
1. It would be helpful to mark line numbers in the text.
2. In Table 1, summary GWAS data for some of Eds were from UK Biobank (UKB) and others
were from FinnGen consortium R9 release data. How to choose these two datasets? Was there
any criterion?
3. In METHODS, SNPs associated with each metabolite at genome-wide significance (P <
 1E-05) was first screened as an IV. How was the P-value threshold determined and was there
a reference available?
4. In the first paragraph of DISCUSSION, the authors tried to discuss in detail the causal
associations they identified. It would be better to divide paragraphs according to diseases or
metabolite types, which makes it more clearer.
Please review this paper.
user
Title: Causal effects of genetically determined metabolites and metabolite ratios on esophageal
diseases: A two-sample Mendelian randomization study
Version: 0 Date: 19 Jun 2024
Reviewer's report:
In this study, the authors explored the causality of genetically determined metabolites (GDMs)
on ED through Mendelian Randomization (MR) study, uncovering several key metabolic
features in ED pathogenesis. These findings have potential as novel biomarkers for ED and
provide insights into the disease's etiology and progression. This study remains several issues
that should be addressed.
1. It would be helpful to mark line numbers in the text.
2. In Table 1, summary GWAS data for some of Eds were from UK Biobank (UKB) and others
were from FinnGen consortium R9 release data. How to choose these two datasets? Was there
any criterion?
3. In METHODS, SNPs associated with each metabolite at genome-wide significance (P <
 1E-05) was first screened as an IV. How was the P-value threshold determined and was there
a reference available?
4. In the first paragraph of DISCUSSION, the authors tried to discuss in detail the causal
associations they identified. It would be better to divide paragraphs according to diseases or
metabolite types, which makes it more clearer.
assistant