Title: Cardiometabolic Index as a Predictor of Gallstone Incidence in U.S. Adults: Insights from
NHANES 2017-2020
Version: 0 Date: 19 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the introduction mentions complications like cholecystitis and pancreatitis, a brief
mention of how these complications directly relate to mortality or quality of life could strengthen
the urgency of addressing GSD as a public health concern.
-The rationale behind excluding individuals due to incomplete CMI information, missing
gallstone data, and insufficient covariate information is clear. However, it would be beneficial
to explain why specific variables (e.g., educational attainment or marital status) were considered
essential for inclusion in the final analysis. This would help justify the exclusion of participants
more transparently.
-The inclusion of dietary factors such as calorie and fat consumption is a strength, but it might
be beneficial to clarify how these variables were adjusted for. For example, how was energy
intake (calories) factored into the analysis of CMI? Were macronutrient intake patterns (e.g.,
carbohydrate vs. fat intake) considered? A brief explanation of how these dietary variables were
handled would provide more context for the readers.
-The CMI threshold of 0.996 is identified as significant, but it is not clear how this threshold was
determined and what it means in practical terms. More explanation about why this particular
value was chosen or how it might be clinically relevant would enhance understanding.
-The results from propensity score matching (PSM) and IPW are described as validating the
findings, but the discussion could go further in explaining the implications of the confidence
intervals (e.g., wide CIs in PSM) and how they relate to the precision of the estimates.
-The genetic component of GSD is mentioned in the context of existing GWAS findings that
identify genetic loci related to cholesterol and lipid metabolism. However, further exploration
of how genetic predispositions might interact with CMI to influence GSD risk would be
beneficial. For instance, how might genetic polymorphisms that affect cholesterol metabolism
(e.g., ABCG5, ABCG8) influence the impact of metabolic factors like CMI? Expanding on the
potential gene-environment interactions could help frame CMI within a more comprehensive
etiological model of GSD.
Title: Cardiometabolic Index as a Predictor of Gallstone Incidence in U.S. Adults: Insights from
NHANES 2017-2020
Version: 0 Date: 19 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the introduction mentions complications like cholecystitis and pancreatitis, a brief
mention of how these complications directly relate to mortality or quality of life could strengthen
the urgency of addressing GSD as a public health concern.
-The rationale behind excluding individuals due to incomplete CMI information, missing
gallstone data, and insufficient covariate information is clear. However, it would be beneficial
to explain why specific variables (e.g., educational attainment or marital status) were considered
essential for inclusion in the final analysis. This would help justify the exclusion of participants
more transparently.
-The inclusion of dietary factors such as calorie and fat consumption is a strength, but it might
be beneficial to clarify how these variables were adjusted for. For example, how was energy
intake (calories) factored into the analysis of CMI? Were macronutrient intake patterns (e.g.,
carbohydrate vs. fat intake) considered? A brief explanation of how these dietary variables were
handled would provide more context for the readers.
-The CMI threshold of 0.996 is identified as significant, but it is not clear how this threshold was
determined and what it means in practical terms. More explanation about why this particular
value was chosen or how it might be clinically relevant would enhance understanding.
-The results from propensity score matching (PSM) and IPW are described as validating the
findings, but the discussion could go further in explaining the implications of the confidence
intervals (e.g., wide CIs in PSM) and how they relate to the precision of the estimates.
-The genetic component of GSD is mentioned in the context of existing GWAS findings that
identify genetic loci related to cholesterol and lipid metabolism. However, further exploration
of how genetic predispositions might interact with CMI to influence GSD risk would be
beneficial. For instance, how might genetic polymorphisms that affect cholesterol metabolism
(e.g., ABCG5, ABCG8) influence the impact of metabolic factors like CMI? Expanding on the
potential gene-environment interactions could help frame CMI within a more comprehensive
etiological model of GSD.
Please review this paper.
user
Title: Cardiometabolic Index as a Predictor of Gallstone Incidence in U.S. Adults: Insights from
NHANES 2017-2020
Version: 0 Date: 19 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the introduction mentions complications like cholecystitis and pancreatitis, a brief
mention of how these complications directly relate to mortality or quality of life could strengthen
the urgency of addressing GSD as a public health concern.
-The rationale behind excluding individuals due to incomplete CMI information, missing
gallstone data, and insufficient covariate information is clear. However, it would be beneficial
to explain why specific variables (e.g., educational attainment or marital status) were considered
essential for inclusion in the final analysis. This would help justify the exclusion of participants
more transparently.
-The inclusion of dietary factors such as calorie and fat consumption is a strength, but it might
be beneficial to clarify how these variables were adjusted for. For example, how was energy
intake (calories) factored into the analysis of CMI? Were macronutrient intake patterns (e.g.,
carbohydrate vs. fat intake) considered? A brief explanation of how these dietary variables were
handled would provide more context for the readers.
-The CMI threshold of 0.996 is identified as significant, but it is not clear how this threshold was
determined and what it means in practical terms. More explanation about why this particular
value was chosen or how it might be clinically relevant would enhance understanding.
-The results from propensity score matching (PSM) and IPW are described as validating the
findings, but the discussion could go further in explaining the implications of the confidence
intervals (e.g., wide CIs in PSM) and how they relate to the precision of the estimates.
-The genetic component of GSD is mentioned in the context of existing GWAS findings that
identify genetic loci related to cholesterol and lipid metabolism. However, further exploration
of how genetic predispositions might interact with CMI to influence GSD risk would be
beneficial. For instance, how might genetic polymorphisms that affect cholesterol metabolism
(e.g., ABCG5, ABCG8) influence the impact of metabolic factors like CMI? Expanding on the
potential gene-environment interactions could help frame CMI within a more comprehensive
etiological model of GSD.
assistant