Title: The relationships between depression, inflammation and self-reported disease activity in
IBD and their impact on healthcare usage.
Version: 3 Date: 30 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the introduction mentions that depression may be an "extraintestinal manifestation of
IBD," this point could be better explained. The authors refer to cytokines, microbiota dysbiosis,
and other factors as mechanisms, but the reader may benefit from more explicit clarification on
why depression is thought to be tied to inflammation in the context of IBD specifically (e.g.,
through cytokine release or HPA axis activation).
-A more concise explanation of how FCP specifically relates to both depression and disease
activity (beyond just being an inflammatory marker) could strengthen the argument for why it
is the focal biomarker in this study.
-The introduction mentions limited evidence on the contemporaneous relationships between
depression, disease activity, and SRDA, but the discussion could be expanded to explain some
of the contradictory findings in prior research. For example, how studies have shown both weak
and strong associations between depression and FCP, and why such discrepancies might exist
(e.g., variations in study populations, methodologies, or measurement tools). This could add
nuance to the presentation of prior literature.
-The discussion contrasts the findings with the conceptual framework of the gut-brain axis,
which suggests that depression might lead to inflammation and vice versa. However, the
relationship between these two variables (depression and inflammation) is described as weak or
nonsignificant, which could be confusing. The authors could clarify whether they are rejecting
the gut-brain axis entirely or suggesting that its effects might be less pronounced in this specific
cohort of IBD patients.
-The authors mention that there were no significant findings when splitting the data by disease
subtype (Crohn’s Disease vs. Ulcerative Colitis). However, it would be helpful to elaborate on
why the relationship between depression and inflammation might differ (or not) between these
two subtypes, especially considering the known differences in disease pathophysiology. A brief
explanation of potential reasons for this lack of differential findings would provide more depth
to the discussion.
-The weak negative correlation between SRDA and FCP is discussed, but it could benefit from
more explanation. Why might SRDA, a subjective measure, only weakly correlate with an
objective marker like FCP? The authors could consider psychological factors, cognitive biases,
or even medication use that may influence patients' perceptions of disease activity independent
of inflammation. This point could be strengthened by referencing literature on the cognitive and
psychological factors influencing symptom reporting in chronic diseases.
Title: The relationships between depression, inflammation and self-reported disease activity in
IBD and their impact on healthcare usage.
Version: 3 Date: 30 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the introduction mentions that depression may be an "extraintestinal manifestation of
IBD," this point could be better explained. The authors refer to cytokines, microbiota dysbiosis,
and other factors as mechanisms, but the reader may benefit from more explicit clarification on
why depression is thought to be tied to inflammation in the context of IBD specifically (e.g.,
through cytokine release or HPA axis activation).
-A more concise explanation of how FCP specifically relates to both depression and disease
activity (beyond just being an inflammatory marker) could strengthen the argument for why it
is the focal biomarker in this study.
-The introduction mentions limited evidence on the contemporaneous relationships between
depression, disease activity, and SRDA, but the discussion could be expanded to explain some
of the contradictory findings in prior research. For example, how studies have shown both weak
and strong associations between depression and FCP, and why such discrepancies might exist
(e.g., variations in study populations, methodologies, or measurement tools). This could add
nuance to the presentation of prior literature.
-The discussion contrasts the findings with the conceptual framework of the gut-brain axis,
which suggests that depression might lead to inflammation and vice versa. However, the
relationship between these two variables (depression and inflammation) is described as weak or
nonsignificant, which could be confusing. The authors could clarify whether they are rejecting
the gut-brain axis entirely or suggesting that its effects might be less pronounced in this specific
cohort of IBD patients.
-The authors mention that there were no significant findings when splitting the data by disease
subtype (Crohn’s Disease vs. Ulcerative Colitis). However, it would be helpful to elaborate on
why the relationship between depression and inflammation might differ (or not) between these
two subtypes, especially considering the known differences in disease pathophysiology. A brief
explanation of potential reasons for this lack of differential findings would provide more depth
to the discussion.
-The weak negative correlation between SRDA and FCP is discussed, but it could benefit from
more explanation. Why might SRDA, a subjective measure, only weakly correlate with an
objective marker like FCP? The authors could consider psychological factors, cognitive biases,
or even medication use that may influence patients' perceptions of disease activity independent
of inflammation. This point could be strengthened by referencing literature on the cognitive and
psychological factors influencing symptom reporting in chronic diseases.
Please review this paper.
user
Title: The relationships between depression, inflammation and self-reported disease activity in
IBD and their impact on healthcare usage.
Version: 3 Date: 30 Dec 2024
Reviewer:  Anwar Ashraf Abouelnasr
Reviewer's report:
Dear Authors, please address the following points below
-While the introduction mentions that depression may be an "extraintestinal manifestation of
IBD," this point could be better explained. The authors refer to cytokines, microbiota dysbiosis,
and other factors as mechanisms, but the reader may benefit from more explicit clarification on
why depression is thought to be tied to inflammation in the context of IBD specifically (e.g.,
through cytokine release or HPA axis activation).
-A more concise explanation of how FCP specifically relates to both depression and disease
activity (beyond just being an inflammatory marker) could strengthen the argument for why it
is the focal biomarker in this study.
-The introduction mentions limited evidence on the contemporaneous relationships between
depression, disease activity, and SRDA, but the discussion could be expanded to explain some
of the contradictory findings in prior research. For example, how studies have shown both weak
and strong associations between depression and FCP, and why such discrepancies might exist
(e.g., variations in study populations, methodologies, or measurement tools). This could add
nuance to the presentation of prior literature.
-The discussion contrasts the findings with the conceptual framework of the gut-brain axis,
which suggests that depression might lead to inflammation and vice versa. However, the
relationship between these two variables (depression and inflammation) is described as weak or
nonsignificant, which could be confusing. The authors could clarify whether they are rejecting
the gut-brain axis entirely or suggesting that its effects might be less pronounced in this specific
cohort of IBD patients.
-The authors mention that there were no significant findings when splitting the data by disease
subtype (Crohn’s Disease vs. Ulcerative Colitis). However, it would be helpful to elaborate on
why the relationship between depression and inflammation might differ (or not) between these
two subtypes, especially considering the known differences in disease pathophysiology. A brief
explanation of potential reasons for this lack of differential findings would provide more depth
to the discussion.
-The weak negative correlation between SRDA and FCP is discussed, but it could benefit from
more explanation. Why might SRDA, a subjective measure, only weakly correlate with an
objective marker like FCP? The authors could consider psychological factors, cognitive biases,
or even medication use that may influence patients' perceptions of disease activity independent
of inflammation. This point could be strengthened by referencing literature on the cognitive and
psychological factors influencing symptom reporting in chronic diseases.
assistant