Title: Dietary inflammatory index in relation to the progression of hepatic steatosis and liver
fibrosis: evaluation by elastography/Fibroscan
Version: 1 Date: 08 Nov 2023
Reviewer:  Zaki A. Sherif
Reviewer's report:
To Authors
If I were to merely look at the Abstract and extract vital information about the rest of the paper,
the following is what I’d come up with:
The study investigated how the inflammatory potential of the diet affects the risk of liver damage
in patients with nonalcoholic fatty liver disease (NAFLD), a condition where fat accumulates in
the liver. This study used a device called Fibro Scan® to measure the degree of liver fibrosis,
which is the scarring of the liver tissue due to chronic inflammation. The study also used a tool
called Dietary Inflammatory Index (DII) to measure the inflammatory potential of the diet based
on the intake of different foods.
In the findings of the study, patients with more severe fat accumulation in the liver (hepatic
steatosis) had higher DII scores, meaning they had more inflammatory diets. This is intuitive
and expected. The study also found that higher DII scores were associated with higher weight,
body mass index (BMI), and liver stiffness, which are indicators of liver damage and fibrosis.
This is also expected.
The study concluded that patients with higher DII scores had a higher risk of developing liver
fibrosis than those with lower DII scores, even after adjusting for other factors. The study
suggested that eating less inflammatory foods may help prevent or slow down the progression
of liver damage and fibrosis in patients with NAFLD. By the way, just judging by the structure
of the English applied in the Abstract, I can state that this paper might need English correction.
Here are some reasons why:
The abstract has many grammatical errors and awkward phrasings that make it hard to read and
understand. For example, the first sentence should say “one of the proposed mechanisms by
which nutrition influences the progression of hepatic steatosis to fibrosis is inflammation.”
In line 42, the last sentence should read “reducing inflammation through food” instead of “with
food”.
The abstract also has some inconsistencies and lack of clarity in the use of terms and
abbreviations. For example, the term “hepatic steatosis” is used interchangeably with “NAFLD”,
but they are not the same. NAFLD is a broader term that includes both steatosis and fibrosis. The
term “inflammatory possible” is unclear and should be replaced with “inflammatory potential” or
“inflammatory effect”. Also, be consistent in the spelling of “Fibroscan” with no space between
“Fibro” and “scan”.
I suggest that the author revise the abstract to address these issues and improve the quality and
readability of the paper.
Now, reading the rest of the manuscript, I found that the Introduction was succinct and well-
written.
Methods and Materials: Lines 89-91: “The study protocol was accepted by the Ethics
Committee of Kermanshah University of Medical Sciences (IR.KUMS.REC.1400.789) and
Mashhad University of Medical Sciences (IR.MUMS.MEDICAL.REC.1397.121).”. Are these
departments equivalent to the IRB (internal Review Committee) oversight committee used in
the USA?
In lines 97-99, you stated that “FibroScan® has been shown to be operator-independent
and producible with the excellent inter-observer agreement and intra-observer agreement
for predicting hepatic steatosis and fibrosis”. Did you mean “reproducible” as opposed to
“producible”? Also, what is the significance of the Fibroscan measurement being done “on the
right lobe of the liver”?
Interestingly, the liver stiffness result is measured in kilopascals (kPa), and normal results are
usually between 2 and 7 kPa1. Therefore, your statement that “greater LSM >5.3 kilopascals
(kPa) was used to diagnose the presence of hepatic fibrosis in patients with NAFLD” is a little
baffling, unless in the context of FibroScan and liver fibrosis assessment, this threshold value
of LSM is used to categorize patients as having or not having significant fibrosis. An AUROC
of 0.879 suggests that this threshold has a good discriminatory power in distinguishing between
individuals with and without hepatic fibrosis. It's important to note that specific cutoff values
and diagnostic criteria can vary depending on the context, the population being studied, and
the clinical guidelines in use, so it's essential to consider the specific guidelines and research
findings relevant to your clinical or research setting.
In lines 111-113, you stated that “DII is a population-based dietary index derived from the
literature regarding the impact of individual nutrients and foods on the pro-inflammatory or anti-
inflammatory mediators including tumor necrosis factor-Alpha …”). I would be better stated as
“The Dietary Inflammatory Index (DII) is a dietary assessment tool that is based on a compilation
of scientific literature regarding the effects of various nutrients and foods on the levels of
pro-inflammatory and anti-inflammatory mediators. These mediators include molecules such
as tumor necrosis factor-Alpha (TNF-#), interleukin-1Beta (IL-1#), IL-4, IL-6, IL-10, and C-
reactive protein (CRP).”
In line 118, you placed omega-6-fatty acid in the anti-inflammatory category. It would have been
better to explain the reason such as Omega-6 fatty acids can have both pro-inflammatory (e.g.,
linoleic acid) and anti-inflammatory (e.g., linolenic acid-GLA) effects in the body, depending
on the specific fatty acids within this group and the overall balance with omega-3 fatty acids.
In line 129, remove the extra parenthesis.
In lines 160-162 of the Results section, you stated “The majority of participants (63.5%) were
female, with a mean age SD of 39.94 12.98 years. Of the subjects, 61 had grade I hepatic steatosis
(35.9%), 66 had grade hepatic steatosis (38.8%), and 43 had grade hepatic steatosis (25.3%). 94
of these individuals had hepatic fibrosis”. Are the 66 patients with grade II and 43 with grade III?
From the findings of this study, one can conclude that the odds of developing hepatic fibrosis
were higher for individuals with higher DII scores in all models. The risk of hepatic fibrosis
increased with higher DII scores, and there was a statistically significant rising trend in all
models. Additionally, each SD increase in the DII score was independently linked to a higher
risk of hepatic fibrosis.
So, overall, these findings suggest a significant association between dietary choices, as measured
by the DII score, and the development of hepatic steatosis and fibrosis in individuals with non-
alcoholic fatty liver disease (NAFLD). The discussion should emphasize the importance of these
results and their implications for understanding the relationship between diet, inflammation, and
liver health in this population. As stated in the Discussion, prior studies (the authors cited many
references) have established a connection between metabolic syndrome and several factors,
including adherence to diets characterized by elevated DII scores, increased body mass index
(BMI) and waist circumference, as well as the presence of hepatic steatosis.
However, the discussion is too long and repetitive, and it does not follow a clear structure.
It should be organized into paragraphs that address the main findings, the comparison with
previous literature, the possible mechanisms, the limitations, and the implications of the study.
The discussion uses too many numbers and references ( a lot of these are also old) that distract
from the main message and make it hard to read. It should use more words to explain the results
and their significance and cite only the most relevant and recent sources. The Conclusion just
states “Further research is required to determine how anti-inflammatory foods might help people
with NAFLD improve their hepatic steatosis and fibrosis status.” But it does not provide a clear
recommendation based on the study results. It should summarize the main findings and their
implications for clinical practice and future research.
Furthermore, the discussion does not acknowledge the limitations of the study, such as
the cross-sectional design, the small sample size, the self-reported dietary intake, and the
potential confounding factors. It should discuss how these limitations affect the validity and
generalizability of the results, and how they can be addressed in future studies. Also, it's
important to emphasize the observational nature of the study and highlight the need for
prospective or clinical trial investigations to establish causation.
Title: Dietary inflammatory index in relation to the progression of hepatic steatosis and liver
fibrosis: evaluation by elastography/Fibroscan
Version: 1 Date: 08 Nov 2023
Reviewer:  Zaki A. Sherif
Reviewer's report:
To Authors
If I were to merely look at the Abstract and extract vital information about the rest of the paper,
the following is what I’d come up with:
The study investigated how the inflammatory potential of the diet affects the risk of liver damage
in patients with nonalcoholic fatty liver disease (NAFLD), a condition where fat accumulates in
the liver. This study used a device called Fibro Scan® to measure the degree of liver fibrosis,
which is the scarring of the liver tissue due to chronic inflammation. The study also used a tool
called Dietary Inflammatory Index (DII) to measure the inflammatory potential of the diet based
on the intake of different foods.
In the findings of the study, patients with more severe fat accumulation in the liver (hepatic
steatosis) had higher DII scores, meaning they had more inflammatory diets. This is intuitive
and expected. The study also found that higher DII scores were associated with higher weight,
body mass index (BMI), and liver stiffness, which are indicators of liver damage and fibrosis.
This is also expected.
The study concluded that patients with higher DII scores had a higher risk of developing liver
fibrosis than those with lower DII scores, even after adjusting for other factors. The study
suggested that eating less inflammatory foods may help prevent or slow down the progression
of liver damage and fibrosis in patients with NAFLD. By the way, just judging by the structure
of the English applied in the Abstract, I can state that this paper might need English correction.
Here are some reasons why:
The abstract has many grammatical errors and awkward phrasings that make it hard to read and
understand. For example, the first sentence should say “one of the proposed mechanisms by
which nutrition influences the progression of hepatic steatosis to fibrosis is inflammation.”
In line 42, the last sentence should read “reducing inflammation through food” instead of “with
food”.
The abstract also has some inconsistencies and lack of clarity in the use of terms and
abbreviations. For example, the term “hepatic steatosis” is used interchangeably with “NAFLD”,
but they are not the same. NAFLD is a broader term that includes both steatosis and fibrosis. The
term “inflammatory possible” is unclear and should be replaced with “inflammatory potential” or
“inflammatory effect”. Also, be consistent in the spelling of “Fibroscan” with no space between
“Fibro” and “scan”.
I suggest that the author revise the abstract to address these issues and improve the quality and
readability of the paper.
Now, reading the rest of the manuscript, I found that the Introduction was succinct and well-
written.
Methods and Materials: Lines 89-91: “The study protocol was accepted by the Ethics
Committee of Kermanshah University of Medical Sciences (IR.KUMS.REC.1400.789) and
Mashhad University of Medical Sciences (IR.MUMS.MEDICAL.REC.1397.121).”. Are these
departments equivalent to the IRB (internal Review Committee) oversight committee used in
the USA?
In lines 97-99, you stated that “FibroScan® has been shown to be operator-independent
and producible with the excellent inter-observer agreement and intra-observer agreement
for predicting hepatic steatosis and fibrosis”. Did you mean “reproducible” as opposed to
“producible”? Also, what is the significance of the Fibroscan measurement being done “on the
right lobe of the liver”?
Interestingly, the liver stiffness result is measured in kilopascals (kPa), and normal results are
usually between 2 and 7 kPa1. Therefore, your statement that “greater LSM >5.3 kilopascals
(kPa) was used to diagnose the presence of hepatic fibrosis in patients with NAFLD” is a little
baffling, unless in the context of FibroScan and liver fibrosis assessment, this threshold value
of LSM is used to categorize patients as having or not having significant fibrosis. An AUROC
of 0.879 suggests that this threshold has a good discriminatory power in distinguishing between
individuals with and without hepatic fibrosis. It's important to note that specific cutoff values
and diagnostic criteria can vary depending on the context, the population being studied, and
the clinical guidelines in use, so it's essential to consider the specific guidelines and research
findings relevant to your clinical or research setting.
In lines 111-113, you stated that “DII is a population-based dietary index derived from the
literature regarding the impact of individual nutrients and foods on the pro-inflammatory or anti-
inflammatory mediators including tumor necrosis factor-Alpha …”). I would be better stated as
“The Dietary Inflammatory Index (DII) is a dietary assessment tool that is based on a compilation
of scientific literature regarding the effects of various nutrients and foods on the levels of
pro-inflammatory and anti-inflammatory mediators. These mediators include molecules such
as tumor necrosis factor-Alpha (TNF-#), interleukin-1Beta (IL-1#), IL-4, IL-6, IL-10, and C-
reactive protein (CRP).”
In line 118, you placed omega-6-fatty acid in the anti-inflammatory category. It would have been
better to explain the reason such as Omega-6 fatty acids can have both pro-inflammatory (e.g.,
linoleic acid) and anti-inflammatory (e.g., linolenic acid-GLA) effects in the body, depending
on the specific fatty acids within this group and the overall balance with omega-3 fatty acids.
In line 129, remove the extra parenthesis.
In lines 160-162 of the Results section, you stated “The majority of participants (63.5%) were
female, with a mean age SD of 39.94 12.98 years. Of the subjects, 61 had grade I hepatic steatosis
(35.9%), 66 had grade hepatic steatosis (38.8%), and 43 had grade hepatic steatosis (25.3%). 94
of these individuals had hepatic fibrosis”. Are the 66 patients with grade II and 43 with grade III?
From the findings of this study, one can conclude that the odds of developing hepatic fibrosis
were higher for individuals with higher DII scores in all models. The risk of hepatic fibrosis
increased with higher DII scores, and there was a statistically significant rising trend in all
models. Additionally, each SD increase in the DII score was independently linked to a higher
risk of hepatic fibrosis.
So, overall, these findings suggest a significant association between dietary choices, as measured
by the DII score, and the development of hepatic steatosis and fibrosis in individuals with non-
alcoholic fatty liver disease (NAFLD). The discussion should emphasize the importance of these
results and their implications for understanding the relationship between diet, inflammation, and
liver health in this population. As stated in the Discussion, prior studies (the authors cited many
references) have established a connection between metabolic syndrome and several factors,
including adherence to diets characterized by elevated DII scores, increased body mass index
(BMI) and waist circumference, as well as the presence of hepatic steatosis.
However, the discussion is too long and repetitive, and it does not follow a clear structure.
It should be organized into paragraphs that address the main findings, the comparison with
previous literature, the possible mechanisms, the limitations, and the implications of the study.
The discussion uses too many numbers and references ( a lot of these are also old) that distract
from the main message and make it hard to read. It should use more words to explain the results
and their significance and cite only the most relevant and recent sources. The Conclusion just
states “Further research is required to determine how anti-inflammatory foods might help people
with NAFLD improve their hepatic steatosis and fibrosis status.” But it does not provide a clear
recommendation based on the study results. It should summarize the main findings and their
implications for clinical practice and future research.
Furthermore, the discussion does not acknowledge the limitations of the study, such as
the cross-sectional design, the small sample size, the self-reported dietary intake, and the
potential confounding factors. It should discuss how these limitations affect the validity and
generalizability of the results, and how they can be addressed in future studies. Also, it's
important to emphasize the observational nature of the study and highlight the need for
prospective or clinical trial investigations to establish causation.
Please review this paper.
user
Title: Dietary inflammatory index in relation to the progression of hepatic steatosis and liver
fibrosis: evaluation by elastography/Fibroscan
Version: 1 Date: 08 Nov 2023
Reviewer:  Zaki A. Sherif
Reviewer's report:
To Authors
If I were to merely look at the Abstract and extract vital information about the rest of the paper,
the following is what I’d come up with:
The study investigated how the inflammatory potential of the diet affects the risk of liver damage
in patients with nonalcoholic fatty liver disease (NAFLD), a condition where fat accumulates in
the liver. This study used a device called Fibro Scan® to measure the degree of liver fibrosis,
which is the scarring of the liver tissue due to chronic inflammation. The study also used a tool
called Dietary Inflammatory Index (DII) to measure the inflammatory potential of the diet based
on the intake of different foods.
In the findings of the study, patients with more severe fat accumulation in the liver (hepatic
steatosis) had higher DII scores, meaning they had more inflammatory diets. This is intuitive
and expected. The study also found that higher DII scores were associated with higher weight,
body mass index (BMI), and liver stiffness, which are indicators of liver damage and fibrosis.
This is also expected.
The study concluded that patients with higher DII scores had a higher risk of developing liver
fibrosis than those with lower DII scores, even after adjusting for other factors. The study
suggested that eating less inflammatory foods may help prevent or slow down the progression
of liver damage and fibrosis in patients with NAFLD. By the way, just judging by the structure
of the English applied in the Abstract, I can state that this paper might need English correction.
Here are some reasons why:
The abstract has many grammatical errors and awkward phrasings that make it hard to read and
understand. For example, the first sentence should say “one of the proposed mechanisms by
which nutrition influences the progression of hepatic steatosis to fibrosis is inflammation.”
In line 42, the last sentence should read “reducing inflammation through food” instead of “with
food”.
The abstract also has some inconsistencies and lack of clarity in the use of terms and
abbreviations. For example, the term “hepatic steatosis” is used interchangeably with “NAFLD”,
but they are not the same. NAFLD is a broader term that includes both steatosis and fibrosis. The
term “inflammatory possible” is unclear and should be replaced with “inflammatory potential” or
“inflammatory effect”. Also, be consistent in the spelling of “Fibroscan” with no space between
“Fibro” and “scan”.
I suggest that the author revise the abstract to address these issues and improve the quality and
readability of the paper.
Now, reading the rest of the manuscript, I found that the Introduction was succinct and well-
written.
Methods and Materials: Lines 89-91: “The study protocol was accepted by the Ethics
Committee of Kermanshah University of Medical Sciences (IR.KUMS.REC.1400.789) and
Mashhad University of Medical Sciences (IR.MUMS.MEDICAL.REC.1397.121).”. Are these
departments equivalent to the IRB (internal Review Committee) oversight committee used in
the USA?
In lines 97-99, you stated that “FibroScan® has been shown to be operator-independent
and producible with the excellent inter-observer agreement and intra-observer agreement
for predicting hepatic steatosis and fibrosis”. Did you mean “reproducible” as opposed to
“producible”? Also, what is the significance of the Fibroscan measurement being done “on the
right lobe of the liver”?
Interestingly, the liver stiffness result is measured in kilopascals (kPa), and normal results are
usually between 2 and 7 kPa1. Therefore, your statement that “greater LSM >5.3 kilopascals
(kPa) was used to diagnose the presence of hepatic fibrosis in patients with NAFLD” is a little
baffling, unless in the context of FibroScan and liver fibrosis assessment, this threshold value
of LSM is used to categorize patients as having or not having significant fibrosis. An AUROC
of 0.879 suggests that this threshold has a good discriminatory power in distinguishing between
individuals with and without hepatic fibrosis. It's important to note that specific cutoff values
and diagnostic criteria can vary depending on the context, the population being studied, and
the clinical guidelines in use, so it's essential to consider the specific guidelines and research
findings relevant to your clinical or research setting.
In lines 111-113, you stated that “DII is a population-based dietary index derived from the
literature regarding the impact of individual nutrients and foods on the pro-inflammatory or anti-
inflammatory mediators including tumor necrosis factor-Alpha …”). I would be better stated as
“The Dietary Inflammatory Index (DII) is a dietary assessment tool that is based on a compilation
of scientific literature regarding the effects of various nutrients and foods on the levels of
pro-inflammatory and anti-inflammatory mediators. These mediators include molecules such
as tumor necrosis factor-Alpha (TNF-#), interleukin-1Beta (IL-1#), IL-4, IL-6, IL-10, and C-
reactive protein (CRP).”
In line 118, you placed omega-6-fatty acid in the anti-inflammatory category. It would have been
better to explain the reason such as Omega-6 fatty acids can have both pro-inflammatory (e.g.,
linoleic acid) and anti-inflammatory (e.g., linolenic acid-GLA) effects in the body, depending
on the specific fatty acids within this group and the overall balance with omega-3 fatty acids.
In line 129, remove the extra parenthesis.
In lines 160-162 of the Results section, you stated “The majority of participants (63.5%) were
female, with a mean age SD of 39.94 12.98 years. Of the subjects, 61 had grade I hepatic steatosis
(35.9%), 66 had grade hepatic steatosis (38.8%), and 43 had grade hepatic steatosis (25.3%). 94
of these individuals had hepatic fibrosis”. Are the 66 patients with grade II and 43 with grade III?
From the findings of this study, one can conclude that the odds of developing hepatic fibrosis
were higher for individuals with higher DII scores in all models. The risk of hepatic fibrosis
increased with higher DII scores, and there was a statistically significant rising trend in all
models. Additionally, each SD increase in the DII score was independently linked to a higher
risk of hepatic fibrosis.
So, overall, these findings suggest a significant association between dietary choices, as measured
by the DII score, and the development of hepatic steatosis and fibrosis in individuals with non-
alcoholic fatty liver disease (NAFLD). The discussion should emphasize the importance of these
results and their implications for understanding the relationship between diet, inflammation, and
liver health in this population. As stated in the Discussion, prior studies (the authors cited many
references) have established a connection between metabolic syndrome and several factors,
including adherence to diets characterized by elevated DII scores, increased body mass index
(BMI) and waist circumference, as well as the presence of hepatic steatosis.
However, the discussion is too long and repetitive, and it does not follow a clear structure.
It should be organized into paragraphs that address the main findings, the comparison with
previous literature, the possible mechanisms, the limitations, and the implications of the study.
The discussion uses too many numbers and references ( a lot of these are also old) that distract
from the main message and make it hard to read. It should use more words to explain the results
and their significance and cite only the most relevant and recent sources. The Conclusion just
states “Further research is required to determine how anti-inflammatory foods might help people
with NAFLD improve their hepatic steatosis and fibrosis status.” But it does not provide a clear
recommendation based on the study results. It should summarize the main findings and their
implications for clinical practice and future research.
Furthermore, the discussion does not acknowledge the limitations of the study, such as
the cross-sectional design, the small sample size, the self-reported dietary intake, and the
potential confounding factors. It should discuss how these limitations affect the validity and
generalizability of the results, and how they can be addressed in future studies. Also, it's
important to emphasize the observational nature of the study and highlight the need for
prospective or clinical trial investigations to establish causation.
assistant