Alcohol and steatosis: The Japanese paradox — Authors' reply
Bibliographic record
Abstract
We thank Lonardo et al., 2016Lonardo A. Ballestri S. Romagnoli D. Nascimbeni F. Alcohol and steatosis: the Japanese paradox.EBioMedicine. 2016; Summary Full Text Full Text PDF PubMed Scopus (1) Google Scholar for their comments on our meta-analysis on the relationship between alcohol consumption and hepatic steatosis (Roerecke et al., 2016Roerecke M. Nanau R. Rehm J. Neuman M. Ethnicity matters: a systematic review and meta-analysis of the non-linear relationship between alcohol consumption and prevalence and incidence of hepatic steatosis.EBioMedicine. 2016; https://doi.org/10.1016/j.ebiom.2016.04.023Summary Full Text Full Text PDF Scopus (19) Google Scholar). We would like to clarify our position on overall risk associated with alcohol consumption and specifically on the risk of hepatic steatosis. First, as we have stated in our paper, we are in agreement with Lonardo et al. that a distinction between alcoholic and non-alcoholic hepatic steatosis has little meaning because alcohol is only one of the risk factors for liver disease, including non-alcoholic fatty liver disease. Different dimensions of alcohol consumption should be distinguished in this regard as non-regular binge drinking among moderate drinkers seems to increase the risk for hepatic steatosis. However, other risk factors also play a role, and the interactions among all risk factors determine the overall risk for liver injury. The large heterogeneity we observed in countries other than Japan underlines that risk factors other than alcohol play a substantial role in risk for hepatic steatosis and precludes us from clearly identifying the role alcohol plays in the development of hepatic steatosis. Thus, categorizing the etiology of liver injury based on one risk factor does not make much sense. Second, when talking about risk associated with alcohol consumption, it makes little sense to use words such as safe. Rather, risk needs to be examined for each disease outcome separately because pathways and risk differ from disease to disease, and the same amount of alcohol may be associated with a low risk for one disease outcome but with high risk for another. For example, the risk for breast cancer is elevated no matter how little alcohol is consumed (Shield et al., 2016Shield K.D. Soerjomataram I. Rehm J. Alcohol use and breast cancer: a critical review.Alcohol. Clin. Exp. Res. 2016; https://doi.org/10.1111/acer.13071Crossref PubMed Scopus (99) Google Scholar), and no level of alcohol consumption is safe in this case. Consequently, guidelines for alcohol consumption are considered ‘low-risk’ drinking guidelines (Stockwell and Room, 2012Stockwell T. Room R. Constructing and responding to low-risk drinking guidelines: conceptualisation, evidence and reception.Drug Alcohol Rev. 2012; 31: 121-125Crossref PubMed Scopus (28) Google Scholar), i.e. no level of alcohol consumption is safe. Third, the term paradox gives evidence that we do not yet fully understand the etiology of liver disease and the role alcohol plays in it. Any comprehensive theory of alcohol's effect on hepatic steatosis or other forms of liver disease should be able to explain the difference in associations our meta-analysis has shown. Ethnicity matters: A Systematic Review and Meta-Analysis of the Non-Linear Relationship Between Alcohol Consumption and Prevalence and Incidence of Hepatic SteatosisFatty liver (hepatic steatosis) is one of the most common diseases globally, with increasing prevalence. The role of alcohol consumption in the development of hepatic steatosis has not been systematically examined. Full-Text PDF Open AccessAlcohol and Steatosis: The Japanese ParadoxIn this issue of EBioMedicine, Roerecke and Colleagues report that, in Japan, alcohol consumption as low as <20 g daily was associated with significant protection from incident and prevalent fatty liver; however, no such association was found in countries other than Japan (Roerecke et al., 2016). This systematic review is based on the analysis of 18 articles (11 of which are from Japan) which recruited, overall, 99,370 participants, 25,662 of whom had steatosis. Full-Text PDF Open Access
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.002 |
| Insufficient payload (model declined to judge) | 0.001 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".