The DOI matches its Crossref record, with a small difference in title or year; 63 of the 64 references it cites were found in a registry or an index; none of the 72 sources its claims cite is checked for support yet.
ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease: Pooling Project of 19 Cohort Studies
Open accessAbstract
IMPORTANCE: The role of ω-3 polyunsaturated fatty acids for primary prevention of coronary heart disease (CHD) remains controversial. Most prior longitudinal studies evaluated self-reported consumption rather than biomarkers. OBJECTIVE: To evaluate biomarkers of seafood-derived eicosapentaenoic acid (EPA; 20:5ω-3), docosapentaenoic acid (DPA; 22:5ω-3), and docosahexaenoic acid (DHA; 22:6ω-3) and plant-derived α-linolenic acid (ALA; 18:3ω-3) for incident CHD. DATA SOURCES: A global consortium of 19 studies identified by November 2014. STUDY SELECTION: Available prospective (cohort, nested case-control) or retrospective studies with circulating or tissue ω-3 biomarkers and ascertained CHD. DATA EXTRACTION AND SYNTHESIS: Each study conducted standardized, individual-level analysis using harmonized models, exposures, outcomes, and covariates. Findings were centrally pooled using random-effects meta-analysis. Heterogeneity was examined by age, sex, race, diabetes, statins, aspirin, ω-6 levels, and FADS desaturase genes. MAIN OUTCOMES AND MEASURES: Incident total CHD, fatal CHD, and nonfatal myocardial infarction (MI). RESULTS: The 19 studies comprised 16 countries, 45 637 unique individuals, and 7973 total CHD, 2781 fatal CHD, and 7157 nonfatal MI events, with ω-3 measures in total plasma, phospholipids, cholesterol esters, and adipose tissue. Median age at baseline was 59 years (range, 18-97 years), and 28 660 (62.8%) were male. In continuous (per 1-SD increase) multivariable-adjusted analyses, the ω-3 biomarkers ALA, DPA, and DHA were associated with a lower risk of fatal CHD, with relative risks (RRs) of 0.91 (95% CI, 0.84-0.98) for ALA, 0.90 (95% CI, 0.85-0.96) for DPA, and 0.90 (95% CI, 0.84-0.96) for DHA. Although DPA was associated with a lower risk of total CHD (RR, 0.94; 95% CI, 0.90-0.99), ALA (RR, 1.00; 95% CI, 0.95-1.05), EPA (RR, 0.94; 95% CI, 0.87-1.02), and DHA (RR, 0.95; 95% CI, 0.91-1.00) were not. Significant associations with nonfatal MI were not evident. Associations appeared generally stronger in phospholipids and total plasma. Restricted cubic splines did not identify evidence of nonlinearity in dose responses. CONCLUSIONS AND RELEVANCE: On the basis of available studies of free-living populations globally, biomarker concentrations of seafood and plant-derived ω-3 fatty acids are associated with a modestly lower incidence of fatal CHD.
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“and DHA (RR, 0.77; 95% CI, 0.64–0.89)”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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In the paper
“lower risk of fatal CHD was evident with DPA (RR, 0.76; 95% CI, 0.65–0.90)”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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In the paper
“Compared with white individuals, ALA was associated with a significantly lower risk of nonfatal MI among African American individuals (P for heterogeneity = .001).”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > Effect Modification
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In the paper
“no significant interaction was identified by FADS desaturase gene variants”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > Effect Modification
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In the paper
“0.90 (95% CI, 0.84–0.96) for DHA”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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In the paper
“lower risk of nonfatal MI was evident with EPA (RR, 0.71; 95% CI, 0.56–0.90)”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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In the paper
“ALA (RR, 1.00; 95% CI, 0.95–1.05), EPA (RR, 0.94; 95% CI, 0.87–1.02), and DHA (RR, 0.95; 95% CI, 0.91–1.00)were not.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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In the paper
“each ω-3 PUFA was associated with an approximately 9% lower risk of fatal CHD, with RRs of 0.91 (95% CI, 0.82–1.00) for EPA”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > EPA, DPA, and DHA for Incident CHD
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In the paper
“0.90 (95% CI, 0.85–0.96) for DPA”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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In the paper
“Associations appeared generally stronger in phospholipids and total plasma.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
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- It may state two separate claims as one. 28
- Probably not a substantial claim. 14
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In the paper
“No significant differences in associations of ω-3 PUFA biomarkers with incident CHD events were observed by age, sex, ω-6 PUFA (LA or AA) concentrations, type 2 diabetes status, statin use, regular aspirin use, year of biomarker sampling, or (for ALA) EPA, DPA, and DHA concentrations (P for heterogeneity >.05 for each)”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > Effect Modification
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In the paper
“The 19 studies comprised 16 countries, 45 637 unique individuals, and 7973 total CHD, 2781 fatal CHD, and 7157 nonfatal MI events, with ω-3 measures in total plasma, phospholipids, cholesterol esters, and adipose tissue.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
Strength:plain· not yet calibratedn = 45,637Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Median age at baseline was 59 years (range, 18–97 years), and 28 660 (62.8%) were male.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > RESULTS
Strength:plain· not yet calibratedn = 28,660Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
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In the paper
“Compared with the main findings, no appreciable differences were observed after excluding cases identified in the first 2 years after biomarker sampling, censoring participants at the first 6 years of follow-up, excluding retrospective studies, or excluding studies with self-reported events”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > Sensitivity Analyses
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In the paper
“Across biomarker types, inverse associations were generally stronger in the phospholipid and total plasma compartments (Table 2); heterogeneity decreased when adipose tissue and cholesterol ester estimates were excluded from meta-analyses.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > EPA, DPA, and DHA for Incident CHD
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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In the paper
“Across these diverse studies, findings were consistent by age, sex, ω-6 PUFA LA and AA levels, year of biomarker sampling, presence or absence of diabetes, statin use, and aspirin use.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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In the paper
“Our findings suggest generally stronger inverse associations with CHD for EPA, DPA, and DHA in phospholipids and total plasma, although fewer estimates and cases were available for adipose and cholesterol esters compartments, decreasing precision.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Compared with priorwork,42 we also took advantage of a far larger number of events (eg, >4-fold larger for fatal CHD)”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [42] Chowdhury R Warnakula S Kunutsor S Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis Ann Intern Med 2014 160 6 398 406 24723079 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“most prior research11 has focused on seafood-derived long-chain ω-3 PUFAs, and potential CHD effects of plant-derived α-linolenic acid (ALA; 18:3ω-3) are far less understood.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > CONCLUSIONS AND RELEVANCE
What the sources say
- Not checked yetcites [11] Pan A Chen M Chowdhury R α-Linolenic acid and risk of cardiovascular disease: a systematic review and meta-analysis Am J Clin Nutr 2012 96 6 1262 1273 23076616 PMC3497923 source
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None of the sources cited for this claim have been checked yet.
In the paper
“most trials provided supplements for a few years or less and were conducted in patients with preexisting CHD or at high risk for CHD and taking multiple cardiovascular drugs.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > CONCLUSIONS AND RELEVANCE
What the sources say
- Not checked yetcites [2] Bucher HC Hengstler P Schindler C Meier G N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials Am J Med 2002 112 4 298 304 11893369 source
- Not checked yetcites [3] Hooper L Thompson RL Harrison RA Omega 3 fatty acids for prevention and treatment of cardiovascular disease Cochrane Database Syst Rev 2004 4 CD003177 15495044 PMC4170890 source
- Not checked yetcites [4] León H Shibata MC Sivakumaran S Dorgan M Chatterley T Tsuyuki RT Effect of fish oil on arrhythmias and mortality: systematic review BMJ 2008 337 a2931 10.1136/bmj.a2931 19106137 PMC2612582 source
- Not checked yetcites [5] Marik PE Varon J Omega-3 dietary supplements and the risk of cardiovascular events: a systematic review Clin Cardiol 2009 32 7 365 372 19609891 PMC6653319 source
- Not matchedcites [6] Trikalinos TA Lee J Moorthy D Effects of Eicosapentanoic Acid and Docosahexanoic Acid on Mortality Across Diverse Settings: Systematic Review and Meta-analysis of Randomized Trials and Prospective Cohorts Rockville, MD Agency for Healthcare Research and Quality 2012 22479722
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [7] Kwak SM Myung SK Lee YJ Seo HG Korean Meta-analysis Study Group Efficacy of ω-3 fatty acid supplements (eicosapentaenoic acid and docosahexaenoic acid) in the secondary prevention of cardiovascular disease: a meta-analysis of randomized, double-blind, placebo-controlled trials Arch Intern Med 2012 172 9 686 694 22493407 source
- Not checked yetcites [8] Rizos EC Ntzani EE Bika E Kostapanos MS Elisaf MS Association between ω-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis JAMA 2012 308 10 1024 1033 22968891 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“A previous review1 also found that a handful of studies have measured objective circulating or tissue ω-3 PUFA levels, but such findings could be limited by publication bias.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > CONCLUSIONS AND RELEVANCE
What the sources say
- Not checked yetcites [1] Mozaffarian D Wu JHY Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events J Am Coll Cardiol 2011 58 20 2047 2067 22051327 source
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the background dietary intake in these trials was not usually measured, and many participants may have had adequate intake from diet alone.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Abstract > CONCLUSIONS AND RELEVANCE
What the sources say
- Not checked yetcites [2] Bucher HC Hengstler P Schindler C Meier G N-3 polyunsaturated fatty acids in coronary heart disease: a meta-analysis of randomized controlled trials Am J Med 2002 112 4 298 304 11893369 source
- Not checked yetcites [3] Hooper L Thompson RL Harrison RA Omega 3 fatty acids for prevention and treatment of cardiovascular disease Cochrane Database Syst Rev 2004 4 CD003177 15495044 PMC4170890 source
- Not checked yetcites [4] León H Shibata MC Sivakumaran S Dorgan M Chatterley T Tsuyuki RT Effect of fish oil on arrhythmias and mortality: systematic review BMJ 2008 337 a2931 10.1136/bmj.a2931 19106137 PMC2612582 source
- Not checked yetcites [5] Marik PE Varon J Omega-3 dietary supplements and the risk of cardiovascular events: a systematic review Clin Cardiol 2009 32 7 365 372 19609891 PMC6653319 source
- Not matchedcites [6] Trikalinos TA Lee J Moorthy D Effects of Eicosapentanoic Acid and Docosahexanoic Acid on Mortality Across Diverse Settings: Systematic Review and Meta-analysis of Randomized Trials and Prospective Cohorts Rockville, MD Agency for Healthcare Research and Quality 2012 22479722
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [7] Kwak SM Myung SK Lee YJ Seo HG Korean Meta-analysis Study Group Efficacy of ω-3 fatty acid supplements (eicosapentaenoic acid and docosahexaenoic acid) in the secondary prevention of cardiovascular disease: a meta-analysis of randomized, double-blind, placebo-controlled trials Arch Intern Med 2012 172 9 686 694 22493407 source
- Not checked yetcites [8] Rizos EC Ntzani EE Bika E Kostapanos MS Elisaf MS Association between ω-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis JAMA 2012 308 10 1024 1033 22968891 source
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Heterogeneity by prespecified subgroups was evaluated by pooling individual study results based on defined strata”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Methods > Statistical Analysis and Pooling
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“We excluded soft CHD end points (eg, angina, revascularization) to minimize bias in ascertainment of these events.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Methods > Assessment of CHD
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“with coefficients of variation less than 10% for most fatty acids and biomarkers”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Results > Characteristics of Studies and Participants
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“In randomized clinical trials, long-chain ω-3 PUFAs benefit multiple major cardiovascular risk factors, including triglyceride levels, blood pressure, heart rate, heart rate variability, endothelial function, and myocardial oxygen demand.1,10”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [1] Mozaffarian D Wu JHY Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events J Am Coll Cardiol 2011 58 20 2047 2067 22051327 source
- Not checked yetcites [10] Mozaffarian D Wu JH (n-3) fatty acids and cardiovascular health: are effects of EPA and DHA shared or complementary? J Nutr 2012 142 3 614S 625S 22279134 PMC3278271 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Several sensitivity analyses were performed.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Methods > Sensitivity Analyses
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Our findings are consistent with prior experimental evidence that long-chain ω-3 PUFAs may have membrane stabilizing actions in the setting of ischemia-induced ventricular fibrillation1,38 and observational evidence indicating that benefits of fish consumption are most related to arrhythmic events39 and fatal CHD.40”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [1] Mozaffarian D Wu JHY Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events J Am Coll Cardiol 2011 58 20 2047 2067 22051327 source
- Not checked yetcites [38] Siscovick DS Lemaitre RN Mozaffarian D The fish story: a diet-heart hypothesis with clinical implications: n-3 polyunsaturated fatty acids, myocardial vulnerability, and sudden death Circulation 2003 107 21 2632 2634 12782612 source
- Not checked yetcites [39] Siscovick DS Raghunathan TE King I Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest JAMA 1995 274 17 1363 1367 7563561 source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Covariates were standardized across studies based on prespecified, harmonized definitions and categorizations”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Methods > Covariates
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“a previous study10 suggests that DPA may inhibit ex vivo collagen-stimulated platelet aggregation, thromboxane production, and cyclooxygenase 1 activity.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [10] Mozaffarian D Wu JH (n-3) fatty acids and cardiovascular health: are effects of EPA and DHA shared or complementary? J Nutr 2012 142 3 614S 625S 22279134 PMC3278271 source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“Our prespecified primary analysis used inverse-variance weights.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Methods > Statistical Analysis and Pooling
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“A standardized analysis protocol was developed and provided to each participating study, including harmonized definitions of populations, exposures, outcomes, covariates, effect modifiers, and methods for pooling across studies.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Methods > Analysis Plan
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In the paper
“A key strength of our analysis was the prespecified, harmonized analytic plan using individual-level data within each study, which allowed consistent assessment of how ALA relates to CHD.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our results support use of phospholipids or total plasma for long-chain ω-3 PUFA exposure and a need for further investigation of optimal biomarkers for assessing ALA.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“few studies were available with African American (n = 2 studies: CHS and MESA) and Chinese subgroups (n = 2 studies: SCHS and MESA).27,33”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [27] Bild DE Bluemke DA Burke GL Multi-Ethnic Study of Atherosclerosis: objectives and design Am J Epidemiol 2002 156 9 871 881 12397006 source
- Not checked yetcites [33] Hankin JH Stram DO Arakawa K Singapore Chinese Health Study: development, validation, and calibration of the quantitative food frequency questionnaire Nutr Cancer 2001 39 2 187 195 11759279 source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Randomized clinical trials of fish oil supplements have found mixed effects, although overall pooled findings indicate a benefit in lowering risk of cardiac death,8 consistent with our findings.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [8] Rizos EC Ntzani EE Bika E Kostapanos MS Elisaf MS Association between ω-3 fatty acid supplementation and risk of major cardiovascular disease events: a systematic review and meta-analysis JAMA 2012 308 10 1024 1033 22968891 source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because our findings reflect habitual ω-3 exposure for primary CHD prevention, our results do not imply that fish oil supplementation will necessarily reduce CHD events, particularly in the context of short-term treatment or in those with preexisting CHD.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Baseline ω-3 PUFA biomarker concentrations reflect habitual dietary intake over the relevant etiologic period.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All cohorts assessed ω-3 PUFA exposure once at baseline, and changes over time would attenuate findings toward the null, causing underestimation of associations.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Because we analyzed observational studies, biomarkers and risk factors were not evenly distributed by randomization of study participants; hence, unmeasured or residual confounding cannot be excluded, and ω-3 biomarker measures may in part be markers of a long-term healthy lifestyle.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“The best compartment for assessing ALA has also been unclear, with possible advantages to adipose tissue16 but relatively little prior evaluation of other compartments.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [16] Baylin A Kim MK Donovan-Palmer A Fasting whole blood as a biomarker of essential fatty acid intake in epidemiologic studies: comparison with adipose tissue and plasma Am J Epidemiol 2005 162 4 373 381 16014782 source
Strength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Most studies18–25,27–35 used centralized adjudication processes or registry linkage rather than self-report alone in ascertaining events, reducing information bias.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [18] ARIC Investigators The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives Am J Epidemiol 1989 129 4 687 702 2646917
- Not checked yetcites [19] Campos H Bailey SM Gussak LS Siles X Ordovas JM Schaefer EJ Relations of body habitus, fitness level, and cardiovascular risk factors including lipoproteins and apolipoproteins in a rural and urban Costa Rican population Arterioscler Thromb 1991 11 4 1077 1088 2065029 source
- Not checked yetcites [20] Fried LP Borhani NO Enright P The Cardiovascular Health Study: design and rationale Ann Epidemiol 1991 1 3 263 276 1669507 source
- Not checked yetcites [21] Day N Oakes S Luben R EPIC-Norfolk: study design and characteristics of the cohort: European Prospective Investigation of Cancer Br J Cancer 1999 80 1 suppl 1 95 103 10466767 source
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- Not checked yetcites [23] Rimm EB Giovannucci EL Willett WC Prospective study of alcohol consumption and risk of coronary disease in men Lancet 1991 338 8765 464 468 1678444 source
- Not checked yetcites [24] Bartali B Benvenuti E Corsi AM Changes in anthropometric measures in men and women across the life-span: findings from the InCHIANTI study Soz Praventivmed 2002 47 5 336 348 12512227 source
- Not checked yetcites [25] Vanharanta M Voutilainen S Lakka TA van der Lee M Adlercreutz H Salonen JT Reduced risk of acute coronary events at high levels of mammalian lignan, enterolactone: a prospective population-based cohort study Lancet 1999 354 2112 2115 10609816 source
- Not checked yetcites [27] Bild DE Bluemke DA Burke GL Multi-Ethnic Study of Atherosclerosis: objectives and design Am J Epidemiol 2002 156 9 871 881 12397006 source
- Not checked yetcites [28] Norberg M Wall S Boman K Weinehall L The Västerbotten Intervention Programme: background, design and implications Global Health Action website 2010 http://www.globalhealthaction.net/index.php/gha/article/view/4643/5514 Accessed May 30, 2016 PMC2844807 20339479 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Our inclusion of all available studies substantially reduces the potential for publication bias.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“In addition, whereas circulating and tissue levels of EPA and DHA are strongly influenced by dietary seafood consumption, DPA concentrations appear to be mainly derived from endogenous elongation of EPA; interconversion between DPA and DHA is very limited.10”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [10] Mozaffarian D Wu JH (n-3) fatty acids and cardiovascular health: are effects of EPA and DHA shared or complementary? J Nutr 2012 142 3 614S 625S 22279134 PMC3278271 source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Use of biomarkers provided measures of exposure free of recall error and allowed separate evaluation of different ω-3 PUFAs and different circulating and tissue lipid compartments.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“However, a meta-analysis11 of prior reports of dietary and biomarker ALA and CHD risk revealed inconsistency, perhaps owing to methodologic and analytic differences in these investigations.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [11] Pan A Chen M Chowdhury R α-Linolenic acid and risk of cardiovascular disease: a systematic review and meta-analysis Am J Clin Nutr 2012 96 6 1262 1273 23076616 PMC3497923 source
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Adipose tissue has been suggested for measurement of fatty acids because it reflects long-term dietary intake (approximately 1 year).56”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [56] Dayton S Hashimoto S Dixon W Pearce ML Composition of lipids in human serum and adipose tissue during prolonged feeding of a diet high in unsaturated fat J Lipid Res 1966 7 1 103 111 5900208 source
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“However, our findings were independent of a range of major cardiovascular risk factors, and the relative specificity for fatal CHD and known biologic effects of ω-3 PUFAs also argue against residual confounding as the sole explanation for our findings.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, EPA and DHA are more highly concentrated in phospholipids than other compartments, and phospholipids also respond rapidly to dietary changes57,58 and may best reflect effects on membrane receptors.1”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
What the sources say
- Not checked yetcites [57] Arterburn LM Hall EB Oken H Distribution, interconversion, and dose response of n-3 fatty acids in humans Am J Clin Nutr 2006 83 6 suppl 1467S 1476S 16841856
- Not checked yetcites [58] Conquer JA Holub BJ Effect of supplementation with different doses of DHA on the levels of circulating DHA as non-esterified fatty acid in subjects of Asian Indian background J Lipid Res 1998 39 2 286 292 9507989
- Not checked yetcites [1] Mozaffarian D Wu JHY Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events J Am Coll Cardiol 2011 58 20 2047 2067 22051327 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The studies included both sexes, multiple races, and a range of socioeconomic statuses across 16 countries, increasing generalizability.”
§ ω-3 Polyunsaturated Fatty Acid Biomarkers and Coronary Heart Disease > Discussion
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
ω-3 PUFA biomarker concentrations reflect dietary intake of these fatty acids.
“biomarker concentrations of seafood and plant-derived ω-3 fatty acids are associated with a lower incidence of fatal CHD.”
The paper relies on this without support.
The 19 included studies are representative of free-living populations globally.
“On the basis of available studies of free-living populations globally”
The paper relies on this without support.
Earlier single-study biomarker analyses generally lacked power to examine effect differences by participant traits, medication use, or genetic variation.
“prior individual biomarker studies were generally underpowered to explore potentially relevant differences in effects depending on underlying participant characteristics, medication use, or genetic variation.”
The paper relies on this without support.
The different biomarker compartments (total plasma, phospholipids, cholesterol esters, adipose tissue) provide comparable measures of ω-3 PUFA exposure for pooling.
“Results were first pooled separately for each biomarker compartment and then pooled together.”
The paper relies on this without support.
Baseline ω-3 PUFA biomarker concentrations reflect habitual dietary intake over the relevant etiologic period.
“Because our findings reflect habitual ω-3 exposure for primary CHD prevention”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Observational studies have demonstrated an inverse association between dietary consumption of either fatty fish or omega-3 fatty acids and incident cardiovascular events 1,2”
From Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk (2020) · cites this paper as [1]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“The origins of this research were based on observations that dietary consumption of fatty fish or omega-3 fatty acids were associated with lower rates of incident cardiovascular events in large cohort studies. 1,2,19,20”
From Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk (2020) · cites this paper as [1]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Different fatty acids are assigned the same nonfatal-MI result
MajorThe abstract assigns the nonfatal-MI quintile result of RR 0.87 to ALA, whereas the Results section assigns that same result to DHA.
“Across quintiles, lower risk of nonfatal MI was evident with EPA (RR, 0.71; 95% CI, 0.56–0.90) and ALA (RR, 0.87; 95% CI, 0.78–0.97)”
“Upper quintiles of EPA and DHA were associated with a lower risk of nonfatal MI (quintile 5 vs quintile 1 comparison: RR, 0.71 [95% CI, 0.56–0.90] vs 0.87 [95% CI, 0.78–0.97]).”
Two heterogeneity values are reported for DHA
MinorFor the fatal-CHD association, DHA is assigned an I2 of both 37% and 31% in consecutive statements.
“There was moderate heterogeneity in this association for EPA and DHA (I2 = 37% for both)”
“low heterogeneity for DPA and DHA (I2 = 0% and 31%, respectively)”
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Metadata
- Authors
- Del Gobbo, L. C., Imamura, F., Aslibekyan, S., Marklund, M., Virtanen, J. K., Wennberg, M., Yakoob, M. Y., Chiuve, S. E., dela Cruz, L., Frazier-Wood, A. C., Fretts, A. M., Guallar, E., Matsumoto, C., Prem, K., Tanaka, T., Wu, J. H. Y., Zhou, X., Helmer, C., Ingelsson, E., Yuan, J.-M., Barberger-Gateau, P., Campos, H., Chaves, P. H. M., Djoussé, L., Giles, G. G., Gómez-Aracena, J., Hodge, A. M., Hu, F. B., Jansson, J.-H., Johansson, I., Khaw, K.-T., Koh, W.-P., Lemaitre, R. N., Lind, L., Luben, R. N., Rimm, E. B., Risérus, U., Samieri, C., Franks, P. W., Siscovick, D. S., Stampfer, M., Steffen, L. M., Steffen, B. T., Tsai, M. Y., van Dam, R. M., Voutilainen, S., Willett, W. C., Woodward, M., Mozaffarian, D., & for the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Fatty Acids and Outcomes Research Consortium (FORCe)
- Affiliations
- Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California
- University of Cambridge (GB)
- University of Alabama at Birmingham (US)
- Uppsala University (SE)
- University of Eastern Finland (FI)
- Umeå University (SE)
- Harvard University (US)
- Brigham and Women's Hospital (US)
- Cancer Epidemiology Centre, Cancer Council Victoria, Victoria, Australia
- USDA/ARS Children’s Nutrition Research Center, Baylor College of Medicine, Houston, Texas
- University of Washington (US)
- Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
- National University of Singapore (SG)
- National Institutes of Health (US)
- The University of Sydney (AU)
- University of Minnesota (US)
- Université de Bordeaux (FR)
- University of Pittsburgh (US)
- Institut National de la Santé et de la Recherche Médicale, Institut de Santé Publique, d'Épidémiologie et de Développement, Centre IInstitut National de la Santé et de la Recherche Médicale U897-Epidemiologie-Biostatistique, Bordeaux, France
- Florida International University (US)
- Cancer Council Victoria (AU)
- Universidad de Málaga (ES)
- Cardiovascular Health Research Unit, Department of Medicine, University of Washington, Seattle
- New York Academy of Medicine (US)
- Saw Swee Hock School of Public Health, National University of Singapore, Singapore
- Tufts University (US)
- ORCID
- Imamura, Fumiaki
- Aslibekyan, Stella
- Marklund, Matti
- Virtanen, Jyrki K.
- Wennberg, Maria
- Yakoob, Mohammad Y.
- Chiuve, Stephanie E.
- Fretts, Amanda M.
- Matsumoto, Chisa
- Prem, Kiesha
- Wu, Jason H. Y.
- Zhou, Xia
- Helmer, Catherine
- Ingelsson, Erik
- Yuan, Jian-Min
- Campos, Hannia
- Chaves, Paulo H. M.
- Djoussé, Luc
- Giles, Graham G.
- Hodge, Allison M.
- Hu, Frank B.
- Jansson, Jan-Håkan
- Johansson, Ingegerd
- Khaw, Kay-Tee
- Koh, Woon-Puay
- Lind, Lars
- Luben, Robert N.
- Rimm, Eric B.
- Risérus, Ulf
- Franks, Paul W.
- Siscovick, David S.
- Stampfer, Meir
- Steffen, Lyn M.
- Steffen, Brian T.
- Tsai, Michael Y.
- Voutilainen, Sari
- Willett, Walter C.
- Woodward, Mark
- Mozaffarian, Dariush
- Venue
- JAMA Internal Medicine
- Publisher
- American Medical Association (AMA)
- Published
- 2016-08-01
- Volume
- 176
- Issue
- 8
- Pages
- 1155
- ISSN
- 2168-6106 (ISSN-L)
- PMC
- PMC5183535
- OpenAlex
- W2469860611
- Cited by
- 404
- References
- 64
- Citations by year
- 2026: 25 · 2025: 26 · 2024: 25 · 2023: 36 · 2022: 41 · 2021: 53 · 2020: 43 · 2019: 53 · 2018: 56 · 2017: 36 · 2016: 8
- FWCI
- 53.39
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- JAMA Internal Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Lund University Publications (Lund University) (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion, cc-by)
- Funders
- Brigham and Women's Hospital
- University of Minnesota
- New York Academy of Medicine
- Florida International University
- University of Washington
- Duke-NUS Medical School
- National Institute for Health and Care Research (NF-SI-0512-10114)
- British Heart Foundation
- University of Oxford
- National University of Singapore
- Agence Nationale de la Recherche (ANR-06-PNRA-0005)
- Lunds Universitet
- Umeå Universitet
- National University Health System
- George Institute for Global Health
- National Institutes of Health (n01hc95164-17-0-1, n01hc085082-026, n01hc085081-021, n01hc085079-024, n01hc085083-027, n01hc95165-34-0-1, 5r01ca049449-18, n01hc085080-026, n01hc95161-24-0-1, n01hc095169-003, n01hc95166-21-0-1, n01hc085086-022, n01hc95162-31-0-1, n01hc95168-27-0-1, n01hc95160-18-0-1, n01hc095167-000, UL1TR001079, n01hc95163-22-0-1, n01hc55222-0-0-0, n02hl64278-6-0-0, n01hc95159-40-0-1, Z99 AG999999)
- Medical Research Council (MC_UU_12015/5, MR/N003284/1)
- National Institute on Alcohol Abuse and Alcoholism (R01AA011181)
- National Institute on Aging (R01AG023629)
- National Heart, Lung, and Blood Institute (N01 HC085086, R01HL060712, N01-HC095169, N01-HC-095165, R21HL088081, N01 HC085079, N01 HC095163, N01 HC085083, N01 HC085080, N02 HL064278, R01HL035464, N01-HC-095159, N01 HC095168, N01-HC-095162, N01-HC-095161, R01 HL026490, R01HL087641, R01HL059367, N01 HC095167, N01HC085082, U01HL080295, N01-HC-095160, R01HL081549, N01 HC055222, N01 HC095166, R01HL034595, N01 HC095164, N01 HC085081, R01HL085710, R01HL086694, R01HL034594, R01HL088521)
- National Human Genome Research Institute (U01HG004402)
- National Cancer Institute (R01CA040360, R01CA144034, R01CA080205, P01CA087969, R01 CA034944, R01‐CA049449, R01CA097193, P01CA055075, UM1CA182876, UM1CA186107, UM1CA167552, U01CA182876, U01CA167552)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK046200)
- National Center for Research Resources (UL1RR025005)
- National Center for Advancing Translational Sciences
- National Institute on Minority Health and Health Disparities (R01MD009164)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Nutritional Studies and Diet
- Life Sciences › Agricultural and Biological Sciences › Aquatic Science › Aquaculture Nutrition and Growth
- Keywords
- coronary artery disease, eicosapentaenoic acid, docosapentaenoic acid, docosahexaenoic acid, alpha-linolenic acid, myocardial infarction, coronary heart disease mortality, primary prevention, plasma phospholipids, cholesterol esters, adipose tissue
- MeSH terms
- Coronary Disease, Docosahexaenoic Acids, Fatty Acids, Unsaturated, Female, Humans, Male, Cohort Studies, Biomarkers, Fatty Acids, Omega-3, Incidence, Odds Ratio, alpha-Linolenic Acid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-01, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-01 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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