Below is the abstract of a journal article that has been bruited about in the popular press. The journal article appeared yesterday. It is one of a long series of attempts to discredit meat eating.
And the present article follows a familiar methodology. I am going to put it bluntly: When there is no overall connection between the variables you are studying, you do comparisons of extremes -- as in tertiles, quartiles or quintiles. You can sometimes "save" your research that way if the extremes differ.
The present article resorts to extreme quintiles so they really had to stretch it to produce a reportable finding. The important thing to know, however, is that such anayses throw away the majority of your data so really tell you nothing. But the resort to extremes does of itself imply that there was NO overall relationship in the data. It's a common analysis but totally discreditable scientifically
The real result of the research therefore is that eating red meat had NO EFFECT on anything
Dietary Meat, Trimethylamine N-Oxide-Related Metabolites, and Incident Cardiovascular Disease Among Older Adults: The Cardiovascular Health Study
Meng Wang et al.
Effects of animal source foods (ASF) on atherosclerotic cardiovascular disease (ASCVD) and underlying mechanisms remain controversial. We investigated prospective associations of different ASF with incident ASCVD and potential mediation by gut microbiota-generated trimethylamine N-oxide, its L-carnitine-derived intermediates γ-butyrobetaine and crotonobetaine, and traditional ASCVD risk pathways.
Among 3931 participants from a community-based US cohort aged 65+ years, ASF intakes and trimethylamine N-oxide-related metabolites were measured serially over time. Incident ASCVD (myocardial infarction, fatal coronary heart disease, stroke, other atherosclerotic death) was adjudicated over 12.5 years median follow-up. Cox proportional hazards models with time-varying exposures and covariates examined ASF-ASCVD associations; and additive hazard models, mediation proportions by different risk pathways.
After multivariable-adjustment, higher intakes of unprocessed red meat, total meat, and total ASF associated with higher ASCVD risk, with hazard ratios (95% CI) per interquintile range of 1.15 (1.01–1.30), 1.22 (1.07–1.39), and 1.18 (1.03–1.34), respectively. Trimethylamine N-oxide-related metabolites together significantly mediated these associations, with mediation proportions (95% CI) of 10.6% (1.0–114.5), 7.8% (1.0–32.7), and 9.2% (2.2–44.5), respectively. Processed meat intake associated with a nonsignificant trend toward higher ASCVD (1.11 [0.98–1.25]); intakes of fish, poultry, and eggs were not significantly associated. Among other risk pathways, blood glucose, insulin, and C-reactive protein, but not blood pressure or blood cholesterol, each significantly mediated the total meat-ASCVD association.
In this large, community-based cohort, higher meat intake associated with incident ASCVD, partly mediated by microbiota-derived metabolites of L-carnitine, abundant in red meat. These novel findings support biochemical links between dietary meat, gut microbiome pathways, and ASCVD.
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