Inflammation is a risk factor for many chronic diseases, including: cardiovascular disease The influence of diet on inflammation (CVD) is an area of increasing scientific interest. In particular, recommendations to limit red meat intake are often based in part on older research suggesting that red meat has a negative impact on inflammation, but more recent research supports this. not.
“The role of a diet that includes red meat on inflammation and disease risk has not been well studied and may lead to public health recommendations that are not based on strong evidence,” said Associate Professor of Pediatrics said Dr. Alexis Wood (Nutrition). his USDA/ARS Pediatric Nutrition Research Center at Baylor College of Medicine and Texas Children’s Hospital. “Our team attempted a more detailed investigation using data on metabolites in the blood, which can provide a more direct link between diet and health.”
Methodology and findings
Wood and her team recently published their findings after analyzing cross-sectional data collected from nearly 4,000 older adults participating in the Multi-Ethnic Study of Atherosclerosis (MESA). of American Journal of Clinical Nutrition. Cross-sectional data are a useful source of evidence on how diet affects health. It uses observed data without affecting the normal lifestyle of freely living people. In this way, it may be easier to retrieve results from such studies and apply them to non-research settings.
In addition to assessing the participants’ self-reported food intake and several biomarkers, the researchers also measured a range of dietary metabolites in their blood. Plasma metabolites help capture the effects of dietary intake as food is processed, digested, and absorbed.
Researchers found that consumption of raw and processed red meat (beef, pork, and lamb) was not directly associated with inflammatory markers when adjusting for body mass index (BMI), and that red meat but not body weight This suggests that it may cause inflammation. Factors contributing to increased systemic inflammation. Of particular interest was the lack of association between red meat intake and C-reactive protein (CRP), a key inflammatory risk marker for chronic disease.
“Our analysis adds to the growing body of evidence that measurement matters. plasma “Rather than relying solely on self-reported dietary intake, we need to use markers such as metabolites to track associations between diet and disease risk,” Wood said. “Our analysis does not support the association of previous observational studies linking red meat intake and inflammation.”
Need for further research
Because observational studies cannot reveal cause and effect, randomized controlled trials (RCTs), which randomly assign individuals to consume or not consume the dietary element of interest, are needed to determine whether red meat does not alter inflammation. Required as additional evidence for proper understanding. . Several RCTs have demonstrated that lean, unprocessed beef can be enjoyed in a heart-healthy dietary pattern.
“When making dietary recommendations based on the latest evidence, we have reached the point where further research is needed before making recommendations to limit red meat intake to reduce inflammation,” Wood said. . “Red meat is popular, accessible, and delicious, and its place in our diets has deep cultural roots. Given this, recommendations for reducing consumption It should be supported by strong scientific evidence, which does not yet exist.”
Reference: “Untargeted metabolomic analysis investigating the association between raw red meat intake and inflammatory markers” Alexis C. Wood, Goncalo Graca, Meghana Gadgil, Mackenzie K. Senn, Matthew A. Allison, Ioanna Tzoulaki, Philip Greenland , Timothy Ebbels, Paul Elliott, Mark O. Guderzi, Russell Tracy, Jerome I. Rotter, David Herrington, September 1, 2023, American Journal of Clinical Nutrition.
DOI: 10.1016/j.ajcnut.2023.08.018
Other contributors to this work include Gonzalo Graca, Meghana Gagil, Mackenzie K. Senn, Matthew A. Allison, Ioanna Tzolaki, Philip Greenland, Timothy Ebels, Paul Elliott, and Mark Elliott. Includes O. Goodarge, Russell Tracy, Jerome I. Lotter, and David Herrington.
This research was supported by the Beef Checkoff. Timber was supported in part by USDA/ARS (Cooperative Agreement 58-3092-5-001). Mark Goodarzi was supported by the Ellis M. Field Chair in Diabetes Research. Jerome Rotter was partially supported by: National Institutes of Health grants from the National Institute of Diabetes and Digestive and Kidney Diseases (DK063491), the National Center for the Advancement of Translational Sciences (UL1TR001881), the CHARGE Consortium, and the National Heart, Lung, and Blood Institute (NHLBI; R01HL105756);