The present experimental data suggest that red meat consumption does not affect glycemic control or inflammation among people who have not been diagnosed with a cardiometabolic disease, based on studies that were less than 16 weeks in duration. These findings held even among subgroup analysis and sensitivity analysis, suggesting that these findings hold up across various groups of people (e.g. individuals with obesity), diet types (e.g. carbohydrate content), and even between processed and unprocessed red meat. As such, these findings suggest that red meat intake alone, as a dietary variable, does not substantially affect glycemic control or inflammation in people without already established cardiometabolic diseases. However, given that the studies included in the meta-analysis ranged from 3 to 16 weeks in length, the present study does not provide insight into longer term red meat consumption.
These data are in line with previous meta-analyses of randomized controlled trials examining the effect of red meat intake on other metabolic variables, specifically blood lipids. For example, one meta-analysis found that red meat intake did not affect measures of blood lipids, lipoproteins, or blood pressure. Another meta-analysis found that red meat did not substantially alter cardiovascular risk factors, unless it was substituted for plant protein, but no other protein sources. The latter is interesting, because subgroup analysis in the present study also supports this finding, as the present study found no benefit when substituting red meat for poultry. However, the present study did not find that substituting red meat for plant protein had any effect.
This study leaves many unanswered questions, as red meat intake does appear to increase the risk of type 2 diabetes in observational studies, but the present study does not show an increase in risk factors associated with type 2 diabetes in randomized trials. In that, it is worth considering that claims of alleged pro-diabetic effects of red meat are based almost exclusively on epidemiological research. Furthermore, one of the most important questions in the context of determining a causal relationship outside of highly controlled RCTs is the unanswered question as to what the mechanism(s) by which red meat increases the risk of diabetes and/or cardiometabolic diseases actually are. In fact, a possible explanation for the epidemiologically observed detrimental effects of red meat is the clustering of established pro-diabetic and pro-CVD lifestyle factors. Specifically, people who eat more red meat are also more likely to smoke, have a higher BMI, consume more processed foods, have high levels of inactivity, and consume lower amounts of fruits, vegetables, and fiber in their diet. While many studies try to adjust for this association, it is by no means clear that the observational data is not critically compromised by confounding.
In addition to the cluster of lifestyle factors that may contribute to risk, several biological mechanisms have been explored, including heme iron, advanced glycation end products, and red meat specific glycans. There has been some association data linking heme iron to increased risk of heart disease, potentially by causing inflammation. However, there is no good evidence in humans to support heme as a main mechanism, and studies done in mouse models may not be applicable because mice are poor absorbers of heme iron, especially when compared to humans. Red meat is also a dietary source of advanced glycation end products, which are proteins or lipids that become glycated after they are exposed to sugars. While these advanced glycation end products have been linked to inflammation in in vitro experimental studies, there is mixed evidence in in vivo studies in humans. For example, one short-term randomized trial found that reducing dietary advanced glycation end product consumption was not beneficial for lowering blood lipids or inflammation. However, a different randomized trial found that a diet lower in advanced glycation end products led to better insulin sensitivity. More recently, a red meat-derived glycan known as Neu5Gc has been examined as a potential mechanism for red meat causing inflammation. Currently, this marker appears to be a good measure of red meat intake, but its precise role in red meat intake, disease risk, and inflammation is not well established in humans.
There are several limitations of the present study that should be taken into consideration when interpreting the findings. The trials included in this study all had a duration of less than 24 weeks, with a median length of 8 weeks. As such, the present study may have not been able to detect changes in inflammation or glycemic control if the effects of red meat take years or decades to manifest. Additionally, heterogeneity was high for the results that it was reported for, suggesting there was high variance in outcomes between studies.
The present study is supported by other experimental studies and corresponding meta-analyses showing that red meat intake does not affect cardiometabolic risk factors, including glycemic control and inflammation. Currently, one possible explanation for the link between red meat and disease risk is that other lifestyle risk factors like smoking and a chronic energy surplus are more likely to be observed among people with high red meat intake.