Red dye given to mice at a human equivalent dose of 7mg/kg caused DNA damage to colon cells. Detrimental effects on the microbiome when administered with a high fat diet were also observed. In conclusion, the scientists stated Red 40 triggers low-grade inflammation in the colon and could play a role in the increasing rates of colon cancer being observed in society today.
ABSTRACT
The incidence of colorectal cancer (CRC) among young people has been on the rise for the past four decades and its underlying causes are only just starting to be uncovered. Recent studies suggest that consuming ultra-processed foods and pro-inflammatory diets may be contributing factors. The increase in the use of synthetic food colors in such foods over the past 40 years, including the common synthetic food dye Allura Red AC (Red 40), coincides with the rise of early-onset colorectal cancer (EOCRC). As these ultra-processed foods are particularly appealing to children, there is a growing concern about the impact of synthetic food dyes on the development of CRC. Our study aimed to investigate the effects of Red 40 on DNA damage, the microbiome, and colonic inflammation. Despite a lack of prior research, high levels of human exposure to pro-inflammatory foods containing Red 40 highlight the urgency of exploring this issue. Our results show that Red 40 damages DNA both in vitro and in vivo and that consumption of Red 40 in the presence of a high-fat diet for 10 months leads to dysbiosis and low-grade colonic inflammation in mice. This evidence supports the hypothesis that Red 40 is a dangerous compound that dysregulates key players involved in the development of EOCRC.
In conclusion, our study, distinguished by meticulous dietary control and selected CRC-related outcome measurements, underscores Red 40's adverse effects. The combination of in vitro and in vivo models facilitates nuanced exploration of CRC-relevant mechanisms. Nonetheless, our study does possess limitations, including the need for more detailed mechanistic insights into observed changes. As we continue to examine how Red 40 triggers low-grade inflammation, with emphasis on relevant microbial species, we acknowledge the challenges in extrapolating results from animal models to human contexts. To this, the current study advances our understanding of Red 40's detrimental effects on health, highlighting the potential of chronic exposure to elevate CRC risk. We demonstrate that Red 40 inflicts DNA damage, particularly in the presence of a HFD, which leads to altered gut microbiota and subsequent inflammation in the distal colon. These findings contribute to the growing body of evidence illustrating Red 40's adverse impact on colorectal carcinogenesis. Future endeavors should incorporate human studies to deepen insights into Red 40's role in EOCRC's natural history, alongside further laboratory investigations to elucidate underlying mechanisms.