The whispers of a growing concern have turned into resounding alarms within the realm of cancer research. Colorectal cancer, a formidable adversary, has begun to rear its head in a younger population, sending shockwaves through the medical community. A disquieting revelation from the American Cancer Society highlights a rising trend in deaths from colorectal cancer among individuals under the age of 55. Amidst the disconcerting statistics, a beacon of understanding emerges, illuminating a potential key factor behind this unsettling surge. In the pages of the February 2019 issue of the journal “Cell,” researchers unveil a revelation that bridges genetics and diet in the development of colorectal cancer.

Genetic Risk and Dietary Triggers: A Disturbing Alliance

The stage for this revelation is set with the APC gene, an integral player in the realm of colon health. The APC gene, responsible for orchestrating regulated cell division within the colon, carries a sinister secret. A genetic defect within this gene paves the way for an increased risk of colon cancer. Yet, the story doesn’t end here. The complexity of genetics unveils a twist—while the APC gene defect is a loaded gun, the introduction of a high-fat diet is the trigger that ignites the devastating cascade of colon cancer development.

The Crucial Culprit: High-Fat Diet

The groundbreaking study in the journal “Cell” speaks volumes about the intimate connection between genetics and diet. Under experimental conditions, animals harboring an APC genetic mutation were fed a high-fat diet. The results painted a stark picture—colon tumors, both benign and malignant, flourished in response to the high-fat diet. In a contrasting scenario, animals with the same genetic mutation but fed a lower fat diet remained unscathed by the threat of colon tumors. The verdict was clear: the APC gene mutation set the stage, but it was the high-fat diet that took center stage as the driving force behind colon cancer development.

Deciphering the Mechanism: Bile Acids and Colon Stem Cells

To uncover the intricate mechanism behind this alliance, the researchers dived deeper into the molecular landscape. A high-fat diet was found to amplify the secretion of bile acids into the intestinal tract. These bile acids, in turn, exerted their influence on a signalling protein within colon stem cells. A crucial protein known as the FXR was inhibited by the action of bile acids. This inhibition created fertile ground for cancer stem cells to propagate uncontrollably, especially in the absence of the check imposed by the APC tumor suppressor gene. The story of cancer unfolded through this interplay, revealing a pivotal chapter in the journey of its genesis.

Unveiling the Preventive Strategies

The revelation serves as a clarion call, reiterating the significance of preventive strategies in the face of colorectal cancer. A gene mutation may set the stage, but it is lifestyle and dietary choices that take the reins. The consumption of a high-fat diet, emblematic of the North American and Western diets, emerges as a central culprit. From high-fat meats to deep-fried temptations, from creamy salad dressings to coconut oil-laden pastries, the high-fat diet contributes significantly to the emergence of colon cancer. This revelation gains greater weight as we witness the unsettling rise of colon cancer among individuals below the age of 55.

Charting a Path to Resilience

The path forward unfolds with clarity—the power to prevent colon cancer resides within our choices. Embracing a healthier dietary landscape becomes the cornerstone. By limiting the intake of detrimental fats, we place ourselves on a trajectory towards resilience. The unsettling statistics can be challenged, and colon cancer’s reach curtailed, through a conscious commitment to well-being. Beyond dietary choices, routine colonoscopy assessments after the age of 50 serve as guardians against the emergence of benign tumors that could evolve into malignant colon cancer.

Epilogue: A Tapestry of Choices

As we traverse the landscape of cutting-edge research, we find ourselves at the crossroads of genetic predisposition and dietary choices. The canvas of human health is painted by intricate strokes—the harmony between genetics and lifestyle. The revelation that a high-fat diet can function as the catalyst in the emergence of colon cancer unveils the importance of redefining our relationship with food. It underscores the potential for empowered choices in sculpting our well-being. Let us heed this revelation as a guiding light, steering us towards vitality and longevity.

References:

1. Ting Fu, Sally Coulter, Eiji Yoshihara, Tae Gyu Oh, Sungsoon Fang, Fritz Cayabyab, Qiyun Zhu, Tong Zhang, Mathias Leblanc, Sihao Liu, Mingxiao He, Wanda Waizenegger, Emanuel Gasser, Bernd Schnabl, Annette R. Atkins, Ruth T. Yu, Rob Knight, Christopher Liddle, Michael Downes, Ronald M. Evans. FXR Regulates Intestinal Cancer Stem Cell Proliferation. Cell, 2019; 176 (5): 10.1016/j.cell.2019.01.036

Eat smart, live well, look great,

Dr. Meschino