Masters of Health Magazine June - July 2026 | Page 19

Tumors as an emergency overflow tank for radiation-induced ROS stress. When the total ROS load exceeds the body’s capacity, tumors upregulate key antioxidant systems to absorb and contain the excess. By isolating and processing the surplus ROS locally, the tumor helps limit widespread oxidative damage to healthy tissues.

In response to this radiation, the body recruits tumor tissue as an emergency overflow tank. These tumors upregulate powerful antioxidant systems to contain and process the excess ROS and damaged biomolecules locally, limiting widespread oxidative damage and inflammation to the rest of the organism. This unifies radiation with all the chemical toxins we’ve discussed: whether the stressor is a chemical (microplastics, PFAS, iron) or electromagnetic radiation, the body responds to the same endpoint — excessive oxidative stress.

Cancer as the body’s second liver

One of my favorite analogies for a cancer tumor is viewing it as the body’s second liver. Indeed, damage to the primary liver often precedes the formation of tumors. Here I discuss several toxins that the liver normally detoxifies when healthy, but that get shuttled to cancer tumors when the liver is overwhelmed.

(1) Fructose

This pattern appears clearly with fructose. (Note that extracted fructose differs from fructose in whole fruit because fruit delivers it alongside fiber and minerals that moderate its effect.) When dietary fructose intake exceeds the liver’s processing capacity, certain tumors upregulate the same key enzymes the liver uses (fructokinase and aldolase B) to metabolize fructose into fat. The tumor essentially takes over part of the liver’s lipogenic and detoxification workload, protecting the primary liver and the rest of the body from fructose-induced oxidative stress and lipotoxicity.

The liver runs fructose through a detox pathway, since fructose is a toxin. I argue that a cancer tumor can be viewed as a back-up liver: it similarly runs fructose through a detox pathway.

(2) Ethanol

The same “second liver” strategy is evident with ethanol. When the liver is fatty, inflamed, or otherwise impaired — often from damaged oils, fructose, or chronic alcohol — many tumors dramatically upregulate alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). These are the exact enzymes the liver uses to convert ethanol into acetaldehyde and then into acetate. By pulling in ethanol and rapidly detoxifying its highly toxic metabolite

(acetaldehyde), tumors help contain the resulting ROS and prevent systemic damage.