Rethinking Cancer: Exploring the Big C as a Metabolic Disease

Cancer has long been viewed primarily as a genetic disease, driven by mutations in our DNA that are inherited or induced through toxic exposure. Yet, it doesn’t give us the total picture of what’s going on. Most cancers arise out of a combination of multiple faulty genes, and many people carrying the same genetic make up will never develop cancer.

Emerging research is challenging this conventional wisdom and offering a new perspective: cancer as a metabolic disease rooted in the malfunction of our cellular powerhouses, the mitochondria.

Most people understand metabolism as simply how the body meets its energy needs through food. This isn’t incorrect. That definition only represents one metabolic process. Metabolism is actually all the chemical processes going on continuously inside your body to allow life and normal functioning.

So that would include the chemical activities that exist inside individual cells to maintain life and function.

Thinking about cancer as metabolic, not simply genetic, is a fascinating paradigm shift in cancer research that is giving more attention to all the contributing factors, including cellular dysregulation. This opens the opportunities around the prevention of cancer within the body, and gives complementary physicians and oncologists more creative opportunities for treatment of this disease condition.

Research has begun looking at the role mitochondria play in cancer development. Mitochondria are tiny, energy-producing organelles found within our cells. They are often referred to as the “cell's powerhouses” because they generate adenosine triphosphate (ATP), the molecule that fuels various cellular processes. Mitochondria are also involved in regulating apoptosis, a process known as “programmed cell death.” When our cells become faulty, a complicated “apoptotic cascade” is initiated - with the key purpose of keeping the faulty cell from propagating in a defective manner, e.g., becoming a cancer.

This is a follow-on from the work of Nobel laureate Otto Warburg, who first described it in the 1920s. He identified “The Warburg” effect, a phenomenon where cancer cells predominantly rely on glycolysis, a less efficient form of energy production, even in the presence of oxygen. In the presence of oxygen in the body, energy production by mitochondria using ATP would usually take place in healthy cells, producing less toxic by-products in the body. Glycolysis, on the other hand, produces a lot of toxic by-products, and is usually triggered in the presence of sugary, acidic foods (like sodas, sugar, ultra-processed foods, excessive meat intake). Glycolysis also plays a key role in pro-inflammatory responses - and inflammation is now being linked to up to 20% of cancers*.

This shift toward glycolysis not only provides cancer cells with a rapid source of energy, but also creates an acidic microenvironment that promotes tumour growth.

Genetic Mutations and the Metabolic Connection

While genetic mutations undoubtedly contribute to cancer development, recent research has shown that many of these mutations are a consequence of mitochondrial dysfunction and metabolic alterations. For instance, impaired mitochondrial function can lead to increased levels of reactive oxygen species (ROS), which can damage DNA and trigger genetic mutations.

The Role Nourishing Foods and Exercise Play in Prevention of Cancer

With cancer being so metabolically linked, it offers real hope in the prevention of cancer, and the maintenance of cancer remission through diet and exercise. Food and movement play critical roles in promoting efficient mitochondrial function. Essential nutrients like vitamins (e.g., B vitamins), minerals (e.g., magnesium), and antioxidants (e.g., coenzyme Q10) are crucial for mitochondrial health. A diet rich in antioxidants, such as vitamins C and E, also helps to counteract oxidative stress and protect mitochondria.

These nutrients are readily obtained from a balanced diet rich in organic and healthy grown fruits and vegetables; well raised and organic lean proteins; and healthy fats like olive oil, hemp oil and Omega 3 Fatty acids.

Exercise improves the cardiovascular system, increasing the efficiency of oxygen delivery to tissues and the utilization of oxygen by mitochondria during energy production. Additionally, resistance training and other forms of exercise promote muscle health and prevent muscle loss (atrophy). Healthy muscles are more metabolically active and contribute to efficient mitochondrial function.

Although it may not suit everyone, high-intensity interval training (HIIT), can also trigger mitochondrial adaptations, leading to improvements in mitochondrial density and function, ultimately enhancing energy production.

And both diet and exercise can reduce chronic stress, which can negatively impact mitochondrial function. Chronic stress can lead to an overproduction of ROS and mitochondrial damage.

Conclusion

While the metabolic approach to cancer is still in its early stages, it offers a promising avenue for prevention, research and treatment options. By targeting the metabolic vulnerabilities of cancer cells, we may be able to develop more effective and non-toxic therapies.

The traditional view of cancer as primarily a genetic disease is changing. Research increasingly supports the notion that it is a metabolic disease driven by mitochondrial dysfunction and altered cellular metabolism. Our bodies are complex, but with the right knowledge, wisdom and information; we can assist our bodies in staving off disease and maintaining health.

References:

*Singh N, Baby D, Rajguru JP, Patil PB, Thakkannavar SS, Pujari VB. Inflammation and cancer. Ann Afr Med. 2019 Jul-Sep;18(3):121-126. doi: 10.4103/aam.aam_56_18. PMID: 31417011; PMCID: PMC6704802.