Is it possible that chromosomal damage is simply a marker for cancer and not the actual cause of the disease? Compelling evidence suggests this is the case, and in the featured lecture, orthopedic surgeon Dr. Gary Fettke reviews some of this evidence.
Having battled cancer himself, Fettke came to realize the influence of nutrition on cancer, and the importance of eating a diet high in healthy fats and low in net carbohydrates (total carbs minus fiber, i.e. non-fiber carbs). Fettke is not the only one promoting the metabolic model of cancer.
Earlier this year I interviewed Travis Christofferson, author of a phenomenal book called “Tripping Over the Truth: The Return of the Metabolic Theory of Cancer Illuminates a New and Hopeful Path to a Cure,” on this topic.
The Metabolic Model of Cancer
The Cancer Genome Atlas project that began in 2006 set out to sequence the genomes of cancer cells. It was the largest government project ever conceived, involving 10,000 times the amount of genetic sequencing done by the Human Genome Project. Alas, the results didn’t conform to their original expectations.
The evidence clearly showed that something other than mere gene mutation was at play. The mutations found in cancer cells were simply too random. Some cancers didn’t even have any genetic mutations driving them. So what then could the driving factor be?
In a nutshell, the nuclear genetic defects typically thought to be responsible for cancer actually occur further downstream. Mitochondrial damage happens first, which then triggers nuclear genetic mutations that may lead to cancer.
Moreover, scientists are now finding that mitochondrial dysfunction is at the core of virtually ALL diseases, placing mitochondrial function at the very center of just about any wellness or disease prevention program.
As Fettke notes, one of the primary considerations is glucose metabolism within your mitochondria — a theory initially brought forth by Dr. Otto Warburg in the 1920s.
In 1931, Warburg won the Nobel Prize in Physiology or Medicine for his discovery that cancer cells have a fundamentally different energy metabolism compared to healthy cells. As it turns out, cancer cells do not have the same metabolic flexibility as healthy ones.
Cancer Cells Are Metabolically Limited to Feed on Sugar
A cell can produce energy either aerobically, in the mitochondria, or anaerobically, in the cytoplasm. Anaerobic metabolism generates excessive levels of lactic acid, which can be toxic.
Warburg discovered that in the presence of oxygen, cancer cells overproduce lactic acid, and this became known as the Warburg Effect. So what does this tell us about the nutritional origins of cancer? In a nutshell, Warburg’s findings tell us that sugar “feeds” cancer while fats “starve” it.
Healthy cells can use either glucose or ketone bodies from fat as an energy source, but cancer is metabolically restricted to using glucose only. Cancer cells for the most part lack metabolic flexibility and simply cannot metabolize ketones, and this is why nutritional ketosis appears to be so effective against cancer.
Cancer could actually be more accurately classified as a mitochondrial metabolic disease. Few people inherit genes that predispose them to cancer. Most inherit genes that prevent cancer. Inherited mutations typically disrupt the function of the mitochondria, and the heightened risk for cancer is a result of that weakness.
The good news is you can optimize your mitochondrial function by addressing certain lifestyle factors such as diet and exercise, and this knowledge opens up a whole new way of looking at and treating cancer.
As explained by Fettke, the metabolic model of cancer is “based around energy and growth; random chromosomal mutations are secondary.” Furthermore:
“All cells require an energy source of adenosine triphosphate (ATP). They also require building materials that are either sourced locally or transported in normal cells convert glucose primarily into ATP and a little into maintenance.
Cancer cells do the opposite. There’s a diversion of glucose away from ATP production to the building materials required for cell growth … The other building materials require protein and fatty acids and cancer steals those from its surroundings.
That invasion of surrounding tissue accounts for how cancer spreads and metastasizes … The driving force behind all of this is oxygen-free radical production.
I believe the free radical production then causes the DNA damage in a random fashion, and account for the chromosomal abnormalities. So, if we can find the source of the oxygen free radicals, we might be onto something.”
Processed Food Diet Is a Major Cancer Promoter
What drives free radical production? Inflammation is a major driver, and our modern processed food diet is highly inflammatory.
Key culprits include polyunsaturated fats (PUFAs), trans fats and added sugar in all its forms, especially processed fructose (such as high-fructose corn syrup), as well as refined grains. Artificial ingredients can also promote inflammation.
By reducing the amount of net carbs you eat, you will accomplish four things that will result in lowered inflammation and reduced stimulation of cancer growth. You will:
- Lower your serum glucose level
- Reduce your mTOR level
- Reduce your insulin level
- Lower insulin growth factor-1 (IGF-1, a potent hormone that acts on your pituitary gland to induce metabolic and endocrine effects, including cell growth and replication. Elevated IGF-1 levels are associated with breast and other cancers)
Indeed, one of the basic reasons why a high-fat, low-net carb diet (nutritional ketosis) works so well is because it drives your inflammation down to almost nothing. And when inflammation disappears, your body can heal.