Cancers are a class of pathology in which cells in your body start growing uncontrollably.  Normally, cell replication in an animal is very carefully managed.  In humans, we grow to adult size, then our production of new cells slows down dramatically.  We are always producing new cells and losing old ones, but it becomes a replacement or repair function, not overall growth, at least in mammals.  Cancer cells form clusters and tumors that grow at the expense of other cells.  They encourage the body to increase blood supply to the tumor.  Often cells from the tumor spread elsewhere–metastasis.  Eventually, this can weaken and kill.

The dominant paradigm of cancer research is based on the observation that cancer cells have high rates of mutation.  But why is the pattern of cancer development and metastasis so similar in all cancers if random mutations are the cause?  Cancers incidences have increased along with obesity, heart disease, diabetes, etc, although we’ve gotten much better at treating cancers once they occur.  Gary Taubes talks about this in one of his New York Times pieces.  There are several factors that may be involved, all related to high sugar consumption.  The elevated incidence of Reactive Oxygen Species (ROS; free oxygen radicals) and associated cellular inflammation caused by a high carbohydrate diet, as discussed by Volek and Phinney, could be a factor.  In Nutrition & Metabolism, Klement and Kämmer review evidence showing that elevated insulin promotes the development of new cancers, then sugar feeds the cancer.

Thomas Seyfried’s exhaustive treatise “Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer” proposes a clear origin, based on his extension of the research of Dr. Otto Warburg, who won a Nobel Prize in 1931.  Warburg observed that cancer cells engage in “fermentation” of glucose even in the presence of oxygen, which is quite abnormal.  Seyfried explains this occurs because something stresses the mitochondria of a cell enough to permanently damage their normal role as the source of most of the cell’s ATP by oxidative phosphorylation.  ATP is essentially like the electricity that powers your home’s energy systems.  To sustain itself, the cell switches to a mechanism that doesn’t need mitochondria, glycolytic fermentation.  Paul Davies and his collaborators call the switch to the ancient pathways their “Atavistic Theory of Cancer,”  but miss the key concept that it’s mitochondrial dysfunction that triggers the switch.  According to Seyfried, the cell switches on “oncogenes.”  Nuclear mutation rates increase dramatically–a symptom, not a cause.  The cell also starts growing and dividing, forming a tumor.  To the body, this looks like a wound, which results in additional blood supply, and white blood cells going to the tumor.  The cancer cells can fuse with the white blood cells.  The hybrid cell ends up with defective mitochondria, cancerous metabolism, and the white blood cell’s ability to go into other parts of the body.  Here’s an article by Seyfried and collaborators that discusses key concepts from his book– “Cancer as a metabolic disease: implications for novel therapeutics.”

Seyfried talks about the agents than can stress mitochondria and cause cancers, but high sugar diets could be the biggest stress, due to way the sugar fructose is metabolized.  According to Dr. Richard Johnson and his collaborators, the uric acid produced by fructose metabolize causes serious mitochondrial stress– “Sugar, Uric Acid, and the Etiology of Diabetes and Obesity.”  Conversely, ketogenic diets, which replace glucose with ketones for most of normal metabolism, would seem to protect you from cancers, preventing both initiation of the cancer and the growth of cancer cells.  Like I say on the Disclaimer page, look at the evidence and form your opinion.  I’m reinforced to stay on a ketogenic (high fat, low carb) diet.

I’ll develop a page or several in the Biology section to better explain this as I learn more and some pending papers appear in print.  Another interesting aspect is that mitochondria are generally considered to have originated as bacteria that were engulfed by early eukaryotes, survived the experience, and became a symbiont within the eucaryote. In exchange for a protected place to live and a supply of substrates (sugar, fat, protein products), the mitochondria produces the ATP the eukaryotic cell needs. Mitochondria still have their own circular genome. Mitochondria can also burst under certain conditions, releasing cytokines that can force the host cell into apoptosis– cellular suicide. Since all the mitochondria in your body are the same genetic individual, inherited from the mother, there are evolutionary relatedness arguments for when and why mitochondria would explode analogous to those used to explain social insect behavior. A crippled mitochondria seems to lose its grip on the kill switch. The nuclear DNA executes a fall-back strategy for it’s survival without the mitochondria. I would like to get some of my people (evolutionary biologists) interested in thinking more about this.

In the meantime, here’s a video in which Thomas Seyfried summarizes the key points from his book–

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