Conventional wisdom holds that cancer is primarily a genetic disease, essentially a ‘bad luck’ scenario whereby mutations in the genetic code are either inherited or develop spontaneously into cancer at some point in life. More and more evidence, however, refutes this claim, instead supporting a theory of metabolic dysfunction being the mechanism that drives cancer.
Traditional cancer treatments (chemotherapy and radiation) are aimed at damaging the genetic material of cancer cells (i.e. DNA) as a strategy to make them die. However, despite billions of dollars in research on cancer treatments, an average of 1,600 people die of cancer in the USA every day. While the DNA-strategies of chemotherapy and radiation are successful in some forms of cancer, overall the success of these therapies is underwhelming.
Perhaps that’s because we’re focused on the wrong thing.
What we know about cancer cells
Cancer is a condition characterized by unregulated cell growth and division. [Reminds me of a quote by one of my favorite writers, a nature writer/environmentalist – Edward Abbey.]
Cancer = Damaged Mitochondria
Cancer cells are characterized by disordered mitochondrial function. Because the mitochondria are damaged, the cancer cells are fully dependent on glucose or glutamine outside of the mitochondria. They are inefficient at making energy and yet have a very high metabolic demand, requiring 400 times the amount of glucose that regular cells do. It’s worth noting that, unlike healthy cells, cancer cells cannot function on ketones.
In fact, this remarkably increased affinity for glucose is the basis for visualizing tumors in vivo by imaging with positron emission tomography (PET). The increased uptake of radio-labeled glucose analogue [18F] fluoro-2-deoxyglucose (FDG) differentiates cancer cells from healthy cells.
Cancer cells must compete with other organs and tissues for glucose to support their growth, inducing changes that decrease the insulin sensitivity of healthy tissues (ref).
Healthy mitochondria are also necessary for regulation of apoptosis, programmed cell death that protects against unregulated cell division (aka cancer). Damaged mitochondria cannot coordinate apoptosis and cannot regulate cell division, thereby allowing the unregulated cell division of cancer.
Mitochondrial Metabolic Model
Perhaps the strongest evidence in support of mitochondrial damage being the driver of cancer comes from Dr. Thomas Seyfried. Dr. Seyfried’s research has demonstrated that transplanting the faulty cancerous DNA into another cell did not result in that cell becoming cancerous. However, transferring cancerous mitochondria into a healthy cell causes a cancerous transformation.
Furthermore, transplanting healthy mitochondria into cancerous cells actually suppresses the cancer. This research clearly demonstrates that the health of the mitochondria is the relevant factor in determining the presence of cancer.
Other evidence supporting the mitochondrial metabolic theory includes:
- Some cancers show no evidence of genetic mutations
- Despite sharing 98.5% of our genes and protein sequences with chimpanzees, there is a notable absence of cancers in chimpanzees.
Summary
There is significant evidence in support of the mitochondrial metabolic theory of cancer, in contrast to the ‘bad luck’ hypothesis that cancer arises from random genetic mutations. Instead, it appears that environmental factors are the predominant driver of cellular injury that leads to the development of cancer.
