Introduction: Genome vs mitochondria
In The Genetic Self: Debunking DNA I described how the cultural and economic imperatives of the Industrial Revolution distorted our understanding of the human genome by positioning nucleic DNA as the master controller of our biochemistry. This fallacy of genetic destiny causes too many people to abandon agency over their own health and talk about themselves as if they were unique victims of some rare genetic defect that causes them to be obese, to age prematurely, or be pre-disposed to any number of chronic diseases.
What most people don’t realize is that very little of what governs bodily biochemistry is controlled by the DNA in the cell nucleus. For example, in The Genetic Self: Epigenetics, I described how the expression of our DNA is controlled by experiences that can switch our genes on and off, and how those epigenetic switches can be inherited from our parents. Moreover, we can create experiences for ourselves that will alter our epigenetic inheritance, thus modifying expression of our own genome.
As for chronic diseases and what are sometimes called the diseases of ageing, the DNA in your nucleus are far less important than the DNA in your mitochondria.
Mitochondrial DNA exist within the cell walls, outside the nucleus, in what is called the cytoplasm. Mitochondria carry genetic information for the production of enzymes and other molecules that govern energy conversion within the body. That is, the mitochondria are the energetic wellspring of life. Without functioning mitochondria, our bodies would be unable to maintain the most basic of metabolic functions.
Whereas a single cell contains only one nucleic genome, it can contain thousands of mitochondria — each with their own set of mitochondrial DNA in various states of disrepair. This makes assessment or sequencing of the mitchondrial DNA more complicated than sequencing the human genome, even though the mitochondrial DNA are shorter. To make matters worse, mitochondrial DNA are more susceptible to damage and more difficult to fix than nucleic DNA.
Which is why it the dominant view of cancer as a genetic disorder is misleading.
Although most medical professionals think of cancer as a manifestation of damaged nucliec DNA, the metabolic theory of cancer suggests that defects begin first in the mitochondria. While it is true that cancer cells carry an accumulation of mutations in nucleic DNA that disrupt regulation of cell division, according to the metabolic theory these nucleic mutations only persist because dysfunctional mitochondria fail to provide the energy necessary to proect and repair them.
Cancer as a metabolic disease
The best evidence that cancer is a mitochondrial rather than a genomic disorder comes from Thomas Seyfried, PhD, a biologist at Boston College. In 2015, he summarized a series of experiments dating back decades that involved transplanting nuclei from cancerous cells into healthy cells that had their nucleus removed. In other words, these experiments were designed to discover if the cancerous genome would reproduce tumor cells in conjunction with healthy mitochondria, of if healthy mitochondria could compensate for a faulty genome. Seyfried finds that “the nuclei of tumor cells can be reprogrammed to form normal tissues when they are transplanted into normal cytoplasm” (Seyfried 2015). That is, healthy mitochondria can suppress the function of genes that would otherwise drive tumor growth.
If Seyfreid is right and metabolic disorders drive cancerous mutations in the genome (rather than the other way around) then we would expect to see effective metabolic therapies for cancer.
In fact, we do.
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