Thomas N. Seyfried

While numerous genetic abnormalities have been described in most human cancers, no specific mutation is reliably diagnostic for any specific type of tumor. On the other hand, few if any tumors are known, which express normal respiration.

I have presented substantial evidence showing that respiratory damage underlies the origin of cancer. Cancer is a disease of energy metabolism. If respiratory injury is the prime cause of cancer then protecting mitochondria and respiration from damage becomes the prime means of preventing cancer.

Emerging evidence suggests that cancer is primarily a metabolic disease rather than a genetic disease. I will present evidence showing how cancer is a disease of defective cellular energy metabolism and that most of the genomic defects found in cancer arise as secondary downstream effects of defective energy metabolism.

Numerous studies show that tumor mitochondria are structurally and functionally abnormal and incapable of generating normal levels of energy.

Considered collectively, these findings indicate that the integrity of the nuclear genome is dependent to a large extent on the functionality and energy production of the mitochondria.

Part of this tissue damage will involve injury to the mitochondria in the affected cells. The prevention of inflammation and damage to the tissue microenvironment will go far in reducing the incidence of most cancers. Hence, simply reducing exposure to cancer risk factors, which produce chronic inflammation and mitochondrial damage, will reduce the incidence of at least 80% of all cancers. In principle, there are few chronic diseases more easily preventable than cancer.

If Warburg’s views on the origins of cancer were correct then much of what is currently being done to manage the disease makes little sense. It is therefore important to carefully consider the evidence that irreversible respiratory injury is the origin of cancer.

In essence, dietary energy restriction and ketone body metabolism delays entropy. As cancer is a disease of accelerated entropy, dietary energy restriction targets the very essence of the disease.

Viewed collectively, the bulk of the experimental evidence indicates that mitochondria structure and function is abnormal in cancer cells. Hence, mitochondrial dysfunction will cause cancer cells to rely more heavily than non-cancer cells on substrate level phosphorylation [aka fermentation of sugar] for energy production in order to maintain membrane pump function and cell viability.

It is interesting in this regard that carcinogenesis, whether arising from viral infection or from chemical agent, produces similar impairment in respiratory enzyme activity and mitochondrial function

It is my opinion that many cancer researchers, through their propensity to focus on gene mutations and mechanisms of action, have made the quest for cancer management far more complicated than it actually is.

There are simply too many inconsistencies with the hypothesis that most cancers arise specifically from gene or chromosomal defects. The most damming evidence against the gene theory comes from the nucleus/cytoplasmic transfer experiments. ... Just because the majority of cancer researchers do not question the theory that guides their work does not mean that the theory is correct. Indeed, it appears that the average cancer researcher is not guided by any grand theory, rather they formulate restricted hypotheses for the next few experiments and tend to go on collecting data without reference to the problem of carcinogenesis.

If cancer is primarily a disease of energy metabolism, then rational strategies for cancer management should be found in those therapies that specifically target tumor cell energy metabolism. These therapeutic strategies should be applicable for the majority of cancers regardless of tissue origin, as nearly all cancers suffer from the same underlying disorder, that is, damaged respiration with compensatory fermentation.

We used linear regression analysis to show that growth of experimental astrocytoma was directly related to the levels of circulating glucose levels. It is clear from the figure that the higher the glucose level, the faster the growth. As glucose levels fall, tumor size (weight) and growth falls. .... In light of these findings, it is difficult to understand why some oncologists would encourage cancer patients to consume high calorie foods and drinks during their treatment. Glucose accelerates tumor growth!

In other words, the well-documented tumor-associated abnormalities in oncogenes, tumor suppressor genes, and chromosomal imbalances can arise as a consequence of the progressive impairment of mitochondrial function.

The data in Table 1.1 shows that we are not winning the war on cancer, regardless of what the pundits say. ... When will this continuum end? It will end, in my opinion, only after we come to recognize cancer as a metabolic disease that can be effectively managed with nontoxic metabolic therapies. My goal is to provide scientific evidence supporting this view.

In contrast to most conventional cancer therapies that expose both normal cells and tumor cells to toxic assaults, dietary restriction and particularly the KD-R [restricted ketogenic diet], are the only known therapies that can target tumor cells while enhancing the health and vitality of normal cells. In this regard, the KD-R as a cancer therapy is conceptually superior to many current conventional cancer therapies.

Delivery of a tumor cell nucleus into a normal cell cytoplasm begets normal cells despite the persistence of tumor-associated genomic abnormalities.