Cancer as a Metabolic Disease

Each year during the anniversary week of Mercola.com, we recognize a Game Changer; someone whose work stands as a great service to humanity by making a significant contribution to improving people’s health.

This year, we present the Game Changer Award to Thomas Seyfried, Ph.D.,1 a professor of biology at Boston College and a leading expert and researcher in the field of cancer metabolism and nutritional ketosis.

His book, “Cancer as a Metabolic Disease” is an important contribution to the field of how cancer starts and can be treated. Seyfried’s work is also heavily featured in Travis Christofferson’s excellent book, “Tripping Over the Truth: The Metabolic Theory of Cancer.”

Each day, some 1,600 people die from cancer in the United States alone. Worldwide, we’re looking at a death toll of about 21,000 people daily. So many of these deaths are unnecessary — they’re preventable and treatable.

Seyfried is one of the pioneers in the application of nutritional ketosis for cancer; a therapy that stems from the work of Dr. Otto Warburg, who was undoubtedly one of the most brilliant biochemists of the 20th century. He received the Nobel Prize in Physiology or Medicine in 1931 for the discovery of metabolism of malignant cells.

Warburg also held a doctorate in chemistry and was personal friends with Albert Einstein and many of the most prominent scientists of his time. His life’s mission was to find a cure for cancer, and he actually did. Unfortunately, few were able to appreciate the importance of his findings.

Seyfried has followed in Warburg’s scientific footsteps, and is conducting important research to advance this science. He has in fact exceeded Warburg’s initial supposition, shedding important light on the metabolic underpinnings of cancer.

Cancer as a Metabolic Disease

The traditionally held view or dogma is that cancer is a genetic disease, but what Warburg discovered is that cancer is really caused by a defect in the cellular energy metabolism of the cell, primarily related to the function of the mitochondria, which are the little power stations within each cell.

The mitochondria were not well understood in Warburg’s time but, today, we have a much better understanding of how they work.

In my view, this information is the game changer that not only treats cancer but virtually every single disease known to man, because at the core of most serious ailments you find mitochondrial dysfunction. As noted by Seyfried:

“A dogma is considered irrefutable truth, and that cancer is a genetic disease is, no question, a dogma. The problem with dogma is that sometimes it blinds you to alternative views and sets up ideologies that are extremely difficult to change.

All of the major college textbooks talk about cancer as a genetic disease. The National Cancer Institute (NCI) website, the first thing they say is cancer is a genetic disease caused by mutations … [and] if cancer is a genetic disease, everything flows from that concept.

It permeates the pharmaceutical industry, academic industry and textbook industry, the entire knowledge base. There’s very little discussion of alternative views to the genetic view. The argument now is that, yes, metabolic problems occur in cancer cells. No one denies that.

But these are all due to the genetic mutations. Therefore we must maintain ourselves on the established track that all of this metabolic stuff could be resolved if we just understood more about the genetic underpinning of the disease.

Now that would be well and good if it were true. But evidence is accumulating that the mutations we see that are the prime focus and the basis for the genetic theory are actually epiphenomenal.

They’re downstream effects of this disturbance in the metabolism that Warburg originally defined back in the 1920s and ’30s.”

How the Metabolic View Alters Cancer Treatment

As Seyfried notes, the problem today is not that scientists and doctors cannot understand the science; it’s that they cannot accept that this could be the truth behind the nature of the disease, because it changes how you approach treatment.

If defective mitochondria are responsible for the origin of cancer, and defective energy metabolism is responsible for the majority of the phenotypes, i.e., the observable characteristics of the disease that you see, then how do you treat the disease?

In my view, one of Seyfried’s most magnificent contributions to this science was his compilation of research from independent and well-respected scientists within various disciplines, who conducted valuable experiments but had no clue how to interpret the results.

Seyfried put all of their work together, forming a strong scientific foundation for the theory that cancer is indeed a metabolic disease, not a genetic one, and that genetic mutations are a downstream effect of defective energy metabolism in the mitochondria.

“Those nuclear transfer experiments were always present in the literature. They were considered anomalies. They were not consistent with the view that cancer is a nuclear genetic disease … but the observation was not interpreted in light of [being] the origin of cancer.

I bundled all those observations together in a new light, looking at the conclusions of those experiments in light of whether the results would support a nuclear gene-based theory versus a mitochondrial metabolic theory …

It was just interpreting a series of experiments in light of the origin of the disease, and then asking what conclusion would these experiments support. Would it support the nuclear genetic theory of cancer, or would it support the mitochondrial metabolic theory of cancer?

In each of these cases, the results more strongly supported the metabolic theory of cancer than the nuclear genetic theory,” Seyfried says.

What the Nuclear Transfer Experiments Showed

The nuclear transfer experiments in question basically involved transplanting the nuclei of a tumor cell into a healthy and normal cytoplasm (the material within a cell, excluding the cell nucleus), which include the mitochondria, the energy-generating organelle of the cell.

The hypothesis is that if cancer is nuclear-gene driven and the phenotype of cancer is dysregulated cell growth, meaning if genetic mutations are responsible for the observable characteristics of the disease, then those abnormal genes should be expressed in the new cytoplasm. But that’s not what happened.

Again and again, what was observed was that when the nuclei of a cancer cell were transferred into a healthy cytoplasm, the new cytoplasm did NOT form cancer. It remained healthy and normal.

“What was interesting is that in many of these nuclear transfer experiments, the organisms aborted at certain periods of development. That abortion seems to be related to how many mutations were in the nucleus that was transferred,” Seyfried says.

“It was true that these cancer nuclei did contain mutations, but those mutations were not causing the hallmark feature of the disease, that is proliferation. Rather, they were causing abortion at some developmental point of the organism that had those nuclei … On the other hand, when the normal nucleus was transferred back into a cancer cytoplasm [which had defective mitochondria], either the cell died or it formed tumor cells.”

Additional evidence has recently been produced by Benny Kaipparettu, Ph.D., and colleagues at Baylor University. When they transplanted normal mitochondria (with its nuclei intact) into cancer cell cytoplasm, it caused the cells to stop growing abnormally. It downregulated the oncogenes that were alleged to be driving the tumor and made the cells grow normally again.

On the other hand, when they took the mitochondria from a tumor cell and moved it into a very slow-growing type of cancer cell, the cancer cells began growing very rapidly. As noted by Seyfried, “When you bundle all these experiments together, you come to the conclusion that nuclear mutations cannot be the drivers of the disease.”

What About BRCA1 and Other Inherited Cancer Genes?

A common argument for the genetic theory is that cancer can be inherited; therefore it must have genetic underpinnings. Li-Fraumeni syndrome,2 which raises your risk of developing cancer at a very young age, and BRCA1, which raises your breast cancer risk are two examples.

“The answer is, yes, on the surface, that would appear to be true,” Seyfried says. “But as Warburg said, there are many secondary causes of cancer but there is only one primary cause, and that’s damage to the respiration. So inherited mutations through the germ lines that cause cancer to affect the mitochondria, it is [still] the mitochondria that is the origin of cancer.

It just so happens that the defect is coming from an inherited gene rather than a chemical carcinogen, radiation, viral infection or an infection of some parasite or whatever, all of which damage respiration; all of which can cause cancer.

Clearly the origin of the disease is a disturbance of the respiratory capacity of that cell which then, if the cell is to survive, must upregulate genes necessary for fermentation. Many of those genes are the so-called oncogenes. The oncogenes are simply fulfilling a rescue event of that cell to function in a fermentation metabolism rather than an oxidative metabolism. We can downregulate oncogenes simply by putting in new respiration.”

If genetic mutations are not the primary cause of cancer but rather a secondary, downstream effect of dysfunctional cell respiration, why and how do mutations occur? As explained by Seyfried, once the cells’ respiration is damaged, that damage then leads to a compensatory fermentation, which requires the upregulation of oncogenes (cancer genes).

Damaged respiration also produces large amounts of reactive oxygen species (ROS) and secondary free radicals that damage DNA proteins and lipids (fats inside your cellular membranes). The ROS also cause mutations in the nuclear genome. So the mutations are the result of defective respiration and subsequent exaggerated ROS production.

Why the War on Cancer Has Not Yet Been Won

At present, the cancer industry is focusing on the downstream effects of the problem, which is why the “war on cancer” has been such a miserable failure.

“Personalized medicines, checkpoint inhibitors, all of these kinds of therapies are basically looking at downstream effects of the disease,” Seyfried says.

“Unfortunately, most of the cells in the tumor are all different from each other genetically. You’re not going to be able to target all of the different cells using these kinds of approaches. Even though you may get success for a few months, or even a year in some people, the majority of people will not respond effectively to these kinds of therapies for the most part.”


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