Cancer is a disease of uncontrolled growth of abnormal cells, also called a malignant growth or tumor. In 1971,1 President Richard Nixon declared war on cancer, signing the National Cancer Act. His goal was to make a national commitment to find a cure, after which Fort Detrick was converted to a cancer research center and renamed the Frederick Cancer Research and Development Center.
Since then a number of chemotherapeutic and surgical treatments have been developed in an effort to treat cancer.2 In 1991, mortality rates from cancer began to decline, falling 0.5% per year from 1990 to 1995.3
In 1998, a major clinical trial reported neoadjuvant chemotherapy in breast cancer allowed women with large tumors to undergo a lumpectomy instead of a full mastectomy.4 The goal was to shrink the tumor using chemotherapy, so a smaller portion of the breast could be surgically removed.
Chemotherapy has been one of the primary treatments used in cancer. The objective has been to destroy the cancer cells so that it does not come back. However, chemo — technically a poison — travels throughout your entire body and affects every single cell, unlike radiation or surgical treatments which target precise locations.5
Short term benefit may lead to long term problems
As mentioned, the initial intention of using chemotherapy before surgical excision of breast cancer tumors was to improve the ability of the surgeon to remove the tumor and spare as much breast tissue as possible. But follow-up research to the original study in 1998 has found that although this treatment increases the number of times breast-conserving therapy may be used, it also increases the number of local recurrences of breast cancer in those same women.6
The authors of the research in The Lancet7 suggest downsizing tumor size using neoadjuvant chemotherapy should also include strategies to mitigate the increased local recurrence. However, other scientists8 suggest neoadjuvant chemotherapy treatment for breast cancer tumors should be abandoned.
Dr. Jayant S Vaidya, consulting surgeon at several hospitals in London, including the University College London Hospitals,9 discussed some key points about the treatment in The BMJ, including the increased pathological response that doesn’t translate into a survival benefit and the reliance on the immediate and dramatic responses seen with newer drugs that may not ultimately benefit patients.10
He was interviewed in a podcast with BMJ Talk Medicine, during which he discussed the original reasons for using neoadjuvant therapy and his analysis of recent research that doesn’t support the use. At 7:33 in the podcast,11 Vaidya discussed how neoadjuvant therapy makes surgery less precise and more difficult for the surgeon to excise the tumor.
While the drugs reduce the size of the tumor, it leaves behind cancer cells in the surrounding tissue and essentially “melts” the tumor margin the surgeon uses to excise the tumor, he said. Additionally, researchers have found breast cancer disseminates using a system they call tumor microenvironment of metastasis (TMEM).12
Scientist have used TMEM to clinically validate markers predictive of metastasis in breast cancer patients. In one study,13 data demonstrated chemotherapy increases the activity of TMEM sites and promotes distant metastasis of breast cancer cells.
Unfortunately, in those who underwent neoadjuvant treatment, expression of TMEM increased, suggesting despite reducing the size of the original tumor, its use increased the risk of metastatic disease.14
Chemo-treated breast cancer grow vesicles promoting spread
Following these studies, an international team of researchers from Ecole Polytechnique Fédérale de Lausanne in Switzerland15 set out to understand how neoadjuvant chemotherapy may result in a higher risk of developing metastatic disease.
Using an experimental model,16 the researchers found two of the more commonly used medications, doxorubicin and paclitaxel,17 induced the release of small vesicles, which contained a protein (Annexin-A6) not released in the vesicles from untreated tumors.
These were then found circulating in the blood and, when reaching a lung tissue, would release their content stimulating cells to release a different protein, attracting monocytes from the immune system. Past studies had demonstrated this may facilitate the growth of cancer cells in lung tissue, the initial step in metastasis.18
The researchers found genetic inactivation of annexin-A6 in the cancer or host cells19 or blocking the monocytes20 could prevent the experimental breast cancers from lung metastasis.
Cancer rates and incidence
Cancer has a significant impact on societies across the world. According to the National Cancer Institute, the most common cancers in order of number diagnosed are breast cancer, lung and bronchus cancer, prostate cancer, colon and rectal cancer and melanoma of the skin.21
The latest information from the CDC from 2016 reports 436 new cases of cancer for every 100,000 men and women and 156 deaths for every 100,000 men and women.22
In the U.S., the CDC data visualization map demonstrates a significant difference between the number of people diagnosed with cancer on the West Coast compared to those on the East Coast of the U.S. Rates on the West Coast are as low as 359.4 per 100,000 while on the East Coast they range up to 509.7 per 100,000.23
Approximately 38.4% of men and women will be diagnosed with some type of cancer during their lifetime.24 In 2017, the economic burden for care was $ 147.3 billion, an increase from $ 137.4 billion in 2010.25
Mitochondria play a crucial role in development of cancer
Simply put, mitochondria are the powerhouses of your cells, producing 90% of the energy generated inside your body.26 Every muscle contraction, biochemical reaction and cellular regeneration requires energy to be completed. When these little powerhouses become dysfunctional it affects your overall health.
Thomas Seyfried, Ph.D., professor of biology at Boston College,27 is a leading expert and researcher in the field of cancer metabolism and nutritional ketosis. His work looks at the mechanism of cancer and the influence mitochondria have on the development and treatment of the disease.
Initially, it was Otto Warburg, Ph.D., a German physiologist, who proposed a difference in cancer cell energy production and metabolism, for which he won the Nobel Prize in 1931.28 He hypothesized cancer growth occurred through an anaerobic breakdown of sugar, called fermentation. This is vastly different from the conversion of sugar to energy in normal cells through glycolysis.
In his work, Seyfried explains how fermentation in the mitochondria of cancer cells uses glucose and glutamine for fermentable fuels as they are unable to use ketones. For further discussion see my past article, “Why Glucose and Glutamine Restrictions Are Essential in the Treatment of Cancer.”
Cancer is frequently a metabolic and not genetic condition
A traditionally held view is cancer is a genetic disease,29 but what Warburg discovered is cancer is really caused by a defect in the cellular energy metabolism of the cell, primarily related to the function of the mitochondria.
In my view, this information is a game changer as it relates to cancer and nearly every other disease, since at the core of most serious health conditions you find mitochondrial dysfunction.
Nuclear transfer experiments involve transplanting the nuclei of one cell into the cytoplasm (the material within a cell, excluding the cell nucleus) of another including the mitochondria. In studying the effect of mitochondrial function in cancer, researchers have transplanted the nuclei of a tumor cell into the cytoplasm of a healthy cell.30
The hypothesis is 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.31
However, what was observed was when the nuclei of cancer cells were transferred into a healthy cytoplasm, the new cytoplasm did not form cancer. It remained healthy and normal. Seyfried writes:32
“Cybrids contain a single nucleus with a mixture of cytoplasm from two different cells. Cybrids with normal mitochondria showed enhanced mitochondrial function including increased ATP synthesis, oxygen consumption and respiratory chain activities despite the presence of the cancerous nuclear genome.
A remarkable finding was that even though genes that encode most mitochondrial proteins are located in the nucleus, introduction of mitochondria derived from the non-cancerous cell to a cancer nuclear environment resulted in suppression of oncogenic pathways and the tumorigenic phenotype.”
Additional evidence produced by Benny Kaipparettu, Ph.D., and colleagues at Baylor University33 showed transplanted normal mitochondria (with their nuclei intact) into cancer cell cytoplasm caused the cells to stop growing abnormally. In essence, this downregulated the oncogenes 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 them into a very slow-growing type of cancer cells, the cancer cells began growing rapidly. As noted by Seyfried,34 “Low dose radiation can cause nuclear mutations but not cancer, whereas high dose radiation damages both the nucleus and mitochondria and can cause cancer.” He goes on to say:35
“In other words, nuclear mutations alone are insufficient for producing tumors, whereas the tumorigenic phenotype can be produced in some cells without nuclear mutations. These findings seriously question the foundation of the somatic mutation theory of cancer.”
Key principles in cancer treatment and prevention
Even though China has a larger population, their cancer rate is higher than the U.S.36 In this informative interview with Thomas Seyfried, Ph.D., who in my view is one of the most prominent and knowledgeable cancer biologists in the world, we discuss the role mitochondria and metabolism play in the development of cancer.
As Seyfried discusses, under an electron microscope mitochondrial structure and number are abnormal, leading to abnormal function. These changes mean cancer mitochondria are only able to use glucose and/or glutamine in a fermentation process to produce enough energy to survive.
The respiratory process used in normal cells using glucose to produce energy is not available to the cancer cells because of the structural abnormality in the mitochondria. This information means targeting glucose and glutamine in the treatment of cancer all but eliminates their source of energy and starves the cells, so they can’t survive.
By bringing the body into ketosis, the cancer cells are unable to use ketones in fermentation and therefore have no mechanism to make energy. Conversely, there is new information demonstrating that cancer is not a genetic disease. As Seyfried describes in the video:
“The nuclear transfer experiments are showing that it cannot be a genetic disease. There has been no scientific argument that I have seen, a rational argument, to discredit the multitude of evidence showing that the mutations are not the drivers but the effects. As a matter of fact, there’s new information now where people are finding so-called genetic drivers of cancer expressed and present in normal cells.”
He goes on to say:
“And now we’re finding many cancers that have no mutations … yet they’re fermenting and they’re growing out of control. So, there’s a number of new observations that are coming out that challenge this concept that cancer is a genetic disease. So, then, once you realize that it’s not a genetic disease, then you have to seriously question the majority of therapies that are being used to try to manage the disease.”
Seyfried believes that cancer is not a genetic disease, mutations are a downstream phenomenon and — most importantly — that we could drop the death rate by 50% in 10 years. This could be accomplished if cancer were treated as a mitochondrial metabolic disease targeting fermentable fuels, rather than using toxic therapies focused on downstream effects.
Most of the current toxic therapies, such as chemotherapy and radiation, are focused on stopping replication of the cells, but by removing the cancer cells’ fuel source, they will also die without the negative, and sometimes devastating, effects of therapy.
Guidelines to reduce your potential risk
Seyfried’s landmark theory of cancer metabolism is available as a free PDF37 and many of his theories of energy production in cancer metabolism are found in his most recent paper,38 “Mitochondrial Substrate-Level Phosphorylation as Energy Source for Glioblastoma: Review and Hypothesis.”
Very simply put, by removing the energy source for the cancer cells, you cause the cells to die. To reduce your risk consider using a cyclical ketosis dietary plan as it improves your metabolic flexibility and reduces your cells’ dependence on glucose, the primary fuel for cancer cells.
Additionally, you may reduce your risk by ditching processed foods of all kinds, eating only whole, organic fruits and vegetables and grass fed, pasture-raised meats and poultry, maintaining optimal levels of vitamin D, reducing your exposure to toxins, drinking pure water, exercising regularly and getting at least eight hours of quality sleep each night.