“Mitochondrial dysfunction is at the heart of cancer. When mitochondria are damaged, cells switch from normal respiration to fermentation for energy production, which leads to dysregulated cell growth”
– Dr. Thomas Seyfried
Ever since cancer has been looked at from the angle of genetic mutations; the idea has been emphasized on DNA alterations that drive the cells to proliferate abnormally. This conventional thinking is referred to as the somatic mutation theory, where it emphasises gene mutations such as oncogenes and tumour-suppressing genes force normal cells to mutate into cancerous cells. The alternative view—though, is the metabolic theory of cancer—stating that a disease is, at root, a disease originating from damaged mitochondria and altered cellular energy metabolism. It offers an alternative view of carcinogenesis with an emphasis on how important cellular metabolism and energy dynamics are.
Why is cancer not a genetic disease?
Mitochondria are often characterised as the cell’s powerhouse in making adenosine triphosphate (ATP) by oxidative phosphorylation (OXPHOS).
In the event of a malfunction in mitochondria, which is what normally powers energy generation, cells are forced to use much less efficient ways to generate energy through glycolysis. This shifting of metabolic process in the presence of oxygen is called the Warburg effect. Otto Warburg initially discovered this phenomenon back in the 1920s and found that even where oxygen is enough, cancer cells mainly produce energy by glycolysis rather than OXPHOS.
The Warburg effect describes a high rate of glucose uptake and increased production of lactate by cancer cells under both anoxic and normoxic conditions. Metabolic reprogramming allows unrestrained growth and proliferation of rapidly dividing cancer cells by generating essential precursors for biosynthetic pathways and balancing cellular redox. The preference for glycolysis instead of OXPHOS in these tumor cells, fundamentally changing mitochondrial function, may be both causative and resultant in cancer development.
The latter may result in an overproduction of reactive oxygen species (ROS)—small, chemically reactive oxygen-containing molecules. ROS are products of cellular metabolism, predominantly from OXPHOS. Although low levels of ROS are implicated in signaling within the cell and in its homeostasis, increased amounts can cause injury to organelles and cellular components, including DNA, proteins, and lipids. Such oxidative stress may then lead to mutational events and genomic instability, all being key factors in carcinogenesis.
Moreover, they are both directly mutagenic and carcinogenic as contributors to the cancer process by their initiation or even promotion, since they could either directly provoke DNA damage by strand breaks or base modification or indirectly make an impact on signaling pathways and DNA repair mechanisms. Meanwhile, ROS may also be pro-survival and pro-proliferative signaling activators, such as NF-κB and HIF-1α, resulting in further promotion in tumorigenesis.
Cancer cells often exhibit changes in various metabolic pathways, including those involving glutamine, fatty acids, and amino acids. These changes function to meet anabolic needs of rapidly dividing cells and help maintain redox balance and epigenetic modifications. Several cancer cells depend on the amino acid glutamine, which is abundantly available, as a source of carbon and nitrogen to drive anabolic processes and for energy production. Glutamine metabolism feeds into the tricarboxylic acid (TCA) cycle, promotes nucleotide and amino acid synthesis, and sustains cellular antioxidants such as glutathione. Secondly, aberrant lipid metabolism is another hallmark feature in cancer cells.
Most cancer cells exhibit increased fatty acid synthesis and uptake for membrane biosynthesis, energy storage, and signaling. Most often than not, the dysregulation of lipid metabolism also generates bioactive lipids that then promote tumor growth and metastasis. Apart from glutamine, other amino acids crucial to the metabolism of cancer cells are serine and glycine. These amino acids serve as input into one-carbon metabolism, which has significant implications in nucleotide synthesis, methylation reactions, and redox balance.
So how can we fight against cancer formation and growth with all the knowledge displayed above?One extremely promising dietary approach is the state of ketosis. This nutritional state, achieved through a low-to-zero carbohydrate diet, focuses on utilising ketones, the breakdown products of fat, as a primary energy source instead of glucose.
The state of ketosis occurs when the body shifts from using glucose to using fat as its main energy source. This metabolic state is induced by significantly reducing carbohydrate intake, prompting the liver to convert fats into ketones. Therefore leaving ketones as the primary fuel for the body and brain.
One of the most intriguing aspects of ketosis is its potential impact on cancer cells. Most cancer cells rely heavily on glucose for energy, the phenomenon of which we have displayed above. By limiting carbohydrate intake and thus glucose availability, a ketogenic diet can effectively starve cancer cells, while normal cells adapt to using ketones for energy.
Ketones are not only an alternative energy source; they are also more efficient and cleaner than glucose. They produce fewer reactive oxygen species (ROS) during metabolism, leading to reduced oxidative stress. This lower oxidative stress translates to less damage to mitochondrial DNA, which is crucial since damaged mitochondria are more prone to mutations that can lead to cancer.
Improved mitochondrial health is a key component in preventing cancerous cell growth. Ketones enhance mitochondrial biogenesis, the process by which new mitochondria are formed within cells. This increased mitochondrial turnover ensures healthier and more efficient cellular energy production, reducing the likelihood of mutations that could initiate cancer.
There is a record of historical support, and scientific studies, about aboriginal people following protective lifestyles involving ketosis. In fact, most aboriginal tribes like those of Africa, Canada, and rainforests have traditionally consumed diets low in carbohydrates for lack of accessibility to carbohydrates. Such populations often show fewer rates of cancer as compared to the modern societies, suggesting that their semi-ketogenic state may be liable for cancer resistance.
This is further illustrated by chimpanzees, only about 2% different in their genes and protein sequences. But in spite of this obvious similarity to man, they seldom fall prey to cancer in their wild environments. A factor that could be playing a role in this low occurrence of cancer among the great apes might be their low intake of processed carbohydrates which would put them on a diet mimicking mild ketosis.
Futhermore, it is widely known that most cancers are associated with inflammation. High levels of hyperprocessed carbohydrates and sugars in the modern diet may initiate an inflammatory process that will lead to damage in the mitochondria and predispose a person to cancer. A ketogenic state is not only anti-inflammatory to the body, but also spares cells from oxidative damage and dysfunction of the mitochondria.
Finally, maintained mitochondrial health is also advanced through reduced intake of alcohol. Alcohol metabolism produces acetaldehyde, which is a toxic chemical that induces ROS that cause mitochondrial impairment. Chronic alcohol consumption damages the electron transport chain in mitochondria, thereby reducing their functionality and eventually increasing the chances of suffering from cancer.
Therefore, we can suggest that lifestyle decisions in the present that include poor diet, alcohol consumption, and reduced exercises are directly escalating the inflammatory and pro-carcinogenic state, implying that cancer is in fact a metabolic disease. This may be the reason that obese people tend to show cancer diagnoses far more than average.
A ketogenic lifestyle, therefore, has the potential to decrease cancer incidence by maintaining mitochondrial health and minimizing inflammation. Key methods include a low-carbohydrate, high-fat diet; regular physical activity; and minimal alcohol consumption. With small adjustments of these habits, a general state of well-being and longevity—possibly free from cancer—could be achieved.
Vitality Blueprint 
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