Lipid Metabolism and Cancer Spread: The Role of Cholesterol and Fatty Acids - Magaziner Center

Lipid Metabolism and Cancer Spread: The Role of Cholesterol and Fatty Acids

As we have stated in many articles on our website, cancer is very clever. Cancer knows how to survive and how to manipulate its environment to protect itself from cancer treatments. One of the ways cancer survives and protects itself from cancer treatments is to capture, mold, and manipulate fat cells to provide itself nourishment and to create a protective cocoon that shields the cancer from cancer treatments. In other words, cancer creates itself a bunker with a well stocked supply of food.

Lipid metabolism is how our bodies absorb fats. We absorb fats for energy and to build the components of our cells. Lipids come in many forms but when there is a problem of lipids most people become very familiar with the diagnosis and dietary and possible statin management suggestions of high cholesterol and high triglyceride levels (your body stores lipids for use at a latter date. When you have too much fat and calories in your diet you have an over abundance of triglycerides.)

How cancer uses lipids

In a September 2019 study (1), researchers examined how cancer utilizes lipids for its survival and reproductive capabilities and suggest possible ways to stop this process. The study suggests:

Cancer cells rely on fatty acids for all biological activities.

Cancer cells can manipulate lipid metabolism to immediately meet the cancer’s cells demands. If cancer treatment is applied, lipid metabolism is switched over to processing fats to provide protection. This ability is key to understanding cancer drug resistance.

Cancer cells can manipulate lipid metabolism to collect or process lipids if exposed to the temporary fluctuations in the availability of nutrients and oxygen. That is the availability of fats in the blood. In other words cancer can adapt to “feast,” or “famine,” and store fats cells.

The researchers go on to say that successful therapies targeting fatty acid metabolism may depend on the type of cancer, and may require targeting multiple sources of fatty acids simultaneously, and perhaps in combination with stringent dietary regimens.

This last sentence suggests one way is to alter diet and use medications (or in our case supplements) to reduce fatty acids in the blood.

Cancer, lipids and the tumor microenvironment

Cancer needs to charge the environment in which it lives to survive. Part of this change is the alteration of Lipid Metabolism. A study in the British Journal of cancer (2) describes the progression of cancer along the lines of this change.

“The development and progression of cancer is typically accompanied by marked changes in the tumor microenvironment. The rapid growth and expansion of tumor tissue often leads to a (self-destructing) poor and aberrant blood supply, resulting in hypoxia (lack of oxygen) and a limited supply of nutrients. To thrive under these changing and challenging conditions, cancer cells adapt their metabolism, including that of lipids. One of the key features of this metabolic adaptation is the elevated de novo synthesis of fatty acids (the cancer is synthesizing lipids from scratch to suit it needs), which is observed in many different cancer types and is generally believed to be required to provide rapidly proliferating cancer cells with a constant supply of fatty acids for membrane biogenesis tissue or tumor making), energy production and protein modification (cancer modifies proteins to suit its needs).”

To treat cancer, researchers suggest you must treat fatty acids and cholesterol and problems of lipid metabolism

A May 2020 study (3) made these observations in its suggestion that cancer treatment should include treatment for fatty acids and cholesterol metabolism

 An accumulating amount of data has indicated abnormal lipid metabolism in cancer stem cells. An alteration of lipid metabolism exerts a great impact on cancer stem cells’ properties such as the capability of self-renewal, differentiation, invasion, metastasis, and drug sensitivity and resistance. Cancer stem cells’ formation and maintenance cannot do without the regulation of fatty acids and cholesterol.

“The Role of Dyslipidemia in Colitis-Associated Colorectal Cancer”

In February 2021,(4)  a study published in the Journal of Oncology, with the title, The Role of Dyslipidemia in Colitis-Associated Colorectal Cancer presented the path from dyslipidemia (an elevation of lipids in the blood) to cancer. The path was a path of inflammation.“Dyslipidemia, characterized by metabolic abnormalities, has become an important participant in colorectal cancer. Dyslipidemia aggravates intestinal inflammation, destroys the protective mucous layer, and disrupts the balance between injury and recovery.”

In the next sentence, the study authors present a paradox that cancer has somehow tricked the body to suit its (cancer) needs. This is the realm of variants and mutations.

“On the other hand, antioxidants induced by oxidative stress enhance glycolysis (the breakdown of glucose) to maintain the acquisition of ATP (Adenosine triphosphate, the molecule that carries energy within cells) allowing epithelial cells (blood vessel and skin cells) with damaged genomes (the genes of the cell) to survive.”

What is happening that the body is responding to oxidative stress by releasing anti-oxidants from glucose to support the energy (ATP) needed to start a repair on damaged cells. Whatch what the cancer does.

Tumor cells are dependent on fat to start metastasis

In December 2016, this headline accompanied the release of a new study: “Tumor cells are dependent on fat to start metastasis.” (5),(6)  The study from Worldwide Cancer Research, a charitable research organization in the United Kingdom, published the findings of  Professor Salvador Aznar Benitah at the Institute for Research in Barcelona (IRB). Here is a summary of those findings:

A study has identified the cells responsible for initiating and promoting metastasis in several types of human tumors.

The results show that a protein, CD36, which absorbs fat from the cell membrane, is an essential factor that determines whether tumor cells become metastatic.

Mice given a high-fat diet developed the most aggressive metastases. The study reports that the metastatic process is enhanced by fat intake.

Why obese patients have poorer outcomes in their cancer treatments

In their paper, Leukemic Stem Cells Evade Chemotherapy by Metabolic Adaptation to an Adipose Tissue Niche, (7) researchers at the University of Colorado Anschutz Medical Campus, may have found a link as to why obese patients have poorer outcomes in their cancer treatments.  According to the researchers, “Adipose tissue (fat) has previously been identified as an extra-medullary (inner) reservoir for normal hematopoietic stem cells and may promote tumor development. Here, we show that a subpopulation of leukemic stem cells can utilize gonadal adipose tissue as a niche to support their metabolism and evade chemotherapy.”  In the study’s accompanying press release (8) it is explained this way:

“researchers found that leukemia stem cells “hide” in fatty tissue, even transforming this tissue in ways that support their survival when challenged with chemotherapy.  It is as if leukemia stem cells not only use fatty tissue as a robbers’ cave to hide from therapy, but actively adapt this cave to their liking.”

Epigenesis is the biological definition of how humans form from a fertilized egg to a multi-organ individual. Cancer also grows through this epigenesis process – mutating and evolving to avoid being killed off by treatments. Therapies that suppress cancer’s abilities to mutate and evolve would be called Epigenetic regulation therapies. Caloric restriction diets and bioactive phytochemicals – spices such as turmeric – would be called weapons of epigenetic cancer targeting.

Caloric restriction diets and bioactive phytochemicals are interventions have been shown to have epigenetic modulatory activities in multiple cancers. Research has suggested that these therapies can decrease the risk of cancer both in preclinical as well as clinical models. Therefore, knowledge of bioactive phytochemicals along with dietary interventions can be utilized for cancer prevention and therapy both alone and with existing drugs to achieve optimum efficacy.

This is not a new idea, a well cited research study from 2003 (9) made these observations on caloric restriction:

Calorie restriction is the most potent, broadly acting cancer-prevention regimen in experimental carcinogenesis models.

Translation of the knowledge gained from calorie restriction research to human chronic disease prevention and the promotion of healthy aging is critical, especially because obesity, which is an important risk factor for several chronic diseases, including many cancers, is alarmingly increasing in the Western world.

Our Cancer Program

Cancer is a very complex disease. In the articles below we continue our discussions which show links between diet, obesity, inflammation, cancer spread, and other challenges related to supportive cancer care.  Knowledge of bioactive phytochemicals along with dietary interventions can be utilized for cancer prevention and therapy both alone and with existing drugs to achieve optimum efficacy. 

At the Magaziner Center for Wellness, our treatments are focused on reducing inflammation, enhancing cellular immune response, and inactivating cancer stem cells since these cells cause cancer recurrences and are much more harmful than the actual tumor cells—all with the goal of improving quality of life, strength, vigor and extending life span. We place particular emphasis on an anti-inflammatory diet and lifestyle, and biologic agents that quiet the inflammatory pathways since inflammation has been found to foster the growth of cancer cells.

Most of our patients have already been through the rigors of conventional treatments but either experienced untoward side effects or unsatisfactory outcomes as the cancer continued to grow. The sooner we begin treatment, the better, since there is usually less damage to the immune system and to the vital organs. Your body then has a better chance to recover.

Our program emphasizes the concept of Thriving While Surviving. We strive to transform cancer from an acute disease into more of a chronic illness, one that can be lived with for many months or even years.

Related articles

Anti-Cancer Properties of Garlic and Onions

Changing Your Diet May Kill Cancer Cells

The Problem of Antibiotic Overuse, Gut Inflammation, and Elevated Cancer Risk


1 Chen M, Huang J. The expanded role of fatty acid metabolism in cancer: new aspects and targets. Precis Clin Med. 2019 Sep;2(3):183-191. doi: 10.1093/pcmedi/pbz017. Epub 2019 Oct 1. PMID: 31598388; PMCID: PMC6770278.
2 Munir R, Lisec J, Swinnen JV, Zaidi N. Lipid metabolism in cancer cells under metabolic stress. British journal of cancer. 2019 Jun;120(12):1090-8.
3 Li H, Feng Z, He ML. Lipid metabolism alteration contributes to and maintains the properties of cancer stem cells. Theranostics. 2020;10(16):7053-7069. Published 2020 May 30. doi:10.7150/thno.41388
4 Chen K, Guo J, Zhang T, Gu J, Li H, Wang J. The Role of Dyslipidemia in Colitis-Associated Colorectal Cancer. Journal of Oncology. 2021 Feb 12;2021.
5 Tumour cells are dependent on fat to start metastasis. Dec 7, 2016. Access.
6 Pascual G, Avgustinova A, Mejetta S, Martín M, Castellanos A, Attolini CS, Berenguer A, Prats N, Toll A, Hueto JA, Bescós C. Targeting metastasis-initiating cells through the fatty acid receptor CD36. Nature. 2017 Jan;541(7635):41.
7 Ye H, Adane B, Khan N, Sullivan T, Minhajuddin M, Gasparetto M, Stevens B, Pei S, Balys M, Ashton JM, Klemm DJ, Woolthuis CM, Stranahan AW, Park CY, Jordan CT. Leukemic Stem Cells Evade Chemotherapy by Metabolic Adaptation to an Adipose Tissue Niche. Cell Stem Cell. 2016 Jul 7;19(1):23-37. doi: 10.1016/j.stem.2016.06.001. Epub 2016 Jun 30. PMID: 27374788; PMCID: PMC4938766.
8 Fatty tissue may be ‘robbers cave’ for cancer stem cells, driving poor prognosis for obese patients Access.
9 Hursting, Stephen D., et al. “Calorie Restriction, Aging, and Cancer Prevention: Mechanisms of Action and Applicability to Humans*.” Annual review of medicine 54.1 (2003): 131-152.


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