A diet high in polyunsaturated fatty acids, especially omega 3s, have been shown to be negatively associated with cancer development
Dietary fatty acids have been recognized as influential factors in the activation of carcinogenic events or disease progression and have been associated with a direct connection to breast cancer prevention.
PUFAs differentially inhibit mammary tumor development by inflicting modifications to the morphology of cell membranes, and influencing signaling pathways, gene expression and apoptosis.
The human body is unable to synthesize long-chain polyunsaturated fatty acids (PUFAs) Omega 3 DHA, docosahexaenoic, and EPA, Eicosapentaenoic acid and Omega 6 Arachidonic Acid at a reasonable rate and therefore, supplementation is required through dietary sources or nutritional supplements. The recommended daily nutritional dose is 2,000 mg EPA+DHA, while therapeutic dosing is 4,000-6,000 milligrams of EPA+DHA per day.
Omega Three Fatty Acids and the Tumor Microenvironment
- Supports Normal Inflammation Control by lowering COX 2, LOX5, PGE2, IL1, IL6,TNFa, CRP.
- Increased inflammation contributes to cancer development, progression and metastasis.
- Increased inflammation is linked to cancer related pain, fatigue, depression and cognitive impairment.
- Increased inflammation is linked to cancer related hypercoagulation and risk of thromboembolism
- Supporting Normal Inflammation control has a wide impact on the behavior of tumor cells and on safety and quality of life for cancer patients and survivors.
- Promotes Expression of M1 Type Tumor Associated Macrophages (TAMs).
- Type M1 TAMs promote tumor regression, inflammation control and immune activation by promoting tumor infiltration by antigen presenting dendritic cells and cytotoxic T cells.
- Type M1 TAMs promote tumor regression, inflammation control and immune activation by promoting tumor infiltration by antigen presenting dendritic cells and cytotoxic T cells.
- Inhibits VEGF (Vascular Endothelial Growth Factor) and Promotes Normal Control of Angiogenesis .
- VEGF promotes the development of new blood vessels to the tumor cells. Inhibition of VEGF and the development of capillaries inhibits tumor growth and profession as well as metastasis.
- VEGF promotes the development of new blood vessels to the tumor cells. Inhibition of VEGF and the development of capillaries inhibits tumor growth and profession as well as metastasis.
- Down regulates tumor promoter Protein Kinase C isoenzymes,
- A group of enzymes that link multiple cellular processes responsible for regulation of tumorigenesis, cell cycle progression and metastasis.
- A group of enzymes that link multiple cellular processes responsible for regulation of tumorigenesis, cell cycle progression and metastasis.
- Inhibits Collagenase,
- A proteolytic enzyme that breaks down the ECM (Extracellular Matrix) and allows invasion of tumor cells into tissues and blood vessels, leading to progression, invasion and metastasis.
- A proteolytic enzyme that breaks down the ECM (Extracellular Matrix) and allows invasion of tumor cells into tissues and blood vessels, leading to progression, invasion and metastasis.
- Promotes Normal Apoptosis signaling.
- Cancer cells lose the ability to initiate apoptosis, the normal process in which a cell recognizes itself as aberrant and self destructs. The inhibition of normal apoptotic signaling in malignant cells is a hallmark of the tumor microenvironment permissive of uncontrolled growth, persistence and immortality due to loss of normal regulation.
- Cancer cells lose the ability to initiate apoptosis, the normal process in which a cell recognizes itself as aberrant and self destructs. The inhibition of normal apoptotic signaling in malignant cells is a hallmark of the tumor microenvironment permissive of uncontrolled growth, persistence and immortality due to loss of normal regulation.
- Lowers Bcl2 and Ras oncogenes.
- These genes inhibit normal apoptosis and promote tumor growth and progression.
- These genes inhibit normal apoptosis and promote tumor growth and progression.
- Acts as a Chemo-sensitizer
- Working synergistically to enhance therapeutic effect of chemotherapy drugs. DHA has a potential to specifically chemo-sensitize tumors.
- Tumour cells can be made more sensitive to chemotherapy than non-tumor cell when membrane lipids are enriched with DHA
- Incorporating DHA during treatment reduces adverse effects of chemotherapy.
- DHA can improve the outcome of chemotherapy when highly incorporated into cell membranes.
- Acts as a Radio-sensitizer.
- By promoting normal membrane structure and function and by influencing the tumor microenvironment DHA acts synergistically to potentiate therapeutic effects of radiotherapy on tumor cells.
- By promoting normal membrane structure and function and by influencing the tumor microenvironment DHA acts synergistically to potentiate therapeutic effects of radiotherapy on tumor cells.
- Promotes Healthy 16-OH Estrogen metabolism.
- Estrogen can be metabolized through multiple pathways. The promotion of 16-Hydroxylation of estrogen produces estrogen metabolites that are not pro-carcinogenic. Omega 3 Fatty Acids promote healthy estrogen metabolism.
- Estrogen can be metabolized through multiple pathways. The promotion of 16-Hydroxylation of estrogen produces estrogen metabolites that are not pro-carcinogenic. Omega 3 Fatty Acids promote healthy estrogen metabolism.
- Inhibits Platelet Aggregation and Thrombin Formation.
- Abnormal hyper-coagulation, increased platelet aggregation and thrombus formation are hallmarks of the tumor microenvironment. Control of platelet aggregation and thrombus formation reduces the risk of life threatening and adverse thrombotic events. 40% of all cancer patients are at risk for the formation of thromboembolisms. Omega 3 Fatty Acids reduce this risk.
- Abnormal hyper-coagulation, increased platelet aggregation and thrombus formation are hallmarks of the tumor microenvironment. Control of platelet aggregation and thrombus formation reduces the risk of life threatening and adverse thrombotic events. 40% of all cancer patients are at risk for the formation of thromboembolisms. Omega 3 Fatty Acids reduce this risk.
- Promotes Normal Cell Membrane Functions and Receptor Binding
- A healthy flexible cell membrane built of omega 3 fatty acids promotes an enhancement of all membrane functions, normalizing and optimizing normal and therapeutic physiology.
- A healthy flexible cell membrane built of omega 3 fatty acids promotes an enhancement of all membrane functions, normalizing and optimizing normal and therapeutic physiology.
- Increases expression of Tumor Suppressor Gene PTEN.
- Increased expression of tumor suppressor genes leads to enhanced control over carcinogenesis, tumorigenesis and metastatic progression.
- Increased expression of tumor suppressor genes leads to enhanced control over carcinogenesis, tumorigenesis and metastatic progression.
- Inhibits Multi Drug Resistance.
- Tumor cells can quickly become resistant to therapeutic anti-neoplastic agents thus decreasing and shortening the efficacy of treatments.
- Tumor cells can quickly become resistant to therapeutic anti-neoplastic agents thus decreasing and shortening the efficacy of treatments.
- Inhibits cachexia preserves muscle mass and bone mass (inhibits proteolysis inducing factor)
- Loss of bone mass (osteopenia) and loss of muscle mass (sarcopenia) are risk factors of aging and of the cancer physiology. Maintaining bone mass and muscle mass are crucial to robust healthy function and quality of life.
- Loss of bone mass (osteopenia) and loss of muscle mass (sarcopenia) are risk factors of aging and of the cancer physiology. Maintaining bone mass and muscle mass are crucial to robust healthy function and quality of life.
- Supports normal mood regulation.
- Depression and anxiety are common in cancer patients. Support of balanced mood allows cancer patients deep and restful sleep, improved quality of life and increased coping capacity and resilience in the face of stress.
- Depression and anxiety are common in cancer patients. Support of balanced mood allows cancer patients deep and restful sleep, improved quality of life and increased coping capacity and resilience in the face of stress.
How to Measure Omega 3 Fatty Acid Status
Serum or plasma omega-3 fatty acid ratios are readily accessible and available from most medical clinical labs. However, I recommend the OmegaQuant Omega-3 Index for measuring omega-3 status(omegaquant.com).
This cost-effective test was developed by a world expert in omega-3s and human health: Bill Harris, PhD, founder of OmegaQuant. Using a finger-stick at-home collection method, the test assesses the fatty-acid composition of the red blood cell membrane—not plasma.
OmegaQuant’s Omega-3 Index is defined as the amount of EPA plus DHA in red blood cell membranes, expressed as the percent of total red blood cell membrane fatty acids. Omega-3 levels of 8-12 percent are associated with better overall health.
For an in-depth discussion of the OmegaQuant Omega-3 Index, listen to the Dr. Bill Harris interview on the The Peter Attia Drive Podcast #83 (December 9, 2019). You can find the podcast at peterattiamd.com/billharris/.
Fish Oil Sourced
DFH Omegavail TG 1000 capsules 2 caps 2x/day = 4 caps = 4000mg
Metagenics EPA DHA 1000 capsules
- 2 caps 2x/day = 4 caps = 4000mg
DFH Omegavail Smoothie (emulsified-flavored liquid)
- Lemon Drop, Key Lime and Citrus Sorbet Flavors
- 3 Tablespoons daily = 4410 mg EPA DHA
Pharmax Ultra EPA DHA Liquid/Orange
- 1 1/2 teaspoons = 4522 mg 2 teaspoons = 5840 mg EPA DHA
Vegetarian sources:
It is challenging to achieve therapeutic dosing with Plant Sourced supplements of Omega 3 Fatty Acids
Algae Oil Sourced
Metagenics Omegagenics EPA DHA 300 Algae
- 300mg EPA DHA per soft gel 3 caps= 900mg 12 caps=3600mg EPA DHA
Plant Sourced Flaxseed Oil
(Flaxseed oil is primarily Alpha Linoleic Omega 3 and must be converted into EPA and DHA Omega 3 by enzymes in the body)
One Tablespoon Flax Oil can provide = 700mg EPA and DHA / 5 tablespoons= 3500mg
Barlean’s Highest Lignan Flax Oil Organic
Flora High Lignan Flax Oil Certified Organic
Selected References:
Azrad M, Turgeon C, and Demark-Wahnefried W. Front Oncol (2013) 3:224.
Bartsch H, Nair J, and Owen RW. Carcinogenesis (1999) 20:2209–18.
Bournoux P, et al. Br.J Cancer 2009 Dec 15:101(12):1978-85.
Tiwary S, Berzofsky J, and Terabe M. Front Immunol.18
Zanoaga O, et al. Exp Ther Med (2018) 15:1167–76.