巴德维疗法治疗癌症的科学依据 The Scientific Basis of Using Flaxseed Oil and Quark or Cottage Cheese to Cure Cancer

The Scientific Basis of Using Flaxseed Oil and Quark or Cottage Cheese to Cure Cancer

Too many in the natural health field, especially writers, scoff at the Budwig Diet’s core protocol as unreal and unsuited for reversing cancer. There are other dietary requirements that are part of her protocol. Lots of sunshine and stress management are also part of Johanna Budwig’s approach to healing the whole person.

That core protocol is flaxseed oil and cottage cheese. Originally it was flaxseed oil and quark, a crumbly textured white cheese resembling ricotta that is common among German speaking nations, Scandinavian countries, and much of the Eastern European region. But quark is not available in America. So here it’s cottage cheese instead of quark.

Even Dr. Andrew Weil was quoted as criticizing the Budwig Diet with “curing cancer with cottage cheese is wishful thinking”. Yet over a 50 year period, Johanna Budwig had a 90% plus cancer cure rate in Germany among 4500 patients afflicted with all types of cancers. Some cancer victims that she cured with her protocol were considered terminal.

The Scientific Basis of Using Flaxseed Oil and Quark or Cottage Cheese to Cure Cancer

As a biochemist and physicist in the early 1950`s, Johanna was a senior scientist in the German Federal Health Office, comparable to the American FDA but with less bureaucratic corruption. Her task was to help determine what might be appropriate for cancer curing medication from German pharmaceutical companies.

One pharmaceutical company forwarded applications to her for a sulfhydryl group, which are proteins (amino acids) that contain sulfur. That company was considering applying the sulfhydryl group toward cancer medication. The data obtained from that company enabled Budwig to get an overview of the problems involved with oxygenating cancer cells through dietary means. Cancer cells cannot thrive in oxygen.

This was an area that the 1931 Nobel Prize winner Otto Warburg had hoped to resolve. He was the one who discovered that cancer cells thrive in an anaerobic environment, but could not survive in an oxygen rich environment. He was looking for a respiratory enzyme that would help oxygenate cancer cells.

Warburg was aware that fats had something to do with inhibiting or enhancing cellular oxygen absorption, but during his time fats were not classified with their biochemical structures and functions. It was around 1951 that Johanna Budwig discovered methods for determining the different properties of fatty acids.

Consequently, she was funded to continue her research categorizing the different properties of fatty acids. Johanna examined the molecular properties of many fats, determining if they were saturated or unsaturated, if they were isolating linoleic acid or lauric acid and if they inhibited or enhanced cellular oxygen absorption. Factually, most of what is known today about fatty acids comes from Johann Budwig’s mid 20th Century research discoveries.

Without these fatty acids, the respiratory enzymes cannot function and the person suffocates, even when he is given oxygen-rich air. A deficiency in these highly unsaturated fatty-acids impairs many vital functions. First of all, it decreases the person’s supply of available oxygen. We cannot survive without air and food; nor can we survive without these fatty acids.

9200000000891198Johanna Budwig had determined that organic cold pressed flaxseed oil was the most suitable fat to combine with an easy to eat protein-sulfur of quark/cottage cheese for the elusive respiratory enzyme that could penetrate cancer cells. These two disparate foods were able to combine and create the oxygen within cancer cells for restoring normalcy.

The Budwig Diet was arrived at from extensive research, which was not even possible until her discoveries of how to determine the properties of fatty acids. Cottage cheese/quark with pure cold pressed flax oil for curing cancer is not merely a culinary quirk.

She was born in 1908 and died in 2003 at the age of 95 from complications due to injuries after a fall in her home. As a result of her research from the 1950’s and on, she was nominated for the Alternative Nobel Prize, Europe’s counterpart to the Swedish Nobel Prize, seven times.

Naturally, her successful treatment of many cancer patients, some of whom were terminal, led to professional envy in Germany. She was harassed through the German court system a couple of times, and both times the courts favored her! She proceeded to expand her knowledge and legitimacy by getting a doctorate in Natural Sciences to become a PhD Naturopath.

This broadened her understanding of how connected all living things are with bio-electrical energy and sunlight. She talks of how seeds that absorb the sun’s energy, such as flax seeds, connect with the human organism’s innate intelligence to convert bio-electric energy for its organic needs – thus the sunshine aspect of her therapy to connect with the flax oil consumption.

Budwig was medically blacklisted because she publicly opposed chemotherapy and radiation on cancer patients. She also didn’t make friends with cooking and salad oil manufacturers when she started exposing the terrible health consequences of using heated, chemically treated processed or hydrogenated oils that were being foisted on the public from the 1950’s on.

Until only recently, virtually all consumers had been suckered into using those oils, which actually contribute toward creating cancer. Ironically, if Budwig’s concerns had been publicized, a lot of poor health turned cancerous from bad oils would have been eliminated.

When it comes to the cottage cheese in this video, realize that low fat was recommended solely because low fat was the dimwitted trend for so long. Whole milk products, raw if possible, are fine. Adhere strictly to the rest of what’s in this video.

If you’re at all interested in the Budwig Diet for cancer or other health issues, you must know the pitfalls. Though simple, it’s precise enough that those who deviate from its guidelines fail. That’s why you should research starting with the following sources for more information:

Covers the Budwig diet well with testimonials and access to her books: http://www.cancertutor.com/budwig/

Basic Introduction to Dr. Budwig`s Diet, Fats, Essential Fatty Acids and Related Subjects

1) http://www.healingcancernaturally.com/budwig_protocol.html#Budwig%20major%20discovery

2) http://www.healingcancernaturally.com/budwig_protocol.html#the-oil-protein-diet-cookbook

German Interview (translated) of Johanna Budwig Circa 1990 http://www.healingcancernaturally.com/lothar-hirneise-johanna-budwig.html

Lothar Hirneise’s site, an apprentice to Johanna Budwig and translator of her books http://www.hirneise.com/index.html

The Miracle of EFA “Oxygen Magnets”

Think of these polyunsaturated EFAs as “oxygen magnets.” The proof of this fact is buried in the world’s leading medical textbooks and medical journals such as Harper’s Illustrated Biochemistry, 26th edition40 and Human Nutrition Clinical Nutrition,41 July 1984. EFAs are integral to the structure and function of cellular respiration. Without high respiration efficiency, cancer is soon to follow. These EFA oxygen magnets in the cell membrane attract the oxygen that’s in your bloodstream and transfer it into the cell just like little oxygen sponges. This process is supposed to be happening in each of your 100 trillion cells. So, no matter how much you breathe or exercise, if you don’t have the proper functional EFAs at the cellular level, your cells will not absorb enough oxygen from your bloodstream. You will be that much more susceptible to cancer.

Without a continuing new supply of these EFAs from food, cellular oxygen transfer is significantly reduced. Imagine what would happen if you had 100 trillion cells that were all deficient in a vital substance they required to be able to absorb oxygen. Here’s an example showing how these essential fats absorb oxygen. At the supermarket, fish goes bad in only a few days because the oil in the fish is highly oxygen-absorbing—it reacts rapidly with the oxygen in the air. Fish spoils rapidly because the EFA-containing oil has the capacity to absorb lots of oxygen. This chemical process is called “oxidation.” This is also true with other types of essential fats. They do their job of absorbing oxygen, but because of it they have a limited life. They simply won’t work after a short period. EFAs become “spent” (rancid). That’s why they need to be replaced every day from our food—Nature designed us this way. There are many ways to add additional oxygen to the bloodstream, such as exercising, drinking “oxygenated” water, or breathing purer air. However, these partial solutions are insufficient for maximum anticancer protection. When the EFA deficiency is solved, every organ becomes its own “oxygen magnet,” like Nature intended.

Breast cancer is the #1 cancer plague to women worldwide. The growing incidence of breast cancer can, for the first time, be explained in light of Dr. Warburg’s discovery about lack of oxygen to the cells. The breasts consist of an exceptionally high amount of fatty tissue. A typical cell membrane in muscle tissue is half fat and contains about one-third EFAs (oxygen transferors). Fatty tissue like the breast contains areas of 80-95% fat concentration. These fatty components of breast tissue require and should have high EFA concentrations, but because of modern food processing, they don’t. Because important organs such as the brain, heart, lungs, and kidneys require EFAs on a priority basis, there may not be enough left over to ensure that breast tissue receives an adequate amount of EFAs. Therefore, oxygen deficiency in the breast tissue will be very significant.

Given this premise, we can deduce that breast tissue should and would be the number one expected cancer site in women worldwide—and it is. This conclusion makes so much sense in explaining the massive rise in breast cancer. Harvard’s Dr. Willett gives us the proof: In a large study concerning the intake of parent omega-6 by over 80,000 nurses it was shown that the group with the lowest intake of linoleic acid (parent omega-6) exhibited the highest incidence of breast cancer.42 Did your ob-gyn tell you that you need this miraculous anticancer nutrient? I doubt it because he probably doesn’t know it.

How Do We Maximize Cellular Oxygenation? - East Valley Naturopathic Doctors
https://www.eastvalleynd.com/treatments_therapies/how-do-we-maximize-cellular-oxygenation/

Singlet Oxygen Generation from the Decomposition of α-Linolenic Acid Hydroperoxide by Cytochrome c and Lactoperoxidase †

Generation of singlet oxygen is first investigated in the decomposition of polyunsaturated lipid peroxide, alpha-linolenic acid hydroperoxide (LAOOH), by heme-proteins such as cytochrome c and lactoperoxidase. Chemiluminescence and electron spin resonance methods are used to confirm the singlet oxygen generation and quantify its yield. Decomposition products of LAOOH are characterized by HPLC-ESI-MS, which suggests that singlet oxygen is produced via the decomposition of a linear tetraoxide intermediate (Russell's mechanism). Free radicals formed in the decomposition are also identified by the electron spin resonance technique, and the results show that peroxyl, alkyl, and epoxyalkyl radicals are involved. The changes of cytochrome c and lactoperoxidase in the reaction are monitored by UV-visible spectroscopy, revealing the action of a monoelectronic and two-electronic oxidation for cytochrome c and lactoperoxidase, respectively. These results suggest that cytochrome c causes a homolytic reaction of LAOOH, generating alkoxyl radical and then peroxyl radical, which in turn releases singlet oxygen following the Russell mechanism, whereas lactoperoxidase leads to a heterolytic reaction of LAOOH, and the resulting ferryl porphyryl radical of lactoperoxidase abstracts the hydrogen atom from LAOOH to give peroxyl radical and then singlet oxygen. This observation would be important for a better understanding of the damage mechanism of cell membrane or lipoprotein by singlet oxygen and various radicals generated in the peroxidation and decomposition of lipids induced by heme-proteins.
　

Oxidative Damage of U937 Human Leukemic Cells Caused by Hydroxyl Radical Results in Singlet Oxygen Formation

.. In addition to 3 (R 5 O)* pathway, the direct decomposition of ROOOOR to 1 O 2 by Russell mechanisms was evidenced in the chemical system 23,24 . More recently, several lines of evidence were provided on the formation of 1 O 2 by the decomposition of lipid and protein ROOH by metal ions, cytochrome c, peroxynitrite, chloroperoxide, and hypochlorous acid [25][26][27][28] . As the yield of 3 (R 5 O)* formation during the decomposition of ROOOOR was found to be 10 3 -10 4 lower compared to the yield of 1 O 2 formation, it was proposed that the Russell mechanism leads predominantly to the formation of 1 O 2 , whereas the formation of 3 (R 5 O)* is rather negligible 29 . ...

Biochem Biophys Res Communication. 1999 Nov
Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB

A 48-h incubation of cultured human fibroblasts with 5 x 10(-5) M oleic acid or polyunsaturated fatty acids (PUFA) from the (n-6) (linoleic, gamma-linolenic and arachidonic acids) or (n-3) (alpha-linolenic and eicosapentaenoic acids) series resulted in an enrichment of the cells with the introduced fatty acid. Cell enrichment with PUFA initiated a rise in the intracellular level of reactive oxygen species (ROS) and lipid peroxidation products (thiobarbituric reactive substances TBARS). Simultaneously, cell enrichment with all the studied PUFA induced an increase in AP1 and NFkappaB binding activity measured by electrophoretic mobility shift assay, whereas no significant effect was observed with the monounsaturated oleic acid. Furthermore, the antioxidants vitamin E (alpha-tocopherol) and N-acetyl cysteine prevented both the arachidonic acid-induced increase in intracellular ROS and TBARS, and the activation of AP1 and NFkappaB. These results indicate that the accumulation of PUFA from (n-6) and (n-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB.

Copyright 1999 Academic Press.

Cellular enrichment with polyunsaturated fatty acids induces an oxidative stress and activates the transcription factors AP1 and NFkappaB - PubMed
https://pubmed.ncbi.nlm.nih.gov/10548500/

Tumour Biology. 2016 Mar;
Alpha-linolenic acid regulates Cox2/VEGF/MAP kinase pathway and decreases the expression of HPV oncoproteins E6/E7 through restoration of p53 and Rb expression in human cervical cancer cell lines

Cervical cancer represents the largest cause of mortality in women worldwide. In our previous report, we have shown how alpha-linolenic acid (ALA), an omega-3 fatty acid, regulated the growth of cervical cancer cells. The present study aimed to explore mechanistic details for the anticancer activity of ALA in cervical cancer cell lines, SiHa and HeLa. ALA significantly modulated the growth kinetics of the cells and reduced cell migration with concomitant decrease in the expression of VEGF, MMP-2, and MMP-9 proteins. Besides this, ALA significantly decreased the expression of phosphorylated p38, pERK1/2, c-JUN, NFκB, and COX2, proteins. Most importantly, ALA reduced the expression of HPV onco-proteins E6 and E7, resulting into restoration of expression of tumor suppressor proteins, p53 and Rb. These results suggested that ALA could be explored for its therapeutic potential in cervical cancer.

Keywords: Alpha-linolenic acid; Cervical cancer; HPV oncoproteins; NF-κB.

Alpha-linolenic acid regulates Cox2/VEGF/MAP kinase pathway and decreases the expression of HPV oncoproteins E6/E7 through restoration of p53 and Rb expression in human cervical cancer cell lines - PubMed
https://pubmed.ncbi.nlm.nih.gov/26440049/

J Oleo Science;
Dietary alpha-linolenic acid inhibits angiotensin-converting enzyme activity and mRNA expression levels in the aorta of spontaneously hypertensive rats

Several studies have shown that dietary alpha-linolenic acid (ALA) is associated with a reduced risk of cardiovascular disease and has an antihypertensive effect. Blood pressure is regulated mainly by angiotensin-converting enzyme (ACE). In the present study, we investigated the effect of dietary ALA on ACE to clarify the mechanism of the antihypertensive effect in spontaneously hypertensive rats (SHR). Six-week-old SHR were fed a diet containing either 10% ALA-rich flaxseed oil or high oleic safflower oil as a control for four weeks. Systolic blood pressure (SBP) was measured by the tail cuff method once weekly. At the end of the feeding period, ACE activity was determined in the heart, aorta, lung and kidney. ACE mRNA in these organs was also measured by real-time PCR analysis. SBP in the ALA group was significantly lower than in the control group at 2, 3, and 4 weeks. The ACE activity and mRNA expression levels in the ALA group were significantly lower than in the control only in the aorta. In conclusion, the present findings suggest that the blood pressure-lowering mechanism of dietary ALA may be involved in the reduction of ACE activity and mRNA expression levels in the aorta of SHR.

Dietary alpha-linolenic acid inhibits angiotensin-converting enzyme activity and mRNA expression levels in the aorta of spontaneously hypertensive rats - PubMed
https://pubmed.ncbi.nlm.nih.gov/19491530/

J Oleo Science;
Dietary alpha-linolenic acid inhibits angiotensin-converting enzyme activity and mRNA expression levels in the aorta of spontaneously hypertensive rats

Several studies have shown that dietary alpha-linolenic acid (ALA) is associated with a reduced risk of cardiovascular disease and has an antihypertensive effect. Blood pressure is regulated mainly by angiotensin-converting enzyme (ACE). In the present study, we investigated the effect of dietary ALA on ACE to clarify the mechanism of the antihypertensive effect in spontaneously hypertensive rats (SHR). Six-week-old SHR were fed a diet containing either 10% ALA-rich flaxseed oil or high oleic safflower oil as a control for four weeks. Systolic blood pressure (SBP) was measured by the tail cuff method once weekly. At the end of the feeding period, ACE activity was determined in the heart, aorta, lung and kidney. ACE mRNA in these organs was also measured by real-time PCR analysis. SBP in the ALA group was significantly lower than in the control group at 2, 3, and 4 weeks. The ACE activity and mRNA expression levels in the ALA group were significantly lower than in the control only in the aorta. In conclusion, the present findings suggest that the blood pressure-lowering mechanism of dietary ALA may be involved in the reduction of ACE activity and mRNA expression levels in the aorta of SHR.

J Nutr Biochemistry. 2012 Apr;23
Alpha-linolenic acid increases cholesterol efflux in macrophage-derived foam cells by decreasing stearoyl CoA desaturase 1 expression: evidence for a farnesoid-X-receptor mechanism of action

Increased cholesterol efflux from macrophage-derived foam cells (MDFCs) is an important protective mechanism to decrease lipid load in the atherosclerotic plaque. Dietary alpha-linolenic acid (ALA), an omega-3 polyunsaturated fatty acid (PUFA), decreases circulating cholesterol, but its role in cholesterol efflux has not been extensively studied. Stearoyl CoA desaturase 1 (SCD1) is the rate-limiting enzyme in the synthesis of monounsaturated fatty acids (MUFAs). Endogenous MUFAs are preferentially incorporated into triglycerides, phospholipids and cholesteryl ester, which are abundant in atherosclerotic plaque. This study investigated the mechanisms by which ALA regulated SCD1 and subsequent effect on cholesterol storage and transport in MDFCs. Small interfering RNA (siRNA) also was applied to modify SCD1 expression in foam cells. Alpha-linolenic acid treatment and SCD1 siRNA significantly decreased SCD1 expression in MDFCs. The reduction of SCD1 was accompanied with increased cholesterol efflux and decreased intracellular cholesterol storage within these cells. Alpha-linolenic acid activated the nuclear receptor farnesoid-X-receptor, which in turn increased its target gene small heterodimer partner (SHP) expression, and decreased liver-X-receptor dependent sterol regulatory element binding protein 1c transcription, ultimately resulting in repressed SCD1 expression. In conclusion, repression of SCD1 by ALA favorably increased cholesterol efflux and decreased cholesterol accumulation in foam cells. This may be one mechanism by which dietary omega-3 PUFAs promote atherosclerosis regression.

Alpha-linolenic acid increases cholesterol efflux in macrophage-derived foam cells by decreasing stearoyl CoA desaturase 1 expression: evidence for a farnesoid-X-receptor mechanism of action - PubMed
https://pubmed.ncbi.nlm.nih.gov/21658928/

Arch Dermatol Research. 1998 Jul;
Linoleic acid and alpha-linolenic acid lightens ultraviolet-induced hyperpigmentation of the skin

This study was conducted to evaluate the effects of unsaturated fatty acids on ultraviolet-induced hyperpigmentation of the skin. An efficient lightening effect was observed following topical application of linoleic acid or alpha-linolenic acid to UV-stimulated hyperpigmented dorsal skin of brownish guinea pigs. The number of melanocytes in the treated skin was similar to the number in the skin of the pigmented control, indicating that the pigment-lightening effect was not due to depletion of melanocytes. In vitro experiments using cultured murine melanoma cells showed that melanin production was inhibited most effectively by alpha-linolenic acid, followed by linoleic acid and then by oleic acid. Furthermore, the turnover of the stratum corneum, which plays an important role in the removal of melanin pigment from the epidermis, was accelerated by linoleic acid and by alpha-linolenic acid. Taken together, the results suggest that the pigment-lightening effects of linoleic acid and alpha-linolenic acid are, at least in part, due to suppression of melanin production by active melanocytes, and to enhanced desquamation of melanin pigment from the epidermis.

Fatty acids (FA) are well known as efficient enhancers for transdermal delivery of drugs; however, their frequent dermal toxicity limits their regular use. In order to utilize the fatty acid as a safe enhancer devoid of its irritant effect, we have synthesized and evaluated a series of fatty acids c …

https://pubmed.ncbi.nlm.nih.gov/18058312

Dietary, but not Topical, Alpha‐linolenic Acid Suppresses UVB‐induced Skin Injury in Hairless Mice when Compared with Linoleic Acid¶ - Takemura - 2002 - Photochemistry and Photobiology - Wiley Online Library
https://onlinelibrary.wiley.com/doi/abs/10.1562/0031-8655%282002%290760657DBNTAL2.0.CO2

Antibacterial activities of fatty acids
Fatty acids tested in enzyme assays were tested for their antibacterial activity against the Gram positive pathogens,S. aureus and S. pyogenes, and against Gram negative bacteria, including E. coli and Pseudomonas aeruginosa (Table 2). The antibacterial activity of fatty acids tested in enzyme assays was monitored by the ability (MIC) of the fatty acids to inhibit cell growth. Unsaturated fatty acids tested exhibited the antibacterial activity with MIC values of 0.05–0.4 mM against Gram positive bacteria of S. aureus and S. pyogenes, while they did not show antibacterial activity on Gram negative bacteria of E. coli and P. aeruginosa. The MIC values are similar to the reported values (0.05–0.5 mM) [9]. The saturated fatty acids tested were not active on either Gram positive or Gram negative bacteria, even at 2 mM. This differential antibacterial activity between unsaturated fatty acids and saturated fatty acids on Gram positive bacteria of S. aureus and S. pyogenes was well correlated with the inhibition of S. aureus FabI in vitro (Table 1).

脂肪酸的抗菌活性
在酶测定中测试的脂肪酸对革兰氏阳性病原体S的抗菌活性进行了测试。金黄色葡萄球菌和化脓性链球菌，以及针对革兰氏阴性细菌，包括大肠杆菌和铜绿假单胞菌（表2）。通过脂肪酸抑制细胞生长的能力（MIC）来监测在酶分析中测试的脂肪酸的抗菌活性。测试的不饱和脂肪酸对金黄色葡萄球菌和化脓性链球菌的革兰氏阳性菌表现出抗菌活性，MIC值为0.05-0.4 mM，而对大肠杆菌和铜绿假单胞菌的革兰氏阴性菌则没有表现出抗菌活性。 MIC值与报告的值相似（0.05–0.5 mM）[9]。测试的饱和脂肪酸对革兰氏阳性细菌或革兰氏阴性细菌均无活性，即使在2 mM时也不起作用。在金黄色葡萄球菌和化脓性链球菌的革兰氏阳性细菌上，不饱和脂肪酸和饱和脂肪酸之间的这种不同的抗菌活性与体外对金黄色葡萄球菌FabI的抑制作用密切相关（表1）。

Fatty acid synthesis is a target for antibacterial activity of unsaturated fatty acids - ScienceDirect
https://www.sciencedirect.com/science/article/pii/S0014579305010124

Metabolic basis for the differential susceptibility of ...

https://www.pnas.org/content/108/37/15378

Sep 13, 2011 · The rationale for the pursuit of bacterial type 2 fatty acid synthesis (FASII) as a target for antibacterial drug discovery in Gram-positive organisms is being debated vigorously based on their ability to incorporate extracellular fatty acids. The regulation of FASII by extracellular fatty acids was examined in Staphylococcus aureus and Streptococcus pneumoniae , representing two important ...

Cited by: 162
Publish Year: 2011

Author: Joshua B. Parsons, Matthew W. Frank, Chitra Subrama

Gram-negative bacteria- cell wall, examples, diseases ...

https://microbenotes.com/gram-negative-bacteria

Apr 11, 2020 · These are bacteria that define the opposite of the gram-positive bacteria in relation to the differential staining technique. During gram staining, the gram-negative bacteria will lose the crystal violet dye color after a wash with alcohol and take up the pink/red color of the counterstain, safranin.. The two classes of bacteria are differentiated through gram staining, because of their cell ...

Metabolic basis for the differential susceptibility of ...

https://www.pnas.org/content/108/37/15378

Cited by: 162
Publish Year: 2011

Author: Joshua B. Parsons, Matthew W. Frank, Chitra Subrama

Breaking the cycle: the role of omega-3 polyunsaturated fatty acids in inflammation-driven cancers

Publication: Biochemistry and Cell Biology • 8 July 2014 •
Chronic inflammation is a cyclical, self-stimulating process. Immune cells called to sites of inflammation release pro-inflammatory signaling molecules that stimulate activation of inducible enzymes and transcription factors. These enzymes and transcription factors then stimulate production of signaling molecules that attract more immune cells and induce more enzymatic and transcriptional activity, creating a perpetual loop of inflammation. This self-renewing pool of inflammatory stimuli makes for an ideal tumor microenvironment, and chronic inflammation has been linked to oncogenesis, tumor growth, tumor cell survival, and metastasis. Three protein pathways in particular, nuclear factor kappa B (NF-kB), cyclooxygenase (COX), and lipoxygenase (LOX), provide excellent examples of the cyclical, self-renewing nature of chronic inflammation-driven cancers. NF-kB is an inducible transcription factor responsible for the expression of a vast number of inflammation and cancer related genes. COX and LOX convert omega-6 (n-6) and omga-3 (n-3) polyunsaturated fatty acids (PUFA) into pro- and anti-inflammatory signaling molecules. These signaling molecules stimulate or repress activity of all three of these pathways. In this review, we will discuss the pro- and anti-inflammatory functions of these fatty acids and their role in chronic inflammation and cancer progression.

Breaking the cycle: the role of omega-3 polyunsaturated fatty acids in inflammation-driven cancers
https://cdnsciencepub.com/doi/abs/10.1139/bcb-2013-0127

Conjugates of Unsaturated Fatty Acids With Propylene ...

Metabolic basis for the differential susceptibility of ...

Gram-negative bacteria- cell wall, examples, diseases ...

Metabolic basis for the differential susceptibility of ...