Welcome To The Cancer Environment
by DanM@cowseatgrass · Published · Updated
When you listen to what the medical ‘experts’ say about cancer, you might come away with the impression that there has been complete agreement – in the vast amounts of scientific literature on the subject – regarding the nature of the disease and as such, the kinds of treatments worthy of consideration.
Even though that impression is not an accurate one, few people are aware of the fact that there is a long history of research and experimentation questioning the validity of the standard paradigm – which views cancer as a genetically driven disease of the cell – opening up the possibility for alternative forms of treatment.
“The somatic mutation theory of carcinogenesis has been the dominant force driving cancer research during the 20th century. In brief, it proposes that successive DNA mutations in a single cell cause cancer…” (C Sonnenschein, A M Soto. 2000)
“…its…continuous invocation of ‘programs’ and ‘mechanisms’ is a reflection of inadequate metaphors borrowed respectively from computer sciences and outdated physics; organisms are neither computers nor machines.” (Carlos Sonnenschein, Ana M Soto, 2013)
The idea however, that cancer is not some kind of random genetic event – but is rather a systemic disease which can be the result of the effects of a wide variety of metabolic stressors – has faced great resistance in both the scientific and medical communities, regardless of the quality of the evidence supporting it.
“We argue that it is necessary to abandon the somatic mutation theory…We propose the adoption of an alternative theory, the tissue organization field theory of carcinogenesis…” (C Sonnenschein, A M Soto. 2000)
“…the tissue organization field theory…incorporates the premise that proliferation and motility are the default state of all cells, and that carcinogenesis is due to alterations on the reciprocal interactions among cells and between cells and their extracellular matrix…There are multiple examples of normalization of cells that once belonged to a cancer…” (Carlos Sonnenschein, Ana M Soto, 2013)
The pushback to this theory arises in part because it threatens the status quo, suggesting that prevention and treatment of cancer need not focus upon discovering ‘responsible’ genes, and seeking out and destroying ‘guilty’ cells. It implies that the dominant approach may be more harmful than helpful.
“In the important realm of experimental cancer research, the proposed change would mean a switch from a subcellular, gene-centric approach to a tissue-based organicist one, in which a combined top-down and bottom-up strategy would include systems biology components.” (Carlos Sonnenschein and Ana M. Soto, 2011)
Destroying or removing ‘cancer cells’ in the currently accepted way – surgery, chemotherapy. and radiation – has been shown to have potentially dangerous repercussions, by increasing the cancer promoting capability of surrounding tissue environments.
“Put another way, cancer results from a breakdown of tissue organization that disrupts the normal inhibitions of proliferation that are inherent in the tissue architecture of a multicellular society of cells.” (C. Sonnenschein, et al., 1999)
Alternatively, it makes sense that any approach which can effectively improve tissue environments, is likely to have the opposite effect, preventing or perhaps even reversing the spread of cancer.
“One of the predictions of the tissue organization field theory is that carcinogenesis can potentially be reversed… Experimentally, the reversal of neoplastic behavior has been accomplished repeatedly when neoplastic cells were placed within the normal tissues from which they originated.” (Maricel V Maffini, et al., 2005)
The significance of this way of understanding is heightened by the knowledge that the worsening of tissue microenvironments influence the likelihood that tumors will spread or metastasize, a circumstance which is overwhelmingly responsible for cancer mortality.
“Metastases are defined as secondary tumors that develop at a distance from their primary originators; they are the cause of death for 90% of cancer patients…the prevailing consensus is that metastases are not explained accurately, and, more importantly, they are far from being successfully managed.” ( Carlos Sonnenschein, Ana M Soto, 2015)
“…behavior of normal cells is ordered by their topological relations in tissues and other homeostatic influences of the organism. Weakening of these ordering relations may contribute to malignant transformation…” (H Rubin, 1990)
Rather than random genetic mutations driving the creation of ‘cancer cells’, it makes sense – based on good quality evidence – to see biological stress as the central factor in the development of an internal cancer environment.
Continuous exposure to stress interfering with the provision of sufficient metabolic energy – or exceeding the amount required to cope with such stress – can be one general way of understanding how the conditions which can change the tissue, damage the cells (as well as DNA), and encourage cancer potential come about.
“We challenge the notion that cancer is a cellular problem caused by mutated genes by assessing…an alternative view that regards carcinogenesis as a developmental process gone awry.” (Ana M Soto, Carlos Sonnenschein, 2005)
“…interactions among different components of a tissue cannot be reduced to cellular events…carcinogenesis takes place at the tissue level of biological organization……while normal cells already carry mutations, they do not end up becoming cancer cells…From this perspective, these mutations would be irrelevant as suggested by the repeated instances where cells from diverse cancer types were normalized when placed within a normal field.” ( Ana M Soto, Carlos Sonnenschein, 2011)
The substances of stress – including cortisol, serotonin, endotoxin, nitric oxide, estrogen, lactate, and various other inflammatory and fibrotic things – which often increase side by side with aging, directly and indirectly impact upon the ability of tissue environments to be able to function in a manner which protects against or even reverses cancer behavior of the cell.
“…damage accumulates with age, as does an increasingly permissive local environment for tumor growth…The order that controls heterogeneity is weakened with age and contributes to the origin and progression of disordered growth.” (H Rubin, 1999)
“…findings reveal unanticipated communication between stress-induced neural signalling and inflammation, which regulates tumour lymphatic architecture and lymphogenous tumour cell dissemination.” (Caroline P. Le, et al., 2016)
Increased circulation of bacterial endotoxin (LPS or lipopolysaccharide) is one thing that is known to promote the inflammatory conditions which can induce cancer development and metastasis.
“Inflammation has been known to be linked to invasion or metastasis of breast cancer, which has poor prognosis…Here we show that T-LAK cell-originated protein kinase (TOPK) mediates pro-inflammatory endotoxin lipopolysaccharide (LPS)-induced breast cancer cell migration and invasion.” (Min-Ah Seol, et al., 2017)
“NF-kappaB is one of the key factors connecting inflammation with cancer progression…LPS increased the invasive ability of pancreatic cancer cells, while blockade of NF-kappaB pathway decreased the LPS-dependent increased invasive ability…” (Mio Ikebe, et al., 2009)
“Our findings suggest that inhibiting LPS-induced TLR4 signaling could improve therapeutic outcomes by preventing cancer metastasis during the perioperative period of CRC (colorectal cancer) resection.” (Rich Y C Hsu, et al., 2011)
The polyunsaturated fats (PUFAs) which get stored in (and released from) the tissue, have been demonstrated to be a fundamental and powerful driver of inflammation as well as the growth and spread of cancer.
“Arachidonic acid (ARA) is metabolized by cyclooxygenase (COX) and cytochrome P450 to produce proangiogenic metabolites. Specifically, epoxyeicosatrienoic acids (EETs) produced from the P450 pathway…promote angiogenesis, tumor growth, and metastasis.” (Amy A Rand, et al., 2017)
“…dietary fat promotes the growth of initiated cells, thus contributing to the higher risk of many human cancers…high-fat diets containing corn oil, soybean oil or safflower oil, which are 55–80% linoleic acid, increase the rate of growth of established tumors…” (Ivan Rusyn, et al., 1999)
“…we find that neutrophil-derived leukotrienes [metabolites of arachidonic acid] aid the colonization of distant tissue by selectively expanding the sub-pool of cancer cells that retain high tumorigenic potential.” (Stefanie K Wculek, Ilaria Malanchi, 2015)
Endotoxin and PUFAs promote nitric oxide (NO), and NO is another powerful mediator of inflammation, which has been shown to play a role in the development of a tissue environment which is increasingly capable of promoting cancer initiation and progression.
“Inducible nitric oxide synthase (iNOS) is associated with poor survival in patients with breast cancer by increasing tumor aggressiveness…targeted therapy with iNOS inhibitors is able to inhibit not only tumor cell proliferation…self-renewal and migration, reducing tumor growth, tumor initiation, and the number of lung metastases.” (Sergio Granados-Principal, et al., 2015)
“…role for NO production from iNOS in human lung cancer because high concentrations of this short molecule may transform to highly reactive compounds such as peroxynitrite; moreover, through the upregulator NF-kB, they can induce a chronic inflammatory state representing an elevated risk for cell transformation to cancer.” (Speranza L, et al., 2007)
Exposure to chronic or acute levels of stress of many different kinds, wastes blood sugar reserves and leads to the increased release of stress substances (including bacterial endotoxin), as well as a rise in systemic levels of polyunsaturated free fatty acids.
The combination of many of the above factors can be seen to be a major determinant of the stress conditions which promote tissue damage, genetic changes, blood sugar dysregulation, and the irregular cell activity of cancer and related metabolic illnesses.
“…chronic periods of stress can be detrimental to health by increasing inflammation and promoting the progression of diseases including cancer…we show that chronic stress restructures lymphatic networks within and around tumours to provide pathways for tumour cell escape.” (Caroline P. Le, et al., 2016)
“Our findings provide a hitherto-undescribed direct role of increased aerobic glycolysis in inducing the cancer phenotype, in which increased glycolytic activity regulates the canonical oncogenic pathways…additional evidence for how hyperglycemia in diseases such as obesity and diabetes could provide a microenvironment that results in higher risk of some cancers.” (Yasuhito Onodera, et al., 2013)
Estrogen levels are known to rise as a result of ongoing exposure to the inflammatory stress substances, potentially causing genetic changes and the development of cancer. Estrogen blood tests do not account for the amount of estrogen trapped in tissue where it causes the most harm.
“…findings suggest that exposure to estrogen…is capable of driving genomic instability, a well-defined early event in breast cancer development. Given that estrogen levels in normal/benign breast tissue are known to be 6-7 times that of circulating estrogen levels, our findings suggest a mechanism through which BRCA1 carriers, through enhanced production of DNA damaging estrogen metabolites, may acquire the genetic alterations that initiate neoplastic transformation in breast tissue…Similarly, levels of estrogen in ovarian tissues greatly exceed that of circulating estrogen, suggesting that this model may also explain the substantially increased risk of ovarian cancer in BRCA1 carriers…” (Kienan I Savage, et al., 2014)
“The knowledge that breast cancer in women is associated with prolonged exposure to high levels of estrogens gives relevance to this model of estrogen induced carcinogenesis…” ( J Russo, Irma H Russo, 2006)
Avoiding consumption of the PUFAs and eating enough high quality protein – from milk, cheese and gelatinous cuts of meat – as well as plenty of simple and easy to digest sugars – from sweet ripe fruit, fruit juice, white sugar and honey – is thought to be a potentially powerful approach to suppressing stress, regulating blood sugar, and lowering exposure to dangerous fats (ingested and stored in tissue), and might also be a logical way to improve tissue organization, redirecting cellular behavior away from cancer progression.
“…these observations may lead to a new paradigm for control and treatment of cancer in situ…it may be possible to redirect tumorigenic cells to normal cell function by exposure to substances present within normal tissues.” (Karen M Bussard, et al., 2010)
“This provides a mechanism through which interaction with the normal mammary microenvironment may suppress tumorigenesis…the normal microenvironment redirects…tumorigenic cells to participate in the regeneration of a normal, functional mammary gland.” (B W Booth, et al., 2010)
Some other things which have been said to be protective include increasing carbon dioxide levels (with bag breathing or adaptation to higher altitudes for example), exposure to daylight, therapeutic use of red light, pregnenolone and progesterone supplementation, vitamin E, vitamin A, caffeine, glycine, aspirin, and a number of other anti-estrogen and anti-serotonin substances including the antihistamine cyproheptadine.
Alternatively, things that lower stress and allow thyroid metabolism to function more effectively (including therapeutic use of white sugar) are likely to be very helpful.
“A deeper understanding of the role(s) of tissue and tumor microenvironments in the pathogenesis of cancer is essential to design more effective strategies for the management of this disease.” (Ezio Laconi, et al., 2008)
“…if a cancer cell exists as a discrete entity distinguishable from a normal cell, it has certainly been very uncooperative in revealing what it has ‘invented’ to deserve the fame it has acquired. More to the point, cells isolated from cancers revert to normalcy when placed in a normal microenvironment.” ( Carlos Sonnenschein, Ana M Soto, 2013)
Copyright 2021, by Dan M @ CowsEatGrass. All rights reserved (except for quotations and images having their own protected copyrights). This copyright protects author-publisher Dan M’s right to future publication of his work in any manner, in any and all media — utilizing technology now known or hereafter devised — throughout the world in perpetuity. Everything described in this publication is for information purposes only. The author-publisher, Dan M, is not directly or indirectly presenting or recommending any part of this publication’s data as a diagnosis or prescription for any ailment of any reader. If anyone uses this information without the advice of their professional health adviser, they are prescribing for themselves, and the author- publisher assumes no responsibility or liability. Persons using any of this data do so at their own risk and must take personal responsibility for what they don’t know as well as for what they do know.
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