The Pregnancy Cancer Connection 2012


This was an article written in 2012 printed in Positive Health online magazine.
It is really a concept introduction for lay people and health professionals to understand the similarities between cancer and pregnancy mechanisms. All still useful ideas.

I need to write new articles on methylation, caspases and cell fusion in cancer to simplify and update the concepts.
Read the new piece written from Feb 2020 on Macrophage Polarization and IDO Enzymes, Immunity, Cancer and Depression to get another viewpoint on cell fusion in the immune process.

The Pregnancy Cancer Connection

by Cal Crilly.

Listed in cancer, originally published in issue 205 – April 2013

The pregnancy link with cancer goes back to John Beard in 1902 who wrote about The Action of Trypsin[1] coming from the foetal pancreas to act on switching off trophoblast function. Trophoblasts are cells that surround the embryo and then form the umbilical cord which grows and creates an entire new set of arteries between mother and child, using the placenta as an organ for transferring maternal-foetal gas, nutrients and waste products.

The blood from the child and mother do not mix, as that can set off an immune reaction so the oxygenated blood from the mother passes the nutrients needed via a thin membrane called the syncytiotrophoblast. To do all of this, arteries and collagen have to be remodelled in the mother to allow 40% of the mother’s blood to feed the baby.

The numbers go like this “At term, maternal blood flow to the placenta is approximately 600-700 ml/minute.

It is estimated that the surface area of syncytiotrophoblasts is approximately 12m2 and the length of foetal capillaries of a fully developed placenta is approximately 320 kilometres at term”[2] which is an enormous amount of arterial remodelling to divert blood to the foetus.

http://commons.wikimedia.org/wiki/File:Gray32.png
Section through ovum imbedded in the uterine decidua. Semidiagrammatic. (After Peters.) am. Amniotic cavity. b.c. Blood-clot. b.s. Body-stalk. ect. Embryonic ectoderm. ent. Entoderm. mes. Mesoderm. m.v. Maternal vessels. tr. Trophoblast. u.e. Uterine epithelium. u.g. Uterine glands. y.s. Yolk-sac.
This image is in the public domain because its copyright has expired. This applies worldwide

Beard noticed that when the pancreas began working in a foetus around the 56th day, the pancreas began helping to breakdown hCG or Human Chorionic Gonadotropin via enzymes, hence Beard used pancreatic enzymes as a cancer cure. The 56th day I cannot confirm and hCG seems to maintain high levels throughout the pregnancy.

The placenta and trophoblasts both release Human Chorionic Gonadotropin as a hormone to maintain the corpus luteum which is like an egg yolk left behind in the ovaries, the corpus luteum then releases the hormone progesterone which signals to the uterus to thicken the endometrium or uterine wall and sustain the zygote (the egg fertilized by sperm to become the embryo) that has implanted itself into the uterine wall.

This is why progesterone is used to prevent pregnancy; higher levels of progesterone convince the body it is pregnant and stop the release of more eggs. I’ll mention that progesterone only birth-control pills have just had a study indicating depression in women using them.[3]

The placenta takes over from the corpus luteum to make progesterone around 8 to 12 weeks, interestingly “progesterone significantly upregulated the HERV-W env expression” HERV-W being the main retrovirus active in the placenta; env is short for the retroviral envelope all retroviruses have to enable cell fusion to occur.[4]

This is all related and I’ll go into details later, the Env of any of our retroviruses seem to cause problems as there is “the potential of Env proteins to induce cell fusions, which may contribute to tumour progression or even aid in metastasizing processes”.[5]

The pregnancy test uses hCG as a marker and if not pregnant can indicate reproductive or germ cell tumours so there is a strong link with too much hCG and cancer; hCG has been used for years as an unproven diet fix to reduce fat but the FDA stepped in to ban it in 2011.

John Beard[6] is still subject to controversy as you’ll find his theories attacked rather impolitely in Quackwatch because Dr Nicholas Gonzalez from the US recently did studies used similar enzyme therapies on pancreatic cancer patients. You can decide from Dr Gonzalez’s list of case studies whether the enzymes work;[67] meanwhile the orthodox  approach is to make anti-hCG vaccines.[8]

Putting aside biased opinions against natural therapies, controlling the trophoblastic actions of a tumour should be basic knowledge in cancer treatment.

http://commons.wikimedia.org/wiki/File:Gray39.png

Scheme of placental circulation.
This image is in the public domain because its copyright has expired. This applies worldwide

The enzymes that influence both trophoblast[9] and tumour functions are these days called caspases[10] and a large majority of chemotherapy options will affect the caspases[11] which in effect tell tumour cells to shut up shop or undergo apoptosis which is cell shutdown.

There is also a long list of non-toxic foods and teas that affect caspases and they are commonly used in alternative treatment of cancer, though the practitioners may not be aware of their caspase properties. What is as interesting are the similarities between embryonic implantation and tumour attachment; both involve angiogenesis or new arterial growth and to do this cells of the uterine wall and its collagen matrix have to be dismantled and removed.

Trophoblasts create angiogenesis[12] to divert blood supply and also release collagen destroying enzymes called metalloproteinases. Tumours also create angiogenesis[13] to divert blood supply and release collagen destroying enzymes called metalloproteinases.

A lot of studies use the trophoblast / tumour similarities as a basis for cancer research; much of the research happened in the last decade because before that the genomic elements like retroviruses that turn up in the placenta and in tumours were seen as junk DNA or infections and cancer research was geared towards affecting oncogenes (cancer promoting genes) and tumour suppressor genes in our DNA.

After the Genome Project it was realized that between 8 to 10% of our DNA is made of retroviruses with retrotransposons or jumping genes like Line1s, SINE1s and Alus bringing the level of jumping genes up to half of our DNA so what did all this ‘junk DNA’ do?

Those retroviruses, oncogenes and tumour suppressor genes all get affected by methylation which is like a chemical button called methyl that binds to DNA to act as a DNA on / off switch. The Genome Project discovered our DNA can be switched on and off by foods we eat and environmental factors after birth and these changes to DNA affect cell functions and tumour development so a new science developed quickly and has been called epigenetics.

Where We Are

It should be mentioned that cancer treatment theories fall into alternative and orthodox ways of thinking and both are opposing camps of thought with seemingly little dialogue between both camps. Alternative therapies generally take the approach of detoxifying the body with the belief that removing poisons and returning cells to a healthy state will stop tumour growth.

Most alternative herbs and foods prevent attachment and angiogenesis, some herbs have cytotoxic properties so I put them into a herbal chemotherapy category. Alternatives can often take the stance that all orthodox therapies are a no-go zone, when sometimes it may be appropriate to remove or poison a tumour.

The other problem is good nutrients can unwittingly feed tumour growth.

Mainstream medicine sees the tumour as something to remove with surgery, poison with chemotherapy or radiate with radiation; all of these approaches either remove the mass or try to kill the tumour. There is an orthodox monopoly on treatment and this makes it impossible to really see what other treatments may work on cancer, since most of the new orthodox drugs are so new there is little evidence that they work in practice; otherwise there would not be such a growing cancer epidemic with so many deaths.

The orthodox monopoly in itself may be a health hazard because cancer interventions in my opinion are too rushed, the conditions for cancer growth need to be managed first before surgery in particular. Cancer is often said to be a “wound that does not heal”, hence preparing the body to heal wounds is necessary before possibly spreading tumour cells via surgery.

Chemotherapy also only works while being taken; once chemotherapy stops the same conditions for tumour growth can remain. The mainstream also pays scant attention to the factors that lay the groundwork for cancer growth so they have the philosophy that all of the body needs to be carpet bombed by drugs. I think if dietary epigenetics was used to prevent cancer spreading, then tumours could be individually targeted with drugs; this would help avoid cancer patients dying from toxic organ failure due to the cancer drugs.

In fact I think all of the chemotherapy is unnecessary, because tumours can be injected with salt to kill them, this is because a tumour is like an egg and shrivels up with salt, salt works by itself,[14] but even more exciting is radiofrequency treatment which in effect cooks the tumour like an egg plus salt injection to enhance the effect.

These were the results of salt injections combined with radiofrequency treatment in a Chinese hospital treating liver cancer patients. “The complete necrosis rate of tumours was 94%, and the necrosis rate of tumours with diameter of 4.0 cm reached 100%.”[15]

So both camps may not be aware of new research that defines some very logical approaches that can go with both modes of thinking. Here I will describe fascinating observations on tumours and pregnancy so this is really a tour guide to send people to new places of thought.

“While on one hand, human placental cells are bestowed with a capacity to proliferate indefinitely and invade extensively, on the other, these cells are also replete with mechanisms to regulate these tumour-like attributes and eventually progress to a senescent apoptotic state. This is therefore, a ‘well-behaved’ tumour.”[16]

“He was the first to point to the parallels between cancer and the trophoblastic cells that envelop and nourish the embryo, characterizing cancer as “irresponsible trophoblast.”[17]

 Hypomethylation v’s Hypermethylation of DNA in Cancer

Immediately I expect to lose everyone’s attention with the word methylation but the “Hypomethylation v’s Hypermethylation of DNA in Cancer” question has had cancer researchers delving deep into these epigenetic changes for years.[18]

Again genes get affected by methylation which is like a chemical button called methyl that binds to DNA to act as a DNA on/off switch. As an example the extremes of methylation in cancer have occupied researchers for years.

“To date, a large amount of research on DNA methylation and disease has focused on cancer and tumour suppressor genes. Tumour suppressor genes are often silenced in cancer cells due to hypermethylation. In contrast, the genomes of cancer cells have been shown to be hypomethylated overall when compared to normal cells, with the exception of hypermethylation events at genes involved in cell cycle regulation, tumour cell invasion, DNA repair, and others events in which silencing propagates metastasis.”[19]

5-aza-2’-deoxycytidine or 5-aza-CdR is a standard laboratory demethylating chemical for making genes switch back on again, so it has been used in clinical trials on cancer patients in the hope tumour suppressor genes would be turned on again and inhibit tumour growth.

Though in this study using 5-aza-CdR on breast cancer cells they said it “draws attention to the potential danger in using demethylating agents in anticancer therapy because of their potential effects on activating a large number of quiescent genes including genes involved in promoting tumour metastases. Nevertheless, it puts forward the opportunity of an opposite approach, namely, inhibition of hypomethylation by hypermethylation therapy”[20]

This is why I refer to laying the groundwork so hypomethylation does not occur post surgery, because in the initial stages of wound healing[21] as in foetal implantation the cells tend to be hypomethylated or genes switched on. The safest and easiest way to address “inhibition of hypomethylation by hypermethylation therapy” is the diet.

Some simplification of DNA may help understanding of these processes.

When we are born we have an individual DNA chain that decides a fair bit of blueprinting if you want to make the plan analogy.

Say each DNA base that make our genes is an equal sign = and a chain of DNA stretched out is represented as a line of   ===================== and is very long but twisted into a helical shape in reality.

Epigenetics discovered the methyl groups are attached to the genes or not, so a gene could methylated and silenced or unmethylated and switched on. What we eat and environmental factors like chemicals, drugs and radiation can change all the genes by switching some off and on. Cancer theorists also have the ‘Stem Cell Theory of Cancer”[22] which reasons that some stem cells (the very first cell type) go wrong and can then become cancerous, since stem cells appear in wounds and cancer, it has logic.

The exciting part of stem cell research has been discovering stem cells can be obtained from either embryos but even better taken from any person, cultured and then used to create new cells in the person if say their nerve channels are broken.They also discovered the basic stem cells from a person can be grown into any type of cell needed.

Different methylation profiles change stem cells into specialised cells in our body, ones that go in different organs, cell layers etc.

Say + is a methyl group to keep a gene quiet.

And Y is an unmethylated gene and switched on.

You start with the DNA chain of the stem cell as a groundplan  ======================

With methylated and unmethylated genes to decide cell types  +YYY+Y+++YYY+YY++Y+

This is from a stem cell study “Notably, even though the iPS (Induced pluripotent stem) cells are derived from fibroblasts, their R-DMRs (reprogrammed cells) can distinguish between normal brain, liver and spleen cells and between colon cancer and normal colon cells. Thus, many DMRs (differentially methylated regions) are broadly involved in tissue differentiation, epigenetic reprogramming and cancer.”[23]

This is the answer to the hypomethylation versus hypermethylation question; you need it all balanced to allow a cell to grow into the right type of cell. If the differentially methylated regions get muddled that is a big part of how a cancer starts. If your diet is low in Folate, B12, B6, Selenium, Choline and a few other nutrients the genes can lose the methyl group. This is how diet affects cancer growth, wound healing and pregnancy. If you have too much Folate, B12, B6, Selenium, Methionine and Choline in particular when pregnant some genes may not switch on.

If your diet is low in Vitamin A the genes can also get switched off hence Retinoic acid, a form of Vitamin A gets used and works quite well on cancers, in particular leukaemia and is a natural demethylating agent that is a cell growth hormone.

Hence Vitamin A is vital for a proper pregnancy along with Folate, B12, B6, Selenium, Methionine and Choline, but too much Vitamin A switches on genes and can cause birth defects, Vitamin A is also great for wound healing, the safest topical one is using rosehip oil.

Under extreme diet changes or exposure to drugs and chemicals people lose all of the methyl groups and genes hypomethylate.

YYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY all on…

When all the genes switch on the stem cells can turn into trophoblast type cells.

These trophoblast cell types can then express the same retroviruses we see in cancer and pregnancy and create angiogenesis or new arterial formation, collagen can get damaged in the process; it seems also an underlying cause of all autoimmune diseases.

“Mouse embryonic stem cells can differentiate into all three germ layers of the embryo but are generally excluded from the trophoblast lineage. Here we show that ES cells deficient in DNA methylation can differentiate efficiently into trophoblast derivatives.”[24]

This is so important if stem cells revert to trophoblast types, from a study clearly named ‘DNA Methylation Changes in Sera of Women in Early Pregnancy Are Similar to Those in Advanced Breast Cancer Patients’ they describe what the trophoblast type cells can do.

“In normal human pregnancy, the uterus and its arterial system, including the decidua and the adjacent third of the myometrium, are invaded by cytotrophoblasts, which initiate conversion of the decidual vascular system from a high-pressure / low-flow system to a low-pressure / high-flow system that meets the needs of the foetus and placenta. The trophoblastic invasion in humans occurs between weeks 8 and 18 of pregnancy. The invasion process into the uterus shows many similarities to the invasion of malignant cells during metastasis in that both types of cells have to pass through a basal membrane.”[25]

Adequate levels of Vitamin D are also needed for cell differentiation, this means Vitamin D can help cancer or trophoblast type cells revert back to normal cell types and grow into mature normal cells. I can’t help but observe the plant analogy that Vitamin D from sunlight may guide our cells.

“These observations suggest that non-toxic agents such as retinoids (Vitamin A) and vitamin D, which have the ability to inhibit growth, induce differentiation, inhibit vimentin expression, reduce cell motility, inhibit uPA and MMP activity, and inhibit invasion and angiogenesis, are potential cancer prevention and intervention agents.”

“These findings are significant, because vitamin D and retinoids are both important chemopreventive agents and their combined use permits a significant increase in drug efficacy at lower doses, thus eliminating the risk of toxicity.”[26] Professionals need to be aware of this if patients are inside and away from sunlight in hospitals and anyone with darker skin is at even higher risk of Vitamin D deficiency. Without Vitamin D the immune system will also fail.

“Activated vitamin D regulates the differentiation of stem cells into monocyte and macrophage immune cells.”[27]

Inflammation, Cell Growth, Retroviruses and Cell to Cell Fusion

“During tissue injury associated with wounding, cell proliferation is enhanced while the tissue regenerates; proliferation and inflammation subside after the assaulting agent is removed or the repair completed. In contrast, proliferating cells that sustain DNA damage and / or mutagenic assault (for example, initiated cells) continue to proliferate in microenvironments rich in inflammatory cells and growth / survival factors that support their growth. In a sense, tumours act as wounds that fail to heal.”[28]

Wound repair is a complex process involving blood factors, immune white blood cells like neutrophils appear first and send out inflammatory cytokines or signalling molecules, while white blood cells like macrophages react to the inflammatory signals and appear on the scene to remove dead cells and at the same time release growth factors.

The immune system generally deals with our own garbage removal more than infections, hence buying shopping trolleys worth of soft drinks or eating foods that clog up the system can predispose the body to immune failure because it needs to deal with the garbage and if any pathogens like bacteria, fungus and parasites get into the system they live off the garbage while the immune system then has to deal with the overload.

This explains the basic philosophy of alternative approaches which concentrate on toxin removal as part of cancer therapy. Our own immune system is also the source of most inflammation so of course getting the rubbish out of the way to calm down our white blood cells is going to avoid repeated release of inflammatory cytokines and growth factors from white blood cells.

When any cell growth happens retroviruses are involved in the process this is why reverse transcriptase the particular enzyme retroviruses use to replicate appears with cell growth.

“Expression of Reverse Transcriptase-coding genes is generally repressed in non-pathological, terminally differentiated cells, but is active in early embryos, germ cells, embryo and tumour tissues, all of which have a high proliferative potential.”[29]

When they say “terminally differentiated cells” they mean cells that have matured and have their identities worked out. In “early embryos, germ cells, embryo and tumour tissues” though there is retroviral activity going on and exactly the sort of lowered methylation that makes these cells potentially turn towards the trophoblast phenotype.

They also experimented with antiretroviral Nevirapine on these cells and stopped them growing as well as rewriting gene expression so stopping retroviruses will change your genes.

“Reverse Transcriptase inhibition induced an extensive reprogramming of the gene expression profile both in cultured cell lines and in preimplantation embryos.”

Recent studies are showing embryonic stem cells have retroviral activity so may be part of the gene switching mechanisms.[3031] Trophoblast cells in pregnancy have enormous retroviral activity in the form of HERV-W or syncytin which also appears in breast and reproductive tumours along with retroviruses like HERV-K which seems to appear in most tumours.

Syncytin is named after syncytium; this is where single cells multinucleate or cluster together to make our organs and cell layers. HERV-W or syncytin is creating cell fusion so gathering cells together. There are 2 types of syncytin retrovirus: one seems to gather cells together while the other affects the remodelling.

“Overexpression of different human endogenous retroviruses (HERVs) has been shown in stem cell tumours, melanomas, human embryonic stem cells as well as in the placenta. The envelope proteins of HERV-W (also known as syncytin 1) and HERV-FRD (syncytin 2) were shown to be involved in cell fusion allowing to generate the syncytiotrophoblast in the human placenta. One of them, syncytin 2, was shown to be immunosuppressive, the immunosuppressive activity was associated with its immunosuppressive (isu) domain. Here we report the expression of another HERV, HERV-K…”[32]

Both HERV-FRD (syncytin 2) and HERV-K are immunosuppressive because the immune system sees them as necessary. If HERV-W or HERV-FRD are not expressing this is a big risk factor for preeclampsia, because without these retroviruses working the blood supply and arterial remodelling does not happen as well and this reduces nutrients to the foetus.[33]

So the retroviruses in pregnancy are vital for cell fusions to occur, but in a tumour this needs to be stopped. Cell fusions by retroviruses apart from pregnancy also create multinucleate cells where single cells in our body are fused together.

This is so new the research has to speak for itself.

There are “cell-cell fusions in connection with human endogenous retroviruses (HERV ) in cancer. Examples of multinucleated cells presented include placental syncytiotrophoblasts, muscle myotubes, bone osteoclasts involved in normal human development and cell-cell fusions detected in tumours. Examples of multinucleated cells in various cancers include germ cell tumours, glioblastoma, melanoma, lung, breast, ovarian and endometrial carcinomas.”[34]

“deregulation of physiological fusogenic proteins in tumour cells may promote cell fusion. For example, syncytin, the Env protein of HERV-W human endogenous retroviruses and putative mediator of trophoblast fusion, was also found to mediate fusion between breast cancer cells and endothelial cells. CD44, a cell surface receptor known to be involved in cell fusion during osteoclastogenesis, is frequently over-expressed in cancer cells and has been linked to poor prognosis and cancer stem cell phenotypes.”

“chronic inflammation has recently been shown to dramatically increase the frequency of cell fusion between hematopoietic cells (blood cells) and various somatic cells such as cardiomyocytes, skeletal muscle, hepatocytes, and Purkinje cells during tissue repair and regeneration. Similar as-yet-unknown mechanisms underlying this observation may also stimulate the fusion between bone marrow-derived cells (BMDC) and tumour cells, because inflammation is often associated with the tumour microenvironment.”

“and cell fusion may be the by-product of “cell-eat-cell” processes, such as phagocytosis of tumour cells by macrophages or entosis”.[35]

Though the immune system is a tricky problem in cancer.

The trophoblast cells in pregnancy express what I call the “this is a baby leave it alone” marker or self antigen HLA-G.[36] Human leukocyte antigens on cell surfaces or HLAs are involved in letting the immune system know this is a self-cell and not foreign to the body. Any mutations or damage to HLAs are a big part of autoimmune disease causation as the immune system can get confused and attack our own cells. During pregnancy the immune system sees HLA-G and leaves trophoblast cells alone to do their work.

“Isoforms of HLA-G saturate the maternal-foetal interface and circulate in mothers throughout pregnancy. Uteroplacental immune privilege for the foetus and its associated tissues is believed to result when immune cells encounter HLA-G.”[37]

The problem with tumours is they also express HLA-G antigens just like trophoblast cells do.

“Convincing clinical evidence indicates that the limited success of T-cell-based immunotherapy of malignant diseases is caused, at least in part, by the ability of malignant cells to escape from immune recognition and destruction. Among the multiple escape mechanisms identified, a major role is played by changes in the expression and/or function of HLA antigens expressed by tumour cells, because they may markedly affect tumour cell-host’s immune system interactions.”[38]

Boosting the immune system in fact can have the complete opposite effect, it can spread the tumour. This is important to know for alternative practitioners who may use things like Echinacea and Astragalus to boost T-cells.

“As the immune surveillance is not sufficient anymore, tumour-associated macrophages contribute to tumour progression. It is notable that tumour-associated macrophages promote the proliferation of tumour cells directly by secreting growth factors. They also participate in tumour progression by acting on endothelial cells and thus promoting the neovascularization of the tumour. Tumour-associated macrophages are indeed key protagonists during angiogenesis and promote each step of the angiogenesis cascade.”[39]

Cell fusions and retroviruses may actually contribute to this process, if tumours are releasing retroviral envelopes then it is quite likely the tumours could be binding macrophages to their edges and using macrophages to burn new arterial channels[40] as this seems to be the case during pregnancy.[41]

“Decidual artery remodelling is essential for a healthy pregnancy.”

“In early stages of remodelling, vascular smooth muscle cells showed dramatic disruption and disorganization before vEVT (endovascular trophoblasts) presence. Leukocytes (identified as uterine natural killer cells and macrophages) were apparent infiltrating vascular smooth muscle cells layers and were matrix metalloproteinase-7 and -9 immunopositive.”[42]

“matrix metalloproteinase-7 and -9” are collagen destroying enzymes that tumours also produce. The cell fusions that occur may mean the tumours bind to our own macrophages. The reason for normal macrophage cell fusion is described here; it means that when infections from viruses, bacteria, fungi, parasites, chemical or radiation exposure or literally anything that damages cells so the dead cells or pathogens need removing may be accompanied by retroviral activity to fuse macrophages into bigger multinucleate cells to do the job.

“Cells of the mammalian monocyte-macrophage lineage form two major types of multinucleated cells: macrophage giant cells in many tissues and osteoclasts in bone. In each case, the physiological roles of these cells involves endocytosis and resorption of relatively large objects, including cell corpses, invading pathogens, foreign bodies, and chunks of mineralized bone. The increased size achieved through cell fusion presumably affords the extra membrane surface area and endosome / lysosome volume to achieve these tasks. In addition, it is conceivable that a larger cell can more safely distance the nuclei and cell body from the noxious degradative cocktails used to dispose of objects within the engulfment apparatus.”[43]

A French study asked this very question?

“Macrophages recognize each other as self  in order to fuse but some essential questions remain: do macrophages fuse with somatic cells to repair tissues and organs? Do macrophages fuse with tumour cells to trigger metastasis?”[44]

Going Back A Century

Cancer is now an epidemic disease, rates nearing one in two. Living longer is a factor but things have changed: we have high-tech medical interventions, vaccines, new drugs, hormone drugs, new chemicals, pesticides, trans fats and GMOs in food, new radiation sources from our electronics, less sunlight, less exercise.

Wealthier people are eating more meat, more sugar, alcohol is massively consumed as always; by the time someone turns up to the hospital with a tumour it’s impossible to know what caused it. In poorer countries they suffer cancers from reckless industrial pollution while going to work can be a chemical hazard. Since the financial collapse, the water and sewage infrastructure of many countries went backwards so cancers from pathogens are also in the mix. The attitude to cancer in itself lends to voodoo, if you tell people they will die they will die.

I’ve been amazed at personal stories told where a patient had surgery and chemotherapy and been dead in less than 2 months and I’ve witnessed others. Our obsession with expensive cancer interventions may be a terrible waste of tax payers’ money while emergency rooms can’t even be funded.

My dad for instance has had surface tumours for 30 years, he has avoided doctors and kept it simple and cheap by making his own salt bags or pads to apply heated salt while sleeping overnight. There are clear studies saying salt injected into tumours works so my dad’s intuitive approach seems to work too.

So in my opinion people with cancer have time; if you can walk perhaps it is healthier to take a holiday first, change your diet and get a bit of fresh air and then come prepared for treatment. Most of our cancers are life-style related, so taking your mind and body somewhere else is a possible road to a cure.

To sum up my thoughts on treatment, anti-inflammatory foods work. Red meats and dairy are actually inflammatory due to a Sialic acid they contain which is foreign to humans, we are mildly allergic to all mammals but not fish, birds or reptiles so any red meats can cause long term inflammation. The Sialic acid from dairy foods can also feed tumours and I suspect the same with eggs and they are both baby foods so avoid them in excess. Phytates or IP6 from legumes, seeds, grains and bran may chelate minerals but inhibits cancer. (I now think unsweetened dairy products like cheese in moderation may be useful to prevent depression due to the trytophan content and prevent IDO enzymes from breaking down tryptophan, this may allow macrophages to keep functioning, refer to the Macrophage Polarization article).

Iron is inflammatory and feeds cancer as well as infections. The nutrients needed for methylation can also affect Iron absorption, to absorb Iron so it is used by the blood and does not become inflammatory we need Folate, B12, B6, Copper and Vitamin C in our diet. Folate, B12, B6, Selenium, methionine, Choline along with Vitamin A and D are needed to balance methylation.

Genetically anyone with mutations to Folate processing genes MTHFR1 and C677T need to be aware this can cause long term hypomethylation and dispose them to trophoblast type cells.

This is where genetic testing can prevent cancers; they can work out methylation levels in people before it becomes a problem. Folate supplementation can encourage cancer growth though hence the need to know if you have problems with those genes. Too much Iron also can affect Selenium levels and the thyroid needs Selenium.

Thyroid hormones encourage both trophoblast and tumour invasion, and a lack of Selenium can cause hyperthyroid and wasting or cachexia. While Iodine without Selenium makes more thyroid hormones, hence Iodine deficiency is also a risk for pregnancy loss because the trophoblasts need thyroid hormones to work.

Since tumours dissolve collagen Lysine tablets or foods with Vitamin C to remake collagen are part of the anti-angiogenesis formula. Proanthocyanidins from berries, Resveratol from grapes, Carotenoids from all the yellow / orange/red veggies have effect.

Green tea, Turmeric and Oleuropein from olives are potent anticancer compounds and anti-inflammatory. Green tea even works better at preventing tumour attachment with Vitamin A.

My favourite anticancer compound is Bromelain, I use it to fix psoriasis. It is one of the best anti-inflammatory chemicals around, it breaks up fibrin and can be used as a blood thinner though any signs of bleeding stop using it. If Bromelain can be used it will prevent tumour attachment to CD44 molecules and also inhibits the inflammatory cytokines.

CD44 is also used for trophoblast attachment so don’t take Bromelain if pregnant.

I want to see the study on what Bromelain does to retroviruses like HERV-W and HERV-K, waiting for that one.

Every one of the food chemicals above from Selenium to Bromelain also affect Caspase enzymes so tell tumours to stop.

These ideas can be researched and used by anyone including people using chemotherapy.

Bromelain for instance actually potentiate drugs.

Doctors using chemotherapy should be using detection scans to target chemotherapy directly to tumours and not all of the body, while being aware they can use all of the above.

I recommend reading Nutrition and cancer: A review of the evidence for an anti-cancer diet by Michael S Donaldson[45] and the book Natural compounds in cancer therapy by John Boik [46] and Nutrition and Cancer State of the Art by Sandra Goodman PhD[47]as a start for further research; they are available online.

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A good lay person’s guide to the retroviral involvement during pregnancy was written in 2012.

I found this article by Carl Zimmer later.

Mammals Made By Viruses

https://www.discovermagazine.com/planet-earth/mammals-made-by-viruses

Da Vinci Fetus