A 3rd Opinion - What does this blood test mean?

[Rinse & rePeat]

“A progesterone deficiency has often been associated with increased susceptibility to cancer, and progesterone has been used to treat some types of cancer.” -Ray Peat

 

[Rinse & rePeat]

Rinse & rePeat:

“Do you think 40 to 50 grams of protein is too much protein having cancer? Is gelatin, nonfat milk and potato good sources of protein to eat with cancer?”

RAY PEAT:
“If the protein is limited to those, and your other calories are from carbohydrates (not fats), that amound should be safe.”

 

[Rinse & rePeat]

“The ratio of saturated fatty acids to polyunsaturated fatty acids is decreased in cancer. Omega-3 fats promote metastasis.” -Ray Peat

 

[Rinse & rePeat]

“When cancers are metastasizing, their phospholipids contain less stearic acid than the less malignant tumors (Bougnoux, et al., 1992), patients with advanced cancer had less stearic acid in their red blood cells (Persad, et al., 1990), and adding stearic acid to their food delayed the development of cancer in mice (Bennett, 1984). The degree of saturation of the body's fatty acids corresponds to resistance to several types of cancer that have been studied (Hawley and Gordon, 1976; Singh, et al., 1995).” -Ray Peat

 

[Rinse & rePeat]

“Rawn points out in his article “The silent risks of blood transfusion,” “Clinical research has identified blood transfusion as an independent risk factor for immediate and long-term adverse outcomes, including an increased risk of death, myocardial infarction, stroke, renal failure, infection and malignancy.”

Complications of Blood Transfusion

www.medstarhealth.org

 

[Rinse & rePeat]

I had no idea!

“The median length of survival was 95.0 (+/- 2.5) months. Twenty-four percent of patients died within 1 year after the transfusion, 30 percent within 2 years, 40 percent within 5 years, and 52 percent within 10 years. The relative risk of death within 10 years increased by 4.1 percent per unit of red cells (p < 0.0001), by 1.2 percent per unit of platelets (p = 0.0003), and by 7.3 percent per unit of fresh-frozen plasma (p = 0.0018) received in 1981, after adjustment for the effects on mortality of age, gender, and number of days of hospitalization in 1981.“

Long-term survival after blood transfusion - PubMed

Receipt of a blood transfusion can be used as a descriptive epidemiologic index of morbidity in the general population, as it is independently predictive of mortality, adding to the predictive value of age, gender, and previous hospitalization. There is a dose-response relationship between the...

pubmed.ncbi.nlm.nih.gov

 

[Rinse & rePeat]

“Transfused blood also has a suppressive effect on the immune system, which increases the risk of infections, including pneumonia and sepsis, he says. Frank also cites a study showing a 42 percent increased risk of cancer recurrence in patients having cancer surgery who received transfusions.”

Blood Transfusions Still Overused and May Do More Harm Than Good in Some Patients - 04/24/2012

Citing the lack of clear guidelines for ordering blood transfusions during surgery, Johns Hopkins researchers say a new study confirms there is still wide variation in the use of transfusions and frequent use of transfused blood in patients who don’t need it.

www.hopkinsmedicine.org

 

[mostlylurking]

My husband had this blood test taken under stressful conditions from a spinal compression fracture, that originally happened from a golf swing. He thought it was just a pulled muscle and went about his business in pain, hoping for it to heal. When it didn't after two months he went to a highly touted back surgeon, who has 5 clinics, and he did 2 x-rays and said his back looked healthy and that there was no cancer. Five weeks later my husband drives himself to the hospital in pain to find that he had two back fractures. A blood test was sent out to Mayo Clinic and was labeled "Smouldering Myeloma" by somebody at the clinic or hospital, I don't know, but the Oncologist at the hospital says he has Myeloma. There has been so many conflicting opinions and dropping the ball with his health, with every twist and turn, this last couple of months, and so much pressure from doctors wanting his business, suggesting a bone marrow transplant, stem cell and gene therapies, before ever meeting him or doing a biopsy. He had a blood test and urine analysis done two weeks earlier at Urgent Care owned by the same hospital with elevated proteins showing up in his urine, which they diagnosed as kidney stones, which was confirmed to be true at the hospital. Can any person on this forum tell anything for certain from his blood test without further testing and a third opinion?

I did a few searches for "multiple myeloma and thiamine". Found a few things of interest I'd like to share:
Type B Lactic Acidosis Associated With Multiple Myeloma Type B Lactic Acidosis Associated With Multiple Myeloma

also this: Thiamine deficiency as a cause of lactic acidosis | Deranged Physiology

Lactic acidosis (aka Warburg's Cancer Metabolism) is caused by thiamine deficiency/functional blockage. Thiamine supplementation lowers lactic acid. Carbon dioxide lowers lactic acid (think acetazolomide); thiamine supplementation increases carbon dioxide very well (probably better than acetazolomide) because it optimizes oxidative metabolism which has carbon dioxide as the end product instead of lactic acid.

also this: Targeting IL-17A in multiple myeloma: a potential novel therapeutic approach in myeloma - PubMed
"We have previously demonstrated that interleukin-17A (IL-17) producing T helper 17 cells are significantly elevated in blood and bone marrow (BM) in multiple myeloma (MM) and IL-17A promotes MM cell growth via the expression of IL-17 receptor."

consider the above info with this one: IL-17, Inflammatory Diseases and the One Vitamin That May Help
"Thiamine Can Limit TH-17 Proinflammatory Response, Potentially Inhibiting IL-17
The following new study from March 2021 below shows for the first time that Thiamine, also known as vitamin B1, is a potent inhibitor (four-fold inhibition) of IL-17 and, of course, the other inflammatory cytokines that are also released right along with IL-17!"
(link provided) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7960760/

If you search for "thiamine and cancer" you will find articles warning about thiamine causing cancer and also articles that say high dose thiamine is anticancer and also articles that say the action of thiamine on cancer being dose dependent and that low dose thiamine gives cancer what it needs to grow but high dose thiamine is anti-carcinogenic.

High Dose Vitamin B1 Reduces Proliferation in Cancer Cell Lines Analogous to Dichloroacetate

The dichotomous effect of thiamine supplementation on cancer cell growth is characterized by growth stimulation at low doses and growth suppression at high doses. Unfortunately, how thiamine reduces cancer cell proliferation is currently unknown. Recent ...

www.ncbi.nlm.nih.gov

"The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting. Clinical and experimental data demonstrate increased thiamine utilization of human tumors and its interference with experimental chemotherapy. Analysis of RNA ribose indicates that glucose carbons contribute to over 90% of ribose synthesis in cultured cervix und pancreatic carcinoma cells and that ribose is synthesized primarily through the thiamine dependent TK pathway (> 70%). Antithiamine compounds significantly inhibit nucleic acid synthesis and tumor cell proliferation in vitro and in vivo in several tumor models. The medical literature reveals little information regarding the role of the thiamine dependent TK reaction in tumor cell ribose production which is a central process in de novo nucleic acid synthesis and the salvage pathways for purines. Consequently, current thiamine administration protocols oversupply thiamine by 200% to 20,000% of the recommended dietary allowance, because it is considered harmless and needed by cancer patients. The thiamine dependent TK pathway is the central avenue which supplies ribose phosphate for nucleic acids in tumors and excessive thiamine supplementation maybe responsible for failed therapeutic attempts to terminate cancer cell proliferation. Limited administration of thiamine and concomitant treatment with transketolase inhibitors is a more rational approach to treat cancer."

The role of thiamine in cancer: possible genetic and cellular signaling mechanisms - PubMed

The relationship between supplemental vitamins and various types of cancer has been the focus of recent investigation, and supplemental vitamins have been reported to modulate cancer rates. A significant association has been demonstrated between cancer and low levels of thiamine in the serum...

pubmed.ncbi.nlm.nih.gov

"The role of thiamine in cancer is controversial. However, thiamine deficiency may occur in patients with cancer and cause serious disorders, including Wernicke's encephalopathy, that require parenteral thiamine supplementation. A very high dose of thiamine produces a growth-inhibitory effect in cancer. Therefore, further investigations of thiamine in cancer are needed to clarify this relationship."

finally, this one:

Linking vitamin B1 with cancer cell metabolism

The resurgence of interest in cancer metabolism has linked alterations in the regulation and exploitation of metabolic pathways with an anabolic phenotype that increases biomass production for the replication of new daughter cells. To support the increase ...

www.ncbi.nlm.nih.gov

"In light of our knowledge regarding alterations of thiamine homeostasis in cancer, the impact of thiamine supplementation on cancer growth has received minimal research attention. In 2001, Comin-Anduix et al. evaluated the effect of increasing thiamine supplementation in multiples of the RDI on an Ehrlich ascites tumor-mouse model [58]. Their findings indicated a statistically significant stimulatory effect of thiamine supplementation on tumor growth compared to non-supplemented controls. Moderate doses of 12.5 to 37.5 times the RDI had the greatest stimulatory effect, peaking at approximately 250% greater tumor cell proliferation with 25 times the RDI. Interestingly, at values above 75 times the RDI, no change was found in tumor cell proliferation, and a slight decrease was found at 2,500 times the RDI. This observation suggests that there is a specific range in which thiamine supports proliferation."

 

[Rinse & rePeat]

I did a few searches for "multiple myeloma and thiamine". Found a few things of interest I'd like to share:
Type B Lactic Acidosis Associated With Multiple Myeloma Type B Lactic Acidosis Associated With Multiple Myeloma

also this: Thiamine deficiency as a cause of lactic acidosis | Deranged Physiology

Lactic acidosis (aka Warburg's Cancer Metabolism) is caused by thiamine deficiency/functional blockage. Thiamine supplementation lowers lactic acid. Carbon dioxide lowers lactic acid (think acetazolomide); thiamine supplementation increases carbon dioxide very well (probably better than acetazolomide) because it optimizes oxidative metabolism which has carbon dioxide as the end product instead of lactic acid.

also this: Targeting IL-17A in multiple myeloma: a potential novel therapeutic approach in myeloma - PubMed
"We have previously demonstrated that interleukin-17A (IL-17) producing T helper 17 cells are significantly elevated in blood and bone marrow (BM) in multiple myeloma (MM) and IL-17A promotes MM cell growth via the expression of IL-17 receptor."

consider the above info with this one: IL-17, Inflammatory Diseases and the One Vitamin That May Help
"Thiamine Can Limit TH-17 Proinflammatory Response, Potentially Inhibiting IL-17
The following new study from March 2021 below shows for the first time that Thiamine, also known as vitamin B1, is a potent inhibitor (four-fold inhibition) of IL-17 and, of course, the other inflammatory cytokines that are also released right along with IL-17!"
(link provided) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7960760/

If you search for "thiamine and cancer" you will find articles warning about thiamine causing cancer and also articles that say high dose thiamine is anticancer and also articles that say the action of thiamine on cancer being dose dependent and that low dose thiamine gives cancer what it needs to grow but high dose cancer is anti-carcinogenic.

High Dose Vitamin B1 Reduces Proliferation in Cancer Cell Lines Analogous to Dichloroacetate

The dichotomous effect of thiamine supplementation on cancer cell growth is characterized by growth stimulation at low doses and growth suppression at high doses. Unfortunately, how thiamine reduces cancer cell proliferation is currently unknown. Recent ...

www.ncbi.nlm.nih.gov

"The objectives of this review are to (a) explain the mechanism by which thiamine (vitamin B1) promotes nucleic acid ribose synthesis and tumor cell proliferation via the nonoxidative transketolase (TK) pathway; (b) estimate the thiamine intake of cancer patients and (c) provide background information and to develop guidelines for alternative treatments with antithiamine transketolase inhibitors in the clinical setting. Clinical and experimental data demonstrate increased thiamine utilization of human tumors and its interference with experimental chemotherapy. Analysis of RNA ribose indicates that glucose carbons contribute to over 90% of ribose synthesis in cultured cervix und pancreatic carcinoma cells and that ribose is synthesized primarily through the thiamine dependent TK pathway (> 70%). Antithiamine compounds significantly inhibit nucleic acid synthesis and tumor cell proliferation in vitro and in vivo in several tumor models. The medical literature reveals little information regarding the role of the thiamine dependent TK reaction in tumor cell ribose production which is a central process in de novo nucleic acid synthesis and the salvage pathways for purines. Consequently, current thiamine administration protocols oversupply thiamine by 200% to 20,000% of the recommended dietary allowance, because it is considered harmless and needed by cancer patients. The thiamine dependent TK pathway is the central avenue which supplies ribose phosphate for nucleic acids in tumors and excessive thiamine supplementation maybe responsible for failed therapeutic attempts to terminate cancer cell proliferation. Limited administration of thiamine and concomitant treatment with transketolase inhibitors is a more rational approach to treat cancer."

The role of thiamine in cancer: possible genetic and cellular signaling mechanisms - PubMed

The relationship between supplemental vitamins and various types of cancer has been the focus of recent investigation, and supplemental vitamins have been reported to modulate cancer rates. A significant association has been demonstrated between cancer and low levels of thiamine in the serum...

pubmed.ncbi.nlm.nih.gov

"The role of thiamine in cancer is controversial. However, thiamine deficiency may occur in patients with cancer and cause serious disorders, including Wernicke's encephalopathy, that require parenteral thiamine supplementation. A very high dose of thiamine produces a growth-inhibitory effect in cancer. Therefore, further investigations of thiamine in cancer are needed to clarify this relationship."

finally, this one:

Linking vitamin B1 with cancer cell metabolism

The resurgence of interest in cancer metabolism has linked alterations in the regulation and exploitation of metabolic pathways with an anabolic phenotype that increases biomass production for the replication of new daughter cells. To support the increase ...

www.ncbi.nlm.nih.gov

"In light of our knowledge regarding alterations of thiamine homeostasis in cancer, the impact of thiamine supplementation on cancer growth has received minimal research attention. In 2001, Comin-Anduix et al. evaluated the effect of increasing thiamine supplementation in multiples of the RDI on an Ehrlich ascites tumor-mouse model [58]. Their findings indicated a statistically significant stimulatory effect of thiamine supplementation on tumor growth compared to non-supplemented controls. Moderate doses of 12.5 to 37.5 times the RDI had the greatest stimulatory effect, peaking at approximately 250% greater tumor cell proliferation with 25 times the RDI. Interestingly, at values above 75 times the RDI, no change was found in tumor cell proliferation, and a slight decrease was found at 2,500 times the RDI. This observation suggests that there is a specific range in which thiamine supports proliferation."

Thanks for posting this. It is so contradictory that I would be leery to go one way or the other. I am gonna ask Ray Peat what he thinks about. This is certainly something to consider!

 

[mostlylurking]

Thanks for posting this. It is so contradictory that I would be leery to go one way or the other. I am gonna ask Ray Peat what he thinks about. This is certainly something to consider!

Please post his response; I'm very interested in what he'll have to say. Please give him the links I found. Thanks!

 

[Rinse & rePeat]

Please post his response; I'm very interested in what he'll have to say. Please give him the links I found. Thanks!

I will!

 

[Rinse & rePeat]

Please post his response; I'm very interested in what he'll have to say. Please give him the links I found. Thanks!

Rinse & rePeat:
“Good morning Dr. Peat! I am reading some controversial studies, this morning, about thiamine and cancer. On one hand they say they are finding cancer patients to be low in B1, but on the other hand they say a very high dose of it kills cancer. Do you know anything about this?”

RAY PEAT:
“Very big doses inhibit carbonic anhydrase, and the resulting increase of CO2 helps

 

[mostlylurking]

Rinse & rePeat:
“Good morning Dr. Peat! I am reading some controversial studies, this morning, about thiamine and cancer. On one hand they say they are finding cancer patients to be low in B1, but on the other hand they say a very high dose of it kills cancer. Do you know anything about this?”

RAY PEAT:
“Very big doses inhibit carbonic anhydrase, and the resulting increase of CO2 helps

I did a quick search for "carbonic anhydrase and high dose thiamine". Here are some of the results:

Thiamine Is A Carbonic Anhydrase Inhibitor As Effective As Acetazolamide

After findings the studies on synergism between thiamine and acetazolamide, and their combined use in a number of diseases I became intrigued. Then the wild thought just came out of nowhere - what if thiamine was also a carbonic anhydrase inhibitor but at different isoenzymes and with different...

raypeatforum.com

also this one seems on topic: Deficiency Of Vitamin B1 (thiamine) Can Cause The Cancer Metabolism

New Developments in High-Dose Thiamine: The Legacy of Antonio Costantini - Hormones Matter

Antonio Costantini pioneered the use of high-dose thiamine for treating a range of neurological and inflammatory conditions.

www.hormonesmatter.com

"The inhibition of carbonic anhydrase isoenzymes by high-dose thiamine and the resulting production of carbon dioxide could lead to reductions in fatigue and other symptomatic improvement through one or more of four potential pathways: (a) by reducing intracranial hypertension and/or ventral brainstem compression; (b) by increasing blood flow to the brain; (c) by facilitating aerobic cellular respiration and lactate clearance through the Bohr effect; or (d) by dampening the pro-inflammatory Th-17 pathway, again through the Bohr effect, potentially mediated by reductions in hypoxia-inducible factor 1."

Although Ray has not written much about thiamine, he does mention it occasionally. Here's a collection of quotes: Ray Peat On Vitamin B1 - Thiamine

 

[Rinse & rePeat]

I did a quick search for "carbonic anhydrase and high dose thiamine". Here are some of the results:

Thiamine Is A Carbonic Anhydrase Inhibitor As Effective As Acetazolamide

After findings the studies on synergism between thiamine and acetazolamide, and their combined use in a number of diseases I became intrigued. Then the wild thought just came out of nowhere - what if thiamine was also a carbonic anhydrase inhibitor but at different isoenzymes and with different...

raypeatforum.com

also this one seems on topic: Deficiency Of Vitamin B1 (thiamine) Can Cause The Cancer Metabolism

New Developments in High-Dose Thiamine: The Legacy of Antonio Costantini - Hormones Matter

Antonio Costantini pioneered the use of high-dose thiamine for treating a range of neurological and inflammatory conditions.

www.hormonesmatter.com

"The inhibition of carbonic anhydrase isoenzymes by high-dose thiamine and the resulting production of carbon dioxide could lead to reductions in fatigue and other symptomatic improvement through one or more of four potential pathways: (a) by reducing intracranial hypertension and/or ventral brainstem compression; (b) by increasing blood flow to the brain; (c) by facilitating aerobic cellular respiration and lactate clearance through the Bohr effect; or (d) by dampening the pro-inflammatory Th-17 pathway, again through the Bohr effect, potentially mediated by reductions in hypoxia-inducible factor 1."

Although Ray has not written much about thiamine, he does mention it occasionally. Here's a collection of quotes: Ray Peat On Vitamin B1 - Thiamine

Thanks! I am going to pass some of this on to Philomath :)

 

[Rinse & rePeat]

Rinse & rePeat:
“Good morning Dr. Peat! I am reading some controversial studies, this morning, about thiamine and cancer. On one hand they say they are finding cancer patients to be low in B1, but on the other hand they say a very high dose of it kills cancer. Do you know anything about this?”

RAY PEAT:
“Very big doses inhibit carbonic anhydrase, and the resulting increase of CO2 helps

Rinse & Repeat:
“Is that high dose of thiamine effect for killing every cancer, like solid tumors as well as blood cancers and lupus?”

RAY PEAT:
“Other C.A. inhibitors such as acetazolamde are more effective.”

 

[mostlylurking]

Rinse & Repeat:
“Is that high dose of thiamine effect for killing every cancer, like solid tumors as well as blood cancers and lupus?”

RAY PEAT:
“Other C.A. inhibitors such as acetazolamde are more effective.”

more info: Carbonic Anhydrase Is A Key Driver Of Aging; Inhibiting It Is Beneficial

and this one: Thiamine Is A Carbonic Anhydrase Inhibitor As Effective As Acetazolamide

 

[Rinse & rePeat]

Mauritio:
Q: Hello Mr Peat,
What do you think about ultrasound for breaking up tumor tissue, as in the link below ?

Could this be a much safer alternative for chemotherapy?

Thanks.

Tumors partially destroyed with sound don't come back

Noninvasive sound technology breaks down liver tumors in rats, kills cancer cells and spurs the immune system to prevent further spread -- an advance that could lead to improved cancer outcomes in humans.

www.sciencedaily.com

RAY PEAT:
A: One advantage is that any damage to good tissue is localized, while chemotherapy damages the brain and other organs.

 

[Rinse & rePeat]

“Decisions about pain control usually disregard the effects of the drugs on tumor growth and general vitality--for example, the opiates stimulate histamine release, which increases inflammation and tumor growth.” -Ray Peat

Cancer: Disorder and Energy

New descriptive sentence from the article here

raypeat.com

 

[Rinse & rePeat]

“Once it is accepted that cancer is a systemic disease, and that a tumor, or the place in the body where a tumor has been removed, is something more than a collection of defective cells, very different therapeutic approaches can be considered. Looking at the events in a failing heart, we can see that the potential repair cells recruited by the stressed heart are diverted by the conditions that they encounter there, and either die or become connective tissue cells, secreting collagen, rather than becoming new muscle cells.

Something that everyone knows about tumors is that they are harder than the normal tissues in which they appear--they can be identified as lumps. Like the failing heart, they become harder than normal, and like the failing heart, the hardening can proceed to calcification. There has been general recognition that inflammation has a role in both heart disease and cancer, but the fact that chronic inflammation leads to fibrosis, and that fibrosis often leads to calcification, is still usually considered not to be relevant to understanding and treating cancer. The tissue hardness that allows oncologists to diagnose cancer (Huang and Ingber, 2005) is ignored when choosing treatments, which isn't surprising, since treatments that destroy cancer cells increase the production of collagen.

Aspirin is commonly recommended for preventing heart attacks, because it helps to prevent abnormal blood clots, but it has other effects that are beneficial in heart disease, for example reducing the generalized fibrosis of the heart that develops after a heart attack (Kalkman, et al., 1995; Wu, et al., 2012). It also protects against fibrosis in other organs, by a variety of mechanisms, and this effect on the extracellular matrix seems to be one of ways in which it protects against cancer. DCA, dichloroacetate, the drug that has been in the news in recent years because it can stop cancer growth, by restoring the oxidation of glucose and stopping the aerobic production of lactic acid, has been found to reduce the fibrosis of a failing heart, by the same mechanism, restoring glucose oxidation. In general, substances that increase collagen production are promoters of cancer and contribute to the progression of heart failure, and other degenerative changes.

The incidence of cancer increases exponentially with age, but when random mutations are seen as the cause of cancer, aging as an essential cause of cancer is disregarded. The total collagen content of the body increases with aging, and the stiffness of that collagen also increases. The total collagen content in cancer patients is higher than in people without cancer (Zimin, et al., 2010). This suggests that the processes in the body that produce aging are acting more intensely in those who develop cancer. As the collagen accumulates in the extracellular matrix, the whole body becomes more favorable for the appearance of cancer.

Plastic surgeons have promoted the idea of injecting collagen into tissues with the argument that they are "replacing collagen lost with aging," but in fact collagen accumulates with aging. It is the greater compactness and stiffness of collagen in old skin that produces noticeable changes such as wrinkling. The difference between calf skin leather, used for soft gloves and purses, and cow hide, used for shoe soles and boots, illustrates the changes that occur with aging. Supermarkets used to categorize chickens as fryers and stewers, or stewing hens. The difference was the age and toughness, very young chickens could be cooked quickly, old laying hens had accumulated more collagen, and especially the cross-linked hardened collagen, and required long cooking to reduce the toughness. Old beef animals are usually sold as cheaper stew meat or hamburger, because the age-hardened collagen can make a steak too rubbery to chew if it's quickly cooked.

In a healthy young organism, tissue injuries are repaired by processes reminiscent of Metchnikov's experiment in which he put a thorn into a jelly fish, and found that wandering cells, phagocytes, converged on the foreign object, surrounding it. If they couldn't eat it, they caused it to be expelled. The importance of that experiment was that it showed that injured tissues emit signals that attract certain types of cell. The process of removing damaged tissues by phagocytosis guides the formation of new tissue, starting with the secretion of collagen, which guides the maturation of the new cells.

Around the middle of the last century, Hans Selye experimented with the antiseptic implantation of a short piece of a narrow glass tube under the skin of rats. The irritation from the glass object caused a collagenous capsule to be formed around it, in the well known "foreign body reaction." He found that a filament of tissue formed in the center of the tube, connecting the two ends of the capsule. The isolated tissue of the filament quickly underwent the degenerative changes seen in aged connective tissues, but if he periodically removed the fluid around it, and allowed fresh lymph fluid to fill the capsule, the filament retained a youthful elasticity, even as the rat aged. Isolation from the organism caused age-like degeneration to develop rapidly. When the organism can't remove a foreign object, the collagenous capsule that encloses it has a high probability of forming a cancer. This "foreign body carcinogenesis" has been studied for many years.

Foreign body carcinogenesis is closely related to chemical carcinogenesis, radiation carcinogenesis, and hormonal carcinogenesis. Chemical carcinogens such as methylcholanthrene are irritating when injected, and stimulate collagen production. Neither type of carcinogenesis is always effective, because this collagen reaction can be protective, by isolating the irritant toxin (Zhang, et al., 2013). Radiation stimulates the secretion of collagen, and causes cross-linking that makes it stiffer, and slows its removal, leading to its accumulation (Sassi, et al., 2001). Some types of cross-linking block the ability of macrophages to remove it, creating something like a diffuse foreign body reaction. Estrogen, for example in the process of causing breast cancer, causes increased collagen synthesis. This is widely recognized, in the association of "breast density" (a high collagen content) with the risk of cancer. Estrogen also causes the formation of the enzymes that cross-link and stiffen the collagen, lysyl oxidase and transglutaminase(Sanada, et al., 1978; Campisi, et al., 2008; Balestrieri, et al., 2012).” -Ray Peat

The Cancer Matrix

If someone tells a cancer patient or an oncologist that cancer is a systemic disease, the thought will be flatly rejected as untrue. They have been taught that cancer is a disease of bad, mutated, cells, which have to be completely eradicated, and that the patient's general health is a separate...

raypeat.com

 

[Rinse & rePeat]

“In 36% of women who had had a breast removed, from 7 to 22 years previously, identifiable (by the same tests used to diagnose breast cancer) cancer cells could be found circulating in their blood stream (Meng, et al., 2004). Tissue biopsies would be able to find the sources of those circulating cells, nests of similar cells throughout the body, which were dying about as fast as they were replicating. In 1969, Harry Rubin described an autopsy study which found that everyone over the age of 50 had at least one diagnosable cancer in some tissue. "Occult microscopic cancers are exceedingly common in the general population and are held in a dormant state by a balance between cell proliferation and cell death and also an intact host immune surveillance"(Goldstein and Mascitelli, 2011). These authors observed that the stress of surgery stimulates tumor growth, by various mechanisms, and that surgery increases the risk of developing cancer in apparently cancer-free patients.“
-Ray Peat