2008 - Age of Awakening / 2016 - Age of disclosures / 2021 - Age of Making Choices & Separation / Next Stage - Age of Reconnection and Transition! /
2024 - Two millenia-old Rational Collectivist societal cycle gives way to the Self-Empowered Individualism. /
2025 Golden Age begins
Showing posts with label cancer. Show all posts
Showing posts with label cancer. Show all posts

Monday, April 15, 2024

Spike protein, a cellular torture!

.

Re-posted WALTER M CHESNUT's article from Substack: "A Cellular Peine Forte et Dure: The Spike Protein Induces Almost Imperceptible Chronic Inflammation with Devastating Consequences The key cytokine is almost certainly CCL2, and this was known in 2010!", by WALTER M CHESNUT APR 15, 2024


Quote:


Upregulation of the Chemokine (C-C Motif) Ligand 2 via a Severe Acute Respiratory Syndrome Coronavirus Spike-ACE2 Signaling Pathway
Upregulation of the Chemokine (C-C Motif) Ligand 2 via a Severe Acute Respiratory Syndrome Coronavirus Spike-ACE2 Signaling Pathway


Why is upregulation of CCL2 (MCP-1) important and why is it dangerous?


CCL2 is expressed in, among other cells, endothelial cells. It is at Ground Zero of what I have called Spike Protein Endothelial Disease (SPED). I believe this to be an initial condition (invasion) that leads to global organ dysfunction and destruction. Please search my Substack for background. CCL2 is involved in much SARS-CoV-2 sequelae.


...

Chemokines in tissue fibrosis


Just as I have previously hypothesized that the Spike Protein is inducing almost imperceptible “micro-tumors,” I have also hypothesized about it causing constant organ damage. This is through inducing almost imperceptible constant inflammation, which, ultimately also explains the accelerated aging I predicted the virus and its Spike Protein would cause. There is now proof of this mechanism.


A study published Friday proves that this low-level, constant inflammation is, indeed, occurring.


...

Cardiovascular symptoms of PASC are associated with trace-level cytokines that affect the function of human pluripotent stem cell derived cardiomyocytes


This slow burn. Eroding all organs little by little. It is Bond-level diabolical. Of course, certain authorities would have us believe that the Bat and the Pangolin have managed to "create" one of the most stealthy and cruel conditions one could conceive – imagine what Humans could do!


We must investigate further. I believe that the Spike, via its amyloidogenic properties, either self-replicates, or is retrotranscribed into host DNA, or both. This is also further evidence that avoiding the Spike Protein (in ALL of its forms) and keeping an anti-inflammatory diet is critical. At least until we have a full understanding of the long-term effects of the Spike Protein and how to deal with them.


Thank you, as always, for your support, readership and dialog.


Wednesday, September 29, 2021

Vaccines and the innate and adaptive immune systems

.

This is my first stab at learning about vaccines. How exactly they work, what do the "adjuvants" do?

Reference:



In a nutshell - modification of the mRNA (nucleoside uridine code) in covid vaccine acts similar to  adjuvants (in other vaccines) weakening the innate immune system in order to give the chance for the adaptive immune system to activate, recognize and store the pathogen's signature.

That explains why vaccinating against a specific pathogen may make one vulnerable (for a time) to some secondary "opportunistic" infections. Or cancer...

Quotes:
In 2005, Drs. Weissman and Kariko discovered a way to protect foreign mRNA from the body’s immune system. That scientific milestone would be key to the advancement of the mRNA vaccines in 2020.

Recently, the University of Pennsylvania Tweeted a picture of the Drs. Weissman and Kariko receiving their Covid vaccination, and reminding us of that milestone. One tweet commenting that they should receive the Nobel prize for their discovery.

The fundamental change discovered by Weissman and Kariko was that nucleoside modification could protect mRNA from the body’s immune defences:

[picture]

Their key discovery, that by modifying the RNA code (modifying the nucleoside uridine), resulted in ablating the innate immune response, involved toll-like receptors (TLR).

This discovery was adopted in the mRNA technology used in Covid vaccines, in order that the foreign vaccine mRNA could enter cells without being destroyed.
...

By modifying the Uridine in the Pfizer vaccine mRNA code, the foreign mRNA is able to bypass part of the body’s first line of defence — the Innate Immune System.

The body possesses two broad parts to its immune system: innate and specific. The innate is the first to go into action against foreign invaders, including foreign mRNA from a vaccine.

How does that simple removal of one letter of code from mRNA achieve that? It does so by affecting Toll Like Receptors (TLR): the alarm signal of the Innate Immune System.

The key TLRs affected are TLR 3, TLR 7 and TLR 8. They act as sentries, whose job is to recognise foreign invaders by way of their form or patterns;
...

Dominguez-Andres et al addressed that question May 6th 2021. They state: ...


...
BNT162b2 vaccine also modulated the production of inflammatory cytokines by innate immune cells upon stimulation with both specific (SARS-CoV-2) and non-specific (viral, fungal and bacterial) stimuli. The response of innate immune cells to TLR4 and TLR7/8 ligands was lower after BNT162b2 vaccination.
...

We observed a significant reduction in the production if IFN-α secreted after stimulation with poly I:C and R848 after the administration of the second dose of the vaccine (Figure 1H, 1I). This may hamper the initial innate immune response against the virus, as defects in TLR7 have been shown to result in and increased susceptibility to COVID-19 in young males (Van Der Made et al., 2020). These results collectively demonstrate that the effects of the BNT162b2 vaccine go beyond the adaptive immune system and can also modulate innate immune responses.

Three concerns are raised by the above.
  1. The ability of the immune system to fight viruses has been diminished; specifically, the ability to fight SARS-CoV-2 may be affected;
  2. Vaccine-induced innate immune tolerance may affect other vaccines; and finally
  3. What other parts of the immune system may be affected.


...
Dr Ryan Cole, a Pathologist, in a recent presentation, stated that he is observing a 20 x uptick in endometrial cancer, and increases in other cancers post SARS-CoV-2 vaccination.
...

The toll-like receptors 7 & 8 are described in the literature as important in eliciting the vital CD8 T cell response. With that in mind, let us remind ourselves what Drs. Weissman and Kariko wrote in 2005 in Suppression of RNA recognition by Toll-like receptors: the impact of nucleoside modification and the evolutionary origin of RNA:

We show that RNA signals through human TLR3, TLR7, and TLR8, but incorporation of modified nucleosides m5C, m6A, m5U, s2U, or pseudouridine ablates activity.

That very technology is being used in SARS-CoV-2 vaccines: It switches off TLR 7 & 8 signalling, that the immune system needs to fight infection and cancer.
Summary

Changes to key parts of the mRNA code in SARS-CoV-2 vaccines may be causal in changing the innate immune response via toll-like receptors. Toll-like receptors are important components in defence against infection and downstream effects may also include inhibition of CD8 T cell response. CD8 is a vital part of the immune system’s ability to eradicate infection and cancer. Those changes may be reflected in recent reactivated Varicella Zoster infections although specific mechanisms are unclear at the moment. Anecdotal reports of significant uptick in cancer presenting to medical consultants may be consistent with aberrant toll-like receptor and dendritic cell changes leading to an inhibition of the anti-cancer CD8 effector response. Further data are required but the prospect of an altered CD8 response to infection and cancer is very concerning and should prompt urgent investigation.
...
-------------------
Updated 2-Oct-2021

Another issue to investigate is cytokine storm and ADE (Anti-body Dependent Enhancement)

See the references in: "Mechanism behind rona virus damage"

Wednesday, June 23, 2021

Ivermectin and cancer

.

Ivermectin: enigmatic multifaceted ‘wonder’ drug continues to surprise and exceed expectations
Abstract Over the past decade, the global scientific community have begun to recognize the unmatched value of an extraordinary drug, ivermectin, that originates from a single microbe unearthed from soil in Japan. Work on ivermectin has seen its discoverer, Satoshi Ōmura, of Tokyo’s prestigious Kitasato Institute, receive the 2014 Gairdner Global Health Award and the 2015 Nobel Prize in Physiology or Medicine, which he shared with a collaborating partner in the discovery and development of the drug, William Campbell of Merck and Co. Incorporated. Today, ivermectin is continuing to surprise and excite scientists, offering more and more promise to help improve global public health by treating a diverse range of diseases, with its unexpected potential as an antibacterial, antiviral and anti-cancer agent being particularly extraordinary.
Ref added 3-Sep-2021: "Ivermectin, a potential anticancer drug derived from an antiparasitic drug", by Mingyang Tanga et al., Pharmacological Research, Volume 163, January 2021, 105207
Highlights
  • Ivermectin effectively suppresses the proliferation and metastasis of cancer cells and promotes cancer cell death at doses that are nontoxic to normal cells.
  • Ivermectin shows excellent efficacy against conventional chemotherapy drug-resistant cancer cells and reverses multidrug resistance.
  • Ivermectin combined with other chemotherapy drugs or targeted drugs has powerful effects on cancer.
  • The structure of crosstalk centered on PAK1 kinase reveals the mechanism by which ivermectin regulates multiple signaling pathways.
  • Ivermectin has been used to treat parasitic diseases in humans for many years and can quickly enter clinical trials for the treatment of tumors.
Abstract Ivermectin is a macrolide antiparasitic drug with a 16-membered ring that is widely used for the treatment of many parasitic diseases such as river blindness, elephantiasis and scabies. Satoshi ōmura and William C. Campbell won the 2015 Nobel Prize in Physiology or Medicine for the discovery of the excellent efficacy of ivermectin against parasitic diseases. Recently, ivermectin has been reported to inhibit the proliferation of several tumor cells by regulating multiple signaling pathways. This suggests that ivermectin may be an anticancer drug with great potential. Here, we reviewed the related mechanisms by which ivermectin inhibited the development of different cancers and promoted programmed cell death and discussed the prospects for the clinical application of ivermectin as an anticancer drug for neoplasm therapy.

Wednesday, May 26, 2021

Hydroxychloroquine and cancer

.

I am posting it as a place-holder to prompt a further digging.
The original video presentation, quoting from memory because the original video depictued in the screenshot below, has been since deleted by youtube (and my account has been blocked by Twitter).

The presenter discussed an in-vitro study using human cultured tissues, with and without Нуdrохуснlоrоquin : (1) lung cancerous tissue (HeLa) and (2) kidney tissue (non-cancerous). The study found that c0rоna virus (normal cv non c19) would attack the lung and the kidney tissue without hcq, while the virus would only attack the cancerous lung tissue but not the non-cancerous kidney tissue when hcq is added.


Further and additional referenced, not the actual presentation:


[TO BE FINISHED LATER]

Thursday, March 4, 2021

Low level radiation is cancer-protective

.

Two papers:

1) https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1349-7006.1992.tb02342.x


Cancer Mortality Survey in a Spa Area (Misasa, Japan) with a High Radon Background Masaaki Mifune Tomotaka Sobue Hiroko Arimoto Yoshiaki Komoto Sohei Kondo Hiroshi Tanooka First published: January 1992

2) https://www.birpublications.org/doi/full/10.1259/bjr.75.895.750637


BJR > Previous Issues > Volume 75, Issue 895 > Radiation increased the longevity of British radiologists Correspondence Radiation increased the longevity of British radiologists J R Cameron 2678 SW 14th Drive, Gainesville, FL 32608, USA

Thursday, August 6, 2020

Research/Patent on Chloroquine treatment against DNA damage

.

"...exposure to chloroquine prior to irradiation increased cell Survival by 30%." 


 Authors: 
Michael B. Kastan, Cordova, TN (US); 
Christopher Bakkenist, Cordova, TN (US);
Mark McCamish, Cupertino, CA (US) 
 Pub. Date: Jan. 20, 2005 

 Note: a Patent is not a proof that the invention works! 

 Quotes:
ABSTRACT The present invention provides methods and compositions for the treatment of DNA damage related disorders. One embodiment is a method for the inhibition of Side effects asSociated with chemotherapeutic and radiotherapeutic agents using chloroquine compounds. Another embodiment is a method for treatment and/or prevention of lethal or Sub-lethal radiation toxicities associated with terrorist acts or war.
BRIEF DESCRIPTION OF THE FIGURES 0007 FIG. 1 shows a Kaplan-Meier survival curve of C57/BL6 mice after exposure to 8 Gy total body irradiation (TBI). Half of the cohort received a dose of chloroquine (dashed line) by either i.p. injection (1.75 mg/kg or 3.5 mg/kg) or in their drinking water (3.5 mg/kg or 7 mg/kg) the day before the TBI. The one mouse which died in the chloroquine-treated group received 1.75 mg/kg by i.p. injection.

0008 FIG. 2 shows that chloroquine treatment enhances survival after TBI by enhancing recovery of hematopoietic progenitor cells. Five mice received 3.5 mg/kg chloroquine (C) by i.p. injection 24 and 4 hours prior to TBI (bars with diagonal Stripes). Five mice received no chloroquine (stippled bars). Fourteen days after irradiation, the cellular ity (open bars) of hematopoietic tissues (spleen, thymus, bone marrow) was assessed by a blinded observer on a scale of 0-3 with 3 being normal cellularity. The bars represent the average cellularity of the tissues from the 5 mice in each group.

0009 FIG.3 shows a Kaplan-Meier survival curve of AT mice after exposure to 8 GyTBI. Half of the cohort received a dose of 3.5 mg/kg chloroquine (CHL; dashed line) by i.p. injection 24 and 4 hours prior to the TBI.

0010 FIG. 4 demonstrates that chloroquine treatment prevents the development of tumors in Eul-myc mice. After weaning, a cohort of transgenic mice expressing the c-myc oncogene were started on chloroquine (CHL) at 7.0 mg/kg in the drinking water ((+), solid line). Within 100 days, all of the mice with no drug in the water had died of leukemia, while none of the cohort of mice on drug had Succumbed. The latter group of mice was then divided into two groups (timing of this event depicted by heavy arrow), one group of which was taken off of chloroquine ((-), dashed line) and the other group of which was started on i.p. injections of 3.5 mg/kg of chloroquine once a week. Within a month, all of the mice taken off of chloroquine had developed malignan cies and all of the mice on the weekly i.p. injections remained tumor-free for months.

0011 FIG. 5 illustrates that chloroquine treatment reduces the development of tumors in mice injected with the potent chemical carcinogen, 3-methylcholanthrene (3-MC). Chloroquine (CHL, 3.5 mg/kg) was given by i.p. injection 24 and 4 hours prior to 3-MC injection in 30 mice and 30 mice received the carcinogen with no chloroquine pretreat ment. The percentage of animals remaining tumor-free is plotted. Statistical significance, log rank test P-0.0001.

0012 FIG. 6 demonstrates that chloroquine treatment reduces the development of tumors in mice exposed to ionizing radiation in a protocol that induces thymic lym phomas. Chloroquine (CHL, 3.5 mg/kg) was given by i.p. injection 24 and 4 hours prior to irradiation in four Successive weeks and animals were subsequently observed for the development of tumors. Statistical Significance, log rank test P=0.0012.

0013 FIG. 7 shows tumor incidence in wildtype mice receiving either placebo or CHQ before 3-MC injection. CHQ markedly protects from tumor development.

0014 FIG. 8 shows tumor incidence in ATM-null mice receiving either placebo or CHQ before 3 MC injection. CHQ does not protect from tumor development.

0015 FIG. 9 shows tumor incidence in p53-null mice receiving either placebo or CHQ before 3 MC injection. CHQ does not protect from tumor development.

0016 FIG. 10 demonstrates the efficacy of two chloroquine compounds in preventing, in Varying degree, the change in coat color in mice treated with 8 GY radiation.






------------ Update 14-Aug-2020 -----------------

"Hydroxychloroquine-loaded hollow mesoporous silica nanoparticles for enhanced autophagy inhibition and radiation therapy",by Yan Li et al., 25-June-2020






Saturday, July 4, 2020

Nail to the coffin of prof Campbell's theory of cancer supposedly triggered by protein

.

A long-time vegan diet promoter Prof-emeritus T.C Campbell of Cornell University, author of The China Study book, used to claim in his studies that adding protein to high carbohydrate mice diet does trigger the cancer while removing it reduces the frequency and size of cancerous tumors. Campbell argues that casein, a protein found in milk from mammals, is "the most significant carcinogen we consume" (see Wiki T. Colin Campbell and Talk by T. Colin Campbell Archived 2011-04-17 at the Wayback Machine, Google Videos, 20:24 mins, accessed December 3, 2010.).

Campbell's theory has been questioned for some time. Most notably, Denise Minger has posted some very in-depth and thorough analyses on-line discussing what exactly may have gone wrong with Campbell's research.

This study found that the reality is in fact quite the opposite to the scientist's claim, showing that a high protein low carbohydrate diet had in fact almost completely protected the genetically-modified cancer-susceptible mice against getting cancer (while the high-carbohydrate control group got 50% cancer!)

"A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation", by
Victor W. Ho, Kelvin Leung, Anderson Hsu, Beryl Luk, June Lai, Sung Yuan Shen, Andrew I. Minchinton, Dawn Waterhouse, Marcel B. Bally, Wendy Lin, Brad H. Nelson, Laura M. Sly and Gerald Krystal, Published in Cancer Research/AACR, July 2011



Quote

Abstract

Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.

Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression. Cancer Res; 71(13); 4484–93. ©2011 AACR.

What was also interesting that an addition of an anti-inflammatory COX-2 inhibitor drug (Celebrex, 1g/kg body) slowed down the tumor growth by about a half, regardless of a diet! Not sure how to interpret it, perhaps that inflammation accelerates the tumor growth in general?

Saturday, March 9, 2019

Ketogenic diet protects against chemotherapy

.

"β-Hydroxybutyrate, a ketone body, reduces the cytotoxic effect of cisplatin via activation of HDAC5 in human renal cortical epithelial cells", Daisuke Mikami et al., Life Sciences
Volume 222, 1 April 2019, Pages 125-132


Quote:

Main methods

In this study, we used human renal cortical epithelial (HRCE) cells. The anti-apoptotic effect of βOHB was evaluated using flow cytometry analysis. The expression of apoptosis-related proteins and HDACs was evaluated by western immunoblot.

Key findings

The results showed that βOHB significantly reduced cisplatin-induced apoptosis in HRCE cells. Furthermore, βOHB significantly reduced cisplatin-induced cleavage of caspase-3, acetylation of histone H3, and phosphorylation of AMP-activated kinase. This anti-apoptotic effect of βOHB was markedly attenuated by an inhibitor of HDAC4/5, and βOHB-mediated suppression of cleavage of caspase3 was significantly blocked by siRNA-induced gene silencing of HDAC5.

Significance

βOHB attenuates cisplatin-induced apoptosis by activation of HDAC5 in HRCE cells, suggesting that βOHB may be a new therapeutic agent for cisplatin nephropathy.

Wednesday, January 16, 2019

New cancer treatment with rosiglitazone+trametinib

.



Cancer Cells Transformed into Harmless Fat in Mouse Study, By Rachael Rettner, January 15, 2019

Quote:

Then, the researchers treated the mice with two drugs: rosiglitazone, which is used in people to treat type 2 diabetes, and trametinib, an anti-cancer drug that inhibits the growth and spread of cancer cells. (Rosiglitazone belongs to a class of drugs known as thiazolidinediones, which bind to receptors that are found mainly in fat tissue and that play a role in a number of biological processes, including the formation of mature fat cells, according to a 2005 paper on the topic. People with diabetes are given the drug because the receptors that it binds to also help increase sensitivity to the hormone insulin, which is involved in regulating blood sugar levels.) The researchers in the new study found that when mice received this drug combination, the cancer cells that had broken free from the initial tumor (called "invasive cancer" cells) changed into fat cells. The drugs also suppressed the growth of the tumor and prevented further metastasis.

Saturday, August 11, 2018

how corporations use scientists to manipulate the public

.
The lawsuit and a verdict against Monsanto described in the article below illustrates the way large corporations use scientists to manipulate public opinion and to hide the inconvenient facts. I expect similar outcomes when the corporations and activists behind "Global Warming/Climate Change" and "Cholesterol/Fat Theory of Heart Disease" will be brought to trial in the similar fashion.

Monsanto ordered to pay $289m as jury rules weedkiller caused man's cancer

Quotes:

Johnson’s lawyers argued over the course of a month-long trial in San Francisco that Monsanto had “fought science” for years and targeted academics who spoke up about possible health risks of the herbicide product.
...
In the extraordinary verdict, which Monsanto said it intends to appeal, the jury ruled that the company was responsible for “negligent failure” and knew or should have known that its product was “dangerous”.

“We were finally able to show the jury the secret, internal Monsanto documents proving that Monsanto has known for decades that ... Roundup could cause cancer,” Johnson’s lawyer Brent Wisner said in a statement.
...
Johnson’s case was particularly significant because a judge allowed his team to present scientific arguments. The dispute centered on glyphosate, which is the world’s most widely used herbicide. The verdict came a month after a federal judge ruled that cancer survivors or relatives of the deceased could bring similar claims forward in another trial.

During the lengthy trial, the plaintiff’s attorneys brought forward internal emails from Monsanto executives that they said demonstrated how the corporation repeatedly ignored experts’ warnings, sought favorable scientific analyses and helped to “ghostwrite” research that encouraged continued usage.
...
Another Roundup cancer trial is scheduled to begin in the fall in St Louis, Missouri. According to Johnson’s lawyers, Monsanto is facing more than 4,000 similar cases across the US.

"Ghostwrite" research means that the corporations hired and paid some scientists to publish falsified or incomplete material in scientific journals in order to portray the company in a favorable light or to obfuscate the wrong-doings.

The following letter outlines the tactics employed by the corporation to manufacture a false outcry in the media and rally the public opinion against the whisteblowers and organisation (in this case IARC / WHO ) that have published damaging facts.

How Monsanto Manufactured ‘Outrage’ at IARC over Cancer Classification

As a side note I find it amusing that the similar to the above-described public-opinion manipulation techniques have been employed since 2016 in the English language media to manufacture an artificial anti-Trump and anti-Republican 'outrage', known as "Trump-Derangement Syndrome". :)

Heretic

Monday, February 12, 2018

New anti-viral melanoma therapy

.

TV interview with medical doctor prof Andrzej Mackiewicz (in Polish)

Quote:

Oncologist prof. Andrzej Mackiewicz, creator of the melanoma vaccine, was a guest of "Dzien Dobry" ["Good Morning"] TVN program. It is a vaccine that heals, not just prevents melanoma! It could have helped several hundred sick people each year if it was officially registered and approved, however that is very expensive. Why is the melanoma vaccine not available to all patients? - We are scientists who have developed a medicine that works, and that seems to pose a huge problem for certain people or authorities - said prof. Mackiewicz on Good Morning TVN.

Wednesday, February 7, 2018

Asparagus - not so good for cancer!

.

Wiki Asparagus

The Guardian article.


Asparagine bioavailability governs metastasis in a model of breast cancer

Quote:

Here we show that asparagine bioavailability strongly influences metastatic potential. Limiting asparagine by knockdown of asparagine synthetase, treatment with -asparaginase, or dietary asparagine restriction reduces metastasis without affecting growth of the primary tumour, whereas increased dietary asparagine or enforced asparagine synthetase expression promotes metastatic progression. Altering asparagine availability in vitro strongly influences invasive potential, which is correlated with an effect on proteins that promote the epithelial-to-mesenchymal transition. This provides at least one potential mechanism for how the bioavailability of a single amino acid could regulate metastatic progression.

Wednesday, July 5, 2017

Study: chemotherapy may spread cancer and trigger more aggressive tumours

.
http://www.telegraph.co.uk/science/2017/07/05/chemotherapy-may-spread-cancer-trigger-aggressive-tumours-warn/

Researchers in the US studied the impact of drugs on patients with breast cancer and found medication increases the chance of cancer cells migrating to other parts of the body, where they are almost always lethal.

Many are given chemotherapy before surgery, but the new research suggests that, although it shrinks tumours in the short term, it could trigger the spread of cancer cells around the body.

It is thought the toxic medication switches on a repair mechanism in the body which ultimately allows tumours to grow back stronger. It also increases the number of ‘doorways’ on blood vessels which allow cancer to spread throughout the body.

Dr George Karagiannis, of the Albert Einstein College of Medicine of Yeshiva University, New York, found the number of doorways was increased in 20 patients receiving two common chemotherapy drugs.

Wednesday, March 30, 2016

Vegetarian diet causes genetic adaptation that raises risk of heart disease and cancer

.
- which was found by an Indian/American study "Positive selection on a regulatory insertion-deletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid" published in Mol Biol Evol (2016) doi: 10.1093/molbev/msw049 on March 29, 2016.

The study found a specific genetic adaptation to vegetarian diet that is detrimental to cardiovascular health and causes higher susceptability to cancer, due to enhanced production of arachidonic acid. Such adaption is not observed among populations consuming diets that are not exclusively plant-based.

From Wiki 
More discussion of the study can be found in:

Science Daily / Are we what we eat?
Evidence of vegetarian diet permanently shaping human genome to change individual risk of cancer, heart disease


Quote:

Summary:
In a new evolutionary proof of the old adage, 'we are what we eat,' scientists have found tantalizing evidence that a vegetarian diet has led to a mutation that -- if they stray from a balanced omega-6 to omega-3 diet -- may make people more susceptible to inflammation, and by association, increased risk of heart disease and colon cancer.

Daily Mail - Vegetarian diet 'raises risk of heart disease and cancer'

Quote:

Vegetarianism over generations can result in genetic mutations which increase the risk of heart disease and cancer.
Researchers found a long-term vegetarian diet means populations are more likely to carry DNA that makes them vulnerable to inflammation.
The mutation is believed to make it easier for vegetarians to absorb necessary fatty acids from plants, but also boosts their production of arachidonic acid, which increases inflammatory disease and cancer.


--------
Added 2/04/2016

This is an important study because it is not only describing statistical correlation which may or may not reflect the real causes, but it also described specific biochemical and genetical mechanisms underlying the effects they have observed. I am tempted to draw the following conclusions, some of them may be a bit stretched, some not. Time will tell.

1) The key factor in the chronic diseases are polyunsaturated fats - not the carbohydrates and not the other types of fats (for example not the mono-unsaturated or saturated fats).

2) Adaptation to a low fat plant based nutrition takes place over many generations of people, works through epigenetic mechanisms, predisposing such populations to efficiently process and convert the little amount of total and mostly polyunsaturated plant fat that they eat. This adaptation allows them to very efficiently convert the small amounts of vegetable oils they consume to some essential fatty acids required for the body, preventing malnutrition related deficiency diseases.

3) The same adaptation allowing low fat plant based food eaters to survive, causes chronic diseases risk once they add too much polyunsaturated fat into their diet, due to hyperactivity of metabolic pathway involving arachidonic acid and prostaglandins. The threshold is probably 5-10% of calories. This threshold applies to polyunsaturated fats of all kinds, including fish fat - BUT IT DOES NOT APPLY TO SATURATED FATS!

4) Both population groups - the one adapted to a low fat plant based diet and the one unadapted could safely consume larger amounts of saturated fats (i.e animal saturated fat, dairy fats, coconut fat etc) if they choose so, without a detriment to their health because saturated fats do not partake in the biochemical pathways involving arachidonic acid and prostaglandins.

5) Population adapted to low fat plant based diet should not consume more than a few percent (in total calories) of polyunsaturated fats such as vegetable oils (and fish oil!), otherwise the risk of chronic diseases increases.

6) Population not adapted to low fat plant based diet, not only can but should consume somewhat higher amounts of polyunsaturated fats including fish fat. How much would be OK and how high is too high? This is to be determined, I am not sure! This will ensure adequate supply of some essential polyunsaturated fatty acids, that their bodies cannot synthesize as efficiently as the adapted group! At the same time, the non-adaptation to low fat makes this group particularly well adapted to consuming larger amounts of polyunsaturated fish fat!

7) For the people who are not adapted to a low fat plant based diet, or those who tried it but could not or would not do it, I would say this: - a high animal fat diet will automatically make it low to moderate in polyunsaturated fats (suitable to both adapted and non-adapted) as long as you avoid using vegetable oils! If in addition, you avoid also consuming excessive amounts of carbohydrates then you will avoid other risk factors involving metabolic dysfunctions involving hyper-insulinemia and glucose overload.

8) Last but not least, I am directing this message to my vegetarian on-line friends and real life friends: - if you find yourself thriving on a low fat plant based diet then you are probably genetically adapted to it, therefore ABSOLUTELY avoid consuming more than a few % of daily calories in form of plant oils and fish (or fish fat)! Stay with it - it will probably work for you, however you most likely DO NOT NEED TO AVOID SATURATED FAT! You do not need to avoid meat, dairy and poultry either but watch out for the polyunsaturated contents of some animal fat! In this respect, if you wanted to add meat to your low fat plant based diet, you are probably better off adding beef rather than chicken or fish!

[3/04/2016]

9) Limiting consumption of polyunsaturated oils, especially Linoleic Acid present in commercial vegetable oils, will likely reduce mitochondrial damage alleviating the risk of metabolic syndrome, even on a high carbohydrate diet. This is key point of the Cardiolipin hypothesis that postulates that the primary cause of metabolic syndrome is mitochondrial degeneration due to incorporation of the linoleic acid into cardiolipin molecules, which makes mitochondria exceedingly vulnerable to oxidative damage. Such oxidative damage may be triggered be glucose overload as in a high carbohydrate diet, or by other factors. This is a two step process the primary factor (a) being the linoleic acid making mitochondria vulnerable and in the second stage (b) carbohydrate overload (or other toxins) actually damages the mitochondria. For further details on Cardiolipin hypothesis read Tucker Goodrich comments under my previous post and this blog.
I thoroughly enjoyed this article by Dr. Kendrick, very much on the topic of polyunsaturated fats: "Greater Cholesterol lowering increases the risk of death" , I hope you too. Here are some quotes:

The original researchers who set up and ran the SDHS did not fully publish their data at the time (one can only speculate as to why this may be so). When this current group of researchers finally managed to get hold of the full data from the SHDS, it was found that replacing saturated fat with polyunsaturated fat did lower cholesterol, however:
REPLACEMENT OF SATURATED FAT SIGNIFICANTLY INCREASED THE RISK OF DEATH FROM CORONARY HEART DISEASE AND ALL CAUSES.

and another one:

The Minnesota Coronary Experiment (MCE), a randomized controlled trial conducted in 1968-73, was the largest (n=9570) and perhaps the most rigorously executed dietary trial of cholesterol lowering by replacement of saturated fat with vegetable oil rich in linoleic acid.
...
Now, a few years later, the researchers who re-analysed the Sydney Diet Heart Study decided to try and find all the unpublished data from the Minnesota Coronary Experiment (MCE). (One can again only speculate as to why the original researchers did not reveal all of their data). The main points from this re-analysis were the following

* Though the MCE intervention lowered serum cholesterol, this did not translate to improved survival

* Paradoxically, MCE participants who had greater reductions in serum cholesterol had a higher, rather than lower, risk of death


Stan (Heretic)

Wednesday, January 9, 2013

Anti-oxidants may promote rather than fight cancer!

.

Hold off those berries and vitamins, suggests DNA discoverer James Watson, in today's article titled "DNA pioneer James Watson takes aim at 'cancer establishments'" article.

From wiki

Quotes:
On the $100 million U.S. project to determine the DNA changes that drive nine forms of cancer: It is "not likely to produce the truly breakthrough drugs that we now so desperately need," Watson argued. On the idea that antioxidants such as those in colorful berries fight cancer: "The time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer."

...

That is why Watson advocates a different approach: targeting features that all cancer cells, especially those in metastatic cancers, have in common.

One such commonality is oxygen radicals. Those forms of oxygen rip apart other components of cells, such as DNA. That is why antioxidants, which have become near-ubiquitous additives in grocery foods from snack bars to soda, are thought to be healthful: they mop up damaging oxygen radicals.

That simple picture becomes more complicated, however, once cancer is present. Radiation therapy and many chemotherapies kill cancer cells by generating oxygen radicals, which trigger cell suicide. If a cancer patient is binging on berries and other antioxidants, it can actually keep therapies from working, Watson proposed.

"Everyone thought antioxidants were great," he said. "But I'm saying they can prevent us from killing cancer cells."







Sunday, November 25, 2012

Ketogenic diet slows progression of cancer...

...in 5 out of 9 patients who exhibited the highest degree of ketosis measured by a level of beta hydroxy butyrate.

The degree of cancer progression slow down or remission correlated with the degree of ketosis and degree of ketosis correlated inversely with the level of insulin.

The study lasted 26-28 days and involved only nine patients who completed the study, all of whom begun with rapidly progressing advanced and incurable cancers.

Fig 2 (part, 1 out of 4 graphs) from the study. β-OH butyrate
(beta hydroxy butyrate) represent a degree of ketosis.

"Targeting insulin inhibition as a metabolic therapy in advanced cancer: A pilot safety and feasibility dietary trial in 10 patients", Eugene J. Fine et al., Nutrition, 1028-1035,2012

Comments:

It is interesting to note that, contrary to a myth about keto diets being supposedly harmful for kidneys,  not only it did not worsen the markers, but improved kidney filtration of one of the patients!

It is important to keep in mind that stopping of a disease progression is not the same as curing it. Ketogenic diet seems to help but I do not consider it to be a universal cure for cancer (it does however cure t2 diabetes!).

Heretic

Saturday, April 30, 2011

Low-level ionising radiation protects against cancer!

.

Quote:

The projections of thousands of late cancer deaths based on LNT, are in conflict with observations that in comparison with general population of Russia, a 15% to 30% deficit of solid cancer mortality was found among the Russian emergency workers, and a 5% deficit solid cancer incidence among the population of most contaminated areas.

Paper :   
Observations on the Chernobyl Disaster and LNT. (thanks Peter for pointing it out)

LNT stands for "Linear Non-Threshold" hypothesis that postulates that no matter how low level of radiation, its harmful effects accumulate and add up over time.

This and other papers posted in this blog ( Gamma radiation protects against cancer, in low doses seems to indicate that this theory is dead.
.

Friday, May 21, 2010

Gamma radiation protects against cancer, in low doses?

.
Cancer mortality reduction by 97% - huge!  Is it true?  Hormesis?

Paper:
  "Effects of Cobalt-60 Exposure on Health of Taiwan Residents Suggest New Approach Needed in Radiation Protection",   W.L. Chen et al.,   Dose Response. 2007; 5(1): 63–75

Quote:

... serendipitous contamination of 1700 apartments in Taiwan with cobalt-60 (T1/2 = 5.3 y). This experience indicates that chronic exposure of the whole body to low-dose-rate radiation, even accumulated to a high annual dose, may be beneficial to human health. Approximately 10,000 people occupied these buildings and received an average radiation dose of 0.4 Sv, unknowingly, during a 9-20 year period. They did not suffer a higher incidence of cancer mortality, as the LNT theory would predict. On the contrary, the incidence of cancer deaths in this population was greatly reduced-to about 3 per cent of the incidence of spontaneous cancer death in the general Taiwan public. In addition, the incidence of congenital malformations was also reduced - to about 7 per cent of the incidence in the general public. These observations appear to be compatible with the radiation hormesis model.

   Figure 1 from the same paper.  Click to magnify and hires.


More readings:

1. by D.W.Miller, MD:  Afraid of Radiation

2.  Keeping the Lights On

3. by William R. Ware, Ph.D.:  Low-Dose Radiation Exposure and Risk of Cancer

4. Caroline Hadley: "What doesn’t kill you makes you stronger", Nature, EMBO reports   VOL 4 | NO 10 | 2003

5. Bernard L. Cohen: "Test of linear no threshold theory of radiation carcinogenesis for inhaled radon decay products", University of Pittsburgh 1994

Fig 1a from Cohen's paper 

To annoy anti-nuclear environuts:    Letter... 

More refs added (02-Mar-2011):

6.  Rheumatology 2000;39:894–902;
"Long-term efficacy of radon spa therapy in rheumatoid arthritis—a randomized, sham-controlled study and follow-up"



7. Int.J.Low Radiation,Vol.1,No.4,2005; "Nuclear shipyard worker study (1980–1988): a large cohort exposed to low-dose-rate gamma radiation"



see also John Cameron's (one of the study author) write-up here

Quote:

In 1980, the US Department of Energy (DOE) gave a contract to the School of Public Health at Johns Hopkins University to study radiation risks to nuclear shipyard workers. This study, which extended for more than a decade, cost the taxpayers $10 million. This was the World's best epidemiological study of nuclear workers. The study has yet to be published more than 12 years after its completion in early 1988.
...
The reader may think that the nuclear shipyard study is contradicted by other human studies. I know of no contradictory studies. One other radiation worker study--the British radiologists study. (Smith and Doll 1981)-- also looked at the death rate from all causes. It gives results consistent with NSWS. (Table 2.)

.

Sunday, June 7, 2009

Can ketogenic diet cure cancer?

(Fatty pork with curry veggies in butter and 'matoes)
There is very little data but what is available, so far is quite encouraging. Strangely enough most medical research institutions do not seem to think so or there would be a mad rush to study it on thousands of patients.

References:

"Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports." Nebeling LC, Miraldi F, Shurin SB, Lerner E.

"Targeting energy metabolism in brain cancer: review and hypothesis", Thomas N Seyfried and Purna Mukherjee, Nutrition & Metabolism 2005,2:30

"Can a High-Fat Diet Beat Cancer?"
By Richard Friebe Monday, Sep. 17, 2007


And finally a paper from my favored scientific publisher specializing in printing fake peer-review journals:

"Tumor growth in patients with tuberous sclerosis complex on the ketogenic diet" Catherine J. Chu-Shore, Elizabeth A. Thiele

Quote:
Three out of five patients, all children, had progression of a known tumor or tumors or the development of a new tumor while on the ketogenic diet. Conclusion: In this limited case series of five TSC patients, the ketogenic diet did not induce tumor regression or suppress the growth of TSC-related tumors.

I am curious, if they emphasize that it didn't help the 3 out of 5, should we interpret it as stating that it did help the other 2 out of 5? (I do not have the access to the full paper to check it).

--------------

Footnote (for an oncologist with a PhD's)

No, it does not work (if it works) by starving a cancer through lowering serum glucose level down to zero. Yes it would of course have killed a patient together with a tumor.

What the ketogenic diet does do is it totally alters a body's predominant metabolic mode shifting it from glucose to ketone bodies and lipids. One side effect of ketogenic diets is the enhancement of the immune system (we all heard of course, I presume of the standard pre-penicillin therapy against TB...)

Another effect is reduction of glucose uptake by the healthy cells that are not yet cancerous and the protective effect resulting from much lower insulin production (and insulin tissue uptake) on the true ketogenic diet versus a low fat high carbohydrate diet. Another and probably even more important effects are those that we do not yet fully understand due to a curious lack of curiosity or competence of some oncologists with the PhD who do not seem to want to pursue any investigation that might actually work...

Based on my mom's experience, the best survival strategy is to listen carefully to the oncologists, write thoroughly down everything they have to say - and do the opposite! It has worked well for my mom since her close encounter with the disease in 1998 when she refused a friendly "slash-burn-and-poison" therapy offer from her local hospital. Eleven years later, so far so good...

Be free and prosper,
Heretic

------ (added later) ----

More references (thanks Cynthia):
"Acetoacetate reduces growth and ATP concentration in cancer cell lines which over-express uncoupling protein 2."
Fine EJ, Miller A, Quadros EV, Sequeira JM, Feinman RD.



CONCLUSION: Seven human cancer cell lines grown in glucose plus acetoacetate medium showed tightly coupled reduction of growth and ATP concentration. The findings were not observed in control fibroblasts. The observed over-expression of UCP2 in cancer lines, but not in controls, provides a plausible molecular mechanism by which acetoacetate spares normal cells but suppresses growth in cancer lines. The results bear on the hypothesized potential for ketogenic diets as therapeutic strategies.

------------------------

Added 12-Nov-2009

Yes!

Read Peter's post: Methylglyoxal on Atkins...

The story can be compressed into two titles:

Ketosis leads to increased methylglyoxal production on the Atkins diet.

A brief critical overview of the biological effects of methylglyoxal and further evaluation of a methylglyoxal-based anticancer formulation in treating cancer patients.

----

Added 15/04/2012
Carbohydrates and the Risk of Breast Cancer among Mexican Women

Starch Intake May Influence Risk for Breast Cancer Recurrence, Jennifer A. Emond, M.S.
Abstract Number: P3-09-01, San Antonio Breast Cancer Symposium, 2011, Title: Change in Carbohydrate Intake and Breast Cancer Prognosis.


Is there a role for carbohydrate restriction in the treatment and prevention of cancer?
Rainer J Klement and Ulrike Kämmerer

.