Ray Peat Email Advice Depository

[Ponylover]

Me: Do you think it is safe to regularly consume cheese made with enzymes/vegetarian rennet if it is well tolerated? Or, will regular consumption cause some damage long term?

Peat: I think it increases the risk of future inflammation.

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Me: Do you think some people can be sensitive to lutein? I think some people have reported feeling depressed and tired after eating lutein, and I think I am responding similarly.

What do you think about this: Sara's Diet - The Lutein-Free Solution

Peat: Beta-carotene can have toxic effects when it accumulates, and since lutein isn’t convertible to vitamin A it’s likely to be more of a problem. Many of the foods with a lot of lutein have lots of other toxic components, so avoiding them might be protective for reasons other than lutein.

Me: That's interesting, thank you. So, could this mean that some people can be sensitive to orange juice, kale, chard, spinach, mustard greens, and eggs?

Peat: I think it’s the whole array that has the effect, and citrus juice has so many antiinflammatory things I think they usually prevent harm from the small amount of carotenoids. With eggs, the concentrated protein itself can precipitate inflammation by lowering glucose. Leaves have multiple irritants and toxins.

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Me: The Mongolian diet seems quite healthy - It's composed primarily of dairy and meat meat - mostly ruminant meat. However, they still seem to have significant health issues and their average life expectancy is 70 years. Why do you think this is?

Peat: Restriction of the amino acids methionine, cysteine, and tryptophan can profoundly extend life. A high protein diet provides too much of those, and chronically elevates cortisol.

Me: That's interesting. You generally recommend 80 - 100 g of protein per day, right?

Peat: Yes; part of that can be gelatin, which lacks those amino acids.

 

[CreakyJoints]

Q: What steps could one take prior to scans (specifically concerning CT scan on the ear/brain) to help mitigate toxic effects to mitochondria? I have heard methylene blue, aspirin, and caffeine might be helpful.

A: Since the brain is most sensitive to radiation damage, the protective substances should be systemic. Thyroid hormone, magnesium, aspirin, and coffee are other protective substances.

---

Q: What are some possible causes and solutions for visual snow?

A: I think it’s the individual retinal cells that define our visual acuity; many people just don’t notice the way their sense receptors interact with the world.

---

Q: Are there any textbooks/journals you wish you could have used as a teacher; or is there a syllabus you would give to new students now, assuming you weren't restricted to a set list?

A: Sources that I’ve mentioned in newsletters over the years are the sort of thing that I have used as background reading for courses. Many years ago, testbooks written by one person were useful when the author happened to be an insightful and imaginative person, but increasingly, textbooks are created by publishers for sales, including everything stylish enough to increase profits. Any syllabus should function as just a direction in which to exercise critical thinking; everything worth knowing becomes more when it’s taken up and used.

---

Q: In A Biophysical Approach to Altered Consciousness, you write positively about Piracetam. Do you have any thoughts on other drugs in this family which have been researched since you wrote this paper? (specifically mentioning Coluracetam, Fasoracetam, Nefiracetam, Phenylpiracetam)

A: I haven’t been paying much attention to those derivatives; too much cholinergic or glutamatergic stimulation is harmful.

Q: Do you therefore believe habitual or occasional usage of Piracetam could be detrimental, since it can deplete choline and glutamate over time? Can this be mitigated by supplementation or is the stimulation itself problematic?

A: I would be more concerned about its chronic effects on the liver.

 

[5a-DHP]

Q: I understand and share you distain for modern medicine's obsession with the 'faulty gene' model of disease; however, for the few disorders that are truly of monogenic origin, do you see any therapeutic potential in the upcoming gene therapies - the adenovirus associated vectors, for example?

A: I think the supposedly monogenic disorders involve deeper problems that would show up in different ways if a single gene were replaced.

 

[Ashoka]

On Eastern Philosophy and Spirituality:

“Yes, it’s worth serious study. I think it makes study of the productions of the western cultures less harmful.”

 

[Ashoka]

On Hegel and Critical Theory:

“American professors who have called themselves marxists, in recent generations, have generally been closer to Hegel in their attitude toward abstractions, protecting some authoritarian commitments, avoiding Lenin’s completely open understanding of matter, which I think was close to Aristotle’s view of substance. I think Hegel’s idea that punishment was for the benefit of the criminal shows that abstraction had precedence over everything. Dialectic thinking makes Idealism as good as it can be, but what it lacks is everything to be discovered in the richness of reality. All the variations of neokantianism and Popperism evade a dialectical understanding, and seem to be motivated by a need to reduce possibilities of knowing.”

 

[Lord Cola]

Me: What do you think is the optimal temperature for milk to be consumed at? Also, why might lukewarm milk produce less gas in my colon than heated milk, while other people seem to digest heated milk better?

RP: The digestive functions all work best at 98 or 99 degrees F; lower temperature slows or stops the digestive functions. Lukewarm is the best temperature for food. Food that we don’t digest becomes available to support the growth of bacteria, which can cause gas and toxic effects.

 

[Beastmode]

Me:
1) Can there be any use of using a continuous blood glucose monitor compared to the ones that prick your finger, which would be more like a snapshot?

2) I know the ranges that are supposedly "healthy" are most like skewed for big pharma purposes (i.e- to sell drugs,) but might there be a range that can be found that aligns with useful metrics (i.e- mood, focus, body temp/pulse, etc?)

3) Have you experimented with this much on yourself to see how it aligns when you're feeling good compared to suboptimal?

p.s- I noticed with a large carb meal last night (masa was the carb,) I noticed it was much easier to digest with some niacinamide (400 mg capsule.)

Ray:
I haven’t had any experience with a continuous glucose monitor. I think the amount of glucose has to be judged in relation to all the conditions.

 

[gaze]

what would you do if the cynoplus/cynomel supply chain gets disrupted, as it often does?

Ray: Novotiral has continued to be available. Most glandular products on the market aren’t what they claim to be, but Armour thyroid, USP, currently seems to be o.k.

 

[rr1]

From a Facebook group, didn't see it posted here.

RE: Tonsil Stones
Ray: Those are white blood cells, usually responding to allergens. I think slight hypothyroidism, possibly low vitamin D, predisposes to them

 

[Zbush]

From a Facebook group, didn't see it posted here.

RE: Tonsil Stones
Ray: Those are white blood cells, usually responding to allergens. I think slight hypothyroidism, possibly low vitamin D, predisposes to them

I've recently found some tonsil stones and they are only on my right tonsil.. Have you found solutions other than maybe low Vit D?

 

[meatbag]

Originally posted here: I asked peat if he believed in luck, heres his response by @Cloudhands
-
I was wondering if you believed in luck. From my perspective the universe seems to collectively interact with me in a symbolically, intelligent manner. Luck almost seems like an energy or substance to could also be viewed as measuring my relationship to the universe and how well it treats me. I also seem to find that not only does having a certain attitude toward things increase my feeling of luck, but different substances and molecules interact with seem to have varying effects. Psychedelic substances such as LSD, mushromms and dimethyltryptamine seem to be the most profound luck enhancers, but other things that improve mitochondrial health such as vitamin B1, B3, pau d'archo, vitamin k2, etc seem to correlate to me having good fortune. Sometimes it feels as if an entity is watching over me and helping me, and I have a strong loving relationship to this entity. Let me know if you think I'm crazy :) thank you

RP: Coffee is another enhancer. F David Peat discusses similar ideas in his book Synchronicity. Andrija Puharich and John Bockris have suggested a variety of interpretations.

 

[CreakyJoints]

RE: Red Light "Overexposure"

Q: I've not seen many satisfactory explanations yet as to why red light therapy or photobiomodulation seems to only work up to a certain point, after which the effects are significantly reduced, if not deleterious. I was wondering a lot about this in light of your recent newsletter about HSP. Is the issue simply a matter of overheating - and does this perhaps explain why strobing/pulsing light seems to enjoy a higher tolerance threshold? Why do you suppose there is a point at which effects are no longer noticed, what is the mechanism?

A: Red light of moderate wattage doesn’t warm the tissues enough to be harmful; its good effects are from restoring oxidative metabolism, and it just takes a short exposure to do that.

 

[llian]

Q:
My mother have Glioblastoma Giant Cells and waa given 2 months only to live. She had surgery to remove 2 tumors but 1 tumor located in Cerebellum can't be removed surgically. How I can treat her without the standard approach?

A:
"Acetazolamide, angiotensin blockers such as losartan, lidocaine, vitamin D, aspirin, and naloxone all have anticancer effects without serious side-effects, and they are inexpensive and available to any doctor..


Study Finds Acetazolamide May Be Effective in Treating Glioblastoma
July 22, 2018
Alison Rodriguez
Acetazolamide, sold under the trade name Diamox, is a drug used to treat altitude sickness, glaucoma, epilepsy, heart failure, and seizures. According to a new study, acetazolamide may also be effective in treating the fast-growing brain tumor glioblastoma.
Acetazolamide, sold under the trade name Diamox, is a drug used to treat altitude sickness, glaucoma, epilepsy, heart failure, and seizures. According to a new study, acetazolamide may also be effective in treating the fast-growing brain tumor glioblastoma.
The drug temozolomide (TMZ) is the most frequently used chemotherapy for treating gliomas; however, not all patients respond to treatment with this drug. TMZ damages DNA in a way that can kill tumor cells, but some tumor cells can block or repair the DNA damage, according to a report.
“Although alkylators like temozolomide (TMZ) improve overall patient survival, many patients experience minimal benefit from their use. These observations underline the critical need for predictors of response to alkylating therapy,” the study explained.
The study found that most patients with glioma who had high levels of the protein BCL-3 (B cell CLL/lymphoma 3) were unresponsive to TMZ because BCL-3 shields cancer cells from the TMZ damage by activating the protective enzyme called carbonic anhydrase II, according to the study.
Although acetazolamide is a carbonic anhydrase inhibitor, it can restore TMZ’s ability to kill the tumor cells. During the study, the researchers added acetazolamide to TMZ , which enabled mice with gliomas to survive longer. Additionally, when this combination treatment was used in several animal models, it resulted in a 30% to 40% increase in survival time, noted the study director Bahktiar Yamini, MD, a neurosurgery professor at the University of Chicago Medicine.
“This finding, when considered with the observation that BCL-3 is a candidate oncoprotein that has never been identified as a glioma driver, indicates that BCL3 loss is a passenger event unrelated to glioma formation,” the researchers stated. “Although the ability of passenger events to promote unintended therapeutic susceptibility has been shown in animal models, the link between loss of BCL-3 and TMZ susceptibility demonstrates the importance of passenger modification to chemosensitivity in a clinical setting.”
Furthermore, when the researchers looked back at previous human studies, they discovered that patients with lower levels of BCL-3 who were treated with TMZ had, overall, survived longer than those who had high levels of the biomarker.
The authors emphasized that, in the future, a prospective randomized clinical trial is necessary in order to validate that the use of BCL-3 to predict which patients will benefit from TMZ. They also suggested that the combination of acetazolamide with TMZ may be an effective subgroup to consider for the trial for patients with high BCL-3 expression.
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Drug Repositioning for the Treatment of Glioma: Current State ...
IntechOpen - Open Science Open Minds › books › drug-repositioni...
by S Tamai · 2020 — Large-scale clinical studies have been performed to investigate the ... Basic research with metformin in glioma cells and glioma stem-like cells (GSCs) has ... The group also showed that treatment with losartan inhibits tumor growth via the ...
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Int J Physiol Pathophysiol Pharmacol. 2017; 9(2): 8–15.
Lidocaine suppresses glioma cell proliferation by inhibiting TRPM7 channels
Tiandong Leng,1 Suizhen Lin,2 Zhigang Xiong,1 and Jun Lin3
Abstract
Background: Malignant glioma is the most common brain cancer with devastating prognosis. Recurrence of malignant glioma following surgery is very common with few preventive and therapeutic options. Novel targets and therapeutic agents are constantly sought for better outcome. Our previous study established that inhibition of transient receptor potential melastatin 7 (TRPM7) channels resulted in significant decrease of human glioma cell growth and proliferation. As local anesthetic lidocaine has been shown to inhibit TRPM7 currents, we hypothesize that lidocaine may suppress glioma cell proliferation through TRPM7 channel inhibition. Methods: TRPM7 currents were recorded in rat C6 glioma cells using the whole cell patch clamp technique. Cell growth and proliferation were assessed under microscopic examination and biochemical assays. Results: Lidocaine inhibits TRPM7-like currents in a dose-dependent and reversible manner. At 1 and 3 mM, it inhibits ~30% and ~50% of TRPM7 currents. At these concentrations, it is effective in inhibiting the proliferation of C6 cells. As expected, the TRPM7 inhibitors gadolinium and 2-Aminoethoxydiphenyl borate have similar effects on TRPM7 currents and proliferation of C6 cells. Similar to its effect on C6 cells, lidocaine inhibits the proliferation of A172 cells, a human glioblastoma cell line. Conclusions: Lidocaine significantly inhibits the proliferation of glioma cells. The effect of lidocaine is mediated, at least in part, by inhibiting TRPM7 channels.
Introduction
Malignant glioma is the most common primary brain tumor with devastating prognosis [1]. Maximal resection is essential for the treatment but surgery itself is a risk factor for recurrence [2]. Recurrence of malignant glioma following surgery is very high with few preventive and therapeutic options. One major advance over last two decades is the development of temozolomide that increased the survival time only by about 2.6 months after surgery when adding to radiotherapy [3,4]. Even so, around 70% malignant glioma is not responsive to temozolomide [5]. Therefore, it is hoped that potential new targets and drugs are able to reduce the growth and proliferation of glioma cells and increase the survival rate of cancer patients.
The melastatin-like transient receptor potential 7 (TRPM7) is a member of TRPM family mediating the entry of Ca2+ and Mg2+ [6]. High expression of TRPM7 has been found in a number of human cancer tissue and cell lines, including head and neck cancer, breast cancer, ovarian cancer, prostate cancer and pancreatic cancer [7-11]. TRPM7 plays an important role in maintaining the homeostasis of Ca2+ and Mg2+ in cancer cells regulating the cell function and cycle [12]. Thus it appears to be an attractive target to suppress the cancer cell proliferation and potentially reduce the recurrence of cancer. Our previous studies have demonstrated that TRPM7 play an important role in the proliferation, migration and invasion of human malignant glioma cells [13], suggesting that TRPM7 might serve as a promising target for malignant glioma treatment.
Lidocaine is a widely used local anesthetic that can be administered to local or regional tissue, epidural or intrathecal space to induce nerve conduction block. It has been shown that lidocaine is neuroprotective against ischemia [14] and Zn2+ induced neurotoxicity [15]. Lidocaine is the only local anesthetic that can be administered intravenously. Intravenous infusion of lidocaine has been found safe and effective in reducing postoperative ileus and pain following colon resection [16]. We have found that lidocaine inhibits TRPM7 currents in HEK293 cells and cultured neurons [15]. A safe and beneficial profile of lidocaine makes it attractive to test its potential effect on cancer cell biology. In the current study, we demonstrated that lidocaine inhibits the proliferation of malignant glioma cells at least in part, by inhibiting TRPM7 channel currents.
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https://www.nmu.edu/grantsandcontra...UserFiles/Pinskey_Excellence_in_Education.pdf
Home | Northern Michigan University › sites › files › UserFiles › P…. subpopulation of GBM cells known as brain tumor stem cells (BTSCs). Although ... Since TMZ affects the most rapidly dividing cells in the tumor and vitamin D targets. BTSCs ... In addition, this work constitutes a large part of my master's thesis."

 

[Riesensackteil]

Dear Dr Raymond Peat,

The caines like Lidocaine can reverse epigenetic changes/demethylate?
Could it possibly prevent reverse transcription of the mRNA when injected like Neural therapy (you have talked about)?

When I take a solution of lidocaine in an enteric capsule and it thus reaches the small intestine, would it have different effects, e.g. on SIBO?
Thanks

Ray: I had constantly bleeding colitis for more than a year, and when I took about 20 to 30 mg of lidocaine (in a 2% solution meant for oral, dental use) the symptoms stopped and haven’t returned in more than 30 years

 

[Beastmode]

The title of the thread was protective vs constructive:

ME:
What are the main determining factors when you know one is happening vs the other?

I ask this because I've been consistent with eating a more pro-metabolic approach over the past 4 years and so many improvements have occurred, yet they don't seem to translate in other areas that haven't.

RAY:
Sometimes deficiencies or imbalances remain, but sometimes it’s a matter of sensitivities that remain even after a deficiency has been corrected, and that take time to be corrected.

 

[metabolizm]

Q: How do you stay positive in the face of the widespread corruption, stupidity and malice that you have witnessed throughout your life?

A: There’s probably a biological tendency to shift attention away from evil toward pleasanter things, but I think it’s important not to indulge too much in positivity. Have you read or listened to Vernon Coleman, The Old Man in a Chair?

 

[Mauritio]

Q: I have tried corn tortillas from nixtamalized corn yesterday. For the first time. I ate like 5 or 6 of them and suffered with horrible stomach cramps after . Today I had a couple of bowel movements and feel surprisingly fine.
Now I'm not sure if I should continue eating them or not .
Maybe it was detox reaction ,maybe it doesnt agree with my body...
Do you have any insights on that or what I could do ?

A:It was probably just that your stomach didn’t expect it; they are more nutritious than things like bread and pasta."


Q: I've read from several people that theres supposedly all kind of mycotoxins a couple hours after the preparation of the nixtamalized corn tortillas .
Do you think that is concerning?

A: Only if you have moldy corn, and the alkali cooking removes much of that, which is drained off. Wheat flour is often contaminated with mycotoxins, so it would probably be good to nixtamalize wheat.

Toxins (Basel). 2019 Apr; 11(4): 227.
Mycotoxins during the Processes of Nixtamalization and Tortilla Production
Sara Schaarschmidt* and Carsten Fauhl-Hassek
Tortillas are a traditional staple food in Mesoamerican cuisine, which have also become popular on a global level, e.g., for wraps or as snacks (tortilla chips). Traditional tortilla production includes alkaline cooking (nixtamalization) of maize kernels. This article summarizes the current knowledge on mycotoxin changes during the nixtamalization of maize and tortilla production. Upon nixtamalization, mycotoxins can be affected in different ways. On the one hand, the toxins can be physically removed during steeping and washing. On the other hand, mycotoxins might be degraded, modified, or released/bound in the matrix by high pH and/or high temperature. This also applies to the subsequent baking of tortillas. Many studies have shown reduced mycotoxin levels in alkali-cooked maize and in tortillas. Most of the available data relate to aflatoxins and fumonisins. The reduction (and detoxification) of aflatoxins during nixtamalization might, however, be partially reversed in acidic conditions. The loss of fumonisin concentrations is to some extent accompanied by hydrolyzation and by lower toxicity. However, some studies have indicated the potential formation of toxicologically relevant modified forms and matrix-associated fumonisins. More data are required to assess the influence of alkaline cooking regarding such modified forms, as well as mycotoxins other than aflatoxins/fumonisin

 

[md_a]

 

[Vileplume]

About vaccine shedding, and the risk to those non-vaccinated:



Ray:
Our own DNA and RNA, proteins, exosomes, etc., are constantly being shed into our environment, so it seems extremely likely that any foreign DNA, RNA, and protein that’s in our blood will appear in our breath, sweat, urine, etc. Pfizer understood that, as indicated in this document. When people started worrying about it, a Pfizer representative said that the document doesn’t mean what it says.
Most people aren’t harmed by the corona virus, so the similar material coming from vaccinated people is likely to be equally harmless. The long range effects that might result from our incorporation of the gene that produces the spike protein would be likely to include inflammation, that would only become a serious problem when our resistance was lowered, by sickness or aging. Prolonged inflammation is carcinogenic, and our ACE2 enzyme (which is inactivated by the spike protein), is one of our protective anti-cancer factors (articles below).
Ideally, vaccinated people would be quarantined until they could show that they weren’t shedding the harmful material, but the govenments aren’t behaving rationally.


https://media.tghn.org/medialibrary/2020/11/C4591001_Clinical_Protocol_Nov2020_Pfizer_BioNTech.pdf
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
A PHASE 1/2/3, PLACEBO-CONTROLLED, RANDOMIZED, OBSERVER-BLIND, DOSE-FINDING STUDY TO EVALUATE THE SAFETY, TOLERABILITY, IMMUNOGENICITY, AND EFFICACY OF SARS-COV-2 RNA VACCINE CANDIDATES AGAINST COVID-19 IN HEALTHY INDIVIDUALS

Study Sponsor:
Study Conducted By:
Study Intervention Number:
Study Intervention Name:
US IND Number:
EudraCT Number:
Protocol Number:
BioNTech
Pfizer
PF-07302048
RNA-Based COVID-19 Vaccines 19736
2020-002641-42 C4591001
1/2/3
Phase:
Short Title: A Phase 1/2/3 Study to Evaluate the Safety, Tolerability, Immunogenicity, and
Efficacy of RNA Vaccine Candidates Against COVID-19 in Healthy Individuals


=============

(page 67, …)

8.3.5. Exposure During Pregnancy or Breastfeeding, and Occupational Exposure
Exposure to the study intervention under study during pregnancy or breastfeeding and occupational exposure are reportable to Pfizer Safety within 24 hours of investigator awareness.
8.3.5.1. Exposure During Pregnancy
An EDP occurs if:

• A female participant is found to be pregnant while receiving or after discontinuing study intervention.
• A male participant who is receiving or has discontinued study intervention exposes a female partner prior to or around the time of conception.
• A female is found to be pregnant while being exposed or having been exposed to study intervention due to environmental exposure. Below are examples of environmental exposure during pregnancy:

• A female family member or healthcare provider reports that she is pregnant after having been exposed to the study intervention by inhalation or skin contact.
Page 67
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
• A male family member or healthcare provider who has been exposed to the study intervention by inhalation or skin contact then exposes his female partner prior to or around the time of conception.
The investigator must report EDP to Pfizer Safety within 24 hours of the investigator’s awareness, irrespective of whether an SAE has occurred. The initial information submitted should include the anticipated date of delivery (see below for information related to termination of pregnancy).

• If EDP occurs in a participant or a participant’s partner, the investigator must report this information to Pfizer Safety on the Vaccine SAE Report Form and an EDP Supplemental Form, regardless of whether an SAE has occurred. Details of the pregnancy will be collected after the start of study intervention and until 6 months after the last dose of study intervention.
• If EDP occurs in the setting of environmental exposure, the investigator must report information to Pfizer Safety using the Vaccine SAE Report Form and EDP Supplemental Form. Since the exposure information does not pertain to the participant enrolled in the study, the information is not recorded on a CRF; however, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
  Follow-up is conducted to obtain general information on the pregnancy and its outcome for all EDP reports with an unknown outcome. The investigator will follow the pregnancy until completion (or until pregnancy termination) and notify Pfizer Safety of the outcome as a follow-up to the initial EDP Supplemental Form. In the case of a live birth, the structural integrity of the neonate can be assessed at the time of birth. In the event of a termination, the reason(s) for termination should be specified and, if clinically possible, the structural integrity of the terminated fetus should be assessed by gross visual inspection (unless preprocedure test findings are conclusive for a congenital anomaly and the findings are reported).
  Abnormal pregnancy outcomes are considered SAEs. If the outcome of the pregnancy meets the criteria for an SAE (ie, ectopic pregnancy, spontaneous abortion, intrauterine fetal demise, neonatal death, or congenital anomaly), the investigator should follow the procedures for reporting SAEs. Additional information about pregnancy outcomes that are reported to Pfizer Safety as SAEs follows:
• Spontaneous abortion including miscarriage and missed abortion;
• Neonatal deaths that occur within 1 month of birth should be reported, without regard to causality, as SAEs. In addition, infant deaths after 1 month should be reported as SAEs when the investigator assesses the infant death as related or possibly related to exposure to the study intervention.

Page 68
PF-07302048 (BNT162 RNA-Based COVID-19 Vaccines) Protocol C4591001
Additional information regarding the EDP may be requested by the sponsor. Further follow-up of birth outcomes will be handled on a case-by-case basis (eg, follow-up on preterm infants to identify developmental delays). In the case of paternal exposure, the investigator will provide the participant with the Pregnant Partner Release of Information Form to deliver to his partner. The investigator must document in the source documents that the participant was given the Pregnant Partner Release of Information Form to provide to his partner.
8.3.5.2. Exposure During Breastfeeding
An exposure during breastfeeding occurs if:

• A female participant is found to be breastfeeding while receiving or after discontinuing study intervention.
• A female is found to be breastfeeding while being exposed or having been exposed to study intervention (ie, environmental exposure). An example of environmental exposure during breastfeeding is a female family member or healthcare provider who reports that she is breastfeeding after having been exposed to the study intervention by inhalation or skin contact.
  The investigator must report exposure during breastfeeding to Pfizer Safety within 24 hours of the investigator’s awareness, irrespective of whether an SAE has occurred. The information must be reported using the Vaccine SAE Report Form. When exposure during breastfeeding occurs in the setting of environmental exposure, the exposure information does not pertain to the participant enrolled in the study, so the information is not recorded on a CRF. However, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.
  An exposure during breastfeeding report is not created when a Pfizer drug specifically approved for use in breastfeeding women (eg, vitamins) is administered in accord with authorized use. However, if the infant experiences an SAE associated with such a drug, the SAE is reported together with the exposure during breastfeeding.
  8.3.5.3. Occupational Exposure
  An occupational exposure occurs when a person receives unplanned direct contact with the study intervention, which may or may not lead to the occurrence of an AE. Such persons may include healthcare providers, family members, and other roles that are involved in the trial participant’s care.
  The investigator must report occupational exposure to Pfizer Safety within 24 hours of the investigator’s awareness, regardless of whether there is an associated SAE. The information must be reported using the Vaccine SAE Report Form. Since the information does not pertain to a participant enrolled in the study, the information is not recorded on a CRF; however, a copy of the completed Vaccine SAE Report Form is maintained in the investigator site file.

Page 69

==============================

SARS-CoV-2 RNA reverse-transcribed and integrated into the human genome
Liguo Zhang, Alexsia Richards, Andrew Khalil, Emile Wogram, Haiting Ma, Richard A Young, Rudolf Jaenisch
Abstract
Prolonged SARS-CoV-2 RNA shedding and recurrence of PCR-positive tests have been widely reported in patients after recovery, yet these patients most commonly are non-infectious. Here we investigated the possibility that SARS-CoV-2 RNAs can be reverse-transcribed and integrated into the human genome and that transcription of the integrated sequences might account for PCR-positive tests. In support of this hypothesis, we found chimeric transcripts consisting of viral fused to cellular sequences in published data sets of SARS-CoV-2 infected cultured cells and primary cells of patients, consistent with the transcription of viral sequences integrated into the genome. To experimentally corroborate the possibility of viral retro-integration, we describe evidence that SARS-CoV-2 RNAs can be reverse transcribed in human cells by reverse transcriptase (RT) from LINE-1 elements or by HIV-1 RT, and that these DNA sequences can be integrated into the cell genome and subsequently be transcribed. Human endogenous LINE-1 expression was induced upon SARS-CoV-2 infection or by cytokine exposure in cultured cells, suggesting a molecular mechanism for SARS-CoV-2 retro-integration in patients. This novel feature of SARS-CoV-2 infection may explain why patients can continue to produce viral RNA after recovery and suggests a new aspect of RNA virus replication.

from Wikipedia:
In cellular life
Self-replicating stretches of eukaryotic genomes known as retrotransposons utilize reverse transcriptase to move from one position in the genome to another via an RNA intermediate. They are found abundantly in the genomes of plants and animals. Telomerase is another reverse transcriptase found in many eukaryotes, including humans, which carries its own RNA template; this RNA is used as a template for DNA replication.[15]
Initial reports of reverse transcriptase in prokaryotes came as far back as 1971 in France (Beljanski et al., 1971a, 1972) and a few years later in the USSR (Romashchenko 1977[16]). These have since been broadly described as part of bacterial Retrons, distinct sequences that code for reverse transcriptase, and are used in the synthesis of msDNA. In order to initiate synthesis of DNA, a primer is needed. In bacteria, the primer is synthesized during replication.[17]
Valerian Dolja of Oregon State argues that viruses, due to their diversity, have played an evolutionary role in the development of cellular life, with reverse transcriptase playing a central role.[18]


1
Oncol Rep. 2011 Nov;26(5):1157-64.
Overexpression of ACE2 produces antitumor effects via inhibition of angiogenesis and tumor cell invasion in vivo and in vitro
Yun Feng 1 , Lei Ni, Huanying Wan, Liang Fan, Xiaochun Fei, Qinyun Ma, Beili Gao, Yi Xiang, Jiaming Che, Qingyun Li
Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. The role of AngII and ACE2 in the metastasis of non-small cell lung cancer (NSCLC) and the effects on matrix metalloproteinases (MMPs) are still unknown. In the present study, the anti-invasive effect and mechanism of ACE2 were investigated in vitro and in vivo. Results of a transwell assay showed that the overexpression of ACE2 reduces the invasive ability of A549 cells in vitro. According to the results of qRT-PCR and western blot analysis, the inhibitory role of ACE2 was mediated through the down-regulation of MMP-2 and MMP-9. Additionally, we confirmed that the overexpression of ACE2 inhibited cell growth and VEGFa production while simultaneously suppressing ACE and angiotensin II type 1 receptor (AT1R) expression in human lung cancer xenografts. These results suggest that the overexpression of ACE2 may potentially suppress the invasion and angiogenesis of NSCLC.

2
J Exp Clin Cancer Res. 2019 Apr 25;38(1):173.
ACE2 inhibits breast cancer angiogenesis via suppressing the VEGFa/VEGFR2/ERK pathway
Qi Zhang 1 2 , Sihong Lu 1 3 , Tianfu Li 1 , Liang Yu 1 , Yunjian Zhang 1 , Huijuan Zeng 1 , Xueke Qian 4 , Jiong Bi 5 , Ying Lin 6
Free PMC article
Abstract
Background: Breast cancer angiogenesis is key for metastasis and predicts a poor prognosis. Angiotensin-converting enzyme 2 (ACE2), as a member of the renin-angiotensin system (RAS), was reported to restrain the progression of hepatocellular carcinoma (HCC) and non-small cell lung cancer (NSCLC) through inhibiting angiogenesis. However, the relationship between ACE2 and breast cancer angiogenesis remains unclear.
Methods: The prognosis and relative gene selection were analysed using the GEPIA, GEO, TCGA and STRING databases. ACE2 expression in breast cancer tissue was estimated by reverse transcription-quantitative polymerase chain reaction (qPCR). Breast cancer cell migration, proliferation and angiogenesis were assessed by Transwell migration, proliferation, tube formation, and wound healing assays. The expression of vascular endothelial growth factor A (VEGFa) was detected by qPCR and Western blotting. The phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR2), mitogen-activated protein kinase 1/2 (MEK1/2), and extracellular signal-regulated protein kinase 1/2 (ERK1/2) was examined by Western blotting. Breast cancer metastasis and angiogenesis in vivo were measured using a zebrafish model.
Results: ACE2 was downregulated in breast cancer patients. Patients with higher ACE2 expression had longer relapse-free survival (RFS). In vitro, ACE2 inhibited breast cancer migration. Meanwhile, ACE2 in breast cancer cells inhibited human umbilical vascular endothelial cell (HUVEC) proliferation, tube formation and migration. In the zebrafish model, ACE2 inhibited breast cancer cell metastasis, as demonstrated by analyses of the number of disseminated foci and the metastatic distance. Neo-angiogenesis was also decreased by ACE2. ACE2 downregulated the expression of VEGFa in breast cancer cells. Furthermore, ACE2 in breast cancer cells inactivated the phosphorylation of VEGFR2, MEK1/2, and ERK1/2 in HUVECs.
Conclusions: Our findings suggest that ACE2, as a potential resister to breast cancer, might inhibit breast cancer angiogenesis through the VEGFa/VEGFR2/ERK pathway.
Trial registration: Retrospectively registered.
Keywords: ACE2; Angiogenesis; Breast cancer; ERK; VEGFR2; VEGFa.
Conflict of interest statement
Ethics approval and consent to participate
Approval and consent obtained for the use of human tissue were obtained from the Institutional Research Ethics Committee of the First Affiliated Hospital of Sun Yat-sen University.
Approval for all the zebrafish experiments was obtained from Sun Yat-sen University Animal Care and Use Committee of the Zebrafish Model Animal Facility, Institute of Clinical and Translational Research, Sun Yat-sen University.

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Tohoku J Exp Med. 2009 Feb;217(2):123-31.
Decreased expression of angiotensin-converting enzyme 2 in pancreatic ductal adenocarcinoma is associated with tumor progression
Lin Zhou 1 , Ruifeng Zhang, Weiyan Yao, Jiancheng Wang, Aihua Qian, Minmin Qiao, Yongping Zhang, Yaozong Yuan
Free article
Angiotensin II (ANG II), the biologically active peptide of the renin-angiotensin system (RAS), is generated by angiotensin-converting enzyme (ACE) and is a regulator of cardiovascular homeostasis. Recently, there has been increasing evidence that ANG II is involved in the regulation of cell proliferation and migration, as well as angiogenesis via the ANG II-type 1 receptor (AT1R). These findings suggest that the ACE-ANG II-AT1R pathway is related to cancer biology. Previous reports have shown that ACE is preferentially expressed in pancreatic ductal adenocarcinoma (PDAC) tissues. Recently a homologue of ACE, angiotensin-converting enzyme 2 (ACE2), was reported to counterbalance the function of ACE, but the expression and role of ACE2 in PDAC are still unclear. In the present study, we analyzed the expression of ACE2 in invasive human PDAC and surrounding non-malignant tissues by Western blot analysis and immunohistochemistry. The ANG II concentration in homogenates of pancreatic tissues was measured with ELISA, and ACE2 protein was detected by Western blot analysis in BxPC3 and SW1990 human pancreatic ductal cancer cells. We have shown for the first time that the expression of ACE2 is decreased in PDAC tissues, in which ANG II was accumulated. Treatment of BxPC3 and SW1990 cells with ANG II decreased the expression of ACE2. Therefore, ANG II may contribute to the down-regulation of ACE2. Moreover, reduction of ACE2 expression by RNA interference promoted the proliferation of cultured pancreatic cancer cells. These findings suggest that ACE2 may have clinical potential as a novel molecular target for the treatment of PDAC.

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Oncol Rep. 2010 Apr;23(4):941-8.
The angiotensin-converting enzyme 2 in tumor growth and tumor-associated angiogenesis in non-small cell lung cancer
Yun Feng 1 , Huanying Wan, Jialin Liu, Ruifeng Zhang, Qinyun Ma, Bing Han, Yi Xiang, Jiaming Che, Huangming Cao, Xiaochun Fei, Weicheng Qiu
Angiotensin II (AngII) is a multifunctional bioactive peptide and previous studies have shown that the renin-angiotensin system (RAS) of both host and tumor are important in tumor growth and angiogenesis in lung cancer. Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS, with 42% amino acid homology to ACE. However, the expression and function of ACE2 in non-small cell lung cancer (NSCLC) are still unclear. In the present study, we analyzed ACE2 expression in NSCLC tissue by Western blot analysis and immunohistochemistry. AngII concentrations in the tissue homogenate were also detected using radio-immunoassay. We also examined the function of ACE2 by transducing A549 cells with MSCV-ACE2. We have shown for the first time that ACE2 expression decreased in NSCLC tissue in which AngII was higher than the matching non-malignant tissues. A concentration of 10(-6) mol/l of AngII significantly increased expression of vascular endothelial growth factor a (VEGFa) and AT1-R and decreased ACE2 expression. We also found that overexpression of ACE2 may have a protective effect by inhibiting cell growth and VEGFa production in vitro. ACE2 may become a target of novel strategies to treat NSCLC.
Cited by 33 articles

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Oncol Rep. 2016 Sep;36(3):1403-10.
ACE2 overexpression inhibits acquired platinum resistance-induced tumor angiogenesis in NSCLC
Qijian Cheng 1 , Ling Zhou 1 , Jianping Zhou 1 , Huanying Wan 1 , Qingyun Li 1 , Yun Feng 1
Angiotensin II (AngII) is a multifunctional bioactive peptide in the renin-angiotensin system (RAS). Angiotensin-converting enzyme 2 (ACE2) is a newly identified component of RAS. We previously reported that ACE2 overexpression may inhibit cell growth and vascular endothelial growth factor (VEGF) production in vitro and in vivo. In the present study, we investigated the effect of ACE2 on tumor-associated angiogen-esis after the development of acquired platinum resistance in non-small cell lung cancer (NSCLC). Four NSCLC cell lines, A549, LLC, A549-DDP and LLC-DDP, were used in vitro, while A549 and A549-DDP cells were used in vivo. A549-DDP and LLC-DDP cells were newly established at our institution as acquired platinum-resistant sublines by culturing the former parent cells in cisplatin (CDDP)-containing conditioned medium for 6 months. These platinum-resistant cells showed significantly higher angiotensin II type 1 receptor (AT1R), ACE and VEGF production and lower ACE2 expression than their corresponding parent cells. We showed that ACE2 overexpression inhibited the production of VEGF in vitro and in vivo compared to their corresponding parent cells. We also found that ACE2 overexpression reduced the expression of AT1R and ACE. Additionally, we confirmed that ACE2 overexpres-sion inhibited cell growth and VEGF production while simultaneously suppressing ACE and AT1R expression in human lung cancer xenografts. Our findings indicate that ACE2 overexpression may potentially suppress angiogenesis in NSCLC after the development of acquired platinum resistance.

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Oncol Rep. 2013 Jun;29(6):2408-14.
doi: 10.3892/or.2013.2370. Epub 2013 Mar 29.
Angiotensin-converting enzyme 2 attenuates the metastasis of non-small cell lung cancer through inhibition of epithelial-mesenchymal transition
Yan-Rong Qian 1 , Yi Guo, Huan-Ying Wan, Liang Fan, Yun Feng, Lei Ni, Yi Xiang, Qing-Yun Li
Angiotensin-converting enzyme 2 (ACE2) is a key enzyme of the renin-angiotensin system (RAS). ACE2 plays a critical counterbalancing role by degrading angiotensin II (Ang II) to Ang 1-7. Recent studies suggest that RAS influences tumor growth and development by its paracrine effects on the tumor microenvironment. Epithelial‑mesenchymal transition (EMT) is now thought to be a process that plays a fundamental role in tumor progression and metastasis. In the present study, we investigated the role of ACE2 in lung cancer metastasis and the mechanism of EMT. This is the first study to elucidate the mechanism through which the overexpression of ACE2 in the A549 lung cancer cell line decreases metastasis formation in vivo and upregulates the expression of E-cadherin both in vitro and in vivo. We also observed the downregulation of vimentin, which supports a role of ACE2 in influencing EMT in lung cancer. Further analysis indicated that ACE2 abrogated the upregulation of TGF-β1-induced EMT markers, such as vimentin and α-smooth muscle actin (αSMA) in vitro in A549 cells. Finally, exposing A549 cells stably expressing ACE2 to DX600, an inhibitor of ACE2, recovered the sensitivity of lung cancer cells to TGF-β1-mediated induction of EMT. Our study demonstrated that ACE2 attenuated the metastasis of lung cancer and may serve as a target for new strategies to inhibit EMT in cancer cells.

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Comparative Study
Lab Invest. 2007 Feb;87(2):189-98.
Roles for host and tumor angiotensin II type 1 receptor in tumor growth and tumor-associated angiogenesis
Nozomi Imai 1 , Tatsuo Hashimoto, Minoru Kihara, Shin-ichiro Yoshida, Ichiro Kawana, Takuya Yazawa, Hitoshi Kitamura, Satoshi Umemura
Angiotensin II (AII) is a multifunctional bioactive peptide, and host renin-angiotensin system (RAS) is closely associated with tumor growth. Recent reports have described that AII is a proangiogenic growth factor, and that Angiotensin II type 1 (AT1) receptor antagonists reduce tumor growth and tumor-associated angiogenesis. In this paper, we investigated the participation of AT1 receptor-signaling in cancer progression using murine Lewis lung carcinoma (LLC) cells, which express AT1 receptor, and AT1a receptor gene-deficient (AT1a-/-) mice. When LLC cells were implanted subcutaneously into wild-type (WT) mice, developed tumors showed intensive angiogenesis with an induction of vascular endothelial growth factor (VEGF) a. Compared with WT mice, tumor growth and tumor-associated angiogenesis was reduced in AT1a-/- mice with reduced expression of VEGFa. In AT1a-/- mice, administration of the AT1 receptor antagonist, TCV-116, showed further reductions of tumor growth, tumor-associated angiogenesis, and VEGFa expression. In vitro study, the expression of VEGFa mRNA and the production of VEGFa protein in LLC cells were significantly increased by AII, which were cancelled by AT1 receptor antagonist, CV-11974. Although the expression of other angiogenic factors, such as angiopoietin-1, angiopoietin-2, epidermal growth factor, and VEGF receptor 2 mRNA, was also investigated in tumor tissues, the expression of VEGFa was most correlated with tumor size among those other angiogenic factors. VEGFa induction by AT1 receptor-signaling in both host and tumor tissues is one of key regulators of tumor growth and tumor-associated angiogenesis. In conclusion, tumor tissue RAS as well as host tissue RAS were found to have an important role in tumor growth. AT1 receptor-signaling blockade may be a novel and effective target in the treatment of cancer.

SARS-CoV-2 RNA can be reverse-transcribed to be part of chimeric viral-human genome

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CDC: 4,178 Americans DEAD Following Experimental COVID Injections – Deaths from COVID Shots now Equal 20 Years of Recorded Deaths Following Vaccines Since 2001


View: https://rumble.com/vgerov-dr.-sucharit-bhakdi-warns-covid-shots-to-decimate-world-population.html


New Report sheds light on Vaccine Doomsday Cult


View: https://www.bitchute.com/video/cdKu2RXGAWyu/



View: https://www.bitchute.com/video/ecOpzGNqNbgZ/

 

[Mauritio]

If one had to get one of the vaccines ...

Q: If one and had to take one of the vaccines, which is the least harmful? My guess : Sputnik or AstraZeneca?

A:
I think both of those include the code for the spike protein, which is the unpredictably dangerous component. As I understand it, Sinovac induces antibodies to the viral substance, in the traditional vaccine manner. This suggests that it is what has always been meant by “vaccine,” while the others are something other than vaccines—gene therapy is a more accurate term. I think people should assimilate the messages of Reiner Fuellmich and Michael Yeadon, at least, before making decisions.

How does the Sinovac vaccine work?​

The Beijing-based biopharmaceutical company Sinovac is behind the CoronaVac, an inactivated vaccine.
It works by using killed viral particles to expose the body's immune system to the virus without risking a serious disease response.
By comparison the Moderna and Pfizer vaccines being developed in the West are mRNA vaccines. This means part of the coronavirus' genetic code is injected into the body, triggering the body to begin making viral proteins, but not the whole virus, which is enough to train the immune system to attack.
"CoronaVac is a more traditional method [of vaccine] that is successfully used in many well known vaccines like rabies," Associate Prof Luo Dahai of the Nanyang Technological University told the BBC.

"mRNA vaccines are a new type of vaccine and there is [currently] no successful example [of them] being used in the population," Prof Luo adds.