p53

How the usual protection from p53 is being compromised

p53

The vast majority of people have never heard of p53 and may be forgiven for mistaking it for one of the next forms you receive after your P45!! p53 just so happens to be a hugely important protein that helps cellular regulation across a wide range of functions.  Mutation of the gene that codes for p53, called TP53, is the most commonly found gene mutation in people suffering with Cancer.  It is not surprising given the functionality of p53.

p53 plays a key role in the regulation or progression through the cell cycle, apoptosis (programmed cell death) and genomic stability by means of several mechanisms. For these reasons it has become known as the “Guardian of the Genome”.

When DNA damage is detected, p53 can pause cell growth and division in order to activate DNA repair proteins.  If p53 can pause the cell cycle sufficiently long for the DNA repair proteins to fix the damage, the cell is allowed to continue the cell cycle. If repair is not made good in this time, the damage is irreparable and p53 initiates apoptosis. This is the basis for p53’s anti-cancer protective role.

As our cells age, the end sections of the DNA (the telomeres) shorten.  At a certain shortening of the telomeres, p53 triggers the senescence response, which means that cell division is slowed down and eventually triggers apoptosis.  This ensures that older cells which are then more likely to become mutated and cancerous are slowed down and strategically removed, hopefully before disease results. In this way, and by maintaining stem cells, p53 clearly plays an important factor in aging too.

p53 counters Reactive Oxygen Species (ROS) inflammation and is triggered by inflammation itself. The balance between inflammation and p53 is crucial in determining the health of our body systems. Chronic inflammation is at the root of all degenerative diseases. Disruption of p53 can therefore lead to a wide range of diseases being allowed to develop.

Without going into every aspect of p53 in detail which would require a thesis, it has a role in controlling inflammatory diseases, normal development, reducing atherosclerosis and is a factor in neurodegenerative disorders. In the latter, controlling inflammation can reduce neurodegeneration, but localised p53 overactivation, as can happen in Alzheimer’s Disease, can also contribute to neurodegeneration too. As with everything, balance is the key.

So why have I brought this up now? Well, it turns out that both the spike protein from SARS-CoV2 and the jabs, and EMFs can adversely impact p53, resulting in increased inflammation, tissue damage, and increased cancers. As the US Forces Dr reported in the video I included on a recent blog, there have been reports of increased cancer in younger people after they’ve had their COVID jabs….

SARS-CoV2

Increased p53 activity reduces the possibility of cell proliferation and differentiation, which hinders lung epithelial reparation, and repair to other injured tissues as well.  This, in turn, increases inflammation, leads to dysfunction of the corresponding organs and predetermines further development of fibrosis. Increased p53 activity can also enhance apoptosis, not only of the virus-infected cells, but also collateral damage to adjacent, accidentally and prematurely  terminated cells, which additionally increases overall tissue injury.

Singh and Singh found that the S2 subunit of SARS-CoV2 spike protein strongly interacts with p53 and BRCA-1/2 proteins. p53 and BRCA proteins are the well-known tumour suppressor proteins, that regulate downstream genes in response to numerous cellular stresses and are frequently mutated in human cancer.

The SARS-CoV2 spike protein causes extreme upregulation of MDM2, a protein which degrades p53. This means that rather than induce apoptosis of cells towards the end of their life they become senescent, and in vascular endothelial cells (blood vessel lining cells) this sets them up to cause vasculopathy and resultant clotting.  Cells that hang around longer than they otherwise would have done are more at risk of becoming cancerous.

Another non-structural protein of SARS-CoV2, nsp3 protein, targets p53 for degradation. p53 may operate as an intracellular antiviral defence mechanism. To circumvent it, SARS viruses adopt a strategy shared by several other viruses with transforming potential. With the reduction of p53 activity as a result of SARS infections and nsp3 activity, this reduces resistance to the spread of infection. With reduced p53 there is also greater potential for cells to become more vulnerable to oncogenic DNA damage. Pre-existing cancer is a known increased risk factor for SARS-CoV2 infection because by virtue of having cancer we know that their p53 is likely to be lowered which reduces viral resistance.

EMFs

Research has determined that DNA damage by EMFs will trigger p53 activation after relatively short exposure times to artificial EMFs. In the past, when artificial EMFs were at a low level, p53 was much more able to cope. In 2016, Prof Johannson of the Karolinka Institute in Sweden stated that the level of artificial EMFs is one quintillion (1018) times higher than the unmodulated artificial EMFs we evolved to live in.  Modulations such as polarisation and digitalisation have made it impossible for our bodies to cope with the artificial EMFs. 5 years later, we are exposed to even more, but nowhere like the amount of EMFs that are planned.

However, p53 is a good example of why biology is not linear and is far more complex than it is often made out to be for the purposes of official safety regulations. It isn’t as simple as saying that EMFs up to a certain power or frequency are safe, and those above are harmful, which defines simple safety thresholds for power and frequency. The frequency is important because if it resonates with a certain ion, ion channel, protein etc within the cells then cellular functions involving those ions/proteins will be altered. When such resonant frequencies are present (as many are within the electrosmog we are engulfed by), damage can occur at very much lower power levels. It means that there are windows of safe and harmful frequencies all mixed up together. Even though p53 will be triggered in response to certain frequencies of EMF it still has its own power threshold, below which it will not be triggered. but because certain EMFs we commonly experience are resonant with ions such as Calcium or Magnesium for example, and their ion channels, these frequencies of sub-threshold power are still capable of causing significant damage over time. In other words, very low power EMFs at specific resonant frequencies can lead to just as much harm as higher power EMFs that overwhelm the ability of p53 to protect the cells.

EMFs and SARS-CoV2 together

UK Cities have tended to get the worst of all factors during the recent Plandamic, hence supposedly the worst stats, although we know all stats this Government publish have questionable reliability. They frequently have communities of people of ethnic origins that have a higher incidence of Vitamin D deficiency that is necessary for a strong immune system. People in cities tend to live much closer together which facilitates transmission of infection. Cities also have higher availability of fast food outlets that increase inflammation and lower health.  Cities have historically had a much higher level of EMFs because all the Telecoms companies provide overlapping coverage as they vie for the most contracts in the highest densities of the population. Cities also have many overlapping WiFi zones, especially in living accommodation tower blocks where every flat his its’ own WiFi, and office buildings that host multiple small businesses that each have their own WiFi too. On top of this established electrosmog, cities have also been the first places to adopt the new 5G.  5G isn’t just another layer of EMFs, but promises to be a considerable increase (if not a multiplier) on what we had before. Cities have also been the first centres where the COVID jabs have been rolled out because it is easier to jab more people in a shorter length of time.

Putting all these factors together, city people who start with a lowered Vitamin D and immune status are exposed to the highest density of SARS-CoV2 and spike protein from infectious people, jabs and those who have been jabbed.  This, in an environment with the highest exposure to EMFs from currently existing WiFi and 2-4G, and now the new 5G is an incredible assault on peoples’ p53 cellular protection.

The incidence of Cancer has been rising steadily for years already, but it is unfortunately no surprise to me that the rate of increase is now seemingly rising too, and are being reported in higher than normal numbers in those who have been jabbed. Given that the WEF have chosen Belfast, Leeds and London as 3 of their 22 global smart cities, I wonder how many more issues with p53 suppression/avoidance at their root will spike at those locations? Other cities are of course increasing 5G too, so maybe the increases will be countrywide across many more cities.

Solutions

I always like to try and finish my blogs on a positive. Clearly, we need to ensure that our p53 system receives the least unnecessary interference, and is allowed to do what it is supposed to.

Keeping our immune system strong will not only help protect us against SARS-CoV2 but other infections that can adversely impact p53 (and us!) too. Natural immunity is always stronger than from acquired immunity from vaccines/jabs. Maintain your immune system with daily supplements of Vitamins D3 (5-10,000iu), C (1-2g), Zinc etc and healthy interactions with our environment and other people – ie no masks. Failure to do this over the Plandemic has caused a big rise in hospitalisations of children with RSV, and no doubt other infections too.  As Dr Zach Bush tells us, we ignore our biome health at our peril, and it requires close interactions with our environment to stay healthy. There are other supplements that people commonly take too such as Echinacea, propolis tincture and others. Do whatever you find works for you, including a healthy diet and lifestyle too of course.

CMO devices from Comosystems are the best researched technology I have come across since I first became interested in EMFs, which is why I agreed to become their official distributor for the UK and Ireland. You can find more information on our UK website here. Those who are interested in buying from countries outside the UK and Ireland will need to order via Comosystems own international website here.  CMO technology doesn’t interfere with the EMFs themselves but works by stabilising the cellular processes that the artificial EMFs disrupt, such as the voltage-gated Calcium channels. They mitigate for all the adverse EMFs that invisibly surround and bombard us.

Prevention is always better than cure, and forewarned is forearmed. P53 is too important a system that protects us to wait until you find out that it is no longer coping. I can’t claim that my suggestions are all-encompassing and all-protective against all p53 disruption, but we can only deal with the known ones as we become aware of them, and give our p53 the best chance of protecting us as it used to before high levels of EMFs and bioweapon attacks.

References

Singh, Nishant & Singh, Anuradha. (2020). S2 subunit of SARS-nCoV-2 interacts with tumor suppressor protein p53 and BRCA: an in silico study. Translational Oncology. 13. 100814. 10.1016/j.tranon.2020.100814.

Cardozo C.M., Hainaut P. Viral Strategies for Circumventing P53: The Case of Severe Acute Respiratory Syndrome Coronavirus. Curr. Opin. Oncol. 2021;33:149–158.

Yuyang Lei, Jiao Zhang, Cara R. Schiavon, Ming He, Lili Chen, Hui Shen, Yichi Zhang, Qian Yin, Yoshitake Cho, Leonardo Andrade, Gerald S. Shadel, Mark Hepokoski, Ting Lei, Hongliang Wang, Jin Zhang, Jason X.-J. Yuan, Atul Malhotra, Uri Manor, Shengpeng Wang, Zu-Yi Yuan, John Y-J. Shyy. SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE 2. Originally published 31 Mar 2021 https://doi.org/10.1161/CIRCRESAHA.121.318902 Circulation Research. 2021;128:1323–1326

Jun Chen and Michael S. Goligorsky. Premature senescence of endothelial cells: Methusaleh's dilemma. American Journal of Physiology-Heart and Circulatory Physiology 2006 290:5, H1729-H1739

Marinelli F, La Sala D, Cicciotti G, Cattini L, Trimarchi C, Putti S, Zamparelli A, Giuliani L, Tomassetti G, Cinti C. Exposure to 900 MHz electromagnetic field induces an unbalance between pro-apoptotic and pro-survival signals in T-lymphoblastoid leukemia CCRF-CEM cells. J Cell Physiol. 2004 Feb;198(2):324-32. doi: 10.1002/jcp.10425. Erratum in: J Cell Physiol. 2004 Mar;198(3):479-80. PMID: 14603534.

Solek, Przemyslaw & Majchrowicz, Lena & Bloniarz, Dominika & Krotoszynska, Ewelina & Koziorowski, Marek. (2017). Pulsed or continuous electromagnetic field induce p53/p21-mediated apoptotic signalling pathway in mouse spermatogenic cells in vitro and thus may affect male fertility. Toxicology. 382. 10.1016/j.tox.2017.03.015.

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