Turbo Cancers Explained

As well as the general rise in new cancers since 2021.

As turbo cancer is not a thing, despite of what Dr McCullough says

, so isn’t any rise in cancer cases and deaths in general, according to Wikipedia, notwithstanding this graph from The Ethical Sceptic for the USA (which is not even the worst-jabbed country in the Western world):

In the video above, Dr. McCullough lists three reasons for the high oncogenicity of mRNA jabs:

1. The mRNA in mRNA jabs impairs cellular DNA repair.

2. The S2 segment of the S spike protein inhibits P53 and DRCA tumor suppressor systems in the cells (“S2 Subunit of SARS-nCoV-2 Interacts with Tumor Suppressor Protein p53 and BRCA: an In Silico Study”, 2020.05.13).

3. DNA plasmid contamination in Moderna and Pfizer mRNA jabs (e.g., “Sequencing of bivalent Moderna and Pfizer mRNA vaccines reveals nanogram to microgram quantities of expression vector dsDNA per dose”, Apr. 2023), as well as SV40 enhancer, promoter, and origin of replication sequences. The repercussions of the latter are manyfold:

   A recent preprint links SV40 enhancer to cancer but more importantly, to AID and somatic hypermutation

Let me now throw in another mechanism of the mRNA jab oncogenicity that may be responsible, bigly, for the turbo part (which doesn’t exist, of course), and also for the non-turbo part. Namely, the damage to cell mitochondria caused by the ill-famous S spike, churned out by the transcription of mRNA contained in the Covid jabs, for many months following the jabbination, to the tune of at least 10-30 time more than in the course of a severe SARS-CoV-2 infection. After two weeks post jabbination, as has been shown in “What If S Spike-Targeting Jabs Never Worked, Like At All?“, the S spikes are being actively expelled from the transfected cells via exosomes, to carry said S spike proteins all around the body, affecting any organ they can reach, for months on end.

This study (“Mitochondrial Dynamics in SARS-COV2 Spike Protein Treated Human Microglia: Implications for Neuro-COVID”, Journal of Neuroimmune Pharmacology, 2021.08.19) sheds light on the effect of S spikes on mitochondria:

We hypothesize that SAR-COV2 induces mitochondrial dysfunction and activation of the mitochondrial-dependent intrinsic apoptotic pathway, resulting in microglial and neuronal apoptosis.

We treated human microglia with SARS-COV2 spike protein and examined the levels of cytokines and reactive oxygen species (ROS) production, determined the efect of SARS-COV2 on mitochondrial bio- genesis and examined the changes in molecular composition of phospholipids. Our results show that SARS- COV2 spike protein increases the levels of pro-infammatory cytokines and ROS production, increases apoptosis and increases the oxygen consumption rate (OCR) in microglial cells. Increases in OCR are indicative of increased ROS production and oxidative stress suggesting that SARS-COV2 induced cell death. Raman spectroscopy yielded signifcant differences in phospholipids such as Phosphatidylinositol (PI), phosphatidylserine (PS), phosphatidylethanolamine (PE) and phosphatidylcholine (PC), which account for ~ 80% of mitochondrial membrane lipids between SARS-COV2 treated and untreated microglial cells. These data provide important mechanistic insights into SARS-COV2 induced mitochondrial dysfunction which underlies neuropathology associated with Neuro-COVID.

Fig. 7 Single Value Decomposition (SVD) analysis of Raman spectra of microglia treated with SARS-COV2 spike protein /heat inactivated SARS-COV2. Spectra was restricted to values above 900 cm -1. SVD analysis decomposes a matrix (stacked Raman spectra) into matrix U, ∑ and VT where U, V are real/complex unitary matrix and ∑ was a positive real diagonal matrix. Matrix U provides the critical spec- tra information and matrix V given the coordinate of SVD cluster for each spectrum base on matrix U. SVD scatter plot are plotted with matrix V where each data point represents one Raman spectrum. The spectra with similar feature form a cluster but spectra with diferent feature get separated in SVD scatter plot. The feature pickup for sepa- ration depends on the matrix U and is plotted as SVD1 and SVD2. SVD1 correspond to the x-axis separation and SVD 2 correspond to y-axis separation in SVD scatter plot

Figure 7A-C, shows spectra which is restricted to values above 900 cm-1 and SVD analysis conducted. Panel A shows SVD analysis and shows the differences between the untreated control and the recombinant SARS-COV2spike protein /HI SARS-COV2 treated microglia. Panel B shows dominant SVD 1 component includes: 1044 cm-1 (phosphate groups), 1446 cm-1 (CH deformation) and 1650 cm-1 (Amide I/ C = C stretching of lipids) and Panel C shows the dominant SVD 2 component includes: 1442 cm-1 (fatty acids) and 1650 cm-1 (Amide I/ C = C stretching of lipids). SVD analysis shows that the control cluster is well separated from recombinant SARS-COV2 spike protein treated cluster, but slightly closer to the HI SARS-COV2 treated cluster in SVD scatter plot, which suggest that the microglia treated with SARS-COV2 spike protein have bigger chemical composition changes as compare to microglia treated with HI SARS-COV2.

This analysis proves that the S spike protein alone is the most damaging, to mitochondria, “ingredient” of the SARS-CoV-2 virus, and it alone causes far greater damage to mitochondria than all other viral (nucleocapsid) proteins:

Mitochondria play a central role in the COVID neuropathogenesis process by virtue of the fact that it is a major reactive oxygen species (ROS) producer, and a target of ROS. The proximity of mtDNA to the ROS-generating electron transport chain makes mtDNA susceptible to oxi- dative damage. Our data shows that treatment with both SARS-COV 2 spike protein and HI SARS-COV2 resulted in a significant increase in mitochondrial respiration. Figure 5 shows a significant increase in both basal and maximal OCR in response to both SARS-COV 2 recombinant spike protein and HI SARS-COV2:

Fig. 5 Measurement of oxygen consumption rate (OCR), in microglia treated with recombinant SARS-COV2 spike protein/ heat inactivated SARS- COV2. OCR was measured in real time, under basal condition, and in response to mitochondria inhibitors: oligomycin (Oligo, 1 μM), cyanide‐4‐(trifluoromethoxy)phenylhydrazone (FCCP, 1.5 μM), and antimycin A plus rotenone (Rot/AA, 0.5 μM). Data represent mean and standard deviation from 3 separate experiments with 5 replicates / sample. A “t- test” was used for statistical analysis. P values are reported in the figure

Our results suggest that SARS-COV2 increased mitochondrial respiration in microglia which could lead to bioenergetic dysfunction and production of ROS and increased oxidative stress. Host responses against SARSCOV2 depend on mitochondrial functions and mitochondrial DNA itself acts as a danger-associated molecular pattern (DAMP) and mitochondrial dysfunction drives a systemic immune response in COVID-19 pathogenesis.

An increase in Reactive Oxygen Species (ROS) may be explained in an alternative way, to contradict the authors’ conclusion about the increased mitochondrial respiration. Namely, it can be explained by an increasingly inefficient oxidative phosphorylation process inside the mitochondria that is responsible for ATP (energy token) production inside eukaryotic cells:

As the oxidative phosphorylation starts producing increasing quantities of ROS/NOS and less ATP, the cells will need to increasingly rely on the much less efficient, in terms of ATP production, and much more glucose-consuming anaerobic glycolysis happening outside of the mitochondria (in the image above). And that is exactly the hallmark of the metabolic origin of cancer theory, first proposed by Otto Warburg:

Warburg hypothesized that cancer growth is caused by tumor cells generating energy (as, e.g., adenosine triphosphate/ATP) mainly by anaerobic breakdown of glucose (known as fermentation, or anaerobic respiration). This is in contrast to healthy cells, which generate energy mainly from oxidative breakdown of pyruvate. Pyruvate is an end product of glycolysis and is oxidized within the mitochondria. Hence, according to Warburg, cancer should be interpreted as a mitochondrial dysfunction.

Cancer, above all other diseases, has countless secondary causes. But, even for cancer, there is only one prime cause. Summarized in a few words, the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar.

— Otto H. Warburg, ^[22]

Warburg continued to develop the hypothesis experimentally and gave several prominent lectures outlining the theory and the data.^[23]

The mainstream science wouldn’t be mainstream without dismissing, out of hand, Warburg’s theory as obsolete, giving preference to the somatic genetic mutation origin of cancer, the Warburg effect being a mere consequence thereof, and not a cause (ibid):

Today, mutations in oncogenes and tumor suppressor genes are thought to be responsible for malignant transformation, and the metabolic changes Warburg thought of as causative are now considered to be a result of these mutations.^[24]

You need to decide for yourself what to think of it. And it can be helped by watching this interview with Dr Thomas Seyfried, a Professor of biology, genetics, and biochemistry at Boston College. He has over 150 peer-reviewed publications and is also the author of books such as, “Cancer as a Metabolic Disease: On the Origin, Management, and Prevention of Cancer”. Listen what Dr. Seyfried has to say on whether cancer’s origin is genetic or metabolic (33:00-36:05 in the video):

For myself, I have decided to trust Dr. Seyfried on that.

So, what do we get? S Spike proteins causing extensive damage to “vaccinee’s” mitochondria, for months on end, which provides the fertile environment for cancers to develop all over the place. And the weakest link usually is the one that gives first. The people that would not, under normal conditions, develop cancer, or which would have non-aggressive cancers further down the road, turn up at the doctor’s offices with aggressive cancers, often with multiple foci, earlier in life. Like people that show up with multiple cancer sites in their colons instead of just one - a recent phenomenon. “Case Report of a Pro-Vaccine Researcher Suggests mRNA Vaccine Might Worsen Lymphoma Cancer” (Gateway Pundit, 2022.10.12):

Goldman and his colleagues published his case report in Frontiers of Medicine last year, titled “Rapid Progression of Angioimmunoblastic T Cell Lymphoma Following BNT162b2 mRNA Vaccine Booster Shot: A Case Report.”

A meta-analysis of nine studies examining changes in 18F-FDG PET/CT scans after Covid-19 (mainly mRNA) vaccination revealed that 37% of vaccinees developed axillary lymphadenopathy on the same side as the shot due to vaccine-related immune responses. Since such vaccine-related axillary lymphadenopathy is similar to certain cancers, so they may get misdiagnosed as cancer. Patients at risk of cancer spread to axillary lymph nodes — e.g., breast cancer, melanoma, and lymphomas —are thus advised to get vaccinated in the arm opposite to the cancer side.

“A study by researchers from Brigham and Women’s Hospital reveals that the incidence of early onset cancers — including breast, colon, esophagus, kidney, liver, and pancreas — has dramatically increased around the world.”

A new review of cancer registry records from 44 countries found that the incidence of early-onset cancers is rising rapidly for colorectal and 13 other types of cancers, many of which affect the digestive system, and this increase is happening across many middle- and high-income nations.

You can’t make this up!