Dr Andrew Goldsworthy Biological Safety Officer for Imperial College London (retired) sent in this fascinating article which might just link to certain aspects of the vaccine-induced magnetism that we have been investigating.
I think this may interest you.
I'm pretty sure you will not find it on the BEEB
In nature, these bacteria live just below the surface of the mud in fresh and saltwater, where they happily feed on organic materials.
They contain magnetite, that make them point like compass needles along the angle of dip of the Earth's magnetic field so that they swim diagonally downwards to find their way back into the mud.
But, the conditions in the small intestine are nearly anaerobic with an abundance of food so your gut is an ideal place for them to live too.
When these bacteria are exposed to alternating magnetic fields they either vibrate or rotate and drill their way through the intestine wall. From there they can enter the nervous system and spread throughout the body where they could cause a variety of disorders, including Parkinson's Disease, Motor Neuron Disease and perhaps many others.
I'm sure we are going to hear a lot more about this in the not-too-distant future.
Most magnetic bacteria belong to the Archaebacteria and differ from other bacteria (Eubacteria) and higher organisms in that the Archaebacteria have a fundamentally different membrane structure based on terpenoids.
This may make it more difficult to design antibiotics and vaccines to combat them, since most of these target specific proteins in the membrane and these are fundamentally different in the Archaebacteria.
It seems possible that Black Seed Oil (which may disrupt the archaebacterial membrane but doesn't depend on specific proteins for its bactericidal activity) may be more effective than traditional treatments and may even cure the disease whereas NHS treatments just do not work and even the NHS admits this
For what it's worth, I have been taking. Black seed oil capsules, three times a day for at least two months and the hand tremors, which I believed to be the beginnings of Parkinson's, have now almost disappeared.
Magnetism and Parkinson's Disease
As I mentioned in my earlier email, there appears to be a link between magnetic particles in the brain and nervous system and Parkinson's Disease.
This has been confirmed using MRI scans. https://www.sciencedaily.com/releases/2018/11/181127171413.htm
But the problem I have with this is that the intense magnetic fields within the scanner (circa 2-3 Tesla) wil draw these particles through the brain cell membranes and so do more damage than the condition they were investigating.
Now may be the time to publish a questionnaire asking anyone who has had an MRI scan, for whatever reason, whether their mental health has been affected. Best wishes
Parkinson’s disease (PD) is the most prevalent movement disorder known and predominantly affects the elderly.
It is a progressive neurodegenerative disease wherein α-synuclein, a neuronal protein, aggregates to form toxic structures in nerve cells.
The cause of Parkinson’s disease (PD) remains unknown.
Intestinal dysfunction and changes in the gut microbiota, common symptoms of PD, are evidently linked to the pathogenesis of PD.
Although a multitude of studies have investigated microbial etiologies of PD, the microbial role in disease progression remains unclear. Here, we show that Gram-negative sulfate-reducing bacteria of the genus Desulfovibrio may play a potential role in the development of PD.
Conventional and quantitative real-time PCR analysis of feces from twenty PD patients and twenty healthy controls revealed that all PD patients harbored Desulfovibrio bacteria in their gut microbiota and these bacteria were present at higher levels in PD patients than in healthy controls.
Additionally, the concentration of Desulfovibrio species correlated with the severity of PD. Desulfovibrio bacteria produce hydrogen sulfide and lipopolysaccharide, and several strains synthesize magnetite, all of which likely induce the oligomerization and aggregation of α-synuclein protein. The substances originating from Desulfovibrio bacteria likely take part in pathogenesis of PD. These findings may open new avenues for the treatment of PD and the identification of people at risk for developing PD.
Our results established a significant correlation between DSV bacteria and PD. The quantity of DSV bacteria in fecal samples correlated with the severity of the disease, and higher amounts of DSV were found in PD samples compared to control samples.
All fecal samples of PD patients were positive for the DSV-specific [FeFe]-hydrogenase gene. DSV bacteria, D. desulfuricans, D. fairfieldensis, and D. piger, were significantly more common in PD samples than in control samples.
Previous attempts to correlate DSV abundance with different intestinal diseases have failed to show correlations (Zinkevich and Beech, 2000; Fite et al., 2004; Scanlan et al., 2009). In our study, all PD patients harbored DSV, but as the primers used for hydA detection were not suitable for qPCR (results not shown), we cannot exclude the possibility that the patients with low levels of the four examined DSV species may have high levels of other DSV species. As 20% of the PD patients had unknown DSV species, these bacteria must be isolated and characterized to enable the development of primers suitable for qPCR. Together, the data strongly suggests that DSV play a role in the pathogenesis of PD.
DSV have an ability to bind to human colonic mucin, and they are found at high levels (approximately 104 to 106 bacteria/g feces) in mucosal samples of the large intestine (Zinkevich and Beech, 2000; Nava et al., 2012; Earley et al., 2015).
An important characteristic of DSV is its ability to perform dissimilatory sulfate reduction by utilizing sulfate as an electron acceptor for respiration, thereby producing hydrogen sulfide (H2S) (Carbonero et al., 2012). H2S can also be produced from cysteine degradation catalyzed by L-cysteine desulfhydrase, present in intestinal pathogens such as Salmonella Typhimurium, Helicobacter pylori, Escherichia coli and in pathogens belonging to genera of DSV, Clostridium, Enterobacter, Klebsiella and Streptococcus.
Additionally, Bilophila wadsworthia and D. desulfuricans can produce H2S through a third pathway as a byproduct of taurine catabolism (Carbonero et al., 2012).
H2S displays Janus-faced characteristics by carrying physiologic signaling events in neuronal cells and showing neuroprotective properties while also being highly toxic at high concentrations (Panthi et al., 2018; Haouzi et al., 2020). In humans, an acute low-dose H2S gas exposition can cause eye irritation and olfactory dysfunction whereas a high-dose exposition can lead to severe central nervous system dysfunction and even death (Rumbeiha et al., 2016; Haouzi et al., 2020).
As a diffusible gas that is more soluble than CO2 or O2, H2S can enter the blood circulation from the gut (Tomasova et al., 2016; Haouzi et al., 2020). It is reasonable to assume that H2S concentrations are raised in the gastrointestinal wall structures in cases where the gut harbors an increased amount of H2S-producing DSV. Elevated H2S concentrations in these structures may result in constipation due to the compound’s ability to inhibit gastrointestinal motility (Singh and Lin, 2015).
In the present study, the constipation prevalence among PD patients was as high as 70%. Notably, constipation is a prevalent ailment in PD and it can precede the motor features of PD and form a risk for PD onset (Abbott et al., 2001; Lin et al., 2014; Stirpe et al., 2016). In one study, constipation was reported to associate with increased quantities of DSV, Cristensenellaceae and Firmicute bacteria in fecal samples of non-PD subjects (Jalanka et al., 2019). However, whether DSV species are a cause or a consequence of constipation in PD remains an unanswered question. Possibly, DSV species take part in the evolution of PD after their quantity exceeds a certain threshold level.
Hydrogen sulfide has been demonstrated to alter intracellular biochemistry to favor α-Syn aggregation. Hydrogen sulfide can release iron from mammalian ferritin in cells and raise iron levels in the cytosolic labile iron pool (Cassanelli and Moulis, 2001; Hälldin and Land, 2008). The resultant effect on α-Syn-expressing nerve cells is of concern as both ferric and ferrous iron are capable of inducing α-Syn aggregates, the main neuropathologic feature of PD (Joppe et al., 2019). Overexpression of endogenously produced H2S can also release mitochondrial cytochrome c into the cytosol, where this cytochrome has been observed to form α-Syn radicals and subsequently induce α-Syn oligomerization, an early stage in α-Syn aggregation (Guo et al., 2015; Kumar et al., 2016; Li et al., 2019).
The colonic mucosa is normally protected from H2S by the sulfide oxidation pathway, including the enzymes sulfide quinone oxidoreductase, persulfide dioxygenase, rhodanese and sulfide oxidase (Picton et al., 2002; Ramasamy et al., 2006; Libiad et al., 2014). If DSV, the dominant SRB in the intestinal mucosa (Zinkevich and Beech, 2000; Nava et al., 2012; Earley et al., 2015), increase in number, H2S will likely be produced at higher levels that may exceed the capacity of the detoxifying enzymes. In addition, inflammation decreases the detoxification capacity of the mucosal tissue, resulting in an increased level of H2S (Flannigan et al., 2013).
The observation that smoking induces a causally protective effect on PD occurrence lends support for the role of H2S and its interaction with detoxifying enzymes in PD pathogenesis (Mappin-Kasirer et al., 2020). It is known that cyanide, present in variable amounts in cigarette smoke, reacts with H2S under the influence of rhodanese to form thiocyanate, thus resulting in lowered H2S levels (Picton et al., 2002).
The enteroendocrine cells of the gut, which display neuron-like properties and are connected to autonomous enteric nerves, express α-Syn (Chandra et al., 2017).
Anatomically, enteroendocrine cells extend their apical cytoplasmic processes towards the gut luminal surface. Thus, it is reasonable to argue that this feature will increase the DSV-borne H2S exposure risk. In addition, overgrowth of DSV may induce colonic mucosal barrier dysfunction by influencing the metabolism of butyrate, a short-chain fatty acid (SCFA), which has been reported to be the major energy substance for the colonic epithelium (Chapman, 2001).
Overgrowth of H2S-producing bacteria such as DSV poses an apparent threat to this barrier function, as sulfides impair the oxidation of butyrate (Babidge et al., 1998). In this context, it has been shown that PD patients exhibit increased intestinal permeability correlating with increased intestinal mucosa staining for α-Syn (Forsyth et al., 2011).
In addition, lipopolysaccharides produced by DSV can apparently increase intestinal permeability and α-Syn expression (Kelly et al., 2014; Fuke et al., 2019; Gorecki et al., 2019). Notably, the mucin layer of the colon consists primarily of glycoproteins, which carry sulfate residues, and degradation products of these sulfomucins serve as a source of sulfate for SRB such as DSV (Derrien et al., 2008). Further, Akkermansia muciniphila and Bifidobacterium, abundant inhabitants of the human gut, can degrade mucin (Derrien et al., 2008; Ruas-Madiedo et al., 2008).
Several studies on gut microbiota in PD have shown increases in the relative abundance of these bacteria (Chiang and Lin, 2019; Shen et al., 2021). Bifidobacteria are commonly available as commercial products, and their abundance in the gut is reported to correlate to the levodopa dose in PD (Wallen et al., 2020). A. muciniphila, in addition to its ability to degrade mucin, seems to promote mucus thickness and stimulate mucus turnover rate, thus apparently freeing considerable amounts of sulfate for SRB (Zhou, 2017).
Support for this interaction between A. muciniphila and SRB is provided by a study on the metabolome profile of PD patients wherein significant changes in sulfur metabolism, including H2S, were verified through computational modeling, and the observed changes were driven by A. muciniphila and B. wadsworthia (Hertel et al., 2019).
As a pathogenetic model, it is justifiable to propose that excessive production of H2S by gut DSV, cross-fed by A. muciniphila, leads to α-Syn oligomerization and aggregation in the adjacent enteroendocrine cells. From there, α-Syn oligomers may make their way to the brain via the vagus nerve. This proposed model agrees with the initial proposal by Braak and colleagues that PD is caused by a pathogen capable of passing through the mucosal barrier of the gastrointestinal tract (Braak et al., 2003).
Routes other than the vagal route for α-Syn oligomer transport come into consideration as well. Elevated levels of oligomeric α-Syn have been detected in plasma samples of PD patients, and it has been documented that α-Syn can cross the blood brain barrier (BBB) in both the blood-to-brain and brain-to-blood direction (El-Agnaf et al., 2006; Sui et al., 2014). If DSV-produced H2S plays a central role in the pathogenesis of PD, it is reasonable to presume that, in addition to DSV, other H2S-producing bacteria, such as H. pylori and Clostridium species, may also induce PD (Murros, 2021). In fact, people with PD have an increased prevalence of H. pylori infections, and eradication of this pathogen has been reported to improve motor functions in PD patients (McGee et al., 2018). Recently, a population-based cohort showed that Clostridium difficile infections temporarily elevate the risk of PD (Kang et al., 2020). Although increased production of H2S may play a pivotal role in PD pathogenesis, inflammation caused by DSV and other infective agents like curli-producing E. coli and Proteus mirabilis evidently play a role as well (Chen et al., 2016; Choi et al., 2018).
Experimentally, an exposure to bacteria that produce the curli protein results in α-Syn depositions in both the gut and the brain (Chen et al., 2016). Furthermore, it has been shown that LPS can accelerate the synthesis of curli fibrils (Swasthi and Mukhopadhyay, 2017). After a primary inflammatory event, a sustained low-level inflammation may develop, resulting in increased intestinal permeability, leakage of inflammatory agents, and ultimately a chronic systemic immune response that may weaken the BBB (Houser and Tansey, 2017).
The potential capability of DSV to produce magnetite (Fe3O4) deserves special attention, as uncoated magnetite nanoparticles can accelerate α-Syn aggregation (Joshi et al., 2015). Most of the DSV contain a [FeFe]-hydrogenase metalloenzyme system, which catalyzes both the oxidation and reduction of molecular hydrogen and protons, respectively (Pereira et al., 2011). Based on studies on D. vulgaris, it has been suggested that the reduction of soluble ferric iron to ferrous iron is a periplasmic process that requires the presence of a [FeFe]-hydrogenase (Park et al., 2008).
An interaction between ferrous iron and amorphous ferric hydroxide can result in magnetite formation, and it has been shown that magnetite can be formed from amorphous ferric hydroxide in the presence of iron- and sulfate-reducing bacteria (Chistyakova et al., 2004; Lenders et al., 2016). D. desulfuricans has the ability to synthesize magnetite (Lovley et al., 1993), and this DSV species was the most frequently found DSV species in the patients included in this study. Notably, magnetite production in anaerobic condition by dissimilatory iron-reducing bacteria is coupled with energy-metabolism and the produced magnetite is extracellular (Konhauser, 1997).
Magnetite nanoparticles can be absorbed into intestinal cells and blood circulation by endocytosis (Fröhlich and Roblegg, 2012; Bergin and Witzmann, 2013). In a study on skin samples of patients having PD, low-temperature magnetometric measurements revealed apparent superparamagnetic magnetite particles in the dermal layer of several PD patients, and it was proposed that these particles were probably gut-borne and produced by DSV (Murros et al., 2019).
Support for the ability of magnetite to accumulate in the brain is provided by a study on 822 brain specimens sampled from seven human cadaver brains (Gilder et al., 2018). However, the possible connection between bacterial magnetite nanoparticles and PD pathogenesis is still speculative; magnetometric data from stool samples and biopsy specimens from the colon and brain of PD patients are currently unavailable.
In the present study, specific DSV species were identified in most of the fecal samples of PD, with the quantities of DSV correlating with the PD severity. In addition, the DSV-specific [FeFe]- hydrogenase gene was found in all PD samples indicating an existence of other unidentified DSV species.
These findings suggest that DSV may be an etiological agent promoting microbiome-related PD pathogenesis. We present the following pathogenetic model. First, DSV colonize the intestine permanently, increase in numbers and produce hydrogen sulfide in amounts exceeding the H2S detoxification capacity of the mucosal sulfide oxidation pathway (especially the rate-limiting sulfide quinone oxidoreductase), while also producing LPS and magnetite (in at least some DSV species) near the enteroendocrine cells.
These agents subsequently induce α-Syn oligomerization and aggregation in the intestinal enteroendocrine cells. Secondly, toxic α-Syn oligomers spread in a prion-like manner, traveling from enteroendocrine cells to the brain mainly via the vagal nerve and possibly via the bloodstream, where they ultimately cause damage to the brain dopaminergic system. In addition, magnetite nanoparticles produced by DSV may pass into the bloodstream from the intestine, cross the BBB, and accelerate α-Syn aggregation in the brain.
This proposed model should be further evaluated in future research.
Future studies could, in the prevention and treatment of PD, focus on developing methods to eradicate DSV from the human intestine by antibiotics, phage therapy, fecal transplantation, diet changes, or a combination of these interventions.
Isolation of DSV from the human intestine is critical, as it allows for designing better primers, antibiotic profiling and phagotype screening.
Isolation of these bacteria also enables genome sequencing of PD-associated DSV and genomic comparison to environmental and healthy-carrier isolates of DSV, potentially aiding in the identification of therapeutic targets among the gene products specific to PD-associated DSV.
FULL ARTICLE HERE:
SEE NOTB FILM ON NEUROLOGICAL DAMAGE POST JAB