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Causes runaway fungus to spread in your body, affecting…
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Important warning if you have taken cortisol in 2018
Today we’re talking about a VERY common fungus.
Sometimes it turns into lupus, but it’s far more common than that.
Officially, the cause of lupus is “unknown,” yet there are times when a disease is left unexplained for political reasons.
The cause implies the cure.
So if a cure is less profitable than the current “treatment,” billions of dollars in profit could be lost if the underlying cause was commonly known.
But, in fact, the cause of lupus has been staring everybody in the face for decades.
Some researchers did connect the right dots in the past, but due to 100+ auto-antibodies found in lupus, the precise mechanism was always hard to define.
The cause of lupus is certainly Aspergillus fumigatus, an invasive fungal species that secretes a few characteristic metabolites.
Of these molecules emitted, the most well-known is gliotoxin.
This small molecule lowers immunity by disrupting NF-κB signaling, facilitating its own survival in the host.
(NF-κB is a protein complex that controls a bunch of things including cellular responses to stress, cytokines, free radicals, bacterial or viral antigens etc. It plays a key role in regulating the immune response to infection.)
Inhibiting NF-κB also happens to be the very same way prescription corticosteroids lower immunity.
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The other notorious A. fumigatus toxin is the 18-kilodalton ribotoxin, the most common fungal protein detected in the urine of people with Aspergillosis.
(Aspergillosis is the name of a wide variety of diseases caused by fungi of the genus Aspergillus.)
This 18-kDa ribotoxin is how Aspergillus induces the obscenely high amount of individual auto-antibodies observed in lupus.
Some Norwegian molecular geneticists have a very logical explanation for this, or just how so many auto-antibodies can be made from just one species.
The best explanation for lupus: Aspergillus ribotoxin binds to ribosomes – where it acts as a hapten in inducing autoimmunity.
(Haptens are minute molecules that elicit an immune response only when attached to a large carrier such as a protein.)
So if you or anyone you know has lupus, you should definitely read this article.
The hapten mechanism is interesting and is in full accord with all things known about lupus.
The 18-kDa ribotoxin is the long-elusive link in the causal chain of events – it seals the deal and finally proves the case.
“Systemic lupus erythematosus (SLE) is an autoimmune disorder with unknown etiology. The major hallmark of this disease is the presence of antibodies against nuclear components, including double-stranded DNA and histones.”
And once a cause is known with certainty, the treatment readily suggests itself and can be carried out with confidence.
To provide the certitude needed I will outline a few key links:
Arie Katz describes three cases of patients with lupus.
Two of these three cases were given prednisolone upon admission, a decision that turned out to be a terrible idea.
Corticosteroids are notorious for lowering immunity towards fungal infections, and these patients certainly had those.
“More than 90% of patients with invasive pulmonary aspergillosis had previously received corticosteroids or cytotoxic agents or had prolonged neutropenia.”
Unwisely, doctors often give patients corticosteroids to lower immunity – this can temporarily relieve symptoms and prevent the rejection of organ transplants.
Yet corticosteroids will reliably facilitate a fungal explosion in infected people.
Two of Dr. Katz’s lupus cases then died from invasive aspergillosis.
Her third case was a kidney transplant patient who was on corticosteroids to prevent rejection.
That patient developed a large fungal node of Aspergillus fumigatus on the kidney and survived after the infected kidney was removed.
That kidney had been transplanted a few years previously, after which corticosteroids were prescribed to prevent rejection.
There are hundreds of such cases. And here are twelve more:
Dr. Hyun-Jin Kim is a Korean lupus specialist and examines many patients with that condition.
Not all of his lupus cases require immediate hospitalization. But, of those who were admitted, all 12 had invasive fungal infections.
Aspergillus spp. was the most common fungus isolated.
Eleven out of the 12 cases had taken corticosteroids in the weeks prior to the visit.
“Most of lupus patients with invasive fungal infections (91.7%) had taken steroids prior to the invasive fungal infections. Three [of the] lupus patients [died]. Notably, these patients were all infected with Aspergillus spp.”
Dr. Hyun-Jin Kim explains the association between lupus and Aspergillus as the patients having “lowered immunity” to fungi.
Though he notes this association, he has the causality backwards.
There are probably thousands of undiagnosed cases – simply because Aspergillus spores are everywhere and they contaminate biopsies.
This is due to the extremely small diameter of Aspergillus spores, which leads to many positive cultures simply being disregarded as “contaminated.”
The tiny size of the spores is also why Aspergillus is commonly found in the lungs and sinuses, ostensibly after being inhaled.
Aspergillus spores are literally floating around everywhere, and a properly functioning immune system is essential to keeping them at bay.
“Thom and Church called them the ‘weeds of the culture room.’ The frequent occurrence of aspergilli as contaminants has caused difficulty in establishing an etiological relation…”
The 15 case reports here are only a fraction of the hundreds reported that link lupus to Aspergillus directly.
This direct link eliminates the necessity of presenting longer chains of induction. But, since these lead to the same conclusion, they strengthen the case.
One such lupus association is with silicosis, which is caused by the inhalation of fine silica particles.
Silicosis has been proven to facilitate pulmonary Aspergillosis in the past, so it would actually be expected to cause lupus.
Silicosis is the second most consistent risk factor for lupus, right behind Aspergillus fumigatus itself.
Enough case reports of lupus patients also having silicosis had been compiled at this point to justify a larger study.
The study group was composed of 265 lupus cases and 355 controls. After a multivariate analysis, a risk ratio of 4.6 was observed.
Although all lupus cases could have aspergillosis, not all would have Aspergillus in the lungs – as shown by the above case reports of kidney infections.
Yet, when approaching from the opposite and more powerful direction in comparison, or finding how many silicosis cases also have lupus, a massive risk ratio of 23.8 is observed.
“Investigators in a population-based, registry-linkage study in Sweden also reported an increased risk of hospitalization with lupus in silicosis patients (relative risk 23.8).”
Of course, silica is harmless sand and cannot be thought to do anything besides physically obstruct.
There are no antibodies towards silicon observed in lupus, and such a thing is not even possible anyway.
But you do see over 100 auto-antibodies in lupus. And a suspiciously large percentage are directed at proteins found near the cell’s nucleus:
After conducting a literature search, Doctor Yaniv Sherer tallied a total of 116 distinct auto-antibody types reported in lupus cases.
It is unlikely that one single lupus case would have all 116 of them, yet 20% of cases had more than 60.
The sheer multiplicity of auto-antibodies is a defining feature of lupus. And of the 116+ distinct types reported, the anti-ribosomal antibody appears to be the most common.
“We believe that the auto-antibodies most likely to exert a pathogenic role are those directed toward nucleosomes, DNA, PARP…”
This is an important fact, especially considering the 18-kDa Aspergillus ribotoxin that’s been shown to bind ribosomes.
But how does it do it? And what about all the other auto-antibodies?
The Aspergillus 18-kDa ribotoxin works like a hapten. There is simply no other way to logically explain it.
“Hapten: a small molecule that, when combined with a larger carrier such as a protein, can elicit the production of antibodies that bind specifically to it (in the free or combined state)” ―Google Dictionary
After Aspergillus ribotoxin binds to the ribosomes – cell organelles that translate mRNA into proteins – the cell would most likely die and undergo apoptosis.
Small protein fragments produced by apoptotic cells are ingested by macrophages.
(A macrophage is a type of cell responsible for detecting and destroying pathogens and apoptotic cells.)
During the normal sequence of events, all engulfed proteins are recognized by macrophages as belonging to “self” and thus no antibodies are formed.
Yet with a hapten or an Aspergillus ribotoxin attached to the ribosome, it will be presumed foreign and antibodies against it will be elicited.
Antibodies formed in this process will bind to the original hapten-protein complex, and also to either the hapten or the protein individually.
It would technically be an antibody when binding the ribotoxin, but also an auto-antibody when binding the host’s ribosome.
Hapten-induced antibodies are dual-target antibodies.
Ribosomes associate directly with messenger RNA, identical to DNA save for uracil replaces thymine.
So it is no coincidence that auto-antibodies to DNA are characteristic of lupus:
“Some are frequent such as anti-dsDNA, which nearly always appears in one stage or another of the disease (13-14), while others have been described in only a few patients.”
Despite the overwhelming plausibility of this scenario, this protein-hapten mechanism, it seems that only one other person has written about it.
A team of Norwegian molecular geneticists outlined the same general mechanism as above.
But they hypothesize that a protein from Epstein-Barr binds to chromosomes.
Yet the subsequent mechanism of auto-antibody formation is identical, and this is really the only logical way to explain so many auto-antibodies.
A protein toxin secreted by a virus, bacterial, or fungal cell must serve as a hapten.
These scientists explained so many lupus antibodies against host DNA by an Epstein-Barr virus protein binding chromosomes in the nucleus – inducing antibodies towards both chromatin and whatever DNA sequence is trapped between.
They cite an instance of this actually occurring in rats after injection of an Epstein–Barr protein.
However, the auto-antibody against ribosomes is more characteristic of lupus than the one against chromatin.
And the “anti-chromatin antibodies” could simply be anti-ribosome antibodies cross-reacting with chromatin, due to the similarity between the two.
(Both ribosomes and chromosomes are nucleic acid + protein complexes.)
“These observations support the hapten-carrier model where a non-self protein can render nucleosomes immunogenic provided that they form physical complexes. This model could also explain the presence of auto-antibodies in SLE patients against other DNA-binding proteins…”
Moreover, chromatin is found in the nucleus separated by two cell membranes. Ribosomes are found in the cytosol surrounded by one.
The way we define lupus today does not preclude two separate causes acting in this manner…
But the evidence certainly points more towards Aspergillus being involved.
Ribosomal auto-antibodies are highly characteristic of lupus, and the Aspergillus ribotoxin actively binds to ribosomes:
Perhaps the best treatment against Aspergillus species is potassium iodide.
This has successfully been used clinically in doses not exceeding a few grams per day.
Potassium iodide is still the treatment of choice for Aspergillus in many countries (those with less pharmaceutical presence than the US).
The iodide ion works because it forms a substrate for myeloperoxidase, an enzyme secreted by neutrophils that can attach to fungal cell walls.
“Aspergillosis was the most common cause and the leading cause of death of invasive fungal infection in patients with lupus.”
Myeloperoxidase uses iodide to form hypoiodous acid, the most powerful antifungal agent produced by the immune system.
Injections of just myeloperoxidase, the bare enzyme, promotes survival in rats by 80% when they are also injected with C. albicans (candida).
Myeloperoxidase needs iodide for full activity.
—–Important Message – —–
They don’t want you to know this
I found a protocol that Big Pharma seems to be actively suppressing.
You need to see this before it is removed. (Seriously)
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